Effects of Malathion on Infectious Disease Susceptibility and the Immune System of Environmental Indicator Species
American Association of Zoo Veterinarians Conference 2004

Sharon K. Taylor1, DVM, PhD; David S. Rotstein2, DVM, MS, DACVP; Scott Willens2, DVM; Michael K. Stoskopf2, DVM, PhD, DACZM; Joseph B. Faulk2; Suzanne Kennedy-Stoskopf2, DVM, PhD, DACZM

1Washington DC Division, National Center for Environmental Assessment, United States Environmental Protection Agency, Research Triangle Park, NC, USA; 2College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA


Abstract

There is increased concern about the sublethal effects of organophosphorus (OP) pesticides on human and animal health.11,17 Malathion, an OP compound, is one of the most widely used pesticides, applied to the environment at an annual rate of 4,486,000 ha in the United States alone.13 It is used most commonly in the control of mosquitoes, flies, household insects, animal ectoparasites, and human lice. Malathion has been labeled with carbon, phosphorus, and sulfur and applied to fields to study its potential translocation and bioaccumulation.10 Small rodents, insects and birds had detectable levels 1 year after treatment.10 While the most studied toxic effect of malathion is on cholinesterase in the nervous system, only a few studies have been conducted on its toxic effect on the immune system. Hermanowicz and Kossmam (1984) observed that humans occupationally exposed to OP compounds have marked impairment of neutrophil chemotaxis and had increased frequency of upper respiratory infections proportionate to the number of years of exposure to organophosphorus compounds.9 Dulout, et al. (1983) demonstrated a dose–response relationship to malathion induced chromosomal aberrations in mouse bone marrow cells.6

Taylor, et al. (1999a) published a model that demonstrated increased infectious disease susceptibility and mortality in Woodhouse’s toads (Bufo woodhousii) externally exposed to field doses of an organophosphorus pesticide.14 Amphibians were selected as the model species for investigation because they are considered highly sensitive, environmental health indicator species that inhabit the aquatic and terrestrial interfaces.14,3,2,15 Worldwide amphibian diversity and population numbers have been reported to be declining.14,18,16 Pesticides are sometimes implicated, yet few studies have been conducted to determine if and how pesticides actually present a hazard to them.7 In addition, most published studies on the effects of pesticides on amphibians have been conducted on embryo and tadpole life stages.8,4,12,5,1

This current project further studies these initial findings on two environmental indicator species of large anurans, the bullfrog (Rana catesbeiana) and the marine toad (Bufo marinus), which inhabit widely different environments. The research showed an increased susceptibility to bacterial infection in these amphibian species following pesticide exposure, strongly suggesting an effect on immune suppression that could correlate with reported effects in humans. This work demonstrates the need to integrate human and wildlife health research and models to better assess potential ecological risks that could result in effects to both humans and wildlife.

The views expressed in this abstract are those of the authors and do not necessarily reflect the views or policies of the U.S. Environmental Protection Agency.

 

Literature Cited

1.  Berrill, M., S. Bertram, B. Pauli, D. Coulson, M. Kolohon, and D. Ostrander. 1994. Comparative sensitivity of amphibian tadpoles to single and pulsed exposures of the forest-use insecticide fenitrothion. Environ. Tox. and Chem. 14: 1011–1018.

2.  Blaustein, A. R., J. M. Kiesecker, D. P. Chivers, and R. G. Anthony. 1997. Ambient UV-B radiation causes deformities in amphibian embryos. Proceedings NAS. 94:13735–13737.

3.  Carey, C., and C. J. Bryant. 1995. Possible interrelations among environmental toxicants, amphibian development, and decline of amphibian populations. Environ. Health Perspect. 103: 13–17.

4.  De Llamas, M. C., A. C. de Castro, and A. M. Pechen de D’Angelo. 1985. Cholinesterase activities in developing amphibian embryos following exposure to the insecticides dieldrin and malathion. Archives of Environ. Contamin. and Tox. 14: 161–166.

5.  Devillers, J., and J. M. Exbrayat. 1992. Ecotoxicity of chemicals to amphibians. Antony Rowe Ltd, Great Britain, 339 pp.

6.  Dulout, F. N., M. C. Pastori, and O. A. Olivero. 1983. Malathion-induced chromosomal aberrations in bone marrow cells of mice. Mutation Res. 122: 163–167.

7.  Hall, R. J., and P. F. P. Henry. 1992. Review: Assessing effects of pesticides on amphibians and reptiles: Status and needs. Herp. J. 2: 65–71.

8.  Hall, R. J., and E. Kolbe. 1980. Bioconcentration of organophosphorus pesticides to hazardous levels by amphibians. J. Tox. and Environ. Health. 6: 853–860.

9.  Hermanowicz, A., and S. Kossman. 1984. Neutrophil function and infectious disease in workers occupationally exposed to organophosphorus pesticides: Role of mononuclear-derived chemotactic factor for neutrophils. Clinical Immun. and Immunopath. 33: 13–22.

10.  Peterle, T. J. 1966. Contamination of the freshwater ecosystem by pesticides. In: Pesticides in the environment and their effects on wildlife, N. W. Moore (ed.). J. of Appl. Ecol., supplement 3: 181–192.

11.  Pruett, S. B. 1992. Immunotoxicity of organophosphorus compounds. In: Organophosphates: Chemistry, Fate, and Effects. J. Chambers, and P. Levi (eds.). 1992. Academic Press pp. 367–386.

12.  Rosenbaum, E. A., A. Caballero de Castro, L. Gauna, and A. M. Pechen de D’Angelo. 1988. Early biochemical changes produced by malathion on toad embryos. Archiv. of Environ. Contamin and Tox. 17: 831–835.

13.  Smith, G. J. 1987. Pesticide use and toxicology in relation to wildlife: organophosphorus and carbamate compounds. United States Department of the Interior, Fish and Wildlife Service, Washington, D. C., Resource Publication 170, 171 pp.

14.  Taylor, S. K., E. S. Williams, and K. W. Mills. 1999a. Effects of malathion on disease susceptibility in Woodhouse’s toads. J. of Wildl. Dis. 35 (3): 536–541.

15.  Taylor, S. K., E. S. Williams, E. T. Thorne, K. W. Mills, D. I. Withers, and A. C. Pier. 1999b. Causes of mortality of the Wyoming toad. J. of Wildl. Dis. 35 (1): 49–57.

16.  Wake, D. B. 1992. Declining amphibian populations. Science. 253: 860.

17.  World Health Organization. 1986. Organophosphorus insecticides. Environmental Health Criteria 63. World Health Organization, Geneva, Switzerland, 181 pp.

18.  Wyman, R. L. 1990. What’s happening to the amphibians? Conserv. Biol. 4: 350–352.

 

Speaker Information
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Sharon K. Taylor, DVM, PhD
Washington DC Division
National Center for Environmental Assessment
United States Environmental Protection Agency
Research Triangle Park, NC, USA


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