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      Social and Physical Environments and Disparities in Risk for Cardiovascular Disease: The Healthy Environments Partnership Conceptual Model

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          Abstract

          The Healthy Environments Partnership (HEP) is a community-based participatory research effort investigating variations in cardiovascular disease risk, and the contributions of social and physical environments to those variations, among non-Hispanic black, non-Hispanic white, and Hispanic residents in three areas of Detroit, Michigan. Initiated in October 2000 as a part of the National Institute of Environmental Health Sciences’ Health Disparities Initiative, HEP is affiliated with the Detroit Community–Academic Urban Research Center. The study is guided by a conceptual model that considers race-based residential segregation and associated concentrations of poverty and wealth to be fundamental factors influencing multiple, more proximate predictors of cardiovascular risk. Within this model, physical and social environments are identified as intermediate factors that mediate relationships between fundamental factors and more proximate factors such as physical activity and dietary practices that ultimately influence anthropomorphic and physiologic indicators of cardiovascular risk. The study design and data collection methods were jointly developed and implemented by a research team based in community-based organizations, health service organizations, and academic institutions. These efforts include collecting and analyzing airborne particulate matter over a 3-year period; census and administrative data; neighborhood observation checklist data to assess aspects of the physical and social environment; household survey data including information on perceived stressors, access to social support, and health-related behaviors; and anthropometric, biomarker, and self-report data as indicators of cardiovascular health. Through these collaborative efforts, HEP seeks to contribute to an understanding of factors that contribute to racial and socioeconomic health inequities, and develop a foundation for efforts to eliminate these disparities in Detroit.

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          Most cited references77

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          Racial Differences in Physical and Mental Health: Socio-economic Status, Stress and Discrimination.

          This article examines the extent to which racial differences in socio-economic status (SES), social class and acute and chronic indicators of perceived discrimination, as well as general measures of stress can account for black-white differences in self-reported measures of physical and mental health. The observed racial differences in health were markedly reduced when adjusted for education and especially income. However, both perceived discrimination and more traditional measures of stress are related to health and play an incremental role in accounting for differences between the races in health status. These findings underscore the need for research efforts to identify the complex ways in which economic and non-economic forms of discrimination relate to each other and combine with socio-economic position and other risk factors and resources to affect health.
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            Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

            Epidemiologic studies have linked long-term exposure to fine particulate matter air pollution (PM) to broad cause-of-death mortality. Associations with specific cardiopulmonary diseases might be useful in exploring potential mechanistic pathways linking exposure and mortality. General pathophysiological pathways linking long-term PM exposure with mortality and expected patterns of PM mortality with specific causes of death were proposed a priori. Vital status, risk factor, and cause-of-death data, collected by the American Cancer Society as part of the Cancer Prevention II study, were linked with air pollution data from United States metropolitan areas. Cox Proportional Hazard regression models were used to estimate PM-mortality associations with specific causes of death. Long-term PM exposures were most strongly associated with mortality attributable to ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. For these cardiovascular causes of death, a 10-microg/m3 elevation in fine PM was associated with 8% to 18% increases in mortality risk, with comparable or larger risks being observed for smokers relative to nonsmokers. Mortality attributable to respiratory disease had relatively weak associations. Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function. Although smoking is a much larger risk factor for cardiovascular disease mortality, exposure to fine PM imposes additional effects that seem to be at least additive to if not synergistic with smoking.
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              Fine particulate air pollution and mortality in 20 U.S. cities, 1987-1994.

              Air pollution in cities has been linked to increased rates of mortality and morbidity in developed and developing countries. Although these findings have helped lead to a tightening of air-quality standards, their validity with respect to public health has been questioned. We assessed the effects of five major outdoor-air pollutants on daily mortality rates in 20 of the largest cities and metropolitan areas in the United States from 1987 to 1994. The pollutants were particulate matter that is less than 10 microm in aerodynamic diameter (PM10), ozone, carbon monoxide, sulfur dioxide, and nitrogen dioxide. We used a two-stage analytic approach that pooled data from multiple locations. After taking into account potential confounding by other pollutants, we found consistent evidence that the level of PM10 is associated with the rate of death from all causes and from cardiovascular and respiratory illnesses. The estimated increase in the relative rate of death from all causes was 0.51 percent (95 percent posterior interval, 0.07 to 0.93 percent) for each increase in the PM10 level of 10 microg per cubic meter. The estimated increase in the relative rate of death from cardiovascular and respiratory causes was 0.68 percent (95 percent posterior interval, 0.20 to 1.16 percent) for each increase in the PM10 level of 10 microg per cubic meter. There was weaker evidence that increases in ozone levels increased the relative rates of death during the summer, when ozone levels are highest, but not during the winter. Levels of the other pollutants were not significantly related to the mortality rate. There is consistent evidence that the levels of fine particulate matter in the air are associated with the risk of death from all causes and from cardiovascular and respiratory illnesses. These findings strengthen the rationale for controlling the levels of respirable particles in outdoor air.
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                Author and article information

                Journal
                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                December 2005
                18 July 2005
                : 113
                : 12
                : 1817-1825
                Affiliations
                [1 ]Health Behavior and Health Education, and
                [2 ]Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, Michigan, USA
                [3 ]ISLES, Inc., Trenton, New Jersey USA
                [4 ]Duke University, Durham, North Carolina, USA
                [5 ]Survey Research Center and Department of Sociology, and
                [6 ]Institute for Social Research and Department of Biostatistics, University of Michigan, Michigan, Ann Arbor, USA
                Author notes
                Address correspondence to A.J. Schulz, Health Behavior and Health Education, School of Public Health, University of Michigan, 5134 SPH II, 1420 Washington Heights, Ann Arbor, MI 48109 USA. Telephone: (734) 647-0221. Fax: (734) 763-7379. E-mail: ajschulz@umich.edu

                The authors declare they have no competing financial interests.

                Article
                ehp0113-001817
                10.1289/ehp.7913
                1314928
                16330371
                93e0d595-e9a5-4e62-bad1-abfe634f285c
                This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.
                History
                : 28 December 2004
                : 29 June 2005
                Categories
                Research
                Mini-Monograph

                Public health
                community-based participatory research partnerships,social and physical environments and cardiovascular disease,racial segregation and cardiovascular disease

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