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Vinyl Fluoride
Vinyl Fluoride A Chattopadhyay, Visva-Bharati University, Santiniketan, India S Podder, North Eastern Hill University, Shillong, India Ó 2014 Elsevier Inc. All rights reserved.
Name: Vinyl fluoride Chemical Abstracts Service Registry Number: CAS 75-02-5 l Synonyms: Fluoroethene, Fluoroethylene, Monofluoroethene, Monofluoroethylene l Molecular Formula: C2H3F l Chemical Structure: l l
the environment through various waste streams. Significant exposure to VF mainly occurs by inhalation at workplaces where VF is produced or used. Skin and eye contacts among workers take place during handling of liquid VF.
Environmental Fate and Behavior H2C
F
Background Vinyl fluoride (VF) was first synthesized by Frederic Swarts, a Belgian chemist in 1901, by the reaction between zinc and 1,1-difluoro-2-bromoethane. Modern preparation involves the reaction of acetylene and hydrogen fluoride (HF) in the presence of a mercury- or aluminum-based catalyst. The US Environmental Protection Agency (EPA) listed VF as a highproduction-volume chemical in 1990. According to National Toxicology Program (NTP), 2005, the annual production of VF in the United States was above 1 million pounds (454 000 kg) in 1990 and approximately 3.3 million pounds (1.5 million kg) in 2001.
Uses Since the 1960s, VF has mainly been used in the production of polyvinyl fluoride (PVF) and other fluoropolymers. Polymers of VF have excellent resistance to degradation by sunlight, chemical attack, and water absorption and exhibit great strength, chemical inertness, and low permeability to air and water. PVF is laminated with aluminum, galvanized steel, and cellulose materials and is used as a protective surface for the exteriors of residential and commercial buildings. PVF laminated with various plastics has been used to cover walls, pipes, and electrical equipments and inside aircraft cabins. PVF is sold under the trademarks Tedlar PVF film and Dalvor. Due to increase in demand for solar panels, the demand for photovoltaic materials such as Tedlar is high, forcing the manufacturer to boost VF production.
Environmental Behavior, Fate, and Pathways At ambient temperature, VF exists as a colorless gas with a faint ethereal odor, which is highly flammable. It is slightly soluble in water, and soluble in alcohol, ether, and acetone. It polymerizes freely and forms explosive mixtures with air. It decomposes on heating to produce HF (Table 1). VF is not known to occur in the environment naturally. Industrial release of VF during its use and production may account for its presence in the environment. VF’s production and use as a prepolymer/copolymer may result in its release to
Encyclopedia of Toxicology, Volume 4
VF is expected to exist solely as a gas in the ambient atmosphere. The gas-phase of VF is degraded in the atmosphere by reaction with photochemically produced hydroxyl radicals. The half-life for this reaction in air is estimated to be 3 days as calculated from its rate constant of 5.56 1012 cm3 moleculesec1 at 25 C. VF also reacts with atmospheric ozone, leading to its atmospheric degradation (estimated half-life of about 16 days). The Henry’s Law constant of VF (0.118 atmm3 mol1) indicates that VF is expected to volatilize rapidly from water surfaces. Due to its volatile property, VF is not persistent in nature and adsorption to sediment is not considered to be a natural process for VF in water. The half-life for volatilization from a model river (1-m deep) and a model pond (2-m deep) are 2 and 23.5 h, respectively. VF is not expected to bioconcentrate in aquatic organisms as it has a bioconcentration factor (BCF) of 4.7, whereas a BCF value greater than 1000 is required for its significant bioaccumulation. As VF remains as a gas under normal conditions, it readily evaporates to the atmosphere when released into soil. When dissolved in an aqueous solution, VF is very mobile in soil. Lack of sufficient data prevents to predict its biodegradation fate in soils.
Toxicokinetics The very low solubility of VF in tissues and blood suggests that it rapidly equilibrates within the body during inhalation exposures. The saturation of VF metabolism occurs at about 75 ppm (143 mg m3) in rats. The rate of metabolism varies among the animal species as in mice, it is three times higher than in rats. VF exposure results in increased exhalation of acetone in experimental rats, which implies an inhibition of Krebs cycle by the fluoroacetate that results from VF metabolism. Fluoride (F) appears to be a metabolite of VF since it was found in the urine of VF exposed rats 6 days after exposure and its concentration in the urine was found to increase with the duration of exposure.
Mechanism of Toxicity VF is readily absorbed after administration by inhalation. Its metabolism is saturable and dose dependent. VF is metabolized via the same pathway as for other carcinogenic vinyl halides like vinyl chloride (VC) and vinyl bromide. VF is metabolized to DNA-reactive intermediates
http://dx.doi.org/10.1016/B978-0-12-386454-3.01182-9
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Vinyl Fluoride
Table 1
Important physical properties of VF
Physical properties
Values
Molecular weight Melting point Specific gravity in gaseous phase (air ¼ 1) Boiling point log P (octanol/water partition coefficient) Relative liquid density (Water ¼ 1) Water solubility (at 25 C) Vapor pressure (at 25 C) Henry’s law constant (at 25 C) Atmospheric OH rate constant (at 25 C)
46.04 g mol1 160.1 C 1.6 72.02 C 1.190 0.91 12.9 mg l1 19.8 mm Hg 0.118 atm-m3 mol1 5.56 1012 cm3 molecule-sec1
fluoroethylene oxide and fluoroacetaldehyde via a human cytochrome P450 2E1 (CYP) dependent pathway. These reactive metabolites react with DNA bases and form promutagenic DNA adducts mainly 1, N6-ethenoadenine and N2,3-ethenoguanine and cause DNA miscoding by modifying base-pairing sites. These cyclic etheno adducts lead to misincorporation of bases upon replication or transcription and cause critical lesions in VF-induced carcinogenesis. The fluoroacetaldehyde is metabolized to fluoroacetic acid, a potent inhibitor of the Krebs cycle. As a consequence, its incorporation into the citric acid cycle disrupts energy metabolism and leads to increased production of mitochondrial acetyl coenzyme A and causes excretion of ketone bodies and free F. So, administration of VF has been shown to increase acetone exhalation and F excretion in urine of experimental animals. On the other hand, fluoroacetaldehyde alkylates the prosthetic heme group of CYP resulting irreversible inactivation of the enzyme, which catalyzes the VF metabolism. The alkylate has been identified as N-(2-oxoethyl) protoporphyrin IX or green porphyrin.
Acute and Short-Term Toxicity
a concentration dependent increase of F excretion in urine was recorded. Changes in VF-induced cell proliferation were recorded at concentrations of 200, 2000, and 20 000 ppm. VF exposure at 2000 ppm for 8 h per day, on 5 days per week for 14 weeks in the newborn rats resulted in increased numbers of preneoplastic foci in liver. When rats and mice were exposed to 25, 250, or 2500 ppm VF 6 h per day, 5 days per week for up to 2 and 1.5 years, respectively, survival decreased. Again, increased urinary excretion of F with concentration and time reaching to a plaetu up to 250 ppm or more were recorded in the animals. Though no other toxic effects were seen in surviving animals, palpable masses in the region of the mammary gland were noted in the VF exposed female mice. VF was found to induce neoplastic lesions mainly as hepatic hemangiosarcomas and hepatocellular carcinomas and bronchioalveolar mammary gland adenocarcinomas in the exposed animals.
Reproductive Toxicity No reproductive organ toxicity was found in the experimental animals after VF exposure.
Animals In experimental animals, VF has very low acute toxicity through the inhalation route as in mice LC50 value after 4 h exposure is found to be 690 000 ppm. Rats exposed to 800 000 ppm for 12.5 h showed slight dyspneic symptoms which disappeared immediately after termination of the exposure.
Human Inhalation exposure to VF may cause respiratory tract irritation, headache, dizziness, unconsciousness, nausea, vomiting, and shortness of breath. Contact with liquid VF could result in burns or tissue damage particularly of skin and eyes from frostbite.
Chronic Toxicity In a 90 days study in rats and mice where animals were exposed to different concentrations of VF for 6 h per day, 5 days per week had no effects on the standard clinical signs of toxicity like body weights, food consumption, clinical observations, and toxicity end points like histopathology up to 20 000 ppm but
Genotoxicity VF is both mutagenic and clastogenic. It was found to induce gene mutations in Salmonella typhimurium with metabolic activation. In addition, VF-induced gene mutations and chromosomal aberrations in Chinese hamster ovary cells (with metabolic activation), sex-linked recessive lethal mutations in Drosophila melanogaster, and micronuclei in bone marrow cells of female mice.
Carcinogenicity VF is an inhalation carcinogen at concentrations of 25 ppm or greater in experimental animals. Structurally VF is closely related to other known vinyl halide carcinogen like VC, which causes rare tumor, hepatic hemangiosarcoma in human. Like VC, it causes the same rare tumor in experimental animals. VF inhalation resulted in increased incidences of hepatic hemangiosarcoma, hepatocellular adenoma, and zymbal gland carcinoma in the rats and hepatic hemangiosarcoma, bronchiolar-alveolar adenoma, hepatocellular adenoma, and harderian gland
Vinyl Fluoride
adenoma in mice. It also causes mammary gland adenocarcinoma in the female mice. Although no adequate human studies of the correlation between exposure to VF and human cancer were found, based on sufficient evidences of carcinogenicity from studies in experimental animals, VF was reasonably anticipated as group 2A human carcinogen. EPA has reviewed the NTP cancer assessment for VF and agreed that VF can reasonably be anticipated to cause cancer in humans.
Clinical Management Good ventilation, local exhaust, or breathing protection should be provided in the workplace. Victims should be brought to fresh air. If breathing difficulty persists, oxygen should be provided. Appropriate personal protective clothing (including cold-insulating gloves) to prevent the skin from becoming frozen from contact with the liquid or with vessels containing the liquid, as well as eye protection with safety goggles, or eye protection in combination with breathing protection should be used in the workplace. Quick drench facilities and/or eyewash fountains should be provided within the immediate work area for emergency use. After accidental exposure, affected body areas should be flushed with plenty of water. Exposed eyes should be rinsed with copious amount of water for several minutes and the patient should be provided with further treatment facility.
Ecotoxicology Since VF exists as a gas under normal ambient conditions, it limits the potential exposure to aquatic organisms. At environmentally relevant concentrations, it is likely to be of low concern for acute toxicity to algae (96 h EC50 ¼ 119.1 mg l1), invertebrates (48 h EC50 ¼ 199.7 mg l1), and fish (96 h LC50 ¼ 197.1 mg l1).
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to the minimum detectable level, with the eventual goal of zero exposure. It has recommended an exposure limit of 1 ppm (1.88 mg m3) as an 8 h time-weighted average, with an upper limit value of 5 ppm (9.4 mg m3) for short-term (15 min) exposure. VF is regulated by US EPA under the Clean Air Act to prevent accidental releases. It has a threshold reporting quantity of 10 000 lb. VF is also regulated by US EPA under the Toxic Substances Control Act. VF is considered as a hazardous material by Department of Transportation (DOT). Special requirements have been set for VF marking, labeling, and transportation by DOT.
Miscellaneous Air samples collected in polytetrafluoroethylene bags can be analyzed for VF concentrations by gas chromatography.
See also: Carcinogen Classification Schemes; Carcinogen–DNA Adduct Formation and DNA Repair; Vinyl Bromide; Vinyl Chloride.
Further Reading Barbin, A., 2000. Etheno-adduct-forming chemicals: from mutagenicity testing to tumor mutation spectra. Mutat. Res. 462, 55–69. Boivin-angele, S., Lefrancois, L., Froment, O., et al., 2000. Ras gene mutations in vinyl chloride-induced liver tumours are carcinogen-specific but vary with cell type and species. Int. J. Cancer 85, 223–227. Environment Protection Agency, 2000. Toxicological Review of Vinyl Chloride (CAS No. 75-01-4). In Support of Summary Information on the Integrated Risk Information System (IRIS). Washington, DC. Melnick, R.L., 2002. Carcinogenicity and mechanistic insights on the behavior of epoxides and epoxide-forming chemicals. Ann. N. Y. Acad. Sci. 982, 177–189. National Toxicology Program, 2011. Report on Carcinogens, twelfth ed. Research Triangle Park, NC. Available at: http://ntp.niehs.nih.gov/ntp/roc/twelfth/roc12.pdf.
Other Hazards During ozonolysis of VF, an explosive solid residue is produced, and the volatile ozonide trapped at 63 C may explode spontaneously, or during handling.
Exposure Standards and Guidelines The US National Institute for Occupational Safety and Health has recommended that exposure to vinyl halides be restricted
Relevant Websites http://cornellbiochem.wikispaces.com – Cornell Wiki: Search for Vinyl Fluoride. http://www.inchem.org – International Programme on Chemical Safety. http://ntp-server.niehs.nih.gov – National Toxicology Program. http://toxnet.nlm.nih.gov – Toxicology Date Network, National Library of Medicine.
Name: Vinyl fluoride Chemical Abstracts Service Registry Number: CAS 75-02-5 l Synonyms: Fluoroethene, Fluoroethylene, Monofluoroethene, Monofluoroethylene l Molecular Formula: C2H3F l Chemical Structure: l l
the environment through various waste streams. Significant exposure to VF mainly occurs by inhalation at workplaces where VF is produced or used. Skin and eye contacts among workers take place during handling of liquid VF.
Environmental Fate and Behavior H2C
F
Background Vinyl fluoride (VF) was first synthesized by Frederic Swarts, a Belgian chemist in 1901, by the reaction between zinc and 1,1-difluoro-2-bromoethane. Modern preparation involves the reaction of acetylene and hydrogen fluoride (HF) in the presence of a mercury- or aluminum-based catalyst. The US Environmental Protection Agency (EPA) listed VF as a highproduction-volume chemical in 1990. According to National Toxicology Program (NTP), 2005, the annual production of VF in the United States was above 1 million pounds (454 000 kg) in 1990 and approximately 3.3 million pounds (1.5 million kg) in 2001.
Uses Since the 1960s, VF has mainly been used in the production of polyvinyl fluoride (PVF) and other fluoropolymers. Polymers of VF have excellent resistance to degradation by sunlight, chemical attack, and water absorption and exhibit great strength, chemical inertness, and low permeability to air and water. PVF is laminated with aluminum, galvanized steel, and cellulose materials and is used as a protective surface for the exteriors of residential and commercial buildings. PVF laminated with various plastics has been used to cover walls, pipes, and electrical equipments and inside aircraft cabins. PVF is sold under the trademarks Tedlar PVF film and Dalvor. Due to increase in demand for solar panels, the demand for photovoltaic materials such as Tedlar is high, forcing the manufacturer to boost VF production.
Environmental Behavior, Fate, and Pathways At ambient temperature, VF exists as a colorless gas with a faint ethereal odor, which is highly flammable. It is slightly soluble in water, and soluble in alcohol, ether, and acetone. It polymerizes freely and forms explosive mixtures with air. It decomposes on heating to produce HF (Table 1). VF is not known to occur in the environment naturally. Industrial release of VF during its use and production may account for its presence in the environment. VF’s production and use as a prepolymer/copolymer may result in its release to
Encyclopedia of Toxicology, Volume 4
VF is expected to exist solely as a gas in the ambient atmosphere. The gas-phase of VF is degraded in the atmosphere by reaction with photochemically produced hydroxyl radicals. The half-life for this reaction in air is estimated to be 3 days as calculated from its rate constant of 5.56 1012 cm3 moleculesec1 at 25 C. VF also reacts with atmospheric ozone, leading to its atmospheric degradation (estimated half-life of about 16 days). The Henry’s Law constant of VF (0.118 atmm3 mol1) indicates that VF is expected to volatilize rapidly from water surfaces. Due to its volatile property, VF is not persistent in nature and adsorption to sediment is not considered to be a natural process for VF in water. The half-life for volatilization from a model river (1-m deep) and a model pond (2-m deep) are 2 and 23.5 h, respectively. VF is not expected to bioconcentrate in aquatic organisms as it has a bioconcentration factor (BCF) of 4.7, whereas a BCF value greater than 1000 is required for its significant bioaccumulation. As VF remains as a gas under normal conditions, it readily evaporates to the atmosphere when released into soil. When dissolved in an aqueous solution, VF is very mobile in soil. Lack of sufficient data prevents to predict its biodegradation fate in soils.
Toxicokinetics The very low solubility of VF in tissues and blood suggests that it rapidly equilibrates within the body during inhalation exposures. The saturation of VF metabolism occurs at about 75 ppm (143 mg m3) in rats. The rate of metabolism varies among the animal species as in mice, it is three times higher than in rats. VF exposure results in increased exhalation of acetone in experimental rats, which implies an inhibition of Krebs cycle by the fluoroacetate that results from VF metabolism. Fluoride (F) appears to be a metabolite of VF since it was found in the urine of VF exposed rats 6 days after exposure and its concentration in the urine was found to increase with the duration of exposure.
Mechanism of Toxicity VF is readily absorbed after administration by inhalation. Its metabolism is saturable and dose dependent. VF is metabolized via the same pathway as for other carcinogenic vinyl halides like vinyl chloride (VC) and vinyl bromide. VF is metabolized to DNA-reactive intermediates
http://dx.doi.org/10.1016/B978-0-12-386454-3.01182-9
939
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Vinyl Fluoride
Table 1
Important physical properties of VF
Physical properties
Values
Molecular weight Melting point Specific gravity in gaseous phase (air ¼ 1) Boiling point log P (octanol/water partition coefficient) Relative liquid density (Water ¼ 1) Water solubility (at 25 C) Vapor pressure (at 25 C) Henry’s law constant (at 25 C) Atmospheric OH rate constant (at 25 C)
46.04 g mol1 160.1 C 1.6 72.02 C 1.190 0.91 12.9 mg l1 19.8 mm Hg 0.118 atm-m3 mol1 5.56 1012 cm3 molecule-sec1
fluoroethylene oxide and fluoroacetaldehyde via a human cytochrome P450 2E1 (CYP) dependent pathway. These reactive metabolites react with DNA bases and form promutagenic DNA adducts mainly 1, N6-ethenoadenine and N2,3-ethenoguanine and cause DNA miscoding by modifying base-pairing sites. These cyclic etheno adducts lead to misincorporation of bases upon replication or transcription and cause critical lesions in VF-induced carcinogenesis. The fluoroacetaldehyde is metabolized to fluoroacetic acid, a potent inhibitor of the Krebs cycle. As a consequence, its incorporation into the citric acid cycle disrupts energy metabolism and leads to increased production of mitochondrial acetyl coenzyme A and causes excretion of ketone bodies and free F. So, administration of VF has been shown to increase acetone exhalation and F excretion in urine of experimental animals. On the other hand, fluoroacetaldehyde alkylates the prosthetic heme group of CYP resulting irreversible inactivation of the enzyme, which catalyzes the VF metabolism. The alkylate has been identified as N-(2-oxoethyl) protoporphyrin IX or green porphyrin.
Acute and Short-Term Toxicity
a concentration dependent increase of F excretion in urine was recorded. Changes in VF-induced cell proliferation were recorded at concentrations of 200, 2000, and 20 000 ppm. VF exposure at 2000 ppm for 8 h per day, on 5 days per week for 14 weeks in the newborn rats resulted in increased numbers of preneoplastic foci in liver. When rats and mice were exposed to 25, 250, or 2500 ppm VF 6 h per day, 5 days per week for up to 2 and 1.5 years, respectively, survival decreased. Again, increased urinary excretion of F with concentration and time reaching to a plaetu up to 250 ppm or more were recorded in the animals. Though no other toxic effects were seen in surviving animals, palpable masses in the region of the mammary gland were noted in the VF exposed female mice. VF was found to induce neoplastic lesions mainly as hepatic hemangiosarcomas and hepatocellular carcinomas and bronchioalveolar mammary gland adenocarcinomas in the exposed animals.
Reproductive Toxicity No reproductive organ toxicity was found in the experimental animals after VF exposure.
Animals In experimental animals, VF has very low acute toxicity through the inhalation route as in mice LC50 value after 4 h exposure is found to be 690 000 ppm. Rats exposed to 800 000 ppm for 12.5 h showed slight dyspneic symptoms which disappeared immediately after termination of the exposure.
Human Inhalation exposure to VF may cause respiratory tract irritation, headache, dizziness, unconsciousness, nausea, vomiting, and shortness of breath. Contact with liquid VF could result in burns or tissue damage particularly of skin and eyes from frostbite.
Chronic Toxicity In a 90 days study in rats and mice where animals were exposed to different concentrations of VF for 6 h per day, 5 days per week had no effects on the standard clinical signs of toxicity like body weights, food consumption, clinical observations, and toxicity end points like histopathology up to 20 000 ppm but
Genotoxicity VF is both mutagenic and clastogenic. It was found to induce gene mutations in Salmonella typhimurium with metabolic activation. In addition, VF-induced gene mutations and chromosomal aberrations in Chinese hamster ovary cells (with metabolic activation), sex-linked recessive lethal mutations in Drosophila melanogaster, and micronuclei in bone marrow cells of female mice.
Carcinogenicity VF is an inhalation carcinogen at concentrations of 25 ppm or greater in experimental animals. Structurally VF is closely related to other known vinyl halide carcinogen like VC, which causes rare tumor, hepatic hemangiosarcoma in human. Like VC, it causes the same rare tumor in experimental animals. VF inhalation resulted in increased incidences of hepatic hemangiosarcoma, hepatocellular adenoma, and zymbal gland carcinoma in the rats and hepatic hemangiosarcoma, bronchiolar-alveolar adenoma, hepatocellular adenoma, and harderian gland
Vinyl Fluoride
adenoma in mice. It also causes mammary gland adenocarcinoma in the female mice. Although no adequate human studies of the correlation between exposure to VF and human cancer were found, based on sufficient evidences of carcinogenicity from studies in experimental animals, VF was reasonably anticipated as group 2A human carcinogen. EPA has reviewed the NTP cancer assessment for VF and agreed that VF can reasonably be anticipated to cause cancer in humans.
Clinical Management Good ventilation, local exhaust, or breathing protection should be provided in the workplace. Victims should be brought to fresh air. If breathing difficulty persists, oxygen should be provided. Appropriate personal protective clothing (including cold-insulating gloves) to prevent the skin from becoming frozen from contact with the liquid or with vessels containing the liquid, as well as eye protection with safety goggles, or eye protection in combination with breathing protection should be used in the workplace. Quick drench facilities and/or eyewash fountains should be provided within the immediate work area for emergency use. After accidental exposure, affected body areas should be flushed with plenty of water. Exposed eyes should be rinsed with copious amount of water for several minutes and the patient should be provided with further treatment facility.
Ecotoxicology Since VF exists as a gas under normal ambient conditions, it limits the potential exposure to aquatic organisms. At environmentally relevant concentrations, it is likely to be of low concern for acute toxicity to algae (96 h EC50 ¼ 119.1 mg l1), invertebrates (48 h EC50 ¼ 199.7 mg l1), and fish (96 h LC50 ¼ 197.1 mg l1).
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to the minimum detectable level, with the eventual goal of zero exposure. It has recommended an exposure limit of 1 ppm (1.88 mg m3) as an 8 h time-weighted average, with an upper limit value of 5 ppm (9.4 mg m3) for short-term (15 min) exposure. VF is regulated by US EPA under the Clean Air Act to prevent accidental releases. It has a threshold reporting quantity of 10 000 lb. VF is also regulated by US EPA under the Toxic Substances Control Act. VF is considered as a hazardous material by Department of Transportation (DOT). Special requirements have been set for VF marking, labeling, and transportation by DOT.
Miscellaneous Air samples collected in polytetrafluoroethylene bags can be analyzed for VF concentrations by gas chromatography.
See also: Carcinogen Classification Schemes; Carcinogen–DNA Adduct Formation and DNA Repair; Vinyl Bromide; Vinyl Chloride.
Further Reading Barbin, A., 2000. Etheno-adduct-forming chemicals: from mutagenicity testing to tumor mutation spectra. Mutat. Res. 462, 55–69. Boivin-angele, S., Lefrancois, L., Froment, O., et al., 2000. Ras gene mutations in vinyl chloride-induced liver tumours are carcinogen-specific but vary with cell type and species. Int. J. Cancer 85, 223–227. Environment Protection Agency, 2000. Toxicological Review of Vinyl Chloride (CAS No. 75-01-4). In Support of Summary Information on the Integrated Risk Information System (IRIS). Washington, DC. Melnick, R.L., 2002. Carcinogenicity and mechanistic insights on the behavior of epoxides and epoxide-forming chemicals. Ann. N. Y. Acad. Sci. 982, 177–189. National Toxicology Program, 2011. Report on Carcinogens, twelfth ed. Research Triangle Park, NC. Available at: http://ntp.niehs.nih.gov/ntp/roc/twelfth/roc12.pdf.
Other Hazards During ozonolysis of VF, an explosive solid residue is produced, and the volatile ozonide trapped at 63 C may explode spontaneously, or during handling.
Exposure Standards and Guidelines The US National Institute for Occupational Safety and Health has recommended that exposure to vinyl halides be restricted
Relevant Websites http://cornellbiochem.wikispaces.com – Cornell Wiki: Search for Vinyl Fluoride. http://www.inchem.org – International Programme on Chemical Safety. http://ntp-server.niehs.nih.gov – National Toxicology Program. http://toxnet.nlm.nih.gov – Toxicology Date Network, National Library of Medicine.