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TETRAETHYL LEAD

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) A gasoline additive that prevents "knocking" of motors (Budavari, 1996).
    B) TEL is a hydrocarbon with an atom of lead attached to it. There are 4 ethyl groups attached to the lead so there are no reactive ligands, and; therefore it is unlikely that the lead is biologically active (Pers Com, 1991).
    C) By the end of 1995, the Clean Air Act completely prohibited the use of lead in all motor vehicle fuels, thus reducing highway fuels to a negligible source of lead (EPA, 2000).

Specific Substances

    1) Tetraethyl plumbane
    2) Lead tetraethyl
    3) TEL
    4) Molecular Formula: C8-H2-O-Pb
    5) METHYLPLUMBANE
    1.2.1) MOLECULAR FORMULA
    1) (C2H5)4 Pb

Available Forms Sources

    A) FORMS
    1) Only one grade is available - of about 98% pure (Lewis, 1997a).
    B) SOURCES
    1) It is produced by alloy formation / dechlorination reaction of ethyl chloride, lead, and sodium (Ashford, 1994b). It is no longer produced in the US (HSDB , 2001).
    C) USES
    1) Tetraethyl lead had been used as a petrol octane booster to prevent "knocking" in motors since 1923. Its concentration is no more than 0.15% in automotive fuel and no more than 0.22 % in aviation fuel (ACGIH, 1991a; Ashford, 1994a; Budavari, 1996).
    a) A gradual ban of tetraethyl lead as a fuel additive in the US was placed in 1978 (ILO, 1998). Tetraethyl lead has been replaced, as an anti-knock compound in automotive fuel, largely by methyl-tert-butyl ether (MBTE) (HSDB , 2001). By the end of 1995, the Clean Air Act completely prohibited the use of lead in all motor vehicle fuels, thus reducing highway fuels to a negligible source of lead (EPA, 2000). Tetraethyl lead is imported to the US for use in aviation fuel (HSDB , 2001).
    b) "A typical motor mix for automotive gasolines consists of about 62 percent tetraethyl lead, 18 percent ethylene dibromide, 18 percent ethylene dichloride, and 2 percent of other ingredients, such as dye, petroleum solvent, and stability improver. A typical aviation mix includes about 61 to 62 percent tetraethyl lead, 35 to 36 percent ethylene dibromide, and 3 percent of dye, solvent, inhibitor, etc" (HSDB , 2001).
    2) It can be used to make other metal alkyls (such as ethylmercury compounds), mixed alkyl leads for gasoline additives, and organomercury fungicides (HSDB , 2001).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Tetraethyl lead is moderately to highly toxic. Acute or chronic EXPOSURE ROUTES include inhalation, ingestion or skin absorption. Exposure to tetraethyl lead often occurs through deliberate inhalation of leaded gasoline (substance abuse). Recent accidental exposure case reports have come from developing countries, such as China.
    B) The central nervous system is the main target organ affected. The effects of tetraethyl lead may be mixed with the effects of the solvent. The exposure-onset interval varies inversely with the dose; symptoms can begin within hours to days (usually within 1 to 5 days, up to as long as 14 days after exposure). Symptoms that begin within 24 hours usually indicate serious exposure or reflect intoxication due to the hydrocarbon (gasoline).
    1) Early exposure effects are generally those of hydrocarbon abuse. These include anorexia, nausea, vomiting, diarrhea, delirium, nervous irritability, headache, restlessness, pallor, tremor, euphoria, lethargy, insomnia, slurred speech and blurred vision.
    2) After the initial effects of asthenia, weakness, fatigue, headache, nausea, vomiting, diarrhea, anorexia and insomnia, the "tetraethyl lead triad" of central nervous system involvement (including ataxia, tremor and hypotonia), bradycardia and decreased body temperature may be noted.
    C) Mild exposure results in anxiety, lassitude, irritability, insomnia, excitement, confusion, lurid (violent or frightening) dreams, anorexia, nausea, vomiting, metallic taste, pallor, mild diarrhea, dizziness, tremulousness, lack of coordination and truncal ataxia.
    D) Moderate exposure can produce disorientation, hyperexcitability, tremors, twitching, chorea, increased reflexes, spasticity, fatigue, muscle pain, bradycardia, hypotension, hypothermia, limited upward gaze and rotary or horizontal nystagmus.
    E) Severe exposure leads to delusions, hallucinations, mania, psychotic behavior, seizures (maniacal, violent convulsions), intense hyperactivity, facial contortions, cerebral edema, coma and death. ENCEPHALOPATHY and vomiting result from severe intoxication; the effects of tetraethyl lead differ from those of inorganic lead poisoning in that metallic taste and hematologic abnormalities are unusual and encephalopathy predominates.
    F) Absorption of as little as 1 gm can be fatal within 3 to 30 days (as the compound slowly degrades to triethyl lead); acute intoxication can have a mortality rate as high as 20 percent.
    G) Effects unrelated to the central nervous system include irritation of the skin, eyes and mucous membranes. Dermal contact can result in dermatitis and burns. Eye exposure produces pain, burns, blurred vision and conjunctivitis. A metallic taste, sneezing, bronchitis and pneumonia have also been noted.
    0.2.3) VITAL SIGNS
    A) Hypothermia, fever, bradycardia, hypotension and irregular respirations have been reported following acute exposure.
    0.2.5) CARDIOVASCULAR
    A) Hypotension and bradycardia have been reported.
    0.2.6) RESPIRATORY
    A) Inhalation of TEL vapors can be fatal. Upper respiratory tract irritation and sneezing may follow dust exposure. Irregular respirations are a non-specific finding.
    0.2.7) NEUROLOGIC
    A) Clinical neurologic effects of TEL intoxication can be divided into MILD, MODERATE, and SEVERE. They usually occur within 1 to 5 days, or as long as 14 days post exposure.
    B) MILD - Anxiety, irritability, insomnia, lurid dreams, anorexia, metallic taste, dizziness, pallor, lassitude, tremor, incoordination, and cerebellar ataxia.
    C) MODERATE - Disorientation, hyperexcitability, hyperreflexia, and lurid dreams, tremors, and chorea.
    D) SEVERE - Delusions, hallucinations, mania, seizures, cerebral edema, coma, and death.
    0.2.8) GASTROINTESTINAL
    A) TEL intoxication usually lacks the common GI manifestations of inorganic lead intoxication. Anorexia, nausea, vomiting, diarrhea and weight loss have been seen after acute exposure.
    0.2.9) HEPATIC
    A) Elevated liver enzymes may occur.
    0.2.10) GENITOURINARY
    A) Renal damage has been reported following acute exposure; urinary retention has occurred infrequently.
    0.2.13) HEMATOLOGIC
    A) Anemia, basophilic stippling, and neutrophilia may occur.
    0.2.14) DERMATOLOGIC
    A) Skin absorption of TEL can occur. Pallor may be observed following acute exposure.
    0.2.15) MUSCULOSKELETAL
    A) Elevated CPK has been reported in severe cases of chronic exposure.
    0.2.17) METABOLISM
    A) ALAD enzyme levels are depressed by TEL.
    0.2.20) REPRODUCTIVE
    A) In contrast to inorganic lead, which is a known human reproductive hazard and also has many reproductive effects in animals, the effect of TEL on human and animal reproduction, if any, is much less clear.
    0.2.21) CARCINOGENICITY
    A) Not known to be a human carcinogen. TEL has been implicated, but not proven as a carcinogen. Epidemiological studies of persons exposed to TEL have reported a possible slight excess of skin cancers and myelomas. These results have not been confirmed by other studies.

Laboratory Monitoring

    A) The blood lead level provides one measure of INORGANIC lead burden which does not necessarily reflect organic lead burden. The normal upper limit is 10 mcg/dL. Inorganic lead levels correlate with CNS signs after chronic exposure.
    B) Metabolic substrates in heme synthesis (ALAD, EP or ZnPP, coprophyrin) may or may not rise after prolonged exposure and are not a reliable test in diagnosis or assessment of severity.
    C) Monitor liver function tests, renal function tests, and hematologic parameters.
    D) The ability to penetrate skin makes reliance on airborne concentrations impractical (Hathaway et al, 1996).
    E) An analysis of the urinary concentration of lead is helpful in evaluating the amount of TEL absorbed during chronic exposure (Hathaway et al, 1996). Urinary lead concentrations are not helpful after acute exposures (He, 1999).

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Emesis is not recommended following ingestion of leaded gasoline or other products containing organolead compounds because of the potential for CNS depression, seizures, and aspiration of the hydrocarbon vehicle.
    B) If large amounts are ingested, consider placing a nasogastric tube to suction stomach contents. Endotracheal intubation should be strongly considered to prevent aspiration.
    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.
    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) Organolead compounds can be absorbed via inhalation.
    C) Consider chelation therapy in patients with blood lead greater than 45 mcg/dL and where symptoms of lead encephalopathy are noted.
    1) BAL (dimercaprol) - 3 to 5 mg/kg/dose deep IM every 4 hours for 2 days; then every 4 to 6 hours for 2 more days; then every 4 to 12 hours up to an additional 7 days.
    2) CALCIUM EDTA - 50 to 75 mg/kg/day deep IM in 3 to 6 divided doses for up to 5 days. EDTA should only be administered after BAL in patients with encephalopathy or children with levels >69 mcg/dL.
    3) DMSA - Initial pediatric dose is 10 mg/kg or 350 mg/m(2) orally every 8 hours for 5 days; reduced to every 12 hours for an additional 2 weeks.
    4) D-PENICILLAMINE - 250 mg 4 times a day PO for up to 5 days. Do not exceed 40 mg/kg/day. OSHA prohibits prophylactic chelation therapy in workers occupationally exposed to lead.
    D) 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.
    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) 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).

Range Of Toxicity

    A) TLV - 0.1 mg/m(3)
    B) Exposure to 100 mg/m(3) for 1 hr or longer periods at a lower rate results in an acute intoxication. Although TEL can cause toxicity through skin absorption, no reliable data exist to relate dermal dose to symptoms in humans.

Clinical Effects

Summary Of Exposure

    A) Tetraethyl lead is moderately to highly toxic. Acute or chronic EXPOSURE ROUTES include inhalation, ingestion or skin absorption. Exposure to tetraethyl lead often occurs through deliberate inhalation of leaded gasoline (substance abuse). Recent accidental exposure case reports have come from developing countries, such as China.
    B) The central nervous system is the main target organ affected. The effects of tetraethyl lead may be mixed with the effects of the solvent. The exposure-onset interval varies inversely with the dose; symptoms can begin within hours to days (usually within 1 to 5 days, up to as long as 14 days after exposure). Symptoms that begin within 24 hours usually indicate serious exposure or reflect intoxication due to the hydrocarbon (gasoline).
    1) Early exposure effects are generally those of hydrocarbon abuse. These include anorexia, nausea, vomiting, diarrhea, delirium, nervous irritability, headache, restlessness, pallor, tremor, euphoria, lethargy, insomnia, slurred speech and blurred vision.
    2) After the initial effects of asthenia, weakness, fatigue, headache, nausea, vomiting, diarrhea, anorexia and insomnia, the "tetraethyl lead triad" of central nervous system involvement (including ataxia, tremor and hypotonia), bradycardia and decreased body temperature may be noted.
    C) Mild exposure results in anxiety, lassitude, irritability, insomnia, excitement, confusion, lurid (violent or frightening) dreams, anorexia, nausea, vomiting, metallic taste, pallor, mild diarrhea, dizziness, tremulousness, lack of coordination and truncal ataxia.
    D) Moderate exposure can produce disorientation, hyperexcitability, tremors, twitching, chorea, increased reflexes, spasticity, fatigue, muscle pain, bradycardia, hypotension, hypothermia, limited upward gaze and rotary or horizontal nystagmus.
    E) Severe exposure leads to delusions, hallucinations, mania, psychotic behavior, seizures (maniacal, violent convulsions), intense hyperactivity, facial contortions, cerebral edema, coma and death. ENCEPHALOPATHY and vomiting result from severe intoxication; the effects of tetraethyl lead differ from those of inorganic lead poisoning in that metallic taste and hematologic abnormalities are unusual and encephalopathy predominates.
    F) Absorption of as little as 1 gm can be fatal within 3 to 30 days (as the compound slowly degrades to triethyl lead); acute intoxication can have a mortality rate as high as 20 percent.
    G) Effects unrelated to the central nervous system include irritation of the skin, eyes and mucous membranes. Dermal contact can result in dermatitis and burns. Eye exposure produces pain, burns, blurred vision and conjunctivitis. A metallic taste, sneezing, bronchitis and pneumonia have also been noted.

Vital Signs

    3.3.1) SUMMARY
    A) Hypothermia, fever, bradycardia, hypotension and irregular respirations have been reported following acute exposure.
    3.3.2) RESPIRATIONS
    A) Irregular respirations have been reported as a nonspecific finding (Ross, 1982).
    3.3.3) TEMPERATURE
    A) FEVER was reported as a nonspecific finding (Ross, 1982).
    B) HYPOTHERMIA may occur following acute exposure (Hathaway et al, 1996) HSDB, 2000).
    3.3.4) BLOOD PRESSURE
    A) HYPOTENSION has been developed following acute exposure (Hathaway et al, 1996) HSDB, 2000).
    3.3.5) PULSE
    A) BRADYCARDIA was reported as a nonspecific finding of acute exposure (Ross, 1982) HSDB, 2000).

Dermatologic

    3.14.1) SUMMARY
    A) Skin absorption of TEL can occur. Pallor may be observed following acute exposure.
    3.14.2) CLINICAL EFFECTS
    A) POISONING
    1) Tetraethyl lead can be absorbed through the skin; lead poisoning can occur from this route of exposure (HSDB, 2000).
    B) PALE COMPLEXION
    1) Pallor may be observed following acute exposure to tetraethyl lead (HSDB, 2000).

Musculoskeletal

    3.15.1) SUMMARY
    A) Elevated CPK has been reported in severe cases of chronic exposure.
    3.15.2) CLINICAL EFFECTS
    A) ENZYMES/SPECIFIC PROTEIN LEVELS - FINDING
    1) CREATINE PHOSPHOKINASE INCREASED
    a) Elevated CPK has been reported in severe cases (Robinson, 1978).
    b) In one study the degree of CPK elevation was similar in groups of patients who abused leaded and unleaded gasoline, suggesting that some component other than tetraethyl lead is responsible for rhabdomyolysis (Burns et al, 1994).
    2) MYALGIA
    a) CASE REPORT - A 19-year-old man with psychosis associated with abuse of leaded gasoline developed muscle weakness and pain associated with elevated CPK and myoglobinuria (Moss & Cooper, 1986).

Reproductive

    3.20.1) SUMMARY
    A) In contrast to inorganic lead, which is a known human reproductive hazard and also has many reproductive effects in animals, the effect of TEL on human and animal reproduction, if any, is much less clear.
    3.20.2) TERATOGENICITY
    A) DEVELOPMENTAL DEFECTS
    1) No studies were found on the effect of TEL alone on female reproduction or on the unborn in humans. There have been isolated reports of CNS and developmental defects in children of women who are gasoline sniffers (Panova, 1976; Hunter et al, 1979). These individual cases were related, however, and possible genetic factors were not excluded. In any event, exposure to TEL would have been complicated by exposure to gasoline and other volatile additives. A syndrome with severe mental retardation has been seen among children of heavy gasoline sniffers (Hunter et al, 1979).
    B) CNS CONGENITAL ANOMALY
    1) Tetraethyl lead is converted to the more stable and more toxic triethyl lead by liver, kidney, and brain. Triethyl lead is the primary toxin to nervous tissue.
    2) Triethyl lead is also converted to inorganic lead. It is felt that inorganic lead plays a significant additive role in toxicity. The lack of some features of intoxication with inorganic lead as a metabolite of TEL and as a primary toxin may be due to pharmacokinetic considerations.
    C) ANIMAL STUDIES
    1) Several reproductive studies have been done in experimental animals; TEL was generally not teratogenic (Odenbro & Kihlstrom, 1977) Odenbro, 1982; (Kennedy, 1975).
    2) TEL given orally to rats at 2.5, 5, and 10 mg/kg/day lowered fetal body weight and increased resorptions, but caused no malformations (McLain & Becker, 1972). Triethyl lead injected into pregnant and nursing mice retarded the growth of the offspring (Grandjean, 1984). Triethyl lead given at 0.5 and 1.54 mg/kg early in pregnancy had no effect in mice (Odenbro & Kihlstrom, 1977).
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) TEL is thought to be transferred through the placenta in rodents but not readily metabolized, because rodents have very low levels of microsomal oxidizing enzymes before birth (Grandjean, 1984). In rodents, it has been speculated that the fetus may be less susceptible to TEL than the mother; this may not necessarily be true in humans (Grandjean, 1984).
    2) RATS - Post-implantation mortality was observed in rats (RTECS, 1990).
    3) Several reproductive studies have been done in experimental animals; TEL was generally not teratogenic. When given to mice early in pregnancy, triethyl lead (the major metabolite of TEL) decreased the frequency of pregnancies (Odenbro & Kihlstrom, 1977), and decreased levels of female steroid hormones (Odenbro, 1982). When given orally at 0.02, 1, and 10 mg/kg/day to pregnant mice, TEL was not teratogenic, but there were reduced numbers of pregnancies at the highest dose which was clearly toxic to the mothers (Kennedy, 1975).
    4) TEL given orally to rats at 2.5, 5, and 10 mg/kg/day lowered fetal body weight and increased resorptions, but caused no malformations (McLain & Becker, 1972). Triethyl lead injected into pregnant and nursing mice retarded the growth of the offspring (Grandjean, 1984). Triethyl lead given at 0.5 and 1.54 mg/kg early in pregnancy had no effect in mice (Odenbro & Kihlstrom, 1977).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS78-00-2 (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: Tetraethyllead
    b) Carcinogen Rating: 3
    1) 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.
    3.21.2) SUMMARY/HUMAN
    A) Not known to be a human carcinogen. TEL has been implicated, but not proven as a carcinogen. Epidemiological studies of persons exposed to TEL have reported a possible slight excess of skin cancers and myelomas. These results have not been confirmed by other studies.
    3.21.3) HUMAN STUDIES
    A) HUMANS
    1) Epidemiological studies of persons exposed to TEL have reported a possible slight excess of skin cancers (IARC, 1973) and myelomas (Haring, 1981). These results have not been confirmed by other studies.
    2) In a case-control study of tetraethyl lead workers covering the period 1956 to 1987, there was a strong dose-dependent association with colorectal cancer. Exposures were estimated relative to the entire TEL manufacturing process, and would have involved both organic and inorganic lead. Evidence for causality from any lead compound was not compelling, however (Fayerweather et al, 1997).
    3) In a 20-year retrospective study of 592 workers, there was no increased prevalence of cancer (Robinson, 1974); however, this study has been criticized because workers who had left employment were not included (Grandjean, 1984).
    3.21.4) ANIMAL STUDIES
    A) ANIMAL STUDIES
    1) In a chronic exposure study where TEL was injected subcutaneously in mice, there was a low incidence of lymphomas (Epstein & Mantel, 1968). These were a normally occurring type of tumor and did not appear earlier than expected. IARC could not evaluate this study and concluded that further studies are needed before any conclusions can be reached about the potential carcinogenicity of TEL (IARC, 1973).

Heent

    3.4.3) EYES
    A) NYSTAGMUS has been reported following acute exposures.
    1) CASE REPORT - Rotary nystagmus and limited upward gaze were reported in a fatally poisoned child (Grant, 1986).
    2) CASE REPORT - Horizontal nystagmus was described in a 19-year-old man who chronically abused leaded gasoline (Edminster & Bayer, 1985).
    3) INCIDENCE - Horizontal nystagmus was reported in 6 of 20 (30%) patients admitted for chronic gasoline sniffing in one series (Goodheart & Dunne, 1994).
    B) IMPAIRED VISION has been reported following toxic exposures.
    1) CASE SERIES - Visual impairment thought to be associated with a weakness of the extrinsic eye muscles developed in 9 of 78 patients exposed to tetraethyl lead (Grant, 1986).
    2) CASE REPORT - Acute visual loss was reported in one patient with chronic dermal contact with gasoline containing tetraethyl lead (Grant, 1986).
    C) AMBLYOPIA has been reported.
    1) CASE REPORT - Amblyopia was reported in a man who washed his upper body daily with gasoline (Grant, 1986).
    D) BLEPHAROSPASM has been reported in animal studies.
    1) Gasoline containing TEL was applied to the eyes of rabbits which caused pain and blepharospasm. With repeat application no damage to the conjunctiva or cornea was reported (Grant, 1986).
    E) IRRITATION may occur following contact with tetraethyl lead dust.
    1) The dust, when in contact with moist skin or ocular membranes, may cause itching, burning, and transient redness. Eye irritation may occur with acute exposure (Sittig, 1985) HSDB, 2000).
    3.4.4) EARS
    A) TINNITUS was reported following inhalation of TEL fumes (Daniels & Latcham, 1984).
    3.4.6) THROAT
    A) Moderate exposures have been reported to cause a feather-like feeling in the throat (He, 1999).

Cardiovascular

    3.5.1) SUMMARY
    A) Hypotension and bradycardia have been reported.
    3.5.2) CLINICAL EFFECTS
    A) BRADYCARDIA
    1) Bradycardia was reported as a nonspecific finding of acute exposure (Ross, 1982) HSDB, 2000).
    B) HYPOTENSIVE EPISODE
    1) Hypotension was reported as a symptom of acute exposure (Hathaway et al, 1996) HSDB, 2000).

Respiratory

    3.6.1) SUMMARY
    A) Inhalation of TEL vapors can be fatal. Upper respiratory tract irritation and sneezing may follow dust exposure. Irregular respirations are a non-specific finding.
    3.6.2) CLINICAL EFFECTS
    A) TOXIC EFFECT OF GAS, FUMES AND/OR VAPORS
    1) ACUTE TOXICITY
    a) Inhalation of TEL vapors are very toxic and fatal lead poisoning may occur via vapor inhalation (HSDB, 2000).
    B) IRRITATION SYMPTOM
    1) The decomposition products of tetraethyl lead (i.e., mono-, di- and triethyl lead compounds), in dust form, may be inhaled and result in irritation of the upper respiratory tract and possibly paroxysmal sneezing (Sittig, 1985).
    C) RESPIRATORY SYMPTOM
    1) IRREGULAR RESPIRATIONS were reported as a nonspecific finding (Ross, 1982).
    D) PNEUMONIA
    1) CHRONIC TOXICITY
    a) Pneumonia may develop in patients who chronically inhale gasoline.
    b) CASE SERIES - In a series of 25 patients admitted for abuse of leaded gasoline, 8 (32%) developed pneumonia (Goodheart & Dunne, 1994).
    c) CASE SERIES - In another series of 70 patients who abused gasoline aspiration pneumonia occurred in about half and 21 (30%) required intubation and ventilation (Currle et al, 1994). Seven patients died of septic complications, most related to aspiration pneumonia.
    d) It was postulated that these patients are predisposed to aspiration by a combination of the encephalopathy, poor coordination of swallowing reflexes, and increased oral secretions.

Neurologic

    3.7.1) SUMMARY
    A) Clinical neurologic effects of TEL intoxication can be divided into MILD, MODERATE, and SEVERE. They usually occur within 1 to 5 days, or as long as 14 days post exposure.
    B) MILD - Anxiety, irritability, insomnia, lurid dreams, anorexia, metallic taste, dizziness, pallor, lassitude, tremor, incoordination, and cerebellar ataxia.
    C) MODERATE - Disorientation, hyperexcitability, hyperreflexia, and lurid dreams, tremors, and chorea.
    D) SEVERE - Delusions, hallucinations, mania, seizures, cerebral edema, coma, and death.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) Acute effects of gasoline sniffing include the following CNS symptoms: insomnia, nightmares, delirium, nervous irritability, restlessness, tremor, euphoria, lethargy, slurred speech, disorientation, hallucinations, seizures and coma (Boeckx et al, 1977) CDC, 1985; HSDB, 2000).
    B) LETHARGY
    1) CNS depression may develop after ACUTE or CHRONIC gasoline sniffing.
    2) INCIDENCE - In a series of 20 patients who chronically abused leaded gasoline, one patient was described as drowsy and 7 (35%) developed stupor or coma on admission (Goodheart & Dunne, 1994).
    C) CHOREOATHETOSIS
    1) Choreoathetoid motions have been reported in acute poisonings with involvement including arms, extensor tendons of the feet, facial muscles, and hands (Ross, 1982). It may also occur following chronic exposure(Goodheart & Dunne, 1994).
    2) INCIDENCE - In a series of 20 patients who chronically abused leaded gasoline, 8 (40%) developed choreoathetosis (Goodheart & Dunne, 1994).
    D) TOXIC ENCEPHALOPATHY
    1) Chronic tetraethyl lead exposure causes a pronounced encephalopathy. It is most commonly seen in the setting of inhalational abuse of leaded gasoline, so the contribution of other constituents is difficult to assess.
    2) MILD effects include anxiety, irritability, insomnia, lurid dreams, anorexia, nausea, vomiting, metallic taste, tremulousness, lack of coordination, and truncal ataxia (Wu & He, 1965; Hathaway et al, 1996).
    3) MODERATE effects include disorientation, hyperexcitability (hypomania), tremors, twitching, chorea, increased reflexes, limited upward gaze, and rotary or horizontal nystagmus (Hathaway et al, 1996).
    4) SEVERE effects include delusions, hallucinations, mania, decreased peripheral nerve conduction velocity, seizures, cerebral edema, coma, and death (Proctor & Hughes, 1978). These episodes may suddenly convert to maniacal or violent convulsive seizures which can end in coma and death (Hathaway et al, 1996).
    5) ONSET - early symptoms include anorexia, mood disturbances, and intermittent vomiting (Tenenbein, 1997).
    6) RISK FACTORS - Young children are at a greater risk of developing significant encephalopathy following exposure; it is rare in older children and adults (Tenenbein, 1997).
    7) RECOVERY - A group of 29 patients who chronically inhaled leaded gasoline, 6 of whom had a history of lead encephalopathy, underwent extensive neurologic and cognitive evaluation while actively abusing gasoline and then reevaluated two years after complete abstinence from gasoline sniffing(Cairney et al, 2005). Blood lead levels improved, and neurobehavioral abnormalities improved or normalized completely. Individuals with more severe baseline neurobehavioral abnormalities showed the greatest improvement but were less likely to show complete reversal of toxic effects.
    E) SEIZURE
    1) Coulehan et al (1983) reported 4 of 23 patients had seizures related to gasoline sniffing(Coulehan et al, 1983).
    2) INCIDENCE - In a series of 20 patients who chronically abused leaded gasoline, 14 (70%) had tonic clonic seizures, and 3 developed status epilepticus (Goodheart & Dunne, 1994a).
    F) PSYCHOTIC DISORDER
    1) Toxic psychosis is common in patients who chronically abuse leaded gasoline. Effects include delusions, paranoia and visual, auditory and tactile hallucinations (Edminster & Bayer, 1985; McCracken, 1987; Moss & Cooper, 1986)(McGrath, 1986; Parker, 1993).
    2) Disorientation, fear, hallucinations, mania, and toxic psychosis developed in industrial workers exposed to TEL in high airborne concentrations (Coulehan et al, 1983; Daniels & Latcham, 1984).
    3) Unlike other solvent abuse, acute and persistent organic psychosis is a feature of TEL exposure (Tenenbein, 1997).
    4) INCIDENCE - In a series of 20 patients who chronically abused leaded gasoline, 12 (60%) had manifestations of delirium (Goodheart & Dunne, 1994). Up until the early and mid 1990's leaded gasoline "sniffing" was a common cause of TEL exposure among native peoples of North America and Canada (Tenenbein, 1997)(Fortenberry, 1985).
    G) TREMOR
    1) Tremor is common in patients who chronically inhale leaded gasoline(Edminster & Bayer, 1985) (McGrath, 1986).
    2) INCIDENCE - In a series of 20 patients who chronically abused leaded gasoline, 4 (20%) had intention tremors(Goodheart & Dunne, 1994) .
    H) MYOCLONUS
    1) INCIDENCE - In a series of 20 patients who chronically abused leaded gasoline, 9 (45%) had myoclonus (Goodheart & Dunne, 1994).
    I) ATAXIA
    1) Ataxia is common in patients who chronically abuse leaded gasoline (Edminster & Bayer, 1985)(McGrath, 1986).
    2) INCIDENCE - In a series of 20 patients who chronically abused leaded gasoline, 13 (65%) had truncal or appendicular ataxia (Goodheart & Dunne, 1994).
    J) HYPERREFLEXIA
    1) Hyperreflexia and clonus are common in chronic gasoline sniffers (Edminster & Bayer, 1985; Moss & Cooper, 1986).
    2) INCIDENCE - In a series of 20 patients who chronically abused leaded gasoline, 12 (60%) developed hyperreflexia (Goodheart & Dunne, 1994).
    K) NEUROPATHY
    1) No defects in sensation were reported in a study of 50 patients who had been sniffing leaded gasoline (Seshia et al, 1978). Peripheral neuropathy is a rare event (Tenenbein, 1997).

Gastrointestinal

    3.8.1) SUMMARY
    A) TEL intoxication usually lacks the common GI manifestations of inorganic lead intoxication. Anorexia, nausea, vomiting, diarrhea and weight loss have been seen after acute exposure.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA, VOMITING AND DIARRHEA
    1) Anorexia, nausea, vomiting, weight loss, and diarrhea have been reported after acute exposure (Boeckx et al, 1977) CDC, 1985; (Hathaway et al, 1996) HSDB, 2000).
    B) CHRONIC POISONING
    1) TASTE PERVERSION
    a) Dysgeusia (metallic taste) may develop with chronic exposure (Proctor & Hughes, 1978).

Hepatic

    3.9.1) SUMMARY
    A) Elevated liver enzymes may occur.
    3.9.2) CLINICAL EFFECTS
    A) LIVER DAMAGE
    1) Elevated liver enzymes have been reported in severe cases of exposure (Robinson, 1978).
    2) EXPOSURE LEVEL - Acute exposure to tetraethyl lead at blood lead levels of 1200 to 1400 mcg/L produced hepatic damage in 50% adolescents exposed (HSDB, 2000).
    3) CHRONIC TOXICITY
    a) INCIDENCE - In 12 patients who chronically abused leaded gasoline who had liver function tests performed, 8 (67%) had evidence of mild hepatocellular dysfunction (Goodheart & Dunne, 1994).

Genitourinary

    3.10.1) SUMMARY
    A) Renal damage has been reported following acute exposure; urinary retention has occurred infrequently.
    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) EXPOSURE LEVEL - Acute exposure to tetraethyl lead at blood lead levels of 1200 to 1400 mcg/L produced renal damage in 50% adolescents exposed (HSDB, 2000).
    B) RETENTION OF URINE
    1) Urinary retention was reported in a single patient (Ross, 1982).

Hematologic

    3.13.1) SUMMARY
    A) Anemia, basophilic stippling, and neutrophilia may occur.
    3.13.2) CLINICAL EFFECTS
    A) TOXIC EFFECT OF HEAVY METAL
    1) INORGANIC LEAD - Hepatic metabolism rapidly oxidized TEL to triethyl lead, and more slowly to inorganic lead. Thus, chronic exposures may present the usual problems of inorganic lead exposure. However, in more moderate/acute exposures, excretion of AMINOLEVULINIC ACID (ALA) and erythrocyte protoporphyrin (EP) are NOT altered (Gutniak et al, 1964).
    B) ANEMIA
    1) CASE SERIES - On admission 14 of 23 patients were noted to be anemic with a hematocrit less than 35%, and only 3 of 14 had basophilic stippling of RBC's (Coulehan et al, 1983).
    C) LEUKOPENIA
    1) Transient neutrophilia was reported as a nonspecific finding (Ross, 1982).
    D) BASOPHILIC STIPPLING
    1) BASOPHILIC STIPPLING may be noted (Hansen & Sharp, 1978).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) The blood lead level provides one measure of INORGANIC lead burden which does not necessarily reflect organic lead burden. The normal upper limit is 10 mcg/dL. Inorganic lead levels correlate with CNS signs after chronic exposure.
    B) Metabolic substrates in heme synthesis (ALAD, EP or ZnPP, coprophyrin) may or may not rise after prolonged exposure and are not a reliable test in diagnosis or assessment of severity.
    C) Monitor liver function tests, renal function tests, and hematologic parameters.
    D) The ability to penetrate skin makes reliance on airborne concentrations impractical (Hathaway et al, 1996).
    E) An analysis of the urinary concentration of lead is helpful in evaluating the amount of TEL absorbed during chronic exposure (Hathaway et al, 1996). Urinary lead concentrations are not helpful after acute exposures (He, 1999).
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) In cases of tetraethyl lead intoxication in humans, urinary lead levels are not high. Whole blood lead levels may be normal or only slightly raised (IARC, 1973).
    2) Obtain a blood lead level (BLL) if chronic use is suspected. Because metabolism of TEL takes weeks, lead levels would not be expected to rise acutely. BLL correlates less well with TEL intoxication than with inorganic lead intoxication. Blood lead, however, probably represents the treatable fraction. BLL may be a better predictor of clinical intoxication (Beattie et al, 1972).
    a) Patients with blood lead in excess of 45 mcg/dL should be treated with chelation, and levels in excess of 80 mcg/dL require immediate hospitalization and chelation (CDC, 1991).
    3) Lead in the lipid fraction of the blood was elevated three-fold more than total blood lead following TEL exposure (Beattie et al, 1972). This may be useful in determining the source of elevated lead levels.
    4) An elevated EP or ZnPP (in the absence of other causes such as iron deficiency anemia, sickle cell anemia, certain hemoglobinopathies, etc.) indicates excess absorption of TEL. Because of the slow conversion of TEL to the inorganic (ionic) form, the finding of a normal EP level does not rule out the possibility of excess TEL absorption.
    5) Metabolic substrates in heme synthesis (ALAD, EP or ZnPP), may or may not rise after prolonged exposure and are not a reliable test in diagnosis or assessment of severity.
    6) Abnormal liver function tests, renal function tests and hematologic parameters are seen in severe cases (Robinson, 1978).
    B) HEMATOLOGIC
    1) Abnormal hematologic parameters are seen in severe cases (Robinson, 1978).
    4.1.3) URINE
    A) URINARY LEVELS
    1) An analysis of the urinary concentration of lead is helpful in determining the amount absorbed from chronic exposure (Hathaway et al, 1996). Urinary lead concentrations do not correlate with acute exposures (He, 1999).
    2) Urinary lead levels rarely exceeded 180 mcg/L in 592 TEL workers with a mean exposure time of 18 years (Robinson, 1974). Levels greater than 150 mcg/L (corrected to a specific gravity of 1.024) are indicative of a severe degree of absorption and if it exceeds 180 mcg/L in a worker they should be removed from exposure (Hathaway et al, 1996). Poisoning is associated with levels of 300 mcg/L or more (Hathaway et al, 1996).
    3) Flemming reported urinary lead of 0 to 140 mcg/L among 60 "normal salesmen" compared to 200 to 1200 mcg/L in 11 TEL workmen with clinical evidence of intoxication (Fleming, 1964).
    4) Diethyl lead in urine was a good indicator of occupational exposure to tetraethyl lead, but total urinary lead was not (Zhang et al, 1994; Hathaway et al, 1996).

Radiographic Studies

    A) CT of the head is indicated prior to lumbar puncture in patients with increased possibility of intracranial mass lesion or elevated cerebrospinal fluid pressure. Especially consider CT of the head in patients with dilated or poorly reactive pupils, papilledema, ocular palsies, focal neurologic signs, recent history of focal seizures, precipitous decrease in level of consciousness, bradycardia, irregular respirations, tonic seizures, diagnosis of CNS immunosuppression (toxoplasma encephalitis or lymphoma), and decerebrate or decorticate posture (Hasbun, et al, 2001; (Steigbigel, 2001).
    B) Withhold spinal tap until status of intracranial pressure has been fully evaluated. Consider intracranial pressure probe.

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) Total lead in the blood is assayed by the usual methods for inorganic lead poisoning, including atomic absorption spectrometry, flame ionization spectroscopy and anodic stripping voltametry.
    2) Organic lead compounds enter lipid portions of the blood. Organic extraction of blood prior to assay for lead reveals this difference in partition (Bligh & Dyer, 1959).
    3) A method for the direct measurement of tetramethyl lead in blood has been published (Andersson et al, 1984).
    4) 4. Tibial lead levels can be measured by X-Ray Fluorescence (Tessler et al, 2001).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) The blood lead level provides one measure of INORGANIC lead burden which does not necessarily reflect organic lead burden. The normal upper limit is 10 mcg/dL. Inorganic lead levels correlate with CNS signs after chronic exposure.
    B) Metabolic substrates in heme synthesis (ALAD, EP or ZnPP, coprophyrin) may or may not rise after prolonged exposure and are not a reliable test in diagnosis or assessment of severity.
    C) Monitor liver function tests, renal function tests, and hematologic parameters.
    D) The ability to penetrate skin makes reliance on airborne concentrations impractical (Hathaway et al, 1996).
    E) An analysis of the urinary concentration of lead is helpful in evaluating the amount of TEL absorbed during chronic exposure (Hathaway et al, 1996). Urinary lead concentrations are not helpful after acute exposures (He, 1999).

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Prehospital use of activated charcoal or emesis is not recommended following ingestion of leaded gasoline or other products containing organolead compounds because of the potential for CNS depression, seizures, and aspiration of the hydrocarbon vehicle.
    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression and seizures.
    B) NASOGASTRIC SUCTION
    1) If large amounts are ingested, consider placing a nasogastric tube to suction stomach contents. This should be preceded by endotracheal intubation in cases of ingestion of large amounts of leaded gasoline or other similar products when CNS depression is present.
    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) GENERAL TREATMENT
    1) Treatment should include recommendations listed in the INHALATIONAL EXPOSURE section where appropriate.

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) DISORDER OF BRAIN
    1) Lead encephalopathy is a medical emergency. Patient should be hospitalized in an intensive care setting. Prompt neurosurgical and toxicological consultation should be obtained to assist in management.
    B) CEREBRAL EDEMA
    1) CLINICAL IMPLICATIONS
    a) Cerebral edema and elevated intracranial pressure (ICP) may occur. Emergent management includes head elevation and administration of mannitol; hyperventilation should be performed if there is evidence of impending herniation.
    2) MONITORING
    a) Patients will usually require endotracheal intubation and mechanical ventilation. Monitor intracranial pressure, cerebral perfusion pressure and cerebral blood flow.
    3) TREATMENT
    a) Most information on the treatment of cerebral edema is derived from studies of traumatic brain injury.
    4) MANNITOL
    a) ADULT/PEDIATRIC DOSE: 0.25 to 1 gram/kilogram intravenously over 10 to 15 minutes (None Listed, 2000).
    b) AVAILABLE FORMS: Mannitol injection (5%, 10%, 15%, 20%, 25%).
    c) MAJOR ADVERSE REACTIONS: Congestive heart failure, hypernatremia, hyponatremia, hyperkalemia, renal failure, pulmonary edema, and allergic reactions.
    d) PRECAUTIONS: Contraindicated in well-established anuria or impaired renal function not responding to a test dose, pulmonary edema, CHF, severe dehydration; caution in progressive oliguria and azotemia. Do not add to whole blood for transfusions; enhanced neuromuscular blockade has occurred with tubocurarine. Keep serum osmolarity below 320 mOsm.
    e) MONITORING PARAMETERS: Renal function, urine output, fluid balance, serum potassium levels, serum osmolarity, and CVP.
    5) HYPERTONIC SALINE
    a) Preliminary studies suggest that hypertonic saline (7.5% saline/6% dextran) 100 ml reduced ICP more effectively than 200 mL of 20% mannitol in adults with elevated ICP after traumatic brain injury(Battison et al, 2005).
    6) ELEVATION
    a) Elevation of the head of the bed to approximately 30 degrees decreases ICP and improves cerebral perfusion pressure (Meixensberger et al, 1997; Schneider et al, 1993; Feldman et al, 1992).
    7) MECHANICAL DECOMPRESSION
    a) Early surgical decompression, ventriculostomy with CSF drainage, or craniectomy may be useful in patients with persistent elevation of ICP (Sahuquillo & Arikan, 2006; Sakai et al, 1998; Polin et al, 1997; Taylor et al, 2001). Most experience with these modalities has been in patients with traumatic brain injury.
    8) HYPERVENTILATION
    a) SUMMARY: Hyperventilation has been associated with adverse outcomes and should not be performed routinely (Muizelaar et al, 1991). It is indicated in patients who have clinical evidence of herniation or if there is intracranial hypertension refractory to sedation, paralysis, CSF drainage and osmotic diuretics (None Listed, 2000a).
    b) RECOMMENDATION:
    1) The PCO2 must be controlled in the range of 25 torr; further lowering of PCO2 may create undesirable effects secondary to local tissue hypoxia.
    2) End-tidal CO2 tension, correlated with an initial ABG measurement, provides a noninvasive means of monitoring PCO2 (Mackersie & Karagianes, 1990).
    3) Most authorities advise that hyperventilation should be considered a temporizing measure only; SUSTAINED hyperventilation should be avoided (Am Acad Neurol, 1997; Bullock et al, 1996; Kirkpatrick, 1997).
    9) DEXAMETHASONE - There is controversy in the literature as to whether dexamethasone is an effective treatment for cerebral edema that is induced by other mechanisms than malignancy and as to the appropriate dose.
    a) LOW DOSE - 16 milligrams/day in divided doses (De Los Reyes et al, 1981).
    b) HIGH DOSES - 1 to 2 milligrams/kilogram/day in divided doses (Heinemeyer, 1987).
    c) Or by other appropriate methods.
    C) 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).
    D) CHELATION THERAPY
    1) CONTROVERSY - Strong differences of opinion exist as to the appropriateness of chelation therapy in exposure to organolead compounds, especially in a symptomatic patient.
    a) Its been suggested that supportive care is the primary therapy in the treatment of physical effects. In most individuals symptoms will improve over several weeks to months, but in some cases neurological damage is irreversible (Tenenbein, 1997).
    2) RECOMMENDATIONS
    a) Chelation therapy is not indicated in patients with acute toxicity only because chelators cannot chelate organic lead because potential ligands are covalently bound by the ethyl groups (Personal Communication, 1991). In one report, chelation therapy for acute TEL encephalopathy did not improve neurological symptoms (He, 1999).
    b) An elevated blood lead probably reflects largely inorganic lead and the presence of lead encephalopathy indicates chelation. Chelation should also be considered in children with blood lead level above 45 mcg/dL and symptomatic adults.
    3) CASE REPORTS
    a) Although generally discouraged in several handbooks and textbooks, experience with industrial exposure (Beattie et al, 1972), a severely poisoned 15-year-old (Robinson, 1978), and a 27-year-old heavy gasoline sniffer (Hansen & Sharp, 1978), demonstrated increased lead excretion with chelation.
    b) Several other case reports and two large case series have demonstrated increased urinary lead excretion and declining blood lead levels with clinical improvement associated with chelation therapy (Edminster & Bayer, 1985; McCracken, 1987; Goodheart & Dunne, 1994; Moss & Cooper, 1986)(McGrath, 1986; Currie et al, 1994).
    E) PROCEDURE EDUCATION
    1) CHILDREN - Chelation therapy is indicated in children with blood lead levels greater than 45 micrograms/deciliter or if signs and symptoms of lead encephalopathy are noted (CDC, 1991).
    2) ADULTS - Chelation should also be considered in symptomatic adults.
    F) DIMERCAPROL
    1) SUMMARY - British-Anti-Lewisite (BAL) or dimercaprol is a small-molecule drug which will cross into cells and prevent the worsening of clinical and biochemical status on the first day of EDTA therapy (Chisolm, 1971).
    2) INDICATIONS - BAL in conjunction with Calcium EDTA is recommended if evidence of encephalopathy exists, or if blood lead levels are higher than 100 mcg/dL in children, or the inability to tolerate oral medications in adults (Dart et al, 2000).
    a) CONTRAINDICATIONS - BAL should NOT be used in adults or children who have an allergy to peanuts or peanut products or if evidence of hepatic dysfunction is present (CDC, 1991; Dart et al, 2000). BAL may also cause hemolysis in patients with glucose-6-phosphate dehydrogenase deficiency (Dart et al, 2000).
    3) DOSE
    a) ADULT: 3 to 5 milligrams/kilogram/dose by deep intramuscular (IM) injection every 4 to 6 hours, then tapered over 1 to 2 days to intervals of every 6 to 12 hours until an oral antidote can be tolerated (Dart et al, 2000).
    b) CHILD: 2.5 to 5 milligrams/kilogram by deep IM dose every 4 to 6 hours or 75 milligrams/square meter IM every 4 hours. Taper the dose over 1 to 2 days to an interval of every 6 to 12 hours until an oral antidote can be tolerated. Discontinue after 5 days; sooner if adverse effects develop (Dart et al, 2000).
    4) ADVERSE EFFECTS - Include headache, tachycardia, nausea, vomiting and pain at the injection site, urticaria, pyrexia, and hypertension (Dart et al, 2000). Treat side effects with antihistamines or cessation of drug.
    G) EDETATE CALCIUM DISODIUM
    1) SUMMARY - The most efficient parenteral chelating agent is calcium disodium ethylene diamine tetraacetic acid (edathamil, EDTA, or CaVersinate).
    2) INDICATIONS - CaNa2EDTA is recommended in conjunction with BAL if evidence of severe lead toxicity with encephalopathy in a child or an adult, if blood lead levels are less than 100 mcg/dL (defined as severe lead poisoning) in children, or if protracted vomiting necessitates parenteral therapy (Dart et al, 2000).
    a) CHILDREN - Only calcium disodium EDTA, not disodium edetate, may be used in children. Disodium edetate may induce tetany and possibly fatal hypocalcemia (CDC, 1991).
    3) PREPARATION - Dilute to less than 0.5 percent solution in dextrose or normal saline. Infuse intravenously slowly over 15 to 20 minutes or by continuous infusion over 6 hours.
    4) DOSE - Calculate dosage on weight or body surface area. In encephalopathy the dose is larger than for all other therapy. There is no proven difference between intramuscular administration, and intravenous therapy given in 4 to 24 hours.
    a) ADULTS: BAL therapy should be initiated first; then give EDTA as 1500 milligrams/square meter/day as a continuous infusion over 24 hours (Dart et al, 2000).
    b) CHILDREN
    1) Lead poisoning without CNS toxicity: a continuous infusion of 1000 milligrams/square meter/day over 24 hours or divided every 8 to 12 hours. Therapy is continued for 5 days, then interrupted for 2 days to evaluate the need for further chelation therapy. Blood lead levels are evaluated every few days after the cessation of therapy until levels are stabilized; chelation may need to be repeated if rebound occurs. Maximum daily dose 50 milligrams/kilogram/day (Dart et al, 2000).
    2) CNS effects present: Initiate BAL therapy first then a continuous infusion of EDTA at 1500 milligrams/square meter/day is given over 24 hours. Maximum daily dose should NOT exceed 75 milligrams/kilogram/day (Dart et al, 2000).
    5) ADVERSE EFFECTS - Toxicity of EDTA is due to 1) renal tubular injury and 2) chelation of other metals. Acute tubular necrosis may occur with a frequency as high as 3/100 cases. It is not directly related to the concentration of lead, nor to the route of administration. EDTA therapy can also result in redistribution of lead to the brain; therefore, BAL is recommended prior to EDTA therapy (Dart et al, 2000).
    a) It is dose related and recommended doses should not be exceeded. Cessation of therapy will usually lead to recovery. EDTA chelates zinc.
    b) While serum zinc returns rapidly to normal, some administer zinc after therapy. EDTA removes iron. If iron stores are marginal or questionable, or ferritin is low, administer iron after therapy.
    6) REBOUND - If the blood lead level rebounds to its pretreatment level or is greater than 50 micrograms/deciliter a repeat course of chelation should be considered.
    7) PRECAUTIONS - Calcium EDTA should only be administered after adequate urine flow is established (Chisolm, 1971). If urine flow has NOT been established in a symptomatic child after 3 hours of fluids, administer the EDTA and initiate simultaneous hemodialysis to remove the EDTA-Pb complex which is nephrotoxic.
    a) Up to 16% of children receiving calcium EDTA and BAL for lead poisoning may develop a nephrotoxic reaction(Moel & Kumar, 1982). At least every other day urinalysis and serum creatinine are recommended.
    8) INTERNAL REDISTRIBUTION - In a rat model of chronic low-level lead exposure, single dose calcium disodium edetate increased urine, brain, and hepatic lead levels and decreased blood and renal lead levels (Cory-Slechta, 1988).
    a) Brain lead level increased by 100 percent over control suggesting concerns about the safety of calcium disodium edetate mobilization test (Chisolm, 1987).
    b) Five daily injections of calcium disodium edetate in rats showed no net loss in brain, hepatic, and bone lead compared with controls (Cory-Slechta, 1988).
    H) SUCCIMER
    1) EFFICACY
    a) It is the preferred treatment in children with blood lead levels higher than 45 mcg/dL and less than 100 mcg/dL without evidence of encephalopathy. It may also be used in children with BLL of 25 to 45 mcg/dL in many healthcare centers, but the precise use is variable (Dart et al, 2000).
    b) ANIMAL DATA - It has been shown to be an effective chelator of lead in rats (Graziano et al, 1978; Kapoor et al, 1989), lead-poisoned workers (Friedheim et al, 1978; Graziano et al, 1985), a patient poisoned with lead contaminated bread (Bentur et al, 1987), children (Graziano et al, 1986; Graziano et al, 1988), and 9 adult lead-poisoned patients (Fournier et al, 1988).
    c) Succimer decreased blood lead concentrations by 35 to 81 percent and induced a 4.5- to 16.9-fold increase in mean daily urinary excretion of lead in a study of 9 adult lead-poisoned patients treated with a dose of 30 milligrams/kilogram/day of DMSA for 5 days (Fournier et al, 1988).
    d) DMSA was reported to be equally efficacious as Calcium EDTA in a 45-year-old man with lead toxicity (Thomas & Ashton, 1991).
    2) SUCCIMER/DOSE/ADMINISTRATION
    a) PEDIATRIC: Initial dose is 10 mg/kg or 350 mg/m(2) orally every 8 hours for 5 days (Prod Info CHEMET(R) oral capsules, 2011).
    1) The dosing interval is then increased to every 12 hours for the next 14 days. A repeat course may be given if indicated by elevated blood levels. A minimum of 2 weeks between courses is recommended, unless blood lead concentrations indicate the need for prompt retreatment.
    2) Succimer capsule contents may be administered mixed in a small amount of food (Prod Info CHEMET(R) oral capsules, 2011).
    b) ADULT: Succimer is not FDA approved for use in adults, however it has been shown to be safe and effective when used to treat adults with poisoning from a variety of heavy metals (Fournier et al, 1988a). Initial dose is 10 mg/kg or 350 mg/m(2) orally every 8 hours for 5 days (Prod Info CHEMET(R) oral capsules, 2011).
    1) The dosing interval then is increased to every 12 hours for the next 14 days. A repeat course may be given if indicated by elevated blood levels. A minimum of 2 weeks between courses is recommended, unless the patient's symptoms or blood concentrations indicate a need for more prompt treatment (Prod Info CHEMET(R) oral capsules, 2011).
    3) MONITORING PARAMETERS
    a) The manufacturer recommends monitoring liver enzymes and complete blood count with differential and platelet count prior to the start of therapy and at least weekly during therapy (Prod Info CHEMET(R) oral capsules, 2011).
    b) Succimer therapy did not worsen preexisting borderline abnormal liver enzyme levels in a prospective evaluation of 15 children with lead poisoning (Kuntzelman & Angle, 1992).
    4) ADVERSE EFFECTS
    a) SUCCIMER/ADVERSE EFFECTS: The following adverse events have occurred in children and adults during clinical trials: nausea, vomiting and diarrhea; transient liver enzyme elevations; rash, pruritus; drowsiness and paresthesia. Events reported infrequently include: sore throat, rhinorrhea, mucosal vesicular eruption, thrombocytosis, eosinophilia, and mild to moderate neutropenia (Prod Info CHEMET(R) oral capsules, 2011).
    b) ODOR: Succimer has a sulfurous odor that may be evident in the patient's breath or urine (Prod Info CHEMET(R) oral capsules, 2005).
    c) HYPERTHERMIA: One adult developed acute severe hyperthermia associated with hypotension; rechallenge resulted in hyperthermia with shaking chills and hypertension (Marcus et al, 1991).
    d) AVAILABLE FORMS: Succimer (Chemet (R)), 100 mg capsules (Prod Info CHEMET(R) oral capsules, 2011).
    5) Outside the US, DMSA has been used in adult patients (without evidence of acute encephalopathy) with chronic TEL exposure. The interval DMSA oral regimen was 0.5 gram three times a day for three days with four days between each three-day treatment period. Repeated courses were given depending on results of urinary lead measurements (Ding & Liang, 1991; He, 1999) Task Group, 1988).
    I) PENICILLAMINE
    1) SUMMARY - Can be used orally as outpatient chelation therapy when the exposure has ceased. Due to lesser efficacy and increased adverse reactions and precautions, succimer is the drug of choice when oral therapy is indicated.
    a) DOSE - ADULTS: 250 milligrams four times a day orally for up to 5 days for long-term therapy; do not exceed 40 milligrams/kilogram/24 hours. CHILD: 20 to 30 milligrams/kilogram/day orally. Administer on an empty stomach with orange juice or applesauce. For treatment in children with blood lead levels of 30 micrograms/deciliter or less, 15 to 30 milligrams/kilogram were administered daily (Shannon et al, 1989a).
    2) ADVERSE EFFECTS
    a) Adverse effects in children receiving D-penicillamine include eosinophilia, leukopenia, thrombocytopenia, elevations of blood urea nitrogen, proteinuria, microscopic hematuria, incontinence, abdominal pain and upset, urticarial eruptions, and erythema multiforme (Marcus, 1982) Shannon et al, 1989; (Sue et al, 1991).
    b) Rashes: Urticaria, toxic erythema, erythema multiforme, and a "ampicillin" type rash. All but the last require cessation of therapy.
    c) Neutropenia: Requires a neutrophil count on a biweekly basis as continued therapy with a neutropenic response may result in aplastic anemia.
    d) Eosinophilia commonly occurs in the first to third week of therapy though usually of little consequence.
    e) CHRONIC - Chronic administration (weeks to months) of penicillamine is associated with a high incidence of adverse reactions including proteinuria, thrombocytopenia, leukopenia, pruritic mucocutaneous rash and gastrointestinal intolerance (Halverson et al, 1978)
    f) PREGNANCY - Penicillamine can cause congenital tissue defects when used throughout pregnancy (Linares et al, 1979; Solomon et al, 1977; Anon, 1981). However, the teratogenic effect when used in low doses or for short periods of time such as in metal chelation has yet to be determined.
    J) UNITHIOL
    1) 2,3-Dimercaptopropane-1-sulfonate (DMPS) is a promising experimental drug which will be available in some centers (Chisolm & Thomas, 1985).
    2) Adverse effects in a series of 23 cases included 2 cases of erythema multiforme requiring steroids and a severe maculopapular rash developing after completion of therapy (Hla et al, 1992).
    K) AIRWAY MANAGEMENT
    1) Because of the high incidence of aspiration pneumonia in patients who chronically abuse leaded gasoline, early aggressive airway management and careful pulmonary toilet are recommended (Currie et al, 1994).
    L) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

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).
    6.8.2) TREATMENT
    A) GENERAL TREATMENT
    1) Treatment should include recommendations listed in the INHALATIONAL EXPOSURE section where appropriate.
    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) GENERAL TREATMENT
    1) Treatment should include recommendations listed in the INHALATIONAL EXPOSURE section where appropriate.
    B) SKIN ABSORPTION
    1) There are no published cases where chelation has been required after dermal exposure.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Abstracts

Case Reports

    A) CHRONIC EFFECTS
    1) HISTORY - A 17-year-old Native American sniffed leaded gasoline intermittently for 10 years (every day or every other day for 3 to 4 weeks). Complaint was a 3 day history of dizziness, lack of coordination, dysarthria, and tremulousness.
    2) PHYSICAL EXAM - Patient was combative, and not oriented to time. There was deliberate speech, hyperreflexic deep tendon reflexes, truncal ataxia, and head tremor. Patient was unable to hold a cup, and was able to walk only with assistance.
    3) LABORATORY - BLL 96 mcg/dL; EP 223 mcg/dL.
    4) COURSE - Three tonic-clonic seizures were reported on day one of hospital course. Therapy improved behavior and ataxia, but slow mentation, slurred speech, and some ataxia remained.
    5) THERAPY - Diazepam for seizure control. EDTA 50 mg/kg/day for two 5-day courses, dimercaprol accompanied the first EDTA course. Patient was discharged on phenobarbital and penicillamine and lost to follow-up.
    B) ADULT
    1) HISTORY - A 47-year-old male cleaned a tank, which had contained leaded (1.4 g/L) fuel 25 years previously, between 12 and 6 days prior to admission. Complaint was restlessness, agitation, and insomnia of 7 days duration. Twenty-four hours prior to admission the patient had nausea, vomiting, constant abdominal pain, and weakness of the lower limbs.
    2) PHYSICAL EXAM - Vital signs, and the neurological exam were within normal limits.
    3) LABORATORY - BLL 80 mcg/dL, EP 49 mcg/dL, ALA dehydrase reduced. EEG: sharp focal activity.
    4) COURSE - Became moody and aggressive, but those symptoms waned and patient was considered normal within one month (Beattie et al, 1972).
    C) PEDIATRIC
    1) Gasoline sniffing (huffing) involving leaded gasoline was found in 59% of school children in Shamattawa, Manitoba (Boeckx et al, 1977). This group of Winnipeg physicians reported 3 juvenile deaths and more than 50 children and young adults with severe encephalopathy and lead levels exceeding 80 mcg/dL (Coodin & Boeckx, 1978); many severe cases have likewise been seen among Arizona Navajos with blood lead levels ranging from 60 to 140 mcg/dL (Colaiaco et al, 1981).

Range Of Toxicity

Summary

    A) TLV - 0.1 mg/m(3)
    B) Exposure to 100 mg/m(3) for 1 hr or longer periods at a lower rate results in an acute intoxication. Although TEL can cause toxicity through skin absorption, no reliable data exist to relate dermal dose to symptoms in humans.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) IN HUMANS - Absorption of only 1 gram of tetraethyl lead may be sufficient to cause death within 3 to 30 days. This is due to the slow degradation of tetraethyl lead to triethyl lead (Baselt, 2000).
    2) Industrial exposure has come primarily to workers cleaning tanks used in the storage of leaded gasoline. From 1923 to 1924, a number of severe cases of TEL poisoning occurred among the men engaged in its manufacture but this has been remarkably low and will drop as manufacturing of this compound declines. More than 100 cases of acute poisoning with 11 deaths were reported (Hamilton & Hardy, 1974).
    3) A case-control study of former workers in a plant manufacturing tetraethyl lead found a strong association to rectal cancer and cancers of the sigmoid colon (Bingham et al, 2001).
    4) IARC included tetraethyl with "LEAD AND ITS COMPOUNDS" in group 3, not classifiable as to its carcinogenicity to humans (Bingham et al, 2001).
    B) CASE REPORTS
    1) GASOLINE SNIFFING - Lead intoxication secondary to gasoline "sniffing" in 23 Navajo adolescents has been reported (Coulehan et al, 1983). Sixty-five percent of the patients first presented with toxic encephalopathy. One death occurred.
    C) ANIMAL DATA
    1) ACUTE
    a) Tetraethyl lead dissolved in tricaprylin was injected subcutaneously into Swiss mice on one to four occasions between birth and 21 days. After a single injection of 2 mg on the first day of life, all of 69 mice died before weaning (IARC, 1973).
    2) CHRONIC
    a) Dogs were exposed to tetraethyl lead at the following concentrations: 42 mg/m(3) (one dog), 22 mg/m(3) (one dog), and 12 mg/m(3) (two dogs). These animals died after 7, 30, 24, and 29 seven-hour exposures, respectively (ACGIH, 1991).
    b) Repeated exposures to sublethal doses were found to cause, in time, symptomatology similar to that seen after a single lethal exposure (ACGIH, 1991).

Maximum Tolerated Exposure

    A) ACUTE
    1) Chronic intoxication has not been observed and gradual onset of symptoms is felt to represent the onset of subacute poisoning.
    2) IN HUMANS -
    a) Exposure to tetraethyl lead at a concentration of 100 mg/m(3) as lead for 1 hour results in acute intoxication (ACGIH, 1991).
    b) In some adolescents with blood lead levels of 1200 to 1400 microgram per liter, renal and hepatic damage can result (HSDB , 2001).
    c) Tetraethyl lead is approximately 3 times more toxic than tetramethyl lead (HSDB , 2001).
    B) CHRONIC
    1) IN HUMANS - Tetraethyl lead causes a separate toxicologic symptom sign complex that overlaps with the initial acute toxic syndrome. The differences include symptomatology, effects on hemoglobin synthesis, and response to chelation therapy (HSDB , 2001).
    2) ANIMAL DATA -
    a) Tetraethyl lead was administered orally to rats over a period of 21 weeks at concentrations of 0.17 mg and at 0.0017 mg/kg five times per week for a total of 100 doses (ACGIH, 1991).
    b) All of the animals survived both exposures, and they showed no change in body weight.
    c) Histologic changes was observed in the liver, pancreas, renal, endocrine, and nervous systems.

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CONCENTRATION LEVEL
    a) Total blood lead concentrations in two persons who died following an inhalation exposure of tetraethyl lead vapor were 3.33 and 4.0 milligrams/liter (Baselt, 2000).
    b) Tetraethyl lead blood concentrations in the same two persons above were 0.15 and 2.43 milligrams/liter (Baselt, 2000).

Workplace Standards

    A) ACGIH TLV Values for CAS78-00-2 (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) Tetraethyl lead, as Pb
    a) TLV:
    1) TLV-TWA: 0.1 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: Skin
    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) 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
    d) Molecular Weight: 323.45
    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 CAS78-00-2 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Tetraethyl lead (as Pb)
    2) REL:
    a) TWA: 0.075 mg/m(3)
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: [skin]
    1) Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.
    f) Note(s):
    3) IDLH:
    a) IDLH: 40 mg Pb/m3
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS78-00-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Tetraethyl lead, as Pb
    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 Assessed under the IRIS program. ; Listed as: Tetraethyl lead
    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): 3 ; Listed as: Tetraethyllead
    a) 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.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Tetraethyl lead (as Pb)
    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 CAS78-00-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Tetraethyl lead (as Pb)
    2) Table Z-1 for Tetraethyl lead (as Pb):
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.075
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: Yes
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: CHRIS, 2001 ITI, 1995 OHM/TADS, 2001 RTECS, 2001
    1) LD50- (SUBCUTANEOUS)MOUSE:
    a) 13,020 mcg/kg -- caused behavioral changes
    2) LD50- (INTRAPERITONEAL)RAT:
    a) 10 mg/kg (OHM/TADS, 2001)
    b) 15 mg/kg
    c) 15.05 mg/kg (OHM/TADS, 2001)
    3) LD50- (ORAL)RAT:
    a) 12,300 mcg/kg -- caused behavioral changes
    b) 14-17 mg/kg
    c) 17-35 mg/kg (OHM/TADS, 2001)
    4) TCLo- (INHALATION)HUMAN:
    a) 1749 g/m(3) for 30M -- caused lacrimation and vomiting
    5) TCLo- (INHALATION)RAT:
    a) 1100 mg/m(3) for 1H/5D intermittent -- affected brain and caused death

Pharmacology Toxicology

Toxicologic Mechanism

    A) Hematologic effects result from both shortened red cell life span and inhibition of hemoglobin synthesis. The latter involves impaired globin synthesis as well as the well-known effect on heme synthesis. Lead inhibits ALA dehydratase leading to an accumulation of ALA.
    1) Lead also inhibits ferrochelatase leading to an accumulation of protoporphyrin. These and other hematologic problems do not occur with mild to acute exposures to TEL, but are present in prolonged and severe TEL intoxications secondary to accumulation of ionic (inorganic) lead.
    B) Whether the toxicity of tetraethyl lead differs from that of inorganic lead because of basic mechanism of injury or simply because the distribution is somewhat different is unknown. The distribution of the lipophillic organic lead compound differs from the ionized form. Available evidence also indicates metabolism of organic lead forms eventually the ionized form.
    1) This metabolism of the lipophillic organic lead compound in sites such as the brain, where the ionized lead would not be found in substantial quantities, may account for the quantitatively different toxicities of TEL. Thus in the absence of evidence to the contrary it can be assumed that a major part of the TEL toxicity results from the ionic lead formed in the tissues.
    2) In rodent models, exposure to tetraethyl lead is associated with decreased brain pyruvate dehydrogenase activity and increased brain glutamate receptors with decreased affinity (Regunathan & Sundaresan, 1984; Regunathan & Sundaresan, 1985).
    C) Triethyl lead is also converted to inorganic lead. It is felt that inorganic lead plays a significant additive role in toxicity. The lack of some features of intoxication with inorganic lead as a metabolite of TEL and as a primary toxin may be due to pharmacokinetic considerations.
    D) Ionic (inorganic) lead present in the soft tissues may damage or interfere with the function of any organ system. The mechanism of functional disturbance of the CNS is poorly understood. Ionic (inorganic) lead inhibits both cholinergic and adrenergic transmitter release in a calcium-dependent fashion.
    E) Inorganic lead damages the proximal tubules with depression of tubular reabsorption of glucose, amino acids, and phosphate. Lead also causes progressive interstitial fibrosis with vascular sclerosis and glomerular atrophy.
    F) Tetraethyl lead is converted to the more stable and more toxic triethyl lead by liver, kidney, and brain. Triethyl lead is the primary toxin to nervous tissue. Triethyl lead has also been shown to adversely affect the development of hippocampal neurons in culture (Audesirk, 1995).

Physicochemical

Physical Characteristics

    A) Tetraethyl lead is a oily colorless liquid with a characteristic slight musty, fruity, or pleasant odor (CHRIS , 2001; HSDB , 2001; Sittig, 1991). It releases a poisonous and flammable vapor (CHRIS , 2001).
    B) The commercial product may be dyed red, orange, or blue (Sittig, 1991).

Molecular Weight

    A) 323.47

Other

    A) ODOR THRESHOLD
    1) Data not available (CHRIS , 2001)

References

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