Cigarette Smoking In Women Research Articles

Impaired action of thyroid hormone associated with smoking in women with hypothyroidism.

The effect of smoking on thyroid function is controversial, and its effect on thyroid hormone action is unknown. We investigated the effects of cigarette smoking in women with various grades of hypothyroidism and in normal women. We studied 138 normal women and 135 women with primary hypothyroidism, of whom 84 had subclinical hypothyroidism and 51 overt hypothyroidism. Sixty of the women with hypothyroidism were reevaluated during thyroxine therapy. The women were categorized as smokers or nonsmokers according to their responses to a questionnaire. Thyroid function was evaluated by measurements of serum thyrotropin, free thyroxine, and triiodothyronine. Peripheral thyroid hormone action was assessed by a clinical score and measurements of ankle-reflex time and serum lipids and creatine kinase. Among the women with subclinical hypothyroidism, the smokers had a higher mean (+/- SD) serum thyrotropin concentration (21.3 +/- 16.6 vs. 12.7 +/- 7.2 mU per liter, P = 0.004) and a higher ratio of serum triiodothyronine to serum free thyroxine (by 30 percent, P = 0.003) than the nonsmokers. Their serum concentrations of total cholesterol and low-density lipoprotein (LDL) cholesterol were higher (by 16 percent, P = 0.013; and 28 percent, P = 0.003, respectively). Among the women with overt hypothyroidism, the serum concentrations of thyrotropin, free thyroxine, and triiodothyronine were similar in the smokers and nonsmokers. As compared with the nonsmokers, the smokers had a clinical score indicating a greater degree of hypothyroidism (P < 0.001), higher serum concentrations of total and LDL cholesterol (by 25 percent, P < 0.001; and 24 percent, P = 0.002, respectively), longer ankle-reflex time (by 25 percent, P < 0.001), and higher serum concentrations of creatine kinase (by 236 percent, P < 0.001). There were dose-response relations between smoking and serum concentrations of total and LDL cholesterol, serum creatine kinase concentrations, and ankle-reflex time in the women with overt hypothyroidism, and between smoking and serum concentrations of total and LDL cholesterol in the women with subclinical hypothyroidism. Smoking increases the metabolic effects of hypothyroidism in a dose-dependent way. This may be explained by alteration of both thyroid function and hormone action.

Dietary change after smoking cessation: a prospective study.

A population sample of 375 men and women cigarette smokers were recruited to take part in a prospective study of smoking cessation to test the hypothesis that stopping smoking is associated with an increased consumption of the essential fatty acid linoleic acid, which explains the concomitant reduction in risk of coronary heart disease. Diet was assessed using a 10 d weighed record in 301 smokers at baseline, 153 at 4-month follow-up, of whom twenty-six had quit smoking, and 122 at 1-year follow-up, of whom twenty had quit. Compared with continuing smokers, those who had quit at the 4-month follow-up (mean 10 and 13 weeks for men and women respectively) had statistically significant increases in body weight (5%), energy intake (13%), total dietary fat (24%), all specific types of dietary fat (26% polyunsaturated fat, 26% linoleic acid, 30% eicosapentaenoic acid, 23% monounsaturated fat and 22% saturated fat) and vitamin E intake (19%). The foods which appeared to contribute to increases in energy and fat intakes at the 4-month follow-up were vegetable oils and polyunsaturated margarines, processed meats and meat pies. By follow-up at 1 year (mean time since quitting 31 and 41 weeks for men and women respectively) there were no detectable differences in energy and total fat intakes. However, intakes of eicosapentaenoic acid and pteroylglutamate (folate) were statistically significantly higher in the quitters compared with the continuing smokers (37% for eicosapentaenoic acid and 16% for folate). We conclude that the short-term increase in dietary intake of linoleic acid, which is not sustained by 1 year, cannot explain the reduction in risk of coronary disease following smoking cessation.

Lung cancer and cigarette smoking in women: A case-control study in Barcelona (Spain): Agudo A, Barnadas A, Pallares C, Martinez I, Fabregat X, Rosello J et al. IREC, c. Jordi Joan 5, 08301 Mataro. Int J Cancer 1994; 59: 165–169

Lung cancer and cigarette smoking in women: A case-control study in Barcelona (Spain): Agudo A, Barnadas A, Pallares C, Martinez I, Fabregat X, Rosello J et al. IREC, c. Jordi Joan 5, 08301 Mataro. Int J Cancer 1994; 59: 165–169

Sociocultural and physiological correlates of cigarette smoking in women.

Cigarette smoking is a major modifiable risk factor for cancer and coronary heart disease and the chief avoidable cause of death in the United States. Over the past few decades, the prevalence of cigarette smoking among males has significantly decreased. However, the same significant decrease has not been seen among women. Researchers have identified sociocultural factors and physiological correlates associated with women's cigarette smoking. It is essential that health care professionals understand the findings of research on women's smoking if they wish to identify and counsel women at risk and to define directions for future research.

Patterns of cigarette consumption and cotinine levels among African American women smokers.

Cigarette smoking intensifies a number of serious health problems, including lung cancer, hypertension, low birth weight, and infant mortality, that disproportionately affect black Americans. Cotinine, a major nicotine metabolite, is one indicator of smoke exposure. It has been reported that black women have higher mean cotinine levels than white women. This divergence may be attributed to biologic factors or to inaccuracy in reporting cigarette use. The purpose of this study was to characterize nicotine dependence and the relationship between self-reported cigarette use and cotinine levels among black women smokers. The sample consisted of 142 black women cigarette smokers recruited individually at urban health centers and worksites. A cotinine/cigarette ratio was determined for light, moderate, and heavy smokers. Underreporting of cigarette consumption, previously defined as cotinine value > 25 ng/ml/cigarette, ranged from 86% among light smokers to 70% among moderate smokers and 21% among heavy smokers. There were significant differences in cotinine/cigarette and nicotine dependence scores across levels of smoking. Average cotinine/cigarette values were higher in black women compared with previous reports for Mexican American women smokers. No comparable values are available for white women. Additional study is needed to begin to explain variations in levels of cotinine, as well as perceived nicotine dependence among black women.

Lung cancer and cigarette smoking in women: a case-control study in Barcelona (Spain).

A case-control study on lung cancer and the habit of cigarette smoking was carried out in Barcelona (Spain). Cases were 103 women newly diagnosed with primary lung cancer in 10 hospitals from the study area. Histologic confirmation was given in 101 cases, of which 53 were adenocarcinoma, 19 squamous-cell carcinoma, 9 small-cell carcinoma and 20 other types. Two controls per case were selected, matched by age, residence and hospital. Compared with the never-smokers, the odds ratios (OR), with corresponding 95% confidence intervals (CI), were 1.61 (0.4 to 6.9) for ex-smokers and 3.61 (1.6 to 8.3) for current smokers. The risk of lung cancer showed a good dose-response relationship with duration of the habit, average number of cigarettes smoked daily and cumulative cigarette consumption. The risk of lung cancer increased by 62% for each 10 pack-years. Depth of inhalation also showed a remarkable effect, independently of the intensity of the habit. Although mortality and incidence rates of lung cancer among women in Spain are lower than in other developed countries, the risk of lung cancer is that which would be expected according to the pattern of the smoking habit in Spanish women.

Cigarette smoking and the outcomes of in vitro fertilization: measurement of effect size and levels of action

To assess whether cigarette smoking in women or men affects the outcomes of IVF-ET and at what functional levels smoking is active. Demographic and smoking data were collected by questionnaire at the onset of consecutive treatment cycles (n = 462) and at the time of ET. In addition to routine endocrine and clinical data, circulating immunoreactive inhibin, follicular fluid E2 endometrial thickness, and morphology were assessed. Reported exposure to cigarettes was validated using a serum cotinine assay. Serum cotinine level at the onset of treatment correlated strongly with the number of cigarettes reported (r = 0.68). The duration and dose of gonadotropin treatment was greater among active smokers than never smokers: 10.2 versus 9.2 days and 24.7 versus 19.8 ampules, respectively. Fertilization, pregnancy, and abortion rates were similar between groups. Multivariate analyses demonstrated negative correlation between female age, but no such effect was seen with female or male smoking. Sperm concentration was significantly reduced in male smokers (prewash: 108 versus 130 x 10(6); postwash: 17.1 versus 21.6 x 10(6)), although fertilization rate was unaffected (66% versus 62%). Follicular function, assessed using serum inhibin and E2, as well as follicular fluid E2 levels showed no significant difference between active smokers and never smokers. Endometrial thickness and morphology also were similar between groups. These data suggest that among couples undergoing IVF neither female nor male smoking has a measurable deleterious effect on conception rate. Female age remains a far more potent prognostic factor in the current study. However, when all the published data are combined, a significant deleterious effect of smoking on conception is suggested, with a common odds ratio of 0.540 (95% confidence interval 0.385 to 0.757).

Factors associated with nicotine dependence among African American women cigarette smokers.

Cigarette smoking contributes to disproportionate morbidity and mortality among African Americans. Purposes of the study were to describe smoking behavior and test a model of nicotine dependence among African American women. Participants (n = 187) smoked a low rate of high nicotine mentholated cigarettes and had a mean salivary cotinine of 402 ng/mL. The proposed model predicted 48% of variance in nicotine dependence with smoking to cope, number of cigarettes/day, positive outcome expectancies about smoking, and interest in quitting, as significant contributors. Suggested interventions include developing alternative coping skills, cognitive restructuring, and techniques focused on the precontemplation stage of smoking cessation.

Cigarette Smoking and Lens Opacities: The Beaver Dam Eye Study

We evaluated the relationship between cigarette smoking behavior and lens opacities in cross-sectional data on 4,926 adults in Beaver Dam, Wisconsin. The frequencies of more severe levels of nuclear sclerosis increased with packyears of cigarette smoking in women and men. For women, the odds ratio (OR) associated with 10 packyears was 1.09 (confidence interval [CI] = 1.04, 1.16) and for men it was 1.09 (CI = 1.05, 1.14) after controlling for age. The frequencies of posterior subcapsular opacities also increased in both sexes with increased packyears. The OR associated with 10 packyears of cigarette smoking was 1.06 (CI = 0.98, 1.14) for women and 1.05 (CI = 1.00, 1.11) for men after controlling for age. There was no significant effect on cortical opacities. Smoking was associated with past cataract surgery. The significant relationships of smoking with lens opacities suggest an etiologic effect. If confirmed prospectively, our results would indicate another benefit of smoking cessation.

Presentation The negative association in women between cigarette smoking and uncomplicated angina pectoris in the Framingham heart study data

As a result of a more complete analysis of available Framingham Heart Study data on the association of cigarette smoking to incidence of uncomplicated angina pectoris than has previously been published in Framingham papers, it was determined that there is a consistently negative risk factor association for women at every follow-up period from 12 to 30 years, with Framingham women cigarette smokers experiencing 30–40% lower rates of uncomplicated angina pectoris than non-smokers, the rates also declining with increasing amounts of cigarettes smoked. Our analysis confirms the absence of a predictive risk factor association in the case of men previously indicated by Framingham investigators. The published declarations by Framingham investigators of an absence of association between cigarette smoking and angina pectoris in Framingham women, is a failure to publicly recognize the distinctive negative association present in the Framingham female data. The Framingham data on the relationship of smoking to angina incidence is clearly at variance with the Surgeon General's sketchy finding of an inconsistent positive association for men and an uncertain relationship for women. It is suggested that special attention should be directed to these results of the Framingham data because of the preeminence of Framingham material world wide, because angina pectoris is the most common manifestation of coronary heart disease, because it will improve the “conventional wisdom” on this subject, and because the negative relationship found for Framingham women does not lend support to the belief held by some that smoking enhances the degree of cornonary atherosclerosis.

90068875 The antiestrogenic effect of cigarette smoking in women

90068875 The antiestrogenic effect of cigarette smoking in women

Alcohol consumption and carotid atherosclerosis in the Lausanne Stroke Registry.

We evaluated the association between alcohol consumption and carotid atherosclerosis in 261 consecutive patients greater than 50 years old admitted to our community-based primary-care center with first ischemic stroke; their characteristics were entered into a computerized data bank (Lausanne Stroke Registry). Reported regular alcohol consumption was compared with the presence and severity of internal carotid artery disease as assessed by duplex scanning with spectral analysis of the Doppler signal and real-time B-mode imaging at the level of the carotid bifurcation. We found an inverse linear relation between light-to-moderate alcohol intake (less than or equal to 4 standard drinks/day) and severity of internal carotid artery stenosis. No conclusion could be drawn for heavier drinkers because there were too few. A logistic regression model showed that hypertension, cigarette smoking, and age in men and diabetes mellitus and cigarette smoking in women strongly counterbalanced the potential benefit of alcohol consumption. Although regular alcohol drinking cannot be advocated on the basis of our findings, light-to-moderate consumption of alcohol is the first factor to be inversely associated with extracranial carotid atherosclerosis in symptomatic patients with cerebrovascular disease.

The antiestrogenic effect of cigarette smoking in women

Epidemiologic results indicate that women who smoke cigarettes are relatively estrogen-deficient. Smokers have an early natural menopause, a lowered risk of cancer of the endometrium, and an increased risk of some osteoporotic fractures. Moreover, women who smoke may have a reduced risk of uterine fibroids, endometriosis, hyperemesis gravidarum, and benign breast disease. Several possible mechanisms for these effects have been identified. Smoking does not appear to be clearly related to estradiol levels, at least in postmenopausal women, although levels of adrenal androgens are increased. Moreover, smoking appears to alter the metabolism of estradiol, leading to enhanced formation of the inactive catechol estrogens.

Proportions of cancer deaths attributable to cigarette smoking in women.

Over two-thirds of a million American women mostly over age 45 were enrolled in a prospective mortality study in 1982 and followed up for four years. In this time period 1,527 women died of six smoking-related cancer sites: oral cavity, esophagus, pancreas, larynx, lung, and bladder. Age-adjusted death rates in nonsmokers were used to obtain smoking-attributable risks and numbers of deaths due to these six cancers. Among current smokers, 601 deaths (85.5% of current smokers' deaths) were attributable to cigarette smoking, and among former smokers 284 (69.3% of ex-smokers' deaths) were attributable to smoking. Cigarette smoking accounted for 885 excess deaths at these sites, giving a population-attributable risk of 57.9%. Over three-quarters of these excess deaths were due to lung cancer. Cigarette smoking, despite increases in smoking cessation, is still responsible for well over half of the deaths from these six types of cancer in women.

Increased 2-hydroxylation of estradiol as a possible mechanism for the anti-estrogenic effect of cigarette smoking.

Epidemiologic data indicate that cigarette smoking is associated with an important anti-estrogenic effect, and increased hepatic metabolism has been suggested as a possible mechanism. We examined the hypothesis that cigarette smoking in women induces an increase in estradiol 2-hydroxylation. This irreversible metabolic pathway yields 2-hydroxyestrogens, which possess minimal peripheral estrogenic activity and are cleared rapidly from the circulation. We found a significant increase in estradiol 2-hydroxylation in premenopausal women who smoked at least 15 cigarettes per day. The extent of the reaction (mean +/- SEM) was 53.6 +/- 2.2 percent among 14 smokers and 35.1 +/- 1.8 percent among 13 nonsmoking controls--an increase of approximately 50 percent (P less than 0.001). The extent of 2-hydroxylation among five smokers did not vary during the follicular and luteal phases of their menstrual cycles. In addition, urinary excretion of estriol relative to estrone was significantly decreased among smokers (P less than 0.01), providing evidence that the smoking-induced increase in 2-hydroxylation diminishes the competing metabolic pathway involving 16 alpha-hydroxylation. This study demonstrates that smoking exerts a powerful inducing effect on the 2-hydroxylation pathway of estradiol metabolism, which is likely to lead to decreased bioavailability at estrogen target tissues. Elucidation of the mechanism responsible for smoking-induced changes in 2-hydroxylation may be useful in the development of strategies to reduce the risk of hormone-dependent tumors.

Prognostic Factors for Mortality in a Population-Based Study of Men and Women With a History of Heart Disease

The role of classical risk factors, particularly high blood pressure, high blood cholesterol levels, and cigarette smoking in predicting incidence of heart disease has been well documented. However, information about the predictive value of these risk factors in persons who already have heart disease is largely derived from selected hospital or case series with limited time of follow-up and predominantly involving men. We examined the role of risk factors in predicting subsequent all-cause and cardiovascular disease mortality in a population of men and women, age 50 to 79 years (mean age, 66 yr), who reported a history of heart disease at baseline examination and who have been followed for nine years. One hundred ninety-one men and 96 women reported a personal history of heart attack or heart failure. In these men, age, high systolic blood pressure, and family history of heart attack were significant independent predictors of mortality attributable to cardiovascular disease and all causes. In contrast, only current cigarette smoking habit and personal history of diabetes significantly predicted increased mortality in these women. High systolic blood pressure in men and cigarette smoking in women appear to be the two major potentially remediable risk factors for mortality in older subjects with a history of heart disease.

Cigarette smoking in women with cancers of the breast and reproductive organs.

This case-control study addressed the relationship between cigarette smoking and cancers of the breast (1,741 cases), endometrium (476 cases), uterine cervix (1,174 cases), and ovary (296 cases). The lifetime smoking history of cases was compared with that of 2,128 controls, and relative risks (odds ratios) for smoking were estimated using multiple logistic regression to adjust for potential confounding by age, marital status, number of pregnancies, and Quetelet's index. With increasing amount smoked there was a statistically significant decrease in endometrial cancer risk and a statistically significant increase in cervical cancer risk. In the highest smoking category (greater than or equal to 15 pack-yr), the endometrial cancer relative risk was 0.57 [95% confidence interval (CI) of 0.37, 0.86] and the cervical cancer relative risk was 1.81 (95% CI of 1.47, 2.22). There was no apparent relationship between smoking and cancers of the breast or ovary.

Normal sister-chromatid exchanges in oral contraceptive users

Sister-chromatid exchanges in peripheral lymphocytes were examined in 115 healthy women, aged 15–43 years. 63 women were on no medication at all, and 52 women used oral contraceptives. 30 metaphases from each culture were scored for SCE. In accord with previous studies, cigarette smoking increased SCE. The use of oral contraceptives had no influence on SCE in non-smoking and in cigarette-smoking women. Thus the results did not indicate any potential mutagenic effect of oral contraceptives.

Relationship of weight loss and cigarette smoking to changes in high-density lipoprotein cholesterol

To determine the effect of weight loss on serum high-density lipoprotein cholesterol (HDL-C), we measured serum HDL-C as well as total cholesterol and triglycerides in 65 subjects 56 women and 9 men, mean age 41.1 +/- 1.5 (+/- SEM yr) before and after a weight reduction program. At entry into the program there was a significant correlation between HDL-C and several indices of overweight--relative weight, body mass index and sum of skinfold thickness. For all subjects, despite a significant weight loss of 4.5 kg or 5.8% of initial body weight and significant decrease in sum of skinfold thickness, there was no significant increase in HDL-C or correlation between changes in HDL-C and change in body weight or skinfold thickness. For women, but not men, a weak negative correlation between change in HDL-C and change in weight or percentage change in weight was observed. However, in the subset of women who were current cigarette smokers a significant (p less than 0.01) correlation was observed between change in HDL-C and change in weight (r = -0.876) and percentage change in weight (r = -0.881). Thus a modest weight loss is not usually associated with a significant increase in serum HDL-C concentration except in cigarette smoking women.

The Respiratory Effects of Regular Cigarette Smoking in Women: A Five-Year Prospective Study

Over a five-year period a consistent habit of smoking or nonsmoking was maintained by 302 women (aged 25 to 54 years at the beginning of the study). There were 130 nonsmokers, 40 ex-smokers, and 15 light, 46 moderate, and 71 heavy smokers. Smokers without serious disability who had stopped smoking had a very low prevalence of respiratory symptoms and showed worsening of pulmonary function over the years similar to life-long non-smokers. Although there is a dose-related response to cigarettes, individual susceptibility also plays an important role in determining the respiratory effect of smoking. A range for change in ventilatory function over a five-year period in apparently healthy nonsmoking women is provided. Using this range, it is possible to identify susceptible smokers who show deterioration in ventilatory function that is more rapid than normal. Repeated spirometric studies may be useful in selecting a group at greatest risk of developing later disabling chronic obstructive pulmonary disease.