Ecotoxicology and environmental safety · 2026
Exposure to personal care products and thyroid function in adults: Unveiling the association and potential mechanism.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Zou Hui, Zhong Jinyan, Wei Xing, Wen Yuquan, Liu Jjayi, Hu Xueping, Yu Jiangnan, Yu Yang, Wan Yunbo, Xiao Lili
Аннотация
BACKGROUND: Personal care products (PCPs) are a ubiquitous source of endocrine-disrupting chemicals, yet their combined impact on thyroid function and the underlying mechanisms remain poorly understood.
METHODS: A total of 2714 adults from the NHANES 2007-2012 were included. Survey-weighted linear regression assessed individual associations and mixture effects were evaluated via quantile g-computation (QGC) and Bayesian kernel machine regression (BKMR). Causal mediation analysis was performed to examine the potential mediating role of systemic inflammation in the observed associations.
RESULTS: Most urinary PCPs metabolites were significantly correlated with reduced thyroid function in a dose-dependent manner, particularly for TT4. One-unit increase in concentrations of bisphenol A, benzophenone-3, butyl paraben, ethyl paraben, methyl paraben, and propyl paraben were associated with percent changes in TT4 of -3.11, -1.28, -1.41, -2.44, -1.46, and -1.55, respectively. QGC and BKMR models consistently identified the PCPs mixture was significantly associated with decreased FT4 and TT4. Bisphenol A, triclosan, and ethyl- and propyl-parabens were the dominant contributors, with a joint effect of -0.014 in FT4 and -0.027 in TT4 per quartile increase in the mixture. Mediation analysis showed that associations of urinary PCPs metabolites, especially triclosan, butyl paraben, ethyl paraben, and methyl paraben, with thyroid function were significantly mediated by neutrophil to platelet ratio (NPR), with mediation proportions ranging from 4.91 % to 25.3 %.
CONCLUSION: Both individual and mixed exposure to PCPs were associated with reduced thyroid function, with effects partially mediated by systemic inflammation. These findings highlight the importance of regulating priority chemicals and assessing combined exposure risks.
METHODS: A total of 2714 adults from the NHANES 2007-2012 were included. Survey-weighted linear regression assessed individual associations and mixture effects were evaluated via quantile g-computation (QGC) and Bayesian kernel machine regression (BKMR). Causal mediation analysis was performed to examine the potential mediating role of systemic inflammation in the observed associations.
RESULTS: Most urinary PCPs metabolites were significantly correlated with reduced thyroid function in a dose-dependent manner, particularly for TT4. One-unit increase in concentrations of bisphenol A, benzophenone-3, butyl paraben, ethyl paraben, methyl paraben, and propyl paraben were associated with percent changes in TT4 of -3.11, -1.28, -1.41, -2.44, -1.46, and -1.55, respectively. QGC and BKMR models consistently identified the PCPs mixture was significantly associated with decreased FT4 and TT4. Bisphenol A, triclosan, and ethyl- and propyl-parabens were the dominant contributors, with a joint effect of -0.014 in FT4 and -0.027 in TT4 per quartile increase in the mixture. Mediation analysis showed that associations of urinary PCPs metabolites, especially triclosan, butyl paraben, ethyl paraben, and methyl paraben, with thyroid function were significantly mediated by neutrophil to platelet ratio (NPR), with mediation proportions ranging from 4.91 % to 25.3 %.
CONCLUSION: Both individual and mixed exposure to PCPs were associated with reduced thyroid function, with effects partially mediated by systemic inflammation. These findings highlight the importance of regulating priority chemicals and assessing combined exposure risks.