In the last few decades, community-based participatory research (CBPR) has emerged as an important approach that links environmental health and justice advocates with research institutions to understand and address environmental health problems. CBPR has generally been evaluated for its impact on policy, regulation, and its support of community science. However, there has been less emphasis on assessing the ways in which CBPR (re)shapes and potentially improves the scientific enterprise itself. This commentary focuses on this under-emphasized aspect of CBPR—how it can strengthen science. Using two case studies of environmental health CBPR research—the Northern California Household Exposure Study, and the San Joaquin Valley Drinking Water Study—we posit that CBPR helps improve the “3 Rs” of science—rigor, relevance and reach—and in so doing benefits the scientific enterprise itself.

Racial or ethnic minority groups and low-income communities have poorer health outcomes than others. They are more frequently exposed to multiple environmental hazards and social stressors, including poverty, poor housing quality, and social inequality. Researchers are grappling with how best to characterize the cumulative effects of these hazards and stressors in order to help regulators and decision makers craft more-effective policies to address health and environmental disparities. In this article we synthesize the existing scientific evidence regarding the cumulative health implications of higher rates of exposure to environmental hazards, along with individual biological susceptibility and social vulnerability. We conclude that current environmental policy, which is focused narrowly on pollutants and their sources, should be broadened to take into account the cumulative impact of exposures and vulnerabilities encountered by people who live in neighborhoods consisting largely of racial or ethnic minorities or people of low socioeconomic status.

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This study examines links between racial residential segregation and estimated ambient air toxics exposures and their associated cancer risks using modeled concentration estimates from the U.S. Environmental Protection Agency’s National Air Toxics Assessment. We combined pollutant concentration estimates with potencies to calculate cancer risks by census tract for 309 metropolitan areas in the United States. This information was combined with socioeconomic status (SES) measures from the 1990 Census. Estimated cancer risks associated with ambient air toxics were highest in tracts located in metropolitan areas that were highly segregated. Disparities between racial/ethnic groups were also wider in more segregated metropolitan areas. Multivariate modeling showed that, after controlling for tract-level SES measures, increasing segregation amplified the cancer risks associated with ambient air toxics for all racial groups combined [highly segregated areas: relative cancer risk (RCR) = 1.04; 95% confidence interval (CI), 1.01–107; extremely segregated areas: RCR = 1.32; 95% CI, 1.28–1.36]. This segregation effect was strongest for Hispanics (highly segregated areas: RCR = 1.09; 95% CI, 1.01–1.17; extremely segregated areas: RCR = 1.74; 95% CI, 1.61–1.88) and weaker among whites (highly segregated areas: RCR = 1.04; 95% CI, 1.01–1.08; extremely segregated areas: RCR = 1.28; 95% CI, 1.24–1.33), African Americans (highly segregated areas: RCR = 1.09; 95% CI, 0.98–1.21; extremely segregated areas: RCR = 1.38; 95% CI, 1.24–1.53), and Asians (highly segregated areas: RCR = 1.10; 95% CI, 0.97–1.24; extremely segregated areas: RCR = 1.32; 95% CI, 1.16–1.51). Results suggest that disparities associated with ambient air toxics are affected by segregation and that these exposures may have health significance for populations across racial lines.

Background: Research indicates that the double jeopardy of exposure to environmental hazards combined with place-based stressors is associated with maternal and child health (MCH) disparities. Objective and Discussion: Our aim is to present evidence that individual-level and place-based psychosocial stressors may compromise host resistance such that environmental pollutants would have adverse health effects at relatively lower doses, thus partially explaining MCH disparities, particularly poor birth outcomes. Allostatic load may be a physiologic mechanism behind the moderation of the toxic effect of environmental pollutants by social stressors. We propose a conceptual framework for holistic approaches to future MCH research that elucidates the interplay of psychosocial stressors and environmental hazards in order to better explain drivers of MCH disparities. Conclusion: Given the complexity of the link between environmental factors and MCH disparities, a holistic approach to future MCH research that seeks to untangle the double jeopardy of chronic stressors and environmental hazard exposures could help elucidate how the interplay of these factors shapes persistent racial and economic disparities in MCH.