Oak Ridge Institute for Science and Education Research Participation Program, U.S. Environmental Protection Agency, Research Triangle Park, NC, USA.
Public Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, U.S. Environmental Protection Agency, Research Triangle Park, NC, USA.
J Toxicol Environ Health B Crit Rev. 2024 Nov 16;27(8):287-314. doi: 10.1080/10937404.2024.2383637. Epub 2024 Jul 29.
Air pollution exposure is ranked as a leading environmental risk factor for not only cardiopulmonary diseases but also for systemic health ailments including diabetes, reproductive abnormalities, and neuropsychiatric disorders, likely mediated by central neural stress mechanisms. Current experimental evidence links many air pollution health outcomes with activation of neuroendocrine sympathetic-adrenal-medullary and hypothalamic-pituitary-adrenal (HPA) stress axes associated with resultant increases in adrenal-derived hormone levels acting as circulating mediators of multi-organ stress reactions. Epidemiological and experimental investigations also demonstrated sex-specific responses to air pollutant inhalation, which may be attributed to hormonal interactions within the stress and reproductive axes. Sex hormones (androgens and estrogens) interact with neuroendocrine functions to influence hypothalamic responses, subsequently augmenting stress-mediated metabolic and immune changes. These neurohormonal interactions may contribute to innate sex-specific responses to inhaled irritants, inducing differing individual susceptibility. The aim of this review was to: (1) examine neuroendocrine co-regulation of the HPA axis by gonadal hormones, (2) provide experimental evidence demonstrating sex-specific respiratory and systemic effects attributed to air pollutant inhalation exposure, and (3) postulate proposed mechanisms of stress and sex hormone interactions during air pollution-related stress.
空气污染暴露被列为不仅是心肺疾病，而且是包括糖尿病、生殖异常和神经精神障碍等全身健康疾病的主要环境风险因素，这可能是通过中枢神经应激机制介导的。目前的实验证据将许多与空气污染有关的健康结果与神经内分泌交感肾上腺髓质和下丘脑垂体肾上腺（HPA）应激轴的激活联系起来，这与肾上腺源性激素水平的升高有关，这些激素作为多器官应激反应的循环介质。流行病学和实验研究也表明，对空气污染物吸入存在性别特异性反应，这可能归因于应激和生殖轴内的激素相互作用。性激素（雄激素和雌激素）与神经内分泌功能相互作用，影响下丘脑反应，从而增强应激介导的代谢和免疫变化。这些神经激素相互作用可能有助于对吸入性刺激物产生先天的性别特异性反应，导致不同的个体易感性。本综述的目的是：（1）检查性腺激素对 HPA 轴的神经内分泌共同调节，（2）提供实验证据，证明归因于空气污染物吸入暴露的性别特异性呼吸和全身效应，以及（3）推测与空气污染相关的应激和性激素相互作用的拟议机制。
