Acute inhalation toxicity of chlorine in rats and mice: Time-concentration-mortality relationships and effects on respiration

The acute inhalation toxicity of chlorine was studied in rats and mice using whole body exposure. Groups of five males and five females were exposed to different concentrations of chlorine for various periods of time and survivors were observed for 14 days thereafter. Satellite groups were sacrificed two days after exposure to obtain intermediate pathological information. Animals of the satellite groups were also used to investigate acute respiratory responses to exposure with chlorine. For rats the relationship between any LC value, concentration, and time of exposure could be described by the following probit equation: P = -16.67 + 1.33 in C -4.31 ln T + 1.01 ln C x ln T yielding the LC-50 values: 5-min LC-50 = 16.9 g/m3, 10-min LC-50 = 5.6 g/m3, 30-min LC-50 = 2.0 g/m3, and 60-min LC-50 = 1.3 g/m3, and LC-01: 5-min LC-01 = 7.3 g/m3, 10-min LC-01 = 3.0 g/m3, 30-min LC-01 = 1.2 g/m3, and 60-min LC-01 = 0.8 g/m3. For mice the response relation could be described by: P = -33.74 + 4.05 ln C + 2.72 ln T yielding the LC-50 values: 10-min LC-50 = 3.0 g/m3 and 30-min LC-50 = 1.5 g/m3. The breathing pattern and the minute volume in rats during exposure. Rapid shallow breathing directly after the start of exposure was followed by apneustic breathing. Near the ned of exposure the breathing pattern changed again in a few animals in a manner suggestive of pulmonary oedema formation. The minute volume decreased to about 20% of the pre-exposure value. Incorrect adaptation of the ventilation - either too much or too little - increased the incidence of lethality. In rats exposed to high concentrations of chlorine death occurred on the day of exposure and on the first and second day thereafter. Only one animal out of 56 deaths died in the second week of the observation period. In mice, 17 out of 59 deaths occurred in the second week of the observation period. Histopathological examination of the lung showed focal oedema and aggregates of polymorpho- or mononuclear inflammatory cells. Additionally, hyperplasia in the lining epithelium of the larynx and trachea was observed in animals killed at day 2. Only animals exposed to the highest concentration of chlorine for 5 or 10 minutes showed hyperplasia in the lining epithelium of the conductive airways at day 14. The estimated LC-01 values seemed to correspond with the onset of irreversible lung damage.
The acute inhalation toxicity of chlorine was studied in rats and mice using whole body exposure. Groups of five males and five females were exposed to different concentrations of chlorine for various periods of time and survivors were observed for 14 days thereafter. Satellite groups were sacrificed two days after exposure to obtain intermediate pathological information. Animals of the satellite groups were also used to investigate acute respiratory responses to exposure with chlorine. Probit equations were obtained which express the relation between LC value, concentration and time of exposure for both rats and mice. The breathing pattern and the minute volume in rats changed during exposure. Rapid shallow breathing directly after the start of exposure was followed by apneustic breathing. Near the end of exposure the breathing pattern changed again in a few animals in a manner suggestive of pulmonary oedema formation. The minutes volume decreased to about 20% of the pre-exposure value. Incorrect adapation of the ventilation - either too much or too little - increased the incidence of lethality.
Chemicals/CAS: chlorine, 13981-72-1, 7782-50-5