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National Research Council (US) Committee on Toxicology. Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2. Washington (DC): National Academies Press (US); 1984.

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Emergency and Continuous Exposure Limits for Selected Airborne Contaminants: Volume 2.

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Chemical formula:Cl2
Molecular weight:70.906
CAS number:7782-50-5
Boiling point:−34.05°C
Density:1.4085 (20°C)
General characteristics:Greenish-yellow gas with suffocating odor
Conversion factors:1 ppm = 2.89 mg/m3
1 mg/m3 = 0.34 ppm


Chlorine is abundant in combined form in the earth's crust (0.19%) and in seawater (3%). It is usually produced by electrolysis of chlorides. Contaminants include hexachloroethane, hexachlorobenzene, and water. Chlorine was among the first of the war gases used in World War I. It is now used as a bleaching agent, as a germicidal agent for purifying water, and in the manufacture of chlorinated hydrocarbons and chlorine-containing chemicals. About 10 million tons of chlorine is produced annually for industrial use. Massive exposure to fumes may occur during transportation accidents, but the development of treatment procedures has resulted in low incidences of morbidity and mortality in industrial operations, as opposed to nonindustrial exposures (ACGIH, 1980; Lawson, 1981; Stecher et al., 1968; Ploysongsang et al., 1982).



An epidemiologic study by Patil et al. (1970) evaluated a population of 500 diaphragm-cell workers exposed to chlorine at a ime-weighted average concentration of 0.146 ± 0.287 ppm (range, 0.006-1.42 ppm). It was concluded that results of chest x rays, ECGs, and pulmonary-function tests were no different between exposed and 382 control workers.

A chlorine study performed on 30 students at the University of Michigan by Anglen et al. (1980) disclosed some sensation of odor, throat irritation, and urge to cough in subjects exposed for 4 h at 0.5 and 1.0 ppm. Exposure at 2 ppm was reported to be much more irritating than that at 0.5 and 1.0 ppm for the same period. The effects were confirmed by a physician.

A study of pulmonary function on four healthy adults accidentally exposed for 2-5 min to chlorine (at unknown concentrations) showed 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.

TABLE 2. Human Exposure to Chlorine.


Human Exposure to Chlorine.


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 decreased body weight, and altered kidney function and revealed a greater sensitivity of females. Although the results suggested that repeated exposure to chlorine at 1 ppm may have produced some toxicity, personal communication with the authors has revealed that chloramine may have been formed from chlorine and ammonia in the inhalation chamber during exposure. Thus, it was not certain whether repeated exposure to chlorine at 1 ppm alone was responsible for the toxic effects observed.

Chlorine itself is not absorbed. The chloride content of the plasma increases for a few hours after gassing, and urinary chloride excretion is increased on the second day after gassing.

In living tissues, chlorine rapidly converts to hypochlorous acid (Zillich, 1972), which easily penetrates the cell wall and reacts with cytoplasmic proteins to form N-chloro derivatives that destroy cell structure (National Research Council, 1975).

Data on animals exposed to chlorine are summarized in Table 3.

TABLE 3. Animal Exposure to Chlorine.


Animal Exposure to Chlorine.


The American Conference of Governmental Industrial Hygienists (1980, 1983) has established a TLV-TWA for chlorine of 1 ppm and a 15-min TLV-STEL of 3 ppm. The TLV-TWA of 1 ppm was recommended “to minimize chronic changes in the lungs, accelerated aging, and erosion of the teeth.” The Occupational Safety and Health Administration (1983) adopted a ceiling limit of 1 ppm as the federal workplace standard for chlorine.


Emergency exposure limits were set by the Committee in 1966 and 1971 primarily on the basis of the chlorine concentrations that produced nasal and eye irritation. Having reviewed available toxicity data on chlorine, the Committee believes that no compelling new information warrants revision of the previously established 60-min EEL and 90-d CEL. However, on the basis of human data that suggest sensory irritation and changes in pulmonary function as results of 8-h exposure to chlorine at 1 ppm, the Committee believes that the 24-h EEL should be lowered to 0.5 ppm.

The present Committee's recommended EELs and CEL for chlorine and the limits proposed in 966 and 1971 are shown below.

60-min EEL3 ppm3 ppm
24-h EEL1 ppm0.5 ppm
90-d CEL0.1 ppm0.1 ppm


  • American Conference of Governmental Industrial Hygienists. 1980. Chlorine. Documentation of the Threshold Limit Values. 4th ed. Cincinnati, Ohio: American Conference of Governmental Industrial Hygienists, Inc. p. 80.
  • American Conference of Governmental Industrial Hygienists. 1983. TLVs(R): Threshold Limit Values for Chemical Substances and Physical Agents in the Work Environment with Intended Changes for 1983-1984. Cincinnati, Ohio: American Conference of Governmental Industrial Hygienists. 93 p.
  • Anglen, D.M., Smith, R.G., Byers, D.H., and Hecker, L.H. 1980. Sensory response of human subjects to low levels of chlorine in air. American Industrial Hygiene Conference Abstracts, May 27-June 1, 1980. Chicago, Ill. p. 92 , abstr. no. 159.
  • Barrow, C.S., Alarie, Y., Warrick, J.C., and Stock, M.F. 1977. Comparison of the sensory irritation response in mice to chlorine and hydrogen chloride. Arch. Environ. Health 32:68-76. [PubMed: 849012]
  • Barrow, C.S., Kociba, R.J., and Rampy, L.W. 1978. A thirty-day inhalation toxicity study of chlorine in Fischer 344 rats. Toxicol. Appl. Pharmacol. 45:290 , abstr. no. 162.
  • Barrow, R.E. and Smith, R.G. 1975. Chlorine-induced pulmonary function changes in rabbits. Am. Ind. Hyg. Assoc. J. 36:398-403.
  • Freitag. 1941. Danger of chlorine gas. Z. Gesamte Schiess Sprengstoffwes.
  • Heyroth, F.F. 1963. Halogens. In: Fassett, D.W., editor; , and Irish, D.E., editor. , eds. Patty's Industrial Hygiene and Toxicology. Vol. II. Toxicology. 2nd revised ed. New York: Interscience Publishers. p. 831-857.
  • Lawson, J.J. 1981. Chlorine exposure: A challenge to the physician. Am. Fam. Physician 23:135-138. [PubMed: 7457311]
  • National Research Council. 1975. Chlorine and Hydrogen Chloride. Washington, D.C.: National Academy of Sciences. 282 p.
  • Occupational Safety and Health Administration. 1983. Toxic and Hazardous Substances. Air contaminants. 29 CFR 1910.1000.
  • Patil, L.R.S., Smith, R.G., Vorwald, A.J., and Mooney, T.F., Jr. 1970. The health of diaphragm cell workers exposed to chlorine. Am. Ind. Hyg. Assoc., J. 31:678 686. [PubMed: 5494432]
  • Pennsylvania Department of Health. Supplement #1 to Short Term Limits for Exposure to Airborne Contaminants. A Documentation 1967-1969. Harrisburg, Pennsylvania: Pennsylvania Dept. Health, Division of Occupational Health. [151] p.
  • Ploysongsang, Y., Beach, B.C., and DiLisio, R.E. 1982. Pulmonary function changes after acute inhalation of chlorine gas. South. Med. J. 75:23-26. [PubMed: 7054876]
  • Potts, W.J., and Lederer, T.S. 1978. Some limitations in the use of the sensory irritation method as an end-point in measurement of smoke toxicity. J. Combust. Toxicol. 5:182-195. [Chem. Abs. 89:141361t, 1978]
  • Rotman, H.H., Flergelman, M.J., Moore, T., Smith, R.J., Anglen, D.M., Kowalski, C.J., and Weg, J., 1983. Effects of low concentrations of chlorine on pulmonary function. Japp Phys. 54:1120-1124. [PubMed: 6853288]
  • Stecher, P.G., editor; , Windholz, M., editor; , and Leahy, D.S., editor. , eds. 1968. The Merck Index: An Encyclopedia of Chemicals and Drugs. 8th ed. Rahway, New Jersey: Merck & Co., Inc. p.236-237.
  • Zielhuis, R.L. 1970. Tentative emergency exposure limits for sulphur dioxide, sulphuric acid, chlorine and phosgene. Ann. Occup. Hyg. 13:171-176. [PubMed: 5465146]
  • Zillich, J.A. 1972. Toxicity of combined chlorine residuals to fresh water fish. J. Water Pollution Control. Fed. 44:212-220. [PubMed: 5062564]
Copyright © National Academy of Sciences.
Bookshelf ID: NBK208300


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