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PURPOSE: To investigate the association between pre- or perinatal factors and breast cancer risk among African American women. METHODS: Participants in the Black Women’s Health Study, a prospective cohort of 59,000 African American women, reported birth weight, preterm birth, twin or triplet status, maternal age at birth, birth order, and having been breastfed during infancy at various times during follow-up from 1997 to 2015. Numbers of incident cases ranged from 312 for breastfed analyses to 1,583 for twin or triplet analyses. Using multivariable Cox proportional hazards regression, we estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between each factor and breast cancer risk overall and by estrogen receptor (ER) status. RESULTS: Compared to birth weights of 5 lbs. 8 oz.−8 lbs. 13 oz., low (8 lbs. 13 oz.) birth weights were associated with increased breast cancer risk; HRs (95% CI) were 1.19 (0.98–1.44) and 1.26 (0.97–1.63), respectively. Associations were similar by ER status. Having been born to a mother aged ≥35 years vs.

To conduct the first epidemiologic study prospectively examining the association between particulate matter air pollution

Breast cancer mortality is higher in Black women than in White women. The prevalence of type 2 diabetes mellitus is also higher, yet data on whether diabetes affects breast cancer mortality in this population are lacking. We investigated the relation of diabetes at the time of breast cancer diagnosis to breast cancer mortality in the Black Women's Health Study, a prospective cohort study.1,621 Black women with invasive breast cancer diagnosed in 1995-2013 were followed by mailed questionnaires and searches of the National Death Index. Multivariable Cox regression analysis was used to compute hazard ratios (HRs) for diabetes in relation to breast cancer mortality and all-cause mortality, with adjustment for age, stage, treatment modality, estrogen receptor (ER) status, and body mass index.There were 368 deaths during follow-up, of which 273 were due to breast cancer. Breast cancer mortality was significantly increased in women who had been diagnosed with diabetes at least 5 years before breast cancer occurrence, HR 1.86 (95% CI 1.20-2.89), with elevations observed for both ER+ and ER- breast cancer. All-cause mortality was also higher in diabetics, with HRs of 1.54 (95% CI 1.12-2.07) overall and 2.26 (95% CI 1.62-3.15) for ≥5-year duration of diabetes relative to non-diabetics.Our results present the first solid evidence of a positive association of type 2 diabetes with breast cancer mortality in Black women. Given the higher prevalence and earlier onset of type 2 diabetes in Black women, it is likely that diabetes contributes to racial disparities in breast cancer mortality.

Endometriosis and mammographic density have been hypothesized to be influenced by sex steroid hormonal exposures in adolescence and early adulthood. We investigated the association between endometriosis and mammographic density, a consistent and independent risk factor for breast cancer. We conducted a cross-sectional analysis among 1,581 pre- and postmenopausal women not previously diagnosed with breast cancer in the Nurses’ Health Study II cohort. We measured average percent mammographic density and absolute dense and non-dense breast area using a validated computer-assisted method. Multivariable linear regression was used to estimate the association between endometriosis and mammographic density among pre- and postmenopausal women separately. Among premenopausal women, average percent mammographic density was 43.1 % among women with endometriosis (n = 91) and 40.5 % among women without endometriosis (n = 1,150). Endometriosis was not associated significantly with mammographic density among premenopausal (% difference = 2.00 percentage points 95 % CI −1.33, 5.33) or among postmenopausal women (% difference = −0.89 percentage points 95 % CI −5.10, 3.33). Among premenopausal women, there was heterogeneity by BMI at age 18 (p value = 0.003), with a suggested association among those who were lean at age 18 (BMI

Bone mineral density (BMD) is a putative marker for lifetime exposure to estrogen. Studies that have explored whether BMD is a determinant of mammographic density (MD) have observed inconsistent results. Therefore, we examined this potential association in a sample of women (n = 1,516) from the clinical sub-cohort in the Mexican teachers’ cohort (n = 115,315). We used multivariable linear regression to assess the association between quartiles of BMD and percent MD, as well as total dense and non-dense area of the breast, stratified by menopausal status. We also examined the associations by body mass index (BMI) (

The association between infectious mononucleosis (IM) and risk of breast cancer is unclear; no prospective studies have examined this relationship. We examined self-reported history and age at IM in relation to risk of invasive breast cancer.Self-reported history and age at IM were examined in relation to risk of invasive breast cancer in a large cohort of women, the Nurses' Health Study II (81,807 women followed from 1989 to 2007). Through questionnaires, women were asked whether they ever had IM and if so, at what age. During follow-up, 2,349 cases of invasive breast cancer were documented. Cox proportional hazards regression was used to estimate relative risks (RR) and 95 % confidence intervals (CI) for the association of IM with breast cancer.The multivariable-adjusted RR for history of IM and risk of invasive breast cancer was 1.00 (95 % CI: 0.90-1.11). Similar null results were obtained when estrogen receptor/progesterone receptor positive and negative tumors were considered separately. There were no clear patterns of association between age at IM and risk of breast cancer: compared to women with no history of IM, those who were ≤15 years old when they had IM were at lower risk (RR: 0.77; 95 % CI: 0.60, 0.97), but there was no association for women who had IM at ages 16-19, 20-24, or 30+. However, an increased RR (1.45; 95 % CI: 1.02-2.04) was observed for women who had IM at ages 25-29.Results of this large prospective study do not support a clear association between history of clinical IM and risk of invasive breast cancer.

As we discussed in our recent manuscript, our findings of modest but significant positive associations between ambient ultraviolet (UV) radiation and non-Hodgkin lymphoma (NHL) risk in the Nurses’ Health Study (NHS) were unexpected and inconsistent with most of the prior literature on this topic [1]. Dr. Grant offers alternative explanations for our results. In response to his comments, we have conducted additional data analyses. First, Dr. Grant questions whether a majority of NHS participants reside in regions of relatively low total and UV-B radiation. We agree that results from the NHS may not be generalizable to other populations, particularly those in the areas of higher UV radiation. Because nurses originally were recruited from 11 US states (i.e., California, Connecticut, Florida, Maryland, Massachusetts, Michigan, New Jersey, New York, Ohio, Pennsylvania, and Texas) [2], a majority of participants (59%) resided in the Northeast at baseline in 1976. A similar proportion of women reported Northeast residence at birth, age 15, and age 30. Over the course of 30 years of follow-up, 55% of the person-time included residence in the northeast region of the USA. We used the distribution of average annual UV-B flux values in our study population, which ranged from 93 to 196 (in R-B counts 910) as nurses changed residence over the 30 years of follow-up, to guide our choice of cutpoints for analysis. We reported that NHL risk was increased among women who resided in regions with UV-B flux[113 compared to those with lower exposure (\113) [1]. In response to Dr. Grant’s comment, we dichotomized the top category of UV-flux at its median value (164) and re-analyzed the data using this 4-category variable. Our findings were similar to the results presented in the manuscript, with increased risks most apparent in the highest category of ambient UV-B exposure. For example, the multivariable-adjusted rate ratio (RR) for NHL associated with UV-B flux [164 at age 15, which included residence in Texas, Florida, Arizona, New Mexico, and Louisiana, compared to UV-B flux\113 was 1.72 (95% confidence interval (CI): 1.30, 2.29). Further, it is important to note that we observed statistically significant linear trends for the association of average annual UV-B flux, assessed at various time points and considered as a continuous variable, and risk of NHL (p-trend\0.05). Moreover, we found no evidence of departure from linearity when restricted cubic splines were examined. Second, Dr. Grant suggests that the association between UV-B radiation and NHL risk may differ by latitude because of differences in the relative amount of UV-B and UV-A radiation. We speculated in our paper that increased risks of NHL could plausibly be mediated through immunosuppressive effects of UV exposure. As previously discussed, modest increased risks were most apparent for individuals living in areas of higher UV-B radiation (i.e., outside of the northeast). Unfortunately, data on ambient UV-A levels were not available for analysis, and therefore, we could not evaluate the relative effects of UV-A vs. UV-B exposure nor could we directly evaluate the immunosuppression K. A. Bertrand (&) F. Laden Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA 02115, USA e-mail: kbertran@hsph.harvard.edu