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

Authors

Liliang Yu, Changlai Lyu, Meiqi Liu, Bin Wang, Daikun Zheng, Yunhao Liu

Published in

Frontiers in public health. Volume 14. Pages 1964801. Epub Sep 17, 2026.

Abstract

The associations between ambient benzene exposure and thyroid dysfunction (hypothyroidism and hyperthyroidism), as well as the role of biological aging, remain largely unknown.
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.
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%).
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.

PMID:
42823953
Bibliographic data and abstract were imported from PubMed on 02 Oct 2026.

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