National Toxicology Program

Selected toxicity information from HSDB, one of the National Library of Medicine's databases. ¹

Names (NTP)

• Tetraethyllead
• TETRAETHYLPLUMBANE (9CI)

Human Toxicity Excerpts

• MAJOR SYMPTOMS OF INTOXICATION WITH TETRAETHYLLEAD ARE REFERABLE TO THE CNS. THE VICTIM SUFFERS FROM INSOMNIA, NIGHTMARES, ANOREXIA, NAUSEA & VOMITING, DIARRHEA, HEADACHE, MUSCULAR WEAKNESS, & EMOTIONAL INSTABILITY. SUBJECTIVE CNS SYMPTOMS SUCH AS IRRITABILITY, RESTLESSNESS, & ANXIETY ARE NEXT EVIDENT. AT THIS TIME THERE IS USUALLY HYPOTHERMIA, BRADYCARDIA, & HYPOTENSION. WITH CONTINUED EXPOSURE, OR IN THE CASE OF INTENSE SHORT-TERM EXPOSURE, CNS MANIFESTATIONS PROGRESS TO DELUSIONS, ATAXIA, EXAGGERATED MUSCULAR MOVEMENTS, &, FINALLY, A MANIACAL STATE. ... IN THE CASE OF SEVERE EXPOSURE, DEATH MAY OCCUR WITHIN A FEW HOURS OR MAY BE DELAYED FOR SEVERAL WEEKS. [Hardman, J.G., L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY: McGraw-Hill, 1996., p. 1654]**PEER REVIEWED**
  
• SYMPTOMS ARE REFERABLE CHIEFLY TO NERVOUS SYSTEM ... & IN SEVERE CASES ACUTE ENCEPHALOPATHY WITH MANIA. OTHER SYMPTOMS ARE VISUAL DIFFICULTIES ... WEAKNESS, TREMORS, MUSCLE PAINS, & EASY FATIGABILITY. [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-139]**PEER REVIEWED**
  
• IN ONE HUMAN CASE OF MASSIVE INGESTION OF PURE TETRAETHYL LEAD, PT SURVIVED 36 HR. INITIAL SIGNS & SYMPTOMS WERE REFERABLE TO GREATLY INCREASED INTRACRANIAL PRESSURE, BUT TERMINAL EVENT WAS PULMONARY EDEMA. [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-226]**PEER REVIEWED**
  
• THE MOST SERIOUS COMPLICATION RESULTING FROM SNIFFING GASOLINE IS LEAD ENCEPHALOPATHY, WHICH CAN BE FATAL. MOST OF THE TOXIC EFFECTS ARE THOUGHT TO BE DUE TO TETRAETHYLLEAD & ITS METABOLITES. [ROSS CA; CAN MED ASSOC J 127 (12): 1195-7 (1982)]**PEER REVIEWED**
  
• A CASE OF POLYNEUROPATHY IN A 14 YR OLD BOY, A CHRONIC GASOLINE SNIFFER, IS REPORTED. CLINICAL EXAM SHOWED SYMMETRICAL MOTOR INVOLVEMENT, MAINLY DISTALLY, & IN LOWER LIMBS. [GALLASSI R ET AL; EUR NEUROL 19 (6): 419-21 (1980)]**PEER REVIEWED**
  
• DURING A 6 YR PERIOD, 23 NAVAJO ADOLESCENTS WERE HOSPITALIZED 47 TIMES FOR PRESUMED LEAD INTOXICATION SECONDARY TO GASOLINE SNIFFING. 67% OF THE PATIENTS PRESENTED WITH TOXIC ENCEPHALOPATHY. OF THE TOTAL EPISODES, 31% INVOLVED TREMOR, ATAXIA, & OTHER NEUROLOGIC SIGNS; 38% INVOLVED ENCEPHALOPATHY WITH DISORIENTATION & HALLUCINATIONS. FREE ERYTHROCYTE PROTOPORPHYRIN LEVELS WERE NOT CONSISTENTLY HIGH, ALTHOUGH BLOOD LEAD LEVELS WERE ALL ELEVATED. ONE DEATH OCCURRED. THREE HAD ELEVATED ZINC PROTOPORPHYRIN LEVELS & ALL 3 WERE ANEMIC. [COULEHAN JL ET AL; PEDIATRICS 71 (1): 112-7 (1983)]**PEER REVIEWED**
  
• ... INFORMATION /COMPARED/ ON HEALTH VARIABLES FOR 153 WHITE MALE 'WAGE ROLL' EMPLOYEES WHO HAD HAD OCCUPATIONAL EXPOSURE TO TETRAETHYLLEAD FOR 20 OR MORE YEARS WITH THOSE FOR A SIMILAR GROUP OF WORKERS MATCHED INDIVIDUALLY FOR AGE & YEARS OF SERVICE WHO HAD NO RECOGNIZED OCCUPATIONAL EXPOSURE TO TETRAETHYLLEAD OR TO ANY OTHER LEAD COMPOUNDS. ... INFORMATION ON HEALTH WAS OBTAINED RETROSPECTIVELY, FROM RESULTS OF PERIODIC PHYSICAL EXAMINATIONS & LABORATORY STUDIES, MEDICAL RECORDS OF ABSENCE FROM WORK DUE TO ILLNESS, & LONG TERM MEDICAL HISTORIES IN FORM OF CUMULATIVE DIAGNOSES. THE PREVALENCE OF SKIN CANCER AMONG EXPOSED WORKERS WAS 7/139 (5%), NOT SIGNIFICANTLY DIFFERENT FROM THAT OF NON-EXPOSED WORKERS (4/139, 2.9%). THERE WERE NO CASES OF CANCER OTHER THAN OF THE SKIN IN EITHER GROUP. (THE WORKING GROUP NOTED THAT WORKERS WHO LEFT EMPLOYMENT FOR REASON, INCL ILLNESS OR RETIREMENT, WERE NOT INCLUDED; THIS STUDY WAS THEREFORE CONSIDERED INADEQUATE TO DETERMINE THE CARCINOGENIC RISK OF EXPOSURE TO TETRAETHYLLEAD.) [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V23 386 (1980)]**PEER REVIEWED**
  
• A study of workers manufacturing tetraethyllead /in an East TX chemical plant/ revealed excesses of respiratory cancer (15 observed, 11.2 expected) & brain cancer (3 observed, 1.6 expected). [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. S7 230 (1987)]**PEER REVIEWED**
  
• IN MANUFACTURING: INTOXICATION BY ... TETRAETHYL LEAD IS NOW RARE; OWING TO VIGOROUS INDUSTRIAL HEALTH MEASURES, ... LEAD POISONING OCCURS AMONG "GASOLINE SNIFFERS." CONTINUED ABSORPTION OF SMALL AMT ... CAN RESULT IN CLASSICAL SYNDROME OF CHRONIC LEAD POISONING. [Goodman, L.S., and A. Gilman. (eds.) The Pharmacological Basis of Therapeutics. 5th ed. New York: Macmillan Publishing Co., Inc., 1975., p. 941]**PEER REVIEWED**
  
• EXTREMELY POISONOUS. ... CAUTION: POTENTIAL SYMPTOMS OF OVEREXPOSURE ARE INSOMNIA, LASSITUDE AND ANXIETY; TREMOR, HYPER-REFLEXIA AND SPASTICITY; BRADYCARDIA, HYPOTENSION, HYPOTHERMIA, PALLOR, NAUSEA, ANOREXIA AND WEIGHT LOSS; DISORIENTATION, HALLUCINATIONS, PSYCHOSIS, MANIA, CONVULSIONS AND COMA; EYE IRRITATION. [Budavari, S. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc., 1996., p. 1572]**PEER REVIEWED**
  
• When the interval between the termination of (either brief or prolonged) exposure and the onset of symptoms is delayed (up to 8 days) the prognosis is guardedly hopeful, but when the interval is short (few hours), an early fatal outcome may result. Recovered patients show no residual damage to the nervous system, although recovery may be prolonged. [Sittig, M. Handbook of Toxic and Hazardous Chemicals and Carcinogens, 1985. 2nd ed. Park Ridge, NJ: Noyes Data Corporation, 1985., p. 846]**PEER REVIEWED**
  
• A MORTALITY STUDY WITH 100% 20 YR FOLLOW UP SHOWED A DEATH RATE 26% LOWER FOR TETRAETHYL LEAD (TEL) WORKERS THAN THE GENERAL POPULATIONS, WITH NO UNUSUAL CAUSES OF DEATH. [ROBINSON TR; INT CONF HEAVY MET ENVIRON, (SYMP PROC) FIRST 3: 357 (1975)]**PEER REVIEWED**
  
• Liquid alkyl lead may penetrate the skin without producing appreciable local injury. However, the decomposition products of tetraethyl lead (TEL) (ie, mono- ,di-, tri-ethyllead compounds) in dust form may be inhaled and result in irritation of the upper respiratory tract and possibly paroxysmal sneezing. This dust, when in contact with moist skin or ocular membranes, may cause itching, burning, and transient redness. TEL itself may be irritating to eyes. [Sittig, M. Handbook of Toxic and Hazardous Chemicals and Carcinogens, 1985. 2nd ed. Park Ridge, NJ: Noyes Data Corporation, 1985., p. 846]**PEER REVIEWED**
  
• Gasoline is a readily obtainable intoxicant that lends itself to habitual abuse by sniffing, a practice found particularly among children and adolescents. The concerted effects of the multiple hydrocarbon and other constituents of gasoline result in a predictable acute toxic syndrome. Organoleads, primarly tetraethyl lead (TEL), cause a separate toxicologic symptom sign complex that overlaps with the initial acute toxic syndrome. The different clinical symptomatology, effects on hemoglobin synthesis, and response to chelation therapy are all in keeping with the view that organolead poisoning is a separate and distinct toxicologic entity from that of classical elemental lead poisoning. [Edminster SC, Bayer MJ; J Emerg Med 3 (5): 365-70 (1986)]**PEER REVIEWED**
  
• A 25 year old man with a five year history of petrol sniffing developed an acute encephalopathy with abnormal body movements and died of aspiration pneumonia. Neuropathological findings included chromatolysis of neurons in the reticular formation and cerebral cortex and loss of neurons. Toxicological studies suggest that the encephalopathy is caused by the tetraethyl lead additive in the petrol. [Kaelan C et al; Aust NZ J Med 16 (6): 804-7 (1986)]**PEER REVIEWED**
  
• ... Sixteen cases of oral acute tetraethyl lead poisoning /were described/. The paper contains clinical data, treatment, and chemical and toxicological analyses of the patients before and after death as well as pathomorphological data of dissected cases. Twelve of sixteen patients died during this poisoning. Clinical symptoms were typical of severe tetraethyl lead poisoning and all attempts of treatment were unsuccessful. The minimal tetraethyl lead dose, which for acute symptoms has been estimated at 6 ml, ie 0.14 g/kg body weight, and minimal lethal dose at 15 ml tetraethyl lead, ie 0.35 g/kg body weight. [Wiernikowski A et al; Folia Med Cracov 28 (1-2): 3-12 (1987)]**PEER REVIEWED**
  
• Intentional use of gasoline as an intoxicant has been frequently reported in diverse clinical literature. Recent investigations have described a high prevalence of this behavior in certain ethnic groups such as American and Canadian Indians living in isolated areas. Encephalopathy due to tetraethyl lead has become a well accepted complication of gasoline sniffing within the last decade. [Fortenberry JD; Am J Med 79 (6): 740-4 (1985)]**PEER REVIEWED**
  
• Exposure to tetraethyllead, resulting in blood lead levels in 4 men of 600-925 ug/l, resulted in inhibited delta-aminolevulinic acid dehydratase in blood but did not enhance excretion of delta-aminolevulinic acid or coproporphyrin. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V23 377 (1980)]**PEER REVIEWED**
  
• SEVEN VICTIMS OF ACCIDENTAL TETRAALKYLLEAD POISONING DIED 5-19 DAYS AFTER POISONING. HISTOLOGICAL EXAM REVEALED DEGENERATIVE ALTERATIONS OF HEART MUSCLE, SWELLING & LIPOFUSCIN DEPOSITS IN MUSCLE FIBER & MYOCARDIAL FRAGMENTATION. [MIZOI Y ET AL; NIPPON HOIGAKU ZASSHI 27 (5): 371-86 (1973)]**PEER REVIEWED**
  
• ... IN MAN, TETRAETHYL LEAD IS APPROX 3 TIMES MORE TOXIC THAN IS TETRAMETHYL LEAD. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V2 158 (1973)]**PEER REVIEWED**
  
• In humans, a tetraethyl lead concentration of 100 mg/cu m, as Pb, for 1 hour may produce frank intoxication. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1514]**PEER REVIEWED**
  
• The longer the exposure time is, the lower is the dangerous concentration. [Zenz, C., O.B. Dickerson, E.P. Horvath. Occupational Medicine. 3rd ed. St. Louis, MO., 1994, p. 529]**PEER REVIEWED**
  
• Food and Environmental Agents: Effect on Breast-Feeding: Reported Sign or Symptom in Infant or Effect on Lactation: Lead: Possible neurotoxicity. /From Table 7/ [Report of the American Academy of Pediatrics Committee on Drugs in Pediatrics 93 (1): 142 (1994)]**PEER REVIEWED**
  
• Acute exposure to tetraethyllead produced renal and hepatic damage in half /of/ adolescents with blood lead levels of 1200-1400 ug/l. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V23 377 (1980)]**PEER REVIEWED**
  

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Non-Human Toxicity Excerpts

• AFTER SINGLE DOSES WITHIN THE LETHAL RANGE WITHIN RANGE OF ... (17 MG/KG BODY WT OF TETRAETHYL LEAD (TEL) ... ) RATS SHOWED IRRITABILITY, HYPERMOBILITY, TREMORS & SPASTICITY. AFTER SINGLE DOSES OF 1.7 MG/KG BODY WT OF TEL ... NO BEHAVIORAL CHANGES WERE SEEN. REPEATED EXPOSURE AT THESE LOWER LEVELS, HOWEVER, WAS ASSOCIATED WITH BEHAVIORAL CHANGES, PERIPHERAL HYPEREMIA & EXCESSIVE BODY WEIGHT GAIN. ... CARDIAC HYPERTROPHY, HYPEREMIA & EDEMA OF BRAIN, & CHANGES IN LIVER, PANCREAS, THYROID, LUNG & THYMUS WERE SEEN IN A FEW RATS. MICROSCOPICALLY, CHANGES ATTRIBUTABLE TO EXPOSURE TO TEL ... WERE NOTED IN THE CENTRAL NERVOUS SYSTEM & LIVER. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V2 156 (1973)]**PEER REVIEWED**
  
• TETRAETHYL LEAD DISSOLVED IN TRICAPRYLIN WAS INJECTED SC INTO MALE & FEMALE SWISS MICE ON 1 TO 4 OCCASIONS BETWEEN BIRTH & 21 DAYS OF AGE. AFTER SINGLE INJECTION OF 2 MG ON THE FIRST DAY OF LIFE, ALL OF 69 MICE DIED BEFORE WEANING. TOTAL DOSES OF 1.2 MG IN 4 DIVIDED DOSES KILLED 92% OF MICE BEFORE WEANING, & TOTAL DOSES OF 0.6 MG GIVEN IN 4 DIVIDED DOSES KILLED 20% OF THE MICE. OF 41 FEMALE MICE THAT SURVIVED FOR 36 WEEKS AFTER TREATMENT WITH 0.6 MG TETRAETHYL LEAD, 5 DEVELOPED MALIGNANT LYMPHOMAS BETWEEN 36 & 51 WEEKS. OF 48 FEMALE CONTROL MICE THAT RECEIVED INJECTIONS OF TRICAPRYLIN ALONE, NONE DEVELOPED LYMPHOMAS. LYMPHOMAS DEVELOPED IN 1 OF 26 MALES THAT RECEIVED A TOTAL DOSE OF 0.6 MG TETRAETHYLLEAD & IN 1 OF 39 CONTROL MALES. (THE WORKING GROUP NOTED THE LOW INCIDENCE OF LYMPHOMAS IN ANIMALS OF ONE SEX ONLY & CONCLUDED THAT A FURTHER STUDY IS WARRANTED IN ORDER TO CONFIRM OR REFUTE THESE RESULTS.) [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V23 363 (1980)]**PEER REVIEWED**
  
• ... HIGH TEST GASOLINE CONTAINING TETRAETHYL LEAD /WAS TESTED/ BY DROPPING ON RABBIT EYES, & ... FOUND IT TO CAUSE IMMEDIATE PAIN & BLEPHAROSPASM ... WHEN APPLICATION WAS REPEATED 10 TIMES IN ... 5 MIN UNDER LOCAL ANESTHESIA, IT PRODUCED CONJUNCTIVAL HYPEREMIA & MODERATE FLOCCULENT DISCHARGE ... . [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 892]**PEER REVIEWED**
  
• CD-1 RANDOM BRED ALBINO MICE & COBS RANDOM BRED RATS WERE TREATED ON DAYS 5-15 (MICE) OR 6-16 (RATS) OF PREGNANCY WITH ORAL DOSES OF ... 0.01, 1 OR 10 MG/KG BODY WEIGHT TETRAETHYLLEAD. NO TERATOGENIC EFFECTS WERE OBSERVED. ... AN INCREASE IN FETAL RESORPTION OCCURRED IN BOTH SPECIES AFTER EXPOSURE TO ... 1 MG/KG BODY WEIGHT TETRAETHYLLEAD. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V23 371 (1980)]**PEER REVIEWED**
  
• IN DARKNESS TETRAETHYLLEAD WAS NOT TOXIC TO THE ALGAE EVEN AT EXTREMELY HIGH CONCENTRATIONS. DEPENDING ON CONCENTRATION, GROWTH, MITOSIS, & CYTOKINESIS OF THE CELLS WERE INHIBITED IN ILLUMINATED CULTURES, RESULTING IN FORMATION OF GIANT CELLS. TETRAETHYLLEAD WAS CONVERTED TO HIGHLY TOXIC DERIVATIVES BY LIGHT IN PRESENCE OR ABSENCE OF LIVING CELLS. [ROEDERER G; ENVIRON RES 23 (2): 371-84 (1980)]**PEER REVIEWED**
  
• THE TOXICITY OF TETRAETHYL LEAD TO DENITRIFICATION OF HETEROTROPHIC MICROORGANISMS EXISTING IN ESTUARINE & MARINE SEDIMENT WAS EVALUATED BY MEASURING ADENOSINE TRI-PHOSPHATE (ATP) LEVELS. A LINEAR CORRELATION EXISTED BETWEEN THE REDUCTION OF ADENOSINE TRI-PHOSPHATE (ATP) & THE DECLINE OF DENITRIFICATION RATE AFTER ADDITION OF ORGANOLEAD COMPOUNDS. [CHARLOU JL ET AL; PROG WATER TECHNOL 12 (4): 501-12 (1980)]**PEER REVIEWED**
  
• ORAL ADMIN OF TETRAETHYLLEAD TO RHESUS MONKEY (MACACA MULATTA) FOR 6 MO AT DOSE LEVEL EQUIVALENT TO 6 MG/KG/DAY OF LEAD DID NOT INDUCE CLINICAL MANIFESTATIONS OF TOXICITY. MINOR ELEVATIONS OF LEAD IN BLOOD & TISSUE WERE FOUND. [HEYWOOD R ET AL; TOXICOL LETT 4 (2): 119-25 (1979)]**PEER REVIEWED**
  
• MALE MICE WERE EXPOSED TO TETRAETHYL LEAD FOR 3 WK IN DRINKING WATER AT 3 OR 4 CONCENTRATIONS RANGING FROM 0.5-10.0 PPM. THE HUMORAL COMPONENT OF THE IMMUNE SYSTEM WAS EVALUATED USING HEMAGGLUTINATION, RADIAL IMMUNODIFFUSION & THE CUNNINGHAM PLAQUE ASSAY. RESULTS INDICATED IMMUNOSUPPRESSIVE EFFECTS AT LOW METAL CONCENTRATIONS. MAX IMMUNOSUPPRESSIVE EFFECT WAS PRODUCED IN MOST INSTANCES AT A METAL CONCN OF LESS THAN 2.0 PPM. [BLAKLEY BR ET AL; TOXICOL APPL PHARMACOL 52 (2): 245-54 (1980)]**PEER REVIEWED**
  
• GROUPS OF WHITE MALE WISTAR RATS WERE ADMIN TETRAETHYLLEAD (TEL) IN DOSES OF 0.0, 10, 20, 40, & 80 MG/KG BODY WT. INTOXICATION OF CNS WAS EXAM BY MEANS OF A POLYGRAPH. AFTER INJECTION, THE GROUP ADMIN 10 MG/KG SURVIVED & TOXIC SYMPTOMS DID NOT APPEAR. RESULTS FROM THE POLYGRAPH CONCERNING SLEEPING-WAKING INDICATED THAT THE AMOUNT OF SLOW WAVE SLEEP (SS) & PARADOXICAL SLEEP (PS) DECREASED GREATLY UNTIL DEATH. BOTH SS & PS DECREASED FOR 5 DAYS AFTER THE INJECTION, AFTER WHICH THEY RETURNED TO NORMAL LEVELS. THE CHANGES IN SLEEPING-WAKING CYCLES CORRELATE DIRECTLY TO THE EXTENT OF POISONING, INASMUCH AS POISONING CAN BE SEEN CREATING A DISTURBANCE IN THE CNS. [MATSUMOTO K ET AL; J HYG 34 (5): 670-6 (1979)]**PEER REVIEWED**
  
• RABBITS INJECTED IP WITH 100-200 MG TETRAETHYLLEAD (TEL) WERE SACRIFICED UPON ONSET OF TOXIC SYMPTOMS. ELECTRONMICROSCOPIC EXAM REVEALED MARKED CYTOLOGICAL CHANGES (ENLARGEMENT OF APICAL VACUOLES & ACCUMULATION OF LYSOSOMES & MICROBODIES) IN EPITHELIAL CELL OF THE PROXIMAL TUBULES. CONFIGURATION CHANGES OF THE ROUGH ENDOPLASMIC RETICULUM LEADING TO FORMATION OF HONEYCOMB LIKE BODIES MAY REPRESENT A HYPERPLASTIC, HYPOACTIVE FORM OF THE ROUGH ENDOPLASMIC RETICULUM & DENOTES A DISRUPTION OF PROTEIN SYNTHESIS. [CHANG LW ET AL; ENVIRON RES 23 (1): 208-23 (1980)]**PEER REVIEWED**
  
• IP ADMIN OF TETRAETHYLLEAD TO RATS (250 UMOL/KG) ON 2 CONSECUTIVE DAYS DECREASED THE CONCENTRATION OF HEPATIC CYTOCHROME P450, THE HEPATIC ACTIVITY OF ARYL HYDROCARBON HYDROXYLASE & ETHOXYCOUMARIN DEETHYLASE. EPOXIDE HYDRATASE ACTIVITY WAS ENHANCED IN THE LIVER, KIDNEY & SMALL INTESTINAL MUCOSA. THE ACTIVITY OF GLUTATHIONE S-TRANSFERASE DECREASED IN THE LIVER BUT INCREASED IN THE KIDNEY & SMALL INTESTINAL MUCOSA. THE GLUCURONIDATION OF O-AMINOPHENOL WAS ENHANCED IN THE KIDNEY. [AHOTUPA M ET AL; ACTA PHARMACOL TOXICOL 44 (5): 359-63 (1979)]**PEER REVIEWED**
  
• ROOT INCUBATION OF GERMINATING WHEAT IN TETRAETHYLLEAD PRODUCED MITOTIC DISTURBANCES AND/OR NUCLEUS STRUCTURE DEGENERATION SYMPTOMS, EG, MARGINATION OF CHROMATIN, DISINTEGRATION OF NUCLEUS STRUCTURE, BINUCLEAR CELLS WITH NUCLEI JOINED BY BRIDGE, NUCLEUS WITH MICRONUCLEUS, FRAGMENTATION OF NUCLEUS, C-MITOSIS, & AGGLUTINATION & ABBREVIATION OF CHROMOSOMES IN MERISTEMS. [GRZYBEK J, KOHLMUNZER S; BROMATOL CHEM TOKSYKOL 13 (3): 305-10 (1980)]**PEER REVIEWED**
  
• Signs of intoxication /in male Japanese quails or mallard ducks exposed orally to LD50 levels of commercially pure tetraethyllead/: Polydipsia, regurgitation, reluctance to leave the swimming pond (in mallards), shakiness, hypoactivity, wing drop, wings spread, ataxia, sitting, reluctance to move, fluffed feathers, ptosis, ataraxia, asthenia, mydriasis, tremors, & anorexia. Regurgitation in mallards occurred as soon as 7 min, other signs appeared as soon as 20 min, & mortalities usually occurred between 1 & 4 days after treatment. Remission took up to 8 days. [U.S. Department of the Interior, Fish and Wildlife Service. Handbook of Toxicity of Pesticides to Wildlife. Resource Publication 153. Washington, DC: U.S. Government Printing Office, 1984., p. 80]**PEER REVIEWED**
  
• ... Animal studies indicate that relatively high levels of lead exposure interfere with resistance to infectious disease. [Gainer JH; Environ Health Perspect Exp 7: 113-9 (1974) as cited in USEPA; Ambient Water Quality Criteria Doc: Lead p.C-71 (1980) EPA 440/5-80-057]**PEER REVIEWED**
  
• Tetraethyl lead was tested for mutagenicity in the Salmonella/microsome preincubation assay using the standard protocol approved by the National Toxicology Program. Tetraethyl lead was tested at doses of 0.001, 0.0033, 0.01, 0.033, 0.1, 0.33, and 1.0 mg/plate in as many as 5 Salmonella typhimurium strains (TA1535, TA1537, TA97, TA98, and TA100) in the presence and absence of rat or hamster liver S-9. Tetraethyl lead was negative in these tests and the highest ineffective dose tested in any Salmonella typhimurium strain was 1.0 mg/plate. [Mortelmans K et al; Environ Mutagen 8: 1-119 (1986)]**PEER REVIEWED**
  
• ... /IT WAS/ FOUND IN RATS THAT TETRAETHYL LEAD (TEL) WAS 2 TO 4 TIMES MORE TOXIC THAN TETRAMETHYL LEAD (TML) BY IV OR IP ROUTE AND THAT TEL WAS 2 TO 3 TIMES MORE TOXIC THAN TML BY ORAL ROUTE. ... AFTER SINGLE DOSES WITHIN THE LETHAL RANGE OF EITHER CMPD (17 MG/KG BODY WT OF TEL; 108 MG/KG BODY WT OF TML) RATS SHOWED IRRITABILITY, HYPERMOBILITY, TREMORS & SPASTICITY. AFTER SINGLE DOSES OF 1.7 MG/KG BODY WT OF TEL OR 10.8 MG/KG BODY WT OF TML, NO BEHAVIORAL CHANGES WERE SEEN. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V2 156 (1973)]**PEER REVIEWED**
  
• Inhalation of tetraethyl lead by one dog at 42 mg/cu m, one at 22 mg/cu m, and two at 12 mg/cu m resulted in death after 7, 30, 24, and 29 seven-hour exposures, respectively. Repeated exposures to sublethal doses were associated with signs of intoxication similar to those seen after a single lethal exposure. Signs of tetraethyl lead poisoning in dogs included tremors and incoordination; with continued exposure, coma and death ensued. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1513]**PEER REVIEWED**
  
• The transplacental effect of tetraethyl lead or lead acetate on the activity of inorganic pyrophosphatase in brain, liver and kidneys of newborn rats varied with the organ, the lead compound, the dose, and the route and time of administration. Enzyme activity was usually decreased in brain and liver, suggesting adverse effects of lead on metabolism in these organs. The inorganic pyrophosphatase activity was generally increased in kidneys. [Tsafaris F, Alexaki E; Vet Hum Toxicol 34 (6): 510-2 (1992)]**PEER REVIEWED**
  

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Human Toxicity Values

• None found

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Non-Human Toxicity Values

• LD50 Rat oral 12,300 ug/kg [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 3100]**PEER REVIEWED**
  
• LC50 Rat ihl 850 mg/cu m/60 mos [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 3100]**PEER REVIEWED**
  
• LD50 Rat ip 15 mg/kg [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 3100]**PEER REVIEWED**
  
• LD50 Rat iv 14,400 ug/kg [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 3100]**PEER REVIEWED**
  
• LD50 Rat parenteral 15 mg/kg [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 3100]**PEER REVIEWED**
  

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Absorption, Distribution and Excretion

• SEVEN VICTIMS OF ACCIDENTAL TETRAALKYLLEAD POISONING DIED 5-19 DAYS AFTER POISONING. THE HIGHEST LEAD CONCN WAS DETECTED IN SPLEEN, LIVER & KIDNEY TISSUE. [MIZOI Y ET AL; NIPPON HOIGAKU ZASSHI 27 (5): 371-86 (1973)]**PEER REVIEWED**
  
• TETRAETHYL LEAD (TEL) IS READILY ABSORBED FROM DIGESTIVE & RESPIRATORY TRACTS & THROUGH THE SKIN, OWING TO THE SOLUBILITY OF TEL IN LIPIDS & TO ITS DIFFUSIBILITY. ... ALTHOUGH PART OF TEL IS METABOLIZED & THE RELEASED INORGANIC LEAD (PB) IS DISTRIBUTED IN OTHER SOFT TISSUES, THE MAJOR PORTION ACCUMULATES IN THE BRAIN OWING TO A SPECIAL AFFINITY BETWEEN THE ORGANIC PB & THE LIPIDS OF NERVE TISSUES. [Venugopal, B. and T.D. Luckey. Metal Toxicity in Mammals, 2. New York: Plenum Press, 1978., p. 189]**PEER REVIEWED**
  
• TISSUE DISTRIBUTION STUDIES OF LEAD IN RATS & DOGS EXPOSED TO LETHAL INHALATION DOSES OF TETRAETHYL LEAD (TEL) OR TETRAMETHYL LEAD (TML) & IN MEN FATALLY POISONED BY TEL REVEALED LEAD (PB) LEVELS OF 0.7-13.0 MG/100 G TISSUE IN LUNG, BRAIN, LIVER & KIDNEY IN THREE SPECIES. HUMAN PB LEVELS IN BRAIN, LIVER & KIDNEY RESEMBLED THOSE SEEN IN CORRESPONDING RAT & DOG TISSUES. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V2 158 (1973)]**PEER REVIEWED**
  
• IN CASES OF ACCIDENTAL POISONING WITH TETRAETHYL LEAD (TEL), LIVER, KIDNEY, PANCREAS, BRAIN & HEART ACCUMULATE TRIETHYLLEAD, & TOTAL TISSUE LEAD (PB) CONCN CORRELATE WITH TRIETHYLLEAD CONCN IN CORRESPONDING TISSUES. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V2 157 (1973)]**PEER REVIEWED**
  
• RATS GIVEN DERMAL APPLICATIONS OF 0.1 ML TETRAETHYL LEAD (TEL) (106 MG LEAD)/RAT SHOWED HIGHEST LEAD LEVELS IN BLOOD, KIDNEY, LIVER, LUNG & BRAIN IN THAT ORDER; ABOUT 6.5% OF DOSE APPLIED WAS ACCOUNTED FOR BY TISSUES, CARCASS & TREATED SKIN. THUS, SUBSTANTIAL PROPORTION OF THE DOSE APPLIED APPEARED TO BE LOST BY EVAPORATION FROM THE SKIN. WHEN RABBITS RECEIVED DERMAL APPLICATION OF 0.75 MG TEL FOR 4 HR & WERE KILLED FROM 6 HR TO 205 DAYS LATER, TISSUE LEAD LEVELS REACHED PEAK AFTER 18 HR EXCEPT IN SPLEEN & BONE, WHERE HIGHEST LEVELS WERE ATTAINED AFTER 7 & 30 DAYS, RESPECTIVELY. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V2 156 (1973)]**PEER REVIEWED**
  
• WITHIN 24 HR OF IV ADMIN OF TETRAETHYL LEAD (TEL) TO RATS 50% OF TOTAL LEAD IN SOFT ORGANS WAS IN THE FORM OF TRIETHYLLEAD, & 70% OF MUSCLE LEAD APPEARED AS TRIETHYLLEAD; HIGHEST LEVELS WERE FOUND IN LIVER, BLOOD, KIDNEY & BRAIN. AFTER 1 WK 90-100% OF TOTAL LEAD IN ORGANS WAS IN FORM OF TRIETHYLLEAD. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V2 155 (1973)]**PEER REVIEWED**
  
• REPEATED ORAL DOSES OF 0.0017-0.17 MG/KG BODY WT OF TETRAETHYL LEAD (TEL) & 0.001-1.08 MG/KG BODY WT TETRAMETHYLLEAD TO RATS 5 TIMES/WK FOR 20 WK RESULTED IN DEPOSITION OF LEAD IN LIVER, KIDNEY, BRAIN, TESTES & OTHER ORGANS. DISTRIBUTION OF LEAD IN TISSUES DIFFERED BETWEEN TEL & TETRAMETHYLLEAD & VARIED WITH DOSE, DOSE SCHEDULE & SEX OF EXPOSED ANIMALS. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V2 155 (1973)]**PEER REVIEWED**
  
• ... AFTER IV INJECTION OF TETRAETHYL LEAD (TEL) INTO RATS 18% OF ADMINISTERED LEAD IS CONVERTED INTO INORG FORM. EXCRETION, PRINCIPALLY AS TRIETHYLLEAD, OCCURS VIA URINE & FECES. AFTER IV INJECTIONS OF 25 MG/KG BODY WT ... INTO RABBITS ... LITTLE OF ... METABOLITE WAS EXCRETED IN URINE. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V2 154 (1973)]**PEER REVIEWED**
  
• ... CAN ENTER THROUGH SKIN BOTH IN LIQUID & VAPOR FORM. [Browning, E. Toxicity of Industrial Metals. 2nd ed. New York: Appleton-Century-Crofts, 1969., p. 175]**PEER REVIEWED**
  
• IN CASES OF TETRAETHYL LEAD (TEL) INTOXICATION IN MAN URINARY LEAD LEVELS ARE HIGH BUT BLOOD LEVELS MAY BE NORMAL OR ONLY SLIGHTLY RAISED. IN PLANT MANUFACTURING TEL NEARLY LINEAR RELATIONSHIP WAS FOUND BETWEEN ATMOSPHERIC LEVEL OF TEL & URINARY LEAD EXCRETION IN EXPOSED WORKERS. /ANOTHER STUDY REPORTED/ ... RAISED BLOOD LEAD LEVELS & RAISED URINARY EXCRETION OF DELTA-AMINOLEVULINIC ACID IN URBAN STREET SWEEPERS & GARBAGE LOADERS WHO ... /WERE/ HEAVILY EXPOSED TO VEHICLE EXHAUST FUMES. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V2 157 (1973)]**PEER REVIEWED**
  
• TETRAETHYL LEAD (12 MG/KG) WAS ADMIN IP TO RABBITS TO DETERMINE CLEARANCE RATES. 24 HR AFTER ADMIN, HIGHEST TOTAL LEAD & TRIETHYLLEAD LEVELS WERE FOUND IN LIVER, FOLLOWED BY KIDNEY, BRAIN, SKELETAL MUSCLE, CARDIAC MUSCLE, SPINAL CORD & BLOOD. APPROX 58% OF THE TETRAETHYLLEAD ADMIN WAS EXCRETED WITHIN 4 DAYS AFTER TREATMENT. [YAMAMURA Y ET AL; SEI MARIANNA IKA DAIGAKU ZASSHI 7 (1): 10-20 (1979)]**PEER REVIEWED**
  
• ONE DAY AFTER THE IV ADMIN OF 12 MG/KG OF TETRAETHYLLEAD INTO RABBITS, TOTAL LEAD IN THE URINE CONSISTED OF 69% DIETHYLLEAD, 27% INORGANIC LEAD, & 4% TRIETHYLLEAD. TOTAL LEAD IN THE FECES CONSISTED OF 85% INORGANIC LEAD, 9% DIETHYLLEAD, & 6% TRIETHYLLEAD 2 DAYS AFTER DOSING, & THE RATIO CHANGED, AFTER 7 DAYS, TO 95, 1, & 4%, RESPECTIVELY. AFTER 24 HR, TRIETHYLLEAD ACCOUNTED FOR 84% OF THE TOTAL LEAD IN THE LIVER, 68% IN KIDNEY, & 59% IN BLOOD, WHEREAS DIETHYLEAD ACCOUNTED FOR 93% OF TOTAL LEAD IN THE BILE, & INORG LEAD MADE UP 90% IN THE CECAL, THE COLONIC, & THE RECTAL CONTENTS. [ARAI F ET AL; SANGYO IGAKU 23 (5): 496-504 (1981)]**PEER REVIEWED**
  
• HUMANS EXPOSED TO (203)PB-TETRAETHYLLEAD SHOWED AN INITIAL DEPOSITION IN LUNG OF 51% TETRAETHYLLEAD. THE CONCENTRATION IN BLOOD FELL BY 2 ORDERS OF MAGNITUDE IN THE FIRST 10 HR AFTER INHALATION OF TETRAETHYLLEAD. DURING THIS TIME APPROX 0.66% OF THE BLOOD ACTIVITY WAS IN PLASMA. [HEARD MJ ET AL; MANAGE CONTROL HEAVY MET ENVIRON, INT CONF PP 103-8 (1979)]**PEER REVIEWED**
  
• CHEMICAL SPECIES OF LEAD IN THE URINE OF PATIENTS POISONED BY TETRAETHYLLEAD WERE IDENTIFIED BY MEANS OF HYDRIDE GENERATION-FLAMELESS ATOMIC ABSORPTION SPECTROMETRY. 21 DAYS AFTER EXPOSURE, THE URINE CONTAINED APPROX 50% DIETHYLLEAD, APPROX 48% INORGANIC LEAD & APPROX 2% TRIETHYLLEAD. [YAMAMURA Y ET AL; IND HEALTH 19 (2): 125-31 (1981)]**PEER REVIEWED**
  
• ... Lipid soluble tetraethyl lead (TEL) is not retained in the blood. After TEL exposure, organic lead (Pb) appears in urine of humans for many weeks. [Nat'l Research Council Canada; Effects of Lead in the Canadian Environment p.614 (1978) NRCC No. 16736]**PEER REVIEWED**
  
• IN ACCIDENTAL HUMAN EXPOSURE TO HIGH LEVEL OF TETRAMETHYL LEAD (TML) PATIENT HAD HIGH LEVELS OF LEAD IN URINE, 4-75 UMOL (933 UG) FOR FIRST 4 DAYS AFTER EXPOSURE & RAISED LEVELS FOR 6 MO, BUT NO SYMPTOMS OR SIGN OF LEAD POISONING. TML IS LESS TOXIC THAN TETRAETHYL LEAD. [GETHING J; BR J IND MED 32 (4): 329-33 (1975)]**PEER REVIEWED**
  
• Organic lead accumulates in the human brain. After acute tetraethyl lead poisoning, however, the lead concentrations are highest in the human liver (24 to 41 ug/g), followed by those in the kidney (8 to 19 ug/g) > pancreas (13 ug/g) > brain (7 to 11 ug/g) > cardiac and skeletal muscle (8 to 9 ug/g) > spleen and adrenal (3 to 6 ug/g). [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1514]**PEER REVIEWED**
  

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Metabolism/Metabolites

• AFTER IV INJECTION INTO RATS, TETRAETHYL LEAD (TEL) IS CONVERTED INTO TRIETHYL LEAD, WHICH IS CONSIDERED TO BE RESPONSIBLE FOR TOXIC EFFECTS SEEN. ... AFTER IV INJECTIONS OF 25 MG/KG BODY WT OF TEL INTO RABBITS, MAIN METABOLITE WAS TRIETHYL LEAD ... [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work)., p. V2 154 (1973)]**PEER REVIEWED**
  
• DEALKYLATION OF TETRAETHYL LEAD OCCURS IN MICROSOMES & REQUIRES OXYGEN & NADPH, & HAS BEEN OBSERVED IN HOMOGENATES OF LIVER, KIDNEY, & BRAIN OF RAT & RABBIT. [The Chemical Society. Foreign Compound Metabolism in Mammals. Volume 2: A Review of the Literature Published Between 1970 and 1971. London: The Chemical Society, 1972., p. 334]**PEER REVIEWED**
  
• BIOLOGICAL DEGRADATION OF TETRAETHYLLEAD TO THE TRIETHYLLEAD CATION BY RAT LIVER MICROSOMES FROM UNTREATED, PHENOBARBITAL PRETREATED & METHYLCHOLANTHRENE PRETREATED RATS WAS STUDIED; NICOTINAMIDE-ADENINE DINUCLEOTIDE PHOSPHATE & OXYGEN ARE ESSENTIAL. [FERREIRA DA SILVA D ET AL; XENOBIOTICA 13 (10): 583-90 (1983)]**PEER REVIEWED**
  
• NICOTINAMIDE-ADENINE DINUCLEOTIDE PHOSPHATE & OXYGEN DEPENDENT MICROSOMAL METABOLISM OF TETRAETHYL-SUBSTITUTED DERIVATIVES OF LEAD GAVE RISE TO ETHYLENE AS A MAJOR PRODUCT & ETHANE AS MINOR PRODUCT IN RATS. REACTIONS WERE CATALYZED BY LIVER MICROSOMAL CYTOCHROME P450 DEPENDENT MONOOXYGENASE. SINCE FORMATION OF ETHANE & ETHYLENE WAS DIFFERENTIALLY INHIBITED BY ANAEROBIOSIS, RESULTS SUGGESTED THAT A LARGE PORTION OF THE ETHANE PRODUCED WAS DERIVED BY A REDUCTIVE MECHANISM. [PROUGH RA ET AL; BIOCHEM J 196 (3): 763-70 (1981)]**PEER REVIEWED**
  
• THE TOTAL LEAD EXCRETED INTO BILE DURING THE FIRST 24 HR AFTER INJECTION OF 12 MG/KG TETRAETHYLLEAD AMOUNTED TO APPROX 8% OF THE INJECTED LEAD. ABOUT 97% OF THE EXCRETED LEAD WAS MADE UP OF DIETHYLLEAD. THE LARGE AMOUNT OF INORGANIC LEAD IN THE FECES WAS DERIVED FROM THE DIETHYLLEAD EXCRETED INTO THE BILE. [ARAI F ET AL; SANGYO IGAKU 25 (3): 175-80 (1983)]**PEER REVIEWED**
  
• Tetramethyl lead (TML) is metabolized more slowly than tetraethyl lead (TEL) to the trialkyl derivative, and hence is considered somewhat less toxic than TEL; however, it is more volatile than TEL, and thus probably is more available for respiratory absorption. [Nat'l Research Council Canada; Effects of Lead in the Canadian Environment p.614 (1978) NRCC No. 16736]**PEER REVIEWED**
  
• The dynamics of diethyl lead urinary excretion in rabbits exposed to various amounts of tetraethyl lead by several different routes of administration was compared to those measured in workers who had sustained occupational exposure to tetraethyl lead. Seventeen male Danish rabbits were administered tetraethyl lead either intravenously or intragastrically at 12 or 3 mg/kg. Animals were also exposed to tetraethyl lead by inhalation at a chamber concentration of 200 micrograms per cu m for 5 hr. Three petroleum company workers whose job involved the addition of tetraethyl lead to gasoline were also studied. Intragastric administration of tetraethyl lead to rabbits at 12 mg/kg produced a time dependent excretion of diethyl lead. Approximately 70 to 90 percent of the total lead excreted was in the form of diethyl lead for the first 7 days following exposure to tetraethyl lead, with maximum diethyl lead excretion occurring on the first day following such exposure. Intravenous administration of tetraethyl lead resulted in lesser amounts of diethyl lead being excreted in the urine, with about 50 percent of the total lead excreted as diethyl lead for the first 7 days following treatment. After administration of 3 mg/kg tetraethyl lead, only small differences in the amount of diethyl lead excreted were observed between intravenously and intragastrically treated animals. Inhalation of tetraethyl lead resulted in maximum diethyl lead excretion on the second day after exposure, with levels of this metabolite constituting about 20 percent of total excreted lead. Exposure to high air levels of tetraethyl lead in petroleum workers resulted in concentration dependent and prolonged urinary excretion of diethyl lead. [Kozarzewka Z, Chmielnicka J; Brit J Indust Med 44: 417-21 (1987)]**PEER REVIEWED**
  
• Oxidative dealkylation of tetraethyl lead in animals and humans catalyzed by hepatic mixed function oxidase enzymes yields trialkyl metabolites; the triethyl derivatives are further metabolized to diethyl lead and to inorganic lead. At 90 days after continuous oral tetraethyl lead treatment, rat liver contained 10.7, 2.6, and 0.42 ug triethyl, diethyl, and inorganic lead/g, respectively, and the kidney contained 3.7, 1.6, and 1.3 ug triethyl, diethyl, and inorganic lead/g, respectively, but blood contained nearly equivalent quantities of the three metabolites. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1514]**PEER REVIEWED**
  

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TSCA Test Submissions

• Tetraethyl lead (CAS # 78-00-2) was evaluated for acute inhalation toxicity in male Charles River CD rats (2/exposure level) administered single whole-body exposures at graduated concentrations of 4.8, 7.3, 10.9, 16.3, and 24.5 mg/l for 1 hour. The undiluted test material infused into a glass bubbler was vaporized and supplied as a dried metered airstream at 2 L/min into the bell jars containing 2 rats each. An approximate lethal dose was 10.9 mg/l. Rats of both lethal and sublethal levels exhibited clinical signs during the exposure including irregular, labored breathing, lumbering gait, and red ears and feet. At lethal concentrations, rats looked ill, had rapid, shallow breathing, puffiness, lethargy and irritability (3/4). Both rats of a 10.9 mg/l exposure showed weight loss, growing irritability, weakness, shaking, screaming and convulsions. One of these rats succumbed at 7 days post-exposure after also displaying flaccid paralysis of both hindlegs. Sublethal concentrations were characterized by dose-related weight loss and nervousness. Upon necropsy, pulmonary edema and congestion were revealed in the decedent rats, while survivors exhibited no gross pathology.[E I Dupont De Nemours & Co; Preliminary Comparative Toxicity Studies with Tetramethyl Lead & Tetraethyl Lead; 07/15/59; EPA Document No. 88-920010199; Fiche No. OTS0555601]**UNREVIEWED**
  
• Tetraethyl lead (CAS # 78-00-2) was evaluated for inhalation toxicity in 4 male Charles River CD rats administered repeated whole-body exposures to 1.1 mg/l tetraethyl lead vapor (0.7 mg/L Pb), 1 hour/day for 5 days. The undiluted test material infused into a glass bubbler was vaporized and supplied as a dried metered airstream at 2.1 L/min into the bell jar containing the rats. Slight weight loss was continuous from the initial treatment and a slight nervousness was noted in 2/4 rats prior to the 5th and last exposure. All rats appeared otherwise normal. On the day following the 5th treatment and for 2 days after, increasing and unanimous shaking, screaming and convulsions culminated in 1 death and sacrifice of the remaining 3 rats. Necropsy revealed pulmonary edema and congestion in the decedent rat and congestion of the brain in all.[E I Dupont De Nemours & Co; Preliminary Comparative Toxicity Studies with Tetramethyl Lead & Tetraethyl Lead; 07/15/59; EPA Document No. 88-920010199; Fiche No. OTS0555601]**UNREVIEWED**
  
• Tetraethyl lead (CAS # 78-00-2) was evaluated for inhalation toxicity and tissue affinity in 4 male Charles River CD rats administered repeated whole-body exposures to 1.1 mg/l tetraethyl lead vapor (0.7 mg/l Pb), 1 hour/day for 5 days. The undiluted test material infused into a glass bubbler was vaporized and supplied as a dried metered airstream at 2.1 L/min into the bell jar containing the rats. Necropsy 3 days following the 5th and final exposure revealed pulmonary edema and congestion in the 1 decedent rat and congestion of the brain in all. Select harvested tissues were dried in a hot air oven at 100 degrees C to a constant weight, ashed and burned with nitric acid, and then heated to burn off the nitrates. The residue in hydrochloric acid was then analyzed for Pb content according to a method of W.W. Woessner and J. Cholak. A group average for 4 rats revealed that lead constituted 0.44, 1.0, 0.82, 7.4, 8.6, 5.14, and 13.0 mg respectively of 100 g bone, brain, fat, kidney, liver, lung, and spleen tissue.[E I Dupont De Nemours & Co; Preliminary Comparative Toxicity Studies with Tetramethyl Lead & Tetraethyl Lead; 07/15/59; EPA Document No. 88-920010199; Fiche No. OTS0555601]**UNREVIEWED**
  

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Footnotes

¹ Source: the National Library of Medicine's Hazardous Substance Database, 10/28/2007.