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Adams, W. J. Aquatic toxicology testing methods. In Handbook of Ecotoxicology, D. J. Hoffman, B. A. Rattner, G. A. Burton Jr., and J. Cairns Jr., eds. Boca Raton, FL: Lewis Publishers, 1995, pp. 25 46. Blaustein, A. R., P. D. Hoffman, D. G. Hokit, J. M. Kiesecker, S. C. Walls, J. B. Hays. UV repair and resistance to solar UV-B in amphibian eggs: A link to population declines Proc. Nat. Acad. Sciences. USA 91: 1791 1795, 1994. Colborn, T., and C. Clement, eds. Chemically-Induced Alterations in Sexual and Functional Development: The Wildlife/Human Connection. Princeton, NJ: Princeton Scienti c, 1992. LeBlanc, G. A., and L. J. Bain. Chronic toxicity of environmental contaminants: Sentinels and biomarkers. Environ. Health Perspect. 105(suppl. 1): 65 80, 1997. Hayes, T. B., A. Collins, M. Lee, M. Mendoza, N. Noriega, A. A. Stuart, and A. Vonk. Hermaphroditic, demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Proc. Nat. Acad. Sciences. 99: 5476 5480, 2002.
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INTRODUCTION
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More than 100,000 chemicals are released into the global environment every year through their normal production, use, and disposal. To understand and predict the potential risk that this environmental contamination poses to humans and wildlife, we must couple our knowledge on the toxicity of a chemical to our knowledge on how chemicals enter into and behave in the environment. The simple box model shown in Figure 27.1 illustrates the relationship between a toxicant source, its fate in the environment, its effective exposure or dose, and resulting biological effects. A prospective or predictive assessment of a chemical hazard would begin by characterizing the source of contamination, modeling the chemical s fate to predict exposure, and using exposure/dose-response functions to predict effects (moving from left to right in Figure 27.1). A common application would be to assess the potential effects of a new waste discharge. A retrospective assessment would proceed in the opposite direction starting with some observed effect and reconstructing events to nd a probable cause. Assuming that we have reliable dose/exposure-response functions, the key to successful use of this simple relationship is to develop a qualitative description and quantitative model of the sources and fate of toxicants in the environment. Toxicants are released into the environment in many ways, and they can travel along many pathways during their lifetime. A toxicant present in the environment at a given point in time and space can experience three possible outcomes: it can be stationary and add to the toxicant inventory and exposure at that location, it can be transported to another location, or it can be transformed into another chemical species. Environmental contamination and exposure resulting from the use of a chemical is modi ed by the transport and transformation of the chemical in the environment. Dilution and degradation can attenuate the source emission, while processes that focus and accumulate the chemical can magnify the source emission. The actual fate of a chemical depends on the chemical s use pattern and physical-chemical properties, combined with the characteristics of the environment to which it is released.
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A Textbook of Modern Toxicology, Third Edition, edited by Ernest Hodgson ISBN 0-471-26508-X Copyright 2004 John Wiley & Sons, Inc.
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TRANSPORT AND FATE OF TOXICANTS IN THE ENVIRONMENT
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Figure 27.1 Environmental fate model. Such models are used to help determine how the environment modi es exposure resulting from various sources of toxicants.
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Conceptually and mathematically, the transport and fate of a toxicant in the environment is very similar to that in a living organism. Toxicants can enter an organism or environmental system by many routes (e.g., dermal, oral, and inhalation versus smoke stack, discharge pipe, or surface runoff). Toxicants are redistributed from their point of entry by uid dynamics (blood ow vs. water or air movement) and intermedia transport processes such as partitioning (blood-lipid partitioning vs. water-soil partitioning) and complexation (protein binding vs. binding to natural organic matter). Toxicants are transformed in both humans and the environment to other chemicals by reactions such as hydrolysis, oxidation, and reduction. Many enzymatic processes that detoxify and activate chemicals in humans are very similar to microbial biotransformation pathways in the environment. In fact, physiologically based pharmacokinetic models are similar to environmental fate models. In both cases we divide a complicated system into simpler compartments, estimate the rate of transfer between the compartments, and estimate the rate of transformation within each compartment. The obvious difference is that environmental systems are inherently much more complex because they have more routes of entry, more compartments, more variables (each with a greater range of values), and a lack of control over these variables for systematic study. The discussion that follows is a general overview of the transport and transformation of toxicants in the environment in the context of developing qualitative and quantitative models of these processes.
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