A particular reference should be made to the findings of pigment deposition. It may be considered a bioindicator of exposure to fossil fuel combustion related to air pollution or agricultural process involving burning for harvesting purposes, wood burning, and cigarette smoking. In those exposed only to cigarette smoke, the pathologic findings were dominated by the findings of brown-colored macrophages (“smoker’s pigment”) within respiratory bronchioles, as well as neighboring alveolar ductus and alveoli. In the smoker group, carbon pigment was also common in the lumina of membranous bronchioles. In the pollution-exposure group, larger numbers of macrophages containing brown or golden pigment, as well as extracellular carbon pigment, were found in the airways walls, particularly the walls of the respiratory bronchioles. Whether the difference in the amount of carbon pigment observed between the groups is dependent on the pollution-induced impairment of mucociliary clearance of normally inhaled particles or, alternatively, represents an extra burden of particles due to the polluted environment, is a matter of dispute. The finding that nonsmokers living in a polluted environment have a tendency to have a larger amount of carbon pigment in their bronchiolar walls tempted us to propose that anthracosis may represent a marker of fossil fuel combustion-related air pollution exposure. To exclude possibilities of bias, the identification of the different types of anthracosis between smokers and nonsmokers was made only after the measurements were performed by a different observer. In addition, our models did not consider differences of carbon pigment, since a single estimate of anthracosis was used during modeling.
The finding of bronchiolar secretory hyperplasia in the pollution-exposed group is in agreement with previous experiments in rats, showing adverse respiratory effects secondary to long-term exposure to urban levels of air pollution. The development of bronchial secretory hyperplasia and a more rigid mucus seems to be a general adaptive response to chronic inhalational insults. Secretory gland hyperplasia, with increased production of acidic mucus, is a well-known finding in the lungs of smokers and in experimental models of chronic inhalation injury.
In conclusion, individuals living in a polluted area had histopathologic evidence of bronchiolar damage. These results suggest that long-term exposure to air pollution may contribute to the pathogenesis of inflammatory airway disease and that urban levels of air pollution have adverse consequences to the respiratory tract.
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