Long-term exposure to low concentrations of ambient benzene with incident thyroid dysfunction and the mediating role of accelerated biological aging.

Abstract

Background The associations between ambient benzene exposure and thyroid dysfunction (hypothyroidism and hyperthyroidism), as well as the role of biological aging, remain largely unknown. Methods We included a total of 385,130 participants from the UK Biobank, and Cox regressions were used to assess the association between benzene exposure and incident thyroid dysfunction. We employed restricted cubic splines to fit potential nonlinear exposure-response relationships. Furthermore, interactions and mediation analyses were conducted to examine the mediating role of biological aging. Results Benzene exposure was dose-responsively associated with an increased risk of thyroid dysfunction, each 1 μg/m3 increase in benzene concentration was linked to hazard ratios (HRs) of 1.19 (95% CI: 1.16, 1.21) for hypothyroidism and 1.21 (95% CI: 1.18, 1.25) for hyperthyroidism. Participants with higher benzene exposure and older biological age showed a greater risk for hypothyroidism compared to those with lower exposure and younger biological age, with a relative excess risk (RERI) of 0.40 (95% CI: 0.13, 0.66). Furthermore, accelerated biological aging significantly mediated the association between benzene exposure and hyperthyroidism. Comparing the highest to the lowest quartile of benzene exposure, the proportion mediated (PM) (95% CI) was 3.07% (2.05, 4.08%). Conclusion Long-term exposure to low concentrations benzene may increase the risk of incident thyroid dysfunction. Accelerated biological aging demonstrated a significant additive interaction with benzene exposure on the risk of hypothyroidism and partially mediated the positive association between benzene exposure and the risk of hyperthyroidism.