title: PM2.5-induced cardiovascular dysregulation in rats is associated with elemental carbon and temperature-resolved carbon subfractions.
abstract: BACKGROUND
  We tested the hypothesis that cardiovascular responses to PM2.5 exposure will be enhanced in hypertensive rats and linked to specific carbonaceous pollutants in an urban industrial setting.
  
  
  METHODS
  Spontaneously hypertensive rats were exposed by inhalation to concentrated PM2.5 in an industrial area of Dearborn, Michigan, for four consecutive summer days. Blood pressure (BP), heart rate (HR) and HR variability (HRV) metrics (SDNN, RMSSD) were assessed by radiotelemetry and compared to 1 h- and 8 h-averaged fluctuations in PM2.5 composition, with a focus on elemental and organic carbon (EC and OC, respectively), and temperature-resolved subfractions (EC1-EC5, PC (pyrolized carbon), and OC1-OC4), as well as other major and minor PM components.
  
  
  RESULTS
  Mean HR and BP were increased, while HRV was decreased over 4 days of exposure. Using 1 h averages, EC (1 μg/m3 increase) was associated with increased HR of 11-32 bpm (4-11% increase), 1.2-1.5 ms (22-27%) decreases in SDNN, 3-14 mmHg (1.5-8%) increases in systolic BP, and 5-12 mmHg (4-9%) increases in diastolic BP. By comparison, associations with OC were negligible. Using 8 h averages, EC subfractions were linked with increased heart rate (EC1: 13 bpm; EC2, EC3, PC: <5 bpm) and SDNN (EC1> > EC2 > EC3, EC4, PC), but with decreased RMSSD (EC2, EC5 > EC3, EC4). Minimal effects were associated with OC and OC1. Associations between carbon subfractions and BP were negligible. Associations with non-carbonaceous components and trace elements were generally non-significant or of negligible effect size.
  
  
  CONCLUSIONS
  These findings are the first to describe associations between acute cardiovascular responses and thermally resolved carbon subfractions. We report that cardiovascular responses to PM2.5 carbonaceous materials appear to be driven by EC and its EC1 fraction.
authors.affiliation: Department of Pathobiology and Diagnostic Investigation, Michigan State University, East Lansing, MI, USA. wagnerja@msu.edu.
authors.forename: James G
authors.initials: JG
authors.lastname: Wagner
authors.forename: Ali S
authors.initials: AS
authors.lastname: Kamal
authors.forename: Masako
authors.initials: M
authors.lastname: Morishita
authors.forename: J Timothy
authors.initials: JT
authors.lastname: Dvonch
authors.forename: Jack R
authors.initials: JR
authors.lastname: Harkema
authors.forename: Annette C
authors.initials: AC
authors.lastname: Rohr
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002244:Carbon / Q000633:toxicity*; D002318:Cardiovascular Diseases / Q000139:chemically induced* / Q000503:physiopathology*; D006973:Hypertension / Q000235:genetics / Q000503:physiopathology; D019570:Inhalation Exposure; D008297:Male; D010316:Particle Size; D052638:Particulate Matter / Q000633:toxicity*; D051381:Rats; D011918:Rats, Inbred SHR; D013686:Telemetry; D013696:Temperature; D014131:Trace Elements
chemical_list: D052638:Particulate Matter; D014131:Trace Elements; D002244:Carbon