PHENOL
PHENOL
CASRN: 108-95-2
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~AAAcpaq6n:37
Human Health Effects:
Toxicity Summary:
HUMAN TOXICITY: Phenol is toxic with a probable oral lethal dose to humans of
50-500 mg/kg. Some individuals may be hypersensitive with lethality or serious
effects at very low exposures. Rapid absorption and severe systemic toxicity can
occur after any route of exposure including skin. Death and severe toxicity are
usually due to effects on the CNS, heart, blood vessels, lung, and kidneys.
However, toxic manifestations may vary somewhat with the route. Observed effects
from acute exposure may include: shock, delirium, coma, pulmonary distress,
phenolic breath, scanty/dark urine, and death. Protracted or chronic exposure
usually results in major damage to the liver, kidneys and eyes. Pigmentary
changes of the skin have been noted. Consumption of water contaminated with
phenol resulted in diarrhea, mouth sores, burning of the mouth, and dark urine.
Phenol is highly caustic to tissues. Skin exposure results in pain, then
numbness, blanching, severe burns, and eschar formation. Ingestion leads to
burning of throat and severe gastrointestinal inflammation. Inhalation can
result in pulmonary irritation and edema. ANIMAL TOXICITY: Toxicity in animals
is similar to that of humans, although additional effects have been observed.
LD50's in animals range from 250-500 mg/kg, differing very little with route of
exposure or species, except for the cat which is unusually susceptible with an
oral lethal dose of 80 mg/kg. Additional reported toxic effects include
irritation and corrosivity of skin and eyes in rabbits, induction of skin tumors
in mice, reproductive effects in rats, and mutagenicity with Salmonella, E coli
and Drosophila. Phenol is also highly toxic to aquatic life and frogs.
METABOLISM: Phenol is metabolized and excreted principally by the kidneys as the
sulfate or glucuronide, although some phenol may be excreted unchanged,
especially at high doses. Other reported metabolites include hydroquinone, other
quinones and catechols.
Evidence for Carcinogenicity:
Evaluation: There is inadequate evidence in humans for the carcinogenicity of
phenol. There is inadequate evidence in experimental animals for the
carcinogenicity of phenol. Overall evaluation: Phenol is not classifiable as to
its carcinogenicity to humans (Group 3).
CLASSIFICATION: D; not classifiable as to human carcinogenicity. BASIS FOR
CLASSIFICATION: Based on no human carcinogenicity data and inadequate animal
data. HUMAN CARCINOGENICITY DATA: None. ANIMAL CARCINOGENICITY DATA: Inadequate.
A4. A4= Not classifiable as a human carcinogen.
Human Toxicity Excerpts:
Oral ingestion can result in mucocutaneous and gastrointestinal corrosion.
Both oral ingestion and extensive application to the skin can cause systemic
toxicity manifested by transient CNS stimulation followed by CNS and
cardiovascular depression; death may result.
CHRONIC SYSTEMIC ABSORPTION OF PHENOL HAS CAUSED GRAY COLORATION OF THE
SCLERA WITH BROWN SPOTS NEAR THE INSERTION OF RECTUS MUSCLE TENDONS, ASSOCIATED
WITH BLUE OR BROWN DISCOLORATION OF THE TENDONS OVER THE KNUCKLES OF THE HANDS.
THIS IS A FORM OF OCHRONOSIS, KNOWN AS CARBOLOCHRONOSIS, OF WHICH 20 CASES ...
/WERE REPORTED/ UP TO 1942 ... .
SYMPTOMATOLOGY: 1. Burning pain in mouth and throat. White necrotic lesions
in mouth, esophagus and stomach. Abdominal pain, vomiting ... and bloody
diarrhea. 2. Pallor, sweating, weakness, headache, dizziness, tinnitus. 3.
Shock: Weak irregular pulse, hypotension, shallow respirations, cyanosis,
pallor, and a profound fall in body temperature. 4. Possibly fleeting excitement
and confusion, followed by unconsciousness ... 5. Stentorous breathing, mucous
rales, rhonchi, frothing at nose and mouth and other signs of pulmonary edema
are sometimes seen. Characteristic odor of phenol on the breath. 6. Scanty,
dark-colored ... urine ... moderately severe renal insufficiency may appear. 7.
Methemoglobinemia, Heinz body hemolytic anemia and hyperbilirubinemia have been
reported ... 8. Death from respiratory, circulatory or cardiac failure. 9. If
spilled on skin, pain is followed promptly by numbness. The skin becomes
blanched, and a dry opaque eschar forms over the burn. When the eschar sloughs
off, a brown stain remains.
The predominant acute action of a toxic dose in man appears to be to the
central nervous system, leading to sudden collapse and unconsciousness.
A 19 yr old female ingested 15 ml of phenol and complained of severe nausea,
burning in the throat, and epigastrium. Laryngoscopic examination revealed
superficial burns and slight edema of the hypopharynx. Despite gastric lavage
with olive oil and intravenous saline administration, she continued to be
nauseated. One hr later she began to vomit blood and to have diarrhea, passing
copious amounts of blood with clots. She gradually became cyanotic and stuporous.
Her blood pressure decreased markedly and her extremities became cold. She
experienced periods of relapse and recovery during treatment but died 17.5 hr
after ingestion.
A woman committed suicide by ingesting 10-20 g of phenol. She became comatose
with partial absence of reflexes, pallor of the skin, accelerated respiration,
weak and rapid pulse, and dilated pupils which did not react to light. Almost
one hour after the ingestion, her heart and respiration stopped and, in spite of
repeated attempts at resuscitation for two hours, she died. Autopsy revealed
marked hyperemia of the tracheal and bronchial mucous membranes. Histologic
examination revealed pulmonary and liver edema as well as hyperemia of the
intestines.
An industrial employee spraying weeds with effluent of a chemical
plant, containing 43% phenol, 20% water, 14% cresols, 11.5% low-boiling
organics, and 11% high-boiling organics suffered burns on thighs and genitalia.
The affected sites were washed with large amounts of warm water (30 min)
followed by ethanol (10 min). Washing and scrubbing were repeated. Within 30
minutes the employee developed symptoms of shock. Reduced body temperature, weak
and irregular pulse, accelerated respiratory rate, stertorous breathing, and
constricted pupils which showed a slow response to light and slow accommodation.
His left leg had convulsive movements for 30 minutes. Tests for a liver function
were normal. Urine was not analyzed for phenol until 4 days after exposure at
which time it was negative. Recovery was complete and the patient was released 7
days later from the hospital.
An employee accidentally spilled 4-5 liters of 78% aqueous phenol on himself.
Following immediate irrigation with alcohol, he exhibited superficial skin
burns, became comatose and died shortly thereafter.
Earlier investigators reported certain signs and symptoms not found in more
recent reports including abortion, acquired ochronosis, difficulty in
swallowing, and tinnitus.
Fatal neonatal hyperbilirubinemia from inhalation of phenolic vapors has
occurred in poorly ventilated nurseries in which phenol was used to disinfect
mattresses and bassinets.
On human eyes, concn phenol has had severe effects ... rendering the
conjunctiva chemotic, and the cornea white and hypesthetic. The lids have become
edematous. ... Severe iritis ... in at least one case. Visual results have been
varied from complete recovery ... to blindness and loss of one eye.
... A 32 yr old male ... spilled a solution of phenol over his scalp, face,
neck, shoulders and back. The victim died 10 min later. There was coagulation
necrosis of the skin and left eye and acute dermatitis veneta with acute passive
congestion of the lungs, liver, spleen, and kidneys.
... 1 ounce of 89% phenol was mistakenly given in a measured container to an
outpatient. ... The patient immediately ... collapsed. Within 30 min she had an
unrecordable blood pressure and sustained respiratory arrest. ... The patient
experienced ventricular tachycardia 1 hr post-ingestion, and resuscitation was
effected ... over first 24 hr ... ventricular arrhythmias, seizures, and
metabolic acidosis. ... Subsequent esophagitis and gastrointestinal bleeding
occurred. The patient survived. ...
Toxic blood level (the concn of drug or chemical
present in the blood that is associated with serious toxic symptoms in humans):
9 mg%; Lethal blood level (the concn of chemical
present in blood that has been reported to cause death, or is so far above
reported therapeutic or toxic concn that one can judge that it might cause death
in humans): 90 u/ml /Table/
Application of moderate amounts to the skin causes epidermal separation and a
severe exposure causes necrosis.
Undiluted /phenol/ cauterizes and whitens the skin and mucous membranes.
PHENOL ... EMPLOYED IN VAGINAL DOUCHE HAS CAUSED LOCAL & SYSTEMIC
POISONING.
14 mg/kg resulted in gastrointestinal effects, and ingestion of 140 mg/kg
caused death.
Phenol is toxic if absorbed and may result in death even if the exposed area
is as small as that of a hand or forearm.
Chemexfoliation (chemical peeling)
is being used to obtain both therapeutic (eg, actinic keratoses) and cosmetic (eg,
removal of fine facial rhytides) benefits. Phenol, one of the most widely used
agents for inducing cutaneous exfoliation, may induce cardiac arrhythmias and is
toxic to the liver and kidneys. Both phenol and trichloroacetic acid may produce
hypertrophic scars and/or keloids and pigmentation irregularities, may
accentuate preexisting abnormalities (eg, telangiectasias, nevi, and pores), and
may be associated with a flare of latent herpesvirus infection. Prolonged
erythema of the treated areas and persistent rhytids have been reported with
both agents.
... Phenol is metabolized to DNA reactants at a low rate by human
lymphocytes; the addition of S9 amplifies the rate of metabolism.
... Phenol damages skin, which increases the rate of penetration; therefore,
it should be applied only on small areas of skin, and occlusive dressings,
bandages, or diapers should not be used. Phenol is not recommended for use in
pregnant women, in infants under 6 months, or for diaper rash. Phenolic
disinfectants have produced epidemics of neonatal hyperbilirubinemia when used
to clean bassinets and mattresses in poorly ventilated nurseries. Fatalities
have been documented in infants. ...
Phenol and substituted phenols vary greatly in their antiseptic and
disinfectant efficacy and safety. Phenol is bacteriostatic in concentrations of
1:500 to 1:800 and bactericidal and fungicidal in concentrations of 1:50 to
1:100. It is not effective against spores. Phenol is seldom used as an
antiseptic or disinfectant. Because it possesses local anesthetic activity and
has an antipruritic effect at concentrations of 0.5% to 1.5%, its primary use is
as a component of topical antipruritic formulations.
Phenol is not a very volatile cmpd. Consequently, most toxic effects occur
from dermal and oral exposure.
Phenol is nephrotoxic to humans and animals, especially following chronic
exposure. ... Humans have experienced nephritis following toxic dermal exposure.
Although esophageal stricture is rare, it is a long term complication that
may develop /as a result of phenol poisoning/.
Several cases of sudden death or intra- or postoperative complications have
been reported after phenol face peels ... .
Major cardiac arrhythmias were noted ... in 10 out of 43 patients during
phenol face peels. However, this item is rather controversial, and some authors
feel that when the procedure is done over more than 1 hour, and when the dose
applied is carefully monitored, phenol face peels are not risky ... .
... A spray of 12.5% phenol dissolved in 25% glycerol in water struck both
eyes of a patient, and induced faint haze in the corneal epithelium, associated
with fine gray stippling visible by slit-lamp biomicroscope, causing temporary
impairment of vision to 6/12 and 6/18. The corneas cleared within 4 days, and
vision returned to normal.
An oral dose of 1 g of phenol may be lethal to man; however, in exceptional
cases, patients have survived the ingestion of 65 g of pure phenol or 120 g of
the crude product. Roughly 50 percent of all reported cases have terminated
fatally.
Application of a bandage containing 2% phenol to the umbilicus of a newborn
baby resulted in death after 11 hour. Another newborn baby treated with 30%
phenol:60% camphor for a skin ulcer experienced circulatory failure, cerebral
intoxication and methemoglobinemia but recovered after a blood transfusion ... .
After an acute percutaneous intoxication of a chemical
worker with phenol, local effects on the skin were seen in conjunction with
several effects due to systemic intoxication, including massive intravascular
hemolysis, tachycardia, respiratory depression, and renal and liver damage. The
latter was concluded from the increased activities of liver enzymes in the serum
... .
... Exposure by inhalation to low concn of phenol (0.004 ppm; 0.015 mg/cu m)
six times for 5 minutes produced increased sensitivity to light in three
volunteers adapted to the dark. Exposure to 0.006 ppm (0.02 mg/cu m) phenol for
15 seconds resulted in the formation of conditioned electrocortical reflexes in
four volunteers ... .
Repeated oral exposure for several weeks (estimated intake, 10-240 mg/day)
due to contamination of groundwater after an accidental spill of phenol resulted
in mouth sores (burning of the mouth), diarrhea and dark urine. Examination six
months after the exposure revealed no residual effect ... .
... Phenol /was applied/ to the skin (over 75% of the body surface area) of
20 adults at 2% in calamine lotion and 4.75% in phenol-camphor liquid petrolatum
preparations. Blood samples were collected pre-exposure and at 2 hour intervals
for 1 to 3 days and analyzed for phenol using the method of Deichmann and
Schafer. In both tests, pre-exposure concentrations of free phenol in the blood
of all subjects averaged 0.15 mg/100 ml and increased to an average of 0.4
mg/100 ml during each of the tests. Pre-exposure concentrations of conjugated
(protein-precipitated) phenol in the blood of all subjects averaged 0.35 mg/100
ml in both experiments. Conjugated phenol concentrations in blood increased over
the range of 0.9 to 1.9 mg/100 ml of blood for both preparations. There were no
detectable differences in the resulting concentrations of free and conjugated
phenol in the blood when either preparation was applied to the skin.
Detoxication by conjugation was initiated immediately, and blood concentrations
of both free and conjugated phenol returned to pre-exposure levels within 24
hours.
... Exposures to airborne phenol and the associated urinary phenol
concentrations from employees in a Bakelite factory /were measured/. Airborne
concentrations of phenol ranged from 0 to 12.5 mg/cu m (3.3 ppm). Urine samples
were collected before and after exposure and analyzed for total, free, and
conjugated phenol and for ethereal glucuronides and sulfates; the concentration
of free phenol varied little with the changes in airborne phenol concentrations.
Ethereal sulfates in the urine generally increased with increasing airborne
phenol concentrations. Increases in urine phenol fractions were observed during
the work shift, but these concentrations decreased to pre-exposure levels within
16 hours. There were no ill effects in any of the workers surveyed.
Skin, Eye and Respiratory Irritations:
Strong irritant to tissue.
Vapor irritates respiratory system and eyes.
Drug Warnings:
DIL PHENOL SOLN (1 TO 2%) ARE USED MEDICINALLY AS ANTIPRURITIC PREPN FOR THE
SKIN. THEIR REPEATED USE OVER LARGE SKIN AREAS OR ON PARTICULARLY MOIST AREAS (AXILLARY
REGION, GROIN, FEET) SHOULD BE AVOIDED.
Soln of phenol (6%) in glycerine are sometimes employed in medical practice
to produce nerve blocks. The spread of phenol beyond the intended site (stellate
ganglion) resulted in infarction on the cervical cord with extensive paralysis
in one patient and neurolosis of the cervical posterior roots with respiratory
arrest in another.
... Phenol ... should be applied only on small areas of skin and occlusive
dressings, bandages, or diapers should not be used.
Phenol should never be used in pregnant women, in infants under 6 mo, or for
diaper rash.
The development of widespread Herpes simplex on the face after phenolic face
peels is not considered rare. Precaution in choosing patients is recommended.
Four cases of acute exacerbation of Herpes simplex are presented in patients who
had recently undergone phenolic face peels.
Medical Surveillance:
... There is some suggestive evidence that a biologic monitoring method may
be useful for detecting an excessive internal dose on an individual ... and/or
on a group basis /for phenol/. Tentative max value in urine <20 mg/g
creatinine, permissible value 300 mg/g creatinine. /From table/
/SRP: Pre-exposure physical examination followed by annual examination of
exposed personnel,/ including studies of liver and kidney function. /Protect/
... those individuals with diseases of central nervous system, liver, kidney,
and lung.
Populations at Special Risk:
Those affected with hepatic or kidney diseases should not be exposed to
phenol for any length of time, because even intermittent exposure to vapors ...
may become dangerous, particularly when ... handled at elevated temp.
Probable Routes of Human Exposure:
WITH RARE EXCEPTIONS, HUMAN EXPOSURE IN INDUST HAS BEEN LIMITED TO ACCIDENTAL
CONTACT OF PHENOL WITH SKIN OR INHALATION OF PHENOL VAPORS.
NIOSH (NOES Survey 1981-1983) has statistically estimated that 320,914
workers are exposed to phenol in the USA(1). Eighty percent of these exposures
are to trade name products containing phenol. Phenol was detected in the general
work atmosphere of a brake pad assembly plant in New Holstein, WI - 0.025 and
0.042 ppm(3). The concn of phenol in bakerlite factories was reported to be 12.5
mg/cu m(2). Phenol was measured in the atmosphere of a dental school laboratory
in Philadelphia, PA during dissection of cadavers at 1.3-5.0 parts per
trillion(4). A study of exposure levels during 25 embalmings found that exposure
to phenol was <0.5 ppm(5). The area air concn of phenol during paint
stripping operations on a Boeing 747 aircraft (120-330 min sampling periods,
n=9) was 3.4-9.5 mg/cu m with a mean of 5.7 mg/cu m(6). For an 8-hr shift, the
exposure levels were 1.1-5.3 mg/cu m with a mean of 2.7 mg/cu m(6).
Protective gloves may be permeable to phenol. The breakthrough times and
permeation rates of 5 mil thicknesses of five common glove materials to solid
phenol were (material, breakthrough time (min), steady state permeation rates (ug/min/sq
cm): latex, 10.4, 0.0151; PVC, 10.6, membrane solubilized; polyurethane, 28.0,
0.233; neoprene, 21.0, 0.201; polynitrile, 185.0, 0.0114(1).
Workplace exposure to phenol will occur via inhalation and dermal absorption
of phenol-containing wastewater, emissions and disinfectants or solvents. The
general population may be exposed to phenol by ingesting food or medicinal
products such as throat lozenges. They will also be exposed by inhalation of
ambient air and cigarette smoke and dermal absorption of phenol contained in
decomposing organic matter and disinfectants and other consumer products(SRC).
Body Burden:
Identified, but not quantified, in 9 of 12 samples of breath in Bayonne and
Elizabeth, NJ as part of the Total Exposure Assessment Methodology (TEAM)
study(1).
Average Daily Intake:
WATER INTAKE: Insufficient data; AIR INTAKE: (assume typical concn in indoor
air of 0.70 ug/cu m) 14 ug; FOOD INTAKE: Insufficient data.
Minimum Fatal Dose Level:
Ingestion of as little as 4.8 g of pure phenol caused death in 10 min.
Antidote and Emergency Treatment:
Because of the rapid onset of symptoms, possible increased phenol absorption
with dilution, and the potential for development of seizures, activated charcoal
(1 g/kg) is preferable to lavage or syrup of ipecac. In vitro studies indicated
that activated charcoal efficiently absorbs phenol. A cathartic should be given
after oral activated charcoal.
Immediate emesis or lavage after phenol ingestion is important to consider,
but are contraindicated in esophageal injury. Egg whites, milk, or gelatin
solution, which serve a protein sources to interact with phenol remaining in the
stomach, may be given. Activated charcoal, followed by a cathartic, may be
preferred to ipecac induced emesis or lavage in decontamination of the GI tract
and preventing systemic absorption of phenol.
Phenol may be extracted from cutaneous tissues by use of alcohol following
either intentional or accidental application. An alcohol bath or dressing of
alcohol applied to the affected area for several minutes will extract most of
the phenol. Phenol has a much greater solubility in alcohol than in the aqueous
tissue fluids and therefore diffuses out of the tissues. If phenol has
penetrated deeply, an oil dressing should be applied after two or three
applications of alcohol. Phenol will also preferentially diffuse into oil.
Animal Toxicity Studies:
Toxicity Summary:
HUMAN TOXICITY: Phenol is toxic with a probable oral lethal dose to humans of
50-500 mg/kg. Some individuals may be hypersensitive with lethality or serious
effects at very low exposures. Rapid absorption and severe systemic toxicity can
occur after any route of exposure including skin. Death and severe toxicity are
usually due to effects on the CNS, heart, blood vessels, lung, and kidneys.
However, toxic manifestations may vary somewhat with the route. Observed effects
from acute exposure may include: shock, delirium, coma, pulmonary distress,
phenolic breath, scanty/dark urine, and death. Protracted or chronic exposure
usually results in major damage to the liver, kidneys and eyes. Pigmentary
changes of the skin have been noted. Consumption of water contaminated with
phenol resulted in diarrhea, mouth sores, burning of the mouth, and dark urine.
Phenol is highly caustic to tissues. Skin exposure results in pain, then
numbness, blanching, severe burns, and eschar formation. Ingestion leads to
burning of throat and severe gastrointestinal inflammation. Inhalation can
result in pulmonary irritation and edema. ANIMAL TOXICITY: Toxicity in animals
is similar to that of humans, although additional effects have been observed.
LD50's in animals range from 250-500 mg/kg, differing very little with route of
exposure or species, except for the cat which is unusually susceptible with an
oral lethal dose of 80 mg/kg. Additional reported toxic effects include
irritation and corrosivity of skin and eyes in rabbits, induction of skin tumors
in mice, reproductive effects in rats, and mutagenicity with Salmonella, E coli
and Drosophila. Phenol is also highly toxic to aquatic life and frogs.
METABOLISM: Phenol is metabolized and excreted principally by the kidneys as the
sulfate or glucuronide, although some phenol may be excreted unchanged,
especially at high doses. Other reported metabolites include hydroquinone, other
quinones and catechols.
Evidence for Carcinogenicity:
Evaluation: There is inadequate evidence in humans for the carcinogenicity of
phenol. There is inadequate evidence in experimental animals for the
carcinogenicity of phenol. Overall evaluation: Phenol is not classifiable as to
its carcinogenicity to humans (Group 3).
CLASSIFICATION: D; not classifiable as to human carcinogenicity. BASIS FOR
CLASSIFICATION: Based on no human carcinogenicity data and inadequate animal
data. HUMAN CARCINOGENICITY DATA: None. ANIMAL CARCINOGENICITY DATA: Inadequate.
A4. A4= Not classifiable as a human carcinogen.
Non-Human Toxicity Excerpts:
... GUINEA PIGS WERE SEVERELY INJURED DUE TO INHALATION FOR 20 DAYS OF PHENOL
VAPOR AT CONCENTRATIONS OF FROM 25 TO 50 PPM. POST MORTEM EVIDENCE OF ACUTE
TOXICITY TO LUNG, HEART, LIVER AND KIDNEYS WAS FOUND.
ON RABBIT EYES, CRYSTALLINE OR CONCN AQ PHENOL CAUSES ALMOST INSTANTANEOUS
WHITE OPACIFICATION OF THE CORNEAL EPITHELIUM. EIGHT HOURS AFTER APPLICATION THE
CORNEA IS ANESTHETIC, THE SURFACE ULCERATED, AND THE STROMA OPAQUE. IN 5 WK
THERE IS ENTROPION, SCARRING OF THE CONJUNCTIVA, AND OPACITY OF THE CORNEA.
PRETREATMENT WITH SINGLE APPLICATION OF ABOUT 75 UG OF
9,10-DIMETHYL-1,2-BENZANTHRACENE (DMBA) WAS NOT ESSENTIAL FOR INDUCTION OF
TUMORS. PHENOL ... /ALONE INDUCED/ PAPILLOMAS & CARCINOMAS, BUT TIME
REQUIRED FOR PRODN OF TUMORS WAS EXTENDED WHEN PRETREATMENT WITH DMBA ...
EXCLUDED. MAX RESPONSE PRODUCED WITH 10% SOLN ... LESS MARKED, BUT POSITIVE,
EFFECT WAS CAUSED BY A 5% SOLN. A MORE CONCENTRATED (20%) SOLN CAUSED DEATH FROM
SYSTEMIC TOXICITY BEFORE TUMORS WERE PRODUCED. BY USING REAGENT GRADE, USP &
PURIFIED PHENOL, IT WAS SHOWN THAT THIS /TUMORIGENIC/ ACTION WAS DUE TO PHENOL
ITSELF, NOT TO A CONTAMINANT.
THE EFFECT OF PHENOL ON THE PERMEABILITY OF ORGANELLE MEMBRANES OF CULTURED
CELLS WAS ASSESSED. BHK (BABY HAMSTER KIDNEY)-(21)C13 CELLS WERE GROWN AS
MONOLAYERS ON GLASS COVER SLIPS & EXPOSED FOR 1 HR TO 1 MG/L & 2 MG/L
PHENOL. AT A CONCN OF 1 MG/ML, PHENOL CAUSED LABILIZATION OF THE LYSOSOMES &
CONSEQUENT LOSS OF ENZYMES, WHICH IS FURTHER ENHANCED AT 2 MG/ML. THE
MITCHONDRIAL MEMBRANES ALSO SHOWED A MARKED INCREASE IN PERMEABILITY AFTER
EXPOSURE TO 1 MG/ML PHENOL, BUT TO A LESSER EXTENT THAN THAT OF LYSOSOMES.
IN SPRAGUE-DAWLEY RATS, ONE-HALF OF THE ANIMALS BECAME DEEPLY COMATOSE WITH
540 UMOL OF IP PHENOL & 100% WITH 600 UMOL. FIVE STAGES OF ENCEPHALOPATHY
WERE READILY DISTINGUISHED WITH SYMPTOMS OF INCREASED & DECREASED MUSCLE
TONUS, RIGHTING REFLEX, & BODY TREMOR UNTIL RECOVERY OR DEATH OF ANIMALS.
In animals, the pathological changes produced by phenol vary with the route
of absorption, vehicle employed, concentration, and duration of exposure. Local
skin disorders include eczema, inflammation, discoloration, papillomas,
necrosis, sloughing, and gangrene. After oral ingestion, the mucous membranes of
the throat and esophagus may show swelling, corrosions, and necrosis, with
hemorrhage and serous infiltration of the surrounding areas. In severe
intoxication, the lungs may show hyperemia, infarcts, bronchopneumonia, purulent
bronchitis, and hyperplasia of the peribronchial tissues. Myocardial
degeneration and necrosis can be present. The hepatic cells may be enlarged,
pale, and coarsely granular with swollen fragmented and pyknotic nuclei.
Prolonged administration of phenol may cause parenchymatous nephritis,
hyperemia, edema of the convoluted tubules, and degenerative changes of the
glomeruli. Blood cells become hyaline, with granules. Marked striation of the
muscle fibers is also seen.
Following initiation with 9,10-dimethyl-1-2,-benzanthracene (DMBA) and
promotion by croton oil through skin painting, mice received 2/wk dermal
applications of 2.5 mg phenol (as a 10% solution in benzene). Mice exhibited
severe skin damage, decreased body weight and increased mortality. After 13
weeks, 22/23 mice had developed papillomas, and 13% had carcinomas of the skin.
In mice treated with DMBA only, 3/21 survivors exhibited papillomas after 42
weeks. Through skin painting with 10% phenol, 5/14 survivors (36%) had
papillomas after 52 weeks. In this group, skin painting was continued to 72
weeks at which time one fibrosarcoma was diagnosed.
The S strain albino mice showed strong promoting activity for tumor formation
after initiation with 0.3 mg 9,10-dimethyl-1,-2,-benzanthracene (DMBA) followed
by repeated skin applications of 20% phenol. 20% phenol soln produced
significant damage to the skin and were weakly carcinogenic when applied alone.
Phenol in a 5% soln had moderate promoting activity, but was not carcinogenic
without previous initiation.
Experiments with Drosophila have shown phenol to be highly mutagenic.
Phenol was evaluated for the induction of sex-linked recessive lethal
mutations in Drosophila melanogaster by the National Toxicology Program.
Canton-S wild-type males were treated with concentrations of phenol that result
in approximately 30% mortality. Following treatment, males were mated
individually to 3 harems of Basc virgin females to produce 3 broods for
analysis. The concentrations of phenol tested by injection (5250 ppm) or feeding
(2000 ppm) were negative in this assay.
Phenol is very toxic to fish and has a nearly unique quality of tainting the
taste of fish if present in marine environments at 0.1-1.0 ppm.
Poisoning from prep containing phenol is occasionally seen in domestic
animals, but especially in cats.
Glaucoma has been induced experimentally in rabbits by injecting 5% phenol in
almond oil subconjunctivally in all four quadrants.
Phenols ... have been implicated ... /in the formation/ of Heinz bodies in
many /animal/ species.
Minor and Becker (1971) injected rats ip on days 8-10 or 11-15 /of gestation/
with up to 200 mg/kg. No adverse fetal effects were observed.
Phenol tested positive for mutagenicity in L5178Y Mouse Lymphoma cells.
Mutation: Esherischia coli back mutation dose 0.1-0.2%.
Inhalation of phenol was related to stimulation of central nervous system,
followed by severe depression. Exposure of animals to phenol resulted in
paralysis in some animal species, but not in others.
In grey mullet exposed to 5 mg phenol/l for 8 days, blood sugar and the
activities of aspartate aminotransferase and lactate dehydrogenase in blood
plasma were above controls; no gross pathology was observed. After an 8 day
exposure to 7.5 mg phenol/l, blood hemoglobin concn, hematocrit value, and
lactate, protein, glyceride, and cholesterol concentrations were below controls
and blood sugar concn and the activities of aspartate aminotransferase and GPT
were above controls. Damage to gills, liver, gallbladder, and kidney was
observed. Higher concentrations (10-28 mg/l) were lethal in several hours; 0.5
mg/l was nontoxic during an 8 day exposure.
Male B6C3F1 mouse bone marrow adherent stromal cells were plated at 4X10+6
cells per 2 ml of DMEM medium in 35 mm tissue culture dishes. The growing
stromal cell cultures were exposed to log 2 doses of phenol for 7 days. The
doses which caused a 50% decrease in colony formation (TD50) was 190x10-6 M for
phenol.
A dog bathed in a phenolic disinfectant developed signs including an
anorexia, excessive salivation, muscular twitching, vomiting, cutaneous
erythema, pruritis and necrosis and a rectal temperature of 40.0 deg C. Topical
and parenteral antibiotic treatment resulted in recovery within one week.
The post-mortem changes associated with ingestion of phenol or cresol are
those that would be expected following exposure to any extremely irritant and
corrosive poison. Centribular necrosis and haemorrhage of the liver are produced
in pigs consuming 'clay' pigeons.
... Phenol was administered to rats or mice at 0, 2500, or 5000 ppm in
drinking water for 103 weeks. An increased incidence of leukemia and lymphomas
was detected only in the low dose male rats.
Molten analytical grade phenol was applied to the intact skin of the pigs at
500 mg/kg, over 35% to 40% of the total body surface area for 1.0 or 2.5
minutes. Phenol was absorbed rapidly through the intact skin. Increasing the
concentration of the applied phenol did not increase the plasma phenol
concentration as much as did increasing the treated surface area. Peak plasma
phenol concentrations (52.6 ppm) were achieved at 1.75 hours postexposure.
Phenol was detected in plasma 8.75 hours after exposure, but it was not
detectable at 23 hours. The metabolism and elimination of parent phenol and its
metabolites were not examined.
... A study was conducted to compare the cardiovascular responses to these
two agents in a rat model. Fifteen rats underwent abdominal epilation. Two to
six days later a surface area comparable to the human face (16 sq cm) was
delineated on the abdomen. Baker's phenol of 50% TCA was applied to this area.
Cardiac rate and rhythm and arterial pressure were monitored. Once stable, the
same agent was applied to the entire abdomen for furthur study. TCA has been
shown to be a safer agent than phenol in this rat model. Assuming that this
model simulates the human response, monitoring would appear to be indicated
during full-face Baker's phenol peeling.
... Under the conditions of this bioassay, phenol was not carcinogenic for
either male or female F344 rats or male and female B6C3F1 mice. Levels of
Evidence of Carcinogenicity: Male Rats: Negative; Female Rats: Negative; Male
Mice: Negative; Female Mice: Negative.
National Toxicology Program Studies:
A bioassay of phenol to test for possible carcinogenicity was conducted by
providing this substance in drinking water to F344 rats and B6C3F1 mice. Groups
of 50 rats and 50 mice of each sex were given drinking water containing 2,500 or
5,000 ppm phenol for 103 wk. As matched controls, groups of 50 rats and 50 mice
of each sex received tap water. ... Under the conditions of this bioassay,
phenol was not carcinogenic for either male or female F344 rats or male and
female B6C3F1 mice. Levels of Evidence of Carcinogenicity: Male Rats: Negative;
Female Rats: Negative; Male Mice: Negative; Female Mice: Negative.
Non-Human Toxicity Values:
LD50 Rat oral 0.53 g/kg
LD50 Cat oral 0.1 g/kg
LD50 Dog oral 0.5 g/kg
Ecotoxicity Values:
TDLO Minnow 30 min 79 ug/l
LC50 Crangon crangon 5600 mg/l 3 min, 20 mg/l 1 hr, 80 mg/l 3 hr, 40 mg/l
6-24 hr, 30 mg/l 48-72 hr, 25 mg/l 96 hr in sea water at 15 deg C /Conditions of
bioassay not specified/
Algae: Chlorella pyrenoidosa toxic: 233 mg/l, 1.06 mg/l /Conditions of
bioassay not specified/
Scenedesmus quadricauda toxicity threshold (cell multiplication inhibition
test) 7.5 mg/l /Conditions of bioassay not specified/
Algae: Microcystis aeruginosa inhibition of cell multiplication noted at 4.6
mg/l /Conditions of bioassay not specified/
Protozoa: Vorticella campanula perturbation level 3 mg/l /Conditions of
bioassay not specified/
Protozoa: Paramecium caudatum: perturbation level, 10 mg/l /Conditions of
bioassay not specified/
Arthropoda: LD0 Daphnia magna 16 mg/l /Conditions of bioassay not specified/
Arthropoda: TLm Daphnia magna 100/100 mg/l 25-50 hr /Conditions of bioassay
not specified/
Arthropoda: TLm Daphnia magna (young) 17/7 mg/l 25-50 hr /Conditions of
bioassay not specified/
Arthropoda: TLm Daphnia magna (adult) 61/21 mg/l 25-50 hr /Conditions of
bioassay not specified/
Arthropoda: Brine shrimp 157/56 mg/l 24-48 hr /Conditions of bioassay not
specified/
Fish: TLm Lepomis macrochirus >15 mg/l 25-50 hr /Conditions of bioassay
not specified/
Fish: TLm Arctopsyche grandis 61/0.001 mg/l 24-96 hr /Conditions of bioassay
not specified/
Fish: TLm Mosquito fish 22.7/56 mg/l 24-96 hr /Conditions of bioassay not
specified/
TLm bluegill (Lepomis macrochirus) 5.7-20 mg/l/96 hr in a flow-through
bioassay
Fish: TLm Bluegill (Lepomis macrochirus) 19/5.7 mg/l 24-96 hr /Conditions of
bioassay not specified/
TLM Mercenaria mercenaria (hard clam) larvae 5.5X10+4/12 days in a static
bioassay.
LC50 Rainbow trout 5.6-11.3 mg/l/24 hr in a static bioassay.
TLM Fathead minnow 41 mg/l/48 hr at 15 deg C; 28 mg/l/48 hr at 25 deg C, both
tests conducted in a flow-through bioassay.
TLM Fathead minnow 36 mg/l/96 hr at 15 deg C; 24 mg/l/96 hr at 25 deg C, both
tests conducted in a flow-through bioassay.
TLm Goldfish 49.9 mg/l/24 hr, 49.1 mg/l/48 hr, 44.5 mg/l/96 hr in soft water
/Conditions of bioasay not specified/
TLm Roach 15 mg/l/24 hr /Conditions of bioassay not specified/
TLm Crassostrea virginica (american oyster) egg 5.825X10+4 ppb/48 hr in a
static bioassay.
TLm Mercenaria mercenaria (hard clam) egg 5.263X10+4 ppb/48 hr in a static
bioassay.
LC50 Golden shiner 35-129 mg/l in a static bioassay.
LC50 Ophicephalus punctatus 46.0 mg/l/48 hr in a static bioassay.
LC50 Fathead minnow >50 mg/l/1 hr, >50 mg/l/24 hr, 33 mg/l/72 hr, 32
mg/l/96 hr in a static bioassay in Lake
Superior Water at 18-22 deg C.
LC50 Goldfish 60-200 mg/l/24 hr in a static bioassay.
TSCA Test Submissions:
Phenol (CAS # 108-95-2) was evaluated for subchronic dietary toxicity. The
test substance was administered to male albino rats (10/group) for 28-days at a
concentration level of 100 ppm (8.22 mg/kg/day); 500 ppm (42.8 mg/kg/day); and
1000 ppm (86.2 mg/kg/day). No deaths or signs of intoxication were noted among
any of the animals. At autopsy, no significant gross pathologic lesions were
found.
Phenol (CAS # 108-95-2) was evaluated for subchronic oral toxicity. The test
substance was administered by gavage to rabbits (sex and strain not indicated)
in a 10% alcohol solution at a dosage level of 0.5 g/kg (1 rabbit, 2 doses); 0.1
g/kg (2 rabbits, 20 doses each); 0.05 g/kg (1 rabbit, 20 doses); and 0.01 g/kg
(1 rabbit, 20 doses). At 0.5 g/kg, the rabbit died and necropsy revealed a
swelled, congested liver, and desquamation of the stomach. At 0.1 g/kg, 1 rabbit
had kidney irritation and the other rabbit had slight liver degeneration.
Phenol (CAS # 108-95-2) was evaluated for subchronic oral toxicity. The test
substance was administered by gavage to rats (sex and strain not indicated) at a
dosage level of 0.5 g/kg (1 rat, 1 dose); 0.3 g/kg (1 rat, 17 doses); 0.2 g/kg
(1 rat, 20 doses); 0.1 g/kg (2 rats, 20 doses each); and 0.01 g/kg (1 rat, 20
doses). At 0.5 g/kg the rat died and at 0.2 g/kg the rat had pneumonia and died.
At 0.2 and 0.1 g/kg, the rats had areas of liver degeneration.
Phenol (CAS # 108-95-2) was evaluated for subchronic oral toxicity. The test
substance was administered to rabbits (number, sex, and strain not indicated) at
dosage levels of 0.001 or 0.1 g/kg for 20 doses. At 0.1 g/kg, slight kidney
change was noted and at 0.001 g/kg, there was no observable change.
Phenol (CAS # 108-95-2) was evaluated for chronic oral toxicity. In the first
experiment, the test substance was administered by gavage to groups of 3 rats
(sex and strain not indicated) at dosage levels of 0.2, 0.1, 0.05, or 0.01 g/kg
for 6 months. At 0.2 g/kg, the animals died or were sacrificed after 1, 6, and
16 doses; all animals had tremors. The animals receiving 1 and 6 doses had
stomach irritation; liver congestion and degeneration; and kidney congestion and
slight hemorrhage. The animal that received 16 doses was moribund when
sacrificed, but no toxicity was detected microscopically. Two animals at 0.1
g/kg, 2 animals at 0.05 g/kg, and 1 animals at 0.01 g/kg survived 136 doses with
no pathological findings. In the second experiment, the test substance was
administered by gavage to groups of 10 rats (sex and strain not indicated) at
dosage levels of 0.1 or 0.05 g/kg for 6 months (5 days a week until 135 or 136
doses had been given). Four rats from each group died; there was no indication
that death was treatment-related. At 0.1 g/kg, there was a cloudy swelling of
the livers and damage to the kidneys with a cloudy swelling of the tubular
epithelium. There was also a slight increase in the weights of the liver and
kidneys. At 0.05 g/kg, 2 animals had injured kidneys, distention of the pelvis,
slight tubular degeneration and a few casts. Blood chemistry indicated a slight
decrease in lymphocytes and bone marrow count was normal.
Phenol (CAS # 108-95-2) was evaluated for reproductive oral toxicity. The
test substance was administered by gavage to mated Charles River Crl:CD VAF/Plus
female rats (10/group) at dosage levels of 0 mg/kg/day (Control); 3 groups at 60
mg/kg/day; 3 groups at 120 mg/kg/day; or 180 mg/kg/day on gestation days 6
through 14. At 120 mg/kg/day, maternal toxicity included reduced body weight
gain and feed consumption. There were treatment-related findings in regards to
clinical signs, developmental toxicity, necropsy findings, organ weights, or
pathology results.
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
A PORTION OF ABSORBED /PHENOL/ DRUG IS OXIDIZED TO HYDROQUINONE &
PYROCATECHOL.
Phenols are subjected to oxidative metabolism leading to ortho- and
para-hydroxylated products. These metabolites are then transformed into
equimolar amounts of two conjugates, sulfates and glucuronides.
Metabolism in rabbits given a lethal dose of phenol (0.5 g/kg) resulted in:
47% oxidation to carbon dioxide and water plus traces of 1,4-dihydroxybenzene
and ortho-dihydroxybenzene, 3% excreted in urine, 50% remaining in the carcass.
Amounts were exhaled in air and excreted in in the feces. Metabolism in rabbits
given a sublethal dose of phenol (0.3 g/kg) resulted in: 23% oxidation to carbon
dioxide and water plus traces of 1,4-dihydroxybenzene and
ortho-dihydroxybenzene, 72% excreted in the urine, 4% remaining in the carcass,
1% excreted in the feces, and trace amounts exhaled in air. Urinary route
resulted in either excretion as free phenol or as conjugate. (Conjugation with
sulfuric acid, glucuronic acid or other acids). /From figure/
The cat was shown to be sensitive to phenol. In addition to sulfate
conjugates, free 1,4-dihydroxybenzene was found as a major metabolite which may
account for the toxicity observed in the cat.
Some species differences have been noted in the metabolism of phenol. Man,
rat, mouse, jerboa, gerbil, hamster, lemming, and guinea pig excreted four
metabolites: sulfate and glucuronic acid conjugates of phenol and of
1,4-dihydroxybenzene. The squirrel and capuchin monkeys excreted phenol
glucuronide, 1,4-dihydroxybenzene glucuronide, and phenol sulfate. The ferret,
dog, hedgehog, and rabbit excreted phenol sulfate, 1,4-dihydroxybenzene sulfate,
and phenyl glucuronide. The Rhesus monkey, fruit bat, and chicken excreted
phenyl sulfate and phenyl glucuronide but not 1,4-dihydroxybenzene conjugates.
The cat excreted only phenyl sulfate and 1,4-dihydroxybenzene sulfate, and the
pig excreted phenyl glucuronide as its major phenol metabolite. Relatively low
doses were utilized in this study.
Concentrations of conjugated phenol in the urine increased following exposure
of humans to phenol from as little as 0.6 mg/cu m (0.16 ppm) to as much as 12.5
mg/cu m (3.3 ppm) without a significant increase in the concentration of free
phenol.
After absorption into the body, most ... phenol is oxidized and conjugated
with sulfuric, glucuronic and other acids.
IN MAN, 90% OF ORAL DOSE OF PHENOL WAS EXCRETED IN 24 HR, MAINLY AS
PHENYLSULFATE (77% OF 24 HR EXCRETION) & PHENYLGLUCURONIDE (16%), WITH VERY
SMALL AMT OF QUINOL SULFATE & GLUCURONIDE. THESE METAB WERE ALSO EXCRETED BY
RAT, MOUSE, JERBON, GERBIL, HAMSTER, LEMMING & GUINEA PIG. /PHENOL/
The sulfate conjugate in urine dominates at low exposure doses, and
glucuronides assume greater importance at higher phenol exposure concentrations.
Below 5 ppm phenol, the sulfate/glucuronide ratio is 3.7:1.
Absorption, Distribution & Excretion:
PHENOL IS ABSORBED BY ALL ROUTES OF ADMIN & CAN REACH CIRCULATION EVEN
WHEN APPLIED TO INTACT SKIN.
ABSORPTION OF 2 G OF PHENOL COULD RESULT FROM 8 HR INHALATION AT ABOUT 50
PPM.
EXPTL OBSERVATIONS HAVE SHOWN THAT RATE OF ABSORPTION FROM SKIN OF ANIMALS
DEPENDS PRIMARILY UPON SIZE OF AREA INVOLVED & DURATION OF CONTACT. CONCN OF
SOLN APPLIED WAS LESS IMPORTANT FACTOR.
RENAL EXCRETION IS PRINCIPAL ROUTE OF ELIMINATION. ... IN MAN 90% OF
NON-TOXIC ORAL DOSE (0.01 MG/KG) OF (14)C-LABELED PHENOL WAS EXCRETED IN 24 HR,
PRINCIPALLY AS SULFATE (77% OF THE EXCRETED LABEL) & AS GLUCURONIDE (16%),
WITH SMALL AMT OF SULFATE & GLUCURONIDE CONJUGATES OF ... HYDROQUINONE. WITH
LARGER DOSES, FREE (UNMETABOLIZED) PHENOL CAN PRESUMABLY BE FOUND IN URINE.
AFTER ABSORPTION INTO BODY ... TRACES OF "FREE" PHENOL ARE
ELIMINATED WITH FECES & EXPIRED AIR.
In volunteers exposed to phenol vapor (5-25 mg/cu m) the retention of vapor
in the lung decreased from ... 80 to 70% in the course of an 8 hr exposure. The
absorption of vapor through the whole skin was approximately proportional to the
concentration of vapor used, the absorption rate being somewhat lower than in
the lung. Almost 100% of the excretion of phenol occured in the urine within 1
day.
In man and all mammals that have been tested, nearly all of the phenol and
its metabolites are excreted in the urine. Only minor amounts are excreted in
air and in the feces.
The skin represents a primary route of entry for phenol vapor, liquid phenol,
and solid phenol. Phenol vapor readily penetrates the skin with an absorption
efficiency approximately equal to that of inhalation. Skin absorption can occur
at low vapor concentrations.
DATA ARE PRESENTED WHICH CORRELATE PHENOL LEVELS IN HUMAN URINE WITH
INHALATORY & SKIN EXPOSURES. NORMAL PHENOL LEVELS IN HUMAN URINE ARE
COMPARED WITH URINE LEVELS RESULTING FROM EXPOSURE TO PHENOL. A CORRELATION IS
MADE BETWEEN URINE PHENOL LEVELS & POTENTIAL HUMAN TOXICITY.
Phenol is absorbed from the gastrointestinal tract and through the skin and
mucous membranes. ... The metabolites are excreted in the urine.
Subjects exposed to phenol vapor (without skin contact) in concn of 5-25
mg/cu m for a total of 7 hr daily retained 60-88% of the inhaled quantity.
Retention ranged from 17.8-62.8 mg and an avg of 99% of this dose was excreted
in the urine in 24 hr.
A fraction of phenol may be excreted by the lung and imparts an aromatic odor
to the breath.
Intoxication can occur after absorption through intact skin, or by ingestion.
Biological Half-Life:
The excretion of phenol was studied in human volunteers exposed to phenol by
inhalation or skin absorption. The human body behaved almost like a single
compartment with respect to phenol absorption and clearance with an excretion
rate constant of K= 0.2/hr This corresponds to a half-life of approximately 3.5
hours.
Mechanism of Action:
Excessive doses of phenol in animals have been shown to depress the vasomotor
center of the brain producing motor disturbances and blood changes of sufficient
magnitude to induce cardiac arrest, respiratory failure, and coma followed by
death.
The effects of monoamine depletors and monoamine denervators on phenol
induced tremor were studied in mice. The tremor induced by phenol was enhanced
by pretreatment with reserpine or tetrabenazine, but not with syrosingopine.
However, alpha-methyl-p-tyrosine, p-chlorophenylalanine or 6-hydroxydopamine did
not affect the tremor. These results suggest that the depletion of central
monoamines as a whole contribute to the enhancement of the tremor induced by
phenol.
... SOMETIMES THERE IS ONLY MILD PAIN OR DISCOMFORT BECAUSE PHENOL
DEMYELINATES OR OTHERWISE DESTROYS MANY TYPES OF NERVE FIBERS.
Death immediately after poisoning ususally occurs from respiratory
depression.
Interactions:
CAMPHOR AND OTHER SUBSTANCES WITH SIMILAR PHYSICOCHEMICAL PROPERTIES INTERACT
WITH PHENOL BOTH TO REDUCE ITS CORROSIVE PROPERTIES AND TO IMPEDE PERCUTANEOUS
ABSORPTION. HOWEVER, SEVERE LOCAL NECROTIC DAMAGE & FATAL SYSTEMIC POISONING
HAVE FOLLOWED USE OF THIS COMBINATION, WHICH WAS ONCE ENDORSED FOR
"ATHLETE'S FOOT".
IN 27 CASES OF PHENOL POISONING BY MOUTH, 10% ETHANOL SOLN WAS JUDGED TO
OFFER NO ADVANTAGE OVER WATER AS LAVAGE FLUID. INDEED, SYMPTOMS APPEARED TO BE
MORE SEVERE WHEN PHENOL & ALCOHOL WERE INGESTED CONCOMITANTLY.
... LOCAL EFFECTS CAN BE STRONGLY MITIGATED BY PRESENCE OF ANY VEHICLE WITH
AFFINITY FOR PHENOL. ...
Benzene induced myelotoxicity can be reproduced by the coadministration of
two principal metabolites, phenol and hydroquinone. Coadministration of phenol
(75 mg/kg) and hydroquinone (25-75 mg/kg) twice daily to B6C3F1 mice for 12 days
resulted in a significant loss in bone marrow cellularity in a manner exhibiting
a dose response. One explanation for this potentiation is that phenol stimulates
the peroxidase dependent metabolism of hydroquinone. Addition of phenol to
incubations containing horseradish peroxidase, hydrogen peroxide, and
hydroquinone resulted in a stimulation of both hydroquinone removal and
benzoquinone formation. Stimulation occurred with phenol as low as 100 uM and
with very low concentrations of horseradish peroxidase. When boiled rat liver
protein was added to identical incubations containing (14)C hydroquinone, the
level of radioactivity recovered as protein bound increased by 37% when phenol
was added. Similar results were observed when (14)C hydroquinone was incubated
in the presence of activated human leukocytes. Hydroquinone binding was
increased by approximately 70% in the presence of phenol. Phenol induced
stimulation of hydroquinone metabolism and benzoquinone formation represents a
likely explanation for the bone marrow suppression associated with benzene
toxicity.
It was found that phenol was not carcinogenic when applied repeatedly
together with benzo(a)pyrene (BAP) since the carcinogenesis of BAP was slightly
inhibited by coapplication.
Pharmacology:
Therapeutic Uses:
Anti-Infective Agents, Local; Disinfectants; Sclerosing Solutions;
Sympatholytics
MEDICATION (VET): ANTISEPTIC CAUSTIC, TOPICALLY AS ANESTHETIC IN PRURITIC
SKIN CONDITIONS.
MEDICATION (VET): PHENOL HAS BEEN USED INTERNALLY AS ANTISEPTIC & GASTRIC
ANESTHETIC ...
DISINFECTANT & ANTISEPTIC (PRIMARILY FORMER USE)
/SRP: Former use:/ Phenol has been used for sclerosing hemorrhoids, but more
effective and safer drugs are available. A 5% soln in glycerin is used in simple
earache. ... Phenol is of some therapeutic value as a fungicide, but more
effective & less toxic agents are available.
MEDICATION (VET): 2-5% CONCN IS RELIABLE DISINFECTANT AGAINST ERYSIPELOTHRIX
RHUSIOPATHIAE EVEN IN PRESENCE OF MANURE; 0.75% KILLS CANINE DISTEMPER VIRUS IN
LESS THAN 10 MIN; 0.2% KILLS ANAPLASMA ORGANISMS IN VACCINES; 2.5% IS FUNGICIDAL
AGAINST A NUMBER OF ORGANISMS; & 5-10% IS USED OCCASIONALLY AS A PREMISE
DISINFECTANT.
IN MOUTHWASHES, HEMORRHOIDAL PREPN & BURN REMEDIES
MEDICATION (VET): 0.125 TO 1.0% CONCN ARE USED IN VACCINES, SERUMS &
PARENTERALS AS PRESERVATIVE
2-3% CONCN ALSO SERVE AS FLY REPELLANT & ARE FREQUENTLY FOUND IN LARGE
ANIMAL WOUND TREATMENT PREPN
Phenol ... is a component (0.1-4.5 %) of various liquids, gels, ointments,
& lotions (including phenolated calomine lotion), throat sprays, gargles,
& lozenges. In most ... phenol is included as a local anesthetic for
pruritis, stings, bites, burns, or sore throat, but some ... are labeled for
antiseptic use.
/Phenol is a/ pharmaceutical necessity as a preservative for injections, etc.
Phenol 30-125 mg is admin intrathecally as a 5% w/w soln in glycerol ... for
the alleviation of spasticity and severe intractable pain in malignant neoplasms
...
AS PHARMACEUTIC AID (ANTIMICROBIAL AGENT)
/Phenol is used in/ chemexfoliation (chemical
peeling) ... to obtain both therapeutic (eg, actinic keratoses) and cosmetic
(eg, removal of fine facial rhytides) benefits.
Drug Warnings:
DIL PHENOL SOLN (1 TO 2%) ARE USED MEDICINALLY AS ANTIPRURITIC PREPN FOR THE
SKIN. THEIR REPEATED USE OVER LARGE SKIN AREAS OR ON PARTICULARLY MOIST AREAS
(AXILLARY REGION, GROIN, FEET) SHOULD BE AVOIDED.
Soln of phenol (6%) in glycerine are sometimes employed in medical practice
to produce nerve blocks. The spread of phenol beyond the intended site (stellate
ganglion) resulted in infarction on the cervical cord with extensive paralysis
in one patient and neurolosis of the cervical posterior roots with respiratory
arrest in another.
... Phenol ... should be applied only on small areas of skin and occlusive
dressings, bandages, or diapers should not be used.
Phenol should never be used in pregnant women, in infants under 6 mo, or for
diaper rash.
The development of widespread Herpes simplex on the face after phenolic face
peels is not considered rare. Precaution in choosing patients is recommended.
Four cases of acute exacerbation of Herpes simplex are presented in patients who
had recently undergone phenolic face peels.
Interactions:
CAMPHOR AND OTHER SUBSTANCES WITH SIMILAR PHYSICOCHEMICAL PROPERTIES INTERACT
WITH PHENOL BOTH TO REDUCE ITS CORROSIVE PROPERTIES AND TO IMPEDE PERCUTANEOUS
ABSORPTION. HOWEVER, SEVERE LOCAL NECROTIC DAMAGE & FATAL SYSTEMIC POISONING
HAVE FOLLOWED USE OF THIS COMBINATION, WHICH WAS ONCE ENDORSED FOR
"ATHLETE'S FOOT".
IN 27 CASES OF PHENOL POISONING BY MOUTH, 10% ETHANOL SOLN WAS JUDGED TO
OFFER NO ADVANTAGE OVER WATER AS LAVAGE FLUID. INDEED, SYMPTOMS APPEARED TO BE
MORE SEVERE WHEN PHENOL & ALCOHOL WERE INGESTED CONCOMITANTLY.
... LOCAL EFFECTS CAN BE STRONGLY MITIGATED BY PRESENCE OF ANY VEHICLE WITH
AFFINITY FOR PHENOL. ...
Benzene induced myelotoxicity can be reproduced by the coadministration of
two principal metabolites, phenol and hydroquinone. Coadministration of phenol
(75 mg/kg) and hydroquinone (25-75 mg/kg) twice daily to B6C3F1 mice for 12 days
resulted in a significant loss in bone marrow cellularity in a manner exhibiting
a dose response. One explanation for this potentiation is that phenol stimulates
the peroxidase dependent metabolism of hydroquinone. Addition of phenol to
incubations containing horseradish peroxidase, hydrogen peroxide, and
hydroquinone resulted in a stimulation of both hydroquinone removal and
benzoquinone formation. Stimulation occurred with phenol as low as 100 uM and
with very low concentrations of horseradish peroxidase. When boiled rat liver
protein was added to identical incubations containing (14)C hydroquinone, the
level of radioactivity recovered as protein bound increased by 37% when phenol
was added. Similar results were observed when (14)C hydroquinone was incubated
in the presence of activated human leukocytes. Hydroquinone binding was
increased by approximately 70% in the presence of phenol. Phenol induced
stimulation of hydroquinone metabolism and benzoquinone formation represents a
likely explanation for the bone marrow suppression associated with benzene
toxicity.
It was found that phenol was not carcinogenic when applied repeatedly
together with benzo(a)pyrene (BAP) since the carcinogenesis of BAP was slightly
inhibited by coapplication.
Minimum Fatal Dose Level:
Ingestion of as little as 4.8 g of pure phenol caused death in 10 min.
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Phenol is an important industrial chemical
and enters the environment in air emissions, wastewater and spills connected
with its use as a chemical
intermediate, disinfectant and antiseptic. It is frequently found in industrial
wastewater. It is also released by wood stoves, in vehicle exhaust and other
anthropogenic processes. Phenol is naturally produced in decaying organic
matter. If released to the environment, phenol's primary removal mechanism is
biodegradation which is generally rapid (days). Since phenol is a benchmark chemical
for biodegradability studies, there is a large body of information on its
degradation which concludes that phenol rapidly degrades in sewage, soil, fresh
water and seawater. Acclimation of resident populations of microorganisms is
rapid. Under anaerobic conditions degradation is slower and microbial adaptation
periods longer. If phenol is released to soil, it will readily leach and
biodegrade. The biodegradation in soil is generally rapid with half-lives of
under 5 days even in subsurface soils. Biodegradation is sufficiently rapid that
most groundwater is generally free of this pollutant. The exception would be in
the cases of spills where high concentrations of phenol destroy degrading
microbial populations. Biodegradation is also the primary removal process for
phenol released into water (half-lives are of the order of hours to days)
although sensitized photolysis may also be important. In one study using
estuarine water, the combination of biodegradation and photolysis resulted in a
half-life in summer and winter of 39 and 94 hr, respectively. Since the pKa of
phenol is 9.994, it will be partially dissociated at higher pHs in water and
moist soils and its transport and reactivity may be pH-dependent. Phenol does
not bioconcentrate in aquatic organisms. In the atmosphere, phenol occurs as a
vapor and reacts with photochemically-produced hydroxyl radicals resulting in a
half-life of approximately 15 hours. During the nighttime, it reacts with
nitrate radicals with a resulting half-life of 12 minutes. Phenol has also been
shown to be readily removed from the atmosphere by rain. Occupational exposure
to phenol is primarily by dermal contact as well as by inhalation. Gloves are
often permeable to this chemical and
do not protect the worker. The general population is exposed via inhalation of
ambient air, ingestion of food and lozenges and dermal contact with disinfects
and other consumer products containing phenol. (SRC)
Probable Routes of Human Exposure:
WITH RARE EXCEPTIONS, HUMAN EXPOSURE IN INDUST HAS BEEN LIMITED TO ACCIDENTAL
CONTACT OF PHENOL WITH SKIN OR INHALATION OF PHENOL VAPORS.
NIOSH (NOES Survey 1981-1983) has statistically estimated that 320,914
workers are exposed to phenol in the USA(1). Eighty percent of these exposures
are to trade name products containing phenol. Phenol was detected in the general
work atmosphere of a brake pad assembly plant in New Holstein, WI - 0.025 and
0.042 ppm(3). The concn of phenol in bakerlite factories was reported to be 12.5
mg/cu m(2). Phenol was measured in the atmosphere of a dental school laboratory
in Philadelphia, PA during dissection of cadavers at 1.3-5.0 parts per
trillion(4). A study of exposure levels during 25 embalmings found that exposure
to phenol was <0.5 ppm(5). The area air concn of phenol during paint
stripping operations on a Boeing 747 aircraft (120-330 min sampling periods,
n=9) was 3.4-9.5 mg/cu m with a mean of 5.7 mg/cu m(6). For an 8-hr shift, the
exposure levels were 1.1-5.3 mg/cu m with a mean of 2.7 mg/cu m(6).
Protective gloves may be permeable to phenol. The breakthrough times and
permeation rates of 5 mil thicknesses of five common glove materials to solid
phenol were (material, breakthrough time (min), steady state permeation rates
(ug/min/sq cm): latex, 10.4, 0.0151; PVC, 10.6, membrane solubilized;
polyurethane, 28.0, 0.233; neoprene, 21.0, 0.201; polynitrile, 185.0, 0.0114(1).
Workplace exposure to phenol will occur via inhalation and dermal absorption
of phenol-containing wastewater, emissions and disinfectants or solvents. The
general population may be exposed to phenol by ingesting food or medicinal
products such as throat lozenges. They will also be exposed by inhalation of
ambient air and cigarette smoke and dermal absorption of phenol contained in
decomposing organic matter and disinfectants and other consumer products(SRC).
Body Burden:
Identified, but not quantified, in 9 of 12 samples of breath in Bayonne and
Elizabeth, NJ as part of the Total Exposure Assessment Methodology (TEAM)
study(1).
Average Daily Intake:
WATER INTAKE: Insufficient data; AIR INTAKE: (assume typical concn in indoor
air of 0.70 ug/cu m) 14 ug; FOOD INTAKE: Insufficient data.
Natural Pollution Sources:
Phenol is present in animal, leaf litter and other organic wastes as a result
of decomposition(1-3). The level of phenol present in poultry manure has been
shown to increase in time as degradation proceeds(2).
Artificial Pollution Sources:
Phenol is produced in large quantities for use as a chemical
intermediate in the production of bisphenol-A, phenolic resins, caprolactam,
aniline, alkylphenols and other chemicals,
as well as a disinfectant and antiseptic(1,2) and may be released to the
environment as emissions and in wastewater as a result of its production and
use(SRC). Wood smoke from fireplaces and wood stoves contain high concns of
phenol and would be expected to be a major source of phenol in winter air in
northern cities(6). Phenol is found in gasoline and diesel engine exhaust and it
was estimated that 3600 kg of phenol were emitted each day in Los Angeles from
these sources during the summer of 1987(3). It is found in cigarette smoke, and
emissions from refuse combustion, brewing, foundries, wood pulping, plastics
mfg, lacquer mfg, and glass fibre mfg(4). Laboratory tests indicate that phenol
would be found in leachate from tires(5). It is also released from some plastics
when heated (e.g., micarta emissions 34% phenol when heated to 280 deg C)(7).
Phenol is a photooxidation product of benzene(4) and would be produced in the
atmosphere from benzene emissions(SRC).
Phenol is obtained from coal tar.
Environmental Fate:
TERRESTRIAL FATE: Based on a recommended classification scheme(4),
experimentally determined Koc values for phenol(1-3) indicate that it would be
highly mobile in soil and may leach. Phenol's vapor pressure, 0.350 mm Hg at 25
deg C(5) and low adsorptivity to soil indicate that volatilization from dry soil
and other surfaces may occur(6,SRC). Phenol will be primarily removed from soil
as a result of biodegradation. Despite its high mobility in soil, biodegradation
is sufficiently rapid that most groundwater is generally free of phenol(7). The
half-lives of phenol in soil is usually <5 days, even in subsurface soil and
aquifer material(7-11), although for acid soils and some surface soils the
half-life may be of the order of 20-25 days(9,11) and in the case of a till
subsoil, 116 days(11). Radiolabeled phenol was rapidly released from soil in a
environmental standard system; after 1 day, half of the label was found in the
air phase as a result of mineralization(13). Degradation will be slower under
anaerobic conditions than under aerobic conditions and acclimation times will
also be longer(12). Phenol may also be removed from soil as a result of
surface-catalyzed reaction or oxidative processes that are not well
understood(14). Phenol is sensitive to indirect photolysis(15,16) and these
reactions may be expected to occur on the soil surface(SRC).
AQUATIC FATE: Because the pKa of phenol is 9.994(7), it will be partially
dissociated at higher pHs and therefore, its transport and reactivity may be pH
dependent(SRC). Based on a recommended classification scheme(4), experimentally
determined Koc values for phenol(1,2,3) indicate that it would not adsorb to
sediment and particulate matter in the water column(SRC). Phenol would not
volatilize from water based on its Henry's Law constant of 3.33X10-7 atm-cu
m/mole(5). Its estimated volatilization half-life in a model river is 107
days(6). Removal will be primarily a result of biodegradation with complete
degradation occurring in a few days(13,14). Degradation is slower in salt water;
the degradation half-life in an estuarine river was 9 days)(12). Phenol may
undergo indirect photolysis in natural waters due to reaction with transients
generated by the absorption of sunlight by, for example, dissolved natural
organic matter and flavins(15-18). Photolysis rates range widely and depend on
the intensity of sunlight, concentration and nature of humic materials and
photosensitzers present in the water and pH(SRC); phenolate ions are more
readily oxidized than undissociated phenol and therefore rates will increase
with pH(15). According to a recommended classification scheme(11), the low
reported BCF values for phenol(8,9) and its rapid elimination(10) suggest that
bioaccumulation of phenol is not an important fate process(SRC).
AQUATIC FATE: The rates of photolysis and microbial degradation in summer (24
deg C, midday surface irradiance 4.9 E/sq m-hr) and winter (10 deg C, midday
surface irradiance 2.9 E/sq m-hr) were determined in estuarine water using
ring-UL-14C-labeled phenol in a flask suspended 3 cm below the surface of water
in an outdoor tank of circulating estuarine water(1). The transformation rate
constants and half-lives of phenol in estuarine water, exposed to light and in
the dark, were (sample description, transformation rate in 1/hr, half-life in
hrs: summer/light, 0.018, 39; winter/light, 0.0074, 94; summer/dark, 0.03, 28;
winter/dark, 0.011, 62(1). The respective mineralization (CO2 appearance) rate
constants and half-lives of phenol in estuarine water, exposed to light and in
the dark, were (sample description, mineralization rate in 1/day. half-life in
days: summer/light, 0.095, 7; winter/light, 0.010, 73; summer/dark, 0.4, 2;
winter/dark, 0.0051, 136(1). Therefore microbial degradation is the primary
transformation process in estuarine waters. The biodegradation half-lives of
phenol in river water and harbor water have been reported to be 264 and 72
hours, respectively(2). An overall degradative half-life of 55 hours has been
suggested for phenol in water(2).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of
semivolatile organic compounds in the atmosphere(1), phenol, which has a vapor
pressure of 0.350 mm Hg at 25 deg C(2) will exist in the vapor phase in the
ambient atmosphere(SRC). Vapor-phase phenol is degraded in the atmosphere by
reaction with photochemically-produced hydroxyl radicals during the day and
nitrate radicals at night(SRC); the half-lives for these reactions in air is
estimated as 14.6 hours and 12 minutes, respectively(3,SRC). Phenol has a low
Henry's Law constant which explains why it is so effectively scavenged from the
air by rain(6). Its presence in rainwater has been confirmed by several
investigators(4-6). Its concn in rain has been shown to decrease markedly as the
rain event progresses(6).
Environmental Biodegradation:
SCREENING TESTS: Phenol is a benchmark chemical
in screening tests and there is abundant data to indicate that phenol
biodegrades fast in aerobic screening tests using a variety of techniques and
inocula, including acclimated and unacclimated activated sludge, sewage, and
soil(SRC). Only selected results are included here. In a 2-week biodegradation
screening test (MITI test) using phenol (100 ppm) and an activated sludge
inoculum, 85% of BOD was removed(1). Phenol was completely removed in 1 day or
less using a soil suspension(2) or activated sludge inocula(3,6). Complete
degradation was observed in 4 days using sediment from an oil refinery settling
pond as an inoculum(4). It was shown that the presence of aromatic compounds
like benzene and naphthalene had a mild inhibitory effect on degradation(4). In
five days, the BOD consumed was 90% and 50% of theoretical using a sewage
inoculum and freshwater and seawater, respectively(5). Another investigator who
obtained 80% of theoretical BOD consumed after 5 days demonstrated that
adaptation of the inoculum has a marked effect on the biodegradation rate(8).
Decreasing the concn of phenol significantly reduces the lag time required to
initiate degradation and increases the removal rate(9). The maximum
mineralization rates of phenol in sewage and landfill leachate were 6.5X10-4 and
2.7X10-4 1/hr, respectively(7). A lag period was observed in landfill leachate.
BIOLOGICAL TREATMENT SIMULATIONS: Phenol readily biodegrades in biological
treatment plants; removals in an aerobic activated sludge reactor (retention
time of 8 hr)(3) and a continuous reactor(6) was close to 100%. Partial
inhibition has been noted at concentrations as low as 50 ppm in aerobic reactors
using industrial wastewater seed and activated sludge seed(4). In a
semi-continuous activated sludge (SCAS) test with phenol, 39% of theoretical BOD
was consumed in 12 hr(1). The COD reduction ranged from 60-99% in a test using a
biofilm reactor with a 0.9 hr retention time(2). Phenol was also completely
removed in an artificial recharge pilot plant(5). In a monitoring study of 37
water pollution control plants in Ontario, Canada, the concn of phenol was
markedly reduced both in number of detections and concn after more progressive
stages of treatment (i.e, primary, secondary, tertiary)(7).
ANAEROBIC BIODEGRADATION: Phenol completely biodegraded in a test to
determine its anaerobic biodegradation potential under methanogenic
conditions(1). Gas production increased rapidly after a 6 day lag period. The
laboratory test was performed at 35 deg C in serum bottles using an anaerobic
digester sludge inoculum in which total gas production was measured over at
least a 60 day period. Sterile controls were used to correct for abiotic gas
production. Another investigator obtained 100% degradation in 28 days with an 18
day lag; on redose, complete degradation was obtained in 10 days with no lag(2).
In 14 days, 100, 91, and 99% mineralization of phenol was obtained on incubation
with 3 digester sludges(3,4).
WATER/SEDIMENT: Phenol completely mineralized in <1 day in water from 3 lakes;
rates increase with increasing concns of phenol and the organic content of the
water (e.g., degraded faster in an eutrophic lake
than an oligotropic one(3). It was completely removed in river water after 2
days at 20 deg C and after 4 days at 4 deg C(4). Degradation is slower in salt
water; the degradation rate in the estuarine Skidway River, GA was 0.079/hr
(half-life 9 days)(1). Laboratory tests were conducted to ascertain the seasonal
mineralization of trace levels of 14C-phenol by heterotrophic microorganisms in
seston and surface sediment at four sites in southwestern Virginia(2). The mean
turnover rates for the four sites between April and May 1986 at 10 deg C were
0.015, 0.023, 0.023, and 0.064 1/hr-mg sediment ash-free dry wt (AFDW).
Mineralization reached a maximum of 1.21X10-4 to 1.16X10-3 mg phenol
mineralized/mg AFDW-hr in October, an increase of 92-625% for seston samples and
46-128% for sediment samples over baseline August levels, despite decreasing
stream temperatures. This autumnal peak in phenol degradation is attributed to
the pulsed input of allochthonous detritus, especially leaf litter which
contains substantial quantities of phenol and related compounds(2).
SOIL: Phenol degradation in soil is completed in 2-5 days, even in subsurface
soils(5). The percent mineralization in an alkaline, para-brown soil under
aerobic conditions was 45.5%, 48%, and 65% after 3, 7, and 70 days,
respectively(1). Half-lives for degr of low concn of phenol in Captina (pH 5.7,
1.1% organic matter) and Palouse silt loam (pH 5.7, 3.6% organic matter) soils
were 2.70 and 3.51 hrs(2). Its disappearance from a Chernozem soil increased
from 10 to 110 days as the concn of phenol increased from 1000 to 9000 ppm(4).
The biodegradation half-life in acidic and basic soil has been reported to be
552 and 98.4 hr, respectively(3). The biodegradation of phenol in subsurface
under a typical Midwest agricultural soil was studied by determining rates in
strata of a 26-m bore(6). Phenol biodegraded rapidly (within 0-1 day) in samples
from the aquifer capillary fringe, saturated zone, and surface soil; lag periods
and lower rates were found in till samples. The half-lives and lag times were
(sample, half-life, lag): surface layers (<2 m) 2.8-4.6 days, 0-1 day lag;
aquifer (>23 m), 1.0-3.5 days, 0 days lag; till (12 m), 116 days, 16 day lag;
subsoil (8 m), 21 days, 2 day lag(6).
Environmental Abiotic Degradation:
The rate constant for the vapor-phase reaction of phenol with photochemically
produced hydroxyl radicals is 2.63X10-11 cu cm/molecule-sec at 25 deg C(2). This
corresponds to an atmospheric half-life of 14.6 hours at an atmospheric
concentration of 5X10+5 hydroxyl radicals per cu cm(SRC). The rate constant for
the vapor-phase reaction of phenol with nitrate radicals is 3.92X10-12 cu
cm/molecule-sec at 23 deg C(1,2). This corresponds to a half-life of 12 minutes
at a nitrate radical concn of 2.4X10+8 per cu cm (over continental areas). The
reaction with nitrate radicals is only important during the nighttime. In the
presence of nitrogen oxides, 2-nitrophenol is formed in these reactions at a
yield of 0.067 and 0.251 for the reaction with hydroxyl radicals and nitrate
radicals, respectively(1).
The pKa of phenol is 9.994(1). Therefore, phenol will be partially
dissociated at the upper end of environmental pH range (e.g., 1% of phenol will
be dissociated at pH 8 and 10% at pH 9) and its reactivity may be pH
dependent(SRC). Phenol does not absorb UV radiation >290 nm(6) and therefore
in the absence of photosensitizers, phenol is not susceptible to direct
photolysis by sunlight(SRC). The phenolate ion absorbs light more strongly and
at longer wavelengths than phenol(7) and therefore may be susceptible to direct
photolysis(SRC). Phenol may undergo indirect photolysis in natural waters due to
reaction with transients generated by the absorption of sunlight by, for
example, dissolved natural organic matter; some of the oxidants that have been
identified include hydroxyl radicals, peroxy radicals(4), singlet oxygen(2) and
reactive excited triplet states(5). Typical half-lives for hydroxyl and peroxy
radical reactions are on the order of 100 and 19.2 hrs of sunlight,
respectively(4). Phenolate ions are more readily oxidized than undissociated
phenol and therefore rates will increase with pH(2). The rate constant of
phenolate ion and phenol with singlet oxygen are 1.55X10+8 L/mol-sec and
2.6X10+6, respectively(2). Assuming a near surface concn of singlet oxygen of
2X10-13 mol/L(3), the half-lives of the phenolate ion and undissociated phenol
would respectively be 6.2 hr and 370 hr(SRC). Another investigator estimated the
half-life for reaction of phenol with photochemically-produced singlet oxygen in
surface waters contaminated by humic substances as 83 days (assuming Switzerland
summer sunlight and singlet oxygen concn 4x10-14 mol/L)(8).
The rates of photolysis in summer (24 deg C, midday surface irradiance 4.9
E/sq m-hr) and winter (10 deg C, midday surface irradiance 2.9 E/sq m-hr) were
determined in distilled water and poisoned estuarine water, both at pH 7.7,
using ring-UL-14C-labeled phenol in a flask suspended 3 cm below the surface of
water in an outdoor tank of circulating estuarine water(3). The transformation
rate constants and half-lives in distilled and estuarine water were (sample
description, transformation rate in 1/hr, half-life in hr: distilled water
(summer), 0.015, 46; distilled water (winter), 0.0040, 173; estuarine water
(summer), 0.016, 43; estuarine water (winter), 0.006, 118(3). The corresponding
mineralization (CO2 appearance) rate constants and half-lives in distilled and
estuarine water were (sample description, mineralization rate in 1/day,
half-life in day: distilled water (summer), 0.04, 16; distilled water (winter),
0.0041, 169; estuarine water (summer), 0.04, 16; estuarine water (winter),
0.0063, 110(3). Riboflavin and other flavins and their more stable
photodegradation products (i.e., lumichrome) are photosensitizers which may be
present in sea water and lake
water(2). The disappearance of phenol in a photoreactor (light >290 nm) in
the presence of riboflavin at pH 5, 7, 9, and 11 was rapid with approximately
53, 38, 23, and 18% degradation occurring respectively in 1 minute. Generally
midday summer sunlight photolysis rate constants at Urbana, IL are approximately
one-half of those determined in the photoreactor(1). In another experiment using
light from a solar simulator, the pseudo first-order rate constants of
lumichrome- sensitized photolysis of phenol was 2.2, 3.5, and 17.0/min at pH
7.0, 8.0 and 9.0, respectively(2).
Phenol has been reported to degrade in water-washed sterile silica sand at a
rate which increases with increasing temperature and decreases with time(1).
After 8 days, approximately 10, 15, and 85% of phenol was removed at 4, 26 and
60 deg C, respectively. The loss could not be a result of volatilization or
photolysis since the flasks were sealed and incubated in the dark. It was
postulated that the loss was a result of a surface-catalyzed reaction or an
oxidative process(1).
Environmental Bioconcentration:
The BCFs reported in aquatic organisms include: goldfish, (Carassius
auratus), 1.9(1); fish (unspecified), 17(7); fish (unspecified), 1.7(10); water
flea (Daphnia magna), 277(2); golden orfe, 20, algae (Clorella fusca), 200(3);
freshwater phytoplankter (Scenedesmus quadricauda), 3.5(4). Phenol was rapidly
eliminated from goldfish(8) and therefore would be unlikely to
bioaccumulate(SRC). When U-14C-phenol was interperitonially administered to
goldfish, the concn decreased to one tenth the initial concn in 2 hr(8). A BCF
of 7.6 was estimated for phenol(SRC), using the log Kow of 1.46(5) and a
recommended regression-derived equation(6). According to a recommended
classification scheme(9), the estimated and reported BCF values and the rapid
elimination of phenol suggests that bioaccumulation of phenol is unlikely(SRC).
Soil Adsorption/Mobility:
The pKa of phenol is 9.994(1), indicating that it will be partially
dissociated at the upper end of environmental pH range and that its mobility may
be pH dependent(SRC). Phenol is reported to have low adsorptivity to clay soils
and silt loam(1) and no adsorption to aquifer material(3) and montmorillonite
and kaolinite clays(11). The Koc for phenol to a Batcombe silt loam soil (pH
6.7, organic carbon 2.51%) was 30(8). It was 16 for a Brookstone clay loam (pH
5.7, organic matter 5.1%) and varied with pH and iron content of the soil(9).
The Freundlich K (1/N) for phenol in Captina (pH 5.7, 1.1 % organic matter) and
Palouse silt loam (pH 5.7, 3.6% organic matter) soils were 0.58 (1.15) and 0.81
(1.00)(2); the Koc values for these soils are 91 and 39(SRC). Using its water
solubility of 82,800 mg/l(4), an estimated Koc of 8.6 was calculated(SRC) using
a recommended regression equation(5). Based on the reported and estimated Koc,
phenol will be expected to generally exhibit very high mobility in soil(6), and
therefore may leach to the groundwater. In a study of the adsorption of phenol
onto siltstone associated with a Wyoming coal deposit suitable for in situ
gasification, the pH of the solution was the major controlling factor with
adsorption occurring at pH's below the pKa of phenol and no adsorption occurring
at pH's above the pKa(7). The log of the Freundlich K value was approximately
-4(7). Therefore, phenol may be transported by groundwater near in situ coal
gasification sites due to the elevated pH's at these sites after
gasification(7).
Volatilization from Water/Soil:
The Henry's Law constant of phenol is 3.33X10-7 atm-cu m/mole(1). 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) is estimated to be 107
days(2,SRC). The liquid phase transfer coefficient for phenol relative to oxygen
was measured to be 0.01 in a laboratory reactor(4). Using the oxygen reaeration
rate for a river, 0.04 1/hr(5), the volatilization half-life would be 72
days(SRC). Phenol's vapor pressure, 0.350 mm Hg at 25 deg C(3) and low
adsorptivity to soil indicate that volatilization from dry soil and other
surfaces may occur(SRC).
Environmental Water Concentrations:
DRINKING WATER: Not detected in finished drinking water in USA(1). Detected
in US drinking water, 1 ppb, mean(2). Identified in the one sample of tap water
analyzed in New Jersey as part of the Total Exposure Assessment Methodology
(TEAM) study(4). Great Britain,
March-Dec 1976, drinking water derived from groundwater sources, 4 sites, 50%
pos; from surface water, 30% pos(3).
GROUNDWATER: Maximum of 1130 ppm in 9 wells in Wisconsin after a spill(1).
Concn of phenol in 2 aquifers 15 months after completion of coal gasification
project 6.5-10,000 ppb(2). Max concn of phenol in Biscayne Aquifer Study Area,
site of an industrial landfill in Dade County, FL was 38 ug/L(3). However. no
phenol was detected in field wells and finished water treatment plants that
utilized water from the aquifer. Phenol was detected in wells in an alluvial
aquifer near Zagreb, Yugoslavia at 10-100 ng/L; the wells were near a wastewater
canal that received untreated wastes from the pharmaceutical industry that
contained phenol levels exceeding 1000 ng/L(3). It was not detected in wells
near the Sava River which contained phenol in the 1-10 ng/L range(3).
SURFACE WATER: Industrial rivers in USA: 0-5 ppb(1,2). Lake
Huron 3-24 ppb(3). Detected, not quantified in 2 of 110 raw water supplies in
1977 analyzed in EPA National Organics Monitoring Survey(4). USEPA STORET
database, 1,754 data points, 13.0% pos, 5.0 ppb median concn(5). Northern
Alberta in region of a pulp mill, fall and summer of 1990 (12 samples), not
detected (detection limit 0.02 ug/L)(6). Phenol was present in the Sava River,
Yugoslavia near Zagreb at a level of about 1-10 ng/L(8). The level of phenol in
the Rio Santiago, Argentina was 40 mg/L(7). This river receives effluents from a
large petrochemical and oil refinery complex, a steel rolling mill and
shipyards.
RAIN/CLOUD WATER: 7 rain events in Portland, OR, Feb-Apr 1984 >280
parts/trillion, mean in rain. Rain samples collected at two sites in Switzerland
were initially 5 and 8 ug/L and rapidly decreased as a function of time as a
result of in- and below-cloud scavenging(3). Phenol in 25 rain samples in
Hannover, Germany between July, 1989 and Feb 1990 ranged from 1.3-15.4 ug/L with
a mean of 5.6 ug/L(2). In cloud and rain water samples collected in the Vosges
Mountains, France in 1991, the mean phenol concn was 3.45 ug/L in cloud water (5
samples) and 1.58 ug/L in rain(4).
Effluent Concentrations:
In a comprehensive survey of wastewater from 4000 industrial and publicly
owned treatment works (POTWs) sponsored by the Effluent Guidelines Division of
the U.S. EPA, phenol was identified in discharges of the following industrial
category (positive occurrences, median concn in ppb): timber products (31;
119.8), leather tanning (14; 158.3), iron and steel mfg (14; 179.8), petroleum
refining (13; 242.8), nonferrous metals (37; 73.0), paint and ink (14; 95.9),
printing and publishing (12; 28.5), coal mining (1; 482.4), organics and
plastics (86; 227.5), inorganic chemicals
(8; 49.3), textile mills (7; 31.9), plastics and synthetics (26; 85.3), pulp and
paper (31; 68.4), rubber processing (12; 156.0), soaps and detergents (4;
179.4), auto and other laundries (4; 33.3), pesticides manufacture (4; 3077.7),
photographic industries (5; 403.1), gum and wood industries (9; 9.7),
pharmaceuticals (17; 73.6), explosives (14; 27.0), plastics mfg (4; 517.5),
foundries (54; 282.6), porcelain/enameling (1; 7.5), aluminum (21; 88.2),
electronics (29; 163.4), oil and gas extraction (15; 120.3), organic chemicals
(54; 63.2), mechanical products (21; 55.3), transportation equipment (5; 174.4),
synfuels (15; 82.6), publicly owned treatment works (151; 77.6), rum industry
(5; 72.2)(1). Industries with highest effluent concns >10 ppm were: organics
and plastics, 530.4 ppm; photographic industries, 32.8; and pesticides
manufacture, 18.8 ppm(1). In a monitoring study of 37 water pollution control
plants in Ontario, Canada (275 samples), phenol was detected in 42.9% of samples
of raw sewage from 29 plants with a geometric mean and max concn of 14.5 and 276
ppm, respectively(2). The concn on phenol in emissions of a municipal waste
incinerator in Germany was 1.40 ug/cu m(3).
Industries with mean phenol concns >0.1 ppm in treated wastewater (max/avg
concn, ppm): iron and steel mfg, 53 ppm max/5.7 ppm avg, leather tanning and
finishing, 1.4/0.63, aluminum forming, 9.7/1.3, electrical/electronic
components, 3.5/<0.74, foundries, 34/2.2, pharmaceuticals, 4.6/0.75,
organics/plastics mfg, not reported/0.110, paint and ink formulation, 1.2/0.14,
rubber processing, 12/3.0(3). Effluent from a chemical
specialties manufacturing plant contained 0.01-0.30 ppm phenol(1) and a 24-hr
composite effluent sample from a plant on the Delaware River contained 7 ppm
phenol(2). Effluent in the EPA STORET database (2,068 data points), 42.1% pos
for phenol, median concn 10.0 ppb(4). US Nationwide Urban Runoff Program (15
cities, 86 samples), frequency of detection, 4% pos (Washington, DC and
Bellevue, WA, 3-10 ppb)(5). Groundwater at 178 CERCLA hazardous waste sites,
13.6% pos(6).
Sediment/Soil Concentrations:
SEDIMENT: EPA STORET database, 318 data points, 9% pos, <1000 ppb median
concn (dry weight)(3). Lake Huron, 13
ppm(1). Not detected in unspecified industrial river in USA(2). Sediment
collected 6 km northwest of the Los Angeles county wastewater treatment plant
discharge zone at Palos Verdes, CA, 10 ppb dry weight(4). Northern Alberta in
region of a pulp mill, fall and summer of 1990 (20 samples) not detected-0.5 ppm
(detection limit 0.08 ppm)(5). SOIL: No data.
Atmospheric Concentrations:
URBAN/SUBURBAN: USA (7 samples), 0.030 ppb, median(1); USA (2 samples), 0.015
ppb(5); USA (2 sites), 0.05-0.35 ug/cu m, <20-289 ug/cu m (with 50% of all
observations <30 ug/cu m(3). The concn of phenol was measured with ground
level 12-hr high volume samplers in Minneapolis and Salt Lake
City between Nov 1988 and Feb 1989 when wood burning would be expected to
contribute to atmospheric phenol(7). Hardwood is burned in Minneapolis and
softwood in Salt Lake City. The phenol
concns at various types of sites were (site description, number of sites, concn
in ng/cu m): suburban residential (Minneapolis), 5, 353-1420 (second highest
level 577); city res (M), 3, 181-367; non-res downtown (M), 3, 257-395; res
suburban (Salt Lake City) 3, 384-520;
city res (SLC), 6, 230-765; non-res downtown (SLC), 2, 251-9(97). The gas phase
concn of phenol during 7 rain events in Portland, OR, Feb-Apr 1984, 220-410
ng/cu m, avg 320 ng/cu m(6). The mean concn and standard deviation of phenol in
155 cities in the USSR in 1989 was 4 ug/cu m and 3 ug/cu m, respectively(4). In
one city, Chelyabinsk, the mean concn was about 8.5 ug/cu m(4). SOURCE DOMINATED
AREAS: USA (83 samples) 5 ppb, median, range 0.44-420 ppb(1); USA (44 samples)
6.88 ppb, median(5). Identified, not quantified, in air along the Niagara River,
Sept 1982(2).
INDOOR AIR: In a Finnish study of chemicals
present in air of normal and "sick" homes, phenol was qualitatively
detected in 56% of the 26 homes screened. A subsequent quantitative study of 50
normal and 38 sick homes, the median phenol concn in the normal homes was 0.70
ug/cu m with 2% of the homes exceeding the median concn by a factor of 5-10(1).
The phenol concn in the sick homes did not exceed this median by as much as a
factor of 5. In 7 of the sick homes chosen as case studies the phenol concn
ranged from 0.34 to 2.66 ug/cu m. PERSONAL AIR: Not identified in 8 samples in
New Jersey as part of the Total Exposure Assessment Methodology (TEAM) study(2).
Food Survey Values:
The concn of phenol in summer smoked sausage and smoked pork belly was 7 ppm
and 28.6 ppm, respectively(1). It was identified, not quantified, as a volatile
in: Mountain cheese(2), fried bacon(3), fried chicken(4), clams(6), short-necked
clams(6) and coffee(5). Phenol may be a component of medicinal preparations such
as throat lozenges(1).
Fish/Seafood Concentrations:
Bottomfish, Commencement Bay, Tacoma, WA, June-Dec 1981, 5 sites, highest avg
concn, 0.14 ppm, max concn, 0.22 ppm(1). In a 1983 survey of composite,
nearshore whole fish samples collected from 13 Lake
Michigan tributaries and Grand Traverse Bay (2 species from each site), phenol
was only detected in common carp (0.16 ppm) and channel catfish (0.06 ppm) from
Grand River, common carp (0.02 ppm) from Muskegon River, and common carp (0.09
ppm) from Pere Marquette River(2). Northern Alberta in region of a pulp mill,
fall and summer of 1990 (22 fish, muscle)- not detected (detection limit 0.03
ppm)(3).
Animal Concentrations:
Natural component of animal matter; rabbit (muscle) 0-1.6 ppm (1).
Other Environmental Concentrations:
Phenol was tentatively identified during the thermal decomposition of 2
samples of polyvinylidene chloride at 22.6 and 27.8 ug/g of polymer heated(1).
Phenol was emitted at 200 deg C. Phenol was present in a sample of fresh poultry
manure at 1.86 ppm(2). After the manure sat for 9 and 28 days at 27-28 deg C,
the concn of phenol rose to 28.0 and 68.1 ppm, respectively. It is thought that
phenol is excreted as glucuronides and the phenol liberated by the action of
microbes or enzymes afterwards(2).
Environmental Standards & Regulations:
FIFRA Requirements:
Phenol is exempted from the requirement of a tolerance when used as a solvent
or cosolvent in accordance with good agricultural practice as inert (or
occasionally active) ingredients in pesticide formulations applied to growing
crops only.
Phenol is exempted from the requirement of a tolerance when used as a solvent
or cosolvent 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. Phenol is found on List D. Case
No: 4074; Pesticide type: antimicrobial; Case Status: OPP is reviewing data from
the pesticide's producers regarding its human health and/or environmental
effects, or OPP is determining the pesticide's eligibility for reregistration
and developing the Reregistration Eligibility Decision (RED) document.; Active
ingredient (AI): Phenol; Data Call-in (DCI) Date(s): 09/30/93; AI Status: The
producers of the pesticide has made commitments to conduct the studies and pay
the fees required for reregistration, and are meeting those commitments in a
timely manner.
Acceptable Daily Intakes:
Calculated acceptable daily intake= 0.1 mg/kg.
TSCA Requirements:
Pursuant to section 8(d) of TSCA, EPA promulagated a model Health and Safety
Data Reporting Rule. The section 8(d) model rule requires manufacturers,
importers, and processors of listed chemical
substances and mixtures to submit to EPA copies and lists of unpublished health
and safety studies. Phenol is included on this list.
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 1000 lb or 454 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).
Releases of CERCLA hazardous substances are subject to the release reporting
requirement of CERCLA section 103, codified at 40 CFR part 302, in addition to
the requirements of 40 CFR part 355. Phenol is an extremely hazardous substance
(EHS) subject to reporting requirements when stored in amounts in excess of its
threshold planning quantity (TPQ) of 500/10,000 lbs.
RCRA Requirements:
U188; As stipulated in 40 CFR 261.33, when phenol, 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. Phenol is produced, as an
intermediate or final product, by process units covered under this subpart.
Listed as a hazardous air pollutant (HAP) generally known or suspected to
cause serious health problems. The Clean Air Act, as amended in 1990, directs
EPA to set standards requiring major sources to sharply reduce routine emissions
of toxic pollutants. EPA is required to establish and phase in specific
performance based standards for all air emission sources that emit one or more
of the listed pollutants. Phenol is included on this list.
Clean Water Act Requirements:
Criterion (permissible level) for ambient water= 0.3 mg phenol/l.
The criterion (permissible level) for protection of freshwater aquatic life
is 600 ug/l (24 hr avg) and a ceiling of 3,400 ug/l.
Toxic pollutant designated pursuant to section 307(a)(1) of the Clean Water
Act and is subject to effluent limitations.
Designated as a hazardous substance under section 311(b)(2)(A) of the Federal
Water Pollution Control Act and further regulated by the Clean Water Act
Amendments of 1977 and 1978. These regulations apply to discharges of this
substance.
Federal Drinking Water Guidelines:
EPA 4000 ug/l
State Drinking Water Guidelines:
(CA) CALIFORNIA 5 ug/l
(FL) FLORIDA 10 ug/l
(MN) MINNESOTA 4000 ug/l
(NH) NEW HAMPSHIRE 4200 ug/l
(WI) WISCONSIN 6000 ug/l
FDA Requirements:
Phenol is an indirect food additive for use as a preservative onlyas a
component of adhesives.
Allowable Tolerances:
Phenol is exempted from the requirement of a tolerance when used as a solvent
or cosolvent in accordance with good agricultural practice as inert (or
occasionally active) ingredients in pesticide formulations applied to growing
crops only.
Phenol is exempted from the requirement of a tolerance when used as a solvent
or cosolvent in accordance with good agricultural practice as inert (or
occasionally active) ingredients in pesticide formulations applied to animals.
Chemical/Physical Properties:
Molecular Formula:
C6-H6-O
Molecular Weight:
94.11
Color/Form:
COLORLESS, ACICULAR CRYSTALS OR WHITE, CRYSTALLINE MASS
Colorless to light pink, interlaced, or separate, needleshaped crystals, or a
... light pink, crystalline mass
Colorless to light pink crystalline solid. [Note: Phenol liquefies by mixing
with about 8% water.]
Odor:
HAS DISTINCT, AROMATIC, SOMEWHAT SICKENING SWEET & ACRID ODOR
WHEN PERFECTLY PURE, PHENOL IS DEVOID OF ODOR OF CRESOL, BUT IT HAS PECULIAR
AROMATIC ODOR WHICH IS NOT DISAGREEABLE
Sweet, tarry odor
Sweet acrid odor.
Taste:
HAS SHARP BURNING TASTE; WHEN IN VERY WEAK SOLN IT HAS A SWEETISH TASTE
Taste threshold: lower-0.0001 ppm, median-0.15 ppm.
Boiling Point:
181.8 deg C @ 760 mm Hg
Melting Point:
40.9 deg C
Critical Temperature & Pressure:
Critical Temp = 694.2 K; Critical Pressure = 6.13 MPa
Density/Specific Gravity:
1.0545 @ 45 deg C/4 deg C
Dissociation Constants:
pKa = 9.994 @ 25 deg C
pKa = 9.89 @ 20 deg C
Heat of Combustion:
-3053.5 kJ/mol @ 25 deg C (crystal); -3122.2 kJ/mol @ 25 deg C (gas)
Heat of Vaporization:
57.82 kJ/mol @ 25 deg C
Octanol/Water Partition Coefficient:
Log Kow = 1.46
pH:
about 6.0 (aq soln)
Solubilities:
1 G/15 ML WATER
1 g/12 ml benzene
Very sol in alcohol, chloroform, ether, glycerol, petrolatum, carbon
disulfide, volatile and fixed oils, aq alkali hydroxides. Almost insoluble in
petr ether.
MISCIBLE IN ACETONE
93,000 MG IN 1 L WATER AT DEG 25 C.
Sparingly sol in mineral oil
Very sol in carbon tetrachloride, methyl alcohol, acetic acid, liquid sulfur
dioxide
82,800 mg/L @ 25 deg C in water
Spectral Properties:
INDEX OF REFRACTION: 1.5408 @ 41 DEG C/D
MAX ABSORPTION (ALC): 276 NM SHOULDER (LOG E= 3.16), 218.5 NM (LOG E= 3.78),
266 NM SHOULDER (LOG E= 3.18), 271 NM (LOG E= 3.28)
IR: 4815 (Coblentz Society Spectral Collection)
UV: 258 (Sadtler Research Laboratories Spectral Collection)
NMR: 3152 (Sadtler Research Laboratories Spectral Collection)
MASS: 199 (Atlas of Mass Spectral Data, John Wiley & Sons, New York)
Surface Tension:
38.20 mN/m @ 50 deg C; 35.53 mN/m @ 75 deg C; 32.86 mN/m @ 100 deg C
Vapor Density:
3.24 (AIR= 1)
Vapor Pressure:
0.3513 mm Hg @ 25 deg C
Viscosity:
3.437 centapoise @ 50 deg C; 1.784 centapoise @ 75 deg C; 1.099 centapoise @
100 deg C
Other Chemical/Physical Properties:
IT IS LIQUEFIED BY MIXING WITH ABOUT 8% WATER
ABSORBS WATER FROM AIR & LIQUEFIES
Heat of fusion: 11.29 kJ/mol @ 40.9 deg C
Latent heat of sublimation: 68.7 kJ/mole (25 deg C).
Heat of formation: -165.0 kJ/mole (25 deg C).
Ionization potential: 8.47 eV.
Heat of solution: -10.9 kJ/mole (20 C).
Heat capacity at constant pressure: 127 J/mole K @ 25 deg C
Coefficient of thermal expansion: 1.090 x 10-3/deg C (20 deg C).
Saturation concentration: 0.77 g/cu m @ 20 deg C, 2.0 g/cu m @ 30 deg C /in
air/.
% IN SATURATED AIR: 0.046% BY VOL @ 25 DEG C; DENSITY OF SATURATED AIR:
1.00104 (AIR= 1); 1 MG/L= APPROX 260 PPM, 1 PPM= APPROX 0.00384 MG/L @ 25 DEG C
& 760 MM HG
When free from water & cresols it congeals at 41 deg C & melts at 43
deg C
Phenol coagulates collodion; liquefies or becomes semiliquid when triturated
with acetanilide, butylchloral hydrate, camphor, monobromated camphor, chloral
hydrate, diuretin, lead acetate, menthol, naphthalene, naphthol, acetophentidin,
pyrogallol, resorcinol, salol, sodium phosphate, thymol, urethane, chloralamide,
terpin hydrate.
Prone to redden on exposure to air and light, hastened on presence of
alkalinity.
Dielectric constant = 12.40 @ 30 deg C
Chemical Safety & Handling:
Hazards Summary:
Phenol is an acutely hazardous substance due primarily to its toxicity.
Because phenol is highly corrosive to skin and systemically toxic by all routes
of exposure, including dermal absorption, it should not be allowed to contact
skin in its normally crystalline or concentrated liquid form. When heated,
phenol can give off vapors which are not only toxic, but flammable as well, if
exposed to an ignition source. Compliance with the OSHA TLV of 5 ppm should
protect against the build-up of both toxic and explosive concentrations of
phenol in air. Under all circumstances where skin contact with phenol is
possible, protective clothing, including gloves and a face shield, should be
worn. This clothing should be made of material which is impervious to phenol eg
neoprene, polyethylene, or rubber. Under conditions where airborne
concentrations of phenol exceed 20 mg/cu meter, a full-face respiratory device
is also required. Warning of potential phenol exposure can come from its
sickeningly sweet, acrid odor, detectable at 0.047 ppm. Containers of phenol may
be leaking if a check of the contents reveals phenol is turning reddish in
color. Toxicity is the prime consideration in the safe storage and shipment of
phenol. Designated as "Poison B" by the DOT, phenol containers are
labeled "Poison". However, no special containers are required due to
phenol's modest fire hazard and low reactivity. Should a phenol fire occur, it
may be combatted with water spray, CO2, dry chemical
or foam extinguishants. Aside from assuring that all containers and shipment
vessels are securely closed, the toxicity and fire hazards of phenol can be
greatly reduced by the prevention of overheating in storage areas. This is
accomplished with proper ventilation. Spills of phenol should be flushed with
water, and caustic soda solution added for neutralization. Phenol should not be
allowed to come into contact with strong oxidizing agents, eg peroxodisulfuric
acid.
DOT Emergency Guidelines:
Health: TOXIC; inhalation, ingestion, or skin contact with material may cause
severe injury or death. Contact with molten substance may cause severe burns to
skin and eyes. Avoid any skin contact. Effects of contact or inhalation may be
delayed. Fire may produce irritating, corrosive and/or toxic gases. Runoff from
fire control or dilution water may be corrosive and/or toxic and cause
pollution. /Phenol, liquid; Phenol, molten; Phenol, solid; Phenol solution/
Fire or explosion: Combustible material: may burn but does not ignite
readily. When heated, vapors may form explosive mixtures with air: indoors,
outdoors, and sewers explosion hazards. Some may polymerize (P) explosively when
heated or involved in a fire. Contact with metals may evolve flammable hydrogen
gas. Containers may explode when heated. Runoff may pollute waterways. Substance
may be transported in a molten form. /Phenol, liquid; Phenol, molten; Phenol,
solid; Phenol solution/
Public safety: CALL Emergency Response Telephone Number on Shipping Paper
first. If Shipping Paper not available or no answer, refer to appropriate
telephone number listed on the inside back cover. Isolate spill or leak area
immediately for at least 25 to 50 meters (80 to 160 feet) in all directions.
Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate
enclosed areas. /Phenol, liquid; Phenol, molten; Phenol, solid; Phenol solution/
Protective clothing: Wear positive pressure self-contained breathing
apparatus (SCBA). Wear chemical
protective clothing which is specifically recommended by the manufacturer.
Structural firefighters' protective clothing is recommended for fire situations
ONLY; it is not effective in spill situations. /Phenol, liquid; Phenol, molten;
Phenol, solid; Phenol solution/
Evacuation: Spill: See the Table of Initial Isolation and Protective Action
Distances for highlighted substances. For non-highlighted substances, increase,
in the downwind direction, as necessary, the isolation distance shown under
"PUBLIC SAFETY". Fire: If tank, rail car or tank truck is involved in
a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider
initial evacuation for 800 meters (1/2 mile) in all directions. /Phenol, liquid;
Phenol, molten; Phenol, solid; Phenol solution/
Fire: Small fires: Dry chemical,
CO2 or water spray. Large fires: Dry chemical,
CO2, alcohol-resistant foam or water spray. Move containers from fire area if
you can do it without risk. Dike fire control water for later disposal; do not
scatter the material. Fire involving tanks or car/trailer loads: Fight fire from
maximum distance or use unmanned hose holders or monitor nozzles. Do not get
water inside containers. Cool containers with flooding quantities of water until
well after fire is out. Withdraw immediately in case of rising sound from
venting safety devices or discoloration of tank. ALWAYS stay away from the ends
of tanks. /Phenol, liquid; Phenol, molten; Phenol, solid; Phenol solution/
Spill or leak: Eliminate all ignition sources (no smoking, flares, sparks or
flames in immediate area). Do not touch damaged containers or spilled material
unless wearing appropriate protective clothing. Stop leak if you can do it
without risk. Prevent entry into waterways, sewers, basements or confined areas.
Absorb or cover with dry earth, sand or other non-combustible material and
transfer to containers. DO NOT GET WATER INSIDE CONTAINER. /Phenol, liquid;
Phenol, molten; Phenol, solid; Phenol solution/
First aid: Move victim to fresh air. Call emergency medical care. Apply
artificial respiration if victim is not breathing. Do not use mouth-to-mouth
method if victim ingested or inhaled the substance; induce artificial
respiration with the aid of a pocket mask equipped with a one-way valve or other
proper respiratory medical device. Administer oxygen if breathing is difficult.
Remove and isolate contaminated clothing and shoes. In case of contact with
substance, immediately flush skin or eyes with running water for at least 20
minutes. For minor skin contact, avoid spreading material on unaffected skin.
Keep victim warm and quiet. Effects of exposure (inhalation, ingestion or skin
contact) to substance may be delayed. Ensure that medical personnel are aware of
the material(s) involved, and take precautions to protect themselves. /Phenol,
liquid; Phenol, molten; Phenol, solid; Phenol solution/
Odor Threshold:
The phenol odor threshold of 19 people was measured and the lowest range of
concentrations detected was 0.022-0.094 mg/cu m (0.006-0.024 ppm).
Threshold odor concentration: 0.047-0.5 ppm; Absolute odor threshold: 0.048
ppm; Recognition threshold: median 0.65 ppm, upper-16.4 ppm; Population
identification threshold: 0.01-0.47 ppm.
In water odor detection threshold: 5.90 ppm /chemically pure/; In air odor
recognition threshold: 4.70x10-2 ppm; /chemically pure/; In air odor detection
threshold: 1.00 ppm /purity not specified/; In air odor recognition threshold
4.70x10-2 ppm /pure/; In air odor threshold (type not specified): 7.70x10+10
molecules/cu cm /purity not specified/; In air odor threshold (type not
specified): 2.60x10+11 molecules/cu cm /purity not specified/; In water taste
threshold (type not specified): 6.00x10+1 ppm /purity not specified/; Odor
threshold (medium & type of threshold not specified): 1.05x10+2 ppm /purity
not specified/; Taste detection threshold in synthetic deodorized butter:
1.00x10-2 ppm /chemically pure/; Taste detection threshold (medium not
specified): 1.00x10-2 ppm /purity not specified/; In beer taste recognition
threshold: 2.71x10+1 moles/l /chemically pure/; In beer taste detection
threshold: 1.25x10+1 ppb /chemically pure/; In water taste detection threshold:
2.50x10+1 ppm /purity not specified/; Taste recognition threshold (medium not
specified): 1.00x10-2 ppm /purity not specified/
Odor Low= 0.1786 mg/m; Odor High= 22.42 mg/m
7.9 ppm in water; 0.05 ppm in air
Skin, Eye and Respiratory Irritations:
Strong irritant to tissue.
Vapor irritates respiratory system and eyes.
Fire Potential:
May be ignited by electrostatic discharge.
NFPA Hazard Classification:
Health: 4. 4= Materials that, on very short exposure, could cause death or
major residual injury, including those that are too dangerous to be approached
without specialized protective equipment. A few whiffs of the vapor or gas can
cause death, or contact with the vapor or liquid may be fatal, if it penetrates
the fire fighter's normal protective gear. The normal full protective clothing
and breathing apparatus available to the typical fire fighter will not provide
adequate protection against inhalation or skin contact with these materials.
Flammability: 2. 2= This degree includes materials that must be moderately
heated before ignition will occur and includes Class II and IIIA combustible
liquids and solids and semi-solids that readily give off ignitible vapors. Water
spray may be used to extinguish fires in these materials because the materials
can be cooled below their flash points.
Reactivity: 0. 0= This degree includes materials that are normally stable,
even under fire exposure conditions, and that do not react with water. Normal
fire fighting procedures may be used.
Flammable Limits:
1.7%-8.6% IN AIR
Flash Point:
175 deg F; 79 deg C, (Closed cup)
85 deg C, (Open cup)
Autoignition Temperature:
1319 deg F (715 deg C)
Fire Fighting Procedures:
Fire extinguishing agents: small fires-dry chemical,
CO2, water spray or foam (alcohol); large fires- water spray, fog, or foam; use
water spray to cool containers in fire area.
If material on fire or involved in fire: Use water in flooding quantities as
fog. Solid streams of water may be ineffective. Cool all affected containers
with flooding quantities of water. Apply water from as far a distance as
possible. Use foam, dry chemical, or
carbon dioxide. Keep run off-water out of sewers and water sources. /Phenol,
solid/
If material on fire or involved in fire: Do not extinguish fire unless flow
can be stopped. Extinguish fire using agent suitable for type of surrounding
fire. (Material itself does not burn or burns with difficulty.) Use water as
flooding quantities as fog. Cool all affected containers with flooding
quantities of water. Apply water from as far a distance as possible. Use foam,
dry chemical, or carbon dioxide. Keep
run-off water out of sewers and water sources. /Phenol, molten/
Toxic Combustion Products:
Toxic and irritating vapors are generated when heated.
Explosive Limits & Potential:
MIXTURES OF AIR CONTAINING 3-10% PHENOL ARE EXPLOSIVE.
When heated, phenol evolves flammable vapors which will form explosive
mixtures with air.
Hazardous Reactivities & Incompatibilities:
Addition of aluminum chloride to a large volume of recovered nitrobenzene
containing 5% phenol caused a violent explosion. Experiment showed that mixtures
containing all three components reacted violently at 120 deg C.
Uncontrolled contact of phenol with peroxodisulfuric acid may cause
explosion.
/A combination of phenol with calcium hypochlorite/ ... is an exothermic
reaction producing toxic fumes which may ignite.
Mixtures of peroxymonosulfuric acid with phenol explode.
A mixture /of phenol with sodium nitrite/ exploded violently on heating in a
test tube.
The combination of phenol with acetaldehyde results in violent condensation.
/From table/
The combination of phenol with 1,3-butadiene and boron trifluoride diethyl
ether complex results in an intense exothermic reaction. /From table/
The combination of phenol with mineral oxidizing acids results in fire. /From
table/
The combination of phenol with isocyanates results in heat generation and
violent polymerization. /From table/
The combination of phenol with nitrides results in heat and flammable gas
generation. /From table/
Strong oxidizers, calcium hypochlorite, aluminum chloride, acids.
Prior History of Accidents:
ACCIDENTAL SPILLAGE OF 37,900 L OF 100% PHENOL IN JULY 1974 CAUSED CHEMICAL
CONTAMINATION OF WELLS IN A RURAL AREA OF SOUTHERN WISCONSIN. HUMAN ILLNESS
CHARACTERIZED BY DIARRHEA, MOUTH SORES, DARK URINE & BURNING OF THE MOUTH
WAS SUBSEQUENTLY REPORTED BY 17 INDIVIDUALS WHO CONSUMED THE CONTAMINATED WATER;
THEIR ESTIMATED INTAKE OF PHENOL WAS 10-240 MG/PERSON/DAY.
A Chessie System freight train derailed in a wooded, rural area near Woodland
Park, Michigan in February 1978. Four tank cars were damaged, spilling approx
300,000 lb of vinylidene chloride, 330,000 lb of phenol, and 125,000 lb of
ethylene oxide. Most of the phenol, which had solidified on the surface, was
removed by a cleanup contractor although residual phenol remained in the soil.
The ethylene oxide vaporized, posing no groundwater contamination problems. The
vinylidene chloride percolated through the sandy soils into the groundwater
about 50 ft below the ground surface. Vinylidene chloride concentrations as high
as 300 mg/l were found in monitoring wells near the derailment site. The
groundwater cleanup program was completed over a three yr period. ...
A description of a fire and explosion in a phenol production plant in 1982 is
presented.
Immediately Dangerous to Life or Health:
250 ppm
Protective Equipment & Clothing:
SAFETY ... MEASURES ... SHOULD INCLUDE: ... EFFECTIVE VENTILATION. ...
SPECIAL PRECAUTION IN TANK CLEANING WHICH SHOULD NOT BE ATTEMPTED WITHOUT PROPER
GEAR; FORCED-AIR SUPPLY, RESCUE HARNESS & LIFELINE, HOSE MASK, BOOTS, RUBBER
APRON & GLOVES, & A "WATCHER" STATIONED AT ENTRANCE OF TANK.
Cloropel, PVC (excellent resistance) or butyl rubber (good resistance) are
recommended chemical suit materials
for protection against phenol.
Wear appropriate personal protective clothing to prevent skin contact.
Wear appropriate eye protection to prevent eye contact.
Eyewash fountains should be provided in areas where there is any possbility
that workers could be exposed to the substance; this is irrespective of the
recommendation involving the wearing of eye protection.
Facilities for quickly drenching the body should be provided within the
immediate work area for emergency use where there is a possibility of exposure.
[Note: It is intended that these facilities provide a sufficient quantity or
flow of water to quickly remove the substance from any body areas likely to be
exposed. The actual determination of what constitutes an adequate quick drench
facility depends on the specific circumstances. In certain instances, a deluge
shower should be readily available, whereas in others, the availability of water
from a sink or hose could be considered adequate.]
Recommendations for respirator selection. Max concn for use: 50 ppm.
Respirator Class(es): Any chemical
cartridge respirator with organic vapor cartridge(s) in combination with a dust
and mist filter. Any supplied-air respirator.
Recommendations for respirator selection. Max concn for use: 125 ppm.
Respirator Class(es): Any supplied-air respirator operated in a continuous flow
mode. Any powered, air-purifying respirator with organic vapor cartridge(s) in
combination with a dust and mist filter.
Recommendations for respirator selection. Max concn for use: 250 ppm.
Respirator Class(es): Any chemical
cartridge respirator with a full facepiece and organic vapor cartridge(s) in
combination with a high-efficiency particulate filter. Any air-purifying,
full-facepiece respirator (gas mask) with a chin-style, front- or back-mounted
organic vapor canister having a high-efficiency particulate filter. Any powered,
air-purifying respirator with a tight-fitting facepiece and organic vapor
cartridge(s) in combination with a high-efficiency particulate filter. Any
self-contained breathing apparatus with a full facepiece. Any supplied-air
respirator with a full facepiece.
Recommendations for respirator selection. Condition: Emergency or planned
entry into unknown concn or IDLH conditions: Respirator Class(es): Any
self-contained breathing apparatus that has a full facepiece and is operated in
a pressure-demand or other positive pressure mode. Any supplied-air respirator
that has a full facepiece and is operated in pressure-demand or other positive
pressure mode in combination with an auxiliary self-contained breathing
apparatus operated in pressure-demand or other positive pressure mode.
Recommendations for respirator selection. Condition: Escape from suddenly
occurring respiratory hazards: Respirator Class(es): Any air-purifying,
full-facepiece respirator (gas mask) with a chin-style, front- or back-mounted
organic vapor canister having a high-efficiency particulate filter. Any
appropriate escape-type, self-contained breathing apparatus.
Preventive Measures:
Workmen should not be permitted to enter empty tank which has been filled
with phenol until it has been thoroughly cleaned and ... air concn ... is below
5 ppm.
Areas in which people handle phenol should be equipped with /SRP: isopropyl/
alcohol solution cans and safety showers.
Contact lenses should not be worn while working with this chemical.
SRP: The scientific literature for the use of contact lenses in industry is
conflicting. The benefit or detrimental effects of wearing contact lenses depend
not only upon the substance, but also on factors including the form of the
substance, characteristics and duration of the exposure, the uses of other eye
protection equipment, and the hygiene of the lenses. However, there may be
individual substances whose irritating or corrosive properties are such that the
wearing of contact lenses would be harmful to the eye. In those specific cases,
contact lenses should not be worn. In any event, the usual eye protection
equipment should be worn even when contact lenses are in place.
If material not on fire and not involved in fire: Keep sparks, flames, and
other sources of ignition away. Keep material out of water sources and sewers.
Build dikes to contain flow as necessary. Neutralize spilled material with
crushed limestone, soda ash, or lime. /Phenol, solid/
If material not on fire and not involved in fire: Keep sparks, flames, and
other sources of ignition away. Keep material out of water sources and sewers.
Build dikes to contain flow as necessary. Do not use water. /Phenol, molten/
Personal Protection: Avoid breathing vapors. Keep upwind. Avoid bodily
contact with the material. ... Do not handle broken packages unless wearing
appropriate personal protective equipment. Wear self-contained breathing
apparatus when fighting fires involving this material. /Phenol, solid/
Environmental considerations: Land spill: Dig a pit, pond, lagoon, or holding
area to contain liquid or solid material. /SRP: If time permits, pits, ponds,
lagoons, soak holes, or holding areas should be contained with a flexible
impermeable membrane liner./ Cover solids with a plastic sheet to prevent
dissolving in rain or fire fighting water. Neutralize with agricultural lime
(CaO), crushed limestone (CaCO3) or sodium bicarbonate (NaHCo)3. /Phenol, solid/
Environmental considerations: Water spill: If dissolved, in region of 10 ppm
or greater concentration, apply activated carbon at ten times the spilled
amount. Use mechanical dredges or lifts to remove immobilized masses of
pollutants and precipitates. /Phenol, solid/
Personnel protection: Avoid breathing vapors. Keep upwind. ... Avoid bodily
contact with the material. ... Do not handle broken packages unless wearing
appropriate personal protective equipment. /Phenol, molten/
Environmental considerations: Air spill: Apply water spray or mist to knock
down vapors. Vapor knockdown water is corrosive or toxic and should be diked for
containment. /Phenol, solid/
SRP: Contaminated protective clothing should be segregated in such a manner
so that there is no direct personal contact by personnel who handle, dispose, or
clean the clothing. Quality assurance to ascertain the completeness of the
cleaning procedures should be implemented before the decontaminated protective
clothing is returned for reuse by the workers.
The worker should immediately wash the skin when it becomes contaminated.
Work clothing that becomes wet or significantly contaminated should be
removed and replaced.
Workers whose clothing may have become contaminated should change into
uncontaminated clothing before leaving the work premises.
Stability/Shelf Life:
PRONE TO REDDEN ON EXPOSURE TO AIR AND LIGHT, HASTENED BY PRESENCE OF ALKALI
Shipment Methods and Regulations:
No person may /transport,/ offer or accept a hazardous material for
transportation in commerce unless that person is registered in conformance ...
and the hazardous material is properly classed, described, packaged, marked,
labeled, and in condition for shipment as required or authorized by ... /the
hazardous materials regulations (49 CFR 171-177)./
The International Air Transport Association (IATA) Dangerous Goods
Regulations are published by the IATA Dangerous Goods Board pursuant to IATA
Resolutions 618 and 619 and constitute a manual of industry carrier regulations
to be followed by all IATA Member airlines when transporting hazardous
materials.
The International Maritime Dangerous Goods Code lays down basic principles
for transporting hazardous chemicals.
Detailed recommendations for individual substances and a number of
recommendations for good practice are included in the classes dealing with such
substances. A general index of technical names has also been compiled. This
index should always be consulted when attempting to locate the appropriate
procedures to be used when shipping any substance or article.
Storage Conditions:
Phenol should be stored in closed containers in an area which is adequate to
ensure that airborne phenol concentrations do not exceed 20 mg/cu m. Conditions
shall be controlled to prevent overheating and the buildup of pressure in phenol
containers. Storage tanks must be electrically grounded and bonded to transfer
lines. Transfer and storage systems shall be designed and operated to prevent
blockage by condensed phenol. Open flames are prohibited when drums of phenol
are heated to melt the contents. The internal pressure will be vented by placing
the drums with the bung up and the bung loosened. The bungs shall be tightened
prior to moving or handling drums. Drums, carboys, or other containers of phenol
shall be closed while being handled or moved. Transfer from such containers
shall be done carefully to avoid splashes, spills, or other possible
circumstances by which an employee may come in contact with phenol. Bulk storage
facilities shall be designed and constructed to contain any leaks or spills.
KEEP WELL CLOSED & PROTECTED FROM LIGHT.
STORE IN COOL, DRY, WELL-VENTILATED LOCATION. SEPARATE FROM OXIDIZERS AND
ACUTE FIRE HAZARDS.
Storage tanks should be equipped with heating coils which pass upward through
the entire vessel ... . Tanks may be constructed by either welding or riveting.
... Underground tanks are not recommended.
Phenolic resins, PVC, neoprene, saran, and polyethylene are generally
unsuitable storage container materials for phenol. /From table/
Cleanup Methods:
Eliminate all ignition sources. Control runoff and isolate discharged
material for proper disposal. Approach release from upwind.
Phenolic cmpd in wastewater are oxidized with hydrogen peroxide catalyzed by
Fe+3-Fe+2. When the wt ratio of PhOH:H2O2 is 1:3 and iron 5-100 ppm, more than
95% of the phenols are removed in 30 min from a 500 ppm phenol soln at pH 5-6
and 25-50 deg C.
Disposal Methods:
Generators of waste (equal to or greater than 100 kg/mo) containing this
contaminant, EPA hazardous waste number U188, must conform with USEPA
regulations in storage, transportation, treatment and disposal of waste.
WASTE LIQUOR CONTAINING 50,000 PPM WAS ADJUSTED TO GIVE EFFLUENT CONTAINING 1
PPM THEN TREATED WITH ACTIVATED SLUDGE TO GIVE FINAL EFFLUENT CONTAINING 0.07
PPM, 10% OF WHICH WAS RECYCLED TO CONDITIONING TANK.
Chemical Treatability of Phenol;
Concentration Process: Reverse Osmosis; Chemical
Classification: Phenol; Scale of Study: Batch Flow; Type of Wastewater Used:
Pure; Results of Study: -5.7% reduction w/CA membrane; 76.5% reduction w/C-PE1
membrane.
Chemical Treatability of Phenol;
Concentration Process: Reverse Osmosis; Chemical
Classification: Phenol; Scale of Study: Pilot scale; Type of Wastewater Used:
Synthetic; Results of Study: In excess of 90% separation at pH 8-10 with optimum
at pH 9 at flux rate of about 70 gpd/sq ft. Results indicate that
hyperfiltration (reverse osmosis) produced higher reduction and flux rates than
ultrafiltration. Increasing pressure improves rejection with little effect on
flux rate. Concentration had little effect on either rejection or flux rate.
Chemical Treatability of Phenol;
Concentration Process: Biological Treatment; Chemical
Classification: Phenol; Scale of Study: Pilot scale; Type of Wastewater Used:
Ultrafiltration; Results of Study: Its maximum rejection was 75% at pH 10;
rejection increased as pH increased. Ionic state of solute rather than membrane
material controlled rejection rate. Increased temp resulted in increased flux
rate but rejection rate was only slightly affected. Solute rejection was not
affected by length of operation.
Chemical Treatability of Phenol;
Concentration Process: Activated carbon; Chemical
Classification: Phenol; Scale of Study: Batch Flow, Laboratory Scale; Type of
Wastewater Used: Pure; Results of Study: 100% reduction; 6% desorbed from carbon
by elutriation with solvent.
Chemical Treatability of Phenol;
Concentration Process: Activated Carbon; Chemical
Classification: Phenol; Scale of Study: Isotherm test; Type of Wastewater Used:
Pure; Results of Study: For pH= 3.0 Carbon capacity= 85 mg/g K= 12, 1/n= 0.38,
r= 0.92; pt for pH= 7.0 Carbon capacity= 80 mg/g, K= 13, 1/n= 0.77, r= 0.91, For
pH= 9.0 carbon capacity= 70 mg/g, K= 22, 1/n= 0.49, r= 0.94.
Chemical Treatability of Phenol;
Concentration Process: Activated Carbon; Chemical
Classification: Phenol; Scale of Study: Continuous flow, Pilot Scale; Type of
Wastewater Used: Hazardous material; Results of Study: 100% reduction with 8.5
min contact time.
A good candidate for rotary kiln incineration at a temperature range of 820
to 1,600 deg C and residence times of seconds for liquids and gases, and hours
for solids. A good candidate for fluidized bed incineration at a temperature
range of 450 to 980 deg C and residence times of seconds for liquids and gases,
and longer for solids.
The use of a microdispersion of air in water for in situ treatment of
hazardous organic wastes was described. An air microdispersion consisting of 60
to 65% air bubbles, 25 to 50 microns in diameter, in water, referred to as
colloidal gas aphrons, was tested for stability and its ability to biodegrade
phenol. Seventy to 82% of the air incorporated into a colloidal gas aphrons
using a nonionic detergent immediately adhered to a saturated coarse sand after
sparging with a fork like probe. Thirty days later, 70 to 80% of initially
retained colloidal gas aphrons were still retained in the saturated sand matrix
as an air dispersion or as coalesced aphrons. In a biodegradation test, a
combination of colloidal gas aphrons and Pseudomonas putida plus microbial
nutrients injected into a saturated anaerobic sand matrix containing 300 mg/l
phenol solution caused degradation of 60% of the phenol within 24 hr. A 33%
colloidal gas aphrons blended with 0.3 g sodium dodecylbenzene sulfonate when
pumped into 310 g of sand saturated with 300 mg/l phenol caused 100% degradation
of phenol after about 24 hr. In a phenol degradation/trough test, a 61%
colloidal gas aphrons was injected into a soil bed containing 300 mg/l phenol at
a flow rate of 250 ml/min with a slow plow of 75 sec per plow pass. Twenty
passes were made at a 10 cm depth. The colloidal gas aphrons effectively treated
6.7 l of water causing a reduction in phenol concentration of 292 to 230 mg/l.
Colloidal gas aphrons offers a unique way to introduce oxygen or ozone for
treating dissolved, and possibly suspended, organic wastes in saturated
impoundment sediments.
The most important method, equally applied by refineries and petrochemical
plants, is the biodegradation of phenol (activated sludge basins, aeration
ponds, trickling filters). With this a 65-99% degradation of phenol is attained.
A further decrease (80-90%) of the phenol content is obtained by treatment with
ozone or activated charcoal.
Occupational Exposure Standards:
OSHA Standards:
Permissible Exposure Limit: Table Z-1 8-hr Time-Weighted Avg: 5 ppm (19 mg/cu
m). Skin Designation.
Threshold Limit Values:
8 hr Time Weighted Avg (TWA) 5 ppm, skin
Excursion Limit Recommendation: Excursions in worker exposure levels may
exceed three times the TLV-TWA for no more than a total of 30 min during a work
day, and under no circumstances should they exceed five times the TLV-TWA,
provided that the TLV-TWA is not exceeded.
BEI (Biological Exposure Index): Total phenol in urine at end of shift is 250
mg/g creatinine. The determinant is usually present in a significant amt in
biological specimens collected from subjects who have not been occupationally
exposed. Such background levels are incl in the BEI value. The determinant is
nonspecific, since it is observed after exposure to some other chemicals.
These nonspecific tests are preferred because they are easy to use and usually
offer a better correlation with exposure than specific tests. In such instances,
a BEI for a specific, less quantitative biological determinant is recommended as
a confirmatory test. (1987 adoption)
A4. A4= Not classifiable as a human carcinogen.
NIOSH Recommendations:
Recommended Exposure Limit: 15 Min Ceiling Value: 15.6 ppm (60 mg/cu m),
skin.
Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 5 ppm (19 mg/cu m).
Immediately Dangerous to Life or Health:
250 ppm
Other Occupational Permissible Levels:
Emergency Response Planning Guidelines (ERPG): ERPG(1) 10 ppm (no more than
mild, transient effects) for up to 1 hr exposure; ERPG(2) 50 ppm (without
serious, adverse effects) for up to 1 hr exposure; ERPG(3) 20 ppm (not life
threatening) up to 1 hr exposure.
Manufacturing/Use Information:
Major Uses:
GENERAL DISINFECTANT IN SOLN OR MIXED WITH SLAKED LIME, ETC, FOR TOILETS,
STABLES, CESSPOOLS, FLOORS, DRAINS, ETC; MFR OF COLORLESS OR LIGHT-COLORED
ARTIFICIAL RESINS, MANY MEDICAL & INDUST ORG CMPD & DYES; REAGENT IN
CHEM ANALYSIS
PHENOL IS BACTERIOSTATIC IN CONCN OF APPROX 0.2%, BACTERICIDAL ABOVE 1%,
& FUNGICIDAL ABOVE 1.3%
CHEM INT FOR PHENOLIC RESINS & BISPHENOL A
CHEM INT FOR CAPROLACTAM VIA CYCLOHEXANONE
CHEM INT FOR ADIPIC ACID
CHEM INT FOR O-HYDROXYBENZOIC ACID
CHEM INT FOR PLASTICIZERS-EG, CRESYL DIPHENYL PHOSPHATE
MEDICATION
MEDICATION (VET)
... Used in germicidal paints and slimicides.
Phenol is a disinfectant effective against vegetative Gram-positive and
Gram-negative bacteria ... and certain viruses.
Chem int for alkylphenols, such as cresols, xylenols, 4-tert-butylphenol,
octylphenols, and nonylphenols; chlorophenols; salycylic acid; aniline.
Manufacturers:
Allied Signal Inc, Hq, 101 Columbia Rd, PO Box 1057, Morristown, NJ 07962,
(201) 455-2000; Allied Signal Engineered Materials Sector; Production site:
Margaret and Bermuda St, Philadelphia, PA 19137
Aristech Chemical Corp, Hq, 600
Grant St, Pittsburgh, PA 15219-2704, (412) 433-2747; Production site: Ironton,
OH 45638
BTL Specialty Resins Corp, Hq, 2112 Sylvan Avenue, Toledo, OH 43606, (419)
244-5856; Production site: Blue Island, IL 60406
Dakota Gasification Company, Hq, 1600 East Interstate Avenue, Bismark, ND,
(701) 221-4400; Production site: Beulah, ND 58523
Georgia Gulf Corporation, Hq, PO
Box 105197, Atlanta, GA 30348, (404) 395-4500; Production sites: Pasadena, TX
77501, Plaquemine. LA 70764
Dow Chemical USA, Hq, 2020 Dow
Center, Midland, MI 48674, (517) 636-1000; Production site: Oyster Creek, TX
77541
General Electric Co, Hq, 3135 Easton Turnpike, Fairfield, CT 06431 (203)
373-2211, GE Plastics, One Plastics Ave, Pittsfield, MA 01201; Production site:
Mount Vernon, IN 47620
Kalama Chemical Inc, Hq, The Bank
of California Center, Suite 1110, Seattle, WA 98164, (206) 682-7890; Production
site: Kalama, WA 98625
Merichem Co, 4800 Texas Commerce Tower, Houston, TX 77002-3068, (713)
224-3030; Production site: 1914 Haden Rd, Houston, TX 77015
Shell Chemical Co, Hq, One Shell
Plaza, PO Box 2463, Houston, TX 77252-2463, (713) 241-6161; Production site:
Deer Park, TX 77536 (Houston plant)
Texaco Refining and Marketing Inc, Hq, 10 Universal City Plaza, Universal
City, CA 91608-1097, (818) 505-2000; Production site: El
Dorado, KS 67042
Methods of Manufacturing:
Oxidation of cumene to the corresponding tert-hydroperoxide, and cleavage to
phenol and acetone (Hock process).
Toluene oxidation to benzoic acid and subsequent oxidizing decarboxylation to
phenol (Dow process).
Sulfonation of benzene to benzene sulfonate and heating in molten alkali
hydroxide.
Dehydrogenation of cyclohexanol-cyclohexanone mixtures (Scientific Design).
Chlorination of benzene and steam hydrolysis of the chlorobenzene (Raschig
process, Raschig-Hooker, Gulf oxychlorination).
Chlorination of benzene and alkaline hydrolysis of the chlorobenzene.
General Manufacturing Information:
Method of purification: Rectification.
... CONCN OF ABOUT 4 PPM WILL IMPART A DECIDED PHENOL TASTE TO VEGETABLES
& FRUIT GROWN WITHIN RADIUS OF MORE THAN A MILE FROM A PLANT WHERE SUCH
VAPORS ESCAPE.
Only the Hock process (cumene oxidation) and toluene oxidation are important
industrially .... other processes were given up for economic reasons. New plants
are now run predominantly on the cumene process.
Formulations/Preparations:
PHENOL, USP ... LIQUEFIED PHENOL, USP IS PHENOL MAINTAINED IN LIQ STATE BY
PRESENCE OF 10% DISTILLED WATER. A NUMBER OF PREPN OF PHENOL IN WATER, OLIVE
OIL, & GLYCERIN, AS WELL AS MIXT OF PHENOL & IODINE, & PHENOL &
CAMPHOR, FORMERLY HAD OFFICIAL STATUS. PHENOLATED CALAMINE LOTION, USP CONTAINS
1% PHENOL.
MOST DERMATOLOGICAL & ANORECTAL PREPN INCORPORATE PHENOL IN A WAX OR
PETROLATUM BASE, WHICH PREVENTS ACCESS TO BACTERIA; OTHERS HAVE TOO LOW A CONCN.
Grades: Fused, crystals or liquid, all as technical (82%, 90%, 95%, other
components mostly cresols); CP & USP.
Phenol is supplied as pure phenol and as 90:10 phenol:water mixt.
ACS loose crystals, ACS double-distilled fused solid, 90% vacuum distilled
grades. Ultrapure, crystalline, nucleic acid grades. USP crystal grade, 99.7%,
liquified with 10% water.
Impurities:
Grades: Fused, crystals or liquid, all as technical (82%, 90%, 95%, other
components mostly cresols); CP & USP.
Consumption Patterns:
CHEM INT FOR PHENOLIC RESINS, 43.0%; CHEM INT FOR BISPHENOL A, 20.9%; CHEM
INT FOR CAPROLACTAM, 17.0%; CHEM INT FOR XYLENOLS, 6.8%; CHEM INT FOR
NONYLPHENOL, 2.7%; CHEM INT FOR ADIPIC ACID, 1.8%; CHEM INT FOR O-HYDROXYBENZOIC
ACID, 1.3%; CHEM INT FOR DODECYLPHENOL, 1.1%; OTHER, 5.4% (1980)
Phenolic resins, 45%; bisphenol-A, 20%; caprolactam, 13%; alkylphenols, 5%;
xylenols and cresols, 5%; aniline, 3%; exports, 4%; misc, 5% (1985)
Adhesives, 60%; plastics, 20% (1985)
About half of USA phenol consumption is directly related to the housing and
construction industries, while an additional 12-15% is related to automotive
applications. ... /The manufacture of/ phenolic resins remains by far the
largest single use of phenol, at 1.182 billion lb in 1987, with growth of 0.5%
to 1.188 billion, in 1988.
CHEMICAL PROFILE: Phenol. Phenolic
resins, 38%; bisphenol-A, 23%; caprolactam, 17%; alkylphenols, 4%; xylenols, 4%;
aniline, 3%; miscellaneous, 5%; exports, 6%.
CHEMICAL PROFILE: Phenol. Demand:
1986: 2,290 million lb; 1987: 3,100 million lb; 1991 /projected/: 3,300 million
lb (Includes exports, imports are negligible).
Bisphenol-A, 35%; phenolic resins, 34%; caprolactam, 15%; aniline, 5%;
alkylphenols, 5%; xylenols, 5%; miscellaneous, 1%.
U. S. Production:
2,577,631X10+3 lb of phenol were produced in 1981.
(1978) 1.22X10+12 G
(1983) 1.18X10+12 G
1.21X10+12 g /From cumene/
7.60X10+10 g /From all other sources/
(1987) 3.24X10+9 lb (phenol, synthetic)
(1990) 3.54 billion lb
(1992) 3.61 billion lb
(1991) 3.60 billion lb
(1993) 3.72 billion lb
1992: 3.74 billion pounds (includes exports, but not imports)
1993: 1,544,222,000 kilograms, of which 1,447,000,000 kilograms was produced
synthetically from cumene by oxidation. /Phenol and its salts/
U. S. Imports:
(1977) 2.56X10+9 G
(1982) 2.60X10+7 G
2.69X10+10 g
(1986) 1.95X10+7 lb (phenol and phenol-alcohols nspf)
1992: Less than 10 million pounds/yr.
U. S. Exports:
(1978) 1.04X10+11 G
(1983) 4.78X10+10 G
(1984) 6.40X10+10 g
(1987) 1.56X10+8 lb (carbolic acid)
1992: 230-350 million pounds/yr.
Laboratory Methods:
Clinical Laboratory Methods:
PHENOL WAS EXTRACTED FROM BLOOD AND ANALYZED BY GAS SOLID CHROMATOGRAPHY
USING THE POROUS POLYMER CHROMOSORB 101 AS THE SOLID ADSORBENT. THE
DETECTABILITY WAS 0.1 MG/L IN 2 ML OF BLOOD.
Analyte: Phenol; Matrix: urine; Procedure: Gas chromatography, flame
ionization detector; Treatment: acid hydrolysis, extraction; Range: 2-300 ug
phenol/ml urine, 2-500 ug p-cresol/ml urine; Controls: pooled urine from
unexposed workers; Est Limit of Detection: 0.5 ug/ml urine; Recovery: 94% @ 15
ug phenol/ml urine, 95% @ 50 ug p-cresol/ml urine; Precision: 0.128, 0.091;
Interferences: o-phenylphenol has GC retention times similar to phenol
Urinary concentration of phenyl sulfate and phenyl glucuronide (0.91) was
slightly higher than those between phenol in the air and phenyl sulfate (0.89)
or phenyl glucuronide (0.87).
Analytic Laboratory Methods:
TITRATION ANALYSIS FOR PREPN CONTAINING PHENOL APPLICABLE TO COMMERCIAL
CRESOLS, SAPONIFIED CRESOL SOLN, COAL TAR DIPS, & DISINFECTANTS, & TO
KEROSENE SOLN OF PHENOLS IN ABSENCE OF SALICYLATES OR BETA-NAPHTHOL. TITRATION
ANAL APPLICABLE TO DETECTION OF PHENOL IN PRESENCE OF SALICYLATES.
IN ENVIRONMENTAL SAMPLES EIGHT PHENOLS WERE CONVERTED INTO CORRESPONDING
BROMOPHENOLS BY REACTION WITH BROMINE. MIN DETECTABLE AMT OF BROMOPHENOLS WITH
AN ELECTRON CAPTURE DETECTOR WAS APPROX 0.01 NG.
Matrix: Air; Procedure: Bubbler collection in dilute sodium hydroxide; GC
analysis. Range: 9.46-37.8 mg/cu m
Analyte: Phenol; Matrix: air; Procedure: gas chromatography, flame ionization
detector; Range: 0.5-6 mg; Est LOD: 10 ug/samp; Precision: 0.044; Interferences:
none identified
NIOSH Method 8305, Phenol and p-Cresol in urine, issued 8/15/94, GC/FID, acid
hydrolysis and extraction, range 2-300 ug/ml urine, estimated limit of detection
0.5 ug/ml.
NIOSH Method 3502, Phenol, GC/FID, issued 8/15/94, air, solid sorbent tube,
working range 5-60 mg/cu m with 100 L air sample, estimated limit of detection
10 ug/sample.
NIOSH Method 2546, Cresol (all isomers) and Phenol, issued 8/15/94, GC/FID,
air, solid sorbent tube, working range 1-60 mg/cu m with 20 L air sample,
estimated limit of detection 1-3 ug/sample.
HPLC with UV detection, reliable quantitation limit 0.041 mg/cu m (0.01 ppm),
recommended sampling volume is 24 L.
EPA Method 8410, Determination of Semi-Volatile Organics by Capillary Column
GC/FT-IR, identification limit 35 ug/L
EPA Method 8270B, Determination of Semi-Volatile Organics by Capillary Column
GC/MS, estimated quantitation limit 10 ug/L in water and 660 ug/kg in soil and
solid waste.
EPA Method 8250A, Determination of Semi-Volatile Organics (After Appropriate
Extraction Techniques) by Capillary Column GC/MS, method detection limit 1.5
ug/L.
EPA Method 8040A, Determination of Phenols (After Appropriate Extraction
Techniques) by Direct Injection Gas Chromatography, method detection limit 2.2
ug/L with ECD detection, 0.14 ug/L with FID detection.
EPA Method 604, Determination of phenol and certain substituted phenols in
municipal and industrial discharges using gas chromatography. Method detection
limit 2.2 ug/L with ECD detection and 0.14 ug/L with FID detection.
EPA Method 604, Determination of semivolatile toxic organic pollutants and
additional compounds amenable to extraction and capillary column GC/MS. Method
detection limit 10 ug/L high solids wastewater and 760 ug/kg soil.
Sampling Procedures:
Analyte: Phenol; Matrix: air; Sampler: bubbler (0.1 N sodium hydroxide); Flow
rate: 0.2-1 l/min; Vol: min: 26 l, max: 240 l; Stability: at least 5 days at 25
deg C
Analyte: Phenol and p-cresol; Matrix: urine; Specimen: 2 spot urine samples,
before and after exposure; Vol: 50-100 ml in polyethylene screw-cap bottle with
preservative; Preservative: few crystals thymol; Controls: pooled urine from
unexposed workers; Stability: stable for 4 days at 25 deg C, 3 mo at -4 deg C
EPA Method 8040: Phenols. For the detection of phenolic compounds, a
representative sample (solid or liquid) is collected in a glass container
equipped with a Teflon-lined cap. Care is taken to avoid sample contact with any
plastic.
Special References:
Special Reports:
LIAO JT F, OEHME FW; LITERATURE REVIEWS OF PHENOLIC CMPD. I. PHENOL: VET HUM
TOXICOL 22 (3): 160-4 (1980). A REVIEW WITH 31 REF ON PHYSICAL & CHEM
PROPERTIES; SOURCES, USES, & EXPOSURES; METABOLISM; TOXICITY & MODE OF
ACTION; & PATHOLOGY OF PHENOL.
USEPA; Ambient Water Quality Criteria Doc: Phenol (1980) EPA 440/5-80-066.
NIOSH; Criteria Document: Phenol (1976) DHEW Pub. NIOSH 76-196.
USEPA; Summary Review of the Health Effects Assoc with Phenol: Health Issue
Assessment. 44p. (1986) EPA/600/8-86/003F. Review of the toxicity, environmental
fate and exposure, and occupational exposure to phenol.
Irons RD, Sawahata T; Bioact Foreign Cmpd 259-81 (1985). A review with 93
references on the bioactivation (mainly oxidation) of phenols, catechols, and
quinones and the toxicity of their oxidation products.
Kristiansen E; Nordic Expert Group for Documentation of Occupat Exposure 48
pp (1984). A critical survey and evaluation of the relevant literature
pertaining to phenol exposure.
Devi CR, Sastry CA; Indian J Environ Prot 7 (4): 271-83 (1987). A review with
many references on the toxicity of phenols, especially from wastewater of
various industries to fish.
O'Donoghue JL; Neurotox Ind Commer Chem 2: 139-53 (1985). A review with 157
references on the neurotoxicity of phenol, pentachlorophenol, hexachlorophene
and 2,4-dichlorophenoxyacetic acid.
USEPA; Chem Profile: Phenol (1985). Aspects covered in this data sheet;
exposure limits; physicochemical properties; fire and explosion hazards;
reactivity; health hazards; uses; handling of spills or releases.
Industrial Accident Assoc; Chemical
Safety Information Sheet: Phenol 2p (1986). A chemical
safety data sheet regarding toxicity, protective equipment, waste disposal,
first aid, fire fighting and hazards.
Safety Practitioner 2 (11): 6-7 (1984). Contents of this data sheet on
phenol: physical properties; fire hazard; uses; hazardous reactions; toxicity
(acute and chronic exposure) ad biological hazards; safety precautions; medical
examination leakage and spillage; handling and storage; first aid measures.
Environment Canada; Tech Info for Problem Spills: Phenol (Draft) (1981).
DHHS/ATSDR; Toxicological Profile for Phenol (1989) ATSDR/TP-89/20
DHEW/NCI; Bioassay of Phenol for Possible Carcinogenicity (1980) Technical
Rpt Series No. 203 DHEW Pub No. (NIH) 80-1759
Synonyms and Identifiers:
Synonyms:
A13-01814
**PEER REVIEWED**
ACIDE CARBOLIQUE (FRENCH)
**PEER REVIEWED**
BENZENOL
**PEER REVIEWED**
CARBOLIC ACID
**PEER REVIEWED**
CARBOLSAURE (GERMAN)
**PEER REVIEWED**
Caswell No. 649
**PEER REVIEWED**
FENOL (DUTCH, POLISH)
**PEER REVIEWED**
FENOLO (ITALIAN)
**PEER REVIEWED**
HYDROXYBENZENE
**PEER REVIEWED**
IZAL
**PEER REVIEWED**
MONOHYDROXYBENZENE
**PEER REVIEWED**
MONOPHENOL
**PEER REVIEWED**
NCI-C50124
**PEER REVIEWED**
OXYBENZENE
**PEER REVIEWED**
PHENIC ACID
**PEER REVIEWED**
PHENOLE (GERMAN)
**PEER REVIEWED**
PHENYL ALCOHOL
**PEER REVIEWED**
PHENYL HYDRATE
**PEER REVIEWED**
PHENYL HYDROXIDE
**PEER REVIEWED**
PHENYLIC ACID
**PEER REVIEWED**
PHENYLIC ALCOHOL
**PEER REVIEWED**
Formulations/Preparations:
PHENOL, USP ... LIQUEFIED PHENOL, USP IS PHENOL MAINTAINED IN LIQ STATE BY
PRESENCE OF 10% DISTILLED WATER. A NUMBER OF PREPN OF PHENOL IN WATER, OLIVE
OIL, & GLYCERIN, AS WELL AS MIXT OF PHENOL & IODINE, & PHENOL &
CAMPHOR, FORMERLY HAD OFFICIAL STATUS. PHENOLATED CALAMINE LOTION, USP CONTAINS
1% PHENOL.
MOST DERMATOLOGICAL & ANORECTAL PREPN INCORPORATE PHENOL IN A WAX OR
PETROLATUM BASE, WHICH PREVENTS ACCESS TO BACTERIA; OTHERS HAVE TOO LOW A CONCN.
Grades: Fused, crystals or liquid, all as technical (82%, 90%, 95%, other
components mostly cresols); CP & USP.
Phenol is supplied as pure phenol and as 90:10 phenol:water mixt.
ACS loose crystals, ACS double-distilled fused solid, 90% vacuum distilled
grades. Ultrapure, crystalline, nucleic acid grades. USP crystal grade, 99.7%,
liquified with 10% water.
Shipping Name/ Number DOT/UN/NA/IMO:
UN 1671; Phenol, solid
UN 2312; Phenol, molten
UN 2821; Phenol solutions
IMO 6.1; Phenol, solid, molten, solutions
Standard Transportation Number:
49 212 20; Phenol, carbolic acid
49 212 10; Phenol, liquid, solution, carbolic acid, liquid (liquid tar acid
containing over 50% phenol)
EPA Hazardous Waste Number:
U188; A toxic waste when a discarded commercial chemical
product or manufacturing chemical
intermediate or an off-specification commercial chemical
product.
RTECS Number:
NIOSH/SJ3325000
Administrative Information:
Hazardous Substances Databank Number: 113
Last Revision Date: 20020118
Last Review Date: Reviewed by SRP on 5/16/1996
http://www.nycwasteless.com/gov-bus/citysense/ede..
Acute Health Effects:
Inhalation can irritate the mouth, nose, throat, and lungs, causing coughing
and/or shortness of breath. Contact can cause severe irritation and burns with
possible permanent damage to eyes and skin. High exposure can cause headache,
dizziness, fatigue, fainting, weakness, nausea, vomiting, and lack of appetite;
may cause collapse and death.
Chronic Health Effects:
May be a carcinogen and mutagen. High or repeated exposure may damage liver,
kidneys, and heart. Effects may include reduced memory or concentration,
personality changes, fatigue, sleep disturbances, and reduced coordination.
http://www.webcom.com/~bi/tables/health-effects-...
Poison: colic, seizures, cardiac arrhythmias, shock, respiratory arrest. 14
Toxic 11, tremors, lower fetal body weight, possible skin
carcinogen, EPA Inhalation data insufficient.16.
ATSDR
- Toxicological Profile: Phenol
... Toxicological Profile for. Phenol. CAS# 108-95-2. December
1998 ... toxicological profile
succintly characterizes the toxicologic and adverse health effects
...
http://www.atsdr.cdc.gov/toxprofiles/tp115.html
More Results From: www.atsdr.cdc.gov
BEAM
... Phenol causes health effects from both short
term (acute less than 14
days) and also long term (chronic greater than 365 days) exposure. ...
http://www.state.me.us/dep/air/beam/factsheets/phenol_fs.htm
More Results From: www.state.me.us
Phenol
[factsheet]
... Office of Drinking Water, Washington, DC. 1990. 9. US Environmental
Protection Agency.
Health and Environmental Effects Profile for Phenol.
EPA/600/x-87/121. ...
http://www.lakes-environmental.com/toxic/PHENOL.HTML
More Results From: www.lakes-environmental.com
IAQ
Fact Sheet: Formaldehyde
... Products made of urea formaldehyde can release formaldehyde gas;
products made of
phenol formaldehyde generally emit lower ... What Are the Health
Effects? ...
http://www.nsc.org/ehc/indoor/formald.htm
More Results From: www.nsc.org
Second
Hand Smoke
... and health effects. A source list of studies on which
this summary is based can be
obtained by contacting or you can download the PDF version by clicking here. ...
http://www.smoke-free.ca/Health/Healtheffectssmoke.htm
More Results From: www.smoke-free.ca
44
Phenol (PDF)
... Synonyms for phenol include carbolic acid, benzophenol, and
hydroxybenzene. Health
Hazards Acute effects: Phenol is irritating and corrosive to the
skin. ...
http://www.ehs.berkeley.edu/pubs/factsheets/44phenol.pdf
More Results From: www.ehs.berkeley.edu
CRC
Press: ATSDR Online
... at about 40 parts of phenol per billion parts of air (ppb),
and begin to smell phenol
in water at about 1–8 parts of phenol ... Because the health
effects ...
http://www.atsdr.net/default.asp?cc=80
More Results From: www.atsdr.net
Testing
Consent Order For Phenol
... 14 specified companies. In the ECA, the companies agreed to perform
certain health effects tests on phenol (CAS No. 108- 95-2).
In ...
http://www.epa.gov/fedrgstr/EPA-TOX/1997/May/Day-23/t13646.htm
More Results From: www.epa.gov
RMHI
| Environmental health hazards checklist
... are harmful and how to avoid or minimize the hazardous health effects
... or other protozoa;
* other contaminants: hydrocarbon pollutants (benzene, phenol ...
http://www.rmhiherbal.org/a/e.envirhaz.html
News
brief: TERA Focuses on Phenol and Acetaldehyde Assessments
... In the case of phenol, Health Canada had proposed an
oral Tolerable
Daily Intake (TDI) for non-cancer health effects. Several issues ...
http://www.riskworld.com/NEWS/97q4/nw7aa052.htm
More Results From: www.riskworld.com
Eco-USA:
Phenol
... should be limited to 0.3 milligrams phenol per liter of water
(0.3 mg/L) to protect
human health from the possible harmful effects of exposure to phenol
by ...
http://www.eco-usa.net/toxics/phenol.shtml
More Results From: www.eco-usa.net
Water
Quality Association Chloramine - Are there negative health ...
... What is CHLORAMINE and are there any negative health effects
... Particularly where the
water supply contains phenol, free chlorine readily reacts to form ...
http://www.wqa.org/sitelogic.cfm?ID=348
Car
Exhaust, Air Pollution; Heath Effects
... Amounts of benzene (in blood) and phenol (in urine) cannot be
used as
yet to predict what degree of harmful health effects may occur. ...
http://www.nutramed.com/environment/carschemicals.htm
More Results From: www.nutramed.com
ATSDR
- Public Health Statement: Phenol (1989)
... the test. The test results cannot be used to tell what health effects
might result from exposure to phenol. Measurement of phenol ...
http://www.cla.sc.edu/geog/hrl/sctrap/toxfaqs/phenol.htm
More Results From: www.cla.sc.edu
Society
of Occupational Medicine - Consultative Documents - ...
... and phenol and at present are allocated OELs. The change
implies that HSC believes
that these three substances could cause the most serious health effects
such ...
http://www.som.org.uk/consdocs/nl85/nl85sp_ecd00eafl.html
More Results From: www.som.org.uk
Effects
of Dinitrophenol on life forms
... Office: 1990 "Toxicological Profile for Phenol" by
Agency for Toxic Substances and
Disease Registry 1986 "Summary Review of the Health Effects
of Phenol" by US ...
http://newton.dep.anl.gov/newton/askasci/1995/environ/ENV167.HTM
Chemical
Network -- Chemical Industry Directory
... Phenol United States Technical Info Symptoms and treatment of phenol
... Perspective on
the Dangers of Plutonium Publication concerning some health effects
...
http://www.chemnet.com/dir/Chemical_resources/Chemical_data/Safety_and_toxicity_data/index4.html
phenol2
... Health Effects: Phenol can cause serious health
effects that increase
as both concentration level and length of exposure increase. ...
http://www.lehigh.edu/kaf3/public/www-data/cchemdata/phenol2.html
More Results From: www.lehigh.edu