Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, Columbia University Irving Medical Center, 630 West 168th Street, Presbyterian Hospital Floor 8, Suite 101, New York, NY, 10032, USA.
Environmental Health Sciences Department, Columbia University Mailman School of Public Health, 630 West 168th Street, Room 16-416, New York, NY, 10032, USA.
Curr Environ Health Rep. 2021 Dec;8(4):281-293. doi: 10.1007/s40572-021-00328-2.
Inhaled environmental exposures cause over 12 million deaths per year worldwide. Despite localized efforts to reduce environmental exposures, tobacco smoking and air pollution remain the urgent public health challenges that are contributing to the growing prevalence of respiratory diseases. The purpose of this review is to describe the mechanisms through which inhaled environmental exposures accelerate lung aging and cause overt lung disease.
Environmental exposures related to fossil fuel and tobacco combustion and occupational exposures related to silica and coal mining generate oxidative stress and inflammation in the lungs. Sustained oxidative stress causes DNA damage, epigenetic instability, mitochondrial dysfunction, and cell cycle arrest in key progenitor cells in the lung. As a result, critical repair mechanisms are impaired, leading to premature destruction of the lung parenchyma. Inhaled environmental exposures accelerate lung aging by injuring the lungs and damaging the cells responsible for wound healing. Interventions that minimize exposure to noxious antigens are critical to improve lung health, and novel research is required to expand our knowledge of therapies that may slow or prevent premature lung aging.
在全球范围内，每年因吸入环境暴露而导致的死亡人数超过 1200 万。尽管在地方层面上做出了努力以减少环境暴露，但吸烟和空气污染仍然是紧迫的公共卫生挑战，导致呼吸道疾病的患病率不断上升。本综述的目的是描述吸入性环境暴露加速肺部衰老并导致明显肺部疾病的机制。
与化石燃料和烟草燃烧有关的环境暴露以及与二氧化硅和煤矿开采有关的职业暴露会在肺部引起氧化应激和炎症。持续的氧化应激会导致关键祖细胞中的 DNA 损伤、表观遗传不稳定、线粒体功能障碍和细胞周期停滞。结果，关键的修复机制受损，导致肺实质过早破坏。吸入性环境暴露通过损伤肺部和破坏负责伤口愈合的细胞来加速肺部衰老。最大限度地减少有害物质暴露的干预措施对于改善肺部健康至关重要，需要开展新的研究来扩展我们对可能减缓或预防肺部过早衰老的治疗方法的认识。
