Phenol

1. NAME

 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. SUMMARY

 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. PHYSICO-CHEMICAL PROPERTIES

 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. USES

 4.1 Uses

 4.1.1 Uses

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 4.1.2 Description

 4.2 High risk circumstance of poisoning

 4.3 Occupationally exposed populations

5. ROUTES OF EXPOSURE

 5.1 Oral

 5.2 Inhalation

 5.3 Dermal

 5.4 Eye

 5.5 Parenteral

 5.6 Other

6. KINETICS

 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. TOXICOLOGY

 7.1 Mode of action

 7.2 Toxicity

 7.2.1 Human data

 7.2.1.1 Adults

 7.2.1.2 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

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8. TOXICOLOGICAL AND BIOMEDICAL INVESTIGATIONS

 8.1 Material sampling plan

 8.1.1 Sampling and specimen collection

 8.1.1.1 Toxicological analyses

 8.1.1.2 Biomedical analyses

 8.1.1.3 Arterial blood gas analysis

 8.1.1.4 Haematological analyses

 8.1.1.5 Other (unspecified) analyses

 8.1.2 Storage of laboratory samples and specimens

 8.1.2.1 Toxicological analyses

 8.1.2.2 Biomedical analyses

 8.1.2.3 Arterial blood gas analysis

 8.1.2.4 Haematological analyses

 8.1.2.5 Other (unspecified) analyses

 8.1.3 Transport of laboratory samples and specimens

 8.1.3.1 Toxicological analyses

 8.1.3.2 Biomedical analyses

 8.1.3.3 Arterial blood gas analysis

 8.1.3.4 Haematological analyses

 8.1.3.5 Other (unspecified) analyses

 8.2 Toxicological analyses and their interpretation

 8.2.1 Tests on toxic ingredient(s) of material

 8.2.1.1 Simple qualitative test(s)

 8.2.1.2 Advanced qualitative confirmation test(s)

 8.2.1.3 Simple quantitative method(s)

 8.2.1.4 Advanced quantitative method(s)

 8.2.2 Tests for biological specimens

 8.2.2.1 Simple qualitative test(s)

 8.2.2.2 Advanced qualitative confirmation test(s)

 8.2.2.3 Simple quantitative method(s)

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 8.2.2.4 Advanced quantitative method(s)

 8.2.2.5 Other dedicated method(s)

 8.2.3 Interpretation of toxicological analyses

 8.3 Biomedical investigations and their interpretation

 8.3.1 Biochemical analysis

 8.3.1.1 Blood, plasma or serum

 8.3.1.2 Urine

 8.3.1.3 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. CLINICAL EFFECTS

 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

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 9.4 Systematic description of clinical effects

 9.4.1 Cardiovascular

 9.4.2 Respiratory

 9.4.3 Neurological

 9.4.3.1 Central nervous system (CNS)

 9.4.3.2 Peripheral nervous system

 9.4.3.3 Autonomic nervous system

 9.4.3.4 Skeletal and smooth muscle

 9.4.4 Gastrointestinal

 9.4.5 Hepatic

 9.4.6 Urinary

 9.4.6.1 Renal

 9.4.6.2 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

 9.4.12.1 Acid-base disturbances

 9.4.12.2 Fluid and electrolyte disturbances

 9.4.12.3 Others

 9.4.13 Allergic reaction

 9.4.14 Other clinical effects

 9.4.15 Special risks

 9.5 Other

 9.6 Summary

10. MANAGEMENT

 10.1 General principles

 10.2 Life supportive procedures and symptomatic/specific treatment

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 PHENOL 

 International Programme on Chemical Safety 

 Poisons Information Monograph 412 

 Chemical 

 1. NAME

 1.1 Substance 

 Phenol 

 1.2 Group

 Hydrocarbons, cyclic, alcohol 

 1.3 Synonyms

 acidum carbolicum; 

 acidum phenolicum; 

 acidum phenylicum; 

 baker's P & S liquid ointment; 

 benzaphenol; 

 benzene phenol; 

 benzenol carbolic acid; 

 carbolic acid; 

 hydroxybenzene (IUPAC); 

 monohydroxybenzene; 

 monophenol; 

 NCI-C50124; 

 Oxybenzene; 

 phenic acid; 

 phenol alcohol; 

 phenyl hydrate; 

 10.3 Decontamination

 10.4 Enhanced elimination

 10.5 Antidote treatment

 10.5.1 Adults

 10.5.2 Children

 10.6 Management discussion

11. ILLUSTRATIVE CASES

 11.1 Case reports from the literature

12. ADDITIONAL INFORMATION

 12.1 Specific preventative measures

 12.2 Other

13. REFERENCES

14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), 

COMPLETE ADDRESS(ES)

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 phenyl hydroxide; 

 phenylic acid; 

 phenylic alcohol 

 1.4 Identification numbers

 1.4.1 CAS number 

 108-95-2 

 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 

 exposure. 

 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. 

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 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. PHYSICO-CHEMICAL PROPERTIES

 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 

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 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 68°C it is entirely water 

 soluble. The vapour is heavier than air (WHO, 

 1994). 

 

 Melting point is 43°C, the commercial product has an 

 impurity that increases the melting point (Windholz, 

 1983). 

 

 Boiling point: 181.75°C 

 Flash point: 80°C (closed cup); 79°C to 85°C (open 

 cup) 

 Relative vapour density: 3.24 (WHO, 1994). 

 Explosive limits are 1.7% to 8.6% (Allen, 1991). 

 Vapour pressure at 20°C is 47 Pascal 

 pKa 10,0 at 25°C 

 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 715°C. 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 

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 of the decomposition of organic materials, liquid 

 manure, and the atmospheric degradation of 

 benzene. 

 

 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, 

 1997). 

 

 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. ROUTES OF EXPOSURE

 5.1 Oral

 Phenol is readily absorbed from the gastrointestinal 

 tract (WHO, 1994). 

 5.2 Inhalation

 Phenol is readily absorbed from the lungs (Allen, 

 1991). 

 5.3 Dermal

 When spilt on the skin, intact or abraded, it is rapidly 

 absorbed and may lead to systemic poisoning (Brooks & 

 Riviere, 1996). 

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 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, 

 1994). 

 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, 

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 1994). 

 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. TOXICOLOGY

 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, 

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 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 

 7.2.1.1 Adults 

 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, 

 1996). 

 7.2.1.2 Children 

 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 

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 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, 

 1993). 

 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 μg/kg/day was 

 recommended as the upper limit of the TDI (WHO, 

 1994) 

 

 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 

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 at high doses. No micronuclei were observed in mice studies 

 at lower dose (IARC, 1989; WHO, 1994). 

 7.6 Interactions

 No data available. 

 8. TOXICOLOGICAL AND BIOMEDICAL INVESTIGATIONS

 8.1 Material sampling plan

 8.1.1 Sampling and specimen collection 

 8.1.1.1 Toxicological analyses 

 8.1.1.2 Biomedical analyses 

 8.1.1.3 Arterial blood gas analysis 

 8.1.1.4 Haematological analyses 

 8.1.1.5 Other (unspecified) analyses 

 8.1.2 Storage of laboratory samples and specimens 

 8.1.2.1 Toxicological analyses 

 8.1.2.2 Biomedical analyses 

 8.1.2.3 Arterial blood gas analysis 

 8.1.2.4 Haematological analyses 

 8.1.2.5 Other (unspecified) analyses 

 8.1.3 Transport of laboratory samples and specimens 

 8.1.3.1 Toxicological analyses 

 8.1.3.2 Biomedical analyses 

 8.1.3.3 Arterial blood gas analysis 

 8.1.3.4 Haematological analyses 

 8.1.3.5 Other (unspecified) analyses 

 8.2 Toxicological analyses and their interpretation

 8.2.1 Tests on toxic ingredient(s) of material 

 8.2.1.1 Simple qualitative test(s) 

 8.2.1.2 Advanced qualitative confirmation test(s) 

 8.2.1.3 Simple quantitative method(s) 

 8.2.1.4 Advanced quantitative method(s) 

 8.2.2 Tests for biological specimens 

 8.2.2.1 Simple qualitative test(s) 

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 8.2.2.2 Advanced qualitative confirmation test(s) 

 8.2.2.3 Simple quantitative method(s) 

 8.2.2.4 Advanced quantitative method(s) 

 8.2.2.5 Other dedicated method(s) 

 8.2.3 Interpretation of toxicological analyses 

 8.3 Biomedical investigations and their interpretation

 8.3.1 Biochemical analysis 

 8.3.1.1 Blood, plasma or serum 

 8.3.1.2 Urine 

 8.3.1.3 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. CLINICAL EFFECTS

 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 

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 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, 

 1996-7). 

 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, 

 1966). 

 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 

 opacification. 

 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, 

 1996). 

 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 

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 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). 

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 9.4.3 Neurological 

 9.4.3.1 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, 

 1994). 

 9.4.3.2 Peripheral nervous system 

 No data available. 

 9.4.3.3 Autonomic nervous system 

 A decrease in body temperature has 

 been reported (WHO, 1994). 

 9.4.3.4 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 

 9.4.6.1 Renal 

 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). 

 9.4.6.2 Other 

 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, 

 1994). 

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 9.4.8 Dermatological 

 Chronic doses may result in ochronosis 

 (yellowing of the skin) and skin eruption (WHO, 

 1994). 

 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 

 9.4.12.1 Acid-base disturbances 

 Metabolic acidosis (WHO, 1994) 

 9.4.12.2 Fluid and electrolyte disturbances 

 Fluid loss secondary to burns or shock. 

 9.4.12.3 Others 

 No data available. 

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 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. MANAGEMENT

 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 

 regimen. 

 Control convulsions with appropriate drug regimen. 

 10.3 Decontamination

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 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 

 cathartic. 

 Endoscopy. 

 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. ILLUSTRATIVE CASES

 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 

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 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., 

 1993). 

 

 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, 

 1994) 

 

 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 

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 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. ADDITIONAL INFORMATION

 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 

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 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 

 (g/L). 

 13. REFERENCES

 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, 

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 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): 

 719-724 

 

 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. 

 

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 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 

 14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE 

 ADDRESS(ES)

 Author: Rachael Inder 

 Pharmacology Department 

 School of Medical Sciences 

 Otago University 

 Dunedin 

 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 

 France 

 

 E-mail: marie-odile.rambourg@wanadoo.fr 

 

 Date: August 1997 

 

 Peer 

 review: Rio de Janeiro, Brazil, September 1997 

 (Group members: R. McKeown, W.A. Temple, W.A. Watson) 

 

 Update: Ad van Heijst 

 Bosch en Duin 

 Netherlands 

 

 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 

 (coordinator)) 

 

 Editor: Mrs J. Duménil 

 International Programme on Chemical Safety 

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 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)

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