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美国成年人尿液有机磷酯代谢物暴露与甲状腺疾病风险之间的关联:2011-2014 年全国健康和营养调查。

Association between urinary organophosphate ester metabolite exposure and thyroid disease risk among US adults: National Health and Nutrition Examination Survey 2011-2014.

机构信息

Department of Epidemiology and Health Statistics, School of Public Health, Fujian Medical University, Fuzhou, Fujian, China.

Laboratory Center, The Major Subject of Environment and Health of Fujian Key Universities, School of Public Health, Fujian Medical University, Fuzhou, China.

出版信息

Front Endocrinol (Lausanne). 2024 Feb 9;15:1329247. doi: 10.3389/fendo.2024.1329247. eCollection 2024.

DOI:10.3389/fendo.2024.1329247
PMID:38405137
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10884265/
Abstract

BACKGROUND

Organophosphate esters (OPEs) may interfere with thyroid function, but the relationship between OPEs and thyroid disease remains unclear. This study aims to elucidate the relationship between OPEs exposure and thyroid disease risk in the general population in the United States.

METHOD

Data were obtained from the 2011-2014 National Health and Nutrition Examination Survey cycle. All participants were tested for seven OPE metabolites in their urine and answered questions about whether they had thyroid disease through questionnaires. Logistic regression was employed to analyze the association between exposure to individual OPE metabolites and thyroid disease. Weighted Quantile Sum (WQS) regression modeling was utilized to assess exposure to mixed OPE metabolites and risk of thyroid disease. Bayesian kernel machine regression(BKMR) models to analyze the overall mixed effect of OPE metabolites.

RESULT

A total of 2,449 participants were included in the study, 228 of whom had a history of thyroid disease. Bis(1,3-dichloro-2-propyl) phos (BDCPP), Diphenyl phosphate (DPHP) and Bis(2-chloroethyl) phosphate (BCEP) were the top three metabolites with the highest detection rates of 91.75%, 90.77% and 86.57%, respectively. In multivariate logistic regression models, after adjustment for confounding variables, individuals with the highest tertile level of BCEP were significantly and positively associated with increased risk of thyroid disease (OR=1.57, 95% CI=1.04-2.36), using the lowest tertile level as reference. In the positive WQS regression model, after correcting for confounding variables, mixed exposure to OPE metabolites was significantly positively associated with increased risk of thyroid disease (OR=1.03, 95% CI=1.01-1.06), with BCEP and DPHP having high weights. In the BKMR model, the overall effect of mixed exposure to OPE metabolites was not statistically significant, but univariate exposure response trends showed that the risk of thyroid disease decreased and then increased as BCEP exposure levels increased.

CONCLUSION

The study revealed a significant association between exposure to OPE metabolites and an increased risk of thyroid disease, with BCEP emerging as the primary contributor. The risk of thyroid disease exhibits a J-shaped pattern, whereby the risk initially decreases and subsequently increases with rising levels of BCEP exposure. Additional studies are required to validate the association between OPEs and thyroid diseases.

摘要

背景

有机磷酸酯(OPEs)可能会干扰甲状腺功能,但 OPEs 与甲状腺疾病之间的关系仍不清楚。本研究旨在阐明美国普通人群中 OPEs 暴露与甲状腺疾病风险之间的关系。

方法

数据来自 2011-2014 年全国健康和营养调查周期。所有参与者的尿液中都检测到了七种 OPE 代谢物,并通过问卷调查回答了他们是否患有甲状腺疾病。采用 logistic 回归分析个体 OPE 代谢物暴露与甲状腺疾病之间的关系。采用加权分位数总和(WQS)回归模型评估混合 OPE 代谢物暴露与甲状腺疾病风险。采用贝叶斯核机器回归(BKMR)模型分析 OPE 代谢物的总体混合效应。

结果

共纳入 2449 名参与者,其中 228 名患有甲状腺疾病。双(1,3-二氯-2-丙基)膦酸酯(BDCPP)、磷酸二苯酯(DPHP)和双(2-氯乙基)磷酸酯(BCEP)是检测率最高的前三种代谢物,分别为 91.75%、90.77%和 86.57%。在多变量 logistic 回归模型中,调整混杂因素后,最高 tertile 水平的 BCEP 与甲状腺疾病风险增加显著相关(OR=1.57,95%CI=1.04-2.36),以最低 tertile 水平为参照。在阳性 WQS 回归模型中,调整混杂因素后,混合 OPE 代谢物暴露与甲状腺疾病风险增加显著相关(OR=1.03,95%CI=1.01-1.06),其中 BCEP 和 DPHP 的权重较高。在 BKMR 模型中,混合 OPE 代谢物暴露的总体效应无统计学意义,但单变量暴露反应趋势表明,随着 BCEP 暴露水平的增加,甲状腺疾病的风险先降低后增加。需要进一步的研究来验证 OPEs 与甲状腺疾病之间的关联。

结论

本研究表明,OPE 代谢物暴露与甲状腺疾病风险增加之间存在显著关联,其中 BCEP 是主要贡献者。甲状腺疾病的风险呈“J”型模式,随着 BCEP 暴露水平的升高,风险先降低后升高。需要进一步的研究来验证 OPEs 与甲状腺疾病之间的关联。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1e3/10884265/090b57cc14a1/fendo-15-1329247-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1e3/10884265/62b678a2fbc6/fendo-15-1329247-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1e3/10884265/d220b679d8a4/fendo-15-1329247-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1e3/10884265/d8fc4cfc4878/fendo-15-1329247-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1e3/10884265/090b57cc14a1/fendo-15-1329247-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1e3/10884265/62b678a2fbc6/fendo-15-1329247-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1e3/10884265/d220b679d8a4/fendo-15-1329247-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1e3/10884265/d8fc4cfc4878/fendo-15-1329247-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1e3/10884265/090b57cc14a1/fendo-15-1329247-g004.jpg

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