NYSA TI Single-Page 4
1959. J Nat Cancer Instit 1964; 32: 115
Abstract
Ham~-ond EC. Smoking in relation to ~ortality and =orbidity. Findings in first 34 ~onths of follow-up in a prospective study started in 1959. J Nat Cancer Instit 1964; 32: 115.
Fields
- Named Organization
- Addiction Research Foundation of Toronto
- Agricultural Research Service
- Agriculture Department (USDA)
- Alcohol, Drug Abuse and Mental Health Administration
- American Association of Advertising Agencies
- American Cancer Society
- American Health Foundation (Health Research)
Plaintiff- American Heart Association (Voluntary health organization that focuses on cardiac health)
Voluntary health organization that focuses on cardiac health and stroke. AHA occasionally teams with tobacco retailers to engage in promotions/fund-raisers (see http://www.smokefree.net/doc-alert/messages/247136.html and http://www.rawbw.com/~jpk/stand/Pictures.html).- American Public Health Association (Public health organization)
Professional organization for people working in public health- ASH (Action on Smoking and Health)
Action on Smoking and Health- ASHRAE (Am Society of Heating, Refrig and AC)
American Society of Heating, Refrigeration and Air Conditioning- Association of National Advertisers (Ad group)
Group of advertising entities nationwide.- Avon (Makeup)
- British Medical Journal (BMJ) (scientific periodical)
scientific periodical- Californians for Nonsmokers' Rights (Americans for Nonsmokers rights precursor)
Precursor organization to Americans for Nonsmokers Rights- Canadian Council on Smoking and Health
- Chilton Research Services
- CPD (Curriculum and Professional Development Dept., TX Ed Agency)
Curriculum and Professional Development Department of the Texas Education Agency- Dell
- Department of Commerce (DOC)
- *Department of Health and Human Services
- *Department of Health, Education, and Welfare (HEW) (use United States Departmen (use @hew_dept)
- *Department of Transportation (use United States Department of Transportation)
- Doctors Ought to Care (Activist physician group on tobacco)
Founded by Alan Blum M.D- Education Department (ED)
- Environmental Protection Agency (EPA)
- Federal Aviation Administration (Ruled on smoking on U.S. flights)
- Federal Communications Commission (FCC)
- Federal Highway Administration
- Federal Trade Commission (Enforcement agency for laws against deceptive advertising)
Enforces laws against false and deceptive advertising, including ads for tobacco products. Ensures proper display of health warnings in ads and on tobacco products;collects and reports to Congress information concerning cigarette and smokeless tobacco advertising, sales expenditures, and the tar, nicotine, and carbon monoxide content of cigarettes.- Federal Trade Commission (FTC)
- Gastroenterology (scientific periodical)
- Harvard Medical School
- *Health and Human Services (HHS) (use United States Department of Health and Hum (US)
- Institute of Psychiatry (London)
- ITC (India Tobacco Company)
India Tobacco Company- Journal of Preventive Medicine (scientific periodical)
- Kaiser-Permanente
- Lakartidningen (Swedish medical journal)
- Lancet
- Ministry of Health (Located in Singapore)
- MRD
- National Academy Press
- National Center for Health Statistics (Keeps statistics on health-related matters)
Plaintiff- National Institute of Education
- National Institute on Drug Abuse (An addiction research center in Baltimore, MD)
An addiction research center located in Baltimore, MD- National Institutes of Health (NIH)
- National Research Council
- Naylor Dana Institute for Disease Prevention (unit of AHF)
- New England Journal of Medicine
- New Scientist (scientific periodical)
- New York State Department of Health
- Newsweek (Weekly News Magazine (U.S.A.))
- Office on Smoking and Health
Responsible for creating reports on the health effects of smoking. Created by the Public Health Service.- Preventive Medicine (periodical)
- Reader's Digest
- Red Cross
- Research Council
- Roper Organization (Consumer Research/Public Relations Org.)
Interested in finding out what drives consumer behavior; surveys consumers on their prime areas of concern; assists corporations with reputation-building and public image based on its findings.- Royal College of Physicians (Monitors the quality of Canadian/U.K. medical education)
- Smokers Clinic
- Tobacco Institute (Industry Trade Association)
The purpose of the Institute was to defeat legislation unfavorable to the industry, put a positive spin on the tobacco industry, bolster the industry's credibility with legislators and the public, and help maintain the controversy over "the primary issue" (the health issue).- U.S. Department of Agriculture
- University of California Los Angeles (UCLA)
- University of California San Francisco
- University of Edinburgh (Located in Scotland)
- University of Houston
- University of London
- University of Manchester
- University of Minnesota
- University of New Mexico
- University of Nottingham
- University of Toronto
- University of Vienna
- University of Western Australia
- University of Western Ontario
- Veterans Administration
- World Conference on Smoking and Health
- World Health Organization (Concerned with global public health)
International organization concered with public health worldwide- Yale University
- Agricultural Research Service
- Named Person
- Armstrong, Bruce K.
- Bailey, Jeffry
- Bishop, Jr., Mike A. (RJR Corp. Public Relations)
Manager Smoking- *Bock, F.G. (Fred)
Associate Cancer- Bray, Jeremy
- Brown, Ron
- Dekker, Marcel
- Elizabeth, Queen, II
- Evans, Richard (smoking in teenagers)
- Fisher, Deborah A.
- Glantz, Stanton A.
- Gritz, Ellen R., Ph.D.
Plaintiff- Hall, Russell
- Harris, John (District Supervisor in Florida Police)
- Heart, Stanford
- Hill, J. Stanley
- Howe, Holly L.
- Jacob, Micheal
- Johnson, Anderson
- Jones, R.T. (BATCO GR&DC)
R. T. Jones was with BATCO-GR&DC. (Source: NM Tobacco Companies Personnel List)- Leathar, D.S.
- Lee, J.D. (ATLA Tobacco Litigation Gp Chair, Knoxville, TC attorney)
J.D. Lee is an attorney in Knoxville, TN and chairman of the ATLA Tobacco Litigation Group in 1994. The telephone number is (615) 544-0101.- Loeb, Barbara Keely
- Mah, Russell
- Mantel, Nathan (Biostatistician, American U., Industry Expert)
PM witness- Parker, Gillian
- Pederson, Linda
- Pellegrino, Ed
- Pindborg, J.J., M.D. (Studied the effects of smoking on Leukoplakia)
- Randell, Jane
- Rawson, Nigel
- Reid, Donald
- Samet, Jonathan M.
- Schwartz, Tony
Plaintiff- Shephard, Roy J.
- Stephens, Thomas
- *Todd, G.F. (use Geoffrey Todd)
- Tso, T.C., Ph.D. (PM Tobacco Working Group)
Defense - Bailey, Jeffry
- Master ID
- TI08350674-1466
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189
Ham~-ond EC. Smoking in relation to ~ortality and =orbidity. Findings
in first 34 ~onths of follow-up in a prospective study started in
1959. J Nat Cancer Instit 1964; 32: 115.
Ravenholt RT. Addiction ~0rtallty in the United States, 1980: tobacco,
alcohol, and other subtances. Population and Development Review 1984;
I0: 697-724.
Radford EP~ Hunt YR. Polonium 210: a volatile radloelement in
cigarettes. Science 1964; 143: 247-249.
I0. Ravenholt RT. Malignant cellular evolution: an analysis of the
causation and prevention of cancer. Lancet 1966; I: 523-526.
II. Ravenholt RT. Circulating mutagens from smoking. (Letter), New Engl J
Med 1982; 307: 312.
TI03350873
191
James L. Repace, M.S.
Office of Air and Radiation
U.S. Environmental Protection Agencyt
Washington, D.C. 20460
U.S.A.
INTRDDUCTION
The major prospective studies on smoking and disease show that the risk of
the diseases of smoking are related to the total dose delivered, regardless
of the time pattern of exposure, that the disease risk increases with
increasing depth of inhalation, and that there is no discernible threshold
for any of the risks (i).
Moreover, there is now evidence, some of it conflicting, that indirect
exposure to tobacco smoke, so-called passive or involuntary smok{ng, the
breathing of indoor a{r polluted with tobacco smoke, may cause cancer and
respiratory impairment (2,3,4). In these epidemiologic studies, the
exposure variable used has typically been the number of c{garettes smoked by
a spouse; relatively little attention has been focused on factors affecting
a non-smoker's exposures or on total doses received. The purpose of this
paper is to discuss these factors.
STUDIES DESIGNED TO QUANTIFY U.S. NON-SMOKERS' EXPOSURE TO ~OBACCO SMOKE
Exposure of non-smokers to tobacco smoke might be expected to be common in
the U.S., because one out of three UoS. adults smokes cigarettes at the
estimated rate of 32 per day (5), while an additional one out of six smokes
cigars or pipes, and because indoor air pollution from tobacco smoke
persists in indoor environments long after smoking ceases (5,6,7).
Repace and Lowrey (5) presented a model of non-smokers' exposure to the
particulate phase of ambient smoke that was supported by controlled experi-
ments and a field survey of the levels of respirable particles indoors and
out, in both smoke-free and smcky environments; this phase contains 60
proven or suspect carcinogens (2,8). This work, which established that
ambient tobacco smoke imposed significant air pollution burdens on
non-smokers, was extended by later work (7) which further demonstrated the
predictive power of this model. The model predicts a range of exposure of
from 0 to 14 mg of cigarette aerosol per day, depending upon the non-
~DISCLAIMER: The op{nions in this article are those of the~_~uthor-~_ t~
crff~ci~l--6~dor~em~nt-q~-th~E~vironmental Protection Agency is intended or
should be inferred.
T[08350874
192
smoker's lifestyle. Exposures of prototyplcal non-smokers were modeled, but
no attempt was made to estimate the average population exposure. It was
shown that the concentrations of ambient tobacco s~oke encountered by U.S.
non-smokers in a variety of microenvironments can, to a good approximation,
be estimated by knowledge of two factors: the average smoker density and the
ventilation rate (5). On the average, a characteristic value of the ratio
of these factors can be assigned to a particular microenvironmental class,
e.g., homes, offices~ restaurants, etc. (9). Therefore, the average daily
REPACE ~" i
exposure of individuals can be estimated from the time-weighted sum of -:-"
concentrations encountered in various microenvironments (9,10) containing
smoke.
It is important to realize that most persons' lifestyles are such that they
spend nearly 90% of their time in just two microenvironmental classes, thus
affording a great simplification of exposure modeling (6,9). Szalai, as
part of The Multinational Comparative Time Budget Research Project, which '-"-"
studied the habits of nearly 30,000 persons in 12 countries (1964-1966), has
compiled data reporting the average time spent in various locations or
.--"-
microenvironments. Szalai's data for 44 cities in the U.S. were reorganized ..~
by Oft (11) who showed that U.S. urban dwellers spend an average of 88% of
their time in just two microenvironments: in homes and in workplaces; more- ""
over, employed persons in the U.S. cities were estimated to spend only 3% of
the day outdoors while housewives spent only 2% outdoors. Repace and Lowrey
(6) used these data to model the average exposures typical non-smokers might
receive in the two most frequented microenvironments.
Exposure of the population to the particulate phase of cigarette smoke can
be modeled to determine both range of concentration and exposure, which is
the concentration multiplied by the average respiration rate (12) of the
exposed persons.
Repace and Lowrey (5,7) have shown that the ambient concentration of tobacco
smoke particles, Q, from cigarette smoking can be usefully represented by an
equilibrium model based upon occupancy of a space by habitual smokers who
smoke 32 cigarettes per day (for every three habitual smokers, there is one
cigarette burning constantly),
Q = 217 Dhs/Cv (~g/m3)
[1],
where Dhs is the habitual smoker density in units of smokers per i00 m3, and
Cv is the ventilatory air change in units of air changes per hour (ach).
The model accurately predicts ambient concentrations of cigarette smoke over
a wide range of smoking rates and ventilation rates (5,6,7).
Ventilation rates given by the American Society of Heating, Refrigerating,
and Ventilating Engineers (ASHRAE) (13) were useful in this model to predict
observed concentrations of tobacco smoke in indoor microenvironments
(5,6,7). ASHRAE Standards are national concensus standards for ventilation
rates in the U.S., and are tied to expected building occupancy. Thus, Eq.
[I] offers the ~osslbility of modeling the range of non-smDkers' exposures
T108350975
193
to ambient tobacco smoke by inserting the ranges of occupancy and air change
rate. Using this method, Repace and Lowrey (6) estimated that the typical
U.S. ~orkplace exposures range from 1.35 to 3.38 mg/8 hrs. for an estimated
average exposure of 2.37 mg/8 hrs. This value is consistent with that
estimated from the concentrations ~easured in a field survey of 23
commercial buildings in the Washington, D.C. and New York City metropolitan
areas, which reported a mean concentration of 242 ± 238 ~g/m3, averaged over
all of the buildings. Assuming an average inhalation rate of 1.47 m3/hr (a
rate corresponding to light work) (12) for those exposed, yields an
estimated exposure of 2.85 mg/8 hrs, or at an inhalation rate of 0.99 m3/hr
(a rate corresponding to alternate sitting and light work) (12), an
estimated exposure of 1.92 mg/8 hrs. Thus, the exposure estimates are
consistent with the limited observations available. Based upon the ratio of
white-collar to blue-collar workers, and upon surveys of smoking policies of
about I000 U.S. corporations, large, medium, and small, Repace and Lowrey
(6) estimated that the exposure probability of U.$. workers to on-the-job
smoking was 63%, and that the average on-the-job exposure to passive smoking
was 1.82 mg/day, when weighted for average hours per day worked.
For comparison, we now examine the estimated average exposure modeled for
the domestic microenvironment.
HODELINC EXPOSDRE OF NON-SNOKERS AT HOME
Similarly, by using data from time budget and census studies, Repace and
Lowrey (6) estimated the average length of time a person spends in the home
microenvironment. This time differs by gender and employment status.
Taking into account the different amounts of time spent in the home by
employed men, employed women, and homemakers, they estimated that the
occupancy-weighted average number of cigarettes smoked in a typical U.S.
home of 340 ms volume during a 16-hr waking day was equal to 22 cigarettes
per day (CPD). Using this figure, Eq. [I] predicts, using an air exchange
rate typical of that expected for U.S. dwellings, a concentration value in
good agreement with measurements of respirable particles obtained in homes
containing one smoker from the Harvard Six City Study by Dockery and
Spengler (14,15). By multiplying by a respiration rate corresponding to
that of alternate sitting and light work, Repace and Lowrey (6) estimated
that a typical U.S. non-smoker is exposed to an average inhaled exposure of
0.45 mg/day, with an exposure probabil~ty of 62%, assuming that occupancy of
the home by smokers and non-smokers is coincident.
NEAN ESTIHATED EXPOSURE FOR A TYPICAL ADOLT FROH TI~ HDST-FREQUENTED
NICROENVIRONMENTS
Repace and Lowrey (6) estimated a probability-weighted average exposure for
a typical U.S. adult by combining the estimated exposure to U.S. adults
ex~osed~i~_~he~wo_~kpi~ce_and_~__h~.~e~_by
each microenvironment by the probability of receivinB it, assuming that the
probabilities are independent, i.e., tha~ exposure at work i~ not correlated
wit~ exposure at home. The results are su~arized in Table I.
TI0~o50,..,76
TABLE I. ESTIMATED PROBABILITIES OF NON-SMOKERS BElOnG ~XPOSED TO
TOBACCO SMOKE AT HOME AND AT WORK (6)
Probability of being exposed at work: 63%;
Probability of not being exposed : 37%.
Probability of being exposed at home: 62%;
Probability of not being exposed : 38%.
Estimated
Daily Annual Average
Probability of being exposed
(Rounded Values)
Estimated Estimated
Daily Daily
Average Probability-
Exposure Weighted
ReceivedExposure
At work and at home:
Neither at work nor at home:
At home only:
At work only:
63% x 62% = 39% 2.27 mg .89 mg
37% x 38% = 14% 0.00 mg .00 mg
37% x 62% = 23% 0.45 mg .lO mg
38% x 63% = 24% 1.82 mg .44 m~
Total: 100% 1.43 mg/day
Table 1 suggests that the typical U.S. non-smoker is in fact a passive
smoker who receives an average exposure of 1.43 mg/day, and that very few
(~15%) persons in the general population appear to escape daily exposure to
tobacco smoke. Table 1 further suggests that indlvlduals having exposure
both at home and at work constitute high exposure groups, with the workplace
likely contributing more exposure than the home by a ratio of 4 to i. These
calculations imply that epidemiological studies of passive smoking should
control for exposures both at home and in the workplace. Further, if
passive smoking does create a risk of smoking-related disease, there may be
disparities in incidence observable by comparing the more-exposed and less-
exposed categories, but if these categories are not separated, as they were
not in the American Cancer Society Study of passive smoking and lung cancer
(16), a potentially large confounding factor has not been taken into
account, particularly since more than one third of U.S. women have been in
the labor force since 1950 (17). Although the Japanese and Greek studies
also did not take working into account, as Hammond and Selikoff (18) have
suggested, this factor may not be as important in such relatively tradition-
al societies (26,27).
TRANSLATING EXPOSURE INTO DOSE
At this point, the estimated range of exposure has been established for
typica~U_.S_._non=s~ok.~s_as_0~t~ 14 ~g~.ay~__t~__ty~_i~.al ~l~qk~lace exposure
has been estimated at 1.82 mg/day, the typical home exposure at 0.45 mg/day,
and the typical exposure at 1.43 mg/day. These may be directly compared
with the 1981 sales-weighted average tar level for U.S. cigarettes of 14
mg/day, or with the level of the lowest tar cigarettes on the market, 0.55
mg or with pre-1960 cigarettes of tar level greater than 30 mg, according to
T108350877
one's preference (191. However, none of these comparisons ~xpress the dose
of tobacco tar to the non-s=oker's bronchial epithelium, rather, they
express the a=ount inhaled daily. It is of interest to calculate the dose
received by a typical non-smoker's lung in each of three cases: the worst
case, the workplace, and the home.
Close association with smokers at work and at home may lead to repeated
daily inhalation of tobacco smoke by non-smokers. This is significant
because repeated daily ezposure of non-smokers to indoor air pollution from
tobacco smoke may lead to a buildup of tar in the lungs to an equilibrium
amount which may far exceed the daily exposure. This is a direct conse-
quence of the very long clearance times for fine-particle aerosols deposited
in the lungs (201. On a single-compartment ra~del (i0) for lung-clearance,
the equilibrium level of tobacco tar in a non-smoker's lungs is given (5,10)
by De~. = ~ ~ D_,,, where D~, is the daily nominal dose, r is the mean life for
pulmonary clearance (1.44 times the half-life), and ~ is the fraction of
inhaled aerosol deposited. We assume the values r = i01 days (20) and ~ =
11%, although a value as high as 20% has been reported (21). In terms of
our modeled Dn (al of 1.82 mg/day for a typical non-smoking worker, (bl of
.45 rag/day for a typical non-smoker at home, (c) 1.43 mg/day for a typical
non-smoker overall, and finally, (d) our worst case, 14.4 mg/day (5) for a
non-smoker working in a piano bar with a chain-smoking spouse, we calculate
respectively, in units of mg of tobacco tar, an equilibrium dose to the
bronchial epithelium of (a) 20 mg, (b) 5 mg, (ci 16 mg, and (d) 160 mg.
On this single-compartment equilibrium model, the estimated doses to the
bronchial epithelium of regularly exposed passive smokers are equivalent to
smoking between a third of a 1981 sales-weighted average tar cigarette per
day and a half-pack per day. In view of the U.S. Surgeon General's
assertions that there is no safe level of consumption of cigarettes, that
there does not appear to be any threshold effect for any of the diseases of
smoking, that risk is closely related to total dosage, regardless of the
time pattern of exposure, and that even the lowest yield of cigarettes
presents significant risks, dosages of this magnitude cannot be dismissed as
inconsequential, being well within the range of observed effects in smokers.
Is there any evidence to support this concept? Earlier work (5) discussed
anecdotal evidence, based on elevated aryl-hydrocarbon hydroxylase and
pigmented alveolar macrophages, that this buildup appears to have been
observed in two non-smokers. Moreover, serum thiocyanate (22) and benzpyrene
(23) levels in some non-smokers have been found to be comparable to the
elevated levels typically found in smokers. However, the most persuasive
evidence has recently been provided by Matsukura (24), who found that
urinary cotinine levels in 472 Japanese passive smokers who lived with
smokers of >40 cigarettes per day or worked with >6 smokers, were virtually
indistinguisable from urinary cotinine of smokers of less than 3 cigarettes
per day. Such a buildup phenomenon appears to offer a plausible explanation
for the findings by White and Froeb (25), Trichopoulos et al. (26), and
Hirayama (27), that the risks of passive smoking were considerable fractions
T108350878
196
REPACE
CONCLUSIONS
Non-smokers' exposures to ambient tobacco smoke can be estimated using an
equilibrium m~del. Estimates of such exposures appear to be consistent with
measurements of concentrations in various indoor microenvironments.
Estimates of exposure probabilities indicate that passive smoking appears to
be a widespread daily phenomenon which only 15% of non-smokers of working
age escape. The results also indicate that estimated average U.S.
workplace-related exposures are about four times higher than estimated
average U.S. domestic exposures.
A single-compartment model for the equilibrium dose of respirable aerosol to
non-smokers' lungs, resulting from regular passive smoking, indicates that
tobacco tar may accumulate to levels reaching an order of magnitude higher
than nominal daily exposures. This phenomenon offers a possible explanation
for the results of epidemiological studies of diseases caused by passive
smoking which indicates risks which are substantial fractions of those of
active smoking. Estimates of the average doses to non-smokers from passive
smoking at home and at work suggest that typical equilibrium doses from
these two most-frequented microenvironments are 20 mg and 5 mg, respective-
ly, and the overall probability-weighted dose to the typical non-smoker
appear to be about 16 mg. The worst-case equilibrium dose is estimated to
be 160 mg of tobacco tar on the bronchial epithelium. The magnitude of
these doses is equivalent in value to the exposure obtained in smoking from
i/3 to ii sales-weighted average tar (14 mg) cigarettes (1981 value) per
day.
Cigarette smoking has been judged by the Surgeon General to be a major cause
of cancers of the lung, larynx, oral cavity, and esophagus~ and a
contributory factor for the development of cancers of the bladder, pancreas~
and kidney, to be causally related to coronary heart disease, and to be the
leading contributory cause of death from chronic bronchitis and other lung
disorders. The U.S. Surgeon General has also stated that there is no safe
cigarette nor safe level of consumption.
Because non-smokers' doses of tobacco smoke from involuntary smoking appear
to be, even on average, well within the range of exposure of active smokers,
there is good reason to believe that indoor air polluted with tobacco smoke
poses a significant threat to the health of non-smokers (28).
US Dept of Health & Human Services. The health consequences of smoking:
the changing cigarette. A report of the Surgeon General. Washington,
D.C.: U.S Dept. of Health & Human Services,. 1981.
US Dept of Health & Human Services. The health consequences of smoking:
Smoking and cancer. A report of the Surgeon General. Washington, D.C.:
U.S. Dept. of Health & Hum_an Services, 1982. (DHHS publication no.
82-50179).
TI08350879
197
3. Kauffman F, Tessier JF, Oriol P. Adult passive smoking in the home
environment: a risk factor for chronic airflow limitation. Am J
Epidemlol 1983; 117: 269-280.
4. Repace JL. The problem of passive smoking. Bull NĄ Acad Med 1981; 57:
936-946.
5. Repace JL, Lowrey AH. Indoor air pollution, tobacco smoke, and public
health. Science 1980; 208: 464-472.
6. Repace JL, Lowrey AH. Modeling exposures of non-smokers to ambient
tobacco smoke. Paper presented at the 76th Annual Meeting of the Air
Pollution Control Association, Atlanta, 1983 June 20-25.
7. Repace JL, Lowrey AH. Tobacco smoke, ventilation, and indoor air
quality. ASHRAE Transactions 1982; 88: 894-914.
8. US Dept of Health, Education and Welfare. Smoking and health. A report
of the Surgeon General. Washington, D.C.: U.S. Dept. of Health
Education and Welfare, 1979. (DHEW publication no. (PHS) 79-50066).
9. Repace JL, Oft WR, Wallace LA. Total human exposure to air pollution.
Presented at the 73rd Annual Meeting of the Air Pollution Control
Association, Montreal 1980 June 22-27.
10. National Research Council. Indoor pollutants. Washington, D.C.:
National Academy Press. 1981.
Ii. Oft, WR. Human activity patterns: a review of the literature for
estimation of exposure to air pollution. Washington, D.C.: U.S.
Environmental Protection Agency, (in press).
12. Altman PL, Ditmer DS. Respiration and circulation. Bethesda, MD:
Federation of American Society for Experimental Biology, 1971.
13. American Society of Heating, Refrigerating, and Ventilating Engineers,
Atlanta. ASHRAE Standards for Natural and Mechanical Ventilation.
1973: 62-73.
14. Dockery D, Spengler JD. Indoor-outdoor relationships of respirable
sulfates and particles. Atmospheric Environ 1981; 15: 335-343.
15. Dockery D, Spengler JD. Personal exposure to respirable particulates
and sulfates. J Air Pollut Control Assoc 1981; 31: 153-159.
16. Garfinkel L. Time trends in lung cancer mortality among non-smokers and
a note on passive smoking. J Nat Cancer Instit 1981; 66: 1061-1066.
17. US_Dept of Comme~ce_. S~9~j~!_i~9~_Ab_%~acts of the United States~ 1980.
Washington, D.C.: U.S. Dept. of Cor~erce, 1980.
18. Ha~_~ond EC, Seliko~f IJ. Passive smoking and lung cancer with co~ents
on two new papers. Environ Res 1981; 24: 444-452.
T108350880
19 8
REP~C'~
19. Bock FG, Repace JL, Lowrey AH. Non-smokers and cigarette smoke: a
=odified perception of risk. Science 1982; 215: 197.
20. Cohen D, Arai SF, Brain JD. Science 1979, 204: 514.
21. Hiller FC, McCusker KT~ Mazunder M~[, Wilson JD, Bone RC.
Respiratory Dis 1982; 125: 406.
Am J
22.
Cohen JD, Bartsch GE. A comparison between carboxyhemoglobin and serum
thiocyanate as indicators of cigarette smoking. Am J Public Health
1980; 70: 284-286.
23. Repetto M, Martinez D. Benzopyrene de cigarettes et son excretion
urinaire. J Europ6en de Toxicologie 1974; 7: 234-237.
24. Matuskura S, et al. Effects of environmental tobacco smoke on urinary
cotinine excretion in non-smokers. New Eng J Med 1984; 311: 828-832.
25. White JR, Froeb HF. Small airways
chronically exposed to tobacco smoke.
720-723.
dysfunction in non-smokers
New Eng J Med 1980; 302:
26. Trichopoulos D, Kalandidi A, Sparros L. Lung cancer and passive
smoking: conclusion of Greek study. Lancet 1983; 2: 677-678.
27. Hirayama T. Non-smoking wives of heavy smokers have a higher risk of
lung cancer: a study from Japan. Br Med J 1981; 282: 183-185.
28. Repace JL, Lowrey AH. A quantitative estimate of non-smokers' lung
cancer risk from passive smoking. Environment International 1985;
ii: 3-22.
NOTE ADDED IN PROOF:
Dr. Hirayama, in a presentation at The Fifth World Conference on Smoking and
Health, suggested that passive smoking in Japan contained an additional
component, innate to the Japanese lifestyle, which he called "direct passive
smoking" to connote the exposure received hy Japanese spouses who associate
with one another in closer proximity than is common in Occidental cultures.
A crude estimate of the magnitude of this effect based on limited data (7)
suggests that exposures received in this manner are of the order of 40%
higher than those received by general mixing from room air circulation.
This may tend to offset the effect of higher infiltration rates in Japanese
dwellings relative to the U.S.
Tl0,3350681
PASSIVE S~OKIRG ARD I~E LUNGS:
A ~EVIEW OF EFFECES OTHER ~ MALIGRANCY
Jonathan M. Samet, M.D.
The Department of Medicine
University of New Mexico Medical Center
Albuquerque, New Mexico 87131
U.S.A.
Frank E. Speizer, M.D.
The Channing Laboratory~ Department of Medicine
Brigham and Women's Hospital, Harvard Medical School
180 Longwood Ave., Boston, Massachusetts 02115
U.S.A.
Passive smoking refers to the involuntary exposure of non-smokers, both
children and adults~ to tobacco combustion products. This review examines
the epidemiologlcal evidence for effects of passive smoking on the lungs,
other than lung cancer and upper airway irritation.
PASSIVE SMOKING A~D (~IILDREN
For children, smoking by parents or other household members is the principal
source of exposure. In the United States, approximately 54 million adults
are current smokers and the majority of homes have at least one smoker
(I,2). Because of this high prevalence of passive smoking, even small
adverse effects have important implications for public health.
Six investigations of varying design have demonstrated an increased risk of
lower respiratory tract infection in infants with smoking parents (Table
|). Four longitudinal studies evaluated the respiratory illness experience
of infants; each showed a significantly increased frequency of bronchitis
and pneumonia during the first year of life when parents smoked (3-6).
Dose-response relationships with ~xtent of parental smoking were demonstra-
ble in three (3,4,6). An effect of passive smoking was not readily identi-
fied after the first year of life. Two controlled follow-up investigations
of children with respiratory syncytial (RS) virus infections during infancy
also demonstrated an effect of passive smoking (7,8).
Studies of older children have demonstrated similar adverse effects of
passive smoking on respirato~/ illness experience. In two large studies in
the United States, parent smoking was associated with a history of serious
Address correspondence to: Jonathan M. Samet, M.D.
TI08350882
