2,2-Dichlor-1,1,1-trifluorethan

Solvents -> Chlorofluorocarbons

Solvents -> Chlorofluorocarbons

1.4638 g/cu cm at 25 °C

Relative density (water = 1): 1.5

1.4638 @25 °C

In water, 2100 mg/L at 25 °C

Solubility in water, g/100ml at 25 °C: 0.21

27.82 °C

28 °C

27.82 °C @760 [mm Hg]

Decomposes on heating. This produces phosgene, hydrogen fluoride and hydrogen chloride.

When heated to decomposition it emits very toxic fumes of /hydrogen chloride and hydrogen fluoride/.

Under certain conditions, /chlorofluorocarbon/ vapors may decompose on contact with flames or hot surfaces, creating the potential hazard of inhalation of toxic decomposition products. /Chlorofluorocarbon/

The appearance of toxic decomposition products serves as warning of the occurrence of thermal decompositon and detection of a sharp acrid odor warns of the presence of these products. /Fluorocarbons/

-107 °C

-107 °C

-107 °C

This chemical does not meet GHS hazard criteria for 2.1% (3 of 144) of reports.

Warning

H336 (32.6%): May cause drowsiness or dizziness [Warning Specific target organ toxicity, single exposure; Narcotic effects]

P260, P261, P264, P270, P271, P304+P340, P308+P316, P319, P403+P233, P405, P501, and P502 (click each P-code to see the statement)

Aggregated GHS information provided per 144 reports by companies from 9 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Danger

Chemical: Ethane, 2,2-dichloro-1,1,1-trifluoro-

Ethane, 2,2-dichloro-1,1,1-trifluoro- is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Ethane, 2,2-dichloro-1,1,1-trifluoro- are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Status: Active Update: 31-03-2022 https://echa.europa.eu/registration-dossier/-/registered-dossier/12060

2,2-dichloro-1,1,1-trifluoroethane: Does not have an individual approval but may be used under an appropriate group standard

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

See CHLOROFLUOROCARBONS.

An eye irritant; Can cause liver injury, narcosis, and cardiac arrhythmias; [ICSC] Effects in high-dose animal studies include anesthesia; [MSDSonline] Several clusters of occupational hepatitis have been reported, e.g., after HCFC-123 leaked in an air-conditioning system in a crane cabin and after HCFC-123 was used as a degreaser; [AIHA]

The Food and Drug Administration (FDA), after consultation with the Environmental Protection Agency (EPA), is amending FDA's regulation on the use of ozone-depleting substances (ODSs) in selfpressurized containers to remove the essential-use designations for flunisolide, triamcinolone, metaproterenol, pirbuterol, albuterol and ipratropium in combination, cromolyn, and nedocromil used in oral pressurized metered-dose inhalers (MDIs). The Clean Air Act requires FDA, in consultation with the EPA, to determine whether an FDA-regulated product that releases an ODS is an essential use of the ODS. FDA has concluded that there are no substantial technical barriers to formulating flunisolide, triamcinolone, metaproterenol, pirbuterol, albuterol and ipratropium in combination, cromolyn, and nedocromil as products that do not release ODSs, and therefore they will no longer be essential uses of ODSs as of the effective dates of this rule. MDIs for these active moieties containing an ODS may not be marketed after the relevant effective date. DATES: Removal of Part 2.125(e)(2)(iii) and 2.125(e)(4)(vii) is effective June 14, 2010. Removal of Part 2.125(e)(1)(v) and 2.125(e)(4)(iv) is effective December 31, 2010. Removal of Part 2.125(e)(1)(iii) is effective June 30, 2011. Removal of 2.125(e)(2)(iv) and Part 2.125(e)(4)(viii) is effective December 31, 2013. /Ozone-Depleting Substances/

Use of ozone-depleting substances in foods, drugs, devices, or cosmetics. (a) As used in this section, ozone-depleting substance (ODS) means any class I substance as defined in 40 CFR part 82, appendix A to subpart A, or class II substance as defined in 40 CFR part 82, appendix B to subpart A. (b) Except as provided in paragraph (c) of this section, any food, drug, device, or cosmetic that is, consists in part of, or is contained in an aerosol product or other pressurized dispenser that releases an ODS is not an essential use of the ODS under the Clean Air Act. (c) A food, drug, device, or cosmetic that is, consists in part of, or is contained in an aerosol product or other pressurized dispenser that releases an ODS is an essential use of the ODS under the Clean Air Act if paragraph (e) of this section specifies the use of that product as essential. For drugs, including biologics and animal drugs, and for devices, an investigational application or an approved marketing application must be in effect, as applicable. ... (e) The use of ODSs in the following products is essential: ... (2) Metered-dose short-acting adrenergic bronchodilator human drugs for oral inhalation. Oral pressurized metered-dose inhalers containing the following active moieties: ... (iv) Pirbuterol. ... (4) Other essential uses. (iii) Anesthetic drugs for topical use on accessible mucous membranes of humans where a cannula is used for application. ... (vi) Metered-dose atropine sulfate aerosol human drugs administered by oral inhalation. ... (viii) Metered-dose ipratropium bromide and albuterol sulfate, in combination, administered by oral inhalation for human use. (ix) Sterile aerosol talc administered intrapleurally by thoracoscopy for human use. /Ozone-Depleting Substances/

Fluorinated Organic Compounds

Fluorinated Organic Compounds

USEPA/ORD; Comments on the Lifetime of Organic Molecules in Air (1980) EPA-600/9-80-003. The lifetimes of halo hydrocarbons and other organics in air are given.

Zakhari S, Aviado DM; Cardiovascular Toxicology of Aerosol Propellants, Refrigerants and Related Solvents; Target Organ Toxicology Series: Cardiovascular Toxicology, XII+ 388 pages; Raven Press: New York, NY 281-326 (1982). Review of the toxicology of aerosol propellants, refrigerants and related solvents on the cardiovascular system of humans.

Vinegar A et al; Dose-dependent metabolism of 2,2,-dichloro-1,1,1-trifluoroethane: A physiologically based pharmacokinetic model in the male Fischer 344 rat; Toxicology and Applied Pharmacology 129 (1): 103-3 (1994). 2,2-Dichloro-1,1,1-trifluoroethane (HCFC-123) is used industrially as a refrigerant, as a foam blowing agent, and as a solvent.

Anders MW; Environmental Health Perspectives 96: 185-191 (1991). Metabolism and toxicity of hydrochlorofluorocarbons: Current knowledge and needs for the future.

For more Special Reports (Complete) data for 2,2-DICHLORO-1,1,1-TRIFLUOROETHANE (10 total), please visit the HSDB record page.

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. 2,2-Dichloro-1,1,1-trifluoroethane is included on this list. Effective date: 10/15/90; Sunset date: 11/9/93.

2,2-DICHLORO-1,1,1-TRIFLUOROETHANE is chemically inert in many situations, but can react violently with strong reducing agents such as the very active metals and the active metals. They suffer oxidation with strong oxidizing agents and under extremes of temperature.

DICHLOROTRIFLUOROETHANE is chemically inert in many situations, but can react violently with strong reducing agents such as the very active metals and the active metals. They suffer oxidation with strong oxidizing agents and under extremes of temperature.

No rapid reaction with air. No rapid reaction with water.

No rapid reaction with air. No rapid reaction with water.

Fresh air, rest. Artificial respiration may be needed. Refer for medical attention.

Rinse skin with plenty of water or shower.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rest.

R-123 is not flammable at ambient temperatures and atmospheric pressure. However, this material will become combustible when mixed with air under pressure and exposed to strong ignition sources. Product will decompose at temperatures above 250 °C. Decomposition products include hydrochloric acid, hydrofluoric acid, and carbonyl halides. Contact with certain finely divided metals may cause exothermic reaction and/or explosive combinations.

Firefighters should wear self-contained, NIOSH-approved breathing apparatus for protection against suffocation and possible toxic decomposition products. Proper eye and skin protection should be provided.

In case of fire in the surroundings, use appropriate extinguishing media.

In case of fire: keep drums, etc., cool by spraying with water.

Keep container closed when not in use. DO NOT store in open, unlabeled or mislabeled containers. Store in a cool, well-ventilated area of low fire risk. Protect container and its fittings from physical damage. Storage in subsurface locations should be avoided. Close valve tightly after use and when empty. If container temperature exceeds boiling point, cool the container before opening.

Always wear recommended personal protective equipment. Evacuate unprotected personnel and provide maximum ventilation. Protected personnel should eliminate all ignition sources if without risk. Only personnel equipped with proper respiratory and eye/skin protection should be permitted in the area. Dike area to contain the spill. Take precautions as necessary to prevent contamination of ground and surface waters. For large spills, pump solvent into appropriate containers. For small spills, recover or absorb spilled material using an absorbent designed for chemical spills such as Hazsorb pillows. Place used absorbents into closed DOT approved containers for disposal. After all visible traces have been removed, thoroughly wet vacuum the area. DO NOT flush into sewer. If the area of the spill is porous, removal of contaminated earth/surface may be required.

Collect leaking and spilled liquid in sealable containers as far as possible. Absorb remaining liquid in sand or inert absorbent. Then store and dispose of according to local regulations. Do not let this chemical enter the environment. Personal protection: chemical protection suit including self-contained breathing apparatus.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.

Because of recent discovery of potential ozone decomposition in the stratosphere by fluorotrichloromethane, this material should be released to the environment only as a last resort. Waste material should be /recovered and/ returned to the vendor, or to licensed waste disposal company.

Collect leaking and spilled liquid in sealable containers as far as possible. Absorb remaining liquid in sand or inert absorbent. Then store and dispose of according to local regulations. Do NOT let this chemical enter the environment. Personal protection: chemical protection suit including self-contained breathing apparatus.

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

Eye washer and instant shower facilities should be located near the work areas where spills and splash hazards exist. /Fluorocarbons/

High concentrations in the air cause a deficiency of oxygen with the risk of unconsciousness or death. Check oxygen content before entering area.

Inhalation of vapors should be avoided. /Chlorofluorocarbon/

For more Preventive Measures (Complete) data for 2,2-DICHLORO-1,1,1-TRIFLUOROETHANE (8 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 140(SRC), determined from a structure estimation method(2), indicates that 2,2-dichloro-1,1,1-trifluoroethane is expected to have high mobility in soil(SRC). Volatilization of 2,2-dichloro-1,1,1-trifluoroethane from moist soil surfaces is expected to be an important fate process(SRC) given a Henry's Law constant of 0.0256 atm-cu m/mole(3). 2,2-Dichloro-1,1,1-trifluoroethane is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 718 mm Hg at 25 °C(4). Primary and ultimate degradation of 24% and 10%, respectively, using the Closed Bottle test(5) suggest that biodegradation is not a fast environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 140(SRC), determined from a structure estimation method(2), indicates that 2,2-dichloro-1,1,1-trifluoroethane is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon a Henry's Law constant of 0.0256 atm-cu m/mole(4). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 3.7 and 4.9 days, respectively(SRC). According to a classification scheme(5), an estimated BCF of 13(SRC), from an estimated log Kow of 2.17(6) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Primary and ultimate degradation of 24% and 10%, respectively, using the Closed Bottle test(7) suggest that biodegradation is not a fast environmental fate process in water(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 2,2-dichloro-1,1,1-trifluoroethane, which has a vapor pressure of 718 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase 2,2-dichloro-1,1,1-trifluoroethane is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is about 2.2 years(SRC), calculated from its rate constant of 2.0X10-14 cu cm/molecule-sec at 25 °C(3). The water solubility of 2,2-dichloro-1,1,1-trifluoroethane of 2100 mg/L at 25 °C(4) indicates that it may undergo atmospheric removal by wet deposition processes; however, any removed by this process is expected to rapidly revolatilize to the atmosphere(SRC). 2,2-Dichloro-1,1,1-trifluoroethane has an estimated atmospheric lifetime of 1.4 years(5,6). 2,2-Dichloro-1,1,1-trifluoroethane does not contain chromophores that absorb at wavelengths >290 nm and, therefore, is not expected to be susceptible to direct photolysis by sunlight in the troposphere(SRC).

Neurotoxin - Acute solvent syndrome

Neurotoxin - Acute solvent syndrome

IDENTIFICATION: HCFC-123 is a synthetic, non-combustible, volatile liquid that is used as a refrigerant in commercial and industrial air conditioning installations, in gaseous fire extinguishants, as a foam blowing agent, and in metal and electronics cleaning. HUMAN EXPOSURE: Exposure to the general public to HCFC-123 is expected to be minimal. There is however, the potential for exposure during the manufacture of HCFC-123 and the manufacture and use of products containing this chemical. Limited information is available on the effects of HCFC-123 on humans. Cases of dizziness, headache and nausea have been reported following a single exposure to an unknown level of airborne HCFC-123, as well as cases of manifest or subclinical liver disease associated with repeated occupational exposures to HCFC-123 vapors at 5-1125 ppm (31.3-7030 mg/cu m) for 1-4 months. There was some evidence of clastogenic activity in human lymphocytes exposed to HCFC-123 at high cytotoxic concn in vitro. The most relevant critical effects for a single, brief exposure to this chemical are CNS depression and incr likelihood of ephinephrine induced cardiac arrythmia. Liver lesions were noted in workers exposed to HCFC-123 levels above 5 ppm(31.3 mg/cu m) for 1-4 mo. ANIMAL STUDIES: The acute toxicity of HCFC-123 in laboratory animals is low. Inhalation for a few minutes to a few hours causes liver lesions in guinea pigs at 1000 ppm (6.25 g/cu m) and central nervous system (CNS) depression in all species examined at 5000 ppm (31.3 g/cu m) and ephinephrine induced cardiac arrythmia in dogs at 20,000 ppm (125 g/cu m). In the rat and hamster, inhalation of more than 30,000 ppm (188 mg/cu m) for 4 hr causes severe CNS depression and death. HCFC-123 is not a skin irritant or sensitizer. It can cause eye irritation in liquid form. In repeated exposure inhalation toxicity studies lasting 2-39 wk in rats, guinea pigs, dogs and monkeys, the main target organs were the liver, the hypothalamic pituitary gonadal endocrine system, and the CNS. There was no evidence that HCFC-123 is teratogenic in laboratory animals or induces reproductive or fetal toxicity at levels of exposure lower than those that cause other systemic effects. Growth was retarded in neonatal rats and monkeys reared by dams exposed to HCFC-123. The main metabolite of HCFC-123, trifluoroacetic acid, was found in the milk of dams. In vitro and in vivo tests for genetic toxicity were negative. In a 2 year inhalation study in rats, there was an incr incidence of precancerous lesions and benign tumors in the liver, pancreas and testes, but no exposure related incr of malignant tumors.

Confusion. Dizziness. Drowsiness. Unconsciousness.

Redness. Pain.

See Inhalation.

Avoid release to the environment because of its impact on the ozone layer. It is strongly advised not to let the chemical enter into the environment because it is persistent. Avoid release to the environment in circumstances different to normal use.

Using a structure estimation method based on molecular connectivity indices(1), the Koc of 2,2-dichloro-1,1,1-trifluoroethane can be estimated to be 140(SRC). According to a classification scheme(2), this estimated Koc value suggests that 2,2-dichloro-1,1,1-trifluoroethane is expected to have high mobility in soil.

URBAN/SUBURBAN: A concentration of 0.2 parts/trillion volume for 2,2-dichloro-1,1,1-trifluoroethane in the Northern Hemisphere was estimated from estimated emission scenarios(1).

RURAL/REMOTE: Non-urban ambient air concentrations of 2,2-dichloro-1,1,1-trifluoroethane in Australia were detected at levels less than 0.01 parts per trillion (62.5 pg/cu m)(1).

/HUMAN EXPOSURE STUDIES/ Acute liver dysfunction has been reported among workers repeatedly exposed to 2,2-dichloro-1,1,1-trifluoroethane (HCFC-123), a substitute for trichlorofluoromethane. Causality between occupational exposure to 2,2-dichloro-1,1,1-trifluoroethane and liver dysfunction was examined. Levels of exposure to 2,2-dichloro-1,1,1-trifluoroethane were estimated retrospectively by reproducing working conditions and by a job record survey. Health surveillance, including liver function and subjective symptoms, was done when two workers first complained of ill health. The mean 2,2-dichloro-1,1,1-trifluoroethane concentration in air was more than 200 ppm with a peak concentration of about 1,000 ppm in a processing area where 2,2-dichloro-1,1,1-trifluoroethane was used. 2,2-dichloro-1,1,1-trifluoroethane of 1824 ppm was detected in the adjunct areas where 2,2-dichloro-1,1,1-trifluoroethane vapor was not generated. Workers (n=14) were then classified into high (n=5) and low (n=9) exposure groups according to the estimated exposure level, which was confirmed by determination of urinary trifluoroacetic acid. Mean serum AST and ALT levels were 236 IU/I and 476 IU/I among the high-exposed workers, and exceeded 500 IU/I in three workers. Various types of symptoms involving the central nervous system and digestive organs, and irritation of the mucous membrane, were also experienced. The degree and prevalence of these health effects were higher in the high exposure group, which indicates the exposure-effect and exposure-response relationships. The consistency and temporality of the relationship between 2,2-dichloro-1,1,1-trifluoroethane exposure and the observed health effects were also confirmed. We conclude that repeated exposure to high concentrations of 2,2-dichloro-1,1,1-trifluoroethane for no more than five weeks causes acute severe liver dysfunction with various symptoms in humans. Biological plausibility must be clarified to confirm the causality.

/HUMAN EXPOSURE STUDIES/ 1,1-Dichloro-2,2,2-trifluoroethane (HCFC-123) was evaluated as a substitute for trichlorofluoromethane (CFC-11), and it appeared that a permissible exposure limit of 50 ppm was justified. When HCFC-123 was introduced as a precision cleaning agent in a controlled operation, marked elevations in serum alanine transaminase and serum aspartase transaminase were noted in exposed workers. Sampling taken during start-up documented personal samples from 24-480 ppm (375 and 21 min, respectively) and area samples of 18-180 ppm (375 and 21 min, respectively). Personal and area samples collected after the liver abnormalities were identified ranged from 5-12 ppm. Exposure data were not available for the period when the abnormalities are suspected to have developed. Two models were developed to estimate exposure during the unmonitored period: (1) the entire plant as a homogenous box and (2) evaporation into smaller work zones. Modeling using the entire building estimated 8-hour time-weighted average (TWA) exposures of 10-35 ppm. Modeled estimates of work area and air exchange rates indicated that degreaser exposed workers could have experienced peak levels of 280-2,100 ppm (8-hour TWAs 252-1,630 ppm). Modeling of the work environment, estimated to be one-third of the volume of the entire open building, indicated peak exposures of 28-210 ppm (8-hour TWAs 25-163 ppm). These ranges estimate the minimum and maximum exposure levels. The best estimates, using 12 air changes per day, suggest peak levels around the degreaser of 635-2,100 ppm (8-hour TWA 499-1,630 ppm) and 63-207 ppm (8-hour TWAs 50-163 ppm) in the work area. These are the first estimates of exposure level associated with these hepatotoxic effects; all are significantly higher than personal and area samples collected for HCFC-123 after the liver abnormalities were identified.

/ALTERNATIVE and IN VITRO TESTS/ Hydrochlorofluorocarbon 1,1-dichloro-2,2,2-trifluoroethane (HCFC-123), a close structural analog of the hepatotoxic anesthetic halotane and a replacement for some ozone-depleting chlorofluorocarbons, is metabolized by liver cytochrome P450 (P450), both in vitro and in vivo. P450 activates HCFC-123, both oxidatively and reductively, to reactive species which attack P450 itself and also damage other targets leading to hepatotoxicity. Previous work in our laboratory has shown that some haloalkanes, including halomethanes CCl4, CCl3Br, CHCl4 and CH2Cl2 as well as halothane, are activated by different hemoproteins to reactive metabolites resulting in the protein's suicidal inactivation. Among these is methemalbumin (MHA), a synthetic complex of hem with human albumin often used as a model for various natural hemoproteins, such as P450. The aim of this study was to use MHA as a model to investigate the mechanism of P450 inactivation by HCFC-123. We found that MHA can reductively activate HCFC-123 to reactive species resulting in the loss of its hem group. During anerobic incubation of MHA with 10 mM HCFC-123, a typical reduced difference spectrum was observed with a 470-nm peak that increased with time, indicating an interaction between HCFC-123 or HCFC-123 metabolites and hem. In similar anerobic incubations, a significant loss of hem was measured using both the pyridine-hemochromogen technique and an ion-pairing reverse-phase HPLC method (37 and 30%, respectively). The loss of hem was time-, but not dose-dependent. No statistically significant loss of protoporphyrin IX, as measured by a fluorescence technique, or of the absolute hem spectrum produced in presence of CO (CO-hem complex) was observed up to 10 mM HCFC-123. Finally, a small but statistically significant inorganic fluoride production was measured in the presence of 20 mM HCFC-123 using an F(-)-specific electrode. Taken together, these results indicate that incubation of the non-enzymatic P450 model MHA with HCFC-123 under anerobic conditions leads to reductive activation of the substrate, resulting in the modification of hem, as was previously shown to occur for halothane. The hem modification is due to interaction of the prosthetic hem group of MHA with HCFC-123 metabolites. These data confirm the results of previous work with rat liver microsomal P450 and confirm suicidal destruction of hem to be the mechanism responsible for the HCFC-123-dependent loss of the enzyme's content and catalytic function.

2,2-Dichloro-1,1,1-trifluoroethane production and use as a refrigerant to replace CFC11(1) in commercial chillers for air conditioning systems, in portable fire extinguishers for the fire protection industry, as a heat transfer agent and in solvents(2) may result in its release to the environment through various waste streams. Limited (and declining) use in oral pressurized metered-dose inhalers(3) will result in its direct release to the environment(SRC). The US EPA lists 2,2-dichloro-1,1,1-trifluoroethane as an acceptable substitute for chlorofluorocarbons in firefighting (nonresidential use) and as a foaming agent as part of its "Significant New Alternatives Policy (SNAP)" program(1) although it is not clear whether it is used for these purposes(SRC).

AEROBIC: Using an aerobic 28-day Closed Bottle biodegradability test, the primary and ultimate degradation of 2,2-dichloro-1,1,1-trifluoroethane was 24% and 10%, respectively(1); therefore, the chemical was not considered readily biodegradable(1,2).

ANAEROBIC: Mixed methanogenic enrichment cultures from aquifer material at Moffett Field, California biotransformed 2,2-dichloro-1,1,1-trifluoroethane at a rate of 0.00090 L/mg-day(1). This slow transformation rate suggests that biodegradation under methanotrophic conditions is not an important environmental fate process(SRC). Microbial degradation of 2,2-dichloro-1,1,1-trifluoroethane was observed in anoxic freshwater and salt marsh sediments but not in aerobic soil; no degradation rates were reported(2).

PURE CULTURE: In a 24-hour screening study, complete degradation for 2,2-dichloro-1,1,1-trifluoroethane was observed by an unidentified methanotroph ENV2041 with a degradation rate of 0.4 umol/hr; incomplete degradation was observed by a mixed methanotropic culture EVN2040 and bacterial strain Mycobacterium vaccae JOB5; no degradation was observed for Methylosinus trichosporium OB3b /table/; however, results are inconclusive due to the discussion, reporting that the mixed ENV2040 did not transform HCFC 123 while ENV2041 and M. trichosporium did(1).

An estimated BCF of 13 was calculated in fish for 1,1-dichloro-1,1,1-trifluorothane(SRC), using an estimated log Kow of 2.17(1) and a regression derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Food and Drug Administration (FDA), after consultation with the Environmental Protection Agency (EPA), is amending FDA's regulation on the use of ozone-depleting substances (ODSs) in selfpressurized containers to remove the essential-use designations for flunisolide, triamcinolone, metaproterenol, pirbuterol, albuterol and ipratropium in combination, cromolyn, and nedocromil used in oral pressurized metered-dose inhalers (MDIs). The Clean Air Act requires FDA, in consultation with the EPA, to determine whether an FDA-regulated product that releases an ODS is an essential use of the ODS. FDA has concluded that there are no substantial technical barriers to formulating flunisolide, triamcinolone, metaproterenol, pirbuterol, albuterol and ipratropium in combination, cromolyn, and nedocromil as products that do not release ODSs, and therefore they will no longer be essential uses of ODSs as of the effective dates of this rule. MDIs for these active moieties containing an ODS may not be marketed after the relevant effective date. DATES: Removal of Part 2.125(e)(2)(iii) and 2.125(e)(4)(vii) is effective June 14, 2010. Removal of Part 2.125(e)(1)(v) and 2.125(e)(4)(iv) is effective December 31, 2010. Removal of Part 2.125(e)(1)(iii) is effective June 30, 2011. Removal of 2.125(e)(2)(iv) and Part 2.125(e)(4)(viii) is effective December 31, 2013. /Ozone-Depleting Substances/

Use of ozone-depleting substances in foods, drugs, devices, or cosmetics. (a) As used in this section, ozone-depleting substance (ODS) means any class I substance as defined in 40 CFR part 82, appendix A to subpart A, or class II substance as defined in 40 CFR part 82, appendix B to subpart A. (b) Except as provided in paragraph (c) of this section, any food, drug, device, or cosmetic that is, consists in part of, or is contained in an aerosol product or other pressurized dispenser that releases an ODS is not an essential use of the ODS under the Clean Air Act. (c) A food, drug, device, or cosmetic that is, consists in part of, or is contained in an aerosol product or other pressurized dispenser that releases an ODS is an essential use of the ODS under the Clean Air Act if paragraph (e) of this section specifies the use of that product as essential. For drugs, including biologics and animal drugs, and for devices, an investigational application or an approved marketing application must be in effect, as applicable. ... (e) The use of ODSs in the following products is essential: ... (2) Metered-dose short-acting adrenergic bronchodilator human drugs for oral inhalation. Oral pressurized metered-dose inhalers containing the following active moieties: ... (iv) Pirbuterol. ... (4) Other essential uses. (iii) Anesthetic drugs for topical use on accessible mucous membranes of humans where a cannula is used for application. ... (vi) Metered-dose atropine sulfate aerosol human drugs administered by oral inhalation. ... (viii) Metered-dose ipratropium bromide and albuterol sulfate, in combination, administered by oral inhalation for human use. (ix) Sterile aerosol talc administered intrapleurally by thoracoscopy for human use. /Ozone-Depleting Substances/

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. 2,2-Dichloro-1,1,1-trifluoroethane is included on this list. Effective date: 10/15/90; Sunset date: 11/9/93.

Adult male Fischer-344 rats were exposed to HCFC 123 (43 g/m3 or 68 g/m3) or to halothane (2-bromo-2-2 chloro-1,1,1-trifluoroethane) (1.05 g/m3) in air for 2 hr. The pattern of proteins immunoreactive with haptens-specific anti-trifluoroacetylprotein antibodies was found to be identical in livers of the rats exposed to HCFC 123 and halothane. Trifluoroacetic acid was detected in urine of rats exposed to HCFC 123 or halothane by nuclear magnetic resonance (NMR) and by gas chromatography with mass spectrometry (GCMS).

Groups of six male Charles River CD rats were exposed to 0, 6, 31, or 125 g/cu m (6 hr/day, 5 days/week) for 4 weeks. ... Urine analysis indicated the presence of trifluoroacetic acid as a major metabolite.

... 1,1-Dichloro-2,2,2-trifluoro-(2-(14C))-ethane (HCFC-123) is a chlorofluorohydrocarbon with potential widespread use and associated human exposure. As a part of the toxicological evaluation of 1,1-Dichloro-2,2,2-trifluoro-(2-(14C))-ethane, its metabolism was studied in rodents in a closed recirculating exposure system. Two male rats were individually exposed for 6 hr. Excretion of radioactivity was monitored for 48 hr after the start of the exposure. Of the radioactivity introduced into the chamber, 14% was recovered in urine within the period of observation. Excretion of metabolites in the urine was very slow. Trifluoroacetic acid was the major metabolite of 1,1-Dichloro-2,2,2-trifluoro-(2-(14C))-ethane and N-trifluoroacetyl-2-aminoethanol and N-acetyl-S-(2,2-dichloro-1,1-difluoroethyl)-L-cysteine were identified as minor urinary metabolites of 1,1-Dichloro-2,2,2-trifluoro-(2-(14C))-ethane. Forty-eight hours after the start of the exposure, covalent binding of radioactive metabolites to protein was highest in liver followed by kidney and lung. Covalent binding above background levels was not observed in pancreas and testis, the target organs of 1,1-Dichloro-2,2,2-trifluoro-(2-(14C))-ethane tumourigenicity. These results suggest that the biotransformation of 1,1-Dichloro-2,2,2-trifluoro-(2-(14C))-ethane in rodents follows a pathway identical to those of the extensively studied structural analogue halothane.

Hydrochlorofluorocarbons (HCFCs) have been identified as chemical replacements of the widely used chlorofluorocarbons (CFCs) that are implicated in stratospheric ozone depletion. Many HCFCs are structural analogues of the anesthetic agent halothane and may follow a common pathway of biotransformation and formation of adducts to protein-centered and other cellular nucleophiles. Exposure of rats to a single dose of halothane (2-bromo-2-chloro-1,1,1-trifluoroethane) or of the candidate CFC substitute HCFC 123 (2,2-dichloro-1,1,1-trifluoroethane) led to the formation of trifluoroacetylated protein adducts (CF3CO-proteins) not only in the liver, but also in the kidney as a novel target tissue for protein trifluoroacetylation. CF3CO-proteins in the kidney amounted to about 5% of those formed in the liver of the same animal. The amount of CF3CO-proteins formed within the kidney was roughly reflected by the capacity of metabolism of halothane or HCFC 123 by rat kidney microsomes in vitro which amounted to about 10% of that observed with liver microsomes. By immunohistochemistry, CF3CO-proteins in the kidney were mainly localized in the tubular segments of the cortex. In the liver, the density of CF3CO-proteins decreased from the central vein towards the portal triad. In vitro incubation of rat liver microsomes with halothane or HCFC 123 resulted in extensive formation of CF3CO-proteins and reproduced faithfully the pattern of liver CF3CO-proteins obtained in vivo. CF3CO-proteins generated in vitro were immunochemically not discernible from those generated in vivo. Glutathione (5 mM) and cysteine (5 mM) virtually abolished CF3CO-protein formation; the release of Br- from halothane and Cl- from HCFC 123 was reduced to much lesser a degree. S-Methyl-glutathione, N-acetyl-cysteine, methionine, and N-acetyl-methionine only slightly affected the formation of CF3CO-proteins or metabolism of either substrate. The data suggest that metabolism and concomitant CF3CO-protein formation of halothane or of candidate CFC replacements like HCFC 123 is not restricted to the liver but also takes place in the kidney. Furthermore, an in vitro system for CF3CO-protein formation has been developed and used to show that protein-centered and glutathione-centered nucleophilic sites compete for intermediates of metabolism of halothane or of HCFC 123.

For more Metabolism/Metabolites (Complete) data for 2,2-DICHLORO-1,1,1-TRIFLUOROETHANE (6 total), please visit the HSDB record page.

2,2-dichloro-1,1,1-trifluoroethane has known human metabolites that include Trifluoroacetaldehyde.

Absorption can be inferred from systemic effects and the elevated urinary fluoride levels seen in toxicity studies in rats. HCFC 123 has been shown to undergo metabolic transformation in rats. Covalent binding to liver protein has been demonstrated.

HCFCs: Used as refrigerants, blowing agents, cleaning agents, and fire extinguishing agents (CFC alternatives); [HSDB]

Used as a refrigerant in air conditioners, a fire extinguisher, a foam blowing agent, and a metal cleaner; [HSDB] Developed as a chlorofluorocarbon replacement; [AIHA]

Metal Degreasing [Category: Clean]

Refrigerant in low pressure chillers for air conditioning systems; in portable fire extinguishers for the fire protection industry; heat transfer agent; solvents. Refrigerant to replace CFC11 in commercial chillers and air conditioning units.

Air conditioning, fire fighting (potential application)

Chlorofluoroalkanes (and also the alternative HCFCs and HFCs) produced on an industrial scale are subject to stringent standards. Impurities must not exceed the following limits (vol %): acids, 0; moisture, <0.001; higher-boiling fractions, <0.05; and other gases, 2. /Chlorofluoroalkanes/

Common impurities reported in several samples of HCFC-123:[Table#6242]

2023: 1,000,000 - <5,000,000 lb

A small amount of HCFC-123 is produced on a small scale - several kilotons/yr. /world production/

Based on the Montreal Protocol, a virtual phase out in the production of HCFC-123 is scheduled by 2020.

Ethane, 2,2-dichloro-1,1,1-trifluoro- is listed as a High Production Volume (HPV) chemical (65FR81686). Chemicals listed as HPV were produced in or imported into the U.S. in >1 million pounds in 1990 and/or 1994. The HPV list is based on the 1990 Inventory Update Rule. (IUR) (40 CFR part 710 subpart B; 51FR21438).

Production volume for non-confidential chemicals reported under the 2006 Inventory Update Rule. Chemical: Ethane, 2,2-dichloro-1,1,1-trifluoro-. Aggregated National Production Volume: 10 to < 50 million lbs.

For more U.S. Production (Complete) data for 2,2-DICHLORO-1,1,1-TRIFLUOROETHANE (6 total), please visit the HSDB record page.

... Made by the fluorination of tetrachloroethylene with either liquid or gaseous HF.

The most important commercial method for manufacturing CFCs and HCFCs is the successive replacement of chlorine by fluorine using hydrogen fluoride. The traditional, liquid-phase process uses antimony pentafluoride or a mixture of antimony trifluoride and chlorine as catalysts. Continuous vapor-phase processes that employ gaseous hydrogen fluoride in the presence of heterogenous chromium, iron, or fluorinated alumina catalysts also are widely used. Carbon tetrachloride, chloroform, and hexachloroethane (or tetrachloroethylene plus chlorine) are commonly used starting materials for one- and two-carbon chlorofluorocarbons. The extent of chlorine exchange can be controlled by varying the hydrogen fluoride concentration, the contact time, or the reaction temperature. /CFCs and HCFCs/

Not Known or Reasonably Ascertainable

Ethane, 2,2-dichloro-1,1,1-trifluoro-: ACTIVE

SRP: The EPA has organized groups of chemicals into two classes according to their ozone-depletion potential. Class I controlled substances are those with an ozone-depletion potential of 0.2 or higher. Class II controlled substances are those with an ozone-potential of less than 0.2. Class II controlled substances are all hydrochlorofluorocarbons (HCFCs).

Class II controlled substances are compounds that have an ozone depletion potential (ODP) less than 0.2, and are all hydrochlorofluorocarbons (HCFCs). HCFCs were developed as transitional substitutes for Class I substances and are subject to a later phaseout schedule than Class I substances. ... Although there are currently 34 controlled HCFCs, only a few are commonly used. The most widely used have been HCFC-22 (usually a refrigerant), HCFC-141b (a solvent and foam-blowing agent), and HCFC-142b (a foam-blowing agent and component in refrigerant blends). ... As a Party to the Montreal Protocol, the U.S. must incrementally decrease HCFC consumption and production, culminating in a complete HCFC phaseout in 2030. The major milestones that are upcoming for developed countries are a reduction in 2010 to at least 75 percent below baseline HCFC levels and a reduction in 2015 to at least 90 percent below baseline. Section 605 of the Clean Air Act sets the U.S. phaseout targets for Class II substances. In 1993, the EPA established the phaseout framework and the "worst-first" approach that focused first on HCFC-22, HCFC-141b, and HCFC-142b because these three HCFCs have the highest ODPs of all HCFCs. To meet the required 2004 reduction, the EPA phased out HCFC-141b in 2003 and froze the production and consumption of HCFC-22 and HCFC-142b. In 2009, EPA reduced the production and import of virgin HCFC-22 and HCFC-142b and limited the use of those compounds to meet the Montreal Protocol's 2010 milestones.

The numbers in the "ODP1" column are from the Montreal Protocol. Some numbers have been updated as per amendments to the protocol. The "ODP2" column numbers are from the stratospheric ozone protection regulations at 40 CFR Part 82, as required by Title VI of the Clean Air Act amendments. These numbers include the amendments of July 18, 2003 (68 FR 42892). Data in the "ODP3" column come from WMO's /World Meteorological Organization/ Scientific Assessment of Ozone Depletion: 2006. ODP values listed are semi-empirical and can be found in Table 8-1 of the document. All GWP values represent global warming potential over a 100-year time horizon. The numbers in the "GWP1" column are from Table 1-6 of The Scientific Assessment of Ozone Depletion, 2002, a report of the World Meteorological Association's Global Ozone Research and Monitoring Project. The GWPs in the "GWP1" column that were not provided Table 1-6 of the 2002 report have not been updated since 1998 and are from The Scientific Assessment of Ozone Depletion, 1998. "GWP2" column numbers are from the Intergovernmental Panel on Climate Change Third Assessment Report: Climate Change 2001, and "GWP3" column numbers are from 40 CFR Part 82, stratospheric ozone protection regulations required by Title VI of the Clean Air Act amendments. The data in the "GWP4" column come from the IPCC Special Report on Safeguarding the Ozone Layer and the Global Climate System: Issues related to Hydrofluorocarbons and Perfluorocarbons ("SROC"). The values listed are for direct radiative forcing and can be found in Table 2.7 in the document. The numbers in the "GWP5" column come from the WMO's Scientific Assessment of Ozone Depletion: 2006. The values listed are for direct radiative forcing and can be found in Table 8-2 of the document.

EPA ensures that HCFC consumption in the U.S. is 75% below the U.S. baseline (as required under the Montreal Protocol) by issuing allowances to producers and importers of HCFCs. The "2010 HCFC Allocation Rule" allocated allowances for each year between 2010 and 2014. To meet the stepdown, the number of allowances for HCFC-22 and HCFC-142b were less than for the 2003-2009 control periods. EPA also issued allowances for HCFC-123, HCFC-124, HCFC-225ca, and HCFC-225cb. The rules also limited the use of virgin HCFC-22 and HCFC-142b to existing refrigeration and air-conditioning equipment. The "Pre-Charted Appliances Rule" banned the sale or distribution of air-conditioning and refrigeration products containing HCFC-22, HCFC-142b, or blends containing one or both of these substances, beginning January 1, 2010. ... The "2010 HCFC Allocation Rule" was challenged in the U.S. Court of Appeals for the D.C. Circuit in Arkema v EPA. In August, 2010, the court decided against EPA. EPA interprets the Court's decision as vacating the portion of the rule that establishes company-by-company production and consumption baselines and calendar-year allowances for HCFC-22 and HCFC-142b. All other aspects of the rule are intact. On August 5, 2011, EPA issued an interim final rule that establishes new company-by-company HCFC-22 and HCFC-142b baselines and allocates production and consumption allowances for 2011.