September, 1989
820K89106
1,2,3-TRICHLOROPROPANE
Drinking Water Health Advisory
Office of Water
U.S. Environmental Protection Agency
I. INTRODUCTION
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
population.
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.
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I
1,2,3 Trichloropropane September, 1989
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II. GENERAL INFORMATION AND PROPERTIES
CAS No. 96-18-4
Structural Formula
Cl Cl Cl
LLJ.
1 1 1
1,2,3-Trichloropropane
Synonyms
0 Allyl trichloride, glycerol trichlorohydrin, glyceryl trichloro-
hydrin, trichlorohydrin (NIOSH, 1986).
Uses
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 25°C) Colorless clear liquid
Boiling Point (25 mm Hg) 156.85°C
Melting Point -14.7°C
Density (20°C) 1.387
Vapor Pressure (20°C) 2 mm Hg
Specific Gravity (20°C) 1.3889
Water Solubility (20°C) 1,900 mg/L
Log Octanol Water Partition 2.63
Coefficient
Odor Threshold (water)
Odor Threshold (air)
Taste Threshold
Conversion Factor 1 ppm = 6 mg/m3
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1,2,3-Trichloropropane September, 1989
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Occurrence
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
locations.
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; 25°C; <0.2 mph air current.
0 Hatsui et al. (1975) determined that trichloropropane (unspecified
isomer) was relatively easy to decompose by microbes in activated
sludge.
III. PHARHACOKIWETICS
Absorption
0 Data regarding the absorption of 1,2,3-TCP could not be located in
the available literature.
Distribution
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.
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1,2,3-Trichloropropane September, 1989
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Metabolism
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.
*
Excretion
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.
IV. -HEALTH EFFECTS
Humans
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.
Animals
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
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1,2,3-Trichloropropane September, 1989
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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
?»r
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1,2,3-Trichloropropane September, 1989
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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
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1,2,3-Trichlc cpropane September, 1989
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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
rate).
Hutagenicity
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.
Carcinogenicity
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.
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1,2,3-Trichloropropane September, 1989
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V. QUANTIFICATION OF TOXICOLOGICAL EFFECTS
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
formula:
(NOAEL or LOAEL) x (BW)
= mg/L { pg/L)
(UF) (_ L/day)
where:
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.
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1,2,3-Trichloropropane September, 1989
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The Longer-term HA for a 10-kg child is calculated as follows:
Longer-term HA = (8 *q' *0 *g> = °'57 mg/L (60°
where:
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
where:
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) ,
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1,2, 3-Trichloropropane September, 1989
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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
where:
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)
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1,2,3-Trichloropropane September, 1989
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where:
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)
where:
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.
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
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
given.
0 The OSHA Permissible Exposure Limit (PEL) for 1,2,3-TCP is 50 ppm
(300 mg/m3) (CFR, 1985).
VII. ANALYTICAL METHODS
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
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1,2,3-Trichloropropane September, 1989
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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.
VIII. TREATMENT TECHNOLOGIES
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 25°C.
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
40.
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
solubility.
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1,2,3-Trichloropropar* September, 1989
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IX. REFERENCES
ACGIH. 1980. American Conference of Governmental Industrial Hygienists.
Documentation of the threshold limit values, 4th ed. Cincinnati, OH:
ACGIH. pp. 410-411.
ACGIH. 1985. American Conference of Governmental Industrial Hygienists.
TLVs. Threshold limit values and biological exposure indices for
1985-86. Cincinnati, OH: ACGIH. pp. 32, 37.
Belyaeva, N.N., T.I. Bonashevskaya, T.L. Harshak and V.Y.A. Brodskii.
1977. Investigation of the effect of certain chlorinated hydrocarbons
on the composition of the hepatocyte population of the rat liver.
Bull. Exp. Biol. Med. (USSR). 83:396-400. (Cited in U.S. EPA, 1983).
CFR. 1985. Code of Federal Regulations. OSHA Occupational Standards.
Permissible Exposure Limits. 29 CFR 1910.1000.
Dewalle, F.B. and E.S.K. Chian. 1978. Presence of trace organics in the
Delaware River and their discharge by municipal and industrial
source. Proc. Ind. Waste Conf. 32:908-919.
Dilling, W.L. 1977. Interphase transfer processes. II. Evaporation
rates of chloromethanes, ethanes, ethylenes, propanes, and propylenes
from dilute aqueous solutions. Comparison with theoretical predic-
tions. Erviron. Sci. Technol. 11:405-409.
Hardin, B.D., G.P. Bond, M.R. Sikov, F.D. Andrew, R.P. Beliles and R.W.
Niemeier. 1981. Testing of selected workplace chemicals for
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