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Dichlorodifluoromethane (CAS No. 75-71-8). Profile from Hazardous Substances Data Bank
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DICHLORODIFLUOROMETHANE
Human Health Effects:
Human Toxicity Excerpts:
... FATAL CASE OF BRONCHOPNEUMONIA /REPORTED/ IN MAN WHO PUNCTURED FREEZING
COIL OF REFRIGERATOR CONTAINING FC-12. IT IS PROBABLE THAT HE ASPIRATED COLD
CONCENTRATED VAPOR OR LIQ, OR WAS EXPOSED TO DEGRADATION PRODUCTS OF REFRIGERANT
CMPD.
... IF INHALED AT 5% BY VOL CONCN INDUCES DIZZINESS IN MAN. IF INHALED AT
15% CONCN, LOSS OF CONSCIOUSNESS RESULTS.
STUDIES ON ... VOLUNTEERS SHOWED THAT INHALATION OF 10,000 PPM OF FC12 FOR
2.5 HR CAUSES 7% REDUCTION IN STANDARDIZED PSYCHOMOTOR SCORES. AT CONCN OF 1000
PPM FOR 8 HR/DAY, 5 DAYS/WK FOR TOTAL OF 17 REPETITIVE EXPOSURES, THERE WERE
NO UNTOWARD SUBJECTIVE RESPONSES & NO ABNORMAL PHYSIOLOGICAL RESPONSES OF
LUNGS OR HEART. CONCN AS HIGH AS 27,000 PPM OF FC12 FOR 15 TO 60 SEC CAUSED
INCR IN AIRWAY RESISTANCE & ELECTROCARDIOGRAPHIC CHANGES.
In brief exptl exposures of humans to F-12 at 198x10+3 mg/cu m vapor concn
in air, tingling sensation, humming in the ears, apprehension, EEG and speech
changes, and deficits in psychological performance were reported. In other test
exposures ... 49x10+3 to 543x10+3 mg/cu m caused cardiac arrhythmia, decreased
consciousness, and amnesia or deficits in performance on psychomotor test scores.
... Women using fluorocarbon-propellant /incl F-12/ aerosol products and receiving
nine or ten times the exposure from normal use /showed/ ... no measureable blood
levels of the fluorocarbons or abnormalities in overall health, respiratory,
or hematologic parameters.
Refrigeration repair workers may be intermittently exposed to fluorocarbons
and their thermal decomposition products. A case of peripheral neuropathy (distal
axonopathy) in a commercial refrigeration repairman prompted an epidemiological
investigation of the health of refrigeration repair workers. No additional cases
of peripheral neuropathy were identified among the 27 refrigeration repair workers
studied. A reference group of 14 non-refrigeration repair workers was also studied.
No differences were noted between groups for the ulnar (motor and sensory),
median (motor and sensory), peroneal, sural, or tibial nerve conduction velocities.
Refrigeration repair workers reported palpitations and lightheadedness significantly
more often than workers in the reference group. No clinical neurological or
electroneurophysiological abnormalities were detected in eight refrigeration
repair workers followed up for three years during continuous employment.
/UV-B Radiation is likely to incr by ozone depletion caused by atmospheric
concentrations of chlorofluorocarbons/. Indications are increasing that UV-B
radiation ... plays a role in the induction and growth of cutaneous melanomas,
a ... dangerous type of skin cancer. ... There are indications that ... suppression
of the immune response by UV-B radiation may occur in humans. The antigen presenting
Langerhans cells in the skin are damaged and allergic responses are depressed.
... There are indications that UV-B radiation increases cataract formation,
an important cause of blindness especially in areas with limited medical facilities.
/Chlorofluorocarbons/
Many gases emitted as a result of industrial and agricultural activities can
accumulate in the earth's atmosphere and ultimately contribute to alterations
in the vertical distribution and concentrations of stratospheric ozone. Among
the most important are those trace gases that have long residence times in the
atmosphere. This allows accumulation in the troposphere and a gradual upward
migration of the gases into the stratosphere where they contribute to depletion
of stratospheric ozone layer. The atmospheric and chemical processes involved
are extremely complex. Trace gases of particular concern include certain long
lived chlorofluorocarbons, such as CFC-11, CFC-12, and CFC-113. Since the transport
of these gases to the stratosphere is slow, their residence times there are
long, and the removal processes are slow, any effect on stratospheric ozone
already seen is probably the result of anthropogenic emissions of these gases
several decades ago. Those gases already in the atmosphere will continue to
exert stratospheric ozone depletion effects well into the next century. /Chlorofluorocarbons/
Increased UV-B radiation would be expected to increase photochemical smog,
and this would aggravate the related health problems in urban and industrialized
areas. /UV-B Radiation/
Deaths resulting from cardiovascular collapse after arrhythmias have been
reported after inhalation of Freons 11 and 12.
This study attempted to determine whether exposure to the fluorocarbons chlorodifluoromethane
or dichlorodifluoromethane during refrigerator repair caused cardiac arrhythmias.
Six repair workers and six plumbers (comparisons) served as study subjects.
They kept diaries about their daily activities including exposure to fluorocarbons,
physical activity, traffic, meals, smoking, and drinking. Ambulatory electrocardiograms
were taken for 24 hours on a day of work exposure and on a comparison day. No
cardiac arrhythmias were found to be clearly connected with exposure to fluorocarbons.
One subject had several ventricle ectopic beats and a connection with exposure
cannot be totally excluded in this worker. Ventricle ectopic beats were somewhat
more common in the refrigerator repair workers than in the plumbers. The number
of ventricle ectopic beats was low, however, when compared with what is known
of ventricle ectopic beats in the normal heart. The average concentrations of
fluorocarbons during work were 170 to 815 cu cm/cu m and the peak concentrations
were 1300 to 10,000 cu cm/ cu m. In two instances the concentrations remained
over 1000 cu cm/cu m for 30 minutes.
A 68 year old man suffered minor burns of both arms and the chest but not
the mouth when he punctured the freezing coil of a refrigerator with an ice
pick, thus releasing dichlorodifluoromethane. His clinical course was characterized
by severe progressive shock, spiking fever, and death in 96 hr. Autopsy revealed
bronchopneumonia and histological changes in the small bronchi thought to represent
the effects of degradation products of the compound and of preexisting degenerative
disease.
Inhalation of Freon compounds at moderate concentrations initially produces
CNS anesthetic effects of intoxication and loss of psychomotor coordination.
In humans, this effect occurred at levels of 2500 ppm for Freon 113 and 10,000
ppm for Freon 12. Higher concentrations produce marked in coordination, slurring
of speech, apprehension, and finally descreasing levels of consciousness. Attendent
hypoxia at high concentrations may also produce tremors, convulsions, and cerebral
edema. Cardiac sensitization occurs at higher concentrations than initial CNS
intoxication.
The effects of CFC-11 and CFC-12 on human volunteers under controlled conditions
/were characterized/. A number of biological end-points, including clinical
hematology and chemistry, ECG, EEG, pulmonary function, neurological parameters,
and cognitive tests were monitored. Single exposures to CFC-11 or CFC-12 at
concentrations of 0.025% (CFC-11, 1.4 g/cu m, CFC-1, 1.2 g/cu m), 0.05% (CFC-11,
2.8 g/cu m, CFC-123, 2.5 g/cu m), and 0.1% (CFC-11, 5.6 g/cu m, CFC-12, 5 g/cu
m, for 1 min to 8 hr, induced no observable effects. There was a statistically-significant
decrease in cognitive test performance in subjects exposed to CFC-11 at 5.6
g/cu m, 8 hr/day, 5 days/week, for 2-4 weeks, but not in subjects exposed to
CFC-12 at 5 g/cu m.
In another study, 11 subjects (7 being maintenance technicians of large cooling
and refrigerating systems) were exposed for 130 min to CFC-12 (weighted exposure
0.46, 49.9, and 87.7 g/cu m. ... This led to acute reduction of ventilatory
lung capacity only at the two highest CFC-12 concentrations, under which conditions
a significant decrease in the heart frequency was also observed.
Ten subjects /were exposed/ to CFC-11, CFC-12, CFC-114, two mixtures of CFC-11
and CFC-12, and a mixture of CFC-12 and CFC-114 (breathing concentrations between
16 and 150 g/cu m) for 15, 45, or 60 seconds, and found significant acute reduction
of ventilatory lung capacity (FEV50, FEF25) on exposure to each chlorofluorocarbon,
as well as bradycardia and increased variability in heart rate in seven subjects,
negative T-waves in two subjects (one was exposed to CFC-11 and CFC-12), and
atrioventricular block in 1 subject (CFC-114). Mixtures exerted stronger respiratory
effects than individual chlorofluorocarbon at the same level of exposure.
Allergic contact eczema /was reported/ in patch tests performed on three patients
that had a prior history of skin reactions to deodorant sprays. All three patients
showed strong positive reactions to 11 deodorant sprays and mild to strong reactions
to CFC-11. One patient showed a mild reaction to CFC-12. Fifteen controls (without
prior history of allergy to deodorants) showed no response to either CFC-11
or CFC-12. These results suggest that individuals may become sensitized to certain
chlorofluorocarbons applied repeatedly to the skin surface.
Effects of chlorofluorocarbons on bronchiolar tone in asthmatic children /were
studied/. Forced expiratory volume, a measure of bronchial tone, was measured
in 18 children with a history of asthma, before and after inhaling aerosols
of the B2-receptor agonist, fenoterol, or a mixture of CFC-11, CFC-12, and CFC-114,
and in the absence of treatment. The levels of exposure were not reported. Exposure
to the chlorofluorocarbon mixture significantly reduced forced expiratory volume
for 2 hr, relative to "no treatment", and for 8 hr relative to exposure to fenoterol
(containing CFC-11 and CFC-12). The results suggest that chlorofluorcarbons
can decrease bronchial tone in asthmatic patients, but that this effect is transient
and of a sufficiently small magnitude to be superseded by the dilating effects
of fenoterol when both fenoterol and chlorofluorcarbon propellants are inhaled
together.
Death rates among 539 workers exposed occupational in constructing and repairing
refrigeration equipment. The chlorofluorocarbons used were CFC-12, HCFC-22,
and CFC-502 (a mixture of CFC-115 and HCFC-22). No increase in total deaths
(18 cases) was seen among those employed more than 6 months, compared to the
expected number (26 cases), nor was there any statistically significant increase
in total tumor deaths or deaths caused by lung cancer or cardiovascular diseases.
When the study was restricted to those exposed for more than 3 or 10 years,
still no significant increases were see. No data on exposure levels were given.
Eighty nine workers were examined during their work with refrigerant equipment.
The refrigerants used were mainly CFC-12 (in 56% of the cases) and HCFC-22 (32%),
the rest being CFC-11, CFC-500 (a mixture of CFC-12 and HCFC 152a), CFC-502
( a mixture of CFC-115 and HCFC 22). The mean exposure time was 10 min. Chlorofluorocarbon
concentrations in the breathing zone were measured for each person individually.
The levels exceeded 750 ppm at least once (as one minute mean values) for 60
of the 89 individuals. Cardiac arrhythmias were registered before, during, and
after the exposure by means of a portable ECG instrument connected to a tape
recorder. No statistically significant difference was found between exposed
and nonexposed period, nor was there any dose-related trend for different individuals
when grouped into different exposure groups. In this study, possible effects
on the central nervous system were also studied by means of simple reaction
time measurements before and after the exposure. No impairment was seen.
Occasionally liquid or gaseous F12 sprays unexpectedly from a pressurized
container or a refrigeratory into a person's eyes, but no significant injuries
from this source are reported. Because of the speed of reflex closure of the
eyes, it seems extremely unlikely that any serious injury would result from
an accidental spray of F-12 in the eyes of conscious or unanesthetized human
beings.
Five percent is said to induce dizziness.
Ordinary occupational and domestic exposure to the gas causes neither ocular
nor respiratory irritation.
Propellant /fluorocarbon/ gases were generated from commercial aerosol units
and applied to the from distance of 50 cm for periods of 15 to 60 sec. At a
measured concn of 95,000 mg/cu m (1700 ppm), there was a biphasic change in
ventilation capacity, the first reduction occurring within a few minutes after
exposure, and second delayed until 13 to 30 min after exposure, and second delayed
until 13 to 30 min after exposure. Most subjects developed bradycardia, and
inversion of the T-wave. /Propellant gases/
EXCESSIVE SKIN CONTACT WITH LIQ FLUOROCARBONS SHOULD BE MINIMIZED TO PREVENT
DEFATTING OF SKIN ... /FLUOROCARBONS/
... The combination of CFC with a sympathomimetic bronchodilator is potentially
dangerous for the treatment of bronchial asthma. For the same reason, sympathomimetic
drugs are contraindicated in cardiac resuscitation of patients suffering from
CFC poisoning. /Fluorocarbon poisoning/
Fluorocarbon vapors are 4 to 5 times heavier than air. Thus high concn tend
to accumulate in low-lying areas, resulting in hazard of inhalation of concentrated
vapors, which may be fatal. /Fluorocarbons/
Under certain condition, fluorocarbon vapors may decompose on contact with
flames or hot surfaces, creating potential hazard of inhalation of toxic decomposition
products. /Fluorocarbons/
EARLY ... HUMAN EXPERIENCE INDICATED THAT HIGH VAPOR CONCN (EG, 20%) MAY CAUSE
CONFUSION, PULMONARY IRRITATION, TREMORS & RARELY COMA, BUT THAT THESE EFFECTS
WERE GENERALLY TRANSIENT & WITHOUT LATE SEQUELAE. ... CAUSE OF DEATH /FROM
ABUSE OF FLUOROCARBONS/ IS IN CONSIDERABLE DOUBT. FREEZING OF AIRWAY SOFT TISSUES
CAN PROBABLY BE ELIMINATED AS A CAUSE OF DEATH EXCEPT IN CASES WHERE THE PRODUCT
WAS SPRAYED DIRECTLY INTO THE MOUTH FROM ITS CONTAINER OR FROM A BALLOON CONTAINING
SOME LIQUID. LARYNGEAL SPASM OR EDEMA, OXYGEN DISPLACEMENT, OR SENSITIZATION
OF MYOCARDIUM TO ENDOGENOUS CATECHOLAMINES WITH SUBSEQUENT VENTRICULAR FIBRILLATION
APPEAR TO BE REASONABLE POSSIBILITIES. /FLUOROCARBON REFRIGERANTS & PROPELLANTS/
Aerosol sprays containing fluorocarbon propellants are another source of solvent
intoxication. Prolonged exposure or daily use may result in damage to several
organ systems. Clinical problems include cardiac arrhythmias, bone marrow depression,
cerebral degeneration, and damage to liver, kidney, & peripheral nerves.
Death occasionally has been attributed to inhalant abuse, probably via the mechanism
of cardiac arrhythmias, especially accompanying exercise or upper airway obstruction.
/Fluorocarbon propellants/
A SPECIAL CLASS OF CHEMICALS SUBJECT TO ABUSE BY INHALATION ARE THE FLUOROHYDROCARBONS
... THE "SNIFFING" OF SUCH AEROSOL SPRAYS IS HAZARDOUS PRACTICE. ... 110 "SUDDEN
SNIFFING DEATHS" /HAVE BEEN IDENTIFIED/ ... IN EACH CASE THE VICTIM SPRAYED
THE AEROSOL INTO A PLASTIC BAG, INHALED THE CONTENTS, BECAME EXCITED, RAN 90
M OR SO, COLLAPSED, & DIED. NECROPSY FINDINGS WERE LARGELY NEGATIVE ...
ALTHOUGH AMOUNT OF PROPELLANT ABSORBED INTO BLOOD FROM USE OF HAIRSPRAY, COSMETIC,
HOUSEHOLD, & MEDICATED AEROSOLS MUST VARY WITH CIRCUMSTANCES, PHYSICIAN
IS ADVISED TO COUNSEL ... PATIENT ON POTENTIAL DANGERS, PARTICULARLY FROM THEIR
USE IN POORLY VENTILATED CONFINED AREAS. IT IS POSSIBLE THAT PATIENTS WITH CARDIAC
OR RESPIRATORY DISORDERS MAY PROVE ESPECIALLY SUSCEPTIBLE. /FLUOROHYDROCARBONS/
Fluorocarbons were initially believed to be compounds low in toxicity. In
the late 1960s there were early reports of deaths caused by intentional inhalation
abuse of various aerosols. Victims frequently discharged the aerosol contents
into a plastic bag and then inhaled the gaseous contents. Suffocation was initially
considered to be the cause of death. In 1970, 110 cases of "sudden sniffing
death" /were reviewed/ without finding evidence of suffocation. The majority
of those deaths (59) involved fluorocarbon propellants. He noted that in several
cases sudden death followed a burst of emotional stress or exercise. No significant
findings were noted at autopsy. /Fluorocarbons/
Fluorocarbon propellants are anesthetic and cardiotoxic. ... Aerosol propellants
produce hallucinogenic effects, and, rarely, contact dermatitis. /Fluorocarbon
propellants/
Fluorocarbon propellants, benzene, 1,1,1-trichloroethane, gasoline, toluene,
and hydrocarbons have been implicated in 110 sudden deaths after inhalant abuse
in which no obvious cardiac or pulmonary pathology existed. Heavy exercise or
stress was associated with 18 of those deaths, /it was/ proposed that these
inhalants act to sensitize the myocardium to endogenous catecholamines. Hypoxia,
hypercarbia, and acidosis may exacerbate these effects. /Fluorocarbon propellants/
Chlorinated hydrocarbons may cause systemic toxicity through percutaneous
absorption. Systemic toxicity includes convulsion, delirium, and central nervous
system depression /From table/. /Chlorinated hydrocarbons/
There are isolated reports of poisoning from exposure to refrigerants and
solvents, and some studies showing a higher incidence of coronary heart disease
among hospital personnel are required to establish causal relationship between
fluorine containing organic compounds, and cardiovascular and bronchopulmonary
diseases among exposed workers. The high incidence of cancer among hospital
personnel repeatedly exposed to fluorine-containing general anesthetics raises
a fundamental need to examine other chlorofluorocarbon-exposed workers for similar
effects. /Fluorocarbons/
Clinical pathologists exposed to fluorocarbons in the preparation of frozen
tissue sections have been seen to develop coronary heart disease. /Fluorocarbons/
There is undisputed evidence that the atmospheric concentrations of chlorofluorocarbons
deplete ozone in the stratosphere. A reduction in ozone concentration will result
in increased transmission of solar ultraviolet radiation through the stratosphere.
Many significant adverse effects of such an increase in exposure to this radiation
have been identified. ... One of the most well-defined human health effects
resulting from stratospheric ozone depletion is an increase in the frequency
of skin cancer expected as a result of even small increases in UV-B radiation
(280-320 nm) reaching the earhs's surface. /Chlorofluorocarbons/
Freons are toxic to humans by several mechanisms. Inhaled fluorocarbons sensitized
the myocardium to catecholamines, frequently resulting in lethal ventricular
arrhythmias. Because they are gases heavier than air, fluorocarbons can displace
atmospheric oxygen, thus resulting in asphyxiation. These compounds also have
a central nervous system (CNS) anesthetic effect analogous to a structurally
similar general anesthetic, halothane. Pressurized refrigerant or liquid fluorocarbons
with a low boiling point have a cryogenic effect on exposed tissues, causing
frostbite, laryngeal or pulmonary edema, and gastrointestinal perforation. Certain
fluorocarbons degrade at high temperatures into toxic products of chlorine,
hydrofluoric acid, or phosgene gases. /Freons/
... HIGH VAPOR CONCN (EG, 20%) MAY CAUSE CONFUSION, PULMONARY IRRITATION,
TREMORS & RARELY COMA ... BUT ... THESE EFFECTS WERE GENERALLY TRANSIENT
& WITHOUT LATE SEQUELAE. /FLUOROCARBON REFRIGERANTS & PROPELLANTS/
Non-occupational exposure and accidental or abusive inhalation of aerosols
/due to Fluorocarbon propellants/ have also been documented, the main symptoms
being CNS depression and cardiovascular reactions. Cardiac arrhythmia, possibly
aggravated by elevated levels of catecholamines due to stress or by moderate
hypercapnia, is suggested as the cause of these adverse response, which may
lead to death. /Aerosols/
Manufacturing processes use hydrofluoric acid from fluorospar in the production
of most fluorine containing organic compounds. Some processes use carbon tetrachloride
from carbon disulfide or as a co product of perchloroethylene and chlorination
of propylene, or chloroform from chlorination of methanol. The major hazards
relate primarily to the inadvertent release of hydrofluoric acid or carbon tetrachloride,
rather than to the manufactured final product. /Fluorocarbons/
... CAUSE OF DEATH /FROM ABUSE OF FLUOROCARBONS/ IS IN ... DOUBT. FREEZING
OF AIRWAY SOFT TISSUES CAN PROBABLY BE ELIMINATED ... EXCEPT IN CASES WHERE
PRODUCT WAS SPRAYED DIRECTLY INTO MOUTH FROM CONTAINER OR BALLOON CONTAINING
SOME LIQ. /FLUOROCARBON REFRIGERANTS & PROPELLANTS/
... CAUSE OF DEATH /FROM ABUSE OF FLUOROCARBONS/ ... IN ... DOUBT. ... LARYNGEAL
SPASM OR EDEMA, OXYGEN DISPLACEMENT, OF SENSITIZATION OF MYOCARDIUM TO ENDOGENOUS
CATECHOLAMINES WITH ... VENTRICULAR FIBRILLATION APPEAR TO BE ... POSSIBILITIES.
/FLUOROCARBON REFRIGERANTS & PROPELLANTS/
The toxicity of Chlorofluorocarbons (CFCs) had been considered to be low;
it is absorbed via the lungs and undergoes little subsequent biotransformation.
In the United States when sudden unexplained deaths of aerosol "sniffers" were
reported they were considered to be possibly due to cardiac arrhythmias induced
by the CFC propellants. /CFCs/
Speizer and coworkers reported that pathology personnel exposed to FC-22 and
FC-12 /dichlorodifluoromethane/ while preparing frozen sections had a greater
prevalence of palpitations than an unexposed control group; ... Continuous electrocardiographic
(EKG) monitoring of several exposed subjects in the course of their work showed
multiple arrhythmias.
Studies on two human volunteers who inhaled CFC-12 at 10,000 ppm for 2.5 hours
showed a 7% reduction in a standardized psychomotor test score but no other
adverse effects.
Blood levels of CFC-12 were below detection limits in normal subjects using
household aerosols; in asthmatic subjects using an aerosol inhaler, blood levels
were much lower than in dogs exposed at the threshold for cardiac sensitization.
Radiolabeled tests showed essentially all the dose of CFC-12 (95%-103%) exhaled
within the first hour after a 12 or 17 minute inhalation at 1000 ppm.; total
metabolites were <0.2% of the administered dose. At 30 minutes, retention
of the labeled dose inhaled in a single breath was 10% versus 23%, 20%, &
12% for comparable doses of trichlorofluoromethane (FC-11), 1,1,2-trichloro-1,2,2-trifluoroethane
(FC-113), & 1,2-dichloro-1,1,2,2-tetrafluoroethane (FC-114), respectively.
For an 8 hr inhalation at 1000 ppm, a pharmacokinetic model based on analyses
in dogs & humans gave an estimate of 55% absorption of the inhaled CFC-12.
This dose would result in roughly 1/20th the blood level required to sensitize
dogs also receiving the stress of IV epinephrine.
Following exposure to CFC-12 at a concentration of 1% (50 g/cu m) for 150
min, a 7% decrease in psychomotor test scores was noted, but no effects were
observed at 0.1% (5 g/cu m).
Medical Surveillance:
Employees should be screened for history of certain medical conditions ...
which might place the employee at increased risk from dichlorodifluoromethane
exposure. Cardiovascular disease: In persons with impaired cardiovascular function,
especially those with a history of cardiac arrhythmias, the inhalation of dichlorodifluoromethane
might cause exacerbation of disorders of the conduction mechanism due to its
sensitizing effects on the myocardium. ... Any employee developing the above-listed
conditions should be referred for further medical examination.
Populations at Special Risk:
Employees /with cardiovascular disease are/ at increased risk.
IT IS POSSIBLE THAT PT WITH CARDIAC OR RESP DISORDERS MAY PROVE ESP SUSCEPTIBLE.
/FLUOROCARBONS/
Probable Routes of Human Exposure:
NIOSH (NOES Survey 1981-1983) has statistically estimated that 435,098 workers
(125,602 of these are female) are potentially exposed to dichlorodifluoromethane
in the US(1). Occupational exposure may be through inhalation and dermal contact
with this compound at workplaces where dichlorodifluoromethane is still used,
such as air conditioning repair shops(SRC). This survey was conducted prior
to the Montreal Protocol which scheduled the production phase-out of this compound
and other chlorofluorocarbons, and is not an accurate measure of the current
occupational exposure(SRC). Due to its long atmospheric residence time, the
general population may be exposed to dichlorodifluoromethane via inhalation
of ambient air(SRC).
Body Burden:
In a pilot study of pollutants in the milk of women living in 4 urban-industrial
areas in the US, dichlorodifluoromethane was identified, not quantified, in
2 of 8 samples(1).
Emergency Medical Treatment:
Emergency Medical Treatment:
| EMT Copyright Disclaimer: |
| Portions of the POISINDEX(R) database are provided here for
general reference. THE COMPLETE POISINDEX(R) DATABASE, AVAILABLE FROM MICROMEDEX,
SHOULD BE CONSULTED FOR ASSISTANCE IN THE DIAGNOSIS OR TREATMENT OF SPECIFIC
CASES. Copyright 1974-1998 Micromedex, Inc. Denver, Colorado. All Rights
Reserved. Any duplication, replication or redistribution of all or part
of the POISINDEX(R) database is a violation of Micromedex' copyrights and
is strictly prohibited.
The following Overview, *** FLUORINATED HYDROCARBONS ***, is relevant for this HSDB record chemical. |
| Life Support: |
o This overview assumes that basic life support measures
have been instituted.
|
| Clinical Effects: |
SUMMARY OF EXPOSURE
0.2.1.1 ACUTE EXPOSURE
o LOW CONCENTRATION - Inhalations such as those caused by
leaking air conditioners or refrigerators usually
result in transient eye, nose, and throat irritation.
Palpitations, light headedness, and headaches are also
seen.
o HIGH CONCENTRATION - Inhalation associated with
deliberate abuse, or spills or industrial use occurring
in poorly ventilated areas has been associated with
ventricular arrhythmias, pulmonary edema and sudden
death.
HEENT
0.2.4.1 ACUTE EXPOSURE
o EYES - Eye irritation occurs with ambient exposure.
Frostbite of the lids may be severe. Ocular
instillation results in corneal burns in rabbits.
o NOSE - Nasal irritation occurs with ambient exposure.
o THROAT - Irritation occurs. Frostbite of the lips,
tongue, buccal mucosa and hard palate developed in a
man after deliberate inhalation.
CARDIOVASCULAR
0.2.5.1 ACUTE EXPOSURE
o Inhalation of high concentrations is associated with
the development of refractory ventricular arrhythmias
and sudden death, believed to be secondary, primarily,
to myocardial sensitization to endogenous
catecholamines. Some individuals may be susceptible to
arrhythmogenic effects at lower concentrations.
RESPIRATORY
0.2.6.1 ACUTE EXPOSURE
o Pulmonary irritation, bronchial constriction, cough,
dyspnea, and chest tightness may develop after
inhalation. Chronic pulmonary hyperreactivity may
occur. Adult respiratory distress syndrome has been
reported following acute inhalational exposures.
Pulmonary edema is an autopsy finding in fatal cases.
NEUROLOGIC
0.2.7.1 ACUTE EXPOSURE
o Headache, dizziness, and disorientation are common.
Cerebral edema may be found on autopsy. A syndrome of
impaired psychomotor speed, impaired memory and
learning, and emotional lability has been described in
workers with chronic occupational exposure to
fluorinated hydrocarbons.
GASTROINTESTINAL
0.2.8.1 ACUTE EXPOSURE
o Nausea may develop. Ingestion of a small amount of
trichlorofluoromethane resulted in necrosis and
perforation of the stomach in one patient.
HEPATIC
0.2.9.1 ACUTE EXPOSURE
o Jaundice and mild elevations in transaminases may
develop after inhalational exposure or ingestion.
Hepatocellular coagulative necrosis has been observed
on liver biopsy.
DERMATOLOGIC
0.2.14.1 ACUTE EXPOSURE
o Dermal contact may result in defatting, irritation or
contact dermatitis. Severe frostbite has been reported
as an effect of freon exposure. Injection causes
transient pain, erythema and edema.
MUSCULOSKELETAL
0.2.15.1 ACUTE EXPOSURE
o Rhabdomyolysis has been reported in a worker
susceptible to malignant hyperthermia after exposure to
fluorinated hydrocarbons and also following intentional
freon inhalation. Compartment syndrome is a rare
complication of severe exposure.
REPRODUCTIVE HAZARDS
o Dichlorodifluoromethane was not teratogenic in rats and
rabbits.
o The reproductive effects of 1,1,1,2-tetrafluoroethane
were studied in rats. No adverse effects on
reproductive performance was noted or on the
development, maturation or reproductive performance of
up to two successive generations.
GENOTOXICITY
o The hydrochlorofluorocarbons, HCFC-225ca and HCFC-225cb,
were not mutagenic in the Ames reverse mutation assay,
or clastogenic in the chromosomal aberration assay with
Chinese hamster lung cells. Neither induced unscheduled
DNA synthesis in liver cells. Both of these agents were
clastogenic in the chromosomal aberration assay with
human lymphocytes.
|
| Laboratory: |
o Fluorinated hydrocarbons plasma levels are not clinically
useful.
o No specific lab work (CBC, electrolyte, urinalysis) is
needed unless otherwise indicated.
o Obtain baseline pulse oximetry or arterial blood gas
analysis.
|
| Treatment Overview: |
SUMMARY EXPOSURE
o Monitor EKG and vital signs carefully. Cardiopulmonary
resuscitation may be necessary.
ORAL EXPOSURE
o These substances may cause frostbite to the upper airway
and gastrointestinal tract after ingestion. Administer
oxygen and manage airway as clinically indicated.
Emesis, activated charcoal, and gastric lavage are not
recommended.
INHALATION EXPOSURE
o MONITOR ECG and VITAL SIGNS carefully. Cardiopulmonary
resuscitation may be necessary. AVOID CATECHOLAMINES.
o PROVIDE A QUIET CALM ATMOSPHERE to prevent adrenaline
surge if the patient is seen before the onset of cardiac
arrhythmias. Minimize physical exertion.
o MONITOR pulse oximetry or arterial blood gases.
o Provide symptomatic and supportive care.
o These substances may cause frostbite of the upper airway
with the potential for severe edema. Administer oxygen
and manage airway early in patients with evidence of
upper airway injury.
o PULMONARY EDEMA (NONCARDIOGENIC): Maintain ventilation
and oxygenation and evaluate with frequent arterial
blood gas or pulse oximetry monitoring. Early use of
PEEP and mechanical ventilation may be needed.
EYE EXPOSURE
o DECONTAMINATION: Irrigate exposed eyes with copious
amounts of tepid water for at least 15 minutes. If
irritation, pain, swelling, lacrimation, or photophobia
persist, the patient should be seen in a health care
facility.
o Ophthamologic consultation should be obtained in any
symptomatic patients.
DERMAL EXPOSURE
o DECONTAMINATION: Remove contaminated clothing and wash
exposed area thoroughly with soap and water. A
physician may need to examine the area if irritation or
pain persists.
o If frostbite has occurred, refer to dermal treatment in
the main body of this document for rewarming.
|
| Range of Toxicity: |
o Freons are very toxic when inhaled in high concentrations
and/or for extended periods. At lower concentrations or
brief exposure, freons may cause transient eye, nose, and
throat irritation. There is significant interpatient
variation and it is difficult to predict which patient
will exhibit symptoms following exposure.
|
Antidote and Emergency Treatment:
Treatment is entirely symptomatic.
... Emergency treatment is supportive and includes decontamination, oxygen,
and any specific therapy required in a particular case such as antiarrhythmics
or anticonvulsants. A few patients may require intermittent positive-pressure
ventilation, dialysis, or treatment for hepatic failure. /Solvent abuse/
... In persons who are intoxicated with fluorocarbons, steps can be taken
to lessen the risk of arrhythmias. ... Before evaluation at the hospital, patients
should be advised to avoid strenuous exercise. In the hospital, patients can
be placed in a quiet, nonthreatening environment and sedated if necessary. If
hypoxic, oxygen should be administered and metabolic abnormalities corrected.
Sympathomimetic drugs should be avoided. Ventricular arrhythmias are best treated
with beta-blocking agents. /Fluorocarbons/
Patients with fluorohydrocarbon poisoning should not be given epinephrine
(Adrenalin) or similar drugs because of the tendency of fluorohydrocarbon to
induce cardiac arrhythmia, including ventricular fibrillation. /Fluorohydrocarbons/
Victims of Freon inhalation require management for hypoxic, CNS anesthetic,
and cardiac symptoms. Patients must be removed from the exposure environment,
and high-flow supplemental oxygen should be utilized. The respiratory system
should be evaluated for injury, aspiration, or pulmonary edema and treated appropriately.
CNS findings should be treated supportively. A calm environment with no physical
exertion is imperative to avoid increasing endogenous adrenegic levels. Exogenous
adrenergic drugs must not be used to avoid inducing sensitized myocardial dysrhythmias.
Atropine is ineffective in treating bradyarrhythmias. For ventricular dysrhythmias,
diphenylhydantoin and countershock may be effective. Cryogenic dermal injuries
should be treated by water bath rewarming at 40 to 42 deg C until vasodilatory
flush has returned. Elevation of the limb and standard frostbite management
with late surgical debridement should be utilized. Ocular exposure requires
irrigation and slit-lamp evaluation for injury. /Freons/
... IF INHALATION OCCURS, EPINEPHRINE OR OTHER SYMPATHOMIMETIC AMINES &
ADRENERGIC ACTIVATORS SHOULD NOT BE ADMIN SINCE THEY WILL FURTHER SENSITIZE
HEART TO DEVELOPMENT OF ARRHYTHMIAS. /FLUOROCARBONS/
Basic treatment: Establish a patent airway. Suction if necessary. Watch for
signs of respiratory insufficiency and assist ventilations as needed. Administer
oxygen by nonrebreather mask at 10 to 15 L/min. Minimize physical activity and
provide a quiet atmosphere. Monitor for pulmonary edema and treat if necessary
... . Anticipate seizures and treat if necessary ... . For eye contamination,
flush eyes immediately with water. Irrigate each eye continuously with normal
saline during transport ... . Do not use emetics. Rinse mouth and administer
5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a
strong gag reflex, and does not drool. Administer activated charcoal ... . Treat
frostbite with rapid rewarming techniques ... . /Chlorinated fluorocarbons (CFCs)
and related compounds/
Advanced treatment: Consider orotracheal or nasotracheal intubation for airway
control in the patient who is unconscious or in respiratory arrest. Positive
pressure ventilation techniques with a bag valve mask device may be beneficial.
Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start an IV
with D5W /SRP: "To keep open", minimal flow rate/. Use lactated Ringer's if
signs of hypovolemia are present. Watch for signs of fluid overload. Consider
drug therapy for pulmonary edema ... . Treat seizures with diazepam ... . Use
proparacaine hydrochloride to assist eye irrigation ... . /Chlorinated fluorocarbons
(CFCs) and related compounds/
Animal Toxicity Studies:
Non-Human Toxicity Excerpts:
... ABOVE 3000 PPM ... ADMIN TO RATS 4 HR/DAY FOR 10 DAYS, CAUSED SLIGHT LIVER
AND BONE MARROW INJURY.
... TWITCHING & TREMORS /OBSERVED IN RATS AT/ CONCN OF 30-40%, LOSS OF
REFLEX AT 50% & ABOVE. AT 70 & 80%, CORNEAL REFLEX WAS ABSENT &
ANIMALS WERE IN DEEP ANESTHESIA. A FEW OF THE ANIMALS WERE EXPOSED AS LONG AS
4-6 HR AT 80% AND ... SUFFERED NO PERMANENT EFFECTS.
... Dogs, monkeys, rats, rabbits & guinea pigs /had continuous exposure/
to 810 ppm of FC 12, 24 hr daily for 90 days. No deaths were attributed to exposure
and pathologic changes ... occurred only in guinea pigs, who showed microscopic
liver injury. ... At 200,000 ppm, guinea pigs, dogs and monkeys exposed some
40 hr weekly for 10-12 weeks showed generalized tremors and other signs of mild
/CNS depression/, as well as slight blood changes, but no pathologic effects.
DOGS, MONKEYS, & GUINEA PIGS EXPOSED TO 20% OF GAS IN AIR FOR SEVERAL
HR A DAY FOR SEVERAL DAYS SHOWED TEMPORARY INTOXICATION WITH TREMORS, ATAXIA,
AND TENDENCY TO STARE, SALIVATE, & LACRIMATE, BUT NO CUMULATIVE TOXIC EFFECT
& NO SPECIFIC OCULAR DISTURBANCE.
In gaseous or vapor form at room temperature or body temperature, F 12 has
very little toxicity to the eye, inside or outside. A bubble of the gas injected
into the anterior chamber of rabbit eyes has not proved damaging to the cornea.
Exposure of a rabbit eye to pure F 12 gas at room temperature for one and one-half
minutes induced a slight irregularity of the corneal epithelium, but the eye
was completely normal the next day.
MICE EXPOSED FOR 3 OR 6 WK, 30 MIN/DAY TO 40,000 PPM, SHOWED ... RESP PATHOLOGY.
RATS FED 160 TO 379 MG/KG, 5 DAYS/WK FOR 18 WK, SHOWED ... SLIGHT ELEVATION
OF PLASMA ALKALINE PHOSPHATASE.
... ADMIN BY GAVAGE TO /GROUPS OF 50 MALE & FEMALE ALBINO/ RATS AT 15
OR 150 MG/KG/DAY FOR 2 YR, /CONTROL GROUPS OF 50 RATS OF EACH SEX RECEIVED VEHICLE
BY INTUBATION/; & IN FOOD TO BEAGLE DOGS AT 8 OR 80 MG/KG/DAY FOR 2 YR.
EXCEPT FOR SLIGHT ADVERSE EFFECT ON GROWTH OF RATS THAT RECEIVED HIGH DOSES,
NO CLINICAL, BIOCHEMICAL, URINARY, HEMATOLOGICAL, OR HISTOPATHOLOGICAL CHANGES
... FOUND IN EITHER SPECIES. NO EVIDENCE OF CARCINOGENIC RESPONSE ... OBSERVED.
IN CHRONIC EXPOSURE STUDIES, MALE & FEMALE RATS ... WERE GIVEN ... DOSES
OF 15 OR 150 MG/KG BY INTUBATION. THE RATS WERE THEN BRED & EVALUATED FOR
FERTILITY, CORPORA LUTEA, IMPLANTATION SITES, RESORPTION SITES, & NUMBER
OF LIVE FETUSES/LITTER. NO DOMINANT LETHALITY WAS FOUND AT EITHER DOSE LEVEL.
FREON 12 WAS NOT MUTAGENIC TO CHINESE HAMSTER OVARY CELLS IN THE PRESENCE
OR ABSENCE OF ACTIVATION SYSTEM.
EFFECTS OF FC 12 ON ELECTRICAL ACTIVITY OF CELLS IN ATRIAL & VENTRICULAR
MYOCARDIUM OF ANESTHETIZED RATS WERE RECORDED. MAJOR DECREASE IN DIASTOLIC POTENTIAL,
AMPLITUDE OF ACTION POTENTIAL, & MODIFICATION IN SHAPE OF THE ACTION POTENTIAL
WAS OBSERVED. RHYTHM ABNORMALITIES CONSISTED OF A DECR IN ATRIOVENTRICULAR CONDUCTION
& CHANGES IN THE MYOCARDIAL PASSIVE EXCITABILITY. CARDIOTOXICITY OF FC 12
IS ASSUMED TO AFFECT PASSIVE OR ACTIVE TRANSMEMBRANE IONIC MOVEMENTS.
Pathologic liver changes were reported in guinea pigs chronically exposed
(continued for 90 days; or eight hr daily, 5 days weekly, for six wk) to F 12
at levels of about 4,000 mg/cu m (0.08 % by vol).
In one chronic (90 day) feeding study of F-12 in rats at 35 and 350 mg/kg/day
... somewhat elevated urinary fluoride and plasma alkaline phosphatase levels.
No changes in dogs at 10 and 100 mg/kg/day were observed.
In a two-yr study using rats intubated with F 12 in corn oil at 15 and 150
mg/kg/day ... some suppresssion of wt gain at the high dose level, but no effects
with respect to clinical signs, liver function, hematology, or histopathology
/were observed/.
Significant mutagenic activity of F 12 at 2.47x10+6 mg/cu m (50%) in air in
a Neurospora crassa test system.
The relative potency of effect of a wide range of halogenated and unsubstituted
hydrocarbons on the CNS and heart of experimental animals were determined. The
chemicals used caused stimulation or depression of the rat CNS after 10 min
inhalation at 0.24-80% (vol/vol), and cardiac sensitization in dogs after 5
minute inhalation at 0.12-80% (vol/vol). The toxicity could not be correlated
with chemical structure, mol wt, the presence or absence of various halogens
or the degree of saturation, but it was inversely related to the saturated vapor
pressure. When the results were expressed on a thermodynamic scale, the chemicals
had similar potencies at relative saturation of 0.004-0.04. The effects of these
chemicals on the CNS and heart are probably structurally non-specific, and the
chemical may be regarded as ... toxicants whose effects are predictable from
their physico-chemical properties.
... INSEMINATED WISTAR ALBINO RATS & ALBINO RABBITS ... /WERE/ ADMIN MIXT
OF 90% FREON 12 ... & 10% FREON 11 BY INHALATION FOR 2 HR/DAY. RATS WERE
EXPOSED ON DAYS 4 TO 16 OF GESTATION & RABBITS ON DAYS 5 TO 20. MIXT WAS
ADMIN IN 20% CONCN (200,000 PPM). NO INDICATIONS OF ANY EMBRYOTOXIC, FETOTOXIC
OR TERATOGENIC CHANGES WERE FOUND WHEN DAMS WERE SACRIFICED & FETUSES REMOVED
ON DAY 20 OF GESTATION (RATS) OR DAY 30 OF GESTATION (RABBITS).
CFC-11, CFC-12, CFC-113, and CFC-114 at 40% in sesame oil were sprayed onto
shaved rabbit skin for 12 exposures with no effect.
CFC-11, CFC-12, CFC-114, and mixtures of CFC-11 and CFC-12 and of CFC-11 and
CFC-22 /were applied/ to the skin, tongue, soft palate and auditory canal of
rats, 1-2 times/day, 5 days/week, for 5-6 weeks. The same compounds were applied
once a day, 5 days/week for 1 month to the eye of rabbits. Slight irritation
was noted only in the skin of the rats and in the eye of the rabbits. The healing
rate of experimental burns on the skin of rabbits, however, was noticeably retarded
by all of the compounds.
Experimental evidence suggests that increased UV-B irradiation at the earth's
surface, resulting from ozone depletion /caused by the atmospheric chlorofluorocarbons/,
would have deleterious effects on both terrestrial and aquatic biota. Despite
uncertanities resulting from the complexities of field experiments, the data
currently available suggest that crop yields and forest productivity are vulnerable
to increased levels of solar UV-B radiation. Existing data also suggest that
increased UV-B radiation will notify the distribution and abundance of plants,
and change ecosystem structure. /UV-B Radiation/
Various studies of marine ecosystems have demonstrated that UV-B radiation
causes damage to fish larvae and juveniles, shrimp larvae, crab larvae, copepods,
and plants essential to the marine food web. These damaging effects include
decreased fecundity, growth, and survival. Experimental evidence suggests that
even small increases in ambient UV-B exposure could result in significant ecosystem
changes. /UV-B Radiation/
Short-term inhalation studies have been reported for CFC-11, CFC-12, CFC-112,
CFC-113, CFC-114, and CFC-115. The results showed low toxicity, and the effects
observed were related mainly to the CNS, respiratory tract, and the liver. Oral
toxicity studies have confirmed the low toxicity.
... Dichlorodifluoromethane ... /was/ tested by inhalation on Sprague-Dawley
rats and Swiss mice. The animals were exposed for 4 hr a day, 5 days a week;
rats were exposed for 104 weeks, and mice were exposed for 78 weeks. Animals
were observed until spontaneous death. Exposure of rats to dichlorodifluoromethane
resulted in no noticeable differences in the incidence of total benign and malignant
tumors, and of the most frequently expected or rate of tumors. Exposure of mice
to dichlorodifluoromethane resulted in a higher number of total tumors in males
and females which was dose related in males, pulmonary adenomas in males and
females at 5000 ppm, and leukemias in males at 5000 and 1000 ppm and in females
at 1000 ppm.
Groups of four male and four female beagle dogs were orally administered CFC-12
(in frozen dog food) at measured doses of 0, 8, or 80 mg/kg per day for 2 years.
None of the dogs died or showed signs of toxicity. No significant differences
between treated and control groups were found in food consumption, body weight,
periodic hematology, clinical chemistry and urine testing, organ weights, or
histopathological findings. An adrenal function test (urinary 17-ketosteroid
excretion) also revealed no effects. There was no evidence of carcinogenicity.
In a three-generation, oral gavage study in rats using CFC-12 (in corn oil)
at average doses of 15 and 150 mg/kg per day. No adverse /were found/ effects
on reproductive capability as measured by the fertility index (percentage of
matings resulting in pregnancy), gestation index (percentage of pregnancies
resulting in birth of live litters), viability index (percentage of rats born
that survived four days), and lactation index (percentage of rats alive at 4
days that survived to be weaned at 21 days).
Long term oral studies of CFC-12 /were conducted/ on rats and dogs. As part
of a multi-generation reproductive and chronic toxicity study, groups of 50
male and 50 female Charles River rats of the F1a generation remained in the
test for 2 years, with an interim kill at 1 year. Starting at 6 weeks of age
controls, low dose, and high dose groups were administered CFC-12 in corn oil
or corn oil alone daily by gavage for 6 weeks and 5 times per week thereafter.
Over the course of the study, actual daily doses of CFC-12 for low dose males
and females declined from 27 to 11 and 25 to 11 mg/kg per day respectively and,
for the high dose males and females, declined from 273 to 130 and 242 to 128
mg/kg per day, respectively. Average doses were 15 mg/kg per day for the low
dose groups and 150 mg/kg per day for the high dose groups. Body weight gain
was depressed in the high dose groups, particularly among the females, and a
slight decline in food efficiency was noted in high dose females, relative to
controls. No overt signs of toxicity were seen, and there were no significant
differences between treated and control groups in survival, periodic measurements
of hematological, clinical chemistry, and urinalysis values, or in organ weights
and histopathological findings. No evidence of carcinogenicity was seen.
Groups of 25 to 27 pregnant Charles River rats were given CFC-12 in corn oil
by gavage at doses of 16.6 or 179 mg/kg per day on days 6-15 of gestation. Neither
dose induced any evidence of embryotoxicity or teratogenicity.
Negative results were also obtained for CFC-11, CFC-12, and CFC-115 in a cell
transformation assay and for CFC-11 and CFC-12 in a mammalian cell mutagenicity
test. CFC-12 was also tested in a plant assay using Tradescantia, and found
to be negative.
A dominant lethal assay was performed as part of a reproduction study on rats
using CFC-12 at doses of 15 and 150 mg/kg per day (gavage) for several weeks.
... Negative results were obtained /in this in vivo assay/ ... .
When administered to groups of 90 male and 90 female /Sprague-Dawley/ rats
and 60 male and 60 female /Swiss/ mice at concentrations of 1000 or 5000 ppm
(57 or 285 g CFC-11/cu m; 49 or 247 g CFC-12/cu m), 4 hr/day, 5 days/week, neither
compound was found to have induced statistically significant differences in
the incidence of total benign or malignant tumors when compared with groups
of unexposed rats or mice. The incidence of all tumors and of some particularly
frequently occurring spontaneous tumors in mice showed a tendency to increase
in animals exposed to CFC-11 and CFC-12 and that the increased incidence was
usually observed in one sex and was not always dose related, possibly due to
a longer survival of the treated mice compared with controls.
When the lids of a rabbit's eye have been held open and a blast of a mixture
of liquid F-12 and lubricating oil from a refrigeratory has been applied directly
to the open eye continously for a second or two, this has caused momentary freezing
of the anterior segment of the eye followed by slight epithelial edema and partial
loss of epithelium, but complete recovery in three days. Spraying of rabbit
eyes with pure liquified F-12 for five to ten seconds caused damage of the corneal
endothelium, shedding in gray sheets from the posterior surface of the cornea,
and this led to swelling of the stroma. However, there was gradual recovery
so that only a small axial nebula persisted after six weeks. Exposure to the
liquid spray continuously for thirty seconds caused much more severe corneal
damage, the cornea ultimately becoming opaque and the globe /atrophic/ ... .
Fluorocarbon inhalation in dogs resulted in dysrhythmias that were enhanced
by anoxia, injected epinephrine, and noise stress. Fatal responses resulted
from inhaled concentrations of 0.35 to 0.61 per cent of Freon 11 and of 5 percent
of Freon 12 and 114.
EARLY ANIMAL ... WORK INDICATED THAT HIGH VAPOR CONCN (EG, 20%) MAY CAUSE
CONFUSION, PULMONARY IRRITATION, TREMORS & RARELY COMA, BUT THAT THESE EFFECTS
WERE GENERALLY TRANSIENT & WITHOUT LATE SEQUELAE. /FLUOROCARBON REFRIGERANTS
& PROPELLANTS/
The immume system of experimental animals is suppressed in specific ways by
UV-B radiation. This results in a decreased resistance to implanted UV-B nduced
tumors and an increased growth of such tumors in mice, in the suppression of
sensitization by contact allergens, and the response to allergens in sensitized
animals. /Chlorofluorocarbons/
Two series of experiments were conducted to determine the effects of bromotrifluoromethane,
bromochlorodifluoromethane, and dichlorodifluoromethane on the isolated, perfused
rabbit heart. Hearts were perfused through the aorta. Left ventricular mechanical
activity was monitored concurrently with action potentials recorded from left
ventricular myocardial fibers. In the first series, mechanical performance curves
were determined for each of 7 hearts using intraventricular balloons to control
end diastolic pressure. The relative effectiveness of these compounds as negative
isotropic agents was bromochlorodifluoromethane > dichlorodifluoromethane
> bromotrifluoromethane. In the 2nd series of experiments, hearts were exposed
to increasing concentrations of each fluorocarbon. Controls were exposed to
equivalent concentrations of nitrogen. Exposure to increasing concentrations
of bromotrifluoromethane decreased peak left ventricular pressure, the integral
of the pressure curve, and the time 20% repolarization of the action potential.
Exposure to increasing concentrations of bromochlorodifluoromethane reduced
peak left ventricular pressure and the maximal rate of rise of the pressure
curve and. Exposure to increasing levels of dichlorodifluoromethane decreased
peak left ventricular pressure and the maximal rate of rise of the pressure
curve.
... Chlorofluorocarbons (CFCs) could sensitize the canine myocardium to adrenaline,
resulting in serious cardiac arrhythmias.
Three propellant chlorofluorocarbons (FC-11, FC-12 /dichlorodifluoromethane/,
FC-22) administered by inhalation at concentrations of 5000 and 1000 ppm for
4 hours daily, 5 days weekly for 78 to 104 weeks to rats and mice had no carcinogenic
effects.
Non-Human Toxicity Values:
LD50 Mouse inhalation 760,000 ppm/30 min
LD50 Guinea pig inhalation >800,000 ppm/30 min
LD50 Rabbit inhalation >800,000 ppm/30 min
LD50 Rat single oral >1 g/kg
LD50 Rat inhalation >800,000 ppm/30 min
Metabolism/Pharmacokinetics:
Absorption, Distribution & Excretion:
ELIMINATION IS RAPID. DOGS EXHALED WITHIN 1 HR ESSENTIALLY ALL FC 12 INHALED
DURING 6-20 MIN EXPOSURE TO 8000-12000 PPM. INHALED FC 12 RAPIDLY APPEARED IN
BLOOD, BILE, CEREBROSPINAL FLUID & URINE OF ANESTHETIZED RABBITS & DOGS.
UNANESTHETIZED DOGS EXPOSED TO 1000-100000 PPM FOR 10 MIN SHOWED RAPID RISE
IN BLOOD CONCN ... DURING 1ST 3 TO 5 MIN WHICH WAS PARALLELED BY A RAPID DECLINE
FOR FIRST 5 MIN AFTER EXPOSURE.
BLOOD LEVELS OF FC 12 WERE BELOW DETECTION LIMITS IN NORMAL SUBJECTS USING
HOUSEHOLD AEROSOLS; IN ASTHMATIC SUBJECTS USING AEROSOL INHALER, BLOOD LEVELS
WERE MUCH LOWER THAN IN DOGS EXPOSED AT THRESHOLD FOR CARDIAC SENSITIZATION.
RADIOLABELED TESTS SHOWED ESSENTIALLY ALL DOSE (95-103%) EXHALED WITHIN 1ST
HR AFTER 12 OR 17 MIN INHALATION AT 1000 PPM. ... FOR AN EIGHT HR INHALATION
AT 1000 PPM, A PHARMACOKINETIC MODEL BASED ON ANALYSES IN DOGS AND HUMANS GAVE
AN ESTIMATE OF 55% ABSORPTION OF THE INHALED FC 12.
AT 1000 PPM ... LEVEL IN /HUMAN/ VENOUS BLOOD WAS 1.2 UG/ML.
Absorption and elimination are dynamic processes involving equilibria among
air, blood, and various tissues. Upon absorption, a biphasic blood-level pattern
occurs, with an initial rapid then slower rise in blood levels, during which
the material is absorbed from blood into tissue.
Human & animal studies indicate rapid excretion of inhaled FC-114. In
a study with radiolabeled FC-114, 30 min retention of the dose inhaled in a
single breath was 12% versus 23%, 10%, & 20% for comparable doses of FC-11,
FC-12, and FC-113, respectively.
... MAIN FACTOR AFFECTING FATE OF FLUOROCARBONS IS BODY FAT, WHERE THEY ARE
CONCENTRATED & SLOWLY RELEASED INTO BLOOD @ CONCN THAT SHOULD NOT CAUSE
ANY RISK OF CARDIAC SENSITIZATION. /FLUOROCARBONS/
There is a significant accumulation of fluorocarbons in brain,
liver and lung compared to blood levels, signifying a tissue distribution of
fluorocarbons similar to that of chloroform. /Fluorocarbons/
Abosrption of fluorocarbons is much lower after oral ingestion (35-48 times)
than after inhalation. ... The lung generally has the highest fluorocarbon concentrations
on autopsy. /Fluorocarbons/
Although fluorocarbons cause cardiac sensitization in certain animal species,
rapid elimination prevents the development of cardiotoxic concentrations from
aerosol bronchodilator use except at exceedingly high doses (12 to 24 doses
in 2 minutes). /Fluorocarbons/
FLUOROCARBON COMPOUNDS ARE LIPID-SOLUBLE AND THUS ARE GENERALLY WELL ABSORBED
THROUGH LUNG. ABSORPTION AFTER INGESTION IS 35 TO 48 TIMES LOWER THAN AFTER
INHALATION. ... FLUOROCARBONS ARE ELIMINATED BY WAY OF LUNG. /FLUOROCARBON COMPOUNDS/
Regardless of the route of entry, chlorofluorocarbons appear to be eliminated
almost exclusively through the respiratory tract. Little, if any, chlorofluorocarbon
or metabolite has ever been reported in urine or feces. /Chlorofluorocarbons/
Biological Half-Life:
The distribution half-life of the common fluorocarbons (Freon 11, Freon 12)
averages 13 to 14 seconds; the elimination half-life is longer (1.5 hours) because
of slower release from fat stores.
Mechanism of Action:
On the basis of an electrophysiological analysis of the action of CFC-12 on
different types of cardiac cells from rats and sheep, the authors conclude that:
1. the cardiac depression observed during inhalation of CFC-12 (and many other
volatile liposoluble compounds) is the consequence of a non-specific impairment
of the membrane properties and notably the inhibition of trans-membrane ionic
currents; 2, CFC-12 action on ionic currents is variable: at high concentrations,
depending on the type of cardiac cell, it can oppose or favor the action of
adrenaline, giving rise to many factors that lead to arrhythmia.
CFC-12 and CFC-114 do not markedly affect oxygen consumption or oxidative
phosphorylation in mitochondria isolated from the liver, lung, brain,
heart, or kidney of rats exposed to about 7.5% chlorofluorocarbons prior to
mitochondrial isolation. Further in vitro studies were conducted with liver
and heart mitochondria in which measurements were taken during exposure of the
mitochondria to CFC-12 at 990 g/cu m (20%) (time of exposure not specified).
No effects on either oxidation or phosphorylation were noted.
Interactions:
AFTER ACUTE EXPOSURE BY INHALATION TO A 13.5% CONCENTRATION FOR 30 SEC, MYOCARDIUM
IN UNANESTHETIZED DOGS WAS SENSITIZED TO SUBSEQUENT INJECTION OF EPINEPHRINE.
IN CONTRAST, A 2.5% CONCENTRATION THAT WAS INHALED 6 HR/DAY FOR 5 DAYS RESULTED
IN NO CARDIAC SENSITIZATION IN DOGS.
/IN HUMANS/ A 10 TO 90% MIXTURE OF CFC 11 & CFC 12, RESPECTIVELY, CAUSED
MORE SEVERE RESPIRATORY EFFECTS THAN EITHER FLUOROCARBON INHALED SINGLY.
IF INHALATION OCCURS, EPINEPHRINE OR OTHER SYMPATHOMIMETIC AMINES & ADRENERGIC
ACTIVATORS SHOULD NOT BE ADMIN SINCE THEY WILL FURTHER SENSITIZE HEART TO DEVELOPMENT
OF ARRHYTHMIAS. /FLUOROCARBONS/
Pharmacology:
Interactions:
AFTER ACUTE EXPOSURE BY INHALATION TO A 13.5% CONCENTRATION FOR 30 SEC, MYOCARDIUM
IN UNANESTHETIZED DOGS WAS SENSITIZED TO SUBSEQUENT INJECTION OF EPINEPHRINE.
IN CONTRAST, A 2.5% CONCENTRATION THAT WAS INHALED 6 HR/DAY FOR 5 DAYS RESULTED
IN NO CARDIAC SENSITIZATION IN DOGS.
/IN HUMANS/ A 10 TO 90% MIXTURE OF CFC 11 & CFC 12, RESPECTIVELY, CAUSED
MORE SEVERE RESPIRATORY EFFECTS THAN EITHER FLUOROCARBON INHALED SINGLY.
IF INHALATION OCCURS, EPINEPHRINE OR OTHER SYMPATHOMIMETIC AMINES & ADRENERGIC
ACTIVATORS SHOULD NOT BE ADMIN SINCE THEY WILL FURTHER SENSITIZE HEART TO DEVELOPMENT
OF ARRHYTHMIAS. /FLUOROCARBONS/
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Dichlorodifluoromethane's former production and use as an aerosol propellent,
foaming agent and refrigerant lead to its release to the environment through
various waste streams. Based on a vapor pressure of 4,850 mm Hg at 25 deg C,
dichlorodifluoromethane is expected to exist solely in the gas-phase in the
ambient atmosphere. Gas-phase dichlorodifluoromethane is extremely stable in
the troposphere. This compound does not react with photochemically produced
hydroxyl radicals, ozone molecules or nitrate radicals in the troposphere. This
compound will gradually diffuse into the stratosphere above the ozone layer
where it will slowly degrade due to direct photolysis from UV-C radiation and
contribute to the catalytic removal of stratospheric ozone. Dichlorodifluoromethane
is expected to have moderate mobility in soils based upon an estimated Koc value
of 356. This compound is expected to volatilize rapidly from dry soil surfaces
based on its measured vapor pressure. Volatilization from moist soil surfaces
is expected based upon a Henry's Law constant of 0.343 atm-cu m/mole. Dichlorodifluoromethane
was degraded under anaerobic conditions in laboratory tests, but does not biodegrade
under aerobic conditions. In water, dichlorodifluoromethane is not expected
to adsorb to sediment or particulate matter given its estimated Koc value. This
compound is expected to volatilize rapidly from water surfaces given its Henry's
Law constant. Estimated half-lives for a model river and model lake are 1 hour
and 4 days, respectively. An estimated BCF of 25 suggests the potential for
bioconcentration in aquatic organisms is low. Occupational exposure may be through
inhalation and dermal contact with this compound at workplaces where dichlorodifluoromethane
is still used, such as air condition repair shops. However, since this compound
is no longer produced in the US, very little occupational exposure is expected.
Due to its long atmospheric residence time, the general population is exposed
to dichlorodifluoromethane through inhalation of ambient air. (SRC)
Probable Routes of Human Exposure:
NIOSH (NOES Survey 1981-1983) has statistically estimated that 435,098 workers
(125,602 of these are female) are potentially exposed to dichlorodifluoromethane
in the US(1). Occupational exposure may be through inhalation and dermal contact
with this compound at workplaces where dichlorodifluoromethane is still used,
such as air conditioning repair shops(SRC). This survey was conducted prior
to the Montreal Protocol which scheduled the production phase-out of this compound
and other chlorofluorocarbons, and is not an accurate measure of the current
occupational exposure(SRC). Due to its long atmospheric residence time, the
general population may be exposed to dichlorodifluoromethane via inhalation
of ambient air(SRC).
Body Burden:
In a pilot study of pollutants in the milk of women living in 4 urban-industrial
areas in the US, dichlorodifluoromethane was identified, not quantified, in
2 of 8 samples(1).
Natural Pollution Sources:
There are no known natural sources of dichlorodifluoromethane(1).
Artificial Pollution Sources:
All of the dichlorodifluoromethane that is produced is eventually lost as
emissions. It is estimated that 3.3% of the dichlorodifluoromethane produced
is lost from plant vents and during packaging, a loss which is immediate(1).
Losses from aerosols occur, on the average, 6 months after sale; losses from
domestic refrigerators and freezers have an average life of 12 yr with a 2%
loss during filling; industrial refrigerator charges have an average lifetime
of 4 yr; all of the dichlorodifluoromethane used in closed cell foams are lost
within 2 yr with 75% being lost during the first year(1). The annual world production
and release of dichlorodifluoromethane in 1982 was 443.7 and 422.8 million kg,
respectively(1). Cumulative production and release estimates up until the end
of 1974 were 4698.5 and 4286.2 million kg(1). By the end of 1982 these figures
had increased to 8196.0 and 7520.2 million kg(1).
The realization that certain chlorofluorocarbons can accumulate in the upper
atmosphere and deplete the earth's ozone layer has had a major impact on chemicals
like dichlorodifluoromethane which are used in large quantities and have the
stability to reach the stratosphere. Uses such as propellants in aerosols which
had accounted for about 75% of the release of dichlorodifluoromethane and trichlorofluoromethane,
the chemicals of greatest concern (refrigerants and foams accounted for about
14 and 12%, respectively), were banned in the US after Dec 15, 1978(1). Previously
dichlorodifluoromethane was the principal propellant for non-food aerosols(1)
and 60% of dichlorodifluoromethane and trichlorofluoromethane production went
into aerosols(1).
Dichlorodifluoromethane's former production and use as an aerosol propellent,
foaming agent and refrigerant(1) lead to its release to the environment through
various waste streams(SRC).
Environmental Fate:
Due to the high vapor pressure of dichlorodifluoromethane, volatilization
to the atmosphere is quite rapid. ... It does not react readily with hydroxyl
radicals, nor does it photodissociate in the troposphere since it exhibits no
absorption of light greater than 200 nm. ... In the stratosphere, dichlorodifluoromethane
is broken down by the absorption of higher energy, shorter wavelength ultraviolet
light.
TERRESTRIAL FATE: Based on a recommended classification scheme(1), an estimated
Koc value of 356(SRC), determined from a log Kow of 2.16(2) and a recommended
regression-derived equation(3), indicates that dichlorodifluoromethane is expected
to have moderate mobility in soil(SRC). Volatilization of dichlorodifluoromethane
is expected from moist soil surfaces(SRC) given a Henry's Law constant of 0.343
atm-cu m/mole(4). Dichlorodifluoromethane is expected to volatilize rapidly
from dry soil surfaces(SRC) based on a vapor pressure of 4,850 mm Hg at 25 deg
C(5). Dichlorodifluoromethane was degraded under anaerobic landfill conditions
in laboratory test digesters(6), suggesting this compound may biodegrade in
soils under anaerobic conditions(SRC).
AQUATIC FATE: Based on a recommended classification scheme(1), an estimated
Koc value of 356(SRC), determined from a log Kow of 2.16(2) and a recommended
regression-derived equation(3), indicates that dichlorodifluoromethane is not
expected to adsorb to suspended solids and sediment in water(SRC). Dichlorodifluoromethane
is expected to volatilize rapidly from water surfaces(3) based on a Henry's
Law constant of 0.343 atm-cu m/mole(4). Estimated half-lives for a model river
and model lake are 1 hour and 4 days, respectively(SRC). According to a classification
scheme(5), an estimated BCF value of 25(SRC), determined from the log Kow(2),
and a regression-derived equation(3), suggests the potential for bioconcentration
in aquatic organisms is low(SRC). Dichlorodifluoromethane was degraded under
anaerobic conditions over a 100 day incubation period by sediment obtained from
the Potomac River(6).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile
organic compounds in the atmosphere(1), dichlorodifluoromethane, which has a
vapor pressure of 4,850 mm Hg at 25 deg C(2), is expected to exist solely as
a gas in the ambient atmosphere. Gas-phase dichlorodifluoromethane is extremely
stable in the troposphere. This compound does not react with photochemically
produced hydroxyl radicals, ozone molecules or nitrate radicals(3,4). This compound
will gradually diffuse into the stratosphere above the ozone layer where it
will slowly degrade due to direct photolysis from UV-C radiation and contribute
to the catalytic removal of stratospheric ozone(SRC). The half-life for this
reaction has been estimated to range from 105 to 169 years(4).
Environmental Biodegradation:
AEROBIC: No evidence of dichlorodifluoromethane biodegradation was found in
a microcosm designed to simulate Narragansett Bay in a month-long experiment(1).
ANAEROBIC: Pure cultures of Methanosarcina barkerii and Methanobacterium thermoautotrophicum
were shown to biodegrade dichlorodifluoromethane via reductive dehalogenation(2).
Pure bacterial cultures isolated from soils obtained from Rockville, MD were
shown to biodegrade dichlorodifluoromethane(4). Dichlorodifluoromethane was
degraded under anaerobic landfill conditions in laboratory test digesters(3).
The degradation product observed was dichlorofluoromethane(3). Dichlorodifluoromethane
was degraded under anaerobic conditions over a 100 day incubation period by
sediment from the Potomac River(4), but was not biodegraded by an aerobic soil.
Environmental Abiotic Degradation:
... Photolysis of dichlorodifluoromethane in the presence of oxygen at 213.9
nm and 25 deg C, leads to the prodn of difluoromethoxide and chloride ... and
chlorine atoms.
... PHOTODISSOCIATION OF FLUOROCARBONS IN STRATOSPHERE PRODUCES SIGNIFICANT
AMT OF CHLORINE ATOMS /SRP: FLUORINE ATOMS AND BROMINE ATOMS/ & LEADS TO
DESTRUCTION OF ATMOSPHERIC OZONE. REDUCTION IN OZONE ALLOWS MORE UV LIGHT TO
REACH EARTH'S SURFACE ... /FLUOROCARBONS/
Gas-phase dichlorodifluoromethane is extremely stable in the troposphere.
This compound does not react with photochemically produced hydroxyl radicals,
ozone molecules or nitrate radicals(1,2). This compound will gradually diffuse
into the stratosphere above the ozone layer where it will slowly degrade due
to direct photolysis from UV-C radiation and contribute to the catalytic removal
of stratospheric ozone(2). The half-life for this reaction has been estimated
to range from 105 to 169 years(2). Dichlorodifluoromethane is not expected to
undergo hydrolysis or direct photolysis in the troposphere due to the lack of
functional groups that could chemically hydrolyze or absorb light at environmentally
significant wavelengths(3).
Environmental Bioconcentration:
... The log octanol/water partition coefficient (log P) of 2.16 indicates
that dichlorodifluoromethane is lipophilic and that bioaccumulation in organisms
may be possible under conditions of constant exposure.
An estimated BCF value of 25 was calculated for dichlorodifluoromethane(SRC),
using a log Kow of 2.16(1) and a recommended regression-derived equation(2).
According to a classification scheme(3), this BCF value suggests that the potential
bioconcentration in aquatic organisms is low(SRC).
Soil Adsorption/Mobility:
... The log octanol/water partition coefficient (log P) of 2.16 ... indicates
that absorption onto organic particulates may be possible.
The Koc of dichlorodifluoromethane is estimated as approximately 356(SRC),
using a log Kow of 2.16(1) and a regression-derived equation(2). According to
a recommended classification scheme(3), this estimated Koc value suggests that
dichlorodifluoromethane is expected to have moderate mobility in soil(SRC).
Volatilization from Water/Soil:
The high vapor pressure and low aqueous solubility of dichlorodifluoromethane
are conductive to rapid volatilization from an aquatic environment. ... Volatilization
is thought to be the major transport process.
The Henry's Law constant for dichlorodifluoromethane is 0.343 atm-cu m/mole(1).
This value indicates that dichlorodifluoromethane will volatilize rapidly from
water surfaces(2). Based on this Henry's Law constant, the volatilization half-life
from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(2)
is estimated as approximately 1 hour(SRC). The volatilization half-life from
a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(2) is
estimated as approximately 4 days(SRC). Dichlorodifluoromethane's Henry's Law
constant(1) indicates that volatilization from moist soil surfaces is expected
occur(SRC). Dichlorodifluoromethane is expected to volatilize rapidly from dry
soil surfaces(SRC) based on the vapor pressure of 4,850 mm Hg at 25 deg C(3).
Environmental Water Concentrations:
GROUNDWATER: Dichlorodifluoromethane was identified, but not quantified in
groundwater under 6 of 13 municipal landfills in Minnesota with suspected leakage
but not in the groundwater under 7 other municipal landfills(1). Dichlorodifluoromethane
was detected in 20 of 2,542 groundwater rural wells at a max concn of about
7 ug/l and in 11 out of 406 urban wells at a max concn of about 70 ug/l in the
US from 1985-1995(2). Dichlorodifluoromethane was detected in shallow wells
in northern Hungary at concns of 0.06-10.36 picomols/l in 1993(3). Dichlorodifluoromethane
was detected at a max concn of 0.6 ug/l in groundwater from Denver, CO(4).
SURFACE WATER: Of the 696 stations reporting pollutants in ambient waters
in EPA's STORET database, 1.0% contained dichlorodifluoromethane at detectable
levels(1). Dichlorodifluoromethane was identified, but not quantified, in the
open waters of Lake Erie(3). The average concn of dichlorodifluoromethane in
surface water at two stations in the Greenland and Norwegian Sea was 218 and
187 ppb, respectively(2). The concn decreased with depth over many km in the
Greenland Sea and was relatively constant in the upper 0.4 km in the Norwegian
Sea before decreasing(2). The deep water concns of dichlorodifluoromethane in
these seas were 37 and 18 ppb(2).
Effluent Concentrations:
Of the 1,144 stations reporting pollutants in ambient waters in EPA's STORET
database, 1.6% contained dichlorodifluoromethane at detectable levels(1). No
dichlorodifluoromethane was found in the effluent of a large community septic
tank (detection limit 0.7 ppb)(2). In the National Urban Runoff Program in which
samples of runoff were collected from 19 cities (51 catchments) in the U.S.,
no dichlorodifluoromethane was found in any samples(3). Leachate from 2 of 6
municipal landfills tested in Minnesota had detectable quantities of dichlorodifluoromethane(4).
Leachate from 1 out of 5 landfills in Wisconsin contained 180 ppb of the chemical(4).
Dichlorodifluoromethane was emitted from a simulated landfill composed of municipal
refuse and wastewater sludges(5).
Sediment/Soil Concentrations:
None of the 204 stations in EPA's STORET database reported any dichlorodifluoromethane
in sediment(1).
Atmospheric Concentrations:
Mean urban concn for dichlorodifluoromethane ranged from 3.5x10-3 to 2.9x10-2
mg/cu m, and an ocean atmosphere mean of 2.7x10-4 mg/cu m.
In a beauty shop, where fluorocarbon pressured cosmetic sprays were apt to
be used, concn of 1.8 mg/cu m.
Dichlorodifluoromethane concn in room air as a result of release of aerosol
can products. Level at periods after 60 sec release of hair spray in a 29.3
cu m room (in mg/cu m): during release: 306.8; 30 min after: 12.4; 60 min after:
0.5. Level at periods after 30 second release of insect spray in a 21.4 cu m
room (in mg/cu m): 1 min: 2,304.0; 60 min: 130.4; 150 min: 56.8. /From table/
Ambient air quality, ground level concn in Los Angeles; July 1970, 0.7 ppb,
Feb 1973, 0.53 ppb; in rural Wash DC; Dec 74-Feb 75: 0.23 ppb.
S Calif Feb-Aug 1973 at 6700 m, 90 parts per trillion ; New Mexico on 5/23/74
at 6400 m 120 parts per trillion; W Ireland June/July 1974 at sea-level, 101.7
parts per trillion; North Atlantic Oct 1974 at sea-level, 115 parts per trillion;
Pullman, Washington Nov 1974 at 0-3600 m, 230 parts per trillion; West of N
Ireland E of Scotland at 7000-8000 m, 231 parts per trillion; off SW Wales Jan
1976 at 900-7300 m, 236 parts per trillion; off SW Wales Jan 1976 at 900-4900
m, 258 parts per trillion; off NE England Feb 1976 at 400-5200 m, 225 parts
per trillion /From table/
RURAL/REMOTE: Sites in the US (431 samples) - 120 parts per trillion, median,
230 parts per trillion, max(1). The average concn of dichlorodifluoromethane
at two stations over the Greenland and Norwegian Sea was 343 parts per trillion(2).
The concn of dichlorofluoromethane in Adrigole, Ireland was 338 parts per trillion(2).
Rural and urban areas of China and rural areas of Oregon contained a median
concn of dichlorofluoromethane was 320 parts per trillion(3). Similarly, median
concns of dichlorodifluoromethane in rural areas of Eastern Washington and the
Caucasus Mountains of the USSR in 1979 was 289 and 313 parts per trillion, respectively(4).
The respective average concns in the morning vs the nighttime in Eastern Washington
was 310 and 318 parts per trillion(4). The background concn of dichlorodifluoromethane
in the northern hemisphere was reported as 530 parts per trillion(5).
RURAL/REMOTE: The average concns of dichlorodifluoromethane in the Northern
and Southern Hemispheres show slight differences(3). In 1976, their values were
218 and 204 parts per trillion(3), respectively. Concns of dichlorodifluoromethane
at the South Pole has increased from 195 to 284 parts per trillion between 1976
and 1980, while over the same period of time the increase in the Pacific Northwest
was from 228 to 322 parts per trillion(1). The annual rate of increase in these
areas is 7%. As the altitude increases, the concn of dichlorodifluoromethane
in the atmosphere at northern mid-latitudes decreased from 350 parts per trillion
at the earth's surface to 250, 100, and 20 parts per trillion at 10, 20, and
30 km(2). The avg concn of dichlorodifluoromethane in coastal regions of Taiwan
was 515 parts per trillion(4).
URBAN/SUBURBAN: Dichlorodifluoromethane was detected at various sites in the
US at a median concn of 0.38 ppb and a max concn of 4.9 ppb(1). Various sites
in the US had dichlorodifluoromethane levels ranging from 0.37 to 4.8 ppb while
sites in continental Europe and Japan had levels of 0.410-11.4 ppb(2). In 1975,
the average concn of dichlorodifluoromethane was 0.23 ppb and rising at an annual
rate of 0.0157 ppb(3). The avg concn of dichlorodifluoromethane in Taipei, Taiwan
was 590 parts per trillion(4). Dichlorodifluoromethane was detected in Japan
(1990-1991) at concns of 0.29-1.7 ppb(5).
Fish/Seafood Concentrations:
None of the 47 stations in EPA's STORET database reported any dichlorodifluoromethane
in biota(1).
Milk Concentrations:
In a pilot study of pollutants in the milk of women living in 4 urban-industrial
areas in the US, dichlorodifluoromethane was found in 2 of 8 samples(1).
Environmental Standards & Regulations:
FIFRA Requirements:
Residues of dichlorodifluoromethane are exempted from the requirement of a
tolerance when used as a propellant in accordance with good agricultural practices
as inert (or occasionally active) ingredients in pesticide formulations applied
to growing crops or to raw agricultural commodities after harvest.
Dichlorodifluoromethane is exempted from the requirement of a tolerance when
used as a propellant in accordance with good agricultural practice as inert
(or occasionally active) ingredients in pesticide formulations applied to animals.
As the federal pesticide law FIFRA directs, EPA is conducting a comprehensive
review of older pesticides to consider their health and environmental effects
and make decisions about their future use. Under this pesticide reregistration
program, EPA examines health and safety data for pesticide active ingredients
initially registered before November 1, 1984, and determines whether they are
eligible for reregistration. In addition, all pesticides must meet the new safety
standard of the Food Quality Protection Act of 1996. Pesticides for which EPA
had not issued Registration Standards prior to the effective date of FIFRA,
as amended in 1988, were divided into three lists based upon their potential
for human exposure and other factors, with List B containing pesticides of greater
concern and List D pesticides of less concern. Dichloromonofluoromethane is
found on List D. Case No: 4042; Pesticide type: insecticide; Case Status: No
products containing the pesticide are actively registered ... The case /is characterized/
as "cancelled." Under FIFRA, pesticide producers may voluntarily cancel their
registered products. EPA also may cancel pesticide registrations if registrants
fail to pay required fees or make/meet certain reregistration commitments, or
if EPA reaches findings of unreasonable adverse effects.; Active ingredient
(AI): Dichloromonofluoromethane; AI Status: The active ingredient is no longer
contained in any registered pesticide products ... "cancelled."
Acceptable Daily Intakes:
EPA RfD= 0.2 mg/kg
CERCLA Reportable Quantities:
Persons in charge of vessels or facilities are required to notify the National
Response Center (NRC) immediately, when there is a release of this designated
hazardous substance, in an amount equal to or greater than its reportable quantity
of 5000 lb or 2270 kg. The toll free number of the NRC is (800) 424-8802; In
the Washington D.C. metropolitan area (202) 426-2675. The rule for determining
when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).
RCRA Requirements:
U075; As stipulated in 40 CFR 261.33, when dichlorodifluoromethane, as a commercial
chemical product or manufacturing chemical intermediate or an off-specification
commercial chemical product or a manufacturing chemical intermediate, becomes
a waste, it must be managed according to Federal and/or State hazardous waste
regulations. Also defined as a hazardous waste is any residue, contaminated
soil, water, or other debris resulting from the cleanup of a spill, into water
or on dry land, of this waste. Generators of small quantities of this waste
may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).
Atmospheric Standards:
This action promulgates standards of performance for equipment leaks of Volatile
Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry
(SOCMI). The intended effect of these standards is to require all newly constructed,
modified, and reconstructed SOCMI process units to use the best demonstrated
system of continuous emission reduction for equipment leaks of VOC, considering
costs, non air quality health and environmental impact and energy requirements.
Dichlorodifluoromethane is produced, as an intermediate or a final product,
by process units covered under this subpart.
Federal Drinking Water Guidelines:
EPA 1000 ug/l
State Drinking Water Guidelines:
(AZ) ARIZONA 1400 ug/l
(FL) FLORIDA 1,400 ug/l
(MA) MASSACHUSETTS 1400 ug/l
(ME) MAINE 1050 ug/l
(MN) MINNESOTA 1000 ug/l
(NC) NORTH CAROLINA 0.19 ug/l
(WA) WASHINGTON 530 ug/l
FDA Requirements:
... Essential uses of chlorofluorocarbons: (1) Metered-dose steroid human
drugs for nasal inhalation; (2) Metered-dose steroid human drugs for oral inhalation;
(3) Metered-dose adrenergic bronchodilator human drugs for oral inhalation;
(4) Contraceptive vaginal foams for human use, and (5) Metered-dose ergotamine
tartrate drug products administered by oral inhalation for use in humans; (6)
Intrarectal hydrocortisone acetate for human use; (7) Polymyxin B sulfate-bacitracin
zinc-neomycin sulfate soluble antibiotic powder without excipients, for topical
use on humans; (8) Anesthetic drugs for topical use on accessible mucous membranes
of humans where a cannula is used for application; (9) Metered-dose nitroglycerin
human drugs administered to the oral cavity; (10) Metered-dose cromolyn sodium
human drugs administered by oral inhalation; (11) Metered-dose ipratropium bromide
for oral inhalation; (12) Metered-dose atropine sulfate aerosol human drugs
administered by oral inhalation. /Chlorofluorocarbons/
Allowable Tolerances:
Residues of dichlorodifluoromethane are exempted from the requirement of a
tolerance when used as a propellant in accordance with good agricultural practices
as inert (or occasionally active) ingredients in pesticide formulations applied
to growing crops or to raw agricultural commodities after harvest.
Dichlorodifluoromethane is exempted from the requirement of a tolerance when
used as a propellant in accordance with good agricultural practice as inert
(or occasionally active) ingredients in pesticide formulations applied to animals.
Chemical/Physical Properties:
Molecular Formula:
C-Cl2-F2
Molecular Weight:
120.91
Color/Form:
LIQUEFIED COMPRESSED GAS
Colorless gas ... [Note: Shipped as a liquified compressed gas].
Odor:
Practically odorless; faint, ether-like odor in high concn
Boiling Point:
-29.8 deg C @ 760 mm Hg
Melting Point:
-158 deg C
Corrosivity:
Noncorrosive
Critical Temperature & Pressure:
Critical temp: 233.2 deg F= 111.8 deg C= 385.0 deg K; Critical pressure: 598
psia= 40.7 atm= 4.12 mn/sq m
Density/Specific Gravity:
1.486 @ -29.8 deg C
Heat of Combustion:
Nonflammable
Heat of Vaporization:
140 Btu/lb= 77.9 cal/g= 3.26X10+5 J/kg (Latent)
Octanol/Water Partition Coefficient:
log Kow= 2.16
Solubilities:
0.28 g/l water @ 25 deg C @ 1 atm
1.9 g/l water @ 25 deg C @ 94.4 psia (the propellant vapor pressure)
13.1 wt% amyl chloride @ 21.1 deg C @ 1 atm
9.0 wt% benzene @ 21.l deg C @ 1 atm
5.0 wt% bromobenzene @ 21.1 deg C @ 1 atm
1.2 wt% bromoform @ 21.1 deg C @ 1 atm
8.5 wt% n-butyl alcohol @ 21.1 deg C @ l atm
13.2 wt% butyl butyrate @ 21.1 deg C @ 1 atm
5.2 wt% carbon tetrachloride @ 21.1 deg C @ 1 atm