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A model describing passive accumulation of organic chemicals from the aqueous environment and contaminated food in fish is developed. This model considers both biological attributes of the fish and physicochemical properties of the chemical that determine diffusive exchange across gill membranes and intestinal mucosa. Important biological characteristics addressed by the model are the fish's gill morphometry, feeding and growth rate and fractional aqueous, lipid, and nonlipid organic composition. Relevant physicochemical properties are the chemical's molar volume and n-octanol/water partition coefficient (Kow), which are used to estimate the chemical's aqueous diffusivity and partitioning to the fish's lipid and nonlipid organic fractions respectively. The model is used to describe and to analyze the bioaccumulation of polychlorinated biphenyls (PCBs) in Lake Ontario alewife (Alosa pseudoharengus), coho salmon (Oncorhynchus kisutch), rainbow trout (Oncorhynchus mykiss), brown trout (Salmo trutta), and lake trout (Salvelinus namaycush).

Simple assumptions for individual toxic response, exchange of toxicant with environmental concentrations and body composition are used in a model to evaluate the effect of lipid variation on toxic response in a subpopulation of similarly sized individuals. This model represents the internal distribution of a chemical such that more hydrophobic chemicals preferentially move into body lipid. Thus, for exposures of equal chemical activity, both increasing body fat and greater hydrophobicities increase the exposure duration that can be withstood without effect. In simulated 96 h bioassays the effect of increased tolerance to higher hydrophobicities was apparent for chemicals whose KOW exceeded 104. These simulations are compared to published observations. Simulations are also compared to other published data for longer‐term bioassays. The effect of interspecies gill morphology on toxic response is also explored. It is concluded that variation in lipid can account for much variation in tolerance in a subpopulation of similarly sized individuals; that gill morphology is another variable influencing toxic response; and that, in general, for similarly exposed organisms, the fattest survives the longest.

A model describing thermodynamically driven kinetic exchange of organic chemicals between fish and the aqueous environment is developed. This model considers both the biological attributes of the fish and the physicochemical properties of the chemical that determine diffusive exchange across gill membranes. Important biological characteristics addressed by the model are the fish's gill morphometry, body weight and fractional aqueous, lipid and structural organic composition. Relevant physicochemical properties are the chemical's aqueous diffusivity, molar volume and n-octanol/water partition coefficient (KOw), which is used as a surrogate to quantify chemical partitioning to the fish's lipid and structural organic fractions. Using this model, excretion rates, gill uptake efficiencies and bioconcentration factors can be predicted for nonmetabolized organic chemicals. Keywords-Bioconcentration DiffusionConvective mass transport Gill morphometry Modeling CHEMICAL EXCHANGE ACROSS GILL MEMBRANESTo characterize the exchange of a nonpolar, nonmetabolized organic chemical across a fish's gills as a diffusion process, the fish's total body burden, Bf = mass/fish, of the chemical is described simply by = SJ, dB' dt where S is the fish's total gill area and Jf is the diffusive flux per unit area of gill surface. According to Fick's first law, the steady-state diffusive flux between two points, zl and z2, without a phase change is given by where J is the mass flux per unit area normal to the direction of diffusion (e.g., mass cm-' s -I ) , D is the solute's diffusion coefficient (e.g., cm2 545 546 M. C. BARBER ET AL. where k, = D , / h , is the toxicant's conductivity through gill epithelium and &, and C, are the concentrations of toxicant at the water-epithelial and the epithelial-capillary interfaces, respectively. An expression for Jf can be formulated using the steady-state relationship Jf = Jw = J, and assuming that: B,/V= Cf = PaCa + PICI f PsCs = (Pa + PIC,/Ca + PsCs/Ca)Ca where Vis the fish's volume (i.e., cm3 = grams for neutrally buoyant fish) and Cf is the concentration of toxicant in the fish's whole body. Moreover, if internal distribution of the toxicant is rapid in comparison to its kinetic uptake and elimination, the above equation can be simplified to A l . The relevant concentration gradient for exchange is B , / V = Cf = (Pa + PIK, + PsKs)Ca (8) between the interlamellar water and the aqueous portion of the capillary blood.

JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. Ecological Society of America is collaborating with JSTOR to digitize, preserve and extend access to Ecology. Ecology, 71(3). 1990, pp. 938-954 0qAbstract. Motivated by problems where variation among individuals is necessary to explain properties of ecological systems, we develop a mathematical model of an individual organism. The model, based primarily upon energetics, is developed specifically for female daphnids, although with appropriate modifications it should be applicable to other aquatic animals such as fish. Mimicking the life history of an individual as it progresses from egg to juvenile to adult instars, the model consists of a coupled pair of nonlinear, nonautonomous ordinary differential equations. The growth of an individual is described through the dynamics of two compartments-lipid and structure-of the organism because of the importance of lipid dynamics in aquatic animals. Energy supply and demand are handled through an energy integrator compartment. Availability of energy is represented by potential flows from the lipid and structural compartments. Energy requirements of maintenance, activity, and reproduction are the sinks. An advantage of employing an individual-based technique is that ample information relating to the individual parameters-most of which are physiological in character-can usually be obtained, and reasonable estimates for model application found.

A method to determine the mortality effects of a hydrophobic chemical on a population is proposed. The ecotoxicological protocol is based on individual organism response and is derived from the static theory of "survival of the fattest." This study, focusing upon effects of mortality and the effects of toxicant stress on population succession, examines the static assessment survival of the fattest in a dynamic population model. A premise in this approach is that risk assessment should not be based solely upon chemical properties of the toxicant and that the biology of the exposed organisms is an important factor in the determination of effects.

Simple assumptions for individual toxic response, exchange of toxicant with environmental concentrations and body composition are used in a model to evaluate the effect of lipid variation on toxic response in a subpopulation of similarly sized individuals. This model represents the internal distribution of a chemical such that more hydrophobic chemicals preferentially move into body lipid. Thus, for exposures of equal chemical activity, both increasing body fat and greater hydrophobicities increase the exposure duration that can be withstood without effect. In simulated 96 h bioassays the effect of increased tolerance to higher hydrophobicities was apparent for chemicals whose KO, exceeded lo4. These simulations are compared to published observations. Simulations are also compared to other published data for longer-term bioassays. The effect of interspecies gill morphology on toxic response is also explored. It is concluded that variation in lipid can account for much variation in tolerance in a subpopulation of similarly sized individuals; that gill morphology is another variable influencing toxic response; and that, in general, for similarly exposed organisms, the fattest survives the longest.

This study of a Daphnia population model suggests that sublethal effects of nonpolar narcotics on growth of individual organisms can result in ultimate extinction of the population at chronic chemical concentrations near the effect concentration that leads to a 50% reduction in individual growth (the 16‐d EC50 for growth). A quantitative dose‐response relationship (QDRR)—a population extinction threshold, relating the minimal chronic chemical concentration that yields population persistence and the octanol/water partition coefficient (Kow)—is generated from numerical simulation studies of a Daphnia population model. The transition from population persistence to extinction is examined in terms of density functions in the lipid, structure, and age variables associated with models of individual daphnids. The densities of populations undergoing transition from persistence to extinction due to increased toxicity suggest that critically stressed populations are age‐bimodal with a component of old, large individuals and a component of small, nonreproductive individuals. The populations that persist near the threshold for extinction are unexpectedly diverse in age density and consist of relatively small individuals.