Inhalational exposure

Announce. Index 12, 9—12 (1981). [A 121-page review of health effects Hterature primarily related to inhalation exposure.]... 

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. 

Toxicity. Lethality is the primary ha2ard of phosphine exposure. Phosphine may be fatal if inhaled, swallowed, or absorbed through skin. AH phosphine-related effects seen at sublethal inhalation exposure concentrations are relatively small and completely reversible. The symptoms of sublethal phosphine inhalation exposure include headache, weakness, fatigue, di22iness, and tightness of the chest. Convulsions may be observed prior to death in response to high levels of phosphine inhalation. Some data are given in Table 2. 

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. 

Vapor Toxicity. Laboratory exposure data indicate that vapor inhalation of alkan olamines presents low hazards at ordinary temperatures (generally, alkan olamines have low vapor pressures). Heated material may cause generation of sufficient vapors to cause adverse effects, including eye and nose irritation. If inhalation exposure is likely, approved respirators are suggested. Monoethan olamine and diethanolamine have OSHA TLVs of 3 ppm. 

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). 

Inhalation exposure to high concentrations of ethylene oxide has been reported to result in respiratory system irritation and edema (236). 

Biologieal exposure indiees (BEI) published by the ACGIH are given in Table 5.13. BEIs represent the levels of determinant whieh are most likely to be observed in speeimens eolleeted from a healthy worker who has been exposed to ehemieals to the same extent as a worker with inhalation exposure to the TLV. Due to biologieal variability it is possible for an individual s measurements to exeeed the BEI without ineuning inereased health risk. If, however, levels in speeimens obtained from a worker on different oeeasions persistently exeeed the BEI, or if the majority of levels in speeimens obtained from a group of workers at the same workplaee exeeed the BEI, the eause of the exeessive values must be investigated and proper aetion taken to reduee the exposure. 

Stripping of these compounds which can then be concentrated by adsorption on activated carbon for subsequent disposal. From a safety standpoint, if a volatile hazardous chemical is spilled, the concern over inhalation exposure may warrant the need for respirators. 

Outdoor inhalation exposure is mainly due to traffic, energy production, heating, and natural factors such as pollen and mineral dusts. These outdoor sources of pollution also affect indoor air quality. The indoor concentration is typically 20-70% of the corresponding outdoor concentration. Occasionally the indoor concentrations of an external pollutant (especially radon) may even exceed the concentrations outdoors. ... 

MMT, monomethyltin DMT, dimethyltin MBT, monobutyltin DBT, dibutyltin TBT, tributyltin MOT, monooctyltin DOT, dioctyltin Exposure via house dust (which has been measured as containing organotins) was also considered it is likely that inhalation exposure indoors includes house dust, which picks up leached organotins from vinyl flooring. 

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. 

No studies were located regarding hepatic effects in animals atter inhalation exposure to methyl parathion. 

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