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When the possible toxic effects of chemical air pollutants are considered, not only the action of a single toxicant must be taken into account, but also the possible interacting systems that may coexist within the host. An experimental approach to this principle of multiple causality in the pathogenesis of pulmonary disease is discussed in this paper. In a series of experiments an animal model system was employed to study the interaction of ozone and an infectious microorganism. The <it>in vivo</it> parameters through which these interactions were determined included rate of bacterial kill, multiplication and invasiveness as well as the enhancement of mortality. Other pulmonary defense mechanisms studied include: chemotaxis, mobilization or suppression of macrophages, phagocytic capability of macrophages, alteration in intra-cellular enzymes and other subtle factors affecting macrophage function and host resistance are also reported. A discussion of the synergistic mechanism of action of these combined agents and an assessment of the role of the infective model system in toxicological appraisal is presented.
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Coffin et al. (1972) studied this question.
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