School of Life Sciences, Faculty of Science, University of Technology Sydney, Ultimo, NSW 2007, Australia; Discipline of Pharmacy, Graduate School of Health, University of Technology Sydney, Ultimo, NSW 2007, Australia.
Discipline of Pharmacy, Graduate School of Health, University of Technology Sydney, Ultimo, NSW 2007, Australia.
Sci Total Environ. 2024 Dec 1;954:176413. doi: 10.1016/j.scitotenv.2024.176413. Epub 2024 Sep 23.
Inhalation of particulate matter (PM), one of the many components of air pollution, is associated with the development and exacerbation of chronic respiratory diseases, such as chronic obstructive pulmonary disease (COPD). COPD is one of the leading causes of global mortality and morbidity, with a paucity of therapeutic options and a significant contributor to global health expenditure. This review aims to provide a mechanistic understanding of the cellular and molecular pathways that lead to the development of COPD following chronic PM exposure. Our review describes how the inhalation of PM can lead to lung parenchymal destruction and cellular senescence due to chronic pulmonary inflammation and oxidative stress. Following inhalation of PM, significant increases in a range of pro-inflammatory cytokines, mediated by the nuclear factor kappa B pathway are reported. This review also highlights how the inhalation of PM can lead to deleterious chronic oxidative stress persisting in the lung post-exposure. Furthermore, our work summarises how PM inhalation can lead to airway remodelling, with increases in pro-fibrotic cytokines and collagen deposition, typical of COPD. This paper also accentuates the interconnection and possible synergism between the pathophysiological mechanisms leading to COPD. Our work emphasises the serious health consequences of PM exposure on respiratory health. Elucidation of the cellular and molecular mechanisms can provide insight into possible therapeutic options. Finally, this review should serve as a stark reminder of the need for genuine action on air pollution to decrease the associated health burden on our growing global population.
吸入颗粒物（PM）是空气污染的众多成分之一，与慢性呼吸道疾病（如慢性阻塞性肺疾病（COPD））的发展和恶化有关。COPD 是全球死亡率和发病率的主要原因之一，治疗选择有限，对全球卫生支出造成重大负担。本综述旨在提供一个机制性的理解，即慢性 PM 暴露后导致 COPD 发展的细胞和分子途径。我们的综述描述了 PM 吸入如何导致肺实质破坏和细胞衰老，这是由于慢性肺炎症和氧化应激引起的。PM 吸入后，据报道，核因子 kappa B 途径介导的一系列促炎细胞因子显著增加。本综述还强调了 PM 吸入如何导致有害的慢性氧化应激在暴露后持续存在于肺部。此外，我们的工作总结了 PM 吸入如何导致气道重塑，表现为促纤维化细胞因子增加和胶原蛋白沉积，这是 COPD 的典型特征。本文还强调了导致 COPD 的病理生理机制之间的相互联系和可能的协同作用。我们的工作强调了 PM 暴露对呼吸健康的严重健康后果。阐明细胞和分子机制可以为可能的治疗选择提供思路。最后，这篇综述应该强烈提醒人们需要采取真正的行动来减少空气污染，以减轻我们不断增长的全球人口所面临的相关健康负担。
