Exposure to traffic pollution, acute inflammation and autonomic response in a panel of car commuters

Environ Res. 2014 Aug:133:66-76. doi: 10.1016/j.envres.2014.05.004. Epub 2014 Jun 4.

Abstract

Background: Exposure to traffic pollution has been linked to numerous adverse health endpoints. Despite this, limited data examining traffic exposures during realistic commutes and acute response exists.

Objectives: We conducted the Atlanta Commuters Exposures (ACE-1) Study, an extensive panel-based exposure and health study, to measure chemically-resolved in-vehicle exposures and corresponding changes in acute oxidative stress, lipid peroxidation, pulmonary and systemic inflammation and autonomic response.

Methods: We recruited 42 adults (21 with and 21 without asthma) to conduct two 2-h scripted highway commutes during morning rush hour in the metropolitan Atlanta area. A suite of in-vehicle particulate components were measured in the subjects' private vehicles. Biomarker measurements were conducted before, during, and immediately after the commutes and in 3 hourly intervals after commutes.

Results: At measurement time points within 3h after the commute, we observed mild to pronounced elevations relative to baseline in exhaled nitric oxide, C-reactive-protein, and exhaled malondialdehyde, indicative of pulmonary and systemic inflammation and oxidative stress initiation, as well as decreases relative to baseline levels in the time-domain heart-rate variability parameters, SDNN and rMSSD, indicative of autonomic dysfunction. We did not observe any detectable changes in lung function measurements (FEV1, FVC), the frequency-domain heart-rate variability parameter or other systemic biomarkers of vascular injury. Water soluble organic carbon was associated with changes in eNO at all post-commute time-points (p<0.0001).

Conclusions: Our results point to measureable changes in pulmonary and autonomic biomarkers following a scripted 2-h highway commute.

Keywords: Asthma; Car commute; Exhaled nitric oxide; Heart rate variability.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Acute Disease
  • Adult
  • Air Pollution / adverse effects*
  • Air Pollution / analysis
  • Asthma / chemically induced
  • Asthma / pathology
  • Automobiles
  • Autonomic Pathways / drug effects*
  • Autonomic Pathways / pathology
  • Biomarkers / analysis
  • Environmental Exposure / adverse effects*
  • Environmental Exposure / analysis
  • Female
  • Humans
  • Inflammation / chemically induced
  • Inflammation / pathology
  • Inflammation Mediators / poisoning*
  • Male
  • Middle Aged
  • Particulate Matter / poisoning
  • Vehicle Emissions / poisoning*
  • Young Adult

Substances

  • Biomarkers
  • Inflammation Mediators
  • Particulate Matter
  • Vehicle Emissions