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Adverse Effect: Direct Mortality Jump down this page to: Steelhead | Chinook Salmon | Delta Smelt | Longfin Smelt | Sacramento Splittail | White Sturgeon | Green Sturgeon | Striped Bass All fishes have an incipient lethal threshold for DO, below which they experience rapid direct mortality. The potential for direct mortality can be defined by the severity and duration of exposure to low DO concentrations. Lethal levels are typically defined by DO concentrations that cause 50% mortality during either 24-hour or 96-hour exposure. DO concentrations below this level can lead to mortality in a short time, ranging from minutes to hours (Breitburg 2002). Laboratory studies of the effect of short-term exposure of fish to low DO concentrations (1- to 24-hour exposures) suggest that there is a narrow threshold concentration above which mortality does not occur and below which mortality rapidly increases. In general, the lethal concentration increases with increasing exposure duration and temperature. Fish exhibit various degrees of physiological adaptation (acclimation) to low DO concentrations that can increase their tolerance and resistance to otherwise lethal levels. Chronic exposure to low but nonlethal concentrations of DO can lead to acclimation through several physiological responses that increase the blood’s oxygen affinity and carrying capacity. Fish may rely on anaerobic metabolism to reduce oxygen requirements and increase their resistance to short-term exposures to severe hypoxia. However, reductions in activity levels may be a more effective survival strategy in response to longer duration exposures when avoidance is ineffective (Breitburg 2002). Acclimation has limited value for fish suddenly encountering low DO concentrations (Davis 1975). Jump to "General Effects" discussion under other adverse effects: Steelhead (Oncorhynchus mykiss) Hypothesis: The lethal threshold for juvenile rainbow trout ranges between 0.7 and 3.5 mg/L, depending on water temperature and length of exposure, as shown in the table. 1. What is the mechanism causing this adverse effect? Studies have been done on the effects of low DO concentrations on the mortality of both the anadromous steelhead and resident freshwater rainbow trout forms of the species. Exposure of steelhead to low DO concentrations can result in mortality if concentrations are low enough and exposure is long enough to impair essential physiological functions. 2. Are there critical thresholds associated with this adverse effect? Generally, mortality increases below 3.0 mg/L and becomes high at 2.0–2.5 mg/L, depending on water temperature (Hicks 2000). The results of several studies that examined the lethal effects of low DO concentrations (3.5 mg/L and below) on rainbow trout for various combinations of exposure duration and water temperature are summarized in this table.
3. How important is this mechanism? The potential for population-level effects associated with exposure to low DO concentrations increases with the severity and duration of exposure and the number of fish exposed to such conditions. Compared to resident fish, migratory fish, such as steelhead, are less likely to experience mortality because of their limited exposure to low DO concentrations in the DWSC. 4. How well is this mechanism understood? This mechanism is well understood based on the large number of studies that have investigated critical thresholds for mortality. These thresholds serve as general guidelines for evaluating the ability of adults and juveniles to tolerate low DO concentrations in their natural environment. However, all the studies discussed above were conducted in the laboratory under controlled conditions and thus may not be directly applicable to wild fish because of the complex responses of fish to low DO concentrations and other factors in their natural environment. Jump to "Steelhead" discussion under other adverse effects: Chinook Salmon (Oncorhynchus tshawytscha) Hypothesis: The lethal threshold (LC50) for salmonids ranges from 0.95 to 3.4 mg/L (Alabaster and Lloyd 1982) depending on water temperature and length of exposure. 1. What is the mechanism causing this adverse effect? Exposure of Chinook salmon to low DO concentrations can result in mortality if concentrations are low enough and exposure is long enough to impair essential physiological functions. 2. Are there critical thresholds associated with this adverse effect? Like all fishes, Chinook salmon have an incipient lethal threshold for DO, below which they experience rapid mortality.
3. How important is this mechanism? The potential for population-level effects associated with exposure to low DO concentrations increases with the severity and duration of exposure and the number of fish exposed to such conditions. Migrating adults are likely to be affected by low DO concentrations because low DO concentrations (5 mg/L and below) are prevalent in September and October when adults begin their upstream migration. Based on evidence presented by Hallock et al. (1970), exposure to low DO concentrations delayed the migration of adult Chinook salmon through the Delta but did not cause direct mortality. Compared to resident fish, migratory fish such as Chinook salmon are less likely to experience mortality from low DO concentrations because of their limited exposure to low DO concentrations in the DWSC. See also Activity While in the Deep Water Ship Channel and Exposure to High Water Temperature for more detailed information. 4. How well is this mechanism understood? This mechanism is well understood based on the large number of studies that have investigated critical thresholds for mortality. These thresholds serve as general guidelines for evaluating the ability of adults and juveniles to tolerate low DO concentrations in their natural environment. However, all of the studies discussed above were conducted in the laboratory under controlled conditions and thus may not be directly applicable to wild fish because of the complex and often site-specific responses of fish to low DO concentrations and other factors in their natural environment. Jump to "Chinook Salmon" discussion under other adverse effects: Delta Smelt (Hypomesus transpacificus) Hypothesis: Delta smelt exposed to DO concentrations below the regulatory minimum for prolonged periods (e.g., 24 hours) suffer increased direct mortality. 1. What is the mechanism causing this adverse effect? No studies on the lethal limits of DO concentrations for delta smelt have been published. The species is generally perceived to be fragile and intolerant of high temperatures that frequently occur in the DWSC (Swanson et al. 1996, 1998). Thus, some physiologists believe that this species cannot tolerate DO concentrations below 50–60% of saturation (e.g., less than 4.55–5.46 mg/L at 20°C) (Swanson pers. comm.). 2. Are there critical thresholds associated with this adverse effect? The incipient lethal threshold for delta smelt has not been determined. 3. How important is this mechanism? The importance of this mechanism is not known because the extent and importance of direct mortality of delta smelt caused be exposure to low DO concentrations is not known. 4. How well is this mechanism understood? This adverse effect is not well understood because no studies on the lethal limits of DO for delta smelt have been published. Jump to "Delta Smelt" discussion under other adverse effects: Longfin Smelt (Spirinchus thaleichthys) Hypothesis: Longfin smelt exposed to DO concentrations below the regulatory minimum for prolonged periods (e.g., 24 hours) suffer increased direct mortality. 1. What is the mechanism causing this adverse effect? No studies on the lethal limits of DO for longfin smelt have been published. Longfin smelt typically inhabit cold, well-oxygenated, pelagic habitats and would not be expected to have evolved the capacity to tolerate low DO concentrations. In general, smelt (family Osmeridae) are not very tolerant of low DO concentrations; thus, longfin smelt would not be expected to retain an ancestral tolerance for low DO concentrations. 2. Are there critical thresholds associated with this adverse effect? The incipient lethal threshold for longfin smelt has not been determined. 3. How important is this mechanism? The extent and importance of direct mortality of longfin smelt attributable to exposure to low DO concentrations are not known. 4. How well is this mechanism understood? No studies on the lethal limits of DO for longfin smelt have been published. Jump to "Longfin Smelt" discussion under other adverse effects: Sacramento Splittail (Pogonichthys macrolepidotus) Hypothesis: Direct mortality to Sacramento splittail from low DO concentrations in the DWSC is rare and occurs only when DO concentrations are well below the regulatory minimum for DO. 1. What is the mechanism causing this adverse effect? Healthy Sacramento splittail probably tolerate DO concentrations well below the regulatory minimum. See the next section for a discussion of laboratory results for Sacramento splittail. 2. Are there critical thresholds associated with this adverse effect? The incipient lethal threshold for DO in Sacramento splittail varies with age and acclimation temperature. Young and Cech (1996) found that Sacramento splittail lost equilibrium (a proxy for mortality in the wild) at DO concentrations of 1.1–1.3 mg/L; older fish lost equilibrium at 0.6 mg/L. 3. How important is this mechanism? This species tolerates low DO concentrations better than most other native species in the Delta. Direct mortality in response to low DO concentrations is probably not an important factor affecting Sacramento splittail because laboratory results suggest that they are able to tolerate DO concentrations below the regulatory minimum, and concentrations in the DWSC are only rarely below their limiting lethal level. 4. How well is this mechanism understood? Young and Cech (1996) documented the tolerances of Sacramento splittail for low-DO and high-temperature conditions. Their study occurred under controlled laboratory conditions that may be more benign (e.g., in the nutritional status or parasite exposure of the test subjects) than those experienced by Sacramento splittail under natural conditions. Thus, Sacramento splittail in the wild may not be as tolerant of low-DO and high-temperature conditions as Young and Cech documented in the laboratory. Nevertheless, the Young and Cech (1996) study suggests that this species has a great tolerance for the low-DO and high-temperature conditions that Sacramento splittail may experience in the DWSC. Jump to "Sacramento Splittail" discussion under other adverse effects: White Sturgeon (Acipenser transmontanus) Hypothesis: White sturgeon exposed to DO concentrations below the regulatory minimum for prolonged periods (e.g., 24 hours) suffer increased direct mortality. 1. What is the mechanism causing this adverse effect? Increased mortality among white sturgeon exposed to hypoxic conditions (58% saturation—4.7–5.7 mg/L) has been observed; white sturgeon exposed to DO concentrations greater than 83% saturation (6.8–8.2 mg/L) in the same study did not suffer increased mortality (Cech et al. 1984). Atlantic sturgeon (A. oxyrinchus) exposed to 3 mg/L DO concentrations suffered nearly complete mortality at 26oC and approximately 25% mortality over a 10-day period at 19°C (Secor and Gunderson 1998). 2. Are there critical thresholds associated with this adverse effect? The precise incipient lethal threshold for white sturgeon has not been determined. Cech et al. (1984) demonstrated significant mortality impacts at DO concentrations as high as 51% of saturation (4.7–5.7 mg/L, at the temperatures they tested) over 10-day exposure periods. Burggren and Randall (1978) found that white sturgeon survived 25–35-minute exposures to very hypoxic (5–10% normoxic) conditions without increasing ventilation frequency or oxygen consumption after exposure. Increased mortality is evident among other Acipenser species exposed to low DO concentrations. For example, Secor and Gunderson (1998) found that Atlantic sturgeon (A. oxyrinchus) display increased mortality under hypoxic conditions (3 mg/L). Shortnose sturgeon (A. brevirostrum) of all ages show complete mortality at DO concentrations less than 2 mg/L (Jenkins et al. 1993, Cech and Doroshov 2004). The incipient lethal threshold of these species may be at higher DO concentrations than those that have been tested. 3. How important is this mechanism? The extent and importance of direct mortality of white sturgeon attributable to exposure to low DO concentrations are not known. 4. How well is this mechanism understood? No published studies have documented the precise lethal limits of DO for white sturgeon. This would require study of several separate groups of white sturgeon held at incrementally different DO concentrations. However, Cech et al. (1984) demonstrated significant mortality impacts at DO concentrations as high as 51% of saturation (4.7–5.7 mg/L, at the temperatures they tested) over 10-day exposure periods, and Burggren and Randall (1978) found that white sturgeon survived 25–35-minute exposures to very hypoxic (5–10% normoxic) conditions. Thus, it is reasonable to believe that white sturgeon can avoid direct mortality effects of even extremely low DO concentrations over very short exposure times, but they do suffer direct mortality from DO concentrations similar to the DWSC’s regulatory minimum when exposed for extended periods. Jump to "White Sturgeon" discussion under other adverse effects: Green Sturgeon (Acipenser medirostris) Although little species-specific information is available for green sturgeon, it is likely that information for white sturgeon is generally applicable to green sturgeon. Jump to "Green Sturgeon" discussion under other adverse effects: Striped Bass (Morone saxatilis) Hypothesis: Striped bass exposed to DO concentrations below the regulatory minimum for prolonged periods (e.g., 24 hours) suffer increased direct mortality. 1. What is the mechanism causing this adverse effect? Exposure of striped bass to low DO concentrations can result in mortality if concentrations are low enough and exposure is long enough to impair essential physiological functions. 2. Are there critical thresholds associated with this adverse effect? Breitburg et al. (2001 in U.S. Environmental Protection Agency 2003) reported a 24-hour LC50 of between 1.1 and 1.6 mg/L for adult and juvenile striped bass and between 1.8 and 2.5 mg/L for larval striped bass. Across a range of temperatures (13–25°C), Krouse (1968 in U.S. Environmental Protection Agency 2003) found DO concentrations of:
Chittenden (1971b in Coutant 1985) observed that striped bass became restless as DO concentrations approached 3 mg/L, followed by inactivity, loss of equilibrium, and death as DO decreased further. 3. How important is this mechanism?
4. How well is this mechanism understood? This mechanism is well understood. Studies documenting thresholds and tolerances of DO are listed above under Are there critical thresholds associated with this adverse effect?. Jump to "Striped Bass" discussion under other adverse effects: |
Given the current understanding of DO dynamics in the DWSC (see figure at right), this mechanism is important in its consequences to individual striped bass but may have low significance to the population because the occurrence of reported lethal DO concentrations (for striped bass) in the DWSC are infrequent and of short duration. DO concentrations in the DWSC rarely fall below 3 mg/L, and even more rarely reach concentrations lethal to striped bass (see above). Mechanisms and deleterious effects associated with chronic exposure to sublethal DO concentrations may be more important.