@article{ref1,
title="Morbidity and mortality resulting from acute inhalation exposures to hydrogen fluoride and carbonyl fluoride in rats",
journal="Inhalation toxicology",
year="2018",
author="Januszkiewicz, Adolph J. and Bazar, Matthew A. and Crouse, Lee C. B. and Chapman, Michael A. and Hodges, Steven E. and McCormick, Steven J. and O'Neill, Arthur J.",
volume="30",
number="3",
pages="114-123",
abstract="OBJECTIVE: Experiments were undertaken to compare morbidity and mortality from brief inhalation exposures to high levels of hydrogen fluoride (HF) and carbonyl fluoride (COF<sub>2</sub>). <br><br>METHODS: Rats from both sexes were exposed for durations of 5 and 10 min to nominal concentrations of 10,000 to 57,000 ppm HF or 500 to 10,000 ppm COF<sub>2</sub>. Respiration was monitored before, during, and after exposure. Animals were observed up to 6 days post-exposure. Terminal blood samples were collected for routine clinical chemistry and hematology. Post-mortem lung fluoride concentrations and lung weights were measured, and gross pathology noted. <br><br>RESULTS: Both gases produced respiratory depression independent of concentration or exposure duration with minute ventilation decreasing to approximately 50% of baseline. Estimated mixed-gender HF and COF<sub>2</sub> 10-min LC<sub>50</sub>'s were 48,661 ppm and 1083 ppm, respectively. HF mortalities were generally delayed 3 to 4 days post-exposure, while COF<sub>2</sub> mortalities occurred during or briefly after exposure. Lung fluoride levels increased with COF<sub>2</sub> dose, though elevated lung weights occurred only at the mid-level exposures. Lung weights were unaffected in the HF-exposed animals, and their lung fluoride concentrations were variable. Clinical chemistry and hematology had few consistent trends with the exception of hemoconcentration primarily in HF-exposed males. These short-term exposure experiments conclude that COF<sub>2</sub> is nearly 45 times more lethal than HF in rats. <br><br>CONCLUSIONS: These experiments suggest that hydrolysis to HF cannot solely explain COF<sub>2</sub> toxicity. Although HF and COF<sub>2</sub> may have common injury mechanisms, they are expressed to markedly different degrees and temporal occurrence.<p /> <p>Language: en</p>",
language="en",
issn="0895-8378",
doi="10.1080/08958378.2018.1465494",
url="http://dx.doi.org/10.1080/08958378.2018.1465494"
}