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Title: Acute exposure to elevated PM2.5 generated by traffic and cardiopulmonary health effects in healthy older adults.

Authors: Fan, Zhihua Tina; Meng, Qingyu; Weisel, Clifford; Laumbach, Robert; Ohman-Strickland, Pamela; Shalat, Stuart; Hernandez, Marta Z; Black, Kathleen

Published In J Expo Sci Environ Epidemiol, (2009 Jul)

Abstract: There are evidences for exposure to vehicular emissions and adverse cardiopulmonary health effects. This study attempted to further explore these effects on elderly. This study monitored personal PM(2.5) concentrations and ambulatory electrocardiograms continuously for 24 h on 1 working day in 3 separate weeks for 11 school crossing guards. Spirometry was also performed before and after the morning shift. The traffic at each work location was video recorded during one of the three morning shifts. The increases in the average personal PM(2.5) concentrations (baseline PM(2.5) was subtracted) of 1.2-87 and 1.1-98 microg/m(3) were observed during the 1-h morning (DeltaPM(2.5-ave-m)) and afternoon shift (DeltaPM(2.5-ave-a)), respectively. Traffic count was not a significant predictor of the DeltaPM(2.5-ave-m) (P=0.78). Mean heart rate variability (HRV), measured as 5-min standard deviation of normal-to-normal (SDNN) beats during the 10-min rest periods, decreased 18-26% (P<0.02) 15 min, 2 and 4 h after the morning shift, but changes in SDNN (DeltaSDNN) were insignificant post-afternoon exposure (-0.3 to -7% with P>0.53). DeltaSDNN were negatively associated with DeltaPM(2.5-ave-m), with the strongest association at 2 h after the morning shift (P<0.01) but insignificant 4 h after the morning exposure. The peak PM(2.5) concentration (DeltaPM(2.5-peak), baseline PM(2.5) was subtracted) was not a significant predictor for DeltaSDNN, and no clear effect of PM(2.5) exposure on heart rate was observed. There was no effect of PM exposure on lung function (P>0.16), either. In conclusion, acute exposure to the PM(2.5) resulting from mobile sources can cause acute decline in HRV in healthy older adults, suggesting one of the biological mechanisms for the adverse cardiovascular health effects associated with traffic-related air pollution. Traffic count may not be an appropriate surrogate measure of acute personal exposure to vehicular emission in traffic congested areas.

PubMed ID: 18841167 Exiting the NIEHS site

MeSH Terms: Air Pollutants/toxicity*; Heart/drug effects*; Humans; Middle Aged; Particle Size; Respiratory System/drug effects*; Vehicle Emissions*

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