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temporary lung-function impairment, which cleared, with no residual lung damage, after 1 mo. Fourteen to sixteen hours after exposure, patients were symptomatic, with cough, chest tightness, and shortness of breath. All had restrictive ventilating defects with impaired diffusing capacity and evidence of obstruction of small airways (Ploysongsang et al., 1982).

Results from a study sponsored by the Chlorine Institute (Rotman et al., 1983) indicate that an 8-h exposure of humans to chlorine at 1 ppm resulted in sensory irritation and changes in pulmonary functions. The literature on the health effects of chlorine has recently been reviewed (National Research Council, 1975).

Data published on airborne exposures of humans to chlorine are summarized in Table 2.


Barrow and Smith (1975) and Barrow et al. (1977) demonstrated that chlorine exposure caused alterations of pulmonary function in rabbits and reduced respiratory rate in mice. The concentration of chlorine to which exposure for 10 min was required to decrease respiratory rate in mice by 50% (RD50) was about 10 ppm. The authors suggested that exposure to a chemical at a concentration that reduced respiratory rate in mice by 50% would be intolerable and incapacitating to humans and that one-tenth of the RD50 might create some discomfort, but would be tolerable. Although this assumption appears to be true for chlorine, studies with other substances have challenged its general applicability. Potts and Lederer (1978) have shown that the pyrolysis products of red oak at concentrations that reduced respiratory rate in mice by 50% did not incapacitate humans. Therefore, use of the RD50 in mice for predicting sensory irritation in humans may very well be compound-specific.

Barrow et al. (1978) also reported studies of male and female Fischer 344 rats (10 of each sex) exposed to chlorine at 1, 3, or 9 ppm for 6 h/d, 5 d/wk, for 6 wk. The results showed decreased body weights in females at all concentrations and in males at 3 and 9 ppm. Three females died before the end of the study. Urinalysis, hematologic tests, and clinical-chemistry measurements were completed for the surviving animals. The urinary specific gravity was increased in females at all exposure concentrations and in males at 3 and 9 ppm. The hematocrit and white-blood-cell count were increased in females exposed at 9 ppm. Clinical-chemistry results included increases in alkaline phosphatase, blood urea nitrogen (BUN), γ-glutamyl transpeptidase (GGTP), and serum glutamic pyruvic transaminase (SGPT) at 9 ppm and in alkaline phosphatase at 3 ppm.

Pathologic examination of rats exposed at 9 ppm showed gross evidence of inflammatory reactions of the upper and lower respiratory tract, including hyperemia and accumulation of inflammatory material in the nasal passages. There were also various degrees of pulmonary atelectasis or consolidation. These observations were also made, but to a much smaller degree, in rats exposed at 3 ppm. The kidneys of rats exposed at 9 ppm were found to be darkened. These data indicated that repeated exposures of rats to chlorine at 3 and 9 ppm resulted in gross pathologic changes of the respiratory tract, significantly

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