National Toxicology Program

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

Names (NTP)

• Endrin
• (1AALPHA,2BETA,2ABETA,3ALPHA,6ALPHA,6ABETA,7BETA,7AALPHA)-2,7:3,6-DIMETHANONAPHTH(2,3-B)OXIRENE, 3,4,5,6,9,9-HEXACHLORO-1-A,2,2A,3,6,6A,7,7A-OCTAHYDRO- (9CI)

Human Toxicity Excerpts

• IN ENGLAND OVER 100 PEOPLE WERE POISONED FROM EATING BREAD MADE FROM FLOUR CONTAMINATED WITH ENDRIN. WITHIN 1-3 HR OF EATING, /SOME/ ... WERE UNCONSCIOUS; OTHERS EXHIBITED EPILEPTIFORM CONVULSIONS. ... ALL RECOVERED WITHOUT COMPLICATIONS ... . [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-285]**PEER REVIEWED**
  
• WORKERS IN A PLANT MFR & FORMULATING ... ENDRIN HAD EPILEPTIFORM CONVULSIONS (3.3%) & HAD ELECTROENCEPHALOGRAMS SUGGESTING BRAIN STEM INJURY (20.5%). THE ELECTROENCEPHALOGRAMS USUALLY RETURNED TO NORMAL WITHIN 3-6 MO AFTER EXPOSURE CEASED. [National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 563]**PEER REVIEWED**
  
• THERE WAS GOOD EVIDENCE THAT THE EXPOSURE OF FACTORY WORKERS TO ENDRIN DURING PESTICIDE MFR SIGNIFICANTLY INCR THE ACTIVITY OF HEPATIC MICROSOMAL ENZYMES, WITH INCR URINARY EXCRETION OF D-GLUCARIC ACID. [The Chemical Society. Foreign Compound Metabolism in Mammals Volume 3. London: The Chemical Society, 1975., p. 621]**PEER REVIEWED**
  
• Workers exposed to endrin exhibited a marked incr in excretion of 6-beta-hydroxycortisol and a marked decr in tissue storage levels of p,p'-1,1-dichloro-2,2-bis(p-chlorophenyl)ethene resulting from general environmental exposure. [NIOSH; Special Occupational Hazard Review: Aldrin/Dieldrin p.89 (1978) DHEW Pub. NIOSH 78-201]**PEER REVIEWED**
  
• SYMPTOMATOLOGY: (Onset of symptoms between 20 min and 12 hr after ingestion): 1. Malaise, headache, nausea, vomiting, dizziness, and tremors. 2. Clonic and tonic convulsions, sometimes without premonitory symptoms. 3. Convulsive episodes may alternate with periods of severe central nervous depression. Death from respiratory arrest may occur during coma, which commonly outlasts the convulsive phase and may persist for a few days. /Dieldrin/ [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-285]**PEER REVIEWED**
  
• SYMPTOMATOLOGY: 4. During the acute phase, leukocytosis, rise in blood pressure, tachycardia, arrhythmias, metabolic acidosis, and fever have been described; Presumably they represent the consequences of hyperactivity of the sympathetic nervous system. 5. Disturbances of sleep, memory, and behavior may persist for several days or weeks after the acute phase of dieldrin poisoning. 6. Generalized cerebral dysrhythmia persisting for months, and both hematuria and albuminuria of about 2 weeks duration have been described in one aldrin poisoning in man. Transient hematuria occurred on the second day of an acute dieldrin poisoning. /Dieldrin/ [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-285]**PEER REVIEWED**
  
• Toxic level in human blood; 0.003 mg% 0.030 ug/ml; Lethal: not specified. [Winek, C.L. Drug and Chemical Blood-Level Data 1985. Pittsburgh, PA: Allied Fischer Scientific, 1985., p. 2]**PEER REVIEWED**
  
• Vital status and cause of death were assessed for 232 of a group of 233 workers engaged in the manufacturing and/or formulation of aldrin, dieldrin, endrin, and (for a limited period) Telodrin. This group is part of the total exposed population of more than 100 workers and was selected for follow up on account of the high exposures in the initial years of manufacturing and formulation and of the long exposure (mean 11 yr) and observation (mean 24 yr) periods. Total observed mortality was 25 versus 38 expected on the basis of the death statistics of the male Dutch population. Of the 9 cancer deaths, 3 were caused by lung cancer, while the remaining 6 were each of a different nature. Although in this group exposures have been high and exposure and the observation periods, long enough for meaningful evaluation, this study revealed no indication of a specific carcinogenic activity of aldrin, dieldrin, or endrin in manufacturing plant workers exposed to these products. [Ribbons PH; Int Arch Occup Environ Health 56 (2): 75-80 (1985)]**PEER REVIEWED**
  
• Ingestion of 12 g of endrin by a 49 year old man caused convulsions persisting for 4 days, hypersalivation, hyperthermia, renal insufficiency, thrombocytopenia and recurrent hypotension. Death followed after 11 days, due to pulmonary complications (infection and hemorrhage) and hypoxemia causing bradycardia and cardiac arrest. Endrin in blood 4 hr, 6 and 11 days after ingestion were, respectively, 450, 86 and 71 ug/l. Endrin concentrations 11 days after ingestion were 0.071 mg/l in blood, 89.5 mg/kg in adipose tissue, 0.87 mg/kg in the heart, 0.89 mg/kg in the brain, 0.55 mg/kg in the kidneys, and 1.32 mg/kg in the liver. [Runhaar EA et al; Hum Toxicol 4 (3): 241-7 (1985)]**PEER REVIEWED**
  
• Its chief toxic effect is as a convulsant; in human beings, the early effects of acute intoxication are sudden epileptiform convulsions, lasting for several min, which can occur from 30 min up to 10 hr following over-exposure. ... Dyisrhythmic changes, often/precede convulsion. ... Removal from exposure generally results in a normal electroencephalogram within one to six mo. In most cases, recovery is rapid, but anorexia, lethargy, weakness, headache, & dizziness may persist for two to four wk. ... In less severe cases of endrin intoxication, the main complaints were headache, dizziness, abdominal distress, nausea, vomiting, insomnia, & occasionally slight mental confusion. Many fatalities have occurred from ingestion of endrin, usually from accidental intake of bread made with contaminated flour. Such cases result in sudden onset of convulsions, with serum endrin levels of 0.053 ppm 30 min after the convulsion & 0.083 ppm after 20 hr. [Zenz, C., O.B. Dickerson, E.P. Horvath. Occupational Medicine. 3rd ed. St. Louis, MO., 1994, p. 623]**PEER REVIEWED**
  
• The most spectacular episodes of poisoning by endrin have been associated with the eating of bread made from contaminated flour. In most instances contamination occurred during shipment of the flour. At least 936 persons have been made sick by eating contaminated bread, and 26 of them died. Isolated accidents often involving the ingestion of formulations are less likely to be reported, but their number has been considerable. For example, 13 cases including six deaths in children /have been reported/. 60 cases of which 41 were suicidal, five were homicidal, 13 were of unknown origin, and one was accidental /have been reported/. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 248]**PEER REVIEWED**
  
• The onset of poisoning may be as little as half an hour or as much as 10 hr after eating contaminated food. The interval usually has been 1 to 4 hr in cases of accidental ingestion and much less in cases of suicide and homicide. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 249]**PEER REVIEWED**
  
• Severe poisoning by endrin involves repeated, violent, epileptiform convulsions, each lasting several minutes and followed by semiconsciousness or coma for 15 to 30 min unless the next fit occurs sooner. Fits may become almost continuous. Usually, there are few or no warning symptoms in severe poisoning, and even in moderate poisoning there may be no warning before the first fit. A less common but very ominous feature of serious poisoning is hyperthermia (41 deg C or more). The high fever was followed by decerebrate rigidity in 1 and 2.5 year old children who developed temperatures 42 deg C and 41.7 deg C, respectively. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 249]**PEER REVIEWED**
  
• Mild illness has involved dizziness, weakness of the legs, abdominal discomfort, and nausea but usually not vomiting. Some patients were temporarily deaf and some were slightly disoriented or aggressive. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 249]**PEER REVIEWED**
  
• Deaths have occurred as little as half an hr after ingestion, and most suicidal cases are dead within an hr or two. Deaths usually have occurred in accidental cases within the first 12 hr. In most survivors, recovery was well advanced 24 hr after poisoning, but a few complained of headache, dizziness, lethargy, weakness, and anorexia for 2 to 4 wk. In one epidemic, many victims improved within the first 5 hours in the hospital, and they were promptly discharged. Except for abnormal electroencephalograms, neurological findings were normal soon after a convulsion. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 249]**PEER REVIEWED**
  
• The mortality rates in outbreaks involving contaminated bread have varied from 0% to 9%. The difference depended in part on dosage. Endrin was found in a concentration of 150 ppm in a sample of bread in an epidemic with no mortality (0/59) and at concentrations of 1339 to 1807 in an epidemic with 9.0% (17/188) mortality. However, the mortality was 1.4% (7/490) in an outbreak in which a bread sample contained only 48 ppm of endrin. The mortality may have been due in part to the fact that patients in the latter epidemics were treated with atropine in the belief that they were suffering from organophosphate poisoning. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 250]**PEER REVIEWED**
  
• Seven intoxications involving endrin, all characterized by one or more convulsions, were encountered in one factory. Although these illnesses were scattered over a period of 8 yr, all of them occurred during the 1st or, in a few instances, during the 2nd year of exposure of each person involved. Clinical recovery following occupational exposure to endrin has been essentially complete within 24 hr. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 250]**PEER REVIEWED**
  
• An outbreak of endrin poisoning from contaminated food in Pakistan in 1984 resulted in a 10% mortality rate from seizures. Seizures occurred within 2 hours following ingestion of contaminated food, and in some instances status epilepticus occurred. endrin serum concentrations in these individuals ranged from 1.5-49.4 ppb. Normal cases recovered in a few days. [Sullivan, J.B. Jr., G.R. Krieger (eds.). Hazardous Materials Toxicology-Clinical Principles of Environmental Health. Baltimore, MD: Williams and Wilkins, 1992., p. 1048]**PEER REVIEWED**
  
• Endrin ... produces dizziness, seizures, tremors, and confusion in acute toxicity. ... Has also been associated with hyperthermia followed by decerebrate rigidity. ... Endrin does not accumulate in human tissues following exposure and is rapidly metabolized. [Sullivan, J.B. Jr., G.R. Krieger (eds.). Hazardous Materials Toxicology-Clinical Principles of Environmental Health. Baltimore, MD: Williams and Wilkins, 1992., p. 1047]**PEER REVIEWED**
  
• The toxicity of endrin resembles that of its stereoisomers, aldrin and dieldrin. In acute oral toxicity tests, endrin proved highly toxic to the mouse, monkey, and rat respective LD50 values were 1.37, 3, and 5.3 mg/kg. Intravenously, in the mouse, endrin proved equally toxic (LD50, 2.3 mg/kg); at equimolar doses, endrin produced convulsions and death quicker than did dieldrin. Dermally, endrin was less toxic; the LD50 for male and female rats was 18 and 15 mg/kg, respectively. [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. 546]**PEER REVIEWED**
  
• In humans, the approximate oral dose producing convulsions lies between 0.2 and 0.25 mg/kg; 1.0 mg/kg resulted in repeated seizures. Human consumption of 1 mg/kg of body weight has resulted In the onset of symptoms in about 3 hours. [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. 546]**PEER REVIEWED**
  
• Single doses of 2.5 mg/kg of endrin administered orally to pregnant hamsters during the period of fetal organogenesis caused a high incidence of fetal death, congenital anomalies, and growth retardation. [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. 546]**PEER REVIEWED**
  

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Non-Human Toxicity Excerpts

• MUTAGENICITY: MUTATION RESEARCH 76: 169 (1980). ESCHERICHIA COLI WP2,UVRA - REVERSE MUTATION STUDIES WITH METABOLIC ACTIVATION: NEGATIVE. [GENE-TOX Program: Current Status of Bioassay in Genetic Toxicology. U.S. Environmental Protection Agency, Washington, DC. Office of Toxic Substances and Pesticides. (For program information, contact Environmental Mutagen Information Center, Oak Ridge National Laboratory, Post Office Box Y, Oak Ridge, Tennessee 37830. Telephone (615) 574-7871), p. ]**PEER REVIEWED**
  
• AN AFFECTED ANIMAL MAY FIRST BECOME APPREHENSIVE & HYPERSENSITIVE OR ... BELLIGERENT. SOON BLEPHAROSPASMS & FASCICULATIONS OF FACIAL & CERVICAL MUSCLES WILL APPEAR, FOLLOWED BY CLONIC SPASMS ... /INCR IN SALIVATION & FROTHING PRECEDES CONVULSIONS PROGRESSING TO DEATH/. [Garner's Veterinary Toxicology. 3rd ed., rev. by E.G.C. Clarke and M.L. Clarke. Baltimore: Williams and Wilkins, 1967., p. 237]**PEER REVIEWED**
  
• THE CARDIOVASCULAR EFFECT OF ENDRIN IN DOGS WAS FOUND ... TO BE DUE TO THE ACTION ON THE CNS ALTHOUGH SOME MAY BE CAUSED BY CHANGES IN CEREBRAL HEMODYNAMICS. ... IN CHRONIC POISONING CHANGES IN RENAL FUNCTION WERE MINIMAL, & DUE TO SECONDARY CHANGES IN SYSTEMIC HEMODYNAMICS. [Clarke, M. L., D. G. Harvey and D. J. Humphreys. Veterinary Toxicology. 2nd ed. London: Bailliere Tindall, 1981., p. 143]**PEER REVIEWED**
  
• WHEN QUAIL WERE FED 1 PPM /ENDRIN/, NO EGGS WERE PRODUCED DURING THE REPRODUCTIVE PERIOD. ENDRIN FED @ 10 PPM REDUCED EGG PRODN IN PHEASANTS & REDUCED SURVIVAL OF THE CHICKS. [National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 567]**PEER REVIEWED**
  
• ENDRIN WAS FED TO RATS @ 2, 6, OR 12 PPM IN THE DIET FOR 2 YR WITHOUT PRODUCING PRIMARY MALIGNANT HEPATIC TUMORS OR INCREASING TUMOR INCIDENCE IN ANY ORGANS. [National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 566]**PEER REVIEWED**
  
• ... ENDRIN ... STUDIED ... IN HAMSTERS & MICE. SINGLE, ORAL DOSES APPROX 1/2 THE RESPECTIVE LD50 DOSES WERE GIVEN ON DAYS 7, 8, OR 9 OF GESTATION IN THE HAMSTER & ON DAY 9 OF GESTATION IN THE MOUSE. ... NUMBER OF DEFECTS WERE PRODUCED IN BOTH SPECIES. [National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 567]**PEER REVIEWED**
  
• IN BEAGLE DOGS 9 MO STUDY DOSAGE LEVELS OF 1-3 PPM YIELDED INCREASED LIVER/BODY RATIO. [National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 572]**PEER REVIEWED**
  
• PREGNANT CD RATS RECEIVED 0.450, 0.330, 0.150, 0.075, OR 0 MG/KG/DAY BY GASTRIC INTUBATION. MARKED REDUCTIONS IN MATERNAL WT GAIN, INCR IN HEPATIC TISSUE RESIDUE. FETAL TISSUE BURDEN INCR AT LOWEST DOSAGE. NOT TERATOGENIC. [KAVLOCK RJ ET AL; TOXICOLOGY 21 (2): 141 (1981)]**PEER REVIEWED**
  
• THE HEPATOCYTE PRIMARY CULTURE/DNA REPAIR ASSAY USING RAT, HAMSTER, & MOUSE HEPATOCYTES EXPOSED TO ENDRIN FOR 18 HR TOGETHER WITH THYMIDINE, INDICATED THAT ENDRIN WAS NOT GENOTOXIC. [MASLANSKY CJ ET AL; J TOXICOL ENVIRON HEALTH 8 (1-2): 121 (1981)]**PEER REVIEWED**
  
• CNS TERATOGEN IN HAMSTERS BUT NOT IN RATS EXPOSED PERINATALLY TO 1.5 MG/KG/DAY ON DAYS 5-14 OF GESTATION CAUSED INCR LOCOMOTION ACTIVITY. RATS EXPOSED PERINATALLY SURVIVED; PUPS GROWTH NOT AFFECTED. [GRAY LE JR ET AL; TOXICOLOGY 21 (3): 187 (1981)]**PEER REVIEWED**
  
• PREGNANT CD 1 MICE RECEIVED 2.0, 1.5, 1.0, OR 0 MG/KG/DAY BY INTUBATION. MATERNAL TOXICITY INCL DEATH, DECR WT GAIN. CONCLUDED ENDRIN WAS NOT TERATOGENIC IN MICE WHEN ADMIN AT MATERNALLY TOXIC DOSE LEVELS THROUGHOUT PERIOD OF ORGANOGENESIS. [KAVLOCK RJ ET AL; TOXICOLOGY 21 (2): 141 (1981)]**PEER REVIEWED**
  
• Ten Ophiocephalus punctatus fish were placed in 20 l solns of 0.005, 0.01, 0.02, 0.04, or 0.08 ppm endrin and kept at 29 + or - 4 deg C at a pH 6.9. The percent survival at 96 hr was 100%, 80%, 70%, 40%, and 0% for the 0.005, 0.01, 0.02, 0.04, and 0.08 ppm groups, respectively. Statistically significant inhibition was noted ... for kidney lactic dehydrogenase. [Sharma SK et al; Bull Envir Contam Toxicol 23 (1-2): 153-7 (1979)]**PEER REVIEWED**
  
• Fetal toxicity was determined in hamsters exposed to endrin ... on either day 8 or days 5-14 of gestation, by administration by oral gavage as a solution in corn oil /at doses of/ ... 0.5-10.0 mg/kg on day 8 and 0.75 to 3.5 mg/kg on days 5-14. ... Single dose /exposures/ ... resulted in significant incidences of fused ribs and meningoencephaloceles at levels of 5 mg/kg or greater. However, no significant effects were noted in either maternal mortality, and weight gain or in fetal mortality or weight gain. ... Multiple doses ... resulted in few fetal defects, although a significant dose-related incr in fetal mortality and decr in fetal weight was seen. Significant maternal lethality and weight reductions were noted at doses of 1.5 mg/kg/day or greater. ... Endrin was found to cross the placenta, and 20 ppb were found in fetuses from litters exposed to 2.5 mg/kg/day. [Chernoff N et al; Toxicology 13: 155-65 (1979)]**PEER REVIEWED**
  
• Rainbow trout (Salmo gairdnerii), bluegill sunfish (Lepomis macrochirus), and sea lampreys (Petromyzon marinus) were subjected to 5.0 ppm of an 18.5% emulsified concn of endrin. Time for death or obvious distress to occur was: 4 hr, trout; 5 hr, bluegill; 14 hr, lamprey. [Applegate, V.C., J.H.Howell, A.E. Hall, Jr., M.A. Smith. Toxicity of 4,346 Chemicals to Larval Lampreys and Fishes. Special Scientific Report-Fisheries No. 207. Washington, DC: U.S.Department of Interior, Fish and Wildlife Service, March 1957., p. 56]**PEER REVIEWED**
  
• COMPARATIVE EFFECTS OF ALDRIN, DIELDRIN, ENDRIN, ISODRIN, & TELODRIN ON DIFFERENT ATPASE ACTIVITIES IN BEEF HEART MITOCHONDRIAL & RAT BRAIN SYNAPTOSOMAL FRACTIONS WERE DETERMINED IN VITRO. BEEF HEART MITOCHONDRIAL (OLIGOMYCIN-SENSITIVE) MG(2+) ATPASE ACTIVITY WAS INHIBITED BY ALL CHEM AT ALL CONCN TESTED. /SRP: ABOUT 30% INHIBITION WAS OBSERVED WITH 100 UM ENDRIN/. RESULTS SUGGEST THAT ATPASE SYSTEM IN RAT HEART & CNS MAY BE SELECTIVELY INHIBITIED BY ALDRIN, BUT NOT BY ITS STRUCTURAL ANALOGS. [MEHROTRA BD ET AL; J APPL TOXICOL 2 (6): 278-83 (1982)]**PEER REVIEWED**
  
• Endrin was tested for mutagenicity in the Salmonella/microsome preincubation assay. Endrin was tested over a wide range of doses (0, 100, 333, 1000, 3333, and 10,000 ug/plate) in four Salmonella typhimurium strains (TA98, TA100, TA1535, and TA1537) in the presence and absence of Aroclor-induced rat or hamster liver S9. Endrin was negative in these tests and the highest ineffective dose level tested (not causing the formation of a precipitate) in any Salmonella tester strain was 333 ug/plate. [Zeiger E et al; Environ Mutagen 9: 1-110 (1987)]**PEER REVIEWED**
  
• The neurotoxic insecticide /endrin/ inhibited gamma-aminobutyric acid-dependent (36)Cl- uptake by mouse brain vesicles. [Bloomquist JR, Soderlund DM; Biochem Biophys Res Commun 133 (1): 37-43 (1985)]**PEER REVIEWED**
  
• Concentrations of 0, 1, and 3 ppm endrin in dry duck mash were fed to mallards (Anas platyrhynchos) starting in Dec. Health and reproduction were measured the following spring and summer. One male fed 3 ppm, died with a diagnostically lethal level of 2.0 ppm (wet wt) in its brain. Birds fed 1 ppm reproduced as well as, if not better than, controls. Birds fed 1 ppm had significantly greater hatching success of fertile eggs than did those fed 0 or 3 ppm, and their clutches hatched significantly earlier than did those of birds fed 3 ppm. Mallards fed 3 ppm appeared to reproduce more poorly than controls, but this finding must be regarded with caution because the results of statistical tests often were not significant. Edrin accumulated in eggs to a mean of 1.1 and 2.9 ppm (wet wt) when fed to hens at 1 and 3 ppm. The concn in the carcasses of adults was similar to that in eggs, but the concn in the fat of adults was approx 4-7 times higher than in eggs. [Spann JW et al; Environ Toxicol Chem 5 (8): 755-9 (1986)]**PEER REVIEWED**
  
• The toxicity to mice of ip administered polychlorocycloalkane insecticides, including endrin, is generally correlated with their potency as in vitro inhibitors of the brain specific (35)S-t-butylbicyclophosphorothionate binding site with correction for metabolic activation and detoxification. These findings from earlier studies areextended to in vivo investigations relating convulsant action to inhibition of the (35)S-t-butylbicyclophosophorothionate binding site in poisoned mice. Radioligand binding assays involved brain P2 membranes. Examination of lindane, technical toxaphene, toxaphene toxicant A, and 10 polychlorocyclodiene insecticides, including endrin , revealed 62 + or - 4% binding site inhibition 30 min after their LD50 doses with 32 +/- 3% inhibition at one-half and 6 + or - 3% inhibition at one-quarter of their LD50 doses. The brain P2 membranes of treated mice contain the parent compound with each of the polychlorcycloalkanes plus activation products of some of the cyclodienes: including 12-ketoendrin from endrin. [Cole LM, Casida JE; Life Sci 39 (20): 1855-62 (1986)]**PEER REVIEWED**
  
• HEPTACHLOR, 1,1,1-TRICHLORO-2,2-BIS(P-CHLOROPHENYL)ETHANE, ENDRIN, & ALDRIN WERE TERATOGENIC IN CHICKEN EGGS & THAT COMBINATIONS OF THESE INSECTICIDES HAD /SYNERGISTIC/ EFFECTS. [Casarett, L.J., and J. Doull. Toxicology: The Basic Science of Poisons. New York: MacMillan Publishing Co., 1975., p. 329]**PEER REVIEWED**
  
• The no-effect level in the rat is 0.05 mg/kg/day (dietary level of 1 ppm), in the mouse 0.038 mg/kg/day (dietary level of 0.3 ppm), and in the dog 0.025 mg/kg/day (dietary level of 1 ppm). [Hayes, W.J., Jr., E.R. Laws, Jr., (eds.). Handbook of Pesticide Toxicology. Volume 2. Classes of Pesticides. New York, NY: Academic Press, Inc., 1991., p. 841]**PEER REVIEWED**
  
• Intratesticular injection of mice with endrin caused chromosomal abnormalities. Studies in mice have demonstrated that endrin produces specific alterations in unmyelinated fiber bundles of peripheral nerves but does not affect myelinated fibers. [Hayes, W.J., Jr., E.R. Laws, Jr., (eds.). Handbook of Pesticide Toxicology. Volume 2. Classes of Pesticides. New York, NY: Academic Press, Inc., 1991., p. 843]**PEER REVIEWED**
  
• A high incidence of fetal organogenesis was reported in golden hamsters fed single doses of 2.5 mg/kg of endrin. ... Congenital anomalies and growth retardation in offspring /were reported/, and rats fed a diet of 100 ppm of endrin for two years developed degenerative changes. [Zenz, C., O.B. Dickerson, E.P. Horvath. Occupational Medicine. 3rd ed. St. Louis, MO., 1994, p. 623]**PEER REVIEWED**
  
• Signs of Intoxication: Ataxia, slowness, drowsiness, tremors, trachael congestion, prostration, convulsions, wing-beat convulsions, and opisthotonos. Signs appeared as soon as 1 hr and mortalities usually occurred between 1 hr and 5 days after treatment. Remission took up to 1 week. /Species not specified/ [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. 38]**PEER REVIEWED**
  
• The 30 day empirical minimum lethal dose for mallards (n =12) is 0.250 mg/kg per day for both sexes. The resulting cumulative toxicity index is 5.64/0.25 = 22, indicating a moderately high degree of cumulative action. The percutaneous LD50 for 10 month old mallard drakes (n =2) after a 24 hr dermal foot exposure to the 97% sample aoppears to be >140 mg/kg. Signs observed after percutaneous treatment included hyperexcitability, tenseness, shakiness, jerkiness, ataxia goose-stepping ataxia, slowness, and stumbling. These signs appeared as soon as 3 hr after the initiation of treatment. Remission took up to 4 days after the end of treatment. Mild dermal irritation was caused by exposure to endrin. When the percutaneous LD50 is compared with the acute oral LD50, endrin appears to have a relatively low order of dermal hazard in mallards. [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. 38]**PEER REVIEWED**
  
• A total of 1600 mice of two strains were used to explore the possible carcinogenicity of endrin. Dietary levels of 0.3 and 3.0 ppm were used, and a few convulsions were observed at the higher level. Although fibrosarcomas, hepatomas, and leukemia were oberved, their incidence was not significantly higher than in the controls. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 248]**PEER REVIEWED**
  
• Endrin is not teratogenic under practical conditions. Dietary levels that do not injure the parents do not injure reproduction. In fact reproduction may continue with little change even at dosage levels that produce some convulsions. The results in wild deer mice are similar. Increased fetal mortality and also increased fetal toxicity (primarily delayed and deviant ossification) /was reported/ in the offspring of rats and mice that were bred for the first time 1 week after receiving four oral doses of endrin emulsion at a rate of 0.58 mg/kg at weekly intervals. The small differences were of unstated statistical significance. Endrin administered pregnancy at half the LD50 level produced a marked increase in fetal deaths of hamsters but not mice. Open eye, webbed foot, cleft palate, and especially fused ribs were seen in young hamster and may have been related to growth retardation. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 248]**PEER REVIEWED**
  
• Differences in the effects of single and repeated doses administered hamsters during pregnancy were reported. A single dose as high as 10 mg/kg on day 8 did not kill the dams or young but did increase in the incidence of fused ribs and meningoencephaloceles. Multiple doses as high as 3.5 mg/kg/day on days 5 to 14 caused maternal weight loss and mortality, and fetal mortality but fewer fetal defects. Single dosages less than 5 mg/kg and repeated dosages of 1.5 mg/kg/day were ineffective. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 248]**PEER REVIEWED**
  
• Hamster pups from dams that had received 1.5 mg/kg/day on gestation days 5 to 14 were more active than controls 15 days after birth, but the difference disappeared by day 34. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 248]**PEER REVIEWED**
  
• An increased in the relative weight of the liver /was observed/ in rats receiving 5 ppm or more of endrin in the diet. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 248]**PEER REVIEWED**
  
• Increased mixed function oxidase activity has been induce in both rats and rabbits by feeding low levels of endrin. ... No enzyme changes /were found/ 12 hr after endrin was administered but did find induction 24 hr and more after administration. Another source of variation is excessive dosage, which may be inhibitory. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 248]**PEER REVIEWED**
  
• Greater benzpyrene hydroxylase activity was found in the liver microsomes of endrin-resistant pine mice than in microsomes from susceptible ones. High levels also were found in the offspring of resistant mice, suggesting that the difference may be inherited. The evidence for inheritance (in contrast to tolerance) is reasonable inasmuch as endrin is excreted rapidly, but final proof would require, among other things, demonstration that the young received no endrin via the placenta and milk. In nature, where the possibilty of outbreeding cannot be excluded, pine mice gradually lost resistance to endrin after application of endrin as a control measure was stopped. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 248]**PEER REVIEWED**
  
• Large, single doses and small, repeated doses of endrin have largely opposite effects on the concentrations of biogenic amines in the brain, but whether the changes are responsible for poisoning or secondary to it is obscure. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 248]**PEER REVIEWED**
  
• Three known mammalian metabolites of endrin are more toxic than the parent compound. The LD50 of 12-ketoendrin is 1.1 and 0.8 mg/kg in male and female rats respectively, and it exerts its full effect during the first 20 hr, compared to 4 to 8 days for endrin. Thus, 12-ketoendrin may be responsible for much of the acute toxicity of endrin or of intermediate metabolites in the rat. However, the fact that the brains of rats killed by endrin contain (in addition to endrin) substantially less 12-ketoendrin than do the brains of rats killed by 12-ketoendrin suggests that endrin is toxic per se. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 247]**PEER REVIEWED**
  
• ... A single resistant mosquito fish may be treated with endrin in such a way that it survives but is able to release enough of the compound into 10 l of clean water to kill five normally susceptible fish of the same species. [Hayes, W.J., Jr., E.R. Laws Jr., (eds.). Handbook of Pesticide Toxicology Volume 1. General Principles. New York, NY: Academic Press, Inc., 1991., p. 471]**PEER REVIEWED**
  
• Young dairy calves are poisoned by 8.8 mg/kg body wt, PO, but tolerate 4.4 mg/kg, while adult cattle tolerate 8.8 mg/kg and are poisoned by 22 mg/kg. Pigs tolerate 22 mg/kg and are poisoned by 44 mg/kg. Horses are poisoned by 22 mg/kg. Because of its effectiveness against insect pests on crops and pasture and consequent low dosage per acre, dieldrin is not likely to poison livestock grazing the treated areas. /Dieldrin/ [Aiello, S.E. (ed). The Merck Veterinary Manual. 8th ed. Merck & Co., Inc., National Publishing Inc., Philadelphia, PA. 1998., p. 2063]**PEER REVIEWED**
  

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Human Toxicity Values

• None found

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Non-Human Toxicity Values

• LD50 Guinea pig male oral 36 mg/kg [Hayes, W.J., Jr., E.R. Laws, Jr., (eds.). Handbook of Pesticide Toxicology. Volume 2. Classes of Pesticides. New York, NY: Academic Press, Inc., 1991., p. 841]**PEER REVIEWED**
  
• LD50 Guinea pig female oral 16 mg/kg [Hayes, W.J., Jr., E.R. Laws, Jr., (eds.). Handbook of Pesticide Toxicology. Volume 2. Classes of Pesticides. New York, NY: Academic Press, Inc., 1991., p. 841]**PEER REVIEWED**
  
• LD50 Rat female dermal 15 mg/kg [Hayes, W.J., Jr., E.R. Laws, Jr., (eds.). Handbook of Pesticide Toxicology. Volume 2. Classes of Pesticides. New York, NY: Academic Press, Inc., 1991., p. 841]**PEER REVIEWED**
  
• LD50 Rabbit female oral 7-10 mg/kg [Hayes, W.J., Jr., E.R. Laws, Jr., (eds.). Handbook of Pesticide Toxicology. Volume 2. Classes of Pesticides. New York, NY: Academic Press, Inc., 1991., p. 841]**PEER REVIEWED**
  
• LD50 Monkey oral 3 mg/kg [Hayes, W.J., Jr., E.R. Laws, Jr., (eds.). Handbook of Pesticide Toxicology. Volume 2. Classes of Pesticides. New York, NY: Academic Press, Inc., 1991., p. 841]**PEER REVIEWED**
  
• LD50 Rat oral 3 mg/kg [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, 1986., p. 231]**PEER REVIEWED**
  
• LD50 Mouse oral 1.3 mg/kg [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, 1986., p. 231]**PEER REVIEWED**
  
• LD50 Mouse iv 2.3 mg/kg [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, 1986., p. 231]**PEER REVIEWED**
  
• LD50 Rat male dermal 18 mg/kg [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, 1986., p. 231]**PEER REVIEWED**
  
• LD50 Rat acute oral 7-15 mg/kg, 3 mg/kg, male and female rat 18 and 7.5 mg/kg [Montgomery, J.H.; Agrochemicals Desk Reference 2nd ed. Lewis Publishers, Boca Raton, FL 1997, p. 208]**PEER REVIEWED**
  
• LD50 Rat oral 3 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. 1464]**PEER REVIEWED**
  
• LD50 Rat skin 12 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. 1464]**PEER REVIEWED**
  
• LD50 Mouse oral / SRP:/ 1.4 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. 1464]**PEER REVIEWED**
  
• LD50 Mouse iv /SRP: 2.3 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. 1464]**PEER REVIEWED**
  
• LD50 Monkey oral 3 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. 1464]**PEER REVIEWED**
  
• LD50 Rabbit oral 7 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. 1464]**PEER REVIEWED**
  
• LD50 Rabbit skin 60 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. 1464]**PEER REVIEWED**
  
• LD50 Guinea pig oral 16 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. 1464]**PEER REVIEWED**
  

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Absorption, Distribution and Excretion

• ... ENDRIN IS CLEARED MUCH MORE RAPIDLY FROM PLASMA THAN DIELDRIN BECAUSE OF MORE RAPID BILIARY EXCRETION. [National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 122]**PEER REVIEWED**
  
• TWELVE WK AFTER APPLICATION OF (14)C ENDRIN TO UPPER LEAF SURFACES OF COTTON PLANTS, 33% OF THE APPLIED RADIOACTIVITY WAS RECOVERED, 26% ON & IN THE LEAVES & THE REMAINDER IN THE OTHER PLANT PARTS & SOIL. [Menzie, C. M. Metabolism of Pesticides, An Update. U.S. Department of the Interior, Fish, Wild-life Service, Special Scientific Report - Wildlife No. 184, Washington, DC: U.S. Government Printing Office, l974., p. 22]**PEER REVIEWED**
  
• ENDRIN IS ACCUM IN THE BODY FAT OF COWS & IS EXCRETED IN SMALL AMT IN THEIR MILK. [Clarke, E.G., and M. L. Clarke. Veterinary Toxicology. Baltimore, Maryland: The Williams and Wilkins Company, 1975., p. 199]**PEER REVIEWED**
  
• VERY LITTLE ENDRIN, AS COMPARED TO OTHER ORGANOCHLORINE INSECTICIDES, IS STORED IN 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. V5 164 (1974)]**PEER REVIEWED**
  
• ORAL ADMIN OF (14)C ENDRIN TO RATS IN DAILY DOSES OF 8 UG IN PEANUT OIL FOR 12 DAYS RESULTED IN EQUIL AFTER 6 DAYS. AFTER 12 DAYS, THE SPLEEN HAD HIGHEST CONCN, 3 PPM, THE BLOOD, 1.1 PPM, THE SKIN & SC ADIPOSE TISSUE, 0.74 PPM, THE PERITONEAL ADIPOSE TISSUE, 0.38 PPM & THE BRAIN, 0.25 PPM. [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. V5 164 (1974)]**PEER REVIEWED**
  
• NO RESIDUES WERE DETECTED IN PLASMA, ADIPOSE TISSUE & URINE OF WORKERS OCCUPATIONALLY EXPOSED TO ENDRIN. [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. V5 165 (1974)]**PEER REVIEWED**
  
• NO EVIDENCE OF EGGSHELL THINNING WAS FOUND FOR ANY OF SPECIES STUDIED. [KLAAS EE ET AL; PESTIC MONIT J 14 (3): 90 (1980)]**PEER REVIEWED**
  
• Following either oral or iv administration of (14)C endrin to rats, it is metabolized to relatively water soluble compounds and excreted mainly in the feces. ... The concentrations in the viscera are about the same as that in fat. ... Over 90% of excreted activity derived from (14)C endrin is found in the feces of intact rats and in the bile of those with bile fistulas. [Hayes, W.J., Jr., E.R. Laws, Jr., (eds.). Handbook of Pesticide Toxicology. Volume 2. Classes of Pesticides. New York, NY: Academic Press, Inc., 1991., p. 842]**PEER REVIEWED**
  
• After absorption, endrin is partly retained in fatty tissues, and partly excreted in urine and feces unchanged and as three metabolites. [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, 1986., p. 231]**PEER REVIEWED**
  
• Following either oral or intravenous administration of (14)C-endrin to rats, it is metabolized to relatively water-soluble compounds and excreted mainly in the feces. The half-life is 2 to 3 days in males and 4 days in females after a dosage of 0.2 mg/kg. With daily oral doses, rats reach maximal storage in 6 days. The concentrations in the viscera are about the same as that in fat. In the rabbit, C-endrin is metabolized to anti-12-hydroxyendrin and to a lesser extent syn-12-hydroxyendrin. The hydroxylated metabolites are excreted mainly as sulfate conjugates but also as glucuronide conjugates. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 247]**PEER REVIEWED**
  
• Over 90% of excreted activity derived from (14)C-endrin is found in the feces of intact rats and in the bile of those with bile fistulas. Under identical circumstances, endrin is excreted faster than dieldrin from intact rats, from bile-fistula rats (in the bile), and from isolated, perfused rat liver preparations. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 248]**PEER REVIEWED**
  
• The greater susceptibility of female rats to endrin is reflected by the slower biotransformation and excretion of (14)C endrin in perfused liver preparations from females. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 248]**PEER REVIEWED**
  

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Metabolism/Metabolites

• IN ANIMALS, ENDRIN IS DEGRADED, LARGELY TO 9-KETOENDRIN & 9-HYDROXYENDRIN, BUT ALSO TO 5-HYDROXYENDRIN. [National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 562]**PEER REVIEWED**
  
• IN A 6-DAY PERIOD, MALES /RATS ADMIN ENDRIN IN ARACHIS OIL/ EXCRETED IN FECES 66% DOSE ... FEMALES ... 37%. ... ANALYSIS /FECES/ REVEALED ... ENDRIN ... ANTI-12-HYDROXYENDRIN ... SYN-12-HYDROXYENDRIN ... 3-HYDROXYENDRIN ... 12-KETOENDRIN ... & DELTA-KETOENDRIN ... . [Menzie, C.M. Metabolism of Pesticides, Update II. U.S. Department of the Interior, Fish Wildlife Service, Special Scientific Report - Wildlife No. 2l2. Washington, DC: U.S. Government Printing Office, 1978., p. 12]**PEER REVIEWED**
  
• IN RATS ADMIN ENDRIN, ANALYSIS OF FECES REVEALED: A POLAR METABOLITE ... TRANS-4,5-DIHYDROISODRIN-4,5-DIOL. ANOTHER POLAR ... NOT IDENTIFIED. ... URINE FROM MALE RATS CONTAINED ENDRIN, 12-KETOENDRIN, ANTI-12-HYDROXYENDRIN & 3-HYDROXYENDRIN (17:19:2:1, RESPECTIVELY). THE EXTRACTS FROM FEMALE RATS DID NOT CONTAIN 12-KETOENDRIN. /SRP: 12-KETOENDRIN IS THE MOST TOXIC/. [Menzie, C.M. Metabolism of Pesticides, Update II. U.S. Department of the Interior, Fish Wildlife Service, Special Scientific Report - Wildlife No. 2l2. Washington, DC: U.S. Government Printing Office, 1978., p. 12]**PEER REVIEWED**
  
• ENDRIN ADMIN TO RATS IN 6 DAY STUDY: ... MAJOR METABOLITE IN FEMALE RAT URINE /WAS/ IDENTICAL TO 12-HYDROXYENDRIN O-SULFATE. IN TISSUES /ANALYZED/ 12-KETOENDRIN /WAS/ MAJOR CMPD IN FAT OF MALES; ENDRIN IN FEMALES /BUT/ 12-KETOENDRIN WAS ALSO PRESENT. IN LIVER OF MALES NO ENDRIN /WAS DETECTED/ & 12-KETOENDRIN /WAS/ MAJOR METABOLITE. [Menzie, C.M. Metabolism of Pesticides, Update II. U.S. Department of the Interior, Fish Wildlife Service, Special Scientific Report - Wildlife No. 2l2. Washington, DC: U.S. Government Printing Office, 1978., p. 12]**PEER REVIEWED**
  
• In the rabbit (14)C endrin is metabolized to anti-12-hydroxy endrin and to a lesser extent syn-12-hydroxyendrin. The hydroxylated metabolites are excreted mainly as sulfate conjugates but also as glucuronide conjugates. [Hayes, W.J., Jr., E.R. Laws, Jr., (eds.). Handbook of Pesticide Toxicology. Volume 2. Classes of Pesticides. New York, NY: Academic Press, Inc., 1991., p. 842]**PEER REVIEWED**
  
• Production of 12-ketoendrin varies greatly from one mammalian species to another, and none has been detected in birds. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 247]**PEER REVIEWED**
  
• After absorption, endrin is partly retained in the fatty tissues and partly excreted in the urine and feces unchanged and as three metabolites. Endrin is more rapidly excreted than dieldrin; rats, on a daily oral dose of 0.32 mg/kg, reached a state of equilibrium after 5 or 6 days. The biologic half-life was 3 days in male rats, 4 days in female rats. [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. 546]**PEER REVIEWED**
  

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TSCA Test Submissions

• None found

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Footnotes

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