Population-based studies suggest a mostly stable trend in overall breast cancer incidence rates,^1,2 although there are documented differences in trends by age at diagnosis and racial/ethnic groups.^1,3-5 Moreover, studies have reported racial/ethnic differences in the incidence rates of breast cancer subtypes, defined according to hormone receptor status or ERBB2 (formerly HER2) receptor status, but these studies have mostly considered few broad molecular subtype, race/ethnicity, or age categories.^6-8 A 2019 report² of temporal changes in breast cancer incidence rates from 2004 through 2016, which used only breast cancer subtypes by hormone receptor status, found that incidence rates increased for hormone receptor–positive breast cancers (corresponding to both luminal A and B molecular breast cancer subtypes) for all races/ethnicities, although rates began to stabilized after 2011 for non-Hispanic Black and American Indian and Alaska Native women. In contrast, hormone receptor–negative tumors (corresponding to both ERBB2-enriched and triple-negative molecular breast cancer subtypes) decreased for women of all racial/ethnic groups by 1.5% to 2.6% per year. Furthermore, differences in trends for women by 2 broad age groups (<50 years vs ≥50 years), were similar, although not statistically significant for the hormone receptor–negative decline in young American Indian and Alaska Native or older Hispanic women.² A previous cross-sectional study also examined breast cancer incidence rates by racial/ethnic and age group differences in 4 breast cancer molecular subtypes based on joint assessment of both hormone receptor status and ERBB2 status using 2010 cancer registry data.⁶ However, studies assessing trends in the incidence rates of breast cancer subtypes are limited, as ERBB2 status was only required to be collected by cancer registries starting in 2010.

Select hair products contain endocrine disrupting chemicals (EDCs) that may affect breast cancer risk. We hypothesize that, if EDCs are related to breast cancer risk, then they may also affect two important breast cancer risk factors: age at menarche and mammographic breast density. In two urban female cohorts (N = 248): 1) the New York site of the National Collaborative Perinatal Project and 2) the New York City Multiethnic Breast Cancer Project, we measured childhood and adult use of hair oils, lotions, leave-in conditioners, root stimulators, perms/relaxers, and hair dyes using the same validated questionnaire. We used multivariable relative risk regression models to examine the association between childhood hair product use and early age at menarche (defined as <11 years of age) and multivariable linear regression models to examine the association between childhood and adult hair product use and adult mammographic breast density. Early menarche was associated with ever use of childhood hair products (RR 2.3, 95% CI 1.1, 4.8) and hair oil use (RR 2.5, 95% CI 1.2, 5.2); however, additional adjustment for race/ethnicity, attenuated associations (hair products RR 1.8, 95% CI 0.8, 4.1; hair oil use RR 2.3, 95% CI 1.0, 5.5). Breast density was not associated with adult or childhood hair product or hair oil use. If confirmed in larger prospective studies, these data suggest that exposure to EDCs through hair products in early life may affect breast cancer risk by altering timing of menarche, and may operate through a mechanism distinct from breast density.

Background: Although advances in early detection and treatment of cancer improve overall population survival, these advances may not benefit all population groups equally and may heighten racial/ethnic differences in survival. Methods: We identified cancer cases in the Surveillance, Epidemiology and End Results program, who were ages ≥20 years and diagnosed with one invasive cancer in 1995 to 1999 (n = 580,225). We used 5-year relative survival rates to measure the degree to which mortality from each cancer is amenable to medical interventions (amenability index). We used Kaplan-Meier methods and Cox proportional hazards regression to estimate survival differences between each racial/ethnic minority group relative to Whites, by the overall amenability index, and three levels of amenability (nonamenable, partly amenable, and mostly amenable cancers, corresponding to cancers with 5-year relative survival rate <40%, 40-69%, and ≥70%, respectively), adjusting for gender, age, disease stage, and county-level poverty concentration. Results: As amenability increased, racial/ethnic differences in cancer survival increased for African Americans, American Indians/Native Alaskans, and Hispanics relative to Whites. For example, the hazard ratios (95% confidence intervals) for African Americans versus Whites from nonamenable, partly amenable, and mostly amenable cancers were 1.05 (1.03-1.07), 1.38 (1.34-1.41), and 1.41 (1.37-1.46), respectively. Asians/Pacific Islanders had similar or longer survival relative to Whites across amenability levels; however, several subgroups experienced increasingly poorer survival with increasing amenability. Conclusions: Cancer survival disparities for most racial/ethnic minority populations widen as cancers become more amenable to medical interventions. Efforts in developing cancer control measures must be coupled with specific strategies for reducing the expected disparities. (Cancer Epidemiol Biomarkers Prev 2009;18(10):2701–8)

Factors beyond the individual level such as those characterizing the residential environment may be important to breast cancer outcomes. We provide a systematic review and results of meta-analysis of the published empirical literature on the associations between breast cancer risk and mortality and features of the residential environment. Using PRISMA guidelines, we searched four electronic databases and manually searched the references of selected articles for studies that were published before June 2013. We selected English language articles that presented data on adult breast cancer incidence or mortality in relation to at least one area-based residential (ABR) independent variable. We reviewed 31 eligible studies, and observed variations in ABR construct definition and measurement, study design, and analytic approach. The most common ABR measures were indicators of socioeconomic status (SES) (e.g., income, education, summary measures of several SES indicators or composite SES). We observed positive associations between breast cancer incidence and urbanization (Pooled RR for urban vs. rural: 1.09. 95% CI: 1.01, 1.19), ABR income (Pooled RR for highest vs. lowest ABR income: 1.17, 95% CI: 1.15, 1.19) and ABR composite SES (Pooled RR for highest vs. lowest ABR composite SES: 1.25, 95% CI: 1.08, 1.44). We did not observe consistent associations between any ABR measures and breast cancer mortality. The findings suggest modest positive associations between urbanization and residential area socioeconomic environment and breast cancer incidence. Further studies should address conceptual and methodological gaps in the current publications to enable inference regarding the influence of the residential environment on breast cancer.

Epigenetic modifications may be one mechanism linking early life factors, including parental socioeconomic status (SES), to adult onset disease risk. However, SES influences on DNA methylation patt...

Maternal smoking in pregnancy (MSP) has been associated with DNA methylation in specific CpG sites (CpGs) in infants and children. We investigated whether MSP, independent of own personal active smoking, was associated with midlife DNA methylation in CpGs that were previously identified in studies of MSP-DNA methylation in children. We used data on MSP collected from pregnant mothers of 89 adult women born in 1959–1964 and measured DNA methylation in blood (granulocytes) collected in 2001–2007 (mean age: 43 years). Seventeen CpGs were differentially methylated by MSP, with multiple CpGs mapping to CYP1A1, MYO1G, AHRR, and GFI1. These associations were consistent in direction with prior studies (e.g., MSP associated with more and less methylation in AHRR and CYP1A1, respectively) and, with the exception of AHRR CpGs, were not substantially altered by adjustment for active smoking. These preliminary results confirm prior prospective reports that MSP influences the offspring DNA methylation, and extends the timeframe to midlife, and suggest that these effects may persist into adulthood, independently of active smoking.