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Exposure to total hydrocarbons (THC) and volatile organic compounds from air pollution is associated with risk of coronary heart disease. THC exposure from oil spills might be similarly associated, but no research has examined this. We assessed the relationship between THC exposure during the response and cleanup of the Deepwater Horizon oil spill (Gulf of Mexico) and heart attack risk among 24,375 oil spill workers enrolled in the Gulf Long-Term Follow-up Study. There were 312 first heart attacks (self-reported physician-diagnosed myocardial infarction, or fatal coronary heart disease) ascertained during the study period (2010–2016). THC exposures were estimated using a job-exposure matrix incorporating self-reported activities and personal air measurements. We used Cox proportional hazards regression to estimate hazard ratios, with inverse-probability weights to account for confounding and censoring. Maximum THC levels of ≥0.30 parts per million (ppm) were associated with heart attack risk, with a 1.8-fold risk for exposure of ≥3.00 ppm versus

Pesticides, common environmental exposures, have been examined in relation to breast cancer primarily in occupational studies or exposure biomarker studies. No known studies have focused on self-reported residential pesticide use. The authors investigated the association between reported lifetime residential pesticide use and breast cancer risk among women living on Long Island, New York. They conducted a population-based case-control study of 1,508 women newly diagnosed with breast cancer between August 1996 and July 1997 and 1,556 randomly selected, age-frequency-matched controls. Comprehensive residential pesticide use and other risk factors were assessed by using an in-person, interviewer-administered questionnaire. Unconditional logistic regression was used to calculate odds ratios and 95% confidence intervals. Breast cancer risk was associated with ever lifetime residential pesticide use (odds ratio = 1.39, 95% confidence interval: 1.15, 1.68). However, there was no evidence of increasing risk with increasing lifetime applications. Lawn and garden pesticide use was associated with breast cancer risk, but there was no dose response. Little or no association was found for nuisance-pest pesticides, insect repellents, or products to control lice or fleas and ticks on pets. This study is the first known to suggest that self-reported use of residential pesticides may increase breast cancer risk. Further investigation in other populations is necessary to confirm these findings.

The hypothesized association between breast cancer and circadian disruption was evaluated in the Electromagnetic Fields and Breast Cancer on Long Island Study. Participants included 576 women with breast cancer diagnosed from August 1996 to June 1997 and 585 population-based controls (87% and 83% participation rates, respectively) aged75 years and living in the same Long Island, New York, home foror = 15 years. An in-person interview ascertained light-at-night exposure histories through shift work (previous 15 years) and at home (previous 5 years). Odds ratios and 95% confidence intervals were estimated by unconditional multivariate logistic regression. Breast cancer was not associated with overall shift work (odds ratio (OR) = 1.04, 95% confidence interval (CI): 0.79, 1.38) or evening shift work (OR = 1.08, 95% CI: 0.81, 1.44). However, overnight shift workers were at lower risk than women never working shifts (OR = 0.55, 95% CI: 0.32, 0.94). Women who frequently turned on lights at home during sleep hours (or = twice/week andor = twice/night) had increased risks (OR = 1.65, 95% CI: 1.02, 2.69). The latter results suggest positive associations with residential light-at-night exposure, or they could reflect response biases. Furthermore, overall and evening shift work were not significant factors, and analyses of overnight shift workers yielded reduced risk estimates. The study thus provides mixed evidence for the light-at-night hypothesis.

Whether use of combined oral contraceptives (OC) protects against benign ovarian tumors is unknown. A case-control study of pathologically confirmed benign ovarian tumors was conducted in the New York City area and included cases diagnosed from January 1, 1992, to December 31, 1993, and controls identified by random digit dialing. There were 196 cases with serous adenomas, 176 with teratomas, 311 with endometriomas, and 65 with mucinous adenomas. Interview data were used to determine contraceptive use. Ever use of OC was associated with a decreased risk of these benign tumors (age- and hospital-adjusted odds ratio = 0.79, 95% confidence interval: 0.60, 1.05). In histologic subgroup analyses, the risk of ovarian tumors was reduced for both current and past OC users. Among tumor subtypes, the risk reduction was greatest for women who had endometriotic lesions. The risk reduction also was greater for women who had used OC for more than 24 months. Protection against benign ovarian tumors may be an additional noncontraceptive benefit of OC use.

To investigate whether use of electric blankets, one of the largest sources of electromagnetic field exposure in the home, is associated with the risk of female breast cancer, the authors analyzed data from a population-based US case-control study. The 2,199 case patients were under age 55 years and had been newly diagnosed with breast cancer between 1990 and 1992. The 2,009 controls were frequency-matched to cases by 5-year age group and geographic area. There was little or no risk associated with ever having used electric blankets, mattress pads, or heated water beds among women under age 45 years (adjusted odds ratio = 1.01, 95% confidence interval 0.86-1.18) or among women aged > or =45 years (adjusted odds ratio = 1.12, 95% confidence interval 0.87-1.43). There was no substantial variation in risk with duration of use; with whether the appliance was used only to warm the bed or used throughout the night; with menopausal status; or with the cases' hormone receptor status or stage of disease. Potential breast cancer risk factors that were associated with electric blanket use did not substantially confound the associations under investigation. These data do not support the hypothesis that electric blanket use increases breast cancer risk among women under age 55 years.

To evaluate whether recreational physical activity is associated with breast cancer among young women, the authors analyzed data from a population-based case-control study. Cases (n = 1,668) were women under age 45 years who had been newly diagnosed with breast cancer between 1990 and 1992 in Atlanta, Georgia, central New Jersey, or Seattle, Washington. Controls (n = 1,505) were frequency-matched to cases by 5-year age group and geographic area of residence. Breast cancer was not associated with recreational activity in any of the three time periods assessed (highest quartile of activity vs. lowest: age- and center-adjusted odds ratio (OR) = 0.94 (95% confidence interval (CI) 0.77-1.15) at ages 12-13 years, OR = 1.08 (95% CI 0.88-1.32) at age 20 years, and OR = 1.18 (95% CI 0.97-1.44) during the past year), with the average of the three time periods (OR = 1.02, 95% CI 0.84-1.25), or with daily climbing of at least two flights of stairs (without stopping) during the past year (daily climbing vs. never climbing: OR = 1.03, 95% CI 0.86-1.23). Estimates were not modified or confounded by body mass index, menopausal status, or caloric intake during the past year. These results do not support a protective role for physical activity in the risk of breast cancer among young women.

In a multicenter population-based case-control study that included 1,588 cases and 1,394 controls less than age 45 years, the authors examined the relation of adult body size and breast cancer risk among young women. Breast cancer patients and healthy controls were identified in Atlanta, Georgia; Seattle/Puget Sound, Washington; and central New Jersey. Cases were newly diagnosed with in situ or invasive breast cancer during the period of May 1, 1990, through December 31, 1992. Anthropometric variables thought to reflect early environmental factors (e.g., height, sitting height, frame size), obesity, and body fat distribution were measured directly. Height, but not sitting height or frame size, was a breast cancer risk factor. Risk of the disease was increased 46 percent among women in the fourth quartile of height (167 cm) compared with women in the first quartile (159 cm). Body weight, but not body fat distribution, was related to breast cancer risk. Risk of the disease was 35 percent lower among women in the highest quartile of Quetelet index (28.8 kg/m2) compared with women in the lowest quartile (22.0 kg/m2). Risk of the disease was increased about 2.1-fold (95 percent confidence interval 1.2-3.8) among women who were thin and tall compared with women who were heavy and short. Thus, breast cancer risk was increased substantially among younger women with a linear body type.

Data from a case-control study that was conducted between 1980 and 1982 were analyzed to investigate the possible association between polycystic ovaries and the risk of breast cancer. The multicenter, population-based study included in-home interviews with 4,730 women with breast cancer and 4,688 control women aged 20-54 years. The age-adjusted odds ratio for breast cancer among women with a self-reported history of physician-diagnosed polycystic ovaries was 0.52 (95% confidence interval 0.32-0.87). The inverse association was not an artifact of infertility, age at first birth, or surgical menopause. Because women with this syndrome have abnormal levels of certain endogenous hormones, the observation of a low risk of breast cancer in this group may provide new insights into hormonal influences on breast cancer.

To investigate whether a history of infertility affects a woman's risk of developing breast cancer, the authors analyzed case-control data collected between 1980 and 1982 as part of the Cancer and Steroid Hormone Study. The 4,730 cases were women aged 20-54 years with a first diagnosis of breast cancer ascertained from eight population-based cancer registries; the 4,688 controls were women randomly selected from the general population of these same eight areas. After controlling for age, age at first birth, and parity, the odds ratio (OR) for breast cancer associated with infertility was 1.01 (95% confidence interval (CI) 0.89-1.15) among gravid women. Controlling for age, the odds ratio was 0.82 (95% CI 0.59-1.14) among nulligravid women. Women who reported that the reason for their infertility was a problem with their ovaries had a risk similar to that for women without a history of infertility (OR = 0.75, 95% CI 0.48-1.24). Women whose physicians reported that the reason for their infertility was anovulation or Stein-Leventhal syndrome also had risks similar to those for women without a history of infertility (OR = 1.26 (95% CI 0.67-2.34) and OR = 1.13 (95% CI 0.46-2.78), respectively). Menopausal status, age at menarche, history of spontaneous abortions, drinking or smoking behavior, use of exogenous hormones, or family history of breast cancer did not appreciably alter the observed odds ratios. If infertility has an effect on breast cancer that is independent of age at first birth, then the effect is small.

It is unclear whether breast cancer risk varies by age and menopausal status in relation to use of hormonal birth control (HBC) and hormone replacement therapy (HRT), taken singly or cumulatively. The authors utilized data from 1,478 cases and 1,493 controls aged 20-98 years with known menopausal status, who had participated in a population-based, case-control study conducted on Long Island during 1996-1997. Exogenous hormone use over the lifecourse was assessed by use of memory aids. The authors examined associations among women in these subgroups: premenopausal (n = 968), postmenopausal65 years (n = 1,045), and postmenopausalor = 65 years (n = 958). Among premenopausal women, risk was increased for ever use of HBC (odds ratio (OR) = 1.37, 95% confidence interval (CI): 1.04, 1.81) or HRT (OR = 1.81, 95% CI: 1.17, 2.81) and was pronounced among women reporting use of both HBC and HRT (OR = 2.59, 95% CI: 1.50, 4.46), long-term HRT use (OR = 3.93, 95% CI: 1.43, 10.84), or estrogen-plus-progestin therapy (OR = 3.51, 95% CI: 1.45, 8.49). There was no effect of ever HBC use among postmenopausal women aged less than 65 years, but risk was modestly elevated for more than 5 years of HRT use (OR = 1.41, 95% CI: 1.00, 1.99). Among postmenopausal women aged 65 years or more, odds ratios for HBC or HRT use were around the null. These results emphasize that timing of exogenous hormone use is important. Women who used these hormones before menopause had elevated risks, but the harmful effects began to decline with age after menopause.

Pregnancy conditions accompanied by high blood pressure, such as preeclampsia and pregnancy-related hypertension, have been associated with a lower risk of breast cancer in several epidemiologic studies. It is unknown whether length of gestation or multiple occurrence of these conditions alters the association with breast cancer. It is also unknown whether the inverse association between preeclampsia and breast cancer risk is modified by menopausal status at breast cancer diagnosis. Using data from a large, population-based case-control study of breast cancer conducted on Long Island, New York, during 1996-1997, the authors examined these questions among ever-parous women (1,310 cases and 1,385 controls) using multivariate logistic models. Preeclampsia was inversely associated with breast cancer (odds ratio = 0.7, 95% confidence interval: 0.5, 1.0); this association was even stronger among women who had multiple occurrences of preeclampsia (odds ratio = 0.3, 95% confidence interval: 0.1, 0.9). The risk reduction was more pronounced among postmenopausal women. Gestation length did not substantially alter the relation between preeclampsia and breast cancer risk. Pregnancy-related hypertension was also inversely associated with breast cancer risk, but the relations were not statistically significant after adjustment for preeclampsia. These data suggest that pregnancy conditions related to hypertension, particularly preeclampsia, play a role in reducing breast cancer risk. Possible biologic mechanisms underpinning these associations should be further explored.

Flavonoids are found in a variety of foods and have anticarcinogenic properties in experimental models. Few epidemiologic studies have examined whether flavonoid intake is associated with breast cancer in humans. In this study, the authors investigated whether dietary flavonoid intake was associated with reduced risk of breast cancer in a population-based sample of US women. They conducted a case-control study among women who resided in Nassau and Suffolk counties on Long Island, New York. Cases and controls were interviewed about known and suspected risk factors and asked to complete a food frequency questionnaire regarding their average intake in the prior 12 months. A total of 1,434 breast cancer cases and 1,440 controls provided adequate responses. A decrease in breast cancer risk was associated with flavonoid intake; the decrease was most pronounced among postmenopausal women for flavonols (odds ratio (OR) = 0.54, 95% confidence interval (CI): 0.40, 0.73), flavones (OR = 0.61, 95% CI: 0.45, 0.83), flavan-3-ols (OR = 0.74, 95% CI: 0.55, 0.99), and lignans (OR = 0.69, 95% CI: 0.51, 0.94). The authors conclude that intake of flavonols, flavones, flavan-3-ols, and lignans is associated with reduced risk of incident postmenopausal breast cancer among Long Island women. These results suggest that US women can consume sufficient levels of flavonoids to benefit from their potential chemopreventive effects.

To examine effects of body size change on postmenopausal breast cancer, the authors conducted a population-based case-control study among 990 cases and 1,006 controls participating in the Long Island Breast Cancer Study Project in 1996-1997. Women who had gained more than 15 kg (33 pounds) since age 20 years were at a 1.6-fold increased risk of breast cancer (95% confidence interval (CI): 1.11, 2.26) relative to their counterparts with stable (+/-3 kg) weight. Subjects who had gained more than 11 kg (24 pounds) during the peri- and postmenopausal years (since age 50 years) had 1.62 times the risk of breast cancer of those whose weight remained unchanged during this time period. This effect of peri- and postmenopausal body size gain was present only among never users of hormone replacement therapy (odds ratio (OR) = 2.02 (95% CI: 1.35, 3.02) as opposed to 0.81 (95% CI: 0.43, 1.53) for ever users; multiplicative interaction: p < 0.01) and was more pronounced among women with estrogen receptor-positive/progesterone receptor-positive breast cancer (OR = 2.17, 95% CI: 1.38, 3.42). Weight loss over the lifetime was associated with decreased risk of postmenopausal breast cancer (OR = 0.55, 95% CI: 0.32, 0.96). These results add to the literature by focusing on the perimenopausal weight trajectory and support efforts urging women to avoid weight gain as they age.

The EMF and Breast Cancer on Long Island Study (EBCLIS) was a case-control study designed to evaluate the possible association between exposure to electromagnetic fields (EMFs) and breast cancer. Eligible women were participants in the population-based Long Island Breast Cancer Study Project, were under 75 years of age at enrollment, were residentially stable, and were identified between August 1, 1996, and June 20, 1997. Of those eligible, 576 cases and 585 controls participated in EBCLIS (87% and 83%, respectively). In-home data collection included various spot and 24-hour EMF measurements, ground-current magnetic field measurements, wire mapping of overhead power lines servicing the home, and an interview. Odds ratios and 95% confidence intervals were based on multivariate logistic regression analyses. All odds ratios were close to 1 and nonsignificant. For the highest quartile of 24-hour EMF measurements, the odds ratio was 0.97 (95% confidence interval (CI): 0.69, 1.37) in the bedroom and 1.09 (95% CI: 0.78, 1.51) in the most lived-in room. For the highest exposure category of ground-current measurements, the odds ratio was 1.13 (95% CI: 0.88, 1.44) in the bedroom and 1.08 (95% CI: 0.85, 1.38) in the most lived-in room. These and other EBCLIS results agree with other recent reports of no association between breast cancer and residential EMF exposures.

To gain insight into whether breast cancer tumors jointly classified by estrogen receptor (ER) and progesterone receptor (PR) status represent diseases with differing etiologies, data from a population-based case-control study of US women 20-44 years of age were analyzed. Cases included 1,556 women diagnosed between 1990 and 1992. Age- and geographic-frequency-matched controls included 1,397 women identified by random digit dialing. Heterogeneity between ER+PR+ and ER-PR- tumors was most pronounced in relation to age, race, and recreational exercise at 12-13 years of age. Multivariate-adjusted odds ratios for ER+PR+ tumors were 0.64 (95% confidence interval (CI): 0.47, 0.89) for 30-34 versus 40-44 years of age, 0.89 (95% CI: 0.63, 1.25) for Black versus White race, and 0.84 (95% CI: 0.68, 1.03) for exercise at 12-13 years of age above versus at or below the median. Corresponding odds ratios for ER-PR- tumors were 1.24 (95% CI: 0.86, 1.77), 1.51 (95% CI: 1.07, 2.14), and 1.15 (95% CI: 0.90, 1.48). Risk of ER-PR- cancer in relation to menstrual and reproductive (parity and lactation) characteristics, alcohol consumption, and family history of breast cancer was similar to that observed for ER+PR+ tumors. These findings only modestly support the hypothesis that hormonally related risk factors have differing relations with ER+PR+ versus ER-PR- tumors among younger women.

Observed weak or null associations between fruit and vegetable intake and breast cancer risk could be due to heterogeneity in endogenous antioxidant capabilities. The authors evaluated potential relations between a functional polymorphism in catalase, an antioxidant enzyme, and breast cancer risk, particularly in relation to fruit and vegetable intake and supplement use. Women (1,008 cases and 1,056 controls) in the Long Island Breast Cancer Study Project (1996–1997) were interviewed, completed a food frequency questionnaire, and provided blood for genotyping. The high-activity catalase CC genotype was associated with an overall 17% reduction in risk of breast cancer compared with having at least one variant T allele (odds ratio ¼ 0.83, 95% confidence interval: 0.69, 1.00). Vegetable and, particularly, fruit consumption contributed to the decreased risk associated with the catalase CC genotype. Associations were more pronounced among women who did not use vitamin supplements, with a significant multiplicative interaction (pinteraction ¼ 0.02) for the CC genotype and high fruit intake (odds ratio ¼ 0.59, 95% confidence interval: 0.38, 0.89), and there was no association among supplement users. These results indicate the importance of diet, rather than supplement use, in concert with endogenous antioxidant capabilities, in the reduction of breast cancer risk. CC genotypes were prevalent in approximately 64% of controls; thus, the preventive potential for fruit consumption has widespread implications. breast neoplasms; catalase; fruit; oxidative stress; vegetables; vitamins

Some studies (but not all) have suggested that there may be an increase in the risk of breast cancer associated with a prior induced abortion. The risk, if present, may vary according to the duration of the pregnancy in which the abortion occurred, or to a woman's age or parity at that time. The authors conducted a case-control study of breast cancer in white women under age 45 years to address the question of breast cancer risk in relation to induced abortion, with the intention of identifying subgroups of women who might be at particularly increased risk. White women who were diagnosed with breast cancer (n = 1,302) from May 1, 1990, through December 31, 1992, in three geographic regions of the United States (Atlanta, Georgia; Seattle/Puget Sound, Washington; and five counties in central New Jersey) were interviewed about their reproductive histories, including the occurrence of induced abortion. Similar information was obtained from control women identified through random digit dialing. Logistic regression analysis was used to estimate the relative risk of breast cancer associated with a history of induced abortion, controlling for the potentially confounding influence of other breast cancer risk factors. Among women who had been pregnant at least once, the risk of breast cancer in those with a prior induced abortion was 20% higher than that in women with no history of abortion (95% confidence interval 1.0-1.5). This small increase in risk varied little according to number of abortions or a woman's current age. The association was present primarily among nulliparous women whose abortions occurred prior to 9 weeks' gestation (estimated relative risk = 2.0, 95% confidence interval 1.2-3.3). There was no excess risk of breast cancer associated with induced abortion among parous women. These data support the hypothesis that there may be a small increase in the risk of breast cancer related to a history of induced abortion among young women of reproductive age. However, the data from this study and others do not permit a causal interpretation at this time; neither do the collective results of the studies suggest that there is a subgroup of women in whom the relative risk associated with induced abortion is unusually high.Previous research has suggested that a history of induced abortion may be associated with an increased risk of breast cancer, but the risk may vary according to factors such as age, parity, or the timing of the abortion. To investigate these relationships further, a case control study was conducted among 1302 White women 20-44 years of age from three geographic areas in the US: Atlanta, Georgia; Seattle/Puget Sound, Washington; and five counties in central New Jersey). The women at these sites, who had been diagnosed with either in situ or invasive breast cancer between May 1, 1990, and December 31, 1992, met the demographic criteria and were available for interview; 1180 White age-matched controls were identified through random digit dialing. Women with breast cancer were more likely than controls to have a lower body mass and family history of breast cancer, to be nulliparous or have had fewer live births, to have had a late age at first birth or an early age at menarche, and to have used oral contraceptives for an extended time period. Among women who had ever been pregnant, the breast cancer risk in those with one or more induced abortion was 1.2 (95% confidence interval [CI], 1.0-1.5) relative to women with no abortion history. The breast cancer risk was greatest (2.0; 95% CI, 1.2-3.3) among nulliparous women whose abortion or abortions occurred prior to 8 weeks' gestation. This risk was slightly higher when the abortion was performed before 20 years of age (1.5) or after 29 years of age (1.4). The data from this study do not permit a causal interpretation at this time, nor do they identify any particular subgroup of women with induced abortion histories at enhanced risk of breast cancer.