per million parts of air (0.5 ppm) for any 15-minute sampling period. This shall be designated as a ceiling concentration.

# (b)
Sampling and analysis Procedures for sampling, calibration of equipment, and analysis of chlorine samples shall be as provided in Appendices I and II, or by any method shown to be equivalent in precision, accuracy, and sensitivity to the methods specified.

# Section 2 -Medical
Medical surveillance shall be made available as specified below for all workers subject to occupational exposure to chlorine.
(a) Preplacement examinations shall include as a minimum:
(1) Medical and occupational histories in sufficient detail to document the occurrence of cardiac disease as well as bronchitis, tuberculosis, pulmonary abscess, and other chronic respiratory diseases.
(2) A medical examination including but not limited to, simple tests of olfactory deficiency.
(3) A chest X-ray, 14 x 17 (posterior-anterior). (1) Periodic examinations shall be made available on an annual basis or at an interval to be determined by the responsible physician.
If it is suspected that a worker has been exposed to high concentrations of chlorine and if he exhibits signs or symptoms of respiratory tract irritation, he shall be referred to a physician. The following warning sign shall be affixed in a readily visible location at or near entrances to areas in which chlorine is present in containers or systems. This sign shall be printed both in English and in the predominant language of non-English-speaking workers. All employees shall be trained and informed of the hazardous areas, with special instruction given to illiterate workers.

# CAUTION! CHLORINE HAZARD AREA UNAUTHORIZED PERSONS KEEP OUT CAUSES BURNS, SEVERE EYE HAZARD MAY BE FATAL IF INHALED PROTECTIVE MASKS FOR CHLORINE LOCATED AT__________________________________
(specific locations to be supplied by employer) (c) All chlorine piping systems shall be plainly marked for positive identification in accordance with American National Standard A13. 1-1975. Associated vessels and critical shut-off valves shall be conspicuously labeled. Chlorine containers in use shall be plainly marked "in use" to distinguish them from those not in use. No container shall ever be presumed to be empty and therefore nonhazardous. (2)
In addition to wearing the respiratory protective devices specified in Table 1-1, personnel performing nonroutine operations where escape of liquid chlorine occurs or emergency operations involving escaping liquid chlorine should wear 1-piece suits which are impervious to chlorine and sealed at the ankles, wrists, and around the face. The suits shall be ventilated with supplied air, or stay time in the work area shall be limited with due consideration of the heat stress factors involved.
Impervious gloves and boots should also be worn. Such protective clothing shall be kept readily available for emergencies.
(3) Impervious gloves shall be worn by persons connecting or disconnecting cylinders of chlorine.
The employer shall supply and maintain all protective clothing in a clean, sanitary, and usable condition.

# (b) Respiratory Protection
Engineering controls shall be used wherever feasible to maintain airborne chlorine concentrations at or below the environmental limit recommended in Section 1 of this document. Compliance with the permissible exposure limit by the use of respirators is only allowed when airborne chlorine concentrations are in excess of the workplace environmental limit while required engineering controls are being installed or tested, when nonroutine maintenance or repair is being accomplished, or during emergencies. When a respirator is thus permitted, it shall be selected and used in accordance with the following requirements:
(1) For the purpose of determining the type of respirator to be used, the employer shall measure, when possible, the airborne concentration of chlorine in the workplace initially and thereafter whenever process, worksite, climate, or control changes occur which are likely to increase the airborne concentration of chlorine.
The employer shall ensure that no worker is overexposed to chlorine because of improper respirator selection, fit, use, or maintenance.
The employer shall provide respirators in accordance with Table 1-1 and shall ensure that the employee uses the respirator provided.
Respiratory protective devices described in (1) Chemical cartridge respirator with full facepiece and cartridge(s) and filter(s) providing protection against chlorine (2) Full-face gas mask, chest-or back-mounted type, with industrialsize chlorine canister (3) Any supplied-air respirator with a full facepiece, hood, or helmet with shroud (4) Any self-contained breathing apparatus with a full facepiece Greater than 25 ppm and Emergencies
(1) Self-contained breathing apparatus with full facepiece, pressure-demand or other positive pressure type (2) Combination respirator which includes a Type C supplied-air respirator with a full facepiece operated in pressure-demand or other positive pressure or continuous-flow mode, and an auxiliary self-contained breathing apparatus, pressure-demand or other positive pressure type Evacuation or Escape (1) Self-contained breathing apparatus with full facepiece (2) Full-face gas mask with industrial-size chlorine canister shall be those approved under the provisions of 30 CFR 11.
The employer shall ensure that employees are instructed on the use of respirators assigned to them and on how to test for leakage. (7) Each indoor area required to be posted in accordance with Section 3(b) shall have emergency respiratory protective devices readily available in nearby locations which do not require entry into a contaminated atmosphere for access.
Certain outdoor locations may be exempted from this requirement depending upon such factors as chlorine capacity, accessibility to facility, nearness to other occupied locations, and ease of evacuation. A decision regarding an exemption shall be made by an OSHA compliance officer. Respiratory protective devices provided shall consist of at least two self-contained breathing apparatus as described in
Respirators specified for use in atmospheres of higher concentrations of chlorine may be used in atmospheres of lower concentrations.
The employer shall ensure that respirators are cleaned, maintained, and stored in accordance with 29 CFR 1910.134.
Canisters shall be discarded after use or whenever an odor or taste is detected, and replaced with fresh canisters. Unused canisters shall be discarded and replaced when the seal is broken or when the shelf life recommended by the manufacturer ends.

# Section 5 -Informing Employees of Hazards from Chlorine
At the beginning of employment, workers whose jobs may involve exposure to chlorine at concentrations greater than one-half of the environmental limit, or who will work in areas required to be posted in accordance with Section 3(b), shall be informed of the hazards, signs, symptoms, and effects of overexposure, emergency procedures, and precautions to take to ensure safe use of chlorine and to minimize exposure to chlorine. Information pertaining to first-aid procedures shall be included. The information shall be posted in the workplace and kept on file, readily accessible to workers at all places of employment where chlorine is involved in unit processes and operations, or is released as a product, byproduct, or contaminant.
A continuing educational program, conducted by a person or persons qualified by reason of experience or special training, shall be instituted to ensure that all workers have current knowledge of job hazards, first-aid procedures, maintenance procedures, and cleanup methods, and that they know how to use respiratory protective equipment and protective clothing.
Retraining shall be repeated at least annually.
In addition, members of emergency teams and employees who work adjacent to chlorine systems or containers where a potential for emergencies due to chlorine exists shall be subjected to periodic drills simulating emergency situations appropriate to the work situation. These shall be held at intervals not exceeding 6 months. Drills should cover, but should not be limited to, the following: Evacuation procedures.
Handling of spills and leaks, including decontamination and use of emergency leak-repair kits.
Location and use of emergency firefighting equipment, and handling of chlorine systems and containers in case of fire.
First-aid and rescue procedures, including procedures for obtaining emergency medical care.
Location, use, and care of protective clothing and respiratory protective equipment.
Location and use of shut-off valves.
Location, reason for, and use of safety showers, eyewash fountains, and other sources of water for emergency use.
Operating procedures.
Entry procedures for confined spaces.
Emergency phone numbers.
Deficiencies noted during the drill shall form the basis for a continuing educational program to ensure that all workers have current knowledge.
Records of drills and training conducted shall be made available for inspection by authorized personnel as required.
Information as required shall be recorded on the "Material Safety Data Sheet" shown in Appendix IV or on a similar form approved by the Occupational Safety and Health Administration, US Department of Labor.

# Section 6 -Work Practices (a) Emergency Procedures
For all work areas in which there is a potential for emergencies, procedures specified below, as well as any other procedures appropriate for a specific operation or process, shall be formulated in advance and employees shall be instructed and drilled in their implementation.
In case of fire, chlorine containers shall be removed to a safe place or cooled with water if leaks do not exist. Fusible plugs in chlorine containers melt at 70-74 C (158-165 F). Every effort shall be made to prevent containers from reaching this temperature.
(5) Water may not be used on chlorine leaks because accelerated corrosion, resulting from the formation of hydrochloric acid when water is present, may quickly make the leak worse. Water spray or fog may, however, be used to help suppress the size of a chlorine cloud near the leak.
Containers leaking liquid chlorine should be oriented so that gaseous chlorine is discharged through the leak until it is controlled. Engineering controls shall be used to maintain chlorine concentrations within the limits of the recommended environmental limit.
The use of completely enclosed processes is the preferred method of control for chlorine.
Local exhaust ventilation may also be effective, either when used alone or in combination with process enclosure. Ventilation systems shall be designed to maintain airborne chlorine concentrations within the limits of the recommended environmental limit to prevent accumulation of chlorine in the workroom, and to remove chlorine from the breathing zones of workmen. Ventilation systems shall be subject to regular preventive maintenance and cleaning to ensure maximum effectiveness. This effectiveness shall be verified by periodic airflow measurements. all holes, ducts, doors, and passthroughs which could allow chlorine to enter other parts of the plant shall be secured and sealed. Central cooling and heating ducts may not extend to chlorine storage areas, but such areas may be cooled by terminal ducts with one-way flap or other appropriate valves to prevent significant reflux of air from the storage area into the duct system. If an enclosed storage area is cooled in this way, the pressure within the enclosure shall be maintained slightly below the atmospheric pressure by forced exhaust to the outside of the area.
(E) Ventilation switches and emergency respiratory protection shall be located outside storage areas in readily accessible locations which will be free of chlorine in an emergency. Fan switches shall be equipped with indicator lights.
(F) Containers shall be secured so they will not fall, upset, or roll.
(G) Chlorine containers shall be protected from flame, heat, corrosion, and mechanical damage.
(H) Incompatible materials which may react violently with chlorine such as hydrogen, ammonia, acetylene, fuel gases, ether, turpentine, most hydrocarbons, finely divided metals, and organic matter, may not be stored immediately adjacent to chlorine. The degree of separation required will be dictated by quantities stored and the type of storage facility (outdoor vs indoor, concrete walls vs wood, etc).
(I) Storage areas should not have low spots in which chlorine could accumulate in case of a leak, unless such places have been designed and constructed for such a purpose.
(J) Containers of chlorine shall be used on a firstin-first-out (FIFO) basis.

# (K)
Full and empty shipping containers shall be so marked, and containers in use shall be plainly marked "in use" to distinguish them from those not in use.
(3) Handling (A) Areas containing chlorine containers and systems shall be checked daily for leaks. All newly made connections shall be checked for leaks immediately after chlorine is admitted. Required repairs and adjustments shall be promptly made. No water shall be applied to the source of leaking chlorine. (G) Containers and valves may not be modified, altered, or repaired except as normally intended by the supplier.
(H) Discharge rates may not be increased by use of hot water, radiant heat, or application of flames or heated objects to the containers.
Air circulated around the containers at workroom temperature may be used. Properly designed chlorine vaporizing equipment (as distinct from storage and shipping containers) may be heated.

# (I)
The amount of chlorine used shall be determined by a positive method, eg, weighing the container.
(J) New gaskets shall be used each time chlorine system connections are made.
(K) Cylinder and ton-container valves may not be opened more than one complete turn. Wrenches longer than 8" shall not be used.

# (L)
Piping systems for chlorine shall be properly designed and manufactured from approved materials meeting or exceeding the provisions of American National Standard B31.1 1973, and shall be equipped with appropriate expansion chambers or pressure relief valves or rupture discs discharging to a receiver or safe area. All precautions shall be taken to prevent hydrostatic rupture of chlorine systems and containers.
(M) Before chlorine is admitted to a new or repaired system, the system shall be thoroughly cleaned, dried, and pressure-tested, using approved procedures. Pressure testing of cylinders designed for portable use shall be repeated at not longer than 5-year intervals.
(N)
Materials for handling moist chlorine shall be selected with great care, considering the enhanced corrosiveness of the chlorine, and the requirements for strength.
(0) A vacuum placed on a chlorine line shall be broken with dry air or nitrogen rather than with chlorine to prevent rendering expansion chambers ineffective. that predetermined procedures will be followed.

# (B)
Confined spaces which have contained chlorine shall be thoroughly cleaned, tested for oxygen deficiency and the presence of chlorine, and inspected prior to entry.
(C) Inadvertent entry of chlorine into a confined space while work is in progress shall be prevented by disconnecting and blanking off chlorine supply lines.

# (D)
Confined spaces shall be ventilated while work is in progress to keep any chlorine concentration below the environmental limit and to prevent oxygen deficiency.
(E) Personnel entering confined spaces where they may be exposed to chlorine shall be equipped with the necessary personal protective equipment and a lifeline tended by another worker outside the space who shall be trained and equipped to perform rescue. If monitoring of an employee's exposure to chlorine reveals that he is exposed at concentrations in excess of the recommended environmental limit, the exposure of that employee shall be measured at least once every 30 days, control measures shall be initiated, and the employee shall be notified of his exposure and the control measures being implemented to correct the situation. Such monitoring shall continue until two consecutive samplings, at least a week apart, indicate that employee exposure no longer exceeds the environmental limit in Section 1(a).
Semiannual monitoring may then be resumed.
(2) In all personal monitoring, samples of airborne chlorine that, when analyzed, will provide an accurate representation of the concentration of chlorine in the air breathed by the worker shall be collected. Procedures for sampling, calibration of equipment, and analysis of chlorine in samples shall be as provided in Appendices I and II, or by any method shown to be equivalent in precision, accuracy, and sensitivity to the methods specified.
(3) For each ceiling determination, a sufficiently large number of samples shall be taken to characterize every employee's peak exposure during each workshift.
Variations in work and production schedules shall be considered in deciding when samples are to be collected.
The number of representative ceiling determinations for an operation or process shall be based on the variations in location and job functions of employees in relation to that operation or process. Chlorine is produced commercially by electrolysis of brine, electrolysis of fused sodium chloride, or by oxidation of chlorides using chemical methods.
 By far the most important production method is the electrolysis of brine using diaphragm cells or mercury cells.   in the beneficiating of ores, and in metal extraction.  Exposure to chlorine can occur in any of these operations.
In addition, exposure to chlorine can occur when hypochlorites are mixed with materials such as toilet bowl cleaners  or vinegar , and when chlorinated hydrocarbons are decomposed thermally  or by actinic rays from welding operations.  Some occupations with potential exposure to chlorine are listed in

# Historical Reports
Interest was focused on the toxic effects of chlorine by its use during World War I as a war gas.
Four reports  centered on the health effects of acute exposure to chlorine as a war gas and the possibility of residual effects from acute chlorine overexposure. Meakins  in 1919 reviewed the after-effects of chlorine war-gas poisoning by following 700 consecutive cases in the admission and discharge books of the clinically and by X-ray at the time of the study. The authors concluded that 9 of the 96 men showed definite asymptomatic or symptomatic residual effects which could be attributed to chlorine gassing. The relationship of disabilities to chlorine gassing was questionable in seven instances. In 80 patients, the disabilities found at the time of the study were concluded to be in no way related to chlorine gassing incurred during the service.
Of the nine men showing definite residual effects , five had pulmonary tuberculosis, with a coexisting emphysema in three. Three of the nine men showed evidence of chronic bronchitis; of these, one had a coexisting emphysema, one had chronic conjunctivitis, and one was free of coexisting conditions. One of the nine men had chronic adhesive pleurisy. In analyzing the five cases of pulmonary tuberculosis, the authors concluded that it was probable that gassing led to reactivation of previously quiescent tuberculous foci.
Seven men who showed disabilities that were questionably related to chlorine gassing had a history of intercurrent respiratory disease or a history of respiratory disease for which the claimants were treated just prior to, or immediately after, the gassing. In these cases, it was not possible to determine the role played by chlorine in the causation of the disabilities which appeared subsequently.
Pearce  in 1919 studied one person who was gassed with chlorine during the war. The man, who first received treatment some 12 months after he was gassed, failed to exhibit on medical examination any impairment of his heart and lungs, except for bronchitis. The respiratory quotient, minute volume of air, depth and rate of respiration, and tension of carbon dioxide in the alveolar air were determined at rest, while walking, and while running at a "dog trot" for a short distance, and were compared with those of the author. At rest, practically "normal" values were obtained.
At exercise, the patient's minute volume of air was greater than expected from the work done, as measured by the oxygen consumption. His breathing was labored and rapid, and he felt faint. The disability in this case was interpreted as being due to a discrepancy between the ability of the blood to obtain oxygen and to rid itself of carbon dioxide. The patient was considered to be able to excrete his carbon dioxide without difficulty but to be unable to get enough oxygen. This condition was thought to be caused by the presence in many of the alveoli of bubbles of foam which prevented a free exchange of air.
No definite improvement was found when the man worked while breathing oxygen at high pressures, however. He was kept under observation for about a year. He gradually developed a more severe bronchitis, together with asthma and emphysema.
No information on his smoking habits or any other significant exposure was given.

# Effects on Humans
(a) Odor Perception
The effect of chlorine on the sense of smell was studied in 1957 by
Styazhkin  who conducted 144 tests on 12 persons ranging in age from 17 to 28 years. They were exposed to chlorine at low concentrations and asked if they detected the gas. Subjects inhaled through the nose from two tanks, one with clean air and one with chlorine, and were asked to designate the one containing chlorine. The threshold of chlorine odor perception occurred at 0.7 mg/cu m (about 0.2 ppm). Leonardos et al  determined odor threshold under controlled laboratory conditions. The odorants were presented to a trained odor panel in a static air system using a low odor background air as the diluting medium. The odor threshold was defined as the first concentration at which all four panel members could detect the odor. The odor threshold for chlorine was reported as 0.314 ppm. Ryazanov  reported that the odor threshold of a group of volunteers ranged from 0.80 to 1.30 mg/cu m (0.3-0.4 ppm). subjects to chlorine at 0.044 ppm, 4 perceived an odor which "became increasingly weak and after 1-24 minutes could no longer be objectified."
When the concentration was raised to 0.09 ppm, 7 of the 10 noticed an odor and recognized the gas, but for 6 of the 7 the odor disappeared after 1-25 minutes (average: 9 minutes). At 0.2 ppm, 13 subjects all noticed an odor, and the duration of the perception was longer by an average of 13 minutes than that for lower concentrations.
Laciak and Sipa  studied olfaction in 173 randomly selected workers; 17 came in contact with chlorine. The 173 workers were asked to identify eugenol, coumarin, iodoform, dinitrobenzene, and methyl salicylate in increasing olfactory dilutions of 1,5,10,20,50,100, and 200. The results were measured in "olfacties," not further described, such that a slight olfactory deficiency meant an average loss of 20 olfacties; a moderate one, 20-100; and a severe deficiency, 100 olfacties to complete anosmia. Four workers had been exposed to chlorine for 1 year or less; of these four, olfactory deficiency was slight in two, moderate in one, and severe in one. Of the 13 workers exposed to chlorine for 2-5 years, 1 suffered slight deficiency, 1 moderate, and 11 severe. The significance of the relationship between chlorine exposure and olfactory deficiency was not discussed.
According to CB Kramer (written communication, June 1974), Dow Chemical Company collected information on odor thresholds for chlorine. In 65 tests, individuals who were industrial hygienists with the company perceived no odor when exposed to chlorine at concentrations ranging from 0.08 to 2.9 ppm; in 16 tests, the odor was described as minimal at an exposure concentration of 1.1-2.7 ppm. Data illustrated individual variation. Furthermore, it was noted that odor perceptions by the same individual made late in the day, after previous exposure, were frequently less discerning than those made earlier the same day.
(b) Case Reports
(1) Severe Exposures
The dramatic response to substantial exposure is well documented in a number of accidents involving chlorine. Romcke and Evensen  in 1940 reported an accident in Norway that released 7-8 tons of chlorine.
The number of those exposed was not given, but 85 were hospitalized and 3 died. The authors commented that some victims had latent periods as long as several hours before they developed symptoms of pulmonary congestion disturbing enough for them to seek medical attention.
The authors also commented that the most severe symptoms of pulmonary edema developed most rapidly in those subjected to physical exertions. In the milder cases, the pulmonary symptoms disappeared in 2-3 days; 54 of the hospitalized patients were discharged in 3 days. In other hospitalized patients, the bronchitic sounds lasted for 8-10 days. Signs of pulmonary edema occurred in 6 patients. Autopsies of two victims revealed intense tracheobronchitis, hyperemia of the brain, and intensely edematous lungs weighing 2,300 and 2,500 g that almost completely covered the heart.
Stout  recounted the occurrence of oral burns from an unusual exposure to chlorine. As a prank, a laboratory student who had filled a bottle with chlorine gas poked it under the nose of a second student. The second student recoiled and gasped for air through his mouth, but inhaled some chlorine instead. The pain in his throat increased during the first day, and he became unable to swallow. Although the inflammation gradually subsided, an unproductive cough continued for several months after the incident. Adventitious pulmonary sounds were present in all: 28 had dry rales on admission, whereas the rest of the patients, with one exception, developed them shortly thereafter. Subsequent moist rales developed in all but two patients. Pulmonary edema was seen in 23 of 30 patients; the others were not observed in the early postexposure period. Respiratory distress subsided, for the great majority, within 72 hours.  However, in five patients, it ceased within 6 days; only one patient had prolonged dyspnea, a symptom to which preexisting heart disease was presumed to have contributed. Substemal pain generally subsided in the first days, leaving a soreness attributed to tracheobronchitis. A dry cough was present initially in every patient, but promptly became quiescent with administration of oxygen and codeine, only to return in most patients after 2-5 days with the production of tenacious mucopurulent sputum, blood-tinged when first produced. Dry rales cleared by the 10th day; moist rales were still present in 20 patients during the second week.
The febrile period lasted 2-13 days.
The following summarizes the clinical test data: chest X-rays showed mottling, patches of irregular densities, and differences in the degree of aeration in both lung fields. X-ray changes in most patients were not remarkable, and it was felt that readings of single roentgenograms could easily have been judged to be normal. In 3, a transient unequal aeration was noted, consistent with obstructive emphysema. In 14, serial changes permitted the diagnosis of pneumonia, basilar in 13. At the time of discharge, all chlorine-related abnormalities visible on chest X-rays were clearing or had cleared. Arterial oxygen saturation was measured 7-8 hours after exposure in eight patients selected for examination because of cyanosis and extensive pulmonary involvement. The values, ranging from 88.1 to 91.2%, were lower than normal (reported as approximately 96%) in six. Serial ECG tracings on 12 patients showed either no abnormality or a preexisting heart disease. For eight patients, vital capacity determined 48 hours after exposure gave values ranging from 16 to 57% of the predicted normal.
A special follow-up clinic  was established and attended by 29 of these patients, usually for 16 months after exposure. Eleven had no abnormal symptoms or signs. One patient had cough and sputum for 6 months, with medium moist rales at the base of the left lung for 3 months. Upon death 10 months after exposure, a post-mortem examination showed a pulmonary embolus, but otherwise normal lungs and bronchi.
A second patient, who had marked congenital kyphoscoliosis with pulmonary fibrosis (there was no comment as to its etiology), had periodic episodes of cough and dyspnea, each lasting a few days to a few weeks. Sixteen patients had what were considered anxiety reactions with phobias, hysterical phenomena, and psychosomatic dysfunctions for 1-16 months: anorexia, nausea, vomiting, weakness, nervousness, dizziness, palpitation, a sense of suffocation, and the odor and taste of chlorine. Two intrauterine pregnancies were reported to be unaffected by the exposure, but no details were given.
There was no correlation between severity of symptoms during the hospital stay and the continuance of symptoms thereafter. No pulmonary function studies were reported from the special follow-up.
Baader  described a freak nighttime industrial accident in which there was a release of "enormous" amounts of "chlorine anhydride".
Fortunately, only 190 of the 900 workers of the mill were at work, but the wind carried the cloud of gas to the town. R>portedly, some 240 people were taken to clinics, 4 workers died, and another 42 persons were in very serious condition. The signs and symptoms present in 46 patients examined by the author were as follows, in order of decreasing frequency: fever, moist rales in some pulmonary fields, dyspnea, blood in sputum, tachycardia, vomiting or nausea, reduced arterial pressure, cyanosis, blood in urine, coated tongue, headache, severe diarrhea, "sticky sweat", fainting, infrasternal pains, constipation, pains below the costal ridge, heart pains, bradycardia, and arrhythmia. One patient who fainted from the exposure developed glucosuria. Three autopsies were performed; aside from pulmonary edema, emphysema, and the presence of bronchopneumonic condensation foci in the lungs, the most striking findings were small hemorrhages in the white matter of the cortex, corpus callosum, internal capsule, and cerebellum.
Hoveid  described a railcar accident in Norway which released 14 tons of chlorine. The exposure resulted in the hospitalization of 85 people.
No information was presented about any others exposed. Three of the 85 died and the others were discharged following treatment as in patients. Information on 75 was secured by mail questionnaires; 4 had died since discharge, and 3 could not be located. The questionnaire asked about "difficulties of any type... caused by this gas exposure," the use of physician services in this regard, and the incidence of recurrences. How long after the incident the questionnaires were mailed was not given, but the spill occurred in 1940 and the article was published in 1956. No difficulties were ascertained in 48 of those who responded, 16 reported difficulties "believed to be a reasonable consequence of the accident," while 11 had a "possible, but somewhat doubtful consequence." The "reasonable consequences" included dyspnea (1 person with dyspnea had pulmonary tuberculosis), bronchitis, "tightness under the chest," and "lacing under the chest." "Possible consequences" included coughing, spontaneous pneumothorax, asthma, emphysema (6 years after exposure), bronchitis (beginning 4 years after exposure), loss of memory, "bad throat," "legs and the strength failing," "poor heart, high blood pressure," and claustrophobia. Half of those with dyspnea did not consult a physician. Eight of 16 with "reasonable consequences" had received oxygen, while 5 of 11 with "possible consequences" and 11 of 48 without difficulties received this therapy; the differences were not statistically significant.
In 1962, Joyner and Durel  reported a spill of about 36 tons of liquid chlorine in Louisiana. Three hours later, chlorine at an airborne concentration of 10 ppm was found in the fringes of the contaminated area;
7 hours after the spill, levels of 400 ppm were recorded 75 yards from the spill, and this was felt not to represent maximal values even at that time.
Approximately 100 persons were treated for exposure to chlorine of various degrees.
Of the 65 casualties handled in one hospital, 15 were admitted.
Three children and one adult were unconscious on admission; an 11-month-old infant died. Ten of the hospitalized patients developed frank and unmistakable pulmonary edema. All heavily exposed victims experienced severe dyspnea, coughing, vomiting, and retching. Most of these patients complained of burning of the eyes and had acute conjunctival injection with profuse tearing and photophobia. Some victims had minor first-degree skin bums, principally of the face.
The authors stated that these burns resulted from gas exposure rather than from splashes. Examination of the chest in all heavily exposed patients revealed diffuse, moist, crackling rales throughout both lung fields which were loud both on inspiration and expiration. Harsh, sibilant rales were also audible in one patient.
Sputum in bedside containers was copious, thin, and very frothy; in one patient, sputum was faintly tinged with blood on the second day after exposure.
Chest X-rays made on hospitalized patients on the third and fourth days after exposure revealed striking changes: fine miliary mottling was distributed bilaterally and symmetrically throughout both lung fields. With therapy, these clinical findings slowly cleared and all hospitalized patients were discharged by the sixteenth day.
In 1969, Weill et al  reviewed the case histories of 12 of those who had been exposed in the spill reported above by Joyner and Durel.  In general, these 12 patients were the ones most severely affected in the community. Three of the 12 were studied 3 years after exposure; all 12 were studied again 7 years after exposure. The 12 study subjects included 11 of the 16 surviving hospitalized patients and the spouse of one subject, an individual who had had prominent symptoms after exposure. Observed values for total lung capacity (TLC), vital capacity (VC), residual volume (RV), and forced expiratory volume at 1 second (FEV 1) were all within two standard deviations of predicted values.
 (A complete listing of pulmonary function abbreviations used here and subsequently is given in Appendix V.) The subjects were essentially asymptomatic from a respiratory standpoint. Chest X-rays were normal in all cases. Minor abnormalities in lung volumes were accounted for by factors other than chlorine exposure.
No definite change in respiratory function was found in the three subjects who were studied both 3 and 7 years after exposure.
Gervais fit al  studied a worker accidentally exposed to chlorine in 1965. There was no estimate of the degree of exposure except that the worker was unable to leave the area by his own efforts. The patient had rales in both lung fields but the chest X-ray was normal. The ECG showed a it was judged to be severe in 7. One developed bacterial pneumonia. Other clinical findings included hemoptysis, rales, wheezes or rhonchi, or both, and edema of the lungs. Within 1-3 weeks, all findings had disappeared except for symptoms of exertional dyspnea, easy fatigability, and cough.
Two months after exposure, all 11 appeared clinically recovered, despite the findings of reduced lung volumes, reduced arterial oxygen partial pressures at rest which were significantly lowered upon mild exercise, and hyperventilation at rest and upon exercise. This symptomatology is consistent with acute alveolo-capillary injury (Table III-l).
Six months later, mean total lung capacity was still reduced, mean vital capacity was further reduced, and mean airway resistance had significantly increased. There was arterial hypoxemia at rest and after exercise, and a decrease in the degree of hyperventilation. At the time of the last two studies lung volumes were returning to normal, although they were still low for up to 3 years after the incident, while airway resistance remained  The profiles developed did not make a strong case for an effect resulting from chlorine exposure; however when the categories were considered individually, those with a history of more severe exposure, hospitalization, or persisting decreased exercise tolerance had a lower diffusion capacity (p < 0.05).
Dixon and Drew  reported a fatal case of chlorine poisoning. A chlorine cloud resulted when a valve was incompletely closed. For reasons which were not clear, a boiler plant operator, age 49, remained in the cloud for about 30 minutes without immediately putting on the canister mask which was available; it is not certain that he used the mask. When he reported for medical assistance, he began vomiting and complained of severe pains in the stomach and chest. There were signs of bronchial irritation and congestion, which were not further described.
After an hour's observation, he was sent home; on the way, he became increasingly ill and died. The interval between initial exposure and death was 3-3.5 hours.
Post-mortem examination revealed pulmonary edema as the cause of death, with coronary insufficiency due to atheroma also reported.
Beach et al  published the case history of a 44-year-old process worker exposed to chlorine gas at an unstated "high" concentration because of a leaking valve. He soon began to choke and then developed severe dyspnea, a persistent cough, and chest pain. His eyes "smarted" and his conjunctivae were markedly injected. Ten hours later, he was cyanotic and had rapid and shallow breathing; he coughed up pink frothy sputum.
Numerous coarse crepitations were heard. He was given "continuous oxygen" for 9 days and prednisolone for 12 days. He remained critically ill for 48 hours and then gradually improved. His dyspnea at rest slowly abated and disappeared by the 10th day. The patient was discharged from the hospital after 13 days. Exercise dyspnea persisted for 5 weeks. Further followup data were not reported.
Uragoda  reported on a water purification plant worker who was exposed to leaking chlorine gas for a period of 20 minutes before he  In summary,  the most heavily exposed residents and neighbors showed a pattern of airway obstruction and uneven ventilation which, for the most part, was transitory. Those moderately or lightly exposed had no physiologic disturbance except for that considered commensurate with age.
Four of the five chlorine workers, with occupational exposure in a chlorine environment for 5-30 years, showed persistent airway obstruction and mild hypoxemia.
There was no comment as to their degree of exposure preceding or during the accident. Only one patient, not a worker, had continuously reduced DLCO, arterial hypoxia, and excessive ventilation, despite a mild chlorine exposure and lack of symptoms.
(2) Less Severe Exposures
Instead of having been exposed to massive amounts of chlorine because of accidents, many workers have been exposed for relatively long periods to chlorine at low airborne concentrations. Some reports    In summary, the above reports  indicate that exposure to chlorine may cause severe irritation, in some cases resulting in death.
Thirteen of the approximately 1,250 exposed persons died. Autopsy following fatalities that resulted from acute exposure to chlorine revealed inflamed bronchi, pulmonary edema, and small foci of bronchopneumonia in the lungs.  Nonfatal doses resulted in severe signs and symptoms including dyspnea and cough, expectoration of bloody froth, sensation of tightness in the chest, cyanosis, conjunctival injection, severe headache, nausea and vomiting, and syncope.  In those persons severely affected, clinical examination and chest X-rays corroborated the presence of pulmonary edema  and oxygen desaturation.  One study  reported serum enzyme abnormalities in SGOT and SGPT but not lactic dehydrogenase (LDH).
The same study  reported sharp transient leukocytosis; less marked leukocytosis was observed in a second study.  The absence of any mention of damage to the skin from gaseous chlorine, except in one article,  suggests that exposures to chlorine at high concentrations are required for this effect. There were no case reports of exposure to liquid chlorine. The bulk of evidence suggests, albeit followup was generally very incomplete, that most persons recover completely and relatively rapidly after massive accidental exposures.  On the other hand, there was some evidence of chronic impairment of pulmonary function following acute exposure.  There is insufficient evidence to conclude that persons chronically exposed to chlorine developed chronic impairment.
All of the reports suffered from a lack of precise data regarding airborne concentrations and exposure durations.. Follow-up data on those exposed was generally very limited.  The widespread use of chlorination of potable water to kill bacteria  has lead to the study of the biochemical mechanism of chlorine-induced alteration of cells.
 In an aqueous milieu such as that found in tissue, molecular chlorine disproportionates rapidly according to the While observed changes in the cellular genetic material following treatment with chlorinating agents are a matter of grave concern, the available information does not provide any evidence concerning the magnitude of these effects in any higher organism or in humans.
No evidence has been found to indicate that chlorine is a carcinogen.
 The overall expected rates of respiratory disease were then compared with the observed rates to determine whether there was any significant difference between the two mills; the prevalence of chronic nonspecific respiratory disease was 32.5% in the pulp mill and 27.4% in the paper mill. This was not judged by the authors to be a significant difference. Formulae based on age and height for predicting forced vital capacity (FVC), FEV, and peak expiratory flowrate (PEFR) were calculated for those in the pulp mill and the paper mill; an analysis of variance for testing the equality of regression coefficients (including the constant term) was done on the two equations for each group and, according to the authors, no significant difference was demonstrated.
Epidemiologic
No difference was noted in results of tests of pulmonary function of 118 pulp-mill workers exposed primarily to sulfur dioxide and the 73 exposed to chlorine or chlorine dioxide. However, when the responses to 12 questions about respiratory symptoms were compared, 3 were answered positively more often by men exposed to chlorine: "gassed at work" (p < 0.05), "phlegm past 3 years" (p < 0.05), and "shortness of"breath grade 3 or more" (p < 0.01).
There are problems in interpreting these results, some of which were pointed out by the authors.
 The industrial hygiene surveys began in 1958; higher chlorine concentrations had probably existed in the past, possibly higher in one mill than in the other, but there were no records.
It is also possible that higher levels occurred during the time surveyed, since the sampling was very limited. It is also not clear where sampling had taken place. The authors commented that many men transferred to the paper mill because they disliked the odors in the pulp mill. Because of this, men working in the paper mill may have been more sensitive to irritant gases. Finally, workers were not only exposed to chlorine, but also to sulfur dioxide and chlorine dioxide, although one usually predominated at any given location.
In 1967, Leduc  reported studies conducted at the request of 620 employees exposed to various irritant gases to determine effects of chronic exposure. There were 15 workers who were exposed to chlorine. The author questioned physicians in localities where workers were exposed to chlorine, specialists, and industrial physicians of factories with similar risks about their experiences with acute chlorine intoxication and any sequelae, and about their observations of ill effects from chronic exposure to chlorine. Private physicians reported treating 5 cases of acute chlorine intoxication; the author's implication was that all 5 were probably not among the 15 chlorine workers in the group requesting the investigation.
The extent of exposure for the five was not quantified. Of the five, one had occasional bronchitis since exposure and one had a 5% disability granted because of bronchitis subsequent to exposure. There were no known sequelae for three; the extent of follow-up was not given. Responses from industrial physicians revealed reports on at least 301 workers; there were 2 fatalities and 2 cases of serious pulmonary edema attributed to chlorine exposure.
After acute intoxication, one worker developed a serious allergic colitis which necessitated several months of hospitalization; it was not further characterized. Fifty-five of the 139 workers had been accidentally exposed one or more times to chlorine at higher concentrations and had required oxygen therapy at least once during their employment. Posterior-anterior chest films were abnormal in 56 of 138 men. The degree of exposure or length of employment of these 56 was not given. One man had a mottled infiltrate in the right apex most consistent with active tuberculosis. Extensive pleural reaction, pulmonary fibrosis, and a high-right diaphragm with plate-like atelectasis and discrete densities in the right lower lobe were separately noted in three other men. Only one subject had abnormal ventilatory function. All but 7 of the 56 revealed evidence of parenchymal or hilar calcifications that were considered to be consistent with old granulomatous disease.
Evaluation of a standard respiratory questionnaire revealed that there was no significant difference between the prevalence of symptoms in those exposed to chlorine who smoked, and in those nonsmokers not exposed to chlorine. A significant difference in maximal midexpiratory flow was seen, however, when chlorine and smoking were considered as additive noxious agents (Table III-3).
The authors stated that before chlorine could be indicted as a specific health hazard, a detailed study of the smokerchlorine cohort would have to be made.
Accidental exposure was defined by the authors as one occurring at least once in the history of each worker and severe enough to require oxygen therapy.
The prevalence of such exposure in smokers correlated positively with a decrease in MMF (p < 0.02).

# Ages of smokers
accidentally exposed averaged 42.5 years, while those with no exposure averaged 35.7 years.
The authors felt that this age difference was insufficient to explain the difference in MMF. Employees with 10-14 years' experience constituted the single largest group, and this group also contained the most workers exposed to more than 0.52 ppm chlorine. There was no correlation between the chlorine concentration and the number of years a person was so exposed.
The exposed and control groups described above were well-matched with respect to age, ranging from 19 to 69 years; 60% of the workers were 30-49 years old.
 The mean age of the two groups combined was 31.2 years.
About 60% of the workers in both groups smoked at the time of the study.
In order to determine whether a significant number of workers with occupational exposure to chlorine had retired due to causes related to chlorine exposure, health data were collected on workers not involved in the study who had terminated employment. No patterns were evident, and it appeared that most workers had resigned or were reassigned for reasons unrelated to health. Of the 329 ECG's from 332 workers, 9.4% were abnormal as compared to 8.5% in controls; the number of ECG's taken in each group was not given.
 The incidence of fatigue (undefined) was greater in workers exposed to chlorine at concentrations greater than 0.5 ppm, but there was no apparent correlation below 0.5 ppm. Nervousness, headache, insomnia, and shyness showed little relationship to chlorine exposure.
Anxiety and dizziness showed moderate correlation with exposure level (p = 0.020).
Histories of neurologic illness and use of alcohol were unrelated to chlorine levels. There was no correlation of exposure with either tremors or abnormal reflexes.

# Animal Toxicity
In 1920, Underhill  described effects of chlorine on dogs.
Animals not subjected to any previous testing were exposed to chlorine gas for 30 minutes at 50-2,000 ppm. They first showed general excitement, as indicated by restlessness, barking, urination, and defecation. Irritation was distinctly visible, as indicated by the blinking of eyes, sneezing, copious salivation, retching, and vomiting. Later, their respiration became labored with frothing at the mouth. Although the dogs frequently drank large quantities of water, they refused food. With increased concentrations of chlorine, the respiratory distress increased until death occurred, usually within 24 hours, apparently from asphyxiation. Table III-4 shows that at a chlorine concentration of 800 ppm half the animals died within 3 days, while at 900 ppm exposure 87% died within this time.
Animals which died after 3 days were classified as "delayed" deaths.
The animals so classified did not exhibit the signs of acute exposure, ie, labored and distressed breathing, for more than 1 or 2 days. They showed signs of loss of appetite, extreme depression, and weakness. In the majority of cases, deaths classed as "delayed" resulted from secondary factors, chiefly bronchopneumonia following the subsidence of acute pulmonary edema. The author considered "the minimum lethal toxicity of chlorine gas under the conditions of the experiment" to occur between 800 and 900 ppm chlorine. Two interpretations of these results were suggested by the author:
the first gassing either rendered the animals less susceptible to the effects of subsequent exposure or killed the weaker individuals. When the deaths from the first gassing were added to those from the second gassing, the final percentage of dying was practically identical with the original standard toxicity figures, a finding supporting the second hypothesis. Gunn  found that exposing cats and rabbits to chlorine at concentrations of 1 part/5,000 parts (200 ppm) to 1 part/10,000 parts (100 ppm) produced a reflex constriction of the bronchi lasting about 1 minute.
The rate of respiration increased concomitantly.
Bell and Elmes  used specific pathogen-free 14-week-old rats (SPF rats) to determine whether chlorine exposure at 40 ppm for 3 hours daily for a total of 43 hours (discrepancy not explained) had any immediate effect or altered the effect of exposure to chlorine at 117 ppm at age 30 weeks (3 hours daily until about half had died, 29 hours). They presented the details about the exposure in another paper.
 At 40 ppm, exposed rats coughed, sneezed, and huddled together; after 3 hours, their noses were running and sometimes blood-stained. Exposure to chlorine at 40 ppm did not make death from chlorine at a subsequently higher concentration (177 ppm) more likely.
A second experiment  compared the effect of chlorine at high concentrations on SPF rats and those with spontaneously occurring lung diseases.
Female SPF and diseased rats were exposed as separate groups to chlorine at 118 ppm for 3 hours followed by 14 hours at 70 ppm. Male SPF and diseased rats were exposed initially to chlorine at 34 ppm for 3 hours daily with incremental increases to 170 ppm; the total duration for male rat exposures was about 60 hours at a mean chlorine concentration of 90 ppm. It was concluded that the presence of preexisting lung disease increased the likelihood of death from exposure to chlorine at high concentrations (p < 0.01). In diseased animals, the cellular response to heavy exposure was much more severe than that in SPF animals.
Proliferation of goblet cells and aspiration of mucus were more intense and extensive in the diseased stock following exposure to chlorine. In animals dying during exposure, diseased rats had a significantly higher incidence of emphysema than did SPF stock. The most noticeable difference between the two groups lay in the reactions of the alveolar part of the lungs to the aspiration of bronchial mucus and debris. In both experiments, the SPF animals showed no increase in number of polymorphonuclear cells, while in were divided into two equal groups and exposed separately 5 hours/day, for 5 days/week, during a period of 3 months. The first group was exposed to airborne mercury at a concentration of 4.5 mg/cu m and the second group was exposed to airborne mercury at the same concentration mixed with 1-3 ppm chlorine.
After about 6 weeks of exposure to mercury vapor (first group), the rats revealed hyperexcitement, sometimes followed by ataxia and tremor.
The rats exposed to airborne mercury vapor mixed with chlorine gas showed mild dyspnea, cough, and diarrhea in the second week. After 2 months of treatment, 10 of the 40 rats in the first group and 4 of 40 rats in the second group had died.
In an earlier experiment,  the authors had demonstrated a fourfold reduction of the mercury vapor concentration in a closed chamber when chlorine gas was added. A fine precipitate, stated to be mercurous chloride-a reaction product of mercury and chlorine gas-was visible on the floor of the chamber and was thought to have accounted for the mercury vapor reduction.
The authors  concluded that the addition of chlorine gas to an atmosphere containing mercury vapor not only reduced mercury absorption, but resulted in a different distribution of the metal in the body, thought to be due to the formation of mercurous chloride. The latter conclusion was supported by autoradiographic studies in which radioactive mercury vapor showed a much different distribution pattern in rats when compared with orally administered radioactive mercurous-203 chloride.
The preceding animal studies were not especially helpful in elucidating the effects of exposure to chlorine at low concentrations. Two studies  provided data indicating a mortality rate in dogs of 85-87% after exposure to chlorine at concentrations of 800-900 ppm; one study  suggested a chlorine LC50 for dogs of 800 ppm after 3 days following a 30minute exposure to chlorine. The remaining studies,  with one exception,  either did not provide any data on chlorine concentrations, or the concentrations were 40 ppm and higher. Arloing et al  exposed guinea pigs to chlorine at 1.7 ppm, 5 hours/day for 87 days. Guinea pigs challenged with tubercle bacilli, with and without a chlorine challenge, were compared with guinea pigs exposed to chlorine alone. In all cases, the animals challenged with either the tubercle bacillus or chlorine alone survived longer than animals exposed to both;
and, animals exposed first to chlorine and then to tubercle bacilli died sooner than those first exposed to tubercle bacilli and then to chlorine; this suggests that an increased susceptibility to infection may occur after an exposure to chlorine.

# Correlation of Exposure and Effects
All the historical studies  and case reports   The color reaction of the methyl orange-chlorine system was seen immediately (bleaching) with color stability lasting at least 24 hours.
 but reproducibility depends on operator technique.
Currently, certain chlorine-specific tubes have been evaluated and certified by NIOSH in accordance with the provisions of 42 CFR 84 (1974).
In order to be certified, detector tubes must exhibit (1) accuracy within 35% at half of the NIOSH test concentration (NTC) and within 25% at 1, 2, and 5 times the NTC (for chlorine, the NTC was 1 ppm); ( 2) channeling (beveled stained-unstained interface) of less than 20%; and (3) tube reader deviation (standard deviation estimate of three or more independent readers) of less than 10% of the average of the readers. A combination pyrolysisfurnace/microcoulometric cell was found to be accurate to 2.5% with a detection limit of 3 ng but it was sensitive to chlorinated hydrocarbons.
 Other electrometric methods,  continuous colorimetric methods,  and sensitized test paper methods are mentioned in the literature.
 In general, automatic and continuous monitoring methods are effective for a narrow range of specific industrial applications, eg, process or fixed position area monitoring, but they are not suited for typical work situations where breathing zone concentrations must be determined.
Although the o-tolidine method Is the most sensitive procedure for determining trace amounts of chlorine,  the methyl orange method is not affected by iron III or compounds containing available chlorine such as chloramine, and yet has 70% of the sensitivity of o-tolidine.
 In addition, o-tolidine has been mentioned as a suspected carcinogen.  The method of choice for atmospheric sampling and analysis of elemental chlorine in working environments is the methyl orange procedure.
 In this procedure, 10 ml of methyl orange sampling solution is placed in a fritted bubbler, and a volume of air is drawn through at a rate of 1-2 liters/minute for 15 minutes. Absorbance is then measured with a spectrophotometer. This procedure is designed to cover the range of 5-10 mg of free chlorine/10 ml of sampling solution. For a 30-liter air sample, this corresponds to approximately 0.05-1.0 ppm in air. The method has an accuracy of +5%. Reagent stability is good and preparation is not lengthy.
Samples remain stable for 24 hours (see Appendix II). Equipment and apparatus needed are uncomplicated, and sampling and analysis are straightforward and easily interpreted.
Minimal performance criteria required for this recommended method and for any proposed alternative method should provide at least one-half the recommended environmental limit as a level of reliable detection. This is required for the purpose of identifying work areas subject to periodic air sampling.

# Environmental Levels and Engineering Controls
Few studies have been published concerning workroom airborne concentrations of chlorine and the extent of engineering controls required to reduce exposures. In 1964, this scarcity of information prompted the environmental health study of a chlorine plant described by Pendergrass.
In the plant studied, chlorine was produced by the electrolysis of brine in 180 Hooker-type cells. The chlorine unit consisted of a cell house, a purification area, a compressor area, and a cell renewal building.
The cell house and purification areas were of primary concern in this study.
The building housing the cells was about 60 x 300 feet with a high ceiling and partial side walls. The purification area was about 25 feet from the cell house and was not enclosed. In normal operations, exposure could occur when chlorine was released to the workroom atmosphere during Feiner and Marlow,  reporting on industrial hygiene in pulp mills, stated that the need for control of chlorine by ventilation in pulp mill-bleaching plants was minimal when chlorine was accurately metered in proportion to the volume of stock to be bleached. However, they recommended covers for bleach chests, hoods for rinse washers, and exhaust ventilation of the enclosures as precautionary measures. The authors did not provide air sampling data to support their statement.
Elkins  reported one sample of "hazardous concentration" out of four samples taken in textile-and paper-bleaching processes. "Hazardous concentration" was assumed to indicate that the threshold limit value of 1 ppm was exceeded. No further data were given.
Joyner and Durel  reported on a spill of about 6,000 gallons of liquid chlorine. Three hours after the spill, the contaminated area was approximately 200 yards in length along a highway. Chlorine at concentrations of 10 ppm was found in the fringes of this area. About 7
hours after the spill, chlorine at a concentration of 400 ppm was found in more heavily contaminated areas 75 yards from the spill. Two and one-half hours later, after treatment of the spill had begun, the airborne chlorine levels dropped to 8 ppm. Joyner and Durel stated  that minor firstdegree burns of the facial skin resulted from exposure to the gaseous chlorine. In a verbal communication of July 1974, Joyner stated that there was no opportunity for persons to contact the liquid; therefore, he was certain that the skin irritation was caused by gaseous chlorine.

# Capodaglio et al  investigated the respiratory function of
workers engaged in chlorine production by means of the electrolysis of brine in mercury cells. They noted that no special precautions were taken to control chlorine in the plant air, although ventilation was present to minimize mercury exposure.
Presumably this would have also prevented exposure to chlorine. The authors  stated that natural and forced ventilation "assured 40 hourly exchanges" in a 40,000-cu m shed. Under these conditions, 18 samples taken for an unspecified period of time showed the average airborne chlorine concentration to be 0.298 ppm. Sixteen spot samples showed an average chlorine concentration of 0.122 ppm.
Smith et al  reported that most chlorine cell rooms had airborne chlorine levels well below 1 ppm, usually in the 0.1 to 0.3-ppm range. No supporting data were given.
The TI-2 Chemical Industry Committee of the Air Pollution Control Association  mentioned that chlorine-manufacturing and processing equipment v>as normally operated with a slightly negative gauge pressure, thus preventing leaks of chlorine into cell room atmospheres. Pressure fluctuations occurring in the system from power outages or compressor failures could have caused chlorine leakage until cells were shutdown.
Connell and Fetch  described vacuum-operated systems for water chlorination. These systems removed much of the hazard which could result from leaks in pressurized chlorine piping. V. DEVELOPMENT OF STANDARD

# Basis for Previous Standards
In order to obtain data on industrial contaminants which might affect Massachusetts' workers, Elkins  prepared in 1939 a list of existing threshold concentrations or maximum allowable concentrations (MAC's), added some tentative proposals for Massachusetts, and sent the list to 19
American and 8 foreign experts. Suggestions and criticisms were received from all but two of the American and four of the foreign experts. The results were tabulated and considered in detail by the Massachusetts Dust and Fume Code Committee. One ppm was proposed for chlorine as a maximum allowable concentration.
There was no written explanation provided to determine if this was intended as a TWA or as a ceiling value.
In 1945, Cook  compiled a list of standards and recommendations for MAC's of industrial atmospheric contaminants. The author noted that 1 ppm was the MAC value for exposure to chlorine in the workplace air in California, Connecticut, Massachusetts, New York, Oregon, and Utah.
According to Cook, 2 ppm was the standard promulgated by the American National Standards Association (now the American National Standards Institute Inc). The American National Standards Institute Inc order department, however, has no record of a standard prior to 1945 (written communication, March 1976).
Cook  reported that early work had indicated 1 ppm should be the maximum allowable concentration for chlorine, and that this recommendation had been generally followed in industry. However, Cook  proposed 5 ppm rather than 1 ppm based on data referred to in the US Bureau of Mines technical paper 248.  This paper described research conducted by the Chemical Warfare Service, American University Experiment Station, and purportedly showed that 15.1 ppm chlorine was necessary to cause throat irritation and 30.2 ppm was necessary to cause coughing, while the chlorine concentration least detectable by odor was 3.5 ppm. This value was likely a TWA concentration since Cook stated that in every case the concentrations given were considered allowable for prolonged exposures, usually assuming a 40-hour week.
In 1947, the American Conference of Governmental Industrial Hygienists (ACGIH)  adopted an MAC for chlorine of 2 ppm. It was not stated whether this MAC was intended as a ceiling concentration or as a TWA concentration. The April 1948 meeting of this same organization  adopted 1 ppm as a threshold limit value (TLV). This TLV for chlorine was clearly specified as a TWA concentration.
In their documentation of TLV's  published in 1962, the ACGIH cited reviews by Heyroth  and Henderson and Haggard  to explain its selection of 1.0 ppm as the TLV for chlorine. Heyroth  cited data from an unpublished dissertation that men could work without interruption in air containing 1-2 ppm chlorine. A translation of this dissertation by Matt  has been reviewed in Chapter III under Effects on Humans.
Heyroth listed 1 ppm as a "maximum permissible" limit in 13 states and 5 ppm in Ohio and Washington. Heyroth  also referred to the Principles of Exhaust Hood Design,  in which DallaValle suggested that the limit be less than 0.35 ppm. The basis for this limit was not identified.
Henderson and Haggard  recommended a maximum concentration of 0.35-1.0 ppm for prolonged exposure. The only reference cited by either Heyroth  or Henderson and Haggard  which gave any support to the TLV of 1 ppm was Matt,  as quoted by Heyroth.
Henderson and Haggard  and a more recent edition of Heyroth  were used as a basis for the 1966 documentation  of the 1-ppm chlorine TLV.
It was recommended as a ceiling value "to minimize chronic changes in the lungs, accelerated aging, and erosion of the teeth," but no data were given to document the occurrence of these chronic changes.
Between 1965 and 1968, ] the 1-ppm TLV was considered a ceiling value by the ACGIH. A revised second edition of the Documentation citing Heyroth  listed a threshold limit of 1 ppm as adopted by the ACGIH and deleted its discussion of concentrations proposed by different states and its reference to DallaValle.  The 1971 documentation of threshold limit values  acknowledged that relatively few studies provided data useful in developing a TLV and proceeded to give a general review of proposed limits without specifically supporting its TLV as a TWA concentration of 1 ppm. Thus it stated that Heyroth  and Flury and Zernik  had proposed 1 ppm, Henderson and Haggard  had suggested 0.35-1 ppm, Cook  had suggested 5 ppm, and Rupp and Henschler  had proposed 0.5 ppm. This documentation  discussed the results of studies by McCord,  Ferris et al,  and Kowitz et al  in which adverse effects were found in humans after exposure to chlorine. However, the exposure levels in these studies  varied from negligible to 15 ppm and did not give support to the TLV of 1 ppm. The Kowitz et al report  concerned a chlorine accident and did not quantify exposures.
In 1971, the Pennsylvania Department of Environmental Resources  adopted a 1-ppm TLV which was a TWA concentration and it also adopted a short-term limit of 3 ppm for 5 minutes.
 Heyroth  and Imperial Chemical Industries, Great Britain, (no specific reference listed) were cited as a basis for the documentation of these short-term limits. Heyroth  reported that chlorine at 3-6 ppm caused a reaction, but that men could work without interruption at 1-2 ppm. The Imperial Chemical
Industries recommendation  stated that exposure to chlorine at 4 ppm for more than a short time might lead to symptoms of illness.
A number of occupational airborne chlorine limits have been set by foreign countries and international groups. East Germany, Hungary, Poland,
Weill et al,  Kaufman and Burkons,  and Heyroth.  The present federal standard (29 CFR 1910.1000) for chlorine is an 8-   relied on statements by exposed individuals about their health. These statements were made an unspecified time after exposure, without other confirmation. He assigned 20% of the persons to the category of those having "difficulties believed to be a reasonable consequence of the accident." Kowitz et al  performed a series of pulmonary function tests on 11 persons after they were discharged following hospitalization for exposure to chlorine and found that, even after 3 years, their lung volumes were still low. The study did not provide a quantitative estimate of the exposure, although the acute respiratory distress had been severe in 7 of the 11, and acute symptoms were documented in the remaining 4. There were no data given for effects at concentrations of chlorine between 0.5 and 1.0 ppm.
In a similar study, Beck  found that 4 of 10 subjects, after exposures of up to 30 minutes, experienced some tickling and stinging in the nose at 0.09 ppm, and one had a weak cough. At 0.2 ppm, 7 of 13 had tickling and stinging in the nose and throat and 3 had slight conjunctival burning. At 1 ppm, 7 of 10 had symptoms of upper respiratory irritation.
In one subject, the exposure had to be terminated in 20 minutes because it was unbearable.
With gradually increasing concentrations of chlorine, three of four subjects exposed felt a stinging in the throat at 0.3 ppm, and at 1.4 ppm, one subject felt neck pain and conjunctival irritation.
Matt  experienced an unpleasant burning in the eyes and nose when he exposed one subject to chlorine at a concentration of 1.3 ppm. He concluded, however, that uninterrupted work was possible at this level.
In contrast, subjective responses of industrial hygienists from the Dow Chemical Company  suggested that chlorine at a higher concentration was required to produce a respiratory response or eye irritation. During air sampling periods of 10 minutes or more, average chlorine concentrations of 1.92-41.0 ppm produced a "minimal", "easily noticed," or "strong" respiratory response. Eye irritation was considered "minimal" at an average concentration of 7.7 ppm (one air sample) and "easily noticed" at concentrations of 8.7-41.0 ppm (4 samples). The above values were qualified, however, by the observation that a previous exposure of the same individual on the same day resulted in a less discerning response subsequently.
Several epidemiologic studies  have attempted to relate previous industrial exposure to the frequency of pulmonary abnormalities and symptoms found.
The study by Ferris et al  indicated that no specific adverse effects resulted from repeated exposures to chlorine at concentrations ranging from 0 to 64 ppm over a period averaging 20.4 years.
Insufficient data were provided, however, to determine TWA exposures. The most extensive prevalence study, which was conducted by Patil et al  and which was the only one reporting time-weighted averages, reported TWA concentrations of chlorine were 0.44 ppm or less for all but 21 of 332 workers. For these 21, the TWA concentrations ranged from 0.52 to 1.42 ppm; 15 were 0.52-1.00 ppm and 6 were 1.00-1.42 ppm, and their durations of It is recognized that many workers handle small amounts of chlorine or work in situations where, regardless of the amounts used, there is only negligible contact with the substance. Under these conditions, it should not be necessary to comply with many of the provisions of this recommended standard, which has been prepared primarily to protect worker health under more hazardous circumstances. Concern for worker health requires that protective measures be instituted below the enforceable limit to ensure that exposures stay below that limit. For these reasons, "exposure to chlorine" has been defined as exposure at or above one-half of the environmental limit, thereby delineating those work situations which do not require the expenditure of health resources for environmental and medical monitoring and associated recordkeeping. One-half of the environmental limit has been chosen on the basis of professional judgment rather than on quantitative data that delineate nonhazardous areas from areas in which a hazard may exist. However, because of nonrespiratory hazards such as those  Use of fully or partially enclosed processes is recommended. 

# Training and Drills
The value of drills and training in handling emergencies and in using equipment for personal protection and control of escaping chlorine was emphasized in the literature.  Danielson  reported on a chlorine spill caused by a rail car bumping into a tank car discharging chlorine. A total of 55 tons of chlorine could have been released into the atmosphere; however, only a few tons escaped because of quick action by employees and supervisory personnel. Danielson  credited the quick action to rigorous and thorough training and drills.

# Leaks
Studies by the Bureau of Mines  indicate that pinhole leaks in chlorine containers are rapidly enlarged by corrosion if moisture is present.
Furthermore, the control of chlorine leaks or spills by the use of water is not effective because of the limited solubility of chlorine in water.  Even the coldest water will supply sufficient heat to cause an increase in the evaporation rate of chlorine.  Therefore, water must never be used on leaking containers of chlorine, or to control spills.
It is illegal to ship a leaking container of chlorine.
Daily checks must be made for leaks in pressurized chlorine systems and containers.  Leaks may be detected by using the vapor from strong ammonia water. A white cloud will be formed near leaks.  If leaking chlorine cannot be removed through regular process equipment, it may be absorbed in alkaline solutions.  These solutions can be prepared as described in Table XIII-3.
 The quantities listed in the table are chemical equivalents and it is desirable to provide excess over these amounts in order to facilitate absorption.
Emergency leak kits designed for standard chlorine containers are available at various locations throughout the country. These kits operate on the principle of capping off leaking valves or, in the case of cylinders and ton containers, of sealing off a rupture in the side wall.
 A record of kit locations is maintained by the Chlorine Institute.  If possible, users of chlorine should have their own appropriate emergency leak kits readily available for use at the process location. It should be noted, however, that the use of leak kits requires some training prior to use in an emergency situation.
Chlorine containers must be used on a first-in, first-out (FIFO)
basis,  because valve packings may harden during prolonged storage and cause leaks when containers are finally used.
Because of the potential danger of excessive hydrostatic pressure in chlorine containers, such containers are filled only partially with liquid chlorine, leaving sufficient gas-filled space to act as an expansion chamber.  Accordingly, gaseous chlorine is discharged from a cylinder if the cylinder is in the upright position, and liquid chlorine is discharged if the cylinder is inverted. Gaseous chlorine is discharged from the upper valve and liquid chlorine from the lower valve in a ton container. To minimize a leak in a container, the container should be oriented so that gaseous chlorine is discharged instead of liquid. The volume of gaseous chlorine formed by vaporization of liquid chlorine is about 450 times its original volume as a liquid.  Protective Clothing and Equipment Whenever liquid or gaseous chlorine is handled or used, it may come in contact with the skin and eyes, or be inhaled. For this reason, personal protective clothing and equipment are necessary. While not specific for chlorine, safety glasses or goggles, hard hats, and safety shoes should be worn or be available as dictated by the special hazards of the area or by plant practice.  Personnel working in areas where chlorine is handled or used should be provided with suitable escape-type respirators. Supplied-air and self-contained breathing apparatus should be used when the concentration of chlorine is not known, as in an emergency.
Canister-type gas masks have limitations. In chlorine concentrations of 2% (20,000 ppm), a canister will protect the user for about 10 minutes.  Canisters should be discarded and replaced whenever they are used, or when the shelf life, as indicated by the manufacturer, expires. Canister masks do not protect in atmospheres deficient in oxygen and should not be used except for escape in chlorine concentrations exceeding 1%.  Self-contained breathing apparatus or supplied-air full-face respirators should be worn when atmospheres contain more than 1% chlorine or where oxygen deficiency may exist. Workers required to use respiratory protection must be thoroughly trained and drilled in its use.  When the concentration of chlorine is not known, as in an emergency, canister masks must not be used.

# Fire and Explosions
Chlorine is classified as nonflammable and nonexplosive. However, it will support combustion of certain materials,   during the manufacture of chlorine,  and in chlorine absorption systems.  The last two incidents  were caused by a mixture of hydrogen and chlorine which was in excess of the explosive limits. Determination of the explosive limits of chlorine-hydrogen mixtures indicates variations of from 3% hydrogen in pure chlorine to 8% hydrogen in a pressurized gas mixture containing 19% chlorine.  It is important that precautionary measures be taken to prevent chlorine from coming into contact with materials with which :Lt may react.

# Hydrostatic Rupture of Containers and Systems
Liquid chlorine has a very high coefficient of thermal expansion.
 A 50 F (28 C) rise in temperature causes a volume increase of about 6%.  If liquid chlorine is trapped in a pipeline between two valves, increasing temperature will cause very high pressures, leading to possible hydrostatic rupture of the line. Accordingly, precautions must be taken to avoid this. It is important that liquid chlorine lines be at the same or higher temperature as the chlorine being fed into the line to prevent condensation, and that the lines be equipped with adequate expansion chambers, pressure relief valves, or rupture discs discharging into a receiver or a safe area. ] Some expansion chambers are heated to ensure that chlorine does not condense therein and destroy the effectiveness of the vapor cushion.
 Should it become necessary to evacuate a chlorine line equipped with expansion chambers, it is important that the vacuum not be broken with liquid or gaseous chlorine, a procedure which would render the expansion chambers ineffective. Dry air or nitrogen must be used for breaking such vacuums.  Warning Properties
The readily identifiable odor of chlorine and the attendant disagreeable reactions it produces appear to be one means by which workers are warned of impending excessive exposure. 105,137,141,156] However, determinations of the threshold of odor have given varying results. For example, Ryazanov  found the threshold of odor of chlorine to be 0.3-0.45 ppm, while Fieldner et al  and Leonardos et al  reported it to be 3.5 ppm and 0.314 ppm, respectively.
The variation of these results probably reflects differences in methods of determination, and possibly differences in the development of odor adaptation.
[ Ventilation systems for transporting chlorine should be constructed of corrosion-resistant materials.

# Unusual Sources
Excessive exposure to chlorine may occur when solutions of hypochlorites are mixed with materials such as toilet bowl cleaners  or vinegar.  Maintenance and custodial personnel should be warned of this possibility and instructed not to mix hypochlorites with any other material.
Chlorine exposure may also occur when chlorinated hydrocarbons are decomposed thermally  or by ultraviolet radiation from electric arcs.  hypochlorous acid with cytosine.
The date and time of sample collection.
(2) Sampling duration.
(3) Volumetric flowrate of sampling.
(4) A description of the sampling location.
(5) Ambient temperature and pressure.
(6) Other pertinent information (eg, worker's name, shift, work process).
Breathing Zone Sampling (a) Breathing zone samples shall be taken as near as practicable to the worker's face without interfering with his freedom of movement.
Care should be taken that the bubbler is maintained in a vertical position during sampling.

# (b)
A portable, battery-operated, personal sampling pump capable of being calibrated to 5% at the required flow in conjunction with a midget fritted bubbler (coarse porosity) holding 10 ml of sampling solution shall be used to collect the sample,
The sampling rate shall be accurately maintained at 1-2 liters/minute for a period of 15 minutes.

# (d)
A "blank" bubbler should be handled in the same manner as the bubblers containing the samples (ie, fill, seal, and transport) except that no air is sampled through this bubbler.

# Calibration of Sampling Trains
Since the accuracy of an analysis can be no better than the accuracy of the volume of air which is measured, the accurate calibration of a sampling pump is essential to the correct interpretation of the volume indicator. The frequency of calibration is dependent on the use, care, and handling to which the pump is subjected. In addition, pumps should be recalibrated if they have been misused, or if they have just been repaired or received from a manufacturer. If the pump receives hard usage, more frequent calibration may be necessary. Ordinarily, pumps should be calibrated in the laboratory both before they are used in the field and after they have been used to collect a large number of field samples.
The accuracy of calibration is dependent upon the type of instrument used as a reference. The choice of calibration instrument will depend largely upon where the calibration is to be performed. For laboratory testing, a 1-liter buret (soapbubble flowmeter) or wet-test meter is between the preselected marks by the time required for the soapbubble to travel the distance. The methyl orange solution is reported  to be less bleached by a rapid addition of halogen without stirring than by slow addition with vigorous mixing. Sulfur dioxide interferes negatively, decreasing the chlorine by an amount equal to one-third the sulfur dioxide concentration.

# Sensitivity and Range
The procedure given is designed to cover the range of 5-100 /xg of free chlorine/100 ml sampling solution. For a 30-liter air sample, this corresponds to approximately 0.05-1.0 ppm in air, the optimum range.

# Precision and Accuracy
Chlorine concentrations have been measured by this procedure with an average error of less than 5% of the amount present.

# Storage
The color of the sampled solutions is stable for 24 hours if protected from direct sunlight, although certain agents  may induce kinetic responses resulting in a slow color change.
X.

# APPENDIX III RECOMMENDED RESEARCH
There is clear need for information in the following areas in order to set a limit for chlorine which is more reliably based on demonstrated dose-response relationships: Chemical substances should be listed according to their complete name derived from a recognized system of nomenclature.
Where possible, avoid using common names and general class names such as "aromatic amine,"
"safety solvent," or "aliphatic hydrocarbon" when the specific name is known.
The "%" may be the approximate percentage by weight or volume (indicate basis) which each hazardous ingredient of the mixture bears to the whole mixture. This may be indicated as a range or maximum amount, ie, "10-40% vol" or "10% max wt" to avoid disclosure of trade secrets.
Toxic hazard data shall be stated in terms of concentration, mode of exposure or test, and animal used, ie, "100 ppm LC50-rat," "25 mg/kg LD50skin-rabbit," "75 ppm LC man," or "permissible exposure from 29 CFR 1910.1000," or, if not available, from other sources of publications such as the American Conference of Governmental Industrial Hygienists or the American National Standards Institute Inc. The "Health Hazard Data" should be a combined estimate of the hazard of the total product. This can be expressed as a TWA concentration, as a permissible exposure, or by some other indication of an acceptable standard. Other data are acceptable, such as lowest LD50, if multiple components are involved.
Under "Routes of Exposure," comments in each category should reflect the potential hazard from absorption by the route in question. Comments should indicate the severity of the effect and the basis for the statement, if possible. The basis might be animal studies, analogy with similar products, or human experiences. Comments such as "yes" or "possible" are not helpful. Typical comments might be:
Skin Contact-single short contact, development of burns; prolonged or repeated contact, pain and tissue destruction.
Eye Contact-burning and tearing "Emergency and First Aid Procedures" should be written in lay language and should primarily represent first aid treatment that could be provided by paramedical personnel or individuals trained in first aid.
Information in the "Notes to Physician" section should include any special medical information which would be of assistance to an attending physician including required or recommended preplacement and periodic medical examinations, diagnostic procedures, and medical management of overexposed workers.

# (f) Section VI. Reactivity Data
The comments in Section VI relate to safe storage and handling of hazardous, unstable substances. It is particularly important to highlight instability or incompatibility to common substances or circumstances such as water, direct sunlight, steel or copper piping, acids, alkalies, etc.
"Hazardous Decomposition Products" shall include those products released under fire conditions. It must also include dangerous products produced by aging, such as peroxides in the case of some ethers. Where applicable, shelf life should also be indicated. Respirators shall be specified as to type and NIOSH or US Bureau of Mines approval class, ie, "Supplied air," "Organic vapor canister," "Suitable for dusts not more toxic than lead," etc. Protective equipment must be specified as to type and materials of construction.
recommended, although other standard calibrating instruments, such as a spirometer, Harriott's bottle, or dry gas meter, can be used.
Instructions for calibration with the soapbubble flowmeter follow. However, if an alternative calibration device is selected, equivalent procedures should be used.
The calibration setup for personal sampling pumps with a midget bubbler is shown in

# % V O L A T IL E S BY V O L E V A P O R A T IO N R A T E (B U T Y L A C E T A T E = - 11 AP P E A R A N C E A N D O DOR