Background: Toxicological research suggests that coarse particles (PM10-2.5) are inflammatory, but responses are complex and may be best summarized by multiple inflammatory markers. Few human studies have investigated associations with PM10-2.5 and, of those, none have explored long-term exposures. Here we examine long-term associations with inflammation and coagulation in the Multi-Ethnic Study of Atherosclerosis.
Methods: Participants included 3,295 adults (45-84 years of age) from three metropolitan areas. Site-specific spatial models were used to estimate 5-year concentrations of PM10-2.5 mass and copper, zinc, phosphorus, silicon, and endotoxin found in PM10-2.5. Outcomes included interleukin-6, C-reactive protein, fibrinogen, total homocysteine, D-dimer, factor VIII, plasmin-antiplasmin complex, and inflammation and coagulation scores. We used multivariable regression with multiply imputed data to estimate associations while controlling for potential confounders, including co-pollutants such as fine particulate matter.
Results: Some limited evidence was found of relationships between inflammation and coagulation and PM10-2.5. Endotoxin was the PM10-2.5 component most strongly associated with inflammation, with an interquartile range (IQR) increase (0.08 EU/m3) associated with 0.15 (95% CI: 0.01, 0.28; p = 0.03) and 0.08 (95% CI: -0.07, 0.23; p = 0.28) higher inflammation scores before and after control for city, respectively. Copper was the component with the strongest association with coagulation, with a 4-ng/m3 increase associated with 0.19 (95% CI: 0.08, 0.30; p = 0.0008) and 0.12 (95% CI: -0.05, 0.30; p = 0.16) unit higher coagulation scores before and after city adjustment, respectively.
Conclusions: Our cross-sectional analysis provided some evidence that long-term PM10-2.5 exposure was associated with inflammation and coagulation, but associations were modest and depended on particle composition.