Assessment of Particulate Exposure and Cardiopulmonary Effects in Diesel Exhaust Exposed Workers

Introduction
The aim of this study was to investigate the potential cardiopulmonary effects of DE exposure using repeated measurements of oxidative stress, lung inflammation markers, and cardiovascular disease markers at a interval of one-month.

Methods
Airr concentrations of DE particulate matter, particulate and gaseous polycyclic aromatic hydrocarbons (PAHs) were measured. 2-naphthol and metals were measured as markers of exposure. Markers of effects measured repeatedly in an interval of one month included oxidative stress (8OHdG), lung inflammation (clara cell protein CC16), and CVD markers (high sensitive C-reactive protein (hs-CRP), homocystein (Hcy) and myoglobin (Myg)).

Results
The particle size in the garage was dominant in large particles. The maximum nanoparticle number measured by CPC was 260,093/cm3 in engine emission, around 73,000/cm3 in the garage workplace, and the minimum nanoparticle number was 10,976/cm3 in office area. Although the particle size in the garage was dominant in large particles, garage workers may be exposed to significant levels of fine and ultrafine particles. The levels of PAHs in vapor phase was much higher than those in particulate phase. The data indicated that PAHs and metals exposure among garage workers were minimal in this study. GEE model with repeated mesurements revealed garage workers had significantly higher slope of increment of 8OHdG during one-month period than drivers, but not for CC16 and hsCRP. GEE models also showed that there was a significant association between DE exposure and myoglobin (p=0.05) and D-dimer (p=0.083) after adjusting for confounding factors.

Discussion
This study found garage workers were mainly exposed to significant levels of fine and ultrafine particles, but the levels of PAHs and metals exposure were minimal in these new technology diesel buses. This study showed exposure to DE may lead to cardiovascular injuries or thrombosis, but not pulmonary damages. The mechanism of cardiovascular injuries may through the induction of oxidative stress.