This paper provides an overview of the contribution of sociologists to the study of racial and ethnic inequalities in health in the U.S. It argues that sociologists have made four principal contributions. First, they have challenged and problematized the biological understanding of race. Second, they have emphasized the primacy of social structure and context as determinants of racial differences in disease. Third, they have contributed to our understanding of the multiple ways in which racism affects health. Finally, sociologists have enhanced our understanding of the ways in which migration history and status can affect health. Sociological insights on racial disparities in health have important implications for the development of effective approaches to improve health and reduce health inequities.

While asthma has emerged as a major contributor to disease and disability in American children, the burden of this disease is unevenly distributed within the population. This paper provides a brief overview of social status variables that predict variation in asthma risks and social exposures such as stress and violence that are emerging as important risk factors. However, the central focus of the paper is on the distal social variables that have given rise to unhealthy residential environments in which the risk factors for asthma and other diseases are clustered. Effective initiatives for the prevention and treatment of childhood asthma need to address these non-medical determinants of the prevalence of asthma.

Despite the widespread assumption that racial differences in stress exist and that stress is a key mediator linking racial status to poor health, relatively few studies have explicitly examined this premise. We examine the distribution of stress across racial groups and the role of stress vulnerability and exposure in explaining racial differences in health in a community sample of Black, Hispanic, and White adults, employing a modeling strategy that accounts for the correlation between types of stressors and the accumulation of stressors in the prediction of health outcomes. We find significant racial differences in overall and cumulative exposure to eight stress domains. Blacks exhibit a higher prevalence and greater clustering of high stress scores than Whites. American-born Hispanics show prevalence rates and patterns of accumulation of stressors comparable to Blacks, while foreign-born Hispanics have stress profiles similar to Whites. Multiple stressors correlate with poor physical and mental health, with financial and relationship stressors exhibiting the largest and most consistent effects. Though we find no support for the stress-vulnerability hypothesis, the stress-exposure hypothesis does account for some racial health disparities. We discuss implications for future research and policy.

We examine several potential mechanisms linking religious involvement to depressive symptoms, major depression, and anxiety. Logistic and OLS regression estimations test five sets of potential psychosocial religion mediators: perceived attitudes toward and motivations for attendance; positive and negative religious coping; religious attitudes, beliefs, and spirituality; congregational support and criticism; and interpersonal and self-forgiveness. Compared to attending services less than once a month or never, attending services once a week but no more is associated with fewer depressive symptoms and anxiety symptoms. Hypothesized mediators, including meaning, interpersonal and self-forgiveness, congregational criticism, social attendance beliefs, and negative coping are independently associated with one or more mental health outcomes.

We examined the association between community violence exposure and childhood asthma risk in a multilevel, multimethod, longitudinal study controlling for individual- and neighbourhood-level confounders and pathway variables. Analyses included 2,071 children aged 0–9 yrs at enrolment from the Project on Human Development in Chicago Neighborhoods. Multilevel logistic regression models estimated the likelihood of asthma, controlling for individual-level (child’s age, sex, race/ethnicity, maternal asthma, socioeconomic status and family violence in the home) and neighbourhood-level confounders (concentrated disadvantage, collective efficacy and social disorder), and pathway variables (maternal smoking, breastfeeding). In adjusted analyses, medium (OR 1.60, 95% CI 1.17–2.19) and high levels (OR 1.56, 95% CI 1.12–2.18) of community violence were associated with increased asthma risk, relative to low levels. The increased asthma risk remained for African Americans when models included community violence and all other individual-level covariates, but attenuated to borderline nonsignificance when further adjusting for collective efficacy. Community violence is associated with asthma risk when controlling for individual- and neighborhood-level confounders. Neither community violence, nor the other individual-level factors, fully accounted for the excess asthma burden among African Americans. These data suggest that public health interventions outside the biomedical model may be needed to reduce asthma in disadvantaged populations.