Cardiopulmonary health effects of traffic-related air pollutants.

摘要

There is emerging evidence that inhaling certain components of ambient particulate matter, specifically traffic pollutants, is associated with adverse health effects. We hypothesized that exposure to air pollution components of diesel exhaust-rich traffic, compared to cars-only traffic, produces greater adverse cardiopulmonary effects. In this case-crossover study, 23 participants were recruited to measure pulmonary function, exhaled NO, blood cytokines, heart rate variability, and blood pressure prior to, immediately after, and 24 hours after intermittent walking along 3 diverse roadways. Exposures lasted for 2 hours between June and September in 2011 and 2012, and personal exposures to pollutants were monitored. The 3 locations differed by traffic type: the George Washington Bridge (GWB) carries truck and car traffic, the Garden State Parkway (GSP) carries only car traffic, and Sterling Forest, NY (SF) acted as a control location. Levels of PM2.5, PM10, black carbon, elemental carbon, organic carbon, and trace elements were found to be highest at GWB and lowest at SF for all pollutants measured. The traffic count was similar between GSP and GWB, and the traffic count of diesel vehicles at GWB was correlated with BC and EC concentrations. Changes in health effects data were calculated using net changes (i.e., post – pre or 24 hr – pre), ratios (i.e., post/pre or 24/pre) or fold changes (i.e., post/pre or 24/pre). Using a repeated measures 1-way ANOVA, p-values were generated based on time point across all 3 locations. Statistically significant changes in biological endpoints were found for blood pressure metrics (SBP, DBP, PP), heart rate variability metrics (SDNN, r-MSSD, HF, LF:HF), and in soluble adhesion cell molecule (s-ICAM) across the exposure locations; suggested associations were found for eNO and IL-1β; no changes were observed for FEV1 , FVC, MAP, LF, CRP, SAA, IL-8, HR, and cortisol. Changes in eNO were observed across location (p = 0.06), and this was significant with the removal of subjects having a BMI > 30 (p = 0.05) and females (p = 0.02). Effect estimates for eNO showed increases in this measurement of 3.4 ppb for every 10 μg/m 3 increase with PM2.5mass concentration. Decreases in SBP, DBP, and PP were observed following exposures at a majority of the locations and time points. This was significant for SBP and PP 24 hrs following exposures (p = 0.02 and 0.01, respectively). The removal of potentially susceptible participants (those with hypertension, BMI > 30, representing minorities, and of female gender) impacted these analyses. Associations between SBP and DBP were significantly observed with EC exposure, as well as with trace element concentrations from non-combustion sources from the PM10 size fraction in the first summer of sampling. Effect estimates for SBP demonstrated decreases of -0.9 mmHg with 10 μg/m3 increases in both PM2.5 mass concentration and PM2.5 EC concentrations. Decreases in SDNN with the removal of males (p = 0.04) and r-MSSD with the removal of minorities (p = 0.05) were also observed, directly following exposures. Decreases in SDNN were not associated with exposures to the pollutants across the locations, but decreases in r-MSSD were observed with increasing levels of EC, BC, crustal components, and markers of tire and brake wear. Other measurements in HRV, including HF, were decreased (p = 0.02) while increases in LF:HF (p = 0.02), were observed directly following exposures; these were associated with inhalation of EC. Although increases in IL-1β were observed 24 hrs following exposure, this was not statistically significant across locations (p = 0.16). Increases in IL-1β were observed with increases in PM10 mass concentration, BC, PM2.5 and PM10 EC, and the PM10 contribution to tire wear, brake wear, and crustal components in the first summer of sampling. Lastly, decreases in s-ICAM were seen 24 hrs following exposures, associated with particle mass obtained using a DataRAM (p = 0.02). In summary, exposures to EC and BC were associated with changes in respiratory and cardiovascular biological endpoints, including eNO, SBP, DBP, PP, SDNN, r-MSSD, HF, and LF:HF. The removal of subjects with a BMI > 30 and hypertension, as well as those representing minorities, significantly affected the results of cardiopulmonary endpoints. Overall, despite the limited number of subjects in this study, significant changes in acute cardiac, respiratory, and immune health effects were observed in a healthy population.