Toxic effects of cadmium microparticles on the respiratory system. An experimental study on rats and mice.

Abstract

Toxic effects of cadmium microparticles on the respiratory system: An experimental study on rats and mice. Scand. j. work environ. & health 3 (1977) 116-121. Experiments on male, specific pathogen-free rats (193) and mice (66) are reported. The test and control animals received a single 15-min exposure to cadmium (cadmium oxide) and aluminum (alumina) microparticles, respectively. The air cadmium content was 10 mg/ m 3 , and 4 fA-g of this metal was retained by the lungs of the rats. The animals were observed for 24 days. The following significant differences appeared between the control and test groups: in the cadmium exposed rats the relative lung weight (percentage of body weight) became temporarily higher; the absolute number of alveolar macrophages decreased at first and then increased; numerous polymorphonuclear and lymphocytic cells appeared in the alveoli. According to these inflammatory phenomena, at the 48th h after exposure, there was an alteration in the clearance kinetics of inhaled bacteria and an increase in the death rate of cadmium exposed animals following a test infection with Salmonella enteritidis (rats) or Pasteurella multocida (mice) aerosols. The mechanism of cadmium toxic action on the respiratory system is discussed.

Alterations in macrophage functions by environmental chemicals.

“…Not all environmental chemicals that reach the lung elicit an automatic influx of reserve macrophages. Exposure to a number of agents reduces the number of free macrophages: lead sequioxide (8), silica (45,50, 51), asbestos (50,52), Pb2O3 (8), Sb and Cd fumes (53), MnO2 (54), Mn3O4 (55), 03 (56), chrysotile (57-59), amosite (60), CdO and CdCl2 (53,61,62), acrolein (63) and NiCl2 (35). These chemical agents are cytolytic to these defense cells.…”

Alterations in Macrophage Functions by Environmental Chemicals

“…A number of respiratory irritants elicit an active influx of granulocytes from the blood. The accumulation of polymorphonuclear (PMN) leukocytes in the alveoli has been reported following acute exposure to diesel exhaust (33), 0,3 (56,76), NO2 (77), iron oxide (78), cotton dust (44,79), cigarette smoke (22,80,81), HCI (82) and CdCl2 (38,61,62,83). This rapid influx of PMN has been shown to be dose-related and is a useful measurement parameter for evaluation of a pulmonary inflammatory response.…”

“…The effects of exposure to NO2 (123,(145)(146)(147), 03 (138,141,(148)(149)(150), S02 (144,151,152), cigarette smoke (5,90,121,137,(153)(154)(155) silica (156), H2SO4 (132), Cd2+ (61,124), alumina (124), Ni2+ (117), Mn2+ (55,157), ethanol (158), PbCl2 (159), and high oxygen tensions (150) have all been investigated using model systems similar to the ones described above. Depressed bactericidal functions has been attributed to exposure to all of these substances except silica, SO2 and 02.…”

“…Exposure to a number of agents reduces the number of free macrophages: lead sequioxide (8), silica (45,50,51), asbestos (50,52), Pb2O3 (8), Sb and Cd fumes (53), MnO2 (54), Mn3O4 (55), 03 (56), chrysotile (57)(58)(59), amosite (60), CdO and CdCl2 (53,61,62), acrolein (63) and NiCl2 (35 100 ,ug/mL but significant cytotoxicity was observed at higher concentrations, > 100 ,ug/mL (60).…”

“…A number of different experimental approaches, using intact animals, have been employed in an effort to determine the degree of efficiency of the pulmonary defense system in the pollutant-exposed, compromised host (61,63,134,141,(218)(219)(220)(221)(222)(223).…”