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. 2015 Jun;123(6):541-8.
doi: 10.1289/ehp.1308069. Epub 2015 Jan 20.

Markers of Inflammation and Coagulation After Long-Term Exposure to Coarse Particulate Matter: A Cross-Sectional Analysis From the Multi-Ethnic Study of Atherosclerosis

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Markers of Inflammation and Coagulation After Long-Term Exposure to Coarse Particulate Matter: A Cross-Sectional Analysis From the Multi-Ethnic Study of Atherosclerosis

Sara D Adar et al. Environ Health Perspect. .
Free PMC article

Abstract

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.

Conflict of interest statement

The authors declare they have no actual or potential competing financial interests.

Figures

Figure 1
Figure 1
Associations between long-term exposures to PM10–2.5 mass and components with biomarkers of inflammation and coagulation before (A) and after (B) adjustment for study site. Abbreviations: Cu, copper; P, phosphorus; PMc, PM10–2.5 mass; Si, silicon; Zn, zinc. Associations with indicators of inflammation are in blue, whereas indicators of coagulation are in white. Inflammation and coagulation scores on the secondary axis, and all other biomarkers are reported as a percent change. All associations were adjusted for age, sex, race, city, marital status, education, employment, household size, home ownership, NSES, alcohol consumption, active and passive smoke, physical activity, family history of stroke or heart attack, BMI, blood pressure, cholesterol, creatinine, diabetes, and anti-inflammatory and blood pressure medications. Associations are scaled to IQRs of 2 and 0.1 μg/m3 for PM10–2.5 and silicon and 4, 11, and 6 ng/m3 for copper, zinc, and phosphorous, respectively. Endotoxin is scaled to 0.08 EU/m3.
Figure 2
Figure 2
Associations between long-term exposures to PM10–2.5 mass and components and an inflammation (A) and coagulation (B) score adjusted for co-pollutants. Abbreviations: Cu, copper; Endo, endotoxin; LAC, light-absorbing carbon; P, phosphorus; PMc, PM10–2.5 mass; Si, silicon; Zn, zinc. All associations were adjusted for age, sex, race, city, marital status, education, employment, household size, home ownership, NSES, alcohol consumption, active and passive smoke, physical activity, family history of stroke or heart attack, BMI, blood pressure, cholesterol, creatinine, diabetes, and anti-inflammatory and blood pressure medications. Associations are scaled to IQRs of 2 and 0.1 μg/m3 for PM10–2.5 and silicon and 4, 11, and 6 ng/m3 for copper, zinc, and phosphorous, respectively. Endotoxin is scaled to 0.08 EU/m3.
Figure 3
Figure 3
Associations between PM10–2.5 mass and components with inflammation score by sex, diabetes, obesity, metabolic syndrome, and race/ethnicity. Significant interactions are noted by asterisk (*). Abbreviations: Cu, copper; E, endotoxin; P, phosphorus; PMc, PM10–2.5 mass; Si, silicon; Zn, zinc. All associations were adjusted for age, sex, race, city, marital status, education, employment, household size, home ownership, NSES, alcohol consumption, active and passive smoke, physical activity, family history of stroke or heart attack, BMI, blood pressure, cholesterol, creatinine, diabetes, and anti-inflammatory and blood pressure medications. Associations are scaled to IQRs of 2 and 0.1 μg/m3 for PM10–2.5 and silicon and 4, 11, and 6 ng/m3 for copper, zinc, and phosphorous, respectively. Endotoxin is scaled to 0.08 EU/m3.

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