CHEMICALS
    1. NAME
     1.1 Substance
       1,1,1-Trichloroethane
     1.2 Group
       Chlorinated aliphatic hydrocarbon
     1.3 Synonyms
       Chloroethene
       Methyl chloroform
       Methyltrichloromethane
       TCE
     1.4 Identification numbers
       1.4.1 CAS number
             71-55-6
       1.4.2 Other numbers
             NCI       c04626
             RTECS     KJ 2975000
             UN        2831
     1.5 Brand names, Trade names
       Electrosol TCE
       Genklene
       Picrin
       Solvent 265B
       Tergo Electrosol TCE
       Trithene
       
       Products containing TCE as a major component include:
       
       Aerothane
       Chlorothene
       CRC  Belt Grip
       CRC  CDT Cutting Oil
       Gamlen Drum Cleaner Solvent
       GNU Genkleen
       Kodak Movie Film Cleaner with Lubricant
       Liquid Paper Correction Fluid
       Molykote
       Nailfix Remover
       Oven Guard
       Superglo Plastic Cement
       Synthetic Lubricating Fluid No. 610
       Textile No. 1
       Yukoff Bumper and Tyre Sheen
     1.6 Manufacturers, Importers
       Dow Chemicals
       Gamlen Chemicals
       ICI
       Tergo Industries
       Robert Bryce and Company
    2. SUMMARY
     2.1 Main risks and target organs
       The major danger is respiratory depression with a risk of 
       cerebral and cardiac anoxia; and depression of the CNS with 
       coma and respiratory insufficiency.  Primary effects are most 
       marked on the nervous system; at levels in excess of 10,000 
       ppm, anaesthesia gradually develops, associated with 

       respiratory depression.  Unprotected, unsupervised exposure in 
       confined and/or unventilated areas is a significant risk.   
       While this solvent is less toxic than some other chlorinated 
       hydrocarbons, care is still warranted during its use.  
       Inhalation abuse is associated with serious risk and has 
       resulted in fatalities.  In these cases cardiac sensitisation, 
       perhaps exacerbated by relative hypoxia, may be responsible 
       for cardiac arrhythmias. Cardiovascular effects including 
       myocardial depression and arrhythmias are the crucial factors 
       in some deaths (see 9.4), especially in those cases related to 
       glue sniffing. 
     2.2 Summary of clinical effects
       Systemic effects: most symptoms and signs reflect the 
       depressant effect on the central nervous system, which include 
       disturbances in equilibrium and coordination, followed by 
       headache and general lassitude.   With increasing 
       concentrations there may be progressive drowsiness and 
       disorientation, progressing finally to coma and respiratory 
       arrest.  With heavy exposures myocardial depression and 
       hypotension can occur.  Cardiac arrhythmia and deaths have 
       occurred.  Serious hepatotoxicity is uncommon even with 
       moderately high levels.
       
       Following inhalation, mild mucous membrane and upper 
       respiratory tract irritation can occur.
       
       Severe irritant effects on the gastrointestinal tract mucosa 
       have been observed following ingestion.
       
       Contact dermatitis has been described.
     2.3 Diagnosis
       It is based on history of exposure and CNS depression.
       
       Environmental monitoring of ambient air can be accomplished 
       most simply with samples taken by Drager tube, charcoal tube 
       or similar.
       
       Breath analysis is the most useful form of biological 
       monitoring, due to the small renal excretion and low blood 
       levels commonly found.  The best approximation to alveolar air 
       is that obtainable immediately after normal expiration 
       (expiratory reserve volume).
       
       Samples should be collected in glass containers or tubes which 
       can be sealed with a suitable closure for subsequent gas 
       analysis.
     2.4 First-aid measures and management principles
       Treatment is basically symptomatic.
       
       The first aid priority is to make a proper assessment of 
       airway, breathing, circulation and neurological status of 
       patient.  If respiration is markedly depressed, maintain a 
       clear airway and support ventilation.  With heavy exposures 
       and/or evidence of significant nervous system effects, monitor 
       blood pressure, and ECG. Mild to moderate hypotension may 
       occur, with ST segment changes on the ECG.  

       
       After oxygenation, intravenous fluids may be helpful. 
       Sympathomimetic pressor agents, including dopamine, should be 
       used only as a last resort, and adrenaline is specifically 
       contraindicated, due to the probable increased risk of cardiac 
       sensitisation to these agents.
    3. PHYSICO-CHEMICAL PROPERTIES
     3.1 Origin of the substance
       Manufactured by the action of chlorine on 1,1-dichloroethane 
       or the catalytic addition of HCl to 1,1-dichloroethylene.
     3.2 Chemical structure
       1,1,1-Trichloroethane
       
       Molecular Weight: 133.4 daltons
       Structural Formula: CH3CCl3 
     3.3 Physical properties
       Boiling point:           74°C
       Melting point:           -30°C to -39°C
       Flash point:             none by standard ASTM
       Autoignition temperature:     537°C
       Relative vapour density: 4.6
       Vapour pressure (20°C):       130 mbar = 13KPa
       Solubility:             insoluble in water; soluble in 
       acetone, benzene, carbon tetrachloride, methanol and 
       ether (Windholz, 1983) Explosive limits:             
       lower limit 7.5% in air (at 25°C)
       upper limit 15.0% in air
       Relative molecular mass: 133.41
     3.4 Other characteristics
       Colourless liquid at room temperature, with a sweet odour.
       
       Vapour hazards: Reacts violently with potassium and sodium.  
       Incompatible with strong oxidising agents, strong bases, 
       magnesium, zinc, aluminium and its alloys, (Bretherick, 1985). 
       At temperatures above 500°C, hydrogen chloride and small 
       amounts of phosgene are formed.  Other combustion/decomposition 
       products include carbon monoxide and carbon dioxide.
       
       Limits of flammability:  7.5%-15% in air.  Will not readily 
       sustain or support combustion; will not ignite from sparking 
       sources such as static electricity or friction grinders.
       
       Fire extinguishing media:  water spray or carbon dioxide, dry 
       chemical powder, alcohol or polymer foam.
       
       Management of spills: Cover with dry lime or soda ash, deposit 
       in closed container and burn in appropriate incinerator.  
       Ventilate area and wash spill site.  Use rubber gloves, boots 
       and self-contained breathing apparatus.
       
       Water pollution: effect of low concentrations on aquatic life 
       is not well known.  Aquatic toxicity rating: TLM 75-150 
       ppm/pinfish saltwater (time period not specified) (Weiss, 
       1980).
       
       Commercial products normally contain 3%-7% stabilisers such as 

       dioxane, isobutyl alcohol, butylene oxide and nitromethane.
    4. USES/CIRCUMSTANCES OF POISONING
     4.1 Uses
       TCE is often used in household aerosol products, such as 
       oven cleaners, stain removers, furniture polish, 
       degreasers, water repellant, suede waterproofer, and 
       also in hairspray, cosmetics, and typewriter correction 
       fluids (Kings et al., 1985; Pointer, 1982), and in 
       crafts.  Thus the potential for misuse of these products 
       must be considered.  In one study, 28% of 110 sudden 
       deaths in glue sniffers were associated with 
       trichloroethane (Bass, 1970).
       
       TCE is also used as a solvent for natural and synthetic 
       resins, oils, waxes, tar and alkaloids; for adhesives, 
       coatings and for textile dyeing operations; and as a dry 
       cleaning extraction solvent; a coolant and lubricant in 
       metal-cutting oils; and a chemical intermediate in 
       manufacturing.
     4.2 High risk circumstance of poisoning
       Work in small, enclosed and/or poorly ventilated spaces, 
       particularly if unsupervised.  Use of excessively large 
       volumes of solvent for cleaning, e.g. pouring directly onto 
       floor or other surfaces to be cleaned.
       
       Solvent abuse.
     4.3 Occupationally exposed populations
       Workers in a range of chemical industries may be exposed to 
       TCE due to its use as a solvent for natural and synthetic 
       resins, oils, waxes, tar, alkaloids, and in adhesives, 
       coatings and textile dyeing. Chemical plant workers may be 
       involved due to its use as a chemical intermediate in some 
       synthetic processes or as an extraction solvent. Workers in 
       the engineering industry may also be exposed; for example 
       those involved in metal degreasing or cutting or removal of 
       oils and waxes. The dry-cleaning industry has also used this 
       compound.
    5. ROUTES OF ENTRY
     5.1 Oral
       Ingestion is possible but infrequently encountered.
     5.2 Inhalation
       This is the most frequent and significant route of entry.  
       Most commonly occupationally-related but may also be involved 
       in inhalational abuse.
     5.3 Dermal
       Exposure can be considerable but while absorption can occur, 
       it is rarely likely to be significant.
     5.4 Eye
       Unlikely to be a significant route given the small amounts and 
       transient nature of inadvertent eye contact.
     5.5 Parenteral
       Cases involving injection are not well documented.
     5.6 Others
       No human data. 
    6. KINETICS
     6.1 Absorption by route of exposure

       Oral
       
       Rapid absorption through gastrointestinal tract.
       
       Skin
       
       Expired air concentrations after topical application of TCE or 
       continuous immersion of the hand for 30 minutes were 0.5 ppm 
       and 10 ppm respectively at 30 minutes post-exposure.  In 
       contrast, respiratory exposure for a similar time to levels 
       sufficient to cause only mild symptoms, i.e. 910 ppm, was 
       associated with expired air concentrations of around 35 ppm at 
       30 minutes post-exposure (Stewart et al, 1961).  The skin is 
       therefore a considerably less significant route of absorption 
       than the lung. Stewart and Dodd (1964) estimated peak alveolar 
       levels of 45 ppm after immersion of both hands in TCE for 30 
       minutes, similar to peak levels observed after respiratory 
       exposure of the same duration to 100-500 ppm in air.  
       Penetration is less with topical application than after total 
       immersion by a factor of about 20.  They concluded that 
       provided the solvent is not confined beneath an impermeable 
       barrier there is little likelihood that toxic amounts will be 
       absorbed during normal industrial use.
       
       The vapour itself is not absorbed in significant amounts 
       through the skin (Riihimaki and Pfaffli, 1978).
       
       Respiratory
       
       Monster (1978) exposed 6 volunteers for 4 hours at 70 ppm and 
       145 ppm with and without exercise periods.  At rest, lung 
       clearance (reflecting absorption rate) decreased significantly 
       over time, from 6 l/min initially to 3.7 l/min at 10 min and 
       1.9 l/min at 4 hours.  Alveolar retention at 4 hours was 
       calculated at 30%.   These findings are consistent with those 
       of Astrand et al. (1973) and Humbert et al. (1977), whose 
       respective findings included a lung clearance of 3.25 l/min 
       after 30 minutes and an alveolar retention of 28% after 4 
       hours at 72 ppm.  Exercise of 100 watts increased lung 
       clearance and the rate of absorption, but a similar decrease 
       in retention and lung clearance over time occurs with exposure 
       under workload.  The relatively low uptake of TCE in contrast 
       to trichloroethylene, and its tendency to decline further 
       during the course of exposure, can be explained by both its 
       much less extensive metabolism (3.5% v. 75%) and its 
       significantly lower partition coefficient between blood and 
       air (5 v. 15), (Monster, 1978).
     6.2 Distribution by route of exposure
       Monster (1978) estimated a partition coefficient of 6 between 
       venous blood and alveolar air, similar to that of 5 estimated 
       by Astrand et al. (1973).
     6.3 Biological half-life by route of exposure
       Respiratory
       
       Monster (1978) found that concentrations in exhaled air 
       following exposure paralleled the decline in blood levels.   

       Due to differences in distribution and elimination 
       characteristics of the various tissues, the elimination half-
       life is not constant;  in the above study the half-life was 
       estimated at 9, 20 and 26 hours at 20, 50 and 100 hours 
       respectively post-exposure.  (The blood concentration was 
       about 8.2 times that in mixed exhaled air, which is, however, 
       about 70% that of alveolar air.)
     6.4 Metabolism
       About 10% is metabolized to trichloroethanol and to a lesser 
       extent to trichloroacetic acid, which are excreted in the 
       urine (Ikeda et al., 1972),  the latter as a glucuronide 
       conjugate.
       
       Monster (1978) estimated that maximum concentrations of 
       trichloroethanol in blood occurred within two hours of the end 
       of exposure and thereafter declined rapidly, with a half-life 
       of approximately 10-12 hours.  In contrast, blood 
       trichloroacetic acid continues to rise until about 40 hours 
       post-exposure, and from about 60 hours declines exponentially 
       with a half-life of 70-85 hours.
     6.5 Elimination by route of exposure
       Respiratory
       
       The greater part of absorbed trichloroethane is excreted 
       unchanged in exhaled air.  The remainder is largely 
       metabolised to trichloroethanol and trichloroacetic acid.  
       Thus Monster found that after 162 hours (about 1 week) the 
       total amount exhaled was estimated to represent 80% of the 
       uptake after exposure to 70 ppm at rest, and a little less 
       with higher exposure levels, with or without workload.  The 
       relatively rapid alveolar elimination of TCE of 75% at 50 hr 
       (in comparison with perchloroethylene, for example), can be 
       explained by its lower blood gas partition coefficient (5 v. 
       15).  In contrast, total urinary excretion of trichloroethanol 
       and trichloroacetic acid were estimated at only 2% and 0.5% 
       respectively of the uptake after 3 days.  (This latter figure 
       rose to 1.5% after 7 days). Trichloroethanol is also excreted 
       in exhaled air but at a level much lower than that in urine.
       
       While the major portion of the trichloroethanol is eliminated 
       in the urine within one day, only about 30% of the total 
       trichloroacetic acid is excreted in urine in the first 3 days 
       after exposure. Thus this compound can accumulate with 
       repeated exposure.
    7. TOXICOLOGY
     7.1 Mode of Action
       The specific mode of action is not well known but is presumed 
       to include effects on cell membranes, due to its lipophilic 
       properties.   In consequence, trans-membrane ion transport 
       systems are affected;  resulting effects include impairment of 
       neuronal impulse coordination.
     7.2 Toxicity
       7.2.1 Human data
             7.2.1.1 Adults
                     Acute Toxicity:
                     

                     Inhalation -  no physiological effects were 
                     observed below 350 ppm (Stewart, 1968).   There 
                     is variation in human response, as evidenced by 
                     particularly susceptible individuals exhibiting 
                     impairment on the modified Romberg Test of 
                     balance at 400 ppm while in another experiment 
                     30 healthy volunteers exposed to 500 ppm for 
                     variable time periods performed this test 
                     normally (Stewart et al, 1961).  At 800-1000 ppm 
                     some subjects showed minor CNS impairment 
                     (Stewart et al, 1961; Torkelson et al, 1958).   
                     Other investigators (Salvini et al, 1971) have 
                     found similar results.  Exposure at 900-1000 ppm 
                     causes mild eye and nasal discomfort, with 
                     slight loss of equilibrium at one hour.   At 
                     2000 ppm loss of equilibrium may occur at 15-30 
                     minutes and loss of coordination after one hour 
                     (American Industrial Hygiene Association, 1964). 
                     Above 1700 ppm disturbances of equilibrium 
                     become more obvious and lassitude and headache 
                     may occur (Stewart et al, 1961).
                     
                     Over 30 deaths and accidental intoxications have 
                     been reported following over-exposure but it is 
                     difficult to assess the levels involved in 
                     fatalities.  In one case, the concentration at 
                     the time of an accident was "well in excess of 
                     5000 ppm" (Kleinfeld and Feiner, 1966), and 
                     circumstantial evidence suggests that this is 
                     applicable to other fatalities.
                     
                     The minimal anaesthetic concentrations are 
                     considered to lie within the range 10,000 to 26,
                     000 ppm (Dornette & Jones, 1960).   A 
                     concentration of 30,000 ppm has been used for 
                     induction of anaesthesia, which was maintained 
                     at levels of 20,000-30,000 ppm.   A five-minute 
                     exposure to 5000 ppm can be expected to produce 
                     marked incoordination, and anaesthesia occurs at 
                     20,000 ppm (Stewart, 1968).  Recovery from light 
                     plane anaesthesia occurs in 3-5 minutes.  With 
                     chronic exposure, significant effects are most 
                     unlikely at levels below the TLV of 350 ppm.   
                     In an exercise reconstructing the circumstances 
                     of a fatal incident, the concentration reached 
                     levels of 62,000 ppm (Hatfield and Maykoski, 
                     1970).
                     
                     Ingestion - Stewart and Andrews (1966) report a 
                     case of an adult male accidentally ingesting 
                     about 28 g of inhibited TCE, an estimated dose 
                     of 0.6 g/kg (Gosselin et al, 1984). The most 
                     notable symptoms were nausea and severe vomiting 
                     and diarrhoea;  the physical examination was 
                     normal.   A slight elevation in serum total 
                     bilirubin (48 IU) was the only other abnormality 

                     noted.   This suggests that, based on a specific 
                     gravity of 1.33, doses of up to about 0.5 ml/kg 
                     may not produce marked systemic effects, 
                     although gastrointestinal irritation may be 
                     considerable. Reversible central nervous 
                     depression has been reported after accidental 
                     ingestion of approximately 0.1 ml/kg of a 95% 
                     trichloromethane solution, (Dornette & Jones, 
                     1960).
                     
                     Skin exposure - cutaneous absorption is probably 
                     too slow to produce significant toxicity 
                     (Stewart & Dodd, 1964).
             7.2.1.2 Children
                     No data available.
       7.2.2 Relevant animal data
             Acute Toxicity:
             
             Inhalation - Adams et al (1950) reported the following 
             maximum non-lethal and no observed effect levels (NOEL) 
             in rats.  These values will approximate the LClo and 
             TClo respectively and have been labelled as such.
             
             LClo       6 min at 30,000 ppm
                       18 min at 18,000 ppm (various species)
                       90 min at 15,000 ppm
                        7 hr  at  8,000 ppm
             TClo     518 min at 18,000 ppm
                        5 hr  at  8,000 ppm
             
             Thus the maximum NOEL is close to the maximum exposure 
             level survived, indicating relatively low acute toxicity 
             for most organs.  This has been supported by other 
             studies (Klaasen and Plaa, 1966, 1967;  Plaa and Larson, 
             1965).
             
             Gehring (1968) also showed that with exposure at 13,500 
             ppm for the median lethal time of 593 minutes 
             (approximately 10 hours), liver function was virtually 
             unaffected unless exposures approached those causing 
             anaesthetic death.
             
             At anaesthetic concentrations (>10,000 ppm), 
             idioventricular rhythms may be induced with adrenaline 
             in animals (Rennick, et al, 1949).
             
             Oral - Torkelson et al (1958) reported the following 
             LD50 values:
             
             Male rats        12.3  g/kg 
             Female rats      10.3  g/kg
             Female mice      11.24 g/kg
             Female rabbits    5.66 g/kg
             Male guinea pigs  9.47 g/kg
             
             Carpenter et al (1949) reported the oral LD50s in four 

             species of laboratory animal of 8.6 - 14.3 g/kg. 
             
             After application to the skin in the rabbit, all animals 
             survived 3.9 g/kg applied for 24 hrs under occlusion. 
             
             Eyes (rabbit) - minor, transient irritation.
             
             Chronic Toxicity:
             
             Inhalation - Adams et al (1950) also studied long-term 
             exposures in rats:
             
             10,000 ppm:   10 mins - staggering gait and weakness 3 
             hrs - irregular perspiration, semiconsciousness
             5,000 ppm:    1 hr - mild but definite narcotic effect
             with reduced activity.  No apparent injury with repeated 
             exposures.  Slight growth retardation.
             3,000 ppm:    No response in rabbits and monkeys over 2 
             months.
             
             Prendergast et al (1967) exposed rabbits and dogs to 2,
             200 ppm for 8 hours per day for 6 weeks.  Although 
             weight loss occurred there were no visible signs of 
             toxicity.
       7.2.3 Relevant in vitro data
             In vitro evaluation of mutagenicity suggests, at most, a 
             weak action (Dow Chemical Company, unpublished data, 
             1981). The data indicate that TCE itself is not likely 
             to be positive in mutagenic tests. Weakly positive Ames 
             test have been reported sporadically (Simmon et al, 
             1977) but may be due to various stabilisers used, some 
             of which are electrophilic in nature.
       7.2.4 Workplace standards
             ACGIH (1986)   TLV-TWA  350 ppm (1900 mg/m3)  
                            TLV-STEL 450 ppm (2450 mg/m3).  
             
             CEC (1986) has recommended corresponding values of 200 
             ppm and 350 ppm respectively.  No BEI or BLV appears to 
             have been set for TCE, unlike trichloroethylene.  
             Recommendations have been made, (Stewart 1961, Lauwerys 
             1986).
       7.2.5 Acceptable daily intake (ADI) and other guideline levels
             Value not found.  Probably not relevant.
     7.3 Carcinogenicity
       No evidence of carcinogenic properties exists.  In one U.S. 
       National Cancer Institute bioassay study (NCI,1977) large 
       doses given by gavage were associated with significantly 
       increased mortality in rats and mice.  However, while 
       assessment was difficult, no statistically significant 
       increase in tumours was observed.  In a second study, 3 of 49 
       animals in the high dose group (4-6 g/kg/day) developed liver 
       cell adenomas and one an hepatocellular carcinoma.
       
       Quast et al (1975) exposed rats to 875 ppm and 1750 ppm by 
       inhalation for 6 hours per day for 1 year and then observed 
       them throughout their lifetimes.   There was no apparent 

       increase in tumours, nor any other adverse effects.
       
       A CEC Committee (1986) considered that the carcinogenic 
       potential of TCE has not been fully evaluated and that 
       stabilisers may contribute to the toxicity in as yet uncertain 
       ways.
     7.4 Teratogenicity
       TCE did not produce teratogenic effects in pregnant rats or 
       mice exposed for 7 hours per day to 875 ppm during the period 
       of organogenesis, ie days 6-15 of gestation, (Schwetz et al, 
       1975). No effects were observed on the average number of 
       implantation sites per litter, litter size, incidence of 
       foetal resorptions, foetal sex ratios or foetal body 
       measurements.  No treatment-related increase in the incidence 
       of skeletal or visceral malformations was observed.  No dose-
       dependent effects on fertility, gestation, viability or 
       lactation indices were observed in a multigeneration 
       reproductive study; nor any teratogenic effects (Torkelson & 
       Rowe, 1981).  Dosage levels tested were 99.4, 2640 and 8520 
       mg/kg daily.
     7.5 Mutagenicity
       Simmon et al (1977) reported mutagenicity in Salmonella 
       typhimurium strain TA100, with or without a microsomal 
       activation system.   They considered that stabilisers or 
       inhibitors may have been responsible.  In a review of 
       organochlorine solvents (CEC, 1986) the authors comment that 
       although the liquid does not produce point mutations in Ames-
       developed strains of S. typhimurium, the vapour gave a 
       positive result in two studies.   However, they suggest that 
       one of these results may have been due to an epoxide 
       stabiliser in the preparation, and the full range of 
       constituents in the other was not detailed.
       
       This group concluded that there is no strong evidence that TCE 
       itself is a potential mutagen but that available data do not 
       allow final conclusions to be made.  They state that no 
       studies have been published on the mutagenicity of TCE in 
       mammalian cells in culture, but there is no evidence from 
       other tests to suggest chromosomal damage; thus negative 
       results were found with a micronucleus and dominant lethal 
       assay in mice, and no indication of sister chromatid exchange 
       in Chinese hamster ovary cells.
     7.6 Interactions
       Some case reports involve concurrent exposure to other 
       compounds, as is commonly the case with solvents. It is not 
       clear however, whether the effects are anything other than 
       simply additive. Some liquid paper products contain both TCE 
       and trichloroethylene (Pointer 1982, King et al, 1985). 
       Deliberate abuse of this product has resulted in death from a 
       combination of nervous system depression and cardiotoxicity, 
       but either of these compounds is capable of such effects at 
       the concentrations encountered with solvent abuse.  It may be 
       that trichloroethylene is the more toxic.
       
       There may be some potentiation of effect by ethanol but this 
       is described more with trichloroethylene than 1,1,1-

       trichloroethane.
    8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
     8.1 Material sampling plan
       8.1.1 Sampling and specimen collection
             8.1.1.1 Toxicological analyses
                     No data available.
             8.1.1.2 Biomedical analyses
                     Environmental monitoring is most simply 
                     accomplished by the use of Draeger tubes or 
                     similar grab sampling.
                     
                     Biological monitoring involves collection of 
                     expired air samples and subsequent analysis.
                     
                     Urinalysis is not helpful, due to the small 
                     amount of urinary excretion of TCE and its 
                     metabolites estimated at 2% of uptake as 
                     trichloroethanol and 0.5% of uptake as 
                     trichloroacetic acid (Monster, 1978).
             8.1.1.3 Arterial blood gas analysis
                     May be useful in the presence of respiratory 
                     depression
             8.1.1.4 Haematological analyses
             8.1.1.5 Other (unspecified) analyses
       8.1.2 Storage of laboratory samples and specimens
             8.1.2.1 Toxicological analyses
             8.1.2.2 Biomedical analyses
             8.1.2.3 Arterial blood gas analysis
             8.1.2.4 Haematological analyses
             8.1.2.5 Other (unspecified) analyses
       8.1.3 Transport of laboratory samples and specimens
             8.1.3.1 Toxicological analyses
             8.1.3.2 Biomedical analyses
             8.1.3.3 Arterial blood gas analysis
             8.1.3.4 Haematological analyses
             8.1.3.5 Other (unspecified) analyses
     8.2 Toxicological Analyses and Their Interpretation
       8.2.1 Tests on toxic ingredient(s) of material
             8.2.1.1 Simple Qualitative Test(s)
             8.2.1.2 Advanced Qualitative Confirmation Test(s)
             8.2.1.3 Simple Quantitative Method(s)
             8.2.1.4 Advanced Quantitative Method(s)
                     Infra-red spectrometry of expired breath.
       8.2.2 Tests for biological specimens
             8.2.2.1 Simple Qualitative Test(s)
             8.2.2.2 Advanced Qualitative Confirmation Test(s)
             8.2.2.3 Simple Quantitative Method(s)
             8.2.2.4 Advanced Quantitative Method(s)
             8.2.2.5 Other Dedicated Method(s)
       8.2.3 Interpretation of toxicological analyses
             While Hall and Hine (1966) reported blood levels of 72 
             mg% and 13 mg% in two fatal cases, others have reported 
             lower levels.  Stahl et al (1969) reported levels of 6.0,
              6.2 and 12.0 mg% in three of six fatal cases, very 
             similar to the 6 mg% reported by Hatfield and Maykoski 
             (1970). Exposure to essentially non-toxic levels of 500 

             ppm for 78 minutes resulted in blood levels of just 
             0.15mg% - 0.65 mg% (Stewart et al, 1961).  Jones and 
             Winter (1983) reported two fatalities in whom post-
             mortem blood levels were 4.2 mg% and 1.8 mg%.
             
             In two of the above cases, the brain concentrations were 
             123 mg% and 8 mg% respectively; in the second case, 
             inhalation of vomitus was thought a contributing factor 
             in the death (Jones and Winter, 1983).
     8.3 Biomedical investigations and their interpretation
       8.3.1 Biochemical analysis
             8.3.1.1 Blood, plasma or serum
                     Abnormal serum bilirubin, SGOT, alkaline 
                     phosphatase and prolonged prothrombin time have 
                     been reported in sniffers of spot remover 
                     containing trichloroethane and trichloroethylene 
                     (Litt & Cohen, 1969).
             8.3.1.2 Urine
                     Elevated urinary urobilinogen has been reported 
                     in one volunteer seven days after exposure to 
                     900 ppm for 20 minutes to trichloroethane at a 
                     concentration increasing continually from 0-2650 
                     ppm.
             8.3.1.3 Other fluids
       8.3.2 Arterial blood gas analyses
             Respiratory acidosis in respiratory insufficiency.
       8.3.3 Haematological analyses
       8.3.4 Interpretation of biomedical investigations
             In blood samples from 66 patients concentrations ranged 
             from 0.1 to 60 mg/l. A broad relationship between blood 
             concentration and the severity of poisoning was observed 
             but there were large variations. There was no strong 
             correlation between blood concentration and clinical 
             features (Meredith et al, 1989).
             
             Using infrared spectrometric analysis of expired breath 
             (Section 8), serial measurements following exposure 
             allow the construction of an excretion curve which can 
             then be compared to the excretion curves of subjects 
             previously exposed to known amounts of solvents.   This 
             gives some indication of the level of exposure.  If a 
             level obtained very soon after exposure is extremely 
             high, serial measurements are unnecessary to establish 
             that exposure was severe.
     8.4 Other biomedical (diagnostic) investigations and their 
       interpretation
     8.5 Overall Interpretation of all toxicological analyses and 
       toxicological investigations
     8.6 References
    9. CLINICAL EFFECTS
     9.1 Acute poisoning
       9.1.1 Ingestion
             Mouth and upper gastrointestinal discomfort followed by 
             nausea, vomiting and severe diarrhoea have been observed 
             following one case where the dose was estimated at 0.6 
             g/kg (Stewart and Andrews, 1966).   A slight elevation 

             in serum total bilirubin at 48 hours in absence of 
             clinical hepatotoxicity was observed.   No significant 
             drowsiness or incoordination was described. Reversible 
             nervous system depression was described after accidental 
             ingestion of about 0.1 ml/kg of a 95% solution (Dornette 
             and Jones, 1960).
       9.1.2 Inhalation
             Some individual variation in susceptibility appears 
             likely at least at lower exposure levels.  Early 
             symptoms may include mild eye and nasal discomfort and 
             impairment of equilibrium and coordination.
             
             Increased lassitude and headache occur with heavier 
             exposures and in severe poisoning progressive CNS 
             depression occurs.   Hepatotoxicity may not become 
             manifest until near-anaesthetic levels are reached.  
             Nausea is apparently not common.   Several deaths have 
             occurred following industrial exposure in confined 
             spaces and also in the context of solvent abuse.  The 
             evidence suggests, particularly in cases of abuse, that 
             the arrhythmogenic and cardiodepressive effects become 
             crucial factors at very high levels.
       9.1.3 Skin exposure
             Stewart and Dodd (1964) tested skin absorption in 
             volunteers by total immersion of the hands.  A mild 
             burning sensation was noted after 10 minutes.  Mild 
             erythema and scaling were noted on removal which settled 
             within 30 to 60 minutes.   This fairly mild skin 
             irritation contrasted with that of some other 
             chlorinated hydrocarbon solvents.   They established 
             that skin absorption is not high.
       9.1.4 Eye contact
             Severe eye irritation has not been reported in man; this 
             is consistent with animal studies where only slight 
             conjunctival irritation without corneal damage has been 
             described.
       9.1.5 Parenteral exposure
             No data available.
       9.1.6 Other
             No data available.
     9.2 Chronic poisoning
       9.2.1 Ingestion
             Not relevant.
       9.2.2 Inhalation
             Chronic effects are considered to be of little 
             consequence with the most usual industrial exposure 
             situations below TLV levels (Kramer et al, 1978). Thus 
             in one controlled study of 151 subjects, no adverse 
             effects and no evidence of hepatotoxic or cardiotoxic 
             effects were found.
       9.2.3 Skin exposure
             Contact dermatitis of the simple irritant type can occur 
             with repetitive exposure.
       9.2.4 Eye contact
             Mild conjunctivitis with chronic vapour exposure.
       9.2.5 Parenteral exposure

       9.2.6 Other
     9.3 Course, prognosis, cause of death
       In mild poisonings subjects may exhibit eye and nasal 
       discomfort, with slight loss of equilibrium and coordination.  
       In moderate cases, increasing headache, lassitude and nausea 
       may occur.   With severe and prolonged exposure, progressive 
       central nervous system and respiratory depression will 
       develop; however considerable evidence indicates that 
       cardiovascular effects including myocardial depression and 
       arrhythmias are the crucial factors in some deaths.
     9.4 Systematic description of clinical effects
       9.4.1 Cardiovascular
             Effects on human cardiac function have been observed 
             when TCE was used as an anaesthetic agent.
             
             Dornette and Jones (1960) reviewed experience with 50 
             anaesthetic administrations.   With concentrations 
             sufficient to produce light anaesthesia (in combination 
             with nitrous oxide), a decrease in systolic blood 
             pressure of 5-10 mm Hg was noted in about half the 
             patients, with greater depression in 6%.  Three of 32 
             monitored patients exhibited premature ventricular 
             contractions of varying degree and/or depressed ST-
             segments in the electrocardiograph.   However, the 
             former occurred only in association with respiratory 
             obstruction and reversion occurred when this was 
             corrected. Thus relative hypoxia contributes to the 
             arrhythmogenic effects.
             
             One of the patients with depressed ST-segments developed 
             cardiac arrest following a steady decline in blood 
             pressure.
             
             It is likely that cardiac arrhythmias could have played 
             a role in some industrial deaths and certainly those 
             involving inhalational abuse, given the rapidity of 
             onset and other features of the cases.  Bass (1970) 
             discussed this possibility in a review of 110 cases of 
             sudden death in solvent sniffers, 29 involving TCE.  The 
             threshold for cardiac conduction defects is probably 
             high since no ECG abnormalities developed after exposure 
             of volunteers to up to 1,000 ppm (Torkelson et al, 
             1958).
       9.4.2 Respiratory
             The vapour is not a serious respiratory tract irritant 
             and few signs of such irritation occur, even at 
             concentrations presenting risks from respiratory 
             depression.  TEC has been used as an anaesthetic.  The 
             pulmonary congestion and oedema found in fatal cases is 
             likely to be a secondary manifestation.  In survivors of 
             severe exposure, recovery is generally prompt with 
             little residual respiratory function deficit.
             
             Kramer el al. (1978) conclude that chronic exposure to 
             levels typical in industry are not a hazard to the 
             respiratory tract. However, Woo et al. (1983) describe a 

             case of cough, dyspnoea and chest pain associated with 
             hypoxia in a man using an aerosolised product containing 
             TCE, and other cases have been reported.  They suggest 
             that aerosol inhalation may result in higher local 
             mucosal concentrations of liquid TCE whose contact with 
             epithelium could have been enhanced by the particular 
             surface active agent included in the product.
       9.4.3 Neurological
             9.4.3.1 CNS
                     Impairment of central nervous system functions 
                     is the most characteristic feature of TCE.  The 
                     earliest symptoms are usually slight impairment 
                     of equilibrium and coordination, followed by 
                     lassitude and headache.  One study by Salvini et 
                     al (1971) involving just 6 subjects found no 
                     statistically significant impairment of 
                     psychophysiological function at levels of 450 
                     ppm, indicating that the TLV is an appropriate 
                     level. Thus assessment of memory, complex 
                     reaction time, manual dexterity and perception 
                     showed no difference from controls.  On the 
                     other hand Gamberale and Hultengren (1973) did 
                     obtain significant differences from controls in 
                     measures of reaction time, perceptual speed and 
                     manual dexterity at 350 ppm.  In a series of 
                     volunteer studies by Stewart et al (1961) it was 
                     found that exposure at 900 ppm for one hour 
                     could cause slightly impaired balance. At 2650 
                     ppm, following gradually increasing exposure 
                     over 15 minutes, two of seven subjects could not 
                     stand and three others became lightheaded, only 
                     one still performing a Romberg test normally.
                     
                     Progressive CNS depression occurs with 
                     increasing concentrations of TCE. Anaesthesia 
                     can be induced at concentrations between 10,000 
                     ppm and 26,000 ppm (Dornette & Jones 1960) and 
                     light anaesthesia is maintained at 
                     concentrations between 6000 and 22,500 ppm.  
                     (They considered that in this series of patients 
                     at least one quarter of the narcotic effect was 
                     attributable to nitrous oxide).  Recovery from 
                     light anaesthesia usually occurred within three 
                     to five minutes.
             9.4.3.2 Peripheral nervous system
                     Peripheral neuropathies have not been directly 
                     associated with TCE exposure.
             9.4.3.3 Autonomic nervous system
                     Effects on the autonomic nervous system may be 
                     possible but have not been clearly described. 
                     Secondary responses may be anticipated to the 
                     apparently negative isotropic and vasodilator 
                     effects of TCE (Herd et al., 1974).
             9.4.3.4 Skeletal and smooth muscle
                     Effects on smooth muscle have been little 
                     researched.  The possibility has been raised by 

                     Herd et al (1974) that the reduced myocardial 
                     contractility observed may be mediated by 
                     changes in distribution in calcium, 
                     administration of which restored function 
                     towards normal.  It is possible that skeletal 
                     muscle function could be affected by similar 
                     mechanisms.
       9.4.4 Gastrointestinal
             Gastrointestinal symptoms with inhalational exposures 
             are not marked although, as with solvent abuse, nausea 
             and in severe cases vomiting can occur. In one ingestion 
             episode, oropharyngeal and gastrointestinal discomfort 
             were followed by nausea, vomiting and severe diarrhoea 
             (Stewart & Andrews, 1966).  In another (Gerace, 1981) 
             burns of the oesophagus were noted.
             
             Rare episodes involving ingestion suggest a severe 
             irritant effect on alimentary tract mucosa.
       9.4.5 Hepatic
             TCE has been used in controlled high doses as an 
             anaesthetic agent. Experience, including a series of 51 
             cases reported by Dornette & Jones (1960), suggests it 
             is not frequently or significantly hepatotoxic, even at 
             such high levels.  This is consistent with a number of 
             animal studies (Adams et al, 1950).  Plaa et al (1958), 
             and Klaasen & Plaa (1966) suggest that it is less 
             hepatotoxic than most other chlorinated hydrocarbons.
             
             Stewart et al. (1961) reported one volunteer with 
             elevated urinary urobilinogen seven days after exposure 
             to 900 ppm for 20 minutes.  This finding was also noted 
             in two of seven subjects exposed for 15 minutes to TCE 
             at a concentration increased continuously from 0 to 2650 
             ppm.
             
             Litt and Cohen (1969) reported abnormal serum bilirubin, 
             SGOT, alkaline phosphatase and prolonged prothrombin 
             time in five teenage males who had sniffed a spot 
             remover containing both TCE and trichloroethylene.  Some 
             had been previous solvent abusers.
             
             Halevy et al (1980) describe an episode where hepatic 
             and renal effects predominated, with little acute CNS 
             symptoms, suggesting exposure levels were not high (see 
             section 11.1, Illustrative cases).  Liver function tests 
             remained elevated for 38 days and biopsy showed 
             cholestasis, eosinophilia and inflammatory cell 
             infiltrate.  A hypersensitivity reaction was suggested 
             as the underlying mechanism.
       9.4.6 Urinary
             9.4.6.1 Renal
                     Effects on the urinary system appear uncommon 
                     and have not been reported in some volunteer 
                     studies (Stewart et al., 1969) and reviews of 
                     workforce populations (Kramer et al., 1978).  
                     However renal effects have been described 

                     following both acute and long-term exposure, and 
                     in one ingestion episode: in this case, 
                     microscopic haematuria and mild proteinuria (1+) 
                     were observed on admission but were resolved 
                     (Stewart & Andrews 1966).
                     
                     Halevy et al (1980) reported a patient with 
                     proteinuria and abnormal renal function indices 
                     (creatinine clearance 70 ml/minute, serum 
                     creatinine 1.55 mg%).  All were reversible 
                     within ten days.
                     
                     Some case-control studies have associated 
                     glomerulonephritis with chronic solvent exposure 
                     (Zimmerman et al., 1975; Lagrue et al., 1977) 
                     although it is difficult to identify the 
                     relevant solvent(s) in sometimes complex 
                     exposures, and negative associations have also 
                     been claimed (Van der Laan, 1980).  Nathan and 
                     Toseland (1979) discussed a patient with 
                     GoodPasture's syndrome attributed to prolonged 
                     glue sniffing in whom TCE abuse exacerbated the 
                     clinical picture; it may also have been one of 
                     the solvents initially involved.
                     
                     Solvent abuse has been implicated in some cases 
                     of renal tubular lesions, and biochemical 
                     markers of tubular effects e.g. urinary ß-
                     glucuronidase were elevated in drycleaning 
                     workers exposed to one chlorinated hydrocarbon 
                     (Franchini et al., 1983).  However TCE does not 
                     appear to have been directly implicated with 
                     this condition.
             9.4.6.2 Others
                     No data available.
       9.4.7 Endocrine and reproductive systems
             There appears to be no evidence of significant adverse 
             effects in humans, although this issue has not been 
             studied in depth.  In one study in mice (Lane et al., 
             1982), 1 g/kg daily via drinking water had no effect on 
             fertility.
       9.4.8 Dermatological
             In volunteer studies involving hand immersion (Stewart & 
             Dodd, 1964), a burning sensation was produced within ten 
             minutes, followed by erythema and scaling on removal; 
             this resolved within 60 minutes.  Chronic exposure can 
             result in irritant contact dermatitis.  Excessive 
             contact can result in blistering and second degree 
             chemical burns (Jones & Winter, 1983).
       9.4.9 Eye, ears, nose, throat: local effects
             Direct eye contact with the liquid can produce mild 
             conjunctivitis, subsiding within a few days (Dow 
             Chemical Company, Medical Records).  Eye irritation may 
             occur with vapour exposure.
       9.4.10 Haematological
              Case histories (Stewart, 1971; Halevy et al., 1980) and 

              workforce population studies (Kramer et al., 1978) 
              suggest that significant haematological toxicity rarely,
               if ever, occurs.
       9.4.11 Immunological
              Parameters of immunological disturbance do not appear 
              to have been well studied.  However glomerular basement 
              membrane antibodies have been isolated in some cases of 
              glomerulonephritis attributed to chronic exposure to 
              solvents which have included TCE in some cases.
       9.4.12 Metabolic
              9.4.12.1 Acid-base disturbances
              9.4.12.2 Fluid and electrolyte disturbances
              9.4.12.3 Others
       9.4.13 Allergic reactions
              Not demonstrated. 
       9.4.14 Other clinical effects
              Not significant.
       9.4.15 Special risks
              Pregnancy - There is little information by which to 
              assess the risk to man. While York et al. (1982) found 
              some foetal developmental delay in rats when dams were 
              exposed to 2100 ppm, postnatal development was normal; 
              there is no evidence of teratogenicity (Schwetz et al., 
              1975; York et al., 1982).  Lane et al. (1982) showed no 
              adverse reproductive or fertility effects in mice.
     9.5 Others
       No data available.
     9.6 Summary
    10. MANAGEMENT
      10.1 General principles
         TCE is primarily a central nervous system depressant and at 
         high levels can cause severe respiratory depression with 
         life-threatening hypoxia, and/or serious cardiac arrhythmia 
         which is exacerbated by endogenous catecholamines.  The most 
         critical aspect of management is immediate support of vital 
         functions; toxicity to other organs is relatively low and 
         there is no specific antidote.
         
         The first priority is to make a proper assessment of the 
         airways, breathing, circulation and neurological status of 
         the patient and to monitor blood pressure and ECG. 
         Sympathomimetic agents, in particular adrenaline, should not 
         be used even in the face of such apparent indications as 
         severe hypotension, as these agents may potentiate the 
         arrhythmogenic effects of TCE, particularly under conditions 
         of hypoxia.
      10.2 Relevant laboratory analyses and other investigations
         10.2.1 Sample collection
                Breath analysis is the most appropriate biological 
                monitoring method.  Expired air can be collected in a 
                container which can be sealed.  Any other specimens 
                collected should be placed in containers which can be 
                sealed to prevent loss of vapour.
         10.2.2 Biomedical analysis
                In severe cases with depressed respiration, arterial 
                blood gas analysis may be a useful monitoring aid.

         10.2.3 Toxicological analysis
                Using analysis of expired breath (Section 8), serial 
                measurements following exposure allow the 
                construction of an excretion curve which can then be 
                compared to the excretion curves of subjects 
                previously exposed to known amounts of solvents.   
                This gives some indication of the level of exposure: 
                if a level obtained very soon after exposure is 
                extremely high, serial measurements are unnecessary 
                to establish that exposure was severe.
         10.2.4 Other investigations
      10.3 Life supportive procedures and symptomatic treatment
         Make a proper assessment of the airways, breathing, 
         circulation and neurological status of the patient. Maintain 
         a clear airway.
         
         If spontaneous respiration is inadequate, perform mouth-to-
         mouth resuscitation or endotracheal intubation and support 
         ventilation using an appropriate mechanical device.
         
         Monitor vital signs. Hypotension may respond to adequate 
         oxygenation and IV fluid replacement.  There appears to be 
         little experience with pharmacological treatment of 
         hypotension or arrhythmia, but ventricular fibrillation has 
         been reversed successfully with defibrillation in at least 
         one case.  Measure arterial blood gases and monitor fluid 
         electrolytes, including calcium.
      10.4 Decontamination
         Inhalation - Move patient to fresh air.  In severe cases 
         administer oxygen by mask or nasal cannula. If spontaneous 
         respiration is inadequate perform endotracheal intubation 
         and support ventilation using an appropriate mechanical 
         device.  There is no evidence that the co-administration of 
         carbon dioxide to act as a respiratory centre stimulant 
         achieves greater clinical improvement or increased 
         elimination, but this has not been well studied.  While the 
         primary purpose of ventilation is to correct hypoxia, it 
         will also result in increased elimination of TCE because the 
         vapour is largely eliminated through the breath.
         
         Ingestion - The minimum systemically toxic oral dose in 
         humans is uncertain but is probably greater than 0.5 g/kg 
         and may be higher.  Decontamination need be considered only 
         above this level.
         
         Ingestion episodes are fortunately very rare and management 
         experience is slight.  In the two most commonly cited cases 
         (Stewart & Andrews, 1966; Gerace, 1981) both vomiting and 
         diarrhoea occurred, within thirty minutes in the latter case 
         (report not yet obtained) which was also associated with 
         oesophageal burns.  Inducing emesis (e.g. with syrup of 
         ipecac) may not be warranted in some cases and may even be 
         contraindicated if there is evidence of severe 
         gastrointestinal pain.
         
         It may be preferable to administer activated charcoal but 

         large volumes may be necessary and will obscure the mucosa 
         from direct visualisation.  Administer a cathartic unless 
         already given with activated charcoal or diarrhoea is 
         evident.  Emesis is contraindicated in coma, with 
         convulsions or evidence of ulceration of the 
         gastrointestinal mucosa. A third alternative for large 
         ingestions is to perform gastric lavage in the absence of 
         severe corrosive injury and with protected airway in 
         comatose or convulsing patients.  Emesis and particularly 
         lavage will be relatively ineffective after one hour. 
         Skin - wash skin with soap and copious amounts of water.
         
         Eye - Exposed eyes should be irrigated with copious amounts 
         of water at room temperature for at least 15 minutes.
      10.5 Elimination
         Established measures to enhance elimination have no role.
      10.6 Antidote treatment
         10.6.1 Adults
                There are no specific antidotes.
         10.6.2 Children
                There are no specific antidotes.
      10.7 Management discussion
         In the great majority of severe TCE poisonings, subjects 
         have either been found dead or dying before adequate 
         resuscitation can be instituted, or they recover fairly 
         rapidly with minimal requirement for active intervention.  
         In only a minority have emergency resuscitative and 
         treatment measures been both immediately indicated and 
         available and their relative efficacy is not well 
         established.  This applies to pharmacological agents for the 
         treatment of hypotension and arrhythmia.  However adrenaline 
         and probably similar agents should be avoided in the 
         treatment of hypotension or bradycardia; electroconversion 
         may be useful in the treatment of ventricular fibrillation, 
         given the success of Wodka and Jeong (1989).  Adequate 
         oxygenation is the mainstay of treatment; in patients with 
         spontaneous respiration, oxygen can be given successfully 
         via a nasal cannula (Pointer, 1982).  The patient should be 
         disturbed or stressed as little as possible.  Follow up 
         should include monitoring of hepatic, renal and neurological 
         function. 
    11. ILLUSTRATIVE CASES
      11.1 Case reports from literature
         One of the first fatalities reported was that by Kleinfeld 
         and Feiner (1966).  Four public utility workers entered an 
         underground vault (14 x 7 x 7 feet) to remove grease from 
         conduits using rags soaked in TCE.  They experienced 
         giddiness and light headedness so retired to fresh air.  One 
         then returned with a circulating fan, but before 
         successfully connecting it he decided once again to leave 
         the vault and shortly thereafter had a respiratory arrest.  
         Blood and tissue analyses were made but levels were not 
         reported. It was estimated that his time in the vault was 
         about 10 minutes and concentrations of TCE were well above 
         5000 ppm.
         

         Hatfield and Maykoski (1970) describe the fatal case of a 
         worker found in the lower portion of a 450 gallon aircraft 
         tip tank.  The blood concentration of TCE was 6 mg% and 
         there was acute passive congestion of pulmonary and cerebral 
         tissues with minimal alveolar oedema.  With the usually 
         employed technique of reaching through the end opening or 
         access port to clean the interior, peak concentrations of 
         800 ppm occurred inside the tank, with breathing zone levels 
         of just 200 ppm.  However a reconstruction of this worker's 
         cleaning habits was made by an individual wearing an airline 
         respirator.  This involved climbing into the tank itself 
         having first poured some solvent into the tank and 
         saturating a cleaning pad.  After a few minutes the solvent 
         in air had reached a concentration of 62,000 ppm.
         
         The above blood level is similar to that of three of the 
         four levels reported from the six fatal cases reported by 
         Stahl et al (1969).  Their fourth case was the exception in 
         that blood and brain levels were just 0.15 and 0.32 mg/100 
         ml respectively.  This youth had been cleaning an air vent 
         in a room of 6 x 8 x 10 feet.  He had been observed to 
         appear quite well over an initial four hour period but was 
         found dead just before a further four hours had elapsed. 
         Because of elevated lactic acid levels in brain tissue, it 
         was considered that in this case oxygen deprivation must 
         have been a critical factor.
         
         Caplan et al. (1976) describes the death of a 40-year-old 
         woman redecorating a small unventilated bathroom.  She was 
         found in the early morning with paint and paint thinner 
         spilled on the floor and mixed with mats and towels.  Tissue 
         levels of TCE included blood 2 mg%, brain 36 mg%, liver 5 
         mg% and lung 1 mg%.  There was acute pulmonary congestion 
         and oedema.  While the recorded blood level was lower than 
         that in most other reported fatalities (with the exception 
         of one of the Stahl et al. series discussed above), it is 
         consistent with the estimate of Stewart et al. (1961) that 
         incapacitating nervous system depression may occur at blood 
         levels of 1.0 to 1.5 mg/100 ml.  A consistent theme with 
         these fatalities is unprotected exposure in relatively small 
         poorly ventilated areas.
         
         Northfield (1981) describes two fatalities in young newly-
         employed workers in the UK. In the first case, air levels 
         ranged from 65 ppm with normal working conditions to 735 ppm 
         in the absence of usual ventilatory measures, the previous 
         employee had been unaffected over a period of several years. 
          Analysis revealed 27 mg% in blood and 118 mg% in lung 
         tissue and there was good circumstantial evidence suggesting 
         solvent sniffing.  The second person worked at a degreasing 
         tank using cans to scoop up cold solvent present at a few 
         inches in depth at the bottom of the tank, and then pour it 
         over metal parts on a perforated tray across the top.  When 
         found he was slumped over the edge of the tank.  
         Environmental monitoring of the undisturbed tank revealed 
         just 200 ppm 15cm from the tank.  However, it was 6000 ppm 

         at 8 to 15 cm below the rim and over 70,000 ppm nearer the 
         base, 8 to 15 cm above the solvent surface.  Measurements 
         were repeated during normal operations, when liquid was 
         disturbed and carried to the tray at the top.  
         Concentrations were 73,000 ppm at 8 cm and 94,000 ppm at 15 
         cm respectively below the tank rim.  It was suggested the 
         worker had either been bending down to wash his hands in 
         solvent or had otherwise lost his balance, in either case he 
         was exposed to rapidly fatal concentrations near the base of 
         the tank.  This underlines the need for properly designed 
         degreasing operations not requiring the worker to bend down 
         into the tank. TCE has a heavy vapour (relative vapour 
         density 4.6) and levels may be very much higher below than 
         above the rim.
         
         Jones and Winter (1983) describe two fatal episodes with 
         associated levels of 4.2 mg% and 1.8 mg% respectively in 
         blood and 123 mg% and 8 mg% in brain tissue.  The latter 
         case involved spraying and wiping motor vehicle upholstery.  
         The worker was found slumped on the floor with his head 
         behind the driver's door, which had been pushed forward.  
         Inhalation of vomitus was a significant factor in the death. 
          An estimated volume of 100 to 200 ml of solvent had been 
         used and a simulation exercise involving deliberate spillage 
         of 100 ml onto a cloth demonstrated just 515 ppm, 15 cm 
         above the floor but rising sharply to 6410 ppm, 2.5 cm above 
         the floor.
         
         There have been several reports of abuse of typewriter 
         correction fluid containing TCE. Whilst there has been a 
         fatal outcome in some cases, recovery from severe effects 
         has occurred in others.
         
         Wodka and Jeong (1989) described a 15-year-old boy found in 
         cardiopulmonary arrest with coarse ventricular fibrillation 
         evident on electrocardiography.  Cardiac defibrillation was 
         attempted twice, with restoration of sinus rhythm and a 
         complication-free recovery.  Echocardiogram showed distal 
         septal wall motion abnormality while electrocardiograms 
         suggested anteroseptal myocardial injury but not persistent 
         ischaemia.  They postulated a mechanism of temporary 
         coronary artery spasm which has been suggested as the cause 
         of infarction and fibrillation in one case of toluene 
         inhalation (Cunningham et al., 1987).
         
         Pointer (1982) discussed the case of a 14-year-old girl 
         found slumped in a city park with partially dried TCF on her 
         hands, face and clothing.  Initially she responded only to 
         deep painful stimuli, but was just mildly drowsy on arrival 
         at hospital.  Low flow oxygen was administered per nasal 
         cannulae and the patient became completely alert within ten 
         further minutes of observation.
         
         Halevy et al. (1980) describe an episode where hepatic and 
         neural effects predominated.  No monitoring was undertaken 
         so that the severity of exposure was uncertain. However, the 

         relatively mild CNS manifestations suggested that exposure 
         had not been great. The major symptoms were dizziness, 
         headache, nausea, abdominal pain and diarrhoea occurring 
         several hours later with fever, jaundice and cough after 48 
         hours.  Investigations included elevated (mainly conjugated) 
         bilirubin, SGOT, LDH and alkaline phosphatase with increased 
         serum creatinine (1.5%), reduced creatinine clearance (70 
         ml/minute), and considerable proteinuria (2.9 gm in 24 
         hours).  Renal function parameters returned to normal with 
         ten days.  Liver function tests reversed only after 38 days 
         and biopsy showed inflammatory cell infiltrate plus 
         eosinophils and cholestasis.  This degree of hepatorenal 
         dysfunction is unusual in the absence of more severe CNS 
         injury and the authors postulated an individual 
         hypersensitivity reaction in this patient.  The time delay 
         between exposure and the initial symptoms is unusual however,
          and perhaps the most convincing evidence of causality was 
         that tests for lymphocyte migration inhibition factor were 
         positive for TCE but negative for ajmalin, a prescribed anti-
         arrythmic agent.
      11.2 Internally extracted data on cases
         No data available.
      11.3 Internal cases
         To be completed by the centre.
    12. ADDITIONAL INFORMATION
      12.1 Availability of antidotes
         Not relevant.
      12.2 Specific preventive measures
         Adequate ventilation conditions are essential, but may need 
         to be supplemented with approved respiratory protective 
         equipment. Use in confined, enclosed spaces should be 
         avoided unless supplied air respirators are available.
      12.3 Other
         Unprotected and unsupervised exposure to high concentrations,
          such as may occur in confined and/or poorly ventilated 
         areas, is the major concern.  Unawareness of this risk, 
         coupled with just   gradually increasing unsteadiness and 
         drowsiness, may result in the worker not instituting 
         suitable evasive measures until finding great difficultly in 
         doing so.
         
         Major signs of severe intoxication are reduced level of 
         consciousness, coma and depressed respiration.
         
         In circumstances of sudden high concentrations, as in 
         inhalation abuse, increased adrenergic activity may be a 
         significant factor and resulting cardiac arrhythmias due to 
         sensitisation to adrenalin can occur.
         
         Essential first aid measures are the assessment and 
         establishment of airway and ventilation. To maintain a clear 
         airway the mouth should be cleared of debris, the tongue 
         pulled forward and an oropharyngeal airway inserted.  If 
         spontaneous respirations are inadequate, perform an 
         endotracheal intubation and support ventilation using 
         appropriate mechanical device.

    13. REFERENCES
    ACGIH (1986)  Documentation of TLV's, methyl chloroform.  
    American Conference Of Governmental Hygienists, Cincinatti, pp 
    269-270.
    
    Adams EM, Spencer HC, Rowe VK, & Irish DD (1950)  Vapor toxicity 
    of 1,1,1-trichloroethane (methylchloroform) determined by 
    experiments on laboratory animals.  Arch Industr Hyg Occup Med, 
    1: 225-236.
    
    American Industrial Hygiene Association, Toxicology Committee 
    (1964)  Emergency exposure limits.  Am Indust Hyg J, 25: 578-586.
    
    Astrand I, Kilbom A, Wahlberg I & Ovrum P (1973)  
    Methylchloroform exposure.  I. Concentration in alveolar air and 
    blood at rest and during exercise.  Work Environ Health, 10: 69-
    81.
    
    Bass M (1970)  Sudden sniffing death.  JAMA, 212: 2075-2079. 
    
    Bretherick L ed. (1985)  Hazards in the chemical laboratory, 4th 
    ed.  London, The Royal Society of Chemistry.
    
    Caplan YH, Backer RC, & Whitaker JQ (1976)  1,1,1-
    trichloroethane: report of a fatal intoxication.  Clin Toxicol 9: 
    69-74.
    
    Carpenter CP, Smyth HF & Pozzani UC (1949)  The assay of acute 
    vapor toxicity, and the grading and interpretation of results on 
    96 chemical compounds.  J Ind Hyg Toxicol 31: 343-349.
    
    CEC (1986)  1,1,1-trichloroethane.  In: Organo-chlorine solvents, 
    Commission of the European Communities, Royal Society of 
    Chemistry, 55-71.
    
    Cunningham SR, Dalzell GWN, McGirr P, Khan MM (1987)  Myocardial 
    infarction and primary ventricular fibrillation after glue 
    sniffing.  Br Med J 294: 739-740.
    
    Dornette WHL & Jones JP (1960)  Clinical experiences with 1,1,1-
    trichloroethane: a preliminary report of 50 anaesthetic 
    administrations.  Anaesthesia and Analgesia, 39: 249-263
    
    Franchini I, Cavatorta A, Falzoi M, Lucertini S & Mutti A (1983) 
    Early indicators of renal damage in workers exposed to organic 
    solvents.  Int Arch Occup Environ Health, 52: 1-9.
    
    Gamberale F & Hultengren M (1973)  Methylchloroform exposure II. 
    Psychophysiological functions.  Work Environ Health, 10: 82-92.
    
    Gehring PJ (1968)  Hepatotoxic potency of various chlorinated 
    hydrocarbon vapors relative to their narcotic and lethal 
    potencies in mice.  Toxicol Appl Pharmacol, 13: 287-298.
    
    Gerace RV (1981)  Near-fatal intoxication by 1,1,1-
    trichloroethane.  Ann Emerg Med, 10: 533-534.

    
    Gosselin RE, Smith RP & Hodge HC eds. (1984)  1,1,1-
    trichloroethane.  In: Clinical Toxicology of Commercial Products, 
    5th ed. Baltimore, Williams & Wilkins, pp II-166.
    
    Halevy J, Pitlik S, Rosenfeld J & Eitan BD (1980)  1,1,1,-
    trichloroethane intoxication: a case report with transient liver 
    and renal damage.  Review of the literature.  Clin Toxicol, 16: 
    467-472.
    
    Hall FB &  Hine CH (1966)  Trichloroethane intoxication: a report 
    of two cases.  J Foren Sci, 11: 404-413.
    
    Hatfield TR & Maykoski RT (1970)  A fatal methyl chloroform 
    (trichloroethane) poisoning.  Arch Environ Health, 20: 279-281.
    
    Herd PA, Lipsky M & Martin HF (1974)  Cardiovascular effects of 1,
    1,1-trichloroethane.  Arch Environ Health, 28: 227-233.
    
    Humbert BE & Fernandez JG (1977)  Exposition au 1,1,1-
    trichloroethane contribution a l'etude de l'absorption de 
    l'ecretion du metabolisme sur des subjets humains.  Arch Mal prof,
     38: 415-425.
    
    Ikeda M, Hatsue O, Imamura T & Komike Y (1972)  Urinary excretion 
    of total trichloroethanol, and trichloroacetic acid as a measure 
    of exposure to trichloroethylene and tetrachloroethylene.  Br J 
    Ind Med, 29: 328-333.
    
    Jones RD & Winter DP (1983)  Two case reports of deaths on 
    industrial premises attributed to 1,1,1-trichloroethane.  Arch 
    Environ Health, 38: 59-61.
    
    King GS, Smialek JE, Troutman WG (1985)  Sudden death in 
    adolescents resulting from the inhalation of typewriter 
    correction fluid.  JAMA, 253: 1604.
    
    Klaasen CD & Plaa GL (1966)  Relative effects of various 
    chlorinated hydrocarbons on liver and kidney function in mice.  
    Toxicol Appl Pharmacol, 9: 139-151.
    
    Klaasen CD & Plaa GL (1967)  Relative effects of various 
    chlorinated hydrocarbons on liver and kidney function in dogs.   
    Toxicol Appl Pharmacol, 10: 119-131.
    
    Kleinfeld M & Feiner B (1966)  Health hazards associated with 
    work in confined spaces.  J Occup Med, 8: 358-364.
    
    Kramer CG, Gerald Ott M, Fulkerson JE, Hicks N & Imbus HR (1978)  
    health of workers exposed to 1,1,1,-trichloroethane: a matched-
    pair study.  Arch Environ Health, 33: 331-342.
    
    Lagrue G, Kalamodine T, Hirbec G, Bernaudin JF, Guerrero J & 
    Zhepova F (1977) Role de l'inhalation de substances toxiques dans 
    la genese des glomerulonephrites.  Nouv Presse Med, 6: 3609-3613.
    

    Lane RW, Riddle BL, Borzelleca JF (1982)  Effects of 1,2-
    dichloroethane and 1,1,1-trichloroethane in drinking water on 
    reproduction and development in mice.  Toxicol Appl Pharmacol, 
    63: 409-421.
    
    Lauwerys RR (1986)  Occupational toxicology.  In: Klaassen CD, 
    Amdur MO & Doull J eds.  Casarett & Doull's Toxicology.  New York,
     Macmillan 
    Litt IF & Cohen MI (1969)  "Danger--vapour harmful": spot-remover 
    sniffing.  N. Eng. J. Med., 281: 543-544.
    
    Meredith TJ, Ruprah M, Liddle A & Flanagan RJ (1989)  Diagnosis 
    and treatment of acute poisoning with volatile substances.  Hum 
    Toxicol, 8: 277-286 
    Monster AC (1978)  Kinetics of chlorinated hydrocarbon solvents.  
    Organisation for Health Research.  TNO.
    
    National Cancer Institute (1977).  Bioassay of 1,1,1-
    trichloroethane for possible carcinogenicity.  NCI-CG-TR-3.
    
    NIOSH (1975)  Occupational exposure to 1,1,1-trichloroethane - 
    criteria for a recommended standard.  U.S. Department of Health 
    Education and Welfare.
    
    Northfield RR (1981)  Avoidable deaths due to acute exposure to 1,
    1,1-trichloroethane.  J Soc Occup Med, 31: 164-166.
    
    Plaa GL & Larson RE (1965)  Relative nephrotoxic properties of 
    chlorinated methane, ethane, and ethylene derivatives in mice.  
    Toxicol Appl Pharmacol, 7: 37-44.
    
    Plaa GL, Evans EA & Hine CH (1958)  Relative hepatotoxicity of 
    seven halogenated hydrocarbons.  J Pharmacol Exp Ther, 123: 224-
    229.
    
    Pointer J (1982)  Typewriter correction fluid inhalation: a new 
    substance of abuse.  J Toxicol - Clin Toxicol, 19: 493-499.
    
    Prendergast JA, Jones RA, Jenkins LJ & Siegel J (1967)  Effects 
    on experimental animals of long-term inhalation of 
    trichloroethylene, carbon tetrachloride, 1,1,1-trichloroethane, 
    dichlorodifluoromethane, and 1,1-dichloroethylene.  Toxicol Appl 
    Pharmacol 10: 270-289
    
    Quast JF, Leong BKJ, Rampy LW & Gehring PJ (1975)  Toxicologic 
    and carcinogenic evaluation of a methylchloroform (1,1,1-
    trichloroethane) formulation by chronic inhalation in rats - 
    interim report after 24 months.   Midland, Michigan, The Dow 
    Chemical Company.
    
    Rennick BR, Balton SD, Moe GS & Seevers MH (1949)  Induction of 
    idioventricular rhythms by 1,1,1-trichloroethane and epinephrine. 
     J Pharmacol Exp Therap, 8: 327.
    
    Riihimaki V & Pfaffli P (1978)  Percutaneous absorption of 
    solvent vapors in man.  Scand J Work Environ Health, 4: 73-85.

    
    Salvini M, Binaschi S & Riva M (1971)  Evaluation of the 
    psychophysiological functions in humans exposed to the 'threshold 
    limit value' of 1,1,1-trichloroethane.  Br J Ind Med, 28: 286-
    292.
    
    Schwetz BA, Leong BKJ & Gehring PJ (1975)  The effect of 
    maternally inhaled trichloroethylene, perchloroethylene, methyl 
    chloroform, and methylene chloride on embryonal and fetal 
    development in mice and rats.  Toxicol Appl Pharmacol, 32: 84-96.
    
    Simmon VF, Kauhanen K & Tardiff RG  (1977)  Progress in genetic 
    toxicology.  Scott D, Bridges BA, & Sobel FH eds.  Elsevier, 
    North Holland Biomedical Press, pp 249 - 58.
    
    Stahl CJ, Fatteh AV & Dominguez AM (1969)  Trichloroethane 
    poisoning: observations on the pathology and toxicology in six 
    fatal cases.  J Forensic Sci, 14: 393-397.
    
    Stewart RD (1968)  The toxicology of 1,1,1-trichloroethane.  
    Annals Occup Hyg, 11: 71-79.
    
    Stewart RD (1971)  Methyl chloroform intoxication.  Diagnosis and 
    treatment.  JAMA, 215: 1789-1792.
    
    Stewart RD & Andrews JT (1966)  Acute intoxication with 
    methylchloroform.  JAMA, 195: 120-122.
    
    Stewart RD & Dodd HC (1964)  Absorption of carbon tetrachloride, 
    trichloroethylene, tetrachloroethylene, methylene chloride, and 1,
    1,1-trichloroethane through the human skin.  Ind Hyg J, 25: 439-
    446.
    
    Stewart RD, Gay HH, Erley DS, Hake CL & Schaffer AW (1961)  Human 
    exposure to 1,1,1-trichloroethane vapor: relationship of expired 
    air and blood concentrations to exposure and toxicity.  Ind Hyg J,
     22: 252-262.
    
    Stewart RD, Gay HH, Schaffer AW, Erley DS & Rowe VK (1969)  
    Experimental human exposure to methyl chloroform vapour.  Arch 
    Environ Health, 19: 467-472.
    
    Torkelson TR and Rowe VK (1981)  Halogenated aliphatic 
    hydrocarbons.  In: Clayton GD & FE eds  Patty's Industrial 
    Hygiene and Toxicology, Vol IIB.  New York, John Wiley & Sons, pp 
    3433-3601
    
    Torkelson TR, Oyen F, McCollister DD & Rowe VK (1958)  Toxicity 
    of 1,1,1-trichloroethane as determined on laboratory animals and 
    human subjects.  Ind Hyg J, 19: 353-362.
    
    Van Der Laan (1980)  Chronic glomerulonephritis and organic 
    solvents: a case control study.  Int Arch Occup Environ Health, 
    47: 1-8.
    
    Weiss G (1980) (Ed.)  Hazardous Chemicals Data Book.  Noyes Data 

    Corporation, Park Ridge, New Jersey, USA, p. 875.
    
    Windholz M ed. (1983)  The Merck Index: an encyclopedia of 
    chemicals, drugs, and biologicals, 10th ed. Rahway, New Jersey, 
    Merck and Co., Inc.
    
    Wodka RM & Jeong WS (1989)  Cardiac effects of inhaled typewriter 
    correction fluid.  Annals Int Med, 110: 91-92.
    
    Woo OF, Healy KM, Sheppard D, & Tong TG (1983)  Chest pain and 
    hypoxemia from inhalation of a TCE aerosol product.  J Toxicol 
    Clin Toxicol, 20: 333-341.
    
    York RG, Sowry BM, Hastings L & Manson JM (1982)  Evaluation of 
    teratogenicity and neurotoxicity with material inhalation 
    exposure to methyl chloroform.  J Toxicol Environ Health, 9: 251-
    266.
    
    Zimmerman SW, Groehler K & Beirne GJ (1975)  Hydrocarbon exposure 
    and chronic glomerulonephritis.  Lancet, 2: 199-201.
    14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
    ADDRESSES
    Author:   Dr D M G Beasley
              National Poisons and Hazardous Chemicals Information 
    Centre
              Otago University Medical School
              P.O. Box 913
              Dunedin
              New Zealand
    
    Date:     February 1991
    
    Reviewer: Professor ANP van Heijst
              Baarnseweg 42a
              3735 MJ Bosch en Duin
              Netherlands
    
    Date:     March 1991
    
    Peer review:   Adelaide, Australia, April 1991

    See Also:
       Toxicological Abbreviations
       Trichloroethane, 1,1,1- (EHC 136, 1992)
       Trichloroethane, 1,1,1- (WHO Food Additives Series 16)
       Trichloroethane, 1,1,1- (IARC Summary & Evaluation, Volume 71, 1999)