drides, and as a doping gas in the semiconductor industry. Diborane was also investigated in the 1950s as a potential rocket fuel.
Data on acute exposures of humans to diborane were limited to case reports of accidental work-related exposures. Signs and symptoms of exposure included chest tightness, shortness of breath and dyspnea, wheezing, nonproductive cough, and precordial pain. Workers exposed to diborane generally experienced a complete recovery within a short period following cessation of exposure. No quantitative information was given regarding the exposure terms of these individuals, and the data were therefore unsuitable for derivation of AEGLs. No reports of human fatalities after diborane exposure were found in the literature. Reported odor thresholds range from 1.8 parts per million (ppm) to 3.6 ppm.
Data on lethal and nonlethal consequences of diborane exposure were available for several animal species, including dogs, rats, mice, hamsters, rabbits, and guinea pigs. Fifteen-minute LC50 values in rats ranged from 159 ppm to 182 ppm, and 4-hour (h) LC50 values ranged from 40 ppm to 80 ppm in rats and 29 ppm to 31.5 ppm in mice. Animals exposed to lethal and nonlethal concentrations developed pulmonary hemorrhage, congestion, and edema, and death was related to these severe pulmonary changes. Recent studies in rats and mice have also uncovered the development of multifocal and/or diffuse inflammatory epithelial degeneration in the bronchioles following exposure to diborane. These pulmonary changes produced by exposure to nonlethal concentrations were completely reversible in rats by 2 weeks (wk) after an acute exposure and were being repaired in the mouse by 2 wk postexposure. The signs of toxicity and repair of pulmonary lesions following acute exposure to nonlethal concentrations in animals were similar to the human case reports. It is likely that the mechanism of toxicity is due to direct interaction of diborane with cellular components, especially because diborane is such a potent reducer. There appears to be a similar mechanism of toxicity among species, because the cause of death from diborane exposure has always been from pulmonary damage, including edema, hemorrhage, and congestion. Mice appeared to be the more sensitive species, and the mice data were therefore used for the derivations of AEGLs.
An AEGL-1 value was not recommended because the AEGL-2 value is below the odor threshold of diborane and no other data pertaining to end points relevant to AEGL-1 definition were available. Absence of an AEGL-1 does not imply that exposure below the AEGL-2 is without adverse effects.