The mechanism by which air pollution causes cardiovascular events is not understood. We postulated that organic emission toxins are transported and stored in the cytosol of adipocytes and cause the release of a chemotaxic factor that signals macrophages to migrate into adipose tissue. This process is known to initiate the secretion of cytokines by both adipocytes and macrophages, which adversely affects vasoreactivity and insulin sensitivity and would account for vascular events and adipocyte hypertrophy, respectively. To test this theoretical concept, we correlated BRFSS data on obesity and social economic factors with air emission (AE) data determined by the Environmental Protection Agency and found in scorecard.com. Only the 38 states that included ozone-depleting chemicals in their data were studied. Obesity, expressed as the percentage of individuals with BMI > 30 kg/m2, is on the y-axes. Figure 1 demonstrates a marked association (p < .001) of air emission expressed as lb/person/mile2 with obesity. Emissions also correlated with multiple measures of low socioeconomic status (SES), which correlated inversely with obesity. To preclude this confounding effect of SES, the percent of BMI > 30 was categorized into tertiles. The states with the lowest and middle tertile of BMI > 30 did not correlate with any SES measures. The AE from these 22 states also correlated significantly with BMI > 30 (p < .001), as demonstrated in Figure 2.
These data, derived from states with low percent BMI > 30 and relatively high SES, support the hypothesis that air emissions, including those affecting ozone, may be associated with factors relating to obesity.
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