September, 1989


                       Drinking Water Health Advisory
                               Office of Water
                    U.S. Environmental Protection Agency
     The Health Advisory Program, sponsored by the Office of Drinking Water
 (ODW), provides information on the health effects, analytical methodology
 and treatment technology that would be useful in dealing with the contami-
 nation of drinking water.  Health Advisories describe nonregulatory concen-
 trations of drinking water contaminants at which adverse health effects
 would not be anticipated to occur over specific exposure durations.  Health
 Advisories contain a margin of safety to protect sensitive members of the

     Health Advisories serve as informal technical guidance to assist
 Federal, State and local officials responsible for protecting public health
 when emergency spills or contamination situations occur.  They are not to
 be construed as legally enforceable Federal standards.  The HAs are subject
 to change as new information becomes available.

     Health Advisories are developed for one-day, ten-day, longer-term
 (approximately 7 years, or 10% of an individual's lifetime) and lifetime
 exposures based on data describing noncarcinogenic end points of toxicity.
 For those substances that are known or probable human carcinogens,
 according to the Agency classification scheie (Group A or B), Lifetime
 Health Advisories are not recommended.  The chemical concentration values
 for Group A or B carcinogens are correlated with carcinogenic risk
 estimates by employing a cancer potency (unit risk) value together with
 assumptions for lifelong exposure and the ingestion of water.  The cancer
 risk is usually derived from the linear multistage model with 95% upper
 confidence limits.  This provides a low-dose estimate of cancer risk to
 humans that is-considered unlikely to pose a carcinogenic risk in excess of
 the stated values.  Excess cancer risk estimates may also be calculated
 using the one-hit, Weibull, logit or probit models.  There is no current
understanding of the biological mechanisms involved in cancer to suggest
 that any one of these models is able to predict risk more accurately than
another.  Because each model is based on differing assumptions, the
estimates that are derived can .differ by several orders of magnitude.

1,2,3 Trichloropropane                                      September, 1989

                                    -2-    . . --     -         -   	~" ...  " .


CAS No.  96-18-4

Structural Formula

                             Cl    Cl    Cl
                            1     1     1
     0  Allyl trichloride,  glycerol  trichlorohydrin, glyceryl trichloro-
        hydrin,  trichlorohydrin  (NIOSH, 1986).
     0  1,2,3-TCP is  used  as  a  paint  and varnish remover, solvent,
        degreasing agent,  and crosslinking agent in the elastomer Thiokiol
        ST (U.S.  EPA,  1983).

Properties (Weast, 1972; Verschueren, 1977; Koneman, 1981; U.S. EPA, 1983)
        Chemical Formula
        Molecular Weight               147.43
        Physical State  (at  25C)       Colorless clear liquid
        Boiling Point (25 mm  Hg)       156.85C
        Melting Point                 -14.7C
        Density (20C)                 1.387
        Vapor Pressure  (20C)          2 mm Hg
        Specific Gravity   (20C)       1.3889
        Water Solubility  (20C)        1,900 mg/L
        Log Octanol Water Partition    2.63
        Odor Threshold  (water)
        Odor Threshold  (air)
        Taste Threshold
        Conversion Factor              1 ppm = 6 mg/m3

 1,2,3-Trichloropropane                                      September, 1989

                                     -3- ~"    I    "	


     0  Drinking water from Carrollton Water Plant in New Orleans, LA,
        contained <0.2 ug/L of 1,2,3-TCP (Keith et al., 1976).  It was
        also detected in Ames, IA, drinking water; however, levels were not
        given, (U.S. EPA, 1976).  Kool et al. (1982) reported that
        1,2,3-TCP had been detected in drinking water in unspecified

     0  Surface water from the Delaware River basin contained trichloro-
        propane (unspecified isomer) at concentrations >1 ug/L in 3% of
        samples (Dewalle and Chian, 1978).   Vakeham et al> (1983) found
        trichloropropane in seawater of Narragansett Bay, RI, but concen-
        trations were not reported.

Environmental Fate

     0  Dilling (1977) reported that the half-life for evaporation of
        1,2,3-TCP from water was about 1 hour under the following
        conditions:   0.92 ppm aqueous solution;  6.5 cm deep;  200 rpm
        stirring;  25C; <0.2 mph air current.

     0  Hatsui et al. (1975) determined that trichloropropane (unspecified
        isomer) was  relatively easy to decompose by microbes  in activated


     0  Data regarding the absorption of 1,2,3-TCP could not be located in
        the available literature.


     0  Volp et al.  (1984) administered 3.6 mg/kg bw C14 1,2,3-TCP (label
        at 1,3 "carbon)  intravenously to male Fischer 344 rats.   Tissues and
        excreta were analyzed for total radioactivity and unchanged
        1,2,3-TCP at various time periods following the administration of
        1,2,3-TCP.  The distribution and excretion of 1,2,3-TCP were
        rapid.  37%  of  the dose was accounted for in adipose tissue within
        15 min.  This consisted of primarily unchanged 1,2,3-TCP.   The
        largest fraction of the dose was detected in the liver  in  the form
        of metabolites  after a 4 hour exposure of 1,2,3-TCP. The  kidneys
        also accumulated radiolabeled 1,2,3-TCP with a peak of  2.8% of the
        total dose at 2 hours, decreasing thereafter to <1% at  the end of
        the 24 hour  period.  The small intestine bad a concentration of
        9.3% of the  dose at 1 hour.  Brain,  lungs, spleen,  testes  and
        epidymides contained <0.5% of the total dose at all times.  The
        primary sites of distribution associated with radiolabeled
        1,2,3-TCP were  initially the adipose tissue, skin and muscle,  then
        subsequently the liver.

1,2,3-Trichloropropane                                      September, 1989

                                     -4-        ~


     0  In the Volp et al. (1984) study described above, 1,2,3-TCP was
        rapidly distributed to all tissues, specifically adipose tissue,
        skin and muscle.  After 4 hours, the concentration of unchanged
        1,2,3-TCP was 90% of the total radiolabeled compound in adipose
        tissue (3.8% of the dose).  This concentration was observed to
        decrease to 37% at the 24 hour period following the administration
        of compound.  The investigators reported that (1) the major
        metabolite of 1,2,3-TCP was carbon dioxide (25% of dose), and (2)
        other minor metabolites were also present but not identified.

     0  In the Volp et al. (1984) study described above 99% of the dose was
        excreted within 6 days.  Most of the excretion (90%) occurred in
        the first 24 hours, with urine being the principal route.  Of the
        total dose of radioactivity, 40% was excreted in urine, 30% in
        expired air, and 18% in the feces in the first 24 hours.  The urine
        contained no detectable 1,2,3-TCP, indicating that *all*of the
        radiolabel was 1,2,3-TCP metabolites.  Of the 30% of the initial
        dose of radioactivity eliminated in expired air, 5% was unchanged
        TCP and 25% was COz.  Almost all of the unchanged TCP (85%) was
        expired within 30 minutes.  In the bile, 30% of the total dose
        appeared within 6 hours, 5% of which was unchanged 1,2,3-TCP.  The
        elimination half-time for unchanged 1,2,3-TCF was 30 to 45 hours
        for all major tissues.  The half-time for elimination of radiolabel
        by all routes was 44 hours.


   Short-term Exposure

     0  Silverman et al. (1946) exposed an average of 12 volunteers (males
        and females) to 1,2,3-TCP and other industrial solvent vapors for
        15 minutes, and found that 100 ppm 1,2,3-TCP (600 mg/m3) caused
        eye and throat irritation and had aja unpleasant odor.  A "border-
        line majority" of the subjects said that 50 ppm (300 mg/m3) would
        be acceptable for an 8-hour workday.  However, this level is based
        on organoleptic quality and not toxicity.

   Long-term Exposure

     0  Pertinent data regarding long-term exposure of humans to 1,2,3-TCP
        could not be located in the available literature.


   ijliOi t ~>g ;g E
        Saito-Suzuki et al. (1982) reported that 500 mg/kg bw 1,2,3-TCP by
        gastric intubation to male Sprague-Dawley rats was lethal.  Smythe

1,2,3-Trichloropropane                                      September,  1989

        et al.  (1962)  reported an oral  LDso  of 0.32 mL/kg bw (444 mg/kg)
        1,2,3-TCP  for  Carworth-Vistar male rats.   An oral LDso  of
        320 mg/kg  for  1,2,3-TCP also has been reported in the  literature
        (RTECS,  1978).

     0   Wright  and Schaffer  (1932)  administered one dose  (route not
        specified)  of  0.2  to 0.5 cc/kg  (278-694 mg/kg}  1,2,3-TCP to  three
        dogs.   All dogs  died within 1-2 days after dosing.   The major  signs
        of toxicity were narcosis and liver  and kidney tissue  necrosis.

     0   Shcherban  and  Piten'ko (1976) reported the following LDao values
        for 1,2,3-TCP  (route not specified):  rats, 505 mg/kg;  mice,
        369 mg/kg;  rabbits,  380 mg/kg;  and guinea pigs, 340  mg/kg.   They
        also reported  that 0.0035 mg/kg was  a completely  nontoxic dose.  No
        other details  were given.

     0   Several  short-term inhalation studies using 1,2,3-TCP  were   .
        available.   Smythe et al. (1962)  reported that  5/6 rats died when
        exposed  to 6,000 mg/m3  (1,000 ppm)  for 4  hours.   McOmie and
        Barnes  (1949)  reported that exposure to a vapor concentration  of
        30,000 mg/m3  (5,000  ppm)  for 20 minutes killed  several  mice
        (8/15 within 2 days).  Four of  the remaining seven mice died from
        liver damage 7 to 10 days later.   When exposed  to 15,000 mg/m3
        (2,500 ppm), 10  minutes/day for 10 days,  7/10 mice died.  Lewis
        (1979) exposed rats  and guinea  pigs  (five/sex)  to 4,800 mg/m3
        (799 ppm),  12,480 mg/m3  (2,080  ppm)  or 30,060 mg/m3  (5,010 ppm)
        for 30 minutes,  resulting in dose-related central nervous system
        (CNS) depression.  Six guinea pigs and two rats at the  high  dose
        30,060 mg/m3  (5,010  ppm)  died.

     0   Sidorenko  et al. (1979)  exposed white male rats (strain not
        specified)  to  1,2,3-TCP 2 to 800  mg/m3  (0.33 to 133  ppm)  for
        periods  ranging  from 2 hours to 86 days.   An increase  in the
        activity of  blood catalase,  acetylcholinesterase, and  the
        excitability of  nerve centers was reported.   These changes were
        observed in  rats after 4 hours  of exposure to 800 mg/m3  (133 ppm)
        and after  40 days of  exposure to  2 mg/m3  (0.33  ppm).

  Dermal/Ocular Effects

     0   Smythe et  al.  (1962)  reported a single skin penetration LDso of
        1.77 mL/kg  (2,458 mg/kg)  1,2,3-TCP for rabbits.   On  a  scale  of 1 to
        10 (1 =  least severe,  10  =  most severe),  1,2,3-TCP rated 1 for skin
        irritation and 4 for  corneal  injury.

     0   McOmie and Barnes (1949)  determined  1,2,3-TCP to  be  an  "intense
        skin irritant" for rabbits,  partially due  to its  lipid  solvent
        properties.  Repeated applications led  to  sloughing  and cracking
        preceded by irritation  and  erythrema.   In  a  15-day period,
        10  applications of 2  mL/100  cm2 led  to  pain,  subdermal  hemorrhage
        and death in 1/7 treated  rabbits.  The  other six  rabbits  survived
1,2,3-Trichloropropane                                      September,  1989


   Lonq-term Exposure

     0  1,2,3-TCP was administered by gavage in corn oil,  5 days/week for
        120 days, to Fischer 344 rats (20/sex/group)  at dose levels of
        8,  16,  32, 63, 125 and 250 mg/kg bw/day (NTP,  1983a).   One control
        group of 30 rats/sex received corn oil.  All animals in the
        250 ing/kg dose group died as a result of treatment, with the main
        findings being renal and hepatic toxicity and necrosis and
        inflammation of the nasal mucosa.  Mortality was also observed in
        the 125 mg/kg dose group.'  Dose-related clinical effects (e.g.,
        thin and hunched appearance, depression, abnormal eyes and urine
        stains) were observed in female rats at doses of *125 mg/kg.*
        Hematological effects (decreased hematocrit,  hemoglobin and
        erthrocyte counts) were seen in both sexes at doses of 16 mg/kg.
        There was a dose-related increase in liver and kidney weights.  At
        125 ng/kg there was also an increase in the weight of testes and a
        decrease in epididymis weight, but no histomorphologic change was
        observed.  Principal target organs were the liver and kidney, with
        histomorphological and clinical chemistry changes observed in dose
        groups 63 mg/kg.  The nasal turbinates were also a target, but it
        was suggested that this may have been due to a local  effect as
        opposed to a systemic effect.  The NOAEL for this study is 8 mg/kg
        and the LOAEL is 16 mg/kg based on hematologic effects.

     0  1,2,3-TCP was administered by gavage in corn oil,  5 days/week for
        120 days, to B6C3Ft mice (20/sex/v.;roup) at dose levels of 8, 16,
        32, 63, 125 and 250 mg/kg bw/day (NTP,  1983b).  One control group
        of  30 mice/sex received corn oil.  Treatment-related deaths due
        primarily to hepatic toxicity occurred particularly in males at the
        250 mg/kg level.  The principal target organs were the liver, lung,
        kidney and stomach, with effects also seen in the spleen and nasal
        passages.  Body weight gain was not affected except for a decrease
        in  two male survivors in the 250 mg/kg group.   Evaluation of the
        hematological and clinical chemistry data revealed no changes of
        biological importance since findings were sporadic in distribution
        and noted by the authors as "incidental to compound
        administration."  Increased weights/or ratios were noted in the
        liver and thymus at doses k!25 mg/kg.  The lowest dose with a
        statistically significant effect was 16 mg/kg, which resulted in a
        lower brain weight ratio in female mice.  This is the basis for
        defining 16 mg/kg as the LOAEL for this study.  The NOAEL is
        8 mg/kg.

   Reproductive Effects

     c  Johannsen et al. (1988)  reported the results of reproduction
        studies in the rat following repeated inhalation exposure.  Groups
        of  10 male and 20 female rats were exposed 6 h/d,  5 d/wk to 5 ppm
        (30 mg/m3) or 15 ppm (90 mg/m3)  1,2,3-trichloropropane vapor
        during premating and mating.  Female rats were also exposed during
        gestation.  Investigators stated that (1) the body weights of both
        .-r--- ~.f t-v.-, c ~prr, (30 ffrr/r3> level WPTP cn^para^le to roptroi
        values, (2) at the 15 ppm (90 mg/m3) level, both sexes exhibited

1,2,3-Trichlc  cpropane                                      September,  1989

        lower mean body weights and significantly (p 4 0.01)  lower mean
        weight gains during the prereating period,  (3)  mating  performance
        was low in all groups of female rats including the controls,  and
        (4)  all measured progeny indices appeared unaffected  by inhalation
        exposure of 1,2,3-trichloropropane.

   Developmental Effects

     0  No treatment-related effects on incidence of grossly  visible
        internal or external malformations occurred  in the offspring  of
        female Sprague-Dawley rats injected  intraperitoneally with
        37 mg/kg bw 1,2,3-TCP in corn oil on days 1  through 15 of  gestation
        (Hardin et al.,  1981).

     0  Hardin et al.  (1981)  administered by intraperitoneal  (i.p.)
        injection 37 mg/kg  bw 1,2,3-TCP in corn  oil  to groups of 10 to
        15 pregnant Sprague-Dawley rats on days  1  through  15  of gestation.
        Exposure caused  maternal toxicity as indicated by  reduced  body
        weight gain or altered  organ weights in  two  or more organs, but did
        not  cause fetotoxicity  (reduced fetal size or  reduced survival


     0  Stolzenberg and  Hime (1980)  reported that  1,2,3-TCP was mutagenic
        to Salmonella  typhJT.r.rium only with  a microsonal activating system
        (S-9).  At the two  concentrations evaluated  on the tester  strain
        TA100,  a dose-dependent increase in  revertant  colony  numbers  was
        observed in the  presence of  S-9 mix  but  not  in its absence.

     0  Results were negative in a dominant  lethal assay in which  80  mg/kg
        bw/day 1,2,3-TCP dissolved in olive  oil  was  administered by gastric
        intubation to  Sprague-Dawley rats for 5  consecutive days (Saito-
        Suzuki et al., 1982).

     0  In a dominant  lethal  assay in which  15 male  Sprague-Dawley rats
        received gavage  doses of 80  mg/kg bw/day for 5 consecutive days
        prior  to mating,  no effects  were seen on reproductive performance
        (frequency of  fertile matings)  (Saito-Suzuki et al.,  1982).   No
        testicular lesions  were observed.

    0  Pertinent data regarding  the carcinogenicity of 1,2,3-TCP could not
       be located at the time of this publication.  The National
       Toxicology Program is currently conducting a 2-year gavage study in
       rats and mice (NTP, 1988).  A judgment of carcinogenicity will be
       deferred until this study is completed.

1,2,3-Trichloropropane                                      September, 1989



     Health Advisories (HAs) are generally determined for one-day, ten-day,
longer-term (up to 7 years) and lifetime exposures if adequate data are
available that identify a sensitive noncarcinogenic end point of toxicity.
The HAs for noncarcinogenic toxicants are derived using the following

               (NOAEL or LOAEL) x (BW)
                                       = 	 mg/L {	 pg/L)
                  (UF) (_	L/day)


        NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Effect Level  (in
                         nig/kg bw/day).

                    BW = assumed body weight of a child (10 kg) or an adult
                         (70 kg).

                    UF = uncertainty factor, (10, 100, 1,000 or 10,000),
                         in accordance with EPA or NAS/ODV guidelines.

            	 L/day = assumed daily water consumption of a child
                         (1 L/day) or an adult (2 L/day).

One-day Health Advisory

     Sufficient data are not available for the derivation of a One-day HA
for 1,2,3-TCP.  Available oral data in rats (Saito-Suzuki et al., 1982;
Smythe et al., 1962) and dogs  (Wright and Schaffer, 1932) define lethal
dosages, but sublethal effects were not investigated.  In absence of
toxicity data, the Longer-term HA value for a child (600 ug/L) is
recommended at this time.

Ten-day Health Advisory

     Sufficient data are not available for the derivation of a Ten-day HA
for 1,2,3-TCP.  Several Russian inhalation studies (Sidorenko et al., 1979;
Belyaeva et al., 1977; Tarasova, 1975) reported that adverse effects
occurred in rats exposed to concentrations as low as 2 mg/m3, but
exposure schedules were not provided and these studies were not available
for review.  In absence of toxicity data, the Longer-term HA value for a
child (600 ug/L) is recommended at this time.
Longer-term Health Advisory

     The NTP studies (1983a,b) have been chosen to serve as the basis  for
the longer-term HA.  Fischer 344 rats and B6C3Fi mice were administered
1,2,3-TCP by gavage 5 days/week for 120 days.  For both rats and mice, the
irtwfxr*- rfr:cp IO.T-PI of f rog/kri was a NOAET., while IP rorr/Vg was a LOAEL based
on hematological effects in the rats and brain weight changes in the mice.

 1,2,3-Trichloropropane                                       September, 1989

     The  Longer-term  HA  for  a  10-kg  child  is  calculated  as  follows:

    Longer-term HA  =  (8  *q'                *0  *g> = '57  mg/L  (60
           8 mg/kg/day = NOAEL, based on absence of significant effects on
                         body and organ weight, hematology, clinical
                         chemistry and histopathology  (NTP, 1983a,b).

                   5/7 = factor to account for exposure of 5 out of 7 days.

                 10 kg = assumed body weight of a child.

                   100 = uncertainty factor, chosen in accordance with EPA
                         or NAS/ODV guidelines for use with a NOAEL from a
                         study in animals.

               1 L/day = assumed daily water consumption of a child.

     The Longer-term HA for a 70-kg adult is calculated as follows:

    Longer-term HA . <8 Bg/     ^70 >g> m 2 "  (2'000

           8 mg/kg/day = NOAEL, based on absence of significant effects on
                         body and organ weight, hematology, clinical
                         chemistry and histopathology  (NTP, 1983a,b) .

                   5/7 = factor to account for exposure of 5 out of 7 days.

                 70 kg = assumed body weight of an adult.

                   100 = uncertainty factor, chosen in accordance with EPA
                         or NAS/ODW guidelines for use with a NOAEL from a
                         study in animals.

               2 L/day = assumed daily water consumption of an adult.

Lifetime Health Advisory

     The Lifetime HA represents that portion of an individual's total
exposure that is attributed to drinking water and is considered protective
of noncarcinogenic adverse health effects over a lifetime exposure.  The
Lifetime HA is derived in a three-step process.  Step 1 determines the
Reference Dose (Rf D) , formerly called the Acceptable Daily Intake (ADI) .
The RfD is an estimate (with uncertainty spanning perhaps an order of
magnitude) of a daily exposure to the human population (including sensitive
subgroups) that is likely to be without appreciable risk of deleterious
     h effects during * lifetime,  and is derived from the NOAEL (or LOAEL) ,

1,2, 3-Trichloropropane                                      September, 1989

identified from a chronic  (or subchronic) study, divided by an uncertainty
factor (s).  From the RfD,  a Drinking Water Equivalent Level (DWEL) can be
determined (Step 2).  A DVEL is a medium-specific  (i.e., drinking water)
lifetime exposure level, assuming 100% exposure from that medium, at which
adverse, noncarcinogenic health effects would not be expected to occur.
The DVEL is derived from the multiplication of the RfD by the assumed body
weight of an adult and divided by the assumed daily water consumption of an
adult.  The Lifetime HA in drinking water alone is determined in Step 3 by
factoring in other sources of exposure, the relative source contribution
(RSC).  The RSC from drinking water is based on actual exposure data or, if
data are not available, a value of 20% is assumed.

     If the contaminant is classified as a known, probable or possible
human carcinogen, according to the Agency's classification scheme of
carcinogenic potential (U.S. EPA,1986b), then caution must be exercised in
making a decision on how to deal with possible lifetime exposure to this
substance.  For human (A) or probable human (B) carcinogens, a Lifetime HA
is not recommended.  For possible human carcinogens (C) , an additional
10-fold safety factor is used in the calculation of the Lifetime HA.  The
risk manager must balance this assessment of carcinogenic potential and the
quality of the data against the likelihood of occurrence and significance
of health effects related to noncarcinogenic end points of toxicity.  To
assist the risk manager in this process, drinking water concentrations
associated with estimated excess lifetime cancer risks over the range of
1 in 10,000 to 1 in 1,000,000 for the 70-kg adult drinking 2 L of water /day
are provided in the Evaluation of Carcinogenic Potential section.

     There are no studies of suitable duration for the derivation of a
DWEL.  Therefore, the subchronic studies by NTP (1983a,b)  will be used.

Step 1:  Determination of the Reference Dose (RfD)
                 RfD = (8                  s -006

         8 mg/kg/day = NOAEL, based on absence of significant effects on
                       body and organ weight, hematology, clinical
                       chemistry and histopathology (NTP, 1983a,b).

                 5/7 = factor to account for exposure of 5 out of 7 days.

               1,000 = uncertainty factor, chosen in accordance with EPA or
                       NAS/ODW guidelines for use with a NOAEL from a study
                       in animals of less than lifetime duration.

Step 2:  Determination of the Drinking Water Equivalent Level (DWEL)

          DWEL = (0.006           <70 W = 0.2 mg/L (200 pg/L)

 1,2,3-Trichloropropane                                      September, 1989



        0.006 mg/kg/day = RfD.

                  70 kg = assumed body weight of an adult.

                2 L/day = assumed daily water consumption of an adult.

 Step 3:  Determination of the Lifetime Health Advisory

            Lifetime HA = (0.2 mg/L)  (20%) = 0.04 mg/L  (40 pg/L)


               0.2 mg/L = DVEL.

                  (20%) = assumed relative source contribution from water.

 Note:   The NTP (1988) is conducting carcinogenicity studies for 1,2,3-TCP
        in animals.  The Lifetime HA for 1,2,3-TCP will be reevaluated
        following a review of the results on the NTP bioassay in animals
        when made available by the NTP.

 Evaluation of Carcinogenic Potential

     0  The rarcinogeni'- potential of 1,2,3-TCP has not beei reported, but
        this chemical is being tested for carcinogenicity by the NTP
        (1988).  IARC has not evaluated the carcinogenic potential of
        1,2,3-TCP.  The evaluation for carcinogenic potential is being
        deferred until the completion of ths NTP studies.


     0  ACGIH (1980, 1985) recommended a Threshold Limit Value (TLV) of
        50 ppm (300 mg/m3) to prevent hepatotoxicity caused by 1,2,3-TCP,
        which is typical of many chlorinated hydrocarbons.  ACGIH (1980,
        1985) recommended a Short-term Exposure Level (STEL) of 75 ppm
        (450 mg/m3)  to prevent eye and mucosal irritation.  ACGIH (1985)
        proposed changing the TLV to 10 ppm (60 mg/m3), but no reason was

     0  The OSHA Permissible Exposure Limit (PEL) for 1,2,3-TCP is 50 ppm
        (300 mg/m3)  (CFR, 1985).


     0  Analysis of  1,2,3-TCP is by a purge-and-trap gas chromatographic
        procedure used for the determination of volatile organohalides in
        drinking water (U.S. EPA, 1985a).  This method calls for the
        bubbling of  an inert gas through the sample and trapping volatile
        compounds on an adsorbent material.  The adsorbent material is

1,2,3-Trichloropropane                                      September, 1989

        heated to drive off the compounds onto a gas chromatographic
        column.  The gas chromatograph is temperature programmed to
        separate the method analytes, which are then detected by a halogen
        specific detector.  Confirmatory analysis is by mass spectrometry
        (U.S. EPA, 1985b).  The detection limit has not been determined for
        either method.

     0  Leighton and Calo (1981) reported experimental measurements of the
        distribution coefficients for 21 chlorinated hydrocarbons,
        including 1,2,3-trichloropropane, in a dilute air-water system.
        (The distribution coefficient is the ratio of the volume of the
        compound in air to the volume of the compound in water after
        purging).  They determined the distribution coefficients for
        1,2,3-trichloropropane to be approximately 20 at 25C.

     0  U.S. EPA (1986a> estimated the feasibility of removing
        1,2,3-trichloropropane from water by packed column aeration,
        employing the engineering design procedure and cost model presented
        at the 1983 National ASCE Conference on Environmental Engineering.
        Based on chemical and physical properties and assumed operating
        conditions, a 90 percent removal effficiency of 1,2,3-trichloro-
        propane was reported for a column with a diameter of 6.7 feet and
        packed with 16 feet of 1-inch plastic saddles.  The air-to-water
        ratio required to achieve this degree of removal effectiveness is

     0  No data were presented for the removal of 1,2,3-trichloropropane
        from drinking water by activated carbon adsorption.  However,
        evaluation of physical/chemical properties indicates that it may be
        amenable to removal by activated carbon adsorption due to its low

 1,2,3-Trichloropropar*                                      September, 1989



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