Scherrer M
Schweiz Med Wochenschr. 1985 Jul 27;115(30):1042-8.
Three atmospheric pollutants are discussed: Sulfur dioxide (SO2) acts as irritant gas on upper airways, trachea and large bronchi. Bronchoconstriction by SO2 is enhanced during work. Dose-response correlation may be observed with SO2 concentrations and bronchial hyperreactivity. Deaths and morbidity rates of patients with COPD parallel peaks of SO2 concentration such as occurred in the 1956 London smog. The mechanisms involved seem to be the same in cross sectional as in long term SO2 effects on human airways. Ozone (O3) is a major irritant pollutant. O3 penetrates deeply into the small airways, kills the macrophages and promotes infections. As peroxide it ruptures the cell membranes and thus lipogenases arise. Neutrophil leukocytes are attracted and transit into the peribronchiolar tissue, an enrichment which may be stopped in hydroxy-urea treated dogs. A marked correlation is observed between peribronchiolar tissue neutrophilia and bronchial hyperreactivity. This may even be a new pathway in the physiopathology of bronchial asthma. Lead is a constituent of exhaust particles and is easily absorbed into the blood. As in the case of drinking-water lead or otherwise absorbed lead, blood lead levels may be markedly reduced by adequate preventive measures. Diastolic and systolic blood pressures correlate significantly with the blood lead level. A further decrease would lower the incidence of myocardial infarctions, strokes and essential hypertension.
二氧化硫（SO₂）对上呼吸道、气管和大支气管起刺激性气体的作用。工作期间，SO₂引起的支气管收缩会增强。SO₂浓度与支气管高反应性之间可观察到剂量反应相关性。慢性阻塞性肺疾病（COPD）患者的死亡率和发病率与SO₂浓度峰值平行，如1956年伦敦烟雾事件中所发生的那样。横断面研究和长期研究中，SO₂对人体气道的影响机制似乎相同。臭氧（O₃）是一种主要的刺激性污染物。O₃可深入小气道，杀死巨噬细胞并促进感染。作为过氧化物，它会破坏细胞膜，从而产生脂肪酶。中性粒细胞被吸引并转移到细支气管周围组织，在接受羟基脲治疗的犬类中，这种富集现象可能会停止。细支气管周围组织嗜中性粒细胞增多与支气管高反应性之间存在显著相关性。这甚至可能是支气管哮喘生理病理学中的一条新途径。铅是废气颗粒的成分之一，很容易被血液吸收。与饮用水中的铅或其他吸收途径的铅一样，采取适当的预防措施可显著降低血铅水平。舒张压和收缩压与血铅水平显著相关。进一步降低血铅水平将降低心肌梗死、中风和原发性高血压的发病率。
