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FACT OR FANCY The Tobacco Institute May 1978

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. Since their usual, unsubstantiated charges have 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. I

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

-3- 0. 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 than three 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). Some persons who disapprove of cigarette smoking say that the larger number of women smoking today accounts for everything from higher lung cancer death rates to an allegedly higher incidence of ulcers, not to mention smaller babies and even larger government disability costs for 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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-5- Do women who smoke while they're pregnant have smaller babies? Q. 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 adequate health care. A baby's sex and whether it is a first or, say, fifth child can also affect weight (13). To control for as many of these differences as possible, Silverman decided to look at weight differences in pairs of infants born to the same

-6- mother. And she located 1016 such pairs, one third of them born to 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. And the second babies of the "changed 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 "changed smokers" produced babies with weights between smokers and 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 consistent with the self-selection hypothesis" (90). O W %3 0 Her findings were consistent with two other studies indicating that W C11 W some women will have smaller babies whether or not they smoke in pregnancy. W

-7- One, a large California project, included women who began smoking after delivering their first children. Those children, born before the mother smoked, were lighter than the nonsmokers' infants in the study (119). The other study, done in Scotland, reported that sisters of women who delivered low-weight infants also tended to have lighter babies (57). 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 attributed to smoking does not occur in the later months -- if indeed 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 difference 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." LBW infants are not necessarily premature (born too 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 Q CJ next highest weight category, 20 times greater than infants of the most ~ W common birth weight category (113). w ~j1

-8- What opponents of smoking fail to point out, however, is that almost all the research 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.) 0

-9- Q, Then why the slogan that pregnant women who smoke endanger two lives? A. 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. And they 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 and 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).

-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). 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 in reading 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

children was on average 16 months behind in general ability when compared with the 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...

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-13- Q, Is it true that smoking mothers can harm their babies after birth -- that children of women who smoke suffer more respiratory illnesses, especially bronchitis and pneumonia? This is a frequent emotion-laden claim 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 child's 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, supported by the Public Health Service, was done by researchers from Yale and Johns Hopkins (88). The third, a survey of 1400 Dutch school children, found that the respiratory symptoms of the children were related to their parents' symptoms, whether or not the parents smoked (63). More recently, a four-year study of 5700 youngsters in England and Scotland identified a so-called "cooking effect" among other environmental

-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. :;4

-15- Q. Is there anything to the charge that smoking can interfere with sexual and reproductive functions of both men and 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 health 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 41 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 longtime 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 population" could prove any point about smoking and sexual dysfunction, he said, "and I have not yet seen such a study..." (60).

-16- Nevertheless, the issue shows that history does have a way of repeating 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 would be pure in your love-instinct, cast this sensualizing fire from you.

-17- Q, Is it true that smoking causes facial wrinkles? As 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 questionst 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).

-19- 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? As 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 used to 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 told an 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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-21- Q, If women are smoking "on a man-sized scale," is that why they are said to be getting more ulcers? A. 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 and aspirin (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 duodenal 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, who, of Q course, have like ca genes. In other words, if one twin has ulcers, chances ~ W C!t ~

-22- are the other twin will also. The presence of ulcers in the second 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" woman -- has not been adequately explored. But various hypotheses exist, many of them involving a predisposition toward ulcer through inheritance or a locked-in way of life. The type of temperament that leads to stress problems also leads toward use of what a former president of the American Gastroenterological Association calls "stress relievers." "The person who smokes 40 cigarettes a day usually also drinks 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 and 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- I Are lung cancer death rates rising more rapidly in women than in men? And is this because more women are said to be smoking? A, Lung cancer death rates reported for U.S. women have been rising 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 (110). However, the proportion of cases of the lung cancer cell type that has been related statistically to smoking has changed little in women 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 Yale has found in a 12-year study of hospital records that the use of sputum smear tests increased dramatically in 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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-25- Q, Do those women who smoke and get lung cancer have anything else in common that could 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 to the varied diseases and conditions associated with cigarettes. 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 possible that the kind of woman who smokes is also the kind of person prone to developing lung cancer. Her life style would certainly, on average, appear to be different from that of the nonsmoker. is most 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 men, researchers have begun to show interest in their work exposure. A physician who for 15 years headed 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 concluded: 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 found 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 found that 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 were working women (9). In cases diagnosed there between 1969 and 1972, less than half the female lung cancer patients were "at home." The I proportion identified as working women had more than doubled, to 36 percent.

-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). And that, of course, is the consuming danger when researchers investi- gate lung cancer in women and look only at whether or not they smoked.

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-29- Q, Is heart disease, like lung cancer, primarily a man's disease? a, It has been said that women seem somehow immune to heart disease until their later years, when they catch up to men in cardiovascular disease. U. 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." The male-female difference is not so pronounced in blacks, among whom both men and 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 cardiovas- cular front to a decrease in the proportion of the population that smokes. Not necessarily so, says a Public Health Service employee, Thomas J. Thom who works with numbers at the government's National Heart, Lung and

-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 women who smoke more likely to have heart attacks and strokes than those who don't? A, 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." As in the larger studies on men before and since, the women identified as Type A's had higher cholesterol levels and blood pressure, often more

-32- rapid blood coagulation. They smoked more than their more easygoing 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).

-33- Q. Is it true that smoking women reach menopause earlier than non- smoking women, and, if so, what difference does it make, really? A, 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 pointed 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 tended to be earlier in black women, in those in lower income brackets and in those who lived in rural areas (70). O ~ ~ W C!t O

-34- There was indication, too, that lean women had slightly earlier meno- 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 to 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 said that the difference they found "could not be explained by the changes recorded in any of the usual risk factors, singly or in combination" (59). O Evidence refuting the menopause/increased CHD risk theory appears in CJ a recent study of younger women with advanced hardening of the arteries (29). w CJ1 M ir

-35- 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 CHD 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). 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 logarithmic analysis of the proportionate changes in men'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. O There was no acceleration of the women's CFID rates after 50. In fact, ~ M they slowed down a little. But the men's rates slowed down even more, N ~ N

-36- indicating that smaller year-to-year increases in the men were 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.

-37- Q, 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 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 and heart disease (28). Increasing social, economic, O 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 CJ 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.

-39- Q, What are the risks of emphysema and chronic bronchitis in women who smoke? A, The answer to this question depends on whom you read. 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 based on a PHS household-interview survey, more than 10 years old, which compared 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 volunteered responses or interviewers' judgments. ~ ~ W W ~ ~

-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. Ttain 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).

-41- Q. 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 had better 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 Cancer Society pamphlet about women says those who smoke lose three times as many work days as women who don't (2). The government data, however, show this only for women who had ever smoked more than two packs daily. These women represented less than 1 percent of all women in the survey (116). That women who smoked more than 40 cigarettes daily reported more of w 3 would seem a including arthritis and chronic sinusitis thing ever ~ , y , W ~ reflection of the•kinds of persons they are and how they live rather than OD an effect of cigarette smoking.

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-43- Q, Does the tobacco industry agree with the more vocal foes of cigarettes on anything? 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 ~ W and opinions as facts. ~ W C!t ~ O

-44- 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. Nor 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. THE TOBACCO INSTITUTE MAY 1978

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