Bioaccumulation of metals from nickel smelter waste in P and F1 generation of exposed animals. Part III. Morphological responses.

Inhalation exposure experiments were conducted on a group of female adult Chinchilla rabbits placed in a field biomonitoring station located downwind from dumped nickel refinery wastes. Their F1 generation offsprings were exposed prenatally and 6 weeks postnatally. After termination of exposure, both P and F1 generation rabbits were sacrificed, their organs removed and subjected to a histologic examination using light and electron microscopy techniques. The histological responses were most marked in P generation female rabbits, namely hypertrophy of the muscle layer of pulmonary artery walls and foci of atelactasis. Electron microscopic examinations of the myocardium of chamber-exposed rats revealed evidence of muscle fibre lesions at sites of intercalary discs and changes in mitochondrial structure as a result of accumulated Ni, Cr and/or other metals. Histologically remarkable was interstitial accumulation of an unidentified electron-dense crystalloid substance situated near blood capillaries and between myofibrils and collagenous fibres; this substance is believed to be a result of metal-protein interaction. The rats injected intravenously with a suspension of metal waste displayed mitochondrial lesions analogous to those observed after inhalation exposure, but no presence of the electron-dence substance could be noted. It is concluded that chronic exposure to metal waste may give rise to cardiovascular lesions.

Biomonitoring of environmental pollution hazards from a nickel smelter waste dump.

Longterm field exposure study was carried out on 10 rabbits placed for 6 months in a bioindication station located about 3 km downwind of a disposal site of nickel smelter waste dump. As revealed by the method of atomic absorption spectrophotometry, all of these animals showed elevated nickel and chromium levels in their body organs and hair. These findings were paralleled by histologic abnormalities in the lungs and liver tissues. Average dustfall values at the site of exposure did not exceed 5.5 g X m-2 X 30 d-1 during the period of observation. Dustfall deposits in this location contained nickel and chromium in amounts that were higher than in control locality. Analogous experiments on Wistar rats were carried out in a laboratory exposure chamber (exposure 4 h/day, 5 days/week, for a period of 6 months). After exposures to 50 mg X m-3 of metallic dust, lung parenchyma of rats was characterized by the presence of dust particles in various phases of phagocytosis as well as the presence of badly damaged or disintegrated alveolar macrophage cells, which pointed to metallic aerosol toxicity for biomembranes. The technique of air pollution biomonitoring on animals, correlated with the data on ambient air concentrations of the suspended particulate matter and its content of trace metals, appears to be a well suitable tool in establishing the potential air pollution hazards to the exposed populations living in the area of concern.

Modulation of peripheral lymphocyte and alveolar macrophage activity by magnesite emissions.

Modulation of alveolar macrophage and peripheral lymphocyte activities in rats exposed to magnesite emissions was tested under field and laboratory conditions. The field exposure test were conducted in a locality near a magnesite ore processing plant, the time observation was 18 weeks. The laboratory exposure tests were performed in an inhalation chamber at a constant magnesite dust aerosol concentration of 50 mg . m-3; the animals were exposed 4 hours a day, 5 days a week for a period of 70 days. Eighteen weeks of exposure to magnesium-polluted ambient air was found to increase the number of alveolar macrophages, to stimulate acid phosphatase activity in these cells, and to enhance activity of peripheral B lymphocytes to form EAC rosettes. The inhalation chamber experiments, evaluated after 46 and 70 days of exposure, resulted in an enhanced acid phosphatase activity of alveolar macrophages, enhanced lactate dehydrogenase activity of peripheral lymphocytes and in an increased percentage of B lymphocytes in blood, depending on exposure time. The activation of peripheral lymphocytes and alveolar macrophages observed in rats exposed under field and laboratory (here in dependence on exposure time) conditions clearly suggest that the cells participating in the induction and expression of the immune response are distinctly modulated in their activity by in vivo exposure to magnesite dust.