[Air burden and respiratory and vascular diseases]

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.