Birru Rahel L, Di Y Peter
Department of Environmental and Occupational Health, University of Pittsburgh Pittsburgh, PA, USA.
Front Physiol. 2012 Aug 28;3:348. doi: 10.3389/fphys.2012.00348. eCollection 2012.
Second hand smoke (SHS) introduces thousands of toxic chemicals into the lung, including carcinogens and oxidants, which cause direct airway epithelium tissue destruction. It can also illicit indirect damage through its effect on signaling pathways related to tissue cell repair and by the abnormal induction of inflammation into the lung. After repeated exposure to SHS, these symptoms can lead to the development of pulmonary inflammatory disorders, including chronic obstructive pulmonary disease (COPD). COPD is a severe pulmonary disease characterized by chronic inflammation and irreversible tissue destruction. There is no causal cure, as the mechanism behind the development and progression of the disease is still unknown. Recent discoveries implicate genetic predisposition associated with inflammatory response contributed to the development of COPD, linked to irregular innate and adaptive immunity, as well as a risk factor for cancer. The use of animal models for both cigarette smoke (CS) and SHS associated in vivo experiments has been crucial in elucidating the pathogenic mechanisms and genetic components involved in inflammation-related development of COPD.
二手烟（SHS）会将数千种有毒化学物质带入肺部，包括致癌物和氧化剂，这些物质会直接破坏气道上皮组织。它还会通过影响与组织细胞修复相关的信号通路以及异常诱导肺部炎症，造成间接损害。反复接触二手烟后，这些症状会导致肺部炎症性疾病的发展，包括慢性阻塞性肺疾病（COPD）。COPD是一种严重的肺部疾病，其特征是慢性炎症和不可逆的组织破坏。由于该疾病发生和发展背后的机制仍不清楚，因此没有因果性的治愈方法。最近的发现表明，与炎症反应相关的遗传易感性促成了COPD的发展，这与先天和适应性免疫异常有关，也是癌症的一个危险因素。在阐明与COPD炎症相关发展所涉及的致病机制和遗传成分方面，使用动物模型进行与香烟烟雾（CS）和二手烟相关的体内实验至关重要。
