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Rationale: A large body of epidemiologic literature has found an association of increased fine particulate air pollution (PM2.5) with acute and chronic mortality. The effect of improvements in particle exposure is less clear.Objectives: Earlier analysis of the Harvard Six Cities adult cohort study showed an association between long-term ambient PM2.5 and mortality between enrollment in the mid-1970s and follow-up until 1990. We extended mortality follow-up for 8 yr in a period of reduced air pollution concentrations.Methods: Annual city-specific PM2.5 concentrations were measured between 1979 and 1988, and estimated for later years from publicly available data. Exposure was defined as (1) city-specific mean PM2.5 during the two follow-up periods, (2) mean PM2.5 in the first period and change between these periods, (3) overall mean PM2.5 across the entire follow-up, and (4) year-specific mean PM2.5. Mortality rate ratios were estimated with Cox proportional hazards regression controlling for individual risk factors.Measurements and Main Results: We found an increase in overall mortality associated with each 10 microg/m3 increase in PM2.5 modeled either as the overall mean (rate ratio [RR], 1.16; 95% confidence interval [CI], 1.07-1.26) or as exposure in the year of death (RR, 1.14; 95% CI, 1.06-1.22). PM2.5 exposure was associated with lung cancer (RR, 1.27; 95% CI, 0.96-1.69) and cardiovascular deaths (RR, 1.28; 95% CI, 1.13-1.44). Improved overall mortality was associated with decreased mean PM2.5 (10 microg/m3) between periods (RR, 0.73; 95% CI, 0.57-0.95).Conclusion: Total, cardiovascular, and lung cancer mortality were each positively associated with ambient PM2.5 concentrations. Reduced PM2.5 concentrations were associated with reduced mortality risk. [ABSTRACT FROM AUTHOR]

OBJECTIVES: We reported previously that 24-hr moving average ambient air pollution concentrations were positively associated with ventricular arrhythmias detected by implantable cardioverter defibrillators (ICDs). ICDs also detect paroxysmal atrial fibrillation episodes (PAF) that result in rapid ventricular rates. In this same cohort of ICD patients, we assessed the association between ambient air pollution and episodes of PAF. DESIGN: We performed a case-crossover study. PARTICIPANTS: Patients who lived in the Boston, Massachusetts, metropolitan area and who had ICDs implanted between June 1995 and December 1999 (n=203) were followed until July 2002. EVALUATIONS/MEASUREMENTS: We used conditional logistic regression to explore the association between community air pollution and 91 electrophysiologist-confirmed episodes of PAF among 29 subjects. RESULTS: We found a statistically significant positive association between episodes of PAF and increased ozone concentration (22 ppb) in the hour before the arrhythmia (odds ratio=2.08; 95% confidence interval=1.22, 3.54; p=0.001). The risk estimate for a longer (24-hr) moving average was smaller, thus suggesting an immediate effect. Positive but not statistically significant risks were associated with fine particles, nitrogen dioxide, and black carbon. CONCLUSIONS: Increased ambient O3 pollution was associated with increased risk of episodes of rapid ventricular response due to PAF, thereby suggesting that community air pollution may be a precipitant of these events. [ABSTRACT FROM AUTHOR]

Familial aggregation of forced expiratory flow during the middle half of the FVC (FEF[25-75%]) and FEF[25-75%]/FVC has been observed in the Boston Early-Onset Chronic Obstructive Pulmonary Disease Study, but linkage results have not been reported for these phenotypes. An autosomal whole genome-wide linkage scan was performed in 72 pedigrees ascertained through a proband with severe, early-onset chronic obstructive pulmonary disease, and linkage analyses of FEF[25-75%]and FEF[25-75%]/FVC were performed using Sequential Oligogenic Linkage Analysis Routines. There was suggestive evidence for linkage of FEF[25-75%]/FVC with chromosome 2 (LOD 2.60 at 216 cM). In a smokers-only analysis, evidence for linkage was observed for postbronchodilator FEF[25-75%] with chromosome 12 (LOD 5.03 at 35 cM) and chromosomes 2 and 12 for FEF[25-75%/FVC (LOD 4.12 at 221 cM and LOD 3.46 at 35 cM, respectively); in the smokers-only model, evidence for linkage also was robust for FEV[1]/FVC on chromosome 2 (LOD 4.13 at 229 cM) and FEV[1] on chromosome 12 (LOD 3.26 at 36 cM). Our analyses provide evidence for linkage of FEF[25-75%] and FEF[25-75%]/FVC on chromosomes 2q and 12p. LOD scores of greater than two were also observed for chromosomes 16, 20, and 22 with the smokers-only analysis, which may suggest gene-by-smoking interactions in these regions. [ABSTRACT FROM AUTHOR]

Acetaminophen decreases glutathione levels in the lung, which may predispose to oxidative injury and bronchospasm. Acetaminophen use has been associated with asthma in cross-sectional studies and a birth cohort. We hypothesized that acetaminophen use would be associated with newly diagnosed adult-onset asthma in the Nurses' Health Study, a prospective cohort study of 121,700 women. Participants were first asked about frequency of acetaminophen use in 1990. Cases with asthma were defined as those with a new physician diagnosis of asthma between 1990 and 1996 plus reiteration of the diagnosis and controller medication use. Proportional hazard models included age, race, socioeconomic status, body mass index, smoking, other analgesic use, and postmenopausal hormone use. During 352,719 person-years of follow-up, 346 participants reported a new physician diagnosis of asthma meeting diagnostic criteria. Increasing frequency of acetaminophen use was positively associated with newly diagnosed asthma (p for trend = 0.006). The multivariate rate ratio for asthma for participants who received acetaminophen for more than 14 days per month was 1.63 (95% confidence interval, 1.11-2.39) compared with nonusers. It would be premature to recommend acetaminophen avoidance for patients with asthma, but further research on pulmonary responses to acetaminophen is necessary to confirm or refute these findings and to identify subgroups whose asthma may be modified by acetaminophen. [ABSTRACT FROM AUTHOR]

Objective: To assess the relationship between cigarette smoking and mortality among women with type 2 diabetes in the Nurses' Health Study cohort.Research Design and Methods: The Nurses' Health Study, a prospective cohort of U.S. female registered nurses, included 7,401 women with type 2 diabetes diagnosed at baseline or during follow-up from 1976 to 1996. Total and cause-specific mortality of these diabetic women were the outcomes of interest.Results: We documented 724 deaths during 20 years of follow-up (67,420 person-years) among women with type 2 diabetes. In multivariate analyses, adjusting for age, history of high blood pressure and high cholesterol, and other cardiovascular risk factors, compared with never smokers, the RRs of mortality were 1.31 (95% CI 1.11-1.55) for past smokers, 1.43 (0.96-2.14) for current smokers of 1-14 cigarettes/day, 1.64 (1.24-2.17) for current smokers of 15-34 cigarettes/day, and 2.19 (1.32-3.65) for current smokers of > or =35 cigarettes/day (P for trend = 0.0002). Women with type 2 diabetes who had stopped smoking for > or =10 years had a mortality RR of 1.11 (0.92-1.35) compared with diabetic women who were never smokers.Conclusions: Cigarette smoking is associated in a dose-response manner with an increased mortality among women with type 2 diabetes. Furthermore, quitting smoking appears to decrease this excess risk substantially. Diabetes patients should be strongly advised against smoking. [ABSTRACT FROM AUTHOR]

Study Objective: Beta(2)-adrenoceptor Gly16 polymorphism has been associated with asthma severity and beta(2)-adrenoceptor receptor downregulation, but not with the diagnosis of asthma. Glu27 polymorphism may limit beta(2)-adrenoceptor downregulation and predict body mass index (BMI), particularly among sedentary persons. In addition, BMI predicts asthma. We hypothesized that these DNA sequence variants predict adult-onset asthma only in sedentary women.Design: Nested case-control study.Setting: Nurses' Health Study, a large, prospective cohort study with participants throughout the United States.Participants: Among lifelong nonsmokers, 171 women with adult-onset, medication-requiring asthma and 137 age-matched control subjects.Measurements: Physical activity and BMI were self-reported by previously validated questionnaire items. Genomic DNA was obtained from buccal brushings collected via first-class mail.Results: Of 76 sedentary women, the adjusted odds ratios of Gly16 allele were 7.4 (p = 0.047) for asthma and 13.8 (p = 0.02) for steroid-requiring asthma. No similar associations were observed among 232 active women (p = 0.91). Sedentary individuals with both Gly16 and Glu27 alleles had a less elevated risk for asthma. BMI was associated with asthma and Glu27 allele among sedentary women.Conclusion: This exploratory analysis suggests an important gene/environment interaction for asthma involving physical activity level. Further study in larger populations is warranted to confirm if sedentary lifestyle unmasks a genetic risk for asthma. [ABSTRACT FROM AUTHOR]

Context: Some epidemiologic studies suggest that elevated fruit and vegetable consumption is associated with a reduced risk of breast cancer. However, most have been case-control studies in which recall and selection bias may influence the results. Additionally, publication bias may have influenced the literature on associations for specific fruit and vegetable subgroups.Objective: To examine the association between breast cancer and total and specific fruit and vegetable group intakes using standardized exposure definitions.Data Sources/study Selection: Eight prospective studies that had at least 200 incident breast cancer cases, assessed usual dietary intake, and completed a validation study of the diet assessment method or a closely related instrument were included in these analyses.Data Extraction: Using the primary data from each of the studies, we calculated study-specific relative risks (RRs) that were combined using a random-effects model.Data Synthesis: The studies included 7377 incident invasive breast cancer cases occurring among 351 825 women whose diet was analyzed at baseline. For comparisons of the highest vs lowest quartiles of intake, weak, nonsignificant associations were observed for total fruits (pooled multivariate RR, 0.93; 95% confidence interval [CI], 0.86-1.00; P for trend =.08), total vegetables (RR, 0.96; 95% CI, 0.89-1.04; P for trend =.54), and total fruits and vegetables (RR, 0.93; 95% CI, 0.86-1.00; P for trend =.12). No additional benefit was apparent in comparisons of the highest and lowest deciles of intake. No associations were observed for green leafy vegetables, 8 botanical groups, and 17 specific fruits and vegetables.Conclusion: These results suggest that fruit and vegetable consumption during adulthood is not significantly associated with reduced breast cancer risk. [ABSTRACT FROM AUTHOR]

Background: Increased physical activity has been associated with reduced risk for cardiovascular disease in the general population, but data are limited on its role among persons with type 2 diabetes mellitus.Objective: To determine whether physical activity decreases risk for cardiovascular disease among diabetic women.Design: Prospective cohort study.Setting: The Nurses' Health Study.Patients: 5125 female nurses with diabetes.Measurements: Physical activity was first assessed in 1980 and was updated in 1982, 1986, 1988, and 1992 through validated questionnaires. Average hours of moderate or vigorous exercise and a metabolic equivalent of task (MET) score were computed.Results: During 14 years of follow-up (31 432 person-years), 323 new cases of cardiovascular disease were documented (225 cases of coronary heart disease and 98 cases of stroke). The age-adjusted relative risks according to average hours of moderate or vigorous activity per week (<1, 1 to 1.9, 2 to 3.9, 4 to 6.9, >/=7) were 1.0, 0.93 (95% CI, 0.69 to 1.26), 0.82 (CI, 0.61 to 1.10), 0.54 (CI, 0.39 to 0.76), and 0.52 (CI, 0.25 to 1.09) (P < 0.001 for trend). These figures did not change materially after adjustment for smoking, body mass index, and other cardiovascular risk factors (1.0, 1.02, 0.87, 0.61, and 0.55, respectively; P = 0.001 for trend). In separate analyses, levels of physical activity were inversely associated with coronary heart disease and ischemic stroke. Among women who did not exercise vigorously, the multivariate relative risks for cardiovascular disease across quartiles of MET score for walking were 1.0, 0.85, 0.63, and 0.56 (P = 0.03 for trend). Faster usual walking pace was independently associated with lower risk.Conclusion: Among diabetic women, increased physical activity, including regular walking, is associated with substantially reduced risk for cardiovascular events. [ABSTRACT FROM AUTHOR]

Background: Diets high in fruits and vegetables have been shown to be associated with a lower risk of lung cancer. beta-Carotene was hypothesized to be largely responsible for the apparent protective effect, but this hypothesis was not supported by clinical trials.Methods: We examined the association between lung cancer risk and fruit and vegetable consumption in 77 283 women in the Nurses' Health Study and 47 778 men in the Health Professionals' Follow-up Study. Diet was assessed with the use of a food-frequency questionnaire that included 15 fruits and 23 vegetables. We used logistic regression models to estimate relative risks (RRs) of lung cancer within each cohort. All statistical tests were two-sided.Results: We documented 519 lung cancer cases among the women and 274 among the men. Total fruit and vegetable consumption was associated with a modestly lower risk of lung cancer among the women but not among the men. The RR for the highest versus lowest quintile of intake was 0.79 (95% confidence interval [CI] = 0.59-1.06) among the women and 1.12 (95% CI = 0.74-1.69) among the men after adjustment for smoking status, quantity of cigarettes smoked per day, time since quitting smoking, and age at initiation of smoking. However, total fruit and vegetable consumption was associated with a lower risk of lung cancer among never smokers in the combined cohorts, although the reduction was not statistically significant (RR = 0.63; 95% CI = 0.35-1.12 in the highest tertile).Conclusion: Higher fruit and vegetable intakes were associated with lower risks of lung cancer in women but not in men. It is possible that the inverse association among the women remained confounded by unmeasured smoking characteristics, although fruits and vegetables were protective in both men and women who never smoked. [ABSTRACT FROM AUTHOR]

Context: Although many studies suggest that physical activity may reduce risk of type 2 diabetes, the role of moderate-intensity activity such as walking is not well understood.Objectives: To examine the relationship of total physical activity and incidence of type 2 diabetes in women and to compare the benefits of walking vs vigorous activity as predictors of subsequent risk of type 2 diabetes.Design and Setting: The Nurses' Health Study, a prospective cohort study that included detailed data for physical activity from women surveyed in 11 US states in 1986, with updates in 1988 and 1992.Participants: A total of 70,102 female nurses aged 40 to 65 years who did not have diabetes, cardiovascular disease, or cancer at baseline (1986).Main Outcome Measure: Risk of type 2 diabetes by quintile of metabolic equivalent task (MET) score, based on time spent per week on each of 8 common physical activities, including walking.Results: During 8 years of follow-up (534, 928 person-years), we documented 1419 incident cases of type 2 diabetes. After adjusting for age, smoking, alcohol use, history of hypertension, history of high cholesterol level, and other covariates, the relative risks (RRs) of developing type 2 diabetes across quintiles of physical activity (least to most) were 1.0, 0.77, 0.75, 0.62, and 0.54 (P for trend <.001); after adjusting for body mass index (BMI), RRs were 1.0, 0.84, 0.87, 0.77, and 0.74 (P for trend = .002). Among women who did not perform vigorous activity, multivariate RRs of type 2 diabetes across quintiles of MET score for walking were 1.0, 0.91,0.73, 0.69, and 0.58 (P for trend <.001). After adjusting for BMI, the trend remained statistically significant (RRs were 1.0, 0.95, 0.80, 0.81, 0.74; P for trend = .01). Faster usual walking pace was independently associated with decreased risk. Equivalent energy expenditures from walking and vigorous activity resulted in comparable magnitudes of risk reduction.Conclusions: Our data suggest that greater physical activity level is associated with substantial reduction in risk of type 2 diabetes, including physical activity of moderate intensity and duration. [ABSTRACT FROM AUTHOR]

Context: Reduction in egg consumption has been widely recommended to lower blood cholesterol levels and prevent coronary heart disease (CHD). Epidemiologic studies on egg consumption and risk of CHD are sparse.Objective: To examine the association between egg consumption and risk of CHD and stroke in men and women.Design and Setting: Two prospective cohort studies, the Health Professionals Follow-up Study (1986-1994) and the Nurses' Health Study (1980-1994).Participants: A total of 37851 men aged 40 to 75 years at study outset and 80082 women aged 34 to 59 years at study outset, free of cardiovascular disease, diabetes, hypercholesterolemia, or cancer.Main Outcome Measures: Incident nonfatal myocardial infarction, fatal CHD, and stroke corresponding to daily egg consumption as determined by a food-frequency questionnaire.Results: We documented 866 incident cases of CHD and 258 incident cases of stroke in men during 8 years of follow-up and 939 incident cases of CHD and 563 incident cases of stroke in women during 14 years of follow-up. After adjustment for age, smoking, and other potential CHD risk factors, we found no evidence of an overall significant association between egg consumption and risk of CHD or stroke in either men or women. The relative risks (RRs) of CHD across categories of intake were less than 1 per week (1.0), 1 per week (1.06), 2 to 4 per week (1.12), 5 to 6 per week (0.90), and > or =1 per day (1.08) (P for trend = .75) for men; and less than 1 per week (1.0), 1 per week (0.82), 2 to 4 per week (0.99), 5 to 6 per week (0.95), and > or =1 per day (0.82) (P for trend = .95) for women. In subgroup analyses, higher egg consumption appeared to be associated with increased risk of CHD only among diabetic subjects (RR of CHD comparing more than 1 egg per day with less than 1 egg per week among diabetic men, 2.02 [95% confidence interval, 1.05-3.87; P for trend = .04], and among diabetic women, 1.49 [0.88-2.52; P for trend = .008]).Conclusions: These findings suggest that consumption of up to 1 egg per day is unlikely to have substantial overall impact on the risk of CHD or stroke among healthy men and women. The apparent increased risk of CHD associated with higher egg consumption among diabetic participants warrants further research. [ABSTRACT FROM AUTHOR]

This study examined prospectively the associations of waist circumference and waist:hip circumference ratio with risk of breast cancer. A total of 47,382 US registered nurses who reported their waist and hip circumferences in 1986 were followed up through May 1994 for identification of incident cases of breast cancer. During 333,097 person-years of follow-up, 1,037 invasive breast cancers were diagnosed. In proportional hazards analyses, waist circumference was nonsignificantly related to risk of premenopausal breast cancer but was significantly associated with postmenopausal breast cancer after adjustment for established breast cancer risk factors (for the highest quintile of waist circumference vs. the lowest, relative risk (RR) = 1.34; 95% confidence interval (CI): 1.05, 1.72). When the analysis was limited to postmenopausal women who had never received hormone replacement therapy, a stronger positive association was found (RR = 1.88; 95% CI: 1.25, 2.85). After the data were further controlled for body mass index, the positive association was only slightly attenuated (RR = 1.83; 95% CI: 1.12, 2.99). Among past and current postmenopausal hormone users, no significant associations were found. Similar but slightly weaker associations were observed between waist:hip ratio and breast cancer risk. These data suggest that greater waist circumference increases risk of breast cancer, especially among postmenopausal women who are otherwise at lower risk because of never having used estrogen replacement hormones. [ABSTRACT FROM AUTHOR]

Whether snoring increases the risk of hypertension remains unclear. The authors examined the association between snoring and risk of hypertension in a cohort of 73,231 US female nurses aged 40-65 years and without diagnosed cardiovascular disease or cancer in 1986. Blood pressure levels and physician-diagnosed hypertension were self-reported through validated questionnaires. During 8 years of follow-up, 7,622 incident cases of physician-diagnosed hypertension were reported. Older age, smoking, body mass index, waist circumference, waist-hip ratio, weight gain, less physical activity, and sleeping on the back were directly associated with regular snoring. After adjustment for age, body mass index, waist circumference, and other covariates, snoring was associated with a significantly higher prevalence of hypertension at baseline (odds ratio = 1.22, 95% confidence interval (CI): 1.16, 1.27 for occasional snoring and odds ratio = 1.43, 95% CI: 1.33, 1.5 for regular snoring). In prospective analyses using incident cases of hypertension as the outcome, the multivariate relative risks of hypertension were 1.29 (95% CI: 1.22, 1.37) for occasional snoring and 1.55 (95% CI: 1.42, 1.70) for regular snoring. In addition, snoring was associated with significantly higher systolic and diastolic blood pressure levels. These data suggest that snoring may increase risk of hypertension in women, independent of age, body mass index, waist circumference, and other lifestyle factors. [ABSTRACT FROM AUTHOR]

Background: Metabolic studies suggest that saturated fatty acids differ in their effects on blood lipids. Objective: The objective was to examine the associations between intakes of individual saturated fatty acids and their food sources in relation to the risk of coronary heart disease (CHI). Design: This was a prospective cohort study of 80082 women in the Nurses' Health Study aged 34-59 y. Subjects had no known cardiovascular disease, cancer, hypercholesterolemia, or diabetes, and completed validated food-frequency questionnaires in 1980. Results: During 14 y of follow-up, we documented 939 incident cases of major (CHI). events. In multivariate analyses in which age, smoking, and other covariates were controlled for, intakes of short- to medium-chain saturated fatty acids (4:0-10:0) were not significantly associated with the risk of (CHI). In contrast, intakes of longer-chain saturated fatty acids (12:0-18:0) were each separately associated with a small increase in risk. The multivariate RR for a 1% energy increase from stearic acid was 1.19 (95% CI: 1.02, 1.37). The ratio of polyunsaturated to saturated fat was strongly and inversely associated with CHD risk (multivariate RR for a comparison of the highest with the lowest deciles: 0.58; 95% CI: 0.41, 0.83; P for trend < 0.0001). Conversely, higher ratios of red meat to poultry and fish consumption and of high-fat to low-fat dairy consumption were associated with significantly greater risk. Conclusion: A distinction between stearic acid and other saturated fats does not appear to be important in dietary advice to reduce CHD risk, in part because of the high correlation between stearic acid and other saturated fatty acids in typical diets. Copyright (c) 1999 American Society for Clinical Nutrition [ABSTRACT FROM AUTHOR]

BACKGROUND: Oxidation of lens proteins plays a central role in the formation of age-related cataracts, suggesting that dietary antioxidants may play a role in prevention. However, the relation between specific antioxidants and risk of cataract remains uncertain. OBJECTIVE: Our objective was to examine prospectively the association between carotenoid and vitamin A intakes and cataract extraction in women. METHODS: A prospective cohort of registered female nurses aged 45-71 y and free of diagnosed cancer was followed; in 1980, 50461 were included and others were added as they became 45 y of age for a total of 77466. Information on nutrient intake was assessed by repeated administration of a food-frequency questionnaire during 12 y of follow-up. RESULTS: During 761762 person-years of follow-up, 1471 cataracts were extracted. After age, smoking, and other potential cataract risk factors were controlled for, those with the highest intake of lutein and zeaxanthin had a 22% decreased risk of cataract extraction compared with those in the lowest quintile (relative risk: 0.78; 95% CI: 0.63, 0.95; P for trend = 0.04). Other carotenoids (alpha-carotene, beta-carotene, lycopene, and beta-cryptoxanthin), vitamin A, and retinol were not associated with cataract in multivariate analysis. Increasing frequency of intakes of spinach and kale, foods rich in lutein, was associated with a moderate decrease in risk of cataract. CONCLUSIONS: Lutein and zeaxanthin and foods rich in these carotenoids may decrease the risk of cataracts severe enough to require extraction. Copyright (c) 1999 American Society for Clinical Nutrition [ABSTRACT FROM AUTHOR]

BACKGROUND: Ingestion of animal protein raises serum cholesterol in some experimental models but not in others, and ecologic studies have suggested a positive association between animal protein intake and risk of ischemic heart disease. Prospective data on the relation of protein intake to risk of ischemic heart disease are sparse. OBJECTIVE: The objective was to examine the relation between protein intake and risk of ischemic heart disease. DESIGN: The study was a prospective cohort study. RESULTS: We examined the association between dietary protein intake and incidence of ischemic heart disease in a cohort of 80082 women aged 34-59 y and without a previous diagnosis of ischemic heart disease, stroke, cancer, hypercholesterolemia, or diabetes in 1980. Intakes of protein and other nutrients were assessed with validated dietary questionnaires. We documented 939 major instances of ischemic heart disease during 14 y of follow-up. After age, smoking, total energy intake, percentages of energy from specific types of fat, and other ischemic heart disease risk factors were controlled for, high protein intakes were associated with a low risk of ischemic heart disease; when extreme quintiles of total protein intake were compared, the relative risk was 0.74 (95% CI: 0.59, 0.94). Both animal and vegetable proteins contributed to the lower risk. This inverse association was similar in women with low- or high-fat diets. CONCLUSIONS: Our data do not support the hypothesis that a high protein intake increases the risk of ischemic heart disease. In contrast, our findings suggest that replacing carbohydrates with protein may be associated with a lower risk of ischemic heart disease. Because a high dietary protein intake is often accompanied by increases in saturated fat and cholesterol intakes, application of these findings to public dietary advice should be cautious. Copyright (c) 1999 American Society for Clinical Nutrition [ABSTRACT FROM AUTHOR]

Background: Few epidemiologic studies are available that quantify the magnitude of the risk of squamous cell carcinoma (SCC) of the skin associated with sun exposure and related factors such as skin type. In addition, several studies have found an association between cigarette smoking and SCC.Purpose: We prospectively examined the risk of developing SCC in relation to phenotype and the effects of sun exposure, as well as to cigarette smoking and other factors, during 8 years of follow-up in a cohort of 107,900 predominantly white women aged 30-55 years at base line in 1976.Methods: Questionnaires regarding medical history and health-related variables were sent to Nurses' Health Study participants every 2 years, beginning in 1976. Information on constitutional factors (natural hair color, childhood and adolescent tendency to sunburn and tan, and lifetime number of severe sunburns), lifestyle factors (regular time spent outdoors in the summer and sunscreen use), the state lived in at birth and at ages 15 and 30 years, and cigarette smoking habits were ascertained by questionnaire. A total of 197 women with first-incident, histologically confirmed, invasive SCCs that were diagnosed from 1982 to 1990 were included in this analysis. Multivariate analysis using proportional hazards models was used to calculate the relative risks (RRs) and corresponding 95% confidence intervals (CIs), with adjustment for confounders.Results: The risk of SCC was increased in women living in California (RR = 1.8; 95% CI = 1.3-2.6) and Florida (RR = 2.1; 95% CI = 1.1-3.9) at base line, compared with those living in the northeastern states. This risk was higher for women living in those states at birth and at 15 years of age (RR = 2.5; 95% CI = 1.4-4.4 for California and RR = 3.0; 95% CI = 0.7-1.2 for Florida). Red (RR = 2.0; 95% CI = 1.1-3.7) and light brown (RR = 1.7; 95% CI = 1.2-2.4) hair colors were associated with an increased risk of SCC, compared with dark brown hair. After adjusting for the number of sunburns, women who tended to burn after 2 or more hours of sun exposure as children had a slightly higher risk of SCC than those who never burned (RR = 1.5; 95% CI = 0.9-2.5 for burn and RR = 1.1; 95% CI = 0.6-2.0 for painful burn), although the actual number of severe burns appeared to be a more important factor (RR = 2.4; 95% CI = 1.5-4.0 for six or more burns). Finally, current cigarette smokers showed a 50% increase in the risk of SCC compared with never smokers (RR = 1.5; 95% CI = 1.1-2.1).Conclusion: Exposure to the sun leading to sunburn, particularly at early ages, should be avoided to decrease the risk of incident SCC. [ABSTRACT FROM AUTHOR]

Objective: To assess the risk of invasive breast cancer associated with total and beverage-specific alcohol consumption and to evaluate whether dietary and nondietary factors modify the association.Data Sources: We included in these analyses 6 prospective studies that had at least 200 incident breast cancer cases, assessed long-term intake of food and nutrients, and used a validated diet assessment instrument. The studies were conducted in Canada, the Netherlands, Sweden, and the United States. Alcohol intake was estimated by food frequency questionnaires in each study. The studies included a total of 322647 women evaluated for up to 11 years, including 4335 participants with a diagnosis of incident invasive breast cancer.Data Extraction: Pooled analysis of primary data using analyses consistent with each study's original design and the random-effects model for the overall pooled analyses.Data Synthesis: For alcohol intakes less than 60 g/d (reported by >99% of participants), risk increased linearly with increasing intake; the pooled multivariate relative risk for an increment of 10 g/d of alcohol (about 0.75-1 drink) was 1.09 (95% confidence interval [CI], 1.04-1.13; P for heterogeneity among studies, .71). The multivariate-adjusted relative risk for total alcohol intakes of 30 to less than 60 g/d (about 2-5 drinks) vs nondrinkers was 1.41 (95% CI, 1.18-1.69). Limited data suggested that alcohol intakes of at least 60 g/d were not associated with further increased risk. The specific type of alcoholic beverage did not strongly influence risk estimates. The association between alcohol intake and breast cancer was not modified by other factors.Conclusions: Alcohol consumption is associated with a linear increase in breast cancer incidence in women over the range of consumption reported by most women. Among women who consume alcohol regularly, reducing alcohol consumption is a potential means to reduce breast cancer risk. [ABSTRACT FROM AUTHOR]

Context: Breast cancer is a major cause of mortality among women. It is important to identify modifiable risk factors for this disease.Objective: To examine body mass index (BMI) at the age of 18 years and at midlife and adult weight change in relation to breast cancer incidence and mortality.Design: Cohort study.Setting: A cohort of 95256 US female nurses aged 30 to 55 years who were followed up for 16 years.Main Outcome Measure: Incident and fatal breast cancer.Results: During 1203498 person-years, 2517 incident breast cancers (60% postmenopausal) were documented. Higher current BMI was associated with lower breast cancer incidence before menopause and was minimally associated with incidence after menopause. However, a stronger positive relationship was seen among postmenopausal women who never used hormone replacement (relative risk=1.59 for BMI >31 kg/m2 vs < or = 20 kg/m2; 95% confidence interval, 1.09-2.32; P for trend <.001). Higher BMI at the age of 18 years was associated with lower breast cancer incidence both before and after menopause. Weight gain after the age of 18 years was unrelated to breast cancer incidence before menopause, but was positively associated with incidence after menopause. This increased risk with weight gain was limited to women who never used postmenopausal hormones; among these women, the relative risk was 1.99 (95% confidence interval, 1.43-2.76) for weight gain of more than 20 kg vs unchanged weight (P for trend <.001). Current BMI and weight gain were even more strongly associated with fatal postmenopausal breast cancer. In this population, the percentage of postmenopausal breast cancer accounted for by weight gain alone was approximately 16% and by hormone replacement therapy alone was 5%, but when the interaction between these variables was considered, together they accounted for about one third of postmenopausal breast cancers.Conclusions: Avoiding adult weight gain may contribute importantly to the prevention of breast cancer after menopause, particularly among women who do not use postmenopausal hormones. [ABSTRACT FROM AUTHOR]

OBJECTIVE--To assess the relationship between coffee consumption and risk of coronary heart disease (CHD) among women. DESIGN--Prospective cohort study with coffee consumption measured in 1980, 1984, and 1986, and follow-up through 1990. SETTING--Female registered nurses in the United States. PARTICIPANTS--A total of 85,747 US women 34 to 59 years of age in 1980 and without history of CHD, stroke, or cancer. MAIN OUTCOME MEASURE--Ten-year incidence of CHD (defined as nonfatal myocardial infarction or fatal CHD). RESULTS--During 10 years of follow-up we documented 712 cases of CHD. After adjustment for age, smoking, and other CHD risk factors, we found no evidence for any positive association between coffee consumption and risk of subsequent CHD. For women drinking six or more cups of caffeine-containing coffee per day in 1980, the relative risk was 0.95 (95% confidence interval, 0.73 to 1.26) compared with women who did not consume this beverage. Similarly, there was no association when the first 4 years of follow-up were excluded, when nonfatal and fatal CHD end points were examined separately, or when we updated coffee consumption in 1984 or 1986 and examined only CHD during the next 2-year interval. Further, there was no association with caffeine intake from all sources combined or with decaffeinated coffee consumption. CONCLUSIONS--These data indicate that coffee as consumed by US women is not an important cause of CHD. [ABSTRACT FROM AUTHOR]

OBJECTIVE--To assess the validity of the 1990 US weight guidelines for women that support a substantial gain in weight at approximately 35 years of age and recommend a range of body mass index (BMI) (defined as weight in kilograms divided by the square of height in meters) from 21 to 27 kg/m2, in terms of coronary heart disease (CHD) risk in women. DESIGN--Prospective cohort study. SETTING--Female registered nurses in the United States. PARTICIPANTS--A total of 115,818 women aged 30 to 55 years in 1976 and without a history of previous CHD. MAIN OUTCOME MEASURE--Incidence of CHD defined as nonfatal myocardial infarction or fatal CHD. RESULTS--During 14 years of follow-up, 1292 cases of CHD were ascertained. After controlling for age, smoking, menopausal status, postmenopausal hormone use, and parental history of CHD and using as a reference women with a BMI of less than 21 kg/m2, relative risks (RRs) and 95% confidence intervals (CIs) for CHD were 1.19 (0.97 to 1.44) for a BMI of 21 to 22.9 kg/m2, 1.46 (1.20 to 1.77) for a BMI of 23 to 24.9 kg/m2, 2.06 (1.72 to 2.48) for a BMI of 25 to 28.9 kg/m2, and 3.56 (2.96 to 4.29) for a BMI of 29 kg/m2 or more. Women who gained weight from 18 years of age were compared with those with stable weight (+/- 5 kg) in analyses that controlled for the same variables as well as BMI at 18 years of age. The RRs and CIs were 1.25 (1.01 to 1.55) for a 5- to 7.9-kg gain, 1.64 (1.33 to 2.04) for an 8- to 10.9-kg gain, 1.92 (1.61 to 2.29) for an 11- to 19-kg gain, and 2.65 (2.17 to 3.22) for a gain of 20 kg or more. Among women with the BMI range of 18 to 25 kg/m2, weight gain after 18 years of age remained a strong predictor of CHD risk. CONCLUSIONS--Higher levels of body weight within the "normal" range, as well as modest weight gains after 18 years of age, appear to increase risks of CHD in middle-aged women. These data provide evidence that current US weight guidelines may be falsely reassuring to the large proportion of women older than 35 years who are within the current guidelines but have potentially avoidable risks of CHD. [ABSTRACT FROM AUTHOR]