Ambient air pollutants and risk of fatal coronary heart disease among kidney transplant recipients.

BACKGROUND

There is increasing evidence that specific ambient air pollutants are associated with coronary heart disease (CHD) morbidity and mortality. Because kidney transplant recipients have prevalent traditional and nontraditional risk factors, they may constitute a sensitive subgroup.

STUDY DESIGN

Retrospective cohort.

SETTING & PARTICIPANTS: This study includes 32,239 nonsmoking adult kidney transplant recipients who underwent transplant in 1997-2003, identified through the US Renal Data System and living in the United States within 50 km of an air pollution monitoring station.

PREDICTOR

Long-term ambient pollutant ozone and particulate matter ≤10 μm (PM(10)), assessed from monthly concentrations of ozone and PM(10) calculated from ambient monitoring data by the US Environmental Protection Agency Air Quality System and interpolated to zip code centroids according to patients' residence.

OUTCOMES

Outcomes of interest were death from CHD and natural-cause mortality.

RESULTS

For the entire transplant cohort, average pollutant levels for ozone and PM(10) were 25.5 ± 4.4 parts per billion (ppb) and 25.3 ± 6.4 μg/m(3), respectively. Correlation between ozone and PM(10) values was low, but statistically significant (P < 0.001). There were deaths from CHD (n = 267) and natural causes (n = 2,076) during the 7-year study period. For each 10-ppb increase in ozone, the risk of fatal CHD increased by 35% (RR, 1.35; 95% CI, 1.04-1.77) in the single-pollutant model and 34% (RR, 1.34; 95% CI, 1.03-1.76) in the 2-pollutant model. No independent association was found between CHD and PM(10). No significant association was identified for PM(10) or ozone level and natural-cause mortality (RR, 1.09; 95% CI, 0.99-1.21).

LIMITATIONS

Exposure assignment based on only residential location.

CONCLUSIONS

For kidney transplant recipients, ambient ozone levels potentially are associated with higher risk of fatal CHD. These findings may have implications for regulations governing air pollution and the development of individual CHD risk-reduction strategies.