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27Background: Stark racial disparities in disease incidence among American women remains a persistent 28 public health challenge. These disparities likely result from complex interactions between genetic, social, 29 lifestyle, and environmental risk factors. The influence of environmental risk factors, such as chemical 30 exposure, however, may be substantial and is poorly understood. 31Objectives: We quantitatively evaluated chemical-exposure disparities by race/ethnicity and age in United 32 States (US) women by using biomarker data for 143 chemicals from the National Health and Nutrition 33 Examination Survey (NHANES) 1999(NHANES) -2014 Methods: We applied a series of survey-weighted, generalized linear models using data from the entire 35 NHANES women population and age-group stratified subpopulations. The outcome was chemical 36 biomarker concentration and the main predictor was race/ethnicity with adjustment for age, socioeconomic 37 status, smoking habits, and NHANES cycle. 38Results: The highest disparities across non-Hispanic Black, Mexican American, Other Hispanic, and other 39 race/multiracial women were observed for pesticides and their metabolites, including 2,5-dichlorophenol, 40 o,p'-DDE, beta-hexachlorocyclohexane, and 2,4-dichlorophenol, along with personal care and consumer 41 product compounds. The latter included parabens, monoethyl phthalate, and several metals, such as mercury 42 and arsenic. Moreover, for Mexican American, Other Hispanic, and non-Hispanic black women, there were 43 several exposure disparities that persisted across age groups, such as higher 2,4-and 2,5-dichlorophenol 44 concentrations. Exposure differences for methyl and propyl parabens, however, were the starkest between 45 non-Hispanic black and non-Hispanic white children with average differences exceeding 4 folds. 46 Discussions: We systematically evaluated differences in chemical exposures across women of various 47 race/ethnic groups and across age groups. Our findings could help inform chemical prioritization in 48 designing epidemiological and toxicological studies. In addition, they could help guide public health 49 interventions to reduce environmental and health disparities across populations.50 51 52The stark racial disparities in disease incidence and health outcomes among American women 53 remains a persistent public health challenge. For example, preterm birth incidence was found to be 54 approximately 60% higher in non-Hispanic Black women relative to non-Hispanic white women (Culhane 55 and Goldenberg 2011). Non-Hispanic Black and Hispanic women are at increased risk of being diagnosed 56 with developing dysglycemia (Marcinkevage et al. 2013) and diabetes (Cowie et al. 2009), relative to non-57 Hispanic white women. Non-Hispanic Black women are also 2-3 times more likely to develop the most 58 aggressive subtype of breast cancer, triple negative, compared to non-Hispanic white women (Carey et al. 59 2006; Stark et al. 2010). Furthermore, relative to non-Hispanic white women, non-Hispanic Black women...

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Among women, breast cancer is the most prevalent form of cancer worldwide and has the second highest mortality rate of any cancer in the United States. The breast cancer related death rate is 40% higher in African American women compared to European American women in the US. The incidence of triple negative breast cancer (TNBC), an aggressive subtype of breast cancer for which there is no targeted therapy, is approximately three times higher in non-Hispanic Black women (NHBW) compared to non-Hispanic White women (NHWW). The drivers of these differences in breast cancer incidence and mortality are still poorly understood, and likely lie in an interaction between genetic and environmental factors. Here, we aimed to identify chemical exposures which may play a role in breast cancer disparities. Using chemical biomonitoring data from the National Health and Nutrition Examination Survey (NHANES) and biological activity data from the EPA’s ToxCast program, we assessed the toxicological profiles of chemicals with higher biomarker concentrations in US NHBW. We conducted a literature search to identify a gene set of breast cancer targets included in ToxCast to analyze the response of prioritized chemicals in these assays. Forty-four chemical biomarkers are significantly higher in NHBW. Investigation of these chemicals in ToxCast resulted in a total of 33,645 assays for analysis, 5,301 of which contained nonzero values for ACC (modl_acc: the concentration at which the dose-response fitted model reaches the cutoff considered “active”) and modl_tp (scaled top value of dose response curve) data. Of these chemicals BPA, PFOS, and thiram are most comprehensively assayed. 2,5-dichlorophenol, 1,4-dichlorobenzene, and methyl and propyl parabens had higher biomarker concentrations in NHBW and moderate testing and activity in ToxCast. The distribution of active concentrations for these chemicals in ToxCast assays are comparable to biomarker concentrations in NHBW. Through this integrated analysis, we have identified that multiple chemicals, including thiram, propylparaben, and p,p’ DDE, with disproportionate exposures in NHBW, have breast cancer associated biological activity at human exposure relevant doses.