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 3 h 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.

The Atlanta Commuters Exposure (ACE) Study was designed to measure in-cabin exposure to roadway particulate pollution and acute health response in a panel of adults with and without asthma following a 2-h scripted route along major highways in Atlanta. This article focuses on methods and results of both continuous and integrated approaches used to measure the concentration of PM 2.5 mass, particle number concentration (PNC), black carbon (BC) mass, and particle-bound PAHs, in-cabin noise, PM elemental composition, elemental carbon, organic carbon, water-soluble organic carbon (WSOC) content, and speciation of a broad range of organic compounds including alkanes, hopanes, and PAHs. Speciated PM data indicates that in-cabin particles derive from three non-co-varying processes: the resuspension of road dust containing crustal elements and previously-deposited brake pad residue with a contribution of normal fuel combustion, incomplete combustion processes producing PAHs and carbon particles, and particles ablated from brake pads that have not previously deposited to the roadside environment. Most in-cabin pollutants were elevated during the warm season with the notable exception of PNC. PNC was not found to be correlated with most other pollutants. In-cabin concentrations were marginally higher when windows were open.

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Background Effects of traffic-related exposures on respiratory health are well documented, but little information is available about whether asthma control influences individual susceptibility. We analyzed data from the Atlanta Commuter Exposure study to evaluate modification of associations between rush-hour commuting, in-vehicle air pollution, and selected respiratory health outcomes by asthma control status. Methods Between 2009 and 2011, 39 adults participated in Atlanta Commuter Exposure, and each conducted two scripted rush-hour highway commutes. In-vehicle particulate components were measured during all commutes. Among adults with asthma, we evaluated asthma control by questionnaire and spirometry. Exhaled nitric oxide, forced expiratory volume in 1 second (FEV1), and other metrics of respiratory health were measured precommute and 0, 1, 2, and 3 hours postcommute. We used mixed effects linear regression to evaluate associations between commute-related exposures and postcommute changes in metrics of respiratory health by level of asthma control. Results We observed increased exhaled nitric oxide across all levels of asthma control compared with precommute measurements, with largest postcommute increases observed among participants with below-median asthma control (2 hours postcommute: 14.6% [95% confidence interval {CI} = 5.7, 24.2]; 3 hours postcommute: 19.5% [95% CI = 7.8, 32.5]). No associations between in-vehicle pollutants and percent of predicted FEV1 were observed, although higher PM2.5 was associated with lower FEV1 % predicted among participants with below-median asthma control (3 hours postcommute: −7.2 [95% CI = −11.8, −2.7]). Conclusions Level of asthma control may influence respiratory response to in-vehicle exposures experienced during rush-hour commuting.