Phosgene human

Toxicity. Sulfur tetrafluoride has an inhalation toxicity comparable to phosgene. The current OSHA standard maximum allowable concentration for human exposure in air is 0.4 mg/m (TWA) (54). On exposure to moisture, eg, on the surface of skin, sulfur tetrafluoride Hberates hydrofluoric acid and care must be taken to avoid bums. One case of accidental exposure of electrical workers to decomposed SF gas containing SF has been cited (108). 

Highly toxic perfluoroisobutylene (PFIB) poses a serious health hazard to the human respiratory tract. PFIB is a thermal decomposition of polytetrafluo-roethylene (PTFE), e.g., Teflon. PFIB is approximately lOx as toxic as phosgene. Inhalation of this gas can cause pulmonary edema, which can lead to death. PFIB is included in Schedule 2 of the Chemical Weapons Convention (CWC), the aim of the inclusion of chemicals such as PFIB was to cover those chemicals, which would pose a high risk to the CWC. 

Lethal human toxicity values have not been established or have not been published. However, based on available information, this material appears to have approximately the same toxicity as Phosgene (C10-A003). 

Industrial Agents Chemicals manufactured for industrial purposes rather than to specifically kill or maim human beings. Hydrogen cyanide, cyanogen chloride, phosgene, and chloropicrin are industrial chemicals that can be military agents as well AC, CK, CG, and PS. Many herbicides and pesticides are industrial chemicals that also can be chemical agents. 

The 30-min and 1-, 4-, and 8-h AEGL-3 values were based on the highest concentration causing no mortality in the rat after a 30-min exposure (15 ppm) (Zwart et al. 1990). A UF of 3 was applied for interspecies extrapolation because little species variability is observed for lethal and nonlethal end points after exposure to phosgene. A UF of 3 was applied to account for sensitive human subpopulations due to the steep concentration-response curve and... 

Diller and Zante (1982) performed an extensive literature review concerning human phosgene exposure, and found that a great majority of data were... 

TABLE 1-3 Effect of Phosgene Exposure in Healthy Humans... 

In their literature review, Diller and Zante (1982) also identified nonlethal effects from phosgene exposure (lethal effects are described in Section 2.1). Nonlethal information synthesized from this review is presented in Table 1-4. From the above data and from animal data for initial lung damage, Diller and Zante (1982) synthesized information for nonlethal effects of phosgene in humans (Table 1-5). 

TABLE 1-4 Acute Irritative Effects of Phosgene Exposure in Humans... 

Developmental and reproductive studies regarding acute human exposure to phosgene were not available. 

IDLH (immediately dangerous to life and health) (NIOSH 1997) represents the maximum concentration from which one could escape within 30 min without any escapeimpairing symptoms or any irreversible health effects. The IDLH for phosgene is based on acute inhalation toxicity data in humans (Diller 1978). 

Galdston, M., Leutscher, J.A., Longcope, W.T., et. al. 1947a. A study of the residual effects of phosgene poisoning in human subjects I. After acute exposure. J. Clin. Invest. 26 145-168. 

The metabolism of chloroform is well understood. Approximately 50% of an oral dose of 0.5 grams of chloroform was metabolized to carbon dioxide in humans (Fry et al. 1972). Metabolism was dose-dependent, decreasing with higher exposure. A first-pass effect was observed after oral exposure (Chiou 1975). Approximately 38% of the dose was converted in the liver, and < 17% was exhaled unchanged from the lungs before reaching the systemic circulation. On the basis of pharmacokinetic results obtained in rats and mice exposed to chloroform by inhalation, and of enzymatic studies in human tissues in vitro, in vivo metabolic rate constants (V, 3,C =15.7 mg/hour/kg, = 0.448 mg/L) were defined for humans (Corley et al. 1990). The metabolic activation of chloroform to its toxic intermediate, phosgene, was slower in humans than in rodents. 

As discussed in Section 2.3.3, the mechanism of chloroform-induced liver toxicity may involve metabolism to the reactive intermediate, phosgene, which binds to lipids and proteins of the endoplasmic reticulum, lipid peroxidation, or depletion of GSH by reactive intermediates. Because liver toxicity has been observed in humans exposed to chloroform levels as low as 2 ppm in the workplace and in several animal species after inhalation and oral exposure, it is possible that liver effects could occur in humans exposed to environmental levels, to levels in drinking water, or to levels found at hazardous waste sites. 

Chloroform is not stored to any appreciable extent in the human body and is mostly metabolized to phosgene and eventually COj (see Section 2.3) however, some chloroform may be stored in fat depots in... 

---