DDT as a Cause of Cat Deaths

The most important aspect of the story as an ecological tale is based on the assumption that the cats not only died of DDT poisoning but did so as a consequence of eating prey that had previously ingested DDT – the now well known concept of “biomagnification”. For example in an early, published version of the cat story, Gordon Harrison (1968, see reference below) states: “the poor house cats at the end of this food chain had concentrated this material, and they began to die”. Harrison attributes the cat story to an unnamed “biologist who had served for five years as a pest control officer in Borneo”. This person was most likely Gordon Conway, an entomologist at the time with expertise in tropical insects who worked in North Borneo from 1961 to 1966 and also referred to the cat story in one his publications (Conway 1972).

Thomas Jukes was one of the most ardent antagonists of biomagnification as the cause of cat deaths from DDT, even defending the use of DDT for anti-malarial programs before the U.S. Senate (United States Congress 1969a) (Ironically, another witness during the hearing described the cat story in an argument against the use of DDT (United States Congress 1969b).) In a letter to the Editor of a medical journal, Jukes argues against the validity of the story which he bases on the toxicity of DDT (Jukes 1971). He provides a reference for the claim that “DDT is one of the least toxic of any of the pesticides to warm-blooded animals”, and provides an LD-50 of 300 mg/kg of body weight for cats. This value is similar to an oral LD-50 of 250 mg/kg (Kegley et al. 2007) and 300 mg/kg (St. Omer 1970) for cats given by other sources. Jukes uses the LD-50 value of 300 mg/kg to calculate that a 5 kg cat would have to eat 60,000 cockroaches in one day to ingest a lethal dose of DDT assuming the cockroaches themselves consumed a lethal dose estimated at 25 micrograms per insect - clearly not possible. Jukes also provides a quote from WHO officials (Brown and Wright 1969) that “DDT as applied has not caused any side effects among domestic animals (the matter of the North Borneo cats as misinterpreted in Time concerned dieldrin, not DDT)”. This claim suggests that, in addition to the DDT use described by Cheng (1967), dieldrin was also used in North Borneo (Sabah). Furthermore, the Time article referred to here is very likely one concerning pesticide use which was printed in the previous year and contains the (unreferenced) cat story (Anonymous 1969).

Jukes also discounts the story as yet another rendition of a similar news account that came out of Vietnam in 1962 (Bigart 1962) that begins: “American DDT spray killed the cats that ate the rats that devoured the crops that were the main props against Communist agitation in the central lowlands”. The author goes on to say that “this highly oversimplified explanation of the disaster in six provinces overrun by field rats is believed by many Vietnamese”. Regardless, Bigart concedes that some cats were killed after huts were sprayed with DDT, but also states that experts believe the explosion in the rat population was more likely due to a combination of favorable factors such as moisture, climate, availability of food “and, chiefly, the Government’s failure to insure adequate supplies of rat poison.”

Similar to the events in Vietnam, there are several other renditions of the cat story from other locales. The situation of this sort that arose closest to the probable site of a cat drop was briefly described in an annual report on conditions in North Borneo (Colony of North Borneo 1959) in which the author remarks: “Field rats were a greater menace than usual, partly as a result of antimalarial spraying which accidentally killed many cats”. This report does not specifically state which insecticide was used but does mention that zinc phoshide was used to kill the rats. Another story of this sort describes a situation in which it was conjectured that insecticide spraying caused the death of cats in Bolivia. This was determined during an investigation of an outbreak of Bolivian hemorrhagic fever (a rodent-borne disease) that was “due to invasion of houses by rodents” (Johnson 1965; Garcia et al. 1979). Furthermore, in a text on malaria, Robert Desowitz, mentioned that cats died in villages in Thailand after homes were sprayed with DDT resulting in an increase in the rat population (Desowitz 1991). Desowitz further commented that there were “numerous reports of village cats dying within one week after malaria-control teams sprayed DDT onto household walls”.

Cat deaths as a result of DDT spraying were also reported in Oaxaca, Mexico (Anonymous 1977) where the exterminators were called los matagatos, “the cat killers”, because “the cats lick the DDT residue off their paws and die of a disease of the nervous system”. Furthermore, Michael Colbourne (1962), who worked for the WHO during the 1950’s, conceded that malaria eradication campaigns in the western Pacific caused the death of some “domestic animals”, although he states, “such killings can be reduced, but not wholly prevented, by adequate precautions.” This remark was one of the few made by a WHO representative on the unintentional deaths of cats via indoor residual spraying of DDT during the height of the eradication program. In 1969, Anthony Brown of the WHO prepared an address to members of a convention on the biological impacts of pesticides in the environment during which he stated, “DDT as applied has not caused any side-effects among domestic animals.” Despite this claim, only several years later, Brown conceded that there were undocumented cases of cats dying from contact with DDT in Bolivia and Sabah “because of their habit of continually cleaning themselves by licking.

These sources confirm that cats died as a result of DDT spraying during malaria eradication programs. However, evidence points to the cause of cat deaths as being related to their propensity for licking their fur and that this trait provided a means for ingesting a lethal dose of DDT obtained directly from contact with the DDT residue clinging to sprayed floors and walls. This explanation also supports Jukes’ argument (Jukes 1971) that a lethal dose could not be acquired via biomagnification without discounting, as Jukes does, that any cats died as a result of DDT spraying. Furthermore, no scientific evidence could be found that any mammal died from the bioaccumulation of DDT through a food chain as suggested in the cat story. Therefore, it is reasonable to assume that this aspect of the story is not true.

References:

[Anonymous.] 1969. Pesticide into pest. Time, 11 July: 56-57.
[Anonymous.] 1977. Malaria makes a comeback. Time, 12 Sept.: 64.
Bigart H. 1962. A DDT tale aids reds in Vietnam. The New York Times (New York, NY), 2 Feb: 3.
Brown AWA, Wright J. 1970. The Present place of DDT in world operations for public health. In: The Biological Impact of Pesticides in the Environment (Gillett JW, ed.). Corvallis, Oregon: Oregon State University Press, 1970.
Brown AWA, “The Ecological Implications of Insecticide Usage in Malaria Programs. Am J Trop Med Hyg. 21(5) (1972):829-34.
Cheng FY. 1967. Observations on Anopheles balabacensis responses to specific patterns of DDT-spraying in Sabah, East Malaysia. World Health Organization, Pub. No. WHO/MAL/615-641, 20 p.
Colbourne MJ. 1962. A Review of malaria-eradication campaigns in the Western Pacific. Ann Trop Med & Parasit 56:33-43
Colony of North Borneo. 1959. Annual Report. Jesseltown, North Borneo: Government Printing Department.
Conway GR.1972. Ecological aspects of pest control in Malaysia. In: The Record of the Conference on the Ecological Aspects of International Development, (Farrar MT, Milton JP eds.) Washington University, December 8-11, 1968, The Natural History Press, Garden City.
Desowitz R. 1991. The Malaria Capers: More Tales of Parasites and People, Research, and Reality. New York: W. W. Norton & Company.
Garcia R, Huffaker CB. 1979. Ecosystem management for suppression of vectors of human malaria and schistosomiasis. Agro-Ecosystems 5:295-315.
Harrison G. 1968. Ecology: the new great chain of being. Natural History, 77(10), December:8-16+.
Johnson KM. 1965. Epidemiology of Machupo virus infection. 3. Significance of virological observations in man and animals. Am J Trop Med Hyg. 14(5):816-8.
Jukes TH. 1971. Letters to the editor: further words about DDT. California Medicine, 114(2):53-7.
Kegley S, Hill B, Orme S. 2007. PAN Pesticide Database, Pesticide Action Network, North America, San Francisco, CA. Available: http://www.pesticideinfo.org [accessed 13 March 2007].
St Omer V V. 1970. Chronic and acute toxicity of the chlorinated hydrocarbon insecticides in mammals and birds. Can Vet J 11 (11): 215-26.
United States Congress. 1969a. Senate. Committee on Commerce. Subcommittee on Energy, Natural Resources, and the Environment. Effects of Pesticides on Sports and Commercial Fisheries: Hearings, Ninety-first Congress, First Session to Consider the Effects of Pesticides on Sports and Commercial Fisheries, Part 1, May 19. Serial No. 91-15. U.S. Government Printing Office, Washington.
United States Congress. 1969b. Senate. Committee on Commerce. Subcommittee on Energy, Natural Resources, and the Environment. Effects of Pesticides on Sports and Commercial Fisheries: Hearings, Ninety-first Congress, First Session to Consider the Effects of Pesticides on Sports and Commercial Fisheries, Part 2, September 29 and 30. Serial No. 91-15. U.S. Government Printing Office, Washington.