TY - CHAP
T1 - Ecotoxicological risk assessment of atrazine in amphibians
AU - Solomon, Keith R.
AU - Carr, J. A.
AU - Du Preez, L. H.
AU - Giesy, J. P.
AU - Gross, T. S.
AU - Kendall, R. J.
AU - Smith, E. E.
AU - Van Der Kraak, G. J.
N1 - Publisher Copyright:
© 2005 American Chemical Society.
PY - 2005
Y1 - 2005
N2 - Although the ecological risks of atrazine in surface waters have been extensively reviewed with respect to its potential effects on a number of components of ecological systems, there is a lack of specific data on amphibians, especially for endpoints related to development and reproduction. To assess whether atrazine causes adverse effects in frogs through endocrine-mediated mechanisms, several hypotheses were tested in laboratory and field studies, using guidelines for the identification of causative agents of disease and eco-epidemiology derived from Koch's postulates and the Hill criteria. These criteria were: Temporality; Strength of Association; Consistency; and Biological Plausibility. Data from the literature and from studies conducted for the purpose of this assessment were used to test the following hypotheses: Atrazine causes adverse effects in amphibians through; 1) estrogen-mediated mechanisms, 2) androgen-mediated mechanisms, 3) thyroid-mediated mechanisms, 4) adverse effects on gonadal development in amphibians, or 5) adverse effects at the population level in exposed amphibians. In a lines-of-evidence approach to address the causal link between atrazine and effects in amphibians, no temporal correlation exists between the occurrence of gonadal effects and the introduction and use of atrazine. The strength of association is not strong. While some concentration-responses have been observed in some studies for some endpoints, these have not been observed under different conditions. The incidence rate of gonadal anomalies and other effects on populations was not related to atrazine exposures. Controlled studies in different laboratories produce inconsistent results and observations are inconsistent among laboratories as well as between laboratory and field studies. The biological plausibility of either of the proposed mechanisms of endocrine disruption is not supported by the laboratory or field observations. The data showed no evidence of effects through thyroid hormone mediated mechanism and little evidence for a mechanism mediated through androgens or estrogens. Overall, there was no compelling evidence to suggest that atrazine causes adverse effects in amphibians that are mediated by endocrine or developmental mechanisms.
AB - Although the ecological risks of atrazine in surface waters have been extensively reviewed with respect to its potential effects on a number of components of ecological systems, there is a lack of specific data on amphibians, especially for endpoints related to development and reproduction. To assess whether atrazine causes adverse effects in frogs through endocrine-mediated mechanisms, several hypotheses were tested in laboratory and field studies, using guidelines for the identification of causative agents of disease and eco-epidemiology derived from Koch's postulates and the Hill criteria. These criteria were: Temporality; Strength of Association; Consistency; and Biological Plausibility. Data from the literature and from studies conducted for the purpose of this assessment were used to test the following hypotheses: Atrazine causes adverse effects in amphibians through; 1) estrogen-mediated mechanisms, 2) androgen-mediated mechanisms, 3) thyroid-mediated mechanisms, 4) adverse effects on gonadal development in amphibians, or 5) adverse effects at the population level in exposed amphibians. In a lines-of-evidence approach to address the causal link between atrazine and effects in amphibians, no temporal correlation exists between the occurrence of gonadal effects and the introduction and use of atrazine. The strength of association is not strong. While some concentration-responses have been observed in some studies for some endpoints, these have not been observed under different conditions. The incidence rate of gonadal anomalies and other effects on populations was not related to atrazine exposures. Controlled studies in different laboratories produce inconsistent results and observations are inconsistent among laboratories as well as between laboratory and field studies. The biological plausibility of either of the proposed mechanisms of endocrine disruption is not supported by the laboratory or field observations. The data showed no evidence of effects through thyroid hormone mediated mechanism and little evidence for a mechanism mediated through androgens or estrogens. Overall, there was no compelling evidence to suggest that atrazine causes adverse effects in amphibians that are mediated by endocrine or developmental mechanisms.
UR - http://www.scopus.com/inward/record.url?scp=79960454219&partnerID=8YFLogxK
U2 - 10.1021/bk-2005-0899.ch012
DO - 10.1021/bk-2005-0899.ch012
M3 - Chapter
AN - SCOPUS:79960454219
T3 - ACS Symposium Series
SP - 124
EP - 137
BT - ACS Symposium Series
PB - American Chemical Society
ER -