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      Income inequality and mortality in metropolitan areas of the United States.

      , , , , , ,
      American Journal of Public Health
      American Public Health Association

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          Abstract

          OBJECTIVES: This study examined associations between income inequality and mortality in 282 US metropolitan areas. METHODS: Income inequality measures were calculated from the 1990 US Census. Mortality was calculated from National Center for Health Statistics data and modeled with weighted linear regressions of the log age-adjusted rate. RESULTS: Excess mortality between metropolitan areas with high and low income inequality ranged from 64.7 to 95.8 deaths per 100,000 depending on the inequality measure. In age-specific analyses, income inequality was most evident for infant mortality and for mortality between ages 15 and 64. CONCLUSIONS: Higher income inequality is associated with increased mortality at all per capita income levels. Areas with high income inequality and low average income had excess mortality of 139.8 deaths per 100,000 compared with areas with low inequality and high income. The magnitude of this mortality difference is comparable to the combined loss of life from lung cancer, diabetes, motor vehicle crashes, human immunodeficiency virus (HIV) infection, suicide, and homicide in 1995. Given the mortality burden associated with income inequality, public and private sector initiatives to reduce economic inequalities should be a high priority.

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          On the measurement of inequality

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            Cumulative impact of sustained economic hardship on physical, cognitive, psychological, and social functioning.

            Although the relation between low income and poor health is well established, most previous research has measured income at only one time. We used income information collected in 1965, 1974, and 1983 from a representative sample of adults in Alameda County, California, to examine the cumulative effect of economic hardship (defined as a total household income of less than 200 percent of the federal poverty level) on participants who were alive in 1994. Because of missing information, analyses were based on between 1081 and 1124 participants (median age, 65 years in 1994). After adjustment for age and sex, there were significant graded associations between the number of times income was less than 200 percent of the poverty level (range, 0 to 3) and all measures of functioning examined except social isolation. As compared with subjects without economic hardship, those with economic hardship in 1965, 1974, and 1983 were much more likely to have difficulties with independent activities of daily living (such as cooking, shopping, and managing money) (odds ratio, 3.38; 95 percent confidence interval, 1.49 to 7.64), activities of daily living (such as walking, eating, dressing, and using the toilet) (odds ratio, 3.79; 95 percent confidence interval, 1.32 to 9.81), and clinical depression (odds ratio, 3.24; 95 percent confidence interval, 1.32 to 7.89) in 1994. We found little evidence of reverse causation -- that is, that episodes of illness might have caused subsequent economic hardship. Sustained economic hardship leads to poorer physical, psychological, and cognitive functioning.
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              Socioeconomic factors and cardiovascular disease: a review of the literature.

              Despite recent declines in mortality, cardiovascular diseases are the leading cause of death in the United States today. It appears that many of the major risk factors for coronary disease have been identified. Researchers are still learning about different modifiable factors that may influence cardiovascular diseases. Socioeconomic status may provide a new focus. The principal measures of SES have been education, occupation, and income or combinations of these. Education has been the most frequent measure because it does not usually change (as occupation or income might) after young adulthood, information about education can be obtained easily, and it is unlikely that poor health in adulthood influences level of education. However, other measures of SES have merit, and the most informative strategy would incorporate multiple indicators of SES. A variety of psychosocial measures--for example, certain aspects of occupational status--may be important mediators of SES and disease. The hypothesis that high job strain may adversely affect health status has a rational basis and is supported by evidence from a limited number of studies. There is a considerable body of evidence for a relation between socioeconomic factors and all-cause mortality. These findings have been replicated repeatedly for 80 years across measures of socioeconomic level and in geographically diverse populations. During 40 years of study there has been a consistent inverse relation between cardiovascular disease, primarily coronary heart disease, and many of the indicators of SES. Evidence for this relation has been derived from prevalence, prospective, and retrospective cohort studies. Of particular importance to the hypothesis that SES is a risk factor for cardiovascular disease was the finding by several investigators that the patterns of association of SES with coronary disease had changed in men during the past 30 to 40 years and that SES has been associated with the decline of coronary mortality since the mid-1960s. However, the declines in coronary mortality of the last few decades have not affected all segments of society equally. There is some evidence that areas with the poorest socioenvironmental conditions experience later onset in the decline in cardiovascular mortality. A number of studies suggest that poor living conditions in childhood and adolescence contribute to increased risk of arteriosclerosis. Some of these studies have been criticized because of their nature, and others for inadequate control of confounding factors.(ABSTRACT TRUNCATED AT 400 WORDS)
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                Author and article information

                Journal
                American Journal of Public Health
                Am J Public Health
                American Public Health Association
                0090-0036
                1541-0048
                July 1998
                July 1998
                : 88
                : 7
                : 1074-1080
                Article
                10.2105/AJPH.88.7.1074
                1508263
                9663157
                76864985-2434-4b39-97d3-b1307f68c50b
                © 1998
                History

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