空气污染与甲状腺功能。

IF 2 4区 医学 Q3 PHYSIOLOGY
Journal of Physiology and Pharmacology Pub Date : 2025-04-01 Epub Date: 2025-05-05 DOI:10.26402/jpp.2025.2.01
M Soloch, W Starczewski, K Brzezinska, M Dotka, W Banach, J Baloniak, D Kozlowska, O Matuszak, D Skrypnik
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引用次数: 0

摘要

空气污染是公认的主要环境健康危害之一。包括NO2、CO、SO2、O3在内的气体分子、颗粒物(PM10、PM2.5)和挥发性有机化合物被认为是特别有害的。尽管如此,全球仍有很大一部分人口居住在空气质量令人不满意的地区。研究表明,空气污染物可能起到内分泌干扰物的作用,可能会干扰甲状腺功能,并通过氧化应激、炎症和激素失调导致甲状腺癌的发展。本文综述了空气污染对甲状腺功能和甲状腺癌风险的影响,重点介绍了流行病学研究和内分泌干扰的机制。空气污染物被怀疑是内分泌干扰物,可能通过受体结合、激素置换以及激素运输、代谢和基因表达的中断来干扰甲状腺功能。暴露于这些污染物,特别是在胎儿发育期间,可损害新生儿甲状腺稳态,增加甲状腺功能减退和长期认知并发症的风险。长期暴露在PM2.5中会增加患甲状腺乳头状癌(PTC)的风险,特别是在高浓度和长期暴露的情况下。二氧化氮和臭氧水平的升高,以及城市中一氧化碳的暴露,也与甲状腺癌的风险增加有关。相反,PM10和SO2呈反比关系。此外,研究表明PM2.5暴露与甲状腺癌风险和死亡率增加之间存在潜在关联,尽管必须考虑多种混杂因素。PM2.5、二氧化氮、一氧化碳等空气污染也会影响甲状腺激素(TH)水平,但研究结果仍不一致,其关系因年龄、性别和肥胖等内部因素而异。虽然有证据表明空气污染与甲状腺功能障碍以及甲状腺癌风险之间存在联系,但研究结果的不一致凸显了进一步研究的必要性。深入了解这些关联背后的机制对于评估健康风险和制定有效的公共卫生干预措施至关重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Air pollution and thyroid function - narrative review.

Air pollution is recognised as one of the primary environmental health hazards. The gas molecules including NO2, CO, SO2, O3, particulate matter (PM10, PM2.5), and volatile organic compounds are being identified as particularly harmful. Despite this, a significant portion of the global population resides in areas with unsatisfactory air quality. Research suggests that air pollutants may act as endocrine disruptors, potentially interfering with thyroid function and contributing thyroid cancer development through oxidative stress, inflammation, and hormonal dysregulation. This paper reviews current literature on the effects of air pollution on thyroid function and thyroid cancer risk, focusing on epidemiological studies and mechanisms of endocrine disruption. Air pollutants are suspected endocrine disruptors that may interfere with thyroid function through receptor binding, hormone displacement, and disruptions in hormone transport, metabolism, and gene expression. Exposure to these pollutants, particularly during fetal development, can impair neonatal thyroid homeostasis, increasing the risk of hypothyroidism and long-term cognitive complications. Prolonged exposure to PM2.5 has been associated with an increased risk of papillary thyroid cancer (PTC), particularly at higher concentrations and with long-term exposure. Elevated levels of NO2 and O3, as well as urban exposure to CO, have also been linked to a heightened risk of thyroid cancer. In contrast, an inverse relationship has been observed for PM10 and SO2. Additionally, studies suggest a potential association between PM2.5 exposure and both increased risk and mortality of thyroid cancer, although multiple confounding factors must be considered. Air pollution with PM2.5, NO2, CO has also been found to affect thyroid hormone (TH) levels, but findings remain inconsistent, with relationships varying based on age, sex, and internal factors such as obesity. While evidence suggests a link between air pollution and thyroid dysfunction, as well as thyroid cancer risk, inconsistencies in findings highlight the need for further research. A deeper understanding of the mechanisms underlying these associations is crucial to assessing health risks and developing effective public health interventions.

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来源期刊
CiteScore
4.00
自引率
22.70%
发文量
0
审稿时长
6-12 weeks
期刊介绍: Journal of Physiology and Pharmacology publishes papers which fall within the range of basic and applied physiology, pathophysiology and pharmacology. The papers should illustrate new physiological or pharmacological mechanisms at the level of the cell membrane, single cells, tissues or organs. Clinical studies, that are of fundamental importance and have a direct bearing on the pathophysiology will also be considered. Letters related to articles published in The Journal with topics of general professional interest are welcome.
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