Physicochemistry and cardiovascular toxicity of metal fume PM 2.5

Occupational exposure to welding fumes causes a higher incidence of cardiovascular disease; however, the association remains unclear. To clarify the possible association, exposure assessment of metal fumes with an aerodynamic diameter of <2.5 μm (PM 2.5) in welding and office areas was characterized in a shipyard in Taiwan. Cardiovascular toxicity caused by PM 2.5 was determined in workers (in both the welding and office areas). Significant amounts of bimodal metal fume particles with count median diameters (CMDs) of 14.1∼15.1 and 126.3∼135.8 nm were produced in the shipyard. Metal fume PM 2.5 resulted in decreased cell viability and increased levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), interleukin (IL)-6, and nitric oxide (NO) in human coronary artery epithelial cells (HCAECs). We recruited 118 welding workers and 45 office workers for a personal PM 2.5 exposure assessment and determination of urinary levels of 8-OHdG, 8-iso-prostaglandin F2α (8-iso-PGF2α), and various metals. We observed that a 10-μg/m 3 increase in the mean PM 2.5 concentration was associated with a 2.15% increase in 8-OHdG and an 8.43% increase in 8-iso-PGF2α in welding workers. Both 8-OHdG and 8-iso-PGF2α were associated with Fe and Zn in the urine. In conclusion, metal fume PM 2.5 could increase the risk of cardiovascular toxicity after inhalation.