Vapors, inhalation exposure

Indene vapor inhalation exposure of human subjects has not been reported. By analogy to related hydrocarbons, inhalation of indene can be expected to cause irritation of the mucous membranes. 

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). 

Exposure occurs almost exclusively by vapor inhalation, which is followed by rapid absorption into the bloodstream. At concentrations of 150—186 ppm, 51—70% of the trichloroethylene inhaled is absorbed. MetaboHc breakdown occurs by oxidation to chloral hydrate [302-17-OJ, followed by reduction to trichloroethanol [115-20-8] part of which is further oxidized to trichloroacetic acid [76-03-9] (35—37). Absorbed trichloroethylene that is not metabolized is eventually eliminated through the lungs (38). The OSHA permissible exposure limit (PEL) eight-hour TWA concentration has been set at 50 ppm for eight-hour exposure (33). 

Exposure to tetrachloroethylene as a result of vapor inhalation is foUowed by absorption into the bloodstream. It is partly excreted unchanged by the lungs (17,18). Approximately 20% of the absorbed material is subsequently metabolized and eliminated through the kidneys (27—29). MetaboHc breakdown occurs by oxidation to trichloroacetic acid and oxaHc acid. 

Polymers. Studies to determine possible exposure of workers to residual epichl orohydrin and ethylene oxide monomers in the polymers have been done. Tests of warehouse air where Hydrin H and Hydrin C are stored showed epichl orohydrin levels below 0.5 ppm. Air samples taken above laboratory mixing equipment (Banbury mixer and 6" x 12" mill) when compounds of Hydrin H or C were mixed gave epichl orohydrin levels below detectable limits, and ethylene oxide levels less than 0.2 ppm, well below permissible exposure limits (46). A subacute vapor inhalation toxicity study in which animals were exposed to emission products from compounded Parel 58 suggests that no significant health effects would be expected in workers periodically exposed to these vapors (47). 

Toxicity. Low toxicity from solvent-vapor inhalation or skin contac t is preferred because of potential exposure during repair of equipment or while connections are being broken after a solvent transfer. Also, low toxicity to fish and bioorganisms is preferred when extraction is used as a pretreatment for wastewater before it enters a biotreatment plant and with final effluent discharge to a stream or lake. Often solvent toxicity is low if water solubility is high. 

Ocular Effects. Some humans experienced mild eye irritation following acute inhalation exposure to trichloroethylene at 200 ppm (Stewart et al. 1970). Itchy watery eyes (Baure and Rabens 1974 El Ghawabi et al. 1973) and inflamed eyes (Schattner and Malnick 1990) have been reported following contact with trichloroethylene vapor. 

Troop exposure to these materials could result from leaking DF containers, accidents that disrupt packaging, spills at production or storage facilities, or accidents during transport. Because DF and DC are relatively volatile compounds, the primary route of exposure is expected to be the respiratory system. However, ingestion also results from inhalation exposures in animals and could occur in humans. DF and DC vapors have a pungent odor and may cause severe and painful irritation of the eyes, nose, throat, and lungs. Data provided are for DF only, DC has similar properties. 

A skin redness reported in experimental animals (rats, rabbits, cats and monkeys) after inhalation exposure to acrylonitrile may be due to a vasodilatory effect, rather than a direct irritant action (Ahmed and Patel 1981). Guinea pigs, which do not exhibit the cyanide-type effects of acrylonitrile poisoning (see Section 2.2.1.4), were observed to have nose and eye irritation from the acrylonitrile vapors (Dudley and Neal 1942). 

During occupational exposure, respiratory absorption of soluble and insoluble nickel compounds is the major route of entry, with gastrointestinal absorption secondary (WHO 1991). Inhalation exposure studies of nickel in humans and test animals show that nickel localizes in the lungs, with much lower levels in liver and kidneys (USPHS 1993). About half the inhaled nickel is deposited on bronchial mucosa and swept upward in mucous to be swallowed about 25% of the inhaled nickel is deposited in the pulmonary parenchyma (NAS 1975). The relative amount of inhaled nickel absorbed from the pulmonary tract is dependent on the chemical and physical properties of the nickel compound (USEPA 1986). Pulmonary absorption into the blood is greatest for nickel carbonyl vapor about half the inhaled amount is absorbed (USEPA 1980). Nickel in particulate matter is absorbed from the pulmonary tract to a lesser degree than nickel carbonyl however, smaller particles are absorbed more readily than larger ones (USEPA 1980). Large nickel particles (>2 pm in diameter) are deposited in the upper respiratory tract smaller particles tend to enter the lower respiratory tract. In humans, 35% of the inhaled nickel is absorbed into the blood from the respiratory tract the remainder is either swallowed or expectorated. Soluble nickel compounds... 

Inhalation exposure route, HCN vapor, in mg/m3, for various periods ... 

Toluene Clear, colorless liquid with a slight fire hazard and moderate explosion hazard. Entry into the body is mostly by vapor inhalation. Acute and chronic exposures occur with concentrations greater than 200 ppm. Irritant to skin and eyes. 

Bruner, R.H., et al., The toxicologic and oncogenic potential of JP-4 jet fuel vapors in rats and mice 12-month intermittent inhalation exposures, Fundam. Appl. Toxicol., 20, 97, 1993. 

Neurotoxicity. No information is available on neurotoxic effects of hexachloroethane in humans following any route of exposure. Acute inhalation exposure in rats caused staggering gait after exposure to high concentrations (5,900 ppm) (Weeks et al. 1979). The usefulness of this data is limited since this concentration was lethal. Tremors have been reported at 260 ppm but not 48 ppm following inhalation exposure of rats in a developmental study and in a study of 6-weeks duration (Weeks et al. 1979). The lack of tremors at 48 ppm in the developmental study serves as the basis for the acute inhalation MRL, and the lack of tremors at 48 ppm in the 6-week study serves as the basis for the intermediate inhalation MRL. One study that evaluated spontaneous motor activity and avoidance behavior in rats during 6 weeks of exposure to 260 ppm hexachloroethane vapors did not reveal adverse effects of hexachloroethane on these neurobehavioral functions (Weeks et al. 1979). 

Nerve agent intoxication requires rapid decontamination to prevent further absorption by the patient and to prevent exposure to others, ventilation when necessary, administration of antidotes, as well as supportive therapy. Skin decontamination is not necessary with exposure to vapor alone, but clothing should be removed to get rid of any trapped vapor. With nerve agents, there can be high airway resistance due to bronchoconstric-tion and secretions, and initial ventilation is often difficult. The restriction will decrease with atropine administration. Copious secretions which maybe thickened by atropine also impede ventilatory actions and will require frequent suctioning. For inhalation exposure to nerve agents, ventilation support is essential. 

The vapor pressures of the three components of Otto Fuel II differ considerably. During vapor generation studies with Otto Fuel II, PGDN was the only component vaporized into inhalation exposure chambers in sufficient quantity to allow direct analysis (Stewart et al. 1974 MacEwen and Vemot 1982). In light of the low toxicity of dibutyl sebacate and 2-nitrodiphenylamine and the fact that they do not vaporize to a detectable extent at test compound generation temperatures up to 45°C, the toxicity of Otto Fuel II has been evaluated in terms of PGDN. Chemical and physical data for PGDN are listed in Table 2-2. 

Ocular Effects. Histopathological examination of the eye and optic nerve after intermediate-duration inhalation exposure revealed no treatment-related lesions in male Sprague-Dawley rats exposed to 500 ppm M-hexanc 22 hours a day for 6 months (IRDC 1981) or in Fischer 344 rats of both sexes exposed to up to 10,000 ppm for 6 hours a day, 5 days a week for 13 weeks (Cavender et al. 1984). Effects caused by direct contact of -hexane vapor with the eye are discussed in Section 2.2.3 (Dermal Exposure). 

Acute inhalation toxicity To determine the potential acute toxicity-lethality following a single 4-h inhalation exposure to a test atmosphere containing the new pharmaceutical excipient (aerosol, vapor or particles)... 

The available information suggests that exposure to di-w-octylphthalate may adversely affect immune function in individuals living in the vicinity of hazardous waste sites if the individuals ingest sufficiently high levels. Because of its low vapor pressure, exposure to high levels of di-w-octylphthalate by inhalation is not likely. 

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