title: Markers of inflammation and coagulation after long-term exposure to coarse particulate matter: a cross-sectional analysis from the multi-ethnic study of atherosclerosis.
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.
authors.affiliation: Department of Epidemiology, University of Michigan, Ann Arbor, Michigan, USA.
authors.forename: Sara D
authors.initials: SD
authors.lastname: Adar
authors.forename: Jennifer
authors.initials: J
authors.lastname: D'Souza
authors.forename: Kari
authors.initials: K
authors.lastname: Mendelsohn-Victor
authors.forename: David R
authors.initials: DR
authors.lastname: Jacobs
authors.forename: Mary
authors.initials: M
authors.lastname: Cushman
authors.forename: Lianne
authors.initials: L
authors.lastname: Sheppard
authors.forename: Peter S
authors.initials: PS
authors.lastname: Thorne
authors.forename: Gregory L
authors.initials: GL
authors.lastname: Burke
authors.forename: Martha L
authors.initials: ML
authors.lastname: Daviglus
authors.forename: Adam A
authors.initials: AA
authors.lastname: Szpiro
authors.forename: Ana V
authors.initials: AV
authors.lastname: Diez Roux
authors.forename: Joel D
authors.initials: JD
authors.lastname: Kaufman
authors.forename: Timothy V
authors.initials: TV
authors.lastname: Larson
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000393:Air Pollutants / Q000633:toxicity*; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation / Q000187:drug effects*; D003430:Cross-Sectional Studies; D004781:Environmental Exposure; D005260:Female; D006801:Humans; D007249:Inflammation / Q000139:chemically induced / Q000453:epidemiology*; D008297:Male; D008875:Middle Aged; D010316:Particle Size; D052638:Particulate Matter / Q000633:toxicity*; D013997:Time Factors; D014481:United States / Q000453:epidemiology
chemical_list: D000393:Air Pollutants; D015415:Biomarkers; D052638:Particulate Matter