Testing Information

Testing Status of Agents at NTP

CAS Registry Number: 8001-35-2 Toxicity Effects

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

Names (NTP)

  • Toxaphene
  • CAMPHECHLOR

Human Toxicity Excerpts

  • INVESTIGATORS: ... REPORTED 4 FATAL CASES OF CHILDREN WHO HAD INGESTED TOXAPHENE. TOXAPHENE PRODUCED CONGESTION AND EDEMA IN THE LUNG, DILATATION OF HEART, AND PETECHIAL HEMORRHAGES IN THE BRAIN. [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 3756]**PEER REVIEWED**
  • SYMPTOMATOLOGY: 1. REFLEX HYPEREXCITABILITY, EVIDENCED BY TREMOR, SALIVATION, & VOMITING. WHEN PRESENT, EMESIS IS APPARENTLY ALWAYS SECONDARY TO REFLEX EXCITATION & NOT TO LOCAL GI IRRITATION. 2. GENERALIZED EPILEPTIFORM CONVULSIONS OF VARIABLE DURATION. ... 3. DEATH DUE TO EXHAUSTION & RESP FAILURE. 4. MILD IRRITATION OF SKIN AFTER DERMAL EXPOSURES BUT LITTLE IF ANY SENSITIZATION. [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-387]**PEER REVIEWED**
  • ... HUMAN VOLUNTEERS INHALED ... 0.0004 MG/L FOR 10 MIN/DAY FOR 15 DAYS, THERE WERE NO SUBJECTIVE OR OBJECTIVE RESULTS. IN ANOTHER STUDY, A MIST CONTAINING TOXAPHENE AT 0.25 MG/L OF AIR WAS INHALED BY 25 PEOPLE FOR 30 MIN/DAY FOR 13 DAYS; THERE WAS NO EVIDENCE OF LOCAL OR SYSTEMIC TOXICITY. [National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 601]**PEER REVIEWED**
  • EIGHT WOMEN WORKING IN AREA WHICH HAD BEEN SPRAYED WITH 2 KG/HA TOXAPHENE BY AIRCRAFT HAD HIGHER INCIDENCE OF CHROMOSOME ABERRATIONS (ACENTRIC FRAGMENTS & CHROMATID EXCHANGES), AS OBSERVED IN LYMPHOCYTE CULTURES, COMPARED WITH AN UNSPECIFIED NUMBER OF CONTROL INDIVIDUALS: 13.1% VERSUS 1.6%. [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. V20 338 (1979)]**PEER REVIEWED**
  • In a survey of 199 employees who worked or had worked with toxaphene between 1949 & 1977, with exposures ranging from 6 mo to 26 yr (mean, 5.23 yr), 20 employees died, 1 with cancer of the colon; none of these deaths appeared to be related to exposure to toxaphene. [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. V20 339 (1979)]**PEER REVIEWED**
  • Allergic bronchopneumonia was observed in 2 workers using toxaphene. [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. V20 338 (1979)]**PEER REVIEWED**
  • Two cases of acute aplastic anemia associated with dermal exposure to toxaphene/lindane mixtures have been reported. One of these cases terminated in death due to acute myelomonocytic leukemia. [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. V20 339 (1979)]**PEER REVIEWED**
  • Short term exposure: Inhalation: 500 mg/cu m for 30 minutes for 10 days in a row caused no effects. Inhalation of spray at unknown levels has caused bronchitis and inflammation of the lung. [Bureau of Toxic Substance Assessment, New York State Department of Health Chemical Fact Sheet for Toxaphene (July/1982)]**PEER REVIEWED**
  • Short term exposure: Skin: If spilled on clothing and allowed to remain, can cause pain and reddening. May be absorbed through skin contributing to symptoms described under ingestion. [Bureau of Toxic Substance Assessment, New York State Department of Health Chemical Fact Sheet for Toxaphene (July/1982)]**PEER REVIEWED**
  • Short term exposure: Ingestion: Is absorbed through the stomach and intestines. 0.6 grams (about 1/50 of an ounce) has caused convulsions. Other symptoms include nausea, vomiting, bluish coloration of the skin, and coma. Estimated lethal dose for an adult is between 2 and 7 grams (1/15-1/4 ounce). [Bureau of Toxic Substance Assessment, New York State Department of Health Chemical Fact Sheet for Toxaphene (July/1982)]**PEER REVIEWED**
  • Long term exposure: Changes in genetic material have been observed in workers exposed to toxaphene. Toxaphene is known to cause cancer in rats and mice. Whether it causes cancer in humans is unknown. [Bureau of Toxic Substance Assessment, New York State Department of Health Chemical Fact Sheet for Toxaphene (July/1982)]**PEER REVIEWED**
  • In man the acute /oral/ lethal dose is given as 2 to 7 g. ... [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. 115]**PEER REVIEWED**
  • It can cause illness by inhalation, skin absorption, and/or ingestion. [Association of American Railroads. Emergency Handling of Hazardous Materials in Surface Transportation. Washington, D.C.: Assoc. of American Railroads, Hazardous Materials Systems (BOE), 1987., p. 688]**PEER REVIEWED**
  • ... A technical toxaphene mixture (Camphechlor) on aromatase (CYP19) activity were investigated in human choriocarcinoma JEG-3 cells. After 18 hr incubation with TCDD, PCB126, Aroclor 1016 or toxaphene, ethoxyresorufin-O-deethylase (EROD), and aromatase activity were determined. To exclude serum effects, incubations were carried out with or without fetal calf serum in the medium. Ethoxyresorufin-O-deethylase activity was induced by both TCDD and PCB126 in the presence or absence of serum, which indicates that JEG-3 cells are responsive toward dioxin-like chemicals. Neither Aroclor 1016 nor toxaphene affected ethoxyresorufin-O-deethylase activity in these cells. ... Aroclor 1016 and toxaphene had no effect on aromatase activity at concentrations up to 1.0 uM for Aroclor 1016 or 3.0 uM for toxaphene. These results show that aromatase activity ran be decreased in a concentration dependent way within the same range where ethoxyresorufin-O-deethylase activity is increased. [Drenth H-J et al; Toxicology and Applied Pharmacology 148 (1): 50-55 (1998)]**PEER REVIEWED**
  • ... Toxaphene significantly inhibited gap junctional intercellular communication in a dose dependent manner. ... Dieldrin and toxaphene inhibited gap junctional intercellular communication by 70 to 80% within 3 hr and 30 minutes of exposure, respectively. No recovery of gap junctional intercellular communication to the control value was observed. [Kang K-S et al; Environmental Health Perspectives 104 (2): 192-200 (1996)]**PEER REVIEWED**

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Non-Human Toxicity Excerpts

  • TOXAPHENE ADMIN BY CAPSULE IN DAILY DOSE OF 4 MG/KG TO 2 DOGS FOR 44 DAYS, & TO 2 (OTHER) DOGS FOR 106 DAYS, INDUCED CNS STIMULATION. THIS OCCURRED OCCASIONALLY & FOR A BRIEF PERIOD AFTER ADMIN. HISTOLOGICAL EXAM OF MANY OF THE ORGANS REVEALED SOME DAMAGE TO THE KIDNEYS (DEGENERATION OF THE TUBULAR EPITHELIUM), & GENERALIZED HYDROPIC DEGENERATIVE LIVER CHANGES, BUT NO DESTRUCTION OF THE CELLS. [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 3754]**PEER REVIEWED**
  • ... 4 GROUPS OF RATS (20 MALES & 20 FEMALES) /WERE FED/ ... 10, 100, 1000, & 1500 PPM OF TOXAPHENE IN THE DIET. AFTER 7.5-10 MO OF FEEDING SOME OF THE RATS FED 1500 PPM & A FEW OF THOSE FED 1000 PPM SUFFERED ... CONVULSIONS. ... THE LIVER WT & LIVER TO BODY WT RATIO WERE SIGNIFICANTLY INCR IN 1000 & 1500 PPM GROUPS. LIVER CHANGES CONSISTED OF SWELLING & HOMOGENEITY OF CYTOPLASM ... THESE CHANGES OCCURRED TO A MODERATE DEGREE IN 1500 PPM GROUP & TO A SLIGHT DEGREE IN THE 1000 PPM GROUP. [Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 3754]**PEER REVIEWED**
  • SIGNS OF INTOXICATION /IN BIRDS FROM ACUTE ORAL ADMIN/: ATAXIA, GOOSE-STEPPING ATAXIA, CIRCLING, LOW OR HIGH CARRIAGE, NECK PULLED IN, PTOSIS OF EYELID, CONSTANT TREMORS ... PHONATION, RELUCTANCE TO MOVE, TENESMUS, HYPERTHERMIA, WINGBEAT CONVULSIONS OR OPISTHOTONOS. THIS IS A FAIRLY SLOW-ACTING CHEMICAL. ALTHOUGH SIGNS WERE SEEN AS SOON AS 20 MIN IN SOME SPECIES, MORTALITIES USUALLY OCCURRED BETWEEN 2 & 14 DAYS AFTER TREATMENT. [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. 83]**PEER REVIEWED**
  • ... LOW TOXICITY TO HONEY BEES. IT IS ONE OF THE MOST TOXIC OF CHLORINATED HYDROCARBON INSECTICIDES TO FISH. [Osol, A. and J.E. Hoover, et al. (eds.). Remington's Pharmaceutical Sciences. 15th ed. Easton, Pennsylvania: Mack Publishing Co., 1975., p. 1195]**PEER REVIEWED**
  • ... IN ACUTE INHALATION STUDIES, 40% ... DUST AT 3.4 G/L OF AIR KILLED APPROX HALF THE EXPOSED RATS WITHIN 1 HR. [National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 601]**PEER REVIEWED**
  • GROUPS OF 50 MALE AND 50 FEMALE 5 WK OLD B6C3F1 MICE WERE FED TECHNICAL GRADE TOXAPHENE IN DIET. INITIALLY, HIGH DOSE ANIMALS RECEIVED 320 MG/KG DIET FOR 19 WK FOLLOWED BY 160 MG/KG DIET FOR FURTHER 61 WK; LOW DOSE ANIMALS RECEIVED 160 MG/KG DIET FOR 19 WK & 80 MG/KG FOR FURTHER 61 WK. A TOXAPHENE FREE DIET WAS THEN FED FOR 10-11 WK. ... MATCHED CONTROLS ... RECEIVED UNTREATED DIET FOR 90-91 WK. THE TIME-WEIGHTED AVG DOSES WERE 99 MG/KG DIET (LOW DOSE) & 198 MG/KG DIET (HIGH DOSE). FURTHER CONTROL DATA WERE OBTAINED FROM ... POOLED CONTROLS FROM OTHER EXPT. ... AN INCR INCIDENCE OF HEPATOCELLULAR CARCINOMAS WAS FOUND IN TREATED MICE: IN MALES: MATCHED CONTROLS, 0/10; POOLED CONTROLS, 4/48 (8%); LOW DOSE, 34/49 (69%); HIGH DOSE, 45/46 (98%); IN FEMALES: MATCHED CONTROLS, 0/9; POOLED CONTROLS, 0/48; LOW DOSE, 5/49 (10%); HIGH DOSE, 34/49 (69%). IN ADDN, NEOPLASTIC NODULES OF LIVER OCCURRED IN 2/10 MATCHED CONTROL MALES, 6/49 LOW-DOSE MALES, 0/9 MATCHED CONTROL FEMALES, 13/49 LOW-DOSE FEMALES & 6/49 HIGH-DOSE FEMALES ... . [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. V20 332 (1979)]**PEER REVIEWED**
  • HIGH DOSE MALE ... /OSBORNE-MENDEL RATS WERE FED/ 2560 MG/KG IN DIET 2 WK, 1280 MG/KG 53 WK, 640 MG/KG FOR FURTHER 25 WK, FOLLOWED BY TOXAPHENE FREE DIET FOR 28 WK. HIGH DOSE FEMALES RECEIVED 1280 MG/KG DIET FOR 55 WK, 640 MG/KG DIET FOR 25 WK, FOLLOWED BY TOXAPHENE-FREE DIET FOR 30 WK. LOW DOSE MALES RECEIVED 1280 MG/KG FOR 2 WK, 640 MG/KG DIET FOR 53 WK, 320 MG/KG DIET FOR 25 WK, FOLLOWED BY TOXAPHENE-FREE DIET FOR 28 WK. LOW-DOSE FEMALES RECEIVED 640 MG/KG DIET FOR 55 WK, 320 MG/KG FOR 25 WK, FOLLOWED BY A TOXAPHENE FREE DIET FOR 30 WK. ... GROUPS OF ... MATCHED CONTROLS WERE GIVEN TOXAPHENE-FREE DIET FOR 108-109 WK ... UNTREATED ... RATS FROM OTHER EXPT SERVED AS POOLED CONTROLS. TIME-WEIGHTED AVG DOSES WERE 556 & 540 MG/KG DIET FOR LOW DOSE MALES & FEMALES, & 1112 & 1080 MG/KG DIET FOR HIGH DOSE MALES & FEMALES, RESPECTIVELY. ... IN MALE RATS, THE COMBINED INCIDENCE OF FOLLICULAR-CELL CARCINOMAS & ADENOMA OF THYROID WAS INCR TO STATISTICALLY SIGNIFICANT EXTENT IN THE HIGH-DOSE GROUP, COMPARED WITH POOLED CONTROLS (P= 0.008), 1/7 IN MATCHED CONTROLS, 2/44 IN POOLED CONTROLS, 7/41 IN LOW-DOSE & 9/35 IN HIGH DOSE ANIMALS. IN FEMALES, INCIDENCES OF FOLLICULAR-CELL ADENOMAS OF THE THYROID WERE 0/6 IN MATCHED CONTROLS, 1/46 IN POOLED CONTROLS, 1/43 IN LOW DOSE ANIMALS & 7/42 IN HIGH-DOSE ANIMALS (P= 0.021 COMPARED WITH POOLED CONTROLS). INCIDENCE OF ADENOMAS, CHROMOPHOBE ADENOMAS OR CARCINOMAS OF PITUITARY IN HIGH-DOSE FEMALES WAS 23/39, COMPARED WITH 17/51 IN POOLED CONTROLS (P= 0.013) ... . [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. V20 335 (1979)]**PEER REVIEWED**
  • RATS ADMIN KAMFOCHLOR BY STOMACH TUBE AT RATES OF 2 MG/KG/DAY OR HIGHER SHOWED CIRCULATORY DISORDERS (HYPEREMIA, EXTRAVASATION, & HEMORRHAGE) OF LUNGS & SPLEEN & DEGENERATIVE LESIONS (REDN OF SPLENIC FOLLICLES), DISTURBED SPERMATOGENESIS, & CYTOTOXIC CHANGES OF LIVER & KIDNEY. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 263]**PEER REVIEWED**
  • THE ILLNESS PRODUCED IN VARIOUS SPECIES BY TOXAPHENE IS DIFFERENT FROM THAT PRODUCED BY 1,1,1-TRICHLORO-2,2-BIS(P-CHLOROPHENYL)ETHANE, AS TREMOR IS ESSENTIALLY LACKING, BUT IS SIMILAR TO THAT PRODUCED BY LINDANE & DIELDRIN ... WHEREAS MOST ANIMALS SHOW HYPERACTIVITY, MUSCLE SPASMS, & CONVULSIONS FOLLOWED BY COMA, SOME SHOW ... DEPRESSION, DROWSINESS & INAPPETENCE WITHOUT ANY INITIAL EXCITEMENT OR FIT. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 261]**PEER REVIEWED**
  • ANOREXIA, OLIGODIPSIA, DIURESIS, GLYCOSURIA, LOSS OF BODY WT, & HYPOTHERMIA HAVE BEEN OBSERVED IN RATS POISONED BY TOXAPHENE. [Hayes, Wayland J., Jr. Pesticides Studied in Man. Baltimore/London: Williams and Wilkins, 1982., p. 261]**PEER REVIEWED**
  • FEEDING OF 5, 50, & 100 MG/KG DIET TOXAPHENE TO CHICKENS FOR 31 WK PRODUCED STERNAL DEFORMATION, RESEMBLING OSTEOMALACIA & NEPHROSIS OF KIDNEY. [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. V20 336 (1979)]**PEER REVIEWED**
  • TOXAPHENE WAS ADMIN BY ORAL INTUBATION TO CD-1 MICE & DC RATS DURING PERIOD OF EMBRYONIC ORGANOGENESIS (DAYS 7-16 OF GESTATION) @ DOSE LEVELS OF 0, 15, 25 & 35 MG/KG/BODY WT/DAY. HIGHEST DOSE PRODUCED ... INCR IN INCIDENCE OF ENCEPHALOCELES AMONG OFFSPRING OF MICE. FETAL MORTALITY ... INCR @ ALL 3 DOSE LEVELS. SMALL DECR IN FETAL BODY WT & IN NUMBER OF STERNAL & CAUDAL OSSIFICATION CENTERS WERE SEEN IN RATS, MOSTLY IN THOSE RECEIVING 25 MG/KG BODY WT DOSE. [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. V20 337 (1979)]**PEER REVIEWED**
  • ADMIN OF 5, 50 OR 500 MG/KG DIET TOXAPHENE TO QUAIL FOR UP TO 4 MO PRODUCED HYPERTROPHY OF THE THYROID, WITH INCREASED UPTAKE OF (131)I & ADRENAL HYPERTROPHY. ... NO EMBRYOTOXICITY WAS OBSERVED IN CHICKEN EMBRYOS HATCHED FROM EGGS PREVIOUSLY INJECTED WITH 400 OR 500 MG/KG TOXAPHENE IN ACETONE; ALTHOUGH WHEN IT WAS DISSOLVED IN CORN OIL, EMBRYOTOXICITY WAS SEEN WITH 300-400 MG/KG. [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. V20 337 (1979)]**PEER REVIEWED**
  • TOXAPHENE IS MUTAGENIC IN SALMONELLA TYPHIMURIUM TEST WITHOUT REQUIRING LIVER HOMOGENATE FOR ... /ACTIVATION/. TOXAPHENE DID NOT INDUCE DOMINANT LETHAL MUTATIONS IN ICR/HA SWISS MICE. WHEN MALES WERE INJECTED IP WITH 36 & 180 MG/KG BODY WT & BRED WITH UNTREATED FEMALES DURING 8 WK, THE FREQUENCY OF EARLY FETAL DEATHS & PREIMPLANTATION LOSS WAS WITHIN CONTROL LIMITS. [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. V20 338 (1979)]**PEER REVIEWED**
  • DOSAGES OF 100 & 2OO PPM TOXAPHENE FED TO FEMALE WEANLING MICE FOR 8 WK DEPRESSED IgG ANTIBODY FORMATION AS COMPARED WITH CONTROLS. [ALLEN AL ET AL; J TOXICOL ENVIRON HEALTH 11 (1): 61-9 (1983)]**PEER REVIEWED**
  • Toxaphene: was admin ... /orally/ to pregnant rats for 2 wk at doses of 12 mg/kg daily. It was demonstrated that /polychlorocamphene/ ... decreased cholinesterase activity of fetal neural structures & hampered differentiation of cardiac neural elements. [Shepard, T.H. Catalog of Teratogenic Agents. 5th ed. Baltimore, MD: The Johns Hopkins University Press, 1986., p. 467]**PEER REVIEWED**
  • ... /Investigators/ gave ... /polychlorcamphene/ to rats from 6 through 15 days (40 mg/kg) or from 1 through 20 (4 mg/kg) & to hamsters in the same doses from days 7 through 11 or on days 1 through 15. The compound showed slightly teratogenic & gonadotoxic activities. [Shepard, T.H. Catalog of Teratogenic Agents. 5th ed. Baltimore, MD: The Johns Hopkins University Press, 1986., p. 467]**PEER REVIEWED**
  • Positive results were obtained for /Salmonella typhimurium/ strains TA98 (frameshift mutation) and TA100 (base pair substitution) only in tests without metabolic activation. ... Toxaphene and toxaphene subfractions are mutagenic to strain TA100 with/without activation by Aroclor induced rat microsomes. [USEPA; Ambient Water Quality Criteria Doc: Toxaphene p.C-33 (1980) EPA 440/5-80-076]**PEER REVIEWED**
  • Mysidopsis behia (mysid shrimp) exposed to 0.14 ug/l during its life cycle exhibited a 82% decrease in the number of young produced. [USEPA; Ambient Water Quality Criteria Doc: Toxaphene p.B-28 (1980) EPA 440/5-80-076]**PEER REVIEWED**
  • Salvelinus fontinalis (brook trout) exposed to 0.068 ug/l/161 days exhibited decreased reproduction, and embryo viability. [Mayer FL et al; Toxaphene Effects on Reproduction, Growth and Mortality of Brook Trout (1975) EPA 600/3-75-013 as cited in USEPA; Ambient Water Quality Criteria Doc: Toxaphene p.B-27 (1980) EPA 440/5-80-076]**PEER REVIEWED**
  • Daphnia magna (cladoceran) exposed to 0.12 ug/l/14 days exhibited reduced reproduction. [Sanders HO; Sublethal Effects of Toxaphene on Daphnids, Scuds and Midges (1980) EPA 600/3-80-006 as cited in USEPA; Ambient Water Quality Criteria Doc: Toxaphene p.B-27 (1980) EPA 440/5-80-076]**PEER REVIEWED**
  • Chironomus plumosus (midge) exposed to 3.2 ug/l/20 days exhibited delayed emergence. [Sanders HO; Sublethal Effects of Toxaphene on Daphnids, Scuds and Midges (1980) EPA 600/3-80-006 as cited in USEPA; Ambient Water Quality Criteria Doc: Toxaphene p.B-27 (1980) EPA 440/5-80-076]**PEER REVIEWED**
  • In 2 yr feeding trials, the no-effect-level for rats was 25 mg/kg diet. [Worthing, C.R. and S.B. Walker (eds.). The Pesticide Manual - A World Compendium. 8th ed. Thornton Heath, UK: The British Crop Protection Council, 1987., p. 119]**PEER REVIEWED**
  • In chronic feeding tests over a 6 mo period, 800 ppm in the daily diet of guinea pigs & rats caused no significant change in the weight curve, urine, blood, mortality or tissue pathology. No indications of toxicity have been observed in monkeys when fed toxaphene at a rate corresponding to 10 ppm of their dietary intake. Approx 60 ppm resulted in toxic symptoms after the second wk of feeding. [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. 115]**PEER REVIEWED**
  • TOXAPHENE DID NOT CAUSE EGGSHELL THINNING IN TESTS ON JAPANESE QUAIL. [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. 83]**PEER REVIEWED**
  • Toxaphene is extremely toxic to fish. ... At water concn as low as 0.00005 ppm, toxaphene treated fish suffer broken-back syndrome, a crippling collagen deformity. ... Toxaphene also is highly toxic to birds ... . [Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. 13(81) 433]**PEER REVIEWED**
  • THE CHRONIC ADMINISTRATION OF ... TOXAPHENE ... TO RATS ENHANCED THE HEPATIC METABOLISM BOTH IN VIVO & IN VITRO, OF 17-BETA-ESTRADIOL & ESTRONE & DECREASED THEIR UTEROTROPIC ACTION. [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. 473]**PEER REVIEWED**
  • A bioassay of technical grade toxaphene for possible carcinogenicity was conducted by administering the test chemical in feed to Osborne-Mendel rats ... . Groups of 50 rats of each sex were administered toxaphene at one of two doses for 80 weeks, then observed for 28 or 30 weeks. Time-weighted average doses for males were 556 or 1,112 ppm; for females they were 540 or 1,080 ppm. Matched controls consisted of groups of 10 untreated rats of each sex ... . All surviving rats were killed at 108-110 weeks. Mean body weights attained by low- and high dose female rats ... were lower than those of matched controls ... . Other clinical signs of toxicity in rats included generalized body tremors at week 53 in high dose male and female animals, and later, leg paralysis, ataxia, epistaxis, hematuria, and vaginal bleeding, predominantly in the dosed groups of rats of each sex. Abdominal distention, diarrhea, dyspnea, and rough hair coats were common to ... dosed rats ... . Sufficient numbers of ... rats ... were at risk for the development of late appearing tumors. ... The test results also suggest carcinogenicity of toxaphene for the thyroid of male and female Osborne-Mendel rats. [DHEW/NCI; Toxicology and Carcinogenesis Studies of Toxaphene p.vii-viii Report# 37 (1979) NIH Pub# 79-837]**PEER REVIEWED**
  • The Chinese hamster V-79 metabolic cooperation assay was used to study the effects of ... toxaphene on gap junctional communication. The cytotoxicity was measured by a colony forming assay using Chinese hamster V79 cells. For the metabolic cooperation assay, appropriate concn of /toxaphene/ were added to cocultures of 6-thioguanine resistant and 6-thioguanine sensitive V79 cells 4 hr after plating, and 6-thioguanine was added 1 hr later. The percentage of the 6-thioguanine resistant cells which formed colonies was used as a measure of metabolic cooperation. ... At concn higher than 5 ug/ml, toxaphene was slightly more cytotoxic than /aldrin and dieldrin/, in both the colony forming assay and the metabolic cooperation assay. At noncytotoxic levels higher that 1 ug/ml, toxaphene failed to induce dose dependent inhibition of metabolic cooperation up to a concn of 4 ug/ml, while higher concn proved to be both cytostatic and cytotoxic. [Trosko JE et al; Molec Toxicol 1 (1): 83-93 (1987)]**PEER REVIEWED**
  • Uptake and distribution of 14(C) toxaphene was studied in the adrenals of rats using whole body autoradiography. An accumulation of radioactivity was seen in the adrenal cortex (zona fasciculata) 1-24 hr after a single gavage of 14(C) toxaphene (16 mg/kg bw). In in vitro studies toxaphene was found to inhibit ACTH stimulated corticosterone synthesis in the cultured rat adrenocortical cells (IC50 2.8X10(-5) M). Moderate but significant inhibition (p< 0.001) of ACTH stimulated corticosterone synthesis was also observed in the adrenocortical cells isolated from rats after a prolonged exposure (5 wk) to low levels (1.2 ppm) of toxaphene in feed. [Mohammed A et al; Toxicol Lett 24 (2-3): 137-43 (1985)]**PEER REVIEWED**
  • In a rat study, groups of 10 male and 10 female animals were fed diets containing 0, 4, 20, 100, or 500 ppm of the test compound for 13 weeks. No clinical signs of toxicity or spontaneous deaths were observed. Toxaphene treatment up to 500 ppm had no effects on weight gain or food consumption. The liver/body weight ratio and hepatic microsomal enzyme activities (phenobarbital type) were increased in both sexes fed 500 ppm of the test compound. Toxaphene at the highest dose also caused kidney enlargement in male but not in female rats. Dose dependent histological changes were seen in the kidney, thyroid, and liver. Changes in the liver and thyroid were considered to be adaptative but the injury in the proximal tubules of the kidney was focally severe. Groups of six male and six female beagle dogs were fed toxaphene in gelatin capsules at 0, 0.2, 2.0, and 5.0 mg/kg body wt/kg body wt/day for 13 weeks. Food consumption and growth rate were not affected. All animals survived the entire treatment period. No clinical signs of toxicity were observed. The liver/body weight ratio and serum alkaline phosphatase were increased in dogs of both sexes fed 5.0 mg/kg. Mild to moderate dose dependent histological changes were observed in the liver and thyroid. Toxaphene was accumulated in a dose dependent manner in the fat and liver of dogs and rats. Based on the biochemical, histological, and residue data, it was concluded that the no-adverse-effect levels of the pesticide were 4.0 ppm (0.35 mg/kg) for the rat and 0.2 mg/kg for the dog. [Chu I et al; Fundam Appl Toxicol 7 (3): 406-18 (1986)]**PEER REVIEWED**
  • Mice with no clinical signs of intoxication exhibited consistent increases in serum acid phosphatase, glutamic pyruvic transaminase, and gamma-glutamyl transpeptidase activities, along with increased neutrophil counts and changes in urinary proteins. [USEPA; Ambient Water Quality Criteria Doc: Toxaphene p.C-26 (1980) EPA 440/5-80-076]**PEER REVIEWED**
  • PHENOBARBITAL SLEEPING TIMES WERE REDUCED IN RATS GIVEN TOXAPHENE ORALLY BY GAVAGE. [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. V20 337 (1979)]**PEER REVIEWED**
  • Oncogenicity: Hazard to wildlife and other chronic effects; Reduction in non-target organisms. [USEPA/OPP; The Status of Chemicals in Special Review Program, Registration Standards Program, and Data Call-In Program p.10 (1986)]**PEER REVIEWED**
  • Toxaphene can be used with reasonable safety if recommendations are followed, but it can cause poisoning when applied or ingested in excessive quantities. Dogs and cats are particularly susceptible. Young calves have been poisoned by 1% toxaphene sprays, while all other farm animals except poultry can withstand 1% or more as sprays or dips. Chickens have been poisoned by dipping in 0.1% emulsions, and turkeys have been poisoned by spraying with 0.5% material. [Aiello, S.E. (ed). The Merck Veterinary Manual. 8th ed. Merck & Co., Inc., National Publishing Inc., Philadelphia, PA. 1998., p. 2064]**PEER REVIEWED**
  • Toxaphene is primarily an acute toxicant and does not persist unduly in the tissues. Adult cattle have been mildly intoxicated by 4% sprays and severely by 8%. Adult cattle have been poisoned from being dipped in emulsions that contained only 0.5% toxaphene (an amount ordinarily safe) because the emulsions had begun breaking down, allowing the fine droplets to coalesce. The large droplets readily adhere to the hair of cattle, and the resultant dosage becomes equivalent to that obtained by spray treatments of much higher concentration. [Aiello, S.E. (ed). The Merck Veterinary Manual. 8th ed. Merck & Co., Inc., National Publishing Inc., Philadelphia, PA. 1998., p. 2064]**PEER REVIEWED**
  • Toxaphene is lethal to young calves at 8.8 mg/kg body wt but not at 4.4 mg/kg. The minimum toxic dose for cattle is 33 mg/kg, and that for sheep between 22 and 33 mg/kg. Spraying Hereford cattle 12 times at 2 wk intervals with 0.5% toxaphene produced a maximum residue of 8 ppm in the fat. Cattle fed 10 ppm of toxaphene in the diet for 30 days had no detectable toxaphene tissue residues, while steers fed 100 ppm for 112 days stored only 40 ppm in their fat (this amount was eliminated in 2 mo after the feeding of toxaphene had been discontinued). [Aiello, S.E. (ed). The Merck Veterinary Manual. 8th ed. Merck & Co., Inc., National Publishing Inc., Philadelphia, PA. 1998., p. 2064]**PEER REVIEWED**
  • Toxaphene is a complex mixture of at least 670 chlorinated camphenes ... Several are more toxic than technical grade toxaphene ... More than a three-fold difference in toxicity was observed for LD50 values in mice after the ip admin of various toxaphene fractions or components that differed in chemical composition, polarity, and solubility ... Toxaphene components A and B have been isolated and found to possess toxicity that is 6 and 14 times greater, respectively, than the technical toxphene mixture ... Toxicant A has been identified as a mixture of 2,2,5-endo,6-exo,8,8,9.10- octachlorobornane and 2,2,5-endo,6-exo,8,9,9,10- octachlorobornane ... and toxicant B has been identified as 2,2,5-endo,6-exo,8,9,10-heptachlorobornane ... It has further been determined that toxicant B and four of its derivatives, each with an additional chlorine atom at position 3-exo,8,9, or 10, may be responsible for the bulk of toxaphene=s acute toxicity ... . [Jansson B, Wideqvist U; Int J Environ Anal Chem 13: 309-322 (1983) as cited in U.S. Dept Health & Human Services/ ATSDR; Toxicological Profile for Toxaphene (Update) p. 67 (1996)]**PEER REVIEWED**
  • ... Only technical toxaphene and CHB-32 were genotoxic in the direct assay, whereas the addition of rat S9 fraction or microsomes of harbor seal and albatross decreased the genotoxic response. Thus, organisms with a low ability to metabolize chlorobornanes, such as whales, may be most affected by the carcinogenic properties of toxaphene. A hypothetical reaction which fits the experimental results is discussed. [Boon JP et al; Comp Biochem Physiol C Pharmacol Toxicol Endocrinol 121 (1-3): 385-403 (1998)]**PEER REVIEWED**
  • The presence of persistent organic pollutants, including the pesticide toxaphene has been reported even in remote regions such as the Arctic and is becoming a health concern. The technical mixture of toxaphene contains over 800 different congeners. The numbers of prevalent congeners, however, decrease along the food chain. About 20 major congeners are found in fish, eight in marine mammals and only two major ones in human, 2-exo,3-endo,5-exo,6-endo,8,8,10,10-octachlorobornane (T2) and 2-exo,3-endo,5-exo,6-endo,8,8,9,10,10-nonachlorobornane (T12). Embryotoxicity of these individual congeners is not known, as previous studies focused on the toxaphene technical mixture. We studied the relative dysmorphogenic activity of toxaphene technical mixture and individual congeners (T2 and T12) using rat embryo culture. Explanted embryos (0-2 somites) were treated for 48 h with concentrations of 0 (DMSO 0.01%), 100, 1000 and 5000 ng/ml of either (a) toxaphene technical mixture; (b) T2; (c) T12; or (d) a 50:50 mixture of T2 and T12. The treatment period corresponds to gestational days (GD) 10-12, a period within the critical time of morphogenesis and organogenesis. Both the technical mixture and the two individual congeners had a significant adverse effects on the total morphological score, somite number, head and crown rump length and the central nervous system scores of embryos. All treatments caused a high incidence of central nervous system defects. The T2 and T12 congeners differed in their spectrum of abnormalities as exposure to T2 caused limb and flexion defects which were not observed with the T12 congener. Differences were also observed in the type of toxicity and the target sites between the technical mixture and the congeners. T2 showed a more potent adverse effect on the morphological score as compared to the technical mixture. Both T2 and T12 were less inhibitory on growth than the technical mixture as indicated by crown-rump length but they showed a stronger inhibitory effect on otic system development. The mixture of T2 + T12 showed a synergistic effect on decreasing crown-rump and head length. Conversely, the combination of T2 and T12 inhibited the strong adverse effect of the individual congeners on otic development. The results suggest environmentally predominant toxaphene congeners can have organ specific embryotoxic effects not predicted by the toxaphene technical mixture. [Calciu C et al; Toxicology 124 (2): 153-62 (1997)]**PEER REVIEWED**
  • Hedli CC [Hedi CC et al; J Appl Toxicol 18 (3): 173-8 (1998)] Exposure of experimental animals to toxaphene induces hepatic cytochrome p450 (CYP). Although chronic administration of toxaphene to mice was found to cause an increased incidence of liver tumors, a mechanism for its carcinogenicity has yet to be elucidated. We investigated two potential mechanisms of toxaphene-induced carcinogenicity: peroxisomal proliferation and DNA binding. Peroxisomal proliferation was evaluated by measuring the level of immunodetectable cytochrome p450 4A1, an isozyme of cytochrome p450 that is specifically induced by peroxisomal proliferators, in hepatic microsomes from CD1 mice that were treated by oral gavage for seven consecutive days with corn oil vehicle or 10, 25, 50 or 100 mg kg(-1) toxaphene. In comparison to control mice, toxaphene-treated mice had increased liver weight, increased liver/body weight ratios and increased levels of total hepatic cytochrome p450 and cytochrome b5. No increase in the level of immunodetectable levels of cytochrome p450 4A1 was found in hepatic microsomes from toxaphene-treated mice when compared to controls. In contrast, increases in immunodetectable cytochrome p450 4A1 were detected in hepatic microsomes from mice treated with the peroxisomal proliferator clofibrate. These findings suggest that toxaphene-induced induction of cytochrome p450 may not involve cytochrome p450 4A1 and that peroxisomal proliferation may not be involved in toxicity. Significant increases in immunodetectable levels of cytochrome p450 2B were, however, detected in toxaphene-treated mice, and are consistent with earlier reports demonstrating that toxaphene, like many other pesticides, induces the phenobarbital-inducible subfamily of cytochrome p450. Analysis of DNA adduct levels in the livers of toxaphene-treated mice by DNA 32P-post-labeling showed no evidence of DNA adduct formation.**PEER REVIEWED**
  • ... Treatment with 2.5, 15 and 60 uM/kg (x3) doses of toxaphene, dieldrin, or dieldrin/toxaphene (equimolar) did not significantly induce a dose-dependent increase in any of the E2-induced responses. The organochlorine pesticides alone and the binary mixture did not bind to the mouse uterine estrogen receptor (ER) in a competitive binding assay using [3H]E2 as the radioligand. In parallel studies, estrogenic activities were determined in MCF-7 cells by using a cell proliferation assay and by determining induction of chloramphenicol acetyl transferase (CAT) activity in MCF-7 cells transiently transfected with plasmids containing ... . Treatment of MCF-7 cells with dieldrin, toxaphene, or an equimolar mixture of dieldrin plus toxaphene (10(-8)-10(-5) M) did not significantly induce cell proliferation or CAT activity in the transient transfection experiment with both plasmids. ... Toxaphene (10(-5) M), dieldrin (10(-5) M), and equimolar concentrations of the dieldrin plus toxaphene mixture (10(-5) M). ... Treatment with 10(-6)-10(-4) M chlordane, dieldrin, toxaphene, or an equimolar mixture of dieldrin/toxaphene did not induce activity, whereas 10(-4) M endosulfan caused a 2000-fold increase in beta-gal activity. Diethylstilbestrol caused a 20-fold increase in activity in yeast transformed with the mouse ER and a single estrogen responsive element upstream of the beta-gal reporter gene. Dieldrin, chlordane, toxaphene, and endosulfan induced a 1.5- to 4-fold increase in activity at a concentration of 2.5 x 10(-5) M. Synergistic transactivation was not observed for any equimolar binary mixture of the pesticides at concentrations of either 2.5 x 10(-5) M or 2.5 x 10(-4) M.[Ramamoorthy K et al; Endocrinology 138 (4): 1520-7 (1997)]**PEER REVIEWED**
  • Organochlorine use over the past 50 years has resulted in the contamination of soil, water, plant and animal species. This contamination has created a long-lasting environmental problem, as the members of the organochlorine class of pesticides are resistant to degradation and have been labeled as persistent bioaccumulators. Studies have shown certain organochlorines to be tumor promoters, liver toxicants and to induce immune cell dysfunction in rats and mice. Our laboratory has shown that the organochlorines heptachlor and chlordane affect leukocytic gene expression and differentiation. In this study, experiments with CEM x 174 cells, a hybrid of human T and B cells, were performed to investigate the effects of the tumor promoter heptachlor and its congeners chlordane and toxaphene on retinoblastoma (Rb) gene expression. The results indicated that heptachlor, chlordane or toxaphene, in the range of 10-50 uM, were able to reduce retinoblastoma protein levels in a concentration-dependent manner. In the case of heptachlor, the reduction could be seen as early as 12 hr and was time-dependent. Analysis of retinoblastoma mRNA levels revealed no detectable difference over the same concentration range. These results suggest that members of the organochlorine class are able to down regulate retinoblastoma expression at the post-transcriptional level, an effect similar to that on p53 tumor suppressor previously reported by our laboratory [Rought SE et al; Toxicol Lett 104 (1-2): 127-35 (1999)]**PEER REVIEWED**
  • The polychlorinated pesticide toxaphene has been identified as a persistent environmental contaminant and is of particular concern in the Great Lakes and Arctic regions of Canada. Inconsistencies in published in vitro genotoxicology studies have hindered risk assessments of toxaphene exposure. When toxaphene mutagenicity was re-evaluated in the Ames Salmonella/microsome assay at 10-10,000 & mgr; g/plate, a dose-dependent increase in His revertants occurred in all five strains of S. typhimurium tested (TA97, TA98, TA100, TA102 and TA104) with higher mutation frequencies observed in the absence of S9 metabolic activation. However, the mutagenic potential of toxaphene was relatively low with concentrations greater than 500 ug/plate required to induce mutation. Toxaphene genotoxicity was also examined in a mammalian system using Chinese hamster V79 lung fibroblasts with metabolic activation provided by human HepG2 hepatoma cells. Genotoxicity of 1-10 ug/ml toxaphene was examined by measuring the frequency of sister chromatid exchange (SCE) and mutation induction at the hypoxanthine guanine phosphoribosyl transferase (HGPRT) gene locus. Although small increases in sister chromatid exchange were observed at toxic concentrations of toxaphene approaching the LD50 (10 ug/ml), they were not found to be statistically significant relative to control. Toxaphene was also unable to induce hypoxanthine guanine phosphoribosyl transferase mutagenesis at the concentrations tested. These results show that while toxaphene is a weak, direct-acting mutagen in the Ames Salmonella Test, convincing evidence of dose-dependent sister chromatid exchange induction and mutagenicity at the hypoxanthine guanine phosphoribosyl transferase gene locus could not be demonstrated in V79 cells. [Schrader TJ et al; Mutat Res 413 (2): 159-68 (1999)]**PEER REVIEWED**

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Human Toxicity Values

  • None found

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Non-Human Toxicity Values

  • LD50 Rat oral 80-90 mg/kg [Worthing, C.R. and S.B. Walker (eds.). The Pesticide Manual - A World Compendium. 8th ed. Thornton Heath, UK: The British Crop Protection Council, 1987., p. 119]**PEER REVIEWED**
  • LD50 Rat percutaneous 780-1075 mg/kg [Worthing, C.R. and S.B. Walker (eds.). The Pesticide Manual - A World Compendium. 8th ed. Thornton Heath, UK: The British Crop Protection Council, 1987., p. 119]**PEER REVIEWED**

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Absorption, Distribution and Excretion

  • IN RAT, 52.6% OF ORAL DOSE OF (36)CL-TOXAPHENE WAS EXCRETED WITHIN 9 DAYS. APPROX 37% ... IN FECES, & 15% IN URINE. ON EXTRACTION, MOST OF RADIOACTIVITY OCCURRED IN WATER FRACTIONS OF URINE & FECES AS IONIC CHLORIDE. ANIMALS GIVEN 2ND DOSE ON 9TH DAY EXCRETED TOXAPHENE IN SIMILAR MANNER, EXCEPT THAT (36)CHLORINE EXCRETION IN FECES WAS REDUCED. LESS THAN 10% OF DOSE WAS FOUND IN SELECTED TISSUES & ORGANS 1 DAY AFTER TREATMENT. [National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 600]**PEER REVIEWED**
  • IT IS: ... ABSORBED THROUGH INTACT SKIN, RESP TRACT & GI TRACT. ... INTESTINAL ABSORPTION IS INCR BY PRESENCE OF DIGESTIBLE OILS, & LIQ PREPN (OIL SOLVENTS) PENETRATE THE SKIN FAR MORE READILY THAN DO DUSTS OR POWDERS. [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-386]**PEER REVIEWED**
  • 3% OF AN ORAL DOSE OF (14)C-TOXAPHENE WAS EXCRETED UNCHANGED IN THE FECES OF RATS. MORE THAN 5% OF THE ADMINISTERED DOSE WAS EXCRETED IN THE URINE AND FECES AS COMPLETELY DECHLORINATED METABOLITES, AND 27% AS PARTIALLY DECHLORINATED METABOLITES; 20% OF THE ACTIVITY WAS FOUND IN EXPIRED AIR. [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. V20 338 (1979)]**PEER REVIEWED**
  • When white leghorn chickens are fed 5, 50, or 100 ppm toxaphene in the diet, residues are detected in eggs. ... The concn of toxaphene in adipose tissue of 8 wk old Hubbard-Hubbard broiler chickens increases with increasing dietary intake. Bioaccumulation factor is about 5. [Booth, N.H., L.E. McDonald (eds.). Veterinary Pharmacology and Therapeutics. 5th ed. Ames, Iowa: Iowa State University Press, 1982., p. 1105]**PEER REVIEWED**
  • Depending upon the dosage, chronic ingestion of toxaphene may result in the accumulation of toxaphene or a chlorinated metabolite in the fatty tissues. Toxaphene is excreted to some extent in urine in conjugation with sulfonate & glucuronide. [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. 115]**PEER REVIEWED**
  • In rats orally treated with toxaphene, fat contained materials similar in gas-liq chromatographic characteristics to toxaphene itself. Liver & feces contained toxaphene products that exhibited greatly altered gas liquid chromatographic characteristics. [Menzie, C.M. Metabolism of Pesticides-Update III. Special Scientific Report- Wildlife No. 232. Washington, DC: U.S.Department of the Interior, Fish and Wildlife Service, 1980., p. 521]**PEER REVIEWED**
  • Studies in laboratory animals indicate that toxaphene is well absorbed by the intestinal tract and probably well absorbed by the lungs. Dermal absorption is low, relative to the other exposure routes. Once absorbed, toxaphene distributes throughout the body. Studies using radiolabeled toxaphene indicate that distribution to fat predominates over distribution to other organs, and levels are detectable in fat tissue for several month following exposure. ... The primary route of excretion is via the feces (70% of an admin dose), but toxaphene is also excreted in the urine. [U.S. Dept Health & Human Services/ ATSDR; Toxicological Profile for Toxaphene (Update) p. 48 (1996)]**PEER REVIEWED**
  • ... The detection of high toxaphene levels in cow's milk (21-45 ppm) after dipping the cattle in a toxaphene soln (0.25% w/w toxaphene plus 0.03% w/v dioxathion) indicates that toxaphene was absorbed following dermal exposure ... . [Keating M; Bull Anim Health Prod Afr 27: 279-286 (1979) as cited in U.S. Dept Health & Human Services/ ATSDR; Toxicological Profile for Toxaphene (Update) p. 49 (1996)]**PEER REVIEWED**
  • In autoradiographic studies of pregnant albino mice iv injected with 14C-toxaphene (16 mg/kg) ... found low levels of activity in fetal tissues. This activity was highly concn in the fetal liver and adrenal gland. These results, as after oral admin, suggest that the transplacental transfer or toxaphene after iv admin is relatively low. [Mohammed A; Arch Toxicol 54: 311-321 (1983) as cited in U.S. Dept Health & Human Services/ ATSDR; Toxicological Profile for Toxaphene (Update) p. 53 (1996)]**PEER REVIEWED**
  • Toxaphene residues in the blood leveled out at 40 ppb, snd sdipose tissue levels wee approximately 4,000 ppb. Not detectable or very low levels of toxaphene residues were found in the urine and kidney tissue. The patter of metabolites in the feces was extremely complex [Andrews P Chemosphere 32 (6): 1043-1053 (1996)]**PEER REVIEWED**

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Metabolism/Metabolites

  • USING BIOASSAY METHODS, IT WAS FOUND THAT RESISTANT FLIES COULD METABOLIZE 4.0 UG OF TOXAPHENE FROM AN ABSORBED DOSE OF 5.4 UG. NO METABOLITES WERE IDENTIFIED. ... IN STUDIES WITH THE COTTON LEAFWORM, THE PRESENCE OF A DEHYDROCHLORINASE & THE BREAKDOWN OF TOXAPHENE WAS DEMONSTRATED. 3 COMPONENTS WERE SEPARATED BY PAPER CHROMATOGRAPHY BUT WERE NOT IDENTIFIED. [Menzie, C.M. Metabolism of Pesticides. U.S. Department of the Interior, Bureau of Sport Fisheries and Wildlife, Publication 127. Washington, DC: U.S. Government Printing Office, 1969., p. 311]**PEER REVIEWED**
  • Rats metabolically dechlorinate toxaphene. In several organisms ... this reaction is a reductive dechlorination, sometimes a dehydrochlorination. In part toxaphene is also metabolized by reduced nicotinamide adenine dinucleotide dependent mixed function oxidase in rat hepatic microsomal enzyme preparations. ... [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-386]**PEER REVIEWED**
  • In vitro studies were conducted with rat liver microsomal preparations. Metabolism of toxaphene was increased by addition of reduced glutathione & nicotinamide-adenine dinucleotide phosphate. In addition to dechlorination, some oxidation to hydroxyl and acidic cmpd occurred. Further study showed that aglycones were released by action of beta-glucuronidase and beta-sulfatase, indicating the presence of water releasing conjugates in vitro. [Menzie, C.M. Metabolism of Pesticides-Update III. Special Scientific Report- Wildlife No. 232. Washington, DC: U.S.Department of the Interior, Fish and Wildlife Service, 1980., p. 521]**PEER REVIEWED**
  • The metabolism of toxaphene in perfused bovine liver was studied. Two beef cows and one dairy calf had blood collected from the jugular vein and the liver was then removed. The blood was defibrinated and filtered; 100 milligrams oxytetracycline was added and then used as perfusate. The liver was cleaned and drained, then attached to the arterial side of a perfusion chamber. An ethanolic solution of toxaphene was added to give a concentration of 20 micrograms per gram in the blood. Samples of the perfusate were taken every 15 minutes until the end of the experiment when the liver was weighed and a sample taken. Recovery of toxaphene and the effect of blood on toxaphene were determined by circulating dosed blood without the liver. Blood samples were analyzed for toxaphene and dechlorinated metabolites were analyzed by gas liquid chromatography. By 15 minutes after dosing, approximately 75% of the toxaphene was taken up by the liver; 105 minutes after dosing, an additional 15% was taken up. The half-life of early rapid rate of decline and later rate of decline of toxaphene from the perfusate was 7 minutes and 86 minutes, respectively. The gas chromatographs showed that toxaphene components produced partially dechlorinated derivatives that degraded further with time. The response ratio between perfusate with liver and circulating blood without liver showed that toxaphene metabolism by the liver occurred by 15 minutes after dosing. [Maiorino RM et al; Arch Environ Contam Toxicol 13 (5): 565-71 (1984)]**PEER REVIEWED**
  • Analysis of the blood and adipose tissue indicated that toxaphene was extensively metabolized. the major residues found in the tissue samples were four chlorinated bornane congeners. [Andrews P Chemosphere 32 (6): 1043-1053 (1996)]**PEER REVIEWED**
  • The capacity of microsomes to metabolize a technical toxaphene mixture decreased in the order Phoca vitulina (harbor seal) >> Lagenorhynchus albirostris (white beaked dolphin) approximately equal to Diomedea immutabilis (Laysan albatross) > Physeter macrocephalus (sperm whale). Harbor seal microsomes metabolized the chlorobornane (CHB) congeners CHB-32 and CHB-62; white beaked dolphin and Laysan albatross microsomes only metabolized CHB-32. Metabolism of CHB-26 and CHB-50 was never observed. The negative chemical ionization (NCI-) mass spectra of some of the hydroxylated metabolites were obtained. The number of peaks in the toxaphene residues of wildlife extracts decreased in the order of increasing in-vitro biotransformation capacity. [Boon JP et al; Comp Biochem Physiol C Pharmacol Toxicol Endocrinol 121 (1-3): 385-403 (1998)]**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.

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Web page last updated on May 14, 2008