Long-term associations of air pollution exposure with liver enzymes among adult employees of the Electricity Generating Authority of Thailand: A longitudinal cohort study

Exposure to particulate air pollution may induce hepatotoxic effects via low-grade inflammation. However, only a few longitudinal epidemiological studies have investigated the long-term effects of air pollution on liver enzyme levels. The present study examined associations between long-term air pollution exposure and serum liver enzymes [alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT)] in employees of the Electricity Generating Authority of Thailand (EGAT) in Thailand's Bangkok Metropolitan Region (BMR). We conducted secondary analyses using the data obtained from 2022 subjects (mean age, 41.2 years as of 2009) of the EGAT3 cohort study (2009–2019). The daily mean concentration of each air pollutant (PM₁₀, O₃, NO₂, SO₂, and CO) was estimated at the sub-district level in BMR from 2008 to 2019 using the Kriging approach. Long-term exposure for each subject was defined as the 1-year average concentrations before the date of the physical examination in 2009, 2014, and 2019. We used linear mixed effects models to assess associations between air pollution and serum liver enzymes. Interquartile range increases in PM₁₀ and O₃ were related to decreased ALP [-2.4% (95%CI: -3.0, −1.9) and −6.6% (−7.3, −5.9), respectively] after potential confounders were adjusted. Positive associations between NO₂, SO₂, and CO with ALP were found [5.7% (4.8, 6.5), 4.5% (4.0, 5.0), and 0.8 (0.3, 1.4), respectively]. Elevated AST was also associated with higher PM₁₀ [1.7% (0.8, 2.5)] and O₃ [5.7% (4.5, 6.9)]. However, AST was negatively associated with NO₂ [-2.9% (−4.0, −1.8)] and SO₂ [-1.7% (−2.3, −1.1)]. In contrast to other air pollutants, we only observed a positive association between O₃ and ALT [3.4% (1.5, 5.3)]. The alteration in liver enzyme levels was significantly associated with long-term exposure to air pollution, which may raise the possibility of hepatocellular damage.