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  • 标题:How risky is risk assessment: The role that life history strategies play in susceptibility of species to stress
  • 本地全文:下载
  • 作者:John D. Stark ; John E. Banks ; Roger Vargas
  • 期刊名称:Proceedings of the National Academy of Sciences
  • 印刷版ISSN:0027-8424
  • 电子版ISSN:1091-6490
  • 出版年度:2004
  • 卷号:101
  • 期号:3
  • 页码:732-736
  • DOI:10.1073/pnas.0304903101
  • 语种:English
  • 出版社:The National Academy of Sciences of the United States of America
  • 摘要:Measurements of toxicity based on individuals, such as the LC50 (concentration that kills 50% of a population), and effects on reproduction are used extensively in determining ecological risk, in particular, for endangered or threatened species. An underlying assumption is that individual-based toxicity metrics for one species can be directly compared with that for another species. However, this assumption overlooks the fact that different species have different life-history strategies and variables, such as lifespan, time to first reproduction, and number of offspring produced over a lifetime. Using a simple model and laboratory-derived parameter values, we tested the impact of differences in life-history traits on predicted responses to stress. The model predicts the delay in population growth. We compared seven invertebrate species by imposing 50% chronic mortality, 50% reduction of offspring, and both of these effects. The model predicted substantial differences in population delay among all of the species. Furthermore, the intrinsic rate of increase of each population was negatively correlated with the delay in population growth; species with high intrinsic rates of increase were less susceptible to equal levels of stress than species with lower intrinsic rates of increase. These results suggest that the susceptibility of species to pollutants is more complicated than previously thought and that differences in life-history variables must be considered in analyses of population persistence for threatened and endangered species.
  • 关键词:toxicity ; conservation biology ; delay-in-population-growth model ; demography
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