Effects of air pollutants on the oxidative metabolism and phagocytic capacity of pulmonary alveolar macrophages.
Isolated rabbit pulmonary alveolar macrophages were found to be a convenient biological model system, relevant for studies of the toxicity of air pollutants. The phagocytic capacity and the oxygen consumption were used as test parameters and studied simultaneously on the same cells. The toxicity of extracts of airborne particles (phi less than 15 microns) collected in urban and rural areas was investigated and compared to a cigarette-smoke condensate. An extract of particles from a car tunnel was found to be the most toxic air sample, inhibiting phagocytosis as well as respiration of the macrophages at a concentration representing 5 m3 air/ml cell suspension. A corresponding sample collected on a roof of a five-storied building in the central area of a city (population 600,000) was found to inhibit phagocytosis but did not affect respiration. Further investigations revealed that one effect of the "tunnel" extract could be explained as an uncoupling of the mitochondrial respiratory control. Compared to the cigarette-smoke condensate, the toxicity of the air samples was infinitesimal.
D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D066298:In Vitro Techniques; D008264:Macrophages / Q000187:drug effects*; D008930:Mitochondria, Liver / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects*; D010587:Phagocytosis / Q000187:drug effects*; D010947:Plants, Toxic; D011650:Pulmonary Alveoli / Q000187:drug effects*; D011817:Rabbits; D051381:Rats; D012906:Smoke / Q000009:adverse effects; D014026:Nicotiana; D001335:Vehicle Emissions / Q000633:toxicity
D000393:Air Pollutants; D012906:Smoke; D001335:Vehicle Emissions