Cardiovascular effects in patrol officers are associated with fine particulate matter from brake wear and engine emissions Public Deposited

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Creator
  • Williams, Ronald W
    • Other Affiliation: U.S. EPA, ORD, National Exposure Research Laboratories, Research Triangle Park, NC, USA
  • Riediker, Michael
    • Other Affiliation: Institute of Occupational Health Sciences, Rue du Bugnon 19, 1005 Lausanne, Switzerland
  • Cascio, Wayne E
    • Affiliation: School of Medicine, Center for Environmental Medicine, Asthma and Lung Biology
    • Other Affiliation: Brody School of Medicine, East Carolina University, Greenville, NC, USA
  • Herbst, Margaret C
    • Affiliation: School of Medicine, Center for Environmental Medicine, Asthma and Lung Biology, Division of Cardiology, Department of Medicine
  • Devlin, Robert B
    • Other Affiliation: U.S. EPA, ORD, National Health and Environmental Effects Research Laboratories, Research Triangle Park, NC, USA
  • Bromberg, Philip A
    • Affiliation: School of Medicine, Center for Environmental Medicine, Asthma and Lung Biology
  • Griggs, Thomas R.
    • Affiliation: School of Medicine, Division of Cardiology, Department of Medicine
    • Other Affiliation: North Carolina State Highway Patrol, Raleigh, NC, USA
Abstract
  • Abstract Background Exposure to fine particulate matter air pollutants (PM2.5) affects heart rate variability parameters, and levels of serum proteins associated with inflammation, hemostasis and thrombosis. This study investigated sources potentially responsible for cardiovascular and hematological effects in highway patrol troopers. Results Nine healthy young non-smoking male troopers working from 3 PM to midnight were studied on four consecutive days during their shift and the following night. Sources of in-vehicle PM2.5 were identified with variance-maximizing rotational principal factor analysis of PM2.5-components and associated pollutants. Two source models were calculated. Sources of in-vehicle PM2.5 identified were 1) crustal material, 2) wear of steel automotive components, 3) gasoline combustion, 4) speed-changing traffic with engine emissions and brake wear. In one model, sources 1 and 2 collapsed to a single source. Source factors scores were compared to cardiac and blood parameters measured ten and fifteen hours, respectively, after each shift. The "speed-change" factor was significantly associated with mean heart cycle length (MCL, +7% per standard deviation increase in the factor score), heart rate variability (+16%), supraventricular ectopic beats (+39%), % neutrophils (+7%), % lymphocytes (-10%), red blood cell volume MCV (+1%), von Willebrand Factor (+9%), blood urea nitrogen (+7%), and protein C (-11%). The "crustal" factor (but not the "collapsed" source) was associated with MCL (+3%) and serum uric acid concentrations (+5%). Controlling for potential confounders had little influence on the effect estimates. Conclusion PM2.5 originating from speed-changing traffic modulates the autonomic control of the heart rhythm, increases the frequency of premature supraventricular beats and elicits pro-inflammatory and pro-thrombotic responses in healthy young men.
Date of publication
Identifier
  • 15813985
  • doi:10.1186/1743-8977-1-2
Resource type
  • Article
Rights statement
  • In Copyright
Rights holder
  • Michael Riediker et al.; licensee BioMed Central Ltd.
License
Journal title
  • Particle and Fibre Toxicology
Journal volume
  • 1
Journal issue
  • 1
Page start
  • 2
Language
  • English
Is the article or chapter peer-reviewed?
  • Yes
ISSN
  • 1743-8977
Bibliographic citation
  • Particle and Fibre Toxicology. 2004 Dec 09;1(1):2
Access
  • Open Access
Publisher
  • BioMed Central Ltd
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