Acute Inhalation

100-2(b)(8), Subpart A, and paragraphs (b)(3) and (b)(4) of this section, the test report must include the following  

CPSC does not provide a detailed guideline for inhalation testing. Their classification definitions are as follows. 

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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. 

The Du Pont HaskeU Laboratory for Toxicology and Industrial Medicine has conducted a study to determine the acute inhalation toxicity of fumes evolved from Tefzel fluoropolymers when heated at elevated temperatures. Rats were exposed to decomposition products of Tefzel for 4 h at various temperatures. The approximate lethal temperature (ALT) for Tefzel resins was deterrnined to be 335—350°C. AH rats survived exposure to pyrolysis products from Tefzel heated to 300°C for this time period. At the ALT level, death was from pulmonary edema carbon monoxide poisoning was probably a contributing factor. Hydrolyzable fluoride was present in the pyrolysis products, with concentration dependent on temperature. 

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). 

Health and Safety Factors. VDE is a flammable gas its combustion products are toxic. Liquid VDE on contact with the skin can cause frostbite. Acute inhalation toxicity of VDE is low median lethal concentrations (LC q) for rats were 128,000 ppm after a single 4-h exposure (52) and 800,000 ppm after a 30-min exposure (53). Cumulative toxicity is low exposure of rats and mice at levels of up to 50,000 ppm for 90 days did not cause any... 

Toxicity of Chlorine Sanitizers. Chlorine-based swimming-pool and spa and hot-tub sanitizers irritate eyes, skin, and mucous membranes and must be handled with extreme care. The toxicities are as follows for chlorine gas, TLV = 1 ppm acute inhalation LC q = 137 ppm for 1 h (mouse) (75). The acute oral LD q (rats) for the Hquid and soHd chlorine sanitizers are NaOCl (100% basis) 8.9 g/kg (76), 65% Ca(OCl)2 850 mg/kg, sodium dichloroisocyanurate dihydrate 735 mg/kg, and trichloroisocyanuric acid 490 mg/kg. Cyanuric acid is essentially nontoxic based on an oral LD q > 20 g/kg in rabbits. Although, it is mildly irritating to the eye, it is not a skin irritant. A review of the toxicological studies on cyanuric acid and its chlorinated derivatives is given in ref. 77. 

Sterner W, Chibanguza G (1976) Acute inhalation toxicity of dibutyltin dichloride in rats, internationai Bio-Research, inc., March. 

Although methods have been established to derive these levels (Barnes and Dourson 1988 EPA 1990c), uncertainties are associated with these techniques. Furthermore, ATSDR acknowledges additional uncertainties inherent in the application of the procedures to derive less than lifetime MRLs. As an example, acute inhalation MRLs may not be protective for health effects that are delayed in development or are acquired following repeated acute insults, such as h q)ersensitivity reactions, asthma, or chronic bronchitis. As these kinds of health effects data become available and methods to assess levels of significant human exposure improve, these MRLs will be revised. 

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... 

The data in animals are insufficient to derive an acute inhalation MRL because serious effects were observed at the lowest dose tested (Hoechst 1983a). No acute oral MRL was derived for the same reason. The available toxicokinetic data are not adequate to predict the behavior of endosulfan across routes of exposure. However, the limited toxicity information available does indicate that similar effects are observed (i.e., death, neurotoxicity) in both animals and humans across all routes of exposure, but the concentrations that cause these effects may not be predictable for all routes. Most of the acute effects of endosulfan have been well characterized following exposure via the inhalation, oral, and dermal routes in experimental animals, and additional information on the acute effects of endosulfan does not appear necessary. However, further well conducted developmental studies may clarify whether this chemical causes adverse developmental effects. 

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

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. 

Methods for Reducing Toxic Effects. The general recommendations for reducing the absorption of trichloroethylene following acute inhalation (HSDB 1994), oral (D Souza et al. 1985 Withey et al. 1983), dermal, or ocular (HSDB 1994) exposure are well established and have a proven efficacy. No additional investigations are considered necessary at this time. 

Kostrzewski P, Jakubowski M, Kolacinski Z. 1993. Kinetics of trichloroethylene elimination from venous blood after acute inhalation poisoning. Clin Toxicol 31 353-363. 

Villaschi S, Giovanetti A, Lombardi CC, et al. 1991. Damage and repair of mouse bronchial epithelium following acute inhalation of trichloroethylene. Exp Limg Res 15 601-614. 

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. 

Hammond SE, Lagerquist CR, Mann JR. 1968. Americium and plutonium urine excretion following acute inhalation exposure to high-fired oxides. Am Ind Hyg Assoc J 29(2) 169-172. 

No endocrine effects were seen in acute inhalation exposure to a triaryl phosphate mixture (Cellulube 220) for rabbits at 2,000 mg/m3 (Carpenter et al. 1959). In studies on rats, hamsters and rabbits no endocrine... 

Acute inhalation exposure to aerosols of certain polyalphaolefin hydraulic fluids produced death in rats associated with respiratory tract irritation, while aerosols of other polyalphaolefin hydraulic fluids produced no apparent respiratory tract irritation or deaths (MacEwen and Vemot 1983 Kinkead et al. 1987b, 1992b). The mechanism by which certain polyalphaolefin fluids may produce respiratory tract irritation is not understood. 

Available data are restricted to acute lethality studies in rats exposed to four water-in-oil emulsion hydraulic fluids or a mineral oil hydraulic fluid for 4—6 hours. No deaths or body weight alterations occurred at exposure concentrations ranging from 180 to 210 mg/m3 for the water-in-oil fluids and 1,130 mg/m3 for the mineral oil fluid. The data are inadequate for acute inhalation MRL derivation. No data regarding intermediate or chronic inhalation exposure to mineral oil hydraulic fluids were located. 

No NOAELs or LOAELs were identified for toxic effects in humans after inhalation exposure to organophosphate ester hydraulic fluids. Reliable NOAELs and LOAELs for acute inhalation exposure are restricted to 4-hour NOAELs for systemic effects in rats exposed to Fyrquel 220 or Durad MP280 and 4-hour LOAELs for mild lethargy in rats exposed to Durad MP280 and Fyrquel 220 (Gaworski et al. 1986). The study identifying these NOAEL and LOAEL values did not measure cholinesterase inhibition, did not allow sufficient follow-up time for the development of delayed neurotoxic effects, and used a... 

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