Metals cause nephrotoxicity with acute and/or chronic exposure; however, few epidemiological studies have examined impacts of exposure to metal fumes on renal injury in welding workers. In total, 66 welding workers and 12 office workers were recruited from a shipyard located in southern Taiwan. Urine samples from each subject were collected at the beginning (baseline) and end of the work week (1-week exposure). Personal exposure to PM2.5 was measured. The 8-h mean PM2.5 was50.3 μg/m3 for welding workers and 27.4 μ g/m3 for office workers. iTRAQs coupled with LC-MS/MS were used to discover the pathways in response to welding PM2.5 in the urine, suggesting that extracellular matrix (ECM)-receptor interactions are a critical mechanism. ECM-receptor interaction-related biomarkers for renal injury, kidney injury molecule (KIM)-1 and neutrophil gelatinase-associated lipocalin (NGAL), were significantly elevated in welding workers post-exposure, as well as were urinary Al, Cr, Mn, Fe, Co, and Ni levels. NGAL was more significantly associated with Al (r = 0.737, p <0.001), Cr (r = 0.705, p <0.001), Fe (r = 0.709, p <0.001), and Ni (r = 0.657, p <0.001) than was KIM-1, suggesting that NGAL may be a urinary biomarker for welding PM 2.5 exposure. Nephrotoxicity (e.g., renal tubular injury) may be an emerging concern in occupational health.
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