Tobacco Documents Online

The results of the British study were inconsistent i with those of Johns Hopkins researchers who followed children born of smoking and nonsmoking mothers in 1962 and 1963. They reported: "At four and seven years there was no significant difference in either physical measurements or intellectual functioning" (29). Despite such studies, there are still those who look only at whether the mother smoked during pregnancy to explain possible differences in children's growth and learning skills. This shortcoming was apparent in the 1977-78 HEW report to Congress on smoking and health (1). The authors discusse& a California study in which children of smoking mothers were found to be shorter at age five than children of nonsmoking mothers (30). But the HEW'writers didn't indicate that the study showed a difference of only 0.9 centimeters, and that the researchers had attributed nearly 90 percent of the varia- tions to "parental stature alone." Only 2 percent of the .9 centimeter difference could possibly be due to association with smoking -- about 7 one-thousandths of an inch -- according to the California investigators. Oral Contraceptives The scientific literature does not support the claim that oral contraceptive users who stop smoking significantly decrease their disease rates. In other words, there is no 56 i

scientific basis for any assurance that oral contraceptive users are not likely to develop certain diseases if they stop smoking. The new warning insert now required by the Federal Food and Drug Administration in oral contraceptive packages in effect implies such assurance. And the FDA came under attack at a Congressional hearing last fall for its decision requiring the new inserts. Several prominent statisticians who had examined the studies relied upon by the agency in its decision testified (31-34). One noted that: The warning as state& implies that there is a causal effect of cigarette smoking on the incidence of cardiovascular disease. No statistical study can establish causality. At best it can establish a high probability of possible interrelationships (33). The studies which the statisticians criticized claimed to have shown that smokers who use oral contraceptives have an increased risk of cardiovascular disease (35-38). Their censure, the statisticians said, was based on statistical weaknesses, inadequate sample size and other methodological problems in the studies. Some of these weaknesses had been noted by the authors of the original reports: These estimates of risk...still need to be inter- preted with caution, as a number of assumptions have necessarily had to be made in their calculation and the margin of error is likely to be fairly wide (35). It is essential to point out that the mortality estimates used in this paper are based on small 57

numbers and may be subject to large sampling errors. These e-stimates are also subject to upward and downward biases, which may not cancel each other out... The net effect of these various factors cannot be estimated without additional research, preferably in different settings (37). These estimates [death-rates] are based on small numbers and are necessarily approximate. Without more data it is not possible to examine the inter- relationships of age, smoking, and duration of oral contraceptive use...(38). Several witnesses expressed concern that a statisti- cal relationship between oral contraceptive use, smoking and illness may influence scientists to overlook other factors that may explain the observed relationship. Two other researchers urged in the British journal Lancet that scientists not let "preconceived ideas affect objectivity" in examination of other possible hypotheses. Left unanswered in research so far, they wrote, is the con- founding question of self-selection (39). And they asked: Is it possible that the women who smoke and use oral contraceptives (particularly the older group) are simply reflective of a more flamboyant lifestyle which may well include more stress, more alcohol, more medication (including "downers" and "uppers"), or marijuana use?...There seems to be nothing in the data which would answer once and for all the question -- is it the smoker or the smoking which creates risk difference and is it the oral contra- ceptive user or oral-contraceptive use which is at the bottom of it all?. They concluded that "somehow epidemiological and laboratory studies must be designed to distinguish among the 58 ,

possible aetiologies." What they called "the mix of factors", s t which include genetics, they wrote, "may be more complex than we think." Smoking and Early Menopause In a widely publicized study which appeared in 1977, Boston researchers reported they had found that smokers undergo menopause earlier than nonsmokers (40). According to some voluntary health associations and anti-smokers, this appeared to present a health hazard, because onset of change of life supposedly deprives a woman of the "protection" she is believed to have from female sex hormones (estrogens) against cardiovascular disease (CVD) in her reproductive years. Rowever, this claim can be disputed for several reasons. First, the CVD vital statistics don't support such a theory. If women actually lost some form of hormonal protec- tion with the onset of menopause, reported CVD death rates presumably would jump during the menopausal age span -- rather than continue the expected steady increase. An editorial in Lancet examined this question a few months after publica- tion of the Boston research. And it pointed out: O W Mortality statistics io not seem to support the suggestion that the menopause has any effect on the ~ risk of CHD (coronary heart disease), siwce the cJ1 W death-rate from the disease increases steadily with rA advancing age (41). O 59

Two researchers who studied trends in CHD mortality data for women in England and Wales concluded that women do not lose protection from CHD after the menopause (42). Secondly, evidence inconsistent with this claim has been presented in a study of premenopausal women with advanced hardening of the arteries (43). The research~ers found that the women did not have estrogen deficiencies, as might be expected in the hormonal protection theory. Instead, they found that a family history of coronary disease, hypertension or diabetes was "the most consistent single factor" found among the women. r Finally, a study of women who underwent surgery for removal of their ovaries -- a procedure resulting in estrogen deprivation -- reported that they had no more coronary artery disease than an age-matched control group (44). The authors wrote that "our data support previous reports which question the protective effect of estrogen on development of atherosclerotic coronary artery disease." Am~ong the facts that are not mentioned by those claiming a smoking-early menopause link is that other variables have been associated with the onset of menopause. For in- stance, a Public Health Service study of 1,200 women f ound that the median menopausal age tended to be lover in black women and in white women areas (45). from lower income brackets and rural , . 60

The PHS study also pointed to a fact that has been discussed in other studies: that lean women undergo menopause slightly earlier, and the thinner their measured skinfolds, the earlier the change in their menses. The leanness factor also was reported by other researchers in a 1976 study (46). And what everyone has forgotten is that women who smoke have been found to (47-49). be leaner than women who do not So one is lef t to wonder, if leaner women experience earlier menopause, is it because they are leaner, or because they smoke, or because of the kind of persons they are? Women and Lung Cancer Some persons who disapprove of cigarette smoking claim that the larger number of women smoking accounts for their rising lung cancer death rates. This claim does not stand up well under critical scrutiny. A major weakness in the claim can be seen in a comparison of international lung cancer patterns. cancer death rates for U.S. women have reportedly rising faster year to year~than those in men since the 1960s (50). The U. S. situation is drastically different 61 I

that in Europe. In a World Health Organization report, a professor of actuarial science reported in 1977 that while men's lung cancer death rates had risen relatively steeply in five European countries, none of the women's rates had risen significantly. In fact, the over-all lung cancer mor- tality in French women had dropped (51). In the United Kingdom declining rates of increase have been observed in younger women; simultaneously, a downhill trend in male rates has been reported in the older age groups (52). Thus, lung cancer occurrence patterns in women differ in various countries and they are also quite dissimilar from those of males. Even when allowance is made for the later popularity of smoking among women, there is still no consistent trend of increasing lung cancer mortality rates. These data are not at all compatible with the contention that the cause of lung cancer in both sexes is the same agent -- cigarette smoking. Some scientists believe that the recent rise in lung cancer in women is more artificial than real, because physicians order diagnostic tests more frequently now for women patients they know to be smokers. For example, a doctor at the Yale Medical School reported that over a 12-year period hospital records indicated a dramatic increase in the use of sputum smear tests for women lung cancer patients. He commented: "This increase in the search rate for women may t 62

possibly play a role in various recent reports of rising rates of lung cancer in women" (53). Therefore, it is highly likely that more lung cancer among women is being diagnosed because of the more frequent application of diagnostic techniques than in the earlier years -- when many cases might not have been so diagnosed. Often overlooked in the hurried attempts to put the full blame for women's lung cancer on smoking is the fact that the proportion of cases of this disease with the cell type that has been most frequently associated with smoking has changed very little in the past 25 years (54,55). This raises the question of why researchers haven't observed an immense increase in squamous-cell lung cancers if the causal agent is cigarette smoking. Simple explanations for this so-called "epidemic" of lung cancer in women based solely on smoking habits are clearly inadequate. Recent studies have suggested that industrial or occupational exposures may be important in lung cancer causa- tion in women. A study in Los Angeles County reported an increased risk of lung cancer in women who worked as beauti- cians, assemblers and waitresses (56). Increased lung cancer mortality rates for women were reported in counties in the U.S. in which certain heavy, industries are located. In some, the rates for women the general U.S. rate (57). were more than a third higher than 63

The need for further occupational, geographic and r socioeconomic studies of women and disease should be recognized from these and similar research findings. A single-minded focus on smoking hampers the search for lung cancer causation. i i

f References for Women and Smoking 1. U.S. Public Health Service. The Health Consequences of Smoking: 1977-78. U.S. Department of Health, Educa- tion and Welfare. Washington, July 27, 1978, 73 pp. 2. Meyer, M.B., et al. Perinatal Events Associated with Maternal Smoking During Pregnancy. American Journal of Epidemiology 103/5: 464-476, May 1976. 3. van den Berg, B.J. In: LBW In Infants of Smokers Not Related Just to Smoking Itself, by Annette Oestreicher. Ob. Gyn. News 13/4: 1, 27, Feb. 15, 1978. 4. Yerushalmy, J. Mother's Cigarette Smoking and Survival of Infant. American~ Journal of Obstetrics and Gynecology 88/4: 505-518, Feb. 15, 1964. 5. Yerushalmy, J. Self-Selection -- A Major Problem in Observational Studies. Proceedings of the 6th Berkeley Symposium on Mathematical Statistics and Probability, Vol. 4: 329-342, 1972. 6. Yerushalmy, J. Infants Their Mothers Started with Low Birth Weight Born Before to Smoke Cigarettes. American Journal of Obstetrics and Gynecology 112/2: 277-284, Jan. 15, 1972. 7 Silverman, D.T. Maternal Smoking and Birth Weight. American Journal of Epidemiology 105/6: 513-521, June 1977. 8 Donovan, J.W. Randomised Controlled Trial of Anti- Smoking Advice in Pregnancy. tive and Social Medicine 31: British Journal of Preven- 6-12, 1977. 9 Yerushalmy, J. The Relation ship of Parents' Cigarette Smoking to Outcome of Pregn ancy -- Implications as to the Problem of Inferring Causation from Observed Associa- tions. American Journal of Epidemiology 93/6: 443-456, June 1971. 10. Robertson, J.S. Health and Education -- Smoking. Public Health 92/2: 54-55, 1978. 11. U.S. Public Health Service. The Health Consequences of Smoking: 1973. U.S. Department of Health, Education and Welfare. Washington, DREW Pub. No. (HSM) 73-8704, 1973, 249 pp. 65