TY - JOUR
T1 - Acute pulmonary and inflammatory response in young adults following a scripted car commute
AU - Golan, Rachel
AU - Ladva, Chandresh
AU - Greenwald, Roby
AU - Krall, Jenna R.
AU - Raysoni, Amit U.
AU - Kewada, Priya
AU - Winquist, Andrea
AU - Flanders, W. Dana
AU - Liang, Donghai
AU - Sarnat, Jeremy A.
N1 - Publisher Copyright:
© 2017, Springer Science+Business Media B.V., part of Springer Nature.
PY - 2018/3/1
Y1 - 2018/3/1
N2 - In-vehicle pollution exposure has been linked to adverse health. We conducted a quasi-controlled panel study, the second Atlanta Commuters Exposures (ACE-2) study, to measure in-vehicle environmental exposures and corresponding changes in acute pulmonary and inflammatory response. ACE-2 was a randomized, crossover study of 60 adults (ages18–39 years) with or without asthma. Each participant conducted a scripted highway commute and either a surface street commute or a clinic exposure scenario, all followed by the same post-exposure health measurements. Exposures were conducted between 7 am–9 am. A range of mainly particulate matter measurements were sampled in-vehicle or indoors. Mixed effect models were used to examine time trends in health endpoints and associations between endpoints and pollutants. Participants were exposed to marginally higher pollutant concentrations during highway compared to surface street commutes. Cu was the only pollutant we measured that was significantly associated with increased eNO, lung function decrement, and increased levels of several cytokines. High-sensitivity C-reactive protein (hs-CRP) levels, soluble intracellular adhesive molecule-1 (sICAM-1) levels, and soluble vascular adhesion molecule-1 (sVCAM-1) levels immediately following exposure were positively associated with elemental carbon, organic carbon, and copper. Forced vital capacity (FVC) decreased relative to pre-commute levels at four repeated measurement time points following highway exposure scenarios (range,− 1.9 to − 2.2%, p < 0.05). Similarly, decrements in forced expiratory volume in 1 s (FEV1) were more pronounced following highway commutes than clinic sessions (− 2 vs. + 1.7%, p = 0.04). We observed transient increases in systemic inflammatory and acute respiratory response following on-road commutes, associated with several primary traffic pollutants, which we believe maybe indicative of exposures to a source or traffic pollutant mixture, namely road dust or brake wear.
AB - In-vehicle pollution exposure has been linked to adverse health. We conducted a quasi-controlled panel study, the second Atlanta Commuters Exposures (ACE-2) study, to measure in-vehicle environmental exposures and corresponding changes in acute pulmonary and inflammatory response. ACE-2 was a randomized, crossover study of 60 adults (ages18–39 years) with or without asthma. Each participant conducted a scripted highway commute and either a surface street commute or a clinic exposure scenario, all followed by the same post-exposure health measurements. Exposures were conducted between 7 am–9 am. A range of mainly particulate matter measurements were sampled in-vehicle or indoors. Mixed effect models were used to examine time trends in health endpoints and associations between endpoints and pollutants. Participants were exposed to marginally higher pollutant concentrations during highway compared to surface street commutes. Cu was the only pollutant we measured that was significantly associated with increased eNO, lung function decrement, and increased levels of several cytokines. High-sensitivity C-reactive protein (hs-CRP) levels, soluble intracellular adhesive molecule-1 (sICAM-1) levels, and soluble vascular adhesion molecule-1 (sVCAM-1) levels immediately following exposure were positively associated with elemental carbon, organic carbon, and copper. Forced vital capacity (FVC) decreased relative to pre-commute levels at four repeated measurement time points following highway exposure scenarios (range,− 1.9 to − 2.2%, p < 0.05). Similarly, decrements in forced expiratory volume in 1 s (FEV1) were more pronounced following highway commutes than clinic sessions (− 2 vs. + 1.7%, p = 0.04). We observed transient increases in systemic inflammatory and acute respiratory response following on-road commutes, associated with several primary traffic pollutants, which we believe maybe indicative of exposures to a source or traffic pollutant mixture, namely road dust or brake wear.
KW - Car commuters
KW - In-vehicle air pollution
KW - Inflammation
KW - Lung function
UR - http://www.scopus.com/inward/record.url?scp=85037172192&partnerID=8YFLogxK
U2 - 10.1007/s11869-017-0530-8
DO - 10.1007/s11869-017-0530-8
M3 - Article
AN - SCOPUS:85037172192
SN - 1873-9318
VL - 11
SP - 123
EP - 136
JO - Air Quality, Atmosphere and Health
JF - Air Quality, Atmosphere and Health
IS - 2
ER -
