1.1 Substance
   1.2 Group
   1.3 Synonyms
   1.4 Identification numbers
      1.4.1 CAS number
      1.4.2 Other numbers
   1.5 Main brand names, main trade names
   1.6 Main manufacturers, main importers
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First aid measures and management principles
   3.1 Origin of the substance
   3.2 Chemical structure
   3.3 Physical properties
      3.3.1 Colour
      3.3.2 State/form
      3.3.3 Description
   3.4 Hazardous characteristics
   4.1 Uses
      4.1.1 Uses
      4.1.2 Description
   4.2 High risk circumstance of poisoning
   4.3 Occupationally exposed populations
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
   5.6 Other
   6.1 Absorption by route of exposure
   6.2 Distribution by route of exposure
   6.3 Biological half-life by route of exposure
   6.4 Metabolism
   6.5 Elimination and excretion
   7.1 Mode of action
   7.2 Toxicity
      7.2.1 Human data Adults Children
      7.2.2 Relevant animal data
      7.2.3 Relevant in vitro data
      7.2.4 Workplace standards
      7.2.5 Acceptable daily intake (ADI)
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
   8.1 Material sampling plan
      8.1.1 Sampling and specimen collection Toxicological analyses Biomedical analyses Arterial blood gas analysis Haematological analyses Other (unspecified) analyses
      8.1.2 Storage of laboratory samples and specimens Toxicological analyses Biomedical analyses Arterial blood gas analysis Haematological analyses Other (unspecified) analyses
      8.1.3 Transport of laboratory samples and specimens Toxicological analyses Biomedical analyses Arterial blood gas analysis Haematological analyses Other (unspecified) analyses
   8.2 Toxicological analyses and their interpretation
      8.2.1 Tests on toxic ingredient(s) of material Simple qualitative test(s) Advanced qualitative confirmation test(s) Simple quantitative method(s) Advanced quantitative method(s)
      8.2.2 Tests for biological specimens Simple qualitative test(s) Advanced qualitative confirmation test(s) Simple quantitative method(s) Advanced quantitative method(s) Other dedicated method(s)
      8.2.3 Interpretation of toxicological analyses
   8.3 Biomedical investigations and their interpretation
      8.3.1 Biochemical analysis Blood, plasma or serum Urine Other fluids
      8.3.2 Arterial blood gas analyses
      8.3.3 Haematological analyses
      8.3.4 Interpretation of biomedical investigations
   8.4 Other biomedical (diagnostic) investigations and their interpretation
   8.5 Overall interpretation of all toxicological analyses and toxicological investigations
   9.1 Acute poisoning
      9.1.1 Ingestion
      9.1.2 Inhalation
      9.1.3 Skin exposure
      9.1.4 Eye contact
      9.1.5 Parenteral exposure
      9.1.6 Other
   9.2 Chronic poisoning
      9.2.1 Ingestion
      9.2.2 Inhalation
      9.2.3 Skin exposure
      9.2.4 Eye contact
      9.2.5 Parenteral exposure
      9.2.6 Other
   9.3 Course, prognosis, cause of death
   9.4 Systematic description of clinical effects
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurological Central nervous system (CNS) Peripheral nervous system Autonomic nervous system Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary Renal Other
      9.4.7 Endocrine and reproductive systems
      9.4.8 Dermatological
      9.4.9 Eye, ear, nose, throat: local effects
      9.4.10 Haematological
      9.4.11 Immunological
      9.4.12 Metabolic Acid-base disturbances Fluid and electrolyte disturbances Others
      9.4.13 Allergic reaction
      9.4.14 Other clinical effects
      9.4.15 Special risks
   9.5 Other
   9.6 Summary
   10.1 General principles
   10.2 Life supportive procedures and symptomatic/specific treatment
   10.3 Decontamination
   10.4 Enhanced elimination
   10.5 Antidote treatment
      10.5.1 Adults
      10.5.2 Children
   10.6 Management discussion
   11.1 Case reports from the literature
   12.1 Specific preventative measures
   12.2 Other

    International Programme on Chemical Safety
    Poisons Information Monograph 412

    1.  NAME

        1.1  Substance 


        1.2  Group

             Hydrocarbons, cyclic, alcohol

        1.3  Synonyms

             acidum carbolicum;
             acidum phenolicum;
             acidum phenylicum;
             baker's P & S liquid ointment;
             benzene phenol;
             benzenol carbolic acid;
             carbolic acid;
             hydroxybenzene (IUPAC);
             phenic acid;
             phenol alcohol;
             phenyl hydrate;
             phenyl hydroxide;
             phenylic acid;
             phenylic alcohol

        1.4  Identification numbers

             1.4.1  CAS number


             1.4.2  Other numbers

                    NIOSH number: SJ 3325000
                    Hazchem code: 2X
                    DOT: 1671/2312/2821

        1.5  Main brand names, main trade names

        1.6  Main manufacturers, main importers

    2.  SUMMARY

        2.1  Main risks and target organs

             Phenol exerts a marked corrosive action on any tissue of
             contact when ingested, inhaled or after skin exposure. Its
             cellular uptake is both rapid and passive due to its
             lipophilic character, and signs of systemic toxicity develop
             soon after exposure. Phenol's main target organs are the
             liver and kidney. It may also effect the respiratory and
             cardiovascular systems.

        2.2  Summary of clinical effects

             After ingestion phenol produces burning pain and white
             necrotic lesions in the mouth, oesophagus and stomach,
             vomiting and bloody diarrhoea. After skin exposure, pain is
             followed by numbness and the skin becomes blanched. The
             systemic clinical effects of phenol are independent on the
             route of exposure, they include: headache, dizziness,
             hypotension, ventricular arrhythmia, shallow respiration,
             cyanosis, pallor; excitation and convulsions may occur
             initially, but it is quickly followed by unconsciousness. A
             fall in body temperature and pulmonary oedema may occur.
             Methemoglobinemia and hemolytic anemia have been reported
             occasionally. The most important effects in short-term animal
             studies are neurotoxicity, liver and kidney damage and
             respiratory effects. The available data do not suggest a
             strong potential for cumulative health effects from chronic

        2.3  Diagnosis

             Phenol poisoning can be recognised by the characteristic
             acrid odour on the breath or it can be detected in the urine,
             which may be dark coloured. Therefore a urine sample and also
             a blood sample should be taken. Phenol is corrosive to mucous
             membranes, eyes and causes burns to the skin.

        2.4  First aid measures and management principles

             EYES: Immediately flush eye(s) with water (preferably
             tepid) for at least 15 minutes.
             INHALATION: Remove patient from the area of exposure to fresh
             air. If unconscious, intubate with a cuffed endo-tracheal
             tube and ventilate mechanically if necessary. If conscious,
             place in Trendelenburg, left lateral position with succion
             equipment ready. Treat convulsions, arrhythmias and
             methaemoglobinemia according to Treatment Guides.

             INGESTION: Do not induce vomiting. Do not dilute since it may
             increase absorption. Gastric aspiration or lavage should be
             weighed with risk. Give polyethylene glycol solution or
             activated charcoal with sorbitol.
             DERMAL: Wearing protective gloves remove contaminated
             clothing immediately, flush excess chemical off the skin with
             water if it is the only available liquid, but preferably 
             wash with polyethyleneglycol molecular weight 300 (Macrogol
             300), isopropyl alcohol, industrial methylated spirits or
             Golytely for at least 30 minutes.
             In all cases of exposure the patient should be transferred to
             a hospital as soon as possible.


        3.1  Origin of the substance

             Natural, obtained from coal tar, or as a degradation
             product of benzene. Synthetic, made by fusing sodium
             benzenesulfonate with NaOH, or by heating monochlorobenzene
             with aqueous NaOH under high pressure (Windholz, 1983)

        3.2  Chemical structure


             Chemical formula:         C6H6O
             Molecular weight:         94.11

        3.3  Physical properties

             3.3.1  Colour

                    Colourless or white (WHO, 1994). 

             3.3.2  State/form

                    Acicular-crystals, or white crystalline mass
                    (WHO, 1994).


           3.3.3  Description

                    The crystals turn pink or red on exposure to
                    air and light, hastened in presence of alkalinity
                    (Windholz, 1983). Phenol has an acrid smell and a
                    sharp burning taste.
                    In the molten state, it is a clear, colourless liquid
                    with a low viscosity. It is soluble in most organic
                    solvents, and solubility is limited in aliphatic
                    solvents.  Phenol's solubility.  In water is limited
                    at room temperature, above 68C it is entirely water
                    soluble. The vapour is heavier than air (WHO,
                    Melting point is 43C, the commercial product has an
                    impurity that increases the melting point (Windholz,
                    Boiling point: 181.75C
                    Flash point: 80C (closed cup); 79C to 85C (open
                    Relative vapour density: 3.24 (WHO, 1994).
                    Explosive limits are 1.7% to 8.6% (Allen, 1991).
                    Vapour pressure at 20C is 47 Pascal
                    pKa 10,0 at 25C
                    pH of aqueous solutions is approximately 6.0
                    It is liquefied by mixing with about 8% water
                    (Windholz, 1983).

        3.4  Hazardous characteristics

             Autoignition temperature is 715C. Phenol is a volatile,
             combustible solid that when heated gives off flammable
             vapours and carbon dioxide. Explosive or violent reactions
             occur with acetylaldehyde; aluminium chloride plus
             nitrobenzene; aluminium chloride-nitromethane; butadine;
             calcium hypochlorite;  peroxomonosulphuric acid;
             peroxodisulphuric acid; sodium nitrate; and sodium
             nitrate-trifluoroacetic acid (Allen, 1991).
             Phenol is sensitive to oxidising agents. Splitting of the
             hydrogen atom from the phenolic hydroxyl group is followed by
             resonance stabilisation of the resulting phenyloxy radical.
             The radical that is formed can be further oxidised. This
             makes phenol suitable as an antioxidant, functioning as a
             radical trapping agent (WHO, 1994).  The taste threshold is
             0.3 mg/L (0.00003%) in water (WHO, 1994).

    4.  USES

        4.1  Uses

             4.1.1  Uses

             4.1.2  Description

                    The main use of phenol is as a feedstock for
                    phenolic resins, bisphenol A and caprolactam (an
                    intermediate in the production of nylon-6). It is used
                    in the manufacture of many products including
                    insulation materials, adhesives, lacquers, paint,
                    rubber, ink, dyes, illuminating gases, perfumes, soaps
                    and toys (IARC, 1989; WHO, 1994).  Also used in
                    embalming and research laboratories. It is a product
                    of the decomposition of organic materials, liquid
                    manure, and the atmospheric degradation of
                    It is found in some commercial disinfectants,
                    antiseptics, lotions and ointments. Phenol is active
                    against a wide range of microorganisms, and there are
                    some medical and pharmaceutical applications including
                    topical anaesthetic and ear drops, sclerosing agent.
                    It is also used in the treatment of ingrown nails in
                    the "nail matrix phenolization method" (Kimata et al.,
                    1995). Another medical application of phenol is its
                    use as a neurolytic agent, applied in order to relieve
                    spasms and chronic pain (Wood, 1978; Geller,
                    It is used in dermatology for chemical face peeling.

        4.2  High risk circumstance of poisoning

             Deliberate, accidental or occupational exposure.

        4.3  Occupationally exposed populations

             Workers involved in the production of phenol by the
             cumene process, or the production of phenol from
             chlorobenzene are at risk. Phenol may be emitted into the air
             during the processing of phenolic resins, production of
             phenol and phenol derivatives, production of caprolactam,
             production of cokes and insulation materials. Wood workers,
             and workers at plywood plants are at risk of exposure. Phenol
             is used in iron and steel foundries - in the manufacture of
             moulds or kernels, or during the operation of an electric
             furnace in a steel factory and also in coal gasification and
             liquefication plants, bakelite factories, and synthetic fibre

             and fibrous glass wool factories. In creosote impregnation
             plants, with highest exposure levels during the cleaning of
             creosote warming chambers. In embalming situations, where the
             embalming solution contains high phenol concentrations
             (Allen, 1991; WHO, 1994).
             In chemical accidents, responders or health staff may be
             exposed by direct contact, by vomitus, or by off-gassing of
             contaminated clothing.


        5.1  Oral

             Phenol is readily absorbed from the gastrointestinal
             tract (WHO, 1994).

        5.2  Inhalation

             Phenol is readily absorbed from the lungs (Allen,

        5.3  Dermal

             When spilt on the skin, intact or abraded, it is rapidly
             absorbed and may lead to systemic poisoning (Brooks &
             Riviere, 1996).

        5.4  Eye

             Phenol is absorbed through the mucous membranes of the
             eye (WHO, 1994).

        5.5  Parenteral

             Therapeutic use: phenol can be administered by
             intrathecal injection to relieve pain and spasticity (Geller,
             1997), and has been used as a sclerosing agent.

        5.6  Other

             No data available.

    6.  KINETICS

        6.1  Absorption by route of exposure

             Phenol is rapidly absorbed through skin, lungs, and the
             gastrointestinal tract.

             Eight humans exposed to 6 to 20 mg/m3 by inhalation for 8
             hours absorbed 70 to 80% of the phenol dose.
             Skin absorption of phenol vapour (5 to 25 mg/m3) occurs
             rapidly. The absorption in 8 humans exposed to phenol vapour
             at concentrations of 6 to 20 mg/m3 , by skin only, for 6
             hours was also 70 to 80%. Concentrations between 5 and 10%
             phenol denature epidermal protein and this can therefore
             partly prevent absorption. The phenol-protein complex is not
             stable and by dissociation of phenol the substance may exert
             its action over a period of time. In an  in vitro study with
             human abdominal skin, 10.9% of the dose was absorbed. The
             period of exposure and the concentration of phenol are both
             factors that determine the extent of absorption, but the area
             of skin exposed affects the extent of absorption more than
             the concentration.  A single dose of 25 mg/kg body weight
             dermally administered to rats, pigs and sheep was more than
             95% absorbed (WHO, 1994).

        6.2  Distribution by route of exposure

             Rapidly distributed to all tissues in exposed animals.
             After a single oral administration of 207 mg/kg phenol to
             rats, the highest concentration ratios between tissue and
             plasma were found in the liver (42%), followed by spleen,
             kidney, adrenal, thyroid and lungs, with a peak tissue level
             occurring after 0.5 hours.
             In rabbits 15 minutes after an oral dose of 0.5 g/kg, the
             highest concentrations of phenol were in the liver, followed
             by the CNS, lungs and blood. After 82 minutes the phenol was
             relatively uniformly distributed in all tissues (WHO,

        6.3  Biological half-life by route of exposure

             The half-life of conjugated phenol in humans is 1 hour
             (Leikin & Paloucek, 1996-7), but there have also been
             reported half-lives of 4 to 5 hours in humans (WHO,

        6.4  Metabolism

             After oral uptake of phenol, there is a large first-pass
             metabolism. It is unclear whether phenol also undergoes first
             pass pulmonary metabolism, there have been conflicting
             results (Dickenson & Taylor, 1996). The liver, lungs and the
             gastrointestinal mucosa are the most important sites of

             phenol metabolism (WHO, 1994).  Conjugation with glucuronic
             acid to phenyl glucuronide and sulphation to phenyl sulphate,
             have been shown to be major metabolic pathways in several
             species. A shift from sulphation to glucuronidation was
             observed in rats after increasing the phenol doses, which is
             thought to be due to a saturation of the overall sulphation
             process, by the limited availability of
             3-phosphoadenosine-5-phosphosulfate. The formation of
             sulphate and glucuronic metabolites occurs in the
             hepatocytes, and then transported to the bile or back into
             the blood (Ballinger et al, 1995).   In vitro studies have
             shown the formation of the reactive metabolites 4,4'-biphenol
             and diphenoquinone by neutrophils and activated leukocytes. 
             Both in vivo and in vitro tests have shown covalent binding
             of phenol to tissue and plasma proteins, some phenol
             metabolites also bind to proteins (WHO, 1994).

        6.5  Elimination and excretion

             Urinary (renal) excretion is the major route of phenol
             elimination in animals and humans. The rate of excretion
             varies with different species, dose and route of
             administration. Three men after an oral administration of
             0.01 mg/kg phenol, excreted 90% of the dose in the urine
             within 24 hours, mainly as phenyl sulfate and phenyl
             glucuronide. A minor part is eliminated in the faeces and
             expired air. Urinary excretion of humans exposed to phenol
             vapour via inhalation or skin, occurred with an excretion
             rate constant of k 0.2/hour. On oxidation to quinones the
             metabolites may tint the urine green.
             The half life is estimated to be between 1 and 4.5 hours with
             52% eliminated unchanged in the urine (Leikin & Paloucek,
             1996-7). The natural presence of phenols in food and drug
             metabolites, makes biological monitoring impossible. A minor
             part is eliminated in expired air and faeces. (Reynolds,
             1993; Ellenhorn & Barceloux, 1988)


        7.1  Mode of action

             Cellular uptake of phenol is due to its lipophilic
             character. It denatures proteins (WHO, 1994). Phenol is known
             to disrupt disulphide bridges in keratin in the skin (Brooks
             & Riviere, 1996).
              In vitro studies have shown the formation of the reactive
             metabolites 4,4'-biphenol and diphenoquinone by neutrophils

             and activated leukocytes. Both  in vivo and  in vitro tests
             have shown covalent binding of phenol to tissue and plasma
             protein, some phenol metabolites also bind to proteins (WHO,
             1994). It produces coagulation necrosis.
             The acute lethality of phenol, associated with exposure to
             high dose concentrations, is customarily attributed to a
             depressant effect on the CNS.

        7.2  Toxicity

             7.2.1  Human data


                             The lethal dose ranges from 1 g to
                             15 g (Reynolds, 1993). Ingestion of 4.8 g
                             resulted in death after 10 minutes in one
                             person (Anderson, 1869).
                             However, an adult survived a 26.7 g dose
                             ingestion after a 15-day stormy hospital
                             course without permanent sequellae (Haddad et
                             al., 1979).
                             Survival has been reported with up to 350
                             mg/kg orally (Christiansen & Klaman,


                             Children have died after the
                             application of 5 % phenol compresses
                             (Ellenhorn, 1996).

             7.2.2  Relevant animal data

                    LD50 (oral) rodent values ranged from 300 to
                    600 mg/kg body weight.
                    LD50 (dermal) values for rats and rabbits range from
                    670 to1400 mg/kg body weight respectively.
                    LC50 (8 hour) for rats by inhalation was more than 900
                    mg/m3 (WHO, 1994).
                    In two multiple dose rat studies, NOAEL values
                    obtained were 40 mg/kg/day and 60 mg/kg /day and the

                    LOAEL values were 53 mg/kg/day and 120 mg/kg/day. In a
                    mouse study the NOAEL was 140 mg/kg/day and the LOAEL
                    was 280 mg/kg/day (WHO, 1994).
                    Chronic vapour exposures in rats ( 0.02 to 1ppm for 2
                    months) produced changes in the blood enzyme activity
                    and time for excitation of extensor muscles. At higher
                    exposures, phenol may lead to decrease in body weight.
                    In various animal species the inhalation of phenol
                    affected the lungs by causing hyperaemia, infarcts,
                    pneumonia, purulent bronchitis and hyperplasia of the
                    peribronchial tissues (WHO, 1994). There does not
                    appear to be a strong potential for cumulative health
                    effects from chronic exposure (WHO, 1994)

             7.2.3  Relevant in vitro data

                    No data available.

             7.2.4  Workplace standards

                    OSHA PEL: TWA 5 ppm (skin)
                    ACGIH TLV: TWA 5 ppm (skin)
                    IDLN: 100 ppm
                    DFG MAK: 5 ppm (19 mg/m3)
                    NIOSH REL: TWA 20 mg/m3; CL 60 mg/m3/15 minutes
                    (Sax & Lewis, 1989)
                    In Britain the occupational exposure standard is 19
                    mg/m3 (long term) and 38 mg/m3 (short term). In the
                    United States the permissible level is 19 mg/m3 and
                    the recommended is 20 mg/m3 (long-term) and the
                    maximum short term is 60 mg/m3 (Reynolds,

             7.2.5  Acceptable daily intake (ADI)

                    A Task Group derived a tolerable daily intake
                    (TDI) using the lowest NOAEL's for kidney and
                    developmental effects in rats which is in the range of
                    12 to 40 mg/kg body weight /day. With an uncertainty
                    factor of 200, the range of 60 to 200 g/kg/day was
                    recommended as the upper limit of the TDI (WHO,
                    The estimated maximal total daily intake of phenol for
                    a 70 kg individual is calculated to be 0.1 mg/kg body
                    weight per day (WHO, 1994).

                    However, according to IRIS (Integrated Risk
                    Information Sytem, 1996), the reference dose (Rfd) is
                    0.6 mg/kg/day, using the NOAEL (reduced fetal body
                    weight in rats) of 60 mg/kg/day, with an uncertainty
                    factor (Uf) of 100.

        7.3  Carcinogenicity

             An IARC review in 1989 found that the carcinogenicity
             evidence for phenol was inadequate (group 3) (WHO, 1994). US
             EPA classifies phenol in group D.
             Two-stage carcinogenicity studies have shown that phenol,
             applied repeatedly to mouse skin, has promoting activity
             (WHO, 1994).

        7.4  Teratogenicity

             Phenol has been identified as a developmental toxicant
             in studies with rats and mice (WHO, 1994).

        7.5  Mutagenicity

             The majority of bacterial mutagenicity tests have
             demonstrated negative results. In mammalian cells, mutations,
             chromosomal damage and DNA effects have been observed. Phenol
             has shown no effect on intercellular communication in
             cultured mammalian cells. The induction of micronuclei in
             bone marrow cells of mice has been observed in some studies
             at high doses. No micronuclei were observed in mice studies
             at lower dose (IARC, 1989; WHO, 1994).

        7.6  Interactions

             No data available.


        8.1  Material sampling plan

             8.1.1  Sampling and specimen collection

            Toxicological analyses

            Biomedical analyses

            Arterial blood gas analysis

            Haematological analyses

            Other (unspecified) analyses

             8.1.2  Storage of laboratory samples and specimens

            Toxicological analyses

            Biomedical analyses

            Arterial blood gas analysis

            Haematological analyses

            Other (unspecified) analyses

             8.1.3  Transport of laboratory samples and specimens

            Toxicological analyses

            Biomedical analyses

            Arterial blood gas analysis

            Haematological analyses

            Other (unspecified) analyses

        8.2  Toxicological analyses and their interpretation

             8.2.1  Tests on toxic ingredient(s) of material

            Simple qualitative test(s)

            Advanced qualitative confirmation test(s)

            Simple quantitative method(s)

            Advanced quantitative method(s)

             8.2.2  Tests for biological specimens

            Simple qualitative test(s)

            Advanced qualitative confirmation test(s)

            Simple quantitative method(s)

            Advanced quantitative method(s)

            Other dedicated method(s)

             8.2.3  Interpretation of toxicological analyses

        8.3  Biomedical investigations and their interpretation

             8.3.1  Biochemical analysis

            Blood, plasma or serum


            Other fluids

             8.3.2  Arterial blood gas analyses

             8.3.3  Haematological analyses

             8.3.4  Interpretation of biomedical investigations

        8.4  Other biomedical (diagnostic) investigations and their

        8.5  Overall interpretation of all toxicological analyses and
             toxicological investigations


        9.1  Acute poisoning

             9.1.1  Ingestion

                    After swallowing a significant concentrated
                    dose, an intense burning of the mouth and throat is
                    felt (necrosis of the skin and mucous membranes of the
                    throat), and pain in the abdominal area, with
                    gastrointestinal irritation including nausea,
                    vomiting, sweating and diarrhoea. The face is usually
                    pale and sweaty, the pupils may be contracted or
                    dilated; cyanosis is usually marked; the pulse is
                    usually weak and slow, occasionally it may be racing;
                    respiration may initially be increased in rate, but
                    later decreased in rate and magnitude; body
                    temperature may fluctuate. Excitation may occur
                    initially, but it is quickly followed by
                    unconsciousness. Occasionally isolated twitching of
                    muscles or convulsions may be observed. Acute renal
                    failure can develop resulting from systemic
                    absorption. Ingestion is usually fatal (Foxall et al.,
                    1989; Allen, 1991; Reynolds, 1993; WHO, 1994).

             9.1.2  Inhalation

                    Phenol vapours are irritating to the upper
                    respiratory tract. Ocular and nasal irritation,
                    tremors and incoordination were reported in rats
                    exposed to phenol via inhalation to 906 mg/m3 for 8
                    hours (WHO, 1994). Wheezing may occur. Other symptoms
                    associated with inhalation include anorexia, weight
                    loss, headache, salivation, vertigo (WHO, 1994) and
                    dark urine (dark/brown/green) (Leikin & Paloucek,

             9.1.3  Skin exposure

                    Phenol is a local anaesthetic, so upon initial
                    contact, no pain is felt. By the time pain is felt,
                    serious burns and absorption through the skin may have
                    occurred (Allen, 1991). Local damage to the skin
                    includes erythema, inflammation, and necrosis. The
                    effects are worse when the application sites are
                    bandaged (WHO, 1994). A white, brown or red
                    discolouration of the skin may occur (Leikin &
                    Paloucek 1996-7). Systemic intoxication can occur from
                    absorption (WHO, 1994); roughly 50 % of all reported
                    cases have a fatal outcome (Horch et al., 1994).
                    In the Kligman maximization test phenol did not cause
                    sensitisation in 24 human volunteers (Kligman,

             9.1.4  Eye contact

                    Phenol is an eye irritant (WHO, 1994). 
                    Solutions can be corrosive to the eyes, and can cause
                    severe ocular damage including corneal

             9.1.5  Parenteral exposure

                    After intraperitoneal and subcutaneous doses of
                    phenol, tremors, convulsions, coma and death have been
                    reported (WHO, 1994). Injection of 30 mL of 89% phenol
                    instead of 10% for celiac plexus nerve block resulted
                    in coma, hypotension, respiratory insufficiency and
                    ventricular tachycardia (Christiansen & Klaman,

             9.1.6  Other

                    No data available.

        9.2  Chronic poisoning

             9.2.1  Ingestion

                    Severe gastrointestinal irritation,
                    cardiovascular, CNS and respiratory effects,
                    hypothermia and decreased body weight. Brown or
                    discoloured urine has also been observed in chronic
                    poisoning (Goldfrank & Bresnitz, 1990).
                    Repeated oral exposure for several weeks (estimated
                    intake 10 to 240 mg/day) resulted in mouth sores,
                    diarrhea and dark urine. Examination 6 months after
                    the exposure revealed no residual effects (Baker et
                    al., 1978).

             9.2.2  Inhalation

                    There does not appear to be a strong potential
                    for cumulative health effects from chronic exposure
                    (WHO, 1994)

             9.2.3  Skin exposure

                    Chronic doses may result in onychronosis
                    (yellowing of the skin) and skin eruption (WHO, 1994).
                    Death has been observed from repeated application of
                    small doses (Olson, 1994).
                    In former times phenol 5 to 10% was used as a skin
                    disinfectant giving rise to the "carbolic marasmus"
                    characterized by anorexia, headache, vertigo,
                    salivation, dark urine and increased skin and scleral
                    pigmentation (Merliss, 1972).

             9.2.4  Eye contact

                    No data available

             9.2.5  Parenteral exposure

                    No data available.

             9.2.6  Other

                    No data available.

        9.3  Course, prognosis, cause of death

             Hypotension, renal failure, apnea, laryngeal oedema and
             ARDS can develop soon after exposure leading to death (WHO,
             1994). Coma and seizures usually occur within minutes to a
             few hours after exposure. Toxic effects may be delayed up to
             18 hours.

        9.4  Systematic description of clinical effects

             9.4.1  Cardiovascular

                    Heart rate at first increases and then becomes
                    slow and irregular. Blood pressure at first increases
                    slightly, then falls markedly (hypotension) (WHO,
                    1994). Cardiovascular collapse, atrial and ventricular
                    arrythmias have been reported (Leikin & Paloucek,
                    1996-7). Deep venous thrombosis has been reported
                    following injection of phenol (WHO, 1994).
                    Cardiac dysrhythmias have been observed in skin
                    peeling and nerve blockade (Forrest & Ramage, 1987;
                    Lober, 1987; Sorkin, 1988; Gaudy et al., 1993; Lalanne
                    et al., 1994; Zamponi & French, 1994).

             9.4.2  Respiratory

                    Respiration may initially be increased in rate,
                    but later decreased in rate. Pulmonary oedema,
                    wheezing, coughing, dyspnea, pneumonia are common
                    signs (Leikin & Paloucek, 1996-7). The cause of death
                    from phenol exposure is often respiratory failure
                    (WHO, 1994).

             9.4.3  Neurological

            Central nervous system (CNS)

                             Initial signs and symptoms include
                             headache, dizziness and tinnitus. Seizures,
                             coma, respiratory depression and death may
                             ensue quickly. Coma and seizures usually
                             occur within minutes to a few hours after
                             exposure or a delay of up to 18 hours. Phenol
                             may also cause demyelination and axonal
                             damage of peripheral nerves (WHO,

            Peripheral nervous system

                             No data available.

            Autonomic nervous system

                             A decrease in body temperature has
                             been reported (WHO, 1994).

            Skeletal and smooth muscle

                             Locomotor activity reduced at 244 mg
                             phenol/kg body weight in female Fischer-344
                             rats (WHO, 1994). Chronic exposure in rats
                             lead to changes in the time for excitation of
                             extensor muscles.

             9.4.4  Gastrointestinal

                    Symptoms include diarrhoea, salivation,
                    vomiting, ulceration and haemorrhage (Leikin &
                    Paloucek, 1996-7). Corrosive damage may involve the
                    entire gastrointestinal tract.

             9.4.5  Hepatic

                    Hepatic necrosis was observed in two(out of
                    six) female Fischer-344 rats when given 244 mg
                    phenol/kg body weight (WHO, 1994).

             9.4.6  Urinary


                             Renal failure has been reported in
                             acute poisoning. Urinalysis may reveal a
                             green to brown discolouration of the urine
                             with albuminuria. Nephritis is reported
                             (Leikin & Paloucek, 1996-7).


                             No data available.

             9.4.7  Endocrine and reproductive systems

                    Increased incidence of preimplantation loss and
                    early postnatal death in the offspring of rats (WHO,

             9.4.8  Dermatological

                    Chronic doses may result in ochronosis
                    (yellowing of the skin) and skin eruption (WHO,

             9.4.9  Eye, ear, nose, throat: local effects

                    The fumes are irritating to the eyes and
                    affects the pupil's response to light (miosis) (WHO,
                    1994). Solutions can be corrosive to the eyes, and can
                    cause severe ocular damage including corneal
                    opacification. Lymph production in the conjunctiva may
                    be increased and will leave the cornea white and
                    hypesthetic (Jaeger, 1987).
                    Necrosis of the mucous membranes of the throat.
                    Phenol applied to the inner ear round window of
                    Sprague-Dawley rats caused morphological damage to the
                    organ of Corti in the basal coil. The outer hair cells
                    appeared to be more sensitive to phenol and as a
                    result of the damage, impairment of inner ear function
                    was noted which was permanent for higher frequencies.
                    One experiment in female mice lead to an increase in
                    ear thickness (WHO, 1994)

             9.4.10 Haematological

                    Heinz body haemolytic anaemia and
                    hyperbilirubinemia have been reported occasionally
                    (WHO, 1994).

             9.4.11 Immunological

                    There are no studies in humans. For four weeks
                    groups of five male CD-1 mice were given drinking
                    water containing 0, 4.7, 19.5 or 95.2 mg phenol/L.
                    Total and differential leukocyte counts were
                    unaffected. The highest dose suppressed the
                    stimulation of cultured splenic lymphocytes by the 
                    B-cell mitogen lipopolysaccharide, the T-cell mitogen
                    phytohaemagglutinin, and the T and B-cell mitogen
                    pokeweed, but not by concanavatin. Suppression of the
                    animal's antibody production in response to a 
                    T-cell-dependent antigen, occurred at the mid and high
                    doses (WHO, 1994).

             9.4.12 Metabolic

           Acid-base disturbances

                             Metabolic acidosis (WHO, 1994)

           Fluid and electrolyte disturbances

                             Fluid loss secondary to burns or shock.


                             No data available.

             9.4.13 Allergic reaction

                    No data available.

             9.4.14 Other clinical effects

                    No data available

             9.4.15 Special risks

                    Phenol has been shown to be a developmental
                    toxicant in rats and mice (WHO, 1994).

        9.5  Other

             No data available.

        9.6  Summary


        10.1 General principles

             When spilt on the skin or in the eyes, there should be
             an immediate washing with water (preferably tepid) for at
             least 10 minutes. If available wash with polyethyleneglycol
             molecular weight 300 (Macrogol 300), isopropyl alcohol,
             industrial methylated spirits or Goletely (PEG 3550) for at
             least 30 minutes (Horch et al., 1994).
             Do not induce vomiting. Dilution may increase absorption.
             Gastric lavage should be carefully weighed against the risk
             of complications. Recommended gastric lavage fluids are
             polyethylene glycol, water, following administration of
             activated charcoal, or vegetable oils, such as olive oil,
             castor oil or cottonseed oil (WHO, 1994).
             Treatment is mainly supportive. If there is a systemic
             intoxication, monitor the respiration and the level of
             oxygenation, the blood pressure and ECG, the level of
             methaemoglobinemia, the hepatic and renal functions. Control
             convulsions and cardiac arrhythmias according to the
             Treatment Guides.

        10.2 Life supportive procedures and symptomatic/specific treatment

             Make a proper assessment of airway, breathing,
             circulation and neurological status.
             Maintain a clear airway.

             If unconscious give artificial respiration.
             If the patient has breathing difficulties, put them in a
             sitting position.
             Monitor vital signs.
             Monitor blood pressure and ECG.
             Monitor fluid and electrolyte balance.
             Monitor acid-base balance.
             Control cardiac dysrhythmias with appropriate drug
             Control convulsions with appropriate drug regimen.

        10.3 Decontamination

             Remove and discard contaminated clothing.
             Irrigate exposed eyes with copious amounts of water.
             Wash skin with copious amounts of water or preferably if
             available wash with polyethyleneglycol molecular weight 300
             (Macrogol 300), isopropyl alcohol, industrial methylated
             spirits or Goletely (PEG 3550) for at least 30 minutes.
             Do not induce vomiting, empty stomach by aspiration followed
             by polyethylene glycol or activated charcoal with

        10.4 Enhanced elimination

             If acute renal failure occurs in phenol poisoning,
             dialysis should probably not be used alone, but in
             conjunction with charcoal hemoperfusion. Without renal
             failure the use of charcoal hemoperfusion may also be useful,
             when the patient has been exposed to 15 to 20 g of phenol
             (Christiansen & Klaman, 1996) 

        10.5 Antidote treatment

             10.5.1 Adults

                    No antidote available.

             10.5.2 Children

                    No antidote available.

        10.6 Management discussion

             No data available.


        11.1 Case reports from the literature

             Occupational - Male
             A 27-year-old male spilt 80% phenol on both knees and arrived
             at the emergency department 30 to 60 minutes after the
             spillage. Both legs had been washed with copious amounts of
             water and he had also undergone further irrigation and
             application of glycerin cream, but continued to be in pain.
             Further irrigation with 6 litres of saline followed and then
             it was suggested to irrigate with polyethylene glycol. By
             mistake Golytely (PEG 3550) was used. The patient reported an
             immediate soothing of the pain and his long term recovery was
             favourable (Wahl et al., 1995).
             Accidental Injection
             A 50-year-old woman inadvertently received a 30 ml dose of
             89% phenol (26.9 g, 0.44 mg/kg body weight). At 23 minutes
             post- injection she was unresponsive, at 27 minutes she had
             respiratory distress and was intubated. At 62 minutes she
             developed shock and dopamine was started followed by
             epinephrine and neosynephrine. At the same time she developed
             ventricular tachycardia and was treated with lidocaine. 4
             hours after the injection she was comatose with a blood
             pressure of 70/58, while receiving large doses of
             vasopressors. At 4.5 hours charcoal hemoperfusion was
             started, and given for 6 hours and 20 minutes. Her clinical
             status improved with the perfusion and she made a complete
             recovery. The perfusion enhanced the elimination of free and
             total phenol (Christiansen & Klaman, 1996).
             Five Year Acute Exposure Study
             A five year evaluation of acute exposure to phenol
             disinfectant (26%) studied 80 cases with an age range of 1 to
             78 years, 75% under 5 years old. There were 60 oral only
             exposures, 7 dermal only, 12 oral/dermal and 1 inhalation.
             65% were assessed at the emergency department and 33% were
             admitted. 14% of oral exposures developed rapid CNS
             depression, without seizures, and 2 patients developed coma
             after ingestion. Burns occurred in 17 oral exposures and 5
             dermal. 17 patients underwent endoscopy. Urine colour change
             was noted in 5 patients following ingestion. There were no
             cardiovascular complications, or oliguria and anuria. In all
             cases there were complete recoveries (Spiller et al.,

             Accidental Ingestion - Male Alcoholic, Addict
             A report from the Invercargill hospital in New Zealand early
             in 1997, reports a 29 year old male, alcoholic, addict, who
             drank 30 mL of 88% phenol from a bottle he found (26.4 g/75
             kg = 350 mg/kg). He had a cardiac arrest requiring DC
             cardioversion, and developed renal failure secondary to
             rhabdomolysis. He developed a denuded oesophagus, large,
             superficial, antral ulceration and received continuous
             haemofiltration and endoscopy. His urine output only
             recommenced 14 days after the ingestion and his renal
             function is expected to return to normal (NZNPIC, 1997).
             Ingestion - Female
             Fatal case reports include a 21 year old female who drank 10
             to 20 g of phenol. She went into a deep coma with partial
             areflexia, a heart rate of 140 and dilated pupils, and had a
             cardiac arrest 60 minutes post ingestion. She received
             repeated gastric lavage with water, glycerin and animal
             charcoal, but died from pulmonary oedema and shock
             (Stajduhar-Carie, 1968).
             Occupational - Fatal Dermal Exposure
             A 17-year-old male had 30% phenol (as industrial waste)
             splashed on his face, neck and right trunk. He was washed
             with water, but 30 minutes later he had a seizure and died.
             His blood phenol level was 2.7 mg/dL. An autopsy showed red
             areas to 15% of his skin area, and pulmonary oedema. (WHO,
             Accidental Immersion
             A man was partially submerged in a solution of 20% phenol in
             dichloromethane for a few seconds. He immediately showered ,
             but collapsed, his extremities were cold and he had 50% burns
             to his body. He developed acute renal failure. Anuria
             followed, with a rise in plasma creatinine, but treatment
             with intravenous furosemide and haemodyalisis (daily for
             seven days, then with decreasing intervals for a further 18
             days), allowed adequate urinary volumes to be produced. He
             also had respiratory distress, treated in intensive care. A
             spill of 80-100% phenol on the hip, thigh and scrotum with a
             contact duration of 20 minutes lead to death, while a
             reported spill of 43.5% to the lower half of the body
             resulted in shock. A  spill of 4 to 5 litres on the upper
             half of the body of 78%, with a contact duration of 2 to 5
             minutes resulted in a coma (WHO, 1994).
            Contaminated Drinking Water
             A chemical spill in Wisconsin in 1974 contaminated
             groundwater which was being used as drinking water. One month
             later there were complaints of health effects, and six months
             later medical histories were taken from 100 people. The
             estimated daily exposure was 10 to 240 mg phenol/person. A
             significantly significant increase in diarrhoea, mouth sores,
             dark urine and burning of the mouth was found.
             Gastrointestinal illnesses were also reported in North Wales,
             when a river used for the preparation of drinking water was
             contaminated with phenol, and when chlorinated, various
             chlorophenols formed (WHO, 1994)
             Accidental Ingestion
             An outpatient was mistakenly given in a measured container
             one ounce of 89 % phenol. The patient immediatly clutched her
             throat and collapsed. Within 30 minutes she had an
             unrecordable blood pressure and sustained respiratory arrest.
             During endotracheal intubation in the ED the mouth and
             hypopharynx were noted to be white. A "lamp oil" odour was
             noted while ventilating the patient with a bag mask. The
             patient experienced ventricular tachycardia one hour after
             ingestion and resuscitation was effected by cardioversion.
             Over the first 24 hours she exhibited ventricular arrhythmia,
             seizures and metabolic acidosis. (Haddad et al., 1979)
             Child Exposure

             A 10-year-old boy had a solution of 40% phenol and 0.8%
             croton oil in hexachlorophene soap and water applied to a
             large nevus covering his 1.9% of his body surface whilst
             under anaesthesia. After 55 minutes of treatment, multifocal
             and coupled premature ventricular complexes were detected by
             ECG. An intravenous infusion of 250 mg bretylium sulfate
             suppressed the dysrhythmia (WHO, 1994).


        12.1 Specific preventative measures

             Phenol should be kept in a tightly closed container, in
             a cool, dry place, away from heat, flame and oxidising
             agents. It is light sensitive and should be kept in the dark
             (WHO, 1994).
             Protective clothing should will be appropriate to the amount
             and form of the phenol being handled. It should be handled
             wearing an approved respirator; viton, butyl rubber or
             neoprene gloves (not nitrile or PVA gloves), safety goggles
             and other protective clothing. Safety showers and

             polyethylene glycol 300 should be near where phenol is being
             handled.(Allen, 1991)

        12.2 Other

             Phenol is not likely to persist in air, soil or sewage,
             sea or surface water. It readily reacts photochemically, is
             rapidly biodegraded aerobically to mainly carbon dioxide, and
             anaerobic biodegradation occurs also at a slower rate. Low
             removal rates of phenol in ground water and soil may occur
             e.g. following spills, with subsequent inhibition of the
             microbial populations.  Phenol is toxic to aquatic organisms:
             the lowest EC50 for water organisms is estimated to be 3.1
             mg/L. The lowest chronic NOEC is estimated to be 0.2


        Allen R, Ed. (1991) Chemical Safety data Sheets, Volume 4b:
        Toxic Chemicals (m-z ).  Royal Society of Chemistry, Cambridge.
        Printed by Staples Printers Rochester Ltd, Kent.
        Anderson W (1869) fatal misadventure with carbolic acid. Lancet,
        1: 179
        Baker EL, Landrigan PJ, Bertozzi PE, Field PH, Basteyns BJ,
        Skinner HG (1978) Phenol poisoning due to contaminated drinking
        water. Arch Environ Health, 83: 98-94
        Ballinger LN, Cross SE & Roberts MS (1995) Availability and Mean
        Transit Times of Phenol and its Metabolites in the Isolated
        Perfused Rat Liver: Normal and Retrograde Studies Using Tracer
        Concentrations of Phenol. J Pharm Pharmacol, 47: 949-956.
        Brooks JD & Riviere JE (1996) Quantitative Percutaneous Absorption
        and Cutaneous Distribution of Binary Mixtures of Phenol and
        para-Nitrophenol in Isolated Perfused Porcine Skin. Fundamental
        and Applied Toxicology, 32: 233-243.
        Christiansen RG & Klaman RN (1996) Successful Treatment of Phenol
        Poisoning With Charcoal Hemoperfusion. Veterinary and Human
        Toxicology, 38(1): 27-28
        Dickenson A & Taylor G (1996) Pulmonary First-Pass and
        Steady-State Metabolism of Phenols. Pharmaceutical Research,
        13(5): 744-748.
        Forrest T & Ramage DT (1987) Cardiac dysrhythmia after subtrigonal
        phenol. Anaesthesia, 42: 77-778

        Foxall PJD, Bending MR, Gartland KPR & Nicholson JK (1989) Acute
        renal failure following accidental cutaneous absorption of phenol:
        application of NMR urinalysis to monitor the disease process.
        Human Toxicol, 9: 491-496
        Gaudy JH, Tricot Z, Sezeur A (1993) [Serious heart rate disorders
        following perioperative splanchnic phenol nerve block]. Cand J
        Anaesth, 40: 357-359 (in French)
        Geller AS (1997) Botulinum Toxin A. Archives of Physical Medicine
        and Rehabilitation, 78: 233
        Goldfrank LR & Bresnitz EA (1990) Toxicologic emergencies, 4th ed,
        East Norwalk, Appleton & Lange
        Haddad LM, Dimond KA, Schweistris JE (1979) Case report: phenol
        poisoning. Burns, 20: 45-50
        Horch R, Spilker G, Stark GB (1994) Phenol burns and intoxication.
        Burns, 20: 45-50
        IARC (1989) Phenol. In: Some organic solvents, resin monomers and
        related compounds, pigments and occupational exposures in paint
        manufacture and painting. Lyon, International Agency for Research
        on Cancer, pp 263-287 (IARC Monographs on the evaluation of
        carcinogenic risks to humans, volume 47)
        Jaeger RW (1987) Poisoning Emergencies: A Primer. St Louis, MO.
        The Catholic Health Association of the United States.
        Kimata Y, Uetake M, Tsukada S & Harii K (1995) Follow-up Study of
        Patients Treated for Ingrown Nails with the Nail Matrix
        Phenolization Method. Plastic and Reconstructive Surgery, 95(4):
        Kligman AM (1966) The identification of contact allergens by human
        assays III The maximum test: a procedure for screening and rating
        contact sensitizers. J Invest Dermatol, 47: 393-409
        Lalanne B, Baubion O, Sezeur A, Tricot C, Gaudy JH (1994)
        [Circulatory arrest after splanchnic neurolysis with phenol in
        unresectable cancer of the pancreas]. Annales de chirurgie, 48:
        1025-1028 (in French)
        Leikin JB & Paloucek FP (1996-1997) Poisoning and Toxicology
        Handbook. 2nd edition American Pharmaceutical Association.
        Lexi-Comp Ltd.
        Lober CW (1987) Chemexfoliation. Indications and cautions. J Am
        Acad Dermat, 17: 109-112

        Merliss RR (1972) Phenol marasmus. J Occup Med, 14: 55-56
        New Zealand National Poisons and Hazardous Chemical Information
        Centre (1997): Report Form, Call Number 90101.
        Olson KR (1994) Poisoning and drug overdose, 2nd Ed, Appleton and
        Lange, Norwalk CT, USA
        Reynolds JEF Ed. (1993) Martindale, The Extra Pharmacopoeia, 30th
        ed. London. The Pharmaceutical Press.
        Sax NI & Lewis RJ (1989) Dangerous properties of industrial
        materials. 7th Ed.  Van Nostrand Reinhold, New York.
        Sorkin MJ (1988) Cardiac arrhythmias during phenol face peel. J
        Dermatol Surg Oncol, 14: 477
        Spiller HA, Quadrani-Kushner DA & Cleveland P (1993) A Five Year
        Evaluation of Acute Exposures To Phenol Disinfectant.  Journal of
        Toxicology and Clinical Toxicology, 31: 307-313.
        Stajduhar-Carie J (1968) Acute Phenol Poisoning: Singular Findings
        in a Lethal Case. Journal of Forensic Medicine, 15: 41-42.
        Wahl M, Lipscomb J & McAllister K (1995) Phenol Burn
        Decontaminated with Golytely. Journal of Toxicology and Clinical
        Toxicology, 33: 494
        WHO (1994) IPCS Health and Safety Guide No. 88. Published by WHO.
        Printed by Wissenschsftliche Verlagsgesellschaft, Stuttgart
        WHO (1994) IPCS Environmental Health Criteria for Phenol (161 )
        First draft prepared by Ms G.K. Montizan. Published by WHO.
        Printed in Finland.
        Windholz M, Ed. (1983) The Merck Index. An  encyclopaedia of
        chemicals, drugs and biologicals , 10th ed. Rahway, New Jersey,
        Merck and Co., Inc
        Wood KA (1978) The use of phenol as a neurolytic agent: a review.
        Pain, 5: 205-225
        Zamponi GW & French RJ (1994) Arrhythmias during phenol therapies:
        a specific action on cardiac sodium channels? (letter).
        Circulation, 89: 914


        Author:     Rachael Inder
                    Pharmacology Department
                    School of Medical Sciences
                    Otago University
                    New Zealand
                    E-mail:  rachael.inder@stonebow.otago.ac.nz
        Date:       April 1997
        Reviewer:   MO Rambourg Schepens
                    Centre Anti-Poisons de Champagne Ardenne
                    Centre Hospitalier Universitaire
                    51092 Reims Cedex
                    E-mail:  marie-odile.rambourg@wanadoo.fr
        Date:       August 1997
        review:     Rio de Janeiro, Brazil, September 1997
                    (Group members: R. McKeown, W.A. Temple, W.A. Watson)
        Update:     Ad van Heijst
                    Bosch en Duin
        Date:       March 1998
        Accepted:   London, United Kingdom, March 1998
                    (Group members: R.E. Ferner, A. van Heijst, M.
                    Mathieu-Nolf, A.J. Nantel, M.O. Rambourg Schepens
        Editor:     Mrs J. Dumnil
                    International Programme on Chemical Safety
        Date:       October 1999

    See Also:
       Toxicological Abbreviations
       Phenol (EHC 161, 1994)
       Phenol (HSG 88, 1994)
       Phenol (ICSC)
       PHENOL (JECFA Evaluation)
       Phenol (IARC Summary & Evaluation, Volume 71, 1999)