Occupational vehicle-related particulate exposure and inflammatory markers in trucking industry workers

- Associations between vehicular air pollutants and inflammatory markers were examined.
- We focused on non-drivers of truck terminal workers as literature is mainly in drivers.
- Short-term exposure to OC and EC may be associated with increased sICAM-1.

BackgroundPrevious studies have suggested an association between particulate air pollution and cardiovascular disease, but the mechanism is still unclear.ObjectiveWe examined the association between workplace exposure to vehicle-related particles and cardiovascular disease related systemic inflammatory markers, C-reactive protein (hs-CRP), soluble intercellular adhesion molecule-1 (sICAM-1), and interleukin-6 (IL-6) in 137 trucking terminal workers (non-drivers) in the U.S. trucking industry.MethodsWe visited two large trucking terminals in 2009 and measured vehicle-related elemental carbon (EC), organic carbon (OC), and particulate matter with aerodynamic diameter ≤2.5 µm (PM2.5), for 5 days consecutively at the main work areas. Each participant provided a blood sample and completed a health questionnaire during the sampling period. Individual workplace exposure level was calculated by 12-h time weighted moving averages based on work shift. The association between each blood marker and exposure to each pollutant during 0-12, 12-24, 24-36, and 36-48 h before the blood draw was examined by multivariable regression analyses.ResultsIn general, OC and EC had a positive association with sICAM-1, especially for exposure periods 12-24 (lag12-24) and 24-36 (lag24-36) h prior to blood draw [β=54.9 (95%CI: 12.3-97.5) for lag12-24 and β=46.5 (95%CI: 21.2-71.8) for lag12-24; change in sICAM-1 (in ng/mL) corresponding to an IQR increase in OC]. A similar pattern was found for EC and PM2.5. We did not find an association between measured pollutants up to 48 h before blood draw and hs-CRP or IL-6.ConclusionIn this group of healthy workers, short-term exposure to vehicle-related air pollutants may be associated with sICAM-1. Our findings may be dependent on the exposure period studied.