Department of Physiopathology and Experimental Medicine, Siena University, Siena, Italy.
Ann N Y Acad Sci. 2012 Jul;1259:104-11. doi: 10.1111/j.1749-6632.2012.06605.x.
Air pollution has been associated with many different diseases, such as cancer, and respiratory, cardiovascular, and cutaneous chronic diseases. These effects are enhanced in people exposed to combined air pollutants, such as ozone and cigarette smoke. Chronic exposure to these pollutants causes an increase in oxidative stress and inflammation and has been associated with an increase in pulmonary diseases and mortality. Clinical and epidemiological studies reported interindividual variability in the adverse health effects of air pollutants, suggesting a genetic predisposition. The identification of subgroups of the population who are particularly vulnerable to air pollution is, therefore, of importance. Mouse models are a useful tool for studying the mechanisms underlying different susceptibility, as they show differences in strain responses to both ozone and cigarette smoke. This review analyses the role of inflammation and the influence of genetic factors on the mechanisms of lung injury caused by ozone and cigarette smoke.
空气污染与许多不同的疾病有关，如癌症，以及呼吸道、心血管和皮肤慢性疾病。这些影响在接触臭氧和香烟烟雾等混合空气污染物的人群中更为明显。慢性暴露于这些污染物会导致氧化应激和炎症增加，并与肺部疾病和死亡率增加有关。临床和流行病学研究报告称，空气污染物对健康的不良影响存在个体间的差异，这表明存在遗传易感性。因此，确定对空气污染特别脆弱的人群亚组非常重要。小鼠模型是研究不同易感性机制的有用工具，因为它们在对臭氧和香烟烟雾的反应方面表现出了品系差异。本综述分析了炎症的作用以及遗传因素对臭氧和香烟烟雾引起的肺损伤机制的影响。
