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. 2008 May;116(5):612-7.
doi: 10.1289/ehp.10565.

Metabolic syndrome and inflammatory responses to long-term particulate air pollutants

Affiliations

Metabolic syndrome and inflammatory responses to long-term particulate air pollutants

Jiu-Chiuan Chen et al. Environ Health Perspect. 2008 May.

Abstract

Background: Human data linking inflammation with long-term particulate matter (PM) exposure are still lacking. Emerging evidence suggests that people with metabolic syndrome (MS) may be a more susceptible population.

Objectives: Our goal was to examine potential inflammatory responses associated with long-term PM exposure and MS-dependent susceptibility.

Methods: We conducted secondary analyses of white blood cell (WBC) count and MS data from The Third National Health and Nutrition Examination Survey and PM10 (PM with aerodynamic diameter < 10 microm) data from the U.S. Environmental Protection Agency Aerometric Information Retrieval System. Estimated 1-year PM10 exposures were aggregated at the centroid of each residential census-block group, using distance-weighted averages from all monitors in the residing and adjoining counties. We restricted our analyses to adults (20-89 years of age) with normal WBC (4,000-11,000 x 10(6)/L), no existing cardiovascular disease, complete PM10 and MS data, and living in current residences > 1 year (n = 2,978; age 48.5 +/- 17.8 years). Mixed-effects models were constructed to account for autocorrelation and potential confounders.

Results: After adjustment for demographics, socioeconomic factors, lifestyles, residential characteristics, and MS, we observed a statistically significant association between WBC count and estimated local PM10 levels (p = 0.035). Participants from the least polluted areas (1-year PM10 < 1st quartile cutoff: 27.8 mug/m3) had lower WBC counts than the others (difference = 145 x 10(6)/L; 95% confidence interval, 10-281). We also noted a graded association between PM10 and WBC across subpopulations with increasing MS components, with 91 x 10(6)/L difference in WBC for those with no MS versus 214, 338, and 461 x 10(6)/L for those with 3, 4, and 5 metabolic abnormalities (trend-test p = 0.15).

Conclusions: Our study revealed a positive association between long-term PM exposure and hematological markers of inflammation and supported the hypothesized MS-dependent susceptibility.

Keywords: air pollution; environmental health; metabolic syndrome; particles; risk factors; susceptibility; white blood cells.

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Figures

Figure 1
Figure 1
Differential inflammatory responses to long-term PM exposure according to the degree of MS. A graded increment of spatial difference in average WBC count compares participants residing in clean air communities (1st quartile of 1-year PM10) with those living in the other, more polluted areas associated with increasing number of MS component abnormalities (p = 0.15 for the trend-test; p = 0.044 after excluding subjects with established hypertension and/or diabetes mellitus).

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