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

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.