subjects in the study of D’Alessandro et al. (1996). That NOAEL supports the choice of 0.5 ppm in the study of Rotman et al. (1983). In fact, the single exercising atopic subject proved to be more sensitive at 0.5 ppm, as indicated by asymptomatic changes in pulmonary function parameters, than were the non-exercising asthmatics exposed at 0.4 ppm.

Because subjects identified as most susceptible to the irritant effects of chlorine were tested (atopic and asthmatic individuals), an intraspecies uncertainty factor (UF) of 1 was applied. The intraspecies UF of 1 is also supported by the fact that bronchoconstriction is induced in pediatric and adult asthmatic subjects at similar levels of challenge (Avital et al. 1991). Therefore, an additional UF to protect pediatric asthmatic subjects is not necessary. Time-scaling was not applied to the AEGL-1 for several reasons. The study conducted by Rotman et al. (1983) actually lasted more than 8 h (two 4-h sessions with a 1-h break between). That reduces the uncertainty usually associated with scaling from shorter to longer time periods. Because effects were not increased following an interrupted 8 h of exposure at 0.5 ppm in the susceptible individual, the 8-h AEGL-1 was also set at 0.5 ppm. The use of the same value across all exposure durations is supported by the fact that the response to the irritant effects of chlorine appears to be concentration-dependent rather than time-dependent. Calculations are presented in Appendix A; results are presented in Table 1–6. Figure 1–1 is a plot of the derived AEGL values and all of the human and animal data on chlorine.

The studies by Joosting and Verberk (1974), Anglen (1981), Rotman et al. (1983), and D’Alessandro et al. (1996) address sensory irritant effects in humans as well as differences in pulmonary function tests during exposures at 1.0 ppm for up to 8 h and 2.0 ppm and 4.0 ppm for 4 h. As previously noted, Rotman et al. (1983) used an exercising atopic individual, and D’Alessandro et al. (1996) used five subjects with nonspecific airway hyper-reactivity, three of which had clinical histories of asthma. For healthy individuals, the concentrations tested by Rotman et al. (1983) and D’Alessandro et al. (1996) resulted in effects below the definition of the AEGL-2. However, in one atopic subject, the 1-ppm concentration for