Adverse Effects
1,1-Difluoroethane (Freon 152A)
CAS No. 75-37-6

 
 

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Activity: Propellent, US EPA List 2 Inert
Structure:

Adverse Effects:
Blood
Heart

Kidney
Mutagenic

Manufacturing/Use Information: Major Uses:

-- INTERMEDIATE

-- The preferred monomer precursor in commercial operations, 1-chloro-1,1-difluoroethane (also known as refrigerant 142b) is synthesized from 1,1-difluoroethane.

-- Refrigerant, aerosol propellant

Manufacturers:
E I duPont de Nemours & Company, Inc.
Production sites:

Chemicals and Pigments Department, Fluoro products Division, Louisville, KY 40201; Corpus Christi, TX 78400
[SRI. 1997 Directory of Chemical Producers -United States of America. Menlo Park, CA: SRI International 1997.. 549]

Methods of Manufacturing:
BY ADDING HYDROGEN FLUORIDE TO ACETYLENE.

Consumption Patterns:
Refrigerants, 39%;
Foam blowing agents, 17%;
Solvents, 14%;
Fluoropolymers, 14%;
Sterilantgas, 2%;
Aerosol propellants, 2%;
Foodfreezant, 1%;
Other, 8%;
Exports, 3%
(1985) /FLUOROCARBONS/ [CHEMICAL PROFILE: FLUOROCARBONS (1986)]

Ref: 1,1-DIFLUOROETHANE CASRN: 75-37-6. Hazardous Substance Data Bank at Toxnet.

Blood (click on for all fluorinated pesticides)

McAlack, J.W. and P.W. Schneider, Jr. 1982. Two-year inhalation study with ethane, 1,1-difluoro (FC-152a) in rats. E.I. Du Pont de Nemours and Co., Inc. Haskell Laboratory for Toxicology and Industrial Medicine. Haskell Laboratory Report No. 8-82. CD rats (30/sex/group) were exposed to 0, 2000, 10,000, or 25,000 ppm 1,1- difluoroethane (HCFC-152a) (99.88% pure) (0, 5399, 26,994, or 67,485 mg/cu.m, respectively) for 6 hours/day, 5 days/week, for 2 years (McAlack and Schneider, 1982). Duration-adjusted concentrations are 0, 964, 4821, or 12,051 mg/cu.m, respectively. Interim sacrifices were performed on 10 rats/sex/group after 3 or 12 months of exposure. The animals were exposed in 4.6-cu.m stainless steel and glass chambers using a one-pass, flow-through mode of air flow (air flow rate = 1200 L/minute). The test atmosphere was generated by diluting HCFC-152a vapor with air. The concentration of the test atmosphere was analyzed approximately every 30 minutes during each exposure period by gas chromatography, and mean chamber concentrations were found to be within 15% of nominal concentrations. Animals were observed twice daily and several times during exposure for clinical signs of toxicity and moribundity. Body weights and food consumption were measured biweekly for the first 14 weeks and monthly thereafter. Hematology, clinical chemistry, and urinalysis were conducted at 1, 3, 6, 12, 18, and 24 months on 10 rats/sex/group. Gross and microscopic evaluation of approximately 40 tissues was conducted in all animals at terminal sacrifice and in the high-concentration and control animals at the 3- and 12-month sacrifices (10 rats/sex). Kidney and nasal tissues from the low- and intermediate-concentration groups were also examined microscopically. The number of cross-sections examined in the nasal tissue ranged from three to six (Trochimowicz, 1992).
There were no statistically significant exposure-related effects on survival or body weight gain. Clinical signs noted at a higher incidence, when summed across exposure periods, in both sexes exposed to 25,000 ppm HCFC- 152a included ocular/nasal discharges and wet/stained perinea. The 25,000-ppm females also exhibited significantly elevated incidences of stained body/face. These observations suggested chronic low-level irritation or stress in the animals exposed to HCFC-152a at the highest exposure level but were not observed consistently across exposure periods or exposure levels nor supported by histopathology. Although several statistically significant hematological changes were noted, none were considered to be toxicologically significant. For example, females exposed to 10,000 and 20,000 ppm HCFC-152a exhibited increased mean corpuscular volumes, and all exposed females exhibited increased serum bilirubin; increased hematocrits and mean corpuscular volumes were seen in males exposed to 10,000 and 25,000 ppm HCFC-152a. However, hematopoietic tissues and red blood cell counts were normal in these animals, which does not support the hemolytic effect that is suggested by the changes listed above. Statistically significant reductions in eosinophils and monocytes also were observed in some of the treated groups...
Ref: US EPA IRIS for 1,1-Difluoroethane.
http://www.fluorideaction.org/pesticides/1,1-difluoroethane.epa.iris.htm

Definitions:
Eosinophil - A white blood cell that contains granules filled with chemicals damaging to parasites, and enzymes that damp down inflammatory reactions.

MONOCYTE - a large white blood cell that plays a role in immune defense by acting as a scavenger that destroys invading microorganisms. Monocytes circulate in the bloodstream; when they migrate to the tissues, they mature into macrophages.

Heart (click on for all fluorinated pesticides)

Freon 152A ... causes sensitization /of the heart/ to epinephrine in the dog. The mouse exposed to FC 152A showed bronchoconstriction, respiratory depression, and decreased compliance, but not cardiac arrhythmia. In the mouse that developed bronchitis and in the rat with pulmonary emphysema, the administration ... provoked abnormalities in the electrocardiogram. These observations were noteworthy, indicating that bronchopulmonary disease increases the cardiotoxicity to FC 152A ... [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982. 3095]
Ref: 1,1-DIFLUOROETHANE CASRN: 75-37-6. Hazardous Substance Data Bank at Toxnet.

Kidney (click on for all fluorinated pesticides)

McAlack, J.W. and P.W. Schneider, Jr. 1982. Two-year inhalation study with ethane, 1,1-difluoro (FC-152a) in rats. E.I. Du Pont de Nemours and Co., Inc. Haskell Laboratory for Toxicology and Industrial Medicine. Haskell Laboratory Report No. 8-82. CD rats (30/sex/group) were exposed to 0, 2000, 10,000, or 25,000 ppm 1,1- difluoroethane (HCFC-152a) (99.88% pure) (0, 5399, 26,994, or 67,485 mg/cu.m, respectively) for 6 hours/day, 5 days/week, for 2 years (McAlack and Schneider, 1982). Duration-adjusted concentrations are 0, 964, 4821, or 12,051 mg/cu.m, respectively. Interim sacrifices were performed on 10 rats/sex/group after 3 or 12 months of exposure. The animals were exposed in 4.6-cu.m stainless steel and glass chambers using a one-pass, flow-through mode of air flow (air flow rate = 1200 L/minute). The test atmosphere was generated by diluting HCFC-152a vapor with air. The concentration of the test atmosphere was analyzed approximately every 30 minutes during each exposure period by gas chromatography, and mean chamber concentrations were found to be within 15% of nominal concentrations. Animals were observed twice daily and several times during exposure for clinical signs of toxicity and moribundity. Body weights and food consumption were measured biweekly for the first 14 weeks and monthly thereafter. Hematology, clinical chemistry, and urinalysis were conducted at 1, 3, 6, 12, 18, and 24 months on 10 rats/sex/group. Gross and microscopic evaluation of approximately 40 tissues was conducted in all animals at terminal sacrifice and in the high-concentration and control animals at the 3- and 12-month sacrifices (10 rats/sex). Kidney and nasal tissues from the low- and intermediate-concentration groups were also examined microscopically. The number of cross-sections examined in the nasal tissue ranged from three to six (Trochimowicz, 1992). ... Urinary fluoride was increased statistically in both sexes at all concentrations, indicating metabolism of HCFC-152a. Biochemical changes (significant increases in serum creatinine in the females exposed to 10,000 and 25,000 ppm HCFC-152a), increased urine volume, and decreased urine osmolality seen throughout the study suggested renal toxicity. The only organ weight or histopathology data to support this functional deficit was decreased kidney weight and renal tubular damage noted in the high-concentration animals at the 3-month sacrifice. The tubular lesions were reported in the original report as "slight cytoplasmic vacuolation, luminal dilation, and the presence of occasional vesiculated nuclei" and were seen in 4/10 males and 7/10 females. These changes were not seen at the other scheduled evaluations, however, and a subsequent peer review of these data (Bruner, 1992) determined that the renal tubular changes reported at the 3-month sacrifice were artifactual changes due to tissue processing rather than a treatment-related nephrotoxicity.
Ref: US EPA IRIS for 1,1-Difluoroethane.
http://www.fluorideaction.org/pesticides/1,1-difluoroethane.epa.iris.htm

Mutagenic (click on for all fluorinated pesticides)

Genetron 23, and Genetron-152A [synonym] exposure increased the mutation rate in progeny of Drosophila melanogaster. Genetron-23 appeared to be more mutagenic. Pronounced phenotypic effects were observed among progeny of exposed males. Part of the observed mutagenic effects of fluorinated hydrocarbon gases may be due to anoxia.
[Foltz VC, Fuerst R; Environ Res 7: 275-85 (1974)]
Ref: Hazardous Substances Data Bank for 1,1-Difluoroethane at Toxnet
http://toxnet.nlm.nih.gov/

 
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