Environmental exposure to manganese and combined exposure to gaseous upper respiratory irritants: mechanism of action and adverse health effects.

Abstract

This review relates to possible explanations of the often-observed findings that exposure to certain air pollutants or their mixture results in an increased rate of acute respiratory diseases. Epidemiological investigations have shown that exposure to manganese (MnO2) concentrations only 10 to 50 times higher than the normal urban concentrations of 0.01 to 0.03 microgram/m3 air might have an adverse health effect on respiratory organs. The assumption that one possible mechanism of action could be that manganese at such exposure levels disturbs certain protective functions in the lung--thus making the organism more susceptible to infections--is supported by toxicological studies. In vitro studies have demonstrated the cytotoxic action of manganese, including the inhibition of activities of alveolar macrophages. Animal experiments showed a decrease in resistance toward respiratory infections that were caused by simultaneous exposure to MnO2 and pathogenic bacteria. In cases of combined exposure to gaseous upper respiratory tract irritants and suspended particles, the involvement of adsorption of gaseous compounds on solid particles as carriers has been suggested. The assumption is that through such a mechanism, water-soluble gaseous irritants can be transported deep into air passages, which such irritants normally do not reach. As the adsorption is reversible, the gaseous compounds can later be released from the particles, inducing a local irritating effect in the small airways and alveoli.