# CRITERIA DOCUMENT: RECOMMENDATIONS FOR AN OCCUPATIONAL EXPOSURE STANDARD FOR PHOSGENE
recommends that worker exposure to phosgene in the workplace be controlled by requiring compliance with the following sections. The standard is designed to protect the health and safety of workers for up to a 10-hour workday, 40-hour workweek over a working lifetime. Compliance with the standard should therefore prevent adverse effects of phosgene on the health and safety of workers. The standard is measurable by techniques that are valid, reproducible, and available to industry and government agencies.
Sufficient technology exists to permit compliance with the recommended standard. The standard will be subject to review and revision as necessary.
"Phosgene" is defined as gaseous or liquified phosgene. Synonyms for phosgene include carbonyl chloride, carbon oxychloride, chlorofomyl chloride, and CG (designation used by military agencies). "Occupational exposure to phosgene" is defined as exposure above half the recommended time-weighted average (TWA) environmental limit. Exposure at lower concentrations will not require adherence to the following Sections except "Overexposure" is defined as known or suspected exposure above either the TWA or ceiling concentrations, or any exposure which leads to development of pulmonary symptoms. Procedures for sampling, calibration of equipment, and analysis of environmental 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 (a) Comprehensive preplacement and annual medical examinations shall be made available to all workers to be occupationally exposed to phosgene unless a different frequency is indicated by professional medical judgment based on such factors as emergencies, variations in work periods, and preexisting health status of individual workers.
(b) These examinations shall include, but shall not be limited to:
(1) Comprehensive or interim medical and work histories.
(2) A comprehensive medical examination giving particular attention to pulmonary function. Preplacement and follow-up pulmonary function tests shall be performed and shall include the forced vital 2 capacity (FVC), the one-second forced expiratory volume (FEV 1), and the forced midexpiratory flow (FEF ; a preplacement chest X-ray shall be obtained. The possibility of increased risk for workers with preexisting cardiovascular or pulmonary diseases should be considered and, when appropriate, the workers should be given counseling on the possibility of increased risk.
Return to work after an absence for sickness due to phosgene overexposure shall require medical approval.
(3) A judgment of the worker's ability to use a negative or positive pressure respirator.
(c) Proper medical management shall be provided for workers overexposed to phosgene.
In case of known or suspected overexposure to phosgene, first aid measures shall be taken immediately, followed by prompt medical evaluation and care. Overexposed persons should not be permitted any unnecessary physical exertion. They should be carried to a vehicle for subsequent transportation to receive medical assistance. Pressurized oxygen and attendants trained in its use shall be available in the event they are needed for persons in respiratory distress. In case of skin or eye contact with liquid phosgene, contaminated clothing shall be removed immediately and the exposed body areas flushed with copious amounts of water. The plant physician or medical consultant shall be informed of any suspected overexposure to phosgene and shall determine the need for X-ray or Open containers with care.
Have respiratory protection available for emergency.

# FIRST AID CALL A PHYSICIAN IMMEDIATELY
In case of inhalation, remove victim to uncontaminated atmosphere.
If breathing stops, administer artificial respiration. Do not allow victim to walk or exercise.
In case of liquid contact, immediately flush skin or eyes with water.
Remove contaminated clothing without delay and dispose of liquid properly.

# (b)
The following warning sign shall be affixed in a readily visible location at or near entrances to areas in which phosgene is stored, handled, used, or formed:

# CONTAINS PHOSGENE EXTREME HEALTH HAZARD
Harmful or fatal if inhaled, may cause delayed lung injury.
In emergency, enter only if wearing respiratory, eye, and skin protection. Phosgene respiratory protection located at (specific locations to be supplied by employer). Unauthorized persons keep out.
This sign shall be printed both in English and in the predominant language of non-English-speaking workers, if any. All employees shall be trained and informed of the hazardous area with special instruction given to illiterate workers.
(c) All systems, piping, and associated equipment containing phosgene shall be plainly marked for positive identification in accordance with American National Standard A13. . Shut-off valves shall be conspicuously labeled. Phosgene containers in use shall be plainly marked "In Use" to distinguish them from those not in use. (1)
In addition to the respiratory protection specified in Table 1-1, personnel performing emergency operations involving exposure to liquid phosgene shall wear one-piece suits, impervious to phosgene and tight at the ankles, wrists, and around the neck and face. The suits shall be ventilated with supplied air, preferably cooled, or time in the work area shall be limited with due consideration to the heat stress factors involved. Impervious gloves and boots shall also be worn. Such protective clothing shall be available at a convenient location outside the contaminated area.
The employer shall insure a sufficient supply and adequate maintenance of protective clothing.

# (b) Eye Protection
Personnel handling liquid phosgene in situations where eye contact can occur shall have eye protection afforded by full-face respiratory protection as specified in Table 1- as amended, shall be established and enforced by the employer. Only appropriate respirators as described in Table 1-1 shall be used.
2ppm
Greater than 2 ppm or emergency situations
(1) Any supplied-air respirator; or
(2) Any self-contained breathing apparatus.
(1) Any supplied-air respirator with a full facepiece, helmet, or hood; or
(2) Any self-contained breathing apparatus with a full facepiece.
(1) Self-contained breathing apparatus with a full facepiece operated in pressure-demand or other positive pressure mode; or  occupational exposure to phosgene shall have at least 2 sets of selfcontained breathing apparatus readily available in nearby locations which do not require entry into, or passage through, a contaminated area for access.
(4) Respirators specified for use in higher concentrations of phosgene may be used in atmospheres of lower concentrations.
(5) Employees shall be trained and drilled in the use of respirators assigned to them and in testing for leakage.
Canisters shall be discarded and replaced with fresh canisters after use. Unused canisters shall be discarded and replaced when the seal is broken or when the shelf life, as recommended by the manufacturer, is exceeded.

# Section 5 -Informing Employees of Hazards from Phosgene
At the beginning of employment, workers who will work in areas required to be posted in accordance with Section 3(b) shall be informed of the hazards from phosgene, symptoms of overexposure, emergency procedures, and precautions to ensure safe use and to minimize exposure. First aid procedures shall be included. This information shall be posted in the work place and kept on file, readily accessible to the worker.
A continuing educational program shall be instituted for workers whose jobs may involve occupational exposure to phosgene. This is to ensure that all such workers have current knowledge of job hazards, maintenance procedures, and clean-up methods, and that they know how to use respiratory protective equipment and protective clothing. Workers should be advised that the detection of the odor of phosgene at any time indicates the need for immediate corrective procedures or withdrawal from the area.
First-line supervisors shall be thoroughly informed of these hazards and procedures and should participate in the education of workers. 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.
Procedures shall Include prearranged plans for:
(A) immediate evacuation of overexposed workers;
(B) transportation of overexposed workers;
(C) any necessary calls for assistance, including alerting medical facilities of the impending arrival of overexposed workers, and calls to suppliers or manufacturers of phosgene for any necessary technical advice;
(D) designation of medical receiving facilities and names of physicians trained in phosgene emergency procedures;
(E) reentry for maintenance or clean-up purposes of areas where phosgene leaks or spills have occurred.
(2) Approved eye, skin, and respiratory protection as specified in Section 4 shall be used by personnel essential to emergency operations.
Water shall not be used on phosgene leaks because accelerated corrosion of metal by phosgene in the presence of moisture will quickly make the leak worse.
If possible, phosgene emissions shall be directed to an alkali scrubber or to process (ie, routed by means of appropriate valving within a closed system to a secondary holding vessel or neutralization system).
Containers leaking liquid phosgene should he positioned so that gaseous phosgene is discharged through the leak until control is effected. enclosed processes is the preferred method of control for phosgene. Local exhaust ventilation may also be effective, used alone or in combination with process enclosure. Ventilation systems shall be designed to prevent the accumulation or recirculation of phosgene in the workroom, to maintain phosgene concentrations within the limits of the recommended standard, and to remove phosgene from the breathing zones of workmen. Exhaust ventilation systems shall discharge to the outside air through a sorption or a decomposition system (eg, scrubbers containing an alkaline scrubbing medium, such as 5% sodium hydroxide solution). Ventilation systems shall be subject to regular preventive maintenance and cleaning to ensure effectiveness, which shall be verified by periodic air-flow measurements.
Tempered makeup air shall be provided to workrooms in which exhaust ventilation is operating.

# (c) Storage
(1) Phosgene shall be stored in unoccupied, adequately ventilated, cool, and dry rooms, or outdoors shielded from the direct rays of the sun and protected from moisture.
(2) Phosgene storage rooms shall be provided with an inspection window to permit viewing of the interior without entry.
Other materials should not be stored with phosgene.
Phosgene containers shall be frequently inspected for leaks and deterioration. If the hydrostatic test date stamped on cylinders is older than 5 years, the cylinder shall be returned to the vendor, or arrangements shall be made to have the necessary test performed.

# (d) Handling and General Work Practices
(1) Written operating instructions and emergency medical procedures shall be formulated and posted where phosgene is handled or used.
(2) Prompt medical attention shall be obtained if there is known or suspected overexposure to phosgene, whether or not symptoms are present.
(3) Returnable phosgene containers shall not be washed out with water.
(4) Safety valves and vents for phosgene equipment shall discharge through absorbers or neutralizers (decomposition system).
The amount of phosgene used from a container shall be determined by a positive method (eg, weighing the preweighed container).
(13) New gaskets shall be used each time phosgene system connections are made.
Welding or burning on tanks or equipment which have contained phosgene shall take place only after such tanks or equipment have been thoroughly purged with a dry inert gas, vented to a sorption or decomposition system. Steam or water shall not be introduced to the tanks, system, or equipment. Phosgene equipment, containers, or piping shall not be repaired while in service.
Before phosgene is admitted to a system, the system shall be thoroughly cleaned, dried, and tested, using previously formulated procedures.
(16) Personnel shall not work alone when phosgene is first admitted to a system or while repairing leaks.
Containers and systems shall be handled and opened with care. Approved eye, skin, and respiratory protection shall be worn while opening, connecting, and disconnecting phosgene containers and systems.
When opening containers or systems, adequate ventilation shall be available to prevent inadvertent exposure to phosgene.
Any odor of phosgene shall be reported to a responsible authority or an alarm sounded as soon as possible after the area has been vacated.
(e)
Work Areas
(1) Where phosgene is stored, piped, handled, or used, eyewash fountains and safety showers shall be located immediately outside the area. They shall be readily accessible and shall be inspected frequently and kept in good working order.
(2) Enclosed phosgene work areas shall be equipped with at least 2 exits, remote from each other, to allow escape into uncontaminated areas in case of emergency. Doors shall open outward.
(3) Unauthorized personnel shall be prohibited from entering areas where phosgene is handled or used.
(4) Wherever possible, phosgene installations shall be outdoors. If it is necessary that such installations be indoors, workers should operate from a pressurized control room supplied with fresh air from an area remote from any possible source of phosgene contamination.
(5) For reentry purposes, at least 2 sets of self-contained breathing apparatus as specified in (2) Phosgene shall not be allowed to enter drains or sewers.
Appreciable discharges of phosgene shall be passed through an adequate decomposition system, such as a scrubbing tower utilizing sodium hydroxide or ammonium hydroxide, or through a sorbent system.
(4) Solid sorbents should be chosen so that desorption of phosgene is unlikely. Heating of the solid sorbent should be avoided.
(g) Confined Spaces
(1) Entry into confined spaces such as tanks, pits, tank cars, barges, process vessels, and tunnels shall be controlled by a permit system. Permits shall be signed by an authorized employer representative certifying that preparation of the confined space, precautionary measures, and personal protective equipment are adequate, and that precautions have been taken to ensure that prescribed procedures will be followed.
(  The development of the recommended standard for occupational exposure to phosgene has revealed deficiencies in the data base in the following areas:
(1) epidemiologic studies of workers exposed to phosgene for extended periods;
(2) chronic animal exposure studies at low levels of phosgene;
(3) improvement of the sensitivity of sampling and analytical methods for personal monitoring;
(4) testing of automatic, continuous monitoring systems and associated alarms.
These gaps in our knowledge of phosgene should be filled.

# III. BIOLOGIC EFFECTS OF EXPOSURE

# Extent of Exposure
Phosgene is a colorless gas at normal temperatures and pressure.
When liquified under pressure or refrigeration, it is a colorless-to-light yellow liquid.  In low concentrations, its odor has been variously described as resembling that of musty hay  or green corn.  Phosgene is easily manufactured by passing chlorine and excess carbon monoxide over activated carbon.  Shortages of chlorine and attendant high prices have somewhat restricted the manufacture of phosgene in recent years.  Some phosgene can also be produced by the decomposition of chlorinated hydrocarbons by heat or by ultraviolet radiation.  Relevant properties of phosgene are presented in Accordingly, much of the literature on phosgene is concerned with its military applications. Phosgene production in the United States in 1957, the first year the US Tariff Commission started reporting phosgene output, was only 5 million pounds.  In 1967, production reached 350 million pounds,  in 1971, 530 million pounds,  while in 1972, it had increased to 657 million pounds.  In contrast to these figures, sales in 1971 were only 11,215,000 pounds  and 11,678,000 pounds in 1972.  The apparent discrepancy between production and sales is due to the fact that the major portion of the phosgene manufactured is for "captive" use (use by the phosgene manufacturer), while the relatively small remainder is sold.  In 1974, phosgene was being produced in 18 plants and capacity was on the increase.  It has been estimated that demand will be 1,630 million pounds in 1978.  The relatively recent revitalization of the phosgene industry and the rapidly increasing demand are due largely to the use of phosgene in the synthesis of isocyanates, which are starting materials for polyurethane resins. Production of isocyanates accounted for about 75% of all phosgene produced in 1967.  In 1974, the uses of phosgene were distributed as follows: production of toluene diisocyanate, 62%; other polymeric isocyanates, 23%; polycarbonates, 6%; pesticides, carbonates, and "specialties," 9%.  Some occupations with potential exposure to phosgene are listed in Table XIII-2.  NIOSH estimates that 10,000 workers have potential occupational exposure to phosgene during its manufacture and use.

# Historical Reports
Berghoff  reported his observations of 2,000 cases of exposure to war gases during World War I. These included chlorine, mustard gas, and phosgene.
The main complaint expressed by those exposed to phosgene was a weakness which developed as early as 2 hours or as late as 3 days after exposure. This weakness lasted for weeks or months. The author also noted that emphysematous patients had a more protracted convalescence than those classified as bronchitic.

# Effects on Humans
Wells et al  published a detailed report on effects of barely detectable concentrations of phosgene on humans. Fifty-six military personnel, without upper respiratory problems, were exposed to increasing concentrations of phosgene until all the subjects could detect phosgene by odor.
The authors reported that 50% of "technically trained" (without further clarification) observers detected phosgene at a concentration of  Five hours after exposure, the patient felt a slight pressure on his chest.
Eight hours after exposure, he became dyspneic and expectorated bloody sputum.
He was admitted to the hospital one hour later. Chest films showed pulmonary edema. Thirteen days of hospitalization, which included treatment with corticosteroids, digitalis, and oxygen, were required to resolve his pulmonary problems.
The fatal accident involved a 55-year-old mason who was presumed to have been exposed to phosgene released by chipping of brick which had possibly adsorbed phosgene. In this case, phosgene was a byproduct in the production of aluminum chloride. An analysis of the apparatus the patient worked on revealed that 2.5 liters of interstitial air volume in the brick at 360-400 C was available for absorbing the phosgene. The amount of dust inhaled by the patient is unknown. He was exposed for 30 minutes and first complained of dyspnea about 2 hours after completing the job. No first aid was given. Five hours after exposure, he was admitted to the hospital in severe respiratory distress. Chest films showed pulmonary edema. Despite phlebotomy and treatment with digitalis and diuretics, the patient died of acute right heart failure about 14 hours after his initial exposure.
Two cases of phosgene exposure were reported by Gerritsen and Buschmann.  They were due to accidental formation of phosgene from chlorinated hydrocarbons. Both cases involved the use of chemical paint removers in poorly ventilated areas heated by portable kerosene stoves.
The first case involved a 52-year-old man who was exposed for an unknown period. He noted respiratory irritation soon after beginning work but persisted working for several hours. Chest symptoms occurred thereafter and the patient, upon examination, exhibited signs of pulmonary congestion.
Approximately 5 hours later, the patient went into frank pulmonary edema and died within a few hours. Autopsy showed extensive degenerative changes in the epithelium of the trachea, bronchi, and bronchioli, together with hemorrhagic edematous focal pneumonia.
The second case  involved a 38-year-old woman, in her 7th month of pregnancy, who was exposed in a similar manner for 3 hours in the afternoon.
That evening hemoptysis occurred. The next morning, symptoms worsened and she was hospitalized. A chest film upon admission showed pulmonary edema. After 8 days' hospitalization, she was released even though her chest film did not yet show a complete return to normal. After 2 months, she gave birth to a healthy child. This is the only case found which reported phosgene exposure during pregnancy.
In attempting to reproduce the circumstances of exposure of the above 2 cases,  it was found that methylene chloride was rapidly decomposed with phosgene being the main decomposition product when methylene chloride was exposed to heat in a poorly ventilated area. The authors stated that this was in contrast to the results reported by Little  when methylene chloride was decomposed by hot surfaces and low amounts of phosgene were produced in comparison with hydrogen chloride and chlorine.
Another case of possible phosgene poisoning resulting in death was reported by Spolyar et al.  The case involved a chlorinated solvent degreaser which was inadvertently filled with trichloroethylene instead of perchloroethylene. The operator of the degreaser was found dead 3 1/2 hours after exposure began and 1 hour after he reported that fumes were escaping from the apparatus. Autopsy showed pulmonary edema consistent with exposure to phosgene. It was assumed that the trichloroethylene vaporized and passed through the firebox of a nearby space heater, with decomposition of the trichloroethylene and the production of phosgene.
Cause of death was consistent with phosgene exposure but it was suggested that trichloroethylene might have contributed to the circulatory collapse. Phosgene was believed to have been generated by the decomposition of trichloroethylene in contact with the hot tip of a burning cigarette. This theory is contradicted by the work of Little  who measured phosgene in the effluent gas of cigarettes and did not detect any in atmospheres containing trichloroethylene, chloroform, carbon tetrachloride, perchloroethylene, or even small amounts of phosgene.
Everett and Overholt  reported a case of phosgene poisoning but gave no details of exposure other than "massive exposure to phosgene."
Initial symptoms were burning of the eyes and coughing. These cleared after a few minutes, but dyspnea occurred in 3 hours. X-ray studies showed pulmonary edema which resolved over 7 days of hospitalization and treatment which included antibiotics, corticosteroids, and oxygen. The patient remained well during the ensuing 2 years.
The Bureau of Engineering Safety, Department of Labor and Industry, State of New Jersey,  reported one fatality among 6 employees exposed to phosgene at unknown concentrations in separate accidents over a 2-year period. The exposures occurred in a plant conducting "phosgenation" where measurements of air concentrations were normally reported to be below 0.1 ppm. Subsequently, all phosgene operations were stopped because of inadequate engineering controls.
Delepine  described 2 cases of fatal phosgene poisoning. The first man had his clothing saturated with phosgene and was treated almost immediately.
He appeared well but experienced symptoms 6 hours after exposure. Treatment (details not given) was temporarily helpful, but the patient died 11 hours later. The second man was exposed as a result of the explosion of a phosgene cylinder. Death occurred 22 hours after exposure.
At autopsy, both cases showed evidence of severe irritation of the respiratory tract with almost complete shedding of the laryngeal, tracheal, and bronchial epithelium.
English  reported a case of poisoning attributed to phosgene in a 67-year-old male with several years- history of chronic bronchitis and a quiescent duodenal ulcer. After an 8-hour exposure in a room heated by a stove burning paraffin in which paint-strippers containing chlorinated hydrocarbons had been used, the worker experienced dyspnea. The next morning, his symptoms increased and he was hospitalized. Chest X-rays showed diffuse bronchiolitis. Despite treatment, dyspnea persisted for 4 days in the hospital. He was discharged after 6 weeks. English stated that phosgene dissolved in saliva irritated the alimentary mucosa and, hence, was responsible for reactivation of a duodenal ulcer in this patient. He cited no authorities for this statement or clinical or experimental evidence to support it. No other references to the effects of phosgene on gastrointestinal mucosa were found other than Cherkes'  statement that stasis and venous hyperemia occur in the gastrointestinal tract as a result of pulmonary edema.
Seidelin  reported a case of probable phosgene inhalation leading to pulmonary edema in a 16-year-old woman. This occurred after she had used a carbon tetrachloride fire extinguisher in an enclosed space. In 1946, Galdston et al  reported studies of 6 cases of acute exposure to phosgene with residual effects up to 19 months after the last known acute exposure. Evaluation of each patient included physical examinations, chest X-rays, pulmonary function tests, and a psychiatric summary. These cases shared a common background of brief single exposures to phosgene at unknown concentrations which usually led to delayed pulmonary edema. One of the cases is interesting in that exposure occurred at a hood which contained an ampule of only 40 ml phosgene.
All were treated at Johns Hopkins Hospital and released, some returning to a normal work routine.
However, follow-up examinations revealed that all had lingering complaints, and although physical examinations and chest X-rays up to 19 months later were generally normal, pulmonary function tests always revealed some abnormalities consistent with beginning pulmonary emphysema.
The authors felt that psychological factors contributed to the lingering symptomatology. Their findings are summarized in Table III-l.
Cherkes,  in an extensive review of the literature concerning the clinical course of acute phosgene exposure, noted that most fatalities occur during the first 24-48 hours. He reported that most patients dying within the first 72 hours died of pulmonary edema or cardiac problems.
Those dying later usually succumbed as a result of complications, such as infection (usually pulmonary), thrombosis, or embolism. He gave no source for these statements other than "according to the data of various authors."
The clinical course following phosgene exposure reported by Cherkes is generally in agreement with other reports following human and animal exposure.  Ardran  pointed out that many victims of phosgene poisoning showed radiological evidence of increased lung volumes. His experiments with dogs  indicated that animals that failed to develop an increase in lung volume after phosgene exposure also failed to develop pulmonary edema.
This test had been used by him clinically.  He reported that, if an expiratory lung film shows evidence of an increase in volume after exposure to phosgene, then pulmonary edema may be expected. He stated that he had looked for this sign in humans exposed to lung irritants and that never, in 20 years, had he found pulmonary edema to develop in the absence of antecedent increased lung volume. There has been no independent Arterial blood oxygen, alveolar air oxygen and carbon dioxide tension studies at rest and after exercise were performed 4-8 months after all other studies were completed. Symptoms, physical and roentgenographic findings were unchanged on reexamination of all available patients (all but one) at that time. From reference 35

# Epidemiologic Studies
Levina et al  described the working environment in the monuron, 3-(p-chlorophenyl)-l,1-dimethylurea, industry. Phosgene is involved in its synthesis and was found to be contaminating 90 workers1 production areas at a concentration of 1.0-2.0 mg/cu m (JO. 2 5 -0 .5 ppm) over a 6-month period under investigation.
According to Smelyanskiy and Ulanova,  the permissible level for the USSR was 0.5 mg/cu m (0.125 ppm). Other contaminants included chlorobenzene, dimethylamine, and parachlorophenylisocyanate. Levina et al  reported no pulmonary problems in these workers, but did not describe searching for them.
Levina and Kurando  reported their studies of a plant manufacturing a weed killer (isopropylphenylcarbamate) using phosgene, isopropyl alcohol, aniline, and caustic soda as raw materials. Although a closed process was used, phosgene was found in 30% of all air samples, most frequently at a concentration of 0.5 mg/cu m (0.125 ppm). A total of 89 workers were studied for evidence of hematological abnormalities.
Methemoglobinemia and anemia were detected which were attributed to the weed killer and aniline. No mention was made of pulmonary problems.
At a plant where phosgene is manufactured, the medical records of all exposed workers (326) were compared with those of 6,288 nonexposed workers.
(AF Myers, written communication, November 1974) Pulmonary function, lung problems, and deaths related to lung problems were tabulated for both groups.
The data were taken to indicate that there were no chronic lung problems related to working in these phosgene operations. By using the age distribution of employees and pensioners and comparing their deaths from lung problems with those expected from a similar age group (described as taken from National Statistics) not exposed to phosgene, no increase in lung-related deaths was noted in the phosgene-industry workers. The They attributed this to differences in the major site of action, ie, the respiratory bronchioles in the first case, and the alveoli in the second.
The authors noted that above a Ct of 30 ppm-minutes gas exchange capacity decreased directly with the logarithmic increase in Ct. Rinehart and Hatch
 noted no significant effect of phosgene on the test animals' pulmonary performance when subjected to exposures less than a Ct of 30 ppm-minutes.
The animals' exposures were varied to cover a Ct product range of 12-360 ppm-minutes.
Gross et al  studied the effect of low concentrations (0.5-4 ppm for 5-480 minutes) on rats. They found that they could produce a chronic pneumonitis which was reversible but left detectable lesions for up to 3 months. They felt they could explain this by the fact that low dosages of phosgene merely irritated the pulmonary alveolar epithelium, resulting in proliferation. The more severe exposures of phosgene usually reported in the literature destroyed the surface epithelium and attacked the underlying alveolar capillaries, thus resulting in pulmonary edema. The authors noted that the severity of the chronic pneumonitis correlated well with the Ct value of the phosgene exposure and seemed to be largely independent of the concentration of the gas in the same bracket of Ct values. Animals in the study by Gross et al  were subjected to Ct products ranging from 13 to 360 ppm-minutes. In the 18 rats exposed to phosgene with Ct products equal to 30 ppm-minutes or less, 5 (28%) showed no abnormalities on pathologic examination; 11 (61%) showed slight chronic pneumonitis; and 2 (11%) showed moderate chronic pneumonitis.
Wirth  studied the effect of low concentrations of phosgene upon cats. He reported that, if the concentration was expressed as mg/cu m, the lethal concentration x the survival time in minutes was approximately 1,000. At low concentrations (5-7 mg/cu m, 1-2 ppm), the constant was as high as 3,000. This shows that the lethal Ct product is considerably higher at low concentrations. The author felt that the increase in Ct product at low concentrations was due to detoxification and that the practical usefulness of the Ct formula was not affected by this, provided it was used within certain concentration limits.
Cordier and Cordier   Other lung changes were found, but, in general, the effect on the pulmonary alveoli was considered to be insignificant. The authors concluded that this concentration, inhaled daily for 10 minutes, seems to be the minimal concentration capable of creating edematous pulmonary zones. This minimum effect level, expressed as a Ct product (25-37.5 ppm-minutes) concurs with the minimum effect level of 30 ppm-minutes later found by Rinehart and Hatch  in experiments with rats using pulmonary uptake of carbon monoxide and ether to measure effect.
Koontz  gassed dogs with phosgene at the minimum lethal dose (undefined by the author) and then studied 95 of those that survived. Onethird died or were killed by other dogs during the course of the experiment. The other two-thirds were killed at intervals from 2 to 60 weeks. About one-half of the dogs showed no or only minor lesions. Those with more significant abnormalities showed transient bronchial plugging and adjacent atelectasis.
Most of the lungs took on a more normal appearance as the time from recovery increased.
Durlacher and Bunting  exposed 31 dogs to phosgene at concen trations averaging 0.29 mg/ liter (72.0 ppm) for 30 minutes. The animals were given a variety of treatments, including oxygen, transfusions, or venesection. The most striking findings were consolidation of one or more lobes of the lungs 4-9 days after exposure. The authors noted that "pulmonary organization occurred...and caused high mortality in spite of oxygen therapy."
The oxygen therapy consisted of maintenance in an atmosphere of 60% oxygen when the arterial oxygen saturation was below 80%.
No specific time for initiation of therapy other than "after exposure" was given.
Gross et al  described their findings concerning pulmonary reactions to toxic gases. They noted that the proliferative lesions produced by phosgene, chlorine, sulfur dioxide, nitrogen dioxide, ozone, and crotonaldehyde differed only quantitatively on a histologic basis. It appeared probable to the authors that, with a proper adjustment of the concentration, even the quantitative difference could be eliminated. They concluded that deep lung irritants preferentially attacked the respiratory bronchioles because of delayed clearance in that region.
In 1920, Underhill  exposed dogs to phosgene and noted the development of pulmonary edema which was maximal at 24-36 hours and resolved in animals surviving 10 days or more. He concluded that the minimum lethal concentration of phosgene for dogs was 310-350 mg/cu m (75-87 ppm). He found that dogs that survived for 3 days usually recovered.
He also concluded that recovery from gassing increased the likelihood of death from regassing of dogs, which differs from the findings of Box and
Cullumbine  in rats. Underhill explained that tolerance is demonstrable only with low concentrations; it does not decrease subsequent reactions to lethal concentrations. Winternitz et al  presented detailed information on the pathology found in these animals at autopsy.
Long and Hatch  reported that a reduction in the rate of respiratory uptake of carbon monoxide was an early and sensitive test of pulmonary impairment following exposure to pulmonary irritants. The test was developed using unanesthetized rats and phosgene as the test irritant.
The animals were exposed to phosgene for 30 minutes at the following levels: 0.5-1, 1-2, 2-3, 3-4, and 4-5 ppm.
The responses included a decrease in pulmonary uptake in CO which was progressive for 6-8 hours, followed by gradual recovery. They found that their test detected changes even at the lowest level of phosgene exposure (0.5-1 ppm) in the absence of microscopic changes at autopsy.
Boyd and Perry  exposed rabbits to phosgene for 30 minutes at a concentration of 270 mg/cu m (67 ppm). They reported a latent period of several hours following exposure.
After the latent period, pulmonary edema developed.
Noweir et al  exposed rats to decomposition products of carbon tetrachloride at its TLV (10 ppm) and demonstrated  that up to 10 ppm of All species showed some degree of edema.
In a subsequent study, Cameron et al  exposed a group of animals to phosgene at an average concentration of 3.47 mg/cu m (0.86 ppm) for a single 5-hour exposure. The animal exposure group consisted of 20 mice, 10 rats, 10 guinea pigs, 10 rabbits, 2 cats, 2 monkeys, and 2 goats. On the morning following exposure, 10% of the rats (1/10) and 60% of the mice (12/20) were dead. There were no other casualties, although one cat and one monkey were very ill with considerable labored breathing. All survivors of the experiment were killed on the morning following exposure.
All animals were then autopsied and one lung from each animal was fixed in formalin for sectioning. Upon examination, 54 out of 56 animals (96.4%)
showed microscopic evidence of pulmonary involvement which was severe in 29 animals (39%), mild in 17 (31%), and slight in 16 (30%). The most frequent lung change noted was edema.
In another study, Cameron et al  reported the results of exposing a variety of animals to phosgene at an average concentration of 0.9 mg/cu m (0.2 ppm) for 5 hours daily for 5 consecutive days. The experimental group consisted of 20 mice, 10 rats, 10 guinea pigs, 10 rabbits, 2 cats, and 2 goats.
No deaths occurred during the exposures. Except for some labored breathing noted in the cats and in one goat, the other animals showed little evidence of distress. At autopsy, pulmonary lesions were seen in 67% of the animals.
In the opinion of the investigators, the great majority of such lesions were slight and of little significance.
Discounting the more susceptible animals (guinea pigs) and correcting for the normal incidence of disease in laboratory animals, the authors estimated that probably between 5 and 10% of the animals showed moderately severe lesions.
Pulmonary edema was noted in 41% of the animals but was considered to be slight in most cases. In 6 animals (1 rabbit, 1 mouse, 1 rat, and 3 guinea pigs), it was extensive. Acute bronchitis was noted in 22% of the animals and bronchial regeneration in 20%.
Their results are
shown in Table III-3.
In their summary statement, the authors  advanced the opinion that there is little doubt that repeated exposure at low concentrations (0.9 mg/cu m) induces damage to the lungs but that such damage was rarely severe. Seemingly in contradiction with this, they also stated that, at this concentration, some fairly severe changes are found in the lungs of experimental animals. The one animal study  devoted to long-term, repeated exposure to phosgene at low concentrations produced pulmonary edema in 41% of the animals. After correcting for the normal incidence of disease in laboratory animals, 5-10% of the animals had moderately severe lesions.
Human exposures to phosgene reported in the literature (summarized in   is the best substantiated in the American literature and gives details of pulmonary function studies in 11 workers with single acute or repeated exposures to phosgene at unknown concentrations.
Unfortunately, other pulmonary irritants were sometimes involved.
Galdston et al  gave evidence that repeated exposures to phosgene can result in residual pulmonary problems. This paper reports on 5 workers who were studied in detail, 2 of whom had abnormal chest films. It is difficult to extrapolate the results found in these workers to what might be expected in the general population of workers exposed to phosgene over long periods of time.
Levina et al  found no pulmonary abnormalities in Soviet workers exposed to 1-2 mg/cu m of phosgene for over a 6-month period. Other inhalants apparently caused hematologic abnormalities. Unfortunately, no mention is made of any pulmonary function studies done on these workers.
In summary, there are no truly pertinent data in the scientific literature concerned with long-term effects on humans exposed to phosgene at low concentrations. Animal data show a 5-10% incidence of severe pulmonary problems in animals exposed at 0.2 ppm. Despite Cherkes'  statement that the dog is the animal most resembling man in terms of susceptibility to phosgene, neither Cherkes nor any other investigator has offered any concrete data to support this contention. In fact, Winternitz  Delepine  English  Steel  Over a 2-year period prior to this investigation, at least 6 employees had been acutely exposed to unknown concentrations of phosgene.
 Four of these were not able to return to work the day after exposure. One death had occurred and was attributed to In 1967, Levina and Kurando  described exposures to phosgene and other chemicals in the manufacture of isopropyl phenylcarbamate, used as a herbicide. Totally enclosed equipment kept under reduced pressure prevented the escape of toxic chemicals to a large degree. Equipment and connections were made of corrosion-resistant materials, with special attention to flanges and valves. Atmospheric pollution was prevented by trapping gases and returning them to process. However, where manual labor was substituted for mechanization or total enclosure, some gas escape was possible. Hazardous processes were separated, and ventilation was reported to be correctly designed and located. Makeup air was supplied. Phosgene was detected in 30% of all air samples taken; of the samples where phosgene was detected, the usual concentration was 0.5 mg/cu m (0.125 ppm), the maximum permissible concentration. Methods of sampling and analysis were not described.
During operations such as quality control sampling, pressure transfer of phosgene, and pump repair, the concentration of phosgene in the workroom air was 1.0 mg/cu m (0.25 ppm). However, these concentrations were described as transient, because the premises were cleared by release of ammonia whenever the odor of phosgene became discernible. Gas masks were worn by personnel engaged in these tasks.
Recommendations for further control included improved sealing of equipment, elimination of manual operations by maximum automation, use of protective clothing, and good personal hygiene.

# Rispoli
 reported 1 and 5 ppm phosgene in a plasticsmanufacturing plant. No details of sampling or analysis were given, but ventilation was described as insufficient.
Reporting on 109 cases of phosgene inhalation over a 12-year period, Thiess and Goldmann  selected the 3 most severe cases for more detailed discussion.
None of the exposures reported were long-term inhalation of low concentrations but were acute accidental exposures at relatively high concentrations.
No determinations of workroom air concentrations were reported, but in 2 of the severe cases some assumptions and calculations were made which might have defined the exposure level involved.
One case described by Thiess and Goldmann  involved a worker removing brick lining, presumably saturated with phosgene, from a reaction vessel. The chemical process for which the reactor was constructed was the chlorination of aluminum oxide in the presence of carbon monoxide for the production of aluminum chloride.
Phosgene was a byproduct of this reaction. Contrary to instructions, the brick lining was removed with a jackhammer from the inside of the furnace and without respiratory protection. Instructions had been given to remove the brick from the outside of the vessel and to wear respiratory protection. The exposure lasted about 30 minutes, during which the worker was presumed to have inhaled dust particles with adsorbed phosgene. Again, assumptions and calculations based on porosity measurements of the brick indicated that a total volume of 2.5 liters was available for absorption of gas by the lining material. This exposure terminated fatally. There is at least a suggestion that the effect of phosgene was enhanced because of its association with particulate matter, but this was not proved. In summary, the workroom air measurements of phosgene in a manufacturing unit showed that, about 25% of the time, operators were exposed to very low but measurable concentrations of phosgene. Sampling procedures used did not determine individual peaks.
Details of controls or of fixed sampling locations were not given. The plant surveyed was reportedly old and built with out-of-date technology.
The decomposition of chlorinated hydrocarbons by means of heat or ultraviolet radiation with the formation of phosgene has been blamed for a number of incidents involving respiratory tract damage in humans. that phosgene was not formed in sufficient quantities by smoking to present a hazard. He also found that various chlorinated hydrocarbons in contact with a heated silica tube did not produce significant quantities of phosgene below 400 C. Even in atmospheres containing small amounts of phosgene, finding no detectable phosgene in effluent gas from cigarettes led to the conclusion that, if any phosgene were formed, it was subsequently decomposed when passed through the combustion zone of the cigarette. It was also hypothesized that the phosgene was absorbed by the tar fraction of the tobacco combustion product.

# Crummett and Stenger
 found that, in contact with heated metals, methyl chloroform (1,1,1-trichloroethane) produced relatively small amounts of phosgene, but much more hydrogen chloride than did carbon tetrachloride.
Dahlberg,  Dahlberg et al,  and Dahlberg and Myrin  extensively investigated the interaction of ultraviolet radiation with chlorinated hydrocarbons. These studies indicated that relatively lower amounts of phosgene were formed compared to the quantities of dichloroacetyl chloride formed simultaneously. Although there have been no environmental limits recommended for dichloroacetyl chloride, it seems likely that it would be a strong irritant to skin and eyes. Actual Noweir et al  found that, at very high temperatures, phosgene itself decomposes, perhaps accounting for concentrations lower than expected. However, phosgene decomposition was greatly reduced in the presence of carbon tetrachloride, indicating that, at least for this chlorinated hydrocarbon, phosgene formed by its decomposition should be relatively stable as long as some carbon tetrachloride remained.
A number of occupational exposures to decomposition products of chlorinated hydrocarbons have been reported. In 1947, Hill  briefly reported an investigation of complaints of workers exposed to fumes arising from a carbon arc-welding operation.
A presumably adequate exhaust ventilation system existed, but the fumes causing the complaints were sometimes strong enough to be detected at some distance from the arc. The workers had not complained prior to the relocation of the operation to a room near a trichloroethylene degreaser. Qualitative tests indicated the presence of phosgene presumably caused by breakdown of trichloroethylene vapor by the ultraviolet radiation of the arc. It was recommended that the degreaser be replaced with alkaline wash equipment and that the use of chlorinated hydrocarbons in the welding room be prohibited.
Spolyar et al  investigated the circumstances causing the death of an employee who had installed a trichloroethylene degreaser and had operated it without the condensing coils functioning. A strong odor of solvent was present in the room when the employee's body was discovered.
An investigation by the authors  took place 3 weeks later, disclosing the following:
(1) Trichloroethylene had been used in a degreaser designed for higher-boiling perchloroethylene, causing excessive loss of solvent.
(2) A fuel-oil-buming space heater was located in the degreaser room, and all windows and doors had been closed on the day of the accident.
(3) Under test conditions, 225-450 ppm trichloroethylene were found near the degreasing tank.
The trichloroethylene vapor passing through the firebox of the space heater could be decomposed with the possible formation of phosgene. A re creation of the situation at the time of the accident, described in Effects on Humans, was undertaken, during which it was noted that one of the solvent heaters in the degreaser became red-hot. Samples taken at that time in the approximate location of an operator's breathing zone showed much higher levels of trichloroethylene and 15 ppm phosgene. The authors  suggested that the decomposition of the trichloroethylene was caused by the degreaser heating element rather than by the space heater, although a back pressure in the smoke pipe of the latter could occur under adverse weather conditions because of the configuration of the stack.
Although some effects due to trichloroethylene were apparent, the authors concluded that the cause of death was consistent with phosgene exposure.
In All phosgene samples contained less than 0.1 ppm, although the trichloroethylene concentrations ranged from a reported 0.0 to 238 ppm and the ozone concentrations ranged from 0.9 to 1.7 ppm. The authors  concluded that ozone rather than phosgene was the source of the complaints.
Exhaust ventilation was installed in the degreasing shop and at the welding positions and operating procedures to prevent solvent drag-out were implemented, resulting in improved working conditions. Physical measurements were based on the olfactory or taste response imparted to tobacco smoke immediately after phosgene inhalation and was considered to be a very sensitive indicator  of the gas, although it suffered from the obvious disadvantage of depending on the exposed worker to determine his exposure.
A method of analysis based upon chloride present after hydrolysis was reported  to depend on aqueous decomposition of phosgene in dilute alkali.
Residual base was titrated or the chloride present was determined by the Volhard or the bichromate method; the hydrogen chloride gas produced upon hydrolysis could also be absorbed in ammoniacal silver nitrate and the resultant silver chloride determined gravimetrically.  However, these procedures were susceptible to physiologically inert, acid-reacting, or chloride-producing components occurring simultaneously with the phosgene.  Iodometric procedures in anhydrous acetone with thiosulfate titration suffered from inherent field limitations due to the anhydrous conditions necessary and evaporation of the volatile solvent.  Gravimetric procedures included (1) a method based on insoluble diphenylurea derived from phosgene and aniline, but which was sensitive to halogen interferences  and limited to a lower detection threshold of about 10 ppm ; and (2) a modified Kjeldahl nitrogen analysis of the diphenylurea which offered little improvement.  Review of colorimetric analytical methods  that were developed indicated that the most sensitive and specific detector was 4-(4'-nitrobenzyl)pyridine (NBP) plus N-benzylaniline although it did not readily lend itself to a liquid reagent system. Later investigators  developed a method using diethylphthalate as an absorber with NBP and Nbenzylaniline and easily determined phosgene at concentrations less than 0.1 ppm in air. Spot tests have been described  for phosgene which generally rely on colored complex formation between heavy metals and diphenylcarbazones.
Various detector papers and treated crayons have been described for determination of phosgene  with the most sensitive prepared A micromanometric method was described  which utilized measurement of gaseous reaction products resulting from hydrolysis of phosgene, but details as to sensitivity and specificity were lacking.
Gas chromatographic techniques provide the most specific and sensitive detection methods for phosgene. A silica gel column at 56.5 C with a hot wire detector was first used to detect phosgene in pyrolysis products on a semiquantitative basis.
 The development of the electron capture detector for the gas chromatograph provided a high degree of specificity for phosgene. This detector was first tried  in conjunction with a dodecylphthalate column at 50 C with resultant 2% standard deviation and detection down to 1 ppb. The authors suggested that this method can possibly be used as the basis for an automatic, continuous monitoring system. A later refinement  used a column of "20% silicon oil DC 200" (probably silicone DC 200) on Chromosorb W at 25 C for detection from below 1 ppb to 0.1 ppm phosgene. Jeltes et al  confirmed detection below 0.005 ppm but pointed out inherent difficulties due to hydrolysis by trace amounts of moisture, leakage of transfer syringes, and problems in transporation and storage of the air samples.
Basu et al  presented operational parameters, retention times, and response factors for gas mixtures including phosgene using a 3-column, 3detector (thermal conductivity) gas chromatographic system with a resultant reproducibility represented by a 1% standard deviation.
Although the gas chromatographic methods display excellent analytical capabilities, field use is hampered by the lack of an adequate personal sampling method. Recent investigations by Barrett et al  of a number of solid sorbents indicated that phosgene can be efficiently collected with activated carbon, alumina, and porous glass, but no satisfactory desorption technique was found.
Methods have been reported for automatic or continuous monitoring of phosgene in air.  The instrumentation requirements make the methods impractical for field use. In-plant applications may be possible but the lower limit of detection may be questionable.
One continuous-sensing instrument which has been found to be generally reliable below 0.1 ppm of phosgene is the Army's M8 portable alarm device for toxic chemical agents. It uses an electrochemical cell as the sensing unit and is designed to give a warning signal when the concentration of phosgene exceeds a certain value. The instrument is therefore not ideally suited for measurement of varying concentrations, but may well have some application as a monitoring or safety device. The device has been tested at concentrations of 0.074 ppm, 0.185 ppm, 0.443 ppm, and 0.625 ppm. The response was found to be linear over this range.
The method of choice for detection of phosgene in the workroom air should provide for a minimum limit of detection of less than 0.05 ppm, reasonable freedom from interference from commonly expected chemicals (see Appendix II) and should permit relatively easy sample collection. The method which best meets these requirements is described in an Analytical Guide by the American Industrial Hygiene Association  and is an improved nitrobenzylpyridine colorimetric method. It involves drawing air through a midget impinger containing 10 ml of a solution of 0. Color stability is good (only 10-15% loss in color density after 8 hours), sampling and analysis equipment needed is simple and readily available, and operator expertise required is minimal.

# V. DEVELOPMENT OF STANDARD

# Basis for Previous Standards
In 1940, Bowditch et al  listed a maximum concentration of 1 ppm (4 mg/cu m) phosgene which was in effect in Massachusetts as a guide to manufacturers interested in maintaining satisfactory working conditions.
In 1945, Cook  compiled a list of maximum allowable concentrations (MAC) of industrial atmospheric contaminants. Cook noted that 1 ppm (4 mg/cu m) was the MAC value for exposure to phosgene in the workroom air adopted by California, Connecticut, New York, Oregon, Utah, and the US Public Health Service. Cook referred to Fieldner et al  and Flury and Zernik  as a basis for the accepted value of 1 ppm (4 mg/cu m ) .
Fieldner et al  indicated that 3 ppm of phosgene in air was irritating to the throat. Flury and Zernik  indicated that 1 ppm was the highest tolerable amount in man, with 1.25-2.5 ppm termed as dangerous to life if the exposure was prolonged.
In 1947, Bloomfield  reviewed the efforts of a committee within the American Conference of Governmental Industrial Hygienists to develop an MAC which could be adopted by all the states. Bloomfield  cited unanimous agreement on a phosgene MAC value of 1 ppm (4 mg/cu m) among 23 respondents.
In 1947, the American Conference of Governmental Industrial Hygienists  adopted an MAC value for phosgene of 1 ppm (4 mg/cu m ) .
It was not stated if this MAC was intended as a ceiling value or as a TWA concentration. The April 1948 meeting of this same organization  adopted 1 ppm as a recommended limit and changed the name to Threshold Limit Values (TLV's).
The TLV of 1 ppm was considered "sufficiently low to cause no more than minimal effects" by the ACGIH according to the 1962 Documentation of the Threshold Limit Values.
 The Documentation  cited Fieldner et al  and Henderson and Haggard  to explain its selection of a TLV of 1 ppm (4 mg/cu m) for phosgene. Fieldner et al  reported that the Chemical Warfare Service at the American University Experiment Station, Washington, DC, considered 1 ppm of phosgene (4 mg/cu m) the maximal concentration safe for prolonged exposure. Henderson and Haggard,  in their review on phosgene, referred to Fieldner et al  and listed 1 ppm (4 mg/cu m) or less as a maximum concentration allowable for prolonged exposure.
Both sources listed 3 ppm as the concentration at which throat irritation first occurs. The Documentation did not quote any other experimental or occupational data to support its recommended TLV.
A change to 0.1 ppm (0.4 mg/cu m) was proposed by the ACGIH in 1964  and 1965  and adopted in 1966.  A TLV of 0.1 ppm (0.4 mg/cu m) was supported in the 1966 Documentation  because of the "seriousness of the response at the experienced levels of phosgene and by analogy with edemagenic agents of similar activity." The Documentation cited Gross et al  who wrote that phosgene, which could produce fatal pulmonary edema or acute chemical pneumonia at a high concentration, could also produce chronic pneumonitis at a low concentration. Gross et al suggested that the chronic pneumonitis is reversible even though residual pneumonitis could be found three months later.  The alveolar epithelium in rats can become irritated after a single 120-minute phosgene exposure at 0.5 ppm.  Studies by Box and Cullumbine  indicated that preliminary nonlethal doses of phosgene produced a transitory effect of increasing tolerance to the gas. It was necessary to damage the lungs of rats and mice to produce this effect. Stokinger et al  reported chronic lung injury of small animals after repeated exposure to ozone.
They stated that this is a separate process from the development of tolerance to subsequent acute exposure. In reviewing Stokinger's article,  the Documentation  stated that "the development of tolerance, however, is believed to be the triggering mechanism of chronic, irreversible pulmonary changes of emphysema and fibrosis from prolonged daily exposure at concentrations that produce no ostensible acute response." The Documentation  assumed that both ozone and phosgene caused pulmonary edema.
The 1971 Documentation  was the same as the 1966 Documentation
 with a few minor style changes and one additional sentence listing a recommendation for the USSR (1959) of 0.1 ppm and mentioning Elkins,  who recommended 0.5 ppm.
There was no discussion of the additional recommendations nor were any new references cited in the bibliography. In 1974, it was recommended  that the TLV of 0.1 ppm be changed to a ceiling concentration of 0.05 ppm (0.2 mg/cu m ) . Documentation for this change was published in the 1974 ACGIH Transactions  and refers to Stokinger's article on ozone toxicity studies  which indicated that there were chronic, irreversible pulmonary changes from prolonged daily exposure even though there was no acute response. None of the references cited specifically supported the ceiling limit of 0.05 ppm (0.2 mg/cu m) which was recommended because of the irritating effect of phosgene on the respiratory tract.
In 1971, Pennsylvania  adopted an environmental limit of 0.1 ppm (0.4 mg/cu m) for phosgene.
It was a maximum average atmospheric concentration for an 8-hour day. A short-term maximum average exposure limit of 1 ppm (4 mg/cu m) for 5 minutes was established.

# Henderson and
Haggard,  Imperial Chemical Industry, and Patty  were cited as the basis for the short-term limit in the Pennsylvania documentation. Those epidemiologic studies  involving exposures at low levels of phosgene suffer from a number of defects, including exposures to multiple irritants and limited analytical or medical data.
In spite of the weaknesses noted, these studies are at least suggestive that the present federal standard is safe for long-term exposures. Therefore, until more conclusive evidence is developed, NIOSH recommends that the present federal standard of 0.1 ppm as a TWA concentration be maintained.
In addition, since phosgene is an acute-acting, irritant gas, it is essential to control the short-term excursions above this average. Animal experiments have demonstrated a threshold for the development of pulmonary lesions after short-term exposure to phosgene. Gross et al  reported that exposure of rats to phosgene at a concentration of 3 ppm for 5 minutes resulted in slight to moderate chronic pneumonitis, while rats exposed at 1.3-1.5 ppm for 10 minutes showed no evidence of recognizable pulmonary lesions. Similarly, rat experiments conducted by Rinehart and Hatch  revealed that exposures to phosgene at a concentration of 1.5 ppm for 20 minutes or less did not result in any evidence of functional respiratory impairment as measured by carbon monoxide or ether uptake. In both studies,  deleterious effects were found at the lowest concentration used, 0.5 ppm, when duration of exposure was 120 minutes or greater.
Although no data are available to substantiate the pulmonary effects of brief exposures to phosgene at low concentrations in humans, these studies suggest that a single exposure of 10-15 minutes' duration at concentrations of or below 1.5 ppm are likely to be safe. It is felt, however, that imposing further limitations on the degree of excursion permitted during a 10-hour workday will provide an additional margin of safety to ensure protection of the worker from the consequences of brief exposures to concentrations of phosgene above the recommended TWA limit. NIOSH is therefore proposing a ceiling limit of 0.2 ppm for any 15-minute period.
In view of the development of pulmonary edema and evidence of chronic lung changes as a result of exposure to phosgene, medical monitoring, including chest X-rays and pulmonary function tests, is required for the protection of the worker.
Professional judgment indicates that local contact with liquid phosgene is likely to cause severe tissue damage which could in part be due to the low temperature of liquid phosgene. Thus skin and eye protection, in addition to respiratory protection, is recommended for those likely to be in contact with liquid phosgene.
It is recognized that many workers are exposed to phosgene at concentrations considerably below the recommended occupational limits.
Under these conditions, it should not be necessary to comply with many of the provisions of this recommended standard. However, concern for worker health requires that protective measures be instituted below the enforceable limits to ensure that exposures do not exceed the standard.
For this reason, "occupational exposure to phosgene" has been defined as exposure above half the recommended TWA, thereby delineating those work situations which do not require the installation of unnecessary controls and the expenditure of health resources for provisions such as environmental and medical monitoring and associated recordkeeping. literature  and the Manufacturing Chemists' Association Chemical Safety Data Sheet SD-95.  In addition, work practices prescribed for other irritating gases have been adapted for phosgene wherever pertinent (eg, those published in the Chlorine Manual ).

# Warning Properties
The American Industrial Hygiene Association  stated that the irritant properties of phosgene were insufficient to give warning of hazardous concentrations, and that olfactory fatigue caused personnel working with phosgene to lose their ability to detect low concentrations by smell. Supporting data for these statements were not reported.
The Manufacturing Chemists' Association  reported that the odor of phosgene can be recognized by some persons at 0.5 ppm, but that the sense of smell is conditioned by the gas so that the odor can only be detected briefly at the time of initial exposure. No substantiating data for these statements were cited, but many materials do have the ability to cause odor fatigue.
Leonardos et al  investigated the odor thresholds of 53 chemicals. They defined the odor threshold as the first concentration at which all members of a trained panel could recognize the odor of a chemical. Their tests indicated an odor threshold for phosgene of 1.0 ppm.
The odor was described as being "hay-like."
In 1938, Wells et al  determined threshold odor detection of phosgene in a number of volunteers. Test concentrations were established with a proportioning instrument known as an osmoscope. Three tests run on 56 subjects showed that all subjects detected the odor of phosgene at or below 37.5 mg/cu m (9.4 ppm), 51.8% detected the odor of phosgene at or below 6.1 mg/cu m (1.5 ppm), and that none detected the odor below 1.8 mg/cu m (0.45 ppm).
Macy,  summarizing the properties and the physiological action of phosgene, stated that the threshold of odor for phosgene was 4.4 mg/cu m (1.1 ppm). Substantiating data were not included in this report. Phosgene presents no fire or explosion hazard, but high temperatures may rupture containers because of increased hydrostatic pressure.
 In case of fire, phosgene containers should be removed to a safe place or cooled with water if phosgene is not escaping.  Spills are best controlled with solutions of caustic soda or with ammonia. It has been reported  that some manufacturers store one ton of ammonia for each ton of stored phosgene for the purpose of neutralizing liquid spills.

# Control of Airborne Phosgene
Phosgene should be used only in completely closed systems. In addition, local exhaust and general ventilation can be effective for control at points of potential escape.  Discharges of ventilation systems or of leaking containers may be passed through scrubbers utilizing caustic soda, ammonia, or steam to prevent phosgene from reaching the outdoor atmosphere.  The possibility of phosgene formation must be considered when installing and operating vapor degreasers containing chlorinated hydrocarbons, since under poor operating conditions, these are potential sources of phosgene.  They should be controlled to prevent exposure of operators to both solvent vapors and phosgene.
During maintenance operations on equipment in which phosgene has been present, there is a potential hazard of exposure to phosgene which is entrapped in the equipment or adsorbed on surfaces or in materials.
Respiratory protection should be supplied to maintenance personnel working on equipment that has carried phosgene, unless it can be established that no phosgene is present.

# Respiratory Protection
Neither chemical cartridge respirators nor half-face masks are recommended for protection against phosgene.  Canister-type gas masks are recommended only for rapid escape from a contaminated area because of the following limitations:
(1) Their useful life is unpredictable because of a number of variables such as breathing rate, ambient humidity, and contaminant concentration.  (2) They cannot be used in atmospheres deficient in oxygen or containing phosgene in concentrations over 2.0% by volume.  Therefore, they are not suitable for controlling emergency exposures where the concentration of phosgene and the oxygen content of the air are unknown.
(3) Users of gas masks have depended on the detection of an odor of the atmospheric contaminant to warn them of loss of protection by the canister or to indicate leaks.  However, phosgene has poor warning properties in low concentrations  and therefore the odor cannot be Gas-mask canisters should be replaced immediately after each use, when the seal is broken, when any leakage is detected, when high breathing resistance develops, or when the recommended shelf life expires, whichever occurs first.  Because of the irritant properties of phosgene, emergency respiratory protection must provide both eye and respiratory protection for the worker.
Full-face masks are the only acceptable devices for employees exposed to phosgene leaks or for the protection of personnel who may be exposed to sudden high concentrations of phosgene. Masks connected to air lines or having a self-contained air or oxygen supply can also be used. Pocket-or mouthpiece-type respirators used for escape in some operations  are not recommended for that purpose.

# Eye Protection
Liquid phosgene is probably a severe eye irritant,  as discussed in Chapter V. Protection should be provided against accidental splashes of the liquid.  Vapor concentrations of phosgene which are said to affect the eyes (1-10 ppm) are likely to affect the respiratory system as well. Accordingly, eye and respiratory protection should be combined by use of full-face respiratory protection.

# Skin Protection
Liquid phosgene is said to cause severe skin burns,  and although this point is inadequately documented, it is a likely effect as discussed in Chapter V.
Skin exposure to liquid phosgene should be prevented by the use of impervious clothing and gloves. Clothing impregnated with phosgene should be removed immediately. near a phosgene leak will produce a visible white cloud.  However, this should not be done unless the worker is wearing a respirator.

# Leak Control
When detected, leaks should be repaired immediately by personnel wearing the proper protective clothing and respiratory protection. Leak repair kits may be assembled  or are commercially available.  Routine inspection should be scheduled to check pumps, lines, and containers for leaks; this practice is especially important during maintenance operations.  Leaking containers should be positioned so that gas rather than liquid phosgene is discharged from the leak.
 This results in less discharge of phosgene and the escaping gas cools the remaining phosgene, thus reducing pressure and leakage. Introducing moisture into phosgene can cause increased pressures sufficient to rupture containers  or can cause leaks through corrosion.  VII. RESEARCH NEEDS  Check the water manometer to ensure that the pressure drop across the sampling train does not exceed 13 inches of water (approximately 1 inch of mercury).
(g) Start a soapbubble up the buret and, with a stopwatch, measure the time it takes the bubble to move from one calibration mark to another.
For a 1000-ml buret, a convenient calibration volume is 500 ml. (c) The 95% confidence limits for 10 degrees of freedom are 0.007 mg at the 0.017-mg level, and 0.003 mg at the 0.10-mg level. The precision was determined by repeated analyses by the same technician.
Rather than air sampling in the field, the precision was determined by analyzing known amounts of phosgene using the same technique as the calibration procedure.

# Interference
Other acid chlorides, alkyl and aryl derivatives which are sub stituted by active halogen atoms and sulfate esters will produce color with this reagent. However, most of these interferents can be removed in a pre scrubber containing 1,l,2-trichloro-l,2,2-trifluoroethane if necessary.
 The method is not subject to interference from carbon tetrachloride,

# Apparatus (a) Sampling
(1) Portable, battery-operated, personal sampling pump.
(2) Midget impinger.
(3) Flexible plastic tubing as appropriate.

# (b) Analysis
(1) Glassware as required for reagent measurement.
(2) Colorimetric spectrophotometer capable of absorbance measurements at 475 nm.
(3) Spectrophotometer cells (cuvettes).

# (c) Calibration
(1) Pressurized cylinder of phosgene gas.
(2) Pressure regulator.
(3) Flow meter.
(4) Appurtenant equipment for gas dilution methods or a midget impinger.
(5) Gas drying tubes.

# Summary of Specifications (a)
The monitoring device must sound an alarm or otherwise warn employees whenever a phosgene concentration of 0.2 ppm is reached or exceeded.

# (b)
The monitoring device must have a response time of 90 seconds or less when exposed to phosgene at a concentration of 0.2 ppm.
(c) Zero drift should be less than 1% of full scale reading in 24 hours. That portion of the signal manifested as background noise should be less than plus or minus 1% of full scale reading.

# (d)
The monitoring device must be accurate to within plus or minus 10% of the reading for the range of 0.05-0.4 ppm phosgene.
(e) Precision and repeatability must be plus or minus 5% of full scale reading.
(f) It is desirable that the instrument respond only to phosgene, but devices which respond to other gases not normally present in the atmosphere may be acceptable. Whenever there is a possibility that gases or vapors, such as hydrogen chloride, chlorine, benzoyl chloride, acetyl chloride, and oxalyl chloride, may be present, it would be desirable to determine in advance the response of the instrument to such gases or vapors.
(g) An operating range of 0-0.4 ppm phosgene is recommended, but other ranges may be selected to suit individual needs.
(h) The device should be capable of 168 hours of continuous, unattended operation.

# (i)
The device and alarm should be intrinsically safe for use in locations where explosion hazards may occur.

# Discussion
The principal requirements for such monitors in addition to responding to phosgene gas are that they be sufficiently rugged to withstand pressure, vibration, normal extremes of temperature, etc, and not be susceptible to plugging or interferences due to contaminants likely to be encountered in most workplaces. They should be so constructed that it is possible to routinely and quickly check the zero setting of the instrument and the response to phosgene at 0. In large plants, where there are considerable distances between work stations, additional monitors may be required to ensure worker safety.
Alternately, a multipoint sampling system bringing sampled air to a single instrument may be satisfactory. Chemical substances should be listed according to their complete name derived from a recognized system of nomenclature. 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, as a permissible exposure, or by some other indication of an acceptable standard. Other data are acceptable, such as lowest LD 50, 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.
"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 this section 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.

# DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE

# PUBLIC HEALTH SER VIC E C E N T E R FO R D ISEA SE C O N T R O L N A T IO N A L INSTITUTE FOR O C C U P A T I O N A L S A F E T Y A N D H E A LT H R O B E R T A. T A F T L A B O R A T O R IE S 4 6 7 6 C O L U M B I A P A R K W
The date and time of sample collection.
(2) Sampling duration.
(3) Volumetric flowrate of sampling.
(4) A description of the sampling location.
(5) Sampling temperature and pressure.
(6) Other pertinent information.

# Breathing Zone Sampling