Aim To investigate the relationship between indium exposure and lung effects markers among indium tin oxide (ITO) manufacturing workers without job change.

Methods We enrolled 179 male workers from ITO target manufacturing and recycling factories in Taiwan. Plasma indium (P-In), urine indium (U-In) and creatinine adjusted U-In (U-In/Creat.) were used as internal dose of indium exposure. Plasma Krebs von den Lungen-6 (KL-6) and surfactant protein D (SP-D) were used as markers of interstitial pneumonitis. Forced vital capacity (FVC), forced expiratory volume at 1 st second (FEV1), and FEV1/FVC were also evaluated by spirometry.

Results After adjusted for covariates by linear regression, plasma, urinary and creatinine adjusted indium were increased in high exposure group (P-In: β=1.13, p<0.001; U-In: β=0.54, p<0.05; U-In/Cre: β=0.63, p<0.01) and low exposure group (P-In: β=0.75, p<0.05; U-In/Cre: β=0.52, p<0.05) with comparison to reference group. Plasma KL-6 was higher in high exposure group (β=0.24, p<0.05) compared to reference group, but not for surfactant protein D (SP-D). Furthermore, FVC and FEV1 were reduced in both high exposure group (FVC: β=−0.08, p<0.01; FEV1: β=−0.05, p<0.05) and low exposure group (FVC: β=−0.06, p<0.05) compared to reference group.

Conclusion Our findings indicate indium exposure was related to restrictive lung dysfunction, decreased lung function for both FEV1 and FVC test but not for FEV1/FVC ratio. Meanwhile, increased plasma KL-6 in high exposure group also supports that indium exposure results in increased risk of interstitial pneumonitis among direct indium exposure workers. Our study provided an explanation to the consequence of indium exposure- interstitial pneumonitis-restrictive lung dysfunction.