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This review explores the role of environments in creating chronic and acute health disorders. A general framework for studying the nesting of social environments and the multiple pathways by which environmental factors may adversely affect health is offered. Treating socioeconomic status (SES) and race as contextual factors, we examine characteristics of the environments of community, work, family, and peer interaction for predictors of positive and adverse health outcomes across the lifespan. We consider chronic stress/allostatic load, mental distress, coping skills and resources, and health habits and behaviors as classes of mechanisms that address how unhealthy environments get "under the skin," to create health disorders. Across multiple environments, unhealthy environments are those that threaten safety, that undermine the creation of social ties, and that are conflictual, abusive, or violent. A healthy environment, in contrast, provides safety, opportunities for social integration, and the ability to predict and/or control aspects of that environment.
Much remains to be understood about how low socioeconomic status (SES) increases cardiovascular disease and mortality risk. Data from the Kuopio Ischemic Heart Disease Risk Factor Study (1984-1993) were used to estimate the associations between acute myocardial infarction and income, all-cause mortality, and cardiovascular mortality in a population-based sample of 2,272 Finnish men, with adjustment for 23 biologic, behavioral, psychologic, and social risk factors. Compared with the highest income quintile, those in the bottom quintile had age-adjusted relative hazards of 3.14 (95% confidence interval (CI) 1.77-5.56), 2.66 (95% CI 1.25-5.66), and 4.34 (95% CI 1.95-9.66) for all-cause mortality, cardiovascular mortality, and AMI, respectively. After adjustment for risk factors, the relative hazards for the same comparisons were 1.32 (95% CI 0.70-2.49), 0.70 (95% CI 0.29-1.69), and 2.83 (95% CI 1.14-7.00). In the lowest income quintile, adjustment for risk factors reduced the excess relative risk of all-cause mortality by 85%, that of cardiovascular mortality by 118%, and that of acute myocardial infarction by 45%. These data show how the association between SES and cardiovascular mortality and all-cause mortality is mediated by known risk factor pathways, but full "explanations" for these associations will need to encompass why these biologic, behavioral, psychologic, and social risk factors are differentially distributed by SES.
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