This sign shall also be printed in the predominant language of non-English-speaking workers. All employees shall be trained and informed of the hazardous areas, with special instructions given to illiterate workers.

# (b)
This sign shall also be posted at or near entrances to areas in which there is occupational exposure to 1,1,1-trichloroethane. (3) Only appropriate respirators as described in Table 1-1 shall be used pursuant to the following requirements:
(A) To determine the class of respirator to be used, the employer shall measure the atmospheric concentration of 1,1,1-trichloroethane in the workplace initially and thereafter whenever process, worksite, climate, or control changes occur which are likely to increase the 1,1,1-trichloroethane concentration. This requirement shall not apply when only self-contained or combination supplied-air and self-contained positive pressure respirators are used.

# (B)
The employer shall ensure that no worker is being exposed to 1,1,1-trichloroethane in excess of the exposure limit because of improper respirator selection, fit, use, or maintenance.
(C) When respirators are required, the employer shall provide respirators in accordance with Table 1-1 and shall ensure that the employee uses the respirator provided.
(D) Respiratory protective devices described in Table 1-1 shall be those approved under the provisions of 30 CFR 11.
(E) Respirators specified for use in higher concentrations of 1,1,1-trichloroethane are permitted in atmospheres of lower concentrations.
(F)
The employer shall ensure that respirators are adequately cleaned, maintained, and stored, and that employees are instructed on the use of respirators and on testing for leakage.
(4) Chemical cartridges and canisters shall not be used for periods of time in excess of those indicated in Table 1-1.
In any case chemical cartridges and canisters should be replaced after each day of use.
Where an emergency may develop that could result in employee injury from overexposure to 1,1,1-trichloroethane, the employer shall provide respiratory protection as listed in Table 1-1.

# (b)
Protective Clothing
In any operation where the worker may come into direct contact with liquid 1,1,1-trichloroethane, protective clothing shall be worn. The clothing should be resistant to 1,1,1-trichloroethane. Gloves, boots, overshoes, and bib-type aprons that cover boot tops shall be provided when necessary. Impervious supplied-alr hoods or suits shall be worn when entering confined spaces such as pits or tanks unless known to be safe. In situations where heat stress is likely to occur, air-supplied suits shall be used. All protective clothing shall be well-aired and inspected for defects prior to reuse. Hands placed in liquid 1,1,1-trichloroethane shall be protected by Impervious gloves. Any liquid 1,1,1-trichloroethane that contacts the skin should be promptly removed.  (1) Containers delivered by closed truck or rail shall not be unloaded until the vehicle in which they arrived has been ventilated.
The absence of any odor of 1,1,1-trichloroethane should not be used as a criterion of adequate ventilation.
(2) Storage containers piping, and valves shall be inspected periodically for leakage
(3) Storage facilities shall be designed to contain spills and prevent contamination of workroom air.
(4) Processes and storage facilities shall not be located near open flames or high-temperature operations, unless precautions are taken to prevent fire and explosion hazards.

# (b) Contaminant Controls
(1) Suitable engineering controls designed to limit exposure to 1,1,1-trichloroethane shall be utilized if needed. Ventilation systems, if used, shall be designed to prevent the accumulation or recirculation of 1,1,1-trichloroethane in the workroom and to effectively remove 1,1,1-trichloroethane from the breathing zones of workers.
Adequate, uncontaminated make-up air shall be provided. Ventilation systems shall be subjected to regular preventive maintenance and cleaning to ensure maximum effectiveness, which shall be verified by periodic airflow measurements.
(2) Portable exhaust ventilation or suitable general ventilation shall be provided, if necessary, to limit environmental concentrations for nonroutine operations that require the application of 1,1,1-trichloroethane. Personnel entering confined spaces shall be furnished with appropriate personal protective equipment and protected by a lifeline tended by another worker outside the space, who shall also be equipped for entry with approved respiratory, eye and skin protection, lifeline, and have contact with a third party.
(E) Written operating instructions and emergency medical procedures shall be formulated and posted in conspicuous locations where accidental exposure to concentrations of 1,1,1-trichloroethane in excess of the environmental limit may occur. These instructions and procedures shall be printed both in English and in the predominant language of non-English-speaking workers, if any. Special instructions shall be given to illiterate workers.

# (d) Showers and Eye Wash Fountains
Showers and eye wash facilities shall be provided and so located as to be readily accessible to workers in all areas where skin or eye splash with 1,1,1-trichloroethane is likely. If 1,1,1-trichloroethane is splashed on the worker, contaminated clothing shall be promptly removed and the skin washed with soap and water. If liquid 1,1,1-trichloroethane contacts the eyes, they shall be thoroughly irrigated with clean water, promptly followed by medical assistance. Such incidents shall be reported to the immediate supervisor by the affected employee or by a fellow worker. exposure in excess of the recommended environmental limit, additional monitoring shall be promptly initiated. If confirmed, control procedures shall be instituted as soon as possible; these may precede and obviate confirmatory monitoring if the employer desires. Affected employees shall be advised that exposures have been excessive and be notified of the control procedures being implemented. Monitoring of these employees shall be conducted at least as often as every 30 days and shall continue until 2 successive samplings at least a week apart confirm that exposure no longer exceeds recommended limits. Normal monitoring may then be resumed.
For each TWA concentration determination, a sufficient number of samples to characterize each worker's exposure during each workshift shall be taken and analyzed.
The number of TWA and ceiling concentration determinations for an operation shall be based on such factors as the variations in location and job functions of workers in that operation.

# (c) Recordkeeping
Environmental monitoring records shall be maintained for at least 20 years. These records shall include methods of sampling and analysis used, types of respiratory protection used, and TWA and ceiling concentrations found. Each employee shall be able to obtain information on his own envi ronmen t al exp o s ur es.
Pertinent medical records shall be retained for 20 years after the last occupational exposure to 1,1,1-trichloroethane. Records of environmental exposures applicable to an employee should be included in that employee's medical records. These medical records shall be made available to the designated medical representatives of the Secretary of Labor, of the Secretary of Health, Education, and Welfare, of the employer, and of the employee or former employee. Further research is needed to more completely characterize the effects of certain levels of 1,1,1-trichloroethane on workers, especially epidemiological, chronic and teratological studies. Animal studies are underway at the National Cancer Institute to determine if 1,1,1trichloroethane is carcinogenic.
Similar studies are being performed by the Dow Chemical Company.

# III. BIOLOGIC EFFECTS OF EXPOSURE
Extent of Exposure 1.1.1-Trichloroethane (CH3 CC1 3) is also known as methyl chloroform and alpha-trichloroethane.
There are two isomers of trichloroethane. The 1,1,2 isomer is also known as ethane trichloride, vinyl trichloride, beta-trichloroethane and monochloroethylenechloride.
 Some reports do not clearly distinguish between the isomers, and some confusion exists in the literature because of

# Indiscriminate use of the term trichloroethane. 
The odor threshold of 1,1,1-trichloroethane was reported by the American National Standards Institute to be around 100 ppm.
 Stewart found a sex difference in odor "acceptance" at 350 ppm.  May  reported that the odor threshold for 1,1,1-trichloroethane of his subjects was 400 ppm, and that they perceived the odor more clearly at 700 ppm.
Arthur D. Little Inc.
 reported the odor recognition threshold, detected by four expert panel members when 1,1,1-trichloroethane was in room air, to be 16 ppm. These data reflect the variability in odor threshold values and highlight the danger of using odor as a criterion for detection of harmful levels of 1,1,1-trichloroethane. Some physical data for 1,1,1-trichloroethane are presented in Production has increased steadily and in 1973, production of 548,394,000 lbs was reported.  There are many uses of 1,1,1-trichloroethane as a solvent and clean ing agent.  In 1969, Gleason et al  tabulated over 40 pro ducts, marketed by 30 companies, which contained it. Among the products were type cleaners, color film cleaners, insecticides, spot removers, cements and adhesives, and fabric cleaning solutions.  One of the most common industrial uses is as a degreasing agent.
Workers involved in the manufacture of 1,1,1-trichloroethane, in its formulation into the many products containing it, and in their final uses, are potentially exposed to 1,1,1-trichloroethane.
In addition to job related exposures, workers may be exposed to 1,1,1-trichloroethane by home use of the many products which contain it. 2-bromo-2-chloro-l,1,1-trifluoroethane (halothane) anesthesia. The investigators  found 1,1,1-trichloroethane to be clinically less potent than either chloroform or 2-bromo-2-chloro-l,1,1-trifluoroethane, and even less potent than trichloroethylene in supplementing nitrous oxide-oxygen for anesthesia.
In an experiment reported in 1961 by Stewart et al, the exposure chamber concentration was increased continuously from 0 to 2,650 ppm for 15 minutes (total exposure).
One of seven exposed subjects became very lightheaded when the concentration reached 2,600 ppm, and at 2,650 ppm, two could not stand, and three others became very lightheaded. Two of the seven subjects did not become lightheaded.
One subject maintained the ability to perform a normal Romberg test (loss of proprioceptive control evidenced by unsteadiness of standing patient when eyes are closed)
throughout the exposure. The other six subjects regained their equilibrium within 5 minutes after cessation of exposure. The five subjects who became lightheaded reported a feeling of malaise for 5 hours after the exposure.
The inhibited 1,1,1-trichloroethane used in this experiment contained 94-97% 1,1,1-trichloroethane, 2.4-3.0% dioxane, 0.12-0.3% butanol, and small amounts of 1,2-dichloroethane, water and other materials.  The only factor that was reported to be statistically significant with regard to 1,1,1-trichloroethane was the interaction between perception of mental strain and 1,1,1-trichloroethane exposure at 450 ppm. Under stress conditions, exposure to 1,1,1-trichloroethane at 450 ppm decreased perceptive capabilities.
 Because of the choice of subjects (healthy students) as well as the lack of controls on intervening variables (food and drinking habits), it would seem that further work is needed to justify a dose-response relationship. repeatedly in four of five subjects exposed 6.5 to 7 hours daily for 5 consecutive days at 500 ppm of a commercial 1,1,1-trichloroethane preparation.
Other subjective symptoms of central nervous system response that were occasionally experienced by the subjects were lightheadedness and mild headache.
The ability of two subjects to perform a modified Romberg test was impaired during the last 5-6 hours of each daily exposure. Their ability to perform the test normally was regained 5-10 minutes after removal from exposure.
The 1,1,1-trichloroethane  used in this experiment contained (in liquid form) 4 vol% of 1,4-dioxane, 0.5 vol% butylene oxide, and 0.5 vol% of nitromethane as inhibitors. The liquid also contained traces of 1,2- Although there were slight increases noted in two patients, the authors  concluded that anesthesia with 1,1,1-trichloroethane of up to 2 hours duration would not be hepatotoxic.
Positive urinary urobilinogen was found 7 hours after exposure in two of seven male subjects exposed for 15 minutes to inhibited 1,1,1-trichloro ethane in a concentration increased continuously from 0-2,650 ppm during the 15-minute exposure.
 On examination of centrifuged urine, five subjects were found to have 1-2 red blood cells per high-power field, com pared to none before exposure.
Elevated urinary urobilinogen was reported by Stewart et al  in one of three male subjects 20 hours after removal from a 20-minute exposure at 900 ppm of inhibited 1,1,1-trichloroethane.
In one experimental exposure of six male subjects at 500 ppm of inhibited 1,1,1-trichloroethane for 78 minutes, 3-6 red blood cells per high power field and a trace of albumin were found in the urine of one subject 20 hours after the exposure. A worker who experienced a sudden onset of nausea, vomiting, "explosive diarrhea" and dizziness 2 hours after leaving work was the subject of a fourth case reported by Stewart.  The previous day the man had worked in the vicinity of an engine cleaning operation where 1,1,1trichloroethane had been used and he had been aware of its odor throughout the day. His illness, however, was not attributed by the author to the effects of 1,1,1-trichloroethane. The illness lasted for 6 hours. Results         When subjects were exposed by Stewart et al  to inhibited 1,1,1triehloroethane 6.5 to 7 hours/day on 5 consecutive days at an average concentration of 507 ppm (420-612 ppm), the concentrations in the alveolar air 16 hours after removal from each daily exposure increased on successive days.
They  did not present the data, but reported that 1,1,1trichloroethane was found in alveolar air for 1 month after the last exposure.
1,1,1-Trichloroethane and tetrachloroethylene were both still present in the breath of one individual at 0.1 ppm 1 month after removal from an exposure to the vapors of these two compounds.
 The individual was  In a second experiment reported by Tada,  the same two subjects were exposed at an average of 420 ppm 1,1,1-trichloroethane, 2 hours/day for three days.
With this exposure, both the TCA concentration in the urine and the total amount excreted per day continued to increase on the 2 days following the last exposure, before beginning to decline on the third and fourth days after exposure. The maximum amount excreted per day was 7.2 mg, averaged for the two subjects.
Excretion of TCA in the urine of two subjects was studied for 8 days and reported by Fukabori  in 1970. These subjects were exposed 2 hours/day to 1,1,1-trichloroethane at average concentrations of 195 ppm on the first day, 376 ppm on the second, 558 ppm on the third, and 832 ppm on the fourth day. The maximum amount of TCA (7.5 mg/day) was excreted on the day following the last exposure. Four days after the last exposure, an average of 2.5 mg TCA/liter of urine was found, compared to a normal value in Japanese men of 0-0.9 mg/liter. TCA was measured by Fukabori  by the alkali-pyridine-benzidine method.
Trichloroacetic acid has been studied in the urine of workers occupationally exposed to 1,1,1-trichloroethane. Chemical analyses or other information about the inhibitors or impurities in the 1,1,1-trichloroethane to which these workers were exposed were not reported.
Marked accumulation of white, frothy, slightly bloody edema fluid was found in the lungs and a small amount of mucoid material was found in the bronchi of one of the fatalities reported by Hall and Hine.
 The man had inhaled (and possibly aspirated) a 1,1,1-trichloroethane cleaning fluid containing dioxane.  The other fatality reported by Hall and Hine
 had habitually inhaled another cleaning fluid containing 1,1,1trichloroethane.
In this case of chronic exposure, passive congestion was found throughout the lungs and there were considerable amounts of thick, dark red blood and thin, frothy fluid in the dependent areas. Thick, yellowish-brown secretions were found in the bronchi. Microscopic findings included some atelectasis in the lung parenchyma, edema and congestion in the lungs and desquamated epithelium in the bronchi.
Slight eye irritation was experienced by one of four subjects during the experimental 30-minute exposure to uninhibited 1,1,1-trichloroethane at 900-1,000 ppm reported by Torkelson et al.  Eye, nose and throat irritation have been experienced during experimental exposures to inhibited 1,1,1-trichloroethane at 400-500 ppm All employees in the exposed group had 1,1,1-trichloroethane (and other solvent) exposures, in varying concentrations, for up to 6 years. The concentration range was 11-838 ppm, with a mean of 115 ppm 1,1,1trichloroethane. Whether this period of exposure would result in toxic systoms is questionable, however. Since only healthy, active workers were selected, and the average length of exposure for the study population was less than 1 year at the stated TWA, no conclusions can be drawn about chronic effects.
The control group had only minimal exposure to nonchlorinated solvents.
Pairs were matched with regard to age, race, sec, work shift, job description and socioeconomic status, and examined within a 10-week period.
 and reported in 1950. The 1,1,1-trichloroethane used in this investigation    Trichloroethane was administered at an average concentration of about 125,000 ppm. Duration of exposure varied from 1.5-6.0 minutes and the total amount of 1,1,1-trichloroethane administered was 10 to 40 ml.

# Ventribular fibrillation, followed by cardiac arrest, occurred in one dog
during its second 3-minute exposure; the first exposure had taken place 2 weeks earlier.
Cardiac arrhythmias, myocardial depression, and tachycardia were reported by Belej et al  to have developed in three anesthetized Rhesus monkeys exposed for 5 minutes at 25,000 ppm of 1,1,1-trichloroethane, and again 10 minutes later when they were similarly exposed at 50,000 ppm.   hours daily for 50 days to 1,1,1-trichloroethane at 73 ppm. After 120 days of exposure, the emphysematous condition was much more pronounced, the interalveolar walls were thin and in some places they had broken down. The vascular walls were thickened and swollen, and around many of them there were accumulations of lymphoid and histiocyte cell elements and isolated plasma cells.
The mucous membrane of the bronchi was swollen, and there were small amounts of mucus and detached epithelial cells in the lumen.
The peribronchial lymphatic nodules were hyperplastic.
In this chronic study, even though conditioned reflex activity was not disrupted in the rats, structural changes in cortical and subcortical areas were noted.
The authors did not report microscopic studies of cat brains in which changes in differential reflexes were found with chronic exposure. In the absence of other information, and because of the nature of the conditioned reflexes they were studying and the methods they used, it is difficult to assess the significance of the behavioral aspects of this study.
Chemosis and hyperemia of the conjunctivas of rabbits after in stillation of 1,1,1-trichloroethane (5% in corn oil) were found by Krantz et al  to be similar to those produced by chloroform administered similarly and simultaneously in the other eye.
A single undiluted application of either uninhibited or inhibited 1,1,1-trichloroethane to the eyes of rabbits was reported by Torkelson et     increased liver weights were reported by Torkelson et al  in 5 male rats exposed 70 times in 99 days to inhibited 1,1,1-trichloroethane at 10.000 ppm 1 hour/day, 5 days/week. Liver weights did not increase in other rats exposed for 0.5, 0.2 or 0.05 hours/day in the same experiment.
increased liver weights were found in female guinea pigs exposed 69 times in the same experiment at 2,000 ppm, for 0.5 or 0.2 hours/day, and in others exposed 69 times at 1,000 ppm, for 3.0 or 1.2 hours/day. Exposures of shorter daily duration at 2,000 or 1,000 ppm did not result in increased liver weights.
In the guinea pigs with increased liver weights, fatty changes were found in the livers.

# No iivei. or kidney effects were reported by Torkelson et al  in
126-130 exposures of rats, guinea pigs, rabbits or monkeys to inhibited 1,1,1-trichloroethane at 500 ppm. The exposures were 7 hours/day, 5 days/week.

# Fatty degeneration of the liver was reported by Adams et al  for
guinea pigs, but not rats or rabbits, exposed 31 times in 44 days for 7 hours/day, to redistilled 1,1,1-trichloroethane at 5,000 ppm. Fatty degeneration was also found in livers of guinea pigs exposed 20 times for 7 hours/day at 3,000 ppm. No liver or kidney effects were reported for rats or monkeys repeatedly exposed (about 50 times) 7 hours/day, 5 days/week at 3.000 ppm. Liver or kidney effects were not reported for guinea pigs similarly exposed at 1,500 ppm over 2 months or at 650 ppm over 3 months. Liver to body weight ratios were also significantly increased in rats exposed to 1,1,1-trichloroethane at 1,000 ppm, but at 250 ppm they were similar to controls.
 Cytoplasmic alterations found by electron microscopy were most severe in centrilobular hepatocytes of the 1,000 ppm group and were mild to minimal in the 250 ppm group. These alterations consisted of vesiculation of the rough endoplasmic reticulum with loss of attached polyribosomes, increased smooth endoplasmic reticulum, microbodies and triglyceride droplets. Some cells had swollen cisternae of the endoplasmic reticulum.
The authors  also observed chronic respiratory disease, in 12 of 40 control rats, in 28 of 40 exposed at 250 ppm, and in 7 of 40 exposed at 1000 ppm. It appears that the respiratory disease was intercurrent rather than related to exposure.
No lesions in dogs or monkeys were ascribed to the exposure by the investigators. In the rats examined after 120 days of exposure, these effects were more prominent, and protein dystrophy of the liver parenchymal cells was found.
[ all major organs and glands were taken for microscopic examination.
Behavioral signs indicative of CNS depression, such as hyperactivity, were sought.
The authors reported no signs or indices attributable to 1,1,1trichloroethane exposure. Several "spontaneous lesions" were found, but on comparison of frequencies between control and experimental groups were not associated with exposure. The portion of the diurnal cycle during which the animals were exposed was not stated. These findings were reported after 24 months and 18-23% of the males and 32-37% of the females were still alive at that time. The doses administered to three rats were 727, 642 and 705 g/kg (approximately 0.5 ml/kg). For two rats in which it could be measured, an average of 97.6% of the administered dose was excreted unchanged in the exhaled air during 25 hours, and in three rats an average of 0.85% (0.55, 0.86, and 1.14%) of the administered radioactivity was found in the urine.  The "behavior" of 1,1,1-trichloroethane and its metabolites was investigated in the expired air, blood and urine of male Wistar rats by Eben and Kimnerle.
 To quantitate concentrations of 1,1,1trichloroethane and its metabolites, a gas chromatograph, equipped with an Ni-63 electron capture detector, was used. The major metabolites studied were TCE and TCA in the urine, 24 hours after exposure, for 3-4 days in the acute group, and 16 hours after exposure, daily, in the subchronic group.
Chloral hydrate concentrations were also determined in the blood and 1,1,1trichloroethane was determined in the blood and breath. It was concluded that the results gave an explanation for 1,1,1trichloroethane-induced depression of myocardial respiration.  (g) Drug Interactions and Potentiation of 1,1,1-Trichloroethane Toxicity 1,1 ,l-'i' richloroethane was found by Van Dyke and Rikans  to stimulate aniline hydroxylase activity when added to the incubation medium of rat liver microsomes.
In the same experiment, it had no effect on aminopyrine demethylase.
Metabolism of hexobarbital, meprobamate, and zoxazolamine, based on loss of righting reflex, was studied by Fuller et al  in male rats and mice, 24 hours after removal from 24 hours of continuous exposures to reagent gra r 1J ,1-trichloroethane at 3,000 ppm. The sleeping times induced by all three drugs were also reduced in rats and mice exposed to 1,1,1-trichloroethane. This indicates that 1,1,1-trichloroethane stimulates the activity of hepatic microsomal enzymes used to metabolize these drugs.
Other studies were conducted with hexobarbital to determine the mechanism by which 1,1,1-trichloroethane reduced the sleeping time.
To functionally block the hypophysis, rats were treated with morphine sulfate (20 mg/kg ip) for 4 days before exposure. This treatment did not alter the effect of 1,1,1-trichloroethane on hexobarbital sleeping time.
In another experiment, adrenalectomized rats retained the 1,1,1-trichloroethane effect on hexobarbital sleeping time.
Other groups of rats were treated with either cycloheximide or actinomycin D to block protein synthesis before they were exposed to 1,1,1trichloroethane.
 Both these drugs blocked the effect of 1,1,1trichloroethane inhalation on hexobarbital sleeping time by preventing reduction of hexobarbital narcosis and an increase in hexobarbital metabolism.
In vitro studies showed that both hexobarbital and zoxazolamlne metabolism by rat livers were increased by exposure of the donor rat to Other experiments were conducted at the 3,000 ppm exposure level.
When 24 hours of total exposure time were completed in three to six exposure periods, each separated by 18-21 hours, a cumulative effect was shown by progressive decreases in sleeping time.  The cause of the decreased hexobarbital sleeping times following 1,1,1-trichloroethane exposures was studied.  It was found that neither barbital nor chloral hydrate induced sleeping times were affected by exposure to 1,1,1-trichloroethane. Oxidation of hexobarbital by 9,000 G supernatant fractions from livers of exposed mice was increased. Reduction of p-nitro-benzoic acid by the same liver fractions was not affected by exposure of the mice to 1,1,1-trichloroethane.
Treatment of mice with atropine, chlorpromazine or tolazoline immediately before and after 12 hours of exposure to 1,1,1-trichloroethane, did not block the effect of exposure on hexobarbital sleeping time.  Administration of two doses of phenobarbital (50 mg/kg ip) by Cornish et al  1 and 2 days before injection of reagent grade 1,1,1trichloroethane at doses of 0.3, 0.5, 1.0 and 2.0 ml/kg, did not enhance the hepatoxicity of 1,1,1-trichloroethane, evaluated by SG0T determinations. Similar increases in SGOT levels were found in control (no phenobarbital treatment) and treated animals at each 1,1,1-trichloroethane dose level. The SGOT levels were significantly increased by 1,1,1trichloroethane with or without phenobarbital pretreatment.
Enhancement of 1,1,1-trichloroethane hepatotoxicity by phenobarbital was reported in 1973 by Carlson.
 In this experiment, the male rats were pretreated with phenobarbital (50 mg/kg/day) for 4 days before an Exposures of rats to redistilled reagent grade 1,1,1-trichloroethane for 2 hours at 10,000 or 15,000 ppm or for 6 hours at 5,000 or 10,000 ppm did not increase serum enzyme levels whether or not there had been ethanol
pretreatment.  The serum enzymes studied in this 1966 report by Cornish and Adefuin  were SGOT, SGPT, and isocitric dehydrogenase.
The ethanol (50%) was administered by stomach tube at 5 g/kg, 16-18 hours before the vapor exposures.
Isopropyl alcohol or acetone administered by gavage to male Swiss-Webster mice 18 hours before ip injection of 1,1,1-trichloroethane did not alter the response of SGPT activity to the administered 1,1,1-trichloro ethane.  The doses of 1,1,1-trichloroethane used in this experiment, by Traiger and Plaa  in 1974, were 1.0, 2.0 and 2.5 ml/kg. The latter dose caused increases in SGPT activity, but the increases were not affected by isopropyl alcohol or acetone pretreatment.

# Correlation of Exposure and Effect

# Summaries of inhalation exposures and effects are presented in
Tables XII-6 to XII-10. The most significant findings concerning the effects of 1,1,1-trichloroethane in man and animals are the depression of the CNS, cardisvoscular toxicity and hepatic toxicity. Irritation of the lungs and mucous membranes also has been reported. Information on experimental exposures of more than 6 months duration, or at 1,1,1trichlorethane concentrations below about 75 ppm, was not found in the literature.
Both experimental studies and occupational experiences indicate that 1,1,1-trichloroethane is irritating to the skin and mucous membranes and that the nervous system, cardiovascular system, and the liver are affected by exposures.

# (a) Central Nervous System Effects
The first reported biologic study of 1,1,1-trichloroethane, by Tauber
 in 1880, established that it had anesthetic properties. Clinical trials in 1958-1960 established that it was not very effective as a surgical anesthetic, and its use for this purpose was discontinued.
The anesthetic properties of 1,1,1-trichloroethane have had occupational significance,  and will continue to be of significance to work practices and requirements for respiratory protective devices.
Concentrations of 1,1,1-trichloroethane required to induce anesthesia under working conditions have not been determined.  The clinical studies are difficult to extrapolate to occupational situations because the patients were usually given sedatives before administration of anesthetic gas, and nitrous oxide was used in the 1,1,1-trichloroethane carrier gas.
[ Changes in cardiovascular function found in dogs exposed to 1,1,1trichloroethane at 8,000 ppm for no more than 5 minutes included an abrupt drop in total peripheral resistance with compensatory cardiac responses.
 Within seconds, the compensatory cardiac responses were dissipated and stroke volume, heart rate, and myocardial contractility decreased.
[ Elevated urinary urobilinogen was also found in one subject following a 20-minute exposure at 900 ppm, and some evidence of possible kidney injury was found in six subjects after exposure at 500 ppm for 78 minutes.

# Serum enzymes were not elevated. 
Evidence of kidney injury (red blood cells and protein in the urine)
and elevated serum bilirubin were also found in a man following ingestion of 1,1,1-trichloroethane.
Autopsy findings in a woman with a history of chronically sniffing 1.1.1-trichloroethane were limited to the respiratory system, stomach, and

# brain. 
Elevated urinary urobilinogen was found In one worker after he had worked with 1,1,1-trichloroethane for 1 hour in a closed room,  and in two of nine women after they had worked with 1,1,1-trichloroethane for several months.

# IV. ENVIRONMENTAL DATA AND BIOLOGIC EVALUATION Environmental Concentrations and Engineering Controls
There is little information available about the concentrations of 1,1,1-trichloroethane to which workers have been routinely exposed.
Concentrations of 1,1,1-trichloroethane developed in cleaning electrical equipment were reported by Burkatskaya et al  in 1973. The sampling and analytical method were not described. The greasy parts were sprayed with or dipped into the solvent. Parts were sprayed for 4-5 minutes and dried with a jet of air for 2-3 minutes. The room had an exhaust fan and a general two-way exhaust that provided 35-40 air changes (time interval not given).
Concentrations of 1,1,1-trichloroethane in the shop area during the spraying period were 27-70 ppm. These concentrations declined rapidly when the spraying and drying process was completed and, after 30 minutes, the room air concentration was not measureable.
Concentrations found in different parts of the room when the dipping tanks opened were 25-55 ppm. When the parts were taken from the bath, about 250 ppm of 1,1,1-trichloroethane were found in the workroom air. were exposed in excess of the TLV (100 ppm) throughout their working day.
During the survey, concentrations of 1,1,1-trichloroethane were "well below toxic levels" (apparently meaning 350 ppm) during normal vapor degreasing.
In this same study,  methods of operation and ventilation were highlighted as important safeguards. The authors reported samples taken near vapor degreasing plants at 21 factories in England. They found that lip exhaust ventilation was provided at three-fourths of the open top tanks surveyed.
Extraction rates varied (tank to tank) from 0 to > 100 cu ft/min. Lips slots were commonly found to be closed, by dropage of heavy objects or deposits of dirt. Conditions were found to be poorest at tanks without lip exhausts, and over half of the operators were receiving concentrations above the TLV. This was aggrevated in some conditions by poor general ventilation. Also, downward drafts caused solvent vapor to be blown out of the tanks and into the workers' breathing zone. The authors suggested that this effect could be limited by the use of covers and screens at the tank.
The authors  found that manual unloading of tanks as well as preparation of work for the tanks, caused a sharp increase of 1,1,1-trichloroethane in the workers' breathing zones.
The following recommendations were made: (1) Degreasing tanks should be sited in well ventilated areas giving particular attention to tanks in confined areas, (2) vapor degreasing tanks should be provided with efficient lip exhaust systems (35 cu ft/min was suggested as an adequate extraction rate) and covered by protective screens to prevent escape of 1,1,1-trichloroethane vapor, (3) work should be arranged so that it can be contained in the freeboard zone of the tank during the removal of excess solvent and stacked to ensure complete drainage of the degreasing solvent, Activated charcoal has been used as a collection medium followed by analysis by gas chromatography.
 Charcoal is nonpolar and will generally adsorb organic vapors in preference to water vapor resulting in less interference from atmospheric moisture than with silica gel. The dechlorination method (alkaline hydrolysis) requires collection of the 1,1,1-trichloroethane contaminated atmosphere by a suitable collection medium followed by alkaline hydrolysis in isopropyl alcohol, and titration of the liberated chloride with silver nitrate.
 The percentage of chlorine hydrolyzed is determined by comparison between samples and known controls. A disadvantage of this method is that chlorine is not easily removed from 1,1,1-trichloroethane and the amount removed depends on the duration of the dechlorination process. Another disadvantage is that it is not specific for 1,1,1-trichloroethane.
In the colorimetric analytical method based on the Fujiwara reaction, a stream of air containing 1,1,1-trichloroethane is passed through a bottle containing pyridine.
 Potassium hydroxide is then added to a portion of the sample, and this mixture is heated in a boiling water bath and cooled during a fixed time period. A portion of the potassium hyroxide solution, to serve as a blank, is similarly heated and cooled. Absorption coefficients of the pyridine layer are determined with a spectrophotometer.
This method requires less time than the dechlorination method, but the problem of specificity with mixtures of chlorinated hydrocarbons remains.
The third chemical method utilizes direct reading detector tubes.
 These are glass tubes packed with chemicals that change color when a measured and controlled flow of air containing 1,1,1-trichloroethane passes through the chemical. Depending on the type of detector tube, the air may be drawn directly through the tube and compared with a calibration chart, or the air may be drawn into a pyrolyzer accessory prior to the detection tube.  In either case, the analysis is not specific for 1,1,1-trichloroethane since liberated halide ions produce the stain and any  The atmosphere of relevant working stations must be sampled and must correspond to the breathing zone of the workers at the working stations. Infrared analysis is subject to interferences from other air contamiants and these interferences are not easily detected or resolved without substantial knowledge of infrared spectrophotometry.
Gas chromatography provides a quantitative analytical method which can be specific for different chlorinated hydrocarbons.
 Every compound has a specific retention time in a given chromatography column, but several compounds in a mixture may have similar retention times.
This problem can be overcome by altering the stationary phase of the chromatography column or by changing the column temperature or other analytical parameters.
Altering conditions usually will change the retention times and separate the components.
A mass spectrometer can be used subsequent to gas chromatography to identify the substance present in a gas chromatographic peak more positively. Linked gas chromatograph-mass spectrometer instruments perform this identification automatically. A charcoal capillary tube has been used to trap and transfer the material associated with a gas chromatographic peak to a mass spectrometer for qualitative identification when only unlinked units are available.
A comparative study of a colorimetric method, a gas chromatographic method, and colorimetric detection tubes for analysis of 1,1,1trichloroethane was reported in 1970 by Fukabori.
 The data are presented in Table XII-11. They suggest that the detector tubes give higher values than the other two methods used. Although considerable data have been collected, they have not been synthesized into useable form to be able to quantitatively evaluate exposure to 1,1,1-trlchloroethane by either breath or urine analysis.

# V. DEVELOPMENT OF STANDARD

# Basis for Previous Standards
The first Threshold Limit Value (TLV) for 1,1,1-trichoroethane was published by the American Conference of Governmental Industrial Hygienists The USSR MAC is 3.66 ppm (20.0 mg/cu m).  The present US federal standard was adopted from "Threshold Limit  Autopsy findings of gross congestion and pulmonary edema in workers overcome by 1,1,1-trichloroethane exposures   Respiratory irritation has been reported in man and several other species. At 400 ppm eye, nose and throat irritation have been experienced by subjects during exposure to 1,1,1-trichloroethane.  Varying degrees of lung congestion were found in all species exposed continuously for 90 days to 1,1,1-trichloroethane at 135 ppm.
 The authors stated, however, in view of pneumonitis in the surviving animals and in the control group, that no positive conclusions could be drawn connecting the 1,1,1trichloroethane exposure to the effects. Irritation of the upper respiratory tract was reported among women during occupational exposure to 1,1,1-trichloroethane.  No other studies of respiratory disease associated with chronic occupational exposure to 1,1,1-trichloroethane have been reported. The recommended ceiling limit should protect workers from acute irritation effects, but it is not known if it will protect them from chronic respiratory effects.
From the data presented above, it is evident that a ceiling should be placed on occupational exposure to 1,1,1-trichloroethane. Evidence of CNS response at 450 ppm  and minimal to no response at 250 to 350 ppm  leads to the conclusion that 350 ppm is a reasonable ceiling concentration.
This ceiling will assure a safe TWA as excursions above the action level will not lead to the chronic effects described in humans and animals.
Although information on workers exposed to 1,1,1-trichloroethane for over 6 years is sui.-e, workers who had experienced TWA's of 217 ppm for up to 6 years showed no adverse effects, and thus it is unnecessary to recommend a TWA limit below 350 ppm to prevent chronic effects.
To provide some assurance that the environmental limit is not exceeded, an action level of 200 ppm is recommended.
It is recognized that many workers handle small amounts of 1,1,1trichloroethane 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 all the provisions of this recommended standard. However, concern for worker health requires that protective measures be instituted below the enforcable limit to ensure that exposures stay below that limit. Therefore,   Airflow through the pump should be within +5% the desired rate. New calibration curves should be established for each sampling pump after making any repairs or modifications to the sampling system.
The volumetric flowrate through the sampling system should be spot-checked and the proper adjustments made before and during each study to ensure obtaining accurate airflow data. The area of the sample peak is determined and preliminary sample results are read from a standard curve prepared as discussed below.

# Determination of Desorption Efficiency
It is necessary to determine the percentage of 1,1,1-trichloroethane on the charcoal that is removed in the desorption process. This desorption efficiency is determined once for a given compound provided the same batch of charcoal is always used.
Activated charcoal, equivalent to the amount in the first section of It is convenient to prepare standards in terms of mg 1,1,1-trichloroethane/0.5 ml of carbon disulfide because samples are desorbed in this amount of carbon disulfide. To minimize error due to the volatility of carbon disulfide, 20 times the weight can be injected into 10 ml of car bon disulfide. For example, to prepare a 0.3 mg/0.5 ml standard, 6.0 mg of 1,1,1-trichloroethane is injected into exactly 10 ml of carbon disulfide in a glass-stoppered flask.
The density of 1,1,1-trichloroethane (1.2528 g/ml) is used to convert 6.0 mg into microliters for easy measurement with a microliter syringe.
A series of standards is prepared, varying in concentration over the range of interest and analyzed under the same gas chromatographic conditions and during the same time period as the unknown samples. Curves are established by plotting concentration versus average peak area.

# Calculations (a)
The weight in mg corresponding to the peak area is read from the standard curve. No volume corrections are needed, because the standard curve is based on mg l,l,l-trichloroethane/0.5 ml carbon disulfide, and the volume of sample injected is identical to the volume of the standards in jected.

# (b)
Separately determine the weights of 1,1,1-trichloroethane on the front and reserve sections of the charcoal tube.
(c) Corrections must be made to the 1,1,1-trichloroethane weights determined on both the front and reserve sections for the weights of the respective sections of the blank charcoal tube.
(1) Subtract the weight of 1,1,1-trichloroethane found on the front section of the blank charcoal tube from the weight of 1,1,1-
The authors did not give any additional information about these incidents. However, Irish  considered that the concentrations may have been near saturation, approximately 167,000 ppm. He gave the exposure time of one
Immediately before sampling, break both ends of the tube to provide openings at least one-half the internal diameter of the tube (2 mm).
The smaller section of charcoal Is used as a reserve and should be positioned nearest the sampling pump.
( (c) A recorder and some method for determining peak area.
(d) Glass stoppered microtubes of 2.5-ml capacity or 2-ml vials that can be sealed with inert caps.
(e) Microsyringe of 10-^1 capacity, and convenient sizes for making standards.
(f) Pipets, 0.5-ml delivery pipets or 1.0-ml pipets graduated in 0.1-ml increments.
(g) Volumetric flasks of 10-ml capacity or convenient sizes for making standard solutions.

# Reagents (a)
"Spectroquality" carbon disulfide.
(b) 1,1,1-Trichloroethane, preferably "chromatoquality" grade.

# EXTREME CAUTION MUST BE EXERCISED AT ALL TIMES WHEN USING CARBON DISFULIDE BECAUSE OF ITS HIGH TOXICITY AND FIRE AND EXPLOSION

# HAZARDS. IT CAN BE IGNITED BY HOT STEAM PIPES. ALL WORK WITH CARBON DISULFIDE MUST BE PERFORMED UNDER AN EXHAUST HOOD. (c) Typical chromatographic operating conditions:
(1) 50 ml/min (70 psig) helium carrier gas flow.
(2) 65 ml/mln (24 psig) hydrogen gas flow to detector.
(3) 500 ml/min (50 psig) airflow to detector. "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.

# P U B L I C H E A L T H S E R V I C E C E N T E R F O R D I S E A S E C O N T R O L N A T I O N A L I N S T I T U T E F O R O C C U P A T I O N A L S A F E T Y A N D H E A L T H R O B E R T A . T A F T L A B O R