Author's response - ACS Publications

Dear Sir: In a feature article (ES&T,. Vol. 16, No. 8, 1982, pp. 448-53A), R. J. Kendall implied that application of paraquat at field usage rates mig...
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ES&T

LETTERS

Wildlife toxicology

Dear Sir: In a feature article (ES&T, Vol. 16, No. 8, 1982, pp. 448-53A), R. J. Kendall implied that application of paraquat at field usage rates might affect developing embryos of wild avian species. He based his assessment on a single study in which mallard eggs were artificially exposed to paraquat (i.e., eggs dipped into aqueous paraquat solutions for 30 s or from direct application of paraquat oil emulsions to eggs). I have several comments on Kendall's assessment. First, the application of paraquat in oil emulsions is not an approved label use, and any data generated by this route of exposure are not relevant to a hazard assessment. Second, the assessment of paraquat effects on birds under field usage is not consistent with the extensive history of safe field usage of paraquat sprays. Third, there are several in vivo studies, including long-term reproduction studies, that show paraquat does not affect the avian embryo. While laboratory trials using artificial egg-dipping techniques indicate that paraquat may affect developing avian embryos if critical concentrations penetrate into the egg, there is no evidence to suggest that this occurs under field use conditions. F.X. Kamienski Chevron Chemical Company 940 Hensely St. Richmond, Calif. 94804 Author's response Dear Sir: It was never stated that paraquat would necessarily affect eggs of wild avian species and, in agreement with Dr. Kamienski, this effect has not been demonstrated under field conditions. However, laboratory studies by Hoffman and Eastin ( / ) have shown that paraquat is embryotoxic and a teratogen in mallard {Anas platyrhynchos) eggs. This study would lead one to suspect a potential hazard to eggs of wild birds exposed to paraquat under field conditions. Further evi62A

Environ. Sci. Technol., Vol. 17, No. 2, 1983

dence of the potential hazard from external application of paraquat to eggs was provided by the study of Lutz-Ostertag and Henou (2), which showed' Japanese quail (Coturnix coturnix japonica) and chicken (Callus domesticus) eggs sprayed with paraquat, in amounts that would simulate field application levels, exhibited over 20% mortality as compared to controls during the incubation period. Certainly, there is evidence available that would at least allow one to suspect the potential hazard of paraquat exposure to eggs of wild birds. Indeed, it was never even implied that dietary (in vivo) exposure to paraquat would cause significant mortality in eggs produced by wild birds ingesting paraquat. The point of the paraquat reference was not to incriminate paraquat but to provide an example to stimulate some critical thinking. For instance, how would one ever identify totally under field conditions if a chemical, such as paraquat, was embryotoxic in eggs of wild birds without the effect being relatively pronounced (e.g., large dieoff after application)? Such difficulties often lead to chemical effects on wildlife, particularly subtle effects on reproduction, going unnoticed for a period of time (e.g., D D T impacts on raptors). Disturbances in embryo survival or health (e.g., embryotoxicity and teratogenicity) that can be determined in laboratory studies can be useful in interpreting impacts of chemicals on wild birds under field conditions. This is not to say that the effect would surely occur under field conditions, such as with the paraquat case, but at least one would suspect a potential hazard. It would seem reasonable, therefore, that an integration of field and laboratory research is of paramount importance here. The message intended by use of the paraquat example is that there is a need for the integration of field and laboratory research to interpret the impact of chemicals on wildlife. Additionally, should not all agricultural

chemicals that are applied in wildlife habitats be able to withstand this type of scrutiny? Ronald J. Kendall

Assistant Professor of Environmental Toxicology Huxley College of Environmental Studies Western Washington University Bellingham, Wash. 98225 References (1) Hoffman, D. J.; Eastin, W. C. J. Arch. Environ. Contam. Toxicol. 1982, / / , 7986. (2) Lutz-Ostertag, Y; Henou, C. C. R. Acad. Sci. Paris 1975, 439-42.

Water chemicals—hypochlorite Dear Sir: In the article "Water Chemicals C o d e x " by Robert Rehwoldt (ES&T, Vol. 16, No. 11, 1982, p. 616A), there is a misinterpretation of the data presented in Table 1. The A W W A publication "1981 Water Utility Operating Data" contains chemical usage data only from the 1397 utilities (of the more than 60 000 water suppliers nationwide) that responded to that survey. In addition, no auditing is performed to ensure that each utility provided accurate or complete information. I write not to point out an error by Rehwoldt, as the author stated ". . . more than 1.2 million tons of chemicals . . . " but to caution readers that the totals reported result from only 2% of the nation's public water supplies. In addition, errors do exist. For example, one community reported a consumption of 438 000 tons of hypochlorite, with an annual production of 473 million gallons of water (a concentration of 140 000 m g / L or three times the strength of household bleach). Eliminating that community, hypochlorite use in the report is only 2222 tons/y. Jon DeBoer, Project Director A W W A Research Foundation 6666 West Quincy Ave. Denver, Colo. 80235