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Research Article: Opposing effects of PM2.5 on TSH levels: effect modification by thyroid peroxidase antibody status in a preconception cohort

Date Published: 2026-06-02

Abstract:
Fine particulate matter (PM2.5) is a significant source of endocrine disrupting chemicals. However, epidemiological evidence linking PM2.5 exposure to thyroid function, particularly thyroid-stimulating hormone (TSH), remains inconsistent. We hypothesized that this inconsistency stems from unmeasured effect modification by thyroid autoimmunity status, specifically the presence of thyroid peroxidase antibodies (TPOAb). To examine whether TPOAb status modifies the association between PM2.5 exposure and thyroid function in women planning pregnancy. This cohort study was conducted in Liaoning, China as a part of the China Medical University Birth Cohort. Serum TSH, FT4, and FT3 were measured, along with TPOAb and TgAb status. PM2.5 exposure was estimated for 1 to 12 month periods prior to blood draw. Linear regression with interaction terms was used to assess effect modification by TPOAb status. A total of 1,357 women were included between January 2019 and December 2023. A significant interaction was observed between half-year average PM2.5 exposure and TPOAb status on TSH levels (P for interaction = 0.003). Critically, the direction of association was opposite: each 10 ?g/m³ increase in PM2.5 was associated with a decrease in TSH among TPOAb-negative women (? = -0.074, 95% CI: -0.122, -0.026), but with an increase in TSH among TPOAb-positive women (? = 0.156, 95% CI: 0.014, 0.299). This effect modification was specific to TSH (no associations with FT4 or FT3), most pronounced for the 6-month exposure window. TPOAb status critically modifies the direction of association between PM2.5 exposure and TSH levels in preconception women. TPOAb-positive women may represent an environmentally susceptible subgroup, highlighting the importance of considering individual autoimmune status in environmental endocrine disruption research.

Introduction:
Fine particulate matter (PM2.5) is a significant source of endocrine disrupting chemicals. However, epidemiological evidence linking PM2.5 exposure to thyroid function, particularly thyroid-stimulating hormone (TSH), remains inconsistent. We hypothesized that this inconsistency stems from unmeasured effect modification by thyroid autoimmunity status, specifically the presence of thyroid peroxidase antibodies (TPOAb).

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