PHENOL AND RELATED AGENTS
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
 -IDENTIFICATION
SYNONYMS
A13-01814 Acide carbolique (French) Baker's P and S liquid Baker's P and S ointment Benzenol Carbolic acid Carbolic oil Carbolsaure (German) Fenol (Dutch, Polish) Fenolo (Italian) Fenosmolin Fenosmoline Hydroxybenzene Liquefied phenol Liquid phenol Monohydroxybenzene Monophenol Oxybenzene Phenic acid Phenol Phenol alcohol Phenol homopolymer Phenol isotopes Phenole (German) Phenolum Phenosmolin Phenyl alcohol Phenyl hydrate Phenyl hydroxide Phenylic acid Phenylic alcohol PnOH CAS 108-95-2 NCI-c 50124 Catechol (benzene-1,2-diol) Chorinated phenols CREOSOTE, COAL TAR CRESOL(O-, M-, AND P-) CRESOL, META- Cresolic acid (cresol synonym) CRS (cresol synonym) Hexachlorophene Hydroquinone (ie, benzene-1,4-diol) JUNIPERUS OXYCEDRUS Guaiacol (ie, 2-methoxyphenol) m-cresol (ie, 3-methylphenol) p-chloro-m-xylenol Paraphenol (ie, 4-phenylphenol) Phenylphenol Phlorglucinol (ie, 1,3-5-trihydroxybenzene) Pyrocatechol (ie, benzene-1,2-diol) Pyrogallol (ie, 1,2,3-trihydroxybenzene) Resorcin (ie, benzene-1,3-diol) Resorcinol (ie, benzene-1,3-diol) Sulfurated phenols Xylenol (ie, dimethylphenol(s))
Catechol (benzene-1,2-diol) Chorinated phenols CREOSOTE, COAL TAR CRESOL(O-, M-, AND P-) CRESOL, META- Cresolic acid (cresol synonym) CRS (cresol synonym) Hexachlorophene Hydroquinone (ie, benzene-1,4-diol) JUNIPERUS OXYCEDRUS Guaiacol (ie, 2-methoxyphenol) m-cresol (ie, 3-methylphenol) p-chloro-m-xylenol Paraphenol (ie, 4-phenylphenol) Phenylphenol Phlorglucinol (ie, 1,3-5-trihydroxybenzene) Pyrocatechol (ie, benzene-1,2-diol) Pyrogallol (ie, 1,2,3-trihydroxybenzene) Resorcin (ie, benzene-1,3-diol) Resorcinol (ie, benzene-1,3-diol) Sulfurated phenols Xylenol (ie, dimethylphenol(s))
IDENTIFIERS
2312-Phenol, molten 1671-Phenol, solid 2821-Phenol solution
4921220 - phenol, carbolic acid 4921210 - phenol, liquid, solution, carbolic
USES/FORMS/SOURCES
Phenol is used primarily in the manufacture of phenolic resins, bisphenol A, caprolactam, alkyl phenols, and other chemicals and drugs. It is also used as a dye and indicator, a medical and veterinary antiseptic, a disinfectant (in solution or mixed with slaked lime), a reagent in chemical analysis, and a preservative for pharmaceuticals (ACGIH, 1991; Budavari, 1996; Sittig, 1991; OHM/TADS , 1999). Phenol is used in the production or manufacture of explosives, fertilizer, coke, illuminating gas, lampblack, paints, paint removers, rubber, asbestos goods, wood preservatives, synthetic resins, textiles, drugs, pharmaceutical preparations, perfumes, bakelite, and other plastics (Sittig, 1991). Phenol is still used in preparations for treatment of localized skin disorders (Castellani's paint), and as a local anesthetic. Dilute phenol solutions have also been injected for celiac plexus nerve block (Christiansen & Klaman, 1996). JUNIPERUS OXYCEDRUS - Cade oil (Juniper tar) is extracted by distillation from the branches and wood of Juniperus oxycedrus plant. The extract has been reported to have keratolytic, antipruritic, and antimicrobial activities in vitro. It has been used in folk medicine (Koruk et al, 2005).
Phenol is available as technical products in fused (82%), crystal (90%), or liquid (95%) form (Lewis, 1997). Sittig (1991) reported phenol's commercial availability as pure crystals or as an aqueous (88%) preparation.
Phenol can be obtained from the distillation of coal tar, or it can be prepared through the fusion of sodium benzenesulfonate with sodium hydroxide or the by heating monochlorobenzene and aqueous sodium hydroxide under high pressure conditions (Budavari, 1996; Lewis, 1998). The majority of the phenol in the US is produced by the oxidation of cumene, which yields acetone as a by-product" (Lewis, 1997). JUNIPERUS OXYCEDRUS (Koruk et al, 2005; Barrero et al, 1991; Bailey & Bailey, 1976): Family: Cupressaceae Description: An evergreen tree which is usually about 12 feet tall, but may reach 30 feet in height. Cade oil (Juniper tar) is extracted by distillation from the branches and wood of Juniperus oxycedrus plant. The plant contains ehteric oils, a trierpene (resin cadinene), and phenols (guaiacol and cresol derivatives). Leaves: Linear, 0.5 to 1 inch long, tapering from the middle. They are about 0.1 inch across, and spiny-pointed. Cones: Usually reddish-brown, may be purplish. They are about 0.5 inch in diameter. There are usually three seeds. Fruits are yellow to red/brown. Distribution: Endemic in the Mediterranean region and in Iran and Turkey. It grows in Europe, Asia, and North America. Toxicity: One source of cade oil (Juniper tar). This oil contains several sequiterpenes which may have phenolic properties. Phenol (carbolic acid) is the chemical substance responsible for the adverse effects of cade oil exposure.
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- USES: Phenol (also known as carbolic acid and phenic acid) is used in the treatment of localized skin disorders and as a local anesthetic. Dilute phenol solutions have been injected for celiac plexus nerve blocks. It is also used extensively in the manufacture of many other chemicals and drugs, as a dye and indicator, antiseptic, disinfectant, a reagent in chemical analysis, and a preservative for pharmaceuticals.
- PHARMACOLOGY: A phenol achieves its affect via several mechanisms.
- TOXICOLOGY: In concentrations of 5% or greater, it rapidly denatures all proteins it contacts. Some phenols, notably dinitrophenol or hydroquinone, will cause methemoglobinemia. There is also some thought that it may cause increased acetylcholine release at the neuromuscular junction causing CNS stimulatory effects.
- EPIDEMIOLOGY: Calls to poison centers concerning phenol are relatively rare, but many workers in various industries may be exposed to low levels of phenol. Severe manifestations and deaths are very rare.
MILD TO MODERATE TOXICITY: Exposure causes irritation to the affected tissue (eg, skin, mucous membranes) and discoloration. SEVERE TOXICITY: Phenol toxicity occurs most frequently after acute ingestion or chronic dermal application. However, systemic toxicity can also result from inhalation of vapors. DERMAL: The major hazard of phenol is its ability to penetrate the skin rapidly, especially in its liquid form. Its strong corrosive effect on body tissue can cause severe chemical burns. However, due to its local anesthetizing properties, skin burns may be painless. Skin absorption can cause systemic symptoms and even death. Chronic exposure may lead to symptoms described for acute poisoning as well as eye and skin discoloration. INGESTION: Phenol ingestion may cause oral, esophageal, and gastric burns. Systemic symptoms of toxicity include nausea, vomiting, diarrhea, dyspnea, tachypnea, pallor, profuse sweating, hypotension, dysrhythmias, acute lung injury, methemoglobinemia, hemolytic anemia, elevated anion gap metabolic acidosis, agitation, lethargy, seizures and coma. PULMONARY: Inhalational exposures can cause digestive disturbances (vomiting, dysphagia, diarrhea, anorexia) and can irritate and even burn the respiratory tract. Signs and symptoms of chronic inhalation exposure may include headache, cough, weakness, fatigue, anorexia, nausea, vomiting, insomnia, nervousness, weight loss, paresthesias, ochronosis, and albuminuria. OCULAR: Direct contact to the eyes may result in symptoms ranging from redness, pain, and blurred vision to severe burns that may lead to partial or even complete loss of vision.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 153 (ERG, 2004)
TOXIC; inhalation, ingestion or skin contact with material may cause severe injury or death. Contact with molten substance may cause severe burns to skin and eyes. Avoid any skin contact. Effects of contact or inhalation may be delayed. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution.
ACUTE CLINICAL EFFECTS
USES: Phenol (also known as carbolic acid and phenic acid) is used in the treatment of localized skin disorders and as a local anesthetic. Dilute phenol solutions have been injected for celiac plexus nerve blocks. It is also used extensively in the manufacture of many other chemicals and drugs, as a dye and indicator, antiseptic, disinfectant, a reagent in chemical analysis, and a preservative for pharmaceuticals. PHARMACOLOGY: A phenol achieves its affect via several mechanisms. TOXICOLOGY: In concentrations of 5% or greater, it rapidly denatures all proteins it contacts. Some phenols, notably dinitrophenol or hydroquinone, will cause methemoglobinemia. There is also some thought that it may cause increased acetylcholine release at the neuromuscular junction causing CNS stimulatory effects. EPIDEMIOLOGY: Calls to poison centers concerning phenol are relatively rare, but many workers in various industries may be exposed to low levels of phenol. Severe manifestations and deaths are very rare. MILD TO MODERATE TOXICITY: Exposure causes irritation to the affected tissue (eg, skin, mucous membranes) and discoloration. SEVERE TOXICITY: Phenol toxicity occurs most frequently after acute ingestion or chronic dermal application. However, systemic toxicity can also result from inhalation of vapors. DERMAL: The major hazard of phenol is its ability to penetrate the skin rapidly, especially in its liquid form. Its strong corrosive effect on body tissue can cause severe chemical burns. However, due to its local anesthetizing properties, skin burns may be painless. Skin absorption can cause systemic symptoms and even death. Chronic exposure may lead to symptoms described for acute poisoning as well as eye and skin discoloration. INGESTION: Phenol ingestion may cause oral, esophageal, and gastric burns. Systemic symptoms of toxicity include nausea, vomiting, diarrhea, dyspnea, tachypnea, pallor, profuse sweating, hypotension, dysrhythmias, acute lung injury, methemoglobinemia, hemolytic anemia, elevated anion gap metabolic acidosis, agitation, lethargy, seizures and coma. PULMONARY: Inhalational exposures can cause digestive disturbances (vomiting, dysphagia, diarrhea, anorexia) and can irritate and even burn the respiratory tract. Signs and symptoms of chronic inhalation exposure may include headache, cough, weakness, fatigue, anorexia, nausea, vomiting, insomnia, nervousness, weight loss, paresthesias, ochronosis, and albuminuria. OCULAR: Direct contact to the eyes may result in symptoms ranging from redness, pain, and blurred vision to severe burns that may lead to partial or even complete loss of vision.
Systemic toxicity and poisoning usually occur by rapid skin absorption, the main route of entry for solid, liquid or vapor phenol; the result can be lethal (ACGIH, 1991; AAR, 1996). Phenol is also toxic through ingestion and inhalation (Budavari, 1996). ABOUT 50% OF CASES OF ACUTE PHENOL OVEREXPOSURE ARE FATAL (ILO, 1998). Symptoms of acute phenol poisoning include headache, dizziness, weakness, dim vision, ringing in the ears, breathing difficulty, cyanosis, SUDDEN COLLAPSE, loss of consciousness, delirium, coma, and death (Clayton & Clayton, 1994; HSDB , 2000; ACGIH, 1992). Many of the internal organs are congested. CNS depression can develop rapidly after phenol ingestion (Spiller et al, 1993). Phenol is CORROSIVE and BURNS tissues on contact. Concentrated phenol may cause second- and third-degree dermal burns (Grant, 1993). Its local anesthetic properties may allow extensive damage to occur before pain is recognized. The affected area may become white and opaque or dull gray, followed by a grey-white sloughing, then necrosis; this may lead to black gangrene (Saydjari et al, 1986; Raffle et al, 1994). In a few clinical cases, newborns have been very sensitive to phenol: A bandage containing a 2% solution was fatal in one case, and an ointment of 30% phenol with 60% camphor caused circulatory failure, cerebral intoxication and methemoglobinemia in another infant (HSDB , 2000). Phenol is extremely irritating to eyes (Budavari, 1996). Severe corneal injury and blindness may occur (Grant, 1993). Phenol can induce cardiac arrhythmias. In one case, arrhythmias and circulatory arrest occurred shortly after injection of a dilute phenol solution in a medical neurolysis procedure (Gaudy et al, 1993). Phenol is a severe respiratory tract irritant by inhalation. Acute overexposure can result in noisy, difficult breathing, cough, rales, acute lung injury, and death due to respiratory failure (Budavari, 1996; ITI, 1995). Phenol can be dangerous if ingested, and can cause nausea, vomiting, severe abdominal pain, corrosion of the mouth, throat, and stomach, pallor, cold sweats, circulatory collapse, and death from respiratory failure (ILO, 1983). Liver damage can occur after phenol exposure (Hathaway et al, 1996), which can result in jaundice (ITI, 1995) and death (Lewis, 1996). Phenol exposure can also produce acute renal failure (Foxall et al, 1989; Wu et al, 1998). Long-lasting behavioral changes occurred in a survivor of acute phenol poisoning (Neundorfer & Wolpert, 1976). Methemoglobinemia may develop after exposure to phenol (ACGIH, 1991). Generally, the effects of phenol exposure in experimental animals parallel those in humans. Almost all organs can be affected by any route of exposure.
- IF PHENOL IS SPLASHED ON THE SKIN
IMMEDIATELY REMOVE ANY CLOTHING UNDER AN EMERGENCY SHOWER. REPEATEDLY SWAB THE AFFECTED AREA WITH FRESH BANDAGES THAT HAVE BEEN SOAKED IN POLYETHYLENE GLYCOL-300 (Clayton & Clayton, 1994). THESE SUPPLIES SHOULD BE AVAILABLE IN THE IMMEDIATE WORK AREA WHEREVER PHENOL IS BEING HANDLED. IMMEDIATE ACTION CAN MAKE A SUBSTANTIAL DIFFERENCE IN ODDS OF SURVIVAL (Clayton & Clayton, 1994). AFTER EMERGENCY PROCEDURES HAVE BEEN PERFORMED ON SITE, GET MEDICAL ATTENTION IMMEDIATELY.
CHRONIC CLINICAL EFFECTS
- Chronic phenol poisoning is now rare, but was a common problem when phenol was more widely used in medicine and surgery (Clayton & Clayton, 1994). Persons exposed to phenol on a daily basis can apparently develop tolerance, because physicians in the time of Lister absorbed and excreted several grams daily with no obvious ill effects (Clayton & Clayton, 1994).
- Repeated exposure to high levels of phenol can cause vomiting, difficulty swallowing, salivation, diarrhea, loss of appetite and weight, headache, fainting, dizziness, mental disturbances (Budavari, 1996) Sax, 1984), kidney and liver damage, muscle pain, weakness, dark urine, skin eruptions, and changes in pigmentation (brown spots on the knuckles) (Clayton & Clayton, 1994).
-FIRST AID
FIRST AID AND PREHOSPITAL TREATMENT
If endoscopy is to be performed, activated charcoal may interfere with visualization of involved areas. However, phenol is adsorbed to activated charcoal in vitro (Decker et al, 1968). Administration of activated charcoal soon after ingestion may be worthwhile. PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002). In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis. The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
CHARCOAL DOSE Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005). Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
ADVERSE EFFECTS/CONTRAINDICATIONS Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information. Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 153 (ERG, 2004)
Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the substance; give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. For minor skin contact, avoid spreading material on unaffected skin. Keep victim warm and quiet. Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.
FIRST AID EYE EXPOSURE: Immediately wash the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately. Contact lenses should not be worn when working with this chemical. DERMAL EXPOSURE: Immediately wash the contaminated skin with soap and water. If this chemical penetrates the clothing, immediately remove the clothing, wash the skin with soap and water, and get medical attention promptly. INHALATION EXPOSURE: Move the exposed person to fresh air at once. If breathing has stopped, perform artificial respiration. Keep the affected person warm and at rest. Get medical attention as soon as possible. ORAL EXPOSURE: If this chemical has been swallowed, get medical attention immediately. TARGET ORGANS: Eyes, skin, respiratory system, liver and kidneys (National Institute for Occupational Safety and Health, 2007).
INHALATION EXPOSURE INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm. If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents. ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed. Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
DERMAL EXPOSURE DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999). Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines. Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
EYE EXPOSURE DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
ORAL EXPOSURE Significant esophageal or gastrointestinal tract irritation or burns may occur following ingestion. The possible benefit of early removal of some ingested material by cautious gastric lavage must be weighed against potential complications of bleeding or perforation. ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old. Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury. SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue). Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years). Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
METHEMOGLOBINEMIA: Determine the methemoglobin concentration and evaluate the patient for clinical effects of methemoglobinemia (ie, dyspnea, headache, fatigue, CNS depression, tachycardia, metabolic acidosis). Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations in patients with anemia, or underlying pulmonary or cardiovascular disorders). Administer oxygen while preparing for methylene blue therapy. METHYLENE BLUE: INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules and 10 mg/1 mL (1% solution) vials. Additional doses may sometimes be required. Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection. NEONATES: DOSE: 0.3 to 1 mg/kg. Concomitant use of methylene blue with serotonergic drugs, including serotonin reuptake inhibitors (SRIs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), norepinephrine-dopamine reuptake inhibitors (NDRIs), triptans, and ergot alkaloids may increase the risk of potentially fatal serotonin syndrome. HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
Ingestion of 1.5 grams of phenol has been reported to be lethal (Lewis, 2000). Probable oral lethal dose was reported at 50 to 500 mcg/kg. Ingestion of 1 gram of phenol has been reported to be lethal(Pohanish, 2002). A minimum lethal dose has been estimated to be 140 mg/kg (Hathaway et al, 1996; HSDB, 2003). An average fatal dose of 15 grams of phenol has been calculated for humans (OHM/TADS , 2000). Death occurred in 10 minutes after the ingestion of as little as 4.8 grams of pure phenol (HSDB, 2003).
CASE REPORT: A 46-year-old woman developed unconsciousness, respiratory failure requiring mechanical ventilation, generalized tonic-clonic seizures, tachycardia, hypotension, leukocytosis, and severe metabolic acidosis after unintentional ingestion of 75 grams of resorcinol instead of glucose. Despite supportive therapy, she died several hours after ingestion (Bulut et al, 2006). CASE SERIES: In a series of 13 adult patients who ingested 16 to 32 grams and were lavaged, the mortality was 15% (Clarke & Brown, 1906). Prior to the use of lavage, Falck reported a 65% mortality in 46 cases (Clarke & Brown, 1906). SPILLS: Small spills of 80% to 100% phenol solutions to cheeks and scalp (Gibson, 1905) and to hip, thigh, and scrotum (Turtle & Dolan, 1922) have been fatal.
Ingestion of 50 to 500 milligrams in infants was reported to be a lethal amount, but no documentation was provided (Deichmann & Gerarde, 1969). Death has been reported from application of 2 coin-sized patches to the groin of a 7-day-old infant (Abrahams, 1900) and from application of a 2% solution for 11 hours to an infant's umbilicus under a closed bandage (Hinkel & Kintzel, 1968). Application of a 2% aqueous solution as a moist dressing on burns over 30% of the body surface area were fatal in one case. Five percent phenol skin compresses to several hundred children led to 2 deaths (Lucas & Lane, 1895).
MAXIMUM TOLERATED EXPOSURE
ORAL Ingestions of 45 grams (Clarke & Brown, 1906), 56 grams (Bennett et al, 1950), and 65 grams (Lewin, 1929) were associated with coma and collapse, but survival. Despite multiple complications, a 44-year-old recovered after hemodialysis and intensive supportive care from an oral ingestion of 150 grams of creosol (Wu et al, 1998). Spiller & Quadrani (1991) reported the largest oral dose producing no effect from a 26% phenol disinfectant solution to be 30 mL (7.8 grams) in a series of 57 cases.
DERMAL (SYSTEMIC EFFECT) HIGH CONCENTRATION: Upper body skin contact to a 78% aqueous solution for 2 to 5 minutes produced coma, but survival (Duverneuil & Ravier, 1962). MEDIUM CONCENTRATION: Application of 2.4 grams of phenol as a 40% solution to a giant hairy nevus of a healthy 10-year-old boy resulted in multi-focal and coupled premature ventricular complexes which responded to bretylium sulfate 250 mg intravenously but not to lidocaine, 100 mg intravenously (Warner & Harper, 1985). LOW CONCENTRATION: A 2.5% solution applied as a leg compress resulted in coma. Application of a 1% lotion for 7 to 17 days to scalp, arms, chest, back, and legs resulted in seizures and coma with survival (Light, 1931).
LOCAL EFFECTS LOW CONCENTRATION: Superficial necrosis and sloughing occurs with 5% solutions applied to skin or mucous membranes. Solutions greater than 1.5% are irritating (Fed Reg, 1982). MEDIUM CONCENTRATION: Keratolytic, neurolytic, and tissue destruction occurs with 10 to 40 percent concentrations. Superficial necrosis and sloughing occurs with 5% to 40% concentrations.
PARENTERAL A 50-year-old man with chronic pain was inadvertently injected with 10 cc phenol 89% (intended dose: 10 cc of 6% phenol) and developed acute respiratory distress syndrome, along with acute renal failure. Treatment included mechanical ventilation for several days and hemodialysis for 12 days. After acute symptoms resolved, the patient developed polyuria for several months. Renal function returned to normal within 6 months, and lung nodules had completely resolved (Gupta et al, 2008). Injection of 30 mL of 89% phenol, equivalent to 26.9 grams or 0.44 g/kg of body weight, resulted in respiratory arrest, shock, ventricular tachycardia and coma in a 50-year-old (Christiansen & Klaman, 1996). The patient survived with medical treatment which included administration of vasopressors, charcoal hemoperfusion, sodium bicarbonate, platelets, and blood transfusions.
- Carcinogenicity Ratings for CAS108-95-2 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Phenol EPA (U.S. Environmental Protection Agency, 2011): D ; Listed as: Phenol IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 3 ; Listed as: Phenol 3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.
NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Phenol MAK (DFG, 2002): Category 3B ; Listed as: Phenol Category 3B : Substances for which in vitro or animal studies have yielded evidence of carcinogenic effects that is not sufficient for classification of the substance in one of the other categories. Further studies are required before a final decision can be made. A MAK value can be established provided no genotoxic effects have been detected. (Footnote: In the past, when a substance was classified as Category 3 it was given a MAK value provided that it had no detectable genotoxic effects. When all such substances have been examined for whether or not they may be classified in Category 4, this sentence may be omitted.)
NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS108-95-2 (U.S. Environmental Protection Agency, 2011):
Oral: Slope Factor: RfD: 3x10(-1) mg/kg-day
Inhalation: Drinking Water:
References: Budavari, 1996; HSDB, 2003; Lewis, 2000; OHM/TADS, 2003; RTECS, 2003 LC50- (INHALATION)MOUSE: LC50- (INHALATION)RAT: LD50- (ORAL)CAT: LD50- (ORAL)DOG: LD50- (INTRAPERITONEAL)MOUSE: LD50- (INTRAVENOUS)MOUSE: LD50- (ORAL)MOUSE: LD50- (SUBCUTANEOUS)MOUSE: LD50- (ORAL)RABBIT: LD50- (SKIN)RABBIT: LD50- (INTRAPERITONEAL)RAT: LD50- (ORAL)RAT: 317 mg/kg 530 mg/kg 414 mg/kg
LD50- (SKIN)RAT: LD50- (SUBCUTANEOUS)RAT: LDLo- (INTRAVENOUS)CAT: LDLo- (ORAL)CAT: LDLo- (SUBCUTANEOUS)CAT: LDLo- (ORAL)DOG: LDLo- (INTRAPERITONEAL)GUINEA_PIG: LDLo- (SUBCUTANEOUS)GUINEA_PIG: LDLo- (ORAL)HUMAN: LDLo- (ORAL)MOUSE: LDLo- (SUBCUTANEOUS)MOUSE: LDLo- (INTRAPERITONEAL)RABBIT: LDLo- (INTRAVENOUS)RABBIT: LDLo- (ORAL)RABBIT: LDLo- (SKIN)RABBIT: LDLo- (SUBCUTANEOUS)RABBIT: TCLo- (INHALATION)RAT: TD- (SKIN)MOUSE: TDLo- (ORAL)HUMAN: TDLo- (ORAL)MOUSE: Female, 2300 mg/kg for 6-15D if preg - teratogenic effects Female, 2600 mg/kg for 6-15D of preg - fetotoxity Female, 2800 mg/kg for 6-15D of preg - fetotoxity 174 mg/kg for 28D-C Female, 4 g/kg for 6-15D of preg
TDLo- (SKIN)MOUSE: TDLo- (INTRAPERITONEAL)RAT: TDLo- (ORAL)RAT: 22750 mg/kg for 13W-C Female, 300 mg/kg for 6-15D of preg -- teratogenic effects Female, 1200 mg/kg for 6-15D of preg -- fetotoxicity
CALCULATIONS
CONVERSION FACTORS 1 ppm = 3.85 mg/m(3) (at 68 degrees F and 760 mmHg) 1 ppm = 2.85 mg/m(3) @ 1 atm and 25 degrees C 1 mg phenol m(3) air = 0.26 ppm (at 20 degrees C and 760 mmHg)
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS108-95-2 (American Conference of Governmental Industrial Hygienists, 2010):
Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
- AIHA WEEL Values for CAS108-95-2 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS108-95-2 (National Institute for Occupational Safety and Health, 2007):
Listed as: Phenol REL: IDLH: IDLH: 250 ppm Note(s): Not Listed
- OSHA PEL Values for CAS108-95-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
Listed as: Phenol Table Z-1 for Phenol: 8-hour TWA: ppm: 5 mg/m3: 19 Ceiling Value: Skin Designation: Yes Notation(s): Not Listed
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS108-95-2 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS108-95-2 (U.S. Environmental Protection Agency, 2010):
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS108-95-2 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS108-95-2 (U.S. Environmental Protection Agency, 2010b):
Listed as: Phenol P or U series number: U188 Footnote: Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.
- EPA SARA Title III, Extremely Hazardous Substance List for CAS108-95-2 (U.S. Environmental Protection Agency, 2010):
Listed as: Phenol Reportable Quantity, in pounds: 1000 Threshold Planning Quantity, in pounds: Note(s): Not Listed
- EPA SARA Title III, Community Right-to-Know for CAS108-95-2 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS108-95-2 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS108-95-2 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 2312 (49 CFR 172.101, 2005):
- DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 1671 (49 CFR 172.101, 2005):
- DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 2821 (49 CFR 172.101, 2005):
- ICAO International Shipping Name for UN2312 (ICAO, 2002):
- ICAO International Shipping Name for UN1671 (ICAO, 2002):
- ICAO International Shipping Name for UN2821 (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS108-95-2 (NFPA, 2002):
Listed as: Phenol Hazard Ratings: Health Rating (Blue): 4 Flammability Rating (Red): 2 Instability Rating (Yellow): 0 Oxidizer/Water-Reactive Designation: Not Listed
-HANDLING AND STORAGE
SUMMARY
Containers of phenol should be protected against physical damage and stored in cool, dry, and well-ventilated locations where the fire hazard is low. Phenol should be separated from other storage, preferably outdoors or in detached storage. Chemical goggles, a self-contained breathing apparatus, rubber gloves, an apron, and boots should be worn for the prevention of contamination (ITI, 1995).
HANDLING
- Phenol should not be handled with bare hands (Budavari, 1996).
- Safety showers and cans of isopropyl alcohol solution should be provided in areas in which people handle phenol (HSDB , 1999).
- "Workmen should not be permitted to enter empty tank which has been filled with phenol until it has been thoroughly cleaned and the air concentration is below 5 ppm" (HSDB , 1999).
STORAGE
Phenol should be stored in tightly-closed containers (Budavari, 1996; Sittig, 1991). Tanks for storing phenol may be constructed by either welding or riveting and should be equipped with heating coils that pass through the entire vessel. Underground tanks are not recommended for the storage of phenol (HSDB , 1999). Phenol should not be stored in containers made of phenolic resins, polyvinyl chlorides, neoprene, saran or polyethylene (HSDB , 1999).
- ROOM/CABINET RECOMMENDATIONS
Containers of phenol should be protected against physical damage and stored in cool, dry and well-ventilated locations away from light, oxidizers and acute fire hazards (such as smoking or open flames). Phenol should be separated from other storage, preferable outdoors or in detached storage (ITI, 1995; NFPA, 1997; OHM/TADS , 1999; Sittig, 1991).
Phenol is incompatible with the following agents (NIOSH , 1999) Pohanish and Green, 1997; (Sittig, 1991; ACGIH, 1991): strong acids aliphatic amines aluminum chloride amides butadiene calcium hypochlorite caustics formaldehyde strong oxidizers
"The hydroxyl group is highly reactive in condensation reactions with formaldehyde" (ACGIH, 1991). Phenol will liquify or become semiliquid when triturated with the following compounds (ACGIH, 1991): acetanilide butylchloral hydrate camphor monobrominated camphor chloral hydrate diuretin lead acetate menthol naphthalene naphthol acetophenetidin pyrgallol resorcinol sodium phosphate thmyol urethane terpin hydrate
Phenol coagulates collodion and proteins (ACGIH, 1991).
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 153 (ERG, 2004)
Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection. fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
- Impervious protective clothing and goggles should be worn in areas where liquid phenol may spill or splash. A full-face mask with forced air supply, along with protective clothing, rubber boots, gloves, and an apron, should be worn in areas of heavy vapor concentration (Sittig, 1991).
- Workers should wash the skin immediately if it becomes contaminated, and clothing that is significantly contaminated should be removed and replaced. Clean clothing should be put on before leaving the work premises if the possibility exists that work clothes may have become contaminated with phenol (NIOSH , 1999; Sittig, 1991).
- In areas where the possibility of coming into contact with phenol exists for workers, eyewash fountains should be provided, regardless of the recommendation to wear eye protection. In the immediate work area, facilities for quickly drenching the body should be provided (NIOSH , 1999; Sittig, 1991).
- "Emergency Response Personal Protective Equipment: Wear special protective clothing and positive pressure self-contained breathing apparatus" (NFPA, 1997).
EYE/FACE PROTECTION
- Eye protection should be worn in order to prevent phenol coming in contact with the eye (NIOSH , 1999).
RESPIRATORY PROTECTION
- Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 108-95-2.
-PHYSICAL HAZARDS
FIRE HAZARD
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 153 (ERG, 2004) Combustible material: may burn but does not ignite readily. When heated, vapors may form explosive mixtures with air: indoors, outdoors and sewers explosion hazards. Those substances designated with a "P" may polymerize explosively when heated or involved in a fire. Contact with metals may evolve flammable hydrogen gas. Containers may explode when heated. Runoff may pollute waterways. Substance may be transported in a molten form.
Phenol is a combustible solid (NFPA, 1997) OHM/TADS (1999) states that phenol is a stable compound and is not dangerously reactive.
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS108-95-2 (NFPA, 2002):
Listed as: Phenol Flammability Rating: 2
- FIRE CONTROL/EXTINGUISHING AGENTS
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 153 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 153 (ERG, 2004)
Dry chemical, CO2, alcohol-resistant foam or water spray. Move containers from fire area if you can do it without risk. Dike fire control water for later disposal; do not scatter the material.
- TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 153 (ERG, 2004)
Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Do not get water inside containers. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire.
- NFPA Extinguishing Methods for CAS108-95-2 (NFPA, 2002):
- If phenol is on fire or is involved in a fire, the fire should not be extinguished unless it is possible to stop the flow. If this is possible, water should be used in flooding quantities as fog. From as far a distance as possible, use water to cool all affected containers. Foam, dry chemical, or carbon dioxide can be used to extinguish fires involving phenol (AAR, 1996; NFPA, 1997; Sittig, 1991)
When exposed to heat, flames, or oxidizing materials, phenol is combustible (Lewis, 1996).
EXPLOSION HAZARD
- When mixed with air, phenol may explode (flash point 174 degrees F/79 degrees C) (Pohanish & Greene, 1997). ITI (1995) reports that phenol, when heated, will evolve flammable vapors which create an explosive mixture with air.
- The potential for an explosive reaction exists when phenol comes into contact with the following compounds (ITI, 1995; Lewis, 1996):
- An explosion occurs when phenol is mixed with aluminum chloride and nitrobenzene (ITI, 1995). Urben (1995) reported an experiment which illustrates these three components reacting violently at 120 degrees C.
- As organic liquids are powerful oxidants, contact with phenol may cause an explosion (Urben, 1995).
- When aromatic compounds come in contact with mixtures containing phenol, an explosion results (Urben, 1995).
- A mixture of phenol and sodium nitrite in a test tube exploded violently upon heating (Urben, 1995).
- Other reactions to phenol include collodian and protein coagulation, and liquification when triturated with the following agents (ACGIH, 2001; HSDB, 2003):
acetanilide butylchloral hydrate camphor monobrominated camphor chloralamide chloral hydrate diuretin lead acetate menthol naphthalene naphthol acetophenetidin pyrogallol resorcinol salol sodium phosphate thmyol urethane terpin hydrate
DUST/VAPOR HAZARD
- When heated, phenol evolves flammable vapors which will form explosive mixtures with air (ITI, 1995).
REACTIVITY HAZARD
- Phenol is incompatible with the following agents (NIOSH, 2003) Pohanish and Green, 1997; (Pohanish, 2002; ACGIH, 2001):
acids (stong) aliphatic amines aluminum chloride amides butadiene calcium hypochlorite caustics formaldehyde oxidizers (strong)
- "The hydroxyl group is highly reactive in condensation reactions with formaldehyde" (ACGIH, 2001).
- When exposed to heat, flames, or oxidizing materials, phenol is combustible (Lewis, 1996).
- The potential for an explosive reaction exists when phenol comes into contact with the following compounds (ITI, 1995; Lewis, 1996):
- Phenol will undergo a violent reaction when in the presence of the following compounds (Lewis, 1996):
- Phenol will emit acrid smoke of irritating fumes when it is heated to decomposition (Lewis, 1996).
- Lead, rubber, certain plastics, and aluminum and its alloys may be corroded by phenol (AAR, 1996).
- Phenol may undergo violent condensation when in the presence of acetaldehyde (ITI, 1995).
- An explosion occurs when phenol is mixed with aluminum chloride and nitrobenzene (ITI, 1995). Urben (1995) reported an experiment which illustrates these three components reacting violently at 120 degrees C.
- An intense exothermic reaction takes place when phenol comes in contact with 1,3-butadiene and boron trifluoride diethyl ether complex (ITI, 1995)
- Phenol undergoes an intense exothermic reaction and ignition when in the presence of calcium hypochlorite (ITI, 1995).
- Phenol will corrode rubber, aluminum and its alloys, and lead (OHM/TADS , 1999).
- As organic liquids are powerful oxidants, contact with phenol may cause an explosion (Urben, 1995).
- When aromatic compounds come in contact with mixtures containing phenol, an explosion results (Urben, 1995).
- The application of the salt-acid nitration mixture of trifluoroacetic to phenol resulted in a potentially-hazardous rapid exothermic reaction in which tar was produced (Urben, 1995).
- A mixture of phenol and sodium nitrite in a test tube exploded violently upon heating (Urben, 1995).
- A fire occurs when phenol is combined with mineral oxidizing acids (HSDB , 1999).
- When phenol is combined with isocyanates, the result is heat generation and violent polymerization (HSDB, 2003).
- "The combination of phenol with nitrides results in heat and flammable gas generation" (HSDB , 1999).
- Phenol, when heated, will evolve flammable vapors which create an explosive mixture with air flash point 174 degrees F/79 degrees C) (ITI, 1995; Pohanish and Greene, 1997).
EVACUATION PROCEDURES
- Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.
- SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 153 (ERG, 2004)
Increase, in the downwind direction, as necessary, the isolation distance of at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids in all directions.
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 153 (ERG, 2004)
If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.
- PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 153 (ERG, 2004)
CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number: MEXICO: SETIQ: 01-800-00-214-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5559-1588; For calls originating elsewhere, call: 011-52-555-559-1588.
CENACOM: 01-800-00-413-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885; For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.
ARGENTINA: CIQUIME: 0-800-222-2933 in the Republic of Argentina; For calls originating elsewhere, call: +54-11-4613-1100.
BRAZIL: PRÓ-QUÍMICA: 0-800-118270 (Toll-free in Brazil); For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).
COLUMBIA: CISPROQUIM: 01-800-091-6012 in Colombia; For calls originating in Bogotá, Colombia, call: 288-6012; For calls originating elsewhere, call: 011-57-1-288-6012.
CANADA: UNITED STATES:
For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions. As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate enclosed areas.
- If the phenol is leaking but is not on fire, evacuation from a downwind area should be considered based upon the amount of material that was spilled, the location, and the weather conditions (AAR, 1996).
- AIHA ERPG Values for CAS108-95-2 (AIHA, 2006):
Listed as Phenol ERPG-1 (units = ppm): 10 ERPG-2 (units = ppm): 50 ERPG-3 (units = ppm): 200 Under Ballot, Review, or Consideration: Yes Definitions: ERPG-1: The ERPG-1 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing more than mild, transient adverse health effects or perceiving a clearly defined objectionable odor. ERPG-2: The ERPG-2 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing or developing irreversible or other serious health effects or symptoms that could impair an individual's ability to take protective action. ERPG-3: The ERPG-3 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing or developing life-threatening health effects.
- DOE TEEL Values for CAS108-95-2 (U.S. Department of Energy, Office of Emergency Management, 2010):
- AEGL Values for CAS108-95-2 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
Listed as: Phenol Final Value: AEGL-1 10 min exposure: ppm: 19 ppm mg/m3: 73 mg/m(3)
30 min exposure: ppm: 19 ppm mg/m3: 73 mg/m(3)
1 hr exposure: ppm: 15 ppm mg/m3: 58 mg/m(3)
4 hr exposure: ppm: 9.5 ppm mg/m3: 37 mg/m(3)
8 hr exposure: ppm: 6.3 ppm mg/m3: 24 mg/m(3)
Definitions: AEGL-1 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic non-sensory effects. However, the effects are not disabling, are transient, and are reversible upon cessation of exposure.
Listed as: Phenol Final Value: AEGL-2 10 min exposure: ppm: 29 ppm mg/m3: 110 mg/m(3)
30 min exposure: ppm: 29 ppm mg/m3: 110 mg/m(3)
1 hr exposure: ppm: 23 ppm mg/m3: 90 mg/m(3)
4 hr exposure: ppm: 15 ppm mg/m3: 57 mg/m(3)
8 hr exposure: ppm: 12 ppm mg/m3: 45 mg/m(3)
Definitions: AEGL-2 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting adverse health effects or an impaired ability to escape.
Listed as: Phenol Final Value: AEGL-3 10 min exposure: 30 min exposure: 1 hr exposure: 4 hr exposure: 8 hr exposure:
Definitions: AEGL-3 is the airborne concentration of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening health effects or death.
- NIOSH IDLH Values for CAS108-95-2 (National Institute for Occupational Safety and Health, 2007):
IDLH: 250 ppm Note(s): Not Listed
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 153 (ERG, 2004) ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 153 (ERG, 2004) Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection. fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
LAND SPILL -- If phenol is spilled onto land, contain the liquid or solid material in a holding area. To prevent solid spills of phenol from dissolving in rain or firefighting material, cover the spill with a plastic sheet. Soil, sand bags, foamed polyurethane, or foamed concrete should be used to dike the surface flow (AAR, 1996). WATER SPILL - In the event of a water spill involving phenol, limit spill travel by using natural barriers or oil spill control booms. Removal of the trapped material can be accomplished with suction hoses (AAR, 1996). AIR SPILL - Water spray or mist should be used to knock down vapors when phenol is spilled into air (AAR, 1996). "Control runoff and isolate discharged material for proper disposal. Approach release from upwind." (NFPA, 1997) Properly protected personnel should dispose of spills immediately by flushing with flooding quantities of water and neutralizing with a caustic soda solution. All contaminated clothing should be removed and isolated at the site (Sittig, 1991). Incineration is the recommended disposal method for phenol (Sittig, 1991). Spills involving phenol should be absorbed with paper and then evaporated on an iron pan in a hood. The paper should be burned and atomized into an incinerator; mixing with a more flammable solvent may improve combustion (ITI, 1995) Solutions made up of less than 1% phenol may respond well to steam stripping, distillation, or placement over carbon to recover phenol economically. Burning, if it is controlled, can be used (OHM/TADS , 1999). Dilute amounts of a phenol solution can be fed to sewage organisms, though shock loadings will be fatal. For the efficient digestion of phenol by bacteria, sludge acclimation is usually required (OHM/TADS , 1999). 100 to 500 ppm potassium permanganate can break phenol's aromatic ring to form aliphatic acids (OHM/TADS , 1999). Phenol is a good candidate for rotary kiln incineration at a temperature range of 820 to 1600 degrees C and a residence time of seconds for liquids and gases and hours for solids. When incineration is carried out at a temperature range of 450 to 980 degrees C and a residence time of seconds for liquids and gases (and longer for solids), phenol is also a good candidate for fluidized bed incineration (HSDB , 1999). "The most important method, equally applied by refineries and petrochemical plants, is the biodegradation of phenol (activated sludge basins, aeration ponds, trickling filters). With this a 65-99% degradation of phenol is attained. A further decrease (80-90%) of the phenol content is obtained by treatment with ozone or activated charcoal" (HSDB , 1999).
-ENVIRONMENTAL HAZARD MANAGEMENT
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- Phenol is composed of colorless or white acicular (needle-shaped) crystals when perfectly pure. It is discolored by exposure to light and air, which makes this compound turn pink or red. Discoloration is hastened by the presence of alkalinity or impurities(ACGIH, 2001; Ashford, 2001; Budavari, 1996). Phenol has a burning taste, and its odor has been described as distinctive and aromatic (Budavari, 1996; Lewis, 2000; Lewis, 2001; Lewis, 1998).
PH
- The pH of an aqueous solution of phenol is approximately 6 (Budavari, 1996; ACGIH, 2001).
VAPOR PRESSURE
- 1 mmHg (at 40.1 degrees C) (Lewis, 1996)
- 1 mmHg (at 40 degrees C) (NFPA, 1997)
- 0.357 mmHg (at 20 degrees C) (NFPA, 1997)
- 0.35 mmHg (at 25 degrees C) (ACGIH, 1991)
- 0.524 mmHg (at 25 degrees C) (Howard, 1989)
- 20 mmHg (at 86 degrees C) (OHM/TADS , 2000)
- 0.3513 mmHg (at 25 degrees C) (HSDB , 1999)
SPECIFIC GRAVITY
- TEMPERATURE AND/OR PRESSURE NOT LISTED
DENSITY
- OTHER TEMPERATURE AND/OR PRESSURE
- TEMPERATURE AND/OR PRESSURE NOT LISTED
1.072 g/cm(3) (Lewis, 2000) 1.07 g/cm(3) (Lewis, 2001) 1.071 g/cm(3) (Budavari, 1996)
FREEZING/MELTING POINT
41 degrees C (Lewis, 1996) 109 degrees F (NIOSH , 1999)
43 degrees C (ACGIH, 1991; Lewis, 1996) 40.85 degrees C (ultrapure material) (Budavari, 1996) 41 degrees C; 106 degrees F (NFPA, 1997; Sittig, 1991). 42.5-43 degrees C (Lewis, 1993) 41-43 degrees C (Ashford, 1994) 40.9 degrees C (HSDB , 1999)
BOILING POINT
- 181.8 degrees C (at 760 mmHg) (HSDB , 1999)
- 182 degrees C; 358 degrees F (ACGIH, 1991; Budavari, 1996; NFPA, 1997; Sittig, 1991)
- 181.75 degrees C (at 760 mmHg) (Howard, 1989).
- 359 degrees F (NIOSH , 1999)
FLASH POINT
- 175 degrees F (closed cup) (Lewis, 1996)
- 79 degrees C; 175 degrees F (closed cup) (ACGIH, 1991; Budavari, 1996; NFPA, 1997; Sittig, 1991).
- 85 degrees C (open cup) (ACGIH, 1991; ITI, 1995)
- 78 degrees C; 172.4 degrees F (closed cup) (Lewis, 1993)
AUTOIGNITION TEMPERATURE
- 715 degrees C; 1319 degrees F (ACGIH, 1991; Lewis, 1996; NFPA, 1997)
EXPLOSIVE LIMITS
1.8% (Sittig, 1991; NIOSH , 1999) 1.7% (Sittig, 1991) 1.5 ppm (OHM/TADS , 2000) 1.3% (NFPA, 1997) 1.8% (NFPA, 1997)
8.6% (ACGIH, 1991; NFPA, 1997; NIOSH , 1999; Sittig, 1991)
SOLUBILITY
soluble (Lewis, 2000; NFPA, 1997) 87,000 mg/L (at 25 degrees C) (Howard, 1989) 1 g/15 mL of water (Budavari, 1996) 6700 ppm (at 25 degrees C) (OHM/TADS , 2000) 9% (at 77 degrees F) (NIOSH , 2000) 93,000 mg in 1 L of water (at 25 degrees C) (HSDB , 2000) 82,800 mg/L (at 25 degrees C) (HSDB , 2000)
Phenol is miscible in acetone, alcohol, and ether (HSDB , 2000; Lewis, 2000). Phenol is soluble in alcohol, ether, chloroform, carbon disulfide, glycerol, petrolatum, fixed or volatile oils, aqueous alkali hydroxides, carbon tetrachloride, methyl alcohol, acetic acid, and liquid sulfur dioxide (Lewis, 2001; HSDB , 2000; ACGIH, 2001). Miscible with oxygenated and chlorinated solvents (Ashford, 2001) 1 g/12 mL of benzene (ACGIH, 2001; Budavari, 1996) Phenol is sparingly soluble in mineral oil (HSDB , 2000). Phenol is almost insoluble in petroleum ethers (ACGIH, 2001).
OCTANOL/WATER PARTITION COEFFICIENT
- Log Kow = 1.46 (Howard, 1989; HSDB , 1999)
SPECTRAL CONSTANTS
OTHER/PHYSICAL
0.05 ppm (Hathaway et al, 1996) In air: 0.04 ppm (Sittig, 1991) In water: 7.9 ppm (Sittig, 1991) Lower odor threshold: 0.016 ppm (OHM/TADS , 2000) Medium odor threshold: 5.9 ppm (OHM/TADS , 2000) Upper odor threshold: 16.7 ppm (OHM/TADS , 1999)
38.20 mN/m (at 50 degrees C) (HSDB , 2000) 35.53 mN/m (at 75 degrees C) (HSDB , 2000) 32.86 mN/m (at 100 degrees C) (HSDB , 2000)
pKa = 10.0 (at 25 degrees C) (ACGIH, 2001; Budavari, 1996) pKa = 9.994 (at 25 degrees C) (HSDB , 2000) pKa = 9.89 (at 20 degrees C) (HSDB , 2000)
1.5425 (at 41 degrees C) (Budavari, 1996). 1.5408 (at 41 degrees C) (HSDB , 2000)
8.50 eV (NIOSH , 2000) 8.47 eV (HSDB , 2000)
- NUCLEAR MAGNETIC RESONANCE
Lower Taste Threshold: 0.0001 (when chlorinated) (OHM/TADS , 2000) Drinking Water Limits: 0.01 (OHM/TADS , 2000)
3.437 centapoise (at 50 degrees C) (HSDB , 2000) 1.784 centapoise (at 75 degrees C) (HSDB , 2000) 1.099 centapoise (at 100 degrees C) (HSDB , 2000)
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