Health effects of sulfur-related environmental air pollution. II. Cellularand molecular parameters of injury

Recently, concern has been raised about effects related to environmental su lfur and/or acidic aerosols. To assess long-term effects on nonrespiratory lung function, 8 beagle dogs were exposed over a period of 13 mo for 16.5 h /day to a neutral sulfite aerosol at a sulfur(IV) concentration of 0.32 mg m(-3) and for 6 h/day to an acidic sulfate aerosol providing a hydrogen con centration of 15.2 mu mol m(-3) for inhalation. Prior to exposure the dogs were kept under clean air conditions for 16 mo to establish physiological b aseline values for each animal. A second group of eight dogs (control) was kept for the entire study under clean air conditions. No clinical symptoms were identified that could be related to the combined exposure. Biochemical and cellular parameters were analyzed in sequential bronchoalveolar lavage (BAL) fluids. The permeability of the alveolocapillary membrane and diethy lenetriaminepentaacetic acid (DTPA) clearance was not affected. Similarly, oxidant burden of the epithelial lining fluid evaluated by levels of oxidat ion products in the BAL fluid protein fraction remained unchanged. Both the lysosomal enzyme beta-N-acetylglucosaminidase and the alpha-1-AT were incr eased (p < .05). In contrast, the cytoplasmic marker lactate dehydrogenase remained unchanged, indicating the absence of severe damages to epithelial cells or phagocytes. Various surfactant functions were not altered during e xposure. Three animals showed elevated levels of the type II cell-associate d alkaline phosphatase (AP), indicating a nonuniform response of type II ce lls. Significant correlations were found between AP and total BAL protein, but not between AP and lactate dehydrogenase, suggesting proliferation of a lveolar type II cells. Absolute and relative cell counts in the BAL fluid w ere not influenced by exposure. Alveolar macrophages showed no alterations with regard to their respiratory burst upon stimulation with opsonized zymo san. The percentage of alveolar macrophages capable of phagocytozing latex particles was significantly decreased (p < .05), while the phagocytosis ind ex was not altered. In view of the results of this and previous studies, we conclude that there is no synergism of effects of these two air pollutants on nonrespiratory lung functions. it is hypothesized that antagonistic eff ects of these air pollutants on phospholipase A(2)-dependent pathways accou nt for compensatory physiological mechanisms. The results emphasize the com plexity of health effects on lung functions in response to the complex mixt ure of air pollutants and disclose the precariousness in the risk assessmen t of air pollutants for humans.