period of time (i.e., years), or it may consist of an induction phase precipitated by a relatively high concentration followed by a challenge phase in which sensitized individuals react to extremely low concentrations of TDI. Only irritation effects were considered in establishing AEGL values, because sensitized individuals are considered to be hypersusceptible. Although individuals with existing TDI sensitization are present in the general population, that presensitization cannot be estimated. If the number of individuals sensitized to TDI in the general population were quantifiable, a different approach to derivation of AEGL values might have been considered. At any of the AEGL levels, there might be individuals who have a strong reaction to TDI, and those individuals might not be protected within the definition of effects for each level.

Human data were available for the derivation of AEGL-1 and AEGL-2. Fifteen asthmatic subjects were exposed to TDI at 0.01 parts per million (ppm) for 1 hour (h), and then after a rest of 45 minutes (min), they were exposed at 0.02 ppm for 1 h. A nonasthmatic referent group of 10 individuals was exposed at 0.02 ppm for 2 h (Baur 1985). None of the individuals had a history of isocyanate exposure, and the asthmatic subjects were not sensitized to TDI. Although no statistically significant differences in lung function parameters were observed among asthmatic subjects during or after exposure, nonpathological bronchial obstruction was indicated in several individuals. In the referent group, there was a significant increase in airway resistance immediately and at 30 min after the initiation of exposure, but none of the subjects developed bronchial obstruction. Both groups reported eye and throat irritation, cough, chest tightness, rhinitis, dyspnea, and/or headache, but time to onset of symptoms was not given. There was also no indication whether symptoms were more severe in asthmatic subjects that inhaled 0.01 or 0.02 ppm. Therefore, the 0.02-ppm concentration was identified as the basis for the 10-min, 30-min, and 1-h AEGL-1 values. The 0.01-ppm concentration was identified as the basis for the 4- and 8-h AEGL-1 values. It should be noted that the AEGL-1 values are below a reported odor detection threshold of 0.05 ppm (Henschler et al. 1962).

Derivation of AEGL-2 was based on human data. Exposure of volunteers to TDI at 0.5 ppm for 30 min resulted in severe eye and throat irritation and lacrimation (Henschler et al. 1962). A higher exposure concentration was intolerable. Extrapolations were made using the equation Cn×t =k (C=concentration, t=time, and k is a constant), where n ranges from 0.8 to 3.5 (ten Berge et al. 1986). In the absence of an empirically derived, chemical-specific exponent, scaling was performed using n=3 for extrapolating to the 10-min time point and n=1 for the 1-h and 4-h time points.



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