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ASPHALT

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Asphalt is a residue of petroleum refining, composed of paraffinic and aromatic hydrocarbons and heterocyclic compounds containing carbon, sulfur, nitrogen, and oxygen.

Specific Substances

    1) Asphalt solids
    2) Asphalt fumes
    3) Asphalt, petroleum
    4) Asphaltum
    5) Bitumen
    6) Blown asphalt
    7) Gilsonite
    8) Judean pitch
    9) Mineral pitch
    10) Petroleum asphalt
    11) Petroleum pitch
    12) Petroleum roofing tar
    13) Pitch
    14) Road asphalt
    15) Tar
    16) ROAD ASPHALT (CUT BACK)
    17) ROAD ASPHALT, LIQUID
    18) ROAD TAR, LIQUID
    19) TAR (ASPHALT)

Available Forms Sources

    A) FORMS
    1) Asphalt (cut back) is a liquid petroleum product. It is also called road asphalt or road tar, liquid. Petroleum asphalt, or petroleum roofing tar, is a steam-refined asphalt (Lewis, 1992; Lewis, 1996).
    B) SOURCES
    1) Asphalt is a residue of petroleum refining, composed of paraffinic and aromatic hydrocarbons and heterocyclic compounds containing carbon, sulfur, nitrogen, and oxygen.
    2) Tar is produced by destructive distillation of coal, oil, lignite, peat, or wood.
    3) Asphalt is a dark-brown to black cement-like material, solid or semisolid in consistency. The predominating constituents are bitumens which occur in nature as such or are obtained as residua in petroleum refining. It is a mixture of paraffinic and aromatic hydrocarbons and heterocyclic compounds containing sulfur, nitrogen, and oxygen (Sax & Lewis, 1987; Lewis, 1996).
    4) It results from evaporation of the lighter hydrocarbons from petroleum and partial oxidation of the residue. Petroleum asphalt, thus, should be differentiated from tar or pitch, which results from the destructive distillation of coal (ACGIH, 2000).
    5) Gamble et al (1999) studied 170 workers exposed to asphalt fumes and found no consistent association between an acute reduction in lung function (pulmonary function measures) or symptoms of pulmonary dysfunction secondary to asphalt exposure.
    C) USES
    1) Asphalt is used in paving, road-coating, roofing, sealing and joint filling, special paints, adhesive in electrical laminates and hot-melt compositions, diluent in low-grade rubber products, fluid loss control in hydraulic fracturing of oil wells, medium for radioactive waste disposal, pipeline and underground cable coating, rust-preventive hot-dip coatings, base for synthetic turf, water-retaining barrier for sandy soils, supporter or rapid bacterial growth in converting petroleum components to protein (Sax & Lewis, 1987; Lewis, 1996).
    2) In the paving and roofing trades, tar or asphalt is applied in a hot liquid form that cools into a semi-solid covering. It becomes liquid at 93 degrees Centigrade, but is often heated to more than 232 degrees Centigrade.

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) WITH POISONING/EXPOSURE
    1) The majority of hot tar burns involve only 3 to 5% of the body surfaces. Partial thickness burns are most common, but patchy areas of full thickness skin losses are commonly observed.
    a) Inhalation of hot asphalt fumes can produce eye and respiratory tract irritation, headache, nausea, and nervousness due to the formation of hydrogen sulfide gas.
    b) Serious hydrogen sulfide poisoning can occur from inhalation of hydrogen sulfide evolved from asphalt in closed tanks. Oral ingestion of cool asphalt is relatively non-toxic.
    c) Asphalt cooled in a closed tank can evolve high concentrations of hydrogen sulfide gas, carbon monoxide, propane, methane, and other aliphatic hydrocarbons, as well as producing a relatively hypoxic atmosphere.
    0.2.4) HEENT
    A) WITH POISONING/EXPOSURE
    1) Exposure to hot asphalt fumes can cause severe irritation of eyes and mucous membranes.
    0.2.6) RESPIRATORY
    A) Prolonged irritation of hot asphalt fumes and release of hydrogen sulfide gas can produce respiratory irritation, pulmonary edema, and hypoxia.
    0.2.7) NEUROLOGIC
    A) WITH POISONING/EXPOSURE
    1) Headache may occur following prolonged inhalation exposure. Coma and seizures can follow hydrogen sulfide inhalation.
    0.2.8) GASTROINTESTINAL
    A) WITH POISONING/EXPOSURE
    1) Bezoars may occur if asphalt is swallowed.
    0.2.10) GENITOURINARY
    A) WITH POISONING/EXPOSURE
    1) Chronic exposure to asphalt fumes may result in renal disease.
    0.2.11) ACID-BASE
    A) WITH POISONING/EXPOSURE
    1) Metabolic acidosis may be seen in cases of hydrogen sulfide exposure.
    0.2.13) HEMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Occupational exposure to asphalt fumes may result in a decreased platelet count.
    0.2.14) DERMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Dermal exposure to hot asphalt produces a lesion which resembles a scald injury. The tar tends to adhere to some areas of skin, but may come off in areas where slight bullae are produced. Partial thickness burns are generally observed, but patchy areas of full thickness skin loss are common.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no reproductive studies were found for asphalt in humans or experimental animals.
    0.2.21) CARCINOGENICITY
    A) Asphalt contains polycyclic aromatic hydrocarbons, and may be carcinogenic with ongoing exposure.

Laboratory Monitoring

    A) In exposures to fumes from asphalt, obtain baseline arterial blood gases, carboxyhemoglobin levels, and electrolytes.

Treatment Overview

    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) 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).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    C) 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.
    D) Sodium nitrite may be efficacious in serious hydrogen sulfide poisoning:
    1) SODIUM NITRITE: Adult: 10 mL (300 mg) of a 3% solution IV at a rate of 2.5 to 5 mL/minute; Child (with normal hemoglobin concentration): 0.2 mL/kg (6 mg/kg) of a 3% solution IV at a rate of 2.5 to 5 mL/minute, not to exceed 10 mL (300 mg).
    2) Repeat one-half of initial sodium nitrite dose one-half hour later if there is inadequate clinical response. Calculate pediatric doses precisely to avoid potentially life-threatening methemoglobinemia. Use with caution if carbon monoxide poisoning is also suspected. Monitor blood pressure carefully. Reduce nitrite administration rate if hypotension occurs.
    E) Hyperbaric oxygen therapy may be considered in severe hydrogen sulfide poisonings unresponsive to standard therapy.
    0.4.4) EYE EXPOSURE
    A) 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.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Immerse tar-covered skin in cool water to limit tissue damage and prevent spread of liquid tar. Cooling should continue only until tar is hardened and cool.
    2) Tar adherent to skin blisters may be removed along with the blister epithelium in a medical facility.
    3) Tar adherent to unblistered skin may be removed in a medical facility using one of these methods.
    a) Apply liberal amounts of polysorbate (Tween 80(R)) over the affected area, cover with wet dressings and allow to remain for 6 hours. Wash away most of the tar with sterile water or saline. Repeat as necessary.
    b) Commercially available sterile surfactant surface active mixture such as De-Solv-it or Shur-Clens may be applied liberally and gently wiped away.
    c) Apply antibiotic creams of polysorbate bases. Cover with wet dressings and allow to remain for 24 hours after each application. Repeat as necessary.
    d) Asphalt may adhere tenaciously to the skin. Attempted removal may cause severe distress and further tissue damage. As asphalt is heated to such high temperatures, it may be thought of as a temporary sterile wound dressing.

Range Of Toxicity

    A) A few breaths of high concentration hydrogen sulfide (700 to 1000 ppm) may produce coma and death. Prolonged inhalation of 50 to 100 ppm hydrogen sulfide can produce toxic symptoms.

Clinical Effects

Summary Of Exposure

    A) WITH POISONING/EXPOSURE
    1) The majority of hot tar burns involve only 3 to 5% of the body surfaces. Partial thickness burns are most common, but patchy areas of full thickness skin losses are commonly observed.
    a) Inhalation of hot asphalt fumes can produce eye and respiratory tract irritation, headache, nausea, and nervousness due to the formation of hydrogen sulfide gas.
    b) Serious hydrogen sulfide poisoning can occur from inhalation of hydrogen sulfide evolved from asphalt in closed tanks. Oral ingestion of cool asphalt is relatively non-toxic.
    c) Asphalt cooled in a closed tank can evolve high concentrations of hydrogen sulfide gas, carbon monoxide, propane, methane, and other aliphatic hydrocarbons, as well as producing a relatively hypoxic atmosphere.

Heent

    3.4.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Exposure to hot asphalt fumes can cause severe irritation of eyes and mucous membranes.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Exposure to hot asphalt fumes can cause severe irritation of eyes (Hoidal et al, 1986; Tavris et al, 1984). Eye irritation was found more often in asphalt workers with symptoms occurring more often as the temperature of the asphalt increased, and with increasing concentrations of asphalt fumes (Norseth et al, 1991).
    2) Female workers in a commercial lighting factory who were exposed to asphalt fumes during production of ballast boxes and coils for fluorescent and high intensity lighting developed symptoms of bilateral conjunctivitis with hyperemic sclera reported in 3 cases (Chase et al, 1994).

Respiratory

    3.6.1) SUMMARY
    A) Prolonged irritation of hot asphalt fumes and release of hydrogen sulfide gas can produce respiratory irritation, pulmonary edema, and hypoxia.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) Subjective complaints of laryngeal/pharyngeal irritation and cough have been reported as acute effects of road workers exposed to asphalt (Norseth et al, 1991).
    b) CHRONIC EXPOSURE - Prolonged inhalation of hot asphalt fumes and hydrogen sulfide gas released can produce respiratory irritation (Burnett et al, 1977; Lewis, 1996).
    B) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Pulmonary edema occurs in about 20% of patients with serious hydrogen sulfide exposure (Burnett et al, 1977).
    C) HYPOXEMIA
    1) WITH POISONING/EXPOSURE
    a) Asphalt cooled in a closed tank can evolve high concentrations of hydrogen sulfide gas, carbon monoxide, propane, methane, and other aliphatic hydrocarbons, as well as producing a relatively hypoxic atmosphere (Hoidal et al, 1986).
    D) ASTHMA
    1) WITH POISONING/EXPOSURE
    a) CHRONIC EXPOSURE - Asphalt workers had an 8 times higher prevalence of physician diagnosed asthma, compared with other outdoor construction workers (Randem et al, 2004).
    E) CHRONIC OBSTRUCTIVE LUNG DISEASE
    1) WITH POISONING/EXPOSURE
    a) CHRONIC EXPOSURE - Chronic obstructive pulmonary disease was significantly more prevalent among asphalt workers, compared with other outdoor construction workers (Randem et al, 2004).
    F) RESPIRATORY DISTRESS
    1) WITH POISONING/EXPOSURE
    a) CHRONIC EXPOSURE - Compared with other outdoor construction workers, asphalt workers had significantly more symptoms of chest tightness, shortness of breath on exertion, and wheezing (Randem et al, 2004).
    G) PULMONARY FUNCTION STUDIES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) CHRONIC EXPOSURE - Compared with outdoor construction workers, the ratio of FEV1/FVC was significantly decreased in asphalt workers (78.1 versus 80.0). There was no statistically significant differences in FEV1 and FVC between the groups; however, asphalt workers tended to have lower lung function parameters (Randem et al, 2004).
    H) LACK OF EFFECT
    1) WITH POISONING/EXPOSURE
    a) CHRONIC EXPOSURE - Gamble et al (1999) studied 170 workers exposed to asphalt fumes and found no consistent association between an acute reduction in lung function (pulmonary function measures) or symptoms of pulmonary dysfunction secondary to asphalt exposure.

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Headache may occur following prolonged inhalation exposure. Coma and seizures can follow hydrogen sulfide inhalation.
    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache may occur following prolonged inhalation exposure.
    B) COMA
    1) WITH POISONING/EXPOSURE
    a) If high concentrations of hydrogen sulfide are present (700 to 1000 ppm), coma, respiratory paralysis, and hypoxia may occur with rapid onset (Gosselin et al, 1984) Ellenhorn et al, 1997 ), the so called "slaughterhouse sledgehammer" effect (Gosselin et al, 1984).
    C) FATIGUE
    1) WITH POISONING/EXPOSURE
    a) In one study, abnormal fatigue was reported as an acute effect of asphalt workers with symptoms occurring more often as the temperature of the asphalt increased, and with increasing concentrations of asphalt fumes (Norseth et al, 1991).

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Bezoars may occur if asphalt is swallowed.
    3.8.2) CLINICAL EFFECTS
    A) BEZOAR
    1) WITH POISONING/EXPOSURE
    a) Gastric concretions and pyloric obstruction have been reported in individuals who have chewed and swallowed asphalt. Apparently this practice was popular among asphalt workers because of its chewiness, tang, and the belief that it whitened the teeth (HSDB , 1990).
    B) LOSS OF APPETITE
    1) WITH POISONING/EXPOSURE
    a) In a comparison study, reduced appetite was one of the acute effects of workers handling asphalt (Norseth et al, 1991).

Genitourinary

    3.10.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Chronic exposure to asphalt fumes may result in renal disease.
    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) WITH POISONING/EXPOSURE
    a) CHRONIC TOXICITY
    1) CASE REPORT - Nephrotic syndrome secondary to glomerulonephritis was described in a road worker who had been exposed to asphalt fumes for more than 10 years (Douglas & Carney, 1998). Proteinuria improved after exposure ceased, but the patient remained hypertensive with an elevated serum creatinine.
    2) Further study of workers occupationally exposed to asphalt as compared to other nonexposed workers indicated an increased risk of renal disease following repeated contact to asphalt or bitumen fumes (Douglas & Carney, 1998).

Acid-Base

    3.11.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Metabolic acidosis may be seen in cases of hydrogen sulfide exposure.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) Metabolic acidosis may be found in cases with significant hydrogen sulfide exposure (Hoidal et al, 1986).

Hematologic

    3.13.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Occupational exposure to asphalt fumes may result in a decreased platelet count.
    3.13.2) CLINICAL EFFECTS
    A) ACQUIRED PLATELET DISORDER
    1) WITH POISONING/EXPOSURE
    a) CHRONIC TOXICITY
    1) CASE SERIES - Female workers exposed to asphalt fumes at a commercial lighting factory were found to have a higher mean platelet volume (MPV) and lower mean platelet count compared with a reference group (Chase et al, 1994). Laboratory analyses improved after modifications were made to the factory's ventilation system.

Dermatologic

    3.14.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Dermal exposure to hot asphalt produces a lesion which resembles a scald injury. The tar tends to adhere to some areas of skin, but may come off in areas where slight bullae are produced. Partial thickness burns are generally observed, but patchy areas of full thickness skin loss are common.
    3.14.2) CLINICAL EFFECTS
    A) THERMAL BURN
    1) WITH POISONING/EXPOSURE
    a) Dermal exposure to hot asphalt produces a lesion which resembles a scald injury. The tar tends to adhere to some areas of skin, but may come off in areas where large bullae are produced (Stratta et al, 1983).
    b) Partial thickness burns are generally observed, but patchy areas of full thickness skin loss are common. Most burns involve 3 to 5% of body surface area (Schiller, 1983).
    c) Burns involving 10% or greater of body surface are likely to be serious and require intravenous fluid resuscitation (Stratta et al, 1983).
    d) CASE SERIES - In one study of 92 patients with asphalt injuries, the mean burn size was 3.87% of the total body surface area with a mean full thickness area of injury of 1.5% (Baruchin et al, 1997). Twenty-four patients had burns of critical areas (described as face, orbits, hands, and feet); the majority of burns, however, were on the upper extremities. 39 (42%) patients required surgical intervention (skin debridement and skin grafting).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) SEQUELA
    1) WITH POISONING/EXPOSURE
    a) A small study of asphalt workers as compared to unexposed male controls, suggested that chronic exposure to PAHs may affect immunological function (Karakaya et al, 1999). The authors, however, noted that extrapolation of these findings may not be possible based on limitations of individual genetic susceptibility, route and dose of exposure, and suggest that further study is required.

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no reproductive studies were found for asphalt in humans or experimental animals.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS8052-42-4 (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) IARC Classification
    a) Listed as: Bitumens, steam-refined, cracking-residue and air-refined
    b) Carcinogen Rating: 2B
    1) The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    2) IARC Classification
    a) Listed as: Bitumens, extracts of steam-refined and air-refined
    b) Carcinogen Rating: 2B
    1) The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    3.21.2) SUMMARY/HUMAN
    A) Asphalt contains polycyclic aromatic hydrocarbons, and may be carcinogenic with ongoing exposure.
    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) Several carcinogenic polycyclic aromatic hydrocarbons have been identified in asphalt at the time of this review (Knecht & Woitowitz, 1989).
    2) There are possible links between asphalt exposure and scrotal cancer (Wahlberg, 1974), Hodgkins disease (Szelc, 1981), and lung cancer (Wilson, 1984); however, these studies generally involved possible mixed exposures with tar or pitch.
    3) Several investigators have suggested that repeated exposure to asphalt or its fumes may result in an increased risk for various types of neoplasms (Knecht & Woitowitz, 1989; Maizlish et al, 1988; Hansen, 1989; Austin et al, 1987).
    4) To estimate excess risks for lung cancer mortality after longtime exposure to bitumen fume, one retrospective study used exposure-response models from a Dutch cohort of road construction and asphalt mixing companies. It was found that the excess lifetime risks for lung cancer in this group of workers was above benchmark values used in standard setting by the Dutch Health Council. However, confounding by smoking could not be ruled out (Hooiveld et al, 2002).
    5) Despite the uncertainty of the human potential of asphalt to cause cancer, ongoing epidemiological studies are recommended to determine cancer risk in man from exposure to asphalt (Chiazze et al, 1991).
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) Roofing asphalt was not carcinogenic in animals, whereas material from older roofs was (Emmett, 1981). Asphalt paints were not carcinogenic (Robinson, 1984), but the condensed volatiles caused tumors in mice (27:351-366). Extracts of asphalt have also been carcinogenic in animal studies (Chiazze et al, 1991).
    B) LACK OF EFFECT
    1) Asphalt fumes have not caused cancer in rats or guinea pigs, and the solid was not carcinogenic on the skin of mice or rabbits (ACGIH, 1986). Injection of the solid material into rodents caused tumors (Heuper & Payne, 1960), but this may not be relevant to normal human exposure.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) In exposures to fumes from asphalt, obtain baseline arterial blood gases, carboxyhemoglobin levels, and electrolytes.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Baseline chest x ray should be obtained in cases of asphalt fume inhalation.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) In exposures to fumes from asphalt, obtain baseline arterial blood gases, carboxyhemoglobin levels, and electrolytes.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Immediately move patient to fresh air and administer oxygen.
    B) Prevent self-exposure and possible death by wearing a self-contained breathing apparatus to rescue the victim.
    6.7.2) TREATMENT
    A) OXYGEN
    1) Administer 100% oxygen.
    B) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 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 (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 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 (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    C) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    D) SODIUM NITRITE
    1) Intravenous sodium nitrite may be beneficial by forming sulfmethemoglobin, thus removing sulfide from combination in tissue. The sodium thiosulfate component of the kit is not efficacious in hydrogen sulfide poisoning. The antidotal efficacy of nitrite therapy is controversial, but is recommended until further studies are available.
    2) INDICATION
    a) Sodium nitrite should be given initially and administered as soon as vascular access is established.
    b) Further administration of sodium nitrite is dictated only by the clinical situation, provided no significant complications (hypotension, excessive methemoglobinemia) are present. Use with caution if carbon monoxide poisoning is also suspected.
    c) The goal of nitrite therapy is to achieve a methemoglobin level of 20% to 30%. This level is not based on clinical data, but represents the tolerated concentration without significant adverse symptoms from methemoglobin in an otherwise healthy individual. Clinical response has been reported to occur with methemoglobin levels in the range of 3.6% to 9.2% (DiNapoli et al, 1989; Johnson et al, 1989; Johnson & Mellors, 1988).
    3) ADULT DOSE
    a) 10 mL of a 3% solution (300 mg) administered intravenously at a rate of 2.5 to 5 mL/minute (Prod Info NITHIODOTE intravenous injection solution, 2011). Frequent blood pressure monitoring must accompany sodium nitrite injection and the rate slowed if hypotension occurs.
    b) If there is inadequate clinical response, an additional dose of sodium nitrite at half the amount of the initial dose may be administered 30 minutes following the first dose (Prod Info NITHIODOTE intravenous injection solution, 2011).
    4) PEDIATRIC DOSE
    a) The recommended pediatric sodium nitrite dose is 0.2 mL/kg of a 3% solution (6 mg/kg) administered intravenously at a rate of 2.5 to 5 mL/minute, not to exceed 10 mL (300 mg) (Prod Info NITHIODOTE intravenous injection solution, 2011).
    b) If there is inadequate clinical response, an additional dose of sodium nitrite at half the amount of the initial dose may be administered 30 minutes following the first dose (Prod Info NITHIODOTE intravenous injection solution, 2011; Berlin, 1970).
    c) PRESENCE OF ANEMIA: If there is a reason to suspect the presence of anemia, the following initial sodium nitrite doses should be given, depending on the child's hemoglobin (sodium nitrite should not exceed the doses listed below; fatal methemoglobinemia may result) (Berlin, 1970):
    1) Hemoglobin: 8 g/dL - Initial 3% sodium nitrite dose: 0.22 mL/kg (6.6 mg/kg)
    2) Hemoglobin: 10 g/dL - Initial 3% sodium nitrite dose: 0.27 mL/kg (8.7 mg/kg)
    3) Hemoglobin: 12 g/dL (average child) - Initial 3% sodium nitrite dose: 0.33 mL/kg (10 mg/kg)
    4) Hemoglobin: 14 g/dL - Initial 3% sodium nitrite dose: 0.39 mL/kg (11.6 mg/kg)
    E) 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).
    F) HYPERBARIC OXYGEN THERAPY
    1) If a serious carbon monoxide poisoning is present (acidosis, coma, pulmonary edema, cardiac ischemia, arrhythmias, or neurologic symptoms and an elevated carboxyhemoglobin level), hyperbaric oxygen is indicated.
    2) Hyperbaric oxygen has been used in 2 reported cases of hydrogen sulfide poisoning where it appeared to be efficacious (Whitcraft et al, 1985; Smilkstein et al, 1985).
    3) The place of hyperbaric oxygen in the treatment of hydrogen sulfide poisoning is presently undefined, but the procedure may be considered for patients with serious poisoning and a poor clinical response to other treatment modalities.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: 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, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    B) Copious irrigation with sterile surface-active solvents (De-Solv-it(R)- Orange-Sol, Inc or Shur-Clens(R)-Whittaker General Medical) and saline may facilitate removal of tar (Stratta et al, 1983).
    C) Polysorbate containing neomycin sulfate has been used to remove corneal or conjunctival tar (Perry, 1993).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) COOLING
    1) Immerse tar-covered skin in cool water to limit tissue damage and prevent spread of liquid tar. Hypothermia may occur with excessive immersion; cooling should be continued only until tar is hardened and cool.
    B) TAR REMOVAL/BLISTERS
    1) Tar adherent to skin blisters may be removed along with blister epithelium in a medical facility.
    C) TAR REMOVAL/UNBLISTERED SKIN
    1) Tar adherent to unblistered tissue may be removed in a medical facility by qualified personnel using one of these methods:
    a) Apply liberal amounts of polysorbate 80 (Tween 80) over the affected area; cover with wet dressings and allow to remain for 6 hours. Wash away emulsified tar with sterile water or saline. Repeat procedure until all of the tar is emulsified and removed (Demling et al, 1980). This is the fastest method, but may not be readily available.
    b) Commercially available sterile surface-active solvent mixtures such as De-Solv-it(R) or Shur-Clens(R) may be applied liberally and gently wiped (Stratta et al, 1983).
    1) CASE REPORT: A 29-year-old man was inadvertently sprayed with asphalt over his entire body and attempts to remove the asphalt from his face, neck, and extremities was unsuccessful with conventional (e.g. mineral oil) therapies, but was quickly and successfully removed with a petroleum based solution (De-Sol-It Multi-Use solvent) which did not cause any further cutaneous or mucous membrane damage.
    a) Methods to remove from dermal surface:
    1) Remove asphalt after 10 to 20 seconds of petroleum-based solvent application,
    2) Gently debride asphalt with forceps or gauze,
    3) Protective clothing and eyewear should be used by personnel assisting in wound decontamination.
    b) The authors suggested further controlled trials to determine if any cutaneous or mucous membrane toxicity exists with the use of this agent for dermal decontamination (Tsou et al, 1996).
    c) Apply antibiotic creams in polysorbate bases (Bose & Tredget, 1982). Cover with wet dressing and allow to remain for 24 hours after each application. Complete removal may take 24 to 72 hours.
    d) Lipophilic substances (Neosporin ointment, petrolatum, mineral oil, lanolin) have been used to dissolve tar, but are less effective than polysorbate bases (Stratta et al, 1983). Emulsification may also take up to 24 to 72 hours to totally remove the asphalt (Baruchin et al, 1997).
    e) A mixture of Unibase(R) and triple antibiotic ointment has been reported to also be effective (Levy et al, 1986).
    f) Tiernan & Harris (1993) reported a case of tar removal using butter placed on gauze which emulsifies the tar and absorbs it onto the gauze. The butter should be warmed to almost liquid consistency prior to being placed on sterile gauze. The tar is absorbed onto the gauze over 20 to 30 minutes. This procedure may be repeated.
    g) Once all the material is removed, the wounds should be treated similar to other dermal burns. The asphalt should be completely removed to avoid the risk of suppuration (Baruchin et al, 1997).
    h) Cooled, previously molten asphalt may adhere so tenaciously to the skin that attempted removal may cause severe distress to the patient, as well as further tissue damage. As asphalt is heated to such high temperatures, it may be sterile and may provide a temporary form of sterile dressing for the wound (James & Moss, 1990).
    6.9.2) TREATMENT
    A) BURN
    1) Following removal of tar, treat as a thermal burn. Intravenous fluid replacement, topical antibiotics, and skin grafting may be required.
    B) ANALGESIC
    1) Analgesics may be required for severe pain.

Abstracts

Case Reports

    A) ADULT
    1) ROUTE OF EXPOSURE
    a) INHALATION: Hoidal et al (1986) reported the cases of 2 workers severely poisoned with hydrogen sulfide gas evolved from asphalt improperly cooled in a closed tank. Both patients rapidly developed coma, and one suffered cardiac arrest with ventricular fibrillation. Both patients were resuscitated, but the more seriously ill victim suffered permanent neurologic damage.

Range Of Toxicity

Summary

    A) A few breaths of high concentration hydrogen sulfide (700 to 1000 ppm) may produce coma and death. Prolonged inhalation of 50 to 100 ppm hydrogen sulfide can produce toxic symptoms.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) A few breaths of high concentrations of hydrogen sulfide (700 to 1000 ppm) may produce coma and death.

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Prolonged inhalation of 50 to 100 ppm hydrogen sulfide can produce toxic symptoms.

Workplace Standards

    A) ACGIH TLV Values for CAS8052-42-4 (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) Asphalt (Bitumen) fume, as benzene-soluble aerosol
    a) TLV:
    1) TLV-TWA: 0.5 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: BEI(P), I
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) BEI(P): The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational. Substances identified as Polycyclic Aromatic Hydrocarbons (PAHs) are part of this notation.
    c) I: Inhalable fraction; see Appendix C, paragraph A (of TLV booklet).
    c) TLV Basis - Critical Effect(s): URT and eye irr
    d) Molecular Weight:
    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 CAS8052-42-4 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Asphalt fumes
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling: 5 mg/m(3) [15-minute]
    d) Carcinogen Listing: (Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix A
    3) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS8052-42-4 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Asphalt (Bitumen) fume, as benzene-soluble aerosol
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    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): 2B ; Listed as: Bitumens, steam-refined, cracking-residue and air-refined
    a) 2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    4) 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): 2B ; Listed as: Bitumens, extracts of steam-refined and air-refined
    a) 2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Asphalt fumes
    a) Ca : NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    6) MAK (DFG, 2002): Category 2 ; Listed as: Bitumen (vapour and aerosol)
    a) Category 2 : Substances that are considered to be carcinogenic for man because sufficient data from long-term animal studies or limited evidence from animal studies substantiated by evidence from epidemiological studies indicate that they can make a significant contribution to cancer risk. Limited data from animal studies can be supported by evidence that the substance causes cancer by a mode of action that is relevant to man and by results of in vitro tests and short-term animal studies.
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS8052-42-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: Lewis, 1992

Pharmacology Toxicology

Toxicologic Mechanism

    A) Dermal or eye exposure to hot asphalt produces direct thermal burn.
    B) Fumes evolved from hot asphalt can contain carbon monoxide, various aliphatic hydrocarbons, and hydrogen sulfide (Hoidal et al, 1986).
    1) Carbon monoxide inhalation produces tissue hypoxia by inhibition of mitochondrial cytochrome oxidase and decrease oxygen delivery and carrying capacity by inducing carboxyhemoglobinemia.
    2) The various aliphatic hydrocarbons displace oxygen from atmospheric air and can produce asphyxia.
    3) Hydrogen sulfide is an inhibitor of mitochondrial cytochrome oxidase and produces cellular hypoxia from inability to utilize oxygen.

Physicochemical

Physical Characteristics

    A) Asphalt is a dark-brown to black cementitious material, solid or semisolid in consistency (Sax & Lewis, 1987; Lewis, 1996).
    B) ODOR: tar or pitch-like odor (HSDB , 1999)
    C) COLOR: dark-brown to black (Sax & Lewis, 1987; Lewis, 1996)

Ph

    1) No information found at the time of this review.

Molecular Weight

    1) No information found at the time of this review.

Other

    A) ODOR THRESHOLD
    1) Currently not available (CHRIS , 2002).

References

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