A genome-wide study identifies genetic loci affecting thyroid hormone levels in Koreans exposed to particulate matter, suggesting new insights into thyroid function.
Although the associations between air pollution exposure and thyroid function have been reported, the interactive effects of the genes involved remain unknown. Therefore, we aimed to identify candidate genetic loci involved in thyroid function by interacting with annual average exposure to particulate matter with a diameter of 10 microns or smaller (PM10) in Korean adults. A total of 1,863 and 1,458 adults were included in the discovery and replication steps, respectively. The average annual concentration of PM10 exposure was considered, and the participants were classified into two groups (low-to-moderate exposure and high-exposure groups) for binary analyses. A genome-wide single-nucleotide polymorphism analysis using a PM10 exposure interaction study was performed to determine thyroid-stimulating hormone levels in Korean adults. Although no SNPs surpassed the stringent genome-wide significance threshold of Pint < 5E-08, one SNP (rs11781213) near MSRA reached a suggestive level of significance of Pint < 5E-07. Two genetic susceptibility loci (FAM84B/PCAT1 and STARD13) were replicated at a nominal significance level of Pint < 1E-05 for the discovery cohort, and Pint < 0.05 for the replication cohort. A genetic variant (rs7169081 G > A) between CGNL1 and GCOM1 was of functional interest. This is the first study reporting genome-wide-air pollution interaction results for thyroid function. The association between long-term PM10 exposure and thyroid hormone levels may be partly explained by identifying several suggestive loci, including MSRA, PCAT1, and GCOM1.
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Park et al. (2026) studied this question.
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