Egg selenium concentrations as predictors of avian toxicity

Citation
A. Fairbrother et al., Egg selenium concentrations as predictors of avian toxicity, HUM ECOL R, 5(6), 1999, pp. 1229-1253
Citations number
26
Categorie Soggetti
Environment/Ecology
Journal title
HUMAN AND ECOLOGICAL RISK ASSESSMENT
ISSN journal
10807039 → ACNP
Volume
5
Issue
6
Year of publication
1999
Pages
1229 - 1253
Database
ISI
SICI code
1080-7039(199912)5:6<1229:ESCAPO>2.0.ZU;2-M
Abstract
Aquatic birds are exposed to selenium through their diet by ingesting aquat ic invertebrates that have accumulated selenium from water and the food cha in. However, dietary composition is highly variable among species, over tim e, and across sites, making it difficult to provide accurate estimations of dietary exposure for particular species at specific locations. Selenium ac cumulates in the egg, resulting in embryo malformation, embryonic death, an d decreased survival of juveniles. If the relationship between egg concentr ation and these reproductive parameters can be defined with sufficient cert ainty, then risk assessments can be performed through analysis of egg selen ium concentrations. Other researchers have proposed egg toxicity thresholds that lead to conclusions of widespread selenium toxicoses in waterbirds. H owever, we believe these values are overly conservative and that it is unli kely that selenium is posing a significant risk to wild birds in areas wher e the current water quality criterion is being met. Through the use of simp le statistical models (logit, probit, and Weibull functions) we are able to express mortality and teratogenicity relationships for mallards (Anas plat yrhynchos) in such a manner that the risk manager can be presented with inf ormation about the probability of reduced duckling survival if mean egg sel enium (MES) concentrations are known. Data analysis indicates that the two endpoints (mortality and teratogenesis) cannot be distinguished statistical ly. Commonly used effects thresholds (the EC10 and EC20) correspond to 16 a nd 21 mg/kg dw MES using the most sensitive endpoint, chick mortality. Both of these values are higher than the 6 mg/kg dw level proposed by Skorupa ( 1998) who based his estimate on field-observational data potentially confou nded by other environmental stress factors. The mortality and teratogenicit y endpoints presented here relate selenium exposure to risk to individuals within a population and do not provide information about the probability of selenium causing changes in population growth rates, either at the local o r regional levels.