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Ecological Risk Assessment
-Cellular and Physiological Approach-

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Ecological risk assessment is the process for evaluating the impacts on organisms when exposed to one or more environmental stressors including chemicals, pathogens and invasive species. Mechanistic knowledge of how a stressor impacts bivalve species facilitates predictive (and thus proactive) approaches to assessing ecological risk. It allows an understanding of processes, such as acclimation, that could affect stressor impact. Also, it enables an evaluation of risk under real-world scenarios where multiple stressors are simultaneously acting upon an organism. Since phenotype results ultimately from the expression of genes and gene complexes, understanding patterns of gene expression evoked in response to environmental change,, yields insights regarding the molecular basis of phenotype, and the ability of organisms to restore cellular homeostasis.

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A mechanistic approach to risk assessment is based on the Adverse Outcome Pathways (AOP) concept, which has received significant attention from the research community since its conception. An AOP seeks to build mechanistic knowledge of how a stressor impacts the biology of an exposed organism. The theoretical framework of the AOP is that an initial perturbation of molecular function (termed a "molecular initiating event"), causes changes at a biochemical and cellular level, resulting in a physiological consequence. 

Modeling data at cellular and whole-organism levels will help in understanding the tolerance limits of individuals against  several stressors. Moreover, they shape the thresholds levels  beyond which disturbance in bivalve homeostasis take places.  As such, risk assessment takes individual-level impacts, which result from suborganismal perturbation, and seek to translate these effects to larger scales. Biomarkers, however, can not be considered useful bioindicators of marine organism health unless they are causally linked to ecologically relevant responses such as population or community-level endpoints.