Effects of occupational exposure to metal fume PM2.5 on lung function and biomarkers among shipyard workers: a 3-year prospective cohort study.

OBJECTIVE: This study investigates the associations of α1-antitrypsin, inter-α-trypsin inhibitor heavy chain (ITIH4), and 8-isoprostane with lung function in shipyard workers exposed to occupational metal fume fine particulate matter (PM2.5), which is known to be associated with adverse respiratory outcomes. METHODS: A 3-year follow-up study was conducted on 180 shipyard workers with 262 measurements. Personal exposure to welding fume PM2.5 was collected for an 8-h working day. Pre-exposure, post-exposure, and delta (∆) levels of α1-antitrypsin, ITIH4, and 8-isoprostane were determined in urine using enzyme-linked immunosorbent assays. Post-exposure urinary metals were sampled at the beginning of the next working day and analyzed by inductively coupled plasma-mass spectrometry. Lung function measurements were also conducted the next working day for post-exposure. RESULTS: An IQR increase in PM2.5 was associated with decreases of 2.157% in FEV1, 2.806% in PEF, 4.328% in FEF25%, 5.047% in FEF50%, and 7.205% in FEF75%. An IQR increase in PM2.5 led to increases of 42.155 µg/g in ∆α1-antitrypsin and 16.273 µg/g in ∆ITIH4. Notably, IQR increases in various urinary metals were associated with increases in specific biomarkers, such as post-urinary α1-antitrypsin and ITIH4. Moreover, increases in ∆ α1-antitrypsin and ∆ITIH4 were associated with decreases in FEV1/FVC by 0.008% and 0.020%, respectively, and an increase in ∆8-isoprostane resulted in a 1.538% decline in FVC. CONCLUSION: Our study suggests that urinary α1-antitrypsin and ITIH4 could indicate early lung function decline in shipyard workers exposed to metal fume PM2.5, underscoring the need for better safety and health monitoring to reduce respiratory risks.

Chronic exposure to metal fume PM2.5 on inflammation and stress hormone cortisol in shipyard workers: A repeat measurement study.

Particulate matter with an aerodynamic diameter of ≤ 2.5 µm (PM2.5) has been linked to adverse health outcomes in welding workers. The objective of this study was to investigate associations of chronic exposure to metal fume PM2.5 in shipyard workers with health outcomes. A longitudinal study was conducted to determine the effects of metal fume PM2.5 on FeNO, urinary metals, urinary oxidative stress, inflammation, and stress hormones in workers. There were 20 office workers and 49 welding workers enrolled in this study who were followed-up for a second year. We observed that Fe, Zn, and Mn were abundant in PM2.5 to which welding workers were personally exposed, whereas PM2.5 to which office workers were personally exposed was dominated by Pb, Cu, and Zn. We observed in the first and/or second visits that urinary 8-iso-prostaglandin F2-α (PGF2α) and 8-hydroxy-2'-deoxy guanosine (8-OHdG) were significantly increased by exposure. An increase in urinary interleukin (IL)-6 and decreases in urinary serotonin and cortisol were observed in the first and/or second visits after exposure. PM2.5 was associated with decreases in urinary 8-OHdG and cortisol among workers. Next, we observed that urinary Ni, Co, and Fe had significantly increased among workers after a year of exposure. Urinary metals were associated with decreases in urinary 8-iso-PGF2α and cortisol among workers. Urinary Ni, Cu, and Fe levels were associated with an increase in urinary IL-6 and a decrease in urinary cortisol among workers. In conclusion, chronic exposure to metal fume PM2.5 was associated with inflammation and a cortisol deficiency in shipyard workers, which could associate with adrenal glands dysfunction.