*SIDS Initial Assessment Report For SIAM*

+---------------------------------+------------------------------------+
| 1\. Chemical Name               | 1,1,1-trifluoroethane              |
+---------------------------------+------------------------------------+
| 2\. CAS No                      | 420-46-2                           |
+---------------------------------+------------------------------------+
| 3\. Sponsor Country             | Oscar Hernandez                    |
|                                 |                                    |
|                                 | Director, Risk Assessment Division |
|                                 |                                    |
|                                 | (7403M)                            |
|                                 |                                    |
|                                 | U.S. Environmental Protection      |
|                                 | Agency                             |
|                                 |                                    |
|                                 | 1200 Pennsylvania Ave., NW         |
|                                 |                                    |
|                                 | #  Washington, DC 20460            |
|                                 |                                    |
|                                 | Phone: 202-564-7641                |
|                                 |                                    |
|                                 | e-mail: <hernandez.oscar@epa.gov>  |
+---------------------------------+------------------------------------+
| 4\. Shared Partnership With     | Honeywell                          |
+---------------------------------+------------------------------------+
| 5\. Roles/Responsibilities of   |                                    |
| the Partners                    |                                    |
+---------------------------------+------------------------------------+
| \- Name of industry             | George Rusch                       |
| sponsor/consortium              |                                    |
|                                 | Honeywell International, Inc.      |
|                                 |                                    |
|                                 | 973-455-3672                       |
|                                 |                                    |
|                                 | george.rusch@honeywell.com         |
+---------------------------------+------------------------------------+
| [- Process used]{.underline}    | Honeywell produced these           |
|                                 | documents; EPA reviewed the        |
|                                 | documents.                         |
+---------------------------------+------------------------------------+
| 6\. Sponsorship History         | The chemical was brought forward   |
|                                 | through the ICCA.                  |
+---------------------------------+------------------------------------+
| 7\. Review Process Prior to the | The U.S. EPA reviewed this case.   |
| SIAM                            |                                    |
+---------------------------------+------------------------------------+

SIDS INITIAL ASSESSMENT REPORT

**1,1,1-TRIFLUOROETHANE**

**CAS No. 420-46-2**

1.  **IDENTITY**

    1.  **Identity** (6, 8, 9, 11, 23, 24, 25)

> Chemical: 1,1,1-Trifluoroethane

## CAS No. 420-46-2

> Molecular Weight: 84
>
> Molecular Formula: C~2~F~3~H~3~
>
> Structural Formula: CH~3~CF~3~
>
> Synonyms: HFC-143a
>
> Ethane, trifluoro-

##  Methyl fluoroform

> FC-143a
>
> R-143a

#  Physical Properties 

> Physical State: Gas
>
> Vapor Pressure: 12620-12720 kPa @ 25˚C
>
> Boiling Point: -47.4 °C \@101.3 kPa
>
> Melting Point: -111.3 °C

## Log K~ow~: 1.74 @ 20 °C

## Water Solubility: 761 mg/L @ 25 °C

> Henry's Law Constant: No Data

# 2. GENERAL INFORMATION ON EXPOSURE

Worldwide production is estimated at 10,000 to 50,000 tons in the year
2006.

## 

The major application is in air conditioning systems and commercial
refrigeration. (19)

> **2.1 Environmental Exposure and Fate**
>
> The low octanol/water partition coefficient (log K~ow~ = 1.74)
> indicates a low potential for bioaccumulation. The low water
> solubility (761 mg/L at 20°C) and high vapor pressure (1262-1272 kPa
> at 25°C) suggest it should migrate to the air. Modeling, using the
> Level III Fugacity model, indicates that when the majority of the
> chemical is released to air, over 99.9 percent will remain in the
> atmosphere. Photodegradation occurs primarily with hydroxyl radicals,
> resulting in a half-life of approximately 9,600 days. (15, 21, 25)
>
> A photochemical trajectory model has calculated a **photochemical
> ozone creation potential (POCP)** of 0.0 for HFC-143a, thus HFC-143a
> should make a negligible contribution to photochemical ozone
> production. (29)
>
> A two-dimensional chemical-radiative-transport model of the global
> atmosphere determined the atmospheric lifetime of HFC-143a to be 47.2,
> which is appreciably lower than 53.5 value previously reported by WMO
> (1999). The difference in values appears to be the result from the
> slow, but not trivial loss in the stratosphere. The direct **global
> warming potential (GWP)** of HFC-143a at 20-, 100- and 500 year time
> horizons was calculated to be 5,695, 4,352, and 1,537, respectively.
> The model took into account evaluated atmospheric lifetimes and
> radiative forcings. The percent difference in GWP for HFC-143a for the
> 100-year time horizon in this study (4,352) was 19% less than that
> reported (5,400) by the WMO (1999). (30,31))
>
> **2.2 Exposure to Humans**
>
> HFC-143a is a gas, and therefore, exposure will be mainly by
> inhalation. Exposure may occur during synthesis, shipping, or filling
> refrigeration equipment. As HFC-143a is a gas, it is used in sealed
> systems.
>
> The Workplace Environmental Exposure Level for HFC-143a is 1000 ppm as
> an 8-hour time-weighted-average (1).
>
> HFC-143a is not used in any commercial products. Therefore the general
> public should not be exposed to it.

3.  **HUMAN HEALTH HAZARDS**

> **3.1 Effects on Human Health**
>
> **3.1.1 Metabolism**
>
> Groups of 3 male Charles River CD BR rats were exposed to HFC-143a for
> 4-5 hours in a recirculating chamber at levels of 100, 390, 1040,
> 2050, 4800 and 40,000 ppm. The chamber concentrations were monitored
> by gas chromatography every 10 minutes. Partition coefficients between
> air and blood, fat, liver, and muscle were measured. At the end of the
> exposure, samples of urine were collected and examined for the
> presence of metabolites by 19F NMR. The partition coefficients were
> 0.66 for blood:air, 1.13 for liver:air, 1.04 for fat:air, and 0.99 for
> muscle:air. Analysis of the gas uptake data with a PBPK model
> suggested that there was measurable metabolism of HFC-143a. The
> estimated Vmax and Km were 4.15 ± 0.1 mg/hr-kg and 4.37 ± 0.18 mg/L,
> respectively. Based on a separate exposure study at 40000, exposure
> appears to be saturated between 20000 and 40000 ppm. Based on 19F NMR,
> the major metabolite in the urine was trifluoroethanol and minor
> metabolites identified included the glucuronide conjugate of
> trifluoroethanol, trifluoroacetic acid, trifluoroacetaldehyde and the
> urea conjugate of trifluoroacetaldehyde. These metabolites were all
> identified in urine from rats exposed to 40000 ppm of HFC-143a for
> 4-hours. No metabolites were identified in the urine from rats exposed
> to 4800 ppm or lower. (13)
>
> In a second study, male Wistar rats were individually exposed by
> inhalation for 4 hours at levels of 5500, 10,000, 16,000, 20,000, or
> 30,000 ppm. The concentration of the test substance in the exposure
> chamber was monitored by gas chromatography. The amount of chemical
> retained in the body was calculated from measurements of the initial
> and final concentration in the chamber. A physiologically-based
> pharmacokinetic computer modeling program was used to calculate the
> kinetic parameters of absorption and metabolism of the test article. A
> significant decrease in liver glutathione was seen in the rats exposed
> to concentrations ≥ 10000 ppm. (15)
>
> Nine occupationally exposed male volunteers were exposed to 500 ppm of
> HFC-143a for two hours during light physical exercise in an exposure
> chamber. Blood, urine, and exhaled air were collected before, during
> and up to two days after the exposure period. The presence of HFC-143a
> in the biological samples was analyzed by head-space gas
> chromatography. Trifluoroacetic acid and fluoride in the urine were
> analyzed using high performance liquid chromatography and an ion
> specific electrode, respectively. The study results showed a low
> metabolic rate and a low solubility in blood for HFC-143a. A plateau
> blood concentration of 1.4 µg/g was found. Two elimination phases were
> observed with half lives of 4 and 300 minutes. (10)
>
> **3.1.2 Acute Toxicity**
>
> Groups of 6 Charles River CR BR male rats were exposed; nose only, to
> concentrations of 97000 or 540000 ppm of the test article for a single
> 4 hour period. They were then observed for 14 days following the
> exposure. During the exposure, oxygen concentrations in the breathing
> air were maintained at 20% by the addition of supplemental oxygen to
> the chamber supply air. The exposure levels were monitored at
> half-hourly intervals using an on-line gas chromatograph with a flame
> ionization detector. There was no lethality. Slight body weight loss
> was noted for the 97000 ppm exposure level group and a more severe
> body weight loss was noted for the rats in the 540000 ppm exposure
> level group on the day following the exposure. By the second day post
> exposure, body weight gain was normal. (4, 7)
>
> The acute toxicity of HFC-143a was assessed by exposing two groups of
> 5 male and 5 female Sprague Dawley rats nose only to either 305000 or
> 591000 ppm of the test article for 4 hours. An additional control
> group was exposed to air for 4 hours. The test atmospheres were
> generated by dilution of the test gas with air and oxygen in such a
> manor that the oxygen level was maintained between 19-21%. The
> exposure level was determined 5 times during the 4-hour exposure. The
> analysis consisted of collection of a sample using a gas sampling
> bulb. Samples were withdrawn using a gas tight syringe and analyzed on
> a gas chromatograph using a thermal conductivity detector. Rats were
> observed for 14 days following the exposure. There was no lethality.
> Increased respiratory depth observed at 350,000 in one male and one
> female and 591,000 ppm in one female. Peripheral vasodilation was
> reported at 591,000 ppm in one male and four females. Aside from a
> slight decrease noted on the day following the exposure, body weight
> and body weight gain appeared normal. The slight loss on the day
> following the exposure was attributed to the restraint system used for
> the exposures. There was no adverse effect on organ weight nor were
> there any gross observations of treatment related abnormalities seen
> during the gross necropsy. (5)
>
> To determine if HFC-143a caused sensitization of the heart to
> epinephrine, groups of 5-6 beagle dogs that were previously trained to
> accept a canvas sling restraining device were exposed to atmospheres
> containing 50000, 100000, 150000, 200000, 250000 and to 300000 ppm of
> the test article. Exposures were conducted using a single pass face
> mask. During the exposure, oxygen concentrations in the breathing air
> were maintained at 20% by the addition of supplemental oxygen to the
> breathing air. Electrocardiogram leads were attached to the dog and
> the EKG was recorded for the 17 minutes of the test. Two minutes after
> breathing air alone, the dog was given an injection of epinephrine
> just below that which could have caused a spontaneous arrhythmia.
> After five additional minutes of exposure to air, the dog was exposed
> to vapors of HFC-143a. After 5 minutes of the exposure to the
> HFC-143a, the dog was given a second injection of epinephrine at the
> same dose as the first injection. Exposure to HFC-143a was continued
> for an additional 5 minutes. A positive response was the development
> of an arrhythmia or at a minimum 5 consecutive ectopic heart beats.
> The threshold for this effect was 300,000 ppm. (4)
>
> As the HFC-143a is a gas at room temperature, skin and eye irritation
> and dermal sensitization data are not available.
>
> **3.1.3 Repeated-Dose Toxicity**
>
> Following a 4-week inhalation toxicity study that was judged to be
> unreliable due to technical problems (27), groups of male Charles
> River CD BR rats were exposed whole body to levels of 2,000, 10,000,
> and 40,000 ppm, 6-hrs/day 5-days/wk for 4 weeks. An air exposed
> control group was also included. The exposure levels were monitored at
> half-hourly intervals using an on-line gas chromatograph with a flame
> ionization detector. There was no mortality, no effects on body weight
> and no adverse clinical signs. Gross pathology and histopathology were
> limited to the testes and epididymides. Changes related to exposure
> were not observed in any group. Therefore 40,000 ppm represented the
> No Observed Effect Level. (4, 28)
>
> Twenty male and 20 Charles River CD BR female rats were exposed to
> concentrations of 0, 2000, 10000 or 40000 ppm of the test article. The
> exposure levels were monitored at half-hourly intervals using an
> on-line gas chromatograph with a flame ionization detector. On the day
> following the last exposure, blood and urine samples were collected
> and the standard serum chemistry, hematology and urinalysis
> evaluations were conducted on all animals. Approximately 35 tissues
> were collected form each animal. They were examined
> histopathologically only from animals in the control and high level
> exposure group Also at termination, samples of liver were collected
> from 5 rats per group for determination of ß-oxidation activity a
> measure of peroxisome proliferation. There were no effects on body
> weight and food consumption. There were no clinical signs. There were
> no effects on ophthalmological examinations, hematology, biochemistry
> and urinalysis. There were no changes in gross pathology and
> histology. There was no proliferation of hepatic peroxisomes. It was
> concluded that the NOEL for this study was 40000 ppm. (4, 17)
>
> **3.1.4 Genetic Toxicity**
>
> Several bacterial mutation assays were conducted with HFC-143a. In the
> first, strains TA 100 and TA 1535 were exposed for 48 hours to a level
> of 500,000 ppm of HFC-143a, both with and without metabolic
> activation. HFC-143a gave a positive response in this assay. However,
> as discussed below, this is the only report of a positive response
> with HFC-143a and the weight of evidence demonstrates that HFC-143a is
> not mutagenic.
>
> In a second study, TA 100, TA 1535, TA 97, TA 98, and e coli WP2 uvrA
> were exposed to 5,000, 15,000, 25,000 and 35,000 ppm both with and
> without metabolic activation. Again the cells were incubated for 48
> hours at 37 ˚C. HFC-1434a was not active in this assay. In a third
> assay, TA 100, TA 1535, TA98, TA 1537, TA 1538 and e coli WP2 uvrA
> were exposed to levels of 100,000, 300,000, 500,000, 700,000, or
> 900,000 of HFC-143a for 48 hours at 37˚C both with and with out
> metabolic activation. Again, HFC-143a was not mutagenic. (2, 4, 14,
> 18)
>
> It was reported that HFC-143a was not active when tested for
> mutagenicity using baby hamster kidney fibroblasts (BHY21). However
> the details of this study were not available. (14)
>
> A chromosome aberration study was conducted in which human lymphocytes
> were exposed to 5,000, 15,000, 25,000 or 35,000 ppm for 3 hours at
> 37˚C both with and with out metabolic activation. Treatment was
> conducted by exposing the cell cultures to atmospheres containing the
> test article at the specified concentrations. The maximum exposure was
> set to be approximately 50% of the lower flammability level for the
> test article. HFC-143a was not active in this test. (3, 4)
>
> Charles River CD-1 mice were exposed, whole body, to the test article,
> 6-hrs/day for two consecutive days at levels of 2,000, 10,000 and
> 40,000 ppm. Bone marrow smears were prepared approximately 24 and 48
> hours after the second exposure, and 1000 polychromatic erythrocytes
> per animal were evaluated for the presence of micronuclei. The
> positive control was cyclophosphamide. The exposures were conducted on
> days 49 and 50 of the 13-week rat exposure study described above.
> Again HFC-143a was not active in this assay. (4, 22)
>
> **3.1.5 Reproductive Toxicity**
>
> HFC-143a has not been evaluated in a reproduction study. However, it
> has been tested in a 13 week subchronic inhalation toxicity study with
> exposures up to 40,000 ppm, 6-hours/day, 5 days/week and included full
> histopathological evaluation of the tissues from the reproductive
> organs (testes, epididymides, ovaries, and uterus). None of these
> studies reported any adverse findings in the reproductive organs. (4,
> 13)
>
> **3.1.6 Developmental Toxicity**
>
> Groups of 25 pregnant Charles River CD BR rats were exposed to 2,000,
> 10,000, or 40,000 ppm of HFC-143a 6 hours/day from day 7 through day
> 16 of gestation. An air control was also included. Exposure levels
> were monitored using a gas chromatograph with a flame ionization
> detector. The day of copulation was designated as Gestation Day 1 (GD
> 1). On GD 20, the maternal animals were killed by CO2 inhalation. The
> ovaries and uteri were examined for the number of corpora lutea, live
> young, embryofetal deaths and resorptions. The uterus of each
> apparently nonpregnant rat was opened and stained with ammonium
> sulfide. Fetuses were weighed, the sex was determined and the fetuses
> were examined for external malformations. Live fetuses were killed and
> examined for visceral malformations by the method of Staples. There
> were no significant findings on maternal mortality, clinical
> observations and gross pathology examinations. Treatment related
> findings were not observed in litter size, embryo-fetal loss and
> litter and fetal weight. Effects on the incidence of malformation were
> not observed at any exposure level. There was however a slight, but
> significant increase in the incidence of fetal visceral variations in
> the litters of all the exposed groups in comparison to the control
> group. Since there was no evidence of any other developmental
> toxicity, the increased incidences were not dose-dependent and fell
> into the historic average of the incidence for variations of this
> effect, they were not considered to be biologically significant. (4,
> 20)
>
> Groups of 24 pregnant New Zealand white rabbits were exposed to 0
> (control), 2,000, 10,000, or 40,000 ppm of HFC 143a 6-hours/day from
> day 6 till day 18 of gestation. Exposure levels were monitored using a
> gas chromatograph with a flame ionization detector. Does were
> artificially inseminated and subsequently injected (iv) with 100 IU of
> hCG. The day of insemination was considered Gestation Day 0 (GD0). On
> GD 29, the maternal animals were killed by iv injection of Socumb
> Euthanasia solution and the internal organs examined for gross
> abnormalities. The ovaries and uteri were examined for the number of
> corpora lutea, live young, embryofetal deaths and resorptions. The
> uterus of each apparently nonpregnant rabbit was opened and stained
> with ammonium sulfide. Fetuses were weighed, the sex was determined
> and the fetuses were examined for external malformations. Live fetuses
> were killed and examined for viseral malformations by the method of
> Staples. One female in the 2000 ppm group aborted on gestation day 17.
> No other findings were observed in adult females within the scheduled
> period, thus the abortion was judged spontaneous. There was no
> indication of developmental toxicity at any exposure level. Fetal
> malformation and variation incidences were similar among all the
> groups. (4, 12)
>
> **3.1.7 Experience with Human Exposure**
>
> Nine male volunteers were exposed to 500 ppm HFC-143a for 2 hours for
> a human toxicokinetic study. The electrocardiogram of the exposed
> volunteers was monitored during and until 20 hours after exposure.
> Irritative and central nervous system symptoms were rated in a
> questionnaire prior to, during and after exposure. The authors stated
> that analyses suggested no increase in symptoms ratings during or
> after exposure. (10)
>
> .
>
> **3.2 Initial Assessment for Human Health**
>
> HFC-143a has a very low mammalian toxicity. A 4-hour exposure of
> 591,000 ppm did not result in lethality. It did not cause any
> significant signs of toxicity in a 13 week inhalation toxicity study
> with exposures up to 40,000 ppm. It also did not cause any
> developmental effects in either rats or rabbits with exposures during
> gestation up to 40,000 ppm. Based on 19F NMR, the major metabolite in
> the urine was trifluoroethanol and minor metabolites identified
> included the glucuronide conjugate of trifluoroethanol,
> trifluoroacetic acid, trifluoroacetaldehyde and the urea conjugate of
> trifluoroacetaldehyde. These metabolites were all identified in urine
> from rats exposed to 40000 ppm of HFC-143a for 4-hours. No metabolites
> were identified in the urine from rats exposed to 4800 ppm or lower.
> Volunteers exposed to 500 ppm for 2-hours did not show or report any
> adverse effects. The current occupational exposure guideline (WEEL) is
> 1000 ppm.

**4. HAZARDS TO THE ENVIRONMENT**

1.  **Aquatic Effects**

### Since HFC-143a will reside in the atmosphere as indicated by a high vapor pressure and limited water solubility, only a few aquatic toxicity tests have been conducted. An acute flow-through toxicity study in the freshwater fish *Oncorhyncus mykiss* estimated the 96-hour LC~50~ to be \> 40 mg/l, the highest concentration evaluated. (32) A static acute toxicity study in the freshwater invertebrate *Daphnia magna* estimated the 48-hour EC~50~ to be 300 mg/l. estimates for the toxicity of HFC-143a have been calculated with the ECOSAR program in the EPIWIN model. For fish, the 96-hr LC~50~ was estimated to be 109 mg/L; for daphnids, the 48-hr EC~50~ was estimated to be 115 mg/L; and for green algae, the 96-hr EC~50~ was estimated to be 71 mg/L. (16)

2.  **Terrestrial Effects**

> No data were found on terrestrial effects.

3.  **Initial Assessment for the Environment**

> Due to the physicochemical properties of HFC-143a, its use in closed
> systems, and its predicted partitioning to air, environmental
> concentrations in the aquatic environment are expected to be low. (26)

**5. CONCLUSIONS AND RECOMMENDATIONS**

1.  **Human Health**

> In acute and repeated-exposure inhalation toxicity studies, HFC-143a
> has been shown to have a low toxicity and low rate of metabolism. In
> two teratology studies, it was not embryo- or fetotoxic nor did it
> produce teratogenicity. Also, evaluation of the reproductive organs
> from a subchronic inhalation exposure study did not reveal any effects
> on these organs. While showing a positive response in an older Ames
> assay, HFC-143a was not mutagenic in a series of subsequent *in vitro*
> or *in vivo* genotoxicity studies.

Because HFC-143a has no applications in consumer products, consumer
exposure is not expected. The occupational exposure limit of 1000 ppm
has been in place for over 10 years.

2.  **Environment**

> HFC-143a is used in closed systems. It also has a water solubility of
> 761 mg/L and a log K~ow~ of 1.74. It is predicted to degrade in the
> atmosphere with a half-life of approximately 9,600 days based on
> reaction with hydroxyl radicals. As HFC-143a does not contain chlorine
> or bromine, it has no potential for stratospheric ozone depletion. Its
> high vapor pressure, low log K~ow~ and low water solubility imply that
> it will not be an environmental hazard in the aquatic environment.
> Finally, releases to the environment are expected to be low.

3.  **Recommendations**

> Human Health: The chemical is currently of low priority for further
> work. HFC-143a has not shown signs of acute toxicity even at a level
> of 591,000 ppm. Due to its flammability, repeat exposure studies were
> conducted at levels of 40,000 ppm and lower. There has been no
> evidence for toxicity in these studies.
>
> Environment: The chemical is currently of low priority for further
> work. Modeling has predicted that it will partition almost exclusively
> into the air and its low log Pow suggests that it will not
> bioaccumulate.

5.  **REFERENCES**

+-----------------------------------------------------------------------+
|   -                                                                   |
| ------- ------------------------------------------------------------- |
|   \(1\)    American Industrial Hygine Association. 1996.              |
|                                                                       |
|          1,1,1-Trifluoroethane Workplace Environmental Exposure Level |
|            Guide. 2700 Prosperity Avenue, Fairfax, VA 22031           |
|                                                                       |
|   \                                                                   |
| (2\)    Benley KS. 1994a. Bacteriall mutagenicity testing of HFC-143a |
|            in the Salmonella typhimurium and Escherichia coli plate   |
|                                                                       |
|           incorporation assay. Unpublished report HLR 787-93. Haskell |
|                                                                       |
|         Laboratory for Toxicology and Industrial Medicine. Du Pont de |
|            Nemours, Newark, Delaware, USA. Du Pont Chemicals,         |
|            Wilmington, Delaware, USA. Allied-Signal, Morristown, New  |
|                                                                       |
|         Jersey, USA. Elf-Atochem, King of Prussia, Pennsylvania, USA. |
|                                                                       |
|   \(3\)    Bentley KS. 1994b. In vitro evaluation of HFC-143a for     |
|            chromosome aberrations in human lymphocytes. Unpublished   |
|            report HLR 788-93. Haskell Laboratory for Toxicology and   |
|            Industrial Medicine. Du Pont de Nemours, Newark, Delaware, |
|            USA. Du Pont Chemicals, Wilmington, Delaware, USA.         |
|                                                                       |
|         Allied-Signal, Morristown, New Jersey, USA. Elf-Atochem, King |
|            of Prussia, Pennsylvania, USA.                             |
|                                                                       |
|                                                                       |
| \(4\)    Brock WJ, Trochimowicz HJ, Farr CH, Millischer RJ, Rusch GM. |
|            1996. acute, subchronic and developmental toxicity and     |
|                                                                       |
|         genotoxicity of 1,1,1-trifluoroethane (HFC-143a). Fundamental |
|            and Applied Toxicology 31:200-209. \<ECETOC\>              |
|                                                                       |
|   \(5\)    Cracknell S. 1992. Forane 143a: acute inhalation toxicity  |
|            study in the rat. Unpublished report 91/ATH007/1159. Life  |
|                                                                       |
|           science Research, Eye, Suffolk, England, UK. Atochem, Paris |
|            la Defense, France.                                        |
|                                                                       |
|   \(6\)    Daubert TE, Danner RP. 1989. Physical and thermodynamic    |
|            properties of pure chemicals data compilation. Taylor and  |
|            Francis, Washington, DC, USA                               |
|                                                                       |
|   \                                                                   |
| (7\)    Du Pont. 1990. Four-hour acute toxicity study with FC-143a in |
|                                                                       |
|           rats. Unpublished report HLR 283-90. Haskell Laboratory for |
|            Toxicology and Industrial Medicine. Du Pont de Nemours,    |
|            Newark, Delaware, USA.                                     |
|                                                                       |
|   \(8\)    European Centre for Ecotoxicology and Toxicology of        |
|                                                                       |
|          Chemicals. 2006. Trifluoroethane (HFC-143a). 4 Avenue E. Van |
|            Nieuwenhuyse (Bte 6), B-1160 Brussels, Belgium.            |
|                                                                       |
|                                                                       |
|  \(9\)    Fujiware K, Nakamura S, Noguchi M. 1998 Critical parameters |
|            and vapor pressure measurements for 1,1,1-trifluoroethane  |
|            (R-143a). J Chem Eng Data 43:55-59.                        |
|                                                                       |
|                                                                       |
|  \(10\)   Gunnare S, Ernstgard L, Sjogren B, Johanson G. 2003. Uptake |
|            and disposition of 1,1,1-Trifluoroethane in man. Poster    |
|            presented at 42nd Annual Meeting of the Society of         |
|            Toxicology, Salt Lake City, Utah, USA March 09-13, 2003.   |
|            Toxicol Sci 72:338                                         |
|                                                                       |
|   \(11\)   Honeywell Material Safety Data Sheet. (December 2005)      |
|                                                                       |
|           Genetron 143a. Honeywell, 101 Columbia Road, Morristown NJ, |
|            USA.                                                       |
|                                                                       |
|                                                                       |
| \(12\)   Holson JF. 1993. An inhalation development toxicity study of |
|            HFC-143a in rabbits, final report. Unpublished report      |
|            WIL-189005. WIL Research Laboratories, Ashland, Ohio, USA. |
|            Elf Atochem, King of Prussia, Pennsylvania, USA.           |
|                                                                       |
|   \(13\)   Keller, DA 1994. Metabolism of HFC-143a in the rat.        |
|            Unpublished report HLR 3-94. Haskell Laboratory for        |
|            Toxicology and Industrial Medicine. Du Pont de Nemours.    |
|            Newark, Delaware                                           |
|                                                                       |
|   \                                                                   |
| (14\)   Longstaff E, Robinson M, Bradbook C, Styles JA, Purchase IFH. |
|            1984. Genotoxicity and carcinogenicity of fluorocarbon     |
|                                                                       |
|          assessment by short-term in vitro tests and chronic exposure |
|            in rats. Toxicol Appl Pharmacol 72:15-31                   |
|                                                                       |
|   \(15\)   Loizou, GD, Eldirdiri, NI, King, LJ. 1996. Physiologically |
|                                                                       |
|         based pharmacokinetics of uptake by inhalation of a series of |
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|                                                                       |
|   \(16\)   Mackay, D. (2001). Multimedia environmental models: the    |
|                                                                       |
|         fugacity approach, 2^nd^ ed. Lewis, Boca Raton, Florida, USA. |
|                                                                       |
|   \                                                                   |
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|   -                                                                   |
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