366 Eutrophication and Oligotrophication nutrient over-enrichment has also been linked to the gradual disappearance of many waterfowl such as black and mute swans (Cygnus atratus, Cited olor strepera), Canada geese (Branta canadensis), coots (Fulica atra), teal (Anas crecca) and gadwells (Anas strepera) Sensitive life history stages of amphibians (e.g., frog eggs) have been killed in increasing hypoxic events within littoral zones of eutrophic lakes It should be noted that waterfowl and other wildlife can also act as eutrophying agents, especially in small lakes and coastal lagoons or poorly flushed embayments Where waterbirds are abundant, exemplified by the increasing problem created by exotic (nonindigenous) Canada geese (Branta canadensis) in small ponds and other waters within urbanizing and agricultural areas of the US, their excreta can be a major nutrient source For example, a small lake draining agricultural lands in the upper Midwest was used by Canada geese and other waterfowl (mostly mallards, Anas platyrhynchos, another exotic species) An analysis by Manny et al (1994) estimated that the lake received B70% of all external carbon sources, 27% of all N, and 70% of all P from the waterbirds Overall, however, based on review of available studies, Hahn et al (2008) reported that in most lakes, bird-mediated nutrient input is generally of minor importance compared with agricultural or sewage contributions Because of human disturbance, wildlife have also become important contributors of fecal bacteria and associated pollutants such as nutrients to some marine shoreline waters as a localized effect (Siewicki et al., 2007) Coastal urbanization has increased impervious surface area, increasing runoff that is channeled into retention ponds or directly into waterways These changes have increased the wildlife carrying capacity of the landscape, while also pushing wildlife (deer, raccoons, waterfowl, shorebirds) away from developed areas and into marsh edges near shellfish beds Aquatic Fauna and Inorganic Nitrogen Toxicity Humans have dramatically altered the Earth’s nitrogen cycle (Smil, 2001), and high levels of inorganic N enrichment to surface waters from fertilizer application and runoff, air pollution, human and animal wastes and other sources have been shown to impair the growth, reproduction, and survival of aquatic animals Aquatic fauna can directly take up unionized ammonia (NH3), NH4 ỵ , nitrite (NO2 ), nitrous acid (HNO2), and NO3 À from the surrounding water Of these, following the excellent review of Camargo and Alonso (2006), NH3 is the most toxic and NH4 ỵ and NO3 are the least toxic, but even NO3 À has a wide range of toxic effects at much lower concentrations that are commonly added to waterways by agriculture and other practices As a generalization, estuarine and marine fauna appear to be comparatively more tolerant of the toxic effects of inorganic nitrogenous compounds than freshwater fauna, likely because of ameliorating effects of chloride and other ions NH3 is highly toxic especially to fish and is thought to act through one or more of the following mechanisms: damage to gill epithelium, causing asphyxiation; stimulation of glycolysis, and suppression of the Krebs cycle, resulting in acidosis and reduced capability of the blood to carry oxygen; uncoupling of oxidative phosphorylation, inhibiting ATP production and depleting ATP in the basilar region of the brain; disrupting blood vessels and osmoregulation, impairing liver and kidney functions; and suppressing the immune system, increasing susceptibility to disease NH4 ỵ ions can exacerbate NH3 toxicity by reducing internal sodium ion concentrations Environmental conditions such as increased pH, warmer temperatures, and low DO can increase fish susceptibility to NH3 toxicity, and mixtures of NH3 with other chemical pollutants such as certain heavy metals can result in additive or synergistic toxic effects Freshwater invertebrates such as molluscs and planarians, and salmonid fishes appear to be most sensitive to NH3 toxicity, and have sustained adverse impacts from chronic exposures to as little as 50 mg NH3 N lÀ1 Water quality recommendations developed in the US and Canada to protect sensitive aquatic life have ranged from 50–350 mg NH3 N lÀ1 for acute (short-term) exposures and 10–20 mg NH3 N lÀ1 for chronic (long-term) exposures Such levels starkly contrast with concentrations commonly discharged in effluent from secondary sewage treatment across the US (103–104 mg NH3 N lÀ1), animal waste spills (104 mg NH3 N lÀ1), etc NO2À also inhibits nitrifying bacteria, which can result in its increased accumulation and intensified toxic effects The main mode of action, especially in fish and crayfish, is conversion of oxygen-carrying hemoglobin or hemocyanin pigments into methemoglobin or methemocyanin forms that can no longer carry oxygen, leading to hypoxia and death Other effects of NO2À toxicity in fish and crayfish have included depletion of chloride levels, leading to severe electrolyte imbalance; potassium ion imbalances that adversely affect membrane potentials, neurotransmission, skeletal muscle contractions, and heart function; formation of mutagenic and carcinogenic N-nitroso compounds; damage to mitochondria in liver cells, resulting in oxygen shortage; and immune system supression Elevated concentrations of certain ions such as chloride in brackish and marine waters are protective because they inhibit NO2À uptake The most sensitive aquatic invertebrates tested so far have included decapod and amphipod crustaceans, ephemeropteran insects, and salmonid and cyprinid fishes Based on acute toxicity data, it has been recommended that NO2 À N concentrations should be maintained below 80–350 mg lÀ1 (depending on the organisms of concern) to protect sensitive aquatic fauna during short-term exposures The main mode of action of NO3 À on aquatic animals is similar to that of NO2À In experiments with aquatic organisms such as fish, reptiles, and amphibians, NO3 À has also been shown to decrease immune response; to induce hematological and biochemical changes; and to adversely affect many metabolic processes by acting as an endocrine disruptor (Guillette and Edwards, 2005; Camargo and Alonso, 2006; McGurk et al., 2006) Because fish and crayfish have lower branchial permeability to NO3 À ions than to NO2 À ions, uptake is more limited The aquatic animals tested as most sensitive to NO3 À toxicity are freshwater caddisflies, amphipods, certain amphibians, and salmonid fishes For example, chronic NO3 À toxicity for freshwater invertebrates can occur at values as low as 230 mg NO3 À N lÀ1 (0.23 mg lÀ1) Lowest chronic toxicity levels reported for adult freshwater invertebrates were 2.8–4.4 mg lÀ1 for two amphipod species; early instar caddisfly larvae sustained adverse effects from chronic toxicity at