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The Health Consequences of Smoking for Women A Report of the Surgeon General - Part 1 of 4
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THE HEALTH
CONSEQUENCES
OF SMOKING
FOR WOMEN
a report of the Surgeon General
U.S. DEPARTMENT OF HEALTH! EDUCATIONANO WELFARE
Public Health Servide
Office of'the Assistant Secretary for, Health
Office on Smoking andiHealth
V
the lowest yield cigarettes are more or less likely to attempt
to quit, or to succeed in quitting, than smokers of
conventionall filtertip or nonfilter cigarettes. The extent to
which the act of switching to a lower "tarn cigarette may
serve as a substitutee for quitting may differ among wom en
and men.
PUBLIC HEALTH RESPONSIBILITIES
This report, which includes data compiled by individuals from
both inside and outside the Government, has confirmed in
every way thejudge:nent of the World Health Organization,
that there cann no longer be any doubt among informed people
that cigarette smoking is a major and removable cause of ill
health and premature death. Eachh individual woman must make her own decision
about this significant health issue. Secretary Harris has
noted that the role of the Government, and all responsible
health professionals, is to assure that this decision Is an
infonnedd one. In issuing this report, we hope to help the
public health community accomplish this purpose.
Julius B. Richmond, M.D.
Assistant Secretary for
Health and Surgeon General
0
viii
PREFACE
This report is more than a factual review of the health
consequences of smoking for women. It is a document which
challenges our society and, In particular, our medical and
public health communities.
This report points out that the first signs of an
epidemic of s;noking-related disease among women are now
appearing.. Because women's cigarette use did not become
widespread until the onset' of YyorldWar II, those women with
the greatest intensity of smoking are now only in their
thirties, forties, and fifties. As these women grow older, and
continue to smoke, their burden of smoking-related disease
will grow larger. Cigarette smoking now contributes to one-
fifth of the newly diagnosed cases of cancer and one-quarter
of all cancer deaths among women--more cancer and more
cancer deaths among women than can be attributed to any
other knownn agent. Within three years, the lung cancer death
rate is expected to surpass that for breast cancer. A similar
epidemic of chronic obstructive lung disease among women has
also begun.
Four main themes emerge from this report to guide
future public health efforts.
First, women are not immune to the damaging effects
of smoking already documented for men. The apparently lower
susceptibility to smoking related diseases among women
smokers is an illusion reflecting the fact that women lagged
one-quarter century behind menn in their widespread use of
cigarettes.
Second, cigarette sm oking is a major threat to the
outcome of pregnancy and well-being of the newborn baby.
Third, women may not start smoking, continue to
smoke, quit smoking, or fail to quit sm oking for precisely the
sam e reasons as men. Unless future research clarifies these
differences, we will find it difficult to prevent initiation or
to promote cessation of cigarette smoking among women.
Fourth, thereduetione of cigarette sm oking. is the
keystone in our nation's long termn strategy to promote a
healthy lifestyle for wo men and men of all races and ethnic
groups.
}MC SCCREiMNT OiN ~ H.CGVG..TIONIND W[LI/:Xr
WwCNIN6TON. DC.COio~i
The Honorable Thomas P. O'Neill,Jr.
Speaker of the House of Representatives
Washingtonj D.C. 20515
Dear Mr. Speaker:
I hereby submit the 12th annual report that the
Department of Health, Education, and Welfare (DHEW)has
prepared for Congress as required by the Public Health
Cigarette Smoking Act of.1969,Public Law 91i-222, and its
predecessor, the Federal Cigarette Labeling and Advertising
Act. This report is one of the most alarming in the series.
It.clearly establishes that women smokers face the same
risks as men smokers of lung cancer, heart disease, lung
disease and other consequences. Perhaps more disheartening
is the harm.which mothers' smoking.causes to their unborn
babies and infants.
The report is not all bad news. It presents recentt
data showing that women are turning away from smoking in
response to the warnings of government, voluntary agencies
and physicians. The precipitate rise in women's deaths from
lung cancer and chronic lung disease demand that this trend
away from cigarettes be.accelerated.. Our scientists expect
that by 1983, the lung cancer death rate will exceed that of
any other type of cancer among women.
Citizens off our free society may decide for themselves
whether to smoke cigarettes. The health consequences of
thi~sdecision make it imperative for their government to
assure that the decision is an informed one. This- series
of reports is one way in which DHEW is striving to meet
this critical responsibility..
m~,
~ /J --~
Patricia Roberts Harris
cancer than women nonsmokers. By 1979, womem accounted
for fully one-fourthof all lung cancer deaths.. Over the next
few years, womem cigarette smokers' risk of lung cancer death
will approach, 8 to 12 times that of women nonsmokers, the
same relative risk as that of men.
Lung cancer has four main histological types:
epidermoid, small cel.l, adenocarcinoma, and large cell
carcinoma. As several studies have shown, the incidence of
each of these types of lung cancer displays a clear
relationship to cigarette smoking amongboth men and women.
Epider:noid and small cell lung cancer appear to be more
prominent among men, while adenocarcinoma of the lung now
appears to be more prominent among women.
The recent acceleration of lung cancer incidence among
women has in fact beenmore rapid than the corresponding
growth of lung cancer among men in the 1930s. Again, this
difference in the initial rate of acceleration of lung cancer
incidencedoes not refute the demonstrated causal relation
between cigarette smoking and lungg cancer among both sexes.
Instead, differences in the rate of increase of lung cancer
incidencemay reflect changes in the carcinogenic properties
of cigarette smoke, thee style of cigarette sm oking, or the
interaction of cigarette smoking with other environmental
hazards. It is noteworthy that those :menwho died of lung
cancer in the 1930s came from a generation that had
gradually converted to cigarettes from other, non-inhaled
forms of tobacco. By contrast, the first regular tobacco
users am ono women weree almost exclusively cigarette sm okers.
The 1979 Report on Smoking and Health documented
numerous instances where cigarette smoking adds to the
hazard's of the workplace envinonmentt among men. Among,
women, this report reveals two such occupational exposures--
asbestos and cotton dust- -which have been clearly
demonstrated to interact with cigarette snoking.The fact
that evidence is limited among women does not imply that
women are protected from the dangerous interactions of
smoking and occupational exposures.
PREGNANCY, INFANT HEALTH, AND REPRODUCTION'
Scientific studies encompassing various races and ethnic
groups, cultures and countries, involving hundreds of thousands
of pregnancies, have shown that cigarette smoking during
pregnancy significantly affects the unborn fetus and the
iii
`
women and men have paralleled those of the general
population. From 1965 to 1979, the proportion of black
women cigarette smokers declined from 34 to 29 percent,
while the proportion of black men smokers declined from 61
to 42 percent. However, differences by race in the onset,
maintenance, and cessation of smoking have not been
adequately explored6 Little Is known about cigarette smoking
among other ethnic and minority groups.
ADOLESCENT 5;9flKNNG
The health consequences of smoking evolve over a lifetime.
Evidence continues to accumulate, for example, that cigarette
smoking produces measurable lung changes even In childhood
and young adulthood. Young cigarette smokers of both sexes
show more evidenceofe small airway dysfunction, and a higher
prevalence of cough, wheezing, phlegm production, and', other
respiratory symptoms. The health damage due to cigarette
smokingg increases when an individual' begins regular smoking
earlier in life. Yet,, as this report documents, the average
age of onset of regular smoking among women has
continuously declined during the last 50 years, and continues
to decline. .
According to a recent survey by the National Institute
of Education, cigarette smoking among adolescent girls now
exceeds that among adolescent boys. In the: 17-19 year age
group, there are almost 5 fe:rtalecigarette smokers for every
4 m ale cigarette sm okers. The causes of this inversion are
far fromn clear. We do nott yet understand the signal events
in the Initiation of smoking among young women. It is
possible that parents set examples concerning lifestyle, healthh
attitude, and risk-taking much earlier in childhood. The
beginning of junior high school or entrance into the work
force may be equally critical events. We do not know enough
about an adolescent's sense of competence and self-m astery,
and how these roles differ among women and men. Although
smoking patterns am onggirls correlate withi parental, peer andd
sibling sm oking habits, educational level, type of schootl
curriculum, academic performance, socioeconomic status, and:
other forms of substance abuse, the practical significance of
these empirical correlations is unclear.:
VI
ACKNOWLEDGEMENTS
This report was prepared by agencies of the U.S.
Department of Health, Education and Welfare under the general
editorship of the Office on Smoking and Health, John M.
Pinney, Director. Consulting scientific editors were David M.
Burns, Assistant Clinical Professor, Pulmonary Division,
University of California at San Diego, San Diego, California
and John H. Holbrook, M.D., Assistant Professor of Internal
Medicine, University of Utah Medical School, Salt Lake City,
Utah.
Introduction and Summary
Office on Smoking and Health
Patterns of Cigarette Smoking
Office on Smoking and Health .
Jeffrey E. Harris, M.D., Ph.D., Assistant Professor,
Department of Economics, Masasachusetts Institute of
Technology, Cambridge, Massachusetts; Clinical
Associate, Medical Services, Massachusetts General
Hospital, Boston, Massachusetts. ..
Overall Mortality ..
National Heart, Lung, and Blood Institute
Eugene Rogot, Division of Heart and Vascular
Diseases, National Heart, Lung, and Blood Institute,
National Institutes of Health, Bethesda, Maryland;
Thomas J. Thom, Division of Heart and Vascular
Diseases, National Heart, Lung and Blood Institute,
National Institutes of Health, Bethesda, Maryland
Morbidity
National, . Center for Health Statistics
Ronald W. Wilson, M.A., Chief, Health Status and
Demographic Analysis Branch, Division of Analysis,
National Center for Health Statistics, Hyattsvllle,
Maryland.
Cardiovascular Diseases
National. Heart, Lung, and Blood Institute.
G.C. McMillan, M.D., Ph.D., Associate Director for
Etiology of Arteriosclerosis and Hypertension,,
Division of Heart and Vascular Diseases, National.
Heart, Lung, and Blood Institute, National Institutes
of Health, Bethesda, Maryland.
xi
Cancer
National Cancer Institute . .
Jesse L. Steinfeldy M.D., Dean, Medical College of
Virginia, Richmond, Virginia. Non-Neoplastic Rronchopulmonary niseases
National Heart, Lung, and Riood.Institute , Richard A. Rordow,M.D., Associate Research
' Physiologist, University of California at San niego,
San Diego, California; Claude J.M. Lenfant, M.n.,
Director, Division of Lung Disease,. National Heart,
Lung, and Rlood Institute, National Lnstitutes of
Health,Rethesda, Maryland
Earbara Marzetta Liu, Division of Lung Disease,
-National Heart, Lung, and Rlood Institote, National
Institutes of Health, Rethesda, Maryland Eric R. Jurrus, Division of Lung Disease, National
..Heart, Lung, and Blood Institute, National Institutes
of Health, Bethesda, Maryland,
Interaction Between Smokingm and r)ccupational
Exposures - - - -
National Institute of Occupational Safety and Health
.. Jeanne M. Steelman, Ph.D., American Health
-"Foundation,New York, New York. ' Steven D. Stetlman, Chief, Division 'of Health &
'Toxicology, A merican Health Foundation, New York,
New York' - -
Pregnancy and Infant. Health - National Institute of Child Health and Human
Development - Eileen. G. Hasselmeyer, Ph.D., R.N., Associate
Director for Scientific Revie w, National Institute of
Child Health and Human Development,National
Institutes of Health, -Rethesda Maryland.
M ary R. Meyer, M.Sc., Associate Professor of
Epidemiology, Johns Hopkins University School of
Hygiene and Public Health, Raltimore, Maryland.
Lawrence D. Longo, M.D., Professor of Physiology and
.Obstertrics and Gynecology, Loma Linda University
School of Medicine, Loma Linda, California
Donald R. M attison, M.D., Senior Investigator,
Pregnancy Research Pranch, National Institute of
Child Health and Humam. Development, National
Institutes of Health, Bethesda, Maryland.
xii
Peptic Ulcer
National Institute of Arthritis, Metabolism and
Digestive Diseases - -
Travis E. Solomon, M.D., Ph.D., Center for Ulcer
Research and Education, VA Wadsworth Medical Center
and UCLA School of Medicine, Los Angeles, California
Janet Elashoff, Ph.D., Center for Ulcer Research and
Education, VA Wadsworth Medical Center and UCLA
School of Medicine, Los Angeles, California.
Interactiuns of Smoking with Drugs, Food
Constituents and Responses to Diagnostic Tests
Cheryl Fossum Graham, M.D., Division of Drug
Experience, Office of Biom etrics and Epidemiology,
Bureau of Drugs, Food and Drug Administration.
Psychosocial and Behavioral Aspects of Smokingg
in. Women - Initiation, Maintenance, and Cessation
'
Ellen P.. Gritz, Ph.D., Research Psychologist,
Veterans Administration Medical Center, Brentwood,
California and Associate Research. Psychologist,
Department of Psychiatry and Behavioral Sciences,
School of Medicine, University of California, Los
Angeles, California. . -
Ann Brunswick, Ph.D., Senior Research. Associate(Sociom edical Sciences), Center for Sociocultural
Research on Drug Use, School of Public Health,
Columbia University, New York, New York. ..
Karen L. Bierman, M.A., Department of Psychology,
University of California, Los Angeles, California.
The editors acknowledge with gratitude the many
distinguished scientists, physicians, and others who
assisted in the preparation of this report by coor-
dinating manuscript preparation, contributing criti-
cal reviews of the manuscripts or helping in other
ways.
Elvin A. Adams, M.D., M.P.H., Practicing Internal
M edicine, Fort Worth, Texas.
Josephine D. Arasteh, Ph.D., Health Scientist
Administrator, Human Learning and Behavior Rranch,
Center for Research for Mothers and Children,
National Institute of Child Health and Human
THE FALLACY OF WOMEN'S IMMUNITY
All of the major prospective studies off smoking and mortality
have reached consistent conclusions.. Deathrates from
coronary heart disease, chronic lung disease, Iung.cancer, and
overall mortality rates are significantly increased among both
women and men smokers. The.serisks increase with the
amount smoked, durationn of smoking, depth of inhalation, and
the "tar" and nicotine delivery of the cigarette smoked.
. In these studies, conducted during the past three
decades, relative mortality risks among female smokers
appeared to be less than those of male smokers. It is now
clear, ho wever, that these studies were comparing the death.rates of a generation of established,
lifelong male sm okerswith a generation of womenn who had not yet taken up smokingg
with full~ intensity. Even those older wom en who reported
smoking a large number of cigarettes per day had not smoked
cigarettes im the same way as their male counterparts. Now
that the cigarette sm oking characteristics of wom en and men
are becoming increasingly simflar, their relative risks of
smoking-related illness will become increasingly similar.
This fallacy of women's apparent immunity is clearly
illustrated' by differences in the timing of the growth in lung
cancer among men and women in this century. _Lung cancer
deaths among males began to increase during the 1930s,as
those aten who had converted from other forms of tobacco to
cigarette smokingg before the turn of the century gradually
accumulated decades of inhaled tobacco exposure. .. By the
tim e of the first retrospective studies of smoking and lung
cancer in 1950, two entire generations of men had already
become lifelong cigarette smokers.. Relatively few womenn
from these generations smoked cigarettes, and even fewer had'd
smokedd cigarettes since their adolescence. Those young
women who had'd taken up smoking intensively during World War
II were only in their twenties and thirties. In 1950, women
accounted for less than one in twelve deaths from~ lung
cancer.
- Thereafter, the age adjusted lung cancer death rate
among women accelerated, and the male predominance in lung
cancer declined. Lung cancer surpassed uterine cervical
cancer as a cause of death in women. By 1968, as the
findings of many large population prospectivee studies were
being published, women accounted for one-sixth of all lung
cancer deaths. These studies found that women cigarette
smokers had 2.5 to 5 ti:nes greater deatNrates from lung
WOMEN AND THE CHANGING CIGARETTE
As this report documents, the proportion of men and women
smokers using brands with lowered "tar" and nicotine
continues to grow. Adolescents of both sexes have followed
this trend~, to the point where nonfilter cigarettes are
relatively rare among young adults.
Although the preponderance of scientific evidence
continues to suggest that cigarettes with lower "tar" and
nicotine are less hazardous, four seriouss warnings are In
order.
First, the reported "tareand nicotine deliveries of
cioarettes are standardized machine measurements. They do
not necessarily represent the sm oker's actual intake of these
substances. Evidence is now mounting that individuals who
switch to cigarettes with lowered "tar" and nicotine inhale
more deeply, smoke a greater proportion of their cigarettes,
and inn some cases smoke more cigarettes. '
Second, "tar" and nicotine are not the only dangerous
chemical components of cigarette smoke. Many conventional
filter cigarettes, in fact, may deliver more carbon monoxide
than nonfilter cigarettes. Third, it has not been established that lower "tar"and
nicotine cigarettes have less harmful effects on the unborn
fetus and baby; on women and men at high risk for developing
coronary heart disease, suchh as those with elevated cholesterol
or high blood pressure; or on workers with adverse
occupational exposures. It has not beenn established that
switching to a lower "tar" and nicotine cigarette has any
salutory effect on individuals who already have sm oking-
relatedillnesses, such as coronary heart disease, chronic
bronchitis, and emphysema.
Fourth, even the lowest yield cigarettes present health
hazards for both. women and men that are very much higher
than smoking no cigarettes at all. The single most effective way for both women and men
smokers to reduce the hazards associated with cigarettes is
to quit smoking.
As this report demonstrates,li6tle is known about thee
effects of these product changes on the initiation,
maintenance and, cessation of sT oking, particularly among
women. It has not been determined whether the availability
of cigarettes with lowered "tar" and nicotine has made it
easier for young womenn to experiment with and becomee
addicted tocigarette.s. It is not known whether smokers of
vii
Concepts of Adolescent Behavior
...... .319
Prevalence and Patterns of
Adolescent Cigarette Uke....... 320
Prevalence ..................... 321
Age of initiation in
,
smoking ........................ 323
Number of cigarettes smoked ..... 326
Type of cJgarette smoked ........ 326
Smoking Cessation. ...............
Smoking prevalence and ethnicity 328
................................328
Alcohol and marijuana use ....... 329
Demographic and Psychosocial Correlates
of Smoking In Adolescence ............. 329
Socioeconomic influences ........ 329
Family patterns ................. 330
Smoking among parents and
- siblings ........ 330
Peer group influenc.e............ 332
Scholastic achievement and
aspirations .................... 334
Dynamic/Personali'tyfactors..... 334
Predictions of future smoking
behavior ....................... 336
Prevention of Smoking and Considera- tions for Future Research............. .338Prevention of the
Initiation of
smoking ........................ 338
Research goals.................. 339
iAaintenanceof Smoking................. 340
Smoking Behavior ................ 340
- Patterns of cigarette -
. smoking................... .340
Smoking prevalence and
ethnicity ................. 345
Pharmacological Effects of
Smoking ........................ 345
Nicotine................... .347
Peripheral effects....347
Central effeats....... 347
A possible role for nico-
tine in smoking mainte-
nance..................... 347
Differences in nicotine
metabolism ................ 350
xxiii
1965 toan estimated 3,900 in 1979. From 1965 to 1979,
the proportion of adult male cigarette smokers declined from
51 to 37' percent. Not only have millions of men quit
smoking,., but the rate of initiatiom of smoking among
adolescent males has now slowed. .
From 1965 to1976, the proportion of adult women
cigarette smokers rem ained virtually unchanged at 32 to 33
percent. Since 1976, however, the proportion of adult women
cigarette smokers appears to have declined to 28 percent.
Although adult women are now beginning to quit sm oking at
rates comparable to adult men, the rate of initiation of
smokingamong younger womenn has not declined.
This report documentss numerous differences by sex in
the perceived role of cigarette smoking, in attitudes to ward
health and lifestyle, and in methods of coping with stress,
anger, and boredom.. Yet thee significance of these
differences, and their relation todiEferences in smoking
patterns, remains poorly understood. .
Although it is freqpently observed that women in
organized smoking cessat'iomn programs have more severe
withdrawal symptoms and lower rates of successful quitting
than men, these observations have not been systematically
confirmed for the general population. In the past, women
may have attempted' to quit or succeededin quitting, smoking
less frequently than men. The recent decline in the propor-
tion off women smokers, however, suggests that women's
attempted and successful quitting rates have now increased.
Althoughh weight gain is a frequently cited consequence
of quitting smoking, the association of weight gain with
cessation of smoking has not been the subject of sufficient
scrutiny. Controlled studies with careful measurement on
representative populations of women do not exist. The impact
of the fear of weightt gain after quitting has not been ade-
quatelyexamined. If weight gainn does result from cessation
of smoking, its exact mechanism must bedetermihed.
Even more problematic are marked differences by sex
in the distribution of smoking prevalence by occupation. Men
with advanced education and professional occupations have
taken the lead io-quitt'ing snoking, but women in
administrative and managerial positions have relatively high
smoking prevalence rates. Although 20 percent or fe wer male
physicians smoke, the proportions of cigarette smokers among
women health professionals, especially nurses and
psychologists, remain disturbinglyhioh.
Recent changes in smoking prevalence among black
V
Director, Pulm onary Division, University of
California, San Diego, California.
Mariauita Mullan, National Instituteof Occupational
Safety and Health, Rockville, Maryland.
Janyce E. Notopoulos, Program Analyst, Office of
Planning and Evaluation, National Institute of
Child Health and: Human Development, National
Institutes of, Health, Bethesda, Maryland.
Albert Oberman,M.D., Director, Division of
Preventive Medicine, School of Medicine, University
of Alabama, Rirmingham, Alabama.
Ralph, S. Paffenberger, Jr., M.D., Professor of
Epidemiology, Department of Health Services,
California State Health. Department, Berkeley
California. . Richard Peto, M.D., P,adcliff Clinic, Oxford
University, Oxford, England.
Malcolm C. Pike, Ph.D., Professor, Community and
Family M edicine, School of P^edicine, University
of Southern Californla at Los Angeles, Los Angeles,
California. - Ovide P.. Pomerleau, Ph.D., Professor ofPsychologvand Psychiatry, University of
Connecticut School of-
Medicine, Farmington, Connecticut. Phill H. Price, M.D., Chief, M etabolic Products
Franch, Division of Ruminant Species, Pureau of
Veterinary Medicine, Food and tlrug Adminl!stration,
Rockvllle, Maryland. Mrs. Dorothy Pechman Rice, Director, National Center
for Health Statistics, Office of the Assistant
Secretary for Health. Hyattsvile, Maryland. Anthony Robbins, M.D., Director, National Institute
of Occupational Safety and Health, Center for nisease
Control, Rockville, Maryland.
Harold P. Roth, M.D., Associate Director for
Digestive Diseases R Nutrition, National Institute of
Arthritis, M etabolism, and Digestive Diseases,
National Institutes of Health, Rethesda, Maryland.
Philip. Sapir, Special Assistant to the Director for
Rehavioral and Social~ Sciences and Chief, Human
Learning and Behavioral Branch, Center for Research
for Mothers and Children, National Institute of Child
Health and Human Development, National. Institutes of
Health,. Bethesda, Maryland.
M arvin A. Schniederman, Ph.D., Associate Director for
xvi
the newborn baby. These damaging effects have been
repeatedly shown to operate independently of all other factors
whichh influence the outcome of pregnancy. The effects are
increased by heavier smoking and are reduced if a womann
stops smoking during pregnancy.
Numerous toxic substances in cigarette smoke, such as
nicotine and hydrogen cyanide, cross the placenta to affect
the fetus directly. The carbon monoxide from cigarette smoke
is transported into the fetal blood and deprives the growing
baby of oxygen. Fetal growth Is directly retarded. The
resulting reduction in fetal weight and size has many
unfortunate consequences. Women who smoke cigarettes during
pregnancy have more spontaneous abortions, and a greater
incidence of bleeding during pregnancy, premature and',
prolonged, rupture of amniotic membranes, abruptio placentae
and placenta previa. Women who smoke cigarettes during
pregnancy have more fetal and neonatall deaths than
nonsmoking pregnant women. A relation between maternal
smoking and Sudden Infant Death Syndrome hass now been
established.
The direct harmful effects of smoking on the fetus
have long term consequences. Children of mothers who
smoked during pregnancy lag measurably in physical growth;
there may also be effects on behavior and cognitive
developm ena. The extent of these deficiencies increases with,
the number of cigarettes smoked. Thedamagingeffectse of maternal sm oking on infants
are not restricted topregnancy. Nicotine, a knowm, poison, is
found in the breast milk of smoking mothers. Childremn whose
parents sm oke cigarettes have more respiratory Infections and
more hospitalizations in the first year of life. Women who smoke cigarettes have more than three
times the risk of dying of stroke due to subarachnoidd
hemorrhage, and as much as two times the risk of dying of
heart attack in comparison to nonsmoking women. The use of
oral contraceptives in addition to smoking, however, causes a
markedly increased risk,, including a 22-fold increase in the
risk of subarachnoid hemorrhagic stroke and a20-fodd'
increase in heart attack in heavy smokers.
WHY DO WO'4EN SrtOKE?
Cigarette consumption in this country is now declining.
Annual per capita consumption has decreasedfrom 4,258 in
iv
NON-NEOPLASTIC BRONCHJPULMUNARY DISEASES........... 160
Definitions ............................ 160
Smoking and Respiratory Mortality ...... 161
Smoking and the Epidemiology and
Pathology of Chronic Obstructive Lung
Disease ............................... 166
Smoking and Respiratory Morbidity...... .173
Smoking and Pulmonary Function......... ..182
Smoking and "Early" Functional
Abnormalities .................. 183
Smoking and Ventilatory
Function....................... ...187
INTERACTION BETWEEN SMOKING AND OCCUPATIONAL
EXPOSURES ............. ..............................203
Smoking Patterns in Women.............. .204
Patterns of Employment................. .208
The Reproductive Roie.................. .213
Specific Interactions Between
Occupational Exposure and Smoking ..... 215
Asbestos ........................215
Cotton Dust ..................... 218
PREGNANCY ArD INFANT HEALTH .........................224
Smoking, Birth Weight, and Fetal Growth
................................224
Placental Ratios ................ 226
Gestation and Fetal Growth ...... 229
Long Term Growth and Development
. ...................................230
Role of Maternal Weight Gain....237
Smoking Fetal and Infant Fbrtality and
Morbidity ............................. 243
Spontaneous Abortion ............ 243
Congenital Malformati'.ons........ 245
Perinatal Mortality ............. 250
Cause of Death .................. 252
Complications of Pregnancy and Labor...254
Preecl.amsia ..................... 256
Preterm Del~ivery, PregnancyComplicati.ons and Perinatal
Mortality by Gestation ........ 258
Long Term Morbidit'yand Mortality...... 263
Sudden Infant Death Syndrome.... 266
xxi
Richard A. Lasco, Ph.D., Pureau of Health, Educat:ion,C.enter for Disease Control, Atlanta, Georgia.
Frances Lazerow, Vice -President, Koba Associates,
Washington, D.C.
Joanne Luoto, M.D.,. N.P.H.. Medical Office, Office on
Smoking and Health, Rockville,. Maryland.
Jack P. Maples, Senior Research Associate, Koba
Associates, Washington, D.C. Marianne P. McCarthy, Ph.D., Director of Technical
Support Services, Koba Associates, Washington, D.C.
Marjorie L. Olson, Secretary (Stenography), Office on
Smoking and Health, Rockville, Maryland.
Kelley L. Phillips, M.D,, M.P.H., F.xpert Consultant,
Officeon Smoking and Health, Rockville, Mayland.
David L. Pitts, Public Health, Advisor, Operations
Pranch, Nutrition Division, Runeau of Sm ailpoxEradication, Center for nisease Control, Atlanta,
Georgia.
Donald. R. Shopland,Technicai Information Officer,
Office on Smoking and Health, Rockville, Maryland.
Linda R. Spiegelman, Administration Assistant,
Office on fmoking and Health, Rockville, Maryland.
Carol M. Sussman, Technical. Publication
WriterJEditor, Office on Smoking and Health,
Rockville, Maryland. RonaldG. Thomas, Pubiic Health Analyst, Office on
Smoking and Health, Rockville, Maryland.
Selwyn. M. Waingrow, Public Health Analyst, Office on
$moking and Health, Rockville, Maryland.
Ann E. Wessel, Public HealtK Analyst, Office on
Smoking and Health.,. Rockville, Maryland.
CaroleG. Winn, Assistant. Chief, Clinical Chemistry
Standardization Section, Clinical Chemistry Division,
MetabolicRiochemistry Rranch, Rureau of
Laboratories, Center for Disease Control, Atlanta,
Georgia.
Development, National Institutes of Health, Bethesda,
M aryland. Lester Breslow, M.D., M.P.H., Dean, School of Public
Health, University of California at Los Angeles, Los
Angeles, California..
A. Sonia Buist, M.D., Associate Professor of Medicine
& Physiology, University of Oregon Health Sciences
Center, Portland, Oregon.
David M. Burns, M.D., Assistant Clinical Professor,
Pulmonary Divisiony University of California at San
Deigo, San DieRo California.
Thomas C. Chalmers, M.D., President and Dean, Mount
Sinai Medical Center, New York, New York.
Florence L. Denmark, Ph.D., Professor of Psychology,
Ph.D. Programs in Psychology, City University of New
York, New York, New York..
Rohert M. Donaldson, Jr., M.D., Chief, Medical
Services, Westhaven Veterans Hopital, Westhaven,
Connecticut.
Joseph T. Doyle, M.D., Professor of Medicine and
Head, Division of Cardiology of the Department of
Medicine, Albany Medical College of Union University,
Albany, New York.
Elizabeth M. Earley, Ph.D., Chief, Section of
Cytogenetics, Division of Pathology, Bureau of
Biologics, Food and Prug Administration, Rockville,
M aryland.
Bernard H. Ellis, Jr., Program Director for Smoking
and Occupationall Activities, Office of Cancer
Communications, National Cancer Institute, National
Institutes of Health, Bethesda, Maryland.
Diane Fink, M.D., Associate Director, M edical
Applications of Cancer Research andCoordinator,
Smoking, Cancer, and Health Program, National
Cancer Institute, National Institutes of Health,
Bethesda, Maryland. Harold E. Fox, M.D., Associate Professor of Clinical
Obstetrics and Gynecology, Department of Obstetrics
and Gynecology, Columbia Presbyterian Medical Center,
an& Medical Director, Western and Upper Manhattan
Perinatal Network, New York, New York.
Joseph H. Gainer, D.V.M., Veterinary Medical Office,
Division of Veterinary Medical Research, Bureau of
Veterinary Medicine, Food and Drug Administration,
Rockville, Maryland.
xiv
Stanley N. Gershoff, Ph.D., Director, Nutrition
Institute and Chairman, Graduate Department of
Nut.rition, Tufts University, Medford, Massachusetts.
Sharon P4. Hall, Ph.D.,. Assistant Professcr,
University of California at San Francisco, Laneley
Porter Neuropsych,iatric Institute, Sam Francisco,
California.
Jane Halpern, M.D., ASPER, Office of Health and
Disability, UnirtedStates Department of Labor,
Washington, D.C.
Peatrix A. Ha mburg, M.D., Research Psychiatrist,
Laboratory of Development. Psychology, National
Institute of Mental Health, National Institutes of
Health, Bethesda, Maryiand.
Virginia C. Harris, M.D., Director, Maternal and
Child Health, Onondago County Health, . Department,
Syracuse, New York.
John H. Holbrook, M.D., Assistant Professor of
Internal Medicine, University of Utah Medical School,
Salt Lake City, Utah.
Stanley James, M.D., Professor of Pediatrics,
Ohstetrics, and Gynecology, College. of Physicians
and Surgeons, Columbia Presbyterian Medical Center,
New York, New York.
Hershel Jick, M.D., Roston Collaborative Drug
Surveillance Program, Boston University Medical
Center,. Waltham, Massachusetts.
Reese T. Jones, u.D.,. Professor of Psychiatry,
Departm ent. of Psychiatry, University of California at
San Francisco, Langley Porter Neuropsychiatric
Institute, San Francisco, California.
Philip Kimbel, k?.D., Head, Pulmonary Diseases
Section, Albert Einsteio-. Med.ical Center,
Philadelphia, Pennsylvania.
Jam W. Kuzma, Ph.D., Chairman and Professor of
Biostatistics, Department of Riostatistics and
Epidemiology, Loma Linda University, Loma Linda,
California. Abraham Liilienfeld, M.D., M.P.H., O.Sc.,llniversity
Distinguished Service Professor, Johns Hopkins School
of Hygiene and Public Health, Paltimore Maryland.
Harold A. M enkes, M.D., Associate Professor of
Medicine, Department of Medicine, Johns Hopkins
University, Paltim ore, Maryland,
Kenneth Moser, M.D., Professor of Medicine andd
xv
CONTENTS
INTRODUCTION ANJ Si.M1MARY ............................1
PART I
PATTERNS OF SMDKING AMOf1G WOMEN AND MEN IN
THE UNITEDSTATES, 1900 .- 1979 .................... 15
The Rise of Cigarette Smoking:
1900-1950 ...................... 17
The Emergence of Filtertip
Cigarettes: 1951-1963 ......... 24
Increasing Public Health
Awareness: 1964-1979 .......... 25
Exposure to Cigarette Smoke -
Among Successive Birth .
Cohorts ........................ 31
Cigarette Smoking Among Vyomen....37
Summary .........................
PART Ii
BIOMEDICAL ASPECTS OF SMOKING
OVERALL MDRTALITY........................... ....53
Mortality Trends ..... .....................Epidemiological Studies................ ..58
American Cancer Society 25 -
State Study .................... 58
Swedish Study ....................60
Canadian Veterans Study ......... 60
Japanese Study of 29 Health Districts ...................... 60
British Doctors Study ........... 61
Framingham Heart Study.......... 61
British - Norwegian Migrant Study .......................... 62
Overall Mortality For Females-Cigarette
Smokers versus Non-Smokers ............ 63
Mortality Ratios................ .63
Amount Smoked and Age ........... 63
Duration of Smoking ............. 72
G
CJ
C~
m
~
CD
N
CJI
xix
Smoking and Stimulation Effects
..............350
Smoking Cessation .................... 352
Demographics............354
Age ..................................354
Education ........355
Income ............................... 355
Occupation ..............355
Psychology of Changing Smoking Habits
......................355
Treatment Studies.................... 356
The Smoking Withdrawal Syndrome ...... 364
Treatment Recoinnendations............ .365
Conclusion............367
Disseminati'.omn of Informati.om About
Smoking ............................. 367
Heal,th Attitudes and Behaviors
......................367
Sources of Information.......... 368
Health care providers ...... 368
Educators......370
Peer group................. 371
Family ..................... 371
Media ..................371
Advertising................ 372
The failure to disseminate
information ...............373
Smoking and weight control.
.......................... 373
Stress at Work375
Smoking Habits of Health
Professionals .................378
Physicians............ 378
Psychologists......... 381
Nurses................ 381
The Pregnant Smoker - A Special
Target ............................385
Sources of Information .......... 386
Physician Advice ..............387
Prevalence of Smoking and
Quitting during Pregnancy ...... 392
Psychosocial Factors in Quitting
R;,om,n ion Recomnendations............396
Sumnary............. ...................397
Science Policy, National Cancer Institute, National
Institutes of Health, Pethesda, Maryland.
Irvina J.. Selikoff, M.D., Professor, Mount Sinai
Medical Center, New York, New York.
S. I. Shihko, Ph.D., Chief, Contaminants and Natural
Toxicants Pranch, Division of Toxicology, Rureau of
Foods, Food and Drug Administration, Rockville,
Maryland.
Jeremiah Stamler, Chairman, Department of Community
Healthh and Preventive Medicine, Northestern
University Medical School, Chicago, Illinois.
Jesse Steinfeld, M.D., Dean, M edical College of
Virginia, Rich mond, Virginia John F. Vanderveen, Ph.D., Director, Division of
Nutrition, Rureau of Foods, Food and Drug
Administration, Rockville, Maryland.
Fve Weinbtatt, Assistant Director, Department of
Research and Statistics, Health Insurance Plan of
Greater New York, New York, New York.
Samuel S. C. Yen, Professor and Chairmany
D epartment of Reproductive Medicine, University
of CaLifornia, San D.iego, Lalolla, California.
The editors also acknowledge the heln of the following
staff who among others assisted in the preparation of the
report.
John. L. Ragrosky, Acting. Associate Director for
Program Operations, Office on Smoking and. Health,
P.ockvilie, Maryland.
JacouelineC). Rlandford, Clerk-Typist, Office on
Smoking an& Health, Rockville, Maryland6
Petty Pudd, Secretary (Typing)., Office on Smoking
and Health, Rockville, Maryland.
John F. Hardesty, Jr., Public Information Officer,
Office on Smoking and Health, Rock.ville, Maryland
Patricia E. Healy, Clerk fTyping),. Office on Smoking,
and Heatth, Rockville, Maryland..
Douglas T. Howard, Jr.,. Ph.D., Senior Editor, Koha
A ssociates, Washington, D.C.
Robert S. Hutchin¢s, Associate Director for
Information and Program Development, nffice on
Smoking and Health, RockviHe, Maryland.
M argaret E. Ketterrnan,. Secretary (Typing), nffice on.
Smoking and Health, Rockvil.le, Maryland.
xvii
man. Each successive birth cohort has also experiencedprogessively smaller sex differences in the
fraction of
lifetim e years of smoking that represents filtertip cigarette
use.
16. Among men born during this century, each
successive birth cohort has thus far experienced fewer
cumulative years of cigarette smoking,higher proportionate
exposure to fiitertipcigarettes, an& lower smoking prevalence
rates.. This relationship between birth date and cigarette
smoke exposure does not hold for women. Women born 1921
to1940. havee experienced substantially higher smoking
prevalence rates that earlier generations. Unless they quit
smoking in substantial numbers, these women, currently aged
40 to 59, will surpass older women in total years of cigarette
smoking per capita, the total years of nonfilter cigarette
smoking per capita, and in the total number of cigarettes
smoked. The health consequences of this enhanced exposure
to cigarette smoke among women are likely to be more
prominent inn the coming decades.
MORTALITY
1. The mortality ratio for women who smoke
cigarettes is about 1.2 or 1.3 compared to nonsmokers.
2. Mortality ratios for women increase with the
amount smoked. In thee largest prospective study the mortality
ratio was 1.63 for the two-pack-a-day smoker as compared
to nonsmokers.
3. Mortality ratios aregenerally proportional to the
duration of cigarette smoking; the longer a woman smokes, the
greater the excess risk of dying.
. 4. Mortality ratios tend to be higher for those women
who begin smoking at a young age compared to those who
begin smoking later.
. 5. Mortality ratios are higher for thosee wom en who
report they inhale smoke than for those who do not inhale.
6. Mortality ratios for women tend to increase with
the "tarn and nicotine content of the cigarette.
7. Mortality ratios for female smokers are less than
for male smokers. This may reflect differences in exposure
to cigarette smoke, such as starting smoking later, smoking
cigarettes with lower "tar" and nicotine content, and smoking
fewer cigarettes per day than men.
8. Women demonstrate the same dose-response
4
Age Began Smoking ...............72
Inhalation ...................... 72
"Tar" and Nicotine Content of
Cigarettes ....... .................
1dORBIDITY .....................................85
Days Lost From Work.................... ..85
Limitati.om of Activity ..................87
Cigarette Smoking and Occupation ....... 87
CADIOVASCULARDISEASES...................... ..96
Fdortality Rates ........................ 96
Atheroclerosis ......................... 100
Risk Factors........................... .101
The Effect of Smoking ...................101
Atherosclerosis ................. 101
- Coronary Heart Disease.......... 102
Cessati'on of Smoking ............ 108
Angina Pectoris ................. 108
Cerebrovascul,ar Disease......... .109
Arteriosclerotic Peripheral
Vascular Disease ............... 111
Aortio- Aneurysm................ .112
- Hypertension ................... 112
Venus Thrombosis ...............113
- High Density Lipoprotein....... 114
,.Oral Contraceptive Use, Smoking and
Cardiovascular Di'sease................ .114
Carbon Monoxide................. ...117
CANCER ................. ................................
Lung ...................................1'29
Geographic Differences .......... 135
Smoking Patterns .4nong lYomen.... 136
Cessation of Smoking ............ 145
Experimental Carcinogenesis ..... 145
Larynx ................................. 145
Oral ............. ..........................
Esophagus ................. ...............1.48
Urina.ry Bladder ..........................149
Kidney ................... ...................Pancreas
................151
xx
INTRODUCTION AND SUMMARY
INTRODUCTION
The 1980 Report on the Health Consequences of Smoking
focuses upon the evidence relating cigarette smokingg to health
effects in wom en. It is not presented as a detailed
discussion of the entire range of effects of smoking on
health. Such aa detailed review of all existing evidence can
be fiound in the 1979 Report of the Surgeon General on
Smoking and Heaith. Instead, this voiume on smokingg and
women's health is offered as a review and reappraisal of
smoking and major health relationships specifically in women.
It Is intended to serve the medical community as a unified
source of existing scientific evidence about health effects of
smoking cigarettes for women.: As an examination of current
knowledge, it will logically lend itself to application in both
the personal and public health arenas. .
Its content is the work. of num erous scientists within
the Department of Heaith, Education, and Welfare, as well as
scientific experts outside that organization. ..
This volume examines the major issues relating tobacco
use to wom en's health inciudingg trends in consumption, the
biomedical evidence of the health effects of cigarette usage
by wom en, and determinants of smoking initiation,
m aintenance, and cessation. This section summarizes the principal findings of this
report. It is hoped that the entire volume will serve to
highlight the established risks of smoking for womenn andd their
children, as well as to define the areas in need of further
investigation.
SUMMARY
PATTERNS OF CIGARETTE SMOKING
1. Women have differed from men in their historical
onset of widespread cigarette use, in the rate of diffusion of
smoking among each new birth cohort, in their intensity of
cigarette smoking and their use of various types of cigarettes.
2. Men took up cigarette smoking rapidly at the
beginning of the twentieth century, especially during World
War I. Cigarettes rapidly replaced other forms of tobacco.
1
By 1925, approximately 50 percent of adult males werecigarette smokers. Smoking among men
accelerated rapidly
during World War II. By 1949, the prevalence of cigarette
use among men approached 70 percent in some urban areas.
3. The onset of widespread cigarette use amongg
women lagged behind that of men by 25 to 30 years. The
proportion of adult women smoking cigarettes did not exceed
one-quarter until the onset of World War II.
4. Between 1951 and 1963, Increasing proportions of
women and men smokers converted to filtertip cigarettes. By
1964, 79 percent of adult womenn smokers and 54 percent of
adult men smokers used filter cigarettes.
5. After reaching a peak value of 4,336 in 1963,
annual per capita consumption of cigarettesdeciined in 1964,
1968-70, and In the period since 1975. The most recent
estimate of 3,900 cigarettes per capita in 1970 .is
approximately equal to that observed in 1952.
6. From 1965 to 1978, .the proportion of adult men
cigarette smokers declined from. 51 to ,37 percent. The
preliminary estimate of adult menys smoking prevalence for
1979 .is 36.9 percent. From 1965 to 1976, the proportion of
adult women smokers remained virtually unchanged at 32 to 33
percent. Since 1976, the proportionn of women smokers has
decllned to below 30 percent. For 1979, the preliminary
estimate of adult women's smoking prevalence is 28.2 percent.
The overall smoking prevalence of 32.3 percent for both sexes
in 1979 represents the lowest recorded value in at least 45
years.
7. The proportion of adult smokers attempting to quit
smoking declined from 1970 to 1975, but increased in 1978-
1979. In contrast to past years, the proportions of women
and men now attempting to quit smoking, and their reported
quitting rates, are indistinguishable. Approxim ately one in
three adult smokers now makes a serious attempt to quit
smoking during thecourseof a year.. Approximately one in
five of those who attempt to qult subsequently succeed.
8. The proportion of adult smokers using lower "tar"
and nicotine brands has increased substantially. In 1979; 39
percent of adult women smokers and 28 percent of adult men
smokers reported primary brands with F.T.C. "tar^ delivery
less than 15.0 milligrams. It is not known whether smokers
of the lowest "tar^ cigarettes are more or less likely to
-attempt to quit smoking, or to succeed in quitting, than
smokers of conventional filtertip or non-filter cigarettes.
9. The average number of cigarettes smoked by women
2
a
and men current smokers has increased. The relationship of
this finding to recent declines in the average F.T.C. ^tare and
nicotine deliveriess of cigarettes is not well understood.
10. With each successive generation, the smoking
characteristics of wom en. and men have become increasingly
similar.
11. Among women, the average age of onset of regular
smokingpnogressively declined with each successive birth
cohort--from 35 years of age for those born before 1900, to
16 years of age among those born 1951 to 1960. The
average age of onset of regular smoking among young women
is now virtually Identical to that of young men.
12. Maximum smoking prevalence rates have declined
substantially in recent birth cohorts of men. Men born 1931
to 1940 .reached a peak smoking proportionn of 61 percent
during 1960-62, while men born 1941 to 1950 reached a peak
smoking proportion of 58 percent in 1968-69. Men born
1951.1 to 1960 reached a peak smoking proportion of 40
percent in 1976. Among recent cohorts of women, peak
smokingg prevalence rates have declined to a much smaller
extent. Women born t931 to 1940 reached aa peak smoking
proportion of 45 percent in 1966-68, while women horn 1941
to 1950~ reached a peak smoking, proportion of 41 percent in
1970-73. Women born 1951 to 1960 reached a peak smoking
proportion of 38 percent In 1976. .Amongg the generation born
1951 to 1960, the proportions of women andmen smoking
cigarettes are now virtually identical.
13. The proportions of women and men smokers in each
age group have declined. Among.those bornn before 1951, this
decline in smokingg prevalence resulted mainly from smoking
cessation. By contrast, the observed decline in smoking
prevalence among younger men born 1951 to 1960 has resulted
from both smoking cessation and a lower rate of smoking
initiation. This decline in the rate of onset of smoking
among youngmen has not been observed for young women. .
14. Recent survey data on, adolescent smoking hahits
reveal that by ages 17to19, smoking prevalence among
women exceeds that of men. This findingg supports the
conclusion that the rate of initiation of smoking among young
men--but not that of young women--is declining. The future
cigarette use of the youngest generations of women.is uncer-
tain.
15. With each successive birth, cohort, the accumulated
years of cigarette smoking per woman has progressively
approached the accumulated years of cigarette smoking per
3
association of cigarette smoking and increased coronary heart:
disease among males. This report reviews the evidence
associatingg cigarette smoking and cardiovascular disease. in
women:
1. Coronary heart disease, including acutemyocardiaL
infarctionn andchronic ischemic heart disease, occurs more
frequently in wom en who smoke.. In general,cigarette
smoking increases the risk by a factor of about two, and in
younger women cigarette smoking may increase the riskk
several fold.
2. Cigarette smoking is a major, independent risk
factor for coronary heart disease in wom en; it also acts
synergistically with other coronary heart disease risk factors
producing a risk greater than the sum of the individual risks.
3. The use of oral contraceptives by women cigarette
smokers increases the risk of a myocardial infarction by a
factor of approximately ten.
4. Women who smoke low "tar"' and nicotinee cigarettes
experience less riskk for coronary heart disease than women
who smoke high "tar" and nicotine cigarettes, but their risk
is still considerably greater than, that of nonsmokers..
5.. Increased levels of high-density lipoprotein (HDL)
are correlated withh a reduced riskk for an acute myocardial.
infarction;; women cigarettee smokers have decreased levels of
HDL.
6. Cigarette smoking is a major, independent risk
factor for the development of arteriosclerotic peripherall
vascular disease inn women. Smoking cessation improves the
prognosis of the disorder and has a favorable impact on
vascular patency following reconstructive surgery.
7. Women cigarette smokers experience an increase& risk,
for subarachnoid hemorrhage; the use of both cigarettes and
oral contraceptives appears to increase synergistically the risk
for subarachnoid hemorrhage.
S. Women who smoke cigarettes may be more likely to
develop severe or malignant hypertension than nonsmoking
women.
CANCER
1. Cigarette smoking is causally associated with
cancer of the lung, larynx, oral cavity, esophagus, and urinary
bladder in womenn as welll as in men; it is associated with
kidney cancer inn women.
6
Long Term Morbidity and Mortalit:y...... 263
Sudden Infant Death Syndrome.... 266
Mechanisms ............................. 267
Experimental Studies ....................270
Tobacco smoke ....................270
. Nicotine ........................ 270
Carbon monoxid~e................. 272
Polycyclic aromatic hydrocarbons
........275
Other components .................276
Fertility .............................. 277
Smoking and Reproduction in
Women .......................... 277
Smoking and Age of Menopause.... .278
Smoking and Reproduction in Men
............ .....................278FertiIizati'.on and Conceptus
~ ~ Transport ... ...................... 2
PEPTIC ULCER ....................................... 297
INTERACTIONS OF SMDKING WITH DRUGS, FOOD
CONSTITUENTS AND RESPONSES TO DIAGNOSIC TESTS ..... 302
Women Smokers and Nonsmokers and Drug Consumption Patterns .. .................. 30Altered Clinical
Response to Drug
Therapy by Smokers Compared to
Nonsmokers ....... ........................304
Oral Contraceptives and Smoking ........ 306
Alterations in Normal Clinical
Laboratory Values in Women Smokers....308
The. Influence of Smoking on the
Nutritional Needs of Women............ .309
PART III
BEHAVIORAL ASPECTS OF SMOKING ......................
PSYCHqSOC1AL AAD BEHAVIORAL ASPECTS OF SMOKING IN
WOMEN: INITIATION, MAINTENANCE, AND CESSATION'....318
Initiation of Smoking in Adolescent
Girls ................................. 318
environmental exposure to a similar health effect due to
smoking,
e). Synergy of exposures, and -
f). Causation of accidents. -
2. Women are entering occupational environments with
greater frequency, and thus may be experiencing greater
exposures to physical andd chemical agents.
3. Cohorts of women with a greater prevalence of
smoking are currently reachingg the ages of maxim al disease
occurrence, replacing earlier cohorts with lower cigarette
-
exposures.
4. Physiologic differences in hormonal status between
males and females constitute a potential source of differing
responses. 5. Women, in the workplace who are pregnant present
a nine- month exposure opportunity, including potential
teratogenic and perinatal mortality effects. 6. Concurrent exposure of women to smoking and
asbestos resulted in a clear excess of cancer of the lung.
7. Women smokers exposed to cotton dust run a higher
risk of developing byssinosis, bronchitic syndromes, and
abnormal pulmonary functionn tests than nonsmoking women.
PREGNANCY
1. Bables born to women who smoke during pregnancy
are, on the average, 200 grams lighter than babies born to
comparable nonsmoking women. 2. The relationship between maternal smoking and
reduced birth weight is independent of all other factors that
influence birth weight including race, parity, maternal size,
socioeconomic status, and sex of child; it is also independent
of gestational age.
3. There is a dose-response relationship between
maternal smoking and reduced birth weight; the more the
women smokes during pregnancy, the greater the reduction in
birth weight. 4. If a woman gives up smoking early duringg
pregnancy, her risk of delivering aa low birth weight baby
approaches that of a nonsmoker.
5. The ratioof placental weight to b.irthweight
increases with, increasingg levels of maternal smoking,
reflecting a considerable decrease in mean birth weight and a
slight increase im, mean placental mass; this may represent an.
9
2. Cigarette smoking accounts for 18 percent of all
cancers newly diagnosed and 25 percent of all cancer deaths
in women. In 1980, 32,0(10of the estimated 117,000 0 deaths,
or over one-quarter of the deaths expected from lung cancer,
will occur in women.
3. Women cigarette smokers have been reported too
have between 2.5 and 5 times greater likelihood of developing
lung cancer than nonsmoking women.
4,. Among womenn the risk of developing, lung cancer
increases with increasing number of cigarettes smoked per
day, duration of the smoking habit, depth of inhalation, "tar"
and nicotine content of the cigarette smoked. The risk is
inverselyrelated to the age at which smoking began.
5. A dose-response relationship has been demonstrated
between cigarette smoking andcancer of the lung, larynx, oral
cavity, pancreas, and urinary bladder in women. 6. The rise in lung cancer death rates is currently
much steeper in wom en that in men. It is projected that the
age adjusted lung cancer death, rate will surpass that of
breast cancer in the early 1980s.
7. The rapid increase in lung cancer rates in women
is similar to but steeper thann the rise seen in men
approxim ately 25 years earlier. This probably reflects the
fact that women first began to smoke in large numbers 25-30
years after the increase in cigarette smoking among men.
Thus, neither menn nor women are protected from developing
lung cancer causedby cigarette smoking.
8. Cigarette smoking has been causally related to all
four of the major histologic types of lung cancer Inn both
women and men, including epidermoidy small cell, large cell
and adenocarcinoma. 9. The usee of filter cigarettes and cigarettes with
lower levels of "tar" and nicotine by women Is correlated
with, . a lower risk of cancer of the lung and larynx compared
to the use of high "tar" and nicotine or unfiltered cigarettes.
The risk posed by =moking low "tar"cigarettes, however, is
clearly greater than that among females who never smoked.
10. After cessation of cigarette smoking, a wom an!s
risk of developing lung and laryngeal cancer has been shown
to drop slowly, equalling that of nonsmokers after 1f)-15
years.
11. Excessive ingestion of alcohol acts synergistically
with cigarette smoking to increase the incidence of oral and
laryngeal cancer in women.
7
adaptation to relative fetal hypoxia.
6. Thepattern of fetal growth retardation that occprswith maternal smoking is a decrease in all dim
ensions
including body length, chest circumference, and head
circumference.
. -
7. Maternal smoking during pregnancy may adversely
affect the child's long-term growth, intellectual development,
and behavioral characteristics.
8. Maternal smoking during pregnancy exerts a direct
growth-retarding effect onthe fetus; this effect does not
appear to be mediated by reduced maternal appetite, eating or
weight gain.
9. The risk of spontaneous abortion, fetall death,, and
neonatal death increasess directly with increasing levels of
maternal smoking: duringg pregnancy; interaction of maternal
smoking with other factors which increase perinatal mortality
may result in an even greater risk.
10. Excess deaths of smokers' infants are found mainly
in the coded cause categories of "unknown" and "anoxia" for
fetal deaths, and the categories of "prem aturity alone^~ and
"respiratory difficulty" for neonatal deaths; this suggests that
the excess deaths aree due to problems of the pregnancy,
rather than to abnormalities of thee fetus or neonate.
11. Increasing levels of maternal smoking result in a
highlys:ignificant increase in the riskk of abruptioplacentae,
placenta previa, bleeding.early or late in pregnancy, premature
and prolonged rupture of membranes, and preterm delivery--
all of which carry high risks of perinatal loss.
12. Although there is little effect of maternalsmokingl on mean gestation, the proportion of fetal
deaths and live
births that occur before term increases directly witbh maternal
smoking level, Up to 14 percent of all preterm deliveries in
the United States may be attributable to maternal smoking.
13. The incidence of pre-eclampsia is decreased among
women who smoke during pregnancy; however, if pre-eclampsia
develops in a smoking woman, the risk of perinatal mortality
is markedly increased.
14. An infant's risk of developing the"sudden infant
death syndrome" is increasedd by maternal smoking during
pregnancy.
15. There are Insufficient data to support a judge ment
on whether maternal and/or paternal cigarette smoking
increases thee risk of congenital malformations.
16. Infants and children born to smoking mothers may
experience more long-term morbidity than those born to non-
10
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NON-NEOPLASTIC BRONCHOPULMONARY DISEASES
1. Recent statistics indicate a risingg death rate due
to chronic obstructive lung disease (COLD) among women. The
data available demonstrate an excess risk of death from COLD
among smoking women over that of nonsmoking women. This
excess riskk is much, greater for heavy smokers than, for light
smokers.
2. Women's total risk of COLD appears to be
somewhat lower than men's, a difference which may be due to
differences in prior smoking habits.
3. The prevalance of chronic bronchitis varies directly
with cigarette smoking, increasing with the number of
cigarettes smoked per day.
4. There is conflictingg evidence regarding differences
in the prevalence of chronic bronchitis in women and men.
Several recent studies suggest that there is no significant
difference in the prevalence of chronic bronchitis between
male and female smokers. This may be the result, however,
of increasingly similar smoking behavior of women and men.
5. The presence of emphysema at autopsy exhibits a
dose-response relationship with cigarette smoking during. life.
6. There is a close relationship between cigarette
smoking and chronic cough or chronic sputum production In
women, which increases with total pack-years smoked.
7. Women current smokers have poorer pulmonary
function by spirometric testing than do female ex-smokers or
nonsmokers, a relationship which is dose-related to the
number of cigarettes smoked.
INTERACTI.ON BETWEEN SMOKING ANDOCCUPATIONAL
EXPOSURE
1. The 1979 Surgeon GeneraRs Report identified the
ways in which smoking cigarettes may interact with the
occupational environment. They include:
a). Facilitat:ionof absorption by physical
contamination of cigarettes,
b). Transformation of workplace chemicals into
more toxic substances,
c) Addition of the exposure to a toxic constituent
of tobacco smoke to a concurrent exposure to the same
constituent present in the workplace,
d) Addition of a health effect due to
8
concern over future social and economic roles. This stress
may be the common mechanism producing the increased rates
of smoking in some groups.
12. The factors associated with successful'quitting., by
adolescents of either sex are lower number of cigarettes
smoked per day, higher educational aspirations andd
achievement, greater acceptance of the health riskk of smoking.
and having more nonsmokers among their friends.
13. It is possible that women and men modify their
smoking In order to maintain a constant nicotine level.
14. Women are more likely than men to smoke in order
to reduce stress.
15. Women at higher education and income levels are
more likely to succeed in quitting. Additional factors
associated with successful quitting are a strong commitment to
change, the use of behavioral techniques and the reliability of
social support for quitting. Wom en have been reported to
show lower rates than men of successful cessation following
organlzed cessationn programs, a difference which Is less
apparent in those programs which include social support.
13
relationships with cigarette smoking as men. An increase inn
mortality occurs with an increaseine number of cigarettes
smoked per day, an earlier age of beginning cigarette
smoking, a longer duration of smoking, inhatation of cigarette
smoke, and a higher etarn and nicotine content of thecigarette. Women who have smoking
characteristics similar tomen may experience mortality rates similar to men.
Caution is necessary in drawing conclusions about themagnitudee
of either the relative risks or the absolute risks of
smoking among womenn compared to men. Existence of a 25-
to-30 year interval between the marked Increase in
consumption of cigarettes between men and women suggests
that current figures may not yet constitute a demonstration of
the maximal health effects of smoking in women.
MORBIDITY
The 1979 Report of the Surgeon General summarized the
information, on smoking and morbidity as follows:
1. Inn general,fematecurrent cigaretta smokers report
more acute and chronic conditions including chronic bronchitis
and/or emphysema, chronic sinusitis, peptic ulcer disease, and
art~eriosclerotic heart disease, than women who never smoked.
2. Thereis a dose-responsereiationship between the
number of cigarettes smoked per day and the frequency of
reporting for most of the chronic conditions.
3. The age-adjustedIncidence of acute conditions
(e.g., influenza) for women, smokers Is 200 percent higher for
women who had ever smoked than, for nonsmokers. Additional data from the Health Interview Survey
(HIS) is
presented:
1. Currently employed women who smoke cigarettes
report more days lost from work due to Illness and injury
than working women who do not smoke.
2. Limitation of activity is reported more commonly
among women under the age of 65 who have ever smoked than
among those who never smoked.
CARDIOVASCULAR DISEASES
Coronary heart disease is the major cause of death among
both males and fem ates in the U.S. population. The 1979Surgeon. General's Report clearly
demonstrated the close
5
4. Insufficient informat.ion exists for assessment of
the impact of smoking on the nutritional needs of women.
BEHAVIORAL ASPECTS OF SA40KING
the people in cigarette advertisements, but they are less
9. Adolescent girls overestimate the percentage of
their peers who smoke and they have a very positive Image of
and nonsmokers associate with. nonsmoking peers.
8. Adolescent smokers associate with peers who smoke
begin smoking if a parent or older sibling also smokes.
7. Female and male adolescents are more likely to
are more likely to become smokers.
families, and families with lower parental educational levels
6. Adolescents from iowincome families, single parent
cigarettes per day.
smokers than their white peers, but they smoke fewer
between the sexes in these patterns of smoking is decreasing.
Adolescent and adult black women are more likely to be
low tar and nicotinecigarettes, smoke fe wer cigarettes per
day and inhale less deeply than do men, but the difference
5. Adolescent and adult womenare more likely to use
than one pack per day is increasing,
1 4. The percentage of women smokers' who smoke more
attempt to quit will be successful.
- 3. The earlier tobacco is used and the greater the
number of cigarettes smoked per day, the less likely an
starting to smoke regularly at a younger age, with~ more than
half of the male and female adolescents who begin to smoke
starting before the 10th grade.
2. Those young women who do begin to smoke are
1. The percentage of 17-18 year old women who
smoke has shown a steady rise between 1968 and 1979; it
now appears, however, that the increase in smoking.prevalence
amongg adolescent femaieshas leveled off and begun to
decline. Young women born after 1952 show a substantlaily
reduced initiation of smoking and will probably have a much
lower prevalence of smoking as adults.
likely than adolescent boys to see smokingg as a social asset.
10. Adolescent girls who smoke tend to be more
outgoing butt feel less able to influence their future. -
11. Adolescents experience stress due to feelings of
unattractiveness, incompetency in school achievement and
personal relations,iimited opportunity for personal growth and
12
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03684944
03684946
FIGURE 1-Annual consumption of cigarettes and flltertip cigarettes per
person aged 18 years and over,19OO-1979,
5000
1900 '10 '20 '30 '40 '50 '60 '70 '80
Saurcee u.S. Oepartment of Agriculture (52)
,
year
Total' per capita consumption data fon 1917-19 and 1940-79 include
overseas forces. Total perr capita consumption for 1979 iss preliminary
estimate: Per capita consumption of filtertip cigarettes derived'from annual
data on the filtertipshare of total cigarette production.
1P.
per
'80
decline during the Great Depression, consumptiom increased
from 665 . cigarettes per capita in 192rr to 3,5?2 cigarettes
per capita in 195Q (,5:2)..:
A continuous, nationally representative series of
smoking prevalence rates during, the period 1oOQto 195r)is
not publicly available. Neverthel;ess,num erous sources can he
pieced together to characterize the differentiail grovrth, of
cigarettee smoking amongg women and men.
Figure 2 depicts estimates of the percentage of male
and femaliee current cigarette smokers In the greater Milwaukee
area, as compiled by the Milwaukee Journal (40).: Im. 1023,
the first reported year of this survey, 51.Rpercent of males
aged iR years and over smoked cigarettes. Sixtypercenty of
male cigarette smokers also smoked pipes or cigars. In total,
R7nercent of adult males used some type of tobacco (40),.
Although earlier survey estim ates of malee smoking rates
are unavailable, It appears that the rise of cigarette
consumption prior to 1023 reflected bothh the conversion of
established male non-cigarette tobacco users to cigarette
smoking and thee recruitment of a ne w generation of younger
male smokers during World War I.: Innovations in cigarette
production and marketing have been cited as Influential fac-
tors in this rapid growtK (41, V), F9),. Camel cigarettes, a
blend of lighter Burley smoking tobaccos with previously
dominant Turkishh cigarette tobaccos, were Introduced in ta13and within months attained a national
market. Two similar
brands, Lucky Strike and Chesterfield, folJowedd in 1016 and1a.14, respectively (41, 50, 69),
rluring WorldWa.r I, the War
Industries noard estimated that solAiers of the Allied Armies
consumed FpO to 70 percent moretobacco than they bad used
in civiliann life (30, a1 ). Cigarettes continued to dominate other forms of
tobacco among male smokers throughout the 19?ns and. 1930s.
py 1935, 62.55 percent of adult males in the greater
Milwaukee area sm oked cigarettes (Figure 2), while the
percentagess of pipe and cigar users had declined substantiallv.
Average cigarette consumption freauency among men smokers
increased from 3.7 packs per week in 1923 to 4.R packs per
week in 1i935, (40).. Consumptionn among men accelerated during World War II
(Figures 1 and 2). In 1°44, more than 95 percent of
cigarettes produced in the U.S. were distributed to overseas
forces, tvpically for free or at low cost, to the point where
subsecuent shortages developed in the domestic market (31,
d1 ),. Py 1 o4R, F7'.1 percent of adult males in the Milwaukee
PATTEttNS OF SMOKING
INTRODUCTION
This chapter traces the evolution of cigarette sm oking among
successive generations of American women and men during the
twentieth century. The available evidence dem onstrates that
women have differed from men in their historicall onset of
widespread cigarette use,, in thee rate of diffusion of s.noking
among each ne wbirth cohort, in their intensity of cigarette
smoking, and their use of various types of cigarettes.
Four main conclusions emerge from this analysis.
First, although men rapidly took up sm oking during the early
decades of this century, the proportion of adult female
cigarette smokers did not exceed one-quarter until the onset
of )Vorld. War II. The peak intensity of smoking occurred
among women born after 1920. Second, as a result of higher
past rates of quitting and lower past rates of initiation among
men, as well as changes in the cigarette consu,med, the
smoking characteristics of women and men are now becoming
increasingly similar. Third, the prevalence of cigarette
smoking among adult Americann women and men is declining.
This conclusion applies to all age groups, but with less
certainty to the youngest generation of women. Fourth,
increasingg public awareness of the health consequences of
smoking has resulted in significant changes in the nature of
the cigarette product.. Yet little is known about the effects
of these product changes on the initiation, maintenance and
cessation of smoking, particularly among women.
Since the last review of cigarette smoking in the 1979
Report of the Surgeon General (26)., two new national surveys
have been performed under the sponsorship of the National
Center for Health Statistics and the National Institute of
Education. This chapter relies in part on the recent,,
preliminary results of these surveys.
The Rise of Cigarette Smoking: 1900 - 1950
Although the use of cigarettes inn the United States was
observed as early as 1854 (44, 50), consumption did not
increase dramatically until after 1,.900. As sho wn in Figure 1,
per capita consumption of all types of cigarettes increased by
more than tenfold from 1900 to 1920. Despite a transient
17
TABLE 1.-Estimates of the prevalence of regular cigarettee smoking
among adudts,United States, selected national surveys,
1935 - 1979.
1935 18.1 52.5
1955 24.5 . 52.6
1965 33.3 51 .11
1970 31.1 43.5
1974 31.9 42.7
1976 32.0 41.9
1978 . 29.9 37.0
1979 28.2 36.9
?0 years and over. Estimates for the years 1965, 1970, 1974, 1978 and
data represent persons 18years and over. 1976 data represent persons
Data for 1979 are preliminary estimates based onn a sample of over
13,000 interviews conducted during.)anuary -)une 1979, provided by
Health Interview Survey, National Center for Health Statlstlcs. 1955
Data for 1978 are revisions of preliminary estimates reported In (26).
SOURCE: (14,18,56,58-61)
1979 represent persons 17 years and over.
23
Although the differential growth of cigarette use among
various socioeconomic groups is not well documented, the
available data during this period suggest that male sm oking
rates declined with increasing incom e, while the relation of
women's smoking to income was less clear. The Milwaukee
Journall in 1945 noted 58 percent of men with monthly rents
over $50 were sm okers, and 75 percent of men with rents
under $30 per month (40)were smokers. Among women, the
corresponding proportions were 32 and 37 percent
respectively. In Mill's and Porter's 1947 survey of Columbus,
Ohio (38), 28.3 percent of white females and 64.9 percent
white males smoked cigarettes, whereas 36.4 percent black
females and 68.9 percent black males smoked cigarettes
(estimates calculated from the 'age distributionn data provided
in Table 6 of (38).. Kirchoff and Rigdon, in a survey of over
21,000 patients, visitors, and employees of hospitals in
Houston and Galveston, noted that 63.2 percent white males,
and 33.4 percent white females, 66.3 percent black males,
and 32.2 black females smoked cigarettes (32).
All of the above findings reinforce the conclusion thatt
the onset of widespread cigarette use among women lagged'
behind that of men by 25 to 30 years. This historical delay
in the growth of cigarette sm oking among women has also
been documented for the United Kingdom (10,48,51).
The Emergence of Filtertip Cigarettes; 1951-1963
As sho wn in. Figure 1, total per capita consumption of
cigarettes declined during 1953 to 1954. This decline was
coincident with the appearance in the popular press of reports
seriously suggesting a link between cigarette smoking and lung
cancer (12,35,36,42). Thereafter, the consumption of
filtertip cigarettes increased rapidly (Figure 1). The 1953
filtertip cigarettes constituted 2.9 percent of cigarette
production. By 1958, their share of production had increased
to 45.3 percent, and by 1963 it was 58.0 percent (52).
The transient decline during 1953 to 1954 in the
number of cigarettes consumed was not clearly matched by a
decrease in the proportion of cigarette smokers (29). At
least in urban areas, the proportion of women smokers
continued to increase. From 1953 to 1958, the prevalence of
adult female smoking increased'from 42.9 to 45.4 percent in
Milwaukee (Figure 2)y from 38.4 to 42.6 percent in Omaha,
from 47.0 to 50.2 in Washington, D.C., and from 39.6 to 44.4
percent in San Jose (39).
24
TABLE 4.-Estimated percentage dlstributlon of adult current ciganette
Smokers accarding to reported daily cons
United States, 1965 - 1979. unptlon ftequency.,
Year . Percent Smoking Percent Smoki'ng
Less Than 15 25 Cigauett<s or
, Cigarettes per More per Day
Day
Women
1,965 44.:5 13.7
1970 39.1 18.0.
1974 38.7 - 18.5
1976 36.5 19.6
1978 36.0 21.0
1979 34.6 22.4
Malas
1965
1970.
29.6
27.8 ,
24.5
27.7
1974 26.3 30.6
1976 . 24.2 31.1
1978 23.4 34.2
1979. 26.4 . 32.2
S6URCE: (26,56,58-61).. Datl.for 1976 represent persons aged 20 year
and over. All other years represent persons aged 17 years and over.
Data for 1979 are preliminary estimates based on interviews conducted
during January - June of that year, provided by the Health InterviewSurv.ey, National. Center for
Health Statistics.
30
estimate yields a 6 percent adult female smoking, prevalence
in 11024 and Moody's estimate yields a 156 percent prevalence
Im. 197Q (53).
The Milwaukee Jlournal series in Figure2 must he
interpreted in lipht of changes inn the type of survey
respondent and the wording of questions designed to elicit
smoking practices (see caotionn to Figure 7). Moreover, this
urban population series may not be representative of all
American women. Nevertheless, the publicly available survey
data sources are consistent with the concius.ion that smokingg
rates among women did not exceed one-auarter until the onset
of World War 11..
Rased on 10,000 applications for insurance policies
during 1030 to 1040, Ley (34) estimated age-standardized- smoking rates of 63..4 percent of men and
20.R percent of
women aged15 years and over. In 1935, Fortune Magazine,
inn the first nation- wide survey (14), reported that 52.5,
percent of adultt men, and 18.1 percent of adult women smoked
cigarettes. (See Table 1 below). Am ong those under 40
years of age, 65.5 percent of men and 26.2 percent of women
were smokers. Among those over 40 years, 19.7 percent of
men and q.3 percent of women were smokers. Urban-rural
differences in smokingg were significant. The proportion of
smokers ranged from 61.4 percent of men and 31~..2 percent of
women in cities with population over one million, to 44.1
percent of inen, and. R.fi percent of women in rural areas with
population under 2,500. A survey of 25n urban women by the
M arket Research Corporation. in 1q37 reported 76 percent
regular smokers and an additional73 percent occasional
smokers (49). After 1940, women's smoking rates accelerated, as new
generations of women, particularly younger women In urban
areas, entered the labor force (see also title "Occupation and
Environment" in this Report). In 1q44, the Gallup Poll
reported 4g pe.rcentt adult malee smokers and 36 percent adult
female smokers (3.). In 1949, the Gallup findings were 54
percent male and 33 percent female (3). Local consumer
surveys ofurhan areas in, 194's revealed 37.6 percent adult
women cigarette smokers in Milwaukee (see also Figure 2)1,
34.3 percent In Omaha, 35.66 percent in Pirmingham, dF.7
percent in Philadelphia, 9R.33 percent in Seattle, and 3d.0
percent in San Jose(39). Conover citing. "tradee journal"
surveys in the three or four yea:rs prior to 1950, reported
smoking prevalence rates of 65. to 7n percent among men and
4n to 45 percent among women (,11),.
22
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TABLE 2.-Estimated rates of attempted and successful quitting among
adult, recent cigarette smokers, United States, 1970 - 1979.
1970
1975
1978
1979
1970
1975
1978
1979
(1).
Percent of
All Recent
Smokers Who
Attempted to
Qui',.t In Past
Year (ii)
Percent of
Smokers
Attempting to
Quit tn Past
Year Who
Reported
Successfully
Quitting (1ti).
Percent of
All Recent
Smokers Who
Reported
Successfully
Quitting in
Past Year
40.9 21.3 8.7
30.2 19.5 5.9
32.7 18.8 6.2
32.9 21.6 7.0.
44.4 . 26.4 11.7
28.3 20.:1 . 5.7
29.1 21.5 6.3
31.4 21.3 6.7
SOURCE: 1970 and 1975 data from surveys of persons aged 21 years and
over, conducted by National Clearinghouse for Smoking and Health
(63,65). 1978 and 1979 data from the Heaith. Interview Survey of per-
sons aged 17 years and over, conducted by the U.S. National Center for
Health Statistics (61). 1979data are preliminary estimates based on
1ntervlews during January - June of that year.
27
At the same time, both women and men rapidly
converted to filtertip cigarettes. By 1958, filter cigarette
use prevailed among 61 percent of women smokers and 42
percent of men smokers in Milwaukee, 54 percent of women
smokers and 43 percent of men smokers in Omaha, 53 percent
of women smokers and 47 percent of men smokers in
Washington, D.C., and 59 percent of women smokers and 42
percent of men smokers in San Jose (39). In a nation-wide
1964 survey reported by the National Clearinghouse for
Smoking and Health (62), 79 percentt of adult female smokers
and 54 percent of adult male smokers used filter cigarettes.
Increasing Public Health Awareness: 1964-1979
Per capita consumption reached a peak of 4,336 in. 1963
(Figure 1). It declined transiently after the appearance in
January 1964 of the first Report of the Advisory Committee
to the Surgeon General (54). Per capita consumption
continued to decline during the subsequent period of increased
publicity concerning the health hazards of smoking (26,29).
Since 1975, per capita consumption has declined at an average
rate of 1.4 percent annually. The most recent 1979 estim ate
of 3,900 cigarettes per capita closely approximates that
observed in 1952. Table 1 summarizes the results of selected, nationally
representative surveys of adult cigarette use during the period
1935to 1979. Except for the Fortune survey of 1935 (14)
and the supplement to the Current Population Survey in 1955
(18), these data were collected under the sponsorship of the
National Center for Health Statistlcs.. The results of other
recent national surveys of adult cigarette use
(:3,4,55,57,58&,62,63,65); revealing very similar trends in the
prevalence of smoking, were described in the 1979 Surgeon
General's Report (26).
Among adult males, the prevalence of regular cigarette
use has declined, continuously since 1965, with more marked
decreases in the intervals 1965 to 1970 and 1976 to 1978.
(The absolute standard errors for all National Center for
Health Statistics estim ates in this table are less than 0.3
percent.). Among adult women, the direction of change in
smoking prevalence is less clear. The estim ates for the
interval 1976 to 1979, however, suggest a recent downturn.
The preliminary 1979 estimate of 32.3 percent for the overall
prevalence of adult cigarette smoking among both sexes
All three indicators of smoking cessation were highest
for mem.n in 1970. Although a relatively large proportion of
women smokers attempted to quit smoking in 1970 (column
(i)), their probability of success in that year was
significantly lower than that of men (column (ii)). Quit
attempt rates for both sexes (.column, (i)) declined by 1975,
but have increased in 1978 to 1979. With respect to the
probability of attempting to quit and the success rate, adult
men and women cigarette smokers are now indistinguishable.
Table. 3displays recent changes in the disribution of
cigarette brands according to F.T.C. "tar" contents. The
proportion of adults smoking cigarettes with F.T.C. "tar"
.delivery less tham 15 milligrams has increased from 9.5
percent of women and 2.9 percent of men in 1970 to 38.5
percent of women and 28.1 percent of men in the first half
of 1979. A corresponding increase in the proportion of
smokers of cigarettes with F.T.C. nicotine delivery less than
1.0 milligram was also observed.
At the sam e tim e, the average cigarette consumption of
adult smokers has increased. Table 4 shows recent changes in
the distribution of daily cigarette consumption among current
smokers. These data must bee interpreted in light of possible
underreporting biases and, in particular, a strong tendency for
respondents to round off their reported daily consumption to
one pack(67).. Nevertheless, the percent of women smoking
less than one pack per day has declined, while the proportion
smoking more than one pack per day has increased. Except
for 1979, a similar trend is observed for men. (The absolute
standard errors of the 1978 and 1979 estim ates are
approximately 1.0 percent.). The data of Table 4 represent the more recent portion
of an apparently long run trend toward increasing daily
cigarette consumption among regular smokers. In 1924,
Milwaukee men smokers consumed an average of 10 cigarettes
per day (40). In 1934, .male smokers in Milwaukee consumed
an average of 13.4 cigarettes per day, whilewomen smokers
consumed 7per day (40). If cigarette consumptiorrn in 1935
was 1,564 per adult (Figure 1 and (52)), and if the overall
percentage of adult smokers was 37.3 percent (14), then. mean
consumption per adult smoker was. 11.5 cigarettes per day. If
consumption per adultt was 3,597 in 1955 and if the
prevalence of regular smoking was 37.6 percent (18), then
mean consumption per adult inn that year was 26.2 cigarettes.
The corresponding calculation based on 1979 per capita
consumption data and adult prevalence date (Figure 1 and
Table 1) yields 33.3 cigarettes per day.
28
t
f
n
5
t
e
t
e
n
5
~$
f
It
1
TABLE 3.-EstimaIedt percentagedlstribution of adult current regular
cigarette smokers according to f.t.c. 'tar' content of
primary brand, United Stated 1970 - 1979.
Year Less Than 5.0 to 10..0.to 15.0 to 20.0 mg
5.6 mg 9.9 mg 14.9 mg 19.9 mg or More
women
1970 9.7 2.0 6.8 . 67.1 23.4
197.5 1.2 1.2 15.0 75.1 7.5
1978. 5.3 8.8 21..1 59.2 5.7
1979 5.6 9.5 23.4 55.4 6.1
Men
1970
0.2
0.9
1.8
61.3
28.1
1975 0.6 1.1 11.0 68.1 19.2
1978 3.3 6.2 13.5 63.5 13.6
1979 2.2 8.5 17.0 60.1 11.8
SOURCE: National Clearinghouse for Smoking and,Health (63,65),
National Center for Health Statistics (61~).. 1979 data are preiiminary
estimates provided by the Natl~onal Center for HealthStatistics. 1970
and 1975 data represent adults aged 21 years and over. 1978 and 1979
data represent adults aged 17 years and over. Estimates exclude those
with unknown primary cigarette brand.
29~
represents the lowest recorded value in at least 45 years.
(The overall prevalence of cigarette smoking in the 1935
Fortune Magazine was 37.3 percent among adults of both
sexes.)
These patterns of change in smoking prevalence applied
to both white and black adults. For white men, the
prevalence of regular smoking declined from 51.5 percent in
1965 to 36.3 percent in 1979. For black men, the prevalence
of regular smoking declined from 60.8 percent in 1965 to
42.0 percent in 1979. For white women, smoking prevalence
declined from 34.2 percent in 1965 to 28.2 percent in 1979.
For black women smoking prevalence declined from 34.4
percent in 1965 to 28.9 percent in 1979. Racial differences
in cigarette use are discussed in greater detail in the chapter
in this report entitled "Psychosocial and Behavioral Aspects of
Smoking in 1'lomen "
Although the Milwaukee area data for 1964 to 1979 do
TABI
woi
19
19
19
19
not closely match these national estim ates, Figure 2 does
show a marked decline in smoking rates for both sexes during
Me
1964 to 1970, a deceleration in the decline of smoking
15
prevalence during 1971 to 1975, and a resumption of the
1<
decline in prevalence among men in the last four years. 1S
The cessation of cigarette smoking has been a 1S
significant factor in explaining this overall decline in sm oking
prevalence (26). Colu:nn (i) of Table 2 presents estim ates of
the percentage of recent smokers who made a "fairly serious
attempt to quit" within one year of the interview date.
(Recent smokers include all current smokers plus those former
smokers reported to have stopped within one year of
interview.) Column(ii) sho ws what proportion, of those
attempting to quit regarded themselves as former smokers.
Column (iii) shows the proportion of all recent smokers
(whether or not they attempted or succeeded quitting)) who
reported themselves as recent former smokers. These data
necessarily reflect respondents' self-assessment of both the
seriousness of a quit attempt an& their degree of success.
Nevertheless, they do provide an indication of the
representative smoker's annual probability of attempting to
quit, the probability of successful cessation given a quit
attempt, and the overall annual smoking cessation rate. (The
absolute standard errors in Table 4 are approximately 1.0
percent, 1.5 percent, and 0.3-0.5 percent for colum ns (i);(ii),
and (iii), respectively.)
26
FIGURE 4.-Changes In the prevalence of cigarette smoking among
sucoessivebirth cohorts of women, 1900-1978.
19Q7-
YEAR
Source: CalculalEd IEOm the rCSUlls ol over 113 00(1 inlerviews 4onduclCtl during lhe.last two
quarter5 0l
1818, promtl¢q tly Division of HeallhJnlerview Slalislms, U.S. Natimnel Center Ior He311h
StalisfC9.
31%
rted
of
no
F .oS
'e r s
fnay
est
Cife
ale
ent
ent
to
fo r
ing
om
~Id
is
n R
Ing
~rn
iar
24)
en
'o r
ta
en
an:
as
d
Dr
al
id
f
d
h
FIGURE 3.-Changes in the prevalence of cigarette smoking among
successive birth.cohorts of inen,,1900-1978.
0
~
N
~
MEN
1921 i-30 ~.
:
-1900
~
1900
0
1930
YEAR
1941-50
5ource. G31cWate0.Irorn tne resulls of o1e113U001nlerviews con0.ucted Ounng 1he last two quarlers
oli
1978. provitletl hyprvislon ol Heal'.h Ihlerview S1911s1ic;,U S Nelional Cenler lortlea IM1
Stabslics-
?
e
FIGURE 6.-Accumulated years of cigarette smoking per person
among successive birth cohorts of women and men, 1978.
o~ 251
0
E
fn 20
19.'
w
ro
U 151
i
I
-1900 1901-101911-201921-3G 1931-40 1941-50 1951-60Blrth Cohort
SOwoc: Seenoles M figures 3 and 4.
37
I
born before 1910, (b) women horn between 1921 and 1940,
who are now approaching 40 to 590 years of age, experienced
the highest smoking prevalence rates. These women have not
vet reached the age wherethe absolute excess deaths of
smokers over nonsmokers are expected to becom e substantial
(1 ). (c) Among successive cohorts of inenn and women, the
age of peak smoking prevalence has declined. Among younger
cohorts, the peak smoking prevalence rates are declining,
although the effect is less marked for women. Men horn
between 19111 and 1o7n reachedd a peak smoking prevalence of
71 percent during. 1946 to 1948, while those born 1941 to
1950 reached a peakk smoking prevalence of 5R percent in
1968 to 1969. Women born 1 021 to 1930 . reached a peakk
prevalence of 44 percent in 19.5R to 196D, while those bornn
in 1041 to 1950 reached. 3 peak smoking prevalence of d1
percent in 197n to 1073. (d). A mong men born 1097 to 1960,
the rate of increase of smoking prevalence was slower than In.
previous cohorts. This slowing of the diffusion of smoking
practices was coincident with the increased publicity
concerning the health risks of smoking and the relatively high
rateo5 ouitting smoking among adult males In the late L9bOs.
A similar effect is not clearly discernible for young women In
this cohort. In both sexes, who are now aporoaching ages 20
to 29, the prevalence of smokingg has apparently peaked.
Smoking rates among men and women in this age group are
now nearly Indistinguishable. Figure 5 depicts the mean age of starting regular
smoking among successive birth cohorts,, calculated from the
same data as for Figures 3 and. 4. The age of onset of
smoking among women declined continuously duringg this
century, to thepoint where it is nearly indistinguishable from
that of men. As aresult, eachh successive cohort of lifelong
continuing women smokers will have an, increasing number of
years of exposure to cigarette smoke.
Figure 6 depicts the accumulated years of cigarette
smoking per capita, up to 1978, for each birth cohort. These
m agnitudes correspond to the total areas under each cohort
prevalence curve In Figures 3 and 4. Among women,
individuals born 1911 to 1.920have thus far experienced the
largest totall exposure per capita. Ho wever, as seen from
Figure 4, unless the smoking prevalence rates of women born
during 1921 to 1940 declinee more rapidly inn the future, the
lifetime exposure of these latter cohorts is likely to exceed
that of the 1911 to 1 070cohort, It is not clear, however,
whether the lifetime exposure of men born from1921 to
35
FIGURE 5.-Mean age of.onset of regular smoking among successive
birth cohorts of women and men..
40
L
>1 35
~ 30
~
~ 25
C/)
~ 1901-10 1911 -p 1921-301931-401~ -~ 195160
Birth Cohort
$OOICE' $E2 nDIB610 FIVlES 3 8n0 4.
36
arette
ncy,
Numerous epidemiological studies and other surveys
performed during the period 195n to 1965 have shown that
for both sexes, especially for wom en, the proportion of heavy
smokers was larger among the younger age groups
(16,1R;21.,22,24,32,3R,62,63). These findings applled to
current daily smoking and lifetime maximum cigarette
consumption. They are consistent with the hypothesis that
regular smokers in past decades consu m ed fe wer cigarettes
per day than contemporary smokers.
The empirical relationships between rates of smoking
cessation (Table 2)ychanges in F.T.C. "tar" and nicotine
delivery of cigarettes (Table 3), and increases In daily
cigarette consumption (Table 4)) are poorly understood (27).
It is not known whether smokers of the lowest"tar"
cigarettes are more or less likely to attempt to quit, or to
succeed in quitting, than smokers of conventional fiitertip or
nonfilter cigarettes. The extent to which the act of switchingg
to a lower "tar" cigarette may serve as a substitute for
quitting may differ among women and men. Tha observedd
increasein daily cigarette consumption among current smokers
could represent the effect of: higher cessation rates among,
lighter smokers; an increase in the smoking frequency of
continuing smokers; or an. increased smokingg frequency of new
entrants into the smoking population; or a combination of
these effects (26). The relationship of these possible
mechanisms to the observed increase in the proportion of
filtertip cigarette andlow"tar" cigarette smokers is not well
elucidated.
Exposure to Cigarette 5 moke A mong Successive Pirth Cohorts
Figures 1 and 4 deplct estim ates of the prevalence of current
cigarette smoking from 19(1p to 197RR among successive birth
cohorts of men and women. Each continuously graphed time
series corresponds to individuals born during a particular
decade. For example, among women horn from, . 1931 to 1?40
(Figure 4), who are now 40 to 49 years old, the prevalence
of smokingg rose ranidly during the post World War II period
and reachedd a peak of 45 percent by 1063. Thereafter, their
overall prevalence of smoking declined to. 3o percent in 1979.
These prevalence data were constructed from the
reported lifetime smoking histories of over 1.3,OOP respondents
to the Health Interview Survey during July to December, 1978.
(For related applications of this methodology, see 9,2P,17).
31
Summary
1. Women have differed from men in their historical
onset of widespread cigarette use, in the rate of diffusion of
quitting rates, are Indistinguishable. Approximately one in
three adult smokers now makes a serious attempt to quit
smoking during the course of a year. Approximately one in
five of those who attempt to quit subsequently succeed.
B. The proportion of adult smokers using tower "tar"
and nicotine brands has increased substantially. In 1979, 39
and men now attempting to quitt smoking, and their reported
1979. In contrast to past years, the proportions of women
smoking declined from 1970 to 1975, but increased in 1978-
7. The proportion of adult smokers attempting to quit
years.
in 1979 represents the lowest recorded value in at least 45
estimate of adult women's smoking, prevalence is 28.2 percent.
The overall smoking prevalence of 32.3 percent for both sexes
declined to below 30 percent. For 1979, the preliminary
percent. Since 1976, the proportion of women smokers has
adult women smokers remained virtually unchanged at 32 to 33
1979 is 36.9 percent. From 1965 to 1976, the proportion of
6. From 1965 to 1978, the proportion of adult men
cigarette smokers declined from 51 to 38 percent. The
preliminary estim ate of adult men's smoking prevalence for
approximately equal to that observed in 1952.
1968-70, and In the period since 1975. The most recent
estimate of 3,900 cigarettes per capita In 1979 is
5. After reaching a peak value of 4,336 in 1963,
annual per capita consumption of cigarettes declined in 1964,
adult men smokers used filter cigarettes.
1964, 79 percent of adult women smokers and 54 percent of
women and men smokers converted to filtertip cigarettes. By
4. Between 1951 and 1963, increasing proportions of
one-quarter until the onset of World War 11.
women lagged~ behind that of men by 25 to 30 years. The
proportion of adult women smoking cigarettes did not exceed'
3. The onset of widespread cigarette use among
use among men approached 70 percent in some urban areas.
during World War II. By 1949, the prevalence of cigarette
By 1925, approximately 50 percent of adult males were
cigarette smokers. Smoking among men accelerated rapidly
War I. Cigarettes rapidly replaced other forms of tobacco.
beginning of the twentieth century, especially during World
elgarette smoking and their use of various types of cigarettes.
2. M en took up cigarette smoking rapidly at the
smoking among each new birth cohort, in their Intensity of
42
1940, now 50 to 69 years of age, will exceed that of
previous generations. With each successive cohort, the ratio
of female to male exposure increasingly approaches one.
As a result of the rapid diffusion of filtertip
cigarettes after 1950 .(Figure1), eachh successivebinth cohort
was exposed to a different proportion of filtertip and
nonfilter cigarettes. Details of the respondent's past history
of cigarette brand use were not obtained in the 1 47A Health
Interview Survey. Suchh data, however, are availablee from a
series of over 4,M!0 intervie ws of current andd form er smokers
aged 71 years and over, conducted by the National
Clearinghouse for Smokingg and Health in 1Q75 ((5). Figure 7
depicts the proportion of years of smoking filtertip cigarettes
among comparablebirth cohorts (the youngest birth cohorts
necessarily differ),. Am ong men, there is a distinct,
monotonically increasing relation betweenn the proportion of
filtertipcigarette exposure and birtK date. The corresoonding
relationship is confounded among.g women, horn before 199(t
reflect their lower sm oking cessation rates and, therefore,
their continued use of filter cigarettes. A woman born in
1925, for example, who begann smoking at age 21 (Figure 5),
and who switched to filtertip cigarettes in 1957 (Figure 1),
has now been smoking filtertip cigarettes for over two thirds
of her smoking career and 4nn percent of her entire life.
The prevalence of cigarette smoking, age of initiation,
lifetime duration of smoking,. and the extent of use of various
types of cigarettes are not the only m easures of cigarette
smoke exposure amongg a particular population. Trends in
depth of inhalation, fraction of cigarette actually smoked, and
other dim ensions of the style of sm oking also affect smoke
exposure. However, as discussed in the 1079 Surgeon
General's Report (76), these are: difficult to determine from
survey data. In vie w of the concern that the accuracv of
contemporaneous survey reports of daily cigarette. consumption
past accounts of the time course of daily cigarette
consumption woutdd be difficult to assess accurately(F7).
N evertheless, the evidence presented in the previouss section is
consistent with the conclusion that the average daily cigarette
consumption among regular cigarette users has increased
am ong each successive birth cohort. As discussed inn the 1979
report of cigarette smoking, trends in depth of inhalation,
fraction of cigarette actuallysmokedy and other dim ensions of
the style of smoking are difficult to gaugee from survey data
(?F ).
38
(14) FORTUNE MAGAZINE. The Fortune Survey. III.
Cigarettes. 12(1): 68, Ut-116, July 1935.
(15) GOTTSEGEN, J.J. Tobacco. A. Study of Its Con-
sumption sumption in the United' States. New York, Pitman
Publishing Corp., 1940.
(16) G RAHAM, E.A. Primary Cancer of the Lung with SpecialConsitleration of Its Etiology. Bulletin
of the
New York Academy of Medicine 27(5): 261-276, May
1951'.
(17) HAENSZEL, W., SHIMKIN, M.B. Smoking Patterns and
. Epidemiology of Lung Cancer in the United States:
'- Are They Compatible? Journal of the National
Cancer Institute 16(6): 1417-1441, June 1956.
(18) HAENSZEL, W.,. SHIMKIN, M.B., MILLER, H.P. Tobacco
Smoking Patterns in the United States. U.S.
'- _Department of Health, Education and Welfare,.
Public Health, Monograph Nb. 45, 1956.
(19) HAMMOND, E.C. Smoking in Relation to the Death- Rates of One Million Men and Women. National
Cancer Institute:Monographs 19: 127-204,
. January 1966. .
(20) HAMMOND, E.C. Life Expectancy of Americam. Men
- in Relation to Their Smoking Habits. Journal
of the National Cancer Institute 43(4):
951 -962, October 1969.
(21 ) HAMMOND, E.C., GARFINKEL, L. Smoking Habits of
- M en and Women. Journal of the National Cancer
Institute 27: 419-442, 1961.
(22) HAMMOND, E.C., GARFINKEL, L. Changes in Cigarette
Smoking. Journal of the National Cancer
Institute 33: 49-64, 1964.
(23) HAMMOND, E.C., GARFINKEL, L. Influence of Health
on Smoking Habits. National Cancer Institute
Monographs 19: 269-285, January 1966.
(24) HAMMOND, E.C., GARFINKEL, L. Changes in Cigarette
Smoking 1959-1965. American Journal of Public
Health 58(1)c 30-45, January 1968.
(25) HAMMOND, E.C., HORN, D. The Relationship Between
. Human. Smoking Habits and Death Rates. Journal
of the American Medical Association 155: 1316-
1328, 1954.
46
rtip
ort
and
ory
Ith
m a
~ers
nal
le 7
tP,s
rts
Ot,
of
ing
n
314
re,
in
5 ),
1 ),
rds
fOn,
bus
ette
~ in
and
pke
eon
ram
of
ion
tte
7).
is
tte
sed
'7q
on,
of
lta
FIGURE 7.-Proportion of years smoking flitertip cigarettes among
successive birth cohorts of women and men, 1975. -
100
90 Zw:
~ ~
U 80i 3 wi i ~
Q
~7°J 7 ;
~ 60~ I I ~ r
;C 50
U) 40
}30
a20i; ;nnl I ~
~ 10 1-j i
-1900 1901-10 1911-20 1921-30 1931-40 1941-50 1951-54
Birth Cohort
Source: Calculaletl from the resulls ol over 4.000 smoking histories o/ men and women who had ever
smoked, collecletl by National Clearinghouse for Smoking and Health (65/.
39
conclusion that the rate of Initiation of smoking among young
men--but not that of young women--Is declining. The future
cigarette use of the youngest generations of women Is uncer-
to cigarette smoke among women are likely to be more
smoked. The health consequences of this enhanced exposure
smoking per capita, the total years of nonfilter cigarette
smoking per capita, and in the total number of cigarettes
to 1940 have experienced substantially higher smoking
prevalence rates that earlier generations. Unless they ouit
smoking In substantial numbers, these women, currently aged
40 to 59, will surpass older women in total years of cigarette
smoke exposure does not hold for women. Women born 1921
successive birth cohort has thus far experienced fewer
cumulative years of cigarette smoking, higher proportionate
exposure to filtertip cigarettes, and lower smoking prevalence
rates. Thiss relationship between birth date and cigarette
16. Among men born during this century, each
use.
lifetime years of smoking that represents filtertip cigarette
progessively sm aller sex differences in the fraction of
man. Each successive birth cohort has also experienced
years of cigarette smoking per woman has progressively
approached the accumulated years of cigarette smoking per
15. With each successive birth cohort, the accumulated
tain.
prominent in the coming decades.
44
Although the accuracy of survey recollection of agee started
smoking, age of sm oking cessation, and the duration of
significant, temporary periodss of abstinence Is not known, no
particular source of recall bias has been identifiied (17,1R).
However, the significantly higher mortality rates of continuing
smokers, as compared to nonsmokers or former smokers
(1,13,19,2n,43,47,48,54), introduces asampling bias that may
understate thee prevalence of past smokingg for the oldest
cohorts. For example, onn the basis of the insurance life
tables recently reported by Co well and Hirst (13), a male
cigarettee smoker at age 32 has an estim ated 75 percent
probability of surviving to age Rny as compared to 49 percent
for a nonsmoker. The estimated probahilities. of surviving to
age. 500 are 90 percent for smokers and 93percent for
nonsmokers, respectively. Therefore, the peak smoking
prevalence rate of in en born before1900,. calculated from
1978survey responses to be 4E6 percent in 1937, could
actually have been as high as 65 percent. Since individuals
who quit smoking have a higher survival than continuing
smokers (1,19,47), the actual point in time at whichh smoking
rates peaked inn this cohort may have been later than 1Q37.
This effect is less likely to be Important among men born
after 1910, who are now approaching 70 years old. A similar
calculation for men born, for example, between 1011-20
reveals that their peak sm oking rate may have been
understated by at most 2 or 3 percentage points. This source of bias is likely to he less important
for
older women. On the basis of age-specific mortality data
reported by Hammond in 1966 (19, Appendix Table 2h), women
continuing to sm oke cigarettes from age 35 would have an
estim ated 49 percent chance of survivingg to age RD years, as
compared to 54 percent for nonsmokers.. The estimated
p.robabll.ities of survival to age 60 would he Q.1 percent for
smokersand 93 percent for nonsmokers. If these survival
data are currently applicable to women smokers and
nonsmokers, then the estimated peak prevalence rate of
smokingg among women born before 1910. could be understated
by only one to two percentage points. Despite these possible biases, the predicted percentages
of current smokers in Figures 3 and 4~4 are consistent with
pastt survey and epidemdological data on the smokingg habits of
different age groups (1.4,. 16-1R,. 21-25, 32,. 37, 3R, 5A).
Comparison of Figures 3 and 4 reveals the following
conclusions. (,a) The most marked differences in smoking
prevalence among men and women appeared in those individuals
32
TABLE 5.-Estimatedpercentage of current, regular cigarette smokers,
Ages 12 - 18, United States, 1968 - 1979.
I of
nost
of
the
of
In
of
iing
(ces
S ).
of
is
7en.
Iing
Q7q
nt.)
be
are
LteS
'ent
in
ent
17
and
of
ime
ing
ded
his
ter
ral
Year
FemaIes
1968
1970
1972
1974.
1979.
1968
1970
1972
1974
1979
Ages 12-14 Ages 15-16 Ages 17-18
0.6 9.6 18.6
3.0. 14.4 22.8
- 2.8 - 16.3 25.3
4.9 - 20.2 25.9
4.4 11.8 26.2
2.9 17.0 30.2
5.7 19.5 37.3
4.6 17.8 30.2
4.2 18.1 31.0
3.2 13.5 19.3
SOURCE:. Natlon-widesurreys performed by National Clearinghouse for
Smoking and Healith, 1968-1974 (64)., and Natlbnal: Ins.titute of
Education , 1979. Current regular smokers In all surveys Include all
those who smoke cigarettes at least weekly. In.1979, approxlmately 90
percent off current regular smokers: used cigarettes on a daily basis.
For 1979 only, 29.7 percent males and 31.9 percent females, aged 19,
were reported as regular smokers.
41
CIGARETTE SMpKING AMONG YOLING WnMEN
Themore marked decline in peak smoking prevalence among
men born between 1951 and 1960, now approaching 20 to 70
years of age, reflected a slowing in the rate of initiation of
smokingg that was not observed in women of the same age
group. This trend.appears too becontinuimg in the next birth
cohort. ' Table 5 reports the results of nation-wide surveys of
teenage cigarette smoking during 1968 to 197q. The most
recent survey, conducted by the National Institute of
Educationn during late 1978 and early lq79, presents the
preliminary results of over ?,fi00 telephone interviews of
individuals aged 12 to 18 years. In this survey, but not in
the others reported in Table 5, women and men. 19 years of
age were also Interviewed. Otherwise, the survey sampling
techniques and interview questions regarding smoking practices
were the same for all the surveys. (See notes to Table s).
The data in Table 5 confirm the conclusion that the rate of
initiation of smokingg among even the youngest men is
declining, an effect that is not present among young women.
These results must be Interpreted in light of sampling
variability. (The absolute standard errors of the 197q
estimates for ages 15-1F and 1.7-1.8'P are about 2 percent.)
As in adult surveys, non-responsebiases must also he
considered. Nevertheless, the findings in Table 5 are
consistent with other nat.ion-wideestim ates of smoking rates
among young women and men. The prevalence of current
regular smoking among respondents 17 to 19 years of age. in
this survey was 2R.1 percent for fem ales and 9?.R percent
for males. The comparable rates for women andd men aged 17
to 19 from the Health Interview Survey were 20.? percent and
27.5 percent, respectively. An analysis of the gro wth of
smoking prevalence among this group, performedd in the same
manner as that of Figures 3 and4, suggested that smoking
rates among this group of wom en gre w. rapidly and exceeded
those of men by 1975. The future smoking habits of this
generation of youngg women cannot be accurately nredicted.Smoking among teenage women is discussed
in greater
detail in the chapter entitled "Psychosocial and Rehavioral
Aspects of Smokingg in. Women" in this Peport.
40
PATTERNS OF SM OKING: REFERENCES
each
Ewer
hate
~nce
efte
921
king
Z it
d
~ette
hette
jttes
Isure
tiore
I
I
(1) ADAMS, E.E. Mortality. In: Smoking and Health.
A Report of the Surgeon General. U.S. Depart-
ment of Health, Education, and Welfare. January
1979, pp. 2-1 to 2-47.
(2) ADVERTISING & SELLING. Marlboro Makes a Direct
Appeal. Advertising and Selling 8:25, March 23,
1927.
(3) AMERICAN INSTITUTE OF PUBLIC OPINION (,GALLUP).
The Gallup Poll Public Opinion, 1935-1971 Series,
pp. 477-1501; 1972-1977 Series, pp. 274-1203.
(4). AMERICAN INSTITUTE OF PUBLIC OPINION (GALLUP).
The Gallup Opinion Index, September 1970, July
1971, July 1972, June 1978.
(5) BAIN; J., JR., WERNER, C. Cigarettes in Fact and
Fancy. Boston, H.M. Caldwell Co., 1906.
(6) BON NER, L. Why Cigarette Makers Don't Advertise
to Women. Advertising & Selling 7: 21, , October
20, 1926.
(7) BORDEN, N.H. The Economic Effects of Ad4ertising,
Chapter VII. The Effect of Advertising on the
Demand for Tobacco Products -- Cigarettes.
Chicago, RichardD.. Irwin, Inc., 1944,, p. 207-
249.
(8). BURKE, H. Women Cigarette Fiends. Ladies Home
Journal 39: 19, June 1922.
(9) BU RBANK, F. ULS. Lung Cancer Death Rates Begin to
Rise Proportionately More Rapidly For Females
Than for Males: A. Dose-Response Effect? Journal
of Chronia Diseases 25: 473 -479, 1972.
(10) CAIRNS, J. The Cancer Problem. Scientific
American 233(5): 64-78, November 1975.
(11). C ONOVER, A.G. Discussion of Elmo Jackson's Paper.
Journal of Farm Economics 32(4, part 2): 923-924,
November 1950.
(12) CONSUMERS UNION. Cigarette Smoking and' Lung Cancer.
Consumer Reports 19:. 54-92, February 1954..
(13) COWELL, M.I., HIRST, B.L. Mortality Differences
Between Smokers and NonSmokers. Worcester,
M assachusetts, State Mutual Life Insurance
Company of America, October 22, 1979.
45
percent of adult women smokers and 28 percent of adult men
smokers reported primary brands with F.T.C. 'tar" delivery
less than 15.0 milligrams. It Is not known whether smokers
of the lowest 'tar" eigarettes are more or less likely to
attempt to quit smoking, or to succeed in quitting, than
smokers of conventional filtertip or non-filter cigarettes.
9. The average number of cigarettes smoked by women
and men current smokers has increased. The relationship of
this finding to recent declines In the average F.T.C. 'tar" and
nicotine deliveries of cigarettes Is not well understood.
10. Withh each successive generation, the smoking
characteristics of women and men have become Increasingly
similar.
11. Among women, the average age of onset of regular
smoking progressively declined with each, successive birth
cohort--from 35 years of age for those born before 1900, to
16 years of age among those born 1951 to 1960. The
average ige of onset of regular smoking among young women
is now virtually Identical to that of young men.
12. Maximum smoking prevalence rates have declined
substantially In recent birth cohorts of men. Men born 1931
to 1940 reached, a peak smoking proportion of 61 percent
during 1960-62, while men born 1941 to 1950 reached a peak
smoking proportion of 58 percent in 1968-69. Men born
1951 to 1960 reached a peak smoking proportion of 40
percent In 1976. Among recent cohorts of women, peak
smoking prevalence rates have declined to a much smaller
extent. Women born 1931 to 1940 reached a peak smoking
proportion of 45 percent in 1966-68, while women born 1941
to 1950 reached a peak smoking proportion of 41 percent in
1970-73. Women born 1951 to 1960 reached a peak smoking
proportion.n of 38 percent In 1976. Among the generation born
1951 to 1960, the proportions of women and men smoking
cigarettes are nowvirtualiy ldentical.
13. The proportions of women and men smokers In each
age group have declined. Among those born before 1951, this
decline In smoking prevalence resulted mainly from smoking
cessation. By contrast, the observed decline In smoking
prevalence among younger men born 1951 to 1960 has resulted
from both smoking cessation and a lower rate of smoking
Initiation. This decline in the rate of onset of smoking
among young men has not been observed for young women.
14. Recent survey data on adolescent smoking habits
reveal that by ages 17 to 19, smoking prevalence among
women exceeds that of men. This finding supports the
43
d
I
0
6.
e
i
(26) HARRIS, J.E. Cigarette Smoking in the United
States, 1950-1978. In: Smoking and Health,
A Report of the Surgeon General. ULS.
Departm ent of Health, Education,- and
Welfare. January 1979, pp. A1 -A29.
(27) HARRIS, J.E. Public Policy Issues in the
Promotion of Less Hazardous Cigarettes. In:
Toward a Less Hazardous Cigarette. Cold
Spring Harbor Laboratory, Banbury Center
Reports (In press)
(28) H OOVER, I.H. Hail to the Chief. Saturday
Evening Post May 5, 1934.
(29), IPPOLITO, R.A., MURPHY, R.D., SANT, D. Staff
Report on Consumer Responses to Cigarette
Health Information. U.S. Federal Trade
Commission Bureau of Economics, August 1979. (30)i JACKSON, E.L. The Consumption of Tobacco
Products: A Descriptive Economic Analysis,
United States 1900-1940. Unpublished Ph.D.
dissertation, Harvard University, 1942.
(31i), JACKSON, E.L. Trends in the Consumption of
Tobacco Products, United States, 1900-1950.
Journal of Farm Economics 32(4, part 2):
881-893, November 1950.
(32). KIRCHOFF, H., RIGDON, R.H. Smoking Habits of
21,612 individuals in Texas. Journal of the
National Cancer Institute 16(5): 1287-1304,
April 1956.
(33) LEWINE, H. Good-Bye to All That. New York:
McGraw-Hill Book Co., 1970.
(34) LEY, H.A., Jr. The Incidence of Smoking and
Drinking Among 10,000 Examinees. Proceedings of the Life Extension Examiners
2: 57-63, 1940.
(35) LIEB, C.W. Can the Poisons In Cigarettes be
Avoided? Reader's Digest 63: 45-47,
December 1953.
(36) MILER, L.M., MONAHAN, J. The Facts Behind the
Cigarette Controversy. Reader's Digest 65:
1-6, July 1954.
(37) MILLS, C.A. Tobacco Smoking:5ome Hints of
Its Biological Hazards. Ohio Medical
Journal 46: 1165-1T70, 1950.
(38) MILLS, C.A., PORTER, M.M. Tobacco Smoking
Habits in an. American City. Journal of the
National Cancer Institute 13: 1283-1297,
April 1953.
47
BIOMEDICAL ASPECTS OF SMOKING
FIG.URE.1.-Age-adiusted death rates' lor all causes.of death
by color and:sex; United Statee, 1950-1977
I500 .
l
5P
NonwM1 n
eMales
/~~
1
~ \
\
000 ~ 109
~ Wn
~te Males
Non wXOeFemales ` __-
700 700
r~ WlilteFemales 500
200 200
1955
1960
1965
'Adjpstedlby the direcv method to theU.SUnpwauon,1940.
SOUflCE;.Data frumitFe Natmnal Center ftr HealtF.SiatOiics..
5h
19]0
1975
03684982
(62) U.S. DEPARTMENT OF HEATLH, EDUCATION, AND
WELFARE, PUBLIC HEALTH SERVICE, NATIONAL
CLEARINGHOUSE FOR SMOKING AND HEALTH. Use
of Tobacco, Practices, Attitudes, Knowledge,
and Beliefs, United States, Fall 1964 and
Spring 1966. July 1969.
(63) U.S. DEPARTMENT OF HEALTH, EDUCATION, AND
WELFARE, PUBLIC HEALTH SERVICE, AND ADULT
HEALTH. NATIONAL CLEARINGHOUSE FOR SMOKING
Use of Tobacco, 1970. June 1973.
(64) U.S. DEPARTMENT OF HEALTH, EDUCATION, AND
WELFARE, PUBLIC HEALTH SERVICE, NATIONAL
CLEARINGHOUSE FOR SMOKING AND HEALTH.
(65) ULS. DEPARTMENT OF HEALTH, EDUCATION, AND
WELFARE, PUBLIC HEALTH SERVICE, NaTIONAL
CLEARINGHOUSE FOR SMOKING AND HEALTH. Adult
'Uke of Tobacco 1975. 1976.
(66) U.S. FEDERAL TRADE COMMISSION. Reports of
°Tar" and Nicotine Content of the Smoke of
Varieties of Cigarettes, 1967-1978.
(67) WARNER, K.E. Possible Increases in the
Underreporting of Cigarette Consumption.
Journal of the Am erican Statistical
Association 73(362): 314-318, June 1978.
(68) WESSEL, C.A. The First Sixty Billions are the
Hardest for the Cigarette Industry. Printer's
Ink 120(5): 3-6, 137-146, January 31. 1924.
(69) WHITTEN, I.T. Brand Performance in the
Cigarette Industry and the Advantage of
Early Entry, 1913 -74. Staff Report to the
U.S. Federal Trade Commission, June 1979.
50
TABLE 2.-Mortalityy ratios for~ female cigarettee
smokers by number of ci&arett.es smoked
per day and age. Females in 74 states.
Number of
cigarettes
per day
Non-smokers
Age Total,35
35-44 45-54 56-64 65-74 75-A4 Age-adjus
1.00. 1.00 1.00 I.nO 1.00 1.00
.9A .95 .99 1.09 1.07 .07
.97 1.22 1.31 I.Ig 1.21 1.19
1.?5 1.54, 1.46 1.51 n5 1.45
1.56 1.96 1.73 1.42 1.63
Ahl Smokers 1.12 1.31 1.27 1.31 1.14 . 1.96
1/ Adjusted by the direct method,using as standard the age
distribution.of, alU women. Not shawn - less than 5 expected deaths.
5(N1RCE: Hamnond, E.C. (6) ..
FIGIIRE 4-Age-adjusted dealh rates' for bronchilis, emohYsema.. and asthma^ by color and
sex:Uniled Slales,1950-1977
30
20
ro
2 1950, 1955 1960 '. 1965 19)0'1995 ~
I
Wh ite Males I
. NonwMte Males
/
~
l
Nomvh l[e Femaln
:1,
/
a
_
l
e J/hue Femalef
30
20
~6tH Rev. 7N Rev Rev
~ Ftljusteb by Ihe dnetr methodto the. U!$. pOPUIanun. 1940
"ICDfithuntl 7th Rev.Nbs.241,y01,502 527,11nr1
8th Rev.Nos.490;493.549,3.
SOVRCE DatatromlheNaUnnalCenterloeHeelViS1ausum
57
um er
th e
ukee
Frette
erbilt
der's
lelvity.
(nited
iience
~terls
IWay.
U.S.
27:
bking
dicaI
~ of
36,
i
stry.
rsity
of
Todd
and
)M1C
'Ious
THE
ited
AND
and
ttee
alth
tion
(55) U.S. DEPARTMENT OF HEALTH, EDUCATION, AND
WELFARE, PUBLIC HEALTH SERVICE, NATIONAL
CENTER FOR HEALTH STATISTICS. Cigarette
Smoking Status--June 1966, August 1967, and
August 1968. Monthly Vital Statistics
Report 18(9): 1-4, Supplement, December
5, 1969.
(56) U6S. DEPARTMENT OF HEALTH, EDUCATION, AND
WELFARE, PUBLIC HEALTH: . SERVICE, NATIONAL
CENTER FOR HEALTH STATISTICS. Changes in
Cigarette Smoking Habits Between 1955 and
1966. Vital and Health Statistics, Series
10, Number 59, April 1970.
(.57) U.S. DEPARTMENT OF' HEALTH, EDUCATION, AND
WELFARE, PUBLIC HEALTH SERVICE, NATIONAL
CENTER. FOR HEALTH STATISTICS. Changes in
Cigarette Consumption. Between. June 1966 and
August 1968. Monthly Vital Statistics Report
19(9): 1-4, Supplement, December 16, 1970.
(58) U6S. DEPARTMENT OF HEALTH, EDUCATION, AND
WELFARE, PUBLIC HEALTH SERVICE, NATIONAL
CENTER FOR HEALTH STATISTICS. Cigarette
Smoking: United States, 1970. Monthly
Vital Statistics Report 21(3): 1- 8,
Supplement, June 2, 1972.
(59) U.S. DEPARTMENT OF HEALTH, EDUCATION, AND
WELFARE, PUBLIC HEALTH SERVICE, NATIONAL
CENTER FOR HEALTH STATISTICS. Current
Estim ates from the Health Interview Survey,
United States - 1976. Vital and Health
Statistics, Series 10, Num ber 119, November
1977.
(60) U.S. DEPARTMENT OF HEALTH, EDUCATION, AND
WELFARE, PUBLIC HEALTH SERVICE, NATIONAL
CENTER FOR HEALTH STATISTICS. Current
Estim ates from the Health Intervie wSurvey,
United States - 1974. Vital and Health
Statistics, Series 10, Num ber 121, December
1978.
(61 )U.S. DEPARTMENT OF HEALTH, EDUCATION, AND
WELFARE, PUBLIC HEALTH SERVICE, NATIONAL
CENTER FOR HEALTH STATISTICS. Changes in
Cigarette Smoking and Current Smoking
Practices Am ong Adults: United States,
1978. Advance Data From Vital andHeatth
Statistics, No. 52, September 19, 1979.
49
and various habits. Information on smoking included: type of
tobacco used, number of cigarettes smoked per day, degree of
inhalation, age at which smoking began, and the brand of
cigarettes usedd from which the "tar" and nicotine content of
the cigarette could be calculated. Nearly 93 percent of the
survivors were successfully followed for a 12 -year period.
Only limited data have been published for the 12-year period
for women; the main body of published data for women is
based on the first 4-year period of the follow-up.
The Swedish Study (1 )
A national probability sample of 55,000 Swedish men and
women was surveyed in. 1963, by a mailed questionnaire to
which 89 percent of the sample responded. Information was
collected on sm oking status at the tim e of the query and at
specified intervals during the previous 9 years according to
type and amount of smoking and degree of inhalation. The
on smoking-related mortality was published in 1975.
questionnaire identified age, sex,, location (urban, nonurban),
Income, and occupation of each subject. A 10-year follow-up
The Canadian Veterans Study (5)
Beginning in 1955, the Department of National Health and
Welfare, Canada, enrolled 78,000 men (~veterans on pension)
and. 14,000 women (mostly widows of veterans) in a study of
smoking-related mortality. Information was obtained on age,
detailedsmoking history, residence, and occupation. During
the 6 years of follow-up, 9,491 of the men and 1,794 of the
women died. No recent follow-up has been reported.
Japanese Study of 29 Health Districts (8)
In late 1965, a total of 265,118 men and women in. 29 health
districts in Japan were enrolled in a prospective study. This
represented from 91 to 99 percent of the population aged 40
and older in these districts. This study provides a unique
opportunity to examine the relationship of cigarette sm oking
to death rates in a population with genetic, dietary, and other
cultural differences from previously examined Western
populations. At the time of the eighth year of follow-up,
60
(39) MILWAUKEE JOURNAL. Consolidated Consumer
Analysis. Annual, 1947-1969.
(40) MILWAUKEE JOURNAL. Consumer Analysis of the
Greater Milwaukee Market. 'diliwaukee
journal, 1924-1979.
(41) NIC HOLLS, W.H. Price Policies in the Cigarette
Industry. Nashville, Tennessee, Vanderbilt
University Press, 1951.
(42) N ORR, R. Cancer by the Carton. Reader's
Digest 61: 7-8, December 1952.
(43) PEARL, R. Tobacco Smoking and Longevity.
Science 87(2253): 216-2T7, March 4, 1938.
(44) PORTER, E.O. The Cigarette in the United
States. South western Social Science
Quarterly 28: 64-75, June 1947.
(45) PRINTERS' INK. Women and Cigarettes. Printer's
.Ink 158(7): 25-27, February 18, 1932.
(46) PRINTERS' INK. Blow Some More My Way.
Printer's Ink 159(2): 20, April 14, 1932.
(47)1 ROGOT, E. Smoking and Mortality among U.S.
Veterans. journal of Chronic Diseases 27:
189-203, 1974.
(48) ROYAL COLLEGE OF PHY5ICIANS OF LONDON. Smoking
or Health. Kent, England: Pitman Medicat.
Publishing Co., Ltd., 1977.
(49) SALES MANAGEMENT. How Critical are Men of
Women who Smoke and Drink? 41(.6):: 36,
September 15, 1937.
(50). TENNANT, R.B. The American Cigarette Industry.
Ne w Haven, Connecticut, Yale University
Press, 1950.
(51) TOBACCO RESEARCH COUNCIL. Statistics of
Smoking in the United Kingdom. G.F. Todd
(Editor). Research Paper No. 1, 1972, and
Supplements 1973-1975.
(52) U.S. DEPARTMENT OF AGRICULTURE, ECONOMIC
RESEARCH SERVICE. Tobacco Situation, various
issues.
(53) U.S. DEPARiIMENT OF COMMERCE, BUREAU OF THE
CENSUS. Historical Statistics of the United
States, Colonial Times to the Present, 1975.
(54),U.S. DEPARTMENT OFHEALTH,. EDUCATION, AND
WELFARE, PUBLIC HEALTH SERVICE. Smoking and
Health, Report of the Advisory Committee
to the Surgeon General of the Public Health
Service, Public Health Service Publication
No. 1103, 1964.
48
Figure3-Agcatlrysled death rales' Ibr malignant neoplasm ol.tracfiea, bronchus and IungJ'
andbreast by color and sev. United Slates,1950-1i977,
BO
70
EO
950 1835 1965 1970 t975
-6th Rev.- .. ]th Hn. Bth Frr.--.
M~~ u.SW .
Ini sm.e .w nn.a. - xe~i2 is~.m e~n H.~~ ao
no.ma
wuxccun. 1ro. r~ rorw.a u...- w..H«Im ss.~.m.
WHITE MALES /
/NONWHITEMALES
/
/ I I
~
WHITE FEMALES
/'
NONWHITE FEMALES
56
OVERALL MORTALITY FOR FEMALES - CIGARETTE SMOKERS
VERSUS NON-SMOKERS .. .
Mortality Ratios
In this report the mortality ratio is the basic means of
comparing cigarette smokers with nonsmokers. It is usually
obtained by dividing a "death rate" (or other mortality
measure) for a classification of smokers by the "death rate"
(or other mortality measure) of a comparable group of
nonsmokers. The "death rate" may differ markedly from one
study to another. In some studies it is calculated by means
of person-years and is a I-year measure; In others it is a
probablity measure; it may be a 5-year, 10-year or, as In the
Framingham Study, a 26-year measure. Differences in
mortality ratios may arise because of these factors.
Because of the arithmetic nature of this ratio, there is
a tendency for lower ratios to result with higher underlying
levels of mortality.. For example, with an underlying mortality
level of 10 percent per year for nonsmokers, the mortality
ratio for aa group of smokers can at most be 10 if all the
smokers died withinthe year. With a mortality level of 50
percent for nonsmokers, the maximum possible ratio Is 2.
Since. "death rates" increase with age, there is a tendency for
the mortality ratios to decline with age, since its range Is
restricted.
For simplicity, ho wever, mortality ratios are used
throughout this review; it is recognized that these ratios are
not strictly' comparable from one study to another nor from
one age group to another.
Amount Smoked and Age
Overall mortality ratios by amount smoked and age are
presented for several of the studies in Tables 2-7. Except
for the Swedish study (Tabla 3), age-adjusted ratios were
calculated for each level of smoking in each study.
Adjustment was by the direct method, using as standard the
age distributrionn of all women In the particular study. For
the S wedish study the age-adjusted values were taken directly
from the report.
Mortality ratios sho wn In Table 2 are considered
especially important since they are derived from the study
with the largest survivorship experience. Mortality ratios
63
CIGARETTE SMOKING AND MORTALITY AMONG WOMEN
INTRODUCTION AND BACKGROUND
Cigarette smoking has been cited as the single most important
environmental factor contributing to premature mortality in the
United States (17). A great many epidemiological studies
support this statem ent.: The emphasis, in general, has been to
study males rather than fem ales. Perhaps themain reason
for this discrepancy is that, in the past, relatively fe w wom en
smoked whereas smoking was common among men. The upward
t~rendd in lungg cancer death rates in males observed in the
1950s by Dorn and, others stimulated epidemiologic studies of
smoking andhealth, especially among males (2,3).
According to the 1979 Surgeon General's Report:
It is important that attention be called specifically to
the mortality that females experience as a result of cigarette
smoking. There has been an increase in smoking among
teenage girls over the past 10 years. At present, the
percentages of teenage boys smoking and teenage girls smoking
are nearly Ident.ical. For some ages, there are more teenage
girl smokers than boy smokers. Over the past 10 years, there
has been, a gradual reduction in the percentage of theaduVt
population that is smoking. Men have quit in greater
numbers than women. There has been only a modest drop in
the percentage of women who are smoking. In Canada and
several European countries, smoking is decreasing among men
but increasing among women.
The present report reviews some of the more important
prospective epidemiological studies on cigarette smoking and
mortality among women.
MORTALITY TRENDS
As background, this section reviews mortality levels by sex
and color inn the United States, by examining recent trends in
overall mortality, and in three causes of death whichh have
been strongly linked to cigarette smoking--ischemic heart
disease, lung cancer and the combined category of bronchitis,
emphysema and, asthma.* These trends are displayed in
Figures I through 4.
"Al2hough asthma may be included in the category,
chronic obstructive lung disease, it is not causally related to
smoking.
53
f ]
e
TAPLF C..-Age-adjusted mortality ratios of female cigarette
smokers, by number of cigarettes smoked per day and
age began smoking. Subjects aged 45-54 at start of
study. 25-State Study.
Number of
clRarettes Age began smoki.ngg
per day ')5+ 15-24
Nonsmokers 1.00 I.nn
I - 9 0.05 O.RR
10 - 19 1.17 1.23
20 - 39 1.33 1 .0; J
40+ .. I.R5
SOURCE: Hanmond, E.C. (6).. I I
..
>'Ratio not shown--less than In expected deaths.
0
73
TABLE F.-Mortality ratios for female cigarette smokers by
_ number of cigarettes smoked per day. Females in
the British Doctors Study.
Number of
cigarettes
per day - Total,
Age-adjustedIJ
Nonsmok:ers
I - 14
15 - 24
25+ 1.001
n.o4
1.54
1.66
Alli Smokers 1.73
I/, Rase&on annual death rates standardized for age.
SOURCE: British Doctors Study; unpubllished data (2).
71
11,R.5F deaths had occurred and there were 1,269,3R2
person-years of observation. For women, however, the main
body of pub.llished data Is based on, 5years of follow-up.
TheRritish Doctors Study (7)
In iiq51., the itritish. Medical Association forwarded to all
Pritish doctors a questionnaire about their smoking habits. A
total of 34,00 0. men and 6,707 women responded. With few
exceptions, alll men who replied In 1951 have been followed
for ?0 years. Further inquiries about changes in tobacco use
and some additional demographic characteristics of the m en
were made in 1QS7, 1066, and 1972. More than in,0n0
deaths have occurred in this population during the past 20
years. For womeny published data are available for 111 years
of follow-up; and unpublished data are available for 27. years
of follow-up.
The Framingham Heart Study (10) The Framingham Study began in 1949 with a cohort of 2,33F
white men and 2,R73 white women who were age 22 to 62 at
the beginning of the study and, were residents of Framingha.m,
~4assachusetts. persons were seiectedby a sample of
households plus enlistment of volunteers. These individuals
were. recalled and examinedd every 9 years thereafter.
The routine ca Miovascular examination consisted of a
medicali history, physical examination, blood chemistries, body
measurements, vital capacity, chest x-ray and a 12-lead
electrocardiopram. Mortalitv and morbidity were documented
in detail fromm the routine biennial examination, hospital
records, death certificates, physician records and the next-
of-kin.
Information on smoking was obtained at the first
examination (and at several thereafter). A series of
monographs and over 741D1YO articles on the Framingham Study
have now 7ecome part of the scientific literature.
nata on the relationship of cigarette smoking to
cardiovascular morbidity andmortai.ity, for both men and
women, have been reported in the Framingham literature, hut
the longest reported follow-up period has been 1R years with
relatively fie w deaths having occurred by then, especially
among the women (11). Data given heiow are based on a
61
longer follow-up period, 766 years, and have not bee
published. The study ispresentty in its 16th biennial cycle.
TheRritlsh-Norwegian Migrant Study (1n),
1°57 for ages 45 to 74, by sex, were as follows.
respondents and deaths occurring amon¢ them from 1963 .. to,
December 31, 1067. The number of morbidity questionnaire
death data for 5 years, from January 1, 1963 through
respondents were then followed for survivorship and cause of
The response ratee to the questionnaire was R#; percent.. Th
of the Rritish and Norwegian immigrants to the United States:
Census. The 12 states Involved contained about three-fourths
which country of birth was recorded in the 1!?60 United Statea
Pritish migrants and 1R,PnO Norwegian migrants to the lJnited
States residing in 12 states. These samples were drawn froni
the 25 percent random sample of the entire population for
cardiorespiratorY disease were sent to approxim ately 97,p00
Including cigarette smoking, as well as symptoms of
Information on personal and demographic characteristics;
In October 1962, morbidity questionnaires requestin
Respondents Deaths Respondents
British 10,103 1,1>:1 9,0{7
Norwegian. 5,002 643 5,337
prevalence study may he briefly summarized. Four syndromes
been published(~13, 14, 15, 1F). The main results of the
with a related cross-sectional study of mortality, inciuding
data on cigarette smoking for women as welll as for men, have
Several reports dealing with the. prevalence survev an
were considered: "persistent couvh and phlegm," "chronlc
bronchitis ;"angina,"and "possihle infarction." The relation
of smoking to the prevalence of these symptoms was clearly
demonstrated for women as well as for men. The mai"
results of the cross-sectional mortality studv indicated
substantial excess mortality for cigarette smokers, 25,
compared to nonsmokers, for both women and men.
62
C
W
~
CD
r;~.
GD
6D
N
TABLE 3.-Mortali.tyratios for female cigarette smokers by
number of cigarette smoked per day and age.
Females in the Swedish study.
Mumber of Age
ci.garettes . . Total, IR-69
per day IR-39 40-49 50-59 FD-69 Age-ad/lusted
Non-smokers 1.0 I.rt 1.0 I:.O 1.0
1- 7 I.n 1.6 1.1 .9 1.0
8~-15 2.3 2.2 1.7' 1.4 1.5
16+ 4.5 7.2 I.g 2.2 2.0
Alll Smokers I.R' I.o 1. 1 1. 1 1.2
SOUR(lE::Cederlof, R., et al (1).
65
I
TABLE 5.-Martality ratios for female cigarette smokers
bynumber of cigarettes smoked per day and age.
Females In.the Framingham Heart Study.
Number of Age
cigarettes Total,. 29-62
per day 29-44 45-54 55-62 Age-Adjusted IJ
Nonsmokers 1.00 1.00 1.00 1.60
<20. 1.42 1.21 I.n7 1.311
20 1.84 1.0 1.13 1.62
21fi 2.25 1.14 ' 1.72
AIISmokers 1.62 1.29 - 1.07- 1.43
1/Adjusted by the direct method using as standard the age
distrlbutionn of all women. -
Not showm - less than 5 expected deaths.
SnURCE: Framingham Heart Study, unpublished data (ln):.
67
For all causes of death (Figure 1), the trend for
females was downwards over the entire period from 19c0-
1977 with a somewhat steeper decline in recent years. The
trend in death rates among males was essentially flat (luring
most of the 1950s and 19[;Rs, but has heen sharply downwards
since the late 1960s.
For ischemic heart disease, the death rate trend for
all sex and color groups was upwards until It flattenedd in the
I°60s. It has been sharply downward since then (pigure 1).
For lung cancer the trend was sharply upwards during
the entire period, especially for females (Figure 1). For bronchitis, emphysema and asthma, the
death rate
has been sharply upwards for all sex and color groups except
non white females. In recent years theree appears to he
leveling off for males but not for white females (Figure 4).
Other investigators have studied these trends, especially In
relation to changes in cigarette smoking habits in the United
States and their potential effect upon mortality from the
smoking- related diseases l9,12). There are inherentt
difficulties in interpreting trend data and in particular in
relating one trend to another.
EPIDEMIOLOG(CAL STUD(ES
During the past gp years, there have beem eight large
prospective epidemiologica(l studies specifically designed to
delineate the relationship between tobacco smokingg and the
devefopm ent of disease. In five of these studies data are
available onn women as welll as men. These studies are
outlined below and in Table 1 f1,2,5,K,R,1~1, To these
published results are added unpublished data from twoo other
studies conducted by the National fieart,. Lung, and plood
Institute, and from the British Doctors Study.
The A merican Cancer Society 25-State Study (a)
The largest study by far Is the American Cancer Society study
of men and women in 25 states. In late I°5n and early 19Fp,
the American Cancer Society enrolled I ,t)7R,g04 men and
women in a prospective study. All segments of the population
were included except groups that could not be traced, easily.
A lengthy initial Questionnaire contained information on age,
sex, race, education, place of residence, family history, past
diseases, present physical complaints, occupational: exposures,
58
TABLE 6.-Mortality ratios for female cigarette smokers by
number of cigarettes smoked per day and age.
Britl'.sh females.
-
Number of
cigarettes
Age
per day
45-54
55-P4
65-74
Nonsmokers 1.00 1.00 . 1..00
<20 1.49 1.09 .79.
20+, 1.85 1.51 d 1.55
All Smokers 1.66 1.25 .98
Total, 45-74
Ag.e-adjusted I,
1.Y5
IJ Adjusted by the. directt method using as standordd the age
distribution of all women. . . .. . . .
SOURCE: Rri'.tish-Norwegi.an Migrant Study, unpublished data (1t!
68
TABLE
Non
<
AII
TABLE 13.-Adjusted mortal ity ratios for males and females
.smoking low tar' and nlcotine cigarettes and subjec
who never smoked regularly.
Sex Mortality ratios
'Low' T/N Nonsmokers
Males ~ . . .. ~ 1.00 0.61
Females ~ - 1.00 ~ 0.74
~
~ Tota1 1.00 0.66
SOURCE: Hanmond, E.C. (7).
78
T.U
generally rose with the amount smoked for each age group
except for the 75 to 84 age group.. The age-ratios were .97
for the 1-to-9-cigarettes-per day group, 1.19 for the 10-
to-19 per day group, 1.45 for the 20-39 group, and 1.63 for
the 40-plus group. For all cigarette smokers the age-
adjusted mortality ratio was 1.26. By age group, mortality
ratios were 1.12 for the 35-to-44 age group, 1.31 for the
45-to-54 age group, 1.27 for the 55-to-65 group, 1.31 for
the 65-to-74 group and 1.14 for the 75-to-84 age groups..
Data from the Swedish study (~Table 3) appear to be
reasonably consistent with the ACS data in Table 2. The 1-
to-7-cigarettes-per-day group had an age-adjusted mortality
ratio of 1.0 (compared with .97 for the 1-to-A group above)
and 2.0 for th 16-plus "group (compared with 1.63 for the
40-plus group above). For three of the four age groups, the
mortality ratios were directly associated with level of
smoking. By age group, the highest mortality ratios were
observed for the two youngest age groups and the lowest for
the two oldest groups. The overall ratio for all cigarette
smokers was 1.2.
For the other studies (Table 4-7) mortality patterns
were generally similar in that mortality ratios tended to be
highest with heaviest sm oking and tended to be lowest at the
oldest ages.
For the Japanese study and the British Doctors Study,
mortality ratios by amount smoked and age were not reported.
However, an overall age-adjusted mortality ratio for female
cigarette smokers was reported In the Japanese study, while in
the British Doctors Study this ratio was obtained fromr unpublished data basedd on 22 years of
follow-up (Table 8).
We list these
studies: along with the overaLl
Study ratios for the other
Total mortali.tyrat.io
age-adjusted
American Cancer Society 1.26
Swedish 1.20
Canadian 1 .31
Japanese 1.28
British Doctors 1.23
Framingham 1.43'
BritishMigrant.s 1.25
Norwegian Migrants 1.28'
70
l
All ratios here are greater than unity. The largest ratio is 1.43 for Framingham. The other seven
ratios are close to one another, ranging from I.? for the ewedishh study ',
to 1.31 for the Canadian study.
Duration of Smoking
Overall mortality ratios for women increased wiithh duration of
the smoking habit based on data from the Canadian and
Swedish studies (1,5). Among Canadian women who smoked
for Kl or more years the mortality ratio, adlusted for age,
was 1.37 compared to a ratio of I.t`R' for women smoking less
than Yt years. In the Swedish studyan excess risk was found
for women smoking 30 or more years (1.4). For those
smoking less than 3n years the ratio was Ln.
Age Regan Smoking
Table Qshows mortality ratios for women who were 455 to 54
by number of cigarettes smoked per day and age began
smoking (6).. Fxceptt for the light cigarette smokers (1-to-
9-per-day),, those taking up the habit at ages 15 to ?.44 had
higher mortality ratios than those who~ started, smoking at
older ages. ' ' -- M ortality data for women smokers, according to age
started, arealso availahlefrom the Swedish study (1 ); age-
adjusted ratios were reported as 1.7, I.6, and 1.1 for age
started less than 17, 17 to Ip, an6 10 plus, respectivelv.
Inhalation
Table IO shows mortality ratios for female cigarette smokers
who were 45 to 54 years of age according to number of
cigarettes smoked per day and degree of inhalation of smoke
(A).No clear pattern emerges. The "moderate-deeo" nroup
had higher mortality ratios than the "none-slight" group in
two of three comparisons.
Table 11 showss mortality ratios for femafe cigarette
smokers by degree of inhalation and age (F). A fairly
consistent qenerall pattern emerges; mortality ratios vary
directly with degree of inhalation. This is seenin, each age
group, except perhaps the I5_to-4d agee group.
TA
72
COMM ENTS
Mortality ratios for women who smoke cigarettes range
from 1.2 in the Swedish study to 1.43 in the Framingham
study. As with men, mortality ratios for women who smoke
cigarettes vary directly with amount smoked, depth of
inhalation, ntare and nicotine content of the cigarette and
duration of sm oking, and varied inversely with the age when
sm oking was started.
In attempting to study cigarette sm oking and mortality
among women, a major difficulty is the lack of large-scale,
epidemiological studies addressed specifically to feTale
populations.. The main findings of this revie w depend heavily
on one study, that of the American Cancer Society. For the
other studies reviewed here, the numbers of women--andof
deaths among them--are often too sparse to permit
m eaningful. statistical analyses. Thus, for example, little can
be said about the survivorship experience of wom en who give
up cigarette smoking. We strongly recommend, where possible,
extending the length of follow-up of women who are alreadyy
enrolled in these prospective studies. It is also highly
recommended that new studies be conducted that are "
specifically addressed to women and smoking-related mortality.
SUMMARY
I. The mortality ratio for womenn who smoke cigarettes
is about 1.2 or 1.3.
2. Mortality ratios for women increase with the amount
smoked. Inn the largest prospective study the mortality ratio
was 1.63 for the two-pack-a-day smoker as compared to
nonsm okers.
3.. Mortality ratios are generally proportional to the
durationn of cigarette smoking; the longer a woman smokes,
the greater the excess risk of dying.
4. Mortality ratios tend to be higher for those women
who begin smoking at a young age as compared to those who
begin smoking later.
5. Mortality ratios are higher for those women who
report they inhale smoke than for those who do not inhale.
6. Mortality ratios for women tend to increase with
the tar and nicotine content of the cigarette.
7. Mortality ratios for female smokers are somewhat
less than for male smokers. This may reflect differences in
80
TABLE 70.-Age-adjusted mortality ratios of femalee
cigarette smokers, by number of cigarettes
smoked per day and degree of Inhalation.
Subjects aged 45-54 at start of study.
25-State Study.
Number of .
clgarettes Degree of inbalation,of smoke
per day None-Slight Moderate-Deep
1 - 9 0..R5 1.04
10 - 19 1.27 1.17
20
- 39
1.41 g
1 . 5?
40+ : 2.i9
X7URCE: Hammond, E.C. (6). ** Ratio not shownr-less than In expected deaths.
TE'
74
Mortality data for female cigarette smokers according
to inhalation are also available from the S wedish study (1);
age-adjusted ratios were reported as 1.1, 1.2, and 1.6 for the
no inhalation, light inhalation, and deep inhalationn groups,
respectively.
"Tar" and Nicotine Content ofCigarettes.
The relationship between overall mortality and the "tar" and
nicotine content of cigarette smoke was recently examined by
Hamm ond, et al. (7). In this study, "tar" and nicotine
levels (TIN) were defined as follows: "High"TJN, 25.8 to
35.7 mg "tar" and 2.0 to 2.7 mg nicotine;: "Mediwm" TIN,
17.6 to 25.7 mg "tar" and 1.2 to 1.9 mg nicotine; "Low'
TJN, less than 17.6 mg "tar" and less than 1.2 mg nicotine.
Table 12 shows the overall mortality ratios of male and
fem alesm okers by these "tar" and nicotine levels. Inn this
instance, the m ortality ratio of the"high" TIN smokers was
represented as 1.00 to illustrate the reduction in overall
mortality that occured with lower TfN cigarettes. There was
a small reduction in the riskk of dying with the use of lower
TIN cigarettes. The mortality ratio was reduced to 0.91 for
the"medium" TIN smokers and was further reducedd to 0.84
for the "low" TIN smokers. The mortality ratios were lower
for women than for men.
In a separate analysis, a comparison was also made
between the mortality ratios of "low" TIN smokers and non-
smokers. These data are presented in Table 13. The
mortality ratio of the "low" TIN group was designated as
1.00. Nonsm okers had overall mortality ratios that were
considerably less than those of "low" T/M smokers.
The combined data from Tables 12 and 13 are shown in
Table. 14 where mortaliity ratios were calculated using non-
smokers as the reference. Combining these data from two
separate analyses that are not exactly comparable results in
figures that are only approximate.
Hammond also compared death rates of smokers of
relatively fe w(I to 9) "high" TfN cigarettes with those of
smokers who smoked relatively large numbers (20 to 39) of
"low" TIN cigarettes (17). The death rates of these two
groups were very similar.
76
exposure to cigarette smoke, such as starting smoking later,
sm oking cigarettes with lower "tar^ and nicotine content, and
smoking fewer cigarettes per day than men.
8. Women demonstrate the same dose-response
relationships with cigarette sm oking as men. An increase in
mortality occurs with an increase in number of cigarettes
smoked per day, an earlier age of beginning cigarette
smoking, a longer duration of smoking, inhalation of cigarette
smoke, and a higher tar and nicotine content of the cigarette.
Women who have smoking characteristics similar to men may
experience mortality rates similar to men.
81
CIGARETTE SMOKING AND MORTALITY AMONG WOMEN:
REFERENCES
(1) BEST, E.W.R. A Canadian study of smoking and
health. Department of National Health and
Wel fare, Epidemiology Division, Health Services
Branch, Blostatistics Division, Research and
Statistics Directorate, 1966, 137 pp.
(2) CEDERLOF, R., FRIBERG, L., HRUBEC, Z., LORICH, U.
The relationship of smoking and som e social
covariables to m ortality and cancer morbidity.
A ten year follow-up in a probability sample of
55,000 Swedish subjects age 18 to 69. Part
I and II. Stockholm, Sweden, The Karolinska
Institute, Departm ent of Environmental Hygiene,
1975, 201 pp.
(3) DOLL, R., GRAY, R., PETO, R. Mortality in rela-
tion to Sm oking: Observations on female doc-
tors. (Unpublished data manuscript, In prepara-
tion).
(4) DORN, H.F. The Increase in cancer of the lung.
Industrial Medicine and Surgery 23(6): 253-257
June 1954.
(5) DORN, H.F. The relationship of cancer of the lung
and the use of tobacco. The Am erican Statistician
(American Statistical Association) 8(5): 7-13,
December 1954.
(6) HAMMOND, E.C. Smoking In relation to the death
rates of one million men and women. In:
Haenszel, W. (Fditor), Epidemiologicab.
Approaches to the Study of Cancer and other
Chronic Diseases, National Cancer Institute
Monograph 19. U.S. Department of Health,
Education, and Welfare, U.S. Public Health
Service, National Cancer Institute, January
1966, pp. 127-204.
(7) HAMMOND, E.C., GARFINKEL, L., SEIDMAN, H., LEW,
E.A. "Tar" and nicotine contentt of cigarette
smoke in relation to death rates. Environ mental
Research 12(3)~: 263-274, December 1976.
(1S)REID, D.D, CONFIELD, J., MARKUSH, R.E., et al.';
Studies of disease among migrants and native'^
population in Great Britain, Norway, and the f
United States. III. Prevalence of Cardiorespira- ~
tory symptoms among migrants and native born in ±
United States. National Cancer Institute Monograph f'
190. U.S. Department of Health, Education and .j
Welfare, U.S. Public Health Service, National "
Prevalence Cancer Institute, Monograph 19: 321- '
346, 1966. ..
(16) ROGOT, E. Cardiorespiratory disease mortality ;,
among British Norwegian migrants to the United
States. American Journal of Epidemiology ~-108(3): 181-191, 1978.
(17) U.S. PUBLIC HEALTH SERVICE. Smoking and Health. -',
A Report of the Surgeon General. U.S. Department ~
of Health, Education, and Welfare, Public Health .
Service, Officeof the Assistant Secretary for -
Health, Office on Smoking and Health. DHEW
Publication No. (PHS) 79-50066, 1979.
84!
(B) HIRAYAMA, T. Smoking inn relation to the death
rates of 265,118 men and women in Japan. A
report of 5 years of follow-up. Presented
at the Am erican Cancer Society's 14th
Science Writers' Seminar, Clearwater Beach,
(9) Florida, March 24-29, 1972, 15 pp.
NATIONAL CENTER FOR HEALTH STATISTICS.
Mortality
from diseases associated with sm oking:
States, 1950-1964. U.S. Department of United
HeaJth,
Education, Welfare,
National Center for Public
Health Health
Statistics, Service,
Public
Health. Service Publication No. 1000-Series 20,
5o. 4, October 1966, 45 pp.
(10) NATIONAL HEART, LUNG, AND BLOOD INSTITUTE.
Proceedings of the conference on the decline in
coronary heart disease mortality. U.S. Depart-
ment of Health, Education, and Welfare, Public
Health Service, National Institutes of Health,
NIH Publication No. 79-1610, May 1979, 399 pp.
(11). NATIONAL. HEART, LUNG, AND BLOOD INSTITUTE. Some
characteristics related to the Incidence of
cardiovascular disease and death: Framingham
Study, 18-year follow-up, In The Framingham.
Study: An Epidemiological. Investigation of
Cardiovascular Disease. Kannel, W.B, and.
Gordon, T. (Editors). DHEWPublication.
No. (NIH) 74-599, February 1974.
(12). NATIONAL HEART, LUNG, AND BLOOD INSTITUTE.
Unpublished data from the Framingham Heart Study
and the British-Norwegian Migrant Study, U.S.
Department of Health, Education, and Welfare,
Public Health Service, National Institutes of
Health, 1979.
(13). PEARL, R.B., LEVINE, D.B., GERSON, E.J. Studies
of disease am ong migrants and native populations
in Great Britain, Norway, and the United States.
II. Conduct of field work in the United States.
National Cancer Institute Monograph 19. U.S.
Department of Health, Education and Welfare,
U.S. Public Health Service, National Cancer
Institute, 1966, pp. 301-320.
(14). REID, D.D. Studies of diseases am ong migrants and
native populations in Great Britain, Norway,
and the United States. I. Background and
design. National Cancer Institute Monograph 19.
U.S. Department of Health, Education, and
Welfare, U.S. Public Health Service, National
Cancer Institute, 1966, pp. 287-199.
83
TABLE 1.-Days lost from work per year due to Illness and injury, per currec
employed person 17 yeara olidand older, by smoking status, sex an
Unllted States, 1965 and 1977. si
Percent off work loss days
1965
Female 17+3..... 5.6 6.6 6.7 4.8
17-44---- 5.5 6.6 . 6.0 ' 4.5
45-64---- 6.0 6.7 7.7 5.3
MaIe
17+3-----
5.7
5.9
6.8
4.6
17-44---- 4.1 4.7 3.6 3.4
45-64---- 7.8- 7.9 9.8 5.6
1977
Female
20+3----- 6.0 6.6 5.4 5.7
20-44---- 6.1 6.8 5.4 5.4
45-64---- 6.4 6.5 5.92 6.5
Male ' '- -
20+3----- 5.3" 5.9 - 6.1 4.2
20-44---- 5.1 6.0 5.5 4.4
45-64---- . 5.6 5.9 6.2 3.9
11nclLdes unknown smoking status. '
2Figure does not meet standards of reliability or precision.
3Ilncludes ages 65 and over.
i
SIXIRCE:. Heaith.Interview Survey, National Center for Health Statistics.
86
Total!) Present Former Never
Smoker Smoker Smoked
t al.
native
i the
pira-
rn in
)graph
and
kional
1 321-
I
tality
Jnited
iotogy
ealth.
kment
l~ealth
for
~HEW
CIGARETTE SMOKING AND MORBIDITY AM ONG WOMEN
The relationship between cigarette smoking and morbidity has
been summarized in the 1979 Surgeon General's Report. That
report contained data from the National Center for HealthStatistios Health Interview Survey (HIS)
sho wing the
relationship for both men and women, between smoking and the
prevalence of selected chronic diseases, the incidence of acute
illness, days lostt from work, days of bed disability, and
perceived health status. This section will present additional
data from the Health Interview Survey on trends in days lost
from work and limitation of activity.
DAYS LOSTi FROM WORK
work-loss days. These calculations were not sex specific.
Certaim modifications in the collection procedures have
lowered the male response rate for the smoking data and may,
thus, make comparisons of more recent data by sexIess than
ideal. However, the data do show that in 1977 the.work-loss
rate: among women who never smoked was higher than in 1965,
while the rates among current smokers remained about the
data, and again the estimate was about 20 percent of all
General's Report presented similar calculations, based on 1974
among current and'former smokers (I). The 1979 Surgeon
and injury could be attributed to the higher rates of loss
approximately 20 percent of all work-loss days due to illness
those who had never sm oked cigarettes. It was estimated that
was obtained by calculating the expected number of work-loss
days if all workers had the same work-loss experience as
the earlier 1965 data to estimate the num ber of "excess"
days lost from work among cigarette smokers. This estimation
The National Clearinghouse for Smokingg and Health used
from~ work by those who never smoked.
reported 6.6 daysIost from work compared to 5.7 days lost
Table 1). Similarly, In the 1977 HIS women who smoke
never sm oked reported losing only 4.8 work -loss days (see
National Health Interview Survey has included questions on
cigarette smoking. For example, in 1965 working women who
smoked reported 6.6 work-loss days; working womenn who had
been observed for both menn and wom en every year that the
Workers who smoke report losing more work days due to
illness and injury than do nonsmokers. This relationship has
85
s
2. Thereis a dose-response relationship between the
women who had ever smoked than for nonsmokers.
(e.g., influenza) for women smokers is 20 percent higher for
3. The age-adJusted incidence of acute conditions
reporting for most of the chronic conditions.
number of cigarettes smoked per day and the frequency of
Additional data from the Health Interview Survey (HIS) is
presented: 'A
1. Currently employed women who smoke cigarettes
report more days lost from work due to illness and injury
than working women who do not smoke. ~^
2. Limitation of activity is reported more comm oniy
among women under the age of 65 who have ever smoked than
among those who never smoked.
9o
TABLE 2.-Percentt of persons with limitation of actiivity duo to chronic con=
ditlons, by cigarette smoking status, sex and age: United State
1965and,1977. -
Tatsi -V Present
Smoker - Former
Smaker Never
Smoked
Percent with limitation
1965
FemaIe
17+------
17.3
12.7
17.3
19.8
17-44---- 8.3 8.8 9.8 7.7
45-64---- 19.5 17.4 22.1 20.2'
65+------ 45.1 39.8 48.6 45.4
MaIe
17+------
17.3
15.3
23.0
17.7
17-44---- 7.3 7.7 8.0 6.2
45-64---- 20.0 20.9 22.1 15.7
65+------ 53.7 52.7 56.3 52~9
1977
Femsle
20+------
17.6
16.0
18.1
18.3
20-44---- 8.0 9.2 8.4 7.0
45-64---- 21.5 24.2 23.9 19.8
65+------ 39.2 36.3 35.5 38'.6
MaIe
20+------
20.0
20.5
24.1
17.6
20-44---- 9.6 12.4 8-3 7.5
45-64---- 25.7 27.5 25.7. 25.7
65+------ 47.5 52.7 47.6 42.5
llncludes known smoking status.
SOURCE: Health Intervlew'Survey, National Center for Health Statistics.
88
urren
x an:
same. This would tend to reduce the number of "excess"
days among women attributable to smoking. There has been a
slight decrease in work-loss among males who never smoked.
Former smokers reported fewer work-loss days in 1977 than
in 1965. Although the difference in work-loss days between
1965 and 1977 is small, it could be attributed to the
assumption that in recent years the former smoker groups
have a greater proportion of people who stopped smoking for
preventive reasons, that is, before they had experienced
serious health consequences.
Further study is needed to determine the association
between "excess" days lost from work by smokers and specific
diseases. Such an analysis would help explain the economic
impact of smoking in the workk place.
LIMITATION OFACTIVITV
The Health Interview Survey also regularly collects data on
the long-term. Impact of chronic illness. Respondents were
asked if chronic illness limited their activities (3).
Estimates of the percent of the population withh limitation of
activity by cigarette smoking status are shown in Table 2 for
1965 and 1977. Detailed interpretation of trend data is
difficult; however, there appears to be a relationshipbetween
smokingand the impact of chronic illness.. In general, the
1977 data, indicate that women under 65 who have ever
smoked are more likely to have a limitation of activity than
those who never smoked. There are no marked differences
between current andd former smokers. Amongelderly women in
1977, there were no differences in limitations of activity by
smokingstatus. .
CIGARETTE SMOKING ANDOCCUPATIONs
The Health Interview Survey provides a considerable data base
on cigarette smoking behavior and occupational status. The
dataa are available from a national probability sample of about
40,000 households for the years 1965, .1966, 1970, 1974,
1976, 1977, 1978, and 1.979. However, only minimal analysis
'See: "Interaction Between Smoking and Occupational
Exposures" in this Re.port..
87
TAfiLE 5.-Estimates of the percentage of current, regular clrtarette ..wters, adulrs ases 11
years and over, according to labor force status and occunation and se.. I1.S., 1n7n.
0
w
~
F ema l e S+a l e
Total Total
17+ 17-44 45-64 17+ 17-44 4S-F4
Total 34.9 36.01 33.7 46.7 40.0 44.4
Currently employed 34.6 36.4 33.7 46.0 4R.7 n4,1
White collar total 34.2 34.9 34.3 41.1 314.4
Pro_fes_sional technical
and kindred 29.1 29.4 26.3 31.7 32.11 30.6
Managers & administrators
except farm 40.9 48.4 3A.3 42.11 47.4 40.n
Sales workers 34.6 35.3 ' 35.7 44.9 4E,R 46.1
Clerical & kindred workers 35.8 35,9 36.4 43.3 45.2 41.5
Rlue collar total 36.5 39.9 33.5 52.8 56.1 49,2
Craftsman & kindred workers 40.4 . 44.4 37.0 51.7 56.1 47.2
Operatlves and kindred workers 36.5 - 40.n 33.5 54.7 57.5 50.7
Laborer, except farm -- 23.3 '25.6 2n,9 50.9 52.0 52.9
Service 35.2 39.3 33.5 49.1 4111.3 51.7
Farm 111.6 25.fi 15.5 34.4 18.7 37.7
Unemployed 38.4 40.8 37.9 52.3 94.4 53.0
Usual activity-housemakers 29.7 37.3 32.3 NA NA
NOTE: Unknown If ever smoked excluded from calculatlon.
Figure does not meet standards of rellabiiity or precislon.
SOURCE: Health Interview Survey, National Center for Health Statistics.
ezosssEo
has been conducted, on this potentially valuable data base (4).
This brief section presents data on smoking patterns for only
two of these periods- -1970 and 1976. Researchers are
encouraged to investigate these date more fully through the
purchase of public use data tapes (2). The im portanceof
this data base increases as new evidence becomes available on
the increased health risks experienced by smokers in certain
occupations. The problems of relatively sm all sample sizes in
high-risk occupations can be partially overcome by combining
several years of the HIS data tapes.. -
Tables 3 and 4 show smoking characteristics of broad
occupational groups--i.e., white collar, blue collar, service
and farm workers--for 1970 and. 1976, respectively. Service
andd blue collar workers, both women andmen, are more likely
to smoke than are white collar and'farm workers, but the
differences are much less among female workers. In 1970,
there were virtually no differences among female white collar,
blue collar, and service workers; more recently, ho wever,there has been a slight increase in
smoking among the latter
two groups. Caution should be used in drawing conclusions
from these data based on differences of only a few
percentage points since such differences can be well within
sampling error. White collar workers who smoke tend to be
heavier smokers than other types of workers, and this pattern
is more narkedamong female white collar workers.
The proportions of cigarette smokers by more detailed
occupational classes are shown in Tables 5 and 6 for 1970
and. 1976. Within three of four subgroupsof white collar
wonkers- -professionals, managers, and sales people- -the.
proportion of smokers among women is the same as for men
in the same occupational group. This also appears to be true
for laborers, who sho w the highest levels of smoking among
both womenn and men.
SUMh1ARY
The 1979 Report of the Surgeon General summarized the
information on smoking and morbidity asfollows:
1. In general, fem ale current cigarette sm okers report
more acute and chronic conditions Including chronic bronchitis
and'/or emphysema, chronic sinusitis, peptic ulcer disease, and
arteriosclerotic heart' disease, than women who never smoked.
89
SMOKING AND CARDIOVASCULAR DISEASE IN, WOMEN
INTRODUCTION
While the mortality and morbidity rates of coronary heart
disease (acute myocardial infarction and chronic ischemic
heart dise:ase): (CHD) are lower for womenn than men, CHD
still represents the major cause of death among women in the
U.5. In 1976, the United States recorded 284,055 female
deaths as attributable to this cause (Table 2). The
difference in m ortality rates between the sexes is more
marked for acute myocardialinfarction, with males of all
ages experiencing 189 deaths and females 111 deaths per
100,000 (Table 1). Observed differences by sex in
susceptibility to coronary heart disease are not fully
understood but appear to be affected by multiple specific-risk
factors within any demographic group. .
McGill and Stern have recently provlded an extensive
revie w of sex differences in susceptibility to atherosclerosis
in hum ans and in experimental anim als, including an analysis
of factors kno wn to predispose to atherosclerosis and its
dependent diseases (24).
MORTALITY RATES
In the United States, the National Center for Health Statistics
has reported mortality rates from acute myocardial infarction
and chronic ischemic heart disease classified by age, sex, and
race, for the years 1968 and 1976 (Tables 1, 2, 3) (32),.
These tables show that mortality rates for acute myocardialinfarctionl
am ong adults up to age 64 are highest for white
men and are succeeded by progressively lower rates for other
men, other women, and finally, white women. Mortality rates
for chronic ischemic heart diseases vary. The rates for white
men are second to those for other men and close to those for
nonwhite women; again, however, rates for white women are
by far the lowest. Bothh white and nonwhite women show
consistently lower rates until extreme old age.. However, the
differences narrow markedly in age in comparison with those
in young adulthood and middle life (Table 1).
Male-to-female mortality ratios for acute myocardial
infarction among adults in their 30s or 40s are approximately
5 to 6 for whites and 2 to 3 for nonwhites; among adults in
96
TAPLE 3.-Percent distribution of the population 17 years and over by cigarette smeking status,
according to sex
and occupation category, United States, 1970.
Sex and occupation category Total Never Former Present Present smoker,--
populationl smoked smoker smokerf Total2 <15
FemaIe
Total populatlon------------.--- 100.0 54.0 11.2 34.4 100,0 39.3
Total currently taployed------ 1n0.0 54.3 11.1 34.5 1n0.n 38.7
White collar workers-------- 100..0 53.7 12.6 34.2 1U0.u 37.6
Plue collar workers------.--- 100.0 55.1 8,5 36.1 100.0 40.7
Servlce workers------------- 100.0 55.7 0.2 35.2 100.n 41.6
Farm workers---------------- 100.0 74.3 7.5 18.6 9n0,0 49.2
Total populatlon--------------- 100.0 ?8.8 . 24.9 46.2 100.0 25.8
Total currently employed------- 100.n 28.g 75.2 46.0 100.0 25.5
Whlte collar workers-------- 100.0 31.6 70,1 39.3 100.0 23.0
Blue collar workers--------- 100.0 24.9 22.4 57.8 100.0 25.5
Service workers------------- 100.0 31.1 70.9 48.1 100.0 31.1
Farm workers---------------- 100.0 40.7 24.8 34.4 100.0 35.5
1Excludes unknown If ever smaked.
2Excludes unknown amount of clcarettes smoked.
*Flgura does not meet standards of reilabillty or precision.
Sr7UIKE: Health Interview Survey, National Center for Health Statistics.
! oi clgarette3 per day2
15-24 25+
42.4 19.2
43.3 18.0
47.g 19,6
44.4 74.9
fit.n 17:4
e33.3 e19.0
45.1 29.1
45.3 29.3
43.4 37.n
46.4 28.0
43.3 25.6
45.1 19.4
izos6sco
TABLE 4.-Percent distribution of the population 20 years and over by cigarette smoking status,
according to
sex and occupation category, United States, 1976.
Sea and nccuprttun category Total Nerer Former Present Present smokers-- 9 of clgarettet per day2
populationt smoked smoker smokers Total2 <15 15-24 25
FemaIe
Total GoCulation--------------
Total currently enqloyed------
Whlte collar workers-------
Blue collar workers --------
Service workers------------
Farm workers---------------
MaIe
1n0.n 54.3 13.9 32.0 100.0 36.5 43.9 19.6
ina.n 50.9 13.3 35.9 100.11 36.5 44.11 19.5
100.0 51.1 14.6 34.3 700.0 35.3 42.4 7?.3
100..0 50.7 10.2 39.11 100.n . 39.0 . 44.3 17.6
100..0 49.1 11.9 39.0 100.11 37.9 48.3 13.7
1n0.0 59.8 31.3 1n0.11 34.6
Total populatlon-----........ - 100.0 29.? 2P.9 41.9 1n0.0 ?4.7 44.R 31.1
Total currently-------------- 10n.n 29.5 )7.1 43.a _ 10p_n ?1.0 45.4 12.8
White collar wnrkers------- 100.0 34.0 79.4 36.6 1UO.n Rn.R 43.< 35.6
plue <otlar workers----rv-c 1n0.n 24.3 25.3 50.4 1nn.n ?1.7 47.4 31.5
Service workers------------ 10n.0 20.4 73.4 47.7 100.0 77.6 40.0 32.4
Farm workers 100.0 34.9 9.8.7 36.9 100.0 70,4 44.0 75.7
1E.cludes unknown If ever smoked. 7Eecludes unknown amount of cigarettes smoked.
FlRure does not meet standards of rellablllty or preclslon.
S(N1RCE: Health lntervlew Survey, Natlonal Center for Health Statistics.
zzos99Eo
TABLE 6.-Estlnates of the percentage of current, regular cl8arette smokers, adults a6ef 20 years and
over, according to labor force status and occunation and sex, U.S., 1976.
Vzos9sCo
Total ,
Currently e,mployed
Whlte collar total '
Prafesslonal technical
. and kindred
Managers & adnlnlstrators
eccept farm
Sales worker,
Clerical & klndred workers
Blue collar total
Craftsman 6 klndred workers
Operatires and kindred workers
Laborer, except farm
Service .
Farm
Unenyloyed
Usual attlvlty-homemakers -
---~ Fanale -MI.-le
Total Total
- 20+ 20-44 45-64 70+ 20-44 45-64
32.0 <6.9 34.6 41.9 47.6 41.3
35.9 37.0 36.1 47.4 . 46.8 39.7
34.3 33.8 36.9 36.6 38.6 35.3
29.1 ~ 79.6 32.7 30.0 31.1 79.9
,
41.6 42.7 40.8 41.0 46.4 36.1
38.1 . 37.0 42.6 39.9 42.6 3P.0
34.8 34.7 36.0 40.4 40.1 44.2
39.0 43.7 33.6 50.4 54.1 44.3
40.5 r 46.9 35.6 48.0 52.1 41.6
37.6 42.5 31.7 52.3 55.3 46.2
56.3 52.6 53.7 56.9 51.7
39.0 42.8 37.2 47.2 51.1 44.P
31.3 51.0 36.9 45.4 35.0
40.0 41.0 39J 56.11 59.9 53.?
29.0 37.1 32.2 NA NA NA
NOTE: Unknown if ever smoked excluded from calculatlon.Flsure d_eef not meet standards of
rellabllity or peclslon. -
SIIURCE: Health Intervlew Survey.;Natl,enal,Cente,.1fo(.HealtIAtH'A{
"i"
TABLE 5: DEATH FRQN ISCHEMIC HEART DISE_ASE_ AND_ S_MO_KING_ H4BITS_ WHEN LAST ASKED
BRITISH PHYSICIANS 1951-1973
ANNDAL DEATH RATE PER 100,000
Total PERSONS STAFDARDIZED FOR AGE X2
Popul. Non-smokers Ex-smokers Current Smokers - Dose Per Day Non-smokers
Number of -- VS.
Deaths 1-14 15-24 ~ 25 others Trend
,
Women 6194 179 138 126 132 304 292 ---. 21.14=.
- - ; (number of cigarettes)
Men* 34440 3191 413 533 501 . 598 . 677 22.59=
=(P<0.001) ' `
Source: *Doll, R. (6A) +Doll, R. (68)
SEOS99E0
(1 gram -= 1 clgarette)
53.56=
A recent study examines the cause-spec.ific mortality
of 6,194 British women physicians over the period 1951 to
1973 (6A). Table 5 presents the results of this study in
conjunction with the previously publishedd results am ong m a1e
physicians during the same period (68). The clear association
of cigarette sm oking and ischemic heart disease previously described in males was confirmed in
female physicians. For
women who reported smoking 15 or more cigarettes per day,
m ortality due to ischemic heart disease was more than double
that of nonsmokers.
Although the results demonstrated a similar effect of
smoking inn the development of ischemicheart disease in both
m ale and female physicians, the association of sroking, with
heart disease was less striking in women physicians. ischemic
heart disease was less prominent as a proportional cause of
death in this population of women than in male colleagues (16
percent vs. 32 percent of all deaths). Ischemic heart disease
mortality was only 26 percent higher for all ever-smoked
women than for never-smoked women. However, for females
who smoked heavily (>25 cigarettes per day), the relative risk
of death from ischemic heart disease was 2.2, a finding
consistent withh that demonstrated in males, who had a relative
risk of 1.6.
In such studies, standardization for amount smoked
daily by each of the sexes does not, however, correct for
differences in. age at initiation of smoking and degree of
inhalation. This fact greatly complicates comparison of the
magnitude of biologic effect in the two sexes. This "cohort
effect" (i.e., unm easured but documented dissimilarities in
total sm oking experience) may lead to an erroneous
interpretation that cigarette smoking is less dam aging to
women than to men. This issue cannot be resolved until
studies examine the effect of smoking in more recent cohorts
of women whose lifetime smoking behavior is more similar to
that of men.
Among 26,467 Swedish women observed during a 10-
year period, the risk of developing fatal coronary heart
disease was significantly higher am ong sm okers than
nonsmokers (49)~. The relative risk was 1.9 at ages 40 to 49
and 1.3 at ages 50 to 59. An extensive mortality study in
Japan also reported a highly significant increase in deaths
from ischemic heart disease among female smokers, with a
mortality ratio for smokers of 1.6 (28).
Coronary heart diseasee morbidity data are available on
women from prospective studies in Framingham, Massachusetts,
TABLF 4.-Coronary heart diseaae mortality ralios related Ib smoklny - profpectiw atudies IAelud
nunber o/ deadls Nown invarenlhesnll ISM Senokers NS -Nom
smokenI
elulbp!, Numbe. aJ FueluwNumbn
IyVeof nafe up ol C~ga~Nfn.Jay
caunlry pppulalqne (Ollevlion lyearel d<a1M1f
Heminord 359 56< Ouef/ionnaile 6 1<g19 Malel Femalef
u.d end /nlb.uoC
eadm.el, 4<5e925 urdeamevo-
1949' lematei ae< uu NS ........ 1.00 1 p0
US.e. .U-a0a1
mrv 19 . 1.21 091
1019..:. IOn 1]2
20 ]0 :....... 1)5 1.52
)ao _._.. 1.// 061
Snu.<e U S. Punl.[ Hea/ln Seiu,ee 143, «1.
C9na.
Pipe,
Maln 16ane1 P
39 dennr
40 e9 5o -59 E4 69 20 19
N5 I Oo 1 0U I UO 1 po
19 ,. l00 150 1.e9 L1<
IU19~~.... 2.39 2.13 1.82 1,41
20.q0,,.... 0]4 2AU 19, 1.49
)a0 351 2./9 1]1 1 <7
Female,
NS . lU0 I0U 100 100
19 _ 1.31 1.15 10C 0.>4
10~19 ..~.,. 204 2.3I 1.>9 098
20.]0.... 362 2 ].89 200 1.2)
je0 . , <].JI 3]3 .202
Fqe Variation Commenta
EEOS6Z9E0
increase in conjunction with the amount and duration of
smoking.. -
AA study of the intramyocardial arteries and arterioles
of the heart in 13 women and 21 men who were nonsmokers,
and 16 women and 27 men who were smokers, indicated that
proliferative lesions in intramyocardial arteries were more
advanced'relative to age in smokers than nonsmokers. Itt was
also found that subendocardial arterioles were thickened in
smokers. A separate analysis by sex was not performed, but
the authors remarked that the lesions developed as rapidly and
as extensively in wom en as in men inn both sm oking andnonsmoking groups (27).
-
Studies of the severity of atherosclerotic plaques in
the arteries of women who smoked in comparison with those
who did not smoke involve too few subjects to be satisfactory.
Investigating the relationship of these arterial lesions and
cigarette smoking In women is fundamental to understanding
the occurrence of heartt attack and other ischemic diseases.
Coronary Heart Disease
Coronary heart disease (acute myocardial infarctionn and
chronic ischemic heart disease) occurs with greater frequency
in smoking than in nonsmoking women. The prospective study
of Hammond and Garfinkel, published in 1969, included data
on approximately 446,000 women between the ages of 40 and
79 (9). The increase in mortality ratios in conjunction with
increasing numbers of cigarettes smoked per day for various
ages is shown below in Table 4 (43,44). Mortaliity ratios
were higher for younger ages and lower for older ages.. The
one-pack-a-day srnokerts risk of deathh from heart attack was
approxim ate.ly twice that of the nonsm oker. The prospective
data of Shapiro and colleagues are based' on a population of
120,000 men and women (35).. Using a sampling factor of
about one-thirtieth, they examined 4,301 women at risk of a
first myocardial infarction between the years 1962 and 1964.
The smokers compared with nonsmokers had roughly twice as
many rapidly fatal heart attacks and heart attacks that were
not fatal within, 48 hours. The ratioo was approximately 2.9
among younger women aged 45 to 54 and 1.8 for the subjects
aged 55 to 64. Heavy smokers had higher ratios, but the
data did nott permit a detailed study of dose relationships or
of the experience of female ex-smokers.
102
for heart attacks at younger and older ages, for recent and
old infarcts, and coronary occlusion without infarct, and for
stenosis, as well as for complicatedd and calcified lesions and
raised plaques in the coronary arteries (40).
Itt should be noted that the grading of atherosclerosis
at autopsy is nott a simple matter because there are several
types of lesions and several ways of evaluating or measuring
them. Moreover, the development of the different sorts of
lesions is not necessarily parallel. Sternby provides a useful
discussion of issues in the grading of atherosclerosis (39).
Nevertheless, the major studies noted above provide strong
evidence that women have less coronary atherosclerosis on the
average than men of the same age in the samepopulatione
w
.
RISK FACTORS
Factors present in Individuals which correlate with future
liability to disease are risk factors for that disease. In the
case of heart attack, for example, it has been sho wn that
age, m ale sex, cigarette sm oking, hypertension, elevated blood
cholesterol, and several, other conditions are positively and
independently associated with the probability of heart attack.
Thelevele of high-density lipoprotein cholesterol in the serum
has a negative correlation with heart attack; thatt is, higher
levels areprotective. The various risk factors have been
identified for both men and womenn and have been shown on
muttivariate analysis to be Independent. A combinationn of risk
factors is synergistic, producing an associated risk greater
than the simple sum of the individual risks. Although the
data for women aremucfi less extensive than for men, they
indicate that cigarette sm oking is a major risk factor for
heart attack in women.
THE EFFECT OF SMOKING
Atherosclerosis
There is little autopsy inform ation about the amount of
atherosclerosis in women smokers. Sackett and his associates
reported on aortic atherosclerosis among bothh men and women: -
of their 450 female subjects, 309 were nonsmokers, 52
smoked less than a half pack per day, and 89 smoked more
(33). Mean, age-adjusted aortic atherosclerosis was found to
101
locial
iomen
4')
~
ore
fo r
~
2hos
i
the
mong
aring
k of
oral
Pmen
fhese
t of
se a se
that
~r In
s (as
Ile ve l
high-
rate
s was
conducted in Ne w York City, Shapiro and colleagues reported a
positive association between the development of angina
pectoris and smoking among men and a nonsignificant positive
trendamong women (35). Among patients with angina
pectoris, sm okinglowers the exercise threshold for the onset
of angina (44). Only male patients have been studied thus
far; equivalent data apparently have not been published for
women with angina and angiographically proven coronary
atherosclerosis.
Corebrovascular Disease
The incidence of stroke as a manifestation of cerebrovascuiar
disease appears to be somewhat greater in men than in
women, but the difference is small (20, 29, 42).
In an autopsy assessment of cerebrovascular
atherosclerosis, Sternby reported more atherosclerosis of thee
com mon carotid artery and the carotid sinus in men than
wornen.. There was also more intracranial atherosclerosis of
certain vessels in m en than women. Ho wever, using the
area-grading m ethod, no sex difference was found in total
intracranial atherosclerosis (39). The International
Atherosclerosis Project also reported a slight excess of
cerebrovascular atherosclerosis am ong m ales (23). On the
whole, the available pathological evidence suggests a minor
increase in cerebrovascular atherosclerosis among men in
comparison with women, although some studies fail to confirm
this conclusion. (see 39).
It is not clear whether smoking is a risk factor among
wo.menn for the development of atherothrombotic stroke. Kannel
has discussed the issue and the current literature in somee
detail~. (18). The Framingham Heart Study has reported a
dose-related correlation between the incidence of
atherothrombotic stroke and cigarette smoking in men but not
in women. The extensive prospective study of Hammond and
Garfinkel, which involved almost 446,000 women and recorded
1,905 deaths fromm cerebrovascular disease during a six-year
period,, found thav smoking was a positive correlate for such
mortality (9); in both -nen and women, the mortality ratio was
increased by roughly 2 or 2.5 times (Table 7) (~43, 44).
That some of these deaths may have involved
subarachnoid hemorrhage rather than brain infarction is
suggested by a recent report that found the incidence of
subarachnoid hemorrhage to be positively associated with
109
Tecumseh, Michigan, and the greater New York areas. The
Tecumseh data of 1967do not sho w a relationship of such
morbidity with smoking (Table 6) (7). The Framingham Heart
Study found an increased risk for women smokers, but the
associations were weak (18, 19).
The study of Shapiro and colleagues considered both
mortality and m orbidity (35). It reported separately on
deaths within 48 hours of onset and on all definite myocardial
infarctions after that tim e interval. Using this classification,
the incidence of coronary heart disease among women smokers
was distinctly higher than it was among nonsmokers.
While there is somevariabiiity in the strength of this
association, the data from the various prospective studies of
m ortaiity and morbidity from coronary heart disease establish
smoking as a positive correlate, or risk factor, for women.
However, the risk ratios tend to be smaller than for men at a
given level of cigarette consumption in all age groups. This
trend may result from the different sm oking patterns reported
by men and women who smoke the same number of cigarettes
per day (6a, 6b, 24). Men generally begin smoking at an
earlier age and have thus smoked for a longer time period
than women. Men also inhale more often than women and are
more likely to smoke more than half of a cigarette. These
smoking styles would expose men to a larger dose of smoke
per cigarette and a larger lifetim e am ount' than that
experienced by women. Case controland retrospective studies of wom en who
havee had heartt attacks have suggested an increased incidence
of heart attack among smokers. For example, a case control
study of 55 women who had heart attacks before age 50 (an
uncomm on event inn women) found that 89 percent were
smokers in contrast to 55 percent in a control group without
myocardial infarction. Heavy smokers (35 or more cigarettes
per day) had an estimated myocardial infarction rate
approxim ately 20 times that of the nonsm okers. As far as
possible, women using oral contraceptives and those with other
identifiable risk factors were excluded from the study(.36).
Spain and his associates conducted a retrospective
autopsy study of women who had died suddenly of coronary
heart disease and compared this verified diagnosis to the
wom en's sm oking habits as reported by the closest living
relative (37). Only witnessed sudden deaths were included
in the data.. Comparisons were made between women who had
died' of coronary heart disease and women who died suddenly
of causes other than heart attack. It was found that 62
no6
their 70s and 80s, they are roughly 1.6 and 1.4. The actual
number of deaths involved is very large; their distribution by ~
age, sex, and race is shown in Table 2. Between 1968 and k'
1976, a striking declinee occurred in the acute myocardial ~
infarction mortality rate for men and women of all ages andr0
races. - i
These are shown as percent changes of rate in Table
.
3. The percent changee has beenn larger at younger ages
(Tables. 2 and 3). The changes for chronic ischemic heart
disease are similar butt less dramatic (Table 3).
ATHEROSCLEROSIS
Differences in heart attack mortality rates among men and
women parallel pathology data concerning atherosclerotic
plaques of the coronary arteries. The International
Atherosclerosis Project systematically collected autopsy
observations on persons from 14 geographicc locations and 19
ethnic groups in different parts of the world, and found that
women from i U of the 19 groups, when compared to their
m ale counterparts, had as much as or even more aortic
atherosclerosis.. Men aver age 39 had more raised plaques in
their coronary arteries than women (23).
These findings indicate that the occurrence of coronary
plaques: was paralleb, to heart attack rates, but that the
occurrencee of aortic lesions was not. Coronary plaque
severity had a male-to-female ratio of 1.61 among whites
and of 1.14 among blacks. Studies of a white population in
Sweden. (39) and of western Europeans from five locations
(17) demonstrate similar findings: a clear excess of coronary
atherosclerosis among men and a similiar severityofi aortic
atherosclerosis among men compared to women.
Autopsy studies thus show a selective liability of the
m alecoronary arterial bed for atherosclerosis, as compared to
the female, especially among white men but also among men
of other races. The pathological f~ihdings are congruent with
the clinical data on heart attack mortality rates. Autopsy
studies also show that, among men or women with manifest
coronary heart disease, women patients have roughly the same
prevalence of advanced atherosclerotic lesions of the
coronaries as men (40). These data suggest that the amount
of atherosclerosis necessary to precipitate a heart attack is
the same, on the average, in both sexes. This generalization
about the amount of coronary atherosclerosis appears to hold
100
colleagues (26). Diabetics were excluded from the report.
There were 164 male and 53 female patients. The late
patency rate of the vascular reconstruction was followed for
I to 4 years.: The authors reported that the number of
cigarettes smoked before surgery did not influence the
outcome, but cessation of smoking after surgery had a
favorable impact. Therewe.re no significant differences in
outcomebetween men and women. The patency rate 4 years
after aortofemorall surgery was. 90 percent in those who
smoked five or fewer cigarettes per day after surgery and 75
percent in those who smoked a greater amount. Following
femoropopliteai reconstruction, the 2-year patency rates were
95 percent for those who stopped smoking, 75 percent for
those smoking as many as 15 cigarettes per day, and 65
percent for those who continued to smoke more than 13
cigarettes per day. .
Aortic Aneurysm
Studies have not been reported for women with respect to
atherosclerotic aortic aneurysm and smoking. Deaths for
women are about one-fifth those for men (9). -
Hypertension
Smoking is not associated with an increased prevalence of
essential hypertension in m en. or women (38). Ho wever,
sm oking does combine with hypertension (and other risk
factors) as a risk factor for heart attack, synergistically
compounding the risk. Two recent case control studies of rapidly progressive,
severe or malignant hypertension have found that there is an
overrepresentation of sm okers among patients with this
uncommon phase of hypertension (3, 12). In one study of 82
patients who developed malignant: hypertension, 67 were
smokers. Thirty-three of those were women. In the study,
77 percent of the fem ale patients with malignant hypertension
smoked, and only about 44 percent of those with essential
hypertension and of the general female population smoked.
The difference is highly significant. A simiiar and parallell
study of 48 patients with malignant hypertension contained 33
men and 15 women; 25 men (76 percent) and 8 women (53
percent) were smokers compared with 44 percent and 30
112
percent of the women suffering sudden cardiac death were
heavy smokers in contrast with only 28 percent of thecontroi
group. For those who smoked heavily, the: mean age at death
was 19 years younger than that of nonsmokers; lighter
smokers died at an intermediate mean age.
In a retrospective study emphasizing psychosocial
variables, Talbott and associates reported on 64 white wom en
who died suddenly of arteriosclerotic heart disease (41).
They found that women who died suddenly smoked more
cigarettes than thee comparison group. The relative risk for
those smoking more than a pack a day compared with those
smoking less than a pack a day was 3.9 (p <.004.),
Smoking, as well as other risk factors, raises the
already som ewhat higher risk of myocardial infarction among
women who use oral contraceptives. During the child-bearing
years, the use of oral contraceptives doubles the risk of
myocardial infarction; women who both smoke and use oral
contraceptives have approxim ately 10 tim es the risk of wom en
who neither sm oke nor use oral contraceptives (13). These
issues are considered below in a separate section.
Cessation of Smoking and "Tar"andNicotine
Content of Cigarettes
Existing data are inadequate to determine the effect of
smoking cessation on the incidence of coronary heart disease
in wom en. Hamm ond and associates (have reported that
mortality rates from coronary heart disease were lower in
women who smoked low-"tar" and low-nicotine cigarettes (as
sold in the196Ds)than in those who smoked medium level
products, and still lower than for those who smoked high-
"tar" and high-nicotine products; even so, the mortality rate
for those women smoking low-"tar", low-nicotine products was
significantly higher than that of nonsmokers (10).
. Evidence considered below suggests that stopping
sm oking is beneficial in the treatm ent of women suffering
from peripheral vascular disease.
Angina Pectoris
The Framingham. Heart Study reported that there was a
positive association between smoking and angina pectoris
among men but not among women (19):. In an extensive study
108
times that of nonusers; and the relative risk for women who
used both cigarettes and oral contraceptives was 22 times as
great. Past users of oral contraceptives also had an increase
In relative risk, but an analysis of risk was not possible
because of the small num ber of cases (30).
The risk of myocardial infarction In wom en is
increased by cigarette smoking and by the use of oral
contraceptives; It is compounded when both are used together.
For example, Mann and associates reported a retrospective
study of 63 women below the age of 45 with acute myocardial
infarction. The proportion of heart attack patients who had
usedd oral contraceptives In the previous months was signifi-
cantly higher than expected. The relative risk for myocardial
infarct:ion among women smoking 25 or more cigarettes per
day was 11.3 times greater than that among nonsmokers.
Moreover, there was evidence for synergism of the two risks
(22).
Jick, et al. reported a case control study of 107
women under age 46 who were discharged fro m the hospital
after suffering nonfatal, acute myocardial infarctions
(14,15,16), The annual risk of nonfatal myocardial infarction
(MI) among healthy women aged 39 to 45 who both smoked
and used estrogens for noncontraceptive purposes was
approximately 1 In 750. They noted that aithoughh an acute
myocardial infarction is uncommon in healthy young women,
the riskk appears to be substantial inn women over the age of
38 who both use estrogens and smoke cigarettes (16).
In this same study, a relative risk of 14 was reported
for oral contraceptive users compared with nonusers (90
percent confidence limits of relative risk from 5.5 to 37)
(15). In women smoking more than 25 cigarettes per day the
relative risk rose to 34 times that of women who were both
nonusers and nonsmokers. While the number of subjects was
small, the authors calculated that for women exposed to either
oral contraceptives or sm oking, but not both, the annual age-
specificrisks for nonfataiMI were roughly 1 per 190,000 at
ages 27 to 37; 1 per 47,000 at ages 38 to 40; 1 per 23,000
at ages 40 to 43; and 1 per 16,000 at ages 44 and 45. If,
however, both cigarettes and oral contraceptives are used, the
annual age-specific risk is estimated to be much higher and
the respective risks become 1 in 8,400; 1 In 920, 1 in 540,
and 1 in 250. The authors report that a dose-response
relationship exists between smoking and risk am ong their
population of female myocardial infarction patients, such that
smoking 1 to 14 cigarettes per day carried a relative riskk of
percent, respectively, of a group of 44 men and 44 women
with nonmalignant hypertension. The difference is significant
for men but does not reach significance for women.
Venous Thrombosis
The section dealing with venous thrombosis of the 1979
Surgeon General's Report noted a case control study by Vessey
and: Doll of 84 women who had venous thromboembolism (44).
There was no significant relationship to smoking, although
there was a trend (p=0.08) reasonably attributable to chance
(45). Similarly, Lawson, Davidson, and Jick reported no
association with smoking among 60 premenopausal women who
used oral contraceptives and who had uncomplicated venous
thromboembolism (21 ).
The Issue is reopened, however, by a recent paper
derived from the Walnut Creek Contraceptive Drug Study. The
authors analyzed 38 cases of venous thromboembolic events
among the approximately 16,700 women followed in the study.
These women were matched with 8,174 controls from the same
cohort, providing each case with 61 to 559 comparison
subjects. The relative riskof cigarette smoking was 2.6 with
a one-sided p vaiueof less than 0.01. On multivariate
analysis, the smoking effect was Independent and remained
significant. Of the 17 idiopathic cases of thromboembolic
disease, 65 percent occurred in sm okers, while 33 percent of
thecontrols were smokers. The relative risk for smokers was
4.2. Both sm oking and', oral contraceptive use were
independent risk factors for venous thromboembolic disease in
this cohort of women (31).
The same section of The 1979 Surgeon General's Report
noted a controversy about whether smokers who suffered
myocardial infarction had a relative protective effect from leg
vein thrombosis in the immediate post infarction period (44).
The authors did not provide an analysis for each sex.
A recent investigation of women undergoing gynecologic
operations has studied the incidence of deep vein thrombosis
of the leg in relation to smoking. In the prospective study
of 231 women, their smoking habits during the month before
the operation were determined. The occurrence of deep vein
thrombosis (DVT)) was assessed by the radioactive fibrinogen
technique, with routine scans on the first, third, and sixth
postoperative days. Of the 231 patients, 99 smoked and 132
did not smoke. Eight of the smokers (8.1 percent)) and 29 of
113
TABLE 7._Deahs from cerebrovaseular dispse releteE to smoking
, (Mortality ratios actual number of deaths shown in parentheses)s
[SM=9mokers NS=Nonsmokers)
PFOSPECT IVESTUDIES
Author, Number
vesr. andtype Oata
nl,y of pnpu rnllection
rererenr..
. . IanOn
Hammond 158,584 DuettinnnaFe
nd marm andlolloe.
Garlinkel 4458]5 upUldeath
1969, lemalas mnificste
U.S.A. 40-)9vears
1]OL u/aBeel
emrv-
Femelea
, Never smnk W 1 DO 1.0n 1.00 1 90
19 ._....__._.....,.. Lh4 1:26 136 0.83
10 19 2 6U ].)0 2.15 10 5] ,
. .
0-30...... ......... . ]90 26> 183 1.28
...
. . 40, .................... .5 )0 .3.52 - -
IUnl<5sot5erwLerpecitied,disparnresbetwaentherotalnumEeroldearhsandthesumV/tM1eindividua!smokingrele
pa_riesereduetothee.clusionoleirneroccasional,miacellaneous.miaed,or aa
snwker; - -Source. U.S. Puhlie Heallb Servia (43. 441.
0VQS99E0
NumOw ol
Fullowyp deathrdue Ci9anttee/ Pipesand
yean underlyirrgle day Cigers
CuD sa
rause. ..
Age variatien - Commenn
6. 4A99 Current Meles t9esedon
l
59
. _ regular
cigarette C0-09 5059 60® ]0-J9 nn
v
deaths
Newrsmoked 1AO 1.00 1.00 190
f9 279 195 1.30 095
ma9.... .. 1.14 149 u 44 092
2030.._ ... 221 2.03 1.82 1.22
' 240_........_..._. 1.64 2.40 1.72
8
400
La-
~IZn r49aul c~.6wauamd . ~~.q
O91S'E
99LCC
GSIN.C'pG295
BIL'84
C4[A6 N99p'4
99[95
965'S
. _.__._ _...........__..ano.vue..eaA S9
08Z9"l 1848'L 9pZA'L 9 199 1 1 ('[60.Z 6GCe1 CS9911 SiCQL 09Ze:1 - .raA:.p9S(
ZLAL
OSCOI
5:669
LLIp
JCCL
9G99 I"6pp
169L
p065 ...... . aeaA.pCS9
9pc[
989,
h.C6C
:0EG
piSC
Z691 Csll
p6tC
9'061 .. ...... Ap9u
CC11 8541 9Zp1 A0t 09L SLp i0C 999 0'[4 aA P95p
56i 866 HBC Op 0L1 p01 lL SOL ' 9[L s.e >ATPSC
C9
Z[
C'9
:p0
91
01 1'1
C2
91 . _..._ ..............._...._._sxaA9CSl
C£ZI 91p1 QlEI tBHI C9SI '1t51 15p1 C'991 9051
8964
G9L5't pLtlCC BG59Z C669'0 080CS e659p 1 0Lp5'p 8Sp6'p pLk9Y
B89p'I LZLL'/ UCLyI 40.'CI 099fi1 09LY1 9LZp'L p.L46"1 9.IZ9' 1
Z595 BS08 I{L9 pnCC 5099 9491 pCCE Hlf9 ti(Hp
0ZZZ L96C Z:ZOC ZCB CpVZ 9651 .898 S65t f[L1
pCC L G91 L 91 L R OL 9 Z8 p.05 L 9Z 6n6 L (5
C9L BIC 'S`ZZ 6[ 5L1 9.OL 91 C:OC 8LL Y5[
SL l9 Cp 9 0 6 1 tI 80 L 9'L saeaA p[.SZ
ti90L p501 >SIL p[SI LY5L 5591 0Ypl 9'CSl L051 vee Ilv
xeavy uuaY mwnNmi nnmq'J 9L6L
d9Z91 p'C91~i 4Z9C1 8YC9'{ i5I[[ 6210C 0C55'C CBLSB 911Ht
Y196
pl6Zl
IC01'1
82pC'I
S90Ct
IZ£CI 59l(I
pHdZZ
1'L991 ....... . .. ...s.raA PB 51
ZItS
iOLOt C0L8
S-ZLS .1 901
SOGC VpLS
p6YL 803C1
Cp89 H6t6 CpL9
6itp C[6/ 0'SICL
['899 9M6
9oZp ........__..._._.__.__.__.... oeae~,>3SS
'CS01 Z"9CC 9991 fl9 YOLZ 9'LSI 899 I`C9C 9331 ueaA:.K S>
'8LC
918
6:C9
IZ1
969
C0p ZSI
GOL
CZp ..sxaAppS[
99 I61 1 8 C 1 59 I"p Z'Z LY 9, yeaA.YF52
CLB t[[L 5661 C9Cl 0H9i ,6561 90CI OLVZ VSHL
896L
IOB6 L69['1 592fL 669811 960LZ 0"SCl'i C06L'1 Lp95`Z OBCOi "-~"-""'-~a^opetueaa5p
0[19 L19011 0116 Cp501 4lHHl'6p9C'L L'SCO'1 L90H1 08ZC1 """""'" ----vaanryi/
560P 6t58 9pL5 5"90p CpZO'l '6pL9 890p 8686 Pp9 '----- --'-"'ue.AnPo
9p61 99HC 2£BZ 1'Zpl IIOS 241E ZlLpl C06p S: 60C anp345
fi99 0'6S1 Z-11t [L[ 1061 8".ILL CLp 6991 Clil aApSSr
E 01
SLp
pOC
'9 1
190
.99Z 0'6
Z9p
OLZ ve.n
nGt
['L p9 :L9 60 FP .9'i fl 8'p HZ "I~ea^YCA
069 ['001 0,11 '.CL11 CtOC 1 891 901, 669L 86p1
~inil I Ie~V+r~OAw ain.~y 916,
aleuuj .aFw alne
, w0 ud Fl.~uf alew
uqlM Vlofi alewad alew
leinL
H
oEeG.eIeaA
(uoi9na/ giql 10 2 1 p sqwnuUoBetes OI'aseasp Ileaq. aiwaVOSt oi,umuo uop, pue'S961 ui
paptlope:'salelS paLwn
aw ul asnio~ pal02pe'saseasp louo9eogisselp leuoilewalqI a4110 uO!sIUad qlublg aql/p 010
/aqwnu3loba.n
OI pau6isse sqleep uo paseq a.e sal~ u0ilaelui IelpLeoOFw aln9e LOi -u01LeInOOtl 000'001'/etl suleap
aLe saRw
- 9d6L-9981'oe3elSPaNup:.avPuaLoloa.d0'aCnw6OM
PsUlOoOa,jq ase.qP Po+4 0l wa4ael *luorya Pue uollo+olul lel W eaa6w einac LoNa W+ 41eaO= 1 31891
TABLE6.-Coronsryhexndiuasemorbid@yasrelatedtosmoking.IRiskratioaactualnumberolCHDmaniFesbtionaahow
ninparentheses)t (SMSmokers
NS = Nonsmokern EX = E.smokers)
Authar, Number
year, 8rdtypeol
country populatlon
Date
Collection
Epstein, 6.568 maa Inltal medical
1967. and female e.vmination
U.S.A. .S_._A. residzots of and repeat
- 7ecnmsen; lalloWup-
Mmh. eeaminatlons.
Source: U.S. Public Health Servine (44).
LE0SB9E0
Fnllnv. Number
up ol
years Incidents
4 96male,92
lemale
CHD includ- NS..........
- ingdeatns, EX.........
,
argine,and Cigarettes
myocareial
Intercnons
Cgerettea/dey
Males
40-59 60andover
... 1.00111 1.000)
..,. 6.331101 1.211111
.... 5.20 136/ 1.90 (23)
Females
.... 1001211 1.00(47)
... 0,89 131 1.31 (5)
Cige:&ie.::: ~::: i 02 1141 0 A2 121
Pipes, agaazs Age verition
Meles
40-59
5M .....,. 1.90 121
60.nd over
SM,...... 0.90I61
Comments
Reeraminasion af
patients was
spread over 1'b -
6 Year p¢riod, but
data are reportM
in terms ul g.year
incidence rates.
A2tuaVnumber uf
CHU incidents
derfved Fdm d.ta
an incidence and
lutzl in emoking
dasv
TABLE 2.-Number of deaths for acute myocardlal Infarctlon and chronic Ischemlc heart dl
specified age groups, by color and sex;.UnltedStates, 1968 and 1976 .aa..
[Number ol deaths due lo acule myoG3rtllallInfarcrOn are Ihose.assiqnetl to category number:41 D
olthe E
Revision o! t11e International Clessification of pl6ea8esd adaplEtl for use In the United
Slales,atlopled in t9llf
for chronic iSChemic heart disease to category number 412of this revislon) .-,'fa
yw, anE aJo
FemalO Ryl; Male Far,ql¢
XAPS Male Fema
1976 Acwe m.oca.mal inla,nron ..
Allqo......_......._...._____.... 319,111 191429 V20<8 295,613 16],820 14t]93'. 23,86< 13.809 IO,j55
25-04vrera.......__...._. .... .. 890 J/B li2 ]2U 598 122' 110 120 50
45d< vrzrs
558<enn
6544 vean ...
1584 veao ..
95yeare~mN Over _ ...
1963
55E4 venl._... _.......
6&)4 yearr ...... .
]584 yere
85 yean erd a.er
19%6
All Aea
2534 ve..a . ...
3314 veen .........
a5.5n v.ne
5594 veerr,
65.)4 v*ar. ... ...
258e ve-
85veanmCa«,.
1966'.
45 s4.aen ..
55E<vean
M .]4 rean . ... . .
]saa ynrs
65 veara xM orn ...._... _ ....... ........
5over. Raxrongerqqe4baU21.
6.223 5.182. 1041 5,338 <,558 ]B0i 885 B2G 261
26.405 21,361 5,U44 23pf9 9,40] 4,072 ' 2y]6 1954 972
62fJ91 46.516 I5,]SJ 55,623 430)243.551 5<68 ]sa4 2024
93:695 61038 0`1.65J. 1 9d00a'. 23,562' 7.129 a.034 3095
89969 46,395 43.574 Ba;852 43,912 40140 ' 1.111 2i4E] 2,5N
40066 18133. 29936 J1,9]9 15A11 32.]26 . 2,129 931 1,198
369610 230D 17 133.593 342999 2Jn5FJ123e82 26611 15,540 11,131
1099 838 261 846 664 182 253 ll6 79
998G 8.132 1348 8,412 . 1.127 ' 1,299 1 569 1.010 558
30032 29.368 66641 32,381 ]5,860 5,401 3,])1 2,508 1283
]6,108 57,38)1a,]21 695n4 53,2111 15,21). 6,604 C;100 2,U34
IW672 ]0,564. 39.108 1m;963 66.205 35,658 ],/N9 aiJ59 3<W
100D12 63838 464]4. 95610 51fJ6 44,1]2 9.699 2,402 2,297
36135 15111 20G24. 3aplv 1.924 19,493 1918 88, 93,
Chmmc uclvmsneam aauace -322,182 1603]5 16201 209,572 143,3)2 146.2W 3281n 1].On9 15,80]
502 381 121 332 266 56 IJO /15 55
293] 2I]3' 664 2,131 1,]3< 403 WO 539 261
13F49 10,391 3159 10,Y1] 5:426 2.16] 1058 1965 1091
30,]65 24.52510]40 269]9 20,996 1.933 5836 3.629 2.33J
0.176 41,612 ' 27,564 60A<I 36;J45 2I23.] 9.136 4.867 4,267
169,860 SU,i 59B`A 101,088 45y]2 55.156 8.772 4,079 4,61
91,]66 3111e9'. 60,259 86]50 29]I] 9131i 5.U10 1992 3,118
300216 151,815 148.401
390 282128
311P ]:350 062.
12953 9.412 3,541
3<i]6 23481 10994
)1905 E1]]0 3n635
108.576 50:145 SqA31
68,5C8 24;Bn1 43>4].
9n
JE181 Wfine Allor6e,
268,494 139,333 13P,]91 31092 16,482 15 610
211 166 45 1Y9 96 83
],I62 1,734 428 1 O50 616 a3e
91]9] 7.545 3182 3Z26 IB61 11359
2J,>43 19,732 8011 8,)]2. 3]49 ],96J
620J6 36,135 24941 9829 5135 ,169a
1oI,l3Y 46,689 6a,5E0. ].3G]345P 3831
64010 23.269 <1,601 ]6]8 1521 3146
While data Implicating sm oking as a risk factor for various
cardiovascular diseases in women are neither as extensive nor
as co mplete as for men, the evidence nonetheless clearly
establishes cigarette smoking as a major correlate for
myocardial infarction, arteriosclerotic peripheral vascular
disease, and subarachnoid hemorrhage in women (44).
119
I
ischemic heart disease of women as compared to men are
paralleledd by less extensive and severe atherosclerosis in the
coronary arteries of adult women. The severity of aortic
atherosclerosis, however, is about the same in both sexes.
The relationship of cigarette sm oking to
atherosclerosis, heart attack, and other ischemic diseases
secondary to atherosclerosis has not beenn studied among
women as extensively as among men; moreover, most studies
have been limited to white women. It is not known whether
atherosclerotic plaques observed at autopsy are more extensive
and severe in women smokers than in nonsmokers. No data
are available concerning the incidence of death from
atheroscleroticc aneurysms of the aorta among women who
sm oke relative to those who do not, and inadequate data exist
to indicate whether cessatiomn of smoking by women is
associatedd with a beneficial reduction in the risk of heart
attack, as has been demonstrated In men. The effect of
smoking on the threshold for the onset of angina pectoris and
on cardiac function in women with coronary heart disease has
not been studied. Nevertheless, compelling data fromm prospective cohort
studies and from casee control investigations indicate that
cigarette smoking is a major risk factor for fatal and non-
fatal heart attacks in women. In general, cigarette smoking
increases the risk by a factor of about two, and in younger
women cigarette sm oking may increase the risk several fold..
Women who smoke low-"tar" and low nicotine cigarettes have
a greater-risk of suffering heart attacks than nonsm okers but
appear to have a smaller risk than women smoking moderate-
to-high "tareand nicotine products.
Smoking is a major risk factor for arteriosclerotic
peripheral vascular disease in women, as it is in men. For
both men and women the successful outcome of surgical repair
of this disorder is enhanced by cessation of sm oking.
Smoking is a major risk factor for subarachnoid hemorrhage
and for the development of malignant hypertension. Smoking
is reported to depress the natural relative elevation of high-
density lipoprotein cholesterol enjoyed by women. In women
who use oral contraceptives, sm oking is a po werfuf synergistic
risk factor for subarachnoid hem orrhage and for myocardial
infarction.
118
the nonsmokers (22 percent) developed DVT. Following an
analysis of other factors, the authors concluded that smoking
provided an apparent "protective" effect against postoperative
DVT, based on the fact that sm okers constituted only 21
percent of the patients with DVT. They also noted that the
women who developed DVT weighed more than those who did
not and that smokers who developed DVT were more overweight
than nonsmokers withDVT (5).
In a continuing prospective study of the relationship of
blood clotting and blood thrombogenic properties to ischemic
heart disease, Meade and associates have reported on a
num ber of blood coagulation variables and their relationship to
smoking among 1,426 men and 638 women in England (25).:
Forty-three percent of the men and 36 percent of the women
were smokers. Smoking was not found to have an effect in
women on factors V or VII, fibrinogen, fibrinolytic activity,
antithrombin III, platelet adhesiveness, or platelet count.
Sm oking decreased fibrinolytic activity in inen and decreased
factor Vlll activity In both men and women. Oral
contraceptive users were found to sho w an increase in
fibrinolytic activity only if the women were nonsmokers.
High-Density L.ipoprotein
High-density lipoprotein (HDL) is a protein complex that
transports cholesterol in the blood. A higher level of HDL
is correlated with a reducedd risk of heart attack. It has
been observed that women who smoke have lower levels of
HDL than expected (1,4,8). .
ORAL CONTRACEPTIVE USE, SMOKING, AND CARDIOVASCULAR
DISEASE
The association of oral contraceptive use and an increased
incidence of certain cardiovascular disorders has attracted
much interest. Smoking has emerged as a strong synergistic
risk factor, and an additional study has focused on smoking as
an Independent risk factor.
The effects of smoking and of estrogen and progestin
contraceptives on the level of high-density lipoprotein in
womenn have been studied by Bradley and associates. They
measured serum HDL among almost 5,000 womenn between the
ages of 21 and 62 (4). They reported that the use of oral
114
0
s
e
e
s
S
e
I
d
s
nonfatal myocardial infarction of 9.2; 15 to 25 cigarettes of
7.9; and 26 or more cigarettes of 21, relative to those who
never smoked (14).
In another recent study of 234 pre-menopausal women
who had suffered a first myocardial infarction and 1,742
control patients drawn from the hospital population, Shapiro
and his coworkers found an association between recent oral
contraceptive use and sm oking (34). They found no evidence
t'hatt past use of oral contraceptives was related to heart
attack or that heightened risk was associated with increased
duration of use of the oral contraceptives. For nonsm okers
who used oral contraceptives, the rate of myocardiaL
infarction increased fourfold compared to nonusers and
nonsmokers; in those women who smoked 25 or more
cigarettes a day but did not use oral contraceptives, the rate increased more than sevenfold; and in
those women who both
smoked heavily and used oral contraceptives the rate increased
at least twentyfold.
CARBON, MONOXIDE
A study of male and female office workers found no sexx
difference in the relationship between carboxyhemoglobin
(COHb) levels and daily consumption of cigarettes. However,
women smoked fewer cigarettes on the average than men. Thee
study found that the COHb levels in smokers were higher
among the sedentary office workers than among physically
active meat porters and that both had higher levels of COHb
than pregnant women who smoked (11). The latter had COHb
levels approximately three tim es higher than that of
nonsmokers. Wald reported from a cross-sectional study that
carboxyhemoglobin levels of smokers are a better indicator of
the risk of atherosclerotic cardiovascular disease than a
reported sm oking history (47). The proportion of both men
and wom en with atherosclerotic disease increased with
increasing levels of COHb.
COMMENT
Women are less likely to experience a myocardial infarction
than m en. Nevertheless, coronary heart disease is still a
leading cause of death and disability in wom en. The lower
mortality rates from acute myocardial infarction and chronic
117
(18) KANNEL, W.B. Epidemiologic studies on smoking
In cerebral and peripheral vascular disease.
In: Wynder, E.L., Hoffman, D.., Gori,
G.R. (Editors).. Proceedings of the Thi7d
World Conference on Smoking and Health., New
York, June 2-5, 1975. Voi,ume I. Modifying
the Risk for the Smoker. U.S. Department
of Health, Education, and Welfare, Public
Health Service, National Institutes of
Health, Education, and Welfare, Public
Health Service, Nati'onal Institutes of
Health, National Cancer Institute, DHEW
Publication No. (NIH) 76-1221~, op.
257-274, 1976.
(19) KAMIEL, W.B., CASTELLI, W.P., MCNAMARA, P.M.
Cigarette smoking andd risk of coronary heart
- disease. Epidemi.ologic clues to pathogene-
sis. The Frami.ngham Study. in: Wynder,
E.L., Hoffman, D. (Editors). Toward a Less
Harmful Cigarette. National Cancer Institute
Monograph No. 28. U.S. Department of Health,
Education, and Welfare,PubIII.cHealth Service,
National Cancer Institute, June 1968, pp.
9-20
(20) KURT7KE, J.F. Epidemiology of cerebrovascu-
lar disease.In: Cerebrovascular survey
report for the Joint Council Subcorrmittee on
Cerebrovascular Disease. The National
I.n.sti'tute of Neurological and Communicative
Disorders and Stroke and the National
Heartt and Lung Institute. Revised January
1976. U~.S. Department of Health, Education,
and Welfare National Institutes of Health,
Public Health Service pp. 213-242.
(21) LAWSON, D.H., DAVIDSON, J.F., JICK, H. Oral
contraceptive use andvenous.thromboemholi.sm:
abscence of ann effect of smoking. Rrit.ish
Medical Journal 2: 729-730, September 17,
1977.
(22)MAMi, ).I., VESSEY, M.P., THORfG00D, M., DOLL,
R. PAyocardial infarction in young women with
special reference to oral~ contraceptive
practice. British Medical Journal 2: 241-245
May 3., 1975.
(23) MCGILL, H.C.,JR. (Editor). The geographic
pathologyof atherosclerosis. GeneralFindings
of the International Atherosclerosis Project.
Laboratory Investigation 18(5):49R-502,
1968.
122
SMOKING AND CANCER IN WOMEN
INTRODUCTION
For more than 40 years cancer has been second only to car-
diovascular disease as a cause of death In the United States.
With the exception of the very elderly, the death rate for
adult men. exceeds that for adult wom en for both groups of
diseases, implying a difference in genetic susceptibility,
environmental exposures or lifestyles between the sexes, or a
combination of genetic and environmental factors.
Placing these generalizations about cause of death in
perspective, current data from the National Center for Health
Statistics (32)) reveal the following statistics:
There are 105 male births each year in the United
States for every 100 female births, but the higher death rate
for males results in a ratio of 100 men to 100 women at
ages 20 to 24 and of 79:100 at ages 65 to 69, and of
47:100 at age 85. Life expectancy in the United States In
1976 was 68.7 years for males compared to 76.11 years for
females.
Heart disease and cancer currently account for 60
percent of deaths in the United States. In contrast to the
decline in the age-adjusted death rates for ischemic heart
disease, the age-adjusted death rate for cancer has increased,.
Hidden in this small rise in the overall cancer statistics is a
remarkable increase--a veritable epidemic--of cancer of the
lung in both men and women. In the past quarter century,
deaths from cancer of the respiratory tract tripled in the
white population and quadrupled in the black population. The
remarkable ;nale-to-femalepreponderence of lung cancer in
the 1940s and 1950s has been decreasing in the 1960s and
1 970s; the rate of increase in lung cancer in males Is
slowing while the rate of increase of lung cancer in females
Is accelerating. As a cause of death, lung cancer In women
is now second only to mammary carcinoma and will likely
displace breast cancer as the leading cause of cancer
mortality in women in the 1980s (1) (see Figure 1).
The 1964.. Surgeon General's Report reached the following
conclusiona "Cigarette smoking is casually related to lung
cancer in men; the magnitude of the effects of cigaretto-
smoking far outweighs all other factors. The data for women,
though less extensive, point in the same directione (45)~
Since then, a number of retrospective and prospectivo-
epidemiologic studies, experimental animal carcinogenesis
0
127
U
CARDIOVASCULAR DISEASES: REFERENCES
(1) ARNTZENIUS, A.C., VAN GENT, C.M., VAN DER VOORT,
H., STEGERHOEK, C.I., STYBLO, K. Reduced high-
density IJpoprotein in women aged 40-41 using con-
traceptives. Consultation Bureau Heart Project.
Lancet: 1221 -1223, June 10, 1978.
(2) BELL, B.A., SYM ON', L. Smoking and subarachnoid
haemorrhage. British Medical Journal 1: 577-578,
March 3, 1979..
(3) BLOXHAN, C.A., BEEVERS, D.G., WALKER, J.M.
Malignant hypertension and cigarette sm oking.
British Medical Journal 1:581 -583, March 3,
1979.
(4) BRADLEY, D.D., WINGERD, J., PETITTI, D.B., KRAUSS,
R.M., RAMCHARAN, S. Serum high-density lipo-
protein cholesterol in wom en using oral con-
traceptives, estrogens, and progestins. Ne w
England Journal of Medicine 299(1): 17-20, July
6, 1978.
(5), CLAYTON, J.K., ANDERSON, J.A., McNICOL, G.P. Effect
of cigarette smoking on subsequent postoperative
thromboembolic disease in gynaecological patients.
British Medical Journal 2(6134): 402, August 5,
1978
(6) COLLABORATIVE GROUP FOR THE STUDY OF STROKE IN
YOUNG WOMEN. Orall contraceptive and increased
risk of cerebral ischemia or thrombosis. New
England Journal of Medicine 288(17): 871-878,
April 26, 1973. .
(6A) DOLL, R., et. al,. Mortality in relation to smoking;
20 years' observations on male British doctors.
British Medical Journal 2: 1525-1536, December
25, 1976.
(7) EPSTEIN, F.H. Some uses of prospective obser-
vations in the Tecumseh Community Health
Study. Proceedings of the Royal. Society of
Medicine 60(1): 56-60, January 1967.
(8) GARRISON, R.J., KANNEL, W.B., FEINLEIB, M.,
CASTELLI, W.P., McNAMARA, P.M., PADGETT, S.J.
Cigarette smoking and HDL cholesterol: The
Framingham Offspring Study. Atherosclerosis
30: 17-25, 1978.
(9) HAMMOND, E.C., GARFINKEL, L. Coronary heart
disease, stroke, and aortic aneurysm: Factors
in the etiology. Archives of Environmental
Health 19(2): 167-182, August 1969.
120
(32) ROSENBERG, H.M., KLF.BBA, A.J. In:Havlick,R.J., Feinlei.b, M. (Editors). Proceedings
of the Conference on the Decline in Coronary
Heart Disease Mortality.. U.S. Department of
Health, Putili.c Health Service, Education,
. and Welfare, NIH Publication No. 79-1610,
pp. 11-39, 1979.
(33) SACKETT, D.L., GIPSON, R.W., RROSS, I.D.J.,
PICXREN, J.W. Rel,ation between aortic
atherosclerosis and the use of cigarettes
and alcohol. An autopsy study. NewEngJand
Journal of Medicine 279(26): 1413-1420,
December 26, 1968.
(34) SHAPIRO, S., SLONE, D., ROSENBERG, L.,
KAUFMAN, D.W., STOLLEY, P.D., MIETTINEN,
O.S. Oral-contraceptive use in relation to
myocardial infarction. Lancet 1:: 743-747,
Apr i l7, 1979.
(35) SHAPIRO, S., WEINBLATT, E., FRANK, C.W.,
SAGER, R.V. Incidence ofc6ronary heart
disease in a population Insured for medical
care (HIP). Myocardial infarction, angina.pectoris,and possi.ble myocardial infarction.
American Journal of Public Health 59
(Supplement 6): 1-101, June 1969.
(36) SLONE, D., SHAPIRO, S., ROSENBERG, L.,
KAUFMAN, D.W., HARTZ, S.C., ROSSI, A.C.,
STOLLEY, P.D., MIETTINEN, O.S. Relation of
cigarette smoking to myocardi.al infarction in
young women. New England Journal of Medicine
298(23): 1273-1276, June 8, 1978.
(37) SPAIN, D.M., SIEGEL, H., PRADESS, V.A. Women
smokers and suddenn death. The relationship
of cigarette smoking to coronary disease.
Journal of the American Medical Association
224(7): 1005-1007, May 14, 1973.
(,38) STAMLER, J., RHO114iERG, P., SCHOENBERGER, J.A.,
SHEKELLE, R.B., DYER, A., SHEKELLE, S.,
STAMLER, R., WANNAMAKER,J. Mu.ltivariate
analysis of the relationship of seven
variables to bloodd pressure. Findings of
the Chicago Heart Association Detection.
Project In Industry, 1967-1972. Journal of
Chronic Diseases 28(10): 527-548, November
1975.
124
TABLE 3.-Percent change Detween 1968 and t B78 In death rates lor ecuta myowrdial Interctlon and
cvonlc ischsmlc heart dlaesses for speellled age groups, by colorund sex: United States ..
crcem cnanges.are based on rales.per 100.000 oopuWation. For 1968ano 1976 rales foracute
myocardial
=a.rcuon are based on oeaths.assignetl to category number 410 oflhe Eighth Revi9iomolthe
Internation al
Cass,ImatronolDiseases.a0apte0iforVse'intheUnlledSlales.atlopletl,in1965.antlthe
Chrnnic6ehemictillarl
mseasea oncalegory number 412 of this revisionil
Tate, White AllOtneo
6ol/r Male
6e.ea
6or5 Male
Beaee
Femle BotM Mele Femalr
Acute myomrEial imlarction
-19.7 -2]] -15.C -190 -21.6 -15.] -73.3-2i]
n]a.ea,:....__.____ .........................._.. -391 -36,1 -5UD -36.6 -338 -<Y.1 -5157-511
n<avean .._ .. _....._.... -383~ -3a8 -C3J. -3A0 -338 -3).2 -U.5 -<18
essav.a., -F15 -M19 -n.3 -29.1 -]9.l -36.5 -33.3-32.3
156a~~.ean . .. . . ... -26A -268 -251 -26a1 -06.8 -2C.6 -2L5 -2a.6
55 ra vea.. -26 7 ~ -20.) -]9Z -26.)' -2C] -19.2 ~58 ~3.2
/53dvear ~ . ... . . .... ...... -]t]~ -188 -21 ] -21 ] -18A -0A.5 -16A -1J8
65.ensann-,n -3U0 -28.2 -289 -?3.1 -Y).1 -29.1 -368 -36.i
eh.onie iunemic nsert eisenc
-5<0
-570
-3a.6
-3U )
-28.2
-15.s
-35.1
-1 e 1.3 1 6 ro. 3.5 -135 -11 < -13.7
n ae aeart ............... . . . .. . .-.. 6] -Z/.3 20D 18.6 25.0 -R.3 -15] -539
l5arears.. ....... ..._.... -59'. -1D -2t1 18 29 -2.5 -]9.1 -132 -N7
a55anan.. . . .... _......_. 1.& 6:2 -11.6 6.1 8.7 -2.3 -19.6 -8.6 -31.7
555a~rus.. ...._ ................_.... 51:1 -SA -16.3 -S.T -3.8 -10.5 -1<.1 -155 -33.7
55~1ereaa.. . . . -nq -1]l -33.6 -166 -lnl -23J -N4 -2r< -271
15Bavees....___ -112~ -62 -1C1 -11.3 -60 -1M.3 -88~ -b] -11.0
65vearsamU~over.._._ . . .... -159'~ -12:3 -1)8 -1L)~ -10.> -18.5 -26.5 -25.5 -268
Snm.c Rosantlrvg ame Rlropa I ~2/. '
20
99
(39) STERNBY, N.H. Atherosclerosis in a defined
population. An autopsy survey in Malmo,
Sweden. Acta Pathologica et Microbiologica
Scandinavica. (Supplement) 194: 16-194,
1968.
(40) STRONG, J.P., SOLRERG, L.A., RESTREPO, C.
Atherosclerosis In persons with coronary
heart disease. Laboratory Investigati.on
18(5): 527-537, May 1968.
(41), TALROTT, E., KULLER, L.H., DETRE, K., PERPER.
J. Riologic and psychosocial risk factors
of sudden death from coronary disease in
white women. TheAmerican journal of
Cardiology 39(6): 85R-864, May 26, 1977.
(42), THE EPIDEMIOLOC,Y STUDY GROUP. Epidemiology
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(43) U.S. PUBLIC HEALTH. SERVICE. The Health
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Disease Control, HEW Publication No. (CDC)
78-8357, 1976.
(44), U.S. PUBLIC HEALTH SERVICE. The Health Conse-
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HealtK, Education, andWelfare, Publia Health
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(45). VESSEY, M.P., DOLL, R. Investigation of rela-
tion between use of oral contraceptives and
thromboemboiic disease. A further report.
British Medical journal 2(.565R.): 651-657,
June 14, 1969.
(46). VESSEY, M., DOLL, R., PETO, R., JOHNSON, R.,
WIGGINS, P. A long-term follow-up study of
women using different methods of contracep-
tion. An interim report. journal of
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(47), WALD., N., HDWARD, S., SMITH, P.G., KJEDLSEN,
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25, 1972. ..
I
125
smoking for both men and women (2). The relative risk for
men was 3.9 and for women, 3.7. The association appeared
to relate to hemorrhage from ruptured cerebral aneurysms
rather than to other conditions thatt may give rise to
subarachnold hemorrhage. A synergism between smoking and
the use of oral contraceptives and subarachnoid hem orrhageis
noted below (30). The Japanese study cited in the discussion
of ischemic heart disease has also reported on 366 deaths
from cerebrovascular disease among women who smoked, (28).
The risk ratios for subarachnoid hemorrhage and cerebral
hemorrhage were both significantly increased among women
smokers (p <.001) as was the risk rate for the category,
"other forms of cerebrovascular disease"(p <.05).
Arteriosclerotic Peripheral Vascular Disease
Clinicians have noted that arteriosclerotic peripheral vascular
disease is more common in men thann women. Sternby hass
reported fromautopsg studies that men generally have
somewhat moree atherosclerosis of the femoral and pelvic
arte.riesthanwomen (39).
Kannel has reviewed the relationship of smoking to the
incidence of arteriosclerotic peripheral vascular disease (18),
In the Framingham Heart Study the incidence of peripheral
vascular disease was increased among smokers of both sexes;
cigarette smoking was as strong an independent risk factor in
women as in men. Heavy smokers had a threefold increased
incidence.
Weiss studied 245 women with arteriosclerotic
peripheral vascular disease (48). Ex-sm okers who had nott
smoked for 5 years or more had nearly a normal risk ratio of
1.06; those who had not smoked for the last 1 to 5 years had
a risk of 1.70; continuing smokers of less than a pack a day,
5.15; pack a day sm okers, 11.53; and those smoking more
than a pack a day, 15.56 (relative to nonsmokers, 1.00). The
increased risk was particularly associated with proxim al
(aortoiliac) disease, and there was less association with distal
(fem oropopliteal) disease. Age-standardized relative risk
ratios for those smoking a pack a day were 30.06 for
proximal and combined proxim al and distal disease and 6.322
for distal disease alone.
A retrospective stud y of 217 patients who underwent
arterial reconstructive procedures of various kinds for
peripheral vascular disease has been reported by Myers and
(24) McGILL, H.C., JR., STERN, M.P. Sex and
Atherosclerosis. ' In: Paoletti, R., Gotto,
A.M.,JR. (Editors).. Atherosclerosis Reviews.
Volume 4. New York, Raven Press 1979, pp.
157-242.
(25) MEADE, T.W., NORTH, W.R.S., CHAKRABARTI, R.,
HAINES, A.P., STIRLING, Y. Population-based
distributions of haemostatic variables.
British Medical Bulletin 33(3): 283-248, 1977.
(.26) MYERS, K.A., KING, R.P., SCOTT, D.F., JOHNSON,
N., Ml7RRIS, P.J. The effect of smoking on
the late patency of arterial reconstructlons
in the legs. British Journal of Surgery
65(4): 267-271, April 1978.
(27)NAEYF_, R.L., TRUONG, L.D. Effects of cigarette
smokingon i.ntramyocardial.arteriesandarteri-
oles In man. American Journal of Clinical
Pathology 68(4.).:493-498, October 1977. (28). 114KAYANI4, Y. Epidemiological research i'.n Japan
on smoking and cardiovascular diseases. In:
Schettler, G., Goto, Y., Hata, Y., Klose, G.
(Editors). Atherosclerosis IV. Proceedings
of the Fourth International Symposium, Tokyo,
1976. Berlin, Springer-Verlag, 1977, .pp.
149-153. -
-
(29). OMAE, T., TAKE.SHITA, M., HIROTA, Y. TheHisayama
study andd joint study on cerebrovascular
diseases in-Japan. In: Scheinberg,P.(Editor)
Cerebrovascular Diseases. Proceedings of the
Tenth Princeton Conference, New Jersey, 1976.
New York, Raven Press, 1976, pp. 255-265.
(30) PETITTI, D.B.,WINGERD, J. Use of oral
contraceptives cigarette smoking, and risk
of subarachnoid haemorrhage. Lancet 2: 234-
236, July 29, 1978.
(31). PETITTI, D.R., WINGERD, J., PELLEGRIN, F.,
RAMCHARAN, S. Oral contraceptives, smoking,
and other factors in relation to risk of
venous thromboembolic disease. American
Journal of Epidemiology 108(6): 480- 485,
December 1978.
123
J
(49) WILHELMSEN, L. Recent studies on smoking and
CVD epidemiology: Scandinavia and some other
Western European countries. In: Steinfeld,
J., Griffiths, W., Rail, K., Taylor, R.M.
. (Editors). Proceedings of the Third World
Conference on Smoking and Heal.th., New York,
June 2-5, 1975. Volume II. Health
ConseQuences, Education, Cessation
Activities and Social Action. U.S.
- Department of Health, Education, andWeifare, Public Health Service, National
Institutes of Health, National Cancer
Institute, HEW Publication No. (NIH) 77-
1413, 1977, pp. 171-177.
126 -~
(10) HAMnY~ND, E.C., GARFINKEL, L., SEIDMAN, H.,
LEW, E.A. "Tar" and nicotine content of
cigarette smoke In relation to death rates.
Environmental Research 12(3): 263-274,
December 1976.
(11) HAWKINS, L.H. Blood carbon monoxide levels as
a function of daily cigarette consumption
andphysicai activity. British journal of
Industrial Medicine 33(2): 123-125, May
1976.
(12) ISLES, C., BROP.N, J.J., CUI~'MING, A.M.M.,
LEVER, A.F., McAREAVEY, D., RORERTSON,
J.I.S., HAWTHORNE, V.M., STEWART, G.M.,
ROBERTSON, I.W.K., WAPSHAW, J. Excess smoking
in maiignant-phasehypertension. Rritish
Medical journal I; 579-581, March 3, 1979.
(13) . JAIN, A.K. Cigarette smoking, use of oral
contraceptives, and myocardi.al infarction.
American journal of Obstetrics and Gynecology
126(3): 301-307, October 1, 1976.
(14), JiCK, H., f11NAN, B., HERkWN, R., ROTHMAN, K.J.
Myocardial infarction and other vascular
diseases In young women. Role of estrogens
and other factors. journal of American
Medical Association 240(23): 2548-2.552,
December 1, 1978.
(15) IICK, H., DINAN, 8., ROTHMAN, K.l. Oral
contraceptives and nonfatal myocardial i.nfarc-,
tion. Journal of the American Medical Asso-
ciation 239(14): 1403-1406, April 3, 1978.
(16). IICK, H., DINAN, B., RnTNMAN, K.J. Noncontra-
ceptive estrogens and non-fatal myocardial
infarction. Journal of American ^ledl cal
Association 239(1:4); 1407-1408, April 3,
1978.
(17): KAGAN, A.R., STERNBY, N.H., UEMUP.A, K., VANECEK
R., VIHERT, A.M., LIFSIC, A.M., MATOVA, E.E.,
ZAKDR, 7_., 7IDANOV, V.S.. Atherosclerosis of the
aorta and coronary arteries in five towns.
Bulletin of the World Health Organization
53(5-6):501-530, 1976.
121
a
0
TABLE 1.-Estimated new cancer cases and deaths for sites associated with cigarette smoking
- 1980
Site Estimated New Cases Estimated Deaths
_. __Total --. Male Female Total Ma r- Femaie
All Sites 785,000* 387,000+ 398,000 405,000 219,500 185,500
------------------------------------------------------------------------------------------
Lung 117,000 85,000 32,000 ' 10 1 300 0 74,800 26,500
Pancreas 24,000 12,500 11,500 20,900 11,100 9,800
Urlnary
Bladder
35,500
26,000
9,500
10,300
7,000
3,300
Oral 25,500 17,900 7,600 8,800 6,100 2,700
Kidney &
Other
'
.
Urinary 16,900 10,500 6,400 7,900 4,800 3,100
Esophagus 8,800 6,200 2,600 7,600 5,500 2,100
Larynx 10,700 9,000 1,700 3,500 2,900 600
A11 Tobacco .
Related 238,400 167,100 71,300 160,300 112,200 48,100
- *Carcinoma In si[u-Is not inciuded. There are 45,000 new cases of uterine cervical
carcinoma in situ each year. Non-metanoma skin cancer Is not Included. Approximately
400,000 new casesof non-melanoma skin cancer occur annually.
SOURCE: Amerlcan Cancer Society (I).
090S89E0
6k
neoplastic transformation. The World Health Organization's
classification of malignant tumors (25) (Table 2). Includes
multiple histologic types, of which epidermoid, small cell,
adenocarcinoma, and large cell carcinoma are causally related
to cigarette smoking and display significant dose-response
relationships in epidemiologic studies (55, 1.0). These four
tumors are the most common histologic types off lung cancer
in: both men and, women. However, there are differences in
the distribution of the different types of lung cancer In men
and women an& in, smokers and nonsmokers. Epidermoid
carcinoma was the most common histologic type of lung cancer
im, the malee smoker, while adenocarcinoma was most common
im the female smoker and in nonsmokers of both sexes in a
series recently published from the Mayo Clinic (Table 3) (39).
Other centershavesimiiar data, although the propor-
tions by histologic type may vary with the pathologic criteria
used, patient population, geographic location, and other
factors.
Earlier epidemiologic studies suggested that cigarette
smokers were more likely to develop squamous-cell and
small-cell lung carcinoma thanother types. However, more
recent investigations indicate that all four major histologic
types of lung cancer- -including.adenocarcinoma, which appears
to be increasing rapidly in recent years--are related to
cigarette smoking in both men and, women (55).
In 1980, of the estimated 117,000 newly diagnosed
cancers of the lung in the United States, 32,000 will he
among women. There.wiil be am estimated 25,500 deaths from
lung cancer in women (1).
In 1950 women accounted for approximately 1 in 12 of
all lung cancer deaths. By 19689 the proportion was 1 in 6;
in 1979 women dying of lung cancer will represent over one-
quarter of all lung cancer victims. White women have death
rates from lung cancer which are similar to those of nonwhite
women, while the rates of white males remain below those of
nonwhite males. These differences may be due to differences
in the smoking habits of blacks and whites described
elsewhere in this report.
M any prospective studies have found that the lung
cancer death rate for smokers was far inn excess of the rates
for nonsm okers in both sexes; and as previously mentioned,
the rates for male smokers dramatically exceeded the rates
for female smokers. However, even the nonsmoking male had
a higher Incidence of, and death rate from, lung cancer than
the nonsmoking female (11). This evidence suggested that
131
I
0
e
an
king
~tive
21
the
did
iight
of
mic
a
to
5).
imen
t In
ity,
~unt.
ased
Oral
I
;that
HDL
has
of
iLAR
ased
cted
st ic
; as
stin
in
hey
the
)ral
estrogens raised the level of HDL significantly above the level
in nonusers while progestin use lowered it. Combination drugs
tended to change the HDL level' according to their relative
estrogen-progestin formulation. The average HDL con-
centration was reduced by smoking.. Among nonsmoking women
the HDL concentration was 63.7 + 16.8 mg/dl. This was
reduced by 2.2 mg/dl for those smoking half a pack per day;
and by 7.3 mg/di for those smoking one or more packs per
day. A reduction in the HDL level among women who smoked
was also reported from Holland. This study foundd an
independent negative association with the HDL levell among oral
contraceptive users (1).
It has been reported from long-term studies that
women using oral'l contraception have a two to threefold
statistically significant increase in risk of venous
thromboembolic disease when compared to those using other
forms of contraception (46). This study concluded thatt
smoking did not significantly increase the incidence of venous
thromboembolism (45). By contrast, the Walnut Creek Study
reported that smoking contributed to venous thromboembolism
among both users and-nonusers of oral. contraceptives (31).
Conclusions about the effect of sm oking on venous
thromboembolic phenomena, therefore, must be regarded ass
uncertain at this tim e since there are fe w relevant studies
and they provide somewhat contrary conclusions.
In 1973, the Collaborative Group for the Study of
Stroke in Young Women estimated that the re]ative risk of
cerebral ischemia or thrombosis was approximately nine times
greater for women who use orall contraceptivess than for those
who do not. A detailed analysis of smoking was not
presented, but one of the study's striking findings was the
high proportion of wom en with stroke who currently or at
some tim e sm okedcigarettes regularly (73.8 percent),
compared with sm oking rates of 43.4 percent among
neighborhood controls aged 17 to 44. The study also found
an increase in hemorrhagic strokes among white women.
Alm ost half of the hem orrhagic strokes were attributable to
bleeding from congenitah aneurysms leading to subarachnoid
hemorrhage (6). Recently an association between smoking and
aneurysmal subarachnoid hemorrhage in both men and women
has been documented (2).
The Walnut Creek Contraceptive Drug Study reported
that in a cohort of approximately 16,700 women, the risk of
subarachnoid hemorrhage for smokers was 5.7 times that of
nonsmokers; the risk for oral contraceptive users was 6.5
115
TAPLE 3.-HllsDologic. Types of Pulmonary Cancers In Smokerss and Non Smokers
Male Female
Type
Total
Smoker s Non-
Smokers
Smokers Non-
Smokers
Epidermoid 992 ' 992 7' 80 13
Small Cell 640, 533 4 100 3
Adenocarcinoma 760~ 492 39 128 101
Large Cell 466 389 16. 46 IS
Bronchiodo-
alveolar
68
35
4
13
16
TOTAL 2,926 2,341 70. 367 148
SOURCE: Resenow and Carr (39).
studies, and studies of human tissues at surgeryand autopsy
have confirmed and extended those conclusions. Cigarette
smoking is the major cause of cancer of the lung. In women.
The risk increases with the number of years the individual
smoked, the number of cigarettes smoked, the "tar" and
nicotine level of the cigarette smoked and, the degree of
inhalation,, and is inversely related to the age at which the
individual began smoking, being higher for those who begin
smoking at younger ages. The risk of developing cancer Is
diminished significantly by quittingg smoking and is lessened
somewhat by switching to low-tar, low-nicotine filter-tip
cigarettes (55, 59). Considerable evidence has also shown
that cigarette smoking is a significant cause--for women and
men--of cancer of the larynx, oral cavity,, esophagus, urinary
bladder, kidney, and pancreas. Much of this information has
been summ arized in previous issues of the "Health
Consequences of Smoking" or the Surgeon Ceneral's Reports
(45-55).
Table 1 Ilsts the new cases and deaths estimated to
occur in. 19800 for those cancers which are causally associated
with cigarettesmok.ing (1). Smoking will contribute to 43
percent of the male and 18 percent of the female newly
diagnosed cancer cases In the United States in 1980 and to 51
percent of the male and 26 percent of the female cancer
deaths. This table does not imply that cigarette smoking
causes each of these individual cancers. It does, however,
Identify the impact of cigarette smoking on the major cancers
now known to be associated with cigarette smoking. Most of
the cases of cancer of the lung and larynx couidhave been
prevented, as could a substantial proportion of the cancer
deaths at the other sites listed.:
In this chapter, selected data on cancer and smoking
among women wi01 be reviewed and summarized. Where
necessary for clarity, data previously reported wlll~~ be
summarized briefly.
LUNG
The lung is a complex organ lined by at least five types of
epithellal cells, each. of which theoretically might give rise to
one or more types of neoplasm. In addition tothe epithelial
cells, blood vessels and connective tissue are prominent in the
lungs. Roth visceral and parietal portions of the lung are
covered by synovial membranes, which also are subject to
129
TABLE 2.-World Health Organization Ciasslfication.of Malignant
. Pleuro-Pudmonary. Neiplasms
I. EpidermoidCarcinomas
IL. Small Cell Anaplastic Carcinomas
III. AdenocarcJnoma:s
I. ~Brochogenic a. acinar
b. papillary witM1h or witliout mucln formation
IV'. Large Cell Carcinocomas
V. Combined Ep6dermoid and Adenocarcinomas
VI. . Carcinofd Tumors
VI1. Bronchial Gland Tumors
- I. Cyl.indromas -~- 2. MucoepiAermoidturmors
VIIL. Papillary Tumors of the Surface Epithelfum
IX. Mixed Tumors and Carcinosarcomas
X. Sarcomas
..
XI. Unclasslfled - -
XII. Melianoma .
X1I1.. Mesotheliomas
SOURCE: Kreyberg, L. (25).
132
TABLE 4.-Age-adjusted lung cancer mortality ratios--
age began smoki'.ng and degrea of Inhalation
Age Regan.Smoking Male Female
IS 16.8 2.5
15.- 19 14.7 5.0
20 - 24 10.1 3.4
25. + _ . 4.1 . . . 2.3
Depth of Inhalation Male Female
Nbne 8.0 2.0
SI'.ight 8.9 2.3
Moderate 13.1 .. 3.5
Heavy 17.0 _ 7.1
9I
TABLE 6.-Lung cancer mortality ratios for females by
duration of smoking: Swedish Study
Duration of
Smoking In -
Years .
Mortality
Ratios
Nonsmokers 1..0
1-29 years 1.6
30+ years 9.6
SOURCE: Cederlof, R. (6).
139
little lower than the consumption of Scottish men 20 years
ago. In. England and Scotland, where the upper socioeconomic
classes have reduced their cigarette consumption in recent
decades, there is a significantly greater lung cancer mortality
rate in the: lower socioeconomic classes among women, (22).
Age-adjusted death rates for lung cancer in women In
select countries indicate that women. In Hong Kong, have the
highest rates, while those In Scotland are second and those In
England and Wales are third. The United States ranked sixth
world wide(.i).
Among nonsmokers, lung cancer is found slightly more
often in urban than In rural areas; however, among, smokers
the marked Increase In lungg cancer found inn urban areas
suggests that urban living exerts a potentiating rather than an
additive effect on the incidence of lung cancer. Urban living
has little independent effect on lung cancer induction in
comparison with even modest smoking, of filtered low-tar and
low-nicotine cigarettes (g, 12).
Smoking Patterns Among Women
Although women tend to have different patterns of smoking
than men, the relative relationships between smoking and lung
cancer are the same. Lung cancer rates for women who
smoke increase with increased dosagee asmeasured by several
dosage measures, inciudingg number of cigarettes smoked per
day, duration of smoking habit, degree of inhalation, age of
initiation of smoking, and the "tar" and nicotine level of the
cigarettes smoked.. These data, obtained from~ several
prospective investigations, aree examined in Tables 4, 5, 6, 7,
9, and 10. The more cigarettes an individual smokes, the
more likely that individual will die of lung cancer (Table 5).
Overall, female cigarette smokers have 2.5 to 5.0 times
greater likelihood of dying from lung cancer than nonsmokers
(Table 7). As discussed earlier, when the full impact of the
cohort effect is felt, this ratio will probably approach that
for men (8 to 12).
Doll, et al. studied, the cause-specific mortality
experience among approximately A,200 female physicians In
England during the period 19511 to 1973 (4a). The results of
this study are presentedin detail in Table 8, which also
Includes data from a previous report on male physicians (a)..
It is apparent thatt smoking and lung cancer are simi-
larly related in men and women. In both sexes, lung cancer
136
TABLE 7.1ung cancer mo:rtality prosDective studies
Cigarette
Non-Smokers Smokers
ACS Male I.0 10.1
Female 1.0 2.6
British. Male 1.0 14.0
Physlclans
Female 1.0 5.0
Swedish Male 1.0 8.7
Study
Female 1.0 4.5
SOURCE: Hamnond., E.C. (14), Doll, R. and Peta, R. (9, 9a), and
Cederlof, et al. (6).
-
140
Age Adjusted Lung Cancer Death - Relative Risks
t?11111111
TABLE 8.-Death rates from lung cancer and smoking habit when last asked British physicians 1951-1973
ANNUAL DEAFH RATE PER 100,000
Total PERSEINS STANDARDIZED FOR AGE
Popul. # Deaths
Non-smokers Ex-Smokers Current Smokers - Dose Per Day
1-14 15-25 25+
Women F194 27 7 23 9 45 2QB
(cigarettes only)
Men 34,440 441 IP 43 52 1n6 224
r
e(P<.001)
SOURCE: Doll, R. (9, 9a).
UUS99E0
(any tohaccofgrams)
(I gram = 1 clWarette)
X 2
Non-smokers Trend
Yf. (nosef
Others Response)
13.47 61.59
41.9' 197.04
' - i
women. might have a decreased susceptibility to lung cancer.
A more careful examination of the data indicates that most of
the differences between male and female lung cancer rates
can be explained by differences in smoking hah.its and occu-
pational exposures. As discussed in other sections of this
report, a smaller percentage of women thann men smoke and,
when they do smoke, they are more likely to adopt smoking
behaviors that have been shown to have a lower risk of deve-
loping lung cancer. That Is, they smoke fewer cigarettes per
day, inhale less, start smokingg later In Ilfe, and are more
likely to smoke low-tar and low-nicotine and filter
cigarettes. In addition, It is Important to consider the cohort
effects on the differences in rates between males and
females. Over 85 percent of those who smoke regularly
began between the ages of 12 and 25 (33). Men first began
to smoke in large numbers just before and during the First
World War. As each succeeding birth cohort passed through
the age of initiation (12 to 25), a larger percentage began
smoking until the groups born between 1915-1930 were
reached (J9a).. Inthe birth cohorts born after 1930, fewer
began to smoke regularly. The risk of developing lung cancer
increases exponentially with age and duration of smoking, with
the increase starting 1 5 to 2P years after the beginning of
regular smoking. This accounts for the dramatic rise in the
male lung cancer death rates noted in the 1930s. As those
birth cohorts withhigher smoking rates replaced those with
lower smoking rates, the age-specific lung cancer rates rose
steadily; and as each of the heavy-smoking birth cohorts grew
older, their lung cancer risk continued to accelerate, resulting
in a very steep rise in the overall male lungg cancer death
rate. The overall cancer rates among men will continue to
rise (albeit more slowly) as those birth cohorts with the
heaviest smoking prevalence replace those with lower
prevalence in the older age groups where the lung cancer
death rates arethe highest. As these birth cohorts with hiRhsmoking prevalence pass through the age
groups and are
replaced by birth cohorts with lo wer smoking prevalence,
declines in lung cancer rates should, he noted.
They should be noted first in the age-specific death
rates for the younger age groups and later in the overall lungg
cancer death rates. The first indications of this change have
been noted, with a decline in the age-specific death rates in
males born after 1930. .It is therefore important to consider
this cohort effect when examining the differences between
lung cancer rates of inen, and women.
?a
9
134
TABLE 10.-Age-adjusted lung cancer mortality (TIN) ratios
for males and females, comparing those who smoked a few high
TIN cigarettes with those who smoked many low T/N cigarettes
1-19 high T/N
cigarettes/day 20-39 iowTJN'.
cigarettes/day
Males ~ 1 .011 0~ 1.6
Femal es 1.00 2.1
The mortality ratio for the category with lowest risk was
made 1.00 so the increase in risk with smoking more cigarettes/day
could be iitustrated. - -
SOURCE: Hammond, E.C. (14),. . . .
143
FIGUREI .-Agsed/ustad death rates' formallgnsnt nsoplasm of tiachee, bronchus end lung"
and breast by color and sex; United Stetes, Ig50-191y, and Projection for whita femafea to
I9B5.
/
WHITEMALES /
/
/~
BFEAST
:
/ I ........ r.... .
/NONWHITEMALES
/
/ .
/ .
/
.00
WHITE EEMFLES
\
/-~ NONWHITEFEMALES
70
m
50
50
27
10'
: 6
1950 1955 1950 1965 19~0 19)5 1980 1965
-BrM,Fev. )rm na. - 81h F- 1883
'Adiusled by.lhe direct mathod to the U.S. populetion, 1940.
^ICObth and 71h Rev. Nos. 162 163 3 and BIh,9ev. No 162.
Source'. Oala from the NalionallCenlenfor Health Stallstics.
^Prolecfion based on average annual rale o/lncrease over lasl 10 years, dEnvetli from Surveibance,
Epidemiology.and End FesulB (SEERM Program, Nallonal Cancer Instiiule.
12r
Women began to take up smoking in large numbers 25 to
30 years later than men (in the early 1,44ns). This rise in
smoking prevalence was produced by predominently young
women first using tobacco as cigarettes. This is in contrast
to the rise in men which included a substantial percentage of
men, of alll ages who switched from. other forms of tobacco
use to cigarettes. The rise in lung, cancer rates in women
occurred as those cohorts with high smoking prevalence
reached the ages where lung cancer occurs with significant
frequency(age 45 and over). Since most of these women
began smoking cigarettes prior to age 25 they would have at
least 20 years of exposure by age 45 in contrast to the
shorter durations of exposure at age 45 for those men who
switched to cigarettes from other forms of tobacco around the
time cigarettes first cam einto widespread use. This greater
duration of exposure at any given age for women in these
first heavy smoking birth cohorts compared to the first
cohorts In men, should resu R. in a more abrupt rise in lung
cancer rates in women. This rapid rise in female lung cancer
death rates began to be observed in the late1 o.5ns. As birth
cohorts with higher smok.ingg prevalence continued to replace
those with lower sm oking prevalence, the rates rose steeply,
reproducing the phenomenon noted in males 20 to 30 years
earlier with. some indication that the rise is even steeper for
women. If one subtracts 25 years from the female cancer
death rates inFigure 1, the rates for women are only slightly
below the rates for men. This small difference is explainedd
by lower prevalence of smoking and less hazardous smoking
patterns of women and their less frequent exposure to
occupational'carcinogens. Thus, close scrutihyof the trends
reveals no substantial protective effect for women on the risk
of developing Iungcancer but rather leads to a sohering.
projection of a reprodutton of the male lung cancer epidemic
in women (Figure 1).
Geographic Differences
Lung cancer death rates, including all histologic types, are
highest in industrialize& countries where there has been a
higher smoking, prevalence for a longer time. Women im,
Scotland have one of the highest death rates from lung cancer
of women of any country. Their tobacco consumption per
smoker approaches that of English and Welsh men (22).
Current tobacco consumption by Scottish women is only a
135
TABLE 5.- Age-adjusted relatlverlsks of lung cancer
by number of cigarettes smoked
Number of Cigarettes Smoked Dailq
1-9 10-19 20-39 40+
ACS Study Male 4.6 8.6 14.7 I8.8
Female 1.3 2.4 4.9 7.5
1-14 15-24 25+
Prltlsh Mala 7.8. 12.725.1
Physicians
Female 1.3 6.4 29.7
SOURCE: Hamoond, P.C. (14) and Doll, R. and Peto, R. (0, 9a),
138
TABLE 9.-Age-ad)usted lung cancer epytall'hy (T/N) ratloss
, for, nules and females, by tar and nlcotine In.eigareCtes smoked
Males Females
High TIN 1.00 1.00
Medivn TIN 0.95 0,79.
Low TfN , O.g1 0.60 .
eThe mortality ratioo fortho- category with highest rlsk was
made 1.00 sn that the relative reductiions in risk with the use
of lower TCN cigarettes could he rtsua n zed. _
SOURCE: Hammond,E.C. (14).
142
TABLE
M1tales
Eemale
eTh
made 1
couid
SOU
cancer mortality rate of the women who smoked fewer
cigarettes, but with high "tar" and nicotine (Table 10). in a retrospective study standardized for
duration of
smoking, number of cigarettes smoked, inhalation and butt
iength,iong-term female smokers of filter cigarettes had a
lower relative risk of developing cancer than smokers of non-
filter cigarettes (59).
Cessation of Smoking
Although the risk of developing lung cancer increases with
age, both for smokers and nonsmokers alike, women in good
health~ who quit smokingg will, over a period of years,
experience a reduction inn their relative risk of deveiopingg
lung cancer. About. 15 years after they have quit smoking,
the risk of developingg lung cancer approximates that of the
nonsmoker.
Experimental Carcinogenesis
Tobacco tars, tobacco smoke, and single or mixtures of
chemicals found in tobacco smoke have been used with various
species of animals In carcinogenesisexperim ents invotving skin
painting, subcutaneous injections, tracheobronchiail implantation,
and/or instiiiation and inhalation. Some experim ents have
reported sex differences in the occurrence of lung tumors
following exposure to chromium oxide (3n).
However, in a recent monograph on lung cancer,
separate reviews on tobacco carcinogenesis, radiation car-
cinogenesis in the respiratory tract, and experimental models
for studies of respiratory tract carcinogenesis did not yield
information suggesting that the male lung of any of the
species studied was more susceptible than the female lung to
carcinogenic action by either tobacco products or radiation
(16.). The reader is referred to previous Smoking and Health
Reports for summaries of experimental tobacco carcinogenesis
studies.
LARYNX
The larynx is a small, complex structure, which produces
speechy controls the flow of air in and out of theiungs, and
145
mortality was at least three times as high in ever-smokers as
In never-smokers, at least twicee as high in current heavy
smokers (more than 25 cigarettes) as in Ilght smokers (less
than 15 cigarettes), and exhibited a significant dose-response
relationship. The magnitude of the smokingg effect on lung
cancer for females and males was approximately the same.
The relative risks for mortality from lung, cancer for
moderate(I5 to 24 cigarettes per day) and heavy (more than
25 cigarettes) smokers were 6.3 and 29.7 among females, and
10.6 and 22.4 for males. .
The authors emphasize, however, that no conclusions
can he dra wn from this data about the magnitude of the
biologic effects of smoking in men compared to women. Since
the authors documentedd differences. In. lifetime smokeexposure
(later age at initiation and lower prevalence of inhalation
among females), lifetime smoking exposures between the sexes
were not directly comparable. This issue will'be resolved
only whenstudies examine the effect of smoking in cohorts of
women whose lifetime smoking behavior more closely matches
that of the men to whom they are compared.
AA number of retrospective studiess have examined the
relationship of smoking and lung cancer in women. The1471
Health Consequences of Smoking reviewed many of these
Investigations and showed a smoker-to-nonsmoker risk ratio
ranging from 0.2 to 6.8for females. The reader is referredtod
this volume for a more detailed discussion of these studies.
Results of these investigations reveal sexx differentials similar
to those found in the larger prospective studies, with males
havingg higher overall lung cancer rates compared to females.
However, the lung cancer rates of smokers are significantly
higher than those of nonsmokers for both sexes.
The women who smokee low-"tar", low-nicotine
cigarettes have a lower age-adjusted lung cancer mortality
rate than women who smoke high-"tar", high-nicotine
cigarettes. Women who smoke medium-"tar", medium-nicotine.
cigarettes have mortality rates In between (,15) (Table9).
However, even the low-"tar" and -nicotine cigarette smoker
has a rate substantially higher than the nonsmoker.
These data suggest some benefit from smokingg low-^tar",
low-nicotine cigarettes. However, a further comparison of
women who smoked less than one pack of high-"tar", high-
nicotine clgarettes daily with women who smoked more than
one pack of low-"tar", low-nicotine cigarettes daily revealed
that the smoker of more than a pack a day of low-"tar",
low-nicotine cigarettes had over twice the. age-adjusted lung
144
smoking and drinking onn laryngeal cancer development (57,
55).
When women quit smoking, their relative risk of
developing laryngeal cancer decreases until 10 years after
cessation when their risk approaches that of the nonsmoker
(58).
A num ber of investigators have found an association
between exposure to asbestos and the subsequent development
of laryngeal carcinoma (55).
ORAL
Oral neoplasms include cancer of the lip, tongue, gums, buccal
mucosa, hard and soft palate, salivary glands, floor of the
mouth, and oropharynx. In the United States for 1980, there
will be 17,900 new cases in men and 7,600 in women,
resulting in 6,100 deaths in men and 2,700 deaths in women.
While different histological types of cancer can occur in this
group, squamous cell carcinoma is by far the most common,
except for the tum ors of the salivary glands. Five-year
survival rates range from 25 percent in those patients whose
tum or is advanced when first diagnosed to 67 percent for
those whose tumor Is localized at diagnosis.
In women, orall cancers account for 1.9 percent of all
neoplasms, while they account for 4.7 percent of all cancer
occurring in men. Death from the various oral cancers
account for 1.4 percent of cancer deaths in women and 2.8
percent of all cancer deaths in men. Cigarette, pipe and(or
cigar sm oking are all associated with increased oral cancers.
Heavy alcohol use (over 7 ounces per day) has been shown to
be an independent causative factor (40, 54). When both are
used together by women or men, synergism results in an even
greater incidence of orall cancer (5). Poor oral hygiene or
inadequate dentition is also a risk factor (18Y..
Most of the prospective epidemiologic studies have
concentratedond men. In Japan a large prospective study
showed the mortality ratio for oral cancer to be 2.88 for the
male cigarette sm oker and 1.22 for the fem ale cigarette
smoker compared with the nonsmoker.
Leukoplakia or an abnormal thickening and keratiniza-
tion of the oral mucous membrane is recognized as a pre-
cancerous condition. While found inn the western world, it is
most common in Asian countries where a mixture of tobacco
and betel nut or lime ash chewing is common, and in those
147
smokers. Thereare no prosoective epidemiologic studies of
female smokers in this country large enough to permit
development of a mortality ratio comparison to nonsmoking
females.
Ingestion of alcohol is also a major etiological factor
in esophageal carcinoma. A dose-response relationship exists
with increasing alcohol ingestion resulting In an increased
incidence of esophageal carcinoma. As in the larynx,
synergism of the carcinogenic effect on the esophagus occurs
with the use of both tobacco and alcohol (5R). Whether or
not nutritional deficiencies, which occur frequently with
severe, chronic alcoholism, play a role inn carcinogenesis
remains unknown, as does the possible contribution of chronic
iron deficiency found In. Plummer binson's Syndrome
(Paterson-Kelly syndrom e, sideropenic dysphagia). -
Ninety-eight percent of esophageal cancers are histo-
logically squamous cell In type.: In an autopsy study,
Auerbach found more abnormaLities of the esophageal
tissues- -including atypical nuciei, disintegrated nuclei,
hyperplasia and hyperactive esophageal glands--of tobacco
smokers as compared with nonsmokers (2).
Esophageal carcinoma can be produced experimentally
by both benz(a)pyrene and the nitrosamines. Both
benz(a)pyrene and a group of nitrosamines have been
identified in tobacco smoke. The appearance of
experimentally-produced squamous cell carcinomas can be
accelerated by dissolving the carcinogen in alcohol, a,
laboratory experim ent duplicated daily by thousands If not
millions of our citizens (55).
URINARY f3LADDER.
Cancer of the urinary bladder will occur in 26,(b0 men and
9,500 women in the Unit°d States during 198n and it will kill
7,000 men and 3,300 women (1). Cancer of the urinary
bladder is frequently muiticentricc in origin. If found while
still localized in the bladder wall, the 5-year survival rate is
72 percent, In contrast to 14 percent for those patients
whose disease has already spread when the diagnosis was first
established (1).
Bladder cancer has been associated with. occupational
exposure to aniline dyes, leading to the study of arom atlc
amines as potential carcinogens. 2-naphthylamine, xenyiamine,
benzidine, and 4-nitrobiphenyl have all been implicated (55).
Q
I
149
countries where reverse chutta (cigar) smoking occurs.
Women In certain regions of India are more likely to engage
In reverse chutta smoking than men, although hoth women and
men develop carcinom a of the hard palate after years of
reverse chutta smoking (3g).
Women and men with mouth, pharynx, and larynx cancer
who continue smoking after surgical treatm entof the firstt
neoplasm have a 40 percent probability of developing another
neoplasm of the head and neck. Only 6 percent of the
patients who quit smoking develop a second cancer in the
region. Less than 10 percent of oral cancer patients are
nonusers of tobacco; almost all have a well-differentiated
carcinoma and a relatively high cure rate (76).
ESOPHAGUS
Carcinoma of the esophagus will be diagnosed in 6,200 men
and 2,600 women In the United States in 19gn (I). The
Am erican Cancer Society estimates that there will be 5,500
deaths in men and 2,1000 deaths In women from this disease
(1). M edian survlval tim e once esophageal carcinoma Is
diagnosed Is 6 months. The 5-year survival rate is only 3
percent. Esophagealcarcinomal rates have declined in the
white population over the past 25 years. However, they have
Increased In the black population inn both sexes. This may
reflect genetic or environm ental. factors. Inn the Caspian
littoral, there Is a remarkablee difference In esophageal
carcinoma incidence in people of comparable background and
socioeconomic status living only 400 kilometers apart. There
is a 30-fold higher incidence In womenn living in the desert
northwest section of Mazandran, Iran, compared with the
fertile Caspian rainbelt 400 kilometers to the west (,23),. -
Data from a number of retrospective studies show that
smoking Increases the risk of developing esophageal carcinoma.
Neither the relative risk of developing esophageal carcinoma
nor the steepness of the dose-response relationshipp with
cigarette smoking is as great as It. is for carcinoma of the
lung or larynx (58). Individuals who stop smokingg or switch
to low-tar, low-nicotine cigarettes will, after a lag period,
experience lower relative risks of developing, esophageal
carcinoma, althoughh the fall-off Is not as steep as withh lung
and laryngeal cancer. In the male, both retrospective and
prospective studies show that pipe and cigar smokers have
mortaiity rates from esophageaJl carcinoma similar to cigarette
148
prevents aspiration during swallowing. In 1980 there will be
an, estimated 1,700 new cases of laryngeal cancer and 60n
deaths from that tumor in U.S. women (Table 1). Laryngeal
cancer has occurred predominantly in men, but more and more
wom en aredevetopinge laryngeal cancer as their smoking and
drinking habits come to approximate those of men. The
male-to-female ratio for laryngeal cancer exceeds that of
lung cancer. Laryngeal cancer occurs In the fifth, sixth, andd
seventh, decades both in menn and women. While the disease is
uncommon, its incidence has continued to rise over the past
quarter century, especially in wom en, substantially because of
changes in their smoking habits.
Cancer can occur either in the glottis (true cord,. 70
percent of cases), or In the suhglottic or supraglottic region
(false cord, 25 percent of cases). Usually the neoplasm is
epidermoidd carcinoma when examined histologically. Since a
tumor that interferes witK speech gives rise to early
symptoms, gtottic cancers are usually diagnosed at an early
stage and are curable in over 60 percent of the cases.: When,
the tumor arises in the subglottic or supraglottic region,
interference with phonation or speech may not occur as early
as whenn neoplasm begins on the glottis. The tu mor may,
therefore, reach a greater size and be accompanied by
significant local tissue invasion and destruction as well as
m etastasis. . Patients with tumors discovered when they are
stil:ll localized in the larynx have approximately an Rn percent
cure rate, while advanced lesions have a 33. percent 5-year
survival rate. ...
. Laryngeal cancer displays a strongg dose-response rela-
tionship with smoking, increasing with the number of
cigarettes smoked per day, the "tar" and nicotine content of
the cigarettes smoked, the depth of inhalation and number of
years cigarettes were smoked the riskk of developingIarynReal
cancer is inversely related to the age at which smoking began
(55). A lower risk for laryngeal cancer has been
demonstratedd in women who used filtered cigarettes for 1n
years or more compared to those who smoked non-filtered
cigarettes. Nonetheless, the risk remained well inn excess of
that experienced by nonsmokers (SR). Excessive use of alcohol by nonsmokers also results in
an increased incidence of larynyeal.cancer. Heavy drinkers of
alcohol- -that Is, greater than seven ounces of whiskey or its
equivalent per day--who also smoke cigarettes have a greater
risk of developing laryngeal cancer than If they either smoked
or drank to excess alone. There is a synergistic effect of
m
,
146
Num erous retrospective studies have sho wn a rela-
tionship between smoking and urinary bladder carcinoma in
both men and women (19). The likelihood of either womenn or
menn developing bladder cancer Increases with the number of
cigarettes smoked, the duration of sm oking, and tar and
nicotine content of the cigarette smoked. Changing to low-
tar, low-nicotine cigarettes or more clearly, cessation ofsmoking, decreases the relative risk of
developing bladder
cancer. The risk' of an ex-smoker developing urinary bladder
cancer approaches that of the nonsmoker years after cessation
(59).
In prospective studies In Japan, and Sweden, women who
smoke are 1.6 to 2.7 tim es as likely to develop bladder
cancer as non smokers (17,5). In an international study of
successive birth cohorts inn theU nited~. States, United Kingdom,
and Denmark, Hoover and Cole found increasing rates of
bladder cancer associated with increased cigarette smoking in
men and womenfn both suburban and rural areas and in all
nationalities studied (19). It has been estimated that 30
percent off urinary bladder cancer in women can bee attributed
to cigarette smoking (55).
KIDNEY
Cancer of the kidney will occur in 10,500 men and 6,400
women In the United States during 1980 (1). Some 4,Rf+0 men
and 3,100 women will die of renal carcinoma (1). The S-
year survival rate. Is between 40 and 50 percent (1). While
the overall classification of kidney carcinoma includes tumors
of the renal pelvis and ureter, the largest number of kidney
carcinomas occur in, the renal parenchyma and are adenocar-
c inomas.
In retrospective studies, adenocarcinomas of the kidney
are found more frequently in smokers compared with non-
smokers in both men and women (55;57). In a large
prospective study among U.S. veterans, the kidney cancer
mortality ratio increased from: 1.0 (the baseline for
nonsmokers) to 1.344 for those who smoked 10 to 19
cigarettes daily and to 2.75 for men who smoke two packs or
more each day(2la). No large scale prospective study of
women and kidney cancer has bee reported to date.
150
(26) MOORE, C. Smoking related to cancer of the mouth,
tongue and lip. In: Steinfield, J., Griffiths,
W., Ball, K., Taylor, R.M. (Editors). Proceedings
of the Third WorldConference on Smoking and Health,
New York, June 2-5, 1975. Volume 11. Health
Consequences, Education, Cessation Activities,
and Social Action. U.S. Department of Health
Education, and Welfare, Public Health Service,
National Institutes of Health, National Cancer
- Institute. DHEW Publication No. (NIH) 77-1413,
1977, pp. 101-104.
(27) MORTEL, C. In: Holland, J., Frei, E. (Editors).
Cancer Medicine. Philadelphia, Pennsylvania,
. Lea and Febiger, 1973.
(28) MOSS, E. Oral and pharyngeal cancer in textile
workers. Annals New York Academy of Sciences
271: 301-307, 1976.
(29) MUSHINSKI, M., STELLMAN, S.D. Impact of new
smoking trends on women's occupational health.
Preventive Medicine 7: 349-365, 1978.
(30) NATIO NAL CANCER INSTITUTE. Carcinogenesis
Technical Report Series, 1977-1979. U.S.
Department of Health, Education, and Welfare,
Public Health Service, National Institutes of
Health, National Cancer Institute.
(31)NATdONAL CENTER FOR HEALTH STATISTICS. Changei
in Cigarette Smoking and Current Smoking
Practices Among Adults: United States, 1978.
Advanca Data. No. 52, September 19, 1979, 16
pp.
(32) NATIONAL CENTER FOR HEALTH STATISTICS. Health,
United States, 1978. Department of Health,
Education and Welfare, Public Health Service,
Office of Health Policy, Research and
Statics, National Center for Health
Statistics, DHEW Publication (PHS) 78-1232,
1979
(33) NATIONAL CLEARINGHOUSE FOR SM OKING AND HEALTH.
Adult use of tobacco, 1975. U.S. Department
of Health, Education and Welfare, Public
Health Service, Center for Disease Control,
Bureau of Health Education, National'
Clearinghouse for Smoking and Health, June
1976, 23 pp.
156
2. Cigarette sm oking accounts for 1R percent of all
cancers newly diagnosed and 25 percent of all cancer deaths
in women. In 1990, 32,000 of the estimated117,000 deaths,
or over one-quarter of the deaths expected from lung cancer,
willl occur in women. -
3. Women cigarette smokers have been reported to
have between 2.5 and 5 times greater likelihood of developing
lung cancer than nonsmoking women.
4. Among women the riskk of devefopingg lung cancer
increases with increasing number of cigarettes smoked per
day, duration of the smokingg habit, depth of inhalation, tar
and nicotine content of the cigarette sm oked. The risk is
Inversely related to the age at which smoking began.
5. A dose-response relationship has been demonstrated
between cigarette smoking and cancer of the lung, larynx, oral
cavity, pancreas, and urinary bladder in women.
6. The rise in lung cancer death rates is currently
much steeper in women that in men. It is projected that the
age adjusted lung cancer death rate witl surpass that of
breast cancer in the early 19AOs.
7. The rapid increase in lung, cancer rates In women
Is similar to butt steeper than the rise seen In men
approxim ately 25 years earlier. This probably reflects the
fact that women first began to smoke in large numbers 25-30
years after the increase inn cigarette smoking among men.
Thus, neither menn nor wom en are protected from developing
lung cancer caused by cigarette smoking.
8. Cigarette smoking has been causally related to all
four of the major histologic types of lungg cancer In both
women and men, including epidermoid, small cell, large cell
and adenocarcinoma.
9. The use of filter cigarettes and cigarettes with
lower levels of tar an& nicotine by women is correlated with
a lower risk of cancer of the lung and larynx compared to
the use of high tar and nicotine or unfiltered cigarettes. The
risk posed by smoking low tar cigarettes, however, is clearly
greater than that among females who never smoked.
1D. After cessation of cigarette smoking, a wom an's
risk of developing lungg and laryngeal cancer has been shown
to dropslowly,equallingp that of nonsmokers after 10-15
years.
11. Excessive ingestion of alcohol acts synergistically
with cigarette smoking to increase the incidence of oral and
laryngeal cancer in women.
152
Stdc,
(1)
(2)
(3.
(4
(5
(6
PANCREAS
Carcinoma of the pancreas will occur In 12,500 men and
11,500 women in the United States during 1980, and 11,100
men and 9,800 women will die of pancreatic carcinoma (1).
During the past 25 years, there has been a steady increase in
both the incidence and mortality due to pancreatic cancer in
both men and women (1,24). Among the common human
neoplasms, the rate of increase of pancreatic cancer over the
past quarter century has been second only to that of the lung.
Most pancreatic carcinomas are adenocarcinomas,
arising from ductal cells (27). Most are relatively
undifferentiated in cell type. The median survival time from
histologic proof of diagnosis to deathh is 3.5 months in men
and 4.5 months in women. Survival time varies little with age
at tim e of diagnosis, duration of sym ptoms, location of Q
primary lesion (head, body, or tail of pancreas) or even
degree of differentiat~ion.The 5-year survival rate is one
percent, the most dismabl survival rate for any of the common
neoplasms of either men or women. 0 ).
Retrospective studies relating smoking to pancreatic
carcinoma have been reviewed in previous reports. In a
prospective study of 143,000 women, the pancreatic cancer
mortality ratio was 1.94 for Japanese women smokers
comparedd to non smokers (17). In Sweden, a smaller
prospective study showed that the mortality ratio for
pancreatic cancer was 2.5 for women smokers compared to
women nonsmokers (6). .
In the United States, the m ate to fem ale ratio of
pancreatic cancer was 1.6 in the 1940s. It has decreased to
the current estimate of 1.17 for 1979 .and is consistent with
the decreasing male to female ratios of lung and laryngeal
carcinomas.
In both retrospective and prospective epidemiologic
studies a dose-res onse relationshi bet e tt
w
n
, p p
e
cigare e ~
smoking and pancreatic carcinoma could be found (56,58). 1
SUMMARY
1.. Cigarette sm oking is causally associated with
cancer of the lung, larynx, orab cavity, esophagus, kidney and
bladder in women as well~ as in men; it is associated with
kidney cancer in women.
151
(52) U.S. PUBLIC HEALTH SERVICE. The Health Consequences
of Sm oking, 1974. U.S. Department of Health,
Education and Welfare, Public Health Service,
Center for Disease Control, DHEW NO. (CDC)
74-8704, 1974, 124 pp.
(53) U.S. PUBLIC HEALTH SERVICE.. The Health Consequences
of Smoking, 1975. U.S. Department of Health,
Education and Welfare, Public Health Service,
Center for Disease Control, DHEW. Publication
No. (CDC) 76-8704, 1976, 235 pp.
(54) U.S. PUBLIC HEALTH SERVICE. The Health Consequences
of Smoking. A Reference Edition. U.S. Health
Department of Health, Education and Welfare,
Public Health Service, Center for Disease
Control, DHEW Publication No. (CDC) 78-8357,
1976, 657 pp.
(55) U.S. PUBLIC HEALTH SERVICE. Sm oking and Health:
A Report of the Surgeon General: 1979. U.S.
Department of Health, Education and Welfare,
Public Health Service, Office of the Assistant
Secretary for Health, Office of Smoking and
Health, DHEW Publication No. (PHS) 79-50066,
1979.
(56) WYNDER, E.L., MABUCHI, K., MARUCHI, N., FORTNER,
J.G. Epidemiology of cancer of the pancreas.
Journal of the National Cancer Institute 50(3):
645-667; 1973.
(57) WYNDER E.L., MABUCHI, K., WHITMORE, F.W., JR.
Epidemiology of adenocarcinoma of the kidney.
Journal of the National Cancer Institute 53(6):
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(10) DOLL, R., PETO, R. Cigarette smoking and bronchial
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regular and lifelong nonsmokers. Journat of
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157
TABLE 1.-Ageadjueted death rates from COLD (ICDA 490-492' and 519.3)
1960-1977 (per 100,000)
WHITE NONWHITE
Male Female Male Female
1977 33.4 10.7 14.8 3.5
1976 33.5 10.1 14.9 . 3.2
1975 32.1 9.1 13.5 3.3
1974 31.1 8.4. 13.7 2.8
1973 31.4 7.8 14.1 3.0
1972 29!9 7.0 14.0 2.9
1971. 28.6 6.5 13.2 3.0
1970 28.2 6.0 13.3 2.6
1969 27.3 5.4 12.8 2.4
1968 22.3 3.8 13.7 2.5
1967 . 19.9 3! 1 11.5 2.0
1966 19.7 3!0 11.0 1.9
1965 18.4 2.7 10.4 1.8
1954. 16.1 2.4 . 9.2 1.6
1963 15.9 2:3 9.5 1.9
1962 13.1 2.0 7.7 1.8
1961 10.9 1.7 7.0 1.3
1960 10.4 1.7 6.7 1.4
Source: National Center for. Health.Statistics. Vital Statistics United States 1960- .
1977 (50)
1EZ
(45) U.S. PUBLIC HEALTH SERVICE. Smoking and Health.
Report of the Advisory Committee to the
Surgeon General of the Public Health Service,
Department of Health, Education and Welfare,
Public Health Service Center for Disease
Control, DHEW Publication No. 1103, 1964, 387
pp
(46) U6S. PUBLIC HEALTH SERVICE. The Health Consequences
of Sm oking. A Public Health Service Review:
1967. U.S. Department of Health, Education
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Services and Mental Health Administration,
DHEW Publication No. 1696, Revised, January
1968, 227 pp.
(47) U.S. PUBLIC HEALTH SERVICE. The Health Consequence
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Health, Education and Welfare, Public Health
Service, Health Services and Mental Health
Admnistration, Publication No. 1696, 1968,
117 pp.
(48) U.S. PUBLIC HEALTH SERVICE. The Health Consequences '
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Administration, DHEW Publication No. 1969-2,
1969, 98 pp.
(49) U.S. PUBLIC HEALTH' SERVICE. The Health Consequences
of Sm oking. U.S. Department of Health, Education
and Welfare, Public Health Service, Health
Services and Mental Health Administration,
DHEW Publication No. (HSM) 71-7513, 1971,
458 pp.
(50) U.S. PUBLIC HEALTH SERVICE. The Health Consequences
of Sm oking. U.S. Department of Health, Education
and Welfare, Public. Health Service, Health
Services and Mental Health Administration, No.
(HSM) 72-7516, 1972, 158 pp.
(51) U.S. PUBLIC HEALTH SERVICE. The Health Consequences
of Smoking, 1973. U.S. Department of Health,
Education and Welfare, PublicHeaith Service,
Health Service and Mental Health Administration,
DHEW Publication No. (HSPA) 73-8704, 1973,249.pp.
(
(
TABLE 2.COLD Mortality ratios+in seven prospective studies
Women in 25 Men in 25
ritish U.S. Canadian Men in California Swedish Subjects
Study B States States
Reference Doetors 45-65 45-64 65-79 Veterans Veterans 9 States Occupations Females Males
(20) (35) (35) (45) (8) (36) (21) (15)
Emphysema .
and/or 24.7 - - - 10.08 - 2.30 4.3
bronchitis
Emphysema
without - 4.89 6.55 11.41 14.17 7.7
bronchitis I
Bronchitis - - - - 4.49 11.3
Bronchitis, - emphysema - - - - - - - - 2.2 3.7'
and asthma '
+ Death rate for smokers divided by death rate of a comparable group of nonsmokers.
'For all ages cnmbined. increased mortality rate Significant only for former smoken.
660SB9E0
lung disease (COLD). Many attempts have been made to
establish criteria for the diagnosis of chronia bronchitis and
emphysema (.1,30,31). The most widely accepted definitions In
the United States arethose of a joint committee of the
Am erican College of Chest Physicians and the Am erican
Thoracic Society (1). "Bronchitis: A non -neoplastic disorder of structure or
function of the bronchi resulting from infectious or
noninfectious irritation. The term bronchitis should be
modified by appropriate words or phrases to indicate its
etiology, its chronicity, the presence of associated airways
dysfunction or type of anatomic change. The term chronic
bronchitis, when unqualified, refers to a conditionn associated
with prolonged exposure to nonspecific bronchial irritants and
accompanied'by mucous hypersecretion and certain structural
alterations in the bronchi. Anatomic changes may include
hypertrophy of the mucous secreting apparatus and epithelial
metaplasia, as well as more classic evidence of inflammation..
In epidemiologic studies, the presence of cough or sputumm
production on most days for at least 3 months of the year
has sometimes been accepted as a criterion for diagnosis "
"Pulmonary Emphysema: An abnormal enlargement of
the air spaces distal to the terminal nonrespiratory bronchiole,
accompanied by destructive changes of the alveolar walls.
The term emphysema may be modified by words or phrases to
indicate its etiology, its anato mic subtype, or any associated
airway dysfunction." "Chronic Obstructive Lung Disease: This term refers
to a disease of uncertain etiology characterized by persistent
slowing of airflow during forced expiration. It is
recommended that a more specific term, such as chronic
obstructive bronchitis or chronic obstructive emphysem a, be
used whenever possible."
It should be noted that these definitions may have
serious inadequacies, particularly when applied to longitudinal
studies assessing the natural history of COLD (62,32). In the
following discussion, these limitations are recognized.
SMOKING AND RESPIRATORY MORTALITY
Recent mortality statistics indicate a striking increasee in
death rate from COLD among women (50). These data
presented in Table 1 indicate a nearly fivefold increaseine reported mortalities due to COLD from
1962 to 1977among
0
0
161
A"
ftgfim~a
TABLE 3.-Death rates from lung cancer and smoking habit when last asked
British physicians 1951 - 1973
ANVUAL
DEATii RATE PER 100,000 X 2
-
Total PERSONS STANDARDIZED FOR AGE Non-smokers Trend
Popul. j{ Deaths Non-
Smokers Ex-
Smokers
Current Smokers - Dose Per Day vs.
All Others (Dose/
Response)
1-14 15-25 >25
'*Women 6,194 13 2 10 21 57 64 12.34* 26.64*
o.
~
(cigarettes only)
***Men 34,440 254 3 44 , 38 50 88 25.58* 47.23
(any tobacco/grams)
(I gram = 1 cigarette) .
* (P>0.001)-- - --
SOURCE: ** Doll, R., in preparation (19)
Doll, R., 1976 (20)
0
L.f0SS9E0
NON-NEOPLASTIC BRONCHOPULMONARY DISEASES
INTRODUCTION
Chronic non-neoplastic bronchopulmonary disorders are a major
cause of death and disability in the United States. Chronic
obstructive lung diseases (COLD) including chronic bronchitis
and emphysema, comprise the majority of these illnesses. In
1977, they were responsible for nearly 46,000 deaths and
millions of dollars in social security disability payments,
ranking second in economic cost only to heart disease (50).
Previous U.S. Public Health Service reports on the
health consequences of smoking have presented evidence that
cigarette smoking is the major cause of COLD (65-74). The
studies on which this is based have focused primarily on male
populations. This reflects the scientific interest generated by
the overwhelming male-to-female ratio inn the prevalence of
COLD at the tim e. these studies began. However, recent
mortality statistics indicate a substantial increase in the death
rate from COLD among women (see Mortality section)..
Although this increased death rate may partially reflect a
greater awareness and recognitiom, of COLD, its magnitude
suggests a true increase in frequency of COLD among women.
The following text reviews a large number of studies analyzing
the relationship of sm oking to COLD. These studies include
appreciable numbers of women, and many suggest that smoking
may affect men and women differently. Nevertheless,
cigarette smoking remains the most important cause of COLD
regardless of sex or other variables.
DEFINITIONS
The terms chronic bronchitis and emphysema have been used
diagnostically for many years. Physicians often use these
terms interchangeably to describe a patient with chronic
airflo w obstruction. These condit~ions are, however, difficult
to distinguishh from each other in patients with chronic airflow
obstruction because (1) both conditions may be present in the
same patient; (2), both disorders are characterized by
expiratory flow obstruction; and (3) patients withh either
disorder frequently have the same symptom- -dyspnea on
exertion. Consequently, the clinician often labels the patient
with chronic airflow obstruction as having chronic obstructive
16o .
TABLE 5.-Means of average degrees of findings in nonsmokers and current smokers standardized for
age of total study population, women.
Subjects Who Current Cigarette
Never Smoked Smokers
Regularly <1 Pk. 1+Pk.
Number of Subjects 252 33 64
Emphysema 0.05 1.37 1.70
Fibrosis 0.37 2.89 3.46
Thickening of arterioles 0.06 1.26 1.57
Thickeningof arteries 0.01 0.40 0.64
`Thepathologic findings recorded were: (1 I degree of empliysema (four-point scale
ranging~from zero for normaUto four for advanced emphysemal; (2) .degree of fibrosis
(seven-point scale ranging from none to advanced diffuse.fibrosis): (3) degree of thicken-
ing of arterioles (four-point scale)t (4) degree of.thickening of arteries (three-point scale);
and(5) padlike attachments to alveolar septa. Padlike attachment is a thickening of
alveolar~ septa in focal areas bydibroblasts..histocytes andd collagen fibrils. This is recorded
as present or absent .
Source: Auerbach,etal..(4),
. -
170
TABLE 8.-Prevalence of cough and sputum production in 500 women related to smoking habit.
Nonsmokers Exsmokers Light Smokers Moderate Smokers Heavy Smokers
No. % No. % No. % No. % No. . %
a. Cough* 11 6.0 1 1.6 11 27.5 32 34.8 66 53.7
b. Sputum" 14 7.7 1 1.6 12 30.0 27 29.3 60 48.8
~ c. Sputum Volume
... .
~n. None 169 92.3 61 1 98.4 - 28 70.0 65 70.7 63 31.2
Morning blob 10 5.5. 0 0.0 7 17.5 19 12.0 29 23.6
Tablespoonful 3 1.6 0 0.0 5 12.5 12 13.0 17 13.8
More than one tablespoonful 1 0.5 0 0.0 0 0.0 4 4.4 12 9.8
I ncludes women with cough wit h or wit hout sputum,
'Includes women with sputum m with or without cough.
$ource: Wolf (751
SOLS89E0
TABLE 9.-Prevalence of respiratory symptoms in men compared withh
women"
Men
(Published Data)'.
Women
(Present
Investigation)
COUGHI Percent Percent
Nonsmokers 4 (46) 6
14-22 (47)
Light smokers 24: (48). 28
Moderate smokers 48-52(48) 35
Heavy smokers . 42 (46) 54
67-74 (47)
58-78 (48)
SPUTUM
Heavy smokers
DYSPNEA
All smokers
Heavysmokers
42 (46). 49
21 (49), 27
33 (50) 33
Numbers in parentheses are reference numbers.
Source: wowr.(7s)
.
176
TABLE 6.-Degree of emphysema* and cigarette smoking"
No. I No. With, Mean Age With,
Cigarettes Over _ Mean Grade . Grade 20 Grade 20
perDay Age 30 ofEmphysema. Emphysema Emphysema
MEN
0 30 6 (0-20) 3 (10%). 66
<21 14 -: 11 (0-45) 5 (36%). 62
?20 41. , -.14 (0-50) - 16 (39%(. . 52
WOMEN
0 ~
<21
? 20
~21~ 2(0-10) ~ 0 ~ - ~ - -
6 - ~ . 6 (0-20) 1 (17%) 70+
22 ~ . 8 (0-30) ~ ~ . 5 (23%) ~ . 40
.Z tesushows significance.at the 1%level for, ihe heavy smokers and nonsmokers.
' Each whole.lung paper, mounted section was graded from 0 to 100 in denominations
of 5 up to grade 50iand then in denominations of. 10 up to grade 100. 'One case.
-
Source: Spain, et aL (60)
172
0
ca
m
fr
~
r+
0
~
relationship between cigarette sm oking and the degree of
emphysema in both men and women. Furthermore, the data
(Table 6) demonstrated a dose-response effect between the
num ber of cigarettes sm oked and the severity of pathological
changes.
Thurlbeck, examined whole-lung sections in 1,742 ran-
dom necropsies In three different cities in different countries
with varying clim ates and environm ents (64). Using a
standard panel of grading pictures, pathologic changes In the
lung were graded from 0-100 by the three readers. In men
and women emphysema was more frequent and more severe in
smokers than nonsmokers; however, male smokers had higher
average emphysema scores and greater frequency of
emphysema than female smokers and nonsmokers. This
difference between men and women was also true when heavy
smokers and ex-smokers of both sexes were compared. The
authors speculate that male-fem aledifferences may exist
because: (a) women are protected by hormonal factors; (b)
men may smoke more heavily than women; (c) men may have
different smoking patterns than women, e.g., inhalation; and
(d) men may be exposed to damaging environmental factors at,
work.
In summary, the prevalence of chroniabronchitis
among women in the United States has been reported to range
from 4 to 10 percent. Women who smokehave a higher
prevalence of chronic bronchitis than those who do not sm oke.
Overall, however, chronic bronchitis is less common among
women than men in the U.S. This may reflect the smaller
proportion of women who smoke, differences in their smoking
behavior, and less occupational exposure to lung irritants.
When comparing current smokers, several studies of different
populations in the United States and England did not find
significant differences in the prevalence of chronic bronchitis
between men and women. Pathological data suggest that
female smokers have a higher frequency of emphysema and
bronchial mucous gland hypertrophy than female nonsmokers.
Furthermore, the severity of emphysema is dose-related to the
number of cigarettes smoked. Distinct female-male dif-
ferences in the frequency and extent of emphysema at autopsy
have been reported, but it is not clear whether these dif-
ferences are due to intrinsic differences in the way men and
women respond to environmental injury or to the differences
In thedegree of environmentall injury experienced by men andd
women.
0
171 1.
SMOKING AND RESPIRATORY MORBIDITY
A large number of recent studies have demonstrated a higher
frequency of respiratory sympto ms, i.e., cough, sputum,
wheezing and dyspnea, in smokers as compared to nonsmokers.
Many of these studies have included appreciable numbers of
women (9,12,16,46,47,48,55,57,75). These investigations have
examined populations varying in age, geographic location,
social class, and exposure to air pollution.
Lebowitz and Burrows examined the quantitative
relationships between cigarette smoking and chronic productive
cough in a large randomized sample of the white non-Mexican
Am erican population of Tucson, Arizona (46). Their data
(Table 7) confirm the close relationship between cigarette
sm oking and chronic cough and/or chronic sputum production in
men and women. The effect of cigarette smoking was closely
related to the total pack-years sm oked (Table 7). These data
support the male to female preponderance in prevalence of
chronic bronchitis noted in several other epidemiologic surveys
(26- 28,49,52,61). However, these data also indicate that
males and females with equivalent smoking histories have
similar rates of chronic cough and/or sputum production.
Woolf examined the frequency of respiratory symptoms
in. women volunteers, aged 25 to 54, drawn from several large
commercial firms (Table 8) (75, 76). The prevalence of
cough and sputum production was significantly greater in
smokers than in nonsm okers (p<0.001). Heavier smokers
complained of cough and/or sputum production more frequently
than nonsm okers or ex-smokers. The prevalence of wheezing
and exertional dyspnea increased progressively with the number
of cigarettessmoked.: In addition, colds that "went to the
chest" occurred more frequently in moderate and heavy
smokers than in nonsmokers (p<0.005 and p<0.001,
respectively). Woolf compared his data with previously
reported data among men (Table 9) and concluded that the
relationship of cigarette smoking to respiratory symptoms was
similar among men and women.
Ferris resurveyed a 1967 sample of Berlin, Ne w
Hampshire residents in 1973 (24). As in. 1967, the preva-
lence of cough and/or sputum production in females and males
was directly related to the num ber of cigarettes smoked daily.
When the group evaluated in 1967 was exam~inedd by current
inhaling and sm okingstatus. (Figure I)., inhalers had a higher
prevalence of symptoms than non-inhalers (24). Furthermore,
the frequency of symptoms was dose-related to the number of
173
white females and a twofold increase among nonwhite females.
Mortality rates from these conditions for white and nonwhite
males have also increased since 1967 (by factors of 1.9 and
1.5, respectively), but the rate of increase has not been as
steep as that for women. _
Seven large prospective studies haveshown a greatly
increased mortality from COLD among smokers as compared to
nonsmokers. (8,15,20,21,35,36,45). These studies, presented in
Table 2, represent over 13 million subject years of
observation and approximately 270,000 deaths from all causes.
The number of deaths related to COLD is probably
underestim ated since some of thee deaths attributed to
pneum onia or myocardial disease may have been due to
complications of COLD. In addition, these mortality figures
do not include an appreciable number of individuals for whom
COLD may have been a major contributory cause of death.
For example, it is not uncommon for individuals to have COLD
and lung cancer simultaneously.
Two of these prospective studies have included signi-
ficant numbers of women. Hammond prospectively followed
1,003,229 subjects aged 35 to 84 (35). Nearly 93 percent of
I
than that of female nonsmokers. The death rate from
from all causes among female smokers was 1.2 times higher
aged 10 to 69 for 10 years (15). The overall mortality rate
nonsm okers. Cederlof, et al. followed 55,000 Swedish subjects
25) had a sevenfold increased mortality rate as compared to
regardless of age when smoking was begun, or smokers of 10
or more cigarettes a day who had begun smoking before age
(defined as either smokers of 20 or more cigarettes a day
cigarette smokers than nonsm okers. "Heavier" smokers
the survivors were observed for a 12-year period. Death
rates from emphysema among women were much higher in
bronchitis, emphysema, and asthma among female smokers was
2.2 times that of female nonsmokers. However, the number
among maiephyslcians over the same period (20). The
study, including previously published results of a similar study
1951 to 1973 (19). Table 3 presents the results of this
physicians in England, observed prospectively over the period
of smoking and cause-specific mortality in 6,194 women
Data collected by Doll, et al. examine the association
cigarette smokers as compared to female nonsmokers.
risk for reported mortality from COLD was present for female
more difficult to evaluate. Nevertheless, a significant excess
these studies; consequently, the relationship with sm oking is
of deaths due to COLD among women was small in both of
163
TABLE 19.-Percenlages of nonsmokers and smokers with abnormal test results in three North American
cities, using combined
reference values*
-
r
MEN WOMEN
Nonsmokers
AS S
Total
AS Smokers
S
Total
AS Nonsmokers
S
Total
AS Smokers
S .
Total
(95)" (27) (122) (12) (115) (236) (145) (46) 1191) (107) (98) (205)
Upper limit+ 1.6 0.2 1.8 1.8 1.8 2.6 2.1 0.6 2.4 1.7 1.7 2.4
Lower limitt 11.6 20.0 10.6 10.6 10.9 8.7 10.0 15.0 9.1 11.1 11.5 9.0
1. Abnormal test FEV/FVC 6 - 11 7 5 7 6 4 20 8 7 25 16
CV/VC 2 7. 3 13 17 15 6 11 7 23 26 25
CC/TLC 2 7 3 20 32 26 6 17 10 20 29 25
AN/L - 1 7 3 17 13 15 7 24 11 27 37 32
RV/TLC 6 11 7 9 9 9 8 9 8 11 13 12
Reference values for nonsmokers derived from asymptomatic nonsmokers ke_rs in the three cities.
'Numbers in parethesis = number of subjects in each group. +Upper and lower limits in the expected
5 percent abnormal results.
AS - asymptomatia; S= symptomat ic Source: euist, ei al. (12) - -
VZLSS9C0
Male Females Male Females Male Female Male Female
A. By age group . 15-29Years (156) 7.2 (182) 8.2 (36) 8.3 (45) 17.7 (78125.7 (82120.8 (34)41.2
(17)41.1
30-44 years (43) 2.3 (82)12.2 (45) 11.1 (41) 4.8 (43)39.5 (40)35.0 (40)47.5 (30)56.7
45-59 years (45)11.1 (119)10.9 (61) 21.3 (63) 20.6 (57143.8 i83)36.2 (54)61.1 (39)51.3
60+ years (105)18.1 (336)14.6 (186)36.0 (77) 20.8 (62)51.6 (82)34.1 (16151.3 (14)57.1
~
of smoking
B. By pack-years
TABLE 7.-Comparison of prevalence of chronic cough+ and/or chronic sputum production+ in men and
women, by smoking habits'
(Number of subjects) % with symptoms
Never smoked Ex-smokers Presently 1-20/day Presently ~20/day
Present smokers Ex-smokers
Never Smoked (350)10.3 (719)12.1 (350)10.3 (719)12.1
' Smoked <6 pack-years . (69) 29.0 (81) 21.0 (59) 5.3 (69)15.9 .
6-20 pack-years (106)35.8 (127)33.1 (77) 14.3 (69)15.9
21-40 pack-years - (96) 47.9 (126)40.5 (86) 34.9 (27)18.5
40+pack-years . (113)61.1 (53) 60.4 (106)35.8 (30)16.7 '
*Subjects with a hitory of childhood respiratory problems have been excluded from the analysis.
Differences in rates byZsmoking significant within
each age-sex group (X and z differences between proportions) and trend withsmokin~q significant
within age-sea groups IX trend). Trend of symptoms by
pack-yeacs slgnificant for male present and ex-smokers and female p resent smokers (X trend). Never
smokers always significantly different from present or
ex-smokers IXZ and zl. -
+Symptoms are thos<reported on as selfcompletion questionnai re and are derived from the National
Heart and Lung Institute modification of the
British Medical Research Council respiratory questions. C_ hro_ ncity" of cough or sputum
production refers to the presence of the symptom "on most days
for at least three months of the year."
Source'. Lebowiu, at al. (46) , . . , . . .
. .
.
.
.
.
. .. .
. ~ . ....::-
. z" .,
,
. .x . .,
.
. _
. .,_ .,_..:_. _
tOIS39E0
cigarettes smoked. Manfreda studied population samples in an -"t
urban and a rural community in. Manitoba, Canada (47).. Their
data presented in Table 10 demonstrate a higher prevalence of
cough, phlegm, and wheezing among men and women who
smoked than in nonsmokers or ex-sm okers. However, no
significant differences in the prevalence of symptoms were '
apparent in the two communities. The relationship betweenn smoking and several
respiratory symptoms was examined by Buist, et al. in -'`
population samples of three North American cities (12). .~
Cough, sputum production, and wheezing occurred more
frequently among smokers than nonsmokers regardless of sex. *-
Bewley and Bland examined the relationships between
smoking and the prevalence of respiratory symptoms in 14,033 f~
children aged 10 to 121/2 in two separate urban areas of the ~
United Kingdom (9). In this questionnaire survey, 2.5 percent
of the girls ackno wledged sm oking at least one cigarette per week ("smoker"). Boys who smoked
outnumbered girls who
smoked by 3:1 and were more frequent smokers of at least one cigarette a day than were females by
11:1. Table 11 -,
shows that even in this young age group, smokers have a
higher frequency of morning cough, cough during the day and
night, and cough for 3 months duration than their nonsmoking
classm ates. -
In a questionnaire study of a large group of American
high school students in Rochester, New York, Rush found a
strong association between current smoking and respiratory
symptoms inn both sexes (57). There were minor differences
between sexes inn the frequency of respiratory symptoms when-
sm oking histories were comparable. Rawbone, et al. in a
questionnaire survey of 10,498 secondary schooll children aged
11 to 17 in London, found a significantly higher frequency of .
cough, colds, and exertional dyspnea in regular smokers as
compared to nonsmokers (55). There was no appreciable
difference in the frequency of cough between male and fe.malesmokers or between male and female
nonsmokers. Colley
examined the influence of smoking, lower respiratory tract
ilJness under 2 years of age, social~~ class of father, and air
pollution on respiratory symptoms in a cohort of 20-year-olds
followed since birth. (.16). Their data (Table 12) suggest that
respiratory symptoms were closely related to current smoking.
Symptoms were also related to a history of lower respiratory
tractt infection in the first 2 years of life but were not
related to social class or air pollution.
178 ,
T.
S
C
d
n
Only a few of the studies examining the relationship of
cigarette sm oking to the frequency and severity of patho-
logical changes have included significant numbers of fem a1e
subjects. Thurlbeck recently reviewed 30 reported surveys of
the frequency of emphysema at necropsy (63).. Emphysema of
some degree was found in about 65 percent of men and 15
percent women. The emphysema found was also more severe
in men than in women.
The predominant pathological finding in chronic
bronchitis is the hypertrophied mucous gland in the submucosa
of the large cartilaginous bronchi. The ratio of bronchial
gland thickness to bronchial wall thickness (Reid index) is
usually increased. In a recent survey of 179 consecutive
necropsies, Ryder foundd significantly greater bronchial mucous
gland volume in smokers comparedto nonsmokers there was no
significant difference in mucous gland voium e between male
and female smokers or male and female nonsmokers (58).
Mueller, examined the prevalence of chronic bronchitis
in one fifth of the adult population of Gleenwood Springs,
Colorado (~49). Among current smokers of varying smoking
categories (Table 4)) there were no significant differences in
the prevalence of chronic bronchitis. Higgins, et al. found
no significant difference in the prevaiencee of chronic
bronchitis between men and women smokers in 186 subjects
randomly chosen from an agricultural community (Table 4)
(40). Similarly, Oswald, found no significant difference in
the prevalence of chronic bronchitis between men and wom en
smokers in 5,844 clerical workers in England (Table 4) (51).
Auerbach, examined the relationship of sm oking to
emphysema In whole-lung and microscopic, sections at necropsy
in 1,436 men and 388 women (4,5). Among the women, there
were 97 current smokers, 16 of whom smoked two packs a
day or more. Data regarding smoking habits were obtained
through intervie ws with relatives. Female sm okers had a
significantly higher rate of emphysema than female nonsmokers
(Table 5). Furthermore, the severity of the emphysema was
dose-related to the num ber of cigarettes sm oked. The
authors found similar relationships in men.
Spain, examined consecutive whole-lung mounts from
necropsies of adult victims (49 women, 85 men) of sudden
and unexpected death (60). Smoking habits were ascertained
by a letter and questionnaire to the next of kin. The degree
of emphysema was graded from 0-100 by two observers
Independently and without prior knowledge of the source of
the specimen or any previous grading. There was a close
168
In summary, recent statistics indicate a rise in the
reported death rate due to COLD among women. The two
large prospective studies that included appreciable num bers of
women found significantly higher mortality rates due to COLD
among women smokers as compared to women nonsmokers.
This relationship was accentuated in heavier sm okers.
Mortality rates from COLD among female smokers are
considerably lower than among male smokers. This may be
due to different smoking patterns and work exposure among
men andwomen.
SMOKING AND THE EPIDEMIOLOGY AND PATHOLOGY OF COLD
The prevalence of chronic bronchitis has been determined in
several populations in the United States and In other countries
(26,27,28,40,42,49,51,52,56,61). Table 4 lists several studies
which have included appreciable numbers of women. These
studies have docum ented. a close relationship between cigarette
smoking and an increased prevalence of chronic bronchitis, and
when looked for, a dose -response relationship was also
present (Table 3). The prevalence of chronic bronchitis in
the United States was determined in four cohort studies and
ranged from 4 to 10 percent among women and 14 to 18
percent among men (26,27,28,49,52,61). In both menn and
women a dose-response relationship between the number of
cigarettes smoked andd the prevalence of chronic bronchitis
was apparent. -
The observed differences between men and women noted
in these. studies may be due in part to the smaller percentage
of women thann men who were smokers inn the population
studied. Moreover these womenn smoked fewer cigarettes than
men. When comparing current smokers, several studies of
different populations in the United States and in England did
not findd significant differences in the prevalence of chronic
bronchitis between men and women (23,38,49).
The relationship between sm oking andd pathologic
changes in the lung have largely been obtained by necropsy
studies. These investigations are often ske wed by physicianand(or hospital interest and may not
accuratelyrepresena a
random population. Moreover, observer variation occurs fre-
quently, even am ong ^experts ^ Data regarding smoking
history are usually derived from a hospital record or from
close relatives and friends; thus they may.be unreliable.
166,
m ale populations and have found a close relationship between
cigarette smoking and the presence of abnormal pulmonary
function (2,6,18,22). Furthermore, the decrement in
performance measured by simple spirometry is dose-related to
the num bers of cigarettes sm oked (6, 18, 22). Relatively fe w
studies have included appreciable numbers of females.
Woolf examined pulmonary function in 500 women
volunteers (75). Smokers demonstrated significantly lower
values for FVC, FEV, FEF 25-75 percent, and specific
conductance than nonsm okers and ex-sm okers who had not
smoked for over a year; this suggests that at least some
abnormalities of pulmonary function are reversible with
smoking cessation.:
Higgins examlhed the relationship of smoking to seven
derivatives of the forced vital capacity curve In 3,109 males
and 3,256 females aged16 and older (41)~. Nonsmokers
performed better than sm okers in both sexes. Values
consistently decreased with increasing cigarette consumption.
The largest differences were in FEV and FEF 25-75 percent.
Seltzer examined the relationship of smoking to FVC in
65,086 white, black, and Asian subjects aged 20 to 79 who
had attended a Kaiser-Permanenrtemultiphasic health clinic
(59). The authors found a significant reduction In FVC
among white women who smoked as compared to nonsmoking
white women.. No such differences were found for black and
Asian subjects, ho wever. No explanation for this racial
difference was apparent from their data.
In a study by Buist, the prevalence of abnorm atities
of FEVI/FVC was higher inn female smokers than nonsmokers
(12). The frequency of abnormalities in FEVI/FVC among
female smokers was twice that of male smokers (Table 12).
Gibson, et al. examined the relationship of smoking to
measurements of the forced vitall capacity in 18,359 men and
women in Australia (34). Nonsmokers hadbetter lung func-
tions than smokers. Among smokers of 10 or more cigarettes
a day, memn showed a greater decrement in lung function than
women.
Burrows examined the relationship of smoking to
measurements of forced expiratory volume in 883 men and
1,166 women in Tucson, Arizona (14). Nonsmokers performed
better than ex-smokers or smokers, and ex-smokers performed
better than smokers in both sexes. Smokers of more than 20
cigarettes per day performed worse than smokers of fe wer
than 20 cigarettes per day. There were no significant dif-
ferences in the regression for FEV1/FVC on pack years in men
188 '
21 19 13774 173'77 19. 3
<10 1020 20-40 >40
.
The dagger indicates significant difference between males and females (P <0.05). A,
tween groups using
20 to 40 cigarettes per day as the reference group (P <0.05). 4
FIGURE 3.-Percentage of male and female cigarette smokers withh an
abnormal change in nitrogen concentration (AN211 per liter according to thelt
daily cigarette consumption. An asterisk indicates a significant difference btr
SoURCE:~. nu~sL rr.~Ll~a)
1£6
cigarettes per day (13). In the groups smoking more than 20
cigarettes a day, a greater proportion of females demonstrated
abnormalities than males. However, the age composition of
each group (maie andd female) was not identical.
A recent study of small airway function in 205 young
volunteer smokers aged 18 to 25 has suggested that smoking
may exert its effects at different anatomic locations In the
lungs of men and women (23). All subjects smoked fairly
heavily (more than 20 cigarettes per day) for a short period
of time (average: 2.4 packlyears). Male smokers showed
frequent abnormalities in tests of small airway function but
female smokers did not exhibit these abnormalities. Both
male and female smokers showed decreased forced expiratory
flows at high lung volumes, suggesting the presence of large-
airway dysfunction in young smokers. Male and female
smokers differed significantly In their response to He-
02 inhalation. Female smokers showed at least as great an
improvement in forced expiratory flows with He-02 as did
female nonsmokers. In contrast male smokers showed a much
smaller response to the He-02 at high lung volumes. Thus,
the predominant female response to habitual cigarette smoking
appears to have been Involvement of the large airways, but
mem who smoked appeared to have developed abnormalities in
small airway function. The reason(s) for the differences In
thedata derived fromm this study and previously cited reports
relating smoking to small airway dysfunction (12,13,47) Is
unclear.
In summary, a limited number of recent' studies have
demonstrated a higher frequency of abnormalities in tests of
small airway function Inn female smokers as compared to
female nonsmokers and ex-smokers. It is not clear whether
these abnormalities are dose-related. Female smokers may
have more frequent abnormalities in the slope of phase III
than male smokers. Male smokers may have more frequent
abnormalities in closing volume than female smokers. The
meaning of these differences Is unclear. One study has
suggested that the earliest effects of smoking on lung func-
tion may occur in the large airways in women and small air-
ways in men.
Smoking and Ventilatory Function
The majority of studies examining the relationship of smoking
to ventilatory capacity have used some measurement of forced
expiratory volume. Most of these studies have focused on
187
I
3.0
FVC
L
2
1.0
(34)
x,X (38)
e~AO x e x
I A
(5)
X NON SMOKER
e HEAVY SMOKER
x
(39).
_x~x
(9e x~x n21
e= x X (22)
e` X~x
(12) A
30 40 50 60 70 80
AGE-YEARS
FIGURE 4.-Changes in forced vital capacity (FVC) by age in various
female cohorts. Results have been standardized to 155 cm. and are body tem-
perature and pressure saturated (BTPS). Numbers in parentheses are number in
that cohort. Heavy smokers are those who smoke 25 or more cigarettes per day.
SOURCE: Ferris (25). ' - '
FI
I
1°0
TABLE 12 -Prevalence(percent)of respiratory symptoms by sex and smoking habit in cohort of 3,898
20-yearaIds followed since birth.
-- Winter Cough Day Cough 3 Winter Phlegm Day
History of Population Morning or Night Months in Morning or Night
Cigarette Smoking Cough in Winter Wlnter Phlagm in Winter
Q.1Ial+ Q.11b1+ Q.1(cl+ Q.21aI+ D.2(b1+
F. M. F. M. F. M. F. M. F. M. F.
Phlegm 3 Persistent
Months in Cough and
Winter Plegm
Q.2(c)+ Q.11t)+2(c)+
M. F.. M. F.
Never smoked
cigarettes 602 1093 1.6 4.0 5.2 6.5 1.5 3.2 4.8 5.2 6.4 3.9 3.7 3.2 0.9 1.9
Exsmokers of -
cigarettes 101 57 3.0 1.8 7.1 10.5 3.0 1.8 11.0 1.9 10.2 9.1 6.0 OA 2.0 0.0
Present smoker of
cigarettes 1009 678 ' 13.0 13.2 13.9 16.0 8.1 7.5 14.1 11,9 11.6 11.2 8.3 5.5 4.9 3.5
No data on cigarette
smoking 92 48 8.7 11.8 9.1 18.8' 4.5 0.0 0.0 6.7 4.8 0.0 4.8 0.0 4.8 0.0
ALL 2022 1876 7.7 7.4 9.8 10.2 5.0 4.7 9.9 7.6 9.3 6.7' 6.2 3.9 3.0 2.4
+1. (a) Do you usually cough first thing in the morning in the winter?
(b) Do you usually cough during the day or at night in the winter?
If "Yes" to either question 1(a) or Ib)
(c) Do you cough like this on most days for as much as three months each winter? 2. (a) Do you
usually bring up any phlegm Ispit from the chest) first thing in the morning in the winter?
(b) Do you usually bring up any phlegm (spit from the chest) during the day or at night in the
winter?
If "Yes" to either question 21a1 or (b)
(c) Do you bring up phlegm Ispit from the chest) an most days for as much as three months each
winter?
Source: Colley, et al. (16)
IILSs9E0
andwomen, suggesting that men and women with equivalent
smokingg habits have similar decrements in FEVI/FVC.
The long-term effects of smoking on pulmonary
function have been scrutinizedd in two prospective studies. In
the Framingham study, 5,209 adults have been followed since
1948 with biennial examinations Including measurem ents of
forced vital capacity (3). Longitudinally, cigarette smokers
sho wed a morerapid decline In forced vital capacity than
nonsmokers. Menn and women who continued to smoke had a
more rapi6 decline in FVC than those who had stopped. The
rate of decline in pulmonary function was appreciably steeper
in male smokers than female smokers. The authors suggest
that these differences could be due to differences in smoking
habits.
In aa longitudinal study of residents of Berlin, New
Hampshire, Ferris examined the changes in pulmonary function
by smoking status inn the various age cohorts (25). Among
females, heavy and moderate smokers had lower values for
FVC and FEVI as compared to nonsmokers, and the values fell
more rapidly with age. These relationships for heavy smokers
(75 or more cigarettes a day)) are presented in Figures 4 and
5.
In summary, womenn smokers perform worse on
spirometric testing than do female ex-smokers or nonsmokers.
This relationship appears to be dose-related to the number of
cigarettes smoked. The differential effects of smoking on
pulmonary function in mal.es and females is unclear. One
study demonstrated that men and wom en with equivalent
smoking, habits have similar decrements in FEV1/FVC. The
long term effect of smoking on pulmonary functionn has been
evaluated in two studies which Included appreciable numbers of
females. Longitudinally, women who smoke show a more rapid
decline in forcedvital, capacity than women who do not
smoke. Women who continue to smoke have a more rapid
decline in forced vitaLl capacity than those who stop; however,
men who continue to sm oke have an even more raoid decline
in pulm onary function thann women who continue to smoke.
The long term relationship between respiratory symptom.s and
airflow obstruction in women is unknown. ()ne large
prospective study could not find a relationship between
symptoms and the ultitnata development of chronic airflow
obstruction in men (37..)..
1189
measured by the number of cigarettes smoked per day and.the
number of years smoked. The majority of studies indicate aa
greater prevalence of respiratory symptoms among men who
smoke than among women who smoke; however, these
differences have not been found in studies carefully controlled
for smoking dosage. -
A limited number of recentt studies have demonstrated
a higher frequency of abnormalities In tests of small airway
function in female smokers as compared to female nonsmokers
and ex-smokers. It is not clear whether theseabnormaiities
are dose-related. Female smokers may have more frequent
abnormalities in the slope of phase III than malesmokers.
Male smokers may have more frequent abnormalities in closing
volume than female smokers. The meaning of such differences
is unclear. One study has suggested that the earliest effects
of smokingg on lung function occur in the large airways of
female smokers and the small airways of male smokers. The
predictive nature of these tests of small airway function in
terms of identifying the smoker who wii.ll develop chronic
airflow obstruction Is unclear. - Women smokers perform worse on spirometric tests of
lung function than do female ex-smokers or nonsmokers. This
relationship appears to be related to the number of cigarettes
smoked andduratdon of smoking. One well-designed study
demonstrated that men and women with equivalent smoking
habits have similar decrements In FEV1/FVC. The long term
effect of smoking on pulmonary function has been evaluated in
twost~udies which included significant numhers of women..
Longitudinally, women who smoke show a more rapid decline in.
forced vital capacity than women who do not smoke. Women
who continue to smoke have a morerapid decline In forced
vital capacity than those who stop; however, m en who continue
to smoke have an even more rapid decline in puim onaryfunc.tion than do women who continue to smoke.
The long-
term relationship between respiratory symptoms and airfiowoF.struction in women is unknown.
In a longitudinal study of elderly Edinburgh residents
aged 61 to 90, Miilne and Williamson found the prevalence of
persistent cough and sputum production was significantly
greater inn smokers of both sexes than in their nonsmoking
counterparts (48). Male prevaiencerates were three times
higher than those In females; however, no attempt was made
to determine the relationship of respiratory symptoms to life
time tobacco exposure.
In summary, many recent studies demonstrate a higher
frequency of respiratory symptoms in women who smoke as
compared to women who do not smoke. This is true in
surveys including children, adolescents, young adults, working
age, and elderly women. The effect of cigarette smoking is
related both in terms of the number of cigarettes and years
smoked. The majority of studies indicate a greater prevalence
of respiratory symptoms among men who smoke than among
women who smoke; however, these differences often disappear
when the study is carefully controlled for smoking history.
SMOKING AND PULMONARY FUNCTION
The insensitivity of cough and sputum production in the
adult as a predictor of future development of COLD has been
emphasized by Fletcher and Peto (32):. Pulmonary function
testing offers an objective method for measuring the adverse
effects of smoking. However, current: tests of pulmonary
function display a marked variability between individuals and
may not detect the devetopm ent of COLD until irreversible
damage of the lung has occured. Also, none of the presently
used, pulmonary function tests can predict which of those
individuals with slightly abnorm al pulmonary function will
progress to debilitating and life threatening emphysem a and
chronic bronchitis. Becklake and Permutt have recently
reviewed the objectives and problems of the tests of lung
function commonly used for early detection of COLD (7).
A large number of studies have established a higher
frequency of pulmonary functional abnormalities in smokers as
compared to nonsm okers. These studies have examined (a) the
relationship of sm oking to abnorm al tests of sm all airway
functionn and (b) the relationship of smoking to measurements
of standard spirometry. The majority of epidemiologic surveys
Investigating the prevalence of functional abnormalities in
smokers have employed'spirometric measurements, usually the
forced expiratory volume (FEV) and vital capacity (VC).
182
3.0
(34) X (38)
FEV ~ p X X~iX_X~~X
A
L X (39/
2.0 (5) (8\ \ ~~ X (72)
~X
18) ~
~~ X`X
d ~~ X
(22)
1.0 X NON SMOKER - (2\ A p HEAVVSMOKER
u
0
30 40. 50 60 . 70 80
AGE-VEARS
n
FIGURE 5.-Changes in forced expiratory volume in.1 second (FEVI,o) by
age in various female cohorts. Results have been standardized to 155 cm and
are body temperature and pressure saturated (BTPS).. Numbers in parenthesis
are number in that cohort. Heavy smokers are those who smoke 25 or more
cigarettes per day. , , . .
SOURCE:. Ferris 1251
191
SUMMARY
Recent statistics indicate a rise in the reported death rate
due to COLD among women. The two large prospective studies
that included appreciable numbers of women found.significantly
higher mortality rates due to COLD among women smokers as
compared to women nonsmokers. This relationship was
accentuated in heavier smokers. Mortality rates from COLD
among female smokers are considerably less than among male
smokers. This may be due to different smoking patterns and
work exposure among menn and women. Women tend to smoke
fewer cigarettes, inhale less deeply, and begin smoking later
in life than men. They more frequently smoke low-"tar"
and-nicotine cigarettes than men, and they work In cleaner
environments than men. Recent data suggest that women are
manifestingg smoking patterns similar to those of men and, that
more women are joining the labor force in occupations in
which exposure to lung irritants may occur. Whether such
women will have mortality rates similar to those of men
remains to be determined. .
The prevalence of chronic bronchitis in women in the
United States has beenn estimated to range between 4 and 10
percent. This is lower than the prevalence in men, probably
reflecting the lower percentage of women who smoke, the
fewer number of cigarettes smoked, and the reduced likelihood
of occupational exposure to lungg irritants. When comparing
current smokers, several studies of different populations in
the United States and England did not find significant
differences in the prevalence of chronic bronchitis between
men and vlomen. Pathological data suggest thatt female
smokers have a higher frequency of emphysema and bronchial
mucous gland hypertrophy than female nonsmokers.
Furthermore, the severity of emphysema is dose-related to the
number of cigarettes smoked in women as well as in, men.
Distinct female-male differences in the frequency and extent
of emphysema at autopsy have been reported, but it is not
clear whether these differences are due to Intrinsic dif-
ferences in the way men and women respond to environmental
injury or to the differences in the degree of environmental
injury experienced by men andwomen.
M any recent studies demonstrate a higher frequency of
respiratory symptoms in women who smoke compared to women
who do not smoke. This is true in surveys including children,
adolescents, young adults, working age, and elderly wom en.
The effect of cigarette smoking is dose-related for dosage
192
NON-NEOPLASTIC BRONCHOPULMONARY DISEASES:
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194
First, smoking patterns among wom en are different
from those among men--women are less likely to smoke, andd
if they do, they smoke fewer cigarettes per day, inhale less,
andare more likely to smoke lower "tar" and nicotine
cigarettes (7, 17, 18). Second, smoking and occupational
exposure may adversely affect the fetus or the health of the
mother during pregnancy. Smoking and occupational exposure
may also interact with methods of contraception chosen by
women.
This chapter reviews each of these reasons for a
differential'l healthimpact on men andwomen and examines
two occupational exposures where interactions with smoking
have been clearly demonstrated for women workers.:
SM OKING PATTERNS IN WOMEN
The m ale-female differences in smoking behavior and the
change in patterns of smoking behavior in women over time
are reviewed in other sections of this report. It is
important, however, to consider the impact of these trends
when evaluating the interaction of smoking and the
environment. Regular cigarette smoking is a behavior that
usually begins between the ages 12 and 25 (18). it is
unusual to begin regular smoking after the age of 25 (7).. In
a cohort of individuals born in the same year, a certainn
percentage of them will beginn smoking by age 25. The
prevalence of smoking In any birth cohort after age 25 is
predominantly determinedby the rateat which people stop
smoking or die. The prevalence changes over time for each
10 year birth oohort since 1910 for both men and women are
presented in the section of this report on patterns of
smoking.
Women first began smoking cigarettes In large numbers
imm ediately before and during the Second World War (18).
Thus, the observed upswing in smoking among women occurred
25 to 30 years after that among men. The birth cohorts with
the highest peakk smokingprevalence were borm from 1910to1930 (men) and' from 1920 to 1950 (women).
As these
cohorts with high prevalence of smoking gro w older, they
replace cohorts with lower smoking prevalence. Since bothh
occupational diseases and smoking related illnesses separately
increase with age, any interaction between the two also could
be expected to increase with age. Men in the birth cohort
from 1910 to 1930 are now In the age range at which a high
204
T.
F
P
N
c
C
c
c
(9) BEWLEY, B., BLAND, J.M. Smoking and respiratory
symptoms in two groups of school children.
Preventative Medicine 5: 63-69, 1976.
(10). BROWN, R., WOOLCOCK, A.J., VINCENT, N.J., MACKLEM,
P.T. Physiological effects of experim entaiairway obstruction with beads. Journal of
Applied Physiology 27: 328-355, 1969. .
(11) BUIST, A.S., FLEET, L.V., ROSS, B.B. A comparison
of conventional spirometric tests and the test
of closing volume In an emphysema screening
center. American Review of Respiratory Disease
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1973
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,
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107:
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(12) BUIST, A.S., GHEZZO, H., ANTHONISEN, N:,
CHERNIAK, R., DUDCIC, S., MACKLEM, P., MANFREDA,
J., MARTIN, R., MARTIN, D., ROSS, B. Relationship
between the single
smoking habit in breath N2 test and age, sex,
the North American cities.
American Review of Respiratory Disease 120:
305- 318, 1979.
(13) BUIST, A.S., ROSS, B.B. Quantitative analysis of
the alveolar plateau In the diagnosis of early
airway obstruction. American Review of
Respiratory Disease 108: 1078-1087, 1973.
(14) BURROWS, B., KNUDSON, R.J., CLINE, M.B., LEBOWITZ,
M.D. Quantitative relationships between
cigarette sm oking and ventilatory function.
American Review of Respiratory Disease 115:
195-205, 1977.
(15) CEDERLOF, R., FRIBERG, L., HRUBEC, Z., LORIER, V.
The relationship of sm oking and some social
covariables to , mortality and cancer morbidity.
A ten year follow-up in a probability sample of
55,000 Swedish subjects age 18-69. Part 1 and
11. Stockholm, Sweden. The Karolenska Institute,
Departm ent of Environmental Hygiene, 1975, 201 pp.
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disease in young adults: Influence of early chiid-
hoodlower respiratory tract illness, social
class, air pollution and sm oking. British
Medical journal 3(5873): 195-198, July 1973.
195
(53)
(54)
PETERS, J.M., FERRIS, B.G., JR. Smoking pulmo-
nary function and respiratory symptoms in a
college-age group.
Diseases 95
774
tor American
1967 Review of Respira-
,
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:
.
PHILLIPS, A.M., PHILLIPS, R.W., THOMPSON, J.L.
Analysis of etiologic factors in survey of 1274
m en. Annals of Internal Medicine 45: 216,
1956.
(55) RAWRONE, R., KEELING, C., JENKINS, A., GUZ, A.
Cigarette smoking among secondary school
children in1975.. journal of Epidemiology and
Community Health 32: 53-58, 1975.
(56) REMINGTON, J. Chronic bronchitis, smoking and
social class. A study am ong working people In
the to wns of East and Mid Cheshire. Rritish
journal of Disease of the Chest 63(4):: 193-
205, 1969.
(57) RUSH, D. Changes In respiratory symptoms related
. to smoking in a teenage population: The re-
sults . of tow linked surveys separated by one
year. International Journal of Epidemiology
- 5(2):173-178., 1976.
(58) RYDER, R., DUNNILL, M., ANDERSON, J. A quan-
titative study of bronchial mucous gland
volume, emphysema and, smoking in a necropsy
population. .. .
(59) SELTZER, C.C., SIEGELAUR, A.B., FRIEDMAN, G.D.,
COLLEN, M.F. Differences in pulmonary func-
tion related to smoking habits and race.
American Review of Respiratory Disease 110 (5)t
598-6n8, November 1974.
SPAIN, P., SIEGEL, H., BRADES, V. Fmphysema in
apparently healthly adults. Journal of the
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1973.
(61) TAGER, I., SPEIZER, F. Risk estimates for
chronic bronchitis in smokers: A study of
male-female differences. American Review of
Respiratory Diseases: 113: 619-625, 1076.
(62) THURLRECK, W.M. Aspects of chronic airflow
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--
(60)
200
(64) THURLBECK, W.M., RYDER, R., STERNLY, N. A com-
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necropsy population in three different coun-
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109: 239-248, 1974.
(65) U.S. PUBLIC HEALTH SERVICE. Smoking and Health.
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Public Health Service, Center for Disease
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Mental Health Administration. DHEWPublica-
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Health Services and Mental Health Administra-
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458 pp.
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Consequences of Smoking. A Report of the
Surgeon General: 1972. U.S. Department of
Health Services and Mental Health Administra-
tiom. DHEW Publication No. (HSM) 72-7516,
1972, 158 pp.
TABLE 1.-Smoking Habits of Working Women by Title and Industry.
FEM4LES PERCENT
Percent of Current Femal'e Non- Ex-
Indu.strr Labor Fnrcea Smokers Smokers Present Smokers
--- <L pzck >1 pack
per day per day
Professionals
Health 4.4 51.2 16.6 25.2 6.9
Teachers 6.8 63.5 14.0~ 19.8 2.7
Other 4.6 53.4 15.1 24.0 7.5
Managarilal, incl. 6.7 42.7 16.4 28.0 12.1
office, rest.,
sa1bs,, adrninistrator
Sales 6.2 46.0 16.2 30.0 8.0
Clerical
Bookkeepers 4.6 53.1 12.2 26.5 8.2
Office machine 1.3 52.8 15.7 23.1 8.4
operators . .
Secretaries 13.3 52.0. 14.7 26.3 7.0
All other 14.2 50.6 . 13.6 27.5 8.3
Crafts 2.4 46.4 13.1 31.8 8.6
Openatiyes 11.8 52.8 10.1 31.6 5.5
Service
Cleaning 2.5 51.9' 12.8' 31.2 4.1
Food 6.6 40.0 13.4 39.8 6.8
Health 6.9 52.1 10.5 32.2 5.2
Private Household 2.8 62.4 10.1 24.7 2.8
Workers
aFigures are subj.ect to sampling errorss and may therefore not agree with
those in, other tables. SOURCE: Unpublishedi data, Heallth Interview Survey, 1976, National Center
for hlealth Statistics (6)
205
(26) FERRIS, R.G., JR., CHEN, H., PULEO, S., MURPHY,
R.L.H., JR. Chronic nonspecific diseases
in Berlin, New Hampshire, 1967-1973.
American Review of Respiratory Disease 1n3:
475-485, 1976.
(27) FERRIS, R.G., JR., HIGGINS, I.T.T., PETERS, J.M.,
VAN GANSE, W.F., GOLDMAN, M. Chronic nonspe-
cific respiratory disease, Berlin, New
Hampshire, 1961 -1967: A cross-sectional
study. American Review of Respiratory
Disease 104: 232-244, 1971.
(28) FERRIS, R.G., JR., HIGGINS, I.T.T., HIGGINS, J.M.,
PETERS, J.M., VAN GANSE, W.F., GOLDMAN, M.
Chronic nonspecific respiratory disease,
Berlin, New Hampshire, 1961-1967: A cross-
sectionall study. Am erican Revie wof
Respiratory Disease: 107: 232-244. 1971.
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F.J.C. Bronchial mucous gland hypertrophy:
Its relation of symptoms and environment.
British Journal Chest Diseases 60: 66, 1966.
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tions, ciassification of chronic pulmonary
emphysema and related conditions. A report
of the conclusions of a. Ciba Guest Symposium.
Thorax 14: 286-299, 1959.
(31 ) FLETCHER, C.M., JONES, N.L., RURRnWS, P.,
NIDEN, A.H. American emphysema and British
bronchitls. A standardized comparative
study. Am erican Review of Respiratory
Disease 90: 1-13, 1964.
(32) FLETCHER, C., PETO, R. The natural history of
chronic airflowobstruction.. British M edical
Journal 1: 1645-1648, 1977.
.
(33) GELR, A.F., GOLD, W.M., WRIGHT, R.R., RP.UCH,
H.R., NADEL, J.A. Physiologic diagnosis of
subclinicall emphysema. American Review of
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(34),SIRSON, J., GALLAGHER, H., JOHANSON, A.,
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population. 2. Spirometric performance and
cigarette smoking habits. Medical Journall
of Australia 1: 354-358, 1979.
1.97
(44).
(45)
I
F (46)
(47)
(48)
(49)
(50)
(51)
(52)
IMBODEN, C.A., JR. Rising mortality from chro-
nic respiratory disease. Am erican Journal of
Public Health 58: 221-222, 1968. (Letter)
KAH N, H.A. The Dorn study of smoking and mor-
tality among U.S. veterans. Report on 81/2
years of observation. In: Haenszel, W.
(Editor). Epidemiological Approaches to the
Study of Cancer and Other Chronic Diseases.
National Cancer Institute Monograph 19. U.S.
Department of Health, Education, and Welfare,
Public Health Service, National Cancer
Institute, January 1966, pp. 1-125.
LEIPOWITZ, M., RURROWS,P. Quantitative rela-
tionships betweenn cigarette smoking and chro-
nic productive cough. Internatlonal Journal
of Epidemiology 6: 107-113, 1977.
MANFREDA, J., NELSON, N., CHERNIACK, R.U.
Prevalence of respiratory abnormalities in a
rural and an urban community. American Review
of Respiratory Disease; 117: 215-226, 197R.
MILLNE, J., WILLIAMSON, J. The relationship of
respiratory function tests to respiratory
symptoms and smoking Inn older people.
Respiration 29: 206-213, 1972.
MUELLER, R.E., KEBLE, D., PLUMMER, J., WALKER,
S.H. The prevalence of chronic bronchitis,
chronic airway obstruction, and respiratory
symptoms in Colorado City. American Review of
Respiratory Disease 103: 2n9-22>s, 1971.
NATIONAL CENTER FOR HEALTH STATISTICS. Vital
Statistics of the United States, 1960-1977.
U.S. Department of Health, Education, and
Welfare, Public Health Service, Office of
Health Policy, Research and Statistics,
National Center for Health Statistics.
OSWALD, N.C., M.EDVEL, V.C. Chronic bronchitis:
the effect of cigarette smoking. Lancet 2:
843-844, October 22, 1955.
PAYNE, M., KJELSP,ERG,M.: Respiratory symptoms,
lungg function and smoking habits In an adult
population. American Journal of Public
Health: 54: 261 -277, 1964.
199
INTERACTION BETWEEN SMOKING AND OCCUPATIONAL
EXPOSURES
The 1979 Surgeon General's Report on the health consequences
of smoking (18) examines the interaction of smoking and
occupational exposure. Ways in which smoking may interact
withh the occupational environment are described and examples
of these interactions are discussed. Briefly, these types of
interaction are: -
1. Tobacco products may serve as vectors by becoming
contaminated with toxic agents foundin the
workplace, thus facilitating entry of the agent by
Inhalation, ingestion, and/or skin absorption of
the agent.
2. Workplace chemicals may be transformed into more
harmful agents by smoking. -
3. Certain toxic agents in tobacco products and/or
smoke may also inhabit theworkpiace, thus
increasing exposure to the agent.
4. Smoking may contribute to an effect comparable to
that which can result from exposure to toxic
agents found in the workplace, thus causing an
additive biological effect.
5. Sm oking may act synergistically with toxic agents
found in the workplace to cause a much more
profound effect than that anticipated simply from
the separate influences of the agent and smoking
added together.
6. Smoking may contribute to accidents in the
workplace.
Although few of the studies discussed in the 1979
Surgeon General's Report included enough women to adequately
determine the health risks for womenn of sm oking and the
occupational environment, it is reasonable to hypothesize that
women with the same occupational exposure and smoking
behavior as men would develop health effects similar to those
demonstrated in men. However, the interaction of smoking
and the occupational environment and its effect on women
differs in at least two ways;
'
(71) U.S. PURLIC HEALTH SERVICE. The Health
Consequences of Smoking: 1973. U.S. Depart-
ment of Health, Education, and Welfare, Public
Health Services, Health Services and Mental
Health Administration. DHEW Publication No.
(HSM) 73-8704, 1973, 249 pp.
(72) U.S. PURLIC HEALTH SERVICE. The Health
Consequences of Smoking: 1974. U.S. Depart-
ment of Health, Education, and Welfare, Public
Health Service, Health Services and M ental
Health Administration. DHEW Publication No.
(CDC) 74-8704, 1974, 124 pp.
(73) U.S. PURLIC HEALTH SERVICE. The Health
Consequences of Smoking: 1975. U.S. Depart-
m ent of Health, Education, and Welfare, Public
Health Service, Health Services and Mental
Health Administration. DHEW Publication No.
(CDC) 76-8704, 1975, 235 pp. . .
(74) U.S. PUBLIC HEALTH SERVICE. Smoking and Health.
A report of the Surgeon General, U S. Depart-
ment of Health, Education, and Welfare, Public
Health Service. Office of the Assistant
Secretary for Health, Office on Smoking and
Heaith. DHEW Publication No. (oH5). 79-50066,
1979, pp. 1257.
(75) WOOLF, C.R. Clinical findings, sputumm examina-
tions, and pulm onary function tests related to
the smoking habits of 500 women. Chest 66:
652-659, 1974.
(76) WOOLF, C., SUERO, J. The respiratory effects of
regular cigarette smokingg in women. American
Review of Respiratory Disease. 103: 26-37,
1971.
(77) SWNDER, E.L., LEMON, F.R., MANTEL, N.
Epidemiology of persistent cough. American
Review of Respiratory Disease 91: 674, 1965.
202
r
s
incidence of disease would be expected, while those women
born from 1920 to 1950 are just beginning to enter the ages
att which there is a high prevalence of disease. As a result,
the adverse effects of sm oking andd occupational exposure
would be expected to occur more frequently in men, reflecting
this difference in the age of the average male and female
smoker. This "cohort effect"might lead to the erroneous
conclusion that women are protected from occupation-smoking
interactions, just as it has been used to suggest that women
are protected from the lung cancers induced by cigarette
smoking in men.
A secondd difference between male and female smoking
habits whicK must be considered is the prevalenceof smoking
by occupation. Table 1 shows that the prevalence of smoking
is reasonably uniform among women employed in many
different occupations (the exceptions are education and
household area workers with low prevalenceand food area
workers with high prevalence). There is not the marked
differencein smoking habits between female blue collar and
white collar workers that has been observed In men (13)
(Table 2). A slightly lower prevalence of sm oking among
professional women compared to other white collar workers
occurs similar to that seen inn men (7).
The section on behavior in this report discusses the
sm oking habits of several groups of healthh professionals. It
shows that women physicians and psychologists smoke more
heavily than their male counterparts. Thus, the relative levels
of sm oking observed in the two sexes are reversed for these
two occupational groups in comparison to the general
population (17). Nurses also have been shown to have a much
higher prevalence of smoking than women of the same age in
the general population (18). A final notable difference is
that among women smoking prevalencedoes not show the
same marked inverse correlation with socioeconomic status
(3). The reasons for these differences are beyond the scope
of this section. However, an understanding of them forms
part of the background for any discussion of the interaction
of smoking and occupational exposures among women.
207
TABLE 4._Prevalenee 9f ehronie bronUriLs by paroking cleuifiatian (rwmben in p.rentbeis repeesent
toul nuMx o1
fild'wiJualc in Inrticular ammkinq 9roup). . SenmaYers NS-nonsmoke.a . EX=ezsmokers
Aurhm, year, Number and type
coVmtryreference of.population
Men - Womem . Comment
Higgins, er al. 1956 94 men and 92NS.........
England(40) , wom.n randomly S..........,
cM1ose from agricultu.al wmmum
tiee
Oswaid,etal.1955 3SO2' maies and. NS.....15.814741 NS.......,.121(f3191Cnronlc boncb'Ck
Englamd(51) 2,242femalec/erkal S._....IB.4'A1,9401 S_..........18.8(B]9[ defineEby.Labituall
worken 4069 yra.. cou96 and sputumm
ofage.. ' ' . productiom
Hubtr, 1965
England (42)
Remin9ton,1969
Enqland.(56)
Ferris,1962
USA. (25, 2].28)1
Payne.19fi4
U S A. (52)
women in a FmnlsE E%....... ........... .16.3 EX......_.13.3 wnt rM1me who 6avt
ruraloommunity40+ 51~14__......... 38.0 S1-14 .............104 stoppeE tur more
60 yn, of ege. 1524._...._.. 41:4 1536 5].0 then 1 monID
.
. >25........, 4.a >25............
41,729 men eon NS......,.5.1198551 NB......3.4(12,3511 Age-edjusted total
22.295nomenpartiEX........9,816.5101 EX......3819591 nranlence Cigarette
cipatib9inmassminl- Cignettes(Y3,243/ Ciyaretes(8.985) dosa9a9radientsignie amne redlograpbp,
5U9..... 9.1 : 549',..... 5.1. ficenttoP<0.001s screening 1D19. 150 10-19.. 10.6.
>N..20b . . . >20... 18.5 .. . .
542 me aM' 625 Dvar91 Dverall Age.ryeCi/it rates
women residents af. NS _...,. 13.8 (1251 NS ....... 9A (3]8)
New Haminhire. EX......, 11.9 U71 El( ...... 10.8 (37)
town ohosen by rar. Cigarettes W.3 (340) Ciqerettes.19.8 (208)
dum szmplin9 o0 1-10.._29.9 610....13.1
canwa 11.20._ 34.2 1140... 22.2
2130...423 2130... - ~ 31>0 .., 61 I t 31 J0... 27.3
.
>41....]5.3 >a1.... - ~
5.140adWtresidents. Dvereul9 Overa114 ' Prevaienceratesesfiof Tecumuen, MicEii .. msted from line
qan graph
Mueller, er al. 19]I 281 rrvn and 328'O.xrall 8J 12811 . OnraI1L,.... 1013281
U.S.A.(49) wnmen residenu o1 NS....._..... 3(jl N3 2(3)
Glenwood Sprlna. EXI......... ., 13 pl EX........... . 5(1)
Cola.. S 1~14 11 (3) S 1~14....... 14 (7)
. 1524...20 (131. 1524..... 2504)
>25...... 38(21) '~ >25._..33 (9)
I
Tager,1976 227 mand 280 oeerall._.14.712nf. Overan... 7.6 12951 A9ead/ustedl preva-
I1.S.A. (81) women In Eae 8os- N9......... 5.8 NS....._. 1.6 lencerate
tdn, Mass. a9e15 or S.-.._...... 34.2 5............1].6.
greater.
TABLE 2.-EStImates of the Percentage afi Current, Regulzr Cigarette Smokers, Adulteages 20
Years and Over, According to Labon Force.5tatus and Occupatlon and .3:
Sex, U.S., 197 1
6
Female stile
Totall Total
20+ 20-44 45-64 20+ 20-44
Total 32.0. 36.9 34.8 41.9 47.6
Currentlyy employed 35.9 37.0 36.1 43.4 46.8
White collar total 34.3 33.8. 36.9 36.6 38.6
Proresslonal technical 29.1 28.6 32:.7. 30,0 311.1
and klndr.ed
Managens &.adminlsHrators
41.6
42.7
40.9
41.0
46.4
except farm
Saies warklers
38.1
37.0
42.6
39.9
42.6
Clerical & kindred wo.ker,s 34.8 34.J 36.0 40,4 40.1
Blue collar total 39.0. 43.7 33.6 50s4 54.1
Craftsman &.kindred wvrkens 40.5 46.9 33.6 48.0 52.1
Operatives andkindred 37.6 42.5 31.2 52'.3 55.3
workers
Laburer, except farm
56.3
52.6
53.7
56.9
Servlce 39.0 42.8 37.2 47.2 51'..1
Farm . - 32.2 51.0~ 36.9 45.4
Unvrylcyed. 40.0 41.0, 39.2 56.8 59.9
Usual actVvity-homemaking
29.0
37.1
32.2
N+, -
NA
45-64
41.3
39.7
35.3
29.9
36.1
38'.0
44.2
44.3
41.6
46.2
51.7
44.8
35.0
53.9
NA
NOTE:Unknnwn, if e r
. moked'excluded from calculation.
Flgure: does not meetstandardS.ofrellability or precision.
SOURCE: Uhpublished data, Health Intenview 5urvey., 1,976, Natlonal Center
for Heallth Statistles (5.), -
206
Volunteers--- Probability -Canadian Total Pop.
/n 25 samnle of pensioners of 79 health
states the Swedish !, dependents districts
populatlon In Japan
686V&9E0
Sample pluf Probability sample
volunteers of Rrltish Po Norwe-
from Framingham, Plan migrants to
Nass.s (whites) U.S. In 12 states
PATTERNS OF EMPLOYMENT
The percentage of women in the United States work force is
steadily growing. In 1973 women represente& 38.4 percent of
the United States work force and in 1978 that percentage had
risen to 41.2 percent (15).
.
Approximately 39 million women are employed, outside
the home. Table 3 clearly indicates that the distribution of
women in the labor force by category of work does not
parallel that of men. lyomenn are more likely than men to be
employed in the clerical and service categories. Men are
more likely to be employed in the management, crafts and
operatives/transport categories than wom en. Table 4 lists the
number of women employed In a wide variety of occupations,
including many of those traditionally believed to be hazardous
for men. In spite of this diversity, the bulk of womenare
employed in a narrow range of jobs. Over one-third of
women in the paid labor force are employed in one of the 10
job categories listed In Table 5. All of these categories have
beenn traditional employment areas for women. Thus, the
recent gains by women in employment opportunity have not yet
had a substantial impact onn the actual distribution patterns of
the female labor force. If a shift does occur in employment
patterns Involving greater proportions of women in occupations
with significant exposures, we would expect a cohort-effect
to be apparent in the developm ent of occupational illness.
That is, those women entering hazardous occupations tradi-
tionally limitedd to male workers would be expected to be
women newly entering the work force and, thus, predominantly
in the younger age groups. As these cohorts age, the
duration of both occupational and smoking exposures would
increase. It is only after these newer cohorts reach the ages
where disease is prevalent that we would be able to observe
the full impact of occupational exposures (or their Interac-
tions with smoking) on the health of women.
Because of this cohort effect, any failure to
.
demonstrate an excess risk of a given occupational exposure
In wom en must be interpreted with considerable caution. It
may mean only that the women exposed'were too young and
the exposure too brief for illness to have yet developed. Thiss
caution is doubly im portant for those attempting to
demonstrate an interaction between occupational exposure an&
smoking on the development of disease in women. Thus, little
comfort can be taken from the current low prevalence of
occupational disease in women. It is reasonable to expect
208 .
03655144
lable 4 Ioontinued)',
# of Wemen
Occupatian In Thousands
Laundry, and dry cleaning
aperat~ives, n.e.c.
Meat cutters and butchers,
eacept''manufocturingMeat cutters and butchers,
manufacturi~ng
Mlne operatives, n.e.c.
Mixing opentlvesPacking. and wrappers,
ascluding meat and produce
Painters, manufactured
artlcles
Phatagraphik process workers
Precision machine operatlves
Drill press openativet
Grinding machine operatlres
Lathe and mlllling machine
operativer
SWRCE: U.S. Oepartment of Labor (17).
/p of Women
Occupation in Thuusands
nursing 238
fLneing aldes,, orderlies,
and attendants
902
Practical nurses 390
Personal servlce warker-s 1,302
Attendantc 175
Barbers 11
Child carewerkers 101
Hairdresser and eosmetoioglsts 483
Housekeepers, excluding private
househnlds
Welfare servlce aidas
92
Protectiveserelte workers 115
Flrefighters 1
Guands 53
Police and detectlres 28
Shenlils and baill7fs 3
Farm wonkers 509
TOTAL - 38,910
211
that any movement of large numbers of women into hazardous
occupations will be followed, after an appropriate time lag, by
a dramatic increase in the prevalence of occupational illness
in women.
THE REPRODUCTIVE ROLE
A third reason for examining the effects of occupational
exposures in women separately from those in men is the
difference in their reproductive roles. Toxic occupational
exposures In both men and wom en can reduce fertility and
increase frequency of teratogenic effects (see Table 6). In
addition, however, the 9-month duration of gestation provides
m any opportunities for the fetus to share any adverse toxic
exposure of Its mother. These risks may interact with the
well-established risks of cigarette smoking during pregnancy
discussed else where in this report. Table 6 provides a list of
hazardous substances in the work environment, some of which
aree suspected of having effects on reproduction. Another specific concern for women is that of
contraception. The type of contraception used often depends
upon decisions by the woman, and substantial numbers of
women in the. United States who useoral'e contraceptives (18).
These drugs have been shown to interact with cigarette
smoking to produce a greatly increased risk of cardiovascular
disease, as discussed in this report. In addition, it is
possible that oral contraceptives may interact in an adverse
manner with physical or chemical agents found in the work
place, or that the combination of smoking, occupational
exposure, and oral contraceptive use may bear special risks.
The answers to those questions can be found only through thee
study of populations of working women. One study approached this issue by examining the
health status of wom en involved in the manufacture of oral
contraceptives. Poller, et al. have shown that women working
in the manufacture of oral contraceptives absorb enough of
the drugs to influence the clotting m echanism as well as alter
m enstrual function (12). Unfortunately, the risk of
cardiovascular disease- -and the effects of sm oking in relation
to it--could not be estimated in this population. Because of
the established excess risk of cardiovascular disease from
concurrent smoking and oral contraceptive use, examination of
cardiovasular risk in this group would be of interest.
213
TABLE 5.-Most Common Female Job Categories, by Percentage of the Female Work
. Force Employed
Percent of Female
Lob Work Force ub
Secretary 8.5 Private Household
Worker '
Retail Sales Clark 4.3 Registered Nurse
Bookkeeper 4.3 Elementary School
Teacher
Waltress ' 3.2 Typist'
, Cleaning Workers
Cashier 3.1 Sewer & Stitcher
SWRCE: U.S. Department of Labor (1i7)',
212
Percent of Female
Work Force
2.9
2.8
2.8
2.6
2.2
2.0
TABLE 4.~umber of Woman In the Current Workforce,. Cl~assifled by Occupation (191g)
# ofi Women
Occupation In Thousands
White-collar workers 24,594
Professional & Technical 6,083
Biological sclentLsts 22
Chemists 17
Nun es, dletlclans,.6 therapists
Heal.th technologlstis and 1,255
technicians 353
Enginccring and sciknce
technlclans 132
Painters and sculptors 83
Photographers 13
Managers and administrators,
except farm ],365Sales. worikers 2,666
Sales clerks, retail trade 1,672Clerieal workers 13,456
Bookkeepers -1,660
Cashlens 1,222.
Secretaries 3,5611
Typi'sts1,009
81ue-collar warkers 5,770
Craflt andd kLndYed workers 694
Prinni:ng craft workers 911
Uphols[er~ers 14
Operatives, exaept transport 4.,317Assemblers 606
Bottling and'canning aperativcs . 25
Checkens, examiners, and
inspectore; m nufacturing 359
Clothing ironers and
pressens 101,
Cutting operative, n.e.c. 84
Dressmakers, except factorry' 113
Drilllers., earth 2
Dry wall installers and
lathers 1
Fllers,, polIsbers,.sanders .
and buffers 38
Furnace tenders, smelters,
and puuners, metal 3
Garage workers, and gas
statlon attendants 20
R of Nbmen
Occupatlon In Thousands
Btu<-colla workers-cont'd.
Opera0lves, xcept transpor.t- contlnued Punch and stamping press 1's=
operat~ives 41
Sawyer 14
Sewers and stitchers 772
Shoemaking machine eperatires 60
Furnace tender, and stokers,
excepL metal (
Textllb operatiee. 224
Spinners, twisters, and wlnder.s 100
Welders and flame cutters 41
Wlndlne operatives, n.e.c. 31
All other operatives, except
transport 1,062
Transportt equipnent operatlves 258
Nonfarm laborers 492
It
Servlce workers 8,D31 1
Private households 1,135
Child care wonkers 471 ,
Cleanerss and servants 514 '
Housekeeper. 111
Service workers, except
househollds 6,901 ~~
Cleaning workers 856
Lodging quarters cleaners 174 Building interlor cleaners,
.
n.e.c.462 )anitprs and sextons 222
Food service workers 2,951
eartenders 111
Waiters, asslstants 45 Cnuke 678
Dishwashers 82
Food counter andfountaln
workers 397
Watters1,252
Food servic< wankers, n.e.c. 384
Health serrice workers 1,660
Dental assistmts 128
Health aides,, excluding
210
lung andpieura was found among those who were severely
exposed and who had worked less than two years. In the
group with severe exposure for more than two years in the
factory, excess deaths from cancer of the lung, pleura, and
non-neoplastic respiratory disease were observed. The authors
calculated the excess annual mortality due to lung cancer.
Women workers with low-to-moderate exposure experienced a
mean excess lung cancer mortality of 63 deaths (per 100,000
years' exposure). Those severely exposed for less than 2
years experienced an excess of 44 deaths, and those severely
exposed for 2 years or longer experienced an excess of 241
deaths. Interestingly, an examination of deaths did not reveall
any significant association with age at first employm ent. in the
asbestos factory. In the sub-sample of workers whose
smoking histories were available, those women who had both
smoked and were heavily exposed had a risk of developing
lung cancer over 30 times that of non-exposed nonsmoking
women. The authors concludedd that the data suggested that
asbestos and cigarette smoking exert multiplicative rather than
m ereiy additive effects.
In summary, the data on smoking and asbestos exposure
in women closely resemble the findings demonstrated for men.
Approximately 250,000 women were employed in the textile
Industry in 1978; that population included approximately
100,000 women engaged In spinning, twisting, and winding
operations. Byssinosis Is a syndrome characterized by
tightness of the chest and shortness of breath in workers
exposed to dust of cotton, flax, and hemp. In addition to
these acute symptoms, workers have been found to develop
chronic bronchitis, and some become severely disabled by their
obstructive lung disease (3). Berry, et al. studied the
workers in 14 cotton and two man-made fiber mills in
Engiand (1). They found that men had a greater prevalence
of byssinosis than wom en, and that smokers of both sexes had
1.4 tim es greater prevalence of byssinosis than nonsmokers.
Byssinosis prevalence was also positively associated with
length of exposure to cotton dust in both women and men and
was positively associated with dust level in the working
environment in women. Berry, et al. were unable to
determine If the observed difference in prevalence by sex
represented a difference in physiologic response or differences
b) Transformation of workplace chemicals into
more toxic substances,
c) Addition of the exposure to a toxic constituent
of tobacco smoke to a concurrent exposure to the same
constituent present in the workplace,
d) Addition of a health effect due to
environ mental exposure to a similar health effect due to
smoking,
e) Synergy of exposures, and
f) Causation of accidents.
2.. Women are entering occupational environments with
greater frequency, and thus may be experiencing greater
exposures to physical and chemical agents.
3. Cohorts of women with a greater prevalence of
sm oking are currently reaching the ages of maximal disease
occurrence, replacing earlier cohorts with lower cigarette
exposures.
4. Physiologic differences in hormonal status between
males and females constitute a potential source of differing
responses.
5. Women In the workplace who are pregnant present
a nine- month exposure opportunity, including potential
teratogenic and perinatal mortality effects. 6. Concurrent exposure of women to sm oking and
asbestos resulted in a clear excess of cancer of the lung.
7. Women sm okers exposed to cotton dust run a higher
risk of developing byssinosis, bronchitic syndrom es, and
abnormal pulmonary function tests than nonsmoking women.
220
in occupational exposure. They also found a higher prevalence
of bronchitis in exposed versus nonexposed workers of both
sexes. Smoking workers had higher bronchitis rates than did
nonsmoking workers. .
Bouhuys, et al. studied 645 active and retired cotton
textile workers (including 372 women), aged 45 and older,
who had worked an average of 35 years. Their respiratory
symptoms and flow-volume curves were compared to those of
community residents who acted as controls (3). Textile
workers of both sexes had significantly increased prevalence
of chronic cough, wheezing, and dyspnea. Work in the textile
mills was the major variable associated with symptom pre-
valence, with smoking as an additional significant variable.
The lung function data confirmed the association of both
smoking and working in the mills with decreased lung function.
Nonsmoking female workers were slightly more likely to report
chronic cough than nonsmoking men, but smoking male workers
were almost twice as likely to report this symptom as smoking
women. A similar pattern' was seen for wheezing and chest
tightness, but not for dyspnea.
Kilburn, et. al. studied the prevalence of byssinosis and
bronchitis in 1,046 women textile workers and showed an
interaction of smoking and work exposure inn producing a
higher prevalence rate of both byssinosis and bronchitis at a
given dust level (5).
In summary, women have clearly been shown to have a
higher risk of developing byssinosis,chronic bronchitis, and
chronic obstructive lung disease because of exposure to cotton
dust in the workplace. Cigarette smoking has been shown to
interact with some work exposures to increase this risk,
although it is not established whether this interaction is
additive or multiplicative. Men employed in occupations where
they are exposed to cotton dust have a greater prevalence of
bronchitis and respiratory disability than women. Clarification
is necessary to determine whether this is a sex difference or
a difference in exposure (either occupational or sm oking).
1. The 1979 Surgeon General's Report identified the
ways in which smoking cigarettes may interact with the
occupational environment. They include:
a) Facilitation of absorption of physical
contamination of cigarettes,
The preceeding discussion presents several areas where
female-male differences may significantly limit the direct
applicability of the results of male smoking studies to the
female population. These areas of potential difference
present research questions which justify significant, ongoing
research activities.
SPECIFIC INTERACTIONS BETWEEN OCCUPATIONAL EXPOSURE
AND SMOKIN6
A revie w of all the potential risks of occupational exposure
for women is beyond the scope of this section. Table 6 lists
a number of agents found in the occupational environment and
their observed organ toxicity. Table 7 presents selected
pulm onary irritants and sensitizers in specific occupational
settings in relation to the number of women employed In those
settings.
There is little specific data on the health effects of a
given occupational exposure in women. Two clear exceptions
exist--exposure to asbestos and to cotton dust. The data
from studies of women exposed to these two compounds
provide examples of established, interactions between smoking
and occupational exposure in women.
Asbestos
Selikoff, et al. prospectively followed a group of 370 male
asbestos insulation workers. He demonstrated a multiplicative
effect of asbestos exposure and cigarette smoking on the risk
of development of lung cancer (4,13). Workers who smoked
cigarettes developed lung cancer at aa rate 92 tim es that of
non-exposed nonsmokers. They observed no deaths from lung
cancer am ong 87 nonsmokers, and 24 deaths from bronchogenic
cancer among 283 regular smokers, aa number well in excess
of the 3 deaths expected. Ne whouse, et al. followed aa
cohort of 900 women first employed between 1936 .and 1942
in anasbestos factory m aking both textiles and insulation
materials (11,2,10). They analyzed the group's mortality
experience between :i:st employment and 1968, with aa
minimum of 26 years' S.illow-up. There was an excess overall
mortality partly accounted for by deaths from cancer,
observed evenamongn those who working imn jobs with low-to-
moderateexposure: to asbestos. An excess of cancer of the
215
(8) NATIONAL CLEARINGHOUSE ON SMOKING AND HEALTH.
Survey of Health Professionals: Smoking and
Health, 1975. U.S. Department of Health,
Education, and Welfare, Public Health Service,
Center for Disease Control. Bureau of Health
Education, National Clearinghouse for Smoking
and Health, June 1976, 42 pp.
(9) NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND
HEALTH. Occupational Diseases (Revised Edition).
U.S. Department of Health, Education, and
Welfare, Public Health Service, Center for Disease
Control, National Institute for Occupational
Safety and Health. Superintendent of Documents,
June 1977, 608 pp.
(10) NEWHOUSE, M.L. Cancer among workers in the
asbestos textile Industry. In: Buguvski, P.,
Gilson, T.C., Timbrell, V., Wagner, J.C., Davis,
W. (Editors). Biological Effects of Asbestos.
International Agency for Research on Cancer,
Scientific Publication No. 8, Lyon, France,
International Agency for Research on Cancer,
1973, pp. 203-208.
(11) NEWHOUSE, M.L., BERRY, G., WAGNER, J.C., TUROK,
M.E. A study of the mortality of female asbestos
workers. British Journai of IndustrialMedicine
29: 134-141, 1972.
(12) POLLER,L., THOMSON, J.M., OTRIDGE, B.W., YEE,
K.F., LOGAN, S.H.M. Effects of manufacturing
. oral contraceptives on blood clotting. British
Medical Journal 1: 1761-1762, June 30, 1979.
(13) PROCTOR, N.H., HUGHES, J.P. Chemical hazards of
the workplace. Philadelphia, J.B. Lippincott
Company, 1978, 533 pp. .. (14) RONES, P., LEON, C. Employment and unemployment
during 1978: An analysis. Special Labor Force
Report 21 8. U.S. Department of Labor Bureau of
Labor Statistics, 1979.
(15) SELIKOFF, I.J., HAMMOND, E.C., CHURG, J. Asbestos
exposure, smoking, and neoplasia. Journal of the
American Medical Association. 204(2): 106-112,
April 8, 1968.
.
222
(16) STELLMAN, J.: DAUM, S.M. Work is dangerous to
health. New York, Pantheon Books, 1973, 448 pp.
(17) U.S. DEPARTMENT OF LABOR. Employment and
unemployment during 1978: An analysis. U.S.
Department of Labor, Bureau of Labor Statistics,
Special Labor Force Report 218, 1979.
(18) U.S. PUBLIC HEALTH SERVICE. Smoking and Health.
A Report of the Surgeon General. U.S. Depart-
ment of Health, Education, and Welfare, Public
Health Service, Office of the Assistant Secretary
for Health, Office on Smoking and Health, DHEW
Publication Nb. (PHS) 79-50066, 1979.
I
223
TABLE 1.-Birth weight under 2,500 grams by maternal smoking habit, relative and attributable risks
from published studies
Relative Attribut-
Study Nonsmokers Propor- Non- risk able
(No.) No. tion Smoker Smoker smoker risk
(%) (%) nonsmoker (%)
Cardiff 7,176 6,238 .465_ 4.1 8.1 198_ 31 US Collaborative White 8,466 9,781 .536 4.3 . 9.5 221 39 ,
Black 11,252 7,777 .409 10.7 17.5 . 164 21,
Californla, Kaiser
Permanente - White 3,189 2,145 .402 3.5 6.4 183 25 Black 934 479 .338 6 4 13.4 209 27
Montreal 3,954 3,004 .432 5.2 11.4 219 _ 34
Ontario 27,316 21,062 .435 4.5 9.1 202 31
N
~
Percentage of total birth weights <2,500 gm attributable to maternal smoking.
Attributable risk in population = b(r-1) divided by b(r-1) -1 where b= propor-
tion of mothers who smoke and r = relative risk of low-weight = smoker rate
nonsmoker rate.
SOURCE: Meyer, (87). , - .
SSISq9E0
INTERACTION BETWEEN SMOKING AND OCCUPATIONAL EXPOSURES:
REFERENCES
.
BERRY, G., MOLYNEUX, M.K.B., TOMBLESON, J.B.L.
Relationships between dust level and byssionsis
and bronchitis In Lancashire cotton mills.
British Journalof Industrial Medicine 31: 18-
27
1974
,
.
BERRY, G., NEWHOUSE, M.L., TUROK, M.E. Combined
effect of asbestos exposure and smoking on
mortality from lung cancer in factory workers.
The Lancet
1972 2(7775): 476-479, September 2,
.
BOUHUYS, A., SCHOENB ERG, .7.B., BECK, G.J.,
SCHILLING, R.S.F. Ep idemiology of chronic lung
disease in a cotton mill community. Lung 154:
167-186, 1977.
(4) HAMMOND, E.C.,SELIKOFF, I.J. Relation of
cigarette smoking to risk of death or
absestos-associated disease among Insulation
workers in the United States. In: Boguvski,
P., Gilson, J.C., Timbreli, V., Wagner, J.C.,
Davis, W. (Editors). Biological Effects of
Asbestos. International Agency for Research on
Cancer, Scientific Publication No. 8, Lyon,
Lyon, France, International Agency for
Research on Cancer, 1973, pp. 312-317.
(5)~ KILBURN, K.H., KILBURN, G.G., MERCHANT, J.A.
Byssinosis: matter from Ilnt to lungs.
American Journal of Nursing 73(11): 1952-1956,
November 1973.
(6) NATIONAL CENTER FOR HEALTH STATISTICS. Health
Interview Survey, 1976. (Unpublished data.)
(7) NATIONAL CLEARINGHOUSE FOR SMOKING AND HEALTH.
Adult Use of Tobacco, 1975. U.S. Department of
Health, Education, and Welfare, Public Center
for Disease Control, Bureau of Health, Education
National Clearinghouse for Smoking and Health,
June 1976.
(1)
(2)
(3)
221
nonsm okers (3, 16, 42, 90, 106, 110, 111).
One study in which rates of low birth weight were
simultaneously adjusted for multiple factors sho wed that
maternal smoking had a more significant relationship to birth
weight than did previous pregnancy history, hospital pay
status, m other's prepregnant weight, height, age-parity, or sex
of child. Adjusted rates of birth weights under 2,500 grams
were 49 per thousand for nonsm okers, 76 per thousand for
smokers of less than a pack per day, and 114 per thousand
for smokers of a pack per day or more. The risk of having
a low-birth-weight baby therefore increased 53 percentt and
130 percent for light and heavy smokers, respectively,
compared with nonsm okers (90).
Population studies that iilustratewhole distributions of
birth weights by maternall smoking levels sho w a do wn ward
shiftt of all birth weights in proportion to the amountt smoked.
(81, 87, 118, 78, 140, 165) (see Figure 1).
These studies show that the relationship between
sm oking and reduced birth weight is independent of all other
factors that influence birth weight, such as race, parity,
maternal size, socioeconomic status, sexx of child, and other
factors that have been studied. It is also independent of
gestational age. There is a dose-response relationship; that
is, the more the woman smokes during pregnancy, the greater
the reduction In birth weight. If a.women gives up smoking
by her fourth month of gestation her risk of delivering a
low-birth-weight baby is similar to that of a nonsmoker.
Placental Ratios
Analyses of placental weights by m aternal sm oking habits have
noted that these weights were either not affected or were
less affected by maternal sm oking than were birth weights
(62, 66, 95, 108, 159). The placental' ratio, the ratio of
placental weight to birth weight, tended to be larger for
smokers than for nonsmokers, mainly because of the dose-
related reduction in birth weights withh increasing num ber of
cigarettes sm oked.
Wingerd and colleagues have studied placental ratios
based on data from 7,000 pregnancies among members of the
Kaiser Foundation Health Plan in Oakland, California (161).
Smoking information was obtained early in pregnancy, and
placentas were handled according to Benirschke's standardized
protocol. Figure 2 sho w placental ratios by sm oking level and
in
226
6a
FIGURE 3. Fetal Biparietal Diameters (BPD) values
Standard Error of. Means (SEM) of nonsmokers and heavy smokers
(10 cigarettes/day) plotted in relation to postmenstrual age against
the normal range (shaded area sepicts 95% confidence interval).
mm
100 r
90
80
70
60
25
30
SOURCE: Persson, P. et al (118)'.
35
231 ~
40
weeks
I
TABLE 7.-Exampfeof pulmonary irritants and inorganic sensitizers in variousocRupations where women
worR *OF WOMEN
SEVERE INORGANIC EMPLOYED
PULMONARY IRRITANT SENSITIZERSOCCUPATION IN THOUSANDS
Beryllium & Compounds Platinum Salts
Phosphorous Trichlontle
tellurium (Hexaflouride)
Zinc (Chlbride9ume)
Ammonia Phlanali<Anhydride
Chlorine
Ozone
Sulfuric Acid
Uranium Compounds
Vanadium Compounds
(Pentoxide)
Acrolein Cobalt, metal
Ammonia fumes & dust
Cadmium dust Phmabc Anhydritle
Chlorine
Chrcmales
DNhloroethylletherEthylene Oxide
Hydrogen Chloride
HqYdro9en Fluoride
H drogen Sulfide: Phosgene
Phosphorous Trichlbride
Phthalic Annydride
Sulfuric Acid
Tellurium (Hr:xafluoride)
.
Zinc Compounds.
Ammonia
Antimony Phthalic Anhydride
Chromic Acid & Chromates Polyuinyl Chloride
ChrOmiVm, metal &
insoluble salis
Hydrogen SulfidePhthaLC.Anhydride
Sulphur. Dioxide
Ammonia
Cadmium tlusUtumes
Chromic Acid & Chromates
Chromium, melaC&
insoluble salts
Fluorine
Hydrogen Chloride
Nitrogen Dioxide
Sulfuric Acid
Zinc Chloride9umes
216
Electronic Maohinery;
Equipment & Supplies
890
-Household Apphances. 67
-Radio, T.V. &.
Communication Equipment
216
-Elecirical Machmery,
Equipment & Supplies
604
Professional & Photo-
graphic.Equipment &
Watches
238
-Scienhfic & Controlling
Instruments
65
-Opticat &.Healtfi Services
SuppLes
119
-Photo{praphic Equipment
& Supplies
36
Rubber & Misc; Plastic
Products
257
-Runber Products 86,
-Misc. Plastic Products 171
ueather & Lealher.
Rroduots 1 77
-FOOtwear,except.rubber 13
-Leatner Products, except
footwear 40
Fabricated Metal Products 299
-Cuneryy hand tDOls, &
otheohardware
52
-Fabricated structurall
metauproalbcts
78
-SCrew machine Products 26
-MetallStampinq 43.
-Mrsc.labncated metal
products
10
PREGNANCY AND INFANT HEALTH
INTRODUCTION
A woman who smokes during pregnancy not only risks her ownn
health, but also changes the conditions under which her baby
develops. Studies have identified specific areas in which the
effects of maternall smoking during pregnancy may occur.
These include fetal growth, most often determined by
comparing birth weights of sm okers' babies with those of
otherwise similar nonsm okers' babies; fetal survival, including
the occurrence of spontaneous abortions, fetal deaths, and
neonatal deaths; pregnancy complications, including those that
predispose to preterm delivery; possible effects on lactation;
and long term effects on surviving children. The relationships
between maternai smoking and these outcomes have been
established by clinical, pathological, and especially
epidemiofogical studies. Understanding of inechanisms by
which smoking may produce the observed effects has been
gained by physiological studies inn humans and experimental
studies in anim ais.
The Chapter on Pregnancy and Infant Health in the
1979 Surgeon General's Report Is a detailed review of past
studies of the effects of smoking In pregnancy, with, a
comprehensive bibliography. This section summarizes current
knowledge in major areas of study, describes important new
studies, and points out areas requiring further research (150).
SMOKING, BIRTH WEIGHT, AND FETAL GROWTH
Babies born to women who smoke during pregnancy are, on the
average, 200 grams lighter than babies born to comparable
women who do not smoke. Since 1957, when Simpson reported
this finding from her original study (142), it has been con-
firmed in more than 45 studies of more than haifa million
births (150). Results of these studies are expressed as mean
birth weights of smokers' and nonsmokers' babies or,
alternatively, as the percentage of babies who weigh less than
a specified amount, usually 2,500 grams.
To illustrate the association between maternal smoking
and an increased proportion of fow-birth-weight infants, the
results of five studies with an aggregated total of aim ost
113,000 births in Wales, the United States, and Canada are
summarized in Table 1.. In these popuiations, 34 to 54 per-
cent of the mothers smoked during pregnancy and on the
average had twice as many fow-birth-weight babies as the
224
FIGURE 2- Ratio of placental weight to birth weight
by length of gestation and materal smoking category.
15.5 t
15.0
Hea~y nnoY.ers
13.5
13.0
0'` I I ! t i--- I F-
37. 38 39 40, 411 42 43'
Wcek ol gpstaunn
SOURCE: W ingerd, J./161 I.
228
FIGURE 4rDistribution of birthlengths.
SOURCE: Persson, P. et al (118)
232
_ non-smokers
____ all smokers_. - ._ heavysmokers
FIGURE 1- Percentage distribution by birth weight
of infants of mothers who did not smoke during preg-
nancy and of those who smokedd one pack or more of
. cigarettes perr day.
INFANT W EIGHT AND PAFENTAL SMOKING'.HABITS
10 '~ -- Non-smoker
-
I -- Smoker
8 }
6 +
4+
2 +
..~~
4 5 6 7 8 9 10 11
BIRTH WEIGHTISCALLE INiPOUNDS:INTERVALS OF 40Z.)
SOURCE r MacMahon,.B.i81)
227
gestation for single live births to black and white women. At
each gestational age, from 37 through 43 weeks, the more the
mother smoked during pregnancy, the higher was thepiacental
ratio. These ratios were higher for black than for white
women and tended to increase as maternal hemoglobin level
decreased (161). Christianson has reported recently (1979) on the
standardized examinations of these placentas. The increase in
placental ratio with m aternal sm oking level was due to
considerable decreases in mean birth weight, accompanied by
slight increases in m ean. piacentalweight. In addition,
smokers' placentas were significantly thinner than those of
nonsmokers, and their minimum diameters were larger (20).
Maternal smoking leads to significant increases In car-
boxyhemoglobin in maternall and fetal blood, with a consequent
reduction in the oxygen carrying capacity of both, and a
reduction of the pressure at which oxygen is delivered to the
fetal tissues (150, 74, 75). Christianson discusses the
similarity between studies of placental ratios by smoking
level, altitude, maternal anemia, and cyanotic maternal heart
disease. He suggests that the changes in placental ratio
represent an adaptation to relative fetal hypoxia (20). An
adaptive advantage for survival might occur because a smaller
fetus would have a decrease oxygen demand. If so, It is
extremely important to know whether this reduction in size is
accompanied by any long-term costs in later growth and
development.
, - -
Gestation and Fetal Growth
In early studies the consistent finding that mean birth weights
were lower and the frequency of births under 2,500 grams
higher for women who smoked during pregnancy thann for
similar nonsmokers raised the dbvious question of whether this
might be due to a sm oking-reiated reduction in gestation.
This is not the case. Studies consistently sho w that mean
gestation is minimally reduced by maternal smoking (less than
2 days) (150, 3, 15, 164) and that birth weight is lower for
infants of smokers than for infants of nonsmokers at each
gestational age (150, 16, 87, 3).
The finding that maternal sm oking does not cause an
overall down wardshift in the distribution of gestational ages,
as was shown for birth weights of smokers' Infants mustt be
due to -direct retardation of fetal growth. In other words,.
229'
these infants are small-for-dates rather than preterm. The
type of fetal growth retardation associated with m aternal
smoking is characterized by an abnormally short crown-heel
length for gestational age (93, 94), Smokers' babies are
smaller than corresponding nonsmokers' babies in all
dimensions measured, Including: length, head circumference,
chest circumference, and shoulder circumference (150, 32, 33,
57, 62, 66, 106, 108, 162, 10).
Previous studies of these m easurements at birth have
inferred that birth size reflects the rate of fetal growth; this
has been confirmed by a definitive study in which fetal
biparietal diameters were measured serially during gestation.
Persson and coworkers studied 5,715 pregnancies prospectively,
making ultrasonic measurements of biparietal diameters (BPD)
from 18 to 20 weeks through term. Separate growth curves
of BPD were constructed for fetuses of smokers and
nonsm okers who were delivered between. 266 and 294 days
after the last menstrual period. The BPD increased faster in
the nonsmoking group; the difference from~ the smoking group
was apparent from the 28th week and was positively
correlated with the average number of cigarettes smoked
(Figure 3). Measurements taken at birth sho wed that the
distributions of birth weights and lengths shifted down wards in
proportion to the level of smoking. Figure 4 illustrates this
shift (118).. These findings corroborate Miller's
characterization of smokers? babies as normally proportioned
but short as well as light for dates, and sm ai{er In all
dimensions than babies of nonsm okers (94). The data are
also consistent with the speculation that relative fetal hypoxia
results in a slower mitotic rate, a baby withh fewer cells,, and
a reduced oxygen demand.
Long-term Growth and Development
Possible long-term consequences of maternal smoking during
pregnancy are also of concern. Severall long-term studies
provide evidencetfiat children of smoking mothers have slight
but measureable deficiencies in physicaP, gro wth,intellectual
and em otional development, and behavior (100).
Because these complex outcomes are affected by many
known and unknown factors, it is important to take these
other factors into account In any attempt to measure long-
term effects of maternal smoking. Numerous well-controlled
studies have shown that the physical growth of smokers'
C
W
Q'7
C7
U1
l~+
~
C
230'
TABLE 2~.-Incidence of neurologica.l abnormalIti:es at about 5 112 years,,
by maternal smokinghab.its
Percent of Children with Diagnosis
. Maternal Smokinv Habits
Dilagnosis 5moker Nonsmoker P
Minimali cerebral dysfunctlon, 20.0 11.0 <.05
Total neurological abnormalities 29.4 19.5 <,q5
EEGborderltne or abnormal .
Low-blrth-weigh¢ children 46.3 32.4 .- NS
Full-birth-weight children 29.2 21.6. NS
SOURCE: Dunn, (38).
234
longitudinal follow-up of the population originally Included in
the British Perinatal Mortality Study, comprising approximately
17,000 births, an estimated 98 percent of all births in
England, Scotland, and Wales during the week of March 3 to
9, 1958. These children were studied again at ages 7 and
11, to describe their behavior, health, physical development,
educational standards, and home environment. At ages 7 and
11 years, physical and mental problems due to whether this
might be due to a smoking-related reduction in gestation.
This is not the case. Studies consistently sho w that mean
gestation is minimally reduced by maternal smoking (less than
2 days) (150, 3, 15, 164) and that birth weight is lower for
infants of smokers than for infants of nonsmokers at each
gestational age (150, 16, 87, 3).
The finding that maternhi sm oking does not cause an
overall downward shift in the distribution of gestational ages,
as was shown for birth weights, leads to the conclusion that
the lower birth weight maternal smoking during pregnancy
were found, and these increased with the num ber of cigarettes
smoked. Children whose mothers smoked 10 or more
cigarettes a day during pregnancy were on average 1.0
centimeter shorter and between 3 to 5 months retarded in
reading, mathematics, and general ability, as compared with
the offspring of nonsm okers. After allowing for associatedd
social and biological factors, alll of these differences were
highly significant, as illustrated in Figure 5(~p >0.001) (17,
32).
Denson's case-control study of hyperkinesis reported a
highly significant association of hyperkinesis with heavy
m aternal sm oking, which at a mean level of 23.3 cigarettes
per day was more than three times the average for two
control groups. The authors concluded that their findings
were"consistent with the hypothesis that smoking during
pregnancy is an important cause of the hyperkinetic syndrome
(35),n
A recent comparison by Saxton of behavioral patterns
of infants of mothers who smoked during pregnancy with
infants of mothers who did'not sm oke found thatt these pat-
terns can be influenced by smoking in pregnancy, and that the
auditory senses are particularly affected. Fifteen sm okers of
moree than 15 cigarettes per day and 17 nonsm okers were
selected for study, m atched for maternall age, social class,
and parity. Aii infants were spontaneous term deliveries of
norm al birth weight. Sex distribution, length of labor,
analgesia, and obstetrical factors were similar for the two
235 '
groups. Examiners who did not know the smoking status of
the mother evaluated the infants at 4 to 6 days of age, using
the Brazelton Neonatal Behavioral Assessm ent Scale. The
scale includes a total of 20 tests and maneuvers.. While many
of these showed' no statistically significant differences,
auditory tests or tests with auditory components were
significantly different. Recorded "overall impressions" of the
infants at the end of the test showed that the smokers'
infants tended to wards "irritability, decreased ability for
self-control, and a general lack of interest, whereas the
nonsm okers group tended to be less irritable and better
orientated." The author concluded that cochlear injury may
have occurred in infants of women who smoke (136).
These studies suggest unfavorable effects of maternal
smoking during pregnancy on the child's long-term gro wth,
intellectual development, and behavioral characteristics.
Although these changes are difficult to study because of the
vast complexity of possible antecedent and confounding
variables, high priority should be given to obtaining conclusive
answers about the long-ter% consequences of fetal exposure
to cigarette smoke. ..
Role of Maternal Weight Gain
In the search for mechanisms through which maternal smoking
reduces birth weight, the question has been asked whether It
might be an indirect result of reduced appetite, less intake of
food'y and lower maternal weight gain (131, 88). Several
early studies reported no differences between smoking and
nonsmoking women in intake of food or in weight gain, and
concluded that the effect of maternal smoking on birth weight
was not mediated in this way (150).
Meyer analyzed the relationships between maternal
smoking, birth weight, m aternai'. weight gain, and gestation,
using data based on 31,788 births from the Ontario Perinatal
Mortality Study (110, 111). She found a significant downward
shift in the distribution of birth weights as maternal smoking
leveli increased, but no similar shift in the distribution of
m aternalweight gain with sm oking. Whereas the usual strong
relationship between the proportion of births under 2,500
grams and maternal smoking level was found, there was no
similar trend for the proportion of mothers who gained', less
than 10 pounds during pregnancy. Finally, the proportion of
infants weighing less than 2,500 grams increased directly with
237
®
1
up
FIGURE 6.- Percentage of birth weights under 2,500
grams by maternal smoking level within materal weight
gain group (five-pounds intervals) by hospital pay staus.eirth of 38+ weeks gestation.
PRIVATE HOSPITAL STATUS
rl NON-SMOKER
0~11 PACK/DAY
®'1tPACK/mAY
0-4 5?J 10-14 1519 20-24 2529 30-34 3539 40
MATERNAL WEIGHT GAIN (pounds)
PWRLIC HOSPITAL STATUS
0
I IN fl YA A rM A ,,-q _R A
-0 5-9 10-14.1519 20-24 25-29 3034 35-39 40+
MATERNAL WEIGHT GAIN Ipoundsl.
SOURCE: Meyen, M.6.(S7)
239
FIGURE 5.-Tests of 11-year-old childern by mothers'
smoking habits after thee fourth month of pregnancy
al Reading comprehension
I n=6 4271 I n=1 L4461 In=1 .09Z1
0 19 10
Amount.smoked penday after 411, month
of pregnancy .
bl.Mathematlcs ability
3 '1
;~ ~ Test for differences between~
111 3 smoking categories after
adlusnng for other lacmrs0 X2 120 F.1=59A: V<0001
n=6.425/ I n=1.4451 I n=1 097)
0 9 10+
Amoum smoked',per day after 4th month
of'oregnancy
144-5
cl.Mprght
Test for differences between
3 smoklhgg categoriess after
adjusrin9 tbr 4lheri factors
%2 12D ',F.1-23-0-. Pf\0001.
Tesl lorr differenresbeiwe.en
. 3 smoking categorres after
adiustingfor omer factors
\%212D.F./=262. P<OU01
In=6:2691. Iri=1.3B91. In°t1.0<81
1430
0 19 10,
Amount smoked per d'y afle, 4ih monthh
ofnregnancy
SOURCE: Butler, N.R. 417)
236
.1
s
Y
FIGURE 7.- Risk of congenital abnormality according to
age and smoking habit.
SOURCE: Himmelberger, D191/59)
TABI
TABLE 5.-Incidenca of congenital abnormal.ity(all single births)
Non-smokers Smokers
Number Percent Number Percent
Total abnormal infants -
' 2.37 2.73
Type of abnormality
- - Anencehaly .- . 18 0.2 1.5 0.2
Spina bifis - 20 0.22 23 0.3
Other C.N.S. abnormallty 38 0.42 36 0.47
CVS abnormality 34 0.37 32 0.42
Cut abnormality 21 0.23 24. 0.32
GeniYo-urlnary abnormality 39 0.43 25 0.33
Bonee abnormality - 65 0.72 52 0.68
Cleft palate and/or hare LIp 10 0.11 20 0.26
Other atinonnality- 19 0.21 18 0.24
x2(,all abnormalities) = 2.22, p= >).)%.
x2(:cleft palate and hare Lip). = 5.36, p= >0.01.
SOURCE: Andrews, J. (2).
246
TABLE 7.-Exmples of Perinatal Mortality Smoking Status Related to Other Subgroup Characteristics
No. of blrths Perinztal or neonatal
deaths 1,000 births Relative
Study Populatlon Non- Category Non-
Smokers Smokers smokers Smokers rlsk
British Perinatal Mortality 11.145 4,660 Social class
Survey, England, all 1,2 (hlgh) 25.8 26.3 1.02
- births 3-5 33.5 46.6 1.39
Washington Co. Maryl md, 7,646 4,641 Father's
white education ~' - 9+ years 14.4 16.1 1.12
<e years 17.6 38.0 2.16
Northern Finland, white 8,898 2346 23.2 23.4 1.01
California, mlddle to Race
upper middle class 6,067 3,726 White 11.0 11.3 1.03
2,219 1,071 Black 17.1 21.5 1.26
Boston City Hospital Race .
Prenatal Clinlc 513 892 White 29.2 31.4 1.09
1,225 1,071 Black 28.6 54.1 1.26
Quebec, 10% Sample of 3,91] 2,967 Maternal aga
registered births <25 12.1 16.1 1.33
25-34 12.6 13.2 1.05
- 35+ 23.0 41.7 1.81
Ratlo ofmorlilT~ratE for emokersN to nonsmokers' babies.
Neonatal only.
SOURCE; Meyer, M.B. (89).
tats9seo
TABLE 4.-Mean birth weights in successive pregnancies, to the same women, by smoking habit
¢
Mean Rirth Weight
Smoking Habits gm Difference
#1 p2 N #1 -- #2 2nd - 1st (gm)
Smoker Smoker . 986 3204 . 3228 +24
Nonsmoker Nonsmoker 988 3356 3388 +32
- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -
Difference: Nonsmoker - Smoker (gm) +152 +160
Smoker Nonsmoker 119 3271 3381 +110
Nonsmoker Smoker lOR 3323 3265 -5R
- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -
Difference: Nonsmoker - Smoker (gm) +52 +116 .
SOURCE: Naeye, (97).
zLtCSseo
TABLE 3.-Birth weight under 2,500 gm by maternal smoking and prepregnancy weight
Births <25p0 gm per 100 Total Births Ratio
Maternai Smoking (Packs per day) Smoker:Nonsmoker
Pre re nant Wel ht Total Births 0 <1 i+ <1 1+
<120 lb (<54 kg) 18,935 6.1 10.2 15.8 1.7 2.6
120-134 lb (54-61 kg) 19,798 4.2 6.3 9.5 1.5 2.3
135+ lb (>61 kg) 10, 456 3.3 5.1 g.7 1.6 2.6
SOURCE: Meyer, (86).
iLiS39C0
from smoking.... However, if, as now seems more likely, the
growth-retarding effect of sm oking Is due to fetal hypoxia,
there is no short-cut to removing this adverse infiuence"
(68). This conclusion in no way obviates the enormous
importance of dietary factors during pregnancy.
Overt maternal malnutrition is associated with inade-
quate growth. Recently, it has been suggested that more
subtle alterations in the maternal supply of essential nutrients
combined withh compromised uteroplacental circulation may
contribute to reduced fetal gro wth. Crosby, et al. (28)
observed that the concentrations of each of 14 amino acids
and carotene were reduced significantly in the blood of
smoking mothers. These workers postulated that, while these
differences were on the order of 10 or 20 percent, they
could be an im portant factor in producing the small-for-
gestational-age infants associated with m aternal smoking. In
a study of over 1,100 pregnant women, Schorah, et al. (139)
noted an Inverse correlation between the number of cigarettes
smoked and the leucocyte ascorbic acid concentration. For
instance, the leukocyte ascorbic acid concentration was about
22 percent less In the blood of women who smoked more than.
20 cigarettes a day as compared with controls. Despite a 15
percent increase in the number of circulating leucocytes in
the blood of smokers, the blood ascorbic acid concentration
was still 10 percent less than in controls. These differences
were even more marked in women from lower socioeconomic
groups. The authors suggested that in addition to the role of
ascorbic acid in fetal nutrition, these lowered concentrations
might be related to the increased incidence of premature
rupture of the amniotic membranes in smoking women.
SMOKING, FETAL AND INFANT MORTALITY, AND MORBIDITY
Spontaneous Abortion
Past studies have demonstrated a statistically significant
association between maternal cigarette sm oking and spon-taneous abortion (60, 66, 89), some showing
a strong dose-
response relationship (114, 148, 167). Spontaneous abortions
are difficult to study because of problems of ascertainment.
In prospective studies, early abortions may be missed, and
bias may occur if one group tends to register earlier than the
other. Retrospective studies allow more complete
ascertainm ent but are subject to errors of recall.
Nevertheless, higher rates of spontaneous abortion have been
243
of paternal sm oking were not statistically significant. In the
total study of 5,200 births, regardless of maternal sm oking
with careful matching of cases withh suitable controls.
the case-control approach is probably the method of choice,
More studies of these possible relationships are
urgently needed. As serious malformations are relatively rare,
social class (84).
state that the trends with paternal smoking were independent
of m aternai smoking level, m aternal and paternal age, and
significantly different (p<.01) by smoking level. The authors
per day, only the differences In facial malformations were
were more frequent if the father smoked over 10 cigarettes
the expected Incidence. Although malform ations In all systems ',
several mal formations with Increasing levels of paternal
smoking; children of heavily smoking fathers had about twice
habits, there was a significant Increase in the Incidence of
nonsmoker risks within subgroups of the population (110,
111). The Increased risk of perinatal mortality for light
smoker; who were young, low-parity, and non-anemic was less
than 10 percent. At the other extreme, m others characterized
by high-parity, public hospital status,previous low-weight
of light sm okers (less than a pack of cigarettes per day) and
of heavy smokers (one pack or more per day) reiativeto
terparts. Their increase inn risk due to sm oking Is relatively
greater. Meyer, et al. measured the perinatal mortality risks
being very young or old during pregnancy, or being black,
have higher risks of perinatal mortality than their coun-
characterized by low social class, lo w level of education,
Table 7 illustrates these points. It shows that women
132, 148, 164).
In general, women with other risk factors were at greater
risk from smoking than otherwise low-risk women (3, 16, 24,
to the pregnancies of certain women than to those of others.
nonsmokers (89). Second, cigarette smoking Is more harmful
distributed between comparison groups of smokers and
nomic status influence the results if they are unequally
important variables such as age, parity, race, and socioeco-
There were two important reasons for variability bet-
ween studies on perinatal IoSs and sm oking. First, other
smoking and the risk of perinatal loss (150, 151).
There Is a direct relationship between level of maternal
250
10,523 live births, which represented a response rate of 53.2
percent. After the effects of age, exposure to anesthetic
gases, and pregnancy history were controlled, the risk of
congenital abnormalities for babies of mothers who smoke was
estimated. A statistically significant risk (pc.05) for
maternal sm oking was found. Figure 7 shows the risk of
congenital abnormality as a function of m aternal age for
nonsmokers, moderate smokers(1 to 19 per day), and heavy
smokers (20 plus per day)~. Relative risks for heavy smokers
compared withnon.smokers were as high as 2.3. Rates of
abnormalities in each general category were higher for the
chiidrenn of smokers (see Table 6). The significant increase
in cardiovascular abnormalities among smokers' children is in
agreement with Fedrick's findings (44) and in general
agreement with the study of Andrews and McGarry (3).
Him melberger, et al. do recognize that their findings are
based on retrospective survey data, obtained by mail, and
therefore subject to bias from various sources, including that
of a high nonresponse rate. However, the study methods have
been designed to eliminate those effects (159).
A recent study by Borlee and Lechat controlled for
confounding variables by matching births with congenital
malformations to control births according to hospital and time
of birth,, maternal age, sexx of child, and socioeconomic level
of parents. Two hundred and two children with malformations
diagnosed at birthh were co mpared, with 175 controls, from a
total of 17,970 consecutive births studied from June 1972
through May 1974. No differences were found between cases
and controls in the distribution of smoking habits, including
the num ber of cigarettes sm okedwith or without filters.
Sixty-six percent of mothers of malformed infants and 68
percent of mothers of controls were nonsm okers. Fathers'
smoking habits were also similar among cases and controls.
Significantly m ore mothers of malformed infants were heavy
coffee drinkers (8 plus cups per day). Because of the
frequent association between heavy coffee drinking and
smoking, both habits should be included in studies of
e.nvironm ental factors possibly related to the risk of conge-
nital malformations (10). The same is true for consumption
of alcohol in populations where drinking is prevalent.
Mau and Netter have reported births by gestation, birth
weight, perinatal mortality, and the incidence of congenital
malformations by smoking habits of fathers in 3,696 cases in
which the mother was a nonsmoker. Trends toward lower
birth weights and m ore preterm births with increasing levels
247 '
Q
0
®
white nonsmokers and higher than the totat[ group of white
sm okers. The 1,001 obese black smoking mothers had babies
whose mean birth weights were generally higher than those of
all black nonsmokers, leading Garnn to conclude that "maternal
obesity (weight-defined) apparently counteracts the smoking
effect on the conceptus" (47). Because birth weight is
strongly correlated with maternal size, a more appropriate
comparison would have been between mean birth weights of
the babies of obese smokers and the babies of obese
nonsmokers. That such a comparison would show the usual
relationship to maternal sm oking level is suggested by Meyer's
analysis of birth weight by maternal sm oking and prepregnancy
weight (Table 3). The correlation between maternal weight
and the proportion of low -birth-weight babies is clear at
each smoking level, and the independent relationship between
smoking level and low-birth-weight Is clear at each level of
m aternal weight. The relative increases in the proportion of
low-weight births with light and with heavy smoking are
aim ost identical in the three strata of prepregnant weight
(90)
Studies of birth weight, m aternal weight, and maternal
weight gain should also be carefully controlled for maternal
age and parity. In studies of successive births to the same
mother included In the Collaborative Perinatal Project of the
NINCDS, Garn found prepregnancy weights- increased with
successive pregnancies by similar amounts for smokers and
nonsmokers (48). Naeye, using the same data base, reported
that maternal weight gain was less in the second pregnancy
than in the first pregnancy for smokers, for nonsmokers, and
for women who changed habits between pregnancies in either
direction (110). Second babies weighed on the average 24
grams more than first babies if the mother smoked both
times, and 32 grams more if the mother smoked neither time
(Table 4). If the mother smoked during the first and not
during the second pregnancy, the second baby weighed an
average of 110 grams more than the first baby, whereas the
second babies of women who smoked during the second
pregnancy but not during the first pregnancy averaged 58
grams less than their first babies (97).
The most careful analyses indicate that the effect of
maternal smoking is a direct one not mediated through an
effect on maternall appetite, eating, or weight gain. In
conclusion, as stated in a Lancet editorial, "the appeal of the
nutritional hypothesis is that women might be more readily
encouraged to eat more during pregnancy than discouraged
TABLE 6.-ComparIson of congenltal abnormality. rates for babies born of
smokers and nonsmokers, byy typee of abnormality.
a
Abnormality Smokers No.nsmoker,s P
% No. % No.
Cu.flovascular 19.07+ (68) 13.65 (95) 0.02
Resplratiory 15.15 (54). 12.07(84.) 0.10
Musculoskeletal 23.84 (85) 19.69 (137) 0.08
GastreintestiInal 13.46 (48) 9.48 (66) 0.04
Central nervous system 11.50 (41) 10.20 (71) 0.27
Uroeenltal 21.-32 (76) 15.81 (110) 0,02
eOne-talll significance level for the test of the dl:flerence betWeen two
proportlbns.
+Ra-te is nunber of congenltali abnormalilles per 1,000 live bllrtbs. Rates basedd
upon 3,565Iiro- births among the smokers and 6,958 Ilre births smont the
nonsmokers.
SOURCE: Himelberger, et al. (59).
249
FIGURE $-TheoratiPal cumulative mortality risk according to
smoking hahrt,.in mothers of different age, parity, and social
class groups. .
Para 1,2;3 Para 0 Para 4. Pera1,7,3
Under 35 years
255
P2ra 0 Pam 4+
35vears+ -
Smoker
Nan Smaker
7
births, or anemia had an increased perinatal mortality risk of
70 to 100 percent when they were heavy smokers (92).
To help visualize the interacting effects of maternal
smoking and of other factors on perinatal mortality risk,
Butler has calculated theoretical mortality risks based on data
from the British Perinatal Mortality Study. In Figure 7,
perinatalmortality risks by social class, m aternai age, and
parity are arranged in order of increasing magnitude. The
differences between smokers' and nonsmokers' risks are
represented by the height of the bars, whichh varies depending
on other risk factors (16).
These studies show that the risk of spontaneous abor-
tion, of fetal death, and of neonatal death increases directly
with increasing levels of maternal smoking during pregnancy.
Studies of sm oking during pregnancy show a range of perinatal
mortality risk ratios (smokers versus nonsmokers)) from a low
of 1.01 to a high of 2.42.
Cause of Death
The increased perinatal mortality associated with maternal
sm oking is concentrated within a fe w cause-specific cate-
gories. Excess stillbirths have been associated with ante-
partum hemorrhage or abruptio placentae and with "unkno wn
cause" (3, 51). Excess neonatal deaths were associated with
imm aturity, asphyxia, atelectasis (25),, and with the
respiratory distress syndrome (3).
Meyer and Tonascla (91) analyzed fetal and neonatal
deaths to identify causes of death which showed an excess if
the mother smoked. Fetal and neonatal deaths by coded cause
and maternal smoking habit are shown in Table 8. For each
cause the observed numbers for smokers were compared with
the number expected at nonsmoker rates. The differences
between observed and:expected numbers indicate the number of
deaths in each category attributable to maternal smoking.
Fetal deaths showed a major smoking-related excess
in the category of "unknown" cause and some increase from
"anoxia" and "maternal cause:1 By contrast, neonatal deaths
related to smoking were inn the category of "prematurity
alone," or in the related category of "respiratory difficuity.e
The tentative conclusion to be drawn here is that fetuses and
neonates whose deaths were related to maternal smoking had
no recognizable pathology, but had died in utero from anoxia,
maternal cause, or unkno wn cause, or had suffered the
consequences of preterm delivery.
252 '
FIGURE 10,-Percentage distribution by weeks of gest-
ationn off births to nonsmokers,, smokers of less than one
pack per day, and smokers of one pack per day or more.
20A+
6.0+
7A +
1k +
0.6+
ry5
I
1
e
i ! i i 1 I II! ~
SOURCE: Meyer, M.B. (B6)
2E0
20: 24 28 J3]6 00 4a.
GESTATION.WEEKS
FIGURE 9rMean plasmavolume in nonsmokers and smokers.
4,0
0 Nnnsmokers
SmnkGrf
3-5
3.0
2.5
I I L I I 1 1
12 16 20 25 30 34 38
Gmt.tion (wsaks)
SOURCE: Pirani &MacGillivray (121)
257 .
associated with maternal smoking in both types of studies (66,
89, 167). _
Kullander and Kallen found higher rates of "spontaneous
abortion" among smoking women, but noted that many of these
pregnancies were unwanted. Analysis of their data showed
that the relative risk of spontaneous abortion of smokers
compared with nonsmokers was 1.20 for wanted and 1.35 for
unwanted pregnancies (66). A case-control study of
spontaneouss abortion with important variables held constant
reported an 80 percent increase in the odds of smoking among
the cases compared with controls (65).
Recent studies corroborated the finding of associations
between smoking and spontaneous abortion risk. In a small
retrospective study in New Zealand, Fergusson found that
women who smoked more than 20 cigarettes a day had almost
twice the nonsmoker risk.of having had a previous spontaneous
abortion, and that the association could not be explained by
differences in maternal age, educational level, parity, race,
socioeconomic status or marital status (46). In a study of
12,013 consecutive pregnancies in Dublin, Ireland, Murphy and
Mulcahy found a positive association between the number of
cigarettes sm oked and the rates of spontaneous abortion,
Independent of the effects of maternal age and parity. The
authors stated that induced abortions are a negligible factor
in Ireland and concluded that maternall smoking leads to
reduced reproduction efficiency at all stages of pregnancy
(96). Himmelberger and colleagues surveyed a group of
professional women in medicine concerning the influence of
m aternal sm oking on their 12,194 pregnancies (59). After
controlling for interfering variables, the risk of spontaneous
abortion for certain subgroups of heavy smokers was estimated
to be as much as 1.7 times that for the nonsmoker.
Spontaneous abortion rates were lowest in the 25 to 29 year
old category, increasing with age to Ievel!s of 33 and 36
percent for nonsm okers and sm okers, respectively, at age 40
plus. The relative increase in risk associated with maternal
smoking was highest at the youngest ages below 25 years and
decreased with increasing age (59).
An editorial in the British Medical Journal summarized
these findings and stated: "Cigarette sm oking, one of the
first manifestations of women' s social emancipation, is
emerging as a possible threat to her procreative role." The
proportion of abnormal karyotypes in abortuses of women who
smoke appears to be reduced rather than.increased (17). The
m echanism underlyingg the sm oking-related excess appears to
TABLE 9.-Preterm births by maternal smoking habit.
Relative and attributable risks, derived from published studies
Preterm Births* Relative
per 100 Risk Attributable
Smokers Total Births Smokers/Non- Risk
Study (proportion) Nonsmokers Smokers smokers ~
Cardiff .465 6.7 9.2 1.36 14
Great Britain .274 4.7 6.9 1.47 11
Montreal .432 7.7 10.6 1.38 14
Ontario .435 7.4 10.1 1.36 14
*Cardiff and Ontario data are for <38 weeks. All others are for <37 weeks..
SOURCE: (150, 3, 16, 42, 90).
6RtS99E0
Whether the reduction in the incidence of preeclampsia
with maternal smoking is due to the hypotensive effects of
thiocyanate, to the reduced size of the baby, to a smaller
increase In maternal blood volum e, or to another process
requires further study.
Preterm Delivery, Pregnancy Complications, and Perinatal
Mortality by Gestation
Studies of large numbers of births to measure mean gestation
by smoking habit have demonstrated differences of only a day
or two. This finding led to the conclusion that maternal
smoking does not affect gestation, (150, 15, 57, 78, 106,
164). On the other hand, abundant evidence has been pre-
sented that a smoking-related increase in preterm delivery
plays an important role In the increased risk of neonatal
death for Infants of smokers.
When the proportion of preterm births is measured,
rather than the mean gestation, smokers have shown con-
sistently higher rates than nonsmokers, as illustrated in. Table
9. Inn four studies In which all births and perinatall deaths
were included, the risk of early delivery Increased from 36 to
47 percent if the mother smoked, and 11 to 14 percent of all
preterm births could be attributed to maternal sm oking (3, 16,
42).
Figure 10, using data from the Ontario Perinatal
Mortality Study, shows percentage distributions by gestational
age of births to nonsm okers, light smokers, and heavy
smokers, plotted on a semtlogarithmic scale to emphasize
differences between smoking-level groups in very preterm
births. There is little difference between the means of these
curves because the great majority of births occur around
term in all groups. There is, ho wever, a significant and
dose-related increase in the proportions of preterm babies
born to women who smoke. These preterm deliveries account
for a small proportion of total births but for a large
proportion of the deaths (150, 86).
As previously reviewed, Meyer and Tonascia have
related the excess fetal and neonatal mortality of sm okers'
infants and the excess incidence of pregnancy complications
among women who smoke to the gestational age of occurrence,
using a life-table approach. A starting population of all
pregnancies in utero at 20 weeks was used to calculate the
probabilities of fetal death, live delivery followed by survival
258
FIGURE 11; Probability of pernatal deathh for smoking
and nonsmoking mothers, by period of gestationalage..
- Bars show 95% confidence intervals.
- NONSMOKERS. SMOKERS
TOTAL BIRTHS 27420 21485
TOTAL DEATHS 634 624
PROBABLITY OF DEATH 023 029
2
¢ 0.1
u+ 0.00
~ 0.02
¢ 0.04
FQ
z 0.02
¢
w
° 0.01
LL 0.000
O 0.001
>
t 0.004
~
m
Q
m
O
2
m
Talal De41119
Smpke'68
NOnsmpNers
2e3'. 19e' 121 110 152 149 187 78
20 24 28 32 36 40 42
GESTATIONwEEKS
SOURCE:.Meyer, M.B. (91)
262
TABLE 10.-Long term effects on morbidity and mortality by level of maternal smoking
Rantakallio Data
A. Morbidity
Nonsmoker Light Smoker Heavy Smoker
Number of Children
Doctor visits per child ~
(mean number)
Hospitalizations per child
(mean number)
<Age 1
Age 1-5 .
Control 1 Control 2 (1-10 per day) (10+ per
1300 258 1302 252
.
.71 .61 . .76 .g3
.
.19 . .15 . .22 .39
.14. . .08 .17 .30
.15 .17 .22 .25
day)
B. Perinatal and Postneonatal Mortality (28 days to 5 years) Per 100 Births, by Maternal Smoking
Nonsmokers -Smokers
Total Births N. . 1844 . - 1844
Perinatal Mortality per 1000 Blrths 23.9 25.7 32.6
Postneonatal mortality . - 3.9 . 11.1 .
All mortality per 1000 live births . 16.5 . 24.7
SOURCE: Rantakalllo, (124).
Control Light Total Heavy
SGZS~9:'~~
COMPLICATIONS OF PREGNANCY AND LABOR
Studies have consistently found a direct relationship between
maternal smoking level and the incidence of placenta previa,
abruptio placentae, bleeding during pregnancy, and premature
rupture of membranes (3, 26, 51, 66, 90, 91, 98, 100, 134,
148, 149). The association Is independent of socioeconomic
and racial background (14~8)y parity (3) and many other
factors (90) (Figure 8).
These complications carry with them a high risk of
fetal and neonatal loss, and aree frequently cited as the cause
of deathh among the offspring of women who smoke. Kullander
and Kallen foundd aa significant increase in the frequency of
abruptio placentae among smokers'children' dying before the
age of I week (66). In a prospeotive study of 9,169
pregnancies by Goujard and colleagues, a large proportion of
the increase in stillbirths among smokers was caused by
abruptlo placentae (51.).
Naeye reviewed the clinical and postmortem material
from the 3,897 fetal and infant deaths in the Collaborative
Perinatal Project of the NINCDS (106) and reported an asso-
ciationn between perinatal mortality rates caused by abruptio
placentae and number of cigarettes smoked by themot'her
(100). Abruptio placentae was the underlying cause identified
in 11 percent of all the deaths in this large study (98).
Analysis of data fromm the Ontario Perinatal Mortality
Study corroborated these findings. Increasing levels of
smoking resulted in a highly significant increase in the risks
of placental abruptions, placenta previa, bleeding in pregnancy,
and premature and prolonged rupture of membranes. Fetal and
neonatal deaths were analyzed for associations between them
and smoking-related excesses of various coded complications
of pregnancy and labor. Although most diagnoses showed no
association with ecess mortality for smokers' babies, a fe w
stood out as highly significant. Excess fetal deaths of
smokers' babies were strongly associated with bleeding during
pregnancy, either before (p=0.01) or after (p=0.0005) 20
weeks' gestation. Inn other coded categories, a significant
excess of fetal deaths occurred am ongsm oking mothers with
abruptio placentae (p=0.0001 ) or other obstetrical problems.
Similar comparisons were made for neonatal deaths. A strong,
significant relationship between sm oking-relatedexcess
neanatall deaths and a history of bleeding before 20 weeks of
gestation was found (p=0.0001,). Other categories that showed
significant increases of smoking-associated neonatal deaths
254 '
or death, or the occurrence of a complication followed by
fetal death or delivery. At 28 weeks (the next point defined
by the data), the population at risk Included those remaining
in utero at that point. Figure 11 sho ws the probability of
perinatal death during each period of gestational age starting
at 20 weeks. Risks for smokers' Infants were significantly
greater in the earlier weeks, but not different after 38- week
gestation (150, 91).
A similar approach was applied to determine the risk
by gestation of abruptio placentae, placenta previa, and
premature rupture of membranes for smokers and nonsmokers.
The risk of all these complications was higher for smokers
throughout gestation, but in all, the differences were most
significant in the weeks of pregnancy from 20 to 32 or 36
weeks (150, 91). The lower limit of 20 weeks was built into
the study design, which included all single births of att least
20 weeks gestation (110, 111).
These studies sho w that excesss deaths of smokers'
infants are found mainly in thecoded cause categories of
"unknown" and "anoxia" for fetal deaths, and in the cate-
gories of "prematurity alone" and "respiratory difficulty" for
neonatall deaths. This finding Indicates that the excess deaths
result not from abnormalities of the fetus or neonate, but
from problems related to the pregnancy. Increasing levels of
m aternal sm oking result In a highly significant increase in the
risks of placental abruptions, placenta previa, bleeding early
or late in pregnancy, prematureand' prolonged rupture of
m embranes, and preterm delivery, all of which carry high
risks of perinatal loss. Although there is little effect of
maternal smoking on mean gestation, the proportion of fetal
deaths and live births that occur before term increases
directly with maternal smoking level. Up to 14 percent of all
preterm deliveries in the United States may be attributable to
m aternal smoking. According to the results of one large
study, the most significant difference betweenn smokers' and
nonsmokers' risk of perinatal mortaflty and pregnancy
compfication occurs at the gestational ages from 20 to 32 or
36 weeks.
These findings lead to the conclusion that maternal
smoking can be a direct cause of fetal or neonatal death. in
an otherwise normal Infant. The immediate cause of most
smoking-related fetal deaths is probably anoxia, which can bee
attributed to placental complications with antepartum bleeding
in 30 percent or more of the cases. In other cases, the
oxygenn supply may simply fall from reduced carrying capacity
261
TABLE 8.-Fetal and Neonatal Deaths by Coded Cause and Maternal Smoking Habit
(English speaking mothers)
C_oded cause Observed Expected Observed- p
Nonsmoker Smoker smoker expected value
difference
N
W
Fetal deaths
Unknown 75 125 - 81.4
Malformatlons 32 24 34.7
Hemolytic disease
Anoxia . . 11
16 15 .
29' 11.9
17.4
Maternal cause . 31 . 45 33.7
All others . 8 ., 13 8.7
TOTAL 173 251 187.9
Neonatal deaths
Unknown
Malformatlons
Hemolytic disease .
Respiratory dlffleulty
Prematurity alone
Maternal cause
All others
TOTAL
43.6 0.003
10.7 N.5.
3.1 N.S.
11.6 N.S.
11.3 N.S.
4.3 N.5
63.1 0.003
52 -
51
56.5
5.5 .
N.S.
22 24 23.9 0.1 N.S.
7 8 7.6 0.4 N.S.
46 63 50.0 13.0 N.S.
33 65 35.8 29.2 0.005
2 . 6 2.2 3.8 . N.S..
16 16 17.4 . 1.4 N.S.
178 233 193.3 . 39.6 0.06
TOTAL BIRTHS 15,240 16,549
N.S. = Significant.
B_ased on nonsmoker rate. . -
p value derived from chi square based an a null hypothesis of no differcnce bet-
ween smokers and nansmokers. SOURCE: Meyer, M.B. (79-116)
EbLS89E0
I
sm oking 10 plus cigarettes per day). Theserates are similar
to those found in other studies in which differences were
statistically significant. Postneonatalmortality, from 28 days
to 5 years, was higher for smokers' children with rates of
11.1 and 3.9 per thousand for smokers'and nonsmokers'
children respectively. Overall death rates of 24.7 per
thousand births in smoking womenn and 16.5 per thousand
births in nonsmoking women were reported for children under
the age of 5, of which 12.6 and 8.8 were neonatal.
In addition, the children of the smokers were
hospitalized' more frequently, had more visits to doctors, and
had longer average durations of hospital stays than children of
nonsm okers. Respiratory diseases caused significantly m ore
hospitalizations am ong sm okers' children. It is of great
interest that the chiidrenborn to a subgroup of wom en who
stopped smoking during the last 3 months of pregnancy sho wed
no Increase of postneonatal mortality or morbidity up to the
age of 5, compared with controls. However, these women had
been very light smokers before quitting. Table 10, derived
from Rantakallio's study, sho ws that the various outcomes
m easured show Increasing rates of morbidity and mortality
with increasing levels of smoking. However, it may not be
possible to distinguish between the adverse effects of
m aternal sm oking during pregnancy,and the adverse effects on
infants and children exposed to cigarette smoke in the home,
because women who smoked'during pregnancy probably also
continued to sm oke after pregnancy.
Because of the known carcinogenic potential of tobacco smoke and the evidence that benzo(a)pyrene
reaches the pla-
centa, Neutel and Buck investigated the relationship of
maternal sm oking during pregnancy to the incidence of cancer
In children aged 7 to 10. A combined population of 89,302
births from the Ontario Perinatal Mortality Study and the
British Perinatal Mortality Survey was used as a base popu-
lation for a prospective study in which 65 cancer deaths and
32 cancer survivors were identified. For cancer of all sites,
the children of sm okers had a relative risk of 1.3, with 95
percentt confidence limits of 0.8 to 2.2. A dose-response
relationship was not observed. The numbers were not large
enough to determine significant differences by site. Excess cancer rates for children of motherss
who smoke and a
possible dose-reiatedprogression were concentrated at ages 0
to 24 months, but these rates were based on small numbers of
cases. The authors conclude that "although a significant excess is not demonstrable, a doubling of
the cancer risk for
A
~
p
E
0
were the admission status of rupture of in embranes only, other
obstetrical complications, and duration of rupture of
membranes over 48 hours (91).
Som e of these studies have shown an Inverse dose-responserelationship, withh the incidence of
preeclampsia declining as
the number of cigarettes sm oked increased (113, 149). Data
from the British. Perinatal Mortality Study were cross-
tabulated by parity, severity of preeclampsia, and maternal
smoking status. Smokers had lower rates of all grades of
preeclampsia than nonsm okers, whether they were primiparae
or multiparae (16). Andrews and McGarry showed that the
inverse relationship between cigarette sm oking and
preeclamptic toxemia was independent of social class, m aternal
weight before pregnancy, and maternal weight gain during
pregnancy (3). Despite the effect of smoking on the inci-
dence ofpreeclampsia, there is a greatly Increased risk of
perinatal mortality if preeciampsia does develop in a smoker
(3, 37, 133). Several authors have suggested that this
negative association may be due to the hypotensiveeffect of
thiocyanate, which is derived from the cyanide present in
cigarette smoke and is regularly found in the blood of smo-
kers (3, 113). Because preeclampsla is predominantly a
complication of first pregnancies, it is possible that the
occasional finding of reduced rates of perinatal m ortality in
young, primiparous, light smokers who are otherwise healthy is
due to this relationship. -
Perani and MacGlllivray performed seven serial
measurements fromm the end of the second trimester until term
in 31 nonsmokers and 29 smokers. After 25 weeks gestation
the plasma volume of smokers failed to keep pace with that
for nonsm okers, the increases in volume being 25 percent less
in smokers (Figure 9). Plasm a volume and total body water
expansion are related to blrth weight, at least inn primigravidas.
After 30 weeks of gestation, total body water in smokers plateaued in contrast to nonsm okers, so
that by term their
body water volume Increase was about 25 percent less. Serum
heat-stable alkaline phosphatase levels in sm okers significantly
exceeded the concentration in nonsmokers from the 37th week
of pregnancy onward. This enzyme Is of placental origin, and
cigarette smoking may contribute to this change by Its effects
on the placenta (1'21).
256 '
TABLE 11.-Selected resuits of gross examinations of placentas from smokers and nonsmokers
Calcification
Patchy Subchorionic Fibrin
Infarcts
Nonsmoker
N=3,461 '
49.5
26.2
24.6
- - - - - - - - - - - - - - - - - - - - - - - - ' - - -
Thickness (mean cm) ~ 2.6
Ratio of smallest diameter to thickness 8.19 -
Shortest distance, edge of rupture of
membranes to placental margin (mean cm)
Percent with zero distance
SOURCE: Christianson, (20).
4.32
25.6
Percent of Placentas with Stated Condition
WHITE BLACK
Smoker
N=2,238
P Nonsmoker
N=.1,300 Smoker
N=652
60.8 <.0001 43.5 59.0 <.0001
35.3 <.0001 30.8 - 37.0 <.01
22.3 <.05 14.4 14.5 NS
- _ - - _
- -
2.12 <.001 2.11 2.06 <.01
8.40 <.001 8.39 8.68 <.01
4.09 <.025 5.08 4.83 NS
27.9 NS 18.6 20.3 <.05
sstss9eo
Is more important cannot be determined.
Naeye, et al. in their analysis of 125 SIDS victims
from the population of the Collaborative Perinatal Project of
the NINCDS, stated: "The gestations that produced the SIDS
victims were characterized by a greater frequency of mothers
who smoked cigarettes and had anemian than was true for the
whoiepoputation of 53,721 infants or for a set of 375
controls matched for important factors (99). Rhead
,
commenting on studies published to date which demonstrate an
increased incidence of maternal cigarette smoking in SIDS,
states: "lt is no w...clear that maternal cigarette smoking
contributes to an infant's risk of dying from SIDSo (127).
MECHANISMS
Clues to the mechanisms by which smoking may increase the
risk of pregnancy complications are available from pathological
and physiological studies of placentas, membranes, blood
vessels, circulatory patterns, and serum levels of substances
important for cell and tissue integrity. For example, it is
possible that placental changes in smokers that serve as
adaptations to the hypoxic effects of carbon monoxide may
also increase the risk of placental complications.
Christianson has reported findings from carefully
standardized gross examinations of 7,651 placentas from smo-
kers and nonsmokers. These examinations revealed that
smokers' placentas were thinner and larger in their minimum
diameter than those of non.sm okers.. This significant change
effectively Increased the surface area of the smokers' pla-
centas and must, therefore, have increased their area of
attachment to the uterine wall. The distance from the edge
of membrane rupture to the placental margin was also less
for smokers, and significantly more smokers than nonsmokers
had zero distance, which is consistent with the diagnosis of
placenta previa (20). These findings suggest a possible
mechanism to account for the significant dose-related increase
in the frequency of the clinical diagnosis of placenta previa
that accompanies maternal smoking (90). A similar increase
in this condition occurs with increasing altitude (79).
Christianson's study also revealed that smokers had
significantly more placental calcification, prim arily of the
maternal surface, and patchy subchorionic fibrin, as shown in
Table 11. These changes are characteristic of maturation and
aging of the placenta and occur as normal gestation proceeds;
267 . '
and reduced unloading pressures for oxygen caused by the
presence of carbon monoxide in maternal and fetal blood.
Neonatal deaths occur as a result of the increased risk of
early delivery among smokers, which may be secondarily
related to bleeding early in pregnancy and prem ature rupture
of membranes (150).
LONG-TERM MORBIDITY AND MORTALITY
Studies of Infant and child morbidity and mortality by the
m other's sm oking habits usually cannot distinguish between the
effects of smoking during pregnancy and the effect of the
infant's or child's passive exposure to cigarette smoke after
birth. Several studies have found that hospitalization rates
for pneumonia and bronchitis were higher during the first year
of life for infants of smoking mothers (22, 23, 58). Rates
in children were higher if the sm oking parents also had cough
and phiegm. Harlap and Davies found that the risk of
contracting pneumonia or bronchitis in the firstt year of life
more than doubled if the parents smoked more than 24
cigarettes a day (58).
A unique and important study of morbidity and mor-
tality in smokers' and nonsmokers' children up to the age of
five has now been published by Rantakallio (123). - The
experience up to age 5 of over 12,000 chiidren born In 1966
in Northern Finland, comprising 96 percent of all births in
two provinces was ascertained through hospital and death
records and questionnaires. Smoking was rare in this popu-
lation, and the smokers tended to be young and otherwise
healthy. Fourteen percent of pregnant women smoked fewer
than 10 cigarettes per day (mean number after the second
month of pregnancy 3.9) and 3 percent smoked more than 10
cigarettes per day (mean number 12.2); the remaining 83
percent of the population were nonsm okers. It was therefore
possible to remove the usual problems of confounding variables
by close individual matching of 1,750 smokers to nonsmoking
"controls". Matching factors included marital status, m aternal
age within 2 years, and place of residence, with the latter
category including many socioeconomic variables to equalize
the probable use of medical facilities and other differences.
Although the author states that perinatal mortality did not
sho w aa statistically significant increase for sm okers, rates
were 244 per thousand for controls, 26 per thousand for light
smokers, and 33 per thousand for "heavy" smokers (defined as
263
These workers suggested that the delayed ovum Implantation
followed a delayed increase in progesterone secretion required
to prepare theut.erus for the implanting blastocyst, and that
the delayed progesterone secretionn results in part from
nicotine-induced disturbed hypothalamus-pituitary balance.
HamosA, et al. observed that, while administration of
100 mg kg-I day-1 nicotine to pregnant rats from day 14
gestation onward failed to affect the mother or fetus,, admi-
nistration of mg.kg-1.day-1, (a dose "comparable" to that of
a 20 cigarette-per-day smoker) resulted in a decrease in
litter size and an increase in stil7birthrate. Although
administration of 100 mg kg-1 dayi nicotine failed to affect
newborn birth weight by 12 days of agee continued maternal
nicotine administration resulted in a 9 percent decrease in
body weight and a 40 percent decrease in weight of the sto-
m ach contents. These decreases presumably resulted from
lower milk production by the nicotine-treated animals (56).
Carboxyhemoglobin concentrations of 4 to 5 percent are asso-
ciated with num erous physiologic alterations In adults (21).
Cigarette smoking raises the carboxyhemoglobin concentration
4 to 5 percent per pack smoked per day. Although CO dif-
fuses across the placenta relatively slowly [the half tlm e
equals 1.5 to 2 hr (74)], fetal carboxyhem oglobin con-
centrations reflect those of the m other, and under steady
state conditions are 10 to 15 percent higher than maternal
levels (76). Elevated cartioxyhemoglobin concentrations in the
fetus are associated with decreased fetal blood oxygen
tensions. These decreased oxygen tensions are associated with
a redistribution of fetal blood flow to the brain, heart, and
adrenal glands (150).
Carboxyhemoglobin concentrations have been described
under several conditions of pregnancy. Davles, et al. (34)
compared carboxyhemoglobin concentrations and "available
oxygen" (a function of 02 content in ml.dl blood-1 ) in women
who stopped smoking for 48 hours during the last trim ester of
pregnancy, with wom en who did not stop sm oking, and with
nonsmoking women. In thosee women who stopped smoking,
carboxyhemoglob.in concentrations decreased. "Available
oxygen" increased about 8 percent due both to an increase in
functioning hemoglobin and a shift in the oxyhemoglobin
saturation curve; this increase in "available oxygen"shouid
however, they occurred earlier in smokers than in nonsmokers
(20). This finding Is compatible with other manifestations of
accelerated aging reported to be associated with cigarette
smoking (112, 30).
Asmussen compared placental vessels in sm oking and
nonsmoking mothers by electronmicroscopy. In the smoking
group thesee vessels were characterized by subintimal edema
with destruction of the Intimal elastio membranes, a marked
decrease in collagen content, and proliferation of myocytes.
Asmussen postulated that similar damage may occur in the
fetal~~ and infant vascular system. To what extent such
changes may predispose to the -subsequent development of
vascular disease remains unknown. The author regarded most
of the changes observed in smokers' vessels as degenerative,
but mentioned the possibility that the thickening of the
basement membrane observed in smokers might be an attempt
at repair (4, 5). Naeye (97) has described an increased
frequency of placental microscopic lesions associated with
sm oking. These include: cytotrophoblastic hyperplasia,
obliterative endarteritis, stromal fibrosis, and small villous
infarction. Smokers also demonstrated an increased frequency
of necrosis and inflammation in the decidua capsularis and in
the decidua basalis at theplacental margin. Placental
features observed less frequently in smoker's placentas were
excessive syncytial knots and various thrombotic phenomena.
Naeye found increasing placental enlargement with
sm oking level, accompanied by decreasing birth weight and aa
consequent increase in the placental ratio. The author stated
that "as smoking increased, placentas developed microscopic
lesions characteristicof underperfusion of theuterusJ"
Naeye's data showed positive trends with maternal smoking
level for some findings and negative trends for others (97).
Many of the changes cit'ed, were of low frequency in all
groups, andd no clear pattern of possible mechanisms of action
emerged.
Other studies that may shed light on these complex
interrelationships include the report by Goujard and colleagues
that heavy alcohol consumption as well as sm oking contributes
to the risk of stillbirth caused by abruptio placentae. In a
prospective survey of 9,169 women, the risk of stillbirth was
21 per 1,000 In smokers who were light or nondrinkers, 20
per 1,000 in nonsmoking drinkers of 45 ml or more of
absolute alcohol per day, and 8.5 per thousand for nonsmokers
who drank less than 45 ml per day. The small number of
sm okers who were also heavy drinkers had stillbirth rates of
269
children of smokers cannot be ruled out "Their equivocal
results were reported to encourage other workers to add to
the data (103). This should certainly be done, with particular
emphasis on the first 2 years of life.
Rantakallio, et al. also analyzed the use rates of
ophthalmological services in their follow-up study of
approximately 12,000 children, relating these rates to prenatal
factors ascertained during pregnancy. The incidence of squint
among smokers''children was 22.5 per thousand, compared with
11.5 per thousand among the children of matched, nonsmoking
controls (p<.05). On the other hand, rates of dacryostenosis
and of other congenital ocular malformations were higher
among the children of controls. The authors state that squint
was inversely correlated with birthh weight and was more
common am ong children with other diseases, especially nervous
or mental diseases (124).
Sudden Infant Death Syndrome
Maternal sm oking habits have been ascertained In several r
studies of the sudden Infant death syndrome(SIDS)~. In all of
these, an association has been found between maternal sm oking ;~
during pregnancy and the incidence of sudden infant death.. .~
Steele and Langworth, inn a study of 80 cases, each with two ~,
m atched controls, which were traced back to the Ontario
~
Perinatal Mortality Study population of 1960-61, found that ,~
sudden Infant deaths were strongly associated with the .~
frequency and level of maternal smoking during pregnancy °-
(p<0.001). Thirty-nine percent of the cases were nonsm okers a3,
versus 60 percent of controls; 36 percent of the cases and ~
27 percent of the controls smoked less than aa pack per day; °
24 percent of the cases and 10 percent of the controls ~
smoked a pack per day or more. The habits of the remaining
(;
1 to 2 percent of mothers were unknown (143).
Bergman and Wiesnor studied 56 families who lost '
babies to the sudden Infant death syndrome and 86 control
families. They reported that a higher proportion of SIDS mothers smoked during pregnancy than
controls (61 percent ;
versus 42 percent), m ore sm oked after pregnancy (59 percent
versus 42 percent), and SIDS m others sm oked a significantly
greater number of cigarettes than controls. These authors'
indicate thatt exposure to cigarette sm oke (passive sm oking) t0
appears to enhance the risk for SIDS for reasons not yet
i
known (9). However, whether prenatal or postnatal exposure
266 '
geniculate, and cortical levels, and may represent Impaired
inhibitory mechanisms, rendering other neurons more excitable.
The question of the possible teratogenicity of CO has
never been resolved. Schwetz, et al. exposed mice to 250
ppm CO for 7 or 24 hours per day, fromm days 6 through 15
of gestation, and rabbits to the same concentration from days
6 through 18 (141). Blood carboxyhemoglobin concentration
ranged from 10 to 15 percent. The fetuses of mice exposed
to CO for 7 and 24 hours per day were slightly heavier and
lighter, respectively, than those of the control animals. The
only increase in teratogenic effects were minor skeletal
variants such as extra lumbar ribs and spurs.
Polycyclic Aromatic Hydrocarbons
The polycyclic aromatic hydrocarbons (PAH) such as
benzo(a)pyrene, are widely distributed mutagens and car-
cinogens. These substances produced by incomplete combustion
of organic material are im portant constituents of tobacco
smoke. Exposure of cells to PAHinduces the enzyme, aryl
hydrocarbon hydroxylase. The Inducibllity of this enzyme
system has been used by some workers to demonstrate,
indirectly, that benzo(a)pyrene and other polycyclic hydro-
carbons reach the placenta and fetus. The placentall concentration of benzo(a)pyrene is highly
correlated with the amount which a pregnant woman smokes
(101, 115). In pregnant rats exposed to this substance higher
doses were required to Induce enzym e activity in the fetus as
compared with the dose required to stimulate placental enzyme
activity (15P), suggesting that the placenta may protect the
fetus from these substances. However, the placenta is not
impermeable to benzo(a)pyrene (138). The placenta is
involved in complex hormonal interrelations between mother
and fetus, and oxidative enzyme pathways in the placenta are
important inn maintaining hormonal and nutrient balance for
normal fetal development. The hydroxylation of polycyclic
hydrocarbons and the active transport of various compounds by
trophoblast cells may share common enzyme systems. Thus,
the induction of various enzymes by polycyclic hydrocarbons
may interfere with normal transport systems.
Another unansweredquestiom concerns the carcinogenic
risk for progeny exposed in utero to polycyclic aromatic
hydrocarbons. The offspring of mice which were injected with
benzo(a)pyrene late in gestation showed an increased incidence
275
some evidence suggests that smoking can alter the amplitude
and tone of contractions measured during the rubin uterotubal
Insufflation test (a combined measure of uterotubal junction
and tubal patency) (102).
In summ ary, cigarette smoking appears to exert an
adverse effect on fertility. Further studies are needed to
quantify the effects, Identify etiologic agent(s), and define
the mechanism(s) of action.
280
FIGURE 72Effect of prenatal CO upon.peak-tdo-peak amplitudes
of the positive1-negative I component of the flash evoked
potential recorded from the RAT visual cortex. .
Vertical bars represent #SEM.
EFFECTS OF PRENATAL CO UPON ADULT
PI-NI AMPLITUDES OF THE VISUAL EVOKED POTENTIAL
0--4 COY n=g .
6-9 C0 d n =15
o-b CONT q n=9 o-oCONTAn=9 '
t 2 4 16
INTENSITY (CANDLEPOWER /9.4><7e)
SOURCE: Dyer et a1440)
.
contribute to im proved fetal oxygenation.
Exposure of rabbits (6) and rats (43) to CO during
gestation resulted in decreasedd fetal weights and increased
perinatal mortality. Such CO-exposed newborn animals showed
less activity as well as decreased lung weights and decreased
concentrations of brain protein, DNA, and the
neurotransmitters norepinephrine and serotonin (49)+ Cellular
hypoxia is the final comm on path way mediating the adverse
effect of CO on the developing fetus.
Recent experimental studies have explored various
aspects of CO-induced biochemical changes in the fetus and
the newborn. Newby, et al. demonstrated a persistent effect
of CO exposure in 8- and 13-day-old rats following a single
5-hour exposure to 1,500 parts per million (0.15 percent CO).
(104).. In these animals alpha methyl-p-tyrosine, a potentt
inhibitor of the enzym e tyrosine hydroxylase, was injected 1
hour before the CO exposure, and the extent of catecholamine
depletion was taken as an Index of the rate of catecholamine
turnover. CO-treated rats sho wed increased steady statedopamine concentrations with decreased rates
of dopamine
turnover. In addition, the CO effect on dopamine turnover
persisted for at least 3 to 6 weeks after a single exposure
of 8-day-old rats. There was no CO effect on norephi-
nephrine concentrations or turnover rates, and the effect was
not produced in rats exposed to 8 percent oxygen instead of
carbon monoxide. This is consistent with the data of Coyle
and Campochiaro, which indicates that a maturational event
occurs in the striatum of the 8-day-old rat (27). Whether
this event represents the age of functional maturity, Initiation
of dopaminergic transmission, or maturation of cholinergic
interneurons Is unclear.
Prenatal CO exposure may have long-term consequences
on central nervous system function.. For instance, Dyer, et
al. exposed female Long-Evans hooded rats to 150 ppm CO
throughout pregnancy (40). At birth the litters and mothers
were placed in roo m air without CO. On day 65 electrodes
were placed In the young rats' skulls, and 2 weeks later
visually evoked potentials were recorded. Figure 12
illustrates the effect of such prenatal exposure on the peak-
to-peak amplitudes of the P1-N1 (first positive to first
negative) component of the visual evoked potential from the
cortex. Females showed a significant increase in P1-N1
amplitude at each of four flash intensities. Although the
exact nature of this amplitude Increase could not be
determined, it suggests altered cell populations at the retinal,
273
t
changes also were associated with an increase in maternal
pulse and, blood pressure. Lehtovirta and Forss measured
changes in placental intervillous blood flow using the 133
xenon method (71). Immediately after smoking, intervillous
flow decreased 22 percent. These data correlate with the
studies of Resnik, et al.. (1979) (126), sho wing nicotine-
induced increases in catacholamines and decreased uterinebiood flow in sheep, and of Haberman,
demonstrating
decreased uteroplacental blood flow In wom en, using ther-
mography (53).
Sastry and his colleagues have carried out a series of
studies on the effect of nicotine on the hum an placenta.
Nicotine added to a caicium-containing medium caused a 33
percent increase in the rate of acetylcholine release from
isolated placental villi (135). The authors postulated that
this effect could account for the decrease in placental amino
acid transport (129, 158)) produced by nicotine- mediated
cholinergic blockade (109). Rowell and Sastry also
demonstrated that nicotine caused a 41 percent decrease inn
uptake of alpha amino isobutyric acid in an experim ental
placental system (130). Their studies indicate that under
normal circumstances acetylcholine exhibits a muscarinic
effect facilitating piac.entall amino acid uptake. Nicotine
blockade of the facilitating effects of acetylcholine on amino
acid uptake m ay result in fetal growth retardation (130).
These data agree with the 1977 work of Crosby, et al. In
humans (28).
Nicotine injection in rats results in prolonged gestation
with lower than normal newborn weights. A possible cause of
this prolongedgestation is nicotine-induced delay in ovum
implantation. Yoshinaga, et al. tested this hypothesis,
administering. 7.5 mg nicotine tartrate twice daily from the
morning of proestrus until the day of sacrifice on days 1 to
5 of pregnancy (166). The nicotine injected animals
demonstrated a delay of about 12 hours Inn ovum cleavage
from the two-to the four-cell stage, and each step of
development after the four-cell stage was thereby delayed.
In addition, ovum entry into the uterus, blastocyst formation,
shedding of the zona pellucida, and implantation were delayed.
Nicotine injection also was associated with a"crowding" of
implantation sites to wardthe tubal ends of the uterine horns.
During the preimplantation period the serum con-
centrations of progesterone, luteinizing hormone, and prolactin
were lower, while the concentrations of estrogen and follicle
stim ulating hormone were higher, than in control anim als.
271
I
regular menses (55). Conversely only 18 percent of
nonsmokers had irregular menses while 24 percent of those
smoking one or more packs of cigarettes per day said they
had irregular menses.. Smoking women were also more likely
to have an unusual vaginal discharge and vaginal bleeding than
nonsm okers. Experimental studies have demonstrated
alterations In luteinizing hormone release and a decreased
ovulatory response in rats exposed to tobacco smoke (80).
The effect of sm oking on ovulation may result from
direct effects of nicotine on the hypothalm us or pituitary.
This would alter the release of gonadotropin releasing hor-
mones from the hypothalamus or impair the pituitary response
to releasing hormones.
Smoking and Age of Menopause
Substantial data demonstrate that smoking lowers the age of -
spontaneous menopause (63, 29, 7, 8, 72, 73). The recent -
study by Jick, et al. revealed aa dose dependent decrease in
the age of menopause in smoking women who live in Sweden -
and the United States (63). The median age of menopause in .
nonsm okers was 50; among those smoking one-half pack it was
49; in those smoking 1 or more pack/day, it was 48. Similar
studies have been published indicating an earier onset of menopause in smoking women in the United
States (29), in
England (7), in Germany (8), and in Sweden (72, 73). The -
mechanism of early menopause in smokers may be related to '~
ovotoxins in cigarette smoke (41) or to toxic alterations in ~
the hormonal regulatory mechanisms controlling the ~
hypothalmic-pituatary-ovarian axis (80). One group of ._
ovotoxins may be polycyclic aromatic hydrocarbons which have ..
been demonstrated to be metabolized by ovarian enzymes to r
toxic products which destroy oocytes in rat and mouse ovaries ?
(83, 52).
Evidence collected by Daniell (31) and Lindquist (72) suggest that the earlier menopause of smokers
is not related
to weight differences between sm okers and nonsm okers but is a direct result of some component of
cigarette smoke.
Smok(ng and Reproduction In Men
Spermatogenesis, sperm morphology, sperm motility (18, 137,
154, 69) and androgen secretion (12, 117) appear to be
278
of neoplasms of the lungs, liver, and mammary glands (105).
Pelkonen, et ai. determined that placental aryl hydrocarbon
hydroxylase activity correlated closely with both theamount'
the mother smoked and newborn weight (116). These authors
suggested that the placental concentration of this enzyme may
be used as a measure of fetal exposure to maternal cigarette
sm oking. Vaught, et al. also reported much higher aryl
hydrocarbon hydroxylase activity In the placental microsomes
of sm okers compared with nonsm okers (152).
Although currently available data do not allow a quan-
titative assessment of the genetic risk to man from cigarette
smoking, such risk may occur since so many components of
cigarette smoke are mutagens (as well as carcinogens)~ (11).
Male cigarette smokers may have an Increased number of
abnormal spermatozoa (154). Paternal and maternal
chromosomal abberrations (107) and sister chromatid exchanges
may be increased in smokers (67). Because the proportion of
smokers in the population is so high (between 30 and 50
percent), even a relatively weak mutagenic effect could have
a significant effect on the gene pool (11).
Other Components
Cyanide, another constituent of cigarette smoke, may contri-
bute to retarded infant gro wth and Increased perinatal mor-
tality. Smokers have increased levels of cyanide and
thiocyanate in body fluids. Serum centrations of vitamin 812,
used in cyanide metabolism are decreased as well. Several
workers have recorded increased thlocyanata concentratlons in
both women who smoke, and their fetuses (2, 144, 158).
Pettigrew, et al. compared cyanide and thiocyanate
concentrations in smokers and nonsmokers, matched for age,
height, parity, andsocloeconomic status (120). Cyanide and
thiocyanate concentrations were two to four times greater in
the blood and urine of smokers and in the urine of smokers'
infants as compared with controls.. Meberg, et al. reported
that thiocyanate concentrations were correlated with 'cigarette
consumption and inversely correlated with birth weight (85)..
Cadmium, another constituent of tobacco smoke, is
concentrated in the placenta of smokers (128). Webster
exposed pregnant mice to 10 to 40 ppm cadmium and noted an
inverse correlation between cadmium concentration and fetal
weight (156). Lauwerys, et al. examined the effects of epidemiology
276
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factors on heavy metal and CO concentrations in the blood,
placenta, and fetus of smoking women (70). Cadmiumm con-
centrations in maternal blood were twofold greater than con-
centrations In fetal blood, sugesting that the placenta acts as
a barrier to this metal. They reported a correlationn between
maternal cadmium and carboxyhemglobinn concentrations(14~,
70). They also found that the cadmium concentration of
smokers' placentas was about 25 percent greater than in a
control group and that the placental cadmium concentration
exceeded that of maternal blood about tenfold (128).
FERTILITY
Fertility results from the successful completion of a complex
type step-wise process beginning with gam etogenesis,(sperm
and egg production) continuing through gamete release
(ejaculation and ovulation), gam ete interaction (fertilization),
conceptus transport through the fallopian tube into the uterus,
and ending with implantation of the embryo into the
endometrial wall. An adverse effect of sm oking on any of
these steps may impair fertility.
Smoking and Reproduction in Women
Several epidemiologic studies have suggested that sm oking
decreases fertility in women (147, 153, 119, 55). The
retrospective study of Tokuhata demonstrated that 21 percent
of women who regularly smoked cigarettes were infertile while
only 14 percent of those who never used tobacco regularly
were (147). After several characteristics (cause of death,
age at andyear of death, education, occupation andd frequency
of marriage as well as husbands' smoking habits, education
and occupation) were controlled, an excess of infertility was
found in women who smoked.
In a study on the return of fertility after discontinuing
contraception, Vessey, et al. founda suggested reduction in
fertility among women smoking 15 or more cigarettes per day
(153). Pettersson, et al. founda tendency to ward a greater
prevalence of secondary amenorrhea among smokers (4.8/100
women)) than among nonsmokers (3.7/100 women) (119).
Hammond found that 49 percent of the nonsmoking women
between 40 and 49 years had regular m enses while only 40
percentt of those smoking more than one pack a day had a
C
W
~
CJ1
N
O
~
277
P
(13) BRITISH MEDICAL JOURNAL. Cigarette smoking and
spontaneous abortion. British Medical Journal
(6108): 259- 260, February 4, 1978.
(14) BUCHET, J.P., ROELS, H., HUBERMONT, G., LAUWERS,
R. Placental transfer of lead, mercury, cadmium,
and carbon monoxide in women: 11 influence of
some epidemiological factors on the frequency
distributions of the biological indices In
maternal and umbilical cord blood. Environmental
Research 15: 494-503, 1978.
(15) BUNCHER, C.R. Cigarette smoking and duration of
pregnancy. American journal of Obstetrics and
Gynecology 103(7): 942-946, April 1, 1969.
(16) BUTLER, N.R., ALBERMAN, E.D. (Editors). Perinatal
Problems. The Second Report of the 1958 Brltish
Perinatal Mortality Survey. London, E. and
S. Livingston, Ltd., 1969, pp. 36-84.
(17) BUTLER, N.R., GOLDSTEIN, H. Smoking in pregnancy
and subsequent child development. British
Medical Journal 4: 573-575, December 8, 1973.
(18) CAMPBELL, J.M., HARRISON, K.L. Smoking and infer-
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342-343, 1979.
(19) CENDRON, H., VALLERY-MASSON, J. Tabac et Comport-
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(20) C HRISTIA NSON, R.E. Gross differences observed in
the placentas of smokers and nonsmokers. American
Journal of Epidemiology 110(2): 178-187, August,
1979.
(21) C OBURN, R.F. (Editor). Carbon Monoxide. Washington,
D.C. National Academy of Sciences, National
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(22) COLLEY, J.R.T., HOLLAND, 19:W., CORKHILL, R.T.
Influence of passive smoking and parentaP phlegm,
on pneumonia and, . bronchitis of early childhood.
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(23) COLLEY; J.R.T. Respiratory symptoms In child-
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British Medical Journal 2: 201-204, 1974.
282
altered in men who smoke. Viczian (154) has demonstrated
decreased sperm density, a cigarette-dose-dependent decrease
in sperm motility, and a cigarette-dose-dependent increased
abnormal sperm morphology among smokers.
In metabolic studies of alcoholic m en admitted to a
clinical research center, an inverse relationship between
number of cigarettes smoked and reduction of testosterone
levels was seen (117). Briggs (12), has reported lower
plasma testosterone among smoking men compared to matched
nonsmoking controls and has shown that cessation of smoking
resulted in increasedtestosterone levels in these m en.
Wintermitaz and Quillen (163) in a study on the acute effects
of smoking in men demonstrated increases in plasma cortisoll
and growth hormoneduring the smoking period. Growth hor-
mone returned to the presm oking level shortly after the
sm oking period, and cortisol fell gradually to the presmoking
level by 90 minutes after cessation of smoking. Urinary
catecholamines were higher on the smoking day than the
nonsmoking day. No acute changes were observed in gona-
dotropins or testosterone in these men.
Studies in experim ental anim ais have also sho wn thatt
tobacco smoke impairs spermatogenesis (41, 155), . Smoking
also lowers sexual activity in male rats (19).
These data suggest two possible mechanisms of action
of smoking on male reproduction. A component of cigarette
smoke may have a direct action on the testes, disrupting
gamete production. This would be consistent with the
suggested effect of cigarette sm oke on the ovary. In addi-
tion, cigarette smoke is known to contaihcompoundswhich are
m utagenic (64). Alternatively, cigarette sm okemay interfere
with the regulatory mechanisms controlling the hypothalamic-
pituitary-testicular axis.: .
Fertilization and Conceptus Transport
The effect of smoking on sperm-egg interaction (fertilization)
has not been studied in mammalian species. Evidence from
mammalian species demonstrates thatt nicotine promotes
polyspermy (the entrance of more than one sperm into the
oocyte) (77). Polyspermy would result In abnormal embryonic
development and early abortion, which is one known effect of
smoking (165).
The effect of smoking on conceptus transport In the
fallopian tubee or entry into the uterus Is unknown; however,.
I
279
(58) HARLAP, S., DAVIES, A.M. Infant admissions to hospi-
tal and maternal smoking. Lancet 1:. 527-532, 1974.
(59) HIMMELBERGER, D.U., BROWN, B.W., COHEN, E.N.
Cigarette smoking during pregnancy and the
occurrence of spontaneous abortion and congenital
abnormality. American Journal of Epidemiology
108(6): 470-479, December 1978.
(60) HOLLINGSWORTH, D.R., MOSER, R.J., CARLSON, J.W.,
THOMPSON, K.T. Abnormal adolescent primiparous
pregnancy: Association of race, human chorionic
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Journal of Obstetrics and Gynecology 126(2):. 230-
237, September 15, 1976.
(61) HUDSON, D.B., MEISAMI, E., TIMIRAS, P.S. Brain deve-
lopm ent in offspring of rats treated with nicotine
during pregnancy, Experientia 29(3): 2860288, 1973.
(62) JARVINEN, P.A., OSTERLUND,K. Effect of smoking
during pregnancy on the fetus, placenta and deli-
very. AnnalesPaediatrlae Fenniae 9: 18-26, 1963.
(63) JICK, H., PORTER, J., MORRISON, A.S. Relation Between
Smoking and. Age of Natural Menopause. Lancet 1:
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(64) KIER, L.D., YAMASAKI, E., AMES, B. Detection of
Mutagenic Activity in Cigarette Smoke Condensates.
Proc. Nat. Acad. SOi. U.S.A. 71: 4159-4163, 1974.
(65) KLINE, J., STEIN, Z.A., SUSSER, M., WARBURTON, D.
Sm oking: A risk factor for spontaneous abortion.
New England Journal of Medicine 297(15): 793-796,
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smoking and pregnancy. Acta Obstetrica et
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(67) LAMBERT, B., LINDBLAD, A., NORDENSKYJOLD, M.,
WERELIUS, B. Increased frequency of sister chroma-
tio exchanges inn cigarette smokers. Hereditas 88:
147-149, 1978.
(68) LANCET: Smoking and intrauterine growth. Lancet
1(8115): 536-537, March 10, 1979.
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286
(71
(7
(7:
(7i
(.7'
(7(
(7i
(7E
(79
(80
(81
(162) WINGERD, J., SCHOEN, E.J. Factors influencing
length at birth and height at five years. Pedia-
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(163) WINTERNITZ, W.W., QUILLEN, D. Acute hormonal
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(164) YERUSHALMY, J. Mother's cigarette smoking and
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(165) YERUSHALMY, J. The relationship of parents'
cigarette smoking to outcom e of pregnancy--
implications as to the problem of inferring
causation from observed associations. Am erican
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(166) YOSHINAGA, K., RICE, C., KRENN, J., PILOT, R.L.
Effects of nicotine on early pregnancy in the rat.
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(167) ZABRISKIE, J.R. Effect of cigarette smoking
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296'
(24) COMSTOCK, G.W., LUNDIN, F.E., JR. Parental
sm oking and perlnatal mortality. Am erican Journal
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July 1, 1967.
(25) COMSTOCK, G.W., SHAH, F.K., MEYER, M.B., ABBEY,
H. Lo w birth weight and neonatal mortality
rate related to maternal sm oking on socioeco-
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M. Cigarette smoking in pregnancy: Associations
with maternal weight gain and fetal growth.
Lancet 1: 385-387, February 21, 1976.
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PREGNANCY: REFERENCES
(1) ALBERMAN, E, CREASY, M., ELLIOTT, M., SPICER, C.
Maternal factors associated with fetal chromosal
anomalies in spontaneous abortions. British
Journal of Obstetrics and Gynecology 83: 621 -
627, August 1976.
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British Journal Obstetrics and Gynecology. 80:
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(7)~ BAILEY, A., ROBINSON, D., VESSEY, M. Smoking and
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(8) BERNHARD, P. Die Wirkung des Ranchers auf Fran und
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(9) BERGMAN, A.B., WIESNER, L.A. Relationship of
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(11 ) BRIDGES, B.A., CHELMMESEN, J., SUGIMURA, T.
cigarette smoking--does it carry a generic risk?
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281
PEPTIC ULCER DISEASE
There is little information dealing specifically with thereiationship betweenn smoking and peptic
ulcer disease inn
women. The data which are available suggest the same trend
toward higher prevalence of peptic ulcer disease among women
who smoke as is observed among men who smoke. Table 1,
extracted from the 1979 .Surgeon General's Report, sho ws that
the prevalence of "peptic ulcer" in female smokers was higher
in two out of three studies of women, which showed a twofold
or 1.6 fold higher prevalence (10).. The onestudy which
failed to demonstrate an increased prevalence was conducted
in rural Poland where very few women smoke (only 7 percent)
(9). The m edian ratio of smoking ulcer patients to
nonsmoking ulcer patients has beenn reported to be 1.7 for
men. (10). Thus, women smokers seem to show greater
susceptability to ulcer disease than do nonsmokers.
The population of wom en with ulcers contains a greater
proportion of smokers than does the group of women without
ulcers. Alp, et al. perform ed a retraspective analysis of 638
patients with gastric ulcer, 230 of whom were wom en. (2).
There were 1.9 times as many smokers in the group of women
ulcer patients as in an age-matched control group. However,
even among the ulcer patients, only 39 percent were smokers.
In a smaller series of 31 female patients admitted to hospi-
tals with hem orrhage from or perforation of gasttic or
duodenal ulcers, the prevalence of smoking was 26 percent in
both ulcer patients (8/31), and controls (.8/31) (1).
In a report examining the effectt of smoking on healing
rates of gastric and duodenal ulcers, Doll, et al. studied 92
women with gastric ulcer and 54 women with duodenal ulcer
(4)4 Smoking was 1.6 times more common in women gastric
ulcer patients as in controls matched for age and place of
residence (p < 0.01). There was no significant excess in the
proportion of smokers in the group with duodenal ulcer. The
effect of smoking on healing rate was reported for men and
women grouped together, so no conclusion regarding specific
effects on women is possible.
Although some studies of etlologicalfactors In
smoking-Induced ulcer disease (gastric acid secretion,
pancreatic secretion, etc.)) have included wom en, the number
of women has been, small, or the data from women have not
been presented separately.
In summary, theevidence currently available documents
an increased'prevalenceof peptic ulcer disease in women who
0
297
TARLE 1.-Prevalence of Peptic Ulcer In Smoking and Non-Smoking Women (Number per 1n(1).
REFFRENCF. WiTH
ULCERS
SNtYfERS
Higgins, M.W. 47 . .?.R '~
(1966) (7)
Friedman, C.D. 1092 6.3
(1°74) (5)
Jedrychowski, W. - . 26 ll.g
(1474) (9)
ezz_C,,sCa
Nf.XJSMJKERS RATIO (Prevalence among Smokers)
(TFrevalence among Nonsmokers)
1.4 ~ 2.0~.
3.9
1.3
(35) DENSON, R., NANSON, J.L., tdCWATTERS, M.A.
Hyperkinesis and maternall smoking. Canadian
Psychiatric Association Journal 20(3): 183-187,
April 1975. - (36) DONOVAN, J.W. Effect on child of maternal smoking
- during pregnancy. Lancet 1: 376, February, 17,
1973. (Letter)
(37), DUFFUS, G.M., MACGILLIVRAY, I. The incidence of
preeclamptic toxaemia in smokers and nonsmokers.
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C.M. Maternall cigarette smoking during preg-
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Physical growth tothe age of 6112 years. Canadian
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C.M. Maternal cigarette sm oking during preg-
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II. Neurological and intellectual maturation
to the age of 61/2 years. Canadian Journal of
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FECHTER, L.D., ANNAU, Z. Prenatal carbon
monoxide and adult evokedpotentials in rats. Journal of Environment,'Science and Health C13:107-120,
1979.
(41) ESSENBERG, J.M., FAGAN, L., MALERSTEIN, A.J.
Chronic poisoning of the ovaries and testes
of albino rats and mice by nicotine and
cigaret~te smoke. Western Journal of Surgery,
Obstetrics and Gynecology 59, 27-32, 1951.
(42) FABIA, J. Cigarettes pendant la grossesse, poids
de naissance et mortalite perinatale (Cigarette
smoking during pregnancy, birthh weight and,
perinatal mortality). Canadian Medical Associa-
tion Journal 109: 1104-1109, December 1, 1973.
(43). FECHTER, L.D., ANNAU, Z. Toxicity of mild pre-
natal carbon monoxide exposure. Science 197
(4304):: 680-682, April 12, 1977.
(.44) FEDRICK
J. Factors associated with low birth
. ,
weight of infants delivered In term. British O
f.7
Journal of Obstetrics and Gynecology 85(1):1-7, 09
January 1978.
(45), FEDRICK, J., ALBERMAN, E.D., GOLDSTEIL*1, H. Possible
Vl
N
teratogenic effect of cigarette smoking. Nature
231: 529-530, June 25, 1971.
?
284
50.5 per 1,000 (95 women with 5 stillbirths). The
proportions of these deaths that were attributable to abruptio
placentae increased with smoking and with drinking (122).
More research is needed to define possible pathways of
actions by which the active components of cigarette smoke
affect pregnancy complications that may lead, in turn, tufetal death inn utero or to preterm birth
with or without
survival. !
EXPERIMENTAL STUDIES
Tobacco Smoke
Tobacco smoke contains more than 4,000 compounds including:
carbon monoxide, oxides of nitrogen, amm onia,polycyclic
aromatic hydrocarbons, hydrogen cyanide, vinyl chloride, and
nicotine. For the pregnant woman and fetus the most impor-
tant of thesee appear to be nicotine, carbon monoxide, and the
polycyclic aromatic hydrocarbons.
Nicotine
The effect of nicotine on sympathetic and parasympathetic
ganglia, skeletal muscles, and the central nervous system is
similar to that of acetylcholine. At all three sites it first
stimulates, then depresses. Minute doses of nicotine stim ulatethe chemoreceptors of the carotid and
aortic bodies, causing
reflex hypertension. Nicotine also releases epinephrinefrom
theadrenal medulla, thereby producing cardiovascular changes.
Thus, it can produce widely differing effects depending upon
the dosage and the particular site that is most sensitive to
stimulation.
Nicotine rapidly crosses the placenta to affect the
fetus (146). Relatively mature rhesus monkey fetuses respond
to nicotine infusion with a rise in blood pressure, bradycardia,
acidosis,, hypercarbia, and hypoxia. (145). Maternal nicotine
administration In rats also has been shown to affect the fetal
central nervous system and its response to electrical
stimulation during the newborn period (61, 82).
Quigley, et al. notedd that in m oderate to heavy smokers,
after 34 weeks gestation, smoking two cigarettes in 10
minutes was associated with a 60 percent increase in maternal
plasma norepinephrine and epinephrine and a 20 percent
increase in serum cortisol concentrations (122). These
4
270 , '
smoke. No data are available concerning specific effects of
smoking in women on gastric acid secretion, gastric emptying,
pancreatic secretion, or other processes which might be
involved in the pathogenesis of peptic ulcer disease.
SUMMARY
The 1979 Surgeon General's Report Included evidence that
cigarette smoking in males was significantly associated with
the incidence of peptic ulcer disease and increased the risk
of dying from peptic ulcer disease by approxim ately two-fold.
The effect of smoking on pancreatic secretion and pyloric
reflux demonstrated among men may provide a mechanism by
which peptic ulcers develop.
1. Female smokers show a prevalence of peptic ulcer
higher than that of nonsmokers by approximately two-fold.
2. The effect of cessation on healing is not known.
0
I
u
0
299
(152) VAUGHT, J.B., GURTOO, H.L., PARKER, N.B., LEBOEUF, R.,
DOCTOR, G. Effects of smoking on benzo(a)pyrene
metabolism by human placental microsomes. Cancer
(153) VESSEY, M.P., WRIGHT, N:H.,.MCPHERSON, K.,WIGGINS, P.
Fertility after stopping different methods of
contraception. British Medical Journal 1(6108):
265-267, 1978.
(154) VICZIAN, M. Results of sperm atozoa studies in
cigarette sm okers. Z. Haut Geschlechtshi. 44(5),
183-187, 1969.
(~155). VICZIAN; M. The effect of cigarette smoke inhalation
on spermatogenesis in rats. Experienta 24: 511-513,
1968
.
(156)~ WEBSTER, W.S. Cadmium-induced fetal growth retar-
dation in the mouse. Archives of Environmental
Health
English. 33(1)> 36-42, January/February 1978.
(157) WELCH, R.M., GOMMI, B., ALVARES, A.P., CONNEY, A.H.
Effect of enzyme induction on the metabolism of
benzo(a)pyrene and 3-methyl-4-
monomethylaminoazobenzene in the pregnant and fetal
rat. Cancer Research 32(5): 973-978, May 1972.
(158) WENNERBERG, P.A., WELSCH, F. Effects of cholinergic
drugs on uptake of 14 C-aminoisobutyric acid by
human term placenta fragments: Implication for ace-
tylcholine recognition sites and observations on the
binding of radioactive cholinergic ligands. Fed.
Proc. 36: 980, 1977.
(159) WILSON, E.W. The effect of smoking in pregnancy on
the placental co-efficient. New Zealand Medical
Journal 74(475): 384-385, 1972.
(160) WILSON, J., MATTHEWS, D.M. Metabolic inter-
relationships between cyanide, thiocyanate and vita-
min B12 in smokers and nonsmokers. Clin. Sci. 31:
1 -7, 1966.
(161) WINGERD, J., CHRISTIANSON, R., LOVITT, W.V., SCHODEN,
E.J. Placental ratio in white and black wom en:
Relation to smoking and anemia. American Journat of
Obstetrics and Gynecology 124(7): 671 -675, Aprll 1,
1976.
?95
C
W
P1
~
N
N
t~.
(142) SIMPSON, W:J.A preliminary report on cigarette
smoking and theincidence of prematurity.
American Journalof Obstetrics and Gynecology
73(4): 808-815, April 1957.
(143) STEELE, R., LANGWORTH, J.T. The relationship of
antenatal and postnatal factors to suddenn unex-
pected death in Infancy. Canadian Medical Assoc-
iation journal 94: 1165- 1171, May 2B, 1966.
(144) STOA, K.F. Studies on thiocyanate in serum. In:
Second Medical Yearbook, Bergeny Norway, University
of Bergen, 1957, pp.. 14.
(J45) SUZUKI, K., HORIGUCHI, T., COMAS-URRUTIA, A.C.,
MUELLER.-HEUBACH, E., MORISHIMA, H.O.,ADAMSONS,
K. Pharmacologic effects of nicotine upon the
fetus and mother in the rhesus monkey. American
Journall of Obstetrics and Gynecology 11i1(8)c
1092-1101, December 15, 1971.
(146) SUZUKI,K., HORIGUCHI, T., COMAS-URRUTIA, A.C.,
- MUELLER-HEURACH, E., MORISHIMA, H.O., ADAMSONS,
K. Placental transfer and distribution of nicotine
in the pregnant rhesus monkey. A merican journal
of Obstetrics and Gynecology 119(2): 25.3-262,
Ma 15
1974
y .
,
(147) TOKU HATA, G. Smoking in relation to infertility
and fetal loss.
3
59 Archives of Environmental Health
1
17:
(148) UNDE ,
35
-3
RWOOD, P., 968.
HESTER, L.L., LAFFITTE, T., JR.,
GREGG, K.V. The relationship of smoking, to the. outcome of pregnancy. American journal of
Obstetrics and Gynecology 91(2): 270-276, January
15, 1965.
(149) UNDERWOOD, P.B., KESLER, K.F., OrLANE, J.M.,
CALLAGAN, D.A. Parental smoking empirically
related to pregnancy outcome. Obstetrics and
Gynecology 29(i): January 1-8, 1967.
(1150). U.S. DHEW. Smoking and Health: A Report of
the Surgeon General, 1979. DHEW Publfcation
N-. ((PHS) 79-50066).
(151.) U.S. PURLIC HEALTH SERVICE. The Health Conse-
quences of Smoking. A Report of the Surgeon
General6 U.S. Department of Health, Education,
and Welfare, DHEW Publication No. (HSM) 73-8704,
1973, pP. 99-1A9. -
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294 '
INTERACTIONS OF SMOKING 1'JITH DRUGS, FOOD CONSTITUENTS
AND RESPONSES TO DIAGNOSTIC TESTS
Since most published studies investigating the effect of
cigarette smoking on measures of health were performed in
mixed populations, it Is difficult to demonstrate specifio-
factors applicable only to women. Neither the differencesbetwe.en men and women regarding the
metabolism and action
of drugs nor the pharmacological basis for differences
between smokers and nonsmokers is well understood. The
same is also true of the observed variations in laboratory
values and nutritional needs. Thus, the associations for
women between smoking, drugs, variations in clinical
laboratory values, and nutritional needs require further study.
Women Smokers and Nonsmokers and Drug Consumption. Patterns
The drug consumption pattern of women as compared to men
has been studied by a num ber of investigators using different
methodologies. The results consistently sho w that women areprescribed and take more prescription
drugs thamn men (7,20).
In one study where 1-year drug histories were used, the per-
centage of women using prescriptionn drugs was 29 percent as
com pared to 13 percent for men (20). Another study which
examined oniydrugs consumed, within 48 hours of the ihter-
vie w sho wed that 60.2 percent of thee wom en had takenn
medication compared to 41.8 percent of the men. (7). The
derived from a self-administered questionnaire asking about
drug use for the past year (25). As Table 1 shows, women
smokers take more of almost every type of drug than
nonsmokers. When the data were organized according to age
only one study have women smokers and nonsmokers been
compared for use of all drug categories;thesedat'a were
coffee and alcoholic beverages than nonsmokers (21,30). In
drugs, especiallyofy the psychotherapeutic type and drink more
Other reports sho w that sm okers tend to use more
smokers or nonsmokers.
quantified information according to whether the subjects were
dispensing patterns. Unfortunately, neither of these studies
studies because they measure actuall self-administration of
drugs rather than counting physician prescriptions or pharmacy
two studies cited are uniquee in the realm of drug usage
302
Toet
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groups, the 15-to-19-year-old group of women showed a
marked elevation in drug use among smokers (Table 2).
Although the data are preliminary, a trend, that female
smokers consume drugs with greater frequency than female
nonsmokers Is suggested. It is beyond the scope of this
chapter to differentiate between the behavioral components of
this phenomenon or to address the argument that women who
smoke are less healthy than nonsmokers. It is beneficial,
however, to examine the few reports that address the
differences in drug actionn between smokers and nonsmokers,
regardless of the reasons for drugg use.
Altered Clinical P,esponse to Drug Therapy by Smokers
Compared to Nonsmokers
The number of studies investigating the differences In the.
clinical responses to a drug by smokers and' nonsmokers are
far fewer in number than thestudies examining.the alterations
In metabolism and biochemistry of drugs in smokers. The
1979 Surgeon General's Report Included ann extensive review of
the alterations In drug disposition that occur in smokers (29)..
That Information. Is useful for clarifying mechanisms by which.
smoking alters drug m etabolism, absorption, excretion, and
other functions. The clinical significance of these alterations
has not been.n clarified, ho wever.
The most exhaustive exam.ination of alterations in
smokers' clinical response to drugs was done by Jick and his
associates In the E4ostom Collaborative Orug Surveillance
Program (PCDSP). Over the past several years, this group
has investigated the clinical response of smokers and
nonsmokers to six different drugs: propoxyphene(L?arvon)
(3); diazepam (Valium ) (4); chlordiazepoxide (Librium) (4);
phenobarbital (4); chlorpromazine (Thorazine) (Q8).; and
theophylline tea (22). The differences observed between
smokers and nonsmokers were consistentamong men and
women, except for the theophylline study, in which thee toxic
effects of therapy were slightly more frequentt amongg women
(13.4 percent) than among men(9.1q percent). Only in the
chlorpromazine (28) study did the studv group (those taking
chlorpromazine) contain more women than men, an observation,
that supports other reports that wom en use major trannuilizing.
agents morefreqpently than men (21).
Since the published RCDSP data is not organized
according to groups of women smokers and nonsmokers, any
0
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Tal
Tal
Tal
sou
304
PEPTIC ULCER: REFERENCES
(1)
(2)
ALLIRONE, A., FLINT, F.J. Rronchitls, aspirin,
smoking and other factors in the aetiology of
peptic ulcer. Lancet 7: 1.79-1F?, July 26,
7958.
ALP, M.H., HISLOP, I.G., GRANT, A.K. Gastric
ulcer in south Australia 1954-1a63. 1.
Epldemiologfcal factors. Medical Journ al of
Australia 2: 117R-1132, December 12, 1970.
(3). RRANpSFtIRG, 0., CHRISTENSEN, N.J., GALRO, H.,
RRANDSRORG, M., LOVGRF.EN, N.A. The effect of
exercise, smoking and propranolol on serum
. gastrin in patients with duodenal ulcer and
vagotimized subjects. Scandinavian Journal of
Clinical and Laboratory Investigation .38(5):
. 441-446, May to78.
(4) DOLL, R., IONES, F.A., PYGOTT, F. Effect of
smoking onn the production and maintenance of
gastricand duodenal ulcers. Lancet 7: 657-
662, March 29, 1958.
(5) FRIEDMAN, G.D., SIEGELAUR, A.B., SFLTZF_R, C.C.
Cigarettes, alcohol, coffee and peptic ulcer.
New England Journal of Medicine 290(9): 469-
473, February 28, 1974. (b) !:RIMES, D.S., GODDARD, J. Effect of cigarette
smoking on gastric emptying. Pritish Medical
Journal 2:. 460-461, August 12, 1078.
(7). HIG G1NS, M.W., KJELSRERG, M. Characteristics of
smokers In Tecumseh, Michigan. II. The
distrihution of selected physical measure ments
andd physiological variables and the prevalence
of certain diseases in smokers and nonsmokers.
American Journal of Epidemiology R6: 60-77,
1967.
(8) IVEY, K.J., TRIGGS, E.. Absorption of nicotine
by the human stomach and its effects on
gastric lon fluxes and potential differences.
A merican Journal of Digestive Oiseases 23(9):
809-814, September 197R.
(9). JERRYCHO11rSK1, W., POPIELA, T. Association be-
tween the occurrence of peptic ulcers and
tohacco smoking. Public Health, London 8R(4):
195-2fN1., 1974.
300
TABLE 2.-Percentage of Positive Responses Among Females
In Age Group15-19
EQU STIONSMDKERSNONSMORERS
n
lakeni phenobarbital or barbiturates? 2.3 . .. 1.0
Takencodeine, morphine, etc.? 16.0 6.5
Taken Benzedrine or Dexedrine? -- ' 4.9-- 0.3
Taken penicillin or other antibiotiesl 33.0 25.8
Taken pills to prevent pregnancyl- 27.0 9.7
30URCE: eAdapted from.SeLtzer (,25)
305
I
I
TABLE 1.-Ratioof Percent Usage of Drug Classes, Wbmen SmokerlNonsmoker Statuse
BHITEBLACJC ASIAN '
Antihilstamine or allergy mtdicine . 0-8 0.9' 0.6
Cough mediicine 1.7 ' 1.8
' 0.7
AstHma medicine _ .
Aspirin-containing drugs ' 0.9
1.2 1I.0
1..2' 0.9
0.9
Pain medicine. 1.2 1.2 1.0
Codeine, morphine, Darvon, Percodan, Demerol 1.5 1.6 . 1.2
Phenobarbital or other barbiturates 1.3 1.8 1.6
Sleeping Pills - 1.2 1.3 1.3'
Tran9uiliusrs- 1.5 1.6 1.9
Anticoagulants 1.3 0.8 0.0
Digi[alis or other heartt medication 1.0 0.8 0.1
Antihypertcnsires 068 1.1 0.9
Diuretics - ' ' 1.1 1.0 1.3
Cortisone-type medicatlon 1.0 1.2 . 1.0
Hormones 1.2 1.3 1.4
Insulin or dlubetic pillls 0.9 0.8 0.9
Iron or anemiua medicatlone 0.9 0.9 0.9
Thyroid medication 1.1 1.3 2.3
Pills to control periiods .' 1.3 _' 1.2 1.5
Contraceptives 1.2 1.1, 1.3
Oenzedritre.or Deaedrlne 1.6 1.11 1.11
Weight reduction medication ' 1.1 0.9 1.3
Penicillinior otherantibiotics 1.2 1.2 1.0
Sulfa drugs 1.1 1.2 0.8
Stomach or digestion meddclne 1.2 1.2 1.3
SOURCE: Adapted from Selbzer (35)'..
303
(9) DALES, L.G., FRIEDMAN, Q.D., SEIGELAUB, A.B.,
SELTZER, A.C., URY, H.K. Cigarette smoking
habits and urine characteristics. Nephron
20; 163-170, 1978.
(10) DESMOND, P.V., ROBERTS, R.K., WILKINSON, Q.R.,
SCHENKER, S. No effect of smoking omn meta-
bolism of chlordiazepoxide. New England
Journal of Medicine 300(4): 199-200
January 25, 1979.
(11 )~ FRIEDMAN, Q.D., SIEGELAUB, A.B., SELTZER, C.C.,
FELDMAN, R., COLLEN, M.F. Smoking habits
andd the leukocyte count. Archives of Environ-
mental Health 26(3): 137-143. March 1973.
(12) GLAUSER, S.C., GEAVSER, E.M., REIDENBERG, M.M.,
RUSY, B.F., TALLARIDA, R.J. Metabolic changes
, - associated with the cessation of cigarette
sm oking. Archives of Environ mental Health
20(3): 377- 381, March 1970.
(13) HELMAN, N., RUBENSTEIN, L.S. The effects of
age, sex, and smoking on erythrocytes and
leukocytes. Am erlcan Journal of Clinical
Pathology 63: 35-44, 1975.
(14) HUNT, S.N., JUSKO, W.J., Y1IRCHAK, A.M. Effect
of, smoking on theophylline disposition..
Clinical Pharmacology and Therapeutics
(Part 1) 19(5)c 546-551, May 1976.
(15) ISA GER, H., HAGERUP, L. Relationship between
cigarette sm oking and high packed cell
volum e and haemoglo6in levels. Scandinavian
Journal of Haemotology 8(4): 24i-244, 1971.
(16) JICK, H., DINAN, B., ROTHMAN, K.J. Noncontra-
ceptive estrogens and nonfatal myocardial
Infarction. Journal of the American Medi-
cal Association 239(14): 1407-1408, April
3, 1978.
(17) JICK, H., DINAN, B., ROTHMAN, K.J. Oral con-
traceptives and nonfatal myocardial infarc-
tion. Journal of the American Medical
Association 239(14)t 1403-1406, April 3,
1978.
312
difference In drug use between these groups Is not reflected
in the data analysis. However, It is Important to note that
these studies, except as noted in the chlorprom azine study,
predominantly involved men. It has been sho wn that women
report more frequent use of the minor tranquilizers suchh as
diazepam and chlordlazepoxide (2n). Thus these studies should
not be interpretedas reflecting drug response among the
general population (20).
The studies on chlorpromazine, diazepamy and
chiordiazepoxideshowed a lessened frequency of the adverse
effect of drowsiness among smokers as compared to
nonsmokers (4,2R). Conversely, no difference was reported
for phenobarbital (4). The analgesic effect of propoxyphene
was reduced in smokers, an effect which was not observed In
smokers on aspirin, codeine, acetaminophen, or combinations of
these drugs (3). Thee evidence for increasedd theophylline metabolism in
smokers is well established and predicts the observed clinical
response to theophylline (14). The PCDSP study of
theophylline sho wed that smokers not only required larger
doses of theophylline for efficacy, but also were less likely
to report adverse effects thann nonsmokers, evenn though, they
required larger doses.
Theoretically, then, because of a decreased clinical
response to a drug, the tendency would be for the smoker to
require Increased doses to achievethe same therapeutic effect
as a nonsmoker. Therapeutic efficacy and adverse side effects in
relationship to gender, smoking history, and drug consu mption
patterns have not been adequately studied, although the
preliminary evidence would Indicate an area of potential toxic
drug effects and/or therapeutic failures.
Oral Contraceptives and Smoking
Chronic estrogen therapy has a profound interaction with
chronic tobacco use. Again, the RCDSP has been most
Instrum entatin. assessing the Influence of these two factors
on the health status of women.
In assessing the relative risk of stroke in women who
smoke and take oral contraceptives, the data from the
Collaborative Group for the Study of StrokeIn Young Women
sho w that smoking alone increased the risk of hemorrhagic
stroke (i.e., subarachnoid)) from, 1.0 for a nonsmoker who did
306
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cn
~
~
~
Alterations in Normal Clinical Laboratory Values in Women
Smokers
Only a fe w investigators have studied clinical laboratory
values in women smokers and nonsmokers (1, 8, 9, 11, 13,
15, 10, 31). Many of these studies show statistically
significant differences in a variety of common param eters.
The clinical significance of these differences may not be
apparent, however, since the actual differences between women
smokers and nonsmokers are small. For example, a study of
packed red cell volume (PCV) and hemoglobin (Hb) in women
smokers and nonsmokers showed the PCV and Hb for
nonsmokers to be 41.95 and 13.85 compared to 42.94 and
14.16 for smokers--a difference significant at P < 0.05, but
a discrimination which physician or patient may find difficult
to assess (15).
Small differences in laboratory values between smokers
and nonsmokers can be seen in a number of serum chemistry
and hematologic tests. One measurement that shows a wide
enough variation between smokers and nonsmokers to be
recognized clinically is the leukocyte count of a smoker
(11,13). It is important to recognize that a WBC of 12,000
per cu/mm is within the normal range for a heavy cigarette
smoker, and that the differential count remains normal (11).
In one study, individuals with chronic bronchitis wereexciuded
from evaluation of leukocyte counts, and the sam e relative
increase in leukocyte count was observed (13).
- In several studies of triglyceride and cholesterol values
In smoking and nonsmoking women, an elevation of both values,
which was not statistically significant, was seen in smokers.
The addition of oral contraceptive use to smoking caused a
significant elevation over the nonsmoker, noncontraceptive
user. The nonsmoker values were 79 + 6.8mg/100 ml for
triglycerides and 157 + 7.5 mg/100 ml for cholesterol. In
the smoker they were 110 + 14.8 mg/T.00 ml and 174.3 + 8.8
m g/100 ml respectively, whereas the smoker using oral
contraceptives had a triglyceride value of 150.0 + 14.1
mg/100 ml and a cholesterol value of 186.1 + 8.4 mg%100 ml.
In this same study, there was no significant difference
between the levels of vitamins A, EE or C in sm oking and
nonsmoking women (31).
A number of investigators have measured vitamin C
levels in sm oking and nonsmoking wom en, with extreme
variation in results. Som e sho wed decreased plasma and
leukocyte vitamin C levels in smokers, and others sho wed no
308
Summary
There is a paucity of data on what short-term effects
cigarette smoking has on drug response, drug interaction, and
the nutritional requirements of wom en.: Preliminary studies
sho w altered responses to drugs and variations in laboratory
measurements. Further study is needed to clarify the
significance of these observations for women who smoke.
310 -
not use oral contraceptives, to 2.6 for a smoker who did not
use oral contraceptives. A sm oker taking oral contraceptives
had a relative risk of 6.1 or 7.6 (depending on the control
group) (5). Similar Increases inn risks do not seem to occur
for thrombotic stroke in the smoker taking oral
contraceptives, but the risk of a thrombotic stroke for a
women using oral contraceptives, alone, is about nine tim es
greater than that for a noncontraceptive user (6).
Again using the BCDSP data, the risk of nonfatal
myocardial infarction among women under 38 is very low
am ong nonsmokers whether or not they use oral contraceptives.
However, the riskk to wom en who both smoke and use oral
contraceptives Is substantially higher, ranging from an
estimated one per 8,400 annually in women aged 27 to 37
years to one per 250 for women aged 44 to 45 years (17).
In a similar study of noncontraceptive estrogens, similar risks
were demonstrated for women who both smoke and use
estrogens (16). These findings areih agreement with studies
done in Great Britain where oral contraceptives were
associated' with an overall Increase in cardiovascular disease
In young women (23). . .
Another group whichh has investigated the link between
sm oking, oral contraception, and myocardial infarction reported
that there is a considerabieinteraction between smoking and
contraceptive use. The group found that rate of acute
myocardial infarction among female smokers on oral
contraceptives is greater than could be accounted for by
either smoking or contraceptives alone (26). In earlier
studies thiss same group concluded that there was a dose-
response relationship between smoking and myocardial
infarction in women, and that among women smoking 35 or
m orecigarettes per day, the rate of myocardial infarction
was estimated to be 20 times higher than among those who
never smoked (27).
These data lend themselves to the prediction of risk In
only a very general way and provide no particular measures by
which a woman--smoker or nonsmoker--can evaluate her own
risk of experiencing one of the adverse effects described.
The following section reviews some of the laboratory
values that are altered by sm oking. Unfortunately, m any of
the largest studies on the correlation between smoking and
alterations in clinical laboratory values have focused on men.
307
0
0
0
Research on gender-role differentiation in childhood
has provided some insight Into developmental differences
between girls and boys. Maccoby suggests that these dif-
ferences may derive from different role models for boys and
girls; from the varying responses of significant adults to their
behaviors; from biological differences; and fromm a combination
of these (111). Block and Maccoby and Jacklin report that
the differences include girls having less confidence in their
ability to handle a new task and less sense of control over
what happens to them (18, 112). Girls also sho w greater
susceptibility to expressed anxiety, greater need for help and
reassurance, greater closeness to friends, and more concern
for what is socially desirable. .
Adolescent behaviors- -social or antisocial, adaptive or
maiadaptive- -are a function both of individual choice and of
theopportunities for growth and development whichh a society
provides its youth (36). "Not oniy is the term 'adolescence'
a social definition, but what society perceives as an
adolescent problem is also socially defined" (53). Similarly,
the develapm ent of values, motivations, and controls that
foster healthy growth and deter the onset of smoking and
other undesirabiebehaviors depends on the opportunities and
resources that society makes available to the adolescent.
Prevalence and Patterns of Adolescent Cigarette Use
National surveys of adolescent smoking behavior have provided
information on gender differences, secular trends, and age
subgroupings within the adolescent period. Surveys of smoking
patterns, ages 12 to 18, have been conducted by the National
Clearinghouse for Smoking and Health. (NCSH) in 1968, 1970,
1972, and 1974 and by the National Institute of Education
(NIE) in 1979 (182, 122). Two other periodic surveys, both
sponsored by the National Institute on Drug Abuse (NIDA),
included cigarette consumption. (2, 99). A number of studies
in specific geographic locales or among specific populations,
such as high school students, have also been carried out
(201). Differing definitions of a current regular adolescent
smoker make comparisons among thesee studies particularly
difficult. In theNCSH and NIE surveys, a regular smoker is
defined as one who smokes cigarettes at least weekly. In the
NIDA surveys, regular smoking is defined as occurring within
the past 30 days.
N
320
Concepts of Adolescent Behavior
Discussion of adolescence with its attendant problems have
seldom differentiatedd between boys and girls, and no theory or
model of adolescent behavior has been developed specifically
for girls. However, gender differences in deveiopment,cognitive processes, sex-role acquisition and
achievement have
recently been examined and a number of psychological
differencies have been identified (67, 197, 26, 29, 52, 95).
The essence of adolescence is growth, transition, and
change. The rate of physical growth in adolescence is more
rapid than at any other stage of development except the
neonatal stage. Adolescent development Is a complicated
process which involves increasing self-awareness, intellectual
and emotional growth, and physiological changes. What adults characterize as risk taking in
adolescence
may be exploration of the limits of Identity and capability.
Adolescents are attempting to resolve the competing and
conflicting demands stemming from childhood experience on the
one hand and expectations of adulthood on the other:
dependency and compliance versus autonomy and independent
decision making; orientation toward family versus orientation
towards peers. They face Increasing demands for social and
cognitive achievement and for developing the self-control
required to handle new psychological, physical, and social
situations. Inadeqpate experiencewith these challenges or
failure to meet them may result In low self-esteem and
increased anxiety and stress.
Numerous formulations contributing to a general model
of adolescent development have emerged. These include life-
span theory and cohort change (125, 53), adolescent sexuality
(132), and differences between early and late adolescence
(82).
Douvan and. Adelson have identified issues that
distinquish adolescence: for girls they are sexuality,
loterpersonal-intimacy, and identity issues; for boys they are
sexuality, autonomy-assertion-Independence and identity issues
(52). In this study, conducted in the 1950s, girls evidenced
conflict betweenn the social roles for which they were
preparing (further education and careers) and the future roles
they desired (marriage.-motherhood). La Farge described a
similar female adolescent conflict between social rules and
individual perceptions (105). Research published in the 1970s
shows that young women still have role conflicts different
from those of young men (67).
319
ts
nd
es
ry
he
FOOD AND DRUG METABOLISM: REFERENCES.
(1) BILLIMORIA, J.D., POZNER, H., METSELAAR, B.,
BEST, F.W:, JAM ES, D.C.D. Effect of ciga-
rette smoking on lipids, lipoproteins, blood
coagulation, fitirinolysis and cellular compo-
nents of hum an blood. Atherosclerosis 21(1):
61-76, January-February 1975.
(2) BLITZER, P.H., RIM M, A.A., GIFFER,E.E. The
effect of cessation of sm oking on body weight
in 57,032 women: Cross sectional and longi-
tudinal analysis. Journal of Chronic Diseases
30(7): 415-429, July 1977.
(3) BOSTON COLLABORATIVE DRUG SURVEILLANCE PROGRAM.
Decreased clinical efficacy of propoxyphene
in cigarette sm okers. CllnicaiPharmacology
and Therapeutics 14(2); 259-263, March-April
1973.
(4). BOSTON COLLABORATIVE DRUG SURVEILLANCE PROGRAM.
Clinical depression of the central nervous
system due to diazepam and chlordiazepoxide
in relation to cigarette sm oking and age.
New England Journal of Medicine 288(6): 277-
280, February 8, 1973. (5) COLLABORATIVE GROUP FOR THE STUDY OF STROKE IN
YOUNG WOMEN. Oral contraceptives and stroke
in young women. Journal of the American
Medical Association 231 (7): 718-722, February
17, 1975.
(6) COLLABORATIVE GROUP FOR THE STUDY OF STROKE IN
YOUNG WOMEN. Oral contraceptives and in-
creased risk of cerebral ischemla or throm-
bosis.. New England Journalof Medicine 288(17):
871.-878, April 26, 1973. (7) CRAIG, T.L., VANNATTA, P.A. Current medica-
tion use and symptoms of depression In a gene-
ral population. Am erican Journal of Psychia-try 135(9): 1036-1039, September 1978.
(8) DALES, L.G., FRIEDMAN, Q.D., SIEGELAUB, A.B.,
SELTZER, A.C. Cigarette smoking and serum
chemistry tests.: Journal of Chronic Diseases
27(:6);: 293-307, August 1974.
a
s,1
d
I
t
1
A
(18). KEOTZ, U., AVANT., Q.R., HOYUMPA, A., SCHENKER,
5., WILKINSON, Q.R. The effects of age and
liver disease on the disposition and elimi-
nation of dlazepam in adult man. Journal of
Clinical Investigation 55: 347-359, February
1975.
(19) LAWSON, D.H., DAVIDSON; J.F., JICK, H. Oral
contraceptive use and venous thromboembolism:
absence of an effect of smoking. British
Medical Journal 2(6089): 729-730, September
17, 1977.
(20) PARRY, H.F., BALTER, M.B., MELLINGER, Q.D.,
CISIN, I.H., MANHEIMER, D.I. National pat-
terns of psychotherapeutic drug use. Archives
of General Psychiatry 28: 769-783, June
1973.
(21 ) PARRY, H.F., CISIN, I.H. BALTER, M.B.,
MELLINGER, Q.D., MANHEIMER, D.I. - Increasing
alcohol intake as a coping mechanism for
psychic stress. In: Cooperstock, R.
(Editor). Social Aspects and Medical Use of
Psychotropic Drugs. Toronto, Addition
Research Foundation, 1974. -
(22). PFEIFER,. H.J., GREENBLATT, D.J. Clinical toxi-
city _ of theophylline in relation to cigarette
smoking. Chest 73(4): 455-459, April 1978.
(23) ROYAL COLLEGE OF GENERAL PRACTITIONERS ORAL
CONTRACEPTION STUDY. Mortality among oral
contraceptive users. Lancet (4): 727-733,
October 8, 1977.
(24), SARTWELL, P.E. Oral'.l contraceptives and throm-
boembolism: A further report. American
Journal of Epidemiology 94(.3):192-201,
September 1971.
.(.25)SELTZER, C.G., FRIEDMAN, Q.D., SIEGELAUB, A.B.
Sm oking and drug consumption in white, black,
and oriental men and women. American Journal
of Public Health 64(5): 466-473, March 1974.
(26) SHAPIRO, S., SLONE, D., ROSENBERG, L.,
KAUFMAN, D., STOLLEY, P.D., MIETTINEN, O.S.
Orall contraceptive use in relation to myocar-
dial infarction. Lancet. (1): 74.3 -747,
April 7, 1979.
(27) SLONE, D., SHAPIRO, S., ROSENBERG, L., KAUFMAN,
D.W., HARTZ, S.C., ROSS1, A.C., STOLLEY,
P.D., MIETTINEN 0.5. Relation of cigarette
smoking to myocardial infarction in young
women. New England Journal of Medicine
298 (23 ): 12 73 -12 76, 197 8.
(28) SWETT, D. Drowisness due to chlorpromazine in
relation to cigarette smoking. Archives of
General Psychiatry 31: 211-213, August.
1974.
(29) U.S. PUBLIC HEALTH. Smoking and Health. A
Report of the Surgeon General. U.S. Depart-
m ent of Health, Education, and Welfare,
Public Health Service, Office of the Assis-
tant Secretary for Health, Office on Smoking
and Health, DHEW Publication No. (PHS) 79-50066, 1979, pp. 1251.
(30) WINGERD, J., SPONZILLI, E.E. Concentratlons
of serum protein fractions in white wom en:
Effects of age, weight, sm oking, tonsillec-
tomy and other factors. Clinical Chemistry
23(7): 1310-1317, 1977.
(31) YEU NG, D.L. Relationships between cigarette .
. smoking, oral contraceptives and plasma vita- -
mins A, E, C and piasm a triglycerides andd
cholesterol. American Journai of Clinical .
Nutrition 29: 1216-1221, 1976.
31.4 '
.
V.
have begun to decline. The prevalence of smoking boys of
this age peaked in 1970 and has shown a steady decline since
that time. These trends may represent fewer adolescents
taking up smoking, but those who do beginning at an earlier
age.
Well over one-half of high school seniors--male and
female--who smoke regularly, reported first smoking In the
ninth grade or earlier (99). It Is hard to know whether this
earlier onset reflects something specific to cigarette smoking
or is attributabie to the more general pattern of earlier onset
of all. "adult-type" behaviors.
This trend toward early initiation of smoking behavior
may have a significant impact on the future health of these
adolescents as many of the health risks associated with
smoking increase with both earlier onset of smoking and
duration of the smoking habit. In addition, the earlier the
use of a substance is begun, the longer it is likely to becontinued and the more heavily it Is
likely to be used (131,
29, 100).
These national surveys do not permit a detailed
examination of the initiation process. "Experimenters," those
who have smoked at least a few puffs of a cigarette, but not
more than 100 cigarettes, are lumped with 'never smokers"--
those who have never taken even a few puffs. "Occasional"
smokers are defined as those who smoke less than one
cigarette a week butt more than 100 cigarettes in a lifetime.
In one study, smoking only a few cigarettes usually leads to
becoming a regular smoker. Occasionall or intermittent
smoking is rare among adults. Examining the proportion of
"experimenters" at each age and following their subsequent
smoking behavior might help clarify the determinants of the
initiation process (120). Their estimate of 8 percent "occasionai smoking" In
adolescence is based on a definition of smoking less than
daily but at least one cigarette a week for as long as 1
month. The difference in definition of occasional smoking
makes comparison with current U.S. data on adoiescents
difficult. From 1968 to 1979, the percentage of current
occasional smokers (less than once per week) varied between
0.4 percent and 1.6 percent for girls, and 0.4 percent and
2.3 percent for boys (122). McKenneli and Thomas estimated
that the mean lengthh of time between smoking the first
cigarette and adopting regular (daily) smoking was slightly
less than 3 years for boys and slightly more than 2 years for
girls (120). The difference is probably due to earlier
325
TARLE 2.{urrent usea ofclprettes, alcohol andncrl)uana, by sea:
thre< natlanal surveys compared
ABes 12~ - 16 ASef 12 - 17--- ABes 17. - 18
NIE. (1979) NIDA, Abelson, et al. High School Senlen
1977 . 1 lohnston, et al. (1977)
A.Jes 1974 1979 A¢es 1974 1977 1975 1977
CURRENI CIGARETiTE USE
12-14 F 5.1% 4.3% 12-13 13% 10%
M 4.2 3.2
15-16 F 211. 6 12.3 14-15 25 22
M 18.1 14.5 '
17-18. F26.4 27.0 16-17 38 35
~M 32.6 19.6
12-18 F 15.9 13.1 12-17 F 24 22 F 35.9% 39.695
M 16.3 11.1 M 27 23 M 37.2 36.6
QIRRENT ALClHM. USE
16-17 F8M 51 52
12-17 F 29 25 F 62.2 65.0 .
12-17 M 39 37 M 75.0 77.8
dIRRENT MNt 13 DANA l ISE
16-17 FAM 20 29 .
12-17 F 111 13 F 22.5 30.0
12-17 M 12 19 M 32.3 40.7
eNote: Defini'.tlon of current use varies by study. Cigarettes: Mllne (1979)--
current regular smoker (one or more cigarettes during the past week over and above a minl-
mom five packs)) and current occasional tmoker (less than one cigarette per week); Abelson,
et al. (1977) and Johnston, et'al. (1977)--smoted within the past 3n.days. Alcohol and
mari/uana--use within the past nontR(smoters and nonsmokers).
SOt1RCES; Abelson, NIDA, etr al., 1977; Johnston, NIDA, et al., 1977; NIE, 1979
324
The 1979 NIE Survey reports that:
The increasing prevalence of teenage smoking was
observed in the period between 1968 and 1968 and 1974 has
come to a halt, and a decrease In the smoking rates of both
boys and girls has taken place. The decrease in boys'
smoking was greater than that of girls, resulting in a higher
smoking rate for girls than for boys in 1979. Smoking among
boys leveled off in the early 1970s, and then began to
decrease. It appears that girls are now following this
pattern: the smoking rate has leveled off among 1 7 and 18
year olds, and probably can be expected to decrease over the
next few years (122).
Other surveys (Table 2) support these trends in ado-
lescent girls' smoking behavior. Differences between studdes
in absolute prevalence rates reported are at least partly due
to the difference in the definition of a smoker, and
differences in survey technique. The National Institute on
Education (NIE) Survey included as current regular smokers,
both those who have smoked one or more cigarettes during the
past week, andd those who have smoked less than one cigarette
in the past week but more than 100 cigarettes inn their
lifetime (NIE Survey).. The prevalence rates of Abelson, et
al. and Johnston, et al. refer to any cigarette sm oking in the
past 30 days. -
The Abelson, et al. data, which were collected 2 years
before that of NIE, show the predicted decline but to a lesser
degree (2, 122), The Johnston, et al. data suggest that there
was an increase in adolescent girls' smoking as measured in
samples of high school seniors between 1975 and 1977 (99).
Johnston"s figures were retrospectively reported and refer only
to youngsters born before and during 1960 and therefore
would not be expected to reflect changes occurring in those
cohorts born after 1962 where the decline has occurred. This
may explain why the Johnston's 1977 sample did not reflect a
downturn, and' reports of later cohorts of high school seniors
should show a stabilization and then a decline in fe male
smoking rates. Results from a study by the same group in
1978 shows the predicted downturn in the smoking hahits of
high school senior girls (from 39.6 in 1977' to 38.1 in 1978)
as well as boys (from 36.6 in 1977 to 34.5 in 1978) (99).
Age at initiation of smoking, The data in Table 1 show that
the prevalence of smoking in girls aged 12-14 increased
steadily between 1968 and 1974 to a level equal to or
slightly higher than boys of the same age. Between 1974 and
1979 .the prevalence of smoking stabilized in girls and may
323
TABLE 1.{stlmates of the percentage of current, regular cigarette smokers,
Ad.olescents, aged 12 to 18, United States, 1968-1979.
Ages 12 - 14 AtL_es 15- 16Ages 1] - 18 Ages12 - 18
Year Male Female
1968 2.9 0.6
1970 5.7 3.0
1972 4.6 2.8
1974 4.2 4.9
1979 3.2 4.3
Male Female Male Female
17.0 9.6 30.2 18.6
19.5 14.4 37.3 22.P
17.8 16.3 30.2 ' 25.3.
18.1 20.2 31.0 21.9
13.5 11.8 19.3 26.2
Vale Female
14.7 8.4
IS.5 11.9
15.7 13.3
15.e 15.3
10.7 12.7
tiDTE:Current regular smoker Includlf respondent who smokes cigarettes at least weekly
SOURCE: 1I51MiEW, 1979 (Appendia); USDHEN, NIE, 1979
322
U
~~...r..<,y , .
TABLE 3.-Percentage of adolescents who smoke by the smoking behavior
of parents and older siblings
Have No Older Sibling Have Older Sibling
w.
-
One/Both . Neither
Parents Smoke Parent Smokes
One or Both Neither Older No Older Older No Older
..
Parents Parent Sibling Sibling Sibling . Sibling
Smoke Smokes Smokes Smokes Smokes Smokes -
Boys: . . ~ ~ . .
12-.14 ~ 2.8 0.0 ~ 6.3 . ~ 2.7 ~ ~ 0.0 ~ 0~.0
15-16 17.6 ~ 4.0 ~ 18.8 , 6.3 21.1 2.1
17-18 . 15.0 ~ ~ 7.9 ~ ~ 25.4 16.7 ~ 31.7 ~ 0.0
Total - 8.2 ~~ 2.9 ~ . 17.0 7.5 ~ . 19.5 ~ ' 0.6
Girls:
1 2-14 .
15-16 3.7 , .
8.2 - ' 0.0 . .
5.7 - ` 8.5 ~.
20.0 - - -
1.3
13.0 .
3.4 -
15.2 ' - 2.9
2.4
17-18 29.7 15.4 32.9 19.6 25.0 6.7,
Total 9.7 4.1 . 20.3 9.7 . 15.3 4.1
BASE: Both Parents Present In Household .
SOURCE: NIE, 1979
sszss9Co
experimentation among boys. The transition from experimentai'
or occasional smoking to regular smoking is an extremely
important one to study because it may provide a crucial
period for intervention before psychosocial or pharmacological
dependency is established.
Number of cigarettes smoked. In the NCSH/NIE survey, a
smaller percentage of girl smokers than boy smokers smoked
10 or more cigarettes per day (61.8 percent versus 73.8 per-
cent in 1974, and. 59.0 percentt versus 65.6 percent in 1979).
The high school senior survey showed male-female rates to be
equivalent at the half-pack per day rate, with, boys exceeding
girls at heavier levels (99). In that study, the proportion of
females currently smoking as much as a half-pack per day
Increased between 7975 and 1977, while the proportion of
males smoking at that rate remained constant. The American
Cancer Society survey also suggested an Increase in the
proportion of heavy smokers among adolescent girls compared
with stable rates in boys between 1969 and 1975 (203). It
reported a fourfold increase in the percentage of girl smokers
who smoked at least a pack a day, from 10 percent to 39
percent, compared with an unchanged rate of 31 percent
among boys. The equality In smoking behavior may be
extending to the number of cigarettes smoked.
Type of cigarette smoked. In adolescent smokers of both
sexes, there has been a definite trend toward smoking
cigarettes with lower ^tar" yields between 1974 and 1979.
Figure 1 shows the decline in the tar and nicotine levels of
the cigarettes smoked by adolescents. Giris appear to be
slightly ahead of boys in the use of lower "tar" cigarettes.
The trend can be attributed to three factors: the increased
marketing of low "tar" cigarettes; the decreased tar levels of
existing cigarettes; and increased awareness of differential
health hazards associated with different kinds of cigarettes
(122). It should be noted, however, that the midpoint on the
cumulative percentage continuum has dropped only about I mg
"tar" between 1974 and 1979, from approximately 17.5 mg to
approximately 16.5 mg, and the percentage of adolescents
smoking the lowest category of "tar" (less than or equal to
10 mg). Is still very small.
326
Prevalence
Table I sum marizes adolescent cigarette smoking prevalence
between 1968 and 1979, .by age and gender, as surveyed by
NCSH and by NIE. Between 1968 and 1974 there was a
significant increase in the percentage of girl smokers in eachh
age category at each point inn time, In contrast to the
relatively stable prevalence of current regular sm oking among
boys. A decline in the average age of smoking initiation for
both sexes is suggested by the small but significant increase
in smoking prevalence among 12 to 14 year olds (186).
Trends inthe data from a national study of high school
seniors also support the hypothesis of an earlier age of
initiation (99).
In the five years from 1974 to 1979, the proportion
of 17 to 18 year old girls who smoked changed little, but the
proportion of boys who smoked dropped by a third. It was
this difference am ong 17 to 18 year olds that created the
overall higher sm oking rate for girls as compared with boys in
1979. However, at ages 15 to 16, the drop from. 1974 to
1979 was greater for girls than boys, suggesting that the
Initiation of smoking Is also beginning to decline in those
girls born after 1962.
The differences in.the within-age-group changes in the
smoking prevalence of girls may represent an isolated effect
on the cohort of girls born in 1963 and 1964. The change
was essentially confined to the 15 to 16 year old subgroups
who were born during these years. The precise nature of the
interactionn of social influences on the development and
m aturation of this cohort Is unclear. Ho wever, other data
suggest that a marked secular change occurred in cigarette
smoking attitudes and behavior which was se.condary to an
increased awareness of the health risks of smoking.
An alternate hypothesis is that the isolated decline in
the 15 to 16 year old subgroup may be an artifact produced
by the combined trends of reduced initiation of smoking and
the initiation at a younger age. Thus, the decline in
prevalence among 15 to 16 year old girls would reflect the
decreasing percentage of young women who are taking up
smoking, but this trend will be masked in the younger age
group by the tendency of those girls who are going to take up
smoking to do so at a younger age.321"
0
f
b
100
a
9ltlrii,M.:1t4 f -..
FIGURE 1.-Oumuletlvo INrcntFy OI WoMaeM malun Ey t0 t.e I W.I of oly.aab smoYq 1 Y)C } 1979
BOYS
90
00j
70
3a
20
10
,10 11 13.5 IS 16 1) 10 19 y?0
10.61 10.01 11 71 i U.11 11.21 I1.11 j1A51
Mg "tai' land meCmn mg nlcotlnel
9OURCE:AGaptetllrom NIE,19V9',ETC,1918
sszs99eo
1974
K-----j( 19)9
GIRLS 100
1115 16 11 IB 19 )20
(0.9) 11.11 (1.11 I1.]1 11.31 (1.45)
Mg °ur^ IanJ medizn mg nirotloe)
p0
60
30
to
TABLE 4.-Smoking parameters observed in Hamburg, Germany In 1971 and 1974
Puff Number Puff Duration Puff Interval Total Puff Duration
(sec) (sec) (sec)
1971 1974 1971 1074 1971 1974 1971 1974
SOURCE: Schulz and Seehofer, 1979.
s9zsa9Co
Men 10.2 10.9 1.47 1.47 52.9 42.1 15.0 16.0
Women 10.9 13.3 1.31 1.17 46.0 40.7 14.3 15.5
All 10.5 11.8 1.41 1.34 50.3 41.5 14.R 15.R
INTRODUCTION
Currently, women are rapidiyapproaching men In rate of Ini-
tiation and prevalence of cigarette smoking, but seem to have
a lower rate for successful cessation of smoking. While an
Increasing percentage of the U.S. population is giving up
of particular importance in the life of the woman smoker.
to the pregnant smoker because the impact of smoking bothh on
the fetus and the pregnant woman makes pregnancy a period
in the health professions is presented. A section Is devoted
A separate analysis of smoking patterns among women
of generating new ideas for research and intervention.
between menn and women smokers are discussed with the hope
maintenance of smoking behavior including pharmacological
effects, sm oking patterns, Information disse mination, and
stress managem ent. The differences in successful quitting
sm oking among girls, andthe factors important in the
attention is directed to the patterns of initiation, the rise in
parative reference to men's use wherever appropriate. Special.
This part discusses tobacco use by women, with com-
successfully.
aa sm aller proportion of women than m en are quitting
smoking, nationwide surveys and cessation studies suggest that
INITIATION OF SMOKING IN' ADOLESCENT GIRLS
A num ber of psychosocial variables correlate highly
with adolescent smoking trends. The.seinclude the attitudes,
perceptions, and behaviors of adolescent girls, their social
setting (family, peer groups) and those broad demographic
factors (race, education, family income, urbanicity) that help
to define an individual's position within the society.
they did, they started later. Neither of these differences
holds true any longer.
girls were less likely to start sm oking than boys, and when
toward earlier onset. For example, before the mid-1970s,
like" behaviors such as alcohol use or sexual activity, is
The trend in adolescent smoking, as in other "adult-
information programs and to social sanctions against smoking.
in sexx roles and gender differences in responses to public
and behaviors reflect broader social forces, Including changes
Cigarette smoking, particularly cigarette smoking among young
girls, is a changing phenomenon. Shifts in smoking attitudes
318
1I
I.
It
t
f
k
0
g
Alcohol and marijuana use. Cigarette use should be viewed in
the context of other substance use behaviors. Abelson, et al.,
provided information on the use of other substance in the age
range of 12 to 17 by current cigarette smokers and by those
not currently smoking (2). Smokers far exceeded nonsmokers
inn reporting use of alcohol, m arijuana and/or hashish, or
"stronger" drugs (hallucinogens, cocaine, heroin, and other
opiates). Positive replies for alcohol were 80.0% versus.
44.8%; For marijuana and/or hashish, 68.3 percent versus 16.7
percent; and for stronger drugs, 26.3 percent versus 4.1
percent' respectively (26, 101, 203). Similar figures for
alcohol use by 13 to 17 year old girls were reported by
Yankelovich, et al., 81 percent of the smokers drank compared with 42 percent of nonsmokers, but
somewhat lower estimates
were reported for marijuana use, 25 percent of the smokers
versus 3 percent of the nonsmokers (203). Strong
associations between alcohol use and cigarette sm oking and/or
between marijuana use and cigarette smoking in adolescents
andd college students have also been identified in a number of
other investigations (83, 94, 145, 168, 172).
Demographic and Psychosocial Correlates of Smokin in
Adolescence. Smoking is a complex behavior. Adolescents
start to smoke for multiple reasons. Strong correlations
between smoking and a number of demographioc and
psychosocial variables have been reported, but the set of
"predisposing factors" has seldom been subjected to
muitivariateanalysi.s. It is rare that more than one or two
variables have been tested simultaneously. What appear to be
separate determinants of smoking behavior (for example, peer
pressure and socioeconomic status) may actually be factors
which exacerbate a more basic variable such as self esteem.
A fe w multivariate analyses have been conducted (107, 109,
132).
Socioeconomic influences. A number of studies have examined
smoking in relation to socioeconomic status. The findings
consistently point to a relationship between lower parental
status--income and education--and higher smoking prevalence
among these parents and their children (20, 122, 141, 151).
Adolescents from low-income families may also begin to
smoke earlier than others (33, 120). The findings that girls
who work have higher rates of sm oking m ay also reflect a
329 -
relationship to lower economic status (10, 122). Srole and
Fischer observed a relationship between downward mobility and
smoking In adults (171). This may be an important dynamic
to explore in adolescent initiation of smoking.
. A relationship between parental education and ado-
lescent smoking also exists (122). When one or both parents
attended college, 9.9 percent of boys and 10.6 percent of
girls smoked, compared with 10.9 percent of boys and 14.8
percent of girls from homes where neither parent attended
col lege.
Family patterns. In single-parent households (19.3 percent of
those households surveyed in 1979)., adolescentt smoking rates
were approximately double those of households In which both
parents were present (122). This relationship holds for both
boys and girls, in every age group, and across all five
NCSH/NIE surveys; it has also been Identified by others
(107). In the 1979 survey, 19.3 percent of the boys and
21.2 percent of the girls in single-parent households are
smokers, compared to 8.6 percent and 10.7 percent of those
in homes with both parents present.
More than one factor is likely to underlie this asso-
ciation. Adult smoking rates are higher for divorced men and
women. Thus, parental modeling may be involved. Smoking is
also inversely related to socioeconomic class, and more
single-parent households fall into lower socioeconomic status
categories than dual-parent households.
Smoking among parents and siblings. Adolescents are more
likely to smoke if either or both parents smoke than If they
do not (10, 15, 20, 151, 199). (See Table 3.) When both
parents smoke, 13.5 percent of sons and 15.1 percent of
daughters smoke; when one parent smokes, 9.1 percent of the
boys and 12.7 percent of girls smoke; and in homes where
neither parent smokes, 5.6 percent of boys and 6.5 percent of
girls smoke (122)..
There are conflicting reports on the relationship bet-
ween the sex of the smoking parent and smoking habits of the
offspring. In two-parent hom es In which, only one parent
smokes, 17 to 18 year olds appear to be more likely to
smoke If the mother does (122). Other studies have
identified a relationship between the child's smoking and that
of the parent of the same sex (15, 199, 10). Allegrante, et
al., found a relationship between the mother's smoking
behavior and that of sans, but not of daughters, and no
330 -
undergraduates who smoke (203, 163). Smoking Is correlated
with a wish to be older (122). Both boys and girls who
differed from thee norms of their high school peers on tests
of self-concept were more likely to smoke cigarettes as well
as to use other drugs (92). .. Adolescent smoking has been consistently correlated
with low educational and occupational aspirations. In a
review which included "locus of control" as a measured
variable, Smith concluded that smokers were more externally
oriented and felt that they had limited control over what
happened to them (167). Pflaum reviewed findings on the
positive relationship between smoking and feelings of
helplessness and hopelessness (137). Adolescent smokers
express less desire and ability than nonsmokers to control
future events, for example, to determine what kind of person
they will become (122). Giris scored slightly higher than
boys on this factor, indicating a greater sense of future
control.
Finally, response to stress has beenn suggested as a
basic dynamic in cigarette smoking (116). Feelings of
unattractiveness, a sense of incompetency and inefficacy in
school achievement and personal relations, limited opportunities
for personal growth and for future social and economic roles
all contribute to stress in adolescence. Changes in social
settings, such as transition from elementary to junior high
school, which occur simultaneously with physical and em otional
changes must also be acknowledged. Theoretical formulations
of life-change events andd their effects on health might also
be worth considering in studying the onset of cigarette
smoking among girls (49).
Prediction of Future Smoking Behavior. In 1979, a longitu-
dinal study was undertaken by the NationaP Institute of
Education involving the re-interview of 46.8 percent (N =
1194) of the 2,553 adolescents first surveyed in. 1974 (122).
In 1974, 152 respondents were smokers and 1,042 were
nonsmokers. By 1979, 27 percent (.N = 41) of the smokers
had quit, while 73 percent (N = 111) had continued to
smoke. During the same time period, 20.8 percent (N = 2t7)
of the nonsmokers had taken up smoking, whdle 79.2 percent
(N = 825) had not. Thus, the proportion of smokers who had
quit was greater than the proportion of nonsmokers who had
taken up the habit. However, because the percentage of
nonsmokers was much higher than the percentage of smokers
the net effect was an increase in the percentage of the
population who were smokers (12.7916 to 27.5%).
336
relationship of the father's smoking behavior to children of
either sex (3). In contrast to all of these findings,
Schneider, et al., were unable to relate parental smoking to
that of offspring (156).
Explanations for the association between parental and
chiidren's smoking behavior Include the effect of role-
modeling, parental permissiveness (real or im agfned), and
availability of cigarettes in the home (119).
Older siblings seem equally Important or more impor-
tant than parents as potential role models for smoking (10,
122, 141). There is a greater likelihood that an adolescent
will smoke if one or more older siblings smoke than if no
older siblings smoke; this is true in those households where
neither parent smokes as well as in those where one or both
parents smoke. In the 1979 survey, boys with older siblings
who smoke were more than three times as likely to smoke as
boys with nonsmoking older siblings. The increase is abouttwofotd for girls (see Table 3). The
highest smoking rate for
girls was found when at least one parent and an older sibling
smoked (20.3 percent). The corresponding rate for boys (17.0
percent) was slightly lower than where an older sibling but
neither parent smoked (19.5 percent).
Peer group infiuence. Adolescents' smoking behavior is highly
correlated with reports of having friends who also smoke (15,
126, 127, 147, 152, 203). Most multivariate analyses have
established this factor as being of prime Importance although
one such analysis found no relationship at all (109, 132, 3).
It has been pointed out that patterns of drug use in
adolescents are very similar among best friends (121 ). It has
not been demonstrated, however, that it is the behavior of
friends rather than Inclinations of the adolescent which
Influences him or her to smoke (3, 122, 156).
Inquiring about the smoking behavior of the "four best
friends" of adolescent respondents, the NIE study reported
that 87.6 percent of boys and 94.0 percent of girls who
smoked stated that at least one of those friends also smoked.
In addition, only 10.2 percent of boys and 5.9 percent of
girls who smoked had no regular smokers among their four
best friends, and an even smaller fraction (2.2 percent of
boys and 0 percent of girls) reported that none of their
friends had even experimented. In a parallel vein, it was
found that nonsmokers also congregate together.-
Approximately one-third of the nonsmokers (33.8 percent of
boys, 32.9 percent of girls) reported having at least one best
332 I
7PE
Table 7.-Estimates of the percentage of current, regular cigarette
smokers among white and black adults, aged 20 years and
over, United States, 1965-1978.
51.5 34.2 60.8 34.4
43.7 . . 31.9 54.0 33.1
41.9 31.8 - 55.3 36.8
41.2 31.8 50.5 35.1
36.4 30.1 42.8 30.2
Results displayed as percentage of respondents with known smoking
status ages 17 years and aver. -
SCJURCE: National Center for Health Statistics: USDHEW, 1979, Appendix.
1965
1970
1974
1976
1978
Note:
V=ss9Co
whether school.,household, or telephone samples are used.
Drop-out, absenteeism, lack of telephone accessibility, and
belonging to a minority group all contribute to the sampling
errors, which Include underrepresentation of population
subgroups whose rates are substantially higher than the norm.
Accurately m easuring these subgroups would enable scientists
to better target interventions. Young black fem ales appear to
be one such group whose smoking rates well exceed the
national average.
There is good reason to expect the heaviest cigarette
use and other "problem behaviors" among those segments of
the adolescent population who feel cut off from socioeconomic
opportunity and m obility. The revie wof correlates of
adolescent smoking shows that many of the variables that
predict cigarette smoking bear a remarkable similarity to ones
identified as predictors of marijuana and/or other illicit drug
use. It is recomm ended that greater attention be given to
models of behavior and socialization processes.
More prospective longitudinal studies need to be
undertaken, based on varied samples of children. Data need
to becoUected about physical and emotional status, psycho-
social outlooks and attitudes, family and peer relations,
academic and recreational activities, family and school set-
tings, and family and residential background. This informationn
must be gathered early in childhood to recordd significant
socialization influences which precede the onset of smoking
behaviors and'd should becoJlected frequently enough to record
significant changes close to the time they occur.
MAINTENANCE OF SMOKING
SM OKING BEHAVIOR
Patterns of cigarette smoking. Smoking patterns differ
between the sexes. Schulz & Seehofer studied the smoking
behavior in male and female smokers observed surreptitiously
in public places.: Puff num ber, duration and interval were
measured (157). Women were found to leave a significantly
longer butt length (approxim ately 2 mm longer)) and had
shorter puff durations than men (see Table 4). However, they
took a greater number of puffs and, therefore, had the same
total puff duration (puff number x puff duration). These
authors do not report gender data on inhalation patterns,
which are crucial to determining dose. Creighton&. Lewis
reported no sex differences in puff volume inn a small study
of the inhalation patterns of eight men and eight women (39).
340 '
Smoking cessation.. Are there differences between girls and
boys in patterns of smoking cessation comparable to those
observed in adults? A greater proportion of adult mates than
adult females have quit smoking (see the section on adult
cessation). The national surveys have shown more ex-smokers
amongg adoiescentt boys thann among girls (122,99). Looking at
either the percentage of ex-smokers among all adolescents or
att the quit rates (number of former smokers divided by
number of ever smokers), boys exceed girls in every survey
between 1968 and 1979 (122). For the two most recent
surveys, the quit rates were as follows: 33.2 percent of
female and 36.0 percent of male smokers had quit in 1974;
30.5 percent of female and 42.3 percent of male smokers had
quit In 1979. In contrast, Reeder found no difference in quit
rates between boys and girls aged 13-19 in national surveys
conducted in 1965 (boys 28 percent, girls 299 percent)) and in
1975 (boys 34 percent, girls 35 percent) (141). Therefore,
it is unclear whether adolescent girls show the same patterns
of quitting smoking found in adult women. It should also be
remembered that research on both smoking cessation and illicit
drug use has shown that quitting is often not a perm anent
state (.164, 140; 98).
Smoking prevalence and ethnicity. There are no data based on
a national sample examining adolescent smoking in different
racial groups. However, beginning in 1969-1970 Brunswick
has conducted a longitudinal personal home interview survey of
a representative sample of 668 urban, non-Hispanic black
youths In Harlem, New York City. She found that' more 16 to
17 year old girls than boys smoked (62 percent versus 50
percent). This wasweli before national rates had sho wn
smoking among girls equalling and then exceeding. that among
boys. This greater smoking prevaiencee in girls continued into
the young adult years. The same subjects were refnterviewed6 to 8 years later, when the youths were
aged 18 to 23.
Sixty-two percent of young black women (N = 258) were
current smokers and 18 percent were currently smoking at
least a pack a day. This Is compared with 57 percent of the
black men 18 to 23 years old (N = 277)whowere current:
smokers, 16 percent of whom regularly smoked at feast a
pack a day. These prevalence rates are well above therates
for adult black women found inn national survey data but are
only slightly higher than the rates found inn adult black men -
(201). This study is of substantial interest, but may not be
representative of national black adolescent smoking patterns.
q
328
Data on smoking patterns were collected in surveys
conducted in 1964, 1966, 1970 and 1975 by the National
Clearinghouse for Smoking and Health (see Table 5). In each
survey a greater proportion of men than women reported
inhaling deeply into thecheste and inhaling almost every puff.
Men therefore may extract a greater dose of nicotine and the
other constituents of cigarette smoke than women do.
However, there is an increasing proportion of wom en who
report smoking their cigarettes "as far as possible," in
contrast to a decline in the proportion of men who reported
this behavior (157). A slightly higher proportion of males
reported letting "very little" of their cigarette burnn without
smoking it: 1970, 20.6 percent male vs. 18.0 percent female;
1975, 20.9 percent vs. 18.6 percent female (181,182). These
changes are often a correlate of heavier smoking. In sum,
the observational data suggest that men and women have equal
total duration of smoking per cigarette, and the national
survey data suggest a larger proportion of males inhale
deeply. In general, men smoke In a more hazardous way than
do women. However, the smoking patterns of women are
changing toward "more hazardous" smoking (see Part I of this
Report).
In contrast to the minor changes that haveoccurred in
the way an indivldual cigarette is smoked, there have been
substantial changes in the percentage of both male. and female
smokers who smoke more than a pack per day (Table 6). A
number of explanations may be offered for the data in these
two tables, (186): (1) more lighter than heavier smokers
may be quitting, resulting in a mean increase in daily
consumption; (2) continuing smokers may be increasing
consumption; (3) smokers newly initiating the behavior may be
smoking more heavily than alreiT~V established smokers; and
(4) declining tar and nicotine contents of cigarettes may be
leading to compensatory increases in number of cigarettes
smoked in order to maintainn nicotine dosage.
The 1975 survey reported a greater percentage of
women smokers smoke filter tip cigarettes, 90.6 percent of
women smokers versus 79.3 percent of men smokers. Women
also seem to be less fixedin their brand preference. Sixty-
one percent of women and only 10 percent of inenn
acknowledge changing brands at least once, and women lead
the trend in adopting king-size, filter-tip and 100 mm
cigarettes. On the other hand, women smoke cigarettes
almost exclusively. Cigars and pipes are currently used by
342
1964 1966 1970 1975
Male Female Male Female Male Female Male Femafe
1. Inhaiing deeply
into the chest 36.5% 22.5% 31.8% 15.59s 34.3% 17.5% 30.3% 16.4y
%':.e~... . .
E
TABLE 5.-Respondent-reported styles of cigarette smoking,
current, regular cigarette smokers, selected
categories, adults, United States, 1964-1975
2. Inhaling almost
every puff 63.1 54.8 63.0 52.1 60.5 47.2 58.5 50.7
3. Smoking cigarette
as far as possible 15.9 7.5 13.5 10.0 9.6 10.4 10.9 12.9
1. In 1964 and 1966, the questiennaire response was "as deeply into the chest as possIble.e in
1970 and 1975, the questionnaire response was phrased "deeply into the chest."
2. In each survey year, the questionnaire response was "inhale aimostevery puff of each
cigarette.'
3. In 1964 and 1966, the respondent was asked to draw a line on a dlagram of a cigarette, indi-
eating the average length of the discarded cigarette butt length. In 1970 and 1975 the verbal
questionnaire response was smoking cigarette "as far as possible." The data for 1964 and 1966
correspond to those respondents indicating a discarded cigarette butt length no greater than 20 nm.
Sfx1RCF: US[1HEW, 1979a, Appendix.
ZGZSSSEQ
friend who smoked, while over two-fifths (43.0 percent of
boys, 44.1 percent of girls) had no best friend who smoked
regularly. Over one-fifth (22.4 percent of boys, 23.0
percent of girls) had no best friends who had even
experimented.
Thus, "peer pressure" to smoke may be operative when
the adolescent belongs to or would like to belong to a group
in which smoking is part of the life-style, (122). When the
peer group behavior does not Inciude smoking, there may be
little pressure on the adolescent to begin to smoke.
Conformity pressures and peer influence are very
strong in early adolescence. Therefore, if smoking were
considered a behavior which was adopted by the majority of
adolescents, experimentationn and Initiation might occur because
of the Importance of conformity in this age period (63).
Unfortunately, there are suggestions that most adolescents
tend to overestimate the proportion of their peers who are
smokers. Eighty-two percent of all girls surveyed in the
1975 American Cancer Society Survey thought of adolescents
as smokers rather than nonsmokers (203). In that same
survey, the professions of teachers, executives, housewives,
and feminist leaders were all characterized as smokers by
approximately two-thirds of girls, with only doctors and
athletes considered nonsmokers.
Heterosexual peer considerations may also be important.
Girl smokers are very likely to have boyfriends who also
smoke (72 percent), compared with nonsmoking girls (27
percent) (203). Similar percentages apply to the fraction of
all male friends who smoke (69 percent for girl smokers and
32 percent for nonsmokers). Yet girls are less likely than
boys to see smoking as a social asset (37 percent versus 55
percent) and they even consider it a drawback (52 percent
girls versus. 31 percent boys).
The kinds of Images projected by the people shown in
cigarette advertisements may support to peer influences to
smoke. Girl smokers characterized such peopleas attractive
(69 percent), enjoying themselves (66 percent), well-dressed
(66 percent), sexy (54 percent), young (50 percent), and
healthy (49 percent).
Prevention efforts aimed at making actual statistics on
smoking prevalence available to teens in order to correct the
above beliefs may help counter the advertising. Popular
personages in various professions and lifestyles which girls
mistakenly perceive as smoker-dominated could be recruited in
this effort.
333 -
I
I
9
d
f
s
v"!
With each increase In age group, the proportion of boys
who initiated smoking became smaller, so that boys who
reached age 17 or 18 as nonsmokers were not likely to start
in the next five years. Only 15.4 percent did so, compared
with 19.3 percent of 15 to 16 year olds, and 21.6 percent of
12 to 14 year olds. For girls, the pattern is less clear.
Fifteenn to 16 year old nonsmokers in 1974 showed the
greatest proportion of initiators (27.1 percent) by 1979. In
the 12 to 144 age group, 22.8 percent took up smoking, and
only 14.7 percent In the 17 to 18 age group did so.
Demographic and psychosocial relationships studied in
1974 were reexamined in this group now aged 17 to 23. The
influence of older siblings became less powerful than the
influence of peers, but educational attainment was still
inversely correlated with smoking status.
Those smokers who had quit had a shorter lifetime
history of smoking and were lighter smokers than those who
were current smokers in 1979. Of the former smokers, 24.7
percent said they had been smoking less than daily just before
quitting, and another 34.5 percent smoked I to 14 cigarettes
per day. Only 7.6 percent of current smokers report less than daily consumption. This suggests that
the former
smokers may have been less dependent (psychologically or
physiologically)) upon.cigarettes and may have found giving up
the habit easier than heavier smokers. In fact, 50 percent of
the former smokers succeeded in quitting on their first
attempt, while 61.6 percent of current smokers had made one
or more unsuccessful attempts to quit. These young smokers were concernedd about health
issues. Sixty percent of current smokers had made at least
one attempt, and another 20 percent would have beenn willing
to quit if there was an easy way to do so. A greater per-
centage of young women than men (91.0 percent and 85.2
percent, respectively) expressed a concern about health
effects of smoking. The risk associated withh oral contra-
ceptive use and smoking and the harmful effects on the fetus
or by smoking during pregnancy (122) may be responsible for
this increased concern. Young women were more likely than
young men to say that all cigarettes are equally hazardous
(33.7 percent and 25.9 percent, respectively).
Multiple regression analysis was used to Identify those
adolescents most likely to take up smoking and discriminantt
function analyses were used to predict future smoking for
each stage- -nonsmoker, experimenter, regular smoker, and ex-
337
cent of smokers) "strongly or mildly agreed" that smoking is
harmful to health (122). Percentages were similar for boys
and girls, and nonsmokers scored higher on, all heatth-related,
questions than smokers. Almost ninety percent of adolescent
smokers (87.9 percent of boys and 89.9 percent of girls)
"strongty or mildly agreed" with the statement, "I believe the
heaithinformation. about smoking is true." Fishbein has
pointed out, however, the potential importance of the
difference between strong and mild agreement with such
statements, and the lack of direct personal attribution involved
(63). Only 60 to 65 percent of adolescent smokers expressed
strong agreement, compared with. approximately 80 percent of
nonsmokers. Either reduction of cognitive dissonance by
denial or actual lack of information may underliethis
response pattern. Finally, a surprisingly high percentage of
smokers feel (strongly or mildly agree) that it is all right to
smoke if "you donft smoke too many." On this item, fewer
girls (25.6 percent) were willing to endorse this statement
than boys (43.3 percent).
Somewhat lower estimates of the acceptance of health
Information comes from the 1975 .American Cancer Society
Survey (ACS) (203). Of all adolescent girls 74 percentt agree
that smoking is as harmful for women as it is for men;
7lpercent agree that smoking is harmful for young people as
well as for older people; 56 percent agree that It is not safe
to smoke low "tar" cigarettes; and 56 percent agree that
smoking is as addictive as Illegal drugs. Comparable figures
are not provided for boys, nor are the data broken down by
smoking and nonsmoking categories. This survey further
reports that 68 percent of the girl sample was not warned
about smoking by their doctors.
While 60 percent of girl smokers began to smoke
before the age of 13, only 48 percent attended an anti-
smoking education program in school, and a mere 4 percent
attended such a program. In thesixthe grade when they were
approximately 12 years old.
These statistics suggest that smoking education and
coping strategies should begin earlier in schools and should
begin earliest for high risk groups.
Research goafs. The best evidence suggests that female
cigarette smoking rates are declining. This change has
occurred in more recent adolescent cohorts- -thoseborn after
1962. National surveys are likely to underestimate true rates
339
0
smoker. The best predictor of future smoking behavior was
the adolescenNs own perception of his or her future smoking
behavior.
The best predictors of future smoking for never-
smokers and experimenters were smoking by an older sibling,
scores on attitude scales, and age. The chance thatt a
nonsmoker will start smoking become smaller as the nonsmoker
grows older. Oncereguiar smoking was initiated, the
variables of higher dosage, lower educational aspirations,
friends who smoked, and lack of acceptance of the health
risks of smoking predicted continued smoking behavior.
In summary, this study revealed that former smokers
seemedd more similar to experimenters than too regular smokers.
Their smoking histories were shorter, had a lower dosage and
did not have much difficulty quitting. Regular smokers, on
the other hand, tried to qpit or expressed an interest in doing
so, andd were bothered by the health hazards associated with
smoking. Five years previously, they were able to accurately
predict their current smoking status. Smoking was also more
likely to be a behavior of their older siblings and peers. And
lastly, both educational aspirations and attainments were lower
for this group.
PREVENTION OF SMOKING AND CONSIDERATIONS FOR FUTURE
RESEARCH
Prevention of the Initiation of smoking . There are a number
of ongoing interventions which attempt to prevent the
Initiat.ion of sm oking (see 34, 59, 60, 119, 186). These
studies are directed at elementary, junior high, and high
school students, and use an ninnocuiation" approach to
prevention. Exposure to a small amount of information about
pressures to smoke Is accompanied by practice In coping and
assertiveness strategies. The main types of influences in
which students are instructedd are peer pressures, parental
modelling, and media pressures. Peer instructors are often
used to maximize influence. Compliance In self-reporting
smoking behavior Is increased by the use of physiotogicalmeasures of smoking, for example, salivary
nicotine or expired
air carbon monoxide, which may or may not be analyzed for
thee entiree subject sample.
Dissemination of Information about the health risks of
smoking seems to be successful, at least on a superficiall
level. Ninety-six percent of all adolescents (and 91.6 per-
s
338 ~
account for the difficulties many individuals experience when
they try to quit smoking (186).
Nicotine. Nicotine is absorbed rapidly from the oral and
intestinal mucosa, lungs, and skin. It is distributed
throughout the body and is metabolized by several organs,
including the liver. It is thenrapidiy cleared, primarily
through the kidney. Nlcotine has effects on several organ
systems, Including the autonomic nervous -system, voluntary
muscles, stomach, intestines, heart, and brain. Most of the
pharmacological actions of nicotine are thought.to result from
Its Interaction with receptors of choiinergic nervous systems.
Analysis of the physiological effects of nicotine is
complicated by the abundance of those effects. Many organs
receive input from several neuronal systems which are altered
directly or indirectly by cholinergic activity. Furthermore,
the effects of nicotine itself depend both on the dose and on
the tim ecourse of drug administration: brief exposure or
low doses cause excitation of cholinergic systems,whlle long
exposure and high doses result In inhibition and paralysis.
Peripheral Effects. Nicotine produces a variety of
changes in the autonomic nervous system due to simultaneous
effects on both sympathetic and parasympathetic systems. The
end result is an increased heart rate and blood pressure;
cold, clammy skin; increased acid production in the stomach;
increased intestinal activity; and biphasic changes In
salivation, with an initial increase follo wed by a decrease.
Nicotine also increases respiration. Central Effects. Nicotine produces tremors and causes
water retention by a central effect on antidiuretic hormone
release. Nicotine-induced nausea and vomiting reflect a
complex interaction between central and peripheral effects.
To date, no specific effects on complex emotions andd beha-
viors have been demonstrated. Animals will self-administer
nicotine under certain circumstances, indicating that it may
have pleasurable effects.
A Possible Role for Nicotine in Smoking Maintenance. A
strong argument has been made for classifying smoking as an
addiction,with nicotine as the leading candidate for the
347
10.3 percent and 7.2 percent of men, respectively, but by less
than 0.5 percent of women. Only 1 percent of women use
snuff or chewing tobacco compared with 3 percent and 5
percent of men, respectively.
m
A
5 moking prevalence and ethnicity. The prevalence of smoking
In the population varies not only with age, sex, and
socioeconomic status, but also with race and cultural
background.
Table 7 presents smoking prevalence among white and
black adults from 1965 to 1978 (186, 187). Smoking has
declined among men of both races, but prevalence has
decreased only slightly among white and black females.
Congruent estimates of prevalence and lower cessation rates
among blacks have been obtained in other studies,
(66,174,190).
Despite their greater prevalence of smoking, black men
and women smoke fewer cigarettes per day than whites
(66,174).
Black women may suffer the worst aspects of sexism
and racism with respect to occupational opportunity and
financiaieompensation. Cigarette smoking may be related to
assertion, independence, andrebeiiion or to identification with
behavioral patterns of black males. Adolescent dynamics have
been studied more than those of adults (see adolescent Section
I). Warnecke et al., found that sociail and psychological
correlates among black women are similar to those observed
among white women (190).
Friedman, et al. examined smoking prevalence among
Oriental menn and women- -Chinese, Japanese, Korean or
unknown from the Kaiser Permanent Health Plan and found a
smaller percentage of cigarette smokers than among whites or
blacks. Asian women had the least frequency of current,
established cigarette smokers--23.1 percent- -compared to
39.2 percent of white women and 42.1 percent of black
women. Asian were also the least likely to inhaie among
most age-sexx groups of smokers. There were fewer cigarette
smokers among Chinese than among Japanese; this was
particularly true for women and younger men.
Pharmacological Effects of S moking.
One or more of the constitutents of cigarette smoke may play
a role In the maintenance of smoking behavior and help
345
I
brain; but by Inhalation, the delivery tim e is 7.5 seconds
(149)~ The plasma half-life of nicotine is approximately 30
minutes, and the pack-a-day smoker lights up approximately
every 30 to 40 minutes of the day. This suggests that the
smoker Is attempting to maintain a constant level of nicotine.
The nature of the reinforcing effect Is so m etim es
described as an alteration of arousal. Stimulation may be
subjectively experienced as increased alertness, a facilitation
of concentration, or an aid to continued efficient performancee
in fatiguing tasks. Sedation, on the other hand, may be
experienced as a tranquilizing or calming effect or as a
reduction of some dysphoric state, such as anger. Smoking
has been described as distinctly pleasurable following a meal
or accompanying xanthines (coffee and tea) or alcohol.
Pharmacologic and psychologic components to these subjective
reports are beginning to be identified (76, 69).
There is an' extensive literature describing acute and
chronic nicotine administration in animals including a limited
number of seif-administration models. Tolerance to nicotine
has also been described (108, 79, 84).
A number of studies have examined the hypothesis that
hum ans self-administer tobacco in order to obtain nicotine.
Studies have also examined compensatory adjustments In the
number of cigarettes and manner of smoking by subjects In
response to experimenter-Induced increases or decreases in
cigarette nicotine content, cigarette size, availability, or
supplemental nicotine administration. Chewing gum containing
nicotine, nicotine tablets, intravenous nicotine and central or
peripheral nicotinic blocking agents have been used to
supplement or block the effects of the nicotine absorbed from
the smoke. A titration effect is said to occur If subjects
change their cigarette sm oke intake In the appropriate
direction in response to these experim ental manipulations.
A modest amountt of compensation has usually been
demonstrated (149, 77). Smokers seem to titrate smoking by
the nicotine, rather than the tar. Experim ents Involving the
Intravenous administration of nicotine have been Inconclusive
with both positive and negative effects on the suppression of
subsequent smoking having been observed.
When compensation occurs, it Is seldom complete. This
may be due to a number of factors: (1), the Inability to
accurately measure the smoke and/or nicotine dose delivered
to the subject; (2) technical problems in experimental design
(77, 186); (3) secondary reinforcing effects of smoking which
mask titration; and (4) the fact that people may smoke for
reasons other than regulation of nicotine level.
I
349:
addictive agent (124). Inhalation of cigarette smoke offers
an effective way to administer nicotine. Absorbed rapidly, it
travels as a highly concentrated bolus through the heart and
directly to the brain and is then rapidly cleared. A smoker
who smokes one pack per day can average around 70,000 such
nicotine "inJections" per year. In behavioral terms, smoking
has many potential conditioned stimuli, ranging from the taste,
sight, and feel of the cigarette itself, to the many social
settings in which smoking takes place. If nicotine were a
strong unconditioned stimulus, particularly when inhaled, then
It would be easily understandable that smoking can become a
rem arkably persistent habit through connection of this
unconditioned stimulus with the many associated stimuli.
Direct proof for nicotine as an addictive agent remains
scant. Recent studies do demonstrate that some animals can
be induced to self-administer nicotine In carefully controlled
settings. Depending upon the conditions selected, this self-
administration can be either a negative or a positive stimulus
to the animals. Studies of humans have shown that smokers
will modulate their cigarette Intake slightly to aiter serum
nicotine concentrations, particularly when levels get too high.
These studies failed to show that Intravenous in'yections of
nicotine have pronounced effects on reducing smoking,
suggesting that nicotine is not the only Important factor.
Some havesuggested that nicotine controls smoking behavior
only at the extremes, and then as an aversive agent (153).
Too much smoking might lead to such high serum.
concentrations of nicotine that toxic effects encourage lower
Intake; and too little smoking or smoking of low-nicotlne
cigarettes could lead to such low concentrations that
withdra wal side effects encourage resumption of smoking.
This hypothesis states that, between those two extremes, other
factors such as psychological and social pressures are far
more influentialin determining smoking patterns.
Although nicotine has effects on essentially all major
organs In the body, including the brain, the role of those
actions in maintaining the smoking habit remains an Important
but unresolved area of research.
The nicotine hypothesis of smoking Is that the phar-
macologlcal actions of nicotine are "reinforcing." The most
likely site of this re warding or reinforcing action Is the
brain, with the precise locus of reinforcement not yet
determined. Inhaling smoke insures rapid delivery of nicotine
to the brain. It takes approximately 13.5 seconds for an
intravenous in(ection of nicotine in the arm to reach the
348
TAHLE 6.-Estimates of the percentage of current, regular cigarette smokers
who tonsume more than one pack per day, adults, United $tates, 1V55-1976,
Supplement to furrent Health Intervlew - National Clearingheuse
Population Survey Survey for Smoking and Health
(TI yrs. and aver) ' (17 yrs. and over) (21 yrs. and over)
21 cigarett es or 25 5lgarettes or 75 cigarettes or _
morc dai ly mo[e d.11Y merc dally
Year Total -Mal e Female Total Male Female Total Male Female
r
r
1955 20.21 25. 5 9.8
1964 25.7 32.4 17.7
1965 19.9 24.5 13.7
7966 21.6 26. 3 . 15.7 27.2 34.7 16.0
1967 21.9 26. 2 . 16.3
1968 22.4 26.5 16.9
1970 23.3 27.6 1R.t 25.? 31.1 17.1
1974 24.72 30.3 19.4
1975 30.1 36.n . 22.8
1976
25.33 30.8 19.4
118 years and uver. .
2llata prevld<d by Health interview 5urvey, National Center for Health Statistlcs.
320 years and over.
SOURCE: USDHEW, 1979, Appendla.
v4zsgsco
basis of this assertion lies partially in the demographic
analyses of cessation rates and partially in the literature on
smoking cessation clinics and experimental programs.
This section presents the results of both demographic
and experim ental analyses of sm oking cessation. A critical
appraisal is made of the relative success of men and women
in giving up smoking and in remaining ex-smokers.
Psychosocial and behavioral factors relating to abstinence and
difficulties encountered in quitting are discussed. Finally,
recommendations are presented for treatment and future
research.
Demographics
The quitting rates of sm okers arecalcuiated by dividing the
number of former smokers by the number of ever smokers
within each relevant demographic category. The statistics are
taken from the 1975 USDHEW survey on Adult Use of Tobacco
(182). Former smokers are defined as those who once
smoked but no longer do so. The term "former smokers"
includes both those who have quit on their own and those who
have received outside help. Quitting rates of womenn lag
behind those of men, for each category reviewed.
Age
The USDHEW tables divide adult age groups into six
categories: ages 21 to 24, 25 to 34, 35 to 44, 45 to 54,
55 to 64, and 65 and over (182). There is a trend toward
increasingly larger percentages of former smokers in each
successive age group. For both men and women, ho wever,
within each age group, the percentage of smokers who havequit is higher for men than It is for
women. For example, in
the youngest age category, the percentage of female smokers
who have quit is 22.6 percent while that for males is 27.9
percent. For a middle-aged category (45 to 54), the female
and male percentages are 32.0 percent and 46.7 percent
respectively. In the oldest age group, 51 percent of female
ever smokers are former smokers, whereas the percentage is
60 percent for males. Bosse and Rose state that the sex
differences in quitting are vanishing at younger ages, but
Dicken argues persuasively that the absolute amount of
convergence is small, and that mem remain substantially more
likely to stop smoking thann women (121, 146):.
354
TABLE 10 -Physician advice- Smoking cessation treatment results by sex.
E_ndot-Treatment Six Month; Long Term
Studv Treatment N 1%1 1%I (%I
1. Burns, 1969 M.D. advice to resp. dis. pts. 66M
- --- -28F
2 Handel, 1973 Antismoking message in 45M
'a med. e.am 55F
.~
M' 3. Burnum.1974 M.D.advlce 84M 29M
- 40W 18F
4. Baricetal.,1976t M.D.advice
Isponto quittersl
. lintervention)
(controi) -
5. Donovan,19371 M.D.advice
1 p <0.05
tPregnancy intervention studies
srYzssseo
134F;
24 83
63 14
47 14
552F 50% reduction
33M> I (3 mo.l
~F > 1 (12 mo./
demographic data showing higher proportions of ex-smokers
among males than females (57). Men were significantly more
likely than women to remain successful abstainers. Men and
women made approximately the same number of attempts to
quit, and current smokers made more attempts than former
smokers (158). Furtherm ore, successful quitters have usually
made at least one abortive attempt to quit before succeeding.
A survey of young women, aged 18 to 35, revealed that light
smokers had the greatest success in stopping smoking (203).
Those factors which consistently see m to differentiate
between those who can quit or reduce intake and those who
cannot, are the presence of strong motivation and commitment
to change, the use of behavioral techniques, and the availa-
bility of social support. Those who successfully quit or
reduce smoking use behavioral techniques such as substituting
candy and gum for cigarettes, and so.ne form of self-
reinforcement of desirable behaviors to maintaln abstinence
(203, 134). Successful reducers use behavioral techniques
m ore. consistently and for a longer period of tim e than those
who fail to reduce smoking (134). Successful quitters
experience cravings when they stop, but the use of substitutes
seems partially to alleviate thesefeeiings (133).
Furthermore, those smokers who do reduce Intake are more
motivated and committed to personal change (134), and long-
term abstainers have niore confidence in their ability to
remain ex-sm okers (57). Successful reducers receive more
positive reinforcement from others and the best known
acquaintances of successful abstainers are former smokers
(134, 57). Warnecke, reported fe male relatives to be the
primary role models for women who quit smoking (190).
Treatment Studies
Most smokers who attempt to quit do not seek outside help to
stop smoking. The population that seeks treatment may be
one thatt experiences severe difficulty in giving up smoking.
Thirty-nine treatm ent studies on sm oking have reported suc-
cess rates for males and females, and have used the cri-
terion of total abstinence, or 90 to 100 percent reduction to
define a successful result.
The studies reviewed here fall into five categories of
treatment:: education, physic ian advice, pharmacotherapy,
psychotherapy, and behavior modification (Tables 9-13). The
356
i
and wom en had a greater desireto smoke in stress-inducing
situations. However, men rated the desire to smoKe
significantly higher than did women on all three of the
questions representing low-arousal situations, whereas women
rated the desire to smoke significantly higher on only one of
the three questions representing the high-arousal extrem e of
the. continuum (68).
Using Frith's questionnaire, Barnes & Fishlinsky were
unable to replicate his findings inn a sample of Canadian
undergraduates (13). Within the male sample, there was no
significant relationship between desire to smoke and the
arousal value of the situation in the question, and female
subjects indicated a greater desire to sm oke in the low-
arousal situations. The authors point out the possible
importance of sampling differences.
Elgerot studied light, medium, and heavy smokers in an
attempt to control potential differences In inhalation patterns
between men and women (cited by Frith as a possible
explanation for his results) (58). Subjects were Swedish
university students. The 42 -item questionnaire was similar,
but not Identical, to Frith's. There was no gender difference
for low-arousal situations. There was no sex difference in
the light and medium smoker subgroups, but women In the
heavy smokers subgroup expressed a greater desire to smoke
in stress-inducing circumstances.
Russell and his colleagues devised a 34 -item
questionnaire covering a wide variety of smoking motives. It
was administered to 175 normal smokers and then subjected to
factor analysis (150).. Six factors, representing sixx types of
smoking, wereidentified.Womene scored significantly lower on
what was termed "sensorlmotor" smoking, and significantly
higher on "sedative" smoking. Thus, the sex difference on
sedative smoking (reduction of arousal) was supported.
Ikard and Tomkins (93) found evidence that women
smoke in situations involving negative affect. Negative affect
smoking i.s defined as smoking which serves to reduce
unpleasant feelings. It includes smoking to reduce the
dysphoric feelings accompanying rejection by a social group as
well as sm oking to satisfy a craving for a cigarette (i.e., aa
deprivation negative affect). Positive affect smoking involves
the arousal of pleasant feelings. For example, smoking from
curiosity would be classified this way because of the feelings
of excitem ent and interest generated. Ikard and Tomkins
sho wed two films, one intended to evoke positive affect (aa
slapstick com edy); and another, to evoke negative affect (a
I
0
0
351
TABLE 12.-Psychotherapy-Smoking cessation treatment results by sex,
Percent Abstinence
' Endo_f-Treatment SixMonths LongTerm
Study Treatmec[ N - 1%), (%) i%)
."I
sL-IzsSsc o
83M
53Fn
11M
12F
BM
12F (12 1
O 2. Mann and Jaois, 1968 Emotional rolepiaying 26F 23di0F (18 mo.l'
- 3 Strelqer and Koch, 1968 Emm'ional rolepiaying 30F OF 14 wks. possl
4 Lichtenstein et aL, 1969 Emotional roleplaying 54F 9F I1-5 wks. post)
1. Moses,1964 Hypnosis,dlscussion 35M
w 15F
~
5 FeeandBenson,1971 Group therapy 306M 56M
204F 38F> 1
6. Bozzetti,1972 Grouptherapy . 7M 57M
7F 43E
7. Tamerin,1972 Grouptherapy 16F 69F
1 p<0 05 'y reduction in smoking
20.05< p<0.1
19F>1 (6-12 mo.)
85M (12 mo.)
57F
TABLE 11 -Pharmacotherapy-Smoking cessation treatment results by sex.
Study
i. Tome,1958'
2. Whiteheadand
Daeies. 1964
3. Wdnelmsen,1966
4. Wenerpvist, 1971
'
1914'
5. Arvldsson,1911'
6. Merry and Preston,
1963'
1. Golledge, 1965'
8. Ross, 1967'
9. Schaubleetal_
196W'
19]T
1nC0.05
Lazsssc 0
Treatment
N Endo_IFreatment
1%1- SixMonths
1%1
Hydroxyalne 23F 4F
Methylphenidate 10M 20M
Diazepam -- 6F OF
Methylscopolamine 291 M 56M
vanpuilizer
200F >
112mo.1
41F
Methylsmmlemine 192M 50M
98F 33F_>
Ancichalinergics Graups, 50M 85M
avarslon Iherapy SOF 85F
Lobeslne 45M 29M
31 F 32F
Labeline & placebo 19M 63M
8F 73F
Lobeline ]28M 40M\ 1
Amphetamine ]45F 29 /F
Lobeline 33M 18M
Amphetamine 35F 26F
Lobeline,smphetamine 14M 57M
and eduqtlon 11F 26F
Lobeline,amphetamme 255M 43M~
288F 33F
'Results based only on those Completing tre9tment or conract<d for lollow-up_
LnngTerm
f%I
OM 112 mo.l
12F 112 mo'I 5E /EO mo'1
48M 1112mo,1
22F ~
21M - 1110-51wks.1
12F /
22.OM
13.5F
1 (60...)
TABLE 9 -Education-Smoking cessation treatment results by sex.
Study
Treatment
N EndofTreatment
1%! Six Months
I%) Long Term
I%1
1. Guilford, 1967" FtveEay Plan' unaided 75M 23M
- - - - - --- 100F 12F?\ 2
Aid
d
e 82M
91F 27M\
29F/I
2. Peterspn el al., 1968'-' Fiv¢Cav Plan 134 M&F 79 M&F 19M (18 mo. follow-up
19F on 121 Ss)
3 Berglund, 1969" Fivetav Plan 895 M&F 87M 32M
84f 27F~2 23F>1 14-18 ma.)
W
~
V 4. Delarue, 1973 Educauon, small groups 472 M&F 34M (12 mo.l
41F
S. Danaher et al., 1978t Eduration; skill training group 11 F 50 (of 8 Ss finishing 50 (9 mo.l
treatment
6. Ochsner & Damrau, 1970 Pamphlete' 20M 85M
33F 52F>1
7
Pyszka et al
1973' Amerlcan Cancer Society Clinics 131M 39 M&F
28M
.,
.
. . . .. .. ..... .. . . . (18mo
1
223F .
20F
8. Kanzler et al., 1976 Smokendens 210M 70M
343F 69F 30 F> 148 moJ
9. Dubren,1977' T.V.spots 92M 15M
218F 7F~>1
-
1pG005 Success =90400%reducuon in smaking_
''
2005 p< 0.10 Results based only on those completing veatment or c_o_ ntaqed for follow-up.
tPreqnancy intervention study
st3z~:sseo
BreatF Eolding,awverant
nintrol,negatrve practice,
aLLentiOn piacEbo
Negative practice or selLcontrol 5QF Neg3bve practicean0 aelf: -
control
Comrol
NonsPeciiro treatment
Elecir.cskock aversion
Electric shock, seW
m9nagcment] pOsltreatment
teerepls[ monitoring. 2 weeks ~ 4M
BF
1lwecks+ 4M
)F
Elearicsoekaversloq . 66M
-aglneA n. reai smokrng 32F
Electrs shock and eontrols 2$M
28F
' Resu/ts based unlY on those completing treatment
"Percent reduRion, little (er F; more for M in imaginetl smoking condition
tTwo weeks post treatment
seszs?9Eo
been told by a physician that it was permissable to continue
smoking quit.
The prospective treatm ent literature yields varying
estimates of the impact of physician advice. Ten to 25 per-
cent of patients advised by a physician to quit or cut down
actually do so (186). Gender does not seem~to exert a par-
ticular influence (55):. The prim ary variables associated with
the ability to quit after physician admonition were good
psychosocial assets, psychological stability, and the ability to
verbalizedepression (55). Success in treatm ent in general seems to relate to
personal characteristics. A shorter sm oking history and lower
cigarette consumption also predict a greater likelihood of
cessation (138, 102, 184).. In addition, those subjects most
likely to succeed in treatm ent are highly motivated, believe
they will succeed', and are confident of their ability to stop
smoking (130, 176, 80).
One group of women that seems to have great
difficulty in giving up smoking in treatment is homemakers.
Homemakers in theage range of 18 to 35 tend to be heavy
smokers and heavy smoking Is one predictor of failure in
treatment (203). Kanzler, et al. found that homemakers were
less successfull at quitting, particularly at long-term follow-
up (102). However, as previously discussed, since homemakers
have quit rates in the mid-rangeof those of women in other
occupations, therefore the difference may apply only to those
homemakers who seek help through treatment programs.
Wilhelmsen found significant male/female differences in
treatment success rates and stated that the poorer per-
formance of women related almost exclusively to the unsuc-
cessful results of homemakers (196). These women explained
that cigarettes served as companions and they reported the
difficulties of being without adult company all day and of
being deprived of outside activities as obstacles to giving up
smoking. Cigarettes have also been described as a means of
temporally partitioning the day, of achieving physical'l autonomy
from children, and of providing role differentiation (72).
Frieze, et al. reported wom en face more life stress
than men and have more symptoms of psychological distress
(67). Waters reports thatt women show more overt signs of
neuroticism than men (192). Furthermore, he finds an asso-
ciation in women between degree of neuroticism and amount
smoked. Burns also found that female smokers had higher
neuroticism scores than did female nonsmokers. No such dif-
ferences were found in men (30).
363
a
G
D
n
L
9
U
k
h
a
suggested that m en and wom en differ in the severity of
smoking withdrawal' symptoms. However, Shiffman analyzed
Guilford's ra w data, and stated that 15 of the 18 m ajor
symptoms reported by subjects demonstrate sex differences
(164, 80). Thirteen of those 15 symptoms were more fre-
quently reported by women. Other studies show similar,
although not statistically significant, trends (179, 135, 202).
Factors contributing to relapse, such as craving and
nervousness, were reported to be. similar for men and women
(179). W6men who experienced the greatest craving during
the initial five days of abstinence were most likely to
relapse (80). Since women score higher than men on
m easures of anxiety as a general rule, it is possible that they
would be more susceptible to relapse if smoking had been
their custo mary m eans of reducing such dysphoria (164).
Women may also pay more attention to somatic symptoms than
men, as they make more frequent use of all health care ser-
vices, specifically for headache and weight gain (110).
It Is likely that the abstinence syndrome is a major
factor in recidivism during the first fe w weeks of cessation
when relapse Is most common and that the number of
cigarettes smoked per day is an important variable in
determining the severity of the withdrawal (91). The issue of
a gender difference in withdrawal severity is a major area
where research is needed. -
Treatment Recom mendations
Perri, et al. recommend that smoking cessation programs with
a behavioral emphasis be comprehensive, multlfaceted,long-
term, and that they Include self-reinforcement and problem-
solving procedures (134). Given thedifficulty for som e
women in simultaneously dieting and attempting to quite
smoking, smoking withdrawal programs should adopt a total
approach to health including advice on dieting, exercise and
the immediate benefits of abstlnence (144).
Marlatt and Gordon write that relapse potential is
greater for individuals whose daily schedule fails to include
some rewarding or pleasurable activity (114). It would
appear use:ful to attend to this issue in smoking treatment
programs.
A social support hypothesis is frequently cited in the
treatm ent literature to explain gender differences in quitting.
It is often suggested that wom en do better than men in
U
365 '
categorization is, by necessity, only a rough separation of
treatment modalities. Evaluation of the gender difference
question, however, does not rest directly on the categorization
schema.
Many of the studies listed in the tables did not report
significance evaluations for male/female quitting rates.
Therefore, a chi square statistic or Fisher exact probability
test was calculated wherever sufficient data were available.
Because of the limited number of studiesidentified', for
analysis and the often limited sample size, results of
borderline (0.05 < p < 0.10)) and acceptable (p < 0.05) levels
of significance are reported for the reader's Information.
The end-of-treatment cessation rates are high for all
types of treatment, but the maintenance of cessation tends
much lower. In 1971, Hunt, et al. demonstrated that
recidivism curves of heroin, alcohol, and sm oking are almost
identical, with long-term cessation faliing off steeply from
the end of treatm ent(.91):. Within three months,
approxim ateiy 35 percent of successful quitters are still not
smoking, and by one year, the figure is closer to 20 percent.
In 1978, another revie wer cited virtually the same figures
(140). There have been reports of improvement In techniques
for obtaining abstinence and in maintaining it, using rapid
sm oking (an aversive conditioning technique)i, hypnosis, and
group therapy. The long-term cure rates of 60 percent or
higher at six months claimed in some studies have not been
reproducible In other settings. The smoking cessation
literature has been retently reviewed in detail (186, 78;59).
Across all treatments, women have more difficulty
giving up smoking than men bothh at tfie., end of treatment and
at iong-te.rm points of measurement. No studies have been
reported in which women do significantiy- better than men.
Several of the larger studies show higher abstinence rates by
menybut many show no difference. Results in the tables are
based primarily on those who complete treatment programs.
Attrition rates arevery difficult to evaluate because most
studies do not discuss the issue of subjects who drop out of
treatment.
Because of thee emphasis placed on theroie of physi-
cian advice in increasing smoking education and promoting
cessation, an estimate of its effectiveness is relevant. From
retrospective data, It is estimated that 35 percent of people
who have beenn advised' by a doctor either to quit (170)~.
Twenty-five percent of those who have not talked to a
physician about smoking quit,, and only 12 percent who have
362
TABLE 14.-Percent Affirmative Responses
TO STATEMENT 'Being Afraid of gaining a lot
of weight keeps people from quitting cigarettes"
SMCM(I~NG STATUS VAMEN~. (%) MEN~ (9s)
N
Cite - National Center for Health Statistics, 1975
377
Never Smoked 59.0 51.5
Formerly Smoked. 63.1 53.6
Currently Smoked - 59.9 47.3
programs which provide a maximum amount of social support,
and tend to do worse in situations where program support is
low or outside factors militate against quitting. For example,
and womenn to quitting smoking, as well as the traditionally
greater willingness of wom en to discuss affective issues, it is
not surprising that ald-female smoking- cessation groups have
been particularly attractive.
Marlatt and Gordon studied the circumstances under
which smoking relapse is most likely to occur (114). They
claim that experiencing stress in the form of aa negative
em otionaistate, social pressure, or interpersonal conflict is
likely to lead to smoking among those who are attempting to
similar process (176). The group also provides an avenue for
affective expression, so that the relevance of cigarettes to
psychosocial events and thepersonai meaning of giving them
up can be discussed. Given the differential reaction of men
45), Tamerin writes that the group . can provide support,
empathy, and shared identification with others going through a
effective for women if they are sexually homogeneous (80,
rates, but women achievedd markedly lower rates. There is
also support for the notion that groups are particularly
of support (54). Guil:ford found that when men and women
participated in group programs, success and failure rates were
the same for both sexes (80). When they did not attend
group programs, men maintained the samesuccess and failure
ticipated in a television stop smoking campaign, butt that
fewer women stopped smoking--presumably because of a lack
Dubren reports that twice as many women as men par-
group or in an individual-to-therapist setting.
do more poorly in treatments characterized by less individual
attention, such as education and pharmacotherapy, compared
with the categories of psychotherapy and behavior
modification, wherecontact is usually maximized, in a small
As the overall categories in Tables 9-13 show, women
quitting sm oking, although spousal support is important (160).
This study provides just one example of the observation that
social support seems to be of lesser consequence to men in
introverted) were less likely to quit than low-scoring women.
social situations and the presence of outgoing tendencies.
Women scoring high on this scale (shyer, m ore socially
(142). This scale measures the degree of discomfort in
Scale of the: Minnesota Multiphasic Personality Inventory
Resnikoff, et al. were able to differentiate between those
women (but not men) who did poorly in group-plus-medication
treatm ent and those who did weilusing the SociaiIntroversion
366
Some studies have shown that women who smoke are
both more subject to psychological stress and more outgoing
quently reported consequence of giving up smoking (T44).
behaviors as smoking and overeating. Weight gain is aa fre-
specifically overeating--if they stop smoking (30, 125, 4).
It Is also possible that underlying stress in wom en impedes
the strength of the determinationrequired to cease such
women that they will engage in symptom substitution--
social stress is illustrated by the fear reported by many
tension and apprehension for women (144). Thatt smoking
might indeed act as a method of coping with psychological and
cess in a smoking withdrawal program was related to lack of
likely to have good adjustment scores. Rode found that suc-
treatm ent successes among women were significantly more
not differ between male treatment successes or failures,
Furthermore, although.the degree of psychiatric adjustment did
worse psychiatric adjustment scores than did men (140).
Russell found that within the treatment group, women had
ment, and that depression was more frequent and severe
among thee women In his sample (148). In a later study,
women cited this reason (135). Russell reports that the
presence of depression was related to dropping out of treat-
Peterson, et al. found that, while 23 percent of the men who
had participated in a smoking program cited nervousness as
the principal reason for resuming smoking, 43 percent of the
shown to affect the success of women in treatment.
. The presence of psychological distress has also been
up smoking.
that thesee characteristics are related to an inability to give
forthright (143). The later authors report that women smo-
kers are also characterized by apprehension and tension, and
more independent-minded, assertive, self-opinionated and
than nonsmokers. There is evidence that women smokers are
women smokers are more extroverted and also more neurotic
scores before taking up the habit. They add that current
They found that smokers had high neuroticism and extroversion
traits In young wom en before the onset of smoking (.31).
women and smoking, Cherry and Kiernan measured personality
than women who do not smoke. In a prospective study on
The Smoking Withdrawal Syndrome
Few of the studies reviewed here mentioned gender as a
factor in connection with withdrawal symptoms, and none
364
40 percent of the adult male population from smoking regu-
larly. Seventy to 80 percent of these sm okers agree that
cigarette smoking is harmful, Is a health hazard that requires
action, and causes disease and death (182). Former smokers
and nonsmokers take a much stronger stand on these three
points, ranging from 87 to 96 percent agreem ent. Gender
differences are very slight..
The value placed on health compared to other positive
life goals was slightly lower for smokers than nonsmokers,
and highest for ex-smokers (197). Out of a maximum factor
score of six, current smokers averaged 4.66 (M = 4.55, F =
4.81), and nonsmokers averaged 4.82 (M = 4.68, F = 4.9)
and ex-sm,okers averaged 4.89 (M = 4.78, F= 5.06):. The
higher scores of women support their traditional concern with
health in our culture but they are incongruent with recentt
smoking trends (J1o),
Fewer current smokers than nonsmokers and ex-smokers
report having personally known someone with coronary heart
disease, lung cancer or emphysemalchronic bronchitis. This
finding m ay be attributable to a process of denial. Only
about one-third of current smokers admitted knowing someone
personally whose "health^ was adversely affected by smoking
while over 60 percent of nonsmokers knew such a person.
Clearly, mechanisms must be operating in smokers to reduce
cognitive dissonance caused by their behavior and their
knowledge of the health consequences of their behavior. One
of these mechanisms may be to deny that the health problems
of others are connected to smoking. Women in our society are more Involved with health care services
(110). They arrange for health care services
and act as role-models for children. -
Sources of Information.
There are a variety of ways that people can learn about the
health. consequences of tobacco use. The information gathered
from and effects of tobacco company advertlsing will be
discussed separately below. The m ajor sources of inform ation
fall into a number of categories.
Health Care Providers. The Influence of physicians and nurses .
as communicators of information and as exemplars of healthy -, .
life styles has been the subject of much research (186). The .,
greater concern about health among women and their greater .
368
n n
------------- -- -----
T 1 {Y ~ T C M(0 ~ 9 N. ~ y~ R. S
TABLE 15 Smoking habits of male and female physicians in selected countries.
Percent Smokers
Pop. Pop. Pop.
Author Country N Never Est. Current Est. Former Est.
1. Bourke, 1972 Ireland M 1359 17.9 19.7' 48.5 67.6' 33.6 12.7'
F 221 51.5 53.9 26.7 38.6' 22.2 7.5'
2. Vuo.l et al., 1971 Finland M 843 38 34 60 27
W - - F 66 26 20 8
V
`-D 3 Wilnelmsen&Eaith-EII,1974 Sweden 7 33 38 29
54 27 19
4. Aaro et al., 1977 Nonway M 740 35.3 53' 371
F 398 21.7 36' 381
5. Westling-Wlkstrandetal.,19]0 USA F 81 42 358 13.6
6. Greenwald ei al., 19712 USA M 3990 323 24 433
F 3990 . 353 36 273
271A
201'
7. USDHEW,1976b USA M 36574 21 39 641 431
341
'$iqmhcant dlfferenc2 between percenta9es paired by
1Smppin9 rate= former smoker
ever smoker. 2Sample consisted of phyndans and their wives whose se profession n was u_ ndefine_d.
3Percen[ages esnmated from graph, not specified in tevt. --- - -4Apprn.imate tosxl of M&F, estimased
to be 93% male.
4oCssseo
er
e
jre
In
e
lof
re
he
l m
ve
~ a
5)
to
~nt
~e n
re
;na rd
~ in
by
of
had
'the
oup
Jes.
rith
)ver
flgh
this
to
;nce
the
:nce
erns
ping
mechanism--a means of reducing negative affect--then it Is
understandable that female physicians, or any other
professional with elevated stress levels, would have higher
current smoking rates than the generaipopulace. It is also
understandable that they might experience more difficulty In
quitting
Psychologists. A survey of psychologists in California state
universities and colleges found that women psychologists were
much more likely to smoke than their male colleagues (47).
The rate of smoking was slightly higher than in male health
professionals, and approxim ately the same for women
psychologists (38 percent) and nurses (183) (see Table 16).
This smoking rate is significantly above the rate among
professional women in general (25.6 percent) and was due to
lower cessation rates among wom en psychologists rather than
higher Initiation rates. The most common reasons given for
smoking are the stress of work or school, and personal stress.
Frieze, et al. state that professional women have to exhibit
"male-like" characterlstics in order to survive In their jobs,
but that these characteristics are often m et with criticism
and hostility (67). Thus, social and occupational demands are
at odds with each other. Furthermore, there is evidence that
female psychologists face very real sex discrimination in the
evaluation of their work.
Dicken and Bryson (47) report a high degree of power
fantasies among women psychologists who smoke. This sup-
ports Fisher's finding thatt wom en sm okers in general seem
preoccupied with the issue of power (64). He speculates that
cigarettes are. used defensively against feelings of
powerlessness, weakness, and inferiority.
Elevated suicide rates are another correlate to the
evidence of excessive stress and difficulty in coping
experienced by some femaieprofessionals. These higher
rates, compared with the general female population, have been
observed among women psychologists, chemists, and physicians
(118, 173). Factors such as ambivalence about success, role
conflict and marginality were offered as dynamics. However,
it is not possible to determine whether these higher suicide
rates are due to the self-selectionn of suicide-prone wom en
into these and possibly other professions, or to the
difficulties encountered in professional training and practice
(.or to an interaction of both).
Nurses. A number of studies have shown a higher rate of
smoking among nurses than in the general female population in
381
contact with health professionals, provides an obvious avenue
of intervention(110). Health professionals should be
continuously reminded of their potential impact and advised to
use it to influence women to reduce smoking. Physicians are
considered the most authoritative source, with the greatest
potential for influencing patient behavior.
From the self-report of adults, physicians are not
delivering enough anti-sm oking Information and advice. In
1975, a full 64.6 percent of male and 60.8 percent of female
current sm okers claim ed that they had never received advice
from any doctor about quitting, cutting down, or continuing
smoking (182). About 19 percent of male and 21 percent of
current female smokers had been advised to quit. Combining
advice to quit and/or cut down, the: percentages rose to 34.8
percent of men and 37.7 percent of women. In 1970, the
percentages of men and women who reported such advice were
30.2 percent and 34 percent, respectively (181). A somewhat
lower estim ate of physician advice was obtained from an
ongoing nation wide study involving approximately 8,000 people(175). Advice to quit or cut down was
reported by 22.4
percent of the subjects, and lack of advice by 77.6 percent;
there were no significantt gender differences. A survey of physicians' opinions about smoking and
health In the mid-1960s revealed that 38 percent claimed
they advised "all" or "almost all" (95 to 100 percent) of
their patients who did not have sm oking-related disorders to
quit or cut down (74). Eighty-eight percent, of physicians
claim ed. they gave such advice to patients with lung andd
pulmonary conditions.-
Nurses spend more time in direct patient contact than
do physicians and can exert a major role in delivering
inform ation as well as serving as exemplars. Most nurses are
aware of this responsibility (73, 61, 129, 183). Only 10
percent of nurses claimed to discuss smoking and health with
"almost alle or "most" (65 to 99 percent) of their patients
or students (129). Another 21.5 percentt claimed to have
discussed it with 35 to 64percent of patients or students.
Only 50 percent of current smokers, compared to 65 percent
each of former smokers and nonsmokers, suggested stopping to
5 percent or more of their patients and students.
While the identical question was not asked of nurses in
the 1975 survey, a number of valuable questions relating to
exemplar status were posed (184). In almost every case,
current smokers took the weakest position on exemplar role,
former smokers were in between, and nonsmokers were
I
I
369
strongest. For all questions, the proportion of nurses-who
agreed "strongly" or "som ewhat" with the statem ents of
exemplar role is reported here. Regarding their own behavior,
69.5, 91.7, and 94.5 percent of current, former and
nonsm oking nurses respectively felt that they should set a
good example by not smoking. This percentage varied
according to work location. Lowest percentages were given
for hospital duty (70.0, 83.3, and 89.2 percent for current,
former and nonsmokers respectively), intermediate for private
physician's office (79.9, 86.7,, and 90.5 percent, respectively),
and highest for private duty (91.1, 91.4, and 94.4 percent,
respectively). A much lower rate of agreement about not
sm oking in public while in uniform was obtained; only 44.4
percent of current smokers, 67.1'percent of former smokers,
and 72.8 percent of nonsmoking nurses concurred. Nurses
believe that it is their responsibility to convince people to
stop smoking; (64 percent of smokers, 74 percent of former
smokers, and 64.8 percent of nonsmokers). Approximately 54
percent of smokers, 81.3 percent of former smokers, and 82
percent of nonsmokers said they had tried to persuade
someone other than patients to quit, and a much higher
percentage reported convincing someone not to start (83.4,
78.6, and 75.8 percent, respectively). Finally, 52.1, 78.2,
and 85.4 percent of the respective groups agreedd strongly or
somewhat that nurses should be more active in speaking to lay
groups.
Given the possible role modeling effect of female nur-
ses, a need exists for adequate preparation of all health
professionals inn smoking and health counseling. This pre-
paration should include education on the health hazards of
sm oking as well as effective methods of counseling patients.
- There is little information available about the role
played by other health care providers in dissemination of
information or discouragement of smoking behavior. Nation-
wide campaigns are currently being aim ed att physicians and
dentists to increase their commitmentt to and involvement with
this task. Other health care providers should be encouraged
to take a more active role and adopt exemplar status as well.
Educators. Adult educators include those irrn schools and
colleges, job training, community organizations (churches and
other religious groups, Young Women's Christian Associations,
and Red Cross, civic organizations, social service groups,
cultural groups) and inn school-based programs for parents.
370
FIGURE 2.-A model of stress at work
SOURCES OF STRESS AT WORK
oor'p~ysiceft orking conditions
Work overload
Time Pressures
Physical danger, etc.
Role in
Roie amb~igu~ity
Role con7hcl
Responsibility for people'
Con/licts reorganizational
boundaries (internal and external), etc
v
verpromo wn
Undetpromotion
Lack ol job security"
Thwarted ambition, elc." '
Belationshios at ork
W
13oor re ons wlf
i 5oss,
subordinates, or colleagues
Difficulties in delegating . .
7esponsibility; ete."
Oraanizalional Structur and Climate-.
i e or no par icipa ion
in decision-making "
Restrictions on behavior (budgets, etc.)
Office politics *
Lack of effective consultation, etc.
60ES99c0
INDIVIDUAL
" CHARACTERISTICS
The Individual:
Level of Anxiety'
Level of neuroticism
Tolerance for ambiguity
Type A
behavioral
patlern
--r niz ti nal
ources o - ress:
Family problems
Life crises
'Financial - difficUtties, etc.
SYMPTOMS OF OCCUPATIONAL
ILL HEAlTH
Diastolic Blood Pressure
Cholesterol level Heart rate
Smoking "
Depressive mood ` - Escapist drinking .
Job dissatislaclion . ,
Reduced aspiration, etc. "
DISEASE
Coronary
heart
disease
Mental
ill
health
Sounce: Adaped from Cooper and Marshall (1976).
" Items marked by asterisk (") are particularly relevant
to female workers.
ort
t I
fiple
lho se
tion
~
sion
itory
t In
les.
fally
men.
that
m In
60)'
omen
idual
ared
avior
'smal l
par-
tha[
lack
omen
were
ttend
ilure
re Is
larly;
(80,
po rt,
gh a
e for
es to
them
f men
)nal ly
it Is
have
abstain. The occurrence of a full-blown relapse, Ao wever,
can be attributed to the cognitive reaction to stress-induced
smoking. Many individuals who aree trying to abstain, view a
single slip as evidence that they have failed, rather than as a
natural and predictable reaction to a stressful situation..
Marlattt and Gordon advocate teaching those who are trying to
quit the importance of not viewing relapse in an all-or-none
manner. Rather, they suggest teaching smokers to nplan for a
relapse," to become psychologically prepared to acceptt a slip
as a natural part of the difficult process of quitting.
Another factor thatt appears to influence the success of
women in treatment programs is the smoking of significant
others in their environm ent. Kanzler, found a significant
trend for women to give up smoking If no one in their daily
environment was a regular sm oker (102). This trend was only
slight for men, although spousal encouragem ent was related to
success in one large study off smoking cessation treatment In
men (160).. Berglund,West, and Warnecke also emphasize the
influence of the sm oking behavior of significant others in
female attempts to quit (4, 194, 190)i. Sensitizing friends
and relatives who are sm okers to this problem and advising
discretion in smoking behavior on their part, might Increase
treatment effectiveness for women.
Conctusions
Treatm ent programs should specifically deal with means of
handling anxiety and tension, ways to combat weight gain, and
prepare sm okersfor mini-relapses. Social support should be
maximized. It may be increased through choice of treatment
mod'ality networks of "buddies," friends and relatives, and the
involvement of spouses.
It should be possible to capitalize on the heavy com-
mitrment of womem to the health care system, both in terms of
their own use and their role as family providers. Health
professionals need to devise targeted interventions for wom en
with this in mind.
DISSEMINATION OF INFORMATION ABOUT SMOKING
Health Attitudes and Behaviors
The extraordinarily serious health consequences of sm oking
havenote deterred almost 30 percent of the adult female and
367
Advertising. In recent years, advertising in the United States
has beenn directed specifically towards the women's market,
review suggests that cigarette advertising does affect
the effects of cigarette advertising is clearly necessary, this
also capable of doing the other. While additionall research on
to influence brand choice and not initiation or consumption,
Fishbein maintains that it Is somewhat unrealistic to assume
that an advertisement which can do one of these things is not
that the tobacco Industry asserts that advertising serves only
Advertising can Influence the initiation of smoking, the choice
of brands smoked, and the level of consumption. Commenting
serve as a discriminativestimulus for sm oking behavior.
Furthermore, he points out that cigarette advertising may
decision to smoke as well as the choice of brand.
Fishbelnn concluded that cigarette advertising influences the
image portrayed, or some other reason--is not known.
brand characterization and availability, identification with the
tisements, but why they do--whether for Information about
and 42.5 percent of females smokers agreed with the state-
ment. It appears that adultt smokers value cigarette adver-
the 1975 Adult Use of Tobacco Survey (182)1 agreed with the
statem ent, "Cigarette advertising should be stopped
completely." The percentages for men were 56.9 percent for
nonsmokers and 56.4 percent' for former smokers, and for
wom en, 68.2 percent for nonsm okers, and 62.5 percent for
former sm okers. However, only 42.6 percent of male smokers
A majority of former and nonsmokers of both sexes In
smoking is a threat to that image (116).
socially valued and successful self-im age, and that giving up
women, people now respond less negatively to a woman
smoking (16). There is evidence that, for some women,
smoking is linked with attitudes and behaviors that comprise a
sense of mystery, sophistication, and power around the beha-
vior of smoking. Although smoking was once frowned upon for
Thus, advertisers have been successful in creating aa
girl nonsmokers or young adult women view advertising.
healthy (by 49 percent). There is no comparable data on ho w
percent), sexy (by 54 percent), young (by 50 percent), and
enjoying themselves. (by 66 percent), well dressed (by 66
tisements.: The latter are seen as attractive (by 69 percent),
impression of theindividuais pictured in cigarette adver-
independent single woman. Most girl sm okers have a positive
with themess as diverse as the emancipation of women, the
first woman (biblical reference), romantic love, and the
cigarette consumption (63).
372
higher on scales m easuring daily stress, m aritai dissatis-
faction, and aging worries, than men. They were also less
likely to display overt anger than either homemakers or men
(87). While incidencerates of coronary heart disease in
working women were not significantly higher than in homemak-
ers, an excess risk of CHD was identified among women who
were employed in ciericall jobs and had children. The risk
factors for CHD in this group inciuded family responsibilities,
suppressed hostility, a nonsupportive supervisor, and low job
mobility over the preceding ten-year period.
Smoking Habits of Health Professionals
There are relatively fe w studies available which present
gender-specific sm oking rates in various professions. Health
professionaiswere selected for analysis because they were
more likely to be aware of the health consequences of
sm oking than the general public; this group has also been
studied more extensively.
Physicians. The smoking habits of male and fe male physicians
inn five nations are presented in Table 15. Smoking rates in
the general population are provided for comparison whenn
supplied by the authors. No breakdowns by gender are
avallable for the United States. Separate estimates of
smoking rate In a smali group of women physicians age 36 to
46 at the time of survey (195) and in a large sample of
predominantly m ale (93 percent) physicians (183) are listed in
the table. In addition, the wives of 3,990 physicians were
queried about their own sm oking habits and those of their
husbands; no information Is provided on the occupation of
these women (75).
Examination of the table shows that smoking rates of
physicians, both male and female, tend to be much lower than
general population rates. The only exception is the higher
rate of current smokers among female physicians In Finland
(189). The percentage of current smokers among the sample
of U.S. fem ale physicians is higher thann that reported in
other countries and approaches the rates in the general
population. Prevalence of smoking has a strong relation to
demographic variables such as profession, income, andd educa-
tion. We would expect physicians to be in the highest cate-
gory on each of thesevariabies and, therefore, to have lower
prevalence rates.
378
Restrictions have no wbeen placed on advertising in
m any countries inn the world, including the Uhited States.
There Is no uniform agreement that the ban on televised
cigarette advertising in the United States and the United
Kingdom significantly reduced, consumption. Ho wever, It is
generally believed that each action of this sort--including the
U.S. Surgeon General's Reports and the Reports of the Royal
College of Physicians, Taxation, and Legislation--has a
cumulative effect on per capita consumption (191, 8, 136)..
The Failure to Disseminate Information. Many of the critical
evaluations of public health campaigns conveying anti-smoking
information maintain that little attitudinal or behavioral
change is ever affected (178). Fishbein (63) argues that
there is insufficient information describing the complex
relationships between cigarette smoking behavior and beliefs,
attitudes, and intentions to make this conclusion. He further
m aintains that It is necessary to know to what extent
decisions regarding initiation, reduction, increase or cessation
are under attitudinal (individual, personal) or normative
(society-influenced) control. The importance of personalizing
the health message, and the failure of the public to
personalize the health messages that they have received is
emphasized. For example over 80 percent of the smokers
agree with the state ment. that smoking is hazardous to health
but on the question, "Are you in any way concerned about the
possible effects of cigarette sm oking on your health?" only 25
percent of current smokers, stated that they were "very
concerned," another 22.6 percent were "fairly concerned,"
18.9 percentt were "only slightly concerned," and a final 31.9
percent were 'not concerned" (197).: Fishbein maintains that
the public is not effectively informed about the general
danger to health posed by smoking and is even less informed
about the connection with specific diseases. He concludes
that the content of an effective message is fourfold: that
continued smoking leads to negative outcomes; that stopping
smoking leads to positive outcomes; that personal relevance
m ust be established; and that norm ative influences must be
appealed to by maintaining that significant others think an
Individual should quit.
Smoking andWeight Control. Women who smoke are, on the
average, thinner than women who do not smoke. The reported
meann weight difference ranges from,l.2 to 4.5 pounds (7, 17,
I
Q
0
I
i
0
373
90). Weight gain has been a frequently docum entedcon-
sequence of quitting smoking, both in males and females (135,
196, 37, 65, 70, 202, 179, 17.)
Studies of males have reported weight gains among
former smokers which range from 1 to 12 pounds greater than
those who continue to smoke. In one such study, the authors
observed that, while 60 percent of continuing smokers gained
weight, among quitting smokers the observed proportion was 85
percent. These figures gave rise to an observed-to-expected
ratio of 1.4, suggesting that those who quit are 40 percent
more likely to gain weight than those who continue to smoke,
but a significant proportion of observed weight gain among
men who quit smoking would have occurred evenn if they had
continued to smoke.. - The single major report on lifetime smoking and weight
patterns in wom en examinedd data provided by approximately
57,000 female members of a national weight-reduction
program (17). Cross-sectional analysis indicated, that current
smokers weighed less than nonsmokers by 1.2 pounds and 4.0
pounds less than former smokers. Inhalers were significantly
less obese by 5.7 pounds than current smokers who did not
inhale.
A 40 -year longitudinal analysis of weight in relation to
reported lifetim e smoking history revealed that between ages
30 and 50 (the two decades after the majority of those who
quit had discontinued smoking), the former smokers gained
m ore weight than continuing smokers, both for Inhalers and
non-inhalers. The calculated weight gain after cessation varied
substantially by amount smoked; heavy smokers who Inhaled
(>41 cigarettes) gained 30 lbs., while light smokers who
inhaled (,1 to 10 cigarettes) gained only 4 pounds. The
observed differences in weight persisted through age 60.
Conclusions of this study may not, inn fact, be directly
applicable to the total female population. This study raises
the issues of reporting and recall bias among this obese
population (m ean group weights ranging from approxim ately
171 to 180 pounds), as well as self-selection into continuing
or former smokers.
The implications of such studies are important. The
Image of the slender, attractive female pervades our culture
and is certainly present in tobacco advertising (Hall and
Havassy, in press). Do wom en perceive weight gain as a
significant and unavoidable sequel to discontinuing smoking?
There is evidence suggesting that fear of weight gain may
keep women from quitting smoking. Women are more
374
TABLE 14.-Clgarette smoking status by work setting for Nurses.
Work_Set[i:ng
Cigarette Smoking Status Total
Current Former Never Percent N
SurgicalUnlts 41.2 19.4 39.4. 100.0 329
Medlcal Units . 37.8 18.2 43.9 99.9 476
Operating, Labor, Delivery. ' Emergency Roum . 39.8 15.2 45.0 100.0 495
Out-Patient Clinic - 42.5 . 15.1 42.5 100.1 113
Other and Mixed 41.3 18.4 40.3 100.0, 1~,078
Elementary or High School 27.5 36.4 36.1 100.0, 217
Doctor's Offlce 24.2 33.8 41.9 99.9' 338
In the Community 26.1, 33.4 40.6 100.1 264
Matennlty Unit'. 36.2 17.2 46.6 100.0 197
Pediatrics Unit or Setting 46.6 8.8 44.6 100 AB0
Psychiatric Unit or Setrting 49.9 16.2 32.0 100.1 135
Nursing Educatlon.5etting 24.6 ' 26.8 ' 48.7100.1. 90
W
~
N
TABLE 16-Percentages of cigarette smokers (S), former smokers (FS), and ever smokers (ES) and
cessation ratio (FS/ES) among psychologists
sychologists nurses and other selected health professionals -
Sample N S FS ES FS/ES
Mare and predommantly male samples
CSUC maie psycna..glsts
Eminent experimental psychologists' 90% male
lLawton & Goldman,196t) -
Psychiatrists % male not reporsed lfamerua & Elsmyer, 1972)
American Pvblic_ Health Association male members
IEyres, 19731
Phys¢lans-93°emale(USPHS.19771
U.S. adult males 1USDHEW, 1976a)
Female and predominant ly female samples
CSUC female psychologists -
Ameriran Public Hea'th Assoeiatlon Iemale members
IEyres,19731
Nmses--98h female (USPHS, 1977)
U.S. adult females (USOHEW, 19761
Note. CSUC =Cabfornia State Unmersity and Colleges.
St7URCE: (47).
258 ' . 28 35 . 62 55
-
72 53 11 64 17
309 42 27 69 39
3,569 21 40 61 66
3,657 21 42 . 63 67
5,702 39 29_ 69 42
86 . 38 19 57 33
1,973 31 31 62 50
2 429 39 22 61 36
6,327 29 14 43 33
OtESq9£0
TABLE 18.-Distrlhutlon of rmsponses of current former smokers
who were ever pregnant to the question ^Did your
doctor suggest that you cut down or stop smoking
clgarettes during yourr last pr.egnancy7
Percent by Year of Last Pregnancy
PhysicAan's Advice (Prlor to 1965{, (1965-69) (1970-75) (1965-75)
Quit smokIng 5.6% 6.3% 10.8% 9.3%
Cut down smoking 5.7 8.4 12.4. 11.4
No advice-givem 70.5 64.1 65.6 65.1
Not emoking at the time 16.4 20.6 9.1 12.9
Had no doctor 0.5 0 0.2 0.1
Den't know or no answer 1.3 0.8 1.3 0.9
N,= 983 466 ]15 291 506
SOURCE: 1975 NQ75 surve.y.
391
According to the three studies providing comparative
data, both fe male and male physicians are quitting at rates
higher than the general population. The percentage of former
smokers among female physicians, and estimates of quit rate,
are lower than among male physicians in all but one of the
studies listed. This trend may represent a time lag in the
smoking behavior of women as compared to that of men, or
there may be a lower quit rate among women physicians.
In two studies, female physicians smoked more
cigarettes per day than women in the general population In
contrast, wives of physicians smoked fewer cigarettes on the
average than their husbands (75). A greater percentage of
the wives of physicians than physicians themselves, were
smokers in every age group except the oldest. The percentage
of current smokers appeared to be inversely related to age in
the group of wives, but virtually stable across age for the
physician-husbands. Husbands and wives tended to have
similar smoking habits.
Based on a small sample of women graduates of a
single U.S. m edical school, Westling- Wikstrand, et al. (195)
reported that 58.8 percent of the current smokers belonged to
the category 'professor," (academic appointm ent of assistant
professor or above, with or without board attainment). when
ranked on professional attainment. The other categories were
"boards" (specialty board certification but not professional
appointments), "no boards" (inn practice without board
certification or professional appointm ent), and "not in
practice." The "professorn group was characterized by
greater likelihood of being single and having fewer ehabits of
nervous tension." Compared to other groups, this group had
the lowest depression scores, average anger scores, and the
highest anxiety scores. The authors comm ent thatt this group
of women was the most similar to their mafecolleagues.
They may also have experienced fewer problems withh
ambivalence about sex roles, self-image, or conflict over
aggressive behavioral patterns. The presence of the high
anxiety scale, however, casts som e doubt on this
generalization.
Women in U.S. m edical schools are subjected to
significantt psychological pressures and often experience
emotional problems and lack of confidence about achieving the
goal of graduation (195). Female physicians also experience
significant role conflict (19). The relevance of indices of stress to smoking patterns
is again one of inference. If sm oking serves as a coping
I
380
concerned with weightt than men are. In the 1975 NC HS
survey, the percentages of female and male smokers who
responded "strongly agree" or "mildly agree" to the statement,
"Being afraid of gaining a lot of weight keeps people from
quitting cigarettes" are shown in Table 14.
Attempts have been made to examine the cause of such
reported weight gains. The mechanism of weight gainn with
cessation of smoking has not, however, been elucidated.
Trahair and others have reportedd that appetite increased with
sm oking cessation;, and the resulting increased caloric intake
caused weight gain. Other studies have suggested that
smoking may, in fact, directly affect metabolism. Glauser, et
al. studied seven males before and one month after cessation.
Body weight and surface area increased, while heart rate,
serum calcium, sugar, and oxygen consumption decreased.
Conversely, ho wever, Sims observed no change in resting
metabolic rate, thermic response to exercise or meals, and no
change in serum T3 or T3 (166).
Further research is necessary to define the degree of
weight gain after cessation of sm oking, the mechanisms by
which it occurs and the ability to modify it by educational or
behavioral interventions during and after cessation attempts.
Stress at Work
A general model of stress at work (38) is worthy of con-
sideration. Examination of the sources of stress at work
(Fig. 2)~ reveals a number of items which are especially
salient for women. Discrimination against women in
employm ent, role conflict, authority problems, inequity in
promotions, exclusion from decision-making processes and the
"old boys" network have been frequently discussed (67).
Individual characteristics may be considered fromm a gender
viewpoint as well; for example, some types of psychological
disorders, such as anxiety and depression, are more prevalent
among women than men (50, 67). The Type A behavior
pattern, which is associated with male cardiovascular disease,
has been shown to be unrelated to sex once socioeconomic
status is taken into consideration (163).
An additional set of stressors originates in the
extraorganizational environment. A prospective study of the
relationship of e:nploym ent status and employm ent-related
behaviors to coronary heart disease (CHD) incidence was con-
ducted by Haynes and Feinleib (197). Working women scored
375
FIGURE 4-Percentage of patients advised to quit or cut down thelr gmoking by the smoking behavior of
the advising obstetrielan Gynecologist
~.0
0
ADVISE ALL +ALMOST ALL PATIENTS
70- a MOST+MANY
FEW +NONE
60-
50-
40 -
30-
20 -
t 0-
45.3 44
21
131;
32.1
50
1 g,Y 18
113.3~
TOTAL CURRENF FORMER
- - SMOKERS SMOKERS
(n=3208) (n-622) (n_l 187)
37.1
NON
SMOKERS
(n=1 401)
BIES99C0
care (41). The beliefs of OB-GYN specialists about the
relationship between maternal smoking and neonatal death aree
presented in Figure 3, along with some of the more common
diseases associated with smoking. Because neonatal death can
result from a great many factors, the attribution of causality
is somewhat lower than for the other conditions represented.
However, it is notable that 23.6 percent of the physicians
deny the existence of any relationship. Congruent with the
estimate from the 1960s, 45.3 percent of OB-GYN special'.i.sts
inn this survey claim ed to instruct all or almost all of their
patients to quit or cut down on smoking (see Figure 4).
Another 13.1 percent delivered such advice to most or many
(65 to 95 percent). A noticeably smailerfraction of
physicians who are current smokers deliver this message than
ex-smokers or nonsmokers.
The 1975 Survey of Adult Use of Tobacco, sponsored
by the National Clearinghouse on Smoking and Health, included
a questionnaire directed at smoking habits in pregnant women.
A preliminary analysis of the results has been made (85)..
Out of 12,029 respondents Interviewed in 1975, a total of
1,225 women (814 current snokers and 411 former smokers)
were administered questions about their smoking habits during
pregnancy.
Each of the 983 respondents (664 current smokers and
319 former smokers) who had ever been pregnant was asked
whether her doctor suggested that she quit sm oking or cut
down during her last pregnancy. Table 18 displays the results
by year of last pregnancy. The percentage of women
reporting such advice from their doctor rose steadily. Only
14.6 percent of women who had last been pregnant from 1965
to 1969 ciaim ed to have been advised by their doctor either
to stop or cut down; 23.7 percent of women last pregnant
from 1970 to 1975 remembered such advice. These estimates
are considerably smaller than those supplied by physicians
themselves(.174, 41). There are several possible explanations
for the discrepancy: the women were reporting
retrospectively, and m emory m ay have been distorted; a
selective under-reporting of advice may have occurred; or the
populations of physicians and patients may be entirely
nonoverlapping. Retrospective data have been shownn to be
unreliable in one pregnancy study (51 ). Unfortunately, sample
sizes were too sm ali to provide reliable estim ates of the
percentage of women who followed the advice of a physician
to stop sm oking during pregnancy. Such data might have
yielded an estimate of the effectiveness of such advice.
388'
+M
7F
w
a
FIGURE 3.-Beliefs of OlrGyn Specialists about the association of Maternal
(Smoking with Neonatal Death and other selected diseases)
100'-'
60 -
40 -
20-
1 7.4
MAJOR l CAUSE
`~ CONTAI8UTIN IG
~ ASSOCIATION
~ NO ASSOCIATION
23.4 23.6
NEONATAL
DEATH
78.2
7.6
CORONARY
ARTERY
DISEASE
93.2
904
92.6
n=5401
4.".:^.7 0 4 t . 0.8 %:a 0.6
CHRONIC PULMONARY LUNG
BRONCHITIS EMPHYSEMA CANCER
4,ZES99C0
hospital In the United States (106). Fifty-two percent of
that group smoked, compared with 36 percent of the medical
nurses (99.3 percent female) and 40 percentt of the student
nurses (95.6 percent female). This survey was aimed at
n
5
0
Identifying smoking within the hospital. Thus, true prevalence
in this sample can only be higher. Compared to other female health professionals (see
Table 16) in the United States, nurses' quit rates are above
some (psychologists, UIS. adult wom en) and below others
(American Public Health Association female members). Knopf
Elkind points out that in the British population other fem ale-
dominatedprofessional, such as primary school teachers,
health visitors and domiciliary midwives, have a noticeably
lower rate of sm oking than hospital nurses and that nurses
sm oke more than other professionals in the U.S. population
(103, 186). Entry into the profession of nursing is
associated with taking up daily smoking but the degree of
occupational stress in a population of 300 British student
nurses was not different for smokers and nonsmokers (88).
This finding does not rule out the use of smoking as a
stress-reduction mechanism, however.
Other factors which might contribute to a high smoking
rate among nurses are work overload and frustration in
professionall relationships with physicians. Knowledge of health consequences of smoking is high
among nurses, but It has been shown that student nurses are
less well-informed than medical students (146). Nurses who
quit sm oking do cite protection of future health as a major
reason (88, 73). Nurses who smoke are less likely than
nonsmokers to agree that not smoking is a preventive measure
against cancer (103). Similar refusal to acknowledge health
risks of smoking Is found among smokers In the general popu-
lation (182). Whether this represents a real lack of
knowledge or a method of reducing cognitive dissonance
through denial is unknown. The problemm is particularly cri-
tical for nurses (and other health professionals) sinee they
serve both as exemplars and as providers of infurmation
(103).
THE PREGNANT SMOKER--A SPECIAL TARGET
The pregnant woman is in a unique life situation. Every
substance she ingests and every behavior that she manifests
can affect the present and future health status of the unborn
385
to 35 percent, which is the figure most often anecdotally
cited. The median is closer to 20 percent. Only one study provides ethnic data on smoking cessa-
tion during pregnancy (104). In this study, it should be
remembered, stopped'smokers are women who smoked prior to,
but nott during the pregnancy, so that quitting may not' have
been pregnancy-specific. Rates are very similar for white,
black and Hispanic women: 24.5 percent, 24.9 percent and
28.7 percent respectively, were stopped sm okers in this study.
- Cutting down on smoking during pregnancy would appear
to be better than no change in behavior, especially for those
adverse effects upon the fetus which show a dose-response
relationship. However, cutting down on number of cigarettes
does not always imply a reduction inn delivered dose of
nicotineor other tobacco smoke constituents (77, 78). When
smoking behavior was measured over the course of pregnancy
in regular smokers (5 to 30 cigarettes per day for at least 5
years), a decrease in num ber of puffs per cigarette occurred
as pregnancy progressed (6). Like puffing rate, the C OHb
concentration also decreased over time in pregnancy.
However, in these subjects there was no significant change in
nicotine dose extracted from the cigarette over the duration
of the pregnancy. Some alteration in puffing pattern,
presum ably in inhalatlon, affected the compensation. Thus,
caution must be exercised in the interpretation of "cutting
down.e
. There is even less information available on the per-
centage of quit-sm okers who return to smoking after delivery.
Table 19 provides two extremely divergent estim ates: 82.2
percent (85) and 13.4 percent (104). Because we are dealing
with relatively smallsample sizes, the reliability of such data
is not very high. Much more Information must be accumulated
before any firm statements about recidivism can be m ade.
Women who quit during pregnancy have an excellent
opportunity to change a behavior for life, with benefits both
to themselves and to their children (see Recommendations).
Psychosocial Factors in Quitting
Health reasons, primarily centering around preventing harm to
the fetus, are m ost often givenn as reasons for quitting.
Yankelovich, et al. (203) report that 62 percent of young
women smokers believe that smoking can harm the fetus and
norms against smoking have been discussed (11). The sickness
394
the United States. The most recent assessm ent of nurses'
smoking behavior was conducted ln 1975 (182, 188). In
Table 6, smoking habits of nurses are compared with those of
adult UIS. women and other groups of health professionals.
Between 1969 and 1975, the proportionn of nurses who
were current sm okers rose from 37 to 39 percent. Every
other category of health professional. (physlcian, dentist, and
pharmacist), had substantially reduced sm oking rates. The
membership of these three professions is predominantly male
and current smoking rates vary from 21 to 28 percent. If
one examines quit rates in 1975 among the four categories of
health professionals, it is clear that the majority of
physicians, dentists, and pharmacists who ever smoked
cigarettes have quit: 64, 61, and 65 percent respectively.
Am ong nurses, only 36 percent have quit, which does, ho wever,
compare favorably with adult women (34 percent) and working
women (30 percent) (183). Noll surveyed smoking behaviors of nurses by work
setting (see Table 17) (129). The overall percentage of
current smokers in this survey was, 37 percent, compared to
a national average (for 1966) of 33.7 percent: in women. There was a smaller percentage of nev.r
smokers (41.3
percent) among nurses in that survey than among the female
population (56.8 percent), suggesting a higher quitting rate at
that time as well. From Table 17 it appears that there Is no
selective recruitm entinto the various nursing specialities; the
proportion of never smokers is fairly equal across work
settings. Differences do appear, ho wever, in the proportion
of current smokers according to workk setting. Highest rates
of sm oking are found inpsychiatric and pediatric settings, and
lowest rates in the four categories connected, to education and
community involvement: nursing education, working in the
community, elementary or high school nursing, and working in
a doctor's office. -
In Great Britain, only 26 percent of maternity nurses
smoked regularly, compared to 37 percent of those in general
nursing (103). In the United Kingdom, approximately the same
proportion of nurses sm oke as women In the general population
44 percent (103, 146).
Elkindreports differences in sm oking among different
types of ward nursing staff. Trained nurses had 41 percent
current smokers, learners had 28 percent, nursery nurses had
14 percent, and auxiliaries had 61 percent current smokers.
Lampman reported a similar excess of smokers among
nurses aides (95.2 percent female) in a large metropolitan
0
383
adolescents of either sex are lower number of cigarettes
smoked per day, higher educational aspirations and
achievem ent, greater acceptance of the health risk of smoking
and having more nonsmokers among their friends.
13. It Is possible that women and men modify their
smoking in order to maintain a constant nicotine level.
14. Women are more likely than men to smoke in order
to reduce stress.
15. Women at higher education and income levels are'
more likely to succeed inn quitting.. - Additional factors
associated withsuccessfui quitting are a strong commitment to
change, the use of behavioral techniques and thereiiability of
social support for quitting. Women have been reported to
show lower rates than men of successful cessation following
organized cessation programs, a difference which is less
apparent in those programs which Include social support.
398 -
month follow-up for those completing treatment (12, 41).
This latter result is very encouraging but is based on a very
small sample in an affluent community where the afore-
mentioned factors of educationaJl level, high socioeconomic
status and orientation toward professional advice are
operative.
Recommendations
Impact of rolemodeling as the child grows.
include better health for the mother and child and the future
pregnancy. Positive aspects of remaining an ex-smoker
smoking cessation rather than just during the time of
4. Much more emphasis must be placed on permanent
pregnancy and birth as a two-person process.
timely in an era when more andd more couples are experiencing
supportive effort of quitting. This should be particularly
the child in the norm ative belief system and in a direct
socioeconomic status. It is Important to involve the father of
used as part of information dissemination and modeling
influences. This is particularly true for wom en of lower
3. Social norms and lay referral systems should be
various health professionals should be raised in this regard.
possible, not solely by the physician. The awareness of
Information should be dispensed by as many different sources
of contact In the prenatal clinic (or doctor's office) as
involve women as the transmitters of information and advice.
In addition, it is important because of gender identification to
nicity in a num ber of geographical and socioeconomic settings.
ticularly good avenues for portraying wom en of varying eth-
2. Mass media, such as television andd film, are par-
benefits of not smoking must be equally emphasized..
the baby alone. The harmfull aspects of sm oking and the
mother's own health should be intricately interwoven in the
theme. Quitting is for the good of both mother and baby, not
directly harmful to the fetus. This information about the
baby's health should be made as specific as possible, and the
harmful to health, and most acknowledge that it can be
1. Pregnant women seem to know that smoking is
pregnant woman and offering her cessation interventions.
which may be useful in improving methods of reaching the
The preceding discussion has revealed a num ber of findings
396 '
(12). Seventy-nine percent of the sample were aware of
some norm relating to smoking in pregnancy: 39 percent
thought they were expected not to smoke at all, and an
additional 40 percent thought they were expected to reduce
their smoking. All of the women could name at least one
source of information: 98 percent had been exposed to
mass-media messages to quit smoking. Smoking seemed to be
undergoing a change in norm status, from generality to
specificity; i.e., from being a general health menace to one
with specific consequences, such as a threat to the health of
the baby.
The issue of normative behavior in smoking andd per-
sonalization of in essageshouid be crucial to inform ationai
campaigns, according to Fishbein's theory (63).: Social support
from a spouse should also be critical, as would be involvement
of significant others. Women about to have their first baby are more likely
to believe educational materials than multiparous women (12,
51a). This finding suggests that different modes of inter-
vention or different emphases should be developed for primi-
parous and multiparous women.
Physician Advice
The physician represents one of the most knowledgeable
figures the pregnant woman will encounter as a source of
information. Consequently, estimates of the frequency with
which the physician delivers advice on smoking are of impor-
tance.
Three such estimates are available from national samples
In the. United States. In the first study, conducted in the
mid-1960s, 37 percent of physicians reported that they
advised all or almost all (95 to 100 percent) of their
pregnant patients to quit smoking or cutt down sharply.
Obstetricians were m ore likely to deliver such advice to
pregnant patients (49 percent) thann were physicians in generall
practice (38 percent) (74). .
The Physician Advice Survey conducted by the Center
for Disease Control examined the beliefs and behavior of
physicians specializing in Obstetrics and Gynecology (OB-GYN)
In the United States (41, 13). The OB-GYN specialty
practice includes preventive m edical careine the form of
specific suggestions regarding hygiene and family planning and,
during pregnancy, active participation in directing perinatal
387
SUMMARY
1. The percentage of 17-18 year old women who
smoke has shown a steady rise between 1968 and 1979; it
now appears, however, that the increase in smoking prevalence
among adolescent females has levefedoff and begun to
decline. Young women born after 1952 show a substantially
reducedinitiation of smoking and will probably have a much
lower prevalence of smoking as adults.
2. Those young women who do begin to smoke are
starting to smoke regularly at a younger age, with more than
half of the male and female adolescents who begin to smoke
starting before the10th. grade. 3. The earlier tobacco is used and the greater the
number of cigarettes smoked per day, the less likely an
attempt to quit will be successful.
4.. The percentage of women smokers who smoke more
than one pack per day is Increasing.
.
5. Adolescent and aduit: women are more likely to use
low tar and nicotine cigarettes, sm oke fe wer cigarettes per
day and inhale less deeply than do men, but the difference
between the sexes in these patterns of smoking is decreasing.
Adolescent and adult black women are more likely to be
smokers than their white peers, but they smoke fe wer
cigarettes per day.
6. Adolescents from low income families, single parent
families, and families with lower parentall educational levela
are more likely to become smokers.
7. Female and maieadolescents are more likely to
begin smoking if a parent or older sibling also smokes.
8. Adolescent smokers associate with peers who smoke
and nonsm okers associate with nonsm oking peers.
9. Adolescent girls overestimate the percentage of
their peers who smoke and they have a very positive image of
the people In cigarette advertisem ents, but they are less
iikelythan adolescent boys to see smoking as a social asset.
10. Adolescent girls who smoke tend to be more
outgoing but feel less able to influence their future.
11. Adolescents experience stress due to feelings of
unattractiveness, incompetency in school achievement and
personal relations, limited opportunity for personal growth and
concern over future social and economic roles. This stress
may be the common mechanism producing the increased rates
of smoking In some groups. 12.. The factors associated with successful quitting by
397
0
fetus she is carrying. If she smokes, the nicotine, carbon
monoxide, and cyanide (andthiocyanate) which she inhales all
cross the placental barrier and enter the bloodstream of the
fetus. The risk factors for both mother and fetus have been
extensively reviewed elsewhere in this volume as well as in
previous reports from the Office of the Surgeon General (see
Pregnancy and Infant Health, Part II of this Report) (186).
It is estimated that betweenn one-quarter and one-third
of pregnant smokers quit smoking for the duration of
pregnancy and that another third cut down.
This section revie ws the current literature on sources
of information availableto the pregnant smoker, summarizes
available data on prevalence of current sm oking and sm oking
cessation during pregnancy, and dlscusses the problem of
cessation from a behavioral vie wpoint.
Sources of Information
posters, and leaflets are inadequate for the delivery of
statistical information; books, which are better sources, were
used muchh less thann these other sources. Baric and
MacArthur present a discussion of health norms ih pregnancy
from a nurse) (12). The authors comment that television,
by a medical source (16 percent from a doctor, and 9 percent
and leaflets; 37 percent had been told by husbands; 34 per-
cent used books and magazines; and 25 percent had been told
as follows: 84 percent had seen it on television; 65 percent
were told by family or friends; 52 percent had seen posters
women, the mode of exposure to smoking information ranked
. In one study of predominantly working class British
i and physician -supplied information (72).
more likely to utilize Impersonal sources such as mass media
transmission of information seems to be more highly valued
and readily adhered to (70). Middle upper class women are
upon mass media or m edical sources (76, 11.). Personal
more on lay referral systems, such as peers and family, than
Wom en in Io wer socioeconomic classes tend to rely
peers and family, community resources, and the media.
through health professionals (prim arily physicians and nurses),
socioeconomic status and parity. Information is distributed
fidence in the information provided seems to be a function of
The same classes of information discussed in the previous
section areavailablee to the pregnant smoker. How the
pregnantt smoker uses these sources and her degree of con-
386 . '
(30) BURNS, B.H. Chronic chest disease, personality,
Thornton, R.E. (Editor). Smoking Behavior.
Edinburgh, Churchill Livingstone, 1978, pp.
cigarettes on hum an. sm oking patterns. In:
(39) CREIG HTO N, D.E., LEWIS, P.H. The effects of different
1976.
Journai of Occupational Psychology 49: 11-28,
of stress: A revie w of the literature relating
to coronary heart disease and mental ill health.
(38) COOPER, C.L., MARSHALL, J. Occupational sources
April 1972.
Archives of Environmental Health 24: 271-276,
and subcutaneous fatness related to sm oking habits.
(37) COMSTOCK, G.W., STONE, R. Changes in body weight
Press, 1974.
on Youth of the President's Science Advisory
Committee. Chicago, The University of Chicago
(36) COLEMAN, J.S.,. Chairman, Panel of Youth. Youth:
Transition to Adulthood, Report of the Panel
The Free Press, 1961.
(35) COLEMAN, J.S. The Adolescent Society. New York,
. ~ Press, in press.
D., Ross, S. (Editors). Behavior Group Therapy:
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the heart in behavioral group therapy. In: Upper,
with children and adolescents: Taking care of
(34) COATES, T.J., PERRY, C. Multifactor risk reduction
Social Science and Medicine 1: 357-382, 1968.
smoking: Data from the Oakland growth study.
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American Society: Social and Psychological
(32) CHILMAN; C.S. Adolescent Sexuality in a Changing
and Social Medicine 30: 123-131, 1976.
(31) CHERRY, N., KIERNAN, K. Personality scores and
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23-27, February 1969.
Journai of Preventive and Social Medicine23(1):
and success In stopping cigarette sm oking. British
289-300.
402
experienced as a part of pregnancy can also be a reason to
give up smoking (12). It has also been reported that women
this finding is unclear.
varies according to time and culture. So thegeneraiity of
of how much weight it is appropriate to gain in pregnancy
a wareness of social expectations In this area (11). The issue
during pregnancy; 24~ percentt of this sample expressed
and MacArthur included control of weight gain as a norm
a reason to continue smoking during pregnancy (Sla). Baric
. A closely related aspect of maternal heaithh is weight
gain. Preventing excessive weight gain has even been given as
associated with quitting (41).
incidence of appetite cravings and aversions, which may be
who smoke before pregnancy show a significantly increased
reducers may be altered during this period. Abstinence
Little is known about problems in quitting during
pregnancy. The role of cigarettes as stimulants or tension
income; being married; being empioyed; more frequentt church
attendance; having a spouse who does not smoke; and no
characteristics: higher educational. level; greater family
Kuzma and Phillips identified a number of similar
49).
sm oking at an older age, having stopped previously for at
least 6 m onths,having heard about harmful effects of smoking
from more sources,, firmly believing that smoking was
harmful to the baby, and finally, being encouraged to stop or
beingg joined in the cessation effort by their husbands (156,
cigarettes before pregnancy (also see 161, 51), having started
related to quitting, followed by sickness in early pregnancy
(12). Other distinguishing characteristics are smoking fe wer
drawn by Baric, et al. and also by Kuzma Phillips (12, 104).
Baric, et al. list educational qualifications as being positively
A composite picture of the successful quitter has been
symptomatology has also not been documented. _ .
information, personalization, and social norms (63).
support--all fit with a model of behavior change involving
belief in stopping for the sake of the fetus, and spousal
levely higher socioeconomic status, wider information base,.
The characteristics described--advanced'educational
illicit drug use (103, 104).
Three studies evaluate smoking cessation interventions
for pregnant women (12, 51, 40). Tables 9 and 10 show
reported abstinence figures for two studies. One study (12):
showed no difference between intervention and control groups,
and the second study showed 50 percent abstinence at 9-
O
W
~
!XJ
Ul
W
N
tJ
(40) DANAHER, B.G. O8-GYN intervention in helping
sm okers quit. In: Schwartz, J.L. (Editor).
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1978. Sponsored by the American Cancer
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Organization and International Union Against
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FORD, J.D. A smoking cessation program for
pregnant women: An exploratory study. American
Journal of Public Health 68(9): 896-898,
September 1978.
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the epidemiology of 'crows feet.e Annals of
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1971.
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12, 1973.
(44). DANIELL, H.W. Wrinkles (Letter). Archives of
Dermatology 111 (7): 927, July 1975.
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of Public Health, Smoking and Health Suppelemnt
64(2): 55-519, March-April 1973.
(46) DICKEN, C. Sex roles, smoking, and smoking cessa-
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403
(20) BORLAND, B.R., RUDOLPH, J.P. Relative effects of
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(26)
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401
In sum, over 50 percent of physicians claim to advise
their pregnant patients to eliminate or sharply curtail their
smoking during pregnancy, but a much smaller percentage of
pregnant women recall such advice.
Prevalence of Smoking and Quitting During Pregnancy
The prevalence of smoking In pregnant women. (before special
cessation efforts). should be roughly equivalent to the pre-
valence of smoking in the female population in the same age
range, corrected for socioeconomic status. Ten studies con-
ducted in developed countries, reported between 1971 and
1973, show a range from 23.4 percent to 47.6 percent in
prevalence of tobacco use (139). The median rate is 42.75
percent smokers for the entire sample. A survey (conducted
during the course of the pregnancy) of 9,553 pregnant women
who represent a cross section of the general population in the
Riverside-San Bernadino-Ontario area (California) was
recently compteted (104). Preliminary results indicate that
44.5 percent of all women surveyed either continued to smoke
during pregnancy or had smoked before, but not during, this
pregnancy. Since the precise tim e of cessation is not clear,
a more conservative estimate is that 33.3 percent of women
continued to.smoke for the duration of their pregnancy. This
estimate is well within the range of those derived from the
Population Report analysis (139).
- There is a paucity of race-specific information on
smoking prevalence during pregnancy. Niswander and Gordon
(128), in a study encompassing 14 U.S. cities, reported
greater prevalence of smoking among white than black women
53.65 percent vs. 41.85 percent, respectively. This is a high
estimate and reversal of the prevalence rates presented in
Table 7. The finding is similar to the previously presented
data in that white wom en sm oked more cigarettes per day
than black women: only 3.3 percent of black women smokers
consume a pack a day or more compared to 13.4 percent of
white wom en in this study. Sm oking is slightly less prevalent
in black than in white women in the sample of Kuzma and
Phillips (104); 57.3 percent of blackk women and, 53.3 percent
of white women have never smoked. For Hispanic women, the
percentage is somewhat higher, 61.9 percent never-smokers.
Table19 summarizess the results of 11 studies reporting rates
of discontinuing smoking during pregnancy. The overall rate
of cessation among regular smokers ranges from~.0.9 percent
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404
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TABLE 19 Percentage of current smokers who alter smoking behavior during pregnancy
Change in Smoking Habi4-Percent of Women
Quit Cut Down No
Author&Dare N Quit Temporarily Only Increased 8hange Mlscellaneous,orCommenl
1. Kullander&Kallen,1971 2,806 09 1.3 97.3 *05Inipated
2 Andr.ews&McGarry,1972 6,733 14.7 Maternitiesonly
3. 9utler et al., 1972 8,341 18.4 Quit by end of 411, month
4. Schwartz et al., 1972 1,188 31 0 10.0
5. Baricetal.,19761 134 14.9 30 82.1 Quitbylstante~natalvish
6. Graham,1976
50
33.3' 333 33.3 '1/3qultorcutdown;
1 /3 cut down temporarily
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No_ te' 1 These two stutlles mey be comppsed of ove.lapping samples.
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3Percenl who smoked prior to, but not during this pregnancy, calculated as part of smoker sarnple.
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418
TARLE 4.- Hortall3y ratios for female cigarette smokers by
number of cigarettes smoked per day and age.
- Females In the Canadian study.
Number of Age
cigarettes
per day
an-54
55-64
65-74
75+
Nonsmokers 1.01) 1.01) 1.nn I.nn
I- 9 1.59 I.o9 1.n5. .c2
In. 2.25 .93 I.)n
All Smokers 1.05 I.n3 I.ISS .95
distrilbuti'.on of all women.
Not shown - less than S expected deaths..
SOIIRCE:9est, E.A'.R., et al (5).
Total, 30
Age-adjusted
t/ Adjusted by the direct methed using as standard the age
TABLE 11.-Smoking and the prevalence of respiratory symptoms in girls from two different cities in
England
Symptom . Residence
Smoker+
N %
Prevalence of symptom with each group
Experimental Nonsmoker
Smokert N % Signific_ance*
N %
Cough in the morning Kent 10 31.3 51 9.8 73 6.9 P<0.001
Derbyshire 14 18.9 50 8.4 138 6.7 P <0.001
a Cough day or night , Kent 17 53.1 148 28.0 195 18.4 P <0.001
. Derbyshire 35 47.3 176 29.5 458 22.1 P<0.001
' Cough for 3 months of year Kent 5 15.6 43 83 55 5.2 P<0.01 *'
. Derbyshire 10 13.5 32 5.4 82 4.0 P <0.001
+Smoker = a child who smoked at least one cigarette a week.
tExperimental smokerca child who had smoked at sometime but less than one cigarette a week.
'Test for significant association of cough and smoking habit. Chisquara 2 x 3 table.
"Smokers and experiemntal smokers combined to give chi-square on a 2 x 2 table.
Source: Bewley, et aL (9) .
OILS89£0
FIGURE 2.-Percentage of adult current cigarette smokers in the
greater Milwaukee area, 1924-19791
80
70
10
UNAI.KEE
0
1900 . 1910
JOUR,
SERIES
MEN
I
1920 . 1930 . 1940 1950 1960 1970 1980 :
YEAR
Source: MIIWaukee Journal comsumer analyses (40)
' Priorto 1941, thewording ot[he question eliciting cigaretteuseand thetype of
respondent are not recorded; From 1941 to-1954, men were asked, "Do yow
smoke cigarettes2" while all respondents were asked, "Do anywomen in your
family smokee cigarettes ?" From 1955.to 1959, all respondents were asked,
"Do any men(women) inyourhousehold smoke.cigaretles with(without) a filten
tip?" From 1960 to 1965 and in 1967, both men andwomeniwere asked"Heve
you bought, for your own use, cigarettes with (wilhout) a filter tip in the past 30
days?" In 1966 and from 1968 to1979, bothimen and women were askedl..
"Have you bought, for yourown use;,cigaretteswith (without) .afiltertip in the
past 7 d8ys?" All percentages reflec(adults aged 18 years and over.
20
FIGURE 2: Ageatlliustetltlealh rates for ischemb tlearftlisease^
by.colonzntl sex; UnileO Stales, 1950-190
I
I WXiteMales
\
NmmLrte
J Males ~ ti ~
~ `~\
\
~
~ NonwhifeF emzlls \`
. ~
Whim F
einala `
EH
50
1950 1966
-Geh Rev.
10G0 R05
-hll Rev ~
1970
1yi5
-AilPmcl Il.y.lho Jinxl mvlhuJ'dw/Lr.US Vnlw/anm4 Iy4p.
"ICD 611i aml hh Hev. No.4ri1 and 8rtl nuv Nirs. 410 413_
SOllnf.E Dnu Ilnm ffiON:mnnnl C. ~uu.. Ioi H>eIN Sominiu
55
BII, ne..
000
200,
100
50
~ Portage La Prairie
Q Charleswood
RV%TLC CV%VCE CC%TLC SIpIII FEV1e%ffVC
FIGURE 2.-Prevalence of lung function.abnormalities among smokers in an
urban (Charleswood)anda rural (Portagela Prairie) community.
SOURCE: MaMieda, et al. (<7)
.
area smokedc.igarettes (Figure 2). This estim ate of the
prevalence of cigarette use among urban men is confirmed by
other local consum er surveys perform ed in that year. For
example, in 1949, adult male smoking rates were 69.1 percent
in Omaha, 67.4 percent in Birmingham, 69.4 percent in
Philadelphia, 63.9 percent in Seattle, and 63.4 percent in San
Jose(.39).. The growth of cigarette smoking among women occurred
much later in the face of strong social taboos. Gottsegen
notedthat "theultra smart set and, women social leaders
began to smoke at the turnn of the century" (15). By 1906,
American "girl stenographers" were reported smoking
cigarettes clandestinely (5). By 1919, somee younger women
in New York were reported smoking at dinner parties "with a
trace of defiance" (52). By 1922, New York women were
smoking openly on the streets and in bus stops (10).
The first advertisement showing a women smoking was
Lorillard's 1919 publicity for Helmar cigarettes (46, 50). In
1'926, aa young wom en in a Liggett and Myers' Chesterfield
advertisement did not smoke but pleaded, "Blow some my way"
(6). In. April, 1927, a Philip Morris advertisem ent for
Marlboro cigarettes noted that "women, when they smoke atail, quickly develop discriminating taste,"
and that Marlboro
cigarettes were as "mild as May" (2). In 1928, a Lucky
Strike advertisem ent. urged' wom en to "reach for a Lucky
instead of a sweet" (33, 43, 50). In 1934, Eleanor Roosevelt
smoked cigarettes publicly (28). By 1940, handbags and
cosmetic compacts were typically designed to hold cigarettes
(17).
Although the Milwaukee Journal (40) reported that 16.7
percent of adult women smoked cigarettes in 1934 (Figure2),
prloo estim ates of wom en's smoking prevalence are sporadic.
Wessel estim ated that wom en. consumed 5 percent of all
cigarettes in 1924 (68). Moody's Investors Service estimatedd
that women smoked 12 percent of cigarettes in. 1929 (45).
The average daily consumption of women smokers, as compared
to men smokers, is not documented for that period. If men
smokers consumed approximately twice as many cigarettes per
day as women smokers (cf. the Milwaukee Journal's 1934
survey report that women's consumption frequency was 135
packs per year as compared to 244 packs per year for male
smokers), and if the estim aties of male smoking prevalence
rates in Figure 2 are takenn as nationally representative, and
if there were approximately 5 percent more adult males thann
adult females during the 1920 to 1930 decade, then Wessel's
21
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(36) HAMMOND, E.C., HORN, D. Smoking and death rates
--Report on forty-four months of follow-up on
187,783 men. 1. Total mortality. Jousnal of
the Am erican Medical Association 166(1n):
1L.59-1172, March 8, 1.958'.
(37) HERNANDEZ,J.A,, ANDERSON, A.E., JR., HOLMES,
W.L., FORAKER, A.G. Pulmonary parenchymal
defects In dogs followingg prolonged cigarette
smoke exposure. American Review of Respiratory
Disease 93(1): 78-83, January 1966.
.(38) HIGGINS, I.T.T. Respiratory symptoms, bronchi-
tis and disability in aa random sample of an
agricultural population. Rritlsh Medical
Journal 2: 1198-1,203, 1957.
(39) HIGGINS, I.T.T., COCHRAN, J.P. Respiratory symp-
toms, bronchitis, and dtsability in a randomsample of ann agricultural community in
Dumfrieshire. 39: 296, 1958.
(40.) HIGGINS, I.T.T., COCHRAN, J.R. Respiratory symp-
toms, bronchitis and disability in a random,
, sample of ann agricultural community In,
Dumfrieshire. 39: 296-301, 1959.
(41) HIGGINS, M.W., KELLER, J.R. Seven measures of
ventilatory lungg function. . American Review of
Respiratory Disease 108: 258-272, 1973.
(4,2) HURTI, E. Prevalence of respiratory symptoms,,
chronic bronchitis and pulmonary emphysema in,
a Finnish rural population. Field survey of
age 40-64 in the Harjavolta area. Aeta
(Supplement) 61:11,1965.
(43) HUTCHEON, M., GRIFFIN, P., LEVISON, H., 7s1MEL,N. Volume of isoflow. A new test in detec-
tlon of mild abnormalities of lungg mechanics.
American. Revie w of Respiratory Disease1.10(4): 458-465, October, 1974.
198
(91) MEYER, M.B., TONASCIA, J.A. Maternal smoking,
pregnancy complications, and perinatal mor-
tal ity. Am erican Journal of Obstetrics and
Gynecology 128(5): 494-502, July 1, 1977.
(92) MEYER, M.B., TONASCIA, J.A., BUCK, C. The
interrelationship of maternal smoking and
increased perinatal mortality with other risk
factors. Further analysis of the Ontario
perinatal mortality study, 1960-1961.
American Journal of Epidemiology
100(6): 443 -452, 1975.
(93) MILLER, H.C., HASSANEIN, K. Maternal smoking
and fetal growth of full term infants.
Pediatric Research 8: 960-963, 1964.
(94). MILLER, H.C., HASSA NEIN, K., HENSLEIGH, P.A.
Fetal gro wth. retardation in relation to
maternal smoking and weight gainn in pregnancy.
American Journal of Obstetrics and Gynecology
125(1): 55-60, May 1, 1976.
(95): MULCAHY, R., MURPHY, J., MARTIN, F. Placental
changes and maternal weight in smoking and
nonsmoking mothers. American Journal of
Obstetrics and Gynecology 106(5):
703-704, March 1, 1970.
(96) MURPHY, J., MULCAHY, R. Cigarette smoking and
spontaneous abortion. British Medical Journal
1(661 8): 988, April 15, 1978 (Letter).
(:97) NAEYE, R. Effects of maternal cigarette
smoking of the fetus and placenta. British
Journal of Obstetrics and Gynecology 85: 732-
737, October 1978.
(98) NAEYE, R.L. Causes of perinatal mortality in the
U.S. Collaborative Perinatal Project. Journal
of the. American Medical Association. 238(3):
228-229, July 18, 1977.
(99) NAEYE, R.L., LADIS, B., DRAGE, J.S. Suddenn
infant death syndrom e. A prospective study.
American Journal of Diseases in Children 130:
1207-1210, November 1976.
(100). NAEYE, R.L., HARKNESS, W.L., UTTS, J. Abruptio
placentae and perinatal death: A prospective
study.. American Journal of Obstetrics and
Gynecology 128(7): 740-746, August 1, 1977.
(101) NEBERT, D.W., WINKER, J., GELBOIN, H.V. Aryl
hydrocarbon hydroxylase activity in human placenta
from cigarette smoking and nonsmoking women.
Cancer Research 29: 1763.-1769, October 1969.
289
(113) PALMGREN, B., WAHLEN, T., WALLANDER, B. Toxaemia
and cigarette sm oking during pregnancy. Prospec-
tive consecutive Investigation of 3927 pregnancies.
Acta Obstetrica et Gynecologica Scandinavica 52:
183-185, 1973.
(114) PALMGREN, B., WALLANDER, B. Cigarettrokning och
abort. Konsekutiv prospektiv undersokning av 4312
graviditeter (Cigarette smoking and abortlon.
Consecutive prospective study of 4,312
pregnancies).. Lakartidningen 68(22): 2611-2616,
May 26, 1971.
(115) PELKONEN, 0., JOUPPILA, P., KARKI, N.T. Effect of
maternal cigarette smoking on 3,4-benzyprene and
n-methylaniline metabolism In human fetal liver
and placenta. Toxicology and Applied Pharmacology
23: 399-407, 1972.
(116) PELKONEN, 0., KARKI, N.T., KOIVISTO, M., TUIMALA, R.,
KAUPPILA, A. Maternal cigarette sm oking, placenta
aryl hydrocarbon hydroxylase and neonatal size.
Toxicological Letters 3: 331-335, 1979.
(117) PERSKY, H., O'BRIEN, C.P., FINE, E., HOWARD, W.J.,
KAHN, M.A., BECK, R.W. The effect of alcohol and
smoking on testicular function and agression in
chronic alcoholics. American journal of
Psychiatry 134: 621-625, 1977.
(118) PERSSON, P.H., GRENNERT,L.,.GENNSER, G., KULLANDERS,
S. A study of smoking and pregnancy with special
reference to fetal gro wth. Acta Obstetrica et
Gynecologica Scandinavica, Supplement 78: 33-39,
1978.
(119) PETTERSSON, F., FRIES, H., NILLIUS, S.J. Epide-
miology of secondary amenorrhea. I. Incidence and
prevalence rates. American journal of Obstetrics
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(120). PETTIGREW, A.R., LOGAN, R.W., WILLOCKS,J. Smoking
In pregnancy--effects on birth weight and on cya-
nide and thiocyanate levels in mother and baby..
British journal of Obstetrics and Gynecology 84:
31-34, 1977.
(121) PIRANI, B.B.K., MACGILLIVRAY, I. Smoking during
pregnancy: its effects on maternal metabolism and
fetoplacental function. American journal of
Obstetrics and Gynecology, 52: 257-263, 1978.
I
291
documentary on Nazi atrocities) to college students who
smoke. To be characterized as either positive- or negative-
affect smokers, the subjects had to smoke during the
appropriate film and indicate a congruent mood on an affect
checklist. The major finding was that 73 percent of the
femalesample of 15 subjects exhibited solely negative-affect
smoking compared to only 36 percent of the sample of 39
males. While 80 percent of the females indicated that they
were likely to smoke in positive as well as negative-affect
conditions,their behavior did not match the self-report In
this experiment. It is difficult to determine if the
environment of the experiment altered normal behavior
patterns or if perhaps,, smokers are not accurate in describing
the types of situations Inn which they smoke.
A nation wide household-Intervie w survey conducted In
1964, 1966, and 1970 also suggested that a higher percentage
of women than men are negative-affect smokers and that
little or no difference exists between men and women in the
percentage who are positive-affect smokers (180, 181) (see
Table 8). A greater percentage of women current smokers
endorsed the statement, "it relaxes me." This supports the
hypothesis that reductionn of negative affect is a m ore
important factor for women smokers. The statements
assessing positive-affect sm oking did not sho w a clear gender
difference. In 1964, slightly more men than women endorsed
the statement "enjoys It" as a reason for sm oking, but in
1966 there was no difference between sexes, and in 1970
slightly more female than male current smokers agreed that
"cigarettes are pleasurable" (79.6 percent of wom en versus
77.0 percent of men).
To summarize: sm oking affects arousal; it is not
known whether womenn smoke to maintain a given arousal level,
to change that level, or to adjust a physical blood level of
nicotine. There are a number of studies which suggest that
women use cigarettes more in high-arousal situations than men
do. Studies which combine self-reporting with experim entai
situations providing aa good, approximation of naturall smoking
conditions are needed to shed som e light on the validity of
evaluations by questionaires alone.
SMOKING CESSATION
There is an assumption in the treatment literature that men
have greater success thann women in quitting smoking. The
352
(132) R USH, D., KASS, E.H. Maternal smoking: A
reassessment of the association with perinatal
mortality. American Journal of Epidemiology 96
(3): 183-196, September 1972.
(133) RUSSELL, C.S., TAYLOR, R., LAW, C.E. Smoking
inn pregnancy, maternall blood pressure, pregnancy
outcom e, baby weight and growth, and other related
factors. A prospective study. British Journal
of Preventive and Social Medicine 22(30): 119-126,
July 1968.
(134) RUSSELL, C.S., TAYLOR, R., MADDISON, R.N. Some
effects of smoking in pregnancy. Journal of
Obstetrics and Gynaecology of the British Common-
wealth 73: 742-746, October 1966.
(135) SASTRY, B.V.R., OLUBADEWO, J.O., BOEHM, F.H.
Effects of nicotine and cocaine on the release
of acetyl-choline from isolated human placental
villi. Arch. Int. Pharmacodyn. Therap. 229:
23-36, 1977.
(136) SAXTON, D.W: The behavior of infants whose mothers
smoke In pregnancy. Early Human Development 2/4:
363 -369, 1978.
(137) SCHIRREN, C., GEY, G. Der Einflusz des Ranchens
auf de Fortpflanzungs-fahigkelt beir Mann und
Fran. Zeitschrift Hant-Geschl. Krkh. 44: 175-
182, 1966.
(138) SCHLEDE, E., MERKER, H.J. Effect of benzo(a)-
pyrene treatment on the benzo(a)pyrene hydroxylase
activity in maternal liver, placenta, and fetus
of the rat during day 13 to day 18 of gestation.
Naunyn-Schmiedeberg's Archives of Pharmacology
272(1): 89-100, December 21, 1972.
(139) SCHORAH, C.J., ZEMROCH, P.J., SHEPPARD, S.,
SMITHELLS, R.W. Leucocyte ascorbic acid and
pregnancy. British Journal of Nutritlon 39:.
139-149, 1978-
(140) SCHWARTZ, D., GOUJARD, J., KAMINSKI, M., RUMEAU-
ROUQUETTE, C. Smoking and pregnancy: Results
of a prospective study of 6,989 women. Revue
Europeened'Etudes Cliniques et Biologiques 17
(9): 867-879, 1972.
(141) SCHWETZ, B.A., SMITH, F.A., LEONG, B.K.J., STAPLES,
R.E. Teratogenic potential of Inhaled carbon
monoxide in mice and rabbits. Teratology 19:
385-392, 1979.
293 1
I
Differences in nicotine metabolism. The metabolism, of nico-
tine may be different In men and women. Measurement of
nicotine and cotinine (the principal metabolite of nicotine)
excreted in the urine after intravenous administration of
nicotine hydrogen tartrate suggested differences in metabolism
based on sex and smoking status (171). In nonsmokers, men
excreted less nicotine but more cotinine than women,
suggesting greater initial metabolism among men. However,
there were no clear differences between male and female
smokers.
Schievelbein, et al., studied nicotine and cotinine
excretion In both regular smokers and nonsmokers after they
sm oked cigarettes with differing tar and nicotine levels (155).
Women excreted significantly lower amounts of nicotine and
cotinine compared with men for three of the four brands
tested. The gender difference was found for the excretion of
nicotine andcotinine when tested separately and together.
The number of cigarettes smoked per day did not differ
between the sexes, but the carboxyhemoglobin (COHb) levels
were lower in the women and COHb levels are often taken as
a correlate of depth of inhalation. The fem ale subjects,
therefore, m ay have received a lower dose of nicotine because
of a different smoking pattern.
Smoking and Stimulation Effects
The literature suggests that women are more likely to smoke
in situations of high arousal than low arousal and when
experiencing ^negative affect" (68, 93)4 The effects of
smoking,, which are often perceived as tranquilizing, might
then be sought as a major coping mechanism. However, it can
also be argued that the stimulant effects of nicotine, which
are usually considered the predominant central nervous system
action, might be equally useful as a mobilizer. These related
and commonly held beliefs will be examined in some depth.
Frith (68)) studied British male and female employees
in a psychiatric institute; they rangedin age from 28 to 50.
Subjects rated the strength of the desire to smoke in 22
hypothetical situations. The 12 high-arousal items involved
either emotional strain and anxiety or demanding mental
activity; the ten low-arousal items concerned boredom and
relaxation or repetitive tasks and physical fatigue. A factor
analysis of the entire questionnaire and t-tests perform ed on
male versus female scores for the most extreme situations onn
the continuum led Frith to state that men had aa greater
desire to smoke in situations inducing boredom and tiredness
350
Education
Higher levels of education are associated with higher rates of
quitting for bothh men and women. Among those with a
college education or higher, 52.1 percent of the men and 48.1
percent of the women who have ever smoked have quit. For
all other levels of education, 40.5 percent of men smokers
and 31.3 percent of women smokers have given up smoking.
Although the discrepancy Is less in the most advanced
education category, the percentage of fem ale quitters is
smaller at both levels of schooling.
--
Income
Higher levels of income are associated in both sexes with
higher rates of cessation. For those ever smokers with
incomes under $10,000, the rates of quitting for men and
women are 34.7 percent and 30.3 percent respectively. For
those with incomes of $10,000 or above, the rates are. 45.7
percent for m en and 36.2 percent for wom en. Quitting rates
of in en exceed those of wom en for all but one ($5,000 to
$7,499), of the seven income levels.
'
Occupation
There is a difference of only 7.6 percentage points between
the proportion of male and femalequitters in the category of
professional, technical, and kindred workers, with the male
quitting rate at 49.4 percent and the female quitting rate at
41.8 percent. A dramatic increase in this difference occurs,
however, among managers, officials, and proprietors. In this
category thee quitting rate for m en is 47.1 percent and that
for women is only 26.5 percent. Am ong sales and clerical
workers, 40.1 percent of the men and 25.8pe.rcent of the
women have quit. The quitting rate of housewives is in the
mid range of the rates for women in other occupations (33.9
percent).
In general, then, wom en are quitting at lower rates
than men across the major demographic categories.
Psychology of Changing Smoking Habits
A two-year follow-up of over 500 former smokers Identified
355
0
I
Yankelovich, et al. have provided a thought-provoking
description of the evolution in values which has occurred over
the past 20 years (203). Smoking is just one behavior which
may have been "suppressed" by social norms describing
appropriate behavior for women in the past, and which now
may be "disinhibited" in a very real sense.
Accompanying this shift In sanctions on female behavior
is an increase In expressed rebelliousness among girl smokers,
which was form erly more characteristic of boys. A higher
percentage of girl smokers than nonsmokers are annoyed by
"experts" who define what is good for them (53 percent
versus 34 percent), agree that there is too much regulation of
people's lives (50 percent versus 39 percent), and do not want
to follow their parent's wishes regarding their behavior
(almost 50 percent versus 26 percent), (203). Factor scores
of boy and girl smokers similarly reflect a more negative
"feeling toward authority" or dislike of adult-imposed
restrictions than those of nonsmokers, and are approximately
equal for both sexes (122). Clausen noted that girls who
smoked were less acquiescent to their parents, more
autonomous, and "strikingly higher in questt for po wer" than
nonsmoking girls (33).
The evolution in values and sex-role behaviors has
resulted in some Interesting differences between boy andgirid smokers, (203). The boy smoker remains
more socially
uneasy, expresses a greater need to be popular with the
opposite sex, and considers smoking more of a sociall asset
than the girl smoker. The girl smoker, compared with her
nonsmoking peer, is more likely to consider parties a favorite
leisure time activity, to have aa boyfriend, and to have had
sexual relationships. In addition, she is less likely to feel
nervous meeting ne w people. Finally, while she is more
willing to admit that smoking is a drawback, she shows less
acceptance than the boy smoker of the stereotype that
adolescents begin to smoke cigarettes to gain peer acceptance
and approval (122). Nonsmokers show the greatest acceptance
ofthisstereotypef and the one which describes the smoker as
a"show -off" who believes that smoking makes one look
"cool" or "grown-up."
In other studies of smoking behavior, self-esteem has
usually been investigated in terms of the adolescent's self-
confidence in interpersonal relationships. Sm oking is ego
enhancing and facilitates social functioning (116). This has
beenn observed specifically amongg adolescent girls and female
335 '
Scholastic achievement and aspirations. Achievement in school
has been one of the most frequently investigated correlates of
signal independence and maturity" (119).
more stress and greater pressure to adopt behaviors that
less aware of the risks of smoking, but they also experience
state, "Educationally deprived young people may be somewhat
wh.ich smoking is not accepted, (119). Furthermore, they
McAI'ister, et al., comment' that high academic achievement Is
probably also associated with admission into a peer group in
that they can control what they will become (122)...
efficacy (.or personal control), are linked to school achieve-
ment. Smokers have been reported to have less confidence
class and other.factors. Sense of competency and sense of
These factors are undoubtedly interrelated with social
131).
activities and have a higher rate of absenteism. (3, 10, 35,
Sm okers are less involved in extracurricular school
study (1193).
percent of girl.s)~. The same trend was found in a previous
of those in other curricula (18.3 percent of boys, 20.1
Smoking rates for boys and girls preparing for college (9.0
percent and 12.0 percent, respectively) were 50 to 60 percent
smoke than students in any other type of curriculum (122).
higher prevalence of smoking (3, 33, 99, 122). High school
students in college preparatory courses were far less likely to
reduced motivation and lower aspiration are associated with a
aspirations andd expectations in reiationn to smoking have found
that reduced motivation and lo wer aspiration are found that
lastic performance as the strongest correlate of smoking in a
sample of high school students (20).. Studies of achievement,
three factors--parent'al-smoking, socioeconomic status, and
scholastic performance--Borland and Rudolph identified scho-
association specifically for girls (35, 203). Comparing the
115, 31, 151, 198, 137j. Two studies have reported this
smoking, with a study as early as 1923 showing an
association between poor school grades and smoking (15, 81,
feelings of self-worth, aspirations and expectations for the
future,, andperceptions of efficacy, competence and the girl's
view of her own smoking behavior.
the world around her. These include attitudes, values, bel~iefs,,
of the girP smoker begins to emerge. Also there is a set of
individuai/personality factors which relate the adolescent to
another. From them, a composite picture of the environment.
Dynamic/personality factors. Up to this point, adolescent
smoking has beenn described and analyzed in terms of discrete
variables, many of which are truly not independent of one
334
TqtsLE 8.~ost frequently endorsed reasons for resuming
smoking. Fall 1964 and Spring 1966 household
Inrterv.lew survey, responses of current smokers.
Q:.. Veopl~e give all sorts of reasons for eitherr not being,abl~e
to or not wanting to stay off cigarettes. What were your
reasons for going backk to elgarette.s7 (Asked iC made a
serious attenpt to stop smoking.)
Selected total
No,wi 1.1 power
It relaxes me
Enjoys It
M .
F
M
F
M
F
M
F
Helps keep weight down M
F
Current Smokers
1964 1966
N % N %
705 55.7. 772 54.9
542 50.6 588 57.1
291 73.(s 279 ' 19.8
209 19.5 191 18.5
212 16.8 181 12.9
245 22.9. 192 18.6
144 11.4. 123 8.7
102 9:.5 90l 8_7
65 5.1 40 2.8
75 7.0. 57 5.5
98 7.743 3.1
F 70 6.546 4.5
Smoke to be sociable M
Note: More than one answer was allowabde for each respondent.
SOURCE: Adapted from DHEW'(1969).
353
the amount sm okedwithin each maternal weight gain group
from less than 5 pounds to 40 pounds or more, as shown in
Figure 6 (87). From Figure 6, one might conclude that
sm oking has a more pronounced effect on low birth weight
when maternal weight gain during pregnancy is less than 20
pounds.
Other studies have indicated a lack of relationship
between smoking and maternal weight gain, while demonstrating
a direct relationship between smoking and fetal growth rate.
The German prospective study of 6,200 pregnant women, exam -
ined every m onth from the first trim ester through delivery,
showed no significant association between smoking habit and
weightt gain. The usual relationships were found between
smoking and small-for-dates babies, with general retardation
of weight, length, and head circumference in proportion to the
number of cigarettes smoked during pregnancy (10). Miller
and Hassanein also found that the effects of smoking on fetal
gro wth did not appear to be related to maternal nutrition
(93). Persson's study sho wing retardation of fetal growth of
smokers' babies by serial' measurement of biparietal diameters
and by weight, length, and other measurements at birth showed
that the low-birth-weights were independent of maternal
weight gain. These authors concluded that the fetal gro wth
retardation resulted fromm a direct pharm acological effect of -
smoking on the fetus "rather than on influence resulting from .
nutritional deprivation" (118).
Hajeri and colleagues studiedd maternal weight gainn in
105 smokers of 10 or more cigarettes a day with a control
group of nonsmokers who were similar with respect to gesta-
tion, age, height, parity, and m aternal weight at conception.
Birth weights, specific for sex, were significantly higher for
infants of nonsm okers, with a mean difference for boys of '
330 grams and for girls of 320 grams (p<..01). Mean
etrauteral weight gain, calculated as the difference between
m aternal weight gain and the weights of fetus and placenta,
was 7,0444 grams for sm okersand 6,899 grams for nonsmokers
(54).
Garn has compared mean birth weights, specific for
gestational age, of babies of obese smokers, all nonsmokers,
and all smokers, using data from the Collaborative Perinatal
Project of the National Institute of Neurologicall Diseases and
Stroke (NINCDS). Obesity was defined as the top 15 percent
of the distribution of prepregnant weights, sho wn separately
for black and white women. Babies of the 1,383 obese white
smokers had mean birth weights similar to the total group of
238
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