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Carbaryl. Caroline Cox. Journal of Pesticide Reform, Volume 13, Number 1, Spring 1993. Northwest Coalition for Alternatives to Pesticides, Eugene, OR.
Carbaryl By Caroline Cox Many pesticides have gained their notoriety because of a particular human or environmental health problem. The organochlorine insecticide DDT, for example, is well known because of its ability to bioconcentrate in carnivorous animals,1 and the fumigant dibromodichloropropane (DBCP) made headlines when it caused sterility in men who worked with it.2 The insecticide carbaryl, however, is striking because its use has been associated with such a large number of health problems. From acute toxicity, suppression of immune system functions, and behavioral pro-blems to cancer, genetic damage, and reproductive problems in both males and females, carbaryl's adverse effects span an enormous range. Carbaryl (1-naphthyl methyl carbamate) is one of the three most commonly used insecticides in the United States with an estimated annual use of between 10 and 15 million pounds.3 (See Figure 2 for agriculture use by state.) It is a broad- spectrum insecticide and is registered for use on more than 100 different crops, animals, ornamental plants, and indoor areas.4 Carbaryl is also sometimes used as a chemical thinning agent for apples.5,6 It has been registered in the U.S. since 1958.4 Previously manufactured by Union Carbide,7 the primary U.S. manufacturer is now Rhone Poulenc Agricultural Company; many of its carbaryl-containing products are marketed under the brand name Sevin.8 Mode of Action Carbaryl is a carbamate insecticide. Like all members of this chemical family, it inhibits the action of an enzyme that is an essential component of insect, fish, bird, and mammal nervous systems. The enzyme, acetyl cholinesterase (AChE), controls the chemical reaction that transforms acetylcholine into choline after acetylcholine has been used to transmit nerve impulses across the junctions between nerves. Without functioning AChE, acetylcholine accumulates and prevents the smooth transmission of nerve impulses.9 This causes loss of normal muscle control, and ultimately death. The AChE inhibition is said to be reversible because the carbaryl disassociates from the AChE within several hours. This happens even if death has already occurred. Insecticides in the organophosphate family (malathion and diazinon, for example) also inhibit AChE, but the inhibition is not as readily reversible.10 Carbaryl can also affect a number of other enzyme systems in living things. For example, the carboxylesterases (detoxification enzymes),11 lactic dehydrogenase (enzymes that utilize sugar),12 and serine esterases (enzymes important to the function of certain immune system components)13 are all inhibited by carbaryl. Acute and Subchronic Toxicity Symptoms of acute carbaryl exposure in humans are malaise, muscle weakness, dizziness, sweating, headache, salivation, nausea, diarrhea, incoordination, and slurred speech. Depression of breathing ability combined with an excess of fluid in the lungs (pulmonary edema) is the usual cause of death when exposure is high.10 Carbaryl's acute oral LD50 (the dose that causes death in 50 percent of a population of test animals) in rats is 255 milligrams per kilogram (mg/kg) of body weight.5 Extrapolated to the weight of an average 70 kilogram (154 pound) human who is assumed to be as sensitive to carbaryl as are rats, this means that a dose of about 18 grams or two-thirds of an ounce would be fatal. Lower doses of carbaryl over a longer period of time cause a variety of adverse effects. In humans, ingestion of 0.13 mg/kg/day (less than a thousandth of the LD50) caused abdominal cramps and a decrease in the ability of the kidneys to resorb amino acids.14 In rats, decreases in weight and body temperature occurred following single injections of doses of less than one-twentieth of the LD50.15 Similar doses given for two years caused kidney abnormalities in rats as well as dogs.16 In addition, drinking water contaminated with 10 parts per million (ppm) of carbaryl caused liver pathologies and reduced blood clotting activity in rats17 and single sublethal doses in rabbits reduced their heart rate and caused changes in their electrocardiograms.18 Behavioral and Neurological Effects Given that carbaryl's primary mode of action disturbs the nervous system, it is not surprising that researchers have measured a variety of neurological and behavioral effects of carbaryl exposure. Case reports of human exposures tell some compelling stories. For example, a professor of medicine at a New England university reported that his twice daily applications of a commercial tick powder with active ingredient carbaryl to his cat had dramatic effects on the cat's personality. The pet, who had never been much of a hunter, began attacking large numbers of birds and mice. The professor's personality underwent a parallel change (in spite of the gloves and mask he wore while dusting the cat) and he was described as being in a "continual rage." Ending the tick powder treatments brought an end to the aggressive behavior in both doctor and cat within a week.19 Two other reports describe patients with a neurological condition called delayed peripheral neuropathy following carbaryl exposure. This condition, normally associated with certain organophosphates and not carbamates like carbaryl, causes nerve degeneration and paralysis of arms or legs several weeks after exposure.20 One of the patients had been exposed through ingestion of a relatively large quantity of carbaryl- containing insecticide.21 The other patient was exposed when his basement was treated for fleas with a carbaryl-containing dust.22 Carbaryl exposure has also caused behavioral and neurological problems in studies of laboratory animals. In rats, single doses of ten mg/kg (less than one-twentieth of the LD50) or less caused decreases in the responses to a battery of behavioral tests,15,23 increased tolerance for electrical shock, and decreased desire to drink water.24 Smaller doses given for two weeks slowed the speed that rats were able to run a maze and increased the number of errors that they made.25 Single sublethal injections of carbaryl reduced the success of monkeys in performing a learning task.26 In pigs, long-term (over 70 days) feeding of sublethal carbaryl doses caused incoordination of movements followed by extensive degeneration of nerves in the brain and muscles.27 Effects on the Immune System Carbaryl's ability to decrease the effectiveness of the immune system has been documented in a variety of laboratory studies. A review of some of the immune system literature published during the 1960s and 1970s cited seven studies that found adverse effects of carbaryl in immune system function of rats and rabbits;28 a second review identified three more studies.29 The studies measured decreases in the cellular activity of the immune system, a reduction in the resistance to infection by certain diseases, a decrease in antibody development, and a decrease in the size of a part of the spleen important in immune system function. Doses were well below lethal toxic doses. More recent studies show similar results. Rats fed carbaryl at doses as low as 1/100 of the LD50 and then infected with a bacteria had a mortality rate almost twice as high as unexposed rats.30 In goldfish cell cultures, synthesis of the immunologically important compound interferon was reduced, leading to enhanced replication of a virus.31,32 In mice cell cultures, carbaryl inhibited enzymes that were essential to proper functioning of macrophages, the cells that engulf and consume foreign bodies.33 Finally, at doses too low to cause inhibition of AChE, carbaryl exposure of human cell cultures reduced proliferation of immune system cells called large granular lymphocytes. This was caused by effects on another immunologically important compound, interleukin. These lymphocytes "contribute significantly to protection against tumor cell growth and infections,"34 so their suppression can have significant consequences. Taken together, the studies suggest striking effects of carbaryl on proper immune system function. Effects on Reproduction Ever since the late 1960s, when two researchers showed that female beagle dogs fed carbaryl had more stillbirths and infant deaths, decreased litter size, smaller pups, and more pups with birth defects than did unexposed mothers,35 carbaryl's reproductive hazards have been of concern.29 Adverse effects in the beagle study were found at doses approximately 1/50 of the LD50. Studies since that time have demonstrated that carbaryl can affect reproduction in a variety of species and in both sexes. Males: Two studies at a carbaryl manufacturing facility have shown that carbaryl exposure affects the quantity and quality of sperm produced by the workers. One study found that more exposed workers had very low sperm counts than in a control group of unexposed workers.36 This result was significant based on one statistical test, but has been criticized because a second statistical test only "closely approached significance." A second study of the same sperm samples found that the number of sperm abnormalities was increased in workers who were being exposed to carbaryl while the study took place.37 Studies of laboratory animals have shown similar effects. A 1980 U.S. Environmental Protection Agency (EPA) review cited four studies (three in rats, one in another rodent) showing decreases in sperm numbers, an increase in sperm abnormalities, and a decrease in sperm mobility caused by carbaryl exposure.38 A 1986 review cited three other studies of rats with similar results.29 Some of these studies found effects at low doses. For example, 7 mg/kg per day (about 1/35 of the LD50) given over a period of nine months reduced sperm mobility and the numbers of sperm-forming cells.39 Females: Female laboratory animals of a number of species fed carbaryl suffer from reproductive problems. A 1986 review summarized 25 studies that had found reproductive problems caused by carbaryl in eight different kinds of animals. These problems included reduced fertility, increased fetal mortality, low birth weights, reduced growth and survival of babies, and birth defects.29 Some effects occur at surprisingly low doses. For example, rats fed carbaryl in doses equivalent to 1/35 of the LD50 for one year had estrous cycles significantly longer than unexposed control rats39 and pregnant monkeys given daily doses as low as 1/100 of the acute lethal dose had increased rates of spontaneous abortions.40 The most recent laboratory study of reproductive effects that NCAP has found (1991) shows a variety of reproductive hazards.41 Rats exposed to carbaryl had smaller litters, smaller babies, and more resorbed fetuses than unexposed rats. (See Figure 4.) These results were found in mice receiving a single carbaryl dose during pregnancy, as well as in those exposed for most of the pregnancy. The study also found an increased frequency of birth defects, including eye, kidney, and skeletal abnormalities, in the fetuses of carbaryl-treated mothers. Carcinogenicity Several recent epidemiology studies have associated exposure to agricultural and household use of carbaryl with an increased risk of cancer in humans. Farmers in Minnesota and Iowa who had ever handled carbaryl had an increased risk of non-Hodgkin's lymphoma; this increased risk was statistically significant for those farmers who had handled the chemical prior to 1965 (with a risk almost four times as high as that of unexposed Minnesota and Iowa residents) or had handled carbaryl without using protective clothing (with a risk about double that of unexposed Minnesotans and Iowans).42 A similar elevated risk associated with exposure to carbamate insecticides as a group was found in a study of Nebraska farmers.43 Exposure to carbaryl used in gardens or backyard orchards in Missouri is associated with an increased risk (2.5-fold) of childhood brain cancer.44 Some of the concerns about carbaryl's carcinogenicity come from the carcinogenicity of nitrosocarbaryl, a compound that forms when carbaryl is combined with certain nitrogen- containing compounds (sodium nitrite, for example). Nitrosocarbaryl belongs to a family of compounds called N- nitrosamines of which 70 percent have been found to be carcinogenic in laboratory tests.45 Nitrosocarbaryl has been shown to form in the stomach of guinea pigs (animals whose stomachs are as acid as human stomachs) when the guinea pigs are given carbaryl and sodium nitrite.46 Nitrosocarbaryl causes skin cancers when painted on the skin of mice47 and cancers of the forestomach in rats.48,49 At least fifteen laboratory studies have been done of carbaryl's carcinogenicity.29,50,51 Three of these studies showed that carbaryl exposure caused an increase in cancer incidence: a 1970 study of rats,52 a 1982 study of carbaryl's ability to enhance lung tumor formation in mice by the carcinogen benzo[a]pyrene,51 and a 1992 study of carbaryl's ability to initiate tumors when painted on the skin of mice.50 The other studies found no relationship between carbaryl exposure and cancer incidence. There are a number of reasons why epidemiology and laboratory studies give conflicting results. First, none of the laboratory studies meets current standards29,53 and properly done studies may show significant results. Second, all of the laboratory studies used technical grade carbaryl while humans in epidemiology studies are exposed to commercial carbaryl products which contain a variety of other ingredients in addition to carbaryl. (See "Secret 'Inert' Ingredients," below) Some of these may be carcinogenic. Third, humans are exposed to mixtures of chemicals rather than the single chemicals used in laboratory tests. Given the studies showing that carbaryl can enhance or initiate cancers caused by other compounds, it may be combinations of chemicals that are important. Finally, humans may be more sensitive to carbaryl than are laboratory animals. For example, human stomachs are more acid than rat stomachs, and therefore are more likely to promote the formation of nitrosocarbaryl.46 Mutagenicity Carbaryl's potential to cause genetic damage (mutagenicity) has been called "weak" by EPA.4 The mutagenicity tests performed with carbaryl, however, provide a different picture. In human cells, carbaryl causes abnormal synthesis of DNA (the molecules from which genes are made).54 In Chinese hamster cells, carbaryl exposure caused sister chromatid exchanges (SCE; exchanges of genetic material within a pair of chromosomes),55 chromosomal aberrations,53 and abnormal cell division.56,57 In a newt, carbaryl exposure caused broken DNA in red blood cells.58 Carbaryl has also caused an increase in the frequency of lethal mutations in fruitflies,59,60 mutations or DNA damage in two species of bacteria,61,62 and chromosome aberrations or mutations in two species of plants (onions and corn).63,64 Several derivatives of carbaryl also are known to be mutagenic. 1-naphthol, the primary breakdown product of carbaryl, caused abnormal mitosis in Chinese hamster cells and DNA breakage when combined with naturally occurring hypochlorous acid in human cells.65 Nitrosocarbaryl (see "Carcinogenicity," above, and Figure 5) was found to be a more potent mutation agent than several other nitrosamines in three bacteria cultures66,67 and is a "potent" agent causing breakage of chromosomes and SCEs in hamster cells.68 Human Exposure People are exposed to carbaryl through using the insecticide in homes and gardens, consuming residues on food, drinking contaminated water, being contaminated due to drift from nearby applications, and working with carbaryl. Detailed information about these effects will be published in the next issue of JPR (13(2); Summer 1993). Effects on Nontarget Species A wide variety of animals, plants, and bacteria are adversely affected by carbaryl. Not only acute toxicity, but many different kinds of chronic effects have been documented in bees, beneficial insects, fish, birds, earthworms, frogs, crop plants, nitrogen-fixing bacteria, and other species. Some effects occur at surprisingly low doses. Detailed information about these effects will be published in the next issue of JPR (Summer 1993). Synergy The anti-ulcer drug Tagamet (cimetidine) has been shown to inhibit the breakdown of carbaryl in both laboratory animals and humans.69 This means that people exposed to both cimetidine and carbaryl will have longer and more pronounced symptoms. For example, a man who was exposed to six home treatments of a carbaryl-containing insecticide and who was also taking cimetidine suffered from headaches, memory loss, muscle weakness and cramps, anorexia, weight loss, and sleep apnea for a seven month period. Some neurological symptoms persisted for over a year.22 The acute and chronic toxicity of niridazole, a drug used to treat schistosomiasis, is also enhanced by carbaryl exposure.70 The common insecticide synergist piperonyl butoxide increases carbaryl toxicity. In fish, acute toxicity of a carbaryl- piperonyl butoxide mixture was over 100 times that of carbaryl alone.71 In addition, carbaryl increases the acute toxicity of the phenoxy herbicide 2,4-D, the insecticides rotenone (a botanical) and dieldrin (an organochlorine) as well as the wood preservative pentachlorophenol.72 Sublethal effects of the organophosphate insecticide phenthoate are also synergized by carbaryl in fish, including AChE inhibition73 and both morphological and behavioral changes.74 While the toxicity of combinations of chemicals is rarely studied, the ability of carbaryl to interact with a large number of chemical classes is striking. Manufacturing One of the intermediaries used in the manufacture of carbaryl is the highly reactive compound methyl isocyanate (MIC).9 On December 3, 1984 a toxic cloud containing MIC and other reaction products escaped from a tank in a Union Carbide plant in Bhopal, India that manufactured carbaryl and aldicarb (another carbamate insecticide).75 Between 2500 and 5000 people died as a result of the accident, and up to 200,000 people were injured. Injuries included respiratory problems, eye damage, fetal and newborn deaths, suppression of the immune system, and changes in blood chemistry.76 A smaller, but similar accident occurred the following year at Union Carbide's aldicarb and carbaryl plant in Institute, West Virginia and 135 people were hospitalized.75 Secret "Inert" Ingredients Most carbaryl-containing pesticide products contain "inert" ingredients whose identity EPA and the pesticide industry claim are trade secrets. There is little publicly available information about most of these "inerts." Some carbaryl formulations contain crystalline silica as an "inert" and others contain petroleum oils.77 EPA has listed petroleum hydrocarbons as an inert with high priority for testing because some petroleum products are suspected or known carcinogens.78 Crystalline silica causes the chronic lung disease silicosis79 and the International Agency for Research on Cancer has classified crystalline silica as having "limited evidence of carcinogenicity in humans" and "sufficient evidence of carcinogenicity" in animals.80 Silica was responsible for what has been called "America's worst industrial disaster" during the 1930s when over 700 workers died of silicosis after working on a tunneling project for Union Carbide in West Virginia.81 Other "inerts" in carbaryl formulations also pose toxicological problems. For example, exposure of prawns to sublethal concentrations of a commercial formulation of carbaryl caused more AChE inhibition than did exposure to carbaryl alone. The researchers believe that the emulsifier in the commercial formulation is responsible for the enhanced toxicity.82 Summary Carbaryl is a neurotoxic carbamate insecticide. In humans, acute effects of carbaryl exposure include headaches, nausea, incoordination, and difficulty breathing. Carbaryl can cause a variety of behavioral effects, some of which are relatively long-term. It also suppresses several functions of the immune system. Men exposed to carbaryl have more abnormal sperm and lower sperm counts than unexposed men. In female laboratory animals, exposure to carbaryl has caused a variety of reproductive problems, including birth defects in beagle dogs and increased rate of miscarriages in monkeys. Exposure to carbaryl has been associated with a higher incidence of the cancer non-Hodgkin's lymphoma in farmers and brain cancer in children. Nitrosocarbaryl, formed when carbaryl and nitrites react, is a potent carcinogen. Both carbaryl and nitrosocarbaryl cause genetic damage in some test systems, as does carbaryl's primary breakdown product, 1-naphthol. Carbaryl acts synergistically with a number of other insecticides and herbicides. An enormous industrial accident occurred at a carbaryl-manufacturing plant in Bhopal, India and other such plants have had significant accidents. Secret ingredients in carbaryl formulations include petroleum oils and crystalline silica, associated with the lung disease silicosis and cancer. n References 1. U.S. Dept. of Health and Human Services. Public Health Service. Agency for Toxic Substances and Disease Registry. 1992. Toxicological profile for 4,4'-DDT, 4,4'-DDE, 4,4'-DDD. (October.) 2. U.S. Dept. of Health and Human Services. Public Health Service. Agency for Toxic Substances and Disease Registry. 1990. Toxicological profile for dibromochloropropanes: 1,2- dibromo-3-chloropropane. (October.) 3. U.S. EPA. Pesticides and Toxic Substances. 1992. Pesticides industry sales and usage: 1990 and 1991 market estimates. Washington, D.C. (Fall.) 4. U.S. EPA. Office of Pesticide Programs. 1984. Guidance for the reregistration of pesticide products containing carbaryl as the active ingredient. Washington, D.C. (September 30.) 5. Abbott, D.L. 1986. A tree physiologist's view of growth regulators. Acta Horticulturae 179:293-298. 6. Jones, K.M. et al. Effects of paclobutrazol and carbaryl on the yield of Hi-Early red 'Delicious' apples. J. Hort. Sci. 66(2):159-163. 7. Farm Chemicals Handbook. 1991. Willoughby, OH: Meister Publishing. 8. Cremlyn, R.J. 1991. Agrochemicals: Preparation and mode of action. Chichester, U.K.: John Wiley and Sons, Ltd. 10. Morgan, D.P. 1989. Recognition and management of pesticide poisonings. Fourth edition. Washington, D.C.: U.S. EPA. Office of Pesticide Programs. Health Effects Division. Pp.12-13. 11. Gay, L. and M. Ehrich. 1990. A comparative study of drug metabolizing enzymes in adrenal glands and livers of rats and chickens. Int. J. Biochem. 22(1):15-18. 12. Parafita, M.A. and P. Fernandez-Otero. 1984. The interaction of carbaryl with the metabolism of isolated hepatocytes: II. Effect on gluconeogenesis. Gen. Pharm. 15(4):333-337. 13. Murphy, S.D. 1986. Toxic effects of pesticides. In Klaassen, C.D., M.O. Amdur, and J. Doull (eds.) Casarett and Doull's Toxicology. New York: Macmillan Company. Cited in Bavari, S. et al. 1991. Modulation of interleukin-2 driven proliferation of human large granular lymphocytes by carbaryl. an anticholinesterase insecticide. Fund. Appl. Toxicol. 17:61-74. 14. Wills, J.H., E. Jameson, and F. Coutston. 1968. Effects of oral doses of carbaryl on man. Clin. Toxicol. 1(30):265- 271. 15. Moser, V.C. et al. 1988. Comparison of chlordimeform and carbaryl using a functional observational battery. Fund. Appl. Toxicol. 11:189-206. 16. Carpenter, C.P. et al. 1961. Mammalian toxicity of 1- napthyl-N-methylcarbamate (Sevin insecticide). J. Agr. Food Chem. 9:30-39. Cited in Cranmer, M.F. 1986. Carbaryl: A toxicological review and risk analysis. Neurotoxicology 7(1):247-332. 17. Lox, C.D. 1984. The effects of acute carbaryl exposure on clotting factor activity in the rat. Ecotoxicol. Environ. Safety 8:280-283. 18. Kossakowski, S. 1987. Electrocardiogram of rabbits experimentally intoxicated with carbaryl. Polsk. Arch. Weteryn. 27:15-20. 19. Rouech, B. 1988. Department of amplification. The New Yorker (February 29):80-81. 20. Lotti, M. 1992. The pathogenesis of organophosphate polyneuropathy. Critical Reviews in Toxicology 21(6):465-487. 21. Dickoff, D.J., O. Gerber, and Z. Turovsky. 1987. Delayed neurotoxicity after ingestion of carbamate pesticide. Neurology 37:1229-1231. 22. Branch, R.A. and E. Jacqz. 1986. Subacute neurotoxicity following long-term exposure to carbaryl. Amer. J. Med. 80:741-745. 23. Anger, W.K. and S. M. Wilson. 1980. Effects of carbaryl on variable interval response rates in rats. Neurobehav. Toxicol. 2(1):21-24. 24. Sideroff, S. I. and J.A. Santolucito. 1972. Behavioral and physiological effects of the anticholinesterase inhibitor carbaryl (1-naphthyl methylcarbamate). Physiol. Behav. 9(3):459-462. 25. Dsi, I. 1974. Neurotoxicological studies of two carbamate pesticides in subacute animal experiments. Toxicol. Appl. Pharm. 27:465-476. 26. Anger, K.W. and J.V. Setzer. 1979. Effects of oral and muscular carbaryl administrations on repeated chain acquisition in monkeys. J. Toxicol. Environ. Health 5:793- 808. 27. Branch, R.A. and E. Jacqz. 1986. Is carbaryl as safe as it's reputation? Amer. J. Med. 80: 659-664. 28. Street, J.C. 1981. Pesticides and the immune system. In Sharma, R.P. (ed.) Immunologic considerations in toxicology. (Volume 1). Boca Raton, FL: CRC Press. Pp. 45-66. 29. Cranmer, M.F. 1986. Carbaryl: A toxicological review and risk analysis. Neurotoxicology 7(1):247-332. 30. Shabanov, M. et al. 1983. Effect of the pesticide carbaryl (Sevin) on the course of experimental Erysipelothrix rhusiopathiae infection in rats. Vet. Med. Nauki. 20:9-15. 31. Shea, T.B. 1983. Characterization of goldfish virus-2, a new iridovirus and the effects of the pesticides carbaryl and toxaphene on its in vitro replication. Northeastern University. Ph.D. dissertation. 32. Shea, T.B. and E.S. Berry. 1984. Suppression of interferon synthesis by the pesticide carbaryl as a mechanism for enhancement of goldfish virus-2 replication. Appl. Environ. Microbiol. 47(2): 250-252. 33. Forgue, M.-F. et al. 1990. 1-Naphthyl n-methyl carbamate effect on intra- and extracellular concentrations of arachidonic acid metabolites and on the chemiluminescence generation by mouse peritoneal macrophages. Int. J. Immunol. 12 (2):155-163. 34. Bavari, S. et al. 1991. Modulation of interleukin-2 driven proliferation of human large granular lymphocytes by carbaryl, an anticholinesterase insecticide. Fund. Appl. Toxicol. 17:61-74. 35. Smalley, H.E. J.M. Curtis, and F.L. Earl. 1968. Teratogenic action of carbaryl in beagle dogs. Toxicol. Appl. Pharm. 13:392-403. 36. Whorton, M.D. et al. 1979. Testicular function among carbaryl-exposed employees. J. Toxicol. Environ. Health 5:929-941. 37. Wyrobeck, A.J. et al. Sperm shape abnormalities in carbaryl-exposed employees. Environ. Health Perspec. 40:255- 265. 38. U.S. EPA. Office of Pesticides and Toxic Substances. 1980. Carbaryl decision document. (December.) Pp. 45-46. 39. Shtenberg, A.I. and M.N. Rybakova. Effect of carbaryl on the neuroendocrine system of rats. Fd. Cosmet. Toxicol. 6:461-467. 40. Dougherty, W.J., L. Goldberg, and F. Coulston. 1971. The effect of carbaryl on reproduction in the monkey (Macacca mulatta). Toxicol. Appl. Pharm. 19(2):365. (Abstract.) 41. Mathur, A. and P. Bhatnagar. 1991. A teratogenic study of carbaryl in Swiss albino mice. Fd. Chem. Toxic. 29(9):629- 632. 42. Cantor, K.P. et al. 1992. Pesticides and other agricultural risk factors for non-Hodgkin's lymphoma among men in Iowa and Minnesota. Cancer Res. 52:2447-2455. 43. Zahm, S.H. et al. 1988. A case-control study of non- Hodgkin's lymphoma and agricultural risk factors in eastern Nebraska. Amer. J. Epidemiol. 128(4):901. 44. Davis, J.R. et al. 1993. Family pesticide use and childhood brain cancer. Arch. Environ. Contam. Toxicol. 24:87-92. 45. Sittig, M. (ed.). 1980. Priority toxic pollutants: Health impacts and allowable limits. Park Ridge, NJ: Noyes Data Corp. Pp. 289-290. 46. Rickard, R.W. and H.W. Dorough. 1984. In vivo formation of nitrosocarbamates in the stomachs of rats and guinea pigs. J. Toxicol. Environ. Health 14:279-290. 47. Deutsch-Wenzel, R.P., et al. 1985. Local application to mouse skin as a carcinogen specific test system for non- volatile nitroso compounds. Cancer Lett. 19:85-92. 48. Lijinsky, W. and D. Schmahl. 1978. Carcinogenicity of N- nitroso derivatives of N-methylcarbamate insecticides in rats. Ecotoxicol. Environ. Safety 2:413-419. 49. Lijinsky, W. and H.W. Taylor. 1976. Carcinogenesis in Sprague-Dawley rats of N-nitrosos-N-alkylcarbamate esters. Cancer Lett. 1:275-279. 50. Shukla, Y., M. Antony, and N.K. Mehrotra. 1992. Carcinogenic and cocarcinogenic studies with carbaryl following topical exposure in mice. Cancer Lett. 62:133-140. 51. Triolo, A.J. et al. 1982. Effect of the insecticides toxaphene and carbaryl on induction of lung tumors by benzo[a]pyrene in the mouse. J. Toxicol. Environ. Health 9:637-649. 52. Andrianova, M.M. and I.V. Alekseev. 1970. Carcinogenic properties of Sevin, maneb, ziram, and zineb. Vop. Pitan. 29:71-74. Cited in reference #29. 53. California Department of Food and Agriculture. Medical Toxicology Branch. 1990. Summary of toxicology data: Carbaryl. Sacramento, CA. (July 31.) 54. Ahmed, F.E., R.W. Hart, and N.J. Lewis. 1977. Pesticide induced DNA damage and its repair in cultured human cells. Mut. Res. 42:161-174. 55. Onfelt, A. and I. Klasterska. 1984. Sister-chromatid exchanges and thioguanine resistance in V79 Chinese hamster cells after treatment with the aneuploidy-inducing agent carbaryl + S9 mix. Mut. Res. 125:269-274. 56. Soderpalm-Berndes, C. and A. Onfelt. 1988. The action of carbaryl and its metabolite naphthol on mitosis in V79 Chinese hamster fibroblasts: Indications of the involvement of some cholinester in cell division. Mut. Res. 201:349-363. 57. Onfelt, A. 1983. Spindle disturbances in mammalian cells. 1. Changes in the quantity of free sulfhydryl groups in relation to survival and c-mitosis in V79 Chinese hamster cells after treatment with colcemid, diamide, carbaryl, and methyl mercury. Chem.-Biol. Interactions 46:201-217. 58. Siboulet, R. et al. 1984. Micronuclei in red blood cells of the newt Pleurodeles waltl Michah: Induction with X-rays and chemicals. Mut. Res. 125:275-281. 59. Brzheskii, V.V. 1972. The study of the mutagenic properties of an insecticide from the carbamate group - Sevin. Genetika 8(6):151-153. 60. Dey, L., et al. 1987. Genotoxic activity of naphthyl carbamate in the larval stages of Drosophila. Current Science 56(16):848-849. 61. Rashid, K.A. and R.O. Mumma. 1986. Screening pesticides for their ability to damage bacterial DNA. J. Environ. Sci. Health B21(4):319-334. 62. Vaishampayan, A. 1985. Mutagenic activity of alachlor, butachlor and carbaryl to a N2-fixing cyanobacterium Nostoc muscorum. J. Agr. Sci. 104:571-576. 63. Grover, I.S., S.S. Ladhar, and S.K. Randhawa. 1989. Carbaryl Q a selective genotoxicant. Environ. Pollut. 58:313- 323. 64. Seehy, M.A., Moussa, M., and E. Badr. 1984. Induction of reverse mutation in waxy locus of Zea mays pollen grains by pesticides. Egypt. J. Genet. Cytol. 13(1):137-142. (abstract.) 65. Kozumbo, W.J., S. Agarwal, and H.S. Koren. 1992. Breakage and binding of DNA by reaction products of hypochlorous acid with aniline, 1-naphthylamine, or 1-naphthol. Toxicol. Appl. Pharm. 115:107-115. 66. Elespuru, R., W. Lijinsky, and J.K. Setlow. 1974. Nitrosocarbaryl as a potent mutagen of environmental significance. Nature 247:386-387. 67. Seiler, J.P. 1977. Nitrosation in vitro and in vivo by sodium nitrite, and mutagenicity of nitrogenous pesticides. Mut. Res. 48:225-236. 68. Thust, R. et al. 1980. Nitrosated urea pesticide metabolites and other nitrosamides: Activity in clastogenicity and SCE assays, and aberration kinetics in Chinese hamster V79-E cells. Mut. Res. 79:239-248. 69. Ward, S.A. et al. 1988. Carbaryl metabolism is inhibited by cimetidine in the isolated perfused rat liver and in man. Clin. Toxicol. 26:269-281. 70. Samaan, H.A. et al. 1990. The modification of the subchronic toxicity of niridazole by some commonly used insecticides in rats. Egypt. J. Pharm. Sci. 31:365-374. 71. Singh, D.K. and R.A. Agarwal. 1989. Toxicity of piperonyl butoxide-carbaryl synergism on the snail Lymnaea acuminata. Int. Revue ges. Hydrobiol. 74:689-699. 72. Statham, C.N. and J.J. Lech. 1975. Potentiation of the acute toxicity of several pesticides and herbicides in trout by carbaryl. Toxicol. Appl. Pharm. 34:83-87. 73. Rao, K.R.S.S. and K.V.R. Rao. 1989. Combined action of carbaryl and phenthoate on the sensitivity of the acetylcholinesterase system of the fish. Ecotoxicol. Environ. Safety 17:12-15. 74. Rao, R.R.S.S. and J.C. Rao. 1987. Independent and combined action of carbaryl and phenthoate on snake head, Channa punctatus (Bloch). Curr. Sci. 56(7):331-332. 75. Everest, L. 1985. Behind the poison cloud: Union Carbide's Bhopal massacre. Chicago IL: Banner Press. 76. Mehta, P.S. et al. Bhopal tragedy's health effects; A review of methyl isocyanate toxicity. JAMA 264(21):2781-2786. 77. MSDS reference for crop protection chemicals. Fourth edition. 1992. New York: Chemical and Pharmaceutical Press. 78. U.S. EPA. Office of Health Effects Assessment. 1986. List of inerts with high priority for testing. Unpublished tables. (July 16.) 79. Patnaik, P.P. 1992. A comprehensive guide to the hazardous properties of chemical substances. New York: Van Nostrand Reinhold. 80. U.S. Dept. of Health and Human Services. Public Health Service. National Institute for Occupational Safety and Health. 1991. Registry of toxic effects of chemical substances. Microfiche edition. (January.) 81. Cherniack, M. 1986. The Hawk's Nest incident: America's worst industrial disaster. New Haven CT: Yale University Press. 82. Reddy, M.S., P. Jayaprada, and K.V. R. Rao. 1990. Recovery of carbaryl inhibited AChE in penaeid prawn, Metapenaeus monoceros. Biochem. 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