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oxidation of tissues, thermal damage from the heat of oxidation, and the effects of HF formed (Cloyd and Murphy, 1965).

In the only documented human exposure, a worker was exposed to the effluent of a chlorine trifluoride-charcoal reactor when he was eating lunch approximately 200 ft downwind from the disposal system. The exposure lasted about 1–2 min. He reported to the medical clinic with symptoms of frontal headache, a bad taste, abdominal pain, and breathing difficulty that persisted for some 2 h. A physician treated him with oxygen therapy for 0.5 h and with APCs (a mixture of aspirin, phenacetin, and caffeine) and the symptoms were relieved. No systemic or local effects were found. The patient reported for work the next day, with no apparent after-effects except fatigue (Longley et al., 1965).


Rats exposed in a dynamic-flow chamber to chlorine trifluoride at 400 ppm died within 40 min; at 800 ppm, the LT50 (lethal time for 50% of the animals) was 15 min. Inhalation exposure of rats at 800 ppm for 15 min was always lethal, whereas exposure at 400 ppm was usually lethal after 35 min of exposure (Dost et al., 1974). In another experiment, 1-h exposure to chlorine trifluoride led to LC50s of 299 (260–344) ppm in male rats and 178 (169–187) ppm in mice (Vernot et al., 1977).

In extensively described experiments, rats were exposed at 480, 96, and 21 ppm; two dogs were also exposed at 21 ppm (Horn and Weir, 1955). The LT50 at 480 ppm was 40 min; at 96 ppm, it was 3.7 h. At 480 ppm, the rats immediately exhibited increased activity. After 2 min, rhinorrhea was noted. From then on, symptoms of respiratory difficulty, eye irritation, and excessive salivation developed. Within 20 min, all were in “acute distress.” In several rats, the cornea looked dull and milky-white where it was not protected by the eyelid. All rats died within 70 min; death was usually preceded by excitement and occasionally by convulsions and coma. The same signs developed, at a lower rate, in the rats exposed at 96 ppm. After 4.5 h of exposure, 70% of the animals were dead. Shortly after the survivors were removed from the chamber, two more died (total mortality, 80%). Some showed excitement and “tonic movements” before death. The gross pathology of the lungs from the animals exposed at 480 and 96 ppm was the same: emphysema, pulmonary edema, vascular congestion, and fusion of the lining cells of the bronchi into a hyaline membrane. The livers exhibited hydropic degeneration and marked vascular congestion. In the 96-ppm group, only the gastrointestinal tract was markedly distended with gas.

Rats and dogs were exposed at 21 ppm 6 h/d for 2 d. About 10 min after exposure began, the dogs had rhinorrhea and lacrimation and kept their eyes tightly closed. During the first day, they coughed up mucous material and had rapid respiration and excessive salivation. When removed from the chamber, they refused to eat or drink, and they kept their eyes tightly closed. The conjunctivae were markedly injected. The animals’ fur felt as though it had been “singed.” Toxic signs also appeared early in the rats, with preening and rhinorrhea. By the end of the first day, rhinorrhea and lacrimation

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