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FACT OR FANCY? • Smoking causes wrinkles in women Smoking causes low-weight babies • Women who smoke harm their babies before and after birth • Women are smoking like men and dying like men Of course you've noticed. It's difficult not to. Women are now the special target of those who would stamp out smoking. And standard, unsubstantiated charges having failed, these crusaders are now trying to hit women where they think them to be most vulnerable -- with threats to their babies and their good looks, and, yes, even their sex lives. In the belief that full, free and informed~discussion of the smoking controversy is in the public interest, The Tobacco Institute has assembled the most frequently heard allegations concerning women and smoking -- and created a dialogue encom- passing the current scientific knowledge on each point. Here, then, are some questions about women and smoking -- and the answers, at least where they are known. t .

-2- 2 Smoking Women Small Babies Pregnancy Outcome Effects on Children Sex and Reproduction Facial Wrinkles Advertising Ulcers Lung Cancer CONTENTS - Page Heart and Vascular Disease Chronic Respiratory Disease Increased Morbidity Summary Reference Sources 3 5 9 13 15 17 19 21 23 29 39 41 43 O W ~ 45 .;a t

C K -3- Q, First of all, is it true that more women are smoking today than ever before? The number of adult American~women who choose to~smoke is apparently larger than ever. But so is the number of women in the U.S. population. The incidence of smoking among,women -- the rate, or percentage of women~ who smoke -- is, however, as low as it was before World War II, when women first began smoking in significant numbers. Public surveys over the last 40 years show an increase from 1935 to 1944, when more than four out of 10 women said they smoked, and a gradual drop to the less thanthree out of 10 estimated by the Public Health Service in 1975 (34, 36-38, 99, 100, 111). The question of the amount of smoking is much more difficult to resolve because there is the known tendency of persons to underestimate the number of cigarettes smoked daily. However, in commenting on a 1975 survey of adult smoking, a consulting psychologist who has directed government smoking surveys since 1967 stated last year in reference to women's smoking levels during the last decade, "No, they're not smoking more cigarettes" (40). Somq-persons who disapprove of cigarette smoking say that the larger number of women smoking today accounts for everything from higher lung w ~ cancer death rates to an allegedly higher incidence of ulcers, not to MIA N mention smaller babies and even larger government disability costs for U1 emphysema. But if the percent of women in the general population who smoke ( is not larger, and if women_smokers are not smoking more, then any higher incidence of disease cannot logically be attributed to cigarettes.

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c e C Do women who smoke while they're pregnant have smaller babies? .t Yes, their babies usually weigh less than the babies of mothers who don't smoke (105)~. Detractors of smoking emphasize the reduced weight of smokers' babies because, they say, birth weight is one of the most important predictors of risk in infancy. And because smokers have smaller newborns whatever the cause -- they are more likely than nonsmokers to bear infants that are low-birth-weight (LBW), an arbitrarily set measure of below 2501 grams (about 5.5 pounds) (113). "It is now generally accepted that maternal smoking is related to a reduction in birth weight," National Institutes of Health researcher Debra Silverman wrote in the June 1977 American Journal of Epidemiology (90). She said: The critical issue is whether smoking causes a reduction in birth weight (the causal hypothesis) or whether smokers are a self-selected group that differs from nonsmokers in ways unrelated to smoking, including the production of lower weight babies (the self-selection hypothesis). ` Some other differences among women which are associated with varying birth weights of their children, or outcomes of their pregnancies -- but do not necessarily cause those variations -- are socioeconomic level, race,age, height, previous obstetric experience and access to ad'equate health care. A baby's sex and whether it is a first or, say, fifth child can also affect weight (13). ' 0 W Q ~ To control for as many of these differences as possible, Silverman N ~ decided to look at weight differences in pairs of infants born to the same ~

-6- mother. mother. And she located 1016 such pairs, one third of them born to Iz women who had begun smoking sometime after their first pregnancies. Silverman reasoned that if smoking alone causes birth-weight reduction, the mean weight differences between first and second babies of mothers who smoked only during the second pregnancy would be signi- ficantly greater when compared to those observed where mothers smoked in both pregnancies, or neither. An&the second babies of the "change& smokers" would be lighter than the first. Neither supposition proved true. There were all the expected differences -- smokers generally had lighter babies than nonsmokers and the "change&smokers" produced babies with weights between smokers an& nonsmokers. But the differences were not large enough to establish that they could not have occurred by chance. Strangely enough, the babies born to smoking mothers who had not smoked in the previous pregnancy were slightly heavier on the average than -their older brothers and sisters had been. But this was thought to have occurred because of the youth of these mothers when they bore their first children. Young mothers produce small babies. Silverman claimed her study failed to confirm that infant weight is dependent,on innate characteristics of the mother rather than any effect of smoking. But she said the observation that future smokers before they began smoking tended to have lighter infants than nonsmokers was "more C W ~ consistent with the self-selection hypothesis" (90). 01 _ IV Her findings were consistent with two other studies indicating that (z some women will have smaller babies whether or not they smoke in pregnancy.

. , . < -7- One, a large California project, included women who began smokingg after deLivering,their first children. Those children, born before the mother smoked, were lighter than the nonsmokers' infants in the study The other study, done in Scotland, reported that sisters of women~who delivere&low-weight infants also tended to have lighter babies (57)~. (114). At least one large-scale study -- of British births in one week in 1958 -- indicated that smoking mothers have heavier babies if they quit or cut down on smoking after the fourth month (14). More recent research, published in 1977, suggests that any fetal weight reduction attribute&to smoking does not occur in the later months -- if indee&it is caused by smoking. Studying more than 1000 pregnant women registered with three maternity units, a British researcher found no statistically significant weight difference between the babies of smoking mothers who quit early in~ pregnancy and those who had quit but resumed smoking in the last four months (26). What little di.fference there was -- an average of 2.8 ounces less -- was, he said, in the opposite direction to that which would be expected if smoking in late pregnancy reduced the birth!weight. The researcher also found that there was no proportional decrease in birth weight with increasing amount smoked by the mother and he said this appeared to support what he called "the other-factor hypothesis." LBWinfants are not necessarily premature (bornitoo soon). They are small for their gestational age and are the subject of concern because their risk of death is almost 10 times greater than that of infants in the next highest weight category, 20 times greater than infants of the most common~birth weight category (113).

-8- What opponents of smoking fail to point out, however, is that a]mnst all the researA on the subject has shown that the LBW babies of women who smoke in pregnancy are healthier than the LBW infants of women who have not smoked. The 1973 Public Health Service report, "The Health Consequences of Smoking," says: If mortality rates were compared for those infants of smokers and nonsmokers weighing less than 2500 grams, the infants of nonsmokers apparently had a considerably higher risk than did those of smokers (105). (Emphasis added.)

t -9- Then why the slogan that pregnant women who smoke endanger two. lives? .9 Who knows -- perhaps because so many well-meaning persons who nowadays seem to want to improve the lives of others accept old myths. But propaganda based on~such ignorance can only delay scientific progress. Some studies have shown a higher rate of spontaneous abortion, stillbirth and infant deaths among smoking women (13,22,35,66). Other studies, however, have shown no differences at all (27, 77, 80, 87, 98, 118). But the conflict in evidence is not considered by those who dis- approve of smoking. Andthey ignore the paradox that the U.S. infant mortality rate continues to drop (101) while the denigrators of cigarettes claim~that more women than ever -- and presumably many mothers-to-be -- are smoking. Nor do the anti-smoking tracts and speakers cite other factors that may affect the unborn child. Even a partial listing would have to include occupational exposures, viruses, X-rays, interval between pregnancies, both obesity an&insufficient weight gain by the mother, use of hormones, aspirin~, antibiotics, vitamins -- and, of course, illicit drugs (12, 21, 49). One of the most recently identified factors is the proximity to airports, unbelievable as it appears (7). .;a U' tV F-D. N

. < , -10- Everyone's heard the old admonition that smoking will stunt a youngster's growth. What about the new claim that youngsters whose mothers smoked while carrying them~are shorter than their contemporaries whose mothers didn't smoke? Those who say this cite research in England that purported to show that children of smoking mothers were shorter, on average, at age 7(39)1. The difference in average height was 1 centimeter, or about three-tenths of an inch. And the same study found that at age 7 the child of a blue- collar family was on average 1.3 centimeters shorter than the child of wealthier parents. The fourth child was 2.3 centimeters shorter than a first born. The same British survey is used for the allegation that smokers' children lag behind imreading ability at age 7 (25). The claimed difference is four months. No such differences were found in a Johns Hopkins study of heights and intellectual abilities of 7-year-old children of smoking and non-.. smoking mothers (46). In Brazil, a study which compared the physical growth rates of LBW babies of smokers as well as nonsmokers with infants of average weight showed that the LBW babies grew faster and had essentially caught up by the second year of life (8). And the British researchers measured little difference in either physical or mental development in the same children four years later, when they were 11. The doctor and the statistician who had designed the study reported in 1973 that what variations there were were small compared to differences associated with social class and family size (15). For instance, comparison showed that a child from a household with no older

C children was on average 16 months behind in general ability when compared with tie child who~had three or more older sisters and brothers at home. The average difference in reading ability was 29 months, in mathematics 14 months. And'the child with no older sisters and brothers was 4 centimeters taller on the average at 11. Coincidentally, other researchers using the same British study data showed that near-sighted children are more than a year ahead of the average at age 11 in math and general ability (78). But those who look only at whether mother smoked or not continue to claim that her smoking,impedes her child's growth and learning skills... W

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., I -13'- (I Q. Is it true that smoking mothers can harm their babies after birth -- that cFiildren of women who smoke suffer more respiratory illnesses, especially bronchitis and pneumonia? A. This is a frequent emotion-lademclaim against cigarettes. Children have more respiratory infections as a whole than adults. They are thought to be more susceptible to airborne germs, smog and other environmental effects. So a number of researchers have set out to investigate the effects of parental smoking -- with conflicting results. Statements that the chilVs health is harmed by a parent's cigarette smoke are usually based on research in Texas (69), and Michigan (17, 18), in England (20) and in Israel (47), dating as far back as 1969. The findings and conclusions of each of these studies, however, have been questioned by the U. S. Public Health Service because of faulty study design (104, 107). Three other studies here and abroad have failed to demonstrate any adverse relationship. One was conducted among second graders in Chattanooga by government health officials (89). Another, supporte&by the Public Health Service, was done by researchers from Yale and Johns Hopkins (88). The third, a survey of 1400 Dutch school children, foun6that the respiratory symptoms of the children were related to their parents' symptoms, whether or not the parents smoked (63). O n a 1 f d f i E 1 d d w t t M 7 W~hk Scotland identified a so-called "cooking effect" among other environmental L11 g n an ers n ore recen y, a our-year stu y o 5 00 youngs cr

-14- and socioeconomic factors in the prevalence of respiratory symptoms and diseases (75). Boys and girls from homes in which gas was used for cooking had more coughs, "colds going into the chest" and bronchitis than children whose homes had electric stoves. The researchers concluded that products of fuel combustion might be the cause of the increased respiratory illness. It is difficult to understand why parental smoking is blamed for a child's coughs or wheezes, in view of these conflicts in research findings.

. C -15- r Is there anything to the charge that smoking can interfere with sexual and reproductive functions of both men an&women -- that it may lower the libido and impair fertility? This favorite attention-getter of anti-smokers shows up from time- to-time, particularly in stories supplied to local newspapers by fund- raising organizations in health fields. There are limited and nonscientific data on animals and less on humans, most representing uncontrolled "clinical" observations and questionnaire surveys of individuals who claimed;"sexual problems." Some eminently refutable claims about impaired sex activity were included in a popular national family heal!th~magazine in 1974 (95). But, in 1975, an international scientific publication, The Journal of Sex Research, published "A Critical Review of Reports on the Effect of Smoking on Sex and Fertility," a comprehensive survey of 4,1 medical papers, dating back to 1923 (93). The authors concluded: EXisting evidence does not support the hypothesis that smoking or tobacco extracts have an effect on sexual activity or procreation~. An Ohio physician~, a liongtime anti-smoking volunteer, with refreshing candor, more recently told an;American Cancer Society meeting in Chicago the same thing. Only "a thoroughgoing statistical analysis of a sizeable Q w population" could prove any point about smoking and sexual dysfunction, he -j '.7. said, "and I have not yet seen such a studg..." (60). ~ N (~') ~

C -16- Nevertheless, the issue shows that history does have a way of repeating -k itself. A contemporary historian devoted two pages in a tobacco history to some claims of 19th century reformers and evangelists (84). While some of them warned that tobacco would render users impotent, others spoke of "tobacco excitement" and cautioned: Ye who wouId be pure in your_love-instinct, cast this sensualizing fire from,you.

c Q, Is it true that smoking causes facial wrinkles? 2 A. Those who may not be familiar with the medical literature, who may have merely repeated what they've been told by others, say smokers have more facial wrinkles than nonsmokers, and so smoking obviously causes wrinkles. One doctor, an internal medicine specialist in Cali- fornia, is the originator of this claim. He reported in 1971 that among his patients, friends and casual visitors, the smokers had more and deeper crow's feet around the eyes than the nonsmokers (24). He admitted that his grading system for the severity of wrinkling was "crude" and said he didn't think that any observer bias could explain the nonsmoker-smoker differences found. "The additional evaluations by fresh, naive observers of the same subjects would seem to support this view," he said. The catch was that the fresh, naive observers in his "scientific" experiment -- who measured wrinkles in pictures of 400 persons -- were two high school sophomores and a 12-year-old. - Shortly after these observations were published, three Navy doctors set out to check the Californian''s conclusions, asking themselves three questionsi 1. If smoking is the most important factor in producing wrinkling, why does it occur in sun-exposed areas and not on all skin areas? 2. Do blacks, whose skin is not susceptible to sun-caused changes, develop similar wrinkles if they smoke? ( 3. If smoking is the "prime" cause of facial wrinkling, how does it create the wrinkles?

-18- They designed a controlled study, and,unlike the California "research," included blacks. They reported that black smokers were no more wrinkled than black nonsmokers, and they concluded in an article published in the Journal of the American Medical Association that sun exposure -- not smoking -- causes early crow's feet (1). The anti-smokers, however, continue to cite what one news service reporter called "the latest weapon in the arsenal of the anti-smoking crusade...an appeal based on the presumed vanity of women" (33).

. . r t Q. There are those who call for an end to cigarette advertising , because, they say, it persuades people to begin smoking, especially the young female, in an era of new freedom for women. Does advertising create new smokers? A, No more than advertising a specific brand of toothpaste causes more people to use toothpaste. Cigarette advertising is brand advertising, aimed at interesting smokers in switching brands and in creating brand loyalty. A Wayne State University economics professor said in a study supported by the American Cancer Society that cigarette advertising is a "competitive weapon that companies have use6to divide the cigarette market; it has not been used as a means for expanding the cigarette market" (44). And the chairman~of Harvard's department of psychology and social relations tol(lan ACS meeting in June 1977 that most of the evidence indicates that advertising does not play a major role in inducing young- sters to smoke (71). But perhaps the best answer lies in the words of a woman -- a New York advertising agency president and ACS consultant who is active in Cancer Society affairs: ...I don't think the increase in cigarette smoking in girls and women is due entirely or even largely to skillful, mani- pulative advertising. Essentially we are dealing with a broad cultural development: a good deal of the behavior that has been man's alone for so long is now open to women...including cigarettes on a man-sized scale (41).

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C -21- Q. If women are smoking "on a man-size&scale," is that why they are said to be getting more ulcers? More women seem in~recent years to be getting ulcers, or, as one government publication said recently probably not entirely tongue-in- check, they are "seizing the longtime badge of success for businessmen" (43). Thirty years ago men had ulcers about 20 times more frequently than women, but the ratio is now about 2 to 1, according to hospital and clinical records studied at the University of California. But that's only because the incidence in males is falling (43). Smoking has been associated with ulcers -- as have stress, heredity, alcohol, coffee andlaspirin (105). Ulcers will strike one in every 20 women at some time in life (55), and they are reported more frequently in women who smoke than in women who don't (116). But few if any gastroenterologists claim a causal association. And no relationship between the amount of smoking and ulcer incidence has been~found (42). "The nature of the relationship between smoking and ulcers is not understood," says Dr. Morton J. Grossman, director of UCLA's Center for Ulcer Research and Education. But, he says, genetic factors clearly contribute to both gastric and duod'enal ulcers, although they are inherited independently. Writing in a current leading medical textbook (42), Dr. Grossman noted the tendency to concordance for ulcers in identical twins, whoy of W' ~ course, have like genes. In other words, if one twin~has ulcers, chances ;b C11 N ~ w

-22- are the other twin will also. The presence of ulcers in the secon& twin is more common in identical twins than in fraternal twin pairs. He called this "strong evidence that the increased familiaL incidence of ulcer is due to genetic factors and not simply to a shared environment." The role of psychic conflict -- job stress or identity crisis, perhaps, in today's "liberated" womarn -- has not been adequately explored. But various hypotheses exist, many of them involving a predisposition toward ulcer through1inheritance or a locked-in way of life. The type of temperament that leads to stress problems also leads towardiuse of what a former president of the American Gastroenterologilcal Association calls "'stress relievers." "The person who smokes 40 cigarettes a day usually alsoidrinks eight cups of coffee and has a few martinis," Dr. Henry D. Janowitz has said in Harper's Bazaar (54). "The additive effect of these an&other stress-coping habits is the cause of trouble." In a recent roundup of developments in ulcer therapy a national news publication pointed out that "despite the progress, modern medicine still can't explain what causes ulcers" (55).

-23- Are Are lung cancer death rates rising more rapi~dly in women than jn men? And is t-his because more women are said'to be smoking? Lung cancer d'eath rates reported for U.S. women have been risingg faster year to year than~those in men since 1961. AnnuaL increases in lung cancer rates for women have exceeded those increases in male rates since 1963' (11i0). However, the proportion of cases of the lung cancer cell type that has been related statistically to smoking has changed little in1women over the past 25 years, and various research reports have shown that from 15 to more than 40 percent of the lung cancer cases in women occur in those who have never smoked (9, 61, 114, 117). Some scientists believe that the recent rise in lung cancer in women is more apparent than real, because physicians order diagnostic tests more frequently now for women patients they know to be smokers. Therefore, they diagnose more lung cancer where it might not have been found in earlier years. An epidemiologist at Yal~e has foundin a 12-year study of hospital records that the use of sputum smear tests increased dramatically im women, from 52 percent of women lung cancer patients in 1953 to 78 percent by 1964 (30, 31). He said: This increase in the search rate for women may possibly play a role in various recent reports of rising rates of lung cancer in women (32). Cigarette smoking, he added'., may contribute more to the diagnosis of lung cancer than~it does to producing the disease itself -- in men as well as women.

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Y t -25- Do those women who smoke and get lung cancer have anything else in common thatrcould have caused the disease? A. Some researchers have hypothesized that it may be the smoker rather than the smoking that should be investigated in relation diseases andconditions associated with cigarettes. to the varied Those who have studied groups of smokers and nonsmokers have found generally that the smokers tend to be different personality types than the nonsmokers: more communicative, more energetic (48), more prone to drink quantities of black coffee and liquor (73), and to like spicy or salty foods in contrast to a blander diet (79). As a group, they are more likely to have had parents with heart disease and hypertension (97). They have had more marriages, more jobs, more residences (68), living in what might be called overdrive (74), as one researcher has put it, searching for aims and purposes (48). But most researchers who have concentrated on women with lung cancer have looked shortsightedly only at whether or not they smoke. And it is possible that the kind of woman who smokes is also the kind of person most prone to developing lung cancer. Her life style would certainly, on average, appear to be different from that of the nonsmoker. Could occupational exposure be responsible for the recent reported increase in lung cancer among women? Consider the recent and increasing exposure of women to environmental~and other stresses outside the home. As a greater proportion~of women has entered:the work force and moved

, -26- from the traditional female jobs into industries where they compete with meny researchers have begun to show interest imtheir work exposure. A physician who for 15 years heade&the National Cancer Institute's environmental cancer program~feels that not enough attention has been paid to the exposure of women to respiratory carcinogens in the workplace. He has written that the adoption of smoking by women can not explain their lung cancer patterns in the U.S. or other countries (53). A statistician with a longtime interest in industrial exposures came to a like conclusion in the American Journal of Public Health (94). "Much more significant than~changes in women's smoking habits," he wrote, "have been the changes in their employment." He said the lung cancer incidence among women in industrial occupations is as high if not higher than that of men. And he conclude&: The secular trend of lung cancer in men runs counter to the smoking-lung cancer hypothesis, while the secular trend of lung cancer in women just as easily supports the hypothesis that the major antecedent of lung cancer may be foun&in occupational exposures rather than in smoking. Further evidence that the anti-smokers may be on the wrong track comes from Boston's Lahey Clinic. A detailed study there foun6that 75 percent of women with lung cancer diagnosed between 1961 and 1964 were "at home" women, and 14 percent of those whose backgrounds were known w ~ were working women (9). In cases*diagnosed there between 1969 and 1972, U1Nless than half the female lung cancer patients were "at home." The W GO proportion identified as working women had more than doubled, to 36 percent.

Y . C, C -27- A retrospective study of lung cancer and smoking in women in one ~ British hospital, 1955-1971, led the investigating,pathologist to conclude that "the current increase in incidence of lung cancer in women may be due not to smoking but to some as yet unrecognized cause" (61). He suggested subsequently in a letter to the journal Lancet that "to concentrate all our efforts on a reduction in the smoking habit may lead us to neglect" other factors associated with lung cancer (62). An&that, of course, is the consuming danger when researchers investi- gate lung cancer in women and look only at whether or not they smoked. A W %4 (

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. • ' -29- A. It has been said that women seem somehow immune to heart disease .S until their later years, when they catch up to men in cardiovascular disease. Ui. S. government figures show that male death rates for ischemic heart disease -- also called coronary heart disease, or CHD, and the major heart killer -- are 3 to 4 times higher than those of females until around age 50 (109). The male and female rates draw closer together thereafter and the male rate is only about 15 percent greater at age 85 and over. Women do not really ever "catch up." .' Is heart disease, like lung cancer, primarily a man's disease?. The male-female difference is not so pronounced in blacks, among whom both men an&women experience more major heart disease at younger ages (102). Heart disease rates for black women, for instance, are 3 to 4 times higher than those of white women under 50. There is no established scientific explanation for this racial disparity nor for the overall male-female difference. Some type of genetic and/or environmental variance is suggested. In~any event, mortality rates for cardiovascular disease have been declining for many years, and the drop in women's rates -- black and white -- has been more dramatic than:those in men. Not surprisingly, some have credited the good news on the cardiova:s- cular front to a decrease in the proportion of the population that smokes. Not necessarily so, says a Public Health Service employee, Thomas J. ThomQ who works with numbers at the government's National Heart, Lung and G:,7 C!' t.~ O F+

, • C . C -30- Blood Institute (96). He notes that the decrease in smoking in men has been greater than that in women~, whereas the CHD death rates have dropped in both sexes, in all age groups. This pattern, he says, "throws some doubt on the notion that giving up cigarette smoking has contributed to the declining trend." Thom describes the trend in CHD death rates as the most significant aspect of the changing pattern of cardiovascular mortality, because CHD accounts for two-thirds of all cardiovascular deaths and because CHD was until a decade or so ago the only major subgroup of the overall cardio- vascular category that was rising.

. -31- Are Q, Are women who smoke more likely to have heart attacks and strokes than those who t3on't? Some studies have shown that there are more smokers than nonsmokers among women with atherosclerosis and other cardiovascular conditions (106). But as a former member of the National Heart Advisory Board wrote recently: No direct proof has been provided to show that cigarettes are atherogenic ((and)) we must question if the increased risk is really due to tobacco (23). He suggested that smoking may be part of a personality pattern that may itself contribute to hardening of the arteries, a forerunner of heart attack and stroke. Although a heart disease-prone personality pattern has been estab- lished in large-scale studies of men (11), so far women have not been so investigated in really significant numbers. One project on the West Coast nearly 20 years ago did, however, examine 257 women, and found four times more clinical heart disease in those exhibiting an overt behavior pattern already labeled in men as Type A -- or more coronary prone (85). The Type A person is chronically in a hurry, pushing constantly in a drive for recognition, advancement, achievement -- suffering from what the two physician researchers who have identified the patterns call "a paucity of time itself." `. O W As in the larger studies on men before an&since, the women identifies4 Cn as Type A's had higher cholesterol levels and blood pressure, often more ~ GJ

-32- rapid blood coagulation. They smoked more than their more easygoing s Type B sisters. And, said the authors, the "strikingly higher incidence of clinical disease" could not be ascribed to any of the measured risk factors, including smoking. They said this strongly suggested "that the Type A behavior pattern is itself in some way largely responsible." The nation's most comprehensive continuing study of heart disease, begun in 1948, includes almost all the adult men and women in Framingham, Massachusetts. All the factors known to be associated with cardiovascular illnesses, except personality type, have been studied. The project's director said recently that smoking "tends to be a minor cardiovascular factor, overall, in women" (58).

M -33- i Q . C Is it true that smoking womenreach menopause earlier than non- smoking women, and, if so, what difference does it make, really? A widely publicized study on smoking and menopause was published in June 1977 and has been much referred to since (56). It indicated , that in groups of hospitalized women ages 44 to 53 a greater proportion of smokers than of nonsmokers had passed menopause in any two-year age group. Among ex-smokers so divided by age group, the percent lay between the smokers and'nonsmokers. The voluntary health associations, other anti-smoking groups and some of the lay press quickly pointe&out that early onset of change of life deprived'a women of the hormonal protection she is believed to have against cardiovascular disease in her reproductive years. The purported "protection" is affected', the theory goes, as her endocrine balance changes at approach of menopause and sex hormone levels diminish thereafter. She smoked. She experienced change of life up to two years earlier. And'she subjected'herself to an early risk of cardio- vascular disease. Or, at least, that's the reasoning of those who bring up the smoking/early menopause relationship. However, statistical relationship does not establish causality, and other differences have been associated with~the age at which menopause occurs. For instance, in a 1966 Public Health Service study of 1200 women the median menopausal age tende&to be earlier in black women, in those in lower income brackets and in those who lived in rural areas (70).

, • • .. ', . -34- There was indication, too, that lean women had slightly earlier meno- .r pauses. And the thinner their measured skinfolds the earlier the change in the menses. The leanness factor - this time measured by a formula of height and weight -- popped up again in the government's Framingham project. The authors reported in 1976 that women who had undergone natural meno- pause (as opposed to surgical) were significantly leaner than controls of the same age who were premenopausal (52). Women who smoke have been found to be leaner -- lighter in weight and thinner in skinfold measurement -- than women who do not (10, 51, 64). Leaner women experience earlier menopauses on average. Is it because they smoke or because they are leaner -- or because of the type of persons they are? Is it the smoke or the smoker? Furthermore, there would appear to be several things wrong with the assumption~that the age at which menopause occurs is important too cardiovascular risk: 1. The vital statistics don't bear it out. 2. The epidemiological evidence so far is not conclusive. In fact, at least two studies have reported no difference in the cardiovascular risk of premenopausal and postmenopausal women (72, 76). And in one study that did show a difference, using data from the Framingham project, the authors sai&that the difference they found "could not be explained by the changes recorde&in any of the usual risk factors, singly or in combination" (59). Evidence refuting the menopause/increased O W ~ w 0 ~ CHD risk theory appears in a recent study of younger women with advanced hardening of the arteries (29).

0 -35- It It found no indication they were deficient in the sex hormone estrogen, as postmenopausal women~might be. Family history of coronary disease, hypertension and diabetes appeared to be the most important risk factors in the occurrence of early atherosclerosis in these premenopausal women~. The failure of vital statistics to support the claim of increased cardiovascular risk after menopause has been~considered by some medical authorities. The Framingham~authors, for instance, commented that "the reported cardiovascular disease death rates rise steadily and with no acceleration through the menopausal span" (59). The British journal Lancet said more recently, in an editorial about CEID in young women: Mortality statistics do not seem to support the suggestion that the menopause has any effect on the risk of CHD, since the death-rate from this disease increases steadily with advancing age (67). i I Those who support the menopause/increased CHD theory claim that it explains why men get so much~more cerebrovascular disease and CHD until the rates begin to converge after age 50. But in early 1978, another hypothesis to explain~that phenomenon was published in the British Medical Journal (50). Two physician researchers in London released a logarithmi~c analysis of the proportionate changes in menm's and women's CHD death rates by five- year age brackets. What they found, they said, indicated that it isn't the ladies that lose "protection" around age 50, it's the men. There was no acceleration of the women's CHD rates after 50. In fact, w they slowed down a little. But the men's rates slowed down even more, CA CJ O ~

-36- indicating indicating that smaller year-to-year increases in the men were i responsible for the narrowing male-female gap. "Apparently, at around the age of 50 men begin to lose a factor that had previously put them at increased risk," they wrote. "Male sex hormones may be risk factors for CHD, and further studies are needed to clarify their role in the aetiology of.CHD in men." They said the trend they had observed in the UK data for the last quarter century "appeared also to be similar in other parts of the Western world, including the USA." This new hypothesis about CHD in men is,of course,no more scientifically established than what one researcher has called the "classically accepted opinion" that early menopause equals increased CHD risk in women.

. C* C -37- Wouldn't Wouldn't stress play a part in explaining why men are more susceptible to cardiovascular disease than:women? A. Many think it does, witness the hypothesis of the Type A person- ality. Hypertension is also thought to play an important part in development of cardiovascular disease - in both sexes. But the woman's blood pressure is on average lower than the man's (65) and may not normally rise as high in stress situations, an artifact from the primitive bread- winner's need for survival. A heightened response to stress in the caveman enabled him to fight t or flee. And now that safeguard of early man is considered a major risk factor. And this is because modern man~no longer fights or runs away and, therefore, does not dissipate the sustained effects of emotional stress on his cardiovascular system (83). This stress factor -- and the general belief that the man has the harder life, with more responsibilities and complications -- has been cited in the past as reason for women's relative freedom from heart problems. Now,of course,there is increasing recognition that the woman's lot is not always the easier one. Two Omaha:cardiologists who wrote recently in the Journal of the American Medical Association include women~in their "invisible entrapment" theory of stress an&heart disease (28). Increasing social, economic, professional and business pressures, they say, can lead to the individual's being boxed into a corner with no way out and no personally acceptable options. The resulting feelings of hopelessness and helplessness increase

-38- the production of stress hormones by the body. The result, in the extreme: heart disease. ~

• . 0 C • ' -39- I What are the risks of emphysema and chronic bronchitis in~women~ who smoke? The answer to this question depends on whom you rea&. The ACS, for instance, says the emphysema rate among women is five times higher for those with a history of smoking (3). The Public Health Service has said that women who smoke have nearly three times as much chronic bronchitis and emphysema as women who don't smoke (108). The Cancer Society's figure, reported in 1976, is no different from the one it reported in 1966. It was derived~from data collected in its so-called million-person survey, begun in 1959, and:is based on a total of 45 deaths -- 24 smokers and 21 nonsmokers -- out of a total of 500,000 women originally enrolled in the continuing study (45). The Public Health~Service claim is base6on a PHS household-interview survey, more than 10 years old, which compare&smoking habits and prevalence of various diseases and conditions claimed for members of 134,000 households (116). The survey report carefully pointed out that the bronchitis reported in the interviews "is not necessarily the same as a physician's diagnosis...It is quite possible that some of the self-diagnosed cases may in fact be 'smokers' cough'." Or, it could, for that matter, be the result of occupational exposure or other environmental pollution. Because emphysema was not among the chronic conditions about which interviewers inquired (115), information on which incidence was derived was based on O W volunteered responses or interviewers' judgments. ~ W W N N

.C -40- The original caveat about the self-diagnosis of bronchitis was .~ forgotten by PHS when it picked the convenient 3-to-1 statistic for its anti-smoking pamphlets. Since then it has been repeated:by many groups providing anti-cigarette material to the public directly and through the local and national media. Also ignored is discovery of a genetic disorder in which an enzyme deficiency seems to determine susceptibility to chronic obstructive lung diseases like chronic bronchitis and emphysema. This inherited metabolic abnormality is thought to be present in about one in 20 persons (103). But there is a recent suggestion that even if the level of the enzyme is high enough to protect the lung, the enzyme system might not be functioning properly (81, 82). There is additional evidence that chronic respiratory diseases are genetically influenced.• 1. The diseases occur more than twice as frequently in whites as in blacks, but strike blacks at earlier ages (102, 109). 2. Children of bronchitic parents are more likely to have the disease, and the tendency is six times higher if both parents have bronchitis (91). 3. Twin studies have shown that if one identical smoking twin has chronic cough, the other tends to as well, whether or not the second twin smokes (19).

Q. C • C -41- t .. Are women who smoke more often sick and absent from work than those who don't? a. This charge probably originated with that 1964-65 Public Health Service household-interview survey (116). The smoker-nonsmoker health findings are spotty, often contradictory (92), but the survey did find that women who said they smoked as much as a half pack a day ha6better health records than those who did not smoke at all. Women smokers overall reported fewer chronic conditions, including 60 percent fewer cases of coronary heart disease. Women who smoked a pack a day or less reported fewer days of restricted activity and days actually sick in bed than did nonsmoking women. But the smoking women, as a whole, did average 1.6 more days lost from work in a year and reported more digestive disorders, for instance, and more injuries, which could account for that average extra 1.6-day work loss. One use made of this PHS data illustrates how statistics can be twisted and misrepresented for scare propaganda. A current American O Cancer Society pamphlet about women says those who smoke lose three times GJ ~ ~ ' as many work days as women who don t (2). The government data, however, Cl1 show this only for women who had ever smoked more than two packs daily. These women represented less than 1 percent of all women imthe survey N W (116). That women who smoked more than~40 cigarettes daily reported more of everything, including arthritis and chronic sinusitis, would seem a reflection of the kinds of persons they are and how they live rather than an effect of cigarette smoking.

03'745314 ~./

r -43- Does Does the tobacco industry agree with the more vocal foes of cigarettes on ariything? A. Yes. It agrees with the American Cancer Society that there should not be a prohibition on cigarettes (86). It agrees with Health, Education and Welfare Secretary Joseph Califano when he says he does not advocate a ban on cigarette adver- tising. (16). It agrees with the American Heart Association that "we still don't know the cause of coronary heart disease" (5). It agrees with the statement in a Public Health Service monograph that "although epidemiological data has clearly established the existence of a correlation between smoking and cancer, a clear-cut causal relationship has not been demonstrated" (112). It agrees with the American Lung Association that there should be a new emphasis on finding the answers about "job-inflicted lung disease" (6). It agrees with all of them that young people should not smoke. And it agrees with the American Cancer Society's stated "conviction" that "adult individuals must make up their own minds about smoking but it requires that individuals know the facts" (4). The industry, however, does quarrel with those who label hypotheses n W and opinions as facts. C11 f.~ F+ CJT

vC -44- 4 S CausaLity has yet to be proved in any of the diseases and conditions linked statistically with cigarette smoking -- in women or men. The controversy must be resolved by scientific research. The tobacco industry does not try to persuade anyone to smoke. Nbr does it discourage anyone who makes up his or her mind to quit. Smoking is an adult custom, to be decided by mature, thinking persons men or women. 4 1 I O -. W THE TOBACCO INSTITUTE ~ MAY 1978 V W N ~

r , r Y C , C -45- ( 1. 2. 3. 4. 5. 6. 7. 8. t 9. 10. 11. 12. 13. 14. REFERENCE SOURCES .r Allen, H.B., et al. Smoker's Wrinkles? Journal of the American Medical Association225/9: 1067-1069, Aug. 27, 1973. American Cancer Society. When a Woman Smokes. Pamphlet, 1975. American Cancer Society. In: Smoking Takes Its Toll of Women. Winston-Salem Journal, Feb. 9, 1976. American Cancer Society. Cancer Facts and Figures/1976. American Heart Association. The American Heart Association Has Something _to Sav. Pamphlet, 1977. American Lung Association. Young Lungs Are for Life. Annual Report 1976-1977. Ando, Y., et al. Effects of Noise on Human Placental Lactogen (HPL) Levels in Maternal Plasma. British Journal of Obstetrics and Gynaecology 84/2: 115-118, February 1977. Barbieri, M.A. A Longitudinal Study of Growth of Low-Birth-Weight Infants. The Journal of Pediatrics 98/2: 320-326, August 1976. Beamis, J.F., et al. Changing Epidemiology of Lung Cancer: Inc•reasing Incidence in Women. Medical Clinics of North America 59/2: 315-325, March 1975. Bjelke, E. Variation in Height and Weight in the Norwegian Population. British Journal of Preventive Medicine, 1971, 25: 192-202. Brand, R.Z. Comparison of Coronary Heart Disease Prediction in the Western Collaborative Group Study Using the Structure&Interview and the Jenkins Activity Survey Assessments of the Coronary-Prone Type A Behavior Pattern. Presented at the 18th Annual Conference onCardio- vascular Disease Epidemiology of the American Heart Association, Orlando, Fla., March 12-16, 1978. Brody, J.E. How a Mother Affects Her Unborn Baby. National Institute of Child Health~and Human Development, National Institutes of Health, Public Health Service, U.S. Department of Health, Education and Welfare. Reprint, 1970. Butler, N.R., and Alberman, E.D. (Editors). Perinatal Problems, E. and S. Livingstone, Ltd., Edinburgh, 1969. O Butler, N.R., et al. Cigarette Smoking in Pregnancy: Its Influence ~ on Birth Weight and Perinatal Mortality. British Medical Journal, ~ 1972, 2: 127-130, April 15, 1972. ci 1-+ ~

-46- 15. Butler, N.R., and Goldstein, H. Smoking in Pregnancy and Subsequent Child Development. British~Medical Journal, 1973, 4: 573-575, Dec. 8, 1973. 16. Califano, J.A., Jr. Testimony before Subcommittee on Health and the Environment, Interstate and Foreign Commerce Committee, U.S. House of Representatives, 95th Congress, Second Session, Feb. 15, 1978. 17. Cameron, P., et al. The Health of Smokers' and Nonsmokers' Children. Journal of Allergy 43/6: 336-341, June 1969. 18. Cameron, P., and Robertson, D. Effect of Home Environment Tobacco Smoke on Family Health. Journal of Applied Psychology 57/2: 142-147, 1973. 19. Cederlof, R., et al. Hereditary Factors, "Spontaneous Cough" and "Smoker's Cough": A Study on 7,800 Twin-Pairs with the Aid of Mailed Questionnaires. Archives of Environmental Health 14/3: 401-406, March 1967. 20. Colley, J.R.T. Respiratory Symptoms in Children and Parental Smoking and Phlegm Production. British Medical Journal, 1974, 2: 201-204, April 27, 1974:. 21. Collins, E., and Turner, G. Maternal Effects of Regular Salicylate Ingestion in Pregnancy. Lancet, 1975, 2: 335-338, Aug. 23, 1975. 22. Comstock, G.W., et al. Low-Birth Weight and Neonatal Mortality Rate Related to Maternal Smoking and Socioeconomic Status. American Journal of Obstetrics and Gynecology 111/1: 53-59, Sept. 1, 1971'. 23. Corday, E., and Corday, S.R. Prevention of Heart Disease by Control of Risk Factors: The Time Has Come to Face the Facts. American, Journal of Cardiology 35/2: 330-333, February 1975. 24. Daniell, H.W. Smoker's Wrinkles: A Study in the Epidemiology of "Crow's Feet." Annals of Internal Medicine 75/6: 873-880, December 1971. 25. Davie, R., et al. From Birth to Seven: The Second Report of the National ChildiDeveloDment Study U58 Cohort). Longman in association with the National Children's Bureau, London, 1972. 26. Donovan, J.W. Randomized Controlled Trial of Anti-Smoking Advice in Pregnancy. British Journal of Preventive and SociaL Medicine 31/1: 6-12, March 1977. 27. Downing, G.C., and Chapman, W'.E. Smoking and Pregnancy: A Statistical O Study of 5,659 Patients. California Medicine 104/3: 187, March 1966. ~ .'1 28. Eliot, R.S., and Forker, A.D. Emotional Stress and Cardiac Disease. (n, Journal of the AmericamMedical Association 236/20: 2325-2326, Nov. Cj 15, 1976 ~

-47- 29. Engel, H.J., et al. Coronary Artery Disease in Young Women. Journal ofythe American Medical Association 230/11: 1531-1534, Dec. 16, 1974. 30. Feinstein, A.R., and Wells, C.K. Cigarette Smoking and Lung Cancer: The Problems of "Detection~Bias" in Epidemiologic Rates of Disease. Abstract. Clinical Research 22/3: 555A, April 1974. 31. Feinstein, A.R. In: "Detection Bias" May Hike Cancer Rate in Smokers. Medical Tribune, June 19, 1974. 32. Feinstein, A.R. In: Smoking Link to Lung Ca Termed Diagnostic Bias. Family Practice News, July 15, 1974. 33. Fogg, S. Scientific Finding: New Wrinkle Seen in Smoking Dispute. Lon. Island Press, Sept. 9, 1973. 34. Fortune. The Fortune Survey, July 1935. 35. Frazier, T.K., et al. Cigarette Smoking and Prematurity: A Prospective Study. American Journal of Obstetrics and Gynecology 81/5: 988-996, May 1961. 36. Gallup, G. American~Institute of Public Opinion, June 7, 1939. Computer printout from Roper Public Opinion Research Center, Williams College, Williamstown, Mass. 37. Gallup, G. American Institute of Public Opinion, Nov. 29, 1944. Computer printout from Roper Public Opinion Research Center, Williams College, Williamstown, Mass. 38. Gallup, G. American Institute of Public Opinion, June 25, 1957. Computer printout from Roper Public Opinion Research Center, Williams College, Williamstown, Mass. 39. Goldstein, H. Factors Influencing the Height of Seven Year Old Children! Results from~the National Child Development Study. Human~Biology 43: 93-111, 1972. 40. Green, D. Testimony before the American Cancer Society's National Commission on Smoking and Public Policy, Philadelphia, June 16, 1977. 41. Green, P. In: Ca News 29/2: 11, Fall 1975. 42. Grossman, M.I. XIV. Diseases of the Digestive System. Section Two. Peptic Ulcer. 640. Pathogensis and Pathophysiology. In: Textbook of Medicine, Fourteenth Editiom, W.B. Saunders Co., Philadelphia, London, Toronto, 1975. 43. Grossman, M.I. In: More Women Than Ever Get Ulcers! Increasing. Female Trend Cause Elusive. NIH Record: 6, July 13, 1976.

C -48- 44. Hamilton, James L. The Effect of Cigarette Advertising Bans on Cigarette Consumption. In: Proceedings of the Third World Conference-on Smokin and Health Vol. II: 829-40. National Cancer Institute, National Institues of Health, Public Health Service, U.S. Department of Health, Education and Welfare, DHEW'Pub. No. (NIH) 77-1413, 1977. 45. Hammond, E. C. Smoking in Relation to the Death Rates of One Million Men and Women. In: Epidemiological Approaches to the Study of Cancer and Other Chronic Diseases. National Cancer TnstTtute-Ronograp 1 19, January T9~- 46. Hardy, J.B., and Mellits, E.D. Does Maternal Smoking During. Pregnancy Have a Long-Term Effect on the Child? Lancet, 1972, 2: 1332-1336, Dec. 23, 1972. 47. Harlap, S., and Davies, A.M. Infant Admissions to Hospital and Maternal Smoking. Lancet, 1974, 1: 529-532, March 30, 1974. 48. Heath, C.W. Differences Between Smokers and Nonsmokers. Archives of Internal Medicine 101/2: 377-388, February 1958. 49. Heinonen, O.P., et al. Cardiovascular Birth Defects an&Antenatal Exposure to Female Sex Hormones. New England Journal of Medicine 296/2: 67-70, Jan~. 13, 1977. 50. Heller, R.F., and Jacobs, H.S. Coronary Heart Disease in Relation to Age, Sex, and Menopause. British Medical Journal, 1978, 1: 472-474, Feb. 25, 1978. 51. Higgins, M.W., and Kjelsberg, M. Characteristics of Smokers and Nonsmokers in Tecumseh, Michigan. II. The Distribution of Selecte& Physical Measurements and Physiological Variables and the Prevalence of Certain Diseases in Smokers and Nonsmokers. American Journal of Epidemiology 86/1: 60-77, July 1967. 52. Hjortland, M.C., et al. Some Atherogenic Concomitants of Menopause: The Framingham~Study. American Journal of Epidemiology 103/3: 304-311, September 1976. 53. Hueper, W.C. Lung Cancer and Smoking in Perspective. In: Lawyers' Medical Encyclopedia of Personal Injuries and A11ie&Specialties, Revised Vol. 5, Pt. B, Sections 37.1a to 38.99. The A1len~Smith Co., Indianapolis, 1972. 54. Janowitz, H.D. In: Ulcers and Colitis: The Price of Success? Harper's Bazaar, November 1975. 55. Jaroslovsky, R. Peptic Prognosis: Mysteries and Myths of Ulcers Give Way to Modern Research. Wall Street Journal, Sept. 29, 1976.

C -49- 56. Jick, H., and Porter, J. Relation Between~Smoking and Age of Natural Menopause: Report from the Boston Collaborative Drug Surveillance Program, Boston University Medical Center. Lancet, 1977, 1: 1354-1355, June 25, 1977. 57. Johnstone, F., and Inglis, L. FamiliaL Trends in Low Birth Weight. British Medical Journal, 1974, 3: 659-61, Sept. 14, 1974. 58. Kannel, W.B., et al. A General Cardiovascular Risk Profile: The Framingham Study. American Journal of Cardiology 38/1: 46-51, July 1976. 59. Kannel, W.B., et al. Menopause and Risk of Cardiovascular Disease: The Framingham Study. Annals of Internal Medicine 85/4: 447-452, October 1976. 60. Kelson, S.R. Testimony before the American Cancer Society's National Commission on Smoking and Public Policy, Chicago, May 25, 1977. 61. Kennedy, A. Relationship Between Cigarette Smoking and Histological Type of Lung Cancer in Women. Thorax 28/2: 204-208, March 1973. 62.. Kennedy, A. Mortality from Lung Cancer. Lancet, 1976, 1: 965, May 1, 1976. 63. Kerrehijn, K.F., et al. Chronic Nonspecific Respiratory Disease in Children in Five Year Follow-Up Study. Acta Paediatrica Scandanavica Supplement 261: 1977. , 64. Kopczynski, J. Height and Weight of Adults in Cracow. • III.. Weight by Age and Cigarette Smoking. Epidemiology of Noninfectious Diseases, Epidemiological Review 26/4: 452-464, 1972. 65. Krantz, J.C., Jr., et al. The Pharmacologic Principles of Medical Practice. Williams and Wilkins, Baltimore, Seventh Edition, 1969. 66. Kullander, S., and Kallen, B. A Prospective Study of Smoking and Pregnancy. Acta Obstetrica et Gynecologica Scandanavica 50/1: 83-94, 1971. 67. Lancet. Editorial• Coronary Heart-Disease in Young Women. Lancet, T97T; -2: 282-283, ~Aug. 6, 1977. 68. Lilienfeld, A.M. Emotional and Other Selected Characteristics of Cigarette Smokers and Nonsmokers as Related to Epidemiological Studies of Lung Cancer and Other Diseases. Journal of National Cancer Institute 22/2: 259-282, February 1959: p C.~ 69. Luquette, A.J., et al. Some Immediate Effects of a Smoking Environment ~ on Children of Elementary School Age. The Journal of School Health ~ 40/10: 533-536, December 1970. ~ N

I -50- 70. MacMahon, B., and Worcester, J. Age at Menopause, U.S., 1960-1962. 1. Vital and -Health Statistics, Data from the National Health Survey, Series 11, No. 19, October 1966. National Center for Health Statistics, Health Services and Mental Health Administration, Public Health Service, U.S. Department of Health, Education and Welfare, DHEW Pub. No. (HSM) 73-1268. Maher, B.A. Testimony before the American Cancer Society's National 72. Commission on Smoking and Public Policy, Boston, June 2, 1977. Manchester, J.H., et al. Premenopausal Castration and;Documented Coronary Atherosclerosis. American Journal of Cardiology 28': 33-38, July 1971. 73. Matarazzo, J.D., an&SasLow, G. Psychological and Related Charac- teristics of,~Smokers and Nonsmokers. Psychological Bulletin 57/6: 493-513, November 1960. 74. McArthur, C., et al. The Psychology of Smoking. Journal of Abnormal Social Psychology 56/2: 267-275, March 1958. 75. Melia, R.J.W., et al. Association Between Gas Cooking and Respiratory Disease in Children. British Medical JournaL, 1977, 2: 149-152, July 16, 1977. 76. Novak, E.R., and Williams, T. J. Autopsy Comparison of Cardiovascular Changes in Castrated and Normal Women. American Journal of Obstetrics and Gynecology 80/11: 863-872, November 1960. 77. O'Lane, J.M. J'Some Fetal Effects of Maternal Cigarette Smoking. Obstetrics and Gynecology 22/2: 181-84, August 1963. 78. Peckham, C.S., et al. Acquired Myopia in 11-Year-Old Children~. British Medical Journal, 1977, 1: 542-544, Feb. 26, 1977. 79. Perrin, M.J., et al. Smoking and Food Preferences. British Medical Journal, 1961, 1: 387-388, Feb. 11, 1961. 80. Peterson, W.F., et al. Smoking and Prematurity: A Preliminary Report Based on Study of 7,740 Caucasians. Obstetrics and Gynecology 26/6: 775-779, December 1965. 81. Pierce, J.A., et al. Antitrypsin Phenotypes in St. Louis.' Journal of the American Medical Association 231/6: 609-612, Feb. 10, 1975. 82. Pierce, J.A. In: Lack of Body Chemical, Emphysema Linked. St. Louis Post-Dispatch, Feb. 10, 1975. - O w 83. Ramey, E. In: Life Span Gap Widening. Washington Post, Jan. 8, 1976.,; C!t

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-52- 97. Thomas, C.B. Familial and Epidemiologic Aspects of Coronary Disease and Hypertension. Journal of Chronic Diseases 7/3: 198-208, March 1958'. 98. Underwood, P.B., et al. Parental Smoking Empirically Relate&to Pregnancy Outcome. Obstetrics an&Gynecology 29/1: 1-8, January 1967. 99. U.S. Public Health Service. Adult Use of Tobacco - 1970. National Clearinghouse for Smoking and Health, Center for Disease Control, U.S. Department of Health, Education and Welfare, DHEW Pub. No. (HSM) 73-827, June 1973. 100. U.S. Public Health Service. Adult Use of Smoking - 1975. Bureau of Health Education, Center for Disease Control, and National Cancer Institute, National Institutes of Health, U.S. Department of Health, Education and Welfare, June 1976.. 101. U.S. Public Health Service. Monthly Vital Statistics Report. Vol. 26, No. 12. National Center for Health Statistics, U.S. Department of Health, Education an&Welfare, DHEW Pub. No. (PHS) 78-1120, March 13, 1978. 102. U. S. Public Health~Service. Monthly Vital Statistics Report: Final Mortality Statistics, 1975. Vol. 25, No. 11, Supplement. National Center for Health Statistics, Health Resources Administration, U.S. Department of Health, Education and Welfare, DHEW Pub. No. (HRA) 77-1120, Feb. 11, 1977. 103. U. S. Public Health Service. The Health Consequences of Smokin : A Report of the Surgeon General: 1971. National Clearinghouse for Smoking and Health, Health Services and Mental Health Administration, U.S. Department of Health, Education and Welfare, DHEW Pub. No. (HSM) 71-7513. 104. U.S. Public Health Service. The Health Consequences of Smoking: A Report of the Surgeon General: 1972. National Clearinghouse for Smoking and Health, Health Services and Mental Health Administration, U.S. Department of Health, Education and Welfare, DHEW Pub. No:. (HSM) 72-7516. 105. U. S. Public Health Service. The Health Consequences of Smoking: January 1973. National Clearinghouse for Smoking and Health, Health Services and Mental Health Administration, U.S. Department of Health, Education and Welfare, DREW Pub. No. (HSM) 73-8704. 106. U1. S. Public Health Service. The Health Consequences of Smoking: January 1974. National Clearinghouse for Smoking and Health, Center for Disease Control, U.S. Department of Health, Education andiWelfare, DHEW Pub. No. (CDC) 74-8704. O W ~ CR W IV .~

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C -54- 117. Wynder, E.L., et al. Lung Cancer in Women: Present and Future Trends. Journal of the National Cancer Institute 51/2: 391-401, August 1973. + 118. Yerushalmy, J. The Relationship of Parents' Cigarette Smoking to Outcome of Pregnancy -- Implications as to the Problem of Inferring Causation from Observed Associations. American Journal of Epidemiology 93/6:- 443-456, June 1971. 119. YerushaLmy, J. Infants with Low Birth Weight Born Before Their Mothers Started to Smoke Cigarettes. American Journal of Obstetrics and Gynecology 112/2: 277-84, Jan. 15, 1972.