摘要:

Epidemiology studies have demonstrated increased pulmonary morbidity such as allergy and infection with episodes of high particulate air pollution (size range 0.1-10 mum diameter, PM10), but the mechanism(s) for this association is not yet well defined. The present study was undertaken to evaluate the effects of EHC-93 urban particles (Ottawa dust) on immune functions of peripheral blood mononuclear cells (PBMCs) and splenocytes from male Fischer 344 rats and C57Bl/6 mice. Immune function endpoints evaluated included cell viability, lymphocyte blastogenesis stimulated by T-cell mitogen (concanavalin A, Con A) or B-cell mitogens [lipopolysaccharide (LPS) or LPS/dextran sulfate], intracellular Ca2+ concentration, interleukin 2 (IL-2) production, and expression of receptors for transferrin (TfR) and IL-2 (IL-2R). In addition, the effect of N-acetylcysteine (NAC), an antioxidant, on the toxicity of EHC-93 particles was evaluated. Total EHC-93 particles, water leachate of EHC-93, and washed EHC-93 suppressed proliferation of PBMCs and splenocytes to T- and B-cell mitogens. Treatment of splenocytes with EHC-93 particles did not alter intracellular Ca2 + concentration or m itogen-induced expression of TfR and IL-2R expression, but increased IL-2 production assayed by enzyme-linked immunosorbent assay (ELISA). In spite of an increase in IL-2 production, exogenous IL-2 when added to cultures was able to reverse the suppression of Con A-induced lymphocyte proliferation by EHC-93 particles. Furthermore, the suppressive effect of EHC-93 particles on mitogen-induced lymphocyte proliferation was completely abolished by addition of the antioxidant NAC to cultures, suggesting a possible role of oxidative factors for the toxicity of EHC-93 particles.

ISSN:1528-7394    

DOI:10.1080/009841000156989

出版商:Informa UK Ltd    

年代:2000

数据来源: Taylor

摘要:

Animals intoxicated by lead present alterations in the fatty acid composition of red blood cells (RBC). Since this altered fatty acid com position of membranes may be a general reflection of lead toxicosis, we have examined 12 clinically healthy leadexposed male subjects for fatty acid composition of RBC membranes along with blood lead, serum calcium, and serum iron concentrations. Twelve unexposed age-matched male subjects were used as controls. Significantly increased levels of arachidonic acid (AA) were found as compared to matching healthy controls in the RBC of the leadexposed subjects. The increase of AA correlated in a dose-dependent manner with elevation in lead, and with serum iron, while a negative correlation was found between AA and serum calcium. The known ability of lead to substitute for calcium, which is essential in activating phospholipase A2for AA release from membrane phospholipids, may be the main reason for increased AA in RBC membranes.

ISSN:1528-7394    

DOI:10.1080/009841000156998

出版商:Informa UK Ltd    

年代:2000

数据来源: Taylor

摘要:

Ethyl methacrylate (ethyl 2-methyl-2-propenoate, EMA) has been implicated in the development of neurologic impairment following occupational exposure. The potential of EMA to produce neurotoxicity was investigated in adult male Sprague-Dawley rats in two experiments. In the first experiment, animals were administered 100, 200, 400, or 800 mg/kg by daily intraperitoneal (ip) injections for 60 d. Control rats received daily ip injections of 1 ml saline/kg. Clinical observations, spontaneous motor activity, and performance in the Morris water maze were assessed. Alterations in clinical parameters in the higher dose groups included lethargy, impaired breathing, decreased weight gain, and increased mortality. Alterations in motor activity were observed at 100 mg/kg, a dose that did not cause alterations in clinical parameters, body weight gain, or mortality. There was also a dose-dependent impairment in performance in the Morris water maze. In the second experiment, animals were administered EMA in drinking water at concentrations of 0.1, 0.2, or 0.5% for 60 d. Control rats were administered tap water. Animals were perfused at the termination of exposure and samples of brain, spinal cord, and sciatic nerve were prepared for histological examination. Spongiform alterations were observed in fiber tracts of the forebrain, brainstem, and spinal cord. Clusters of axonal swellings were scattered throughout the dorsal, ventral, and lateral columns of the spinal cord, and typically involved internodal segments of two or three neighboring axons. Shrunken axons with separated myelin lamellae and large axons with thinner than normal myelin sheaths were apparent in the sciatic nerve. The patterns of alterations in the white matter of the spinal cord and the sciatic nerve are consistent with myelinopathy, but additional experiments are necessary to confirm whether oligodendroglia and Schwann cells are the primary sites of injury. In addition to the alterations associated with myelin, there was a decrease in the density of neurons in the ventral horn of the spinal cord. While the observed effects of EMA on the nervous system of rats are consistent with neurologic symptom s of workers exposed to EMA, additional experiments are necessary to determine if the level and route of exposures associated with occupational use produce these impairments in experimental animals.

ISSN:1528-7394    

DOI:10.1080/009841000157005

出版商:Informa UK Ltd    

年代:2000

数据来源: Taylor

摘要:

The effect of arsenic compounds depends on the chemical form and is specific for certain organs. The lack of specific biological indicators for the effects of each arsenic species makes it difficult to differentiate their toxicity. Five prospective biological indicators of system ic toxicity were examined at time points ranging from 15 m in to 24 h using male Sprague-Dawley rats, B6C3F1 mice, Golden-Syrian hamsters, and Hartley guinea pigs, following intraperitoneal dosing with 0.1 and 1 mg/kg sodium arsenite. Rats and mice were also dosed with 1 mg/kg sodium arsenate. Total blood arsenic levels were determined in all animal species to show that exposure occurred and as an index of the severity of the change is an indicator of toxicity. Total blood arsenic levels were increased in all animal species. This increase was dose, arsenic species, and animal dependent. Renal pyruvate dehydrogenase activity was significantly decreased at early time points in mice, hamsters, and guinea pigs, and at later time points in rats dosed with arsenite. Rats and mice dosed with arsenate also exhibited PDH decrease at early time points. Blood hematocrit and glucose were increased in the rat and guinea pig, respectively, after arsenite administration. Creatinine and urea nitrogen were found to be unresponsive to arsenic in most animal species. Data suggested that the mouse and secondly the hamster appear to be the most appropriate animal models for the study of acute arsenic toxicity. the acute toxicity of DMA is lower than that of the inorganic (Marafante et al., 1985). Each of these arsenic species has commercially and each has its own toxicity. Assigning toxic a particular species has been complicated by the finding that can, in some cases, metabolize one arsenic species to other et al., 1999). Environmental inorganic arsenic compounds metabolized, sometimes to other toxic intermediates (Cullen et Exposure to gallium arsenide (Webb et al., 1986) and exposure (Fowler & Weissberg, 1974) lead to pulmonary and blood toxicity, The arsenic species that induce toxicity in either case are not known. The development of biological indicators that differentiate As(III), As(V), and AsH3toxicity could make it possible to the mechanisms of toxicity of some arsenic compounds. An indicator of arsenic exposure would show significant upon very-low-dose exposure and would respond quantitatively manner to each different chemical species of arsenic.

ISSN:1528-7394    

DOI:10.1080/009841000157014

出版商:Informa UK Ltd    

年代:2000

数据来源: Taylor