Return to 1,1-Difluoroethane
Index Page
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.
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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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