Inhalation exposure acute

Limited information was located regarding the distribution of vanadium in humans following inhalation exposure. Acute animal studies suggest that there is an initial accumulation of vanadium in the lungs, kidneys, and liver of rats, as well as high levels in the blood. However, retention of vanadium occurs primarily in the bone. Though there were no animal data on longer exposure to vanadium via the inhalation route, it seems likely that experimental studies would show distribution patterns similar to these seen with chronic human exposures. 

Respiratory effects have also been observed in animals after acute- and intermediate-duration inhalation exposure acute, but not intermediate, oral exposure and acute, but not intermediate, dermal exposure to 2-butoxyethanol. No adverse respiratory effects have been reported in animals after inhalation, oral, or dermal exposure to 2-butoxyethanol acetate (Truhaut et al. 1979) however, the data are limited. In acute-duration inhalation studies on 2-butoxyethanol, respiratory effects consisted of rapid and shallow breathing prior to death in rats exposed to 867 ppm for 4 hours, audible respiration and nasal discharge in... 

Toxicity studies on trifluoroethanol show acute oral LD q, 240 mg/kg acute dermal LD q, 1680 mg/kg and acute inhalation L(ct) Q, 4600 ppmh. Long-term subchronic inhalation exposure to 50—150 ppm of the alcohol has caused testicular depression in male rats, but no effects were noted at the 10 ppm level (32). Although the significance of the latter observations for human safety is unknown, it is recommended that continuous exposure to greater than 5 ppm or skin contact with it be avoided. 

Acute inhalation exposure of rats to 200,000 ppm VF for 30 minutes or more produced weak anaesthesia and no deaths (90). In rats VF is only slightly metabolized at a rate of one-fifth that of vinyl chloride (91—95). An extensive program of toxicity testing of vinyl fluoride is ia progress (96,97). 

Inhalation is the chief route of worker exposure. Comparative data from acute or subchronic inhalation exposures with rats (98) indicate that nitromethane and nitroethane are the least toxic of the nitroparaffins by this route and do not induce methemoglobin formation. The nitropropanes are less well tolerated 2-nitropropane is more toxic than 1-nitropropane and is more likely to cause methemoglobinemia. 

Health and Safety Factors, Toxicology. Phosphoms trichloride severely bums skin, eyes, and mucous membranes. Contaminated clothing must be removed immediately. Vapors from minor inhalation exposure can cause delayed onset of severe respiratory symptoms after 2—24 h, depending on the degree of exposure. Delayed, massive, or acute pulmonary edema and death can develop as consequences of inhalation exposure. 

Health nd Safety Factors. Thionyl chloride is a reactive acid chloride which can cause severe bums to the skin and eyes and acute respiratory tract injury upon vapor inhalation. The hydrolysis products, ie, hydrogen chloride and sulfur dioxide, are beheved to be the primary irritants. Depending on the extent of inhalation exposure, symptoms can range from coughing to pulmonary edema (182). The LC q (rat, inhalation) is 500 ppm (1 h), the DOT label is Corrosive, Poison, and the OSHA PEL is 1 ppm (183). The safety aspects of lithium batteries (qv) containing thionyl chloride have been reviewed (184,185). 

Although a number of studies have reported the effects of inhalation exposure to methyl parathion in humans, no inhalation MRLs were derived based on human data because of the lack of adequate quantitative exposure information. Animal data were also insufficient to support the derivation of an acute-, intermediate-, or chronic-duration inhalation MRL. 

No studies were located regarding gastrointestinal, hematological, musculoskeletal, or dermal effects in humans or animals after inhalation exposure to methyl parathion. Dean et al. (1984) reported that seven children exposed to methyl parathion by many routes exhibited pinpoint pupils, abdominal pain, and diarrhea. The respiratory, cardiovascular, hepatic, and renal effects reported by Fazekas (1971) that were found in humans acutely exposed to methyl parathion intoxication resulted from exposure by all three routes however, the results did not distinguish between the routes. 

George J, Andrade C, Joseph T. 1992. Delayed effects of acute oral and chronic inhalational exposure to methyl parathion on learning and memory in rats. Indian J Exp Biol 30 819-822. 

Where sufficient toxicologic information is available, we have derived minimal risk levels (MRLs) for inhalation and oral routes of entry at each duration of exposure (acute, intermediate, and chronic). These MRLs are not meant to support regulatory action but to acquaint health professionals with exposure levels at which adverse health effects are not expected to occur in humans. They should help physicians and public health officials determine the safety of a community living near a chemical emission, given the concentration of a contaminant in air or the estimated daily dose in water. MRLs are based largely on toxicological studies in animals and on reports of human occupational exposure. 

There have been no reports of renal toxicity associated with acute inhalation exposure to endosulfan in laboratory animals. However, acute oral and dermal exposure to endosulfan has been reported to cause damage to the kidneys of rats, rabbits, and dogs (FMC 1958, 1980a Gupta and Chandra 1975 Hoechst... 

An MRL of 2 ppm was derived for acute inhalation exposure (14 days or less) to trichloroethylene. 

Cardiovascular Effects. Chronic cardiovascular disease has not been reported in workers occupationally exposed to low levels of trichloroethylene (El Ghawabi et al. 1973), although deaths following acute high-level inhalation exposures to trichloroethylene have been attributed to cardiac arrhythmias. Case studies have described cardiac arrhythmias that in some instances led to death after occupational exposure (Bell 1951 Kleinfeld and Tabershaw 1954 Smith 1966), poisoning (Dhuner et al. 1957 Gutch et al. 1965), or... 

Gastrointestinal Effects. Case reports indicate that acute inhalation exposure to trichloroethylene results in nausea and vomiting (Buxton and Hayward 1967 Clearfield 1970 David et al. 1989 DeFalque 1961 Gutch et al. 1965 Milby 1968). Anorexia, nausea, vomiting, and intolerance to fatty foods have also been reported after chronic occupational exposure to trichloroethylene (El Ghawabi et al. 1973 Schattner and Malnick 1990 Smith 1966). Trichloroethylene-induced efiects on the autonomic nervous system may contribute to these effects (Grandjean et al. 1955). Some of the people exposed to trichloroethylene and other chlorinated... 

Dermal Effects. Some humans experienced dry throats following acute inhalation exposure to trichloroethylene at 200 ppm (Stewart et al. 1970). Persons working with trichloroethylene for intermediate periods sometimes develop skin rashes and dermatitis (Bauer and Rabens 1974 El Ghawabi et al. 1973). It is reported that some people may be particularly sensitive to trichloroethylene and develop allergies when exposed to high levels in the air or on their skin during oeeupational exposures of intermediate duration (Cziijak et al. 1993 Goh and Ng 1988 Nakayama et al. 1988 Phoon et al. 1984). Exposure to... 

Further information gained from accidental human exposures could be utilized in defining the lowest air level that affects humans. Similarly, studies on the acute effects of dermal exposure to trichloroethylene in animals may be useful in determining the risk for these exposures in humans at hazardous waste sites. However, there appear to be sufficient data available on neurological effects after acute inhalation exposure. 

Siegel J, Jones RA, Coon RA, et al. 1971. Effects on experimental animals of acute, repeated, and continuous inhalation exposures to dichloroacetylene mixtures. Toxicol Appl Pharmacol 18 168-174. 

Renal Effects. Animal studies indicate that degenerative changes in the kidneys may result from acute inhalation exposure to 241 Am. Repeated intraperitoneal injection of241 Am resulted in histopathologic changes in the kidneys of rats. 

No reports were located regarding death in humans resulting from acute-, intermediate-, or chronic-duration inhalation exposure to americium. 

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