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Background Research on psychosocial stress and risk of breast cancer has produced conflicting results. Few studies have assessed this relation by breast cancer subtype or specifically among Black women, who experience unique chronic stressors. Methods We used prospective data from the Black Women’s Health Study, an ongoing cohort study of 59,000 US Black women, to assess neighborhood- and individual-level psychosocial factors in relation to risk of breast cancer. We used factor analysis to derive two neighborhood score variables after linking participant addresses to US Census data (2000 and 2010) on education, employment, income and poverty, female-headed households, and Black race for all households in each residential block group. We used Cox proportional hazards regression to estimate hazard ratios (HR) and 95% confidence intervals (CI) adjusted for established breast cancer risk factors. Results During follow-up from 1995 to 2017, there were 2167 incident invasive breast cancer cases (1259 estrogen receptor positive (ER +); 687 ER negative (ER−)). For ER− breast cancer, HRs were 1.26 (95% CI 1.00–1.58) for women living in the highest quartile of neighborhood disadvantage relative to women in the lowest quartile, and 1.24 (95% CI 0.98–1.57) for lowest versus highest quartile of neighborhood socioeconomic status (SES). For ER+ breast cancer, living in the lowest quartile of neighborhood SES was associated with a reduced risk of ER+ breast cancer (HR = 0.83, 95% CI 0.70–0.98). With respect to individual-level factors, childhood sexual abuse (sexual assault ≥ 4 times vs. no abuse: HR = 1.35, 95% CI 1.01–1.79) and marital status (married/living together vs. single: HR = 1.29, 95% CI 1.08–1.53) were associated with higher risk of ER+, but not ER− breast cancer. Conclusion Neighborhood disadvantage and lower neighborhood SES were associated with an approximately 25% increased risk of ER− breast cancer in this large cohort of Black women, even after control for multiple behaviors and lifestyle factors. Further research is need to understand the underlying reasons for these associations. Possible contributing factors are biologic responses to the chronic stress/distress experienced by individuals who reside in neighborhoods characterized by high levels of noise, crime and unemployment or the direct effects of environmental toxins.

Evidence linking active or passive smoking to the incidence of adult-onset asthma is inconsistent with both positive and inverse associations being reported. Most previous studies of active smoking have not accounted for passive smoke exposure, which may have introduced bias. To assess the separate associations of active and passive smoking to the incidence of adult-onset asthma in the U.S. Black Women's Health Study, a prospective cohort of African American women followed since 1995 with mailed biennial questionnaires. Active smoking status was reported at baseline and updated on all follow-up questionnaires. Passive smoke exposure during childhood, adolescence, and adulthood was ascertained in 1997. Asthma cases comprised women who reported doctor-diagnosed asthma with concurrent asthma medication use. Cox regression models were used to derive multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) for former and current smoking and for passive smoking among nonsmokers compared with a reference category of never active or passive smokers. Among 46,182 participants followed from 1995 to 2011, 1,523 reported incident asthma. The multivariable HRs for former active smoking, current active smoking, and passive smoking only were, respectively, 1.36 (95% CI, 1.11-1.67), 1.43 (95% CI, 1.15-1.77), and 1.21 (95% CI, 1.00-1.45), compared with never active/passive smoking. In this large population with 16 years of follow-up, active smoking increased the incidence of adult-onset asthma, and passive smoke exposure increased the risk among nonsmokers. Continued efforts to reduce exposure to tobacco smoke may have a beneficial effect on the incidence of adult-onset asthma.

Background In the U.S., poorer breast cancer survival in Black women relative to white women has persisted for over 30 years, with recent data showing a 38% higher mortality in Black women with breast cancer. Stage at diagnosis is the most powerful predictor of survival. However, despite rates of mammographic screening having become approximately equal in the two groups, Black women are more likely to be diagnosed at later stages. We examined whether perceived experiences of discrimination due to race in receipt of health care is associated with a late stage at diagnosis of breast cancer. Methods Nested within the prospective Black Women’s Health Study (BWHS), this case-only study included 1,617 self-identified U.S. Black women diagnosed with a first invasive breast cancer in 2003 through 2022. Eligible cases had completed a BWHS questionnaire in 2003 in which participants were asked whether they received differential health care due to their race or insurance status. The primary outcome in the present research was stage at breast cancer diagnosis, obtained from medical records and cancer registry data. Odds ratios (OR) for the association of perceived racial discrimination in health care with later stage at diagnosis were estimated in logistic regression analyses, with each of stages II, III, and IV compared with stage I diagnosis. Results In multivariable analyses controlled for age, body mass index, socioeconomic factors, and mammographic screening, perceived racial discrimination in healthcare was associated with an increased odds of breast cancer diagnosis at stage IV versus stage I (OR = 2.10, 95% CI 1.15–3.83). The association was present even among women who reported having a mammogram in the two years before diagnosis. No associations were observed for stage II or III versus stage I. Conclusions The findings support reducing healthcare discrimination to alleviate the disproportionate burden of worse prognosis and survival experienced by Black women.

Better information on lung cancer occurrence in lifelong nonsmokers is needed to understand gender and racial disparities and to examine how factors other than active smoking influence risk in different time periods and geographic regions. We pooled information on lung cancer incidence and/or death rates among self-reported never-smokers from 13 large cohort studies, representing over 630,000 and 1.8 million persons for incidence and mortality, respectively. We also abstracted population-based data for women from 22 cancer registries and ten countries in time periods and geographic regions where few women smoked. Our main findings were: (1) Men had higher death rates from lung cancer than women in all age and racial groups studied; (2) male and female incidence rates were similar when standardized across all ages 40+ y, albeit with some variation by age; (3) African Americans and Asians living in Korea and Japan (but not in the US) had higher death rates from lung cancer than individuals of European descent; (4) no temporal trends were seen when comparing incidence and death rates among US women age 40-69 y during the 1930s to contemporary populations where few women smoke, or in temporal comparisons of never-smokers in two large American Cancer Society cohorts from 1959 to 2004; and (5) lung cancer incidence rates were higher and more variable among women in East Asia than in other geographic areas with low female smoking. These comprehensive analyses support claims that the death rate from lung cancer among never-smokers is higher in men than in women, and in African Americans and Asians residing in Asia than in individuals of European descent, but contradict assertions that risk is increasing or that women have a higher incidence rate than men. Further research is needed on the high and variable lung cancer rates among women in Pacific Rim countries.

Objective Limited evidence suggests that higher levels of serum vitamin D (25(OH)D) protect against SARS-CoV-2 virus (COVID-19) infection. Black women commonly experience 25(OH)D insufficiency and are overrepresented among COVID-19 cases. We conducted a prospective analysis of serum 25(OH)D levels in relation to COVID-19 infection among participants in the Black Women’s Health Study. Methods Since 1995, the Black Women’s Health Study has followed 59,000 U.S. Black women through biennial mailed or online questionnaires. Over 13,000 study participants provided a blood sample in 2013–2017. 25(OH)D assays were performed in a certified national laboratory shortly after collection of the samples. In 2020, participants who had completed the online version of the 2019 biennial health questionnaire were invited to complete a supplemental online questionnaire assessing their experiences related to the COVID-19 pandemic, including whether they had been tested for COVID-19 infection and the result of the test. We used logistic regression analysis to estimate odds ratios (OR) and 95% confidence intervals (CI) for the association of 25(OH)D level with COVID-19 positivity, adjusting for age, number of people living in the household, neighborhood socioeconomic status, and other potential confounders. Results Among 5,081 eligible participants whose blood sample had been assayed for 25(OH)D, 1,974 reported having had a COVID-19 test in 2020. Relative to women with 25(OH)D levels of 30 ng/mL (75 nmol/l) or more, multivariable-adjusted ORs for COVID-19 infection in women with levels of 20–29 ng/mL (50–72.5 nmol/l) and <20 ng/mL (<50 nmol/l) were, respectively, 1.48 (95% CI 0.95–2.30) and 1.69 (95% CI 1.04–2.72) (p trend 0.02). Conclusion The present results suggest that U.S. Black women with lower levels of 25(OH)D are at increased risk of infection with COVID-19. Further work is needed to confirm these findings and determine the optimal level of 25(OH)D for a beneficial effect.

Selection pressure due to exposure to infectious pathogens endemic to Africa may explain distinct genetic variations in immune response genes. However, the impact of those genetic variations on human immunity remains understudied, especially within the context of modern lifestyles and living environments, which are drastically different from early humans in sub Saharan Africa. There are few data on population differences in constitutional immune environment, where genetic ancestry and environment are likely two primary sources of variation. In a study integrating genetic, molecular and epidemiologic data, we examined population differences in plasma levels of 14 cytokines involved in innate and adaptive immunity, including those implicated in chronic inflammation, and possible contributing factors to such differences, in 914 AA and 855 EA women. We observed significant differences in 7 cytokines, including higher plasma levels of CCL2, CCL11, IL4 and IL10 in EAs and higher levels of IL1RA and IFN[alpha]2 in AAs. Analyses of a wide range of demographic and lifestyle factors showed significant impact, with age, education level, obesity, smoking, and alcohol intake, accounting for some, but not all, observed population differences for the cytokines examined. Levels of two pro-inflammatory chemokines, CCL2 and CCL11, were strongly associated with percent of African ancestry among AAs. Through admixture mapping, the signal was pinpointed to local ancestry at 1q23, with fine-mapping analysis refined to the Duffy-null allele of rs2814778. In AA women, this variant was a major determinant of systemic levels of CCL2 (p = 1.1e-58) and CCL11 (p = 2.2e-110), accounting for 19% and 40% of the phenotypic variance, respectively. Our data reveal strong ancestral footprints in inflammatory chemokine regulation. The Duffy-null allele may indicate a loss of the buffering function for chemokine levels. The substantial immune differences by ancestry may have broad implications to health disparities between AA and EA populations.

African American (AA) women are more likely than white women to be obese and to be diagnosed with ER− and triple-negative (TN) breast cancer, but few studies have evaluated the impact of obesity and body fat distribution on breast cancer subtypes in AA women. We evaluated these associations in the AMBER Consortium by pooling data from four large studies. Cases were categorized according to hormone receptor status as ER+, ER−, and TN (ER−, PR−, and HER2−) based on pathology data. A total of 2104 ER+ cases, 1070 ER− cases (including 491 TN cases), and 12,060 controls were included. Odds ratios (OR) and 95 % confidence intervals (CI) were computed using logistic regression, taking into account breast cancer risk factors. In postmenopausal women, higher recent (most proximal value to diagnosis/index date) BMI was associated with increased risk of ER+ cancer (OR 1.31; 95 % CI 1.02–1.67 for BMI ≥35 vs. <25 kg/m 2 ) and with decreased risk of TN tumors (OR 0.60; 95 % CI 0.39–0.93 for BMI ≥35 vs. <25). High young adult BMI was associated with decreased premenopausal ER+ cancer and all subtypes of postmenopausal cancer, and high recent waist-to-hip ratio with increased risk of premenopausal ER+ tumors (OR 1.35; 95 % CI 1.01–1.80) and all tumor subtypes combined in postmenopausal women (OR 1.26; 95 % CI 1.02–1.56). The impact of general and central obesity varies by menopausal status and hormone receptor subtype in AA women. Our findings imply different mechanisms for associations of adiposity with TN and ER+ breast cancers.

Background Moderate to heavy alcohol consumption is associated with an increased risk of breast cancer. The etiologic role of genetic variation in genes involved in ethanol metabolism has not been established, with little information available among women of African ancestry. Methods Our analysis from the African American Breast Cancer Epidemiology and Risk (AMBER) Consortium included 2889 U.S. Black women who were current drinkers at the time of breast cancer diagnosis (N cases = 715) and had available genetic data for four ethanol metabolism genomic regions ( ADH, ALDH, CYP2E1 , and ALDH2 ). We used generalized estimating equations to calculate genetic effects, gene* alcohol consumption (≥ 7drinks/week vs. < 7/week) interactions, and joint main plus interaction effects of up to 23,247 variants in ethanol metabolism genomic regions on odds of breast cancer. Results Among current drinkers, 21% of cases and 14% of controls reported consuming ≥ 7 drinks per week. We identified statistically significant genetic effects for rs79865122-C in CYP2E1 with odds of ER- breast cancer and odds of triple negative breast cancer, as well as a significant joint effect with odds of ER- breast cancer (≥ 7drinks per week OR = 3.92, < 7 drinks per week OR = 0.24, p joint  = 3.74 × 10 −6 ). In addition, there was a statistically significant interaction of rs3858704-A in ALDH2 with consumption of ≥ 7 drinks/week on odds of triple negative breast cancer (≥ 7drinks per week OR = 4.41, < 7 drinks per week OR = 0.57, p int  = 8.97 × 10 –5 ). Conclusions There is a paucity of information on the impact of genetic variation in alcohol metabolism genes on odds of breast cancer among Black women. Our analysis of variants in four genomic regions harboring ethanol metabolism genes in a large consortium of U.S. Black women identified significant associations between rs79865122-C in CYP2E1 and odds of ER- and triple negative breast cancer. Replication of these findings is warranted.

Evidence of an association between plasma 25‐hydroxyvitamin D [25(OH)D] levels and risk of hypertension, predominantly from studies of White individuals, suggests an inverse relationship. Limited data are available on Black individuals, who are more likely to have vitamin D deficiency. In the Black Women's Health Study (BWHS), a prospective study of 59 000 self‐identified Black women from across the US, we assessed levels of a validated predicted vitamin D score in relation to incident hypertension. We followed 42 239 participants who were free of cardiovascular disease and cancer from 1995 to 2019, during which time 19 505 incident cases of hypertension were identified. Cox proportional hazards model were used to calculate multivariable‐adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for the association of predicted vitamin D with the risk of incident hypertension. In age‐adjusted analyses, there was a strong inverse dose‐response association between predicted vitamin D score and hypertension risk, with an HR of .66 (95% CI: .63‐.68, p trend < .0001) for the highest quartile of predicted vitamin D relative to the lowest. After control for potential confounders including body mass index, physical activity, and cigarette smoking, the HR was attenuated to .91 (95% CI: .87–.95, p trend = .002). In this prospective cohort study of Black women, predicted vitamin D score was weakly inversely associated with the incidence of hypertension. This observed association may reflect an inability to fully control for confounding factors.

Background Use of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) has been hypothesized to be associated with reduced risk of breast cancer; however, results of epidemiological studies have been mixed. Few studies have investigated these associations among African American women. Methods To assess the relation of aspirin use to risk of breast cancer in African American women, we conducted a prospective analysis within the Black Women’s Health Study, an ongoing nationwide cohort study of 59,000 African American women. On baseline and follow-up questionnaires, women reported regular use of aspirin (defined as use at least 3 days per week) and years of use. During follow-up from 1995 through 2017, 1919 invasive breast cancers occurred, including 1112 ER+, 569 ER−, and 284 triple-negative (TN) tumors. We used age-stratified Cox proportional hazards regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for associations of aspirin use with risk of ER+, ER−, and TN breast cancer, adjusted for established breast cancer risk factors. Results Overall, the HR for current regular use of aspirin relative to non-use was 0.92 (95% CI 0.81, 1.04). For ER+, ER−, and TN breast cancer, corresponding HRs were 0.98 (0.84, 1.15), 0.81 (0.64, 1.04), and 0.70 (0.49, 0.99), respectively. Conclusions Our findings with regard to ER− and TN breast cancer are consistent with hypothesized inflammatory mechanisms of ER− and TN breast cancer, rather than hormone-dependent pathways. Aspirin may represent a potential opportunity for chemoprevention of ER− and TN breast cancer.