Chapter 29. Ecotoxicology

• Ecotoxicology is the study of the fate and effects of toxic substances on an ecosystem.
• Chemodynamics is, in essence, the study of chemical release, distribution, degradation, and fate in the environment.
• A chemical can enter any of the four matrices: the atmosphere by evaporation, the lithosphere by adsorption, the hydrosphere by dissolution, or the biosphere by absorption, inhalation, or ingestion (depending on the species). Once in a matrix, the toxicant can enter another matrix by these methods.
• The biological availability (or bioavailability) of a chemical is the portion of the total quantity of chemical present that is potentially available for uptake by organisms.
• Pollution may result in a cascade of events, beginning with effects on homeostasis in individuals and extending through populations, communities, ecosystems, and landscapes.
• Terrestrial toxicology is the science of the exposure to and effects of toxic compounds in terrestrial ecosystems.
• Aquatic toxicology is the study of effects of anthropogenic chemicals on organisms in the aquatic environment.

Ecotoxicology is the study of contaminants in the biosphere and their effects on constituents of the biosphere. It has an overarching goal of explaining and predicting effect or exposure phenomena at several levels of biological organization (Figure 29–1). Relevant effects to nonhuman targets range from biomolecular to global. As the need to predict major effects to populations, communities, ecosystems, and other higher level entities has become increasingly apparent, more cause–effect models relevant to these higher levels of biological organization are added to the conventional set of toxicology models applied by pioneering ecotoxicologists. Contaminant chemical form, phase association, and movement among components of the biosphere are also central issues in ecotoxicology because they determine exposure, bioavailability, and realized dose.

Relevant exposure routes are the conventional ingestion, inhalation, and dermal absorption. But, unique features of exposure pathways must be accommodated for species that ingest a wide range of materials using distinct feeding mechanisms, breathe gaseous or liquid media using different structures, and come into dermal contact with a variety of gaseous, liquid, and solid media.

Prediction of oral exposure can be limited because species feed on different materials; however, conventional principles about oral bioavailability remain relevant. Many techniques applied to determining human oral bioavailability are available to the ecotoxicologist. As an example, some birds are uniquely at high risk of lead poisoning because they ingest and then use lead shot as grit. The birds grind shot in their gizzards under acidic conditions, releasing significant amounts of dissolved lead.

Estimation of chemical speciation is central to predicting bioavailability of water-associated contaminants. Speciation can determine the bioavailability of dissolved metals. Movements of nonionic and ionizable organic compounds across the gut or gills are strongly influenced by lipid solubility and pH partitioning, respectively. Consequently, determination of a compound's lipophilicity or calculation of pH- and pKa-dependent ionization facilitates some predictive capability for bioavailability. The free ion activity model (FIAM) states that uptake and toxicity of cationic trace metals are best predicted from their free ion activity or concentration, although exceptions exist.

Bioavailability, bioaccumulation, or exposure concentrations for sediment-associated toxicants are also approached by considering chemical speciation and phase partitioning. Metals in sediments are either incorporated into one of the many solid phases or dissolved in the interstitial waters surrounding the sediment particles. Bioavailable metals have been estimated by normalizing sediment metal concentrations to easily extracted iron and manganese concentrations because solid iron and manganese oxides sequester metals in poorly bioavailable solid forms.

Another issue of importance to the ecotoxicologist is the possibility of biomagnification, the increase in contaminant concentration as it moves through a food web. Biomagnification can result in harmful exposures to species situated high in the food web such as birds of prey.

One approach to this complex topic of ecotoxicologic effects is to organize effects according to biological levels of organization. One may consider effects, in ascending order, at the subcellular (molecular and biochemical), cellular, organismal, population, community, and ecosystem levels of organization. Ecotoxicology deals with, theoretically at least, all species, and in line with other aspects of natural resource management, the primary concern is one of sustainability. The policies and regulations surrounding chemical effects in natural ecosystems are designed to protect ecological features such as population dynamics, community structures, and ecosystem functions.

Molecular and Biochemical Effects

This lowest level of organization includes fundamental processes associated with the regulation of gene transcription and translation, biotransformation of xenobiotics, and the deleterious biochemical effects of xenobiotics on cellular constituents including proteins, lipids, and DNA.

Gene Expression and Ecotoxicogenomics

Xenobiotics can affect gene transcription through interactions with transcription factors and/or the promoter regions of genes. In the context of environmental toxicology, perhaps the most studied xenobiotic effects involve ligand-activated transcription factors. These intracellular receptor proteins recognize and bind specific compounds, thus forming a complex that binds to specific promoter regions of genes, thereby activating transcription of mRNAs, and ultimately translation of the associated protein.

Estrogen Receptor

The dominant natural ligand for this nuclear receptor is estradiol (E2). Binding of E2 with estrogen receptor (ER) produces a complex that can then bind to estrogen response elements (ERE) of specific genes that contain one or more EREs, thereby causing gene transcription. Genes regulated in this manner by E2–ER play various important roles in sexual organ development, behavior, fertility, and bone integrity.

A number of chemicals can serve as ligands for ER; in most cases these “xenoestrogens” activate gene transcription acting as receptor agonists. Some of these xenoestrogens include diethylstilbestrol (DES), DDT, methoxychlor, endosulfan, surfactants (nonyl-phenol), some PCBs, bisphenol A, and ethinyl E2, a synthetic estrogen observed in municipal effluents and surface waters. Environmental exposures to these chemicals are sufficient to perturb reproduction or development.

Aryl Hydrocarbon Receptor

The aryl hydrocarbon receptor (AHR) is a member of the basic helix–loop–helix Per ARNT Sim (bHLH-PAS) family of receptors/transcription factors that is involved in development, as sensors of the internal and external environment in order to maintain homeostasis, and in establishment and maintenance of circadian clocks. Characterized genes that are upregulated by the AHR system code for enzymes involved in the metabolism of lipophilic chemicals, including organic xenobiotics and some endogenous substrates such as steroid hormones. These enzymes include mammalian CYP1A1, 1A2, and 1B1 and their counterparts in other vertebrates, glutathione transferase, glucuronosyltransferase, alcohol dehydrogenase, and quinone oxidoreductase.

Some ubiquitous pollutants that act as AHR ligands and markedly upregulate gene transcription via the AHR–ARNT signaling pathway include the polycyclic aromatic hydrocarbons (PAHs) and the polyhalogenated aromatic hydrocarbons (pHAHs). In general, pHAH-type AHR ligands are more potent AHR ligands and enzyme inducers than PAHs.

Genomics and Ecotoxicogenomics

Ecotoxicogenomics has great potential for elucidating impacts of chemicals of ecological concern and ultimately for playing an important role in ecological risk assessments (ERA) and regulatory ecotoxicology. Specific areas to which this emerging field can contribute include prioritization of chemicals investigated in ERA, identification of modes of action of pollutants, identification of particularly sensitive species, and effect prediction at higher levels of organization.

Protein Damage

Acetylcholinesterase (AChE) degrades the neurotransmitter acetylcholine, and controls nerve transmission in cholinergic nerve tracts. The widely used organophosphate and carbamate classes of insecticides kill by inhibiting AChE, and this mechanism is operative for “nontarget” organisms including invertebrates, wildlife, and humans. Of particular ecological concern have been the ingestion of AChE-inhibiting insecticides with food items or granular formulations (mistaken as seed or grit) by birds and aquatic animal exposures from agricultural run-off. In addition to enzyme inhibition, chemicals can damage proteins in other ways, including oxidative damage and the formation of stable adducts similar to those formed with DNA.

Oxidative Stress

Oxidative stress has been defined as the point at which production of ROS exceeds the capacity of antioxidants to prevent damage. Numerous environmental contaminants act as prooxidants and enhance production of ROS. The resulting oxidative damage can account wholly or partially for toxicity. Mechanisms by which chemicals enhance ROS production include redox cycling, interactions with electron transport chains (notably in mitochondria, microsomes, or chloroplasts), and photosensitization. Redox cycling chemicals include diphenols and quinones, nitroaromatics and azo compounds, aromatic hydroxylamines, paraquat, and certain metal chelates, particularly of copper and iron.

Photosensitization is an important mechanism in aquatic systems. Ultraviolet (UV) radiation (specifically UVB and UVA) can penetrate surface waters to varying depths, depending on the wavelength of the radiation and the clarity of the water. The UV radiation generates ROS and other free radicals via excitation of photosensitizing chemicals, including common pollutants of aquatic systems.

ROS can drive redox status to a more oxidized state, potentially reducing cell viability. These ROS-mediated impacts and others have been associated with several human diseases including atherosclerosis, arthritis, cancer, and neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. With the exception of cancer, the role of ROS in specific diseases in wildlife has received little attention. It is reasonable to assume that oxidative stress accounts in part for the toxicity of diverse pollutants to free-living organisms.

DNA Damage

Cancer is an important health outcome associated with chemical exposures in wildlife. In the context of ecotoxicology, the most widely studied form of damage has been the formation of stable DNA adducts, particularly by PAHs. PAHs must be activated to reactive metabolites to form these adducts.

Cellular, Tissue, and Organ Effects

Cells

Most free-living organisms routinely experience energy deficits. For example, food resources are often scarce during the winter for many animals, which adapt by conserving energy (by hibernating or lowering metabolism) or by storing energy beforehand (as is the case for many migratory birds). Thus, the effects of pollutants on mitochondrial energy metabolism can be of particular importance to wildlife.

Lysosomes, which are involved in the degradation of damaged organelles and proteins, sequester many environmental contaminants, including metals, PAHs, and nanoparticles. The accumulation of xenobiotics by lysosomes can elicit membrane damage, which warns of pathological effects in both invertebrates and vertebrates.

Chemical effects on nuclei have been examined in ecological contexts. Micronuclei are chromosomal fragments that are not incorporated into the nucleus at cell division, and chemical exposures can markedly increase their frequency. Elevated micronuclei numbers have been observed in erythrocytes in fish and in hemocytes in clams from a PCB-polluted harbor.

Target Organs

An important target organ in ecotoxicology of nonmammalian aquatic vertebrates and many invertebrates is the gill, which is the major site of gas exchange, ionic regulation, acid–base balance, and nitrogenous waste excretion. Gills are immersed in a major exposure medium for these animals (surface water), so metabolically active epithelial cells are in direct contact with this medium. They also receive blood supply directly from the heart. Common structural lesions in gills include cell death (via necrosis and apoptosis), rupture of the epithelium, hyperplasia, and hypotrophy of various cell pop-ulations that can lead to lamellar fusion, epithelial swelling, and lifting of the respiratory epithelium from the underlying tissue.

Organismal Effects

Mortality

Chemical pollution of the environment does not generally attain levels sufficient to outright kill wildlife. The ecotoxicologic concerns are the long-term, chronic impacts of chemicals on organismal variables such as reproduction and development, behavior, and disease susceptibility, and how such impacts parlay into effects at the population and higher levels of organization. However, mortality is an endpoint in exposure studies.

Reproduction and Development

Contaminant effects on development are often difficult to discern in field studies, due to the small size of embryos and the fact that developmental impacts are generally either lethal or greatly reduce survival. Because early life stages of most organisms are generally more sensitive to xenobiotics than other life stages, developmental impacts merit careful attention by ecotoxicologists.

Chlorinated hydrocarbons continue to generate concerns although many (DDT and other insecticides, and PCBs) have had their production and use sharply curtailed. The dioxins (TCDD) and coplanar PCBs compromise cardiac development, among other effects in vertebrates, and these developmental perturbations are largely receptor-mediated and dependent on binding of the chemical (such as TCDD) with the AHR.

Hydrocarbons, in large part PAHs, associated with oil spills, contaminated sediments, paper mill effluents, and creosote used for wood treatment have profound developmental effects in fish embryos. In many cases, the effects observed visually appear similar to those observed in fish embryos exposed to dioxins and coplanar PCBs, and include malformed hearts (“tube hearts”), craniofacial deformities, hemorrhaging, and edema of the pericardium and yolk sac, the latter resulting in a distended, faintly blue yolk sac that gives this syndrome the name “blue sac disease.”

Disease Susceptibility

The potential impacts of environmental contaminants on immune systems that render organisms more susceptible to disease are of great concern. Numerous laboratory studies have demonstrated chemical impacts on immune systems in animals of ecological relevance. These include pesticides in amphibians, PCBs in channel catfish, heavy metals in rainbow trout, PAHs in bivalves, and flame retardants (polybrominated diphenyl ethers) in American kestrels.

Behavior

Relatively subtle effects on behaviors associated with mating and reproduction, foraging, predator–prey interactions, preference/avoidance of contaminated areas, and migration have potentially important ramifications for population dynamics. In some cases, the biochemical mechanisms underlying behavioral effects have been elucidated, which may assist our understanding of these issues and provide useful biomarkers for behavioral toxicants in field studies.

Chemicals causing behavioral effects in wildlife are known to be neurotoxicants. Behavioral effects of insecticides have been observed in fish. For example, impacts of the organophosphate diazinon on olfactory-mediated behaviors such as the alarm response and homing in the Chinook salmon have been observed, as well as similar thresholds for the effects of another organophosphate (chlorpyrifos) on swimming and feeding behaviors and on AChE inhibition in coho salmon (O. kistich). Mercury, particularly as methylmercury, comprises another potent neurotoxin that has been shown to perturb behavior in wildlife.

Environmental contaminants not generally thought of as neurotoxicants have also been shown to perturb behavior. For example, cadmium and copper have been shown to impact olfactory neurons and associated behaviors (preference/avoidance to chemicals, including pheromones) in several fish species. Copper exposure in zebrafish also led to loss of neurons in the peripheral mechanosensory system (“lateral line”), which could lead to altered behaviors associated with schooling, predator avoidance, and rheotaxis (physical alignment of fish in a current). Clearly, numerous mechanisms of chemical toxicity can result in behavioral impacts, including direct toxicity to neurons, alterations in hormones that modulate behaviors, and impaired energy metabolism. Also, impaired behavior may comprise a sublethal impact with substantive ecological consequence.

Cancer

Beginning in the 1960s, numerous cases of cancer epizootics in wildlife that are associated with chemical pollution, particularly in specific fish populations, have been reported in North America and northern Europe. As in humans, cancer in these animals occurs largely in relatively older age classes and therefore is oftentimes considered a disease unlikely to directly impact population dynamics or other ecological parameters. However, this may not always be the case, particularly in species that require many years to attain sexual maturity and/or have low reproductive rates.

Lifestyle is a major contributor to differential cancer susceptibility; benthic (bottom-dwelling) species such as brown bullhead (Ameriurus nebulosus) and white sucker (Catostomus commersoni) in freshwater systems and English sole (Parophrys vetulus) and winter flounder (Pseudopleuronectes americanus) in marine systems generally exhibit the highest cancer rates in polluted systems. The bulk of chemicals in these systems associated with cancer epizootics, such as PAHs, PCBs, and other halogenated compounds, reside in sediments; benthic fish live in contact with these sediments and prey in large measure on other benthic organisms.

It is noteworthy that many reports of elevated cancer rates in free-living animals occur in fish, with few reports of potentially chemically related cancers to our knowledge in other vertebrates. It is likely that elevated exposures play an important role in the relatively high frequency of reports of cancers in benthic fish; relative inherent sensitivities among mammals, birds, reptiles, and amphibians, and fish are unclear.

Population

A population is a collection of individuals of the same species that occupy the same space and within which genetic information can be exchanged. Population ecotoxicology covers a wide range of topics with core research themes being (1) epidemiology of chemical-related diseases, (2) effects on general population qualities including demographics and persistence, and (3) population genetics.

The level of belief warranted for possible contaminant-related effects in nonhuman populations is assessed by applying routine epidemiological methods. Rules of thumb for gauging the level of belief warranted by evidence that emerged from human epidemiology are also applied in population ecotoxicology (Table 29–1).

Some species populations fluctuate within a range of densities. These fluctuations are characteristic of the species' strategy for maintaining itself in various types of habitats and toxicant exposure could potentially change this range. Combined with decreases in population densities driven by external forces such as weather events, these toxicant-induced modifications of the average population densities and dynamics can increase the risk of a population's density falling so low that local extinction occurs. Toxicants can change a species population's vital rates, such as age- and sex-dependent death, birth, maturation, and migration rates. Combined, these changes determine the population density and distribution of individuals among ages and sexes during exposure.

Individuals of the same species often are grouped into subpopulations within a habitat and all of these subpopulations together comprise a metapopulation (Figure 29–2). Subpopulations in the metapopulation have different levels of exchange and different vital rates that depend on the nature of their habitat. Spatial distances and obstacles or corridors for migration influence migration among patches; habitat quality determines vital rates.

The genetics of exposed populations are studied to understand changes in tolerance to toxicants and to document toxicant influence on field populations. Some populations have the capacity to become more tolerant of toxicants via selection. Genetic qualities are also used to infer past toxicant influence in an exposed population. Another piece of evidence demonstrating past toxicant influence on populations can be a change in genetic diversity. A drop in genetic diversity in populations is thought to be an adverse effect because genetic diversity is required in populations to evolutionarily adapt to environmental changes. Toxicants can influence genetic diversity by purely stochastic means.

Community

An ecological community is an interacting assemblage of populations occupying a defined habitat at a particular time. Populations in a community interact in many ways and, because these many interactions are complex, a community has properties that are not predictable from those of its component populations.

Communities take on characteristic structures as predicted by the Law of Frequencies: the number of individual organisms in a community is related by some function to the number of species in the community. Ecotoxicants can alter the resulting community structure in predictable ways by either directly impacting the fitness of individuals in populations that make up the community or by altering population interactions.

Recently, structural and functional qualities in communities have been combined to generate multimetric indices such as the Index of Biotic Integrity (IBI). Ecological insight is used to select and then numerically combine community qualities such as species richness, health of individual animals in a sample, and the number of individuals in a sample belonging to a particular functional group, such as number of piscivorous fish. The IBI score for a study site is calculated and compared with that expected for an unimpacted site in order to estimate its biological integrity.

Another central theme in community ecotoxicology is toxicant transfer during trophic interactions. Toxicant concentrations can decrease (biodiminution), remain constant, or increase (biomagnification) with each trophic transfer within a food web. Metals that biomagnify are mercury and the alkali metals, cesium and rubidium. Zinc, an essential metal that is actively regulated in individuals, can exhibit biomagnification or biominification depending on whether ambient levels are below or above those required by the organism to function properly.

Most individuals in a community can feed on different species depending on their life stage, seasons, and relative abundances of prey species. These trophic interactions are best described as occurring in a trophic web, not a trophic chain.

Ecosystem to Biosphere

Ecosystems, the functional unit of ecology, are composed of the ecological community and its abiotic habitat. The ecotoxicologist is interested in understanding how toxicants diminish an ecosystem's capacity to perform essential functions and to understand toxicant movement within different ecosystem components enough to assess exposure.

Conventional ecosystem studies involve descriptions of contaminant concentrations and movements in easily defined ecosystems such as lakes, forests, or fields. Some toxicants, especially those subject to wide dispersal by air or water, cannot be completely understood in this framework, so a landscape scale might be chosen instead. As an example, acid precipitation might be examined in the context of an entire watershed, mountain range, or even a continental region. Still other ecotoxicants require a global context in order to fully understand their movements and accumulation. As an example, hexachlorobenzene concentration in tree bark collected worldwide showed a clear latitudinal gradient.

Toxicity Tests

Toxicity testing encompassing representative animals and plants at different levels of organization offers a practical approach to characterize chemical effects on biological systems. Toxicity tests address the potential direct effects of toxic substances on individual ecosystem components in a controlled and reproducible manner. Ecotoxicology tests feature a wide variety of aquatic (including algae, invertebrates, tadpoles, bivalves, shrimp, and fish), avian (quail and duck), and terrestrial (soil microorganisms, crops, honey bees, earthworms, and wild mammals) species. Species are selected based on their traditional use as laboratory animals, but also on ecological relevance, which further complicates global harmonization of ecological testing. In addition, testing of aquatic species requires monitoring of water quality, investigation of the solubility and stability of the test substance under the conditions of testing, and determination of nominal versus measured concentrations.

In acute toxicity testing, single species are exposed to various concentrations of the test agent. The most common endpoint in acute tests is death. Abnormal behavior and other gross observations are commonly noted, and nonlethal endpoints occasionally apply. Data from different test concentrations are used to derive concentration–response curves. The LC50 represents the concentration of test substance killing 50 percent of the tested animals and EC50 the concentration of test substance affecting 50 percent of the test population during a specified period of time, such as growth; the IC50 is the concentration causing a 50 percent reduction in a nonquantal measurement (such as movement) for the test population. Other quantitative values are the lowest observed effect concentration (LOEC), that is, the lowest concentration where an effect is observed, and the no observed effect concentration (NOEC), the highest concentration resulting in no adverse effects.

Short-term laboratory studies conducted with single species are useful for rapid screening, provide information on thresholds for effects, selective and comparative toxicity, and can be used as range finders to guide subsequent, often more involved, studies. Long-term and reproductive studies evaluate the effects of substances on organisms over extended periods of time and/or sequential generations (chronic toxicity, life cycle, and reproduction).

Unique to ecotoxicology are the more elaborate microcosm, mesocosm, and field studies. Microcosms are representative aquatic or terrestrial ecosystems created under laboratory conditions that include a number of relevant species (such as protozoa, plankton, algae, plants, and invertebrates). Simulated field studies or mesocosms can be created in the laboratory or in the field (e.g., artificial streams and ponds) or consist of enclosures of existing habitats, containing representative soil, water, and biota. Lastly, full-scale field studies (aquatic organisms, terrestrial wildlife, and pollinators) evaluate the effects of a substance on wildlife under real-life scenarios of actual use conditions of a product (e.g., pesticide field usage rate), and thus are more complicated, subject to considerable variability, and require extensive knowledge of the local population and community dynamics.

As a final point, plant studies are a significant component of ecological toxicity testing, particularly for pesticide registration, and involve tiered testing of both target area and nontarget terrestrial and aquatic plants.

Biomarkers

The term “biomarker” is most often employed to refer to molecular, physiologic, and organismal responses to contaminant exposure that can be quantified in organisms inhabiting or captured from natural systems. Biomarkers do not directly provide information concerning impacts on the higher levels of organization that ecotoxicology ultimately endeavors to discern. Nevertheless, biomarkers often provide important ancillary tools for discerning contaminant exposures and potential impacts of ecological importance. Biomarkers can provide sensitive early warning signals of incipient ecological damage.

Chemical specificity among biomarkers is also highly variable and is imbued with trade-offs. Many biomarkers are invasive and require sacrifice of the organism in order to obtain needed tissues. This can be problematic, particularly in cases involving rare species or charismatic species such as marine mammals. In such cases, and in others where feasible, the use of noninvasive biomarkers is either preferred or required. Biomarkers can provide powerful tools as early warning signals of ecological damage, to assist in assessments of environmental contamination, and in determining the effectiveness of various environmental management decisions such as clean-ups. However, careful case-specific thought is required for the selection of biomarkers.

Population

Demographic surveys or experiments can be conducted for exposed populations. Some studies explore age-specific vital rates but others are designed to explore vital rates for different ages such as nestling, fledgling, juvenile, and adult. Most result in data sets that can be analyzed profitably using either a simple life table or more involved matrix analysis. The matrix method allows one to describe the population state and also to understand the sensitivity of the population to effects on vital rates for various ages or stages. The value of such studies lies in the ability to integrate effects on several factors into a projection of population consequences. Demographic studies are becoming more common in ecotoxicology, especially with species amenable to laboratory manipulation.

Conventional studies of increased tolerance after generations of exposure and molecular genetic surveys of exposed populations are the primary approaches by which genetic consequences are assessed. Increased tolerance is usually detected by subjecting individuals from the chronically exposed population and a naïve population to toxicant challenge and formally testing for tolerance differences. Alternatively, a change associated with a tolerance mechanism might be examined in chronically exposed and naïve populations. Close examinations of population genetics associated with contaminated habitats are also used to infer consequences of multigenerational exposure.

Community and Ecosystem

Most studies of community and ecosystem effects use modified methods developed in community and systems ecology. The approach affording the most control and ability to replicate treatments involves laboratory microcosms. A microcosm is a simplified system that is thought to possess the community or ecosystem qualities of interest. The experimental control and reproducibility associated with microcosms come at the cost of losing ecological realism. Gaining back some realism by giving up some degree of tractability, outdoor mesocosms are also applied to community and ecosystem ecotoxicology. Mesocosms are larger experimental systems, usually constructed outdoors that also attempt to simulate some aspect of an ecosystem such as community species composition. Field studies are the third means of exploring effects at the community or ecosystem level. The high realism of associated findings from field studies is balanced against the difficulty of achieving true replication and sufficient control of other factors influencing the system's response. Field studies can involve manipulations such as introducing toxicant into replicate water bodies; however, the majority of field studies involve biomonitoring of an existing, notionally impacted, community or ecosystem.

Landscape to Biosphere

Technologies for acquiring, processing, and analyzing large amounts of information have been essential. Archived and new imagery from satellites and high-altitude platforms are now integrated with off-the-shelf geographic information systems (GIS) software with affordable computers. Remote sensing data from satellites or aircraft provide information for wide spatial areas and the rapidly emerging, ground- or water-based observing system networks have begun to produce extremely rich data streams.

ERA applies ecotoxicologic knowledge to support environmental decision making. A widely dispersed ecotoxicant such as acid precipitation or widely used product such as an herbicide might require assessment of risk at a landscape or subcontinental scale. Ecotoxicants requiring a global ERA might include greenhouse gases contributing to global warming, hydrofluorocarbons depleting the ozone layer, and persistant organic pollutants that accumulate to harmful concentrations in polar regions far from their release point at industrialized latitudes.

Adaptations are based on the context of an ERA. Some ERAs address existing situations. Considerable field information might be available for such a retroactive ERA and epidemiological methods might be applied advantageously. In contrast, predictive ERAs assess possible risk associated with a future or proposed toxicant exposure.

Exposure characterization describes or predicts contact between the toxicant and the assessment endpoint. Depending on the ERA context, this could involve a simple calculation of average exposure, or a temporally and spatially explicit description of amounts present in relevant media. Toxicant sources, transport pathways, kinds of contact, and potential costressors are also defined.

Ecological effects characterization describes the qualities of any potential effects of concern, the connection between the potential effects and the assessment endpoint, and how changes in the level of exposure might influence the effects manifesting in the assessment endpoint. Normally, a statement about the strength of evidence associated with the descriptions and uncertainties is presented in the ecological effects characterization.

It is important to consider interconnections between human health and ecological integrity, or health. By determining how chemicals and other anthropogenic stressors degrade ecosystems and impact human health and well-being, and vice versa, a holistical understanding of the results of environmental contamination is obtained. For example, a conceptual model attempts to elucidate the interconnections linking natural and social systems in a circular manner with continuous feedbacks. The natural system produces both positive outputs (such as natural resources and raw materials) and negative outputs (such as hurricanes and disease vectors) to the social system. The culture and institution of the social system in turn transform the natural system outputs in various ways and subsequently deliver various positive outputs (consumer goods and conservation efforts) and negative outputs (pollution and deforestation) to the natural system. These outputs influence the quantity and quality of life (human and nonhuman) of the natural system, and the circular flow of resources continually creates conditions that influence the well-being of individuals, societies, and ecosystems.

This rather abstract model formalizes the interconnections between human and ecological health that most of us intuitively sense. Some of these connections are obvious. Chemical contamination of seafoods valued by humans is one example. Others are less clear but potentially very significant, such as human impacts on aquatic systems that foster the propagation of human disease vectors, or human impacts on global climate that may concomitantly impact humans and ecosystems in varied and complex ways. Collaboration among biomedical, environmental, and social scientists and policy-makers will catalyze the integrated protection of human and ecosystem health.