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At least 631 records · Page 35Linked to original sources
PubMed1988

SCE increases after an accidental acute inhalation exposure to EtO and recovery to normal after 2 years.

Sister-chromatid exchanges (SCEs) were studied in 3 workers accidentally exposed for about half an hour to high levels of ethylene oxide (more than 700 ppm) during a sterilizing process. The 3 workers had clinical symptoms of exposure and were tested for SCE frequencies 5 days and 2 years after the accident: 2 had also been tested 6 months earlier. All 3 showed a similar increase in SCEs after the accident, to a mean of 13.8 SCEs/cell compared with 8.6 for a control group. The incidence of 'high-frequency cells' was markedly elevated but decreased over 2 years, when the mean SCE frequencies had also returned to pre-accident levels.

Accidents↗
PubMed1984

Subchronic inhalation exposure of dearomatized white spirit and C10-C11 isoparaffinic hydrocarbon in Sprague-Dawley rats.

Groups of 35 male and 35 female Sprague-Dawley rats were exposed to either Dearomatized White Spirit (DAWS) vapor at concentrations of 1.97 and 5.61 g/m3 or C10-C11 Isoparaffinic Hydrocarbon (IPH) vapor at concentrations of 1.91 and 5.62 g/m3. These concentrations were targeted for the recommended occupational exposure limits and three times that value, respectively. Exposures were 6 hr-day, 5 days/week for 12 weeks. Following Weeks 4, 8, and 12 of exposure, a total of 10, 10, and 15 rats, respectively, from each group were sacrificed. Clinical chemistry and hematology parameters were measured in blood samples taken immediately prior to sacrifice, and selected organs were removed and weighted. Twenty-three organs and tissues from each animal were examined microscopically. There were no deaths during the course of this study related to either DAWS or IPH. Mean body weights were significantly lower than controls in male rats following exposure to 5.61 g/m3 DAWS, and 5.62 or 1.91 g/m3 IPH. Body weights were not affected in females. The primary effects from DAWS or IPH exposure were observed in the kidneys of male rats only from both exposure groups beginning at Week 4. Evidence of mild tubular toxicity, such as regenerative tubular epithelia and dilated tubules containing proteinaceous casts, was observed at the corticomedullary junction. The incidence and severity appeared to increase with increasing concentration and exposure duration. There were scattered instances of statistically significant increases in liver and kidney weights in both males and females. With the exception of the mild male rat tubular nephrotoxicity, other significant toxic effects were not observed at levels tested.

Alkanes↗
PubMed1987

Evaluation of the effects of inhalation exposure to 1,3-dichloropropene on fetal development in rats and rabbits.

1,3-Dichloropropene (DCP), which has found widespread use as a soil fumigant, was evaluated for its potential effects on embryonal and fetal development in rats and rabbits. Pregnant Fischer 344 rats and New Zealand White rabbits were exposed to 0, 20, 60, or 120 ppm of 1,3-dichloropropene for 6 hr/day during gestation Days 6-15 (rats) or 6-18 (rabbits). Exposure-related decreases in maternal weight gain and feed consumption were observed in rats at all treatment levels. Decreased weight gain was also observed among rabbits at 60 and 120 ppm. A slight, but statistically significant, increase in the incidence of delayed ossification of the vertebral centra in rats exposed in utero to 120 ppm of DCP was considered of little toxicologic significance in light of the maternal toxicity observed at this exposure concentration. No evidence of a teratogenic or embryotoxic response was observed in either species at any exposure level tested. Thus, it was concluded that DCP was not teratogenic at exposure levels up to 120 ppm in either rats or rabbits.

Aerosols↗
PubMed1980

Dose-dependent neurochemical effects of 1,1,2-trichloro-1,2,2-trifluoroethane inhalation exposure in rats.

Male Wistar rats were exposed to 200, 1000 or 2000 ppm of 1,1,2-trichloro-1,2,2-trifluoroethane vapour for 2 weeks, 5 day/week, 6 h daily and showed a dose-dependent accumulation of the compound in perirenal fat and brain. In the first week increased NADPH-diaphorase activity was observed and there was decreased cerebral glutathione at the highest dose. During the second week these effects disappeared while RNA tended to increase, and glutathione peroxidase activity to decrease at the highest dose. After a withdrawal period of 7 days, no fluorohydrocarbon was detected and the neurochemical effects had disappeared except that brain RNA at the highest exposure was below the control range.

Animals↗
PubMed1982

Conditioned taste aversion induced by inhalation exposure to methyl bromide in rats.

The toxic effect of methyl bromide vapor was assessed by a conditioned taste aversion regime. Rats kept under a water deprivation schedule for 7 days, were permitted access to 0.3% (w/v) sodium saccharin, and were exposed to methyl bromide at 0, 25, 50, and 100 ppm for 4 h. 3 days after the exposure, saccharin preference tests were carried out, revealing dose-dependent saccharin aversion in the exposure group. This result suggests that the conditioned taste aversion method is effective for assessing the toxicity of gaseous substances such as methyl bromide.

Animals↗
PubMed1983

Effect of long-term inhalation exposure to cadmium oxide fumes on cardiac muscle ultrastructure in rats.

The ultrastructure of the cardiac muscle of rats exposed 5 h daily, 5 days a week to cadmium oxide (CdO) fumes at a concentration of 0.16 mg Cd/m3 for 3 and 6 months and at a concentration of 1 mg Cd/m3 for 3 and 4 months has been evaluated. The structure of muscle cells, arterioles and capillaries remained unchanged. There were distinct alterations of the intercalated disc structure dependent upon the level and time of exposure. The damage to intercalated discs varied from the enlargement of the fissure between membranes (within unspecialized segments) to disruption of the complex junctions.

Animals↗
PubMed1989

Concentration-dependent depletion of non-protein sulfhydryl (NPSH) content in lung, heart and liver tissue of rats and mice after acute inhalation exposure to butadiene.

The effects of different exposure concentrations of butadiene on the cellular non-protein sulfhydryl (NPSH) content of liver, lung and heart tissue were investigated in B6C3F1 mice and Sprague-Dawley rats. Groups of male animals of both species were exposed for 7 h to 10, 50, 100, 250, 500, 1000 and 2000 ppm butadiene. Immediately after exposure, NPSH content of liver, lung and heart tissue was determined according to a modified Ellman procedure. A comparison of both species shows that a dose-dependent NPSH depletion can be observed in mice for all tissues examined. In rats, liver NPSH content shows a major reduction at high exposure concentrations only. In mice, depletion of NPSH content of liver, lung and heart tissue starts at exposure concentrations of about 250 ppm butadiene. A reduction in NPSH content of about 80% is observed for lung tissue at 1000 ppm and for liver and heart tissue at exposure concentrations of 2000 ppm butadiene. The data on tissue concentrations of NPSH obtained after exposure of rats and mice to butadiene reflect the quantitative differences in butadiene metabolism and in biological effectivity of reactive butadiene intermediates between both species.

Animals↗
PubMed1989

Accumulation of mixed mineral dusts in the lungs of rats during chronic inhalation exposure.

The effects of mixed dust exposure on pulmonary clearance during chronic exposure has been investigated using rats exposed to combinations of toxic and relatively nontoxic dusts: quartz (at respirable dust concentrations of 1 and 10 mg/m3) plus titanium dioxide (at 30 and 20 mg/m3, respectively), and amosite asbestos (2.5 mg/m3) plus titanium dioxide (15 mg/m3). The rats were exposed for 5 days per week, and for up to 16 weeks (for quartz) or up to 32 weeks (for asbestos). The lung burdens were compared with previously published results for exposure to single dusts under the same exposure regimens. The main feature of all these comparisons was the absence of significant differences between the lung burdens (at 3, 10, and 38 days postexposure) for single-dust and mixed-dust exposures. There was, however, some reduction in the postexposure clearance (as shown by the lung burdens at 94, 150, and 260 days postexposure) of titanium dioxide which appeared to be due to the presence of quartz in the lung. For the quartz plus titanium dioxide experiments, the lymph nodes were dissected and analyzed separately. These results showed that transfer to lymph nodes accounted for most of the postexposure clearance for titanium dioxide, and almost all for the quartz.

Animals↗
PubMed1998

DNA adducts in mouse testis and lung after inhalation exposure to 1,3-butadiene.

1,3-Butadiene is a widely used industrial chemical and also an environmental contaminant. Recent findings have shown that butadiene can also be a male germ cell mutagen. In this study, DNA adduct formation in testis and lung has been explored by using N7-alkylated guanines as a marker of biological effective dose. The adducts measured were the four structurally different guanine N7-adducts alkylated by butadienemonoepoxide, the main metabolite of 1,3-butadiene. This study demonstrates the dose-dependent adduct formation in lung and testis. At lower exposures (50 and 200 ppm) the adduct levels were about the same in the two organs, but at 500 ppm the adduct level was significantly (p < 0.03) higher in testis than in lung. The enantiomeric composition of the adducts detected was also different. In lung, all 4 possible adducts were present (S-C-1" dominating, 49%), but in testis only two out of four adducts were detected (S-C-2" being the most abundant adduct, 71%). These novel observations indicate that the DNA repair is different in these two organs studied and that heritable genetic effects observed may be mediated through the DNA adducts.

Alkylation↗
PubMed2004

Inhalational exposure to nerve agents.

The respiratory system plays a major role in the pathogenesis of nerve agent toxicity. It is the major route of entry and absorption of nerve agent vapor, and respiratory failure is the most common cause of death follow-ing exposure. Respiratory symptoms are mediated by chemical irritation,muscarinic and nicotinic receptor overstimulation, and central nervous system effects. Recent attacks have demonstrated that most patients with an isolated vapor exposure developed respiratory symptoms almost immediately. Most patients had only mild and transient respiratory effects, and those that did develop significant respiratory compromise did so rapidly. These observations have significant ramifications on triage of patients in a mass-casualty situation, because patients with mild-to-moderate exposure to nerve agent vapor alone do not require decontamination and are less likely to develop progressive symptoms following initial antidote therapy. Limited data do not demonstrate significant long-term respiratory effects following nerve agent exposure and treatment. Provisions for effective respiratory protection against nerve agents is a vital consideration in any emergency preparedness or health care response plan against a chemical attack.

Chemical Warfare Agents↗