MOBILE VIEW  | 

THIOPHENOL

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) Thiophenol may be classified as a phenylmercaptan.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C6-H6-S

Available Forms Sources

    A) FORMS
    1) Thiophenol is available at 99% purity (HSDB, 2000).
    2) It exhibits a color ranging from colorless to water-white to light yellow (CHRIS, 2000; Howard, 1993).
    3) It has a repulsive, penetrating, burnt rubber, stench, garlic-like odor, especially when impure (Budavari, 1996a; CHRIS, 2000)and a low odor threshold (0.00094 mcg/L) (HSDB, 2000).
    4) It is a solid at temperatures below 5 degrees F (HSDB, 2000).
    B) SOURCES
    1) It is produced by reduction reaction using benzenesulphonyl chloride and phosphorus (Ashford, 1994a).
    2) It is prepared by reduction reaction using benzenesulfonyl chloride and zinc dust in sulfuric acid (Budavari, 1996a).
    3) It is manufactured by reaction of hydrogen sulfide with chlorobenzene to produce thiophenol and diaryl sulfides (Clayton & Clayton, 1994a).
    C) USES
    1) Thiophenol is used as a chemical intermediate in the manufacture of pesticides, pharmaceuticals, and amber dyes; as a mosquito larvicide; and in solvents used for removing polysulfide sealants (Clayton & Clayton, 1994a; Hathaway et al, 1996; ACGIH, 1991a).

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Thiophenol is toxic by ingestion, inhalation and skin absorption. Symptoms are typical of a central nervous system stimulant, followed by CNS post-convulsive depression. It can cause a choking sensation, coughing, dyspnea, labored breathing, wheezing, cyanosis, pulmonary edema and pneumonia. Weakness, headache, dizziness, nausea and vomiting can result from overexposure.
    B) The central nervous system effects of overexposure start with restlessness, progressing to hyperpnea, incoordination, muscular weakness, skeletal muscle paralysis, cyanosis, lethargy and/or sedation and respiratory depression, followed by coma and death at the higher doses.
    C) It is a severe skin, eye, respiratory, and gastrointestinal system irritant, producing redness, pain, inflammation and severe burns of eyes, skin and mucous membranes. Severe dermatitis may be produced from prolonged or repeated skin contact. Skin absorption may cause systemic effects, but at roughly a 10-fold higher dose than by inhalation and ingestion.
    D) Exposure to thiophenol may damage kidney, liver, lung and spleen.
    0.2.3) VITAL SIGNS
    A) Because of this compound's extremely low olfactory threshold, exposures may be substantially lower than clinical signs may indicate. In animals at higher levels of exposure, respiratory rate increases initally followed by cyanosis, respiratory depression, and death.
    0.2.4) HEENT
    A) Severe eye irritation or burns may occur. It is irritating to the mucous membranes, nose, and throat. Headache has been reported.
    0.2.6) RESPIRATORY
    A) Dyspnea and coughing may occur. Lung changes including hemorrhages were seen in mice after inhalation. Pulmonary edema may be a cause of death.
    0.2.7) NEUROLOGIC
    A) CNS excitation, followed by CNS depression, occurred in animals. Thiophenol had a pronounced soporific (sleep-inducing) effect.
    0.2.8) GASTROINTESTINAL
    A) Nausea and vomiting may occur following ingestion.
    0.2.9) HEPATIC
    A) Fatty degeneration and necrosis of the liver occurred from inhalation in mice.
    0.2.10) GENITOURINARY
    A) Hyaline casts in the tubules and kidney changes were seen in animals.
    0.2.13) HEMATOLOGIC
    A) Methemoglobin can be produced by thiophenol in vitro, but is not likely to occur in the body.
    0.2.14) DERMATOLOGIC
    A) Burns or severe irritation may occur.
    0.2.15) MUSCULOSKELETAL
    A) Progressive incoordination, weakness, and paralysis were produced in animals.
    0.2.20) REPRODUCTIVE
    A) A NOAEL for developmental toxicity was > 40 mg/kg/day in the rabbit. Post-implantation mortality was observed in rats.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    0.2.22) OTHER
    A) Thiophenol may be hazardous by the oral, dermal, or inhalation route.

Laboratory Monitoring

    A) Monitor CBC, urinalysis, and liver and kidney function. Monitor arterial gases, pulmonary function, and chest x-ray if pulmonary irritation is present.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Do NOT induce emesis.
    B) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    C) 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.
    D) Carefully observe patients with ingestion exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    0.4.3) INHALATION EXPOSURE
    A) 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.
    B) 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.
    C) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    0.4.4) EYE EXPOSURE
    A) In rabbits, flushing the eyes with 0.5% silver nitrate followed by copious irrigation with water has proven beneficial.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) 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).
    2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    3) 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.

Range Of Toxicity

    A) Minimum lethal human exposure is unknown.

Summary Of Exposure

    A) Thiophenol is toxic by ingestion, inhalation and skin absorption. Symptoms are typical of a central nervous system stimulant, followed by CNS post-convulsive depression. It can cause a choking sensation, coughing, dyspnea, labored breathing, wheezing, cyanosis, pulmonary edema and pneumonia. Weakness, headache, dizziness, nausea and vomiting can result from overexposure.
    B) The central nervous system effects of overexposure start with restlessness, progressing to hyperpnea, incoordination, muscular weakness, skeletal muscle paralysis, cyanosis, lethargy and/or sedation and respiratory depression, followed by coma and death at the higher doses.
    C) It is a severe skin, eye, respiratory, and gastrointestinal system irritant, producing redness, pain, inflammation and severe burns of eyes, skin and mucous membranes. Severe dermatitis may be produced from prolonged or repeated skin contact. Skin absorption may cause systemic effects, but at roughly a 10-fold higher dose than by inhalation and ingestion.
    D) Exposure to thiophenol may damage kidney, liver, lung and spleen.

Vital Signs

    3.3.1) SUMMARY
    A) Because of this compound's extremely low olfactory threshold, exposures may be substantially lower than clinical signs may indicate. In animals at higher levels of exposure, respiratory rate increases initally followed by cyanosis, respiratory depression, and death.
    3.3.2) RESPIRATIONS
    A) Increased respirations were seen in several animal species (ACGIH, 1992).
    B) Cyanosis and respiratory depression, coma and death occurred in animals following initial respiratory stimulation (ACGIH, 1992).

Heent

    3.4.1) SUMMARY
    A) Severe eye irritation or burns may occur. It is irritating to the mucous membranes, nose, and throat. Headache has been reported.
    3.4.2) HEAD
    A) Headache has been reported (Clayton & Clayton, 1994) ACGIH, 1992).
    3.4.3) EYES
    A) IRRITATION - Thiophenol induced severe eye irritation in the rabbit in the Standard Draize Test (RTECS, 1997). Eye injury, erythema, edema of the conjunctivae, and discharge occurred and were completely reversed by two months (Clayton & Clayton, 1994).
    B) BURNS to the eyes may occur upon contact with the liquid (CHRIS, 1997). Corneal opacities developed in rabbits, but were reversed by two months (Grant, 1993). More severe damage occurred when the eyes were flushed with water (Grant, 1993).
    3.4.5) NOSE
    A) IRRITATION - Thiophenol is irritating to the mucous membranes (CHRIS, 1997).
    3.4.6) THROAT
    A) IRRITATION - Thiophenol is irritating to the mucous membranes (CHRIS, 1997).

Respiratory

    3.6.1) SUMMARY
    A) Dyspnea and coughing may occur. Lung changes including hemorrhages were seen in mice after inhalation. Pulmonary edema may be a cause of death.
    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) Coughing and difficulty breathing may occur upon inhalation (CHRIS, 1997).
    B) PULMONARY HEMORRHAGE
    1) Lung changes were seen in mice after inhalation of high doses (ACGIH, 1992). Some hemorrhaging occurred (Clayton & Clayton, 1994).
    C) ACUTE LUNG INJURY
    1) Pulmonary edema may be a cause of death (EPA, 1985).

Neurologic

    3.7.1) SUMMARY
    A) CNS excitation, followed by CNS depression, occurred in animals. Thiophenol had a pronounced soporific (sleep-inducing) effect.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL STIMULANT ADVERSE REACTION
    1) Animals showed signs of initial CNS stimulation, including restlessness and increased respiration (ACGIH, 1992).
    B) CENTRAL NERVOUS SYSTEM DEFICIT
    1) CNS stimulation was followed by CNS depression in animals: ataxia, weakness, cyanosis, lethargy, sedation, respiratory depression, coma and death. Headaches and dizziness have been reported (ACGIH, 1992).
    2) Thiophenol had a pronounced soporific (sleep-inducing) effect in animals, which persisted for one to two days (ACGIH, 1992).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea and vomiting may occur following ingestion.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Nausea and vomiting may occur after inhalation or ingestion and may occur at low levels in some people due to its low odor threshold and disagreeable odor (EPA, 1985) CHRIS, 1997).

Hepatic

    3.9.1) SUMMARY
    A) Fatty degeneration and necrosis of the liver occurred from inhalation in mice.
    3.9.2) CLINICAL EFFECTS
    A) HEPATIC NECROSIS
    1) Fatty degeneration and necrosis of the liver occurred in mice after inhalation (Clayton & Clayton, 1981).

Genitourinary

    3.10.1) SUMMARY
    A) Hyaline casts in the tubules and kidney changes were seen in animals.
    3.10.2) CLINICAL EFFECTS
    A) RENAL TUBULAR DISORDER
    1) Some kidney changes, including hyaline casts in the tubules, were seen in animals (ACGIH, 1992).

Hematologic

    3.13.1) SUMMARY
    A) Methemoglobin can be produced by thiophenol in vitro, but is not likely to occur in the body.
    3.13.2) CLINICAL EFFECTS
    A) METHEMOGLOBINEMIA
    1) Thiophenol at 0.25 mM converted oxyhemoglobin to methemoglobin in vitro, but it is likely that the cell can adapt to this response (Amrolia et al, 1989).

Dermatologic

    3.14.1) SUMMARY
    A) Burns or severe irritation may occur.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) Thiophenol is a definite skin irritant in humans, and severe skin irritation was produced in rabbits (ACGIH, 1992).
    B) CHEMICAL BURN
    1) Thiophenol may burn the skin (CHRIS, 1997).

Musculoskeletal

    3.15.1) SUMMARY
    A) Progressive incoordination, weakness, and paralysis were produced in animals.
    3.15.2) CLINICAL EFFECTS
    A) PARALYSIS
    1) Acute exposures in animals produced progressive incoordination, muscular weakness, and paralysis of the skeletal muscles in the hind limbs (ACGIH, 1992).

Reproductive

    3.20.1) SUMMARY
    A) A NOAEL for developmental toxicity was > 40 mg/kg/day in the rabbit. Post-implantation mortality was observed in rats.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) Post-implantation mortality was observed in rats administered a dose of 500 mg/kg on days 6 through 15 of pregnancy.
    2) A NOAEL for developmental toxicity was > 40 mg/kg/day in the rabbit (Final report on the Developmental Toxicity of Thiphenol in New Zealand Rabbits TER92134 NTIS#PB94-201183).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS108-98-5 (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):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Genotoxicity

    A) Thiophenol was mutagenic in the Ames Salmonella assay.

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor CBC, urinalysis, and liver and kidney function. Monitor arterial gases, pulmonary function, and chest x-ray if pulmonary irritation is present.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count and liver and kidney function tests is suggested for patients with significant exposure.
    4.1.3) URINE
    A) URINALYSIS
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring urinalysis is suggested for patients with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Monitor CBC, urinalysis, and liver and kidney function. Monitor arterial gases, pulmonary function, and chest x-ray if pulmonary irritation is present.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) DO NOT INDUCE EMESIS - because this agent could possibly produce burns.
    B) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    C) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) 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).
    1) 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).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) 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.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) OBSERVATION REGIMES
    1) 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.
    2) Carefully observe patients with ingestion exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    B) MONITORING OF PATIENT
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Many chemicals cause irritation of the eyes, skin, and respiratory tract. In severe cases respiratory tract irritation can progress to ARDS/acute lung injury, which may be delayed in onset for up to 24 to 72 hours in some cases.
    2) Irritation or burns of the esophagus or gastrointestinal tract are also possible if caustic or irritant chemicals are ingested.
    B) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    C) MONITORING OF PATIENT
    1) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    2) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) In rabbits, flushing the eyes with 0.5% silver nitrate followed by copious irrigation with water has proven beneficial.
    6.8.2) TREATMENT
    A) OBSERVATION REGIMES
    1) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) BURN
    1) APPLICATION
    a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.
    2) DEBRIDEMENT
    a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
    b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
    c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).
    3) TREATMENT
    a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
    b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
    c) WOUND DRESSING:
    1) Depending on the site and area, the burn may be treated open (face, ears, or perineum) or covered with sterile nonstick porous gauze. The gauze dressing should be fluffy and thick enough to absorb all drainage.
    2) Alternatively, a petrolatum fine-mesh gauze dressing may be used alone on partial-thickness burns.
    d) DRESSING CHANGES:
    1) Daily dressing changes are indicated if a burn cream is used; changes every 3 to 4 days are adequate with a dry dressing.
    2) If dressing changes are to be done at home, the patient or caregiver should be instructed in proper techniques and given sufficient dressings and other necessary supplies.
    e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.
    4) TETANUS PROPHYLAXIS
    a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.
    B) SUPPORT
    1) 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.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Summary

    A) Minimum lethal human exposure is unknown.

Minimum Lethal Exposure

    A) ADULT
    1) GENERAL/SUMMARY
    a) The minimum lethal human dose to this agent has not been delineated.
    B) ANIMAL DATA
    1) In guinea pigs, dermal application of 2 mL/kg were lethal in 24 hours (Clayton & Clayton, 1994).
    1) NOAEL - (oral) Rabbit 10 mg/kg/day - decreased body weight of pregnant dams
    2) NOAEL - (oral) Rabbit >40 mg/kg/day - developmental effects not observed at the highest dosing.
    3) (From Final Report on the Developmental Toxicity of Thiophenol in New Zealand White Rabbits TER 92134 NTIS# PB94-201183)
    2) In rats, repeated IP injections of 3.5 mg/kg in 9 doses over a 3 week period caused fibrous thickening of the splenic capsule, enlargement of the spleen, and mild degenerative changes in the kidneys (Clayton & Clayton, 1994).

Maximum Tolerated Exposure

    A) ADULT
    1) GENERAL/SUMMARY
    a) The maximum tolerated human exposure to this agent has not been delineated.
    2) SPECIFIC SUBSTANCE
    a) The following maximum exposure tolerance data are for ETHYL MERCAPTAN, a compound that is thought to have similar toxicity:
    3) The maximum tolerated human exposure to ethyl mercaptan has not been delineated. Volunteers exposed to 4 ppm (10 mg/m(3)) 3 hours daily for 5 to 10 days reported intermittent nausea; an increase in the olfactory threshold; altered taste sensations to bitter and sweet substances; fatigue; and irritation of the lips, nose, and throat. No unpleasant effects were noted with a similar exposure to 0.5 ppm (1 mg/m(3)) (ACGIH, 1991).
    B) ANIMAL DATA
    1) Rats exposed to a 3.3% concentration of ethyl mercaptan became comatose, but recovered within 30 minutes (Gosselin et al, 1984).
    2) Application of one drop of thiophenol to rabbit eyes caused severe irritation, moderate redness, conjunctiva chemosis for 3 or 4 days. Normal conjunctiva returned in 10 to 16 days. Corneal opacities increased during 2 to 3 weeks. Recovery occurred in 2 months (Grant, 1993).
    a) If the rabbit eyes were flushed with water after application of thiophenol, more severe injury was observed: corneal opacity lasted several weeks and requiring 3 to 4 months to clear (Grant, 1993).
    b) If the rabbit eyes were flushed with 0.5% silver nitrate solution immediately after application of thiophenol followed by copious irrigation with water to remove the precipitated silverthiol compoind, less severe injury was observed: slight conjunctival inflammation and relatively small transient, diffuse corneal opacification were noticed (Grant, 1993).
    3) The following maximum exposure tolerance data are for ETHYL MERCAPTAN, a compound which is thought to possess similar toxicity:
    a) Rabbits, rats, and mice chronically exposed to about 40 ppm (100 mg/m(3)) developed minimal changes in organ weights and minor cardiovascular system regulatory disorders. This was considered to be about the threshold effect concentration for ethyl mercaptan (ACGIH, 1991).

Workplace Standards

    A) ACGIH TLV Values for CAS108-98-5 (American Conference of Governmental Industrial Hygienists, 2010):
    1) 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.
    a) Adopted Value
    1) Phenyl mercaptan
    a) TLV:
    1) TLV-TWA: 0.1 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Skin
    3) Definitions:
    a) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): CNS impair; eye and skin irr
    d) Molecular Weight: 110.18
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS108-98-5 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Benzenethiol
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling: 0.1 ppm (0.5 mg/m(3)) [15-minute]
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS108-98-5 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Phenyl mercaptan
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) 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): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Benzenethiol
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS108-98-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: ACGIH, 1991 HSDB, 2000 ITI, 1995 RTECS, 2000
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 25 mg/kg
    2) LD50- (INTRAPERITONEAL)RAT:
    a) 25.2 mg/kg (HSDB, 2000)
    b) 9800 mcg/kg -- General depressed activity; Coam; Respiratory depression
    3) LD50- (ORAL)RAT:
    a) 46,200 mcg/kg -- General depressed activity; Coam; Respiratory depression
    4) LD50- (SKIN)RAT:
    a) 300 mg/kg -- Tremor; Respiratory depression; Primary irritation

Physical Characteristics

    A) It has a repulsive, penetrating, burnt rubber, stench, garlic-like odor, especially when impure (Budavari, 1996; CHRIS , 2000).
    B) It exhibits a color ranging from colorless to water-white to light yellow (CHRIS , 2000; Lewis, 2000).
    C) It is a solid at temperature below 5 degrees F (HSDB , 2000).

Ph

    A) Thiophenol is feebly acidic with a pKa value of 6.62 (Budavari, 1996; HSDB , 2000).

Molecular Weight

    A) 110.18

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