DRAFT
August, 1987
1,3-DICHLOROPROPENE
Health Advisory
Office of Drinking Water
U.S. Environmental Protection Agency
I. INTRODUCTION
The Health Advisory (HA) Program, sponsored by the Office of Drinking
Water (ODW), provides information on the health effects, analytical method-
ology and treatment technology that would be useful in dealing with the
contamination of drinking water. Health Advisories describe nonregulatory
concentrations 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.
Health Advisories do not quantitatively incorporate any potential carcinogenic
risk from such exposure. For those substances that are known or probable
human carcinogens, according to the Agency classification scheme (Group A or
B), Lifetime HAs 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
lifetime exposure and the consumption of drinking water. The cancer unit
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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II. GENERAL INFORMATION AND PROPERTIES
CAS No. 542-75-6
Structural Formula
C1CH2 H C1CH2 Cl
\ ' \ /
c = c c » c
/ \ / \
H Cl H H
(trans) (cis)
1,3-Dichloropropene
(approximately 46% trans/42% cis)
Synonyms
Dichloro-1,3-propene; 1,3-dichloro-1-propene; Telone? Telone II;
Dow Telone; cis/trans-1,3-dichloropropene; 1,3-D; DCP; D-D
(approximately 28% cis/27% trans).
Uses
0 The pesticide 1 , 3-dichloropropene (DCP) is a broad spectrum soil
fumigant to control plant pests. Its major use is for nematode
control on crops grown in sandy soils of the Eastern, Southern and
Western U.S.
0 The usage of DCP has increased due to cancellation of the once widely
used product containing ethylene dibromide (EDB) and dibromochloro-
propane (DBCP) (U.S. EPA, 1986a).
0 Estimated usage of DCP containing products in 1984 to 1985 ranged from
about 34 to 40 million pounds (U.S. EPA, 1986a).
Properties (Dow Chemical USA, 1977, 1982; Patty, 1981)
Chemical Formula
Molecular Weight 11.0.98 (pure isomers )
Physical State (25°C) Pale yellow to yellow liquid
Boiling Point about 104°C (104.3°C, cis; 112°C, trans)
Density (25°C) 1.21 g/mL
Vapor Pressure (25°C) 27.3 mm Hg
Specific Gravity about 1.2 (20/20°C)
Water Solubility (25°C) 0.1 to about 0.25% (1 to 2.5 g/L)
reported; miscible with most organic
solvents
Log Octanol/Water Partition 25
Coefficient
Flash Point about 28°C
Conversion Factor (25'C) 1 mg/L.= 220 ppm; 1 ppm » 4.54 mg/m3
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Occurrence
0 In California (Maddy et al.f 1982), 54 wells were examined in areas
where Telone or D-D were used for several years. The well water did
not have measurable amounts of DCP (<0.1 ppb).
0 Monitoring data from New York have shown positive results for DCP in
ground water (U.S. EPA, 1986b).
Environmental Fate
* Available data indicate that DCP does leach to ground water. However,
the relative hydrolytic instability of the parent compound would
mitigate the potential for extensive contamination (U.S. EPA, 19865;
U.S. EPA, 1986c).
0 The half-life of 1,3-DCP in soil was reported by Laskowski et al.
(1982) to be approximately 10 days while Van Dijk (1974) reported
3 to 37 days depending on soil conditions and analytical methods.
III. PHARMACOKINETICS
Absorption
0 Toxicity studies indicate that DCP is absorbed from skin, respiratory
and gastrointestinal systems (Patty, 1981).
0 Oral administration of DCP in rats resulted in approximately 90%
absorption of the administered dose (Hutson et al., 1971).
Distribution
0 Radiolabeled [C14] D-D (55% DCP) was administered orally in arachis
oil in rats. After 4 days, most of the administered dose was recovered
for the most part in urine and there were insignificant amounts (less
than 5%) remaining in the gut, feces, skin and carcass (Hutson et al.,
1971).
Metabolism
0 cis-Dichloropropene in corn oil was given as a single oral dose
(20 mg/kg bw) to two female Wistar rats. Urine and feces were
collected separately. The main urinary metabolite (92%) was N-acetyl-
S-[ (cis)-3-chloroprop-2-enyl] cysteine. The cis-DCP has also been
shown to react with glutathione in the presence of rat liver cystol
to produce S[(cis)-3-chloroprop-2-enyl]glutathione. The cis-DCP is
probably biotransformed to an intermediate glutathione conjugate and
then follows the mercapturic acid pathway and is excreted in the
urine as a cysteine (Climie and Morrison, 1978).
0 In a study conducted by Dietz et al. (1984) rats and mice administered
(via gavage) up to 50 and 100 mg DCP/kg bw, respectively, demonstrated
no evidence of metabolic saturation.
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Excretion
In two studies (Hutson et al., 1971; Cliraie and Morrison, 1978)
f4c]cis- and/or trans-DCP, administered orally in rats, were excreted
primarily in the urine in 24 to 48 hours. When pulmonary excretion
was evaluated (Hutson et al., 1971), the cis and trans isomers were
3.9% and 23.6% of the administered dose, respectively. Most of the
cis-DCP was excreted in the urine.
IV. HEALTH EFFECTS
Humans
The only known human fatality occurred a few hours after accidental
ingestioh of D-D mixture. The dosage was unknown. Symptoms were
abdominal pain, vomiting, muscle twitching and pulmonary edema.
Treatment by gastric lavage failed (Gosselin et al., 1976).
Inhalation of high vapor concentrations result in gasping, refusal to
breathe, coughing, substernal pain and extreme respiratory distress
at vapor concentrations over 1,500 ppm {Gosselin et al., 1976).
Venable et al. (1980) studied 64 male workers exposed to three carbon
compounds including DCP to determine if fertility was adversely
affected. The exposed study population was divided into <5 years
exposure and >5 years exposure. Sperm counts and percent normal
sperm forms were the major variables evaluated. Although the study .
participation rate for the exposed group was only 64%, no adverse
effects on fertility were observed.
Animals
Short-term Exposure
0 DCP is moderately toxic via single-dose oral administration. A
technical product containing 92% cis-/trans-DCP was fed as a 10%
solution in corn oil to rats. The oral LDsos in male and female rats
were 713 and 740 mg/kg, respectively (Torkelson and Oyen, 1977). In
another study, the oral LD5Q in the mouse for both males and females
was 640 mg/kg (Toyoshima et al., 1978).
Dermal/Ocular Effects
e The percutaneous LD^gS for male and female mice were greater than
1,211 mg/kg (Toyoshima et al., 1978).
e The percutaneous administration of DCP in rabbits (3 g/kg) resulted
in mucous nasal discharge, depressed respiration and decreased body
movements. The LD5g by this route was 2.1 g/kg (Torkelson and Oyen,
1977).
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Primary eye irritation and primary dermal irritation studies in
rabbits indicated that DCP causes severe conjunctival irritation,
moderate transient corneal injury and slight skin erythema/edema.
Eye irritation was reversible 8 days post-instillation. The dermal
in rabbits was 504 mg/kg (Dow, 1978; Hanley et al., 1987).
Long-term Exposure
0 Rats, guinea pigs, rabbits and dogs were exposed to 4.5 or 13.6 mg/m3
DCP in air for 7 hours per day, and 5 days per week for 6 months.
The only effect noted was a slight apparently reversible microscopic
renal lesion in male rats exposed to the high dose (Torkelson and
Oyen, 1977).
0 Fischer 344 rats and CD-1 albino mice were exposed to Telone II
(Production Grade) by inhalation exposure, 6 hours per day for 13
weeks at concentrations of 11.98, 32.14, and 93.02 ppm. Gross pathology
revealed an increased incidence of kidney discoloration in the treated
male rats relative to the control group. The significance of this
lesion is unknown (Coate et al., 1979).
0 Solutions of Telone (78.5% DCP) in propylene glycol were administered
by gavage to 1 0 rats/sex/dose for six days per week for a period of 1 3
weeks. The dose levels were 1, 3, 10 and 30 mg/kg/day. The control
groups were given propylene glycol. The daily administration of DCP
to rats by stomach intubation up to a dosage of 30 mg/kg/day did not
result in any major adverse effects. No significant effects on body
weight, food consumption, hematology and histopathology were noted.
However, at the 10 mg/kg/day dose, the relative weight of the kidney
of males was still higher than controls. The authors conclude that
the no-toxic-effect level for DCP was between 3 and 10 mg/kg/day.
The actual observed No-Observed-Adverse-Effect-Level (NOAEL) was
3 mg/kg/day (Til et al, 1973).
0 The National Toxicology Program (NTP, 1985) evaluated the chronic
toxicity and carcinogenicity of Telone II in rats and mice. These
studies utilized Telone II fumigant containing approximately 89%
cis- and trans-DCP. Groups of 52 male and female F344/N rats (doses
0, 25 or 50 mg/kg) and 50 male and female B6C3F! mice (doses 0, 50
or 100 mg/kg) were gavaged with Telone II in corn oil, 3 days per
week up to 104 weeks. Arcillary studies were conducted in which
dose groups containing five male and female rats were killed after
receiving Telone II for 9, 16, 21, 24 or 27 months. Toxic effects
(noncarcinogenic) included basal cell or epithelial hyperplasia of
the forestomach of rats and mice at all treatment levels of DCP.
Epithelial hyperplasia of the urinary bladder of mice occurred at
both treatment levels in males and females. Kidney hydronephrosis
also occurred in mice. The study in male mice was considered inade-
quate due to the deaths of vehicle control animals. Many chronic
toxicity parameters (hematology/ clinical chemistry) were not deter-
mined. The DCP used in the NTP study had a different stabilizer from
the current Telone II.
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Reproductive Effects
0 Groups of male and female Wistar rats were exposed to technical D-D
at 0, 64, 145 and 443 mg/m3 (0, 14, 12 and 94 ppm) for 5 days per
week over 10 weeks. Male mating indices, fertility indices and
reproductive indices were not affected by D-D exposure. No gross
morphological changes were seen in sperm. Female mating, fertility
and other reproductive indices were normal. Litter sizes and weights
were normal and pup survival over 4 days was not influenced by exposure
(Clark et al., 1980).
Developmental Effects
0 Hanley et al. (1987) investigated the effects of inhalation exposure
to DCP on fetal development in rats. Pregnant Fischer 344 rats were
exposed to 0, 20, 60 and 120 ppm DCP for 6 hr/day during gestation
days 6 to 15. Maternal body weight gain was depressed in all of the
DCP-exposed rats in a dose-related manner. Therefore, the Lowest-
Observed-Adverse-Effect-Level (LOAEL) for this effect was 20 ppm DCP.
There was also significant depression of feed consumption in all
exposed rats, along with decreases in water consumption in rats
exposed to 120 ppm DCP. At 120 ppm there were significant increases
in relative kidney weights and decreases in absolute liver weights in
all exposed rats. There was a statistical increase in the incidence
of delayed ossification of the vertebral centra of rats exposed to
120 ppm DCP. This effect is of little toxicological significance due
to maternal toxicity observed at 120 ppm DCP.
0 Hanley et al. (1987) also studied the effects of inhalation exposure
to DCP on fetal development in rabbits. Pregnant New Zealand White
rabbits were exposed to 0, 20, 60 or 120 ppm DCP for 6 hr/day during
gestation days 6 through 18. In rabbits, evaluation of maternal
weight gain over the entire exposure period indicated significant
exposure-related decreases in both the 60- and 120-ppm groups.
Therefore, the NOAEL was 20 ppm DCP. Statistically significant
decreases in the incidence of delayed ossification of the hyoid and
presence of cervical spurs among the exposed group were considered
within normal variability in rabbits.
Mutagenicity
0 Tests of commercial formulations containing DCP (DeLorenzo et al.,
1975; Flessel, 1977; Neudecker et al., 1977; Brooks et al., 1978;
Sudo et al., 1978; Stolzenberg and Hine, 1980), a mixture of pure
cis-DCP and trans-DCP (DeLorenzo et al., 1975), and pure cis-DCP
(Brooks et al, 1978) were positive in the Salmonella typhimurium
strains TA1535 and TA100 with and without metabolic activation.
These results indicate that DCP acts by base-pair substitution and
is a direct acting mutagen.
0 DCP may be a mutagen that acts via frame shift mutation indicated
by studies (DeLorenzo et al, 1975) in which positive results were
obtained for TA1978 (with and without metabolic activation) for a
commercial mixture of DCP and a mixture of pure cis- and trans-DCP.
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e A commercial mixture of DCP and pure cis-DCP were also positive with
and without metabolic activation in Salmonella typhimurium strain TA98
(Flessel, 1977; Sudo et al., 1978; Brooks et al., 1978).
• sudo et al. (1978) tested DCP in a reverse mutation assay with
J3. coli B/r Wp2 with negative results.
0 DCP was negative for reverse mutation in the mouse host-mediated test
with S. typhimurium G46 in studies by Shirasu et al. (1976) and Sudo
et al7 (1978).
Carcinogenicity
0 F344 rats of each sex were gavaged with Telone II in corn oil at
doses of 0, 25 and 50 mg/kg/day for 3 days per week. A total of
77 rats/sex were used for each dose group (52 animals/sex/group were
dosed for 104 weeks in the main oncogenicity study, and an ancillary
study where 5 animals/sex/ group were sacrificed after 9, 16, 21, 24
and 27 months' exposure to DCP). No increased mortality occurred in
treated animals. Neoplastic lesions associated with Telone II included
squamous cell papillomas of the forestomach (male rats: 1/52; 1/52;
9/52; female rats: 0/52; 2/52; 3/52), squamous cell carcinomas of
the forestomach (male rats: 0/52; 0/52; 4/52) and neoplastic nodules
of the~liver (male rats: 1/52; 6/52; 7/52). The increased incidence
of forestomach tumors was accompanied by a positive trend for fore- N
stomach basal cell hyperplasia in male and female rats of both treated
groups (25 and 50 mg/kg/day). The highest dose level tested in rats
(50 mg/kg/day) approximated a maximum tolerated dose level (NTP, 1985).
0 B6C3Fi mice of each sex were gavaged with Telone II in corn oil at
doses of 0, 50 and 100 mg/kg/day for 104 weeks. A total of 50 mice/sex
were used for each dose group. Due to excessive mortality in control
male mice from myocardial inflammation approximately 1 year after the
initiation of the study, conclusions pertaining to oncogenicity were
based on concurrent control data and NTP historical control data.
Neoplastic lesions associated with the administration of Telone II
included squamous cell papillomas of the forestomach (female mice:
0/50; 1/50; 2/50), squamous cell carcinomas of the forestomach (female
mice: 0/50; 0/50; 2/50), transitional cell carcinomas of the urinary
bladder (female mice: 0/50; 8/50; 21/48), and alveolar/bronchiolar
adenomas (female mice: 0/50; 3/50; 8/50). The increased incidence
of forestomach tumors was accompanied by an increased incidence of
stomach epithelial cell hyperplasia in males and females at the
highest dose level tested (100 mg/kg/day), and the increased incidence
of urinary bladder transitional cell carcinoma was accompanied by a
positive trend for bladder hyperplasia in male and female mice of
both treated groups (50 and 100 mg/kg/day) (NTP, 1985).
0 Thirty female Ha:ICR Swiss mice received weekly subcutaneous injections
of cis-DCP. The dose was 3 mg DCP/mouse in 0.05 mL trioctanoin
delivered to the left flank. After 77 weeks, there was an increased
incidence of fibrosarcomas at the site of injection. Six of the
30 exposed mice developed the tumors. There were no similar lesions
in the controls (Van Duuren, 1979).
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V. QUANTIFICATION OF TOXICOLOGICAL EFFECTS
Health Advisories (HAs) are generally determined for one-day, ten-day,
longer-term (approximately 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:
HA = (NOAEL or LOAEL) x (BW) = _ mg/L ( _ ug/L)
(UF) x ( _ L/day)
where:
NOAEL or LOAEL = No- or Lowest-Observed-Adverse-Effect-Level
in rag/kg bw/day.
BW = assumed body weight of a child (10 kg) or
an adult (70 kg).
UF » uncertainty factor (10, 1 00 or 1,000), in
accordance with NAS/ODW guidelines.
_ L/day - assumed daily water consumption of a child
(1 L/day) or an adult (2 L/day).
One-day Health Advisory N
There are not sufficient data to derive a One-day Health Advisory value
for DCP. It is recommended that the Longer-term HA value for a 10-kg child
(30 ug/L, calculated below) be used at this time as a conservative estimate
of the One-day HA value.
Ten-day Health Advisory
There are not sufficient data to derive a Ten-day HA value for DCP. It
is recommended that the Longer-term HA value for a 10-kg child (30 ug/L) be
used as a conservative estimate of the Ten-day HA value.
Longer-term Health Advisory
The Til et al. (1973) 90-day subchronic feeding study in rats has been
selected to serve as the basis for calculating the Longer-term HA for DCP.
This study resulted in a LOAEL of 10.0 mg/kg/day based on increased relative
kidney weight in males. No adverse biological effects were noted at the
next lowest dose (3.0 mg/kg/day). Therefore, the NOAEL is 3.0 mg/kg/day.
Based on the NOAEL of 3.0 mg/kg/day determined in this study, the Longer
term HAs are calculated as follows:
For a 10-kg child:
Longer-term HA - (3*° agAq/day) (10 kg) = QfQ3 mg/L (30 ug/L)
(100) (10) (1 L/day)
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where:
3.0 mg/kg/day = NOAEL based on the absence of increased relative kidney
weights in rats.
10 kg = assumed body weight of a child.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
10 = modifying factor, selected since this was the only
useful feeding study available and the study design was
not ideal for assessing exposure via drinking water.
1 L/day = assumed daily water consumption of a child.
For a 70-kg adult:
Longer-term HA = (3.0 mg/kg/day) (70 kg) = ,105 mg/L (105 ug/L)
(100) (10) (2 L/day)
where:
3.0 mg/kg/day = NOAEL based on the absence of increased relative kidney
weights in rats.
70 kg = assumed body weight of an adult.
100 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
10 = modifying factor, selected since this was the only
useful feeding study available and the study design was
not ideal for assessing exposure via drinking water.
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 w.ter and is considered protective of noncar-
cinogenic adverse health effects over a lifetime exposure. The Lifetime HA
is derived in a three-step process. Step 1 determines the Reference Dose
(RfD), formerly called the Acceptable Daily Intake (ADI). The RfD is an esti-
mate of a daily exposure to the human population that is likely to be without
appreciable risk of deleterious effects over a lifetime, and is derived from
the NOAEL (or LOAEL), 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 DWEL 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 DWEL 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
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adult. The Lifetime HA 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 for synthetic organic chemicals and a value of 10%
is assumed for inorganic chemicals. If the contaminant is classified as a
Group A or B carcinogen, according to the Agency's classification scheme of
carcinogenic potential, then caution should be exercised in assessing the
risks associated with lifetime exposure to this chemical. For Group C
carcinogens, an additional safety factor of 10 is added to the DWEL.
The Lifetime HA for a 70-kg adult has been determined on the basis of
the study in rats by Til et al. (1973), as described above.
Using the NOAEL of 3.0 mg/kg/day, as determined in that study, the
DWEL is calculated as follows:
Step 1: Determination of the Reference Dose (RfD)
RfD = (3.0 mg/kg/day) _ Q.0003 mg/kg/day
(1,000) (10)
where:
3.0 mg/kg/day = NOAEL based on the absence of increased relative kidney
weights in rats.
1,000 = uncertainty factor, chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study
of less-than-lifetime duration.
10 = modifying factor selected since this was the only useful
feeding study available and the study design was not
ideal for assessing exposure via drinking water.
Step 2: Determination of the Drinking Water Equivalent Level (DWEL)
DWEL = (0.0003 mg/kg/day) (70 kg) , ,011 mg/L (n ug/L)
(2 L/day)
where:
0.0003 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 HAs are not recommended for Group A or B carcinogens. DCP is
a Group B, probable human carcinogen. The estimated cancer risk associated
with lifetime exposure to drinking water containing DCP at 11 ug/L is
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1,3-Dichloropropene August, 1987
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approximately 5.5 x 10-5. This estimate represents the upper 95% confidence
limit using the linearized multistage model. The actual risk is unlikely to
exceed this value.
Evaluation of Carcinogenic Potential
0 DCP may be classified as a B2, probable human carcinogen based on
sufficient evidence of tumor production in two rodent species and two
routes of administration.
0 Data on an increased incidence of squamous cell papilloma or carcinoma
of the forestomach in rats exposed to DCP (NCI, 1985) were used for a
quantitative assessment of cancer risk due to DCP. Based on the data
from this study and using the linearized multistage model, a carcinogenic
potency factor (q<*) for humans of 1.75 x 10"^ (mg/kg/day)~^ was
calculated.
0 The drinking water concentrations corresponding to increased lifetime
cancer risks of 10~4, 10~5 and 10~6 (one excess cancer per one million
population) for a 70-kg adult consuming 2 L/day are 20 ug/L, 2 ug/L
and 0.2 ug/L, respectively.
0 The forestomach tumor data in male rats used to calculate the q-|*
value (NCI, 1985) consisted of the 2-year study data excluding the
ancillary studies data. The ancilliary studies involved serial
sacrifice of animals (at 9, 16, 21, 24 and 27 months). It is not
appropriate to include these data in the lifetime predictive model
used (multistage).
0 For comparison purposes, drinking water concentrations associated
with an excess risk of 10~6 were 0.2 ug/L, 3.6 mg/L, 0.03 ug/L and
0.004 ug/L for the one-hit, Weibull, probit and logit models,
respectively.
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
0 The ACGIH recommended 1 ppm (5 mg/m3) as a Threshold Limit Value for
DCP (Patty, 1981).
VII. ANALYTICAL METHODS
0 No specific methods have been published by U.S. EPA for analysis of
DCP in water. However, EPA Method 524.2 (U.S. EPA, 1986d) and EPA
Method 502.2 (USEPA, 1986e) both for volatile organic compounds in
water should be suitable for analysis of DCP. Both are standard
purge and trap capillary column gas chromatographic techniques.
VIII. TREATMENT TECHNOLOGIES
0 There are no specific publications on treatment of 1,3-DCP. However,
adequate treatment by granular activated carbon (GAC) should be
possible. Freundlich carbon absorption isotherms for DCP indicate
reasonably high adsorption capacity (U.S. EPA, 1980).
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1 , 3-Dichloropropene August, 1987
IX. REFERENCES
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dichloropropenes: mutation studies with 1,3-D and cis-1 , 3-dichloropropene
and the influence of glutathione on the mutagenicity of cis-1 , 3-dichloro-
propene in Salmonella typhimurium; Group research report (Shell Research,
Ltd.) TLGR.0081 78. Unpublished study by Shell Chemical Co., Washington,
DC. MRID 61059.
Clark, D., D. Blair and S. Cassidy.* 1980. A 10 week inhalation study of
mating behavior, fertility and toxicity in male and female rats: Group
research report (Shell Research, Ltd.) TLGR.80.023. Unpublished study
Dow Chemical U.S.A., Midland, MI. MRIDs 117055, 103280, 39691.
Climie, I.J.G., and B.J. Morrison.* 1978. Metabolism studies on (Z)1 , 3-dichloro-
propene in the rat: Group research report (Shell Research, Ltd.) TLGR.010U
78. Unpublished study by Dow Chemical U.S.A., Midland, MI. MRID 32984.
Coate, W.B., D.L. Keenan, R.J. Hardy and R.W. Voelker.* 1979. Inhalation-
toxicity study in rats and mice: Telone II: Project No. 174-127.
Final report. Unpublished study by Hazleton Laboratories America, Inc.,
for Dow Chemical U.S.A., Midland, MI. MRID 119191.
DeLorenzo, F., S. Degl Innocenti and A. Ruocco.* 1975. Mutagenicity of
pesticides containing 1 , 3-dichloropropene: University of Naples, Italy.
Submitted by Dow Chemical U.S.A., Midland, MI. MRID 119179.
Dietz, F.K., E.A. Hermann and J.C. Ramsey. 1984. The pharmacokinetics of
14c-1 , 3-dichloropropene in rats and mice following oral administration.
Toxicologist. 4:585 (Abstract no.).
Dow Chemical U.S.A.* 1977. Telone II soil fumigant: Product chemistry.
MRID 00119178.
Dow Chemical U.S.A.* 1978. Summary of human safety data. Summary of studies
099515-1 and 09951 5-J. Unpublished study Dow Chemical U.S.A., Midland, MI.
MRID 39676.
Dow Chemical U.S.A. 1982. A data sheet giving the chemical and physical
properties of the chemical. A complete statement of the names and
percentages by weight of each active inert ingredient in the formulation
to be shipped. Dow Chemical U.S.A., Midland, MI. MRID 115213.
Flessel, P.* 1977. Letter dated Apr. 8, 1977: Subject: Mutagen testing
program, mutagenic activity of Telone II in the Ames Salmonella assay.
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•Confidential Business Information submitted to the Office of Pesticide
Programs.
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