Dissolved Oxygen Depletion in the Stockton Deep Water Ship Channel: Biological and Ecological Effects Conceptual Model

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Secondary Driver: Exposure to Toxic Substances

Jump down this page to: Steelhead | Chinook Salmon | Delta Smelt | Longfin Smelt | Sacramento Splittail | White Sturgeon | Green Sturgeon | Striped Bass

General Effects

Fish species may be negatively affected by chemical pollution such as urban or agricultural runoff (Kuivila and Foe 1995; Werner et al. 2000; Kuivila and Moon 2004). The toxicity of particular chemicals to fish often changes depending on water quality parameters, including DO concentrations, pH, salinity, and hardness (Meehan 1991; Palawski et al. 1985; Richards and Rago 1999). Toxic substances and low DO concentrations change the physiology of fish and can affect the function and behavior of fish in the field (Cox and Coutant 1981). In general, organisms living near their environmental tolerance limits (such as low DO concentrations) are more susceptible to additional chemical stress, especially when exacerbated by increased temperatures or low food supplies (Heugens et al. 2002). An increase in susceptibility to toxic substances may be caused by an increase in respiration attributable to low DO concentrations. Fish respiring more bring more water, and therefore more toxicants, across the gills and into their systems (Lloyd 1961 in Chapman 1986).

One of the leading hypotheses for the recent (post-2000) rapid decline of fish native to the Delta is that they are negatively affected by agricultural pesticides and urban runoff. Large volumes of saline subsurface agricultural drainwater enters the San Joaquin every year that includes largely ions of sodium and sulfate in addition to chromium, mercury, selenium, and other trace elements in concentrations near or exceeding maximum limits of the EPA for protecting aquatic life (Saiki et al. 1992).

Jump to "General Effects" discussion under other Secondary Drivers:
Low DO Tolerance | Alternative Habitats | Occurrence of Sensitive Life Stages | Food Web | Parasites and Pathogens | Activity Levels | High Water Temperatures

Species-Specific Effects

Steelhead (Oncorhynchus mykiss)

Hypothesis:

Low DO increases the susceptibility of steelhead to the toxic effects of various chemical pollutants. Conversely, some pollutants can increase the susceptibility of steelhead to the adverse effects of low DO.

1. How does this driver operate?

Low DO concentrations can increase the susceptibility of fish to the toxic effects of chemical pollutants by increasing ventilation rate and thus the rate at which these chemicals are absorbed by the blood (Alabaster and Lloyd 1982). Other pollutants (e.g., heavy metals) can exacerbate the effects of low DO by damaging the gills and their ability to extract oxygen from the water (Holeton 1980).

2. Are there critical thresholds associated with this driver?

Critical thresholds associated with toxins such as zinc, lead, copper, and phenols have been established for rainbow trout.

  • Rainbow trout weighing from 1 to 11 grams, subjected to water temperature of 17.5°C and DO of 5.78 mg/L, had an increased susceptibility to adverse effects from toxins such as zinc, lead, copper, and phenols. When the DO concentration was reduced to 3.8 mg/L, the toxic effect was even greater (Lloyd 1961 in Chapman 1986).
  • Rainbow trout ranging from 13 to 15 cm in length, exposed to water temperatures of 17 to 17.5°C and DO of 9.74 mg/L, had a more rapid death in cyanide when oxygen concentrations were reduced (Downing and Merkens 1955 in Chapman 1986).
  • Ammonia toxicity is exacerbated at low DO concentrations, resulting in mortality at DO concentrations from 8.6 to 2.6 mg/L (Thurston et al. 1981 in Chapman 1986).
  • Exposure of juvenile Chinook salmon to high concentrations of ions and trace elements in agricultural drainwater from the San Joaquin River resulted in 23% mortality and a reduction in growth (compared to other water sources) after 28 days of exposure. Exposure to other sources, including a water sample taken from the San Joaquin River, resulted in 0% mortality after 28 days. The study was inconclusive because of the potential influence of other factors on mortality and growth. (Saiki et al. 1992).

3. How important is this driver?

Contaminants, such as ammonia, enter the lower San Joaquin River from non-point sources and wastewater treatment plants upstream of the DWSC (Lehman et al. 2004). The importance of this driver is unclear because of limited understanding of the effects of toxicants on salmonids and the effects of multiple stressors on fish in their natural environment. Exposure of adults and juveniles to low DO and elevated levels of contaminants in the DWSC would be limited because these life stages would be expected to move quickly through the DWSC to upstream spawning areas or more favorable downstream rearing areas.

4. How well is this driver understood?

A large body of literature exists on the acute and chronic effects of various chemical pollutants on fish (including salmonids) and other aquatic organisms. This literature forms the basis for state and federal regulatory criteria governing the discharge requirements of wastewater treatment plants and other point and non-point sources of pollution. However, few studies have been conducted to evaluate the interactive effects of low DO and various chemical pollutants (alone or in combination) on aquatic organisms.

Jump to "Steelhead" discussion under other Secondary Drivers:
Low DO Tolerance | Alternative Habitats | Occurrence of Sensitive Life Stages | Food Web | Parasites and Pathogens | Activity Levels | High Water Temperatures

Chinook Salmon (Oncorhynchus tshawytscha)

Hypothesis:

Chinook salmon exposed to low DO concentrations (sublethal levels) and toxic substances are more susceptible to mortality than fish that are exposed to low DO concentrations alone.

1. How does this driver operate?

Chinook salmon subjected to high water temperatures and decreased DO concentrations are more likely to experience the adverse effects of chemical pollution from contaminated runoff or sediments. An increase in susceptibility to toxins may be caused by an increase in respiration attributable to low DO concentrations. Increased gill ventilation rates resulting from hypoxic conditions bring more water and, therefore, toxicants into contact with the gills, increasing the uptake of toxicants into the bloodstream (Lloyd 1961 in Chapman 1986).

2. Are there critical thresholds associated with this driver?

  • Juvenile Chinook salmon exposed to elevated concentrations of major ions (ammonia, calcium, chloride, magnesium, sodium, sulfate) and trace elements (boron, chromium, copper, molybdenum, selenium) in agricultural drainwater experienced 75% higher mortality rates and weighed 28% less than control fish after 28-day exposure periods (Saiki et al. 1992). All other water samples, including a water sample taken from the San Joaquin River, resulted in no mortality after 28 days. The study was inconclusive, in that it could not identify whether the major ions or trace elements were the reason for the increased mortality and decreased growth (Saiki et al. 1992).
  • Ammonia toxicity increases with decreasing DO concentrations from 8.6 to 2.6 mg/L (Thurston et al. 1981 in Chapman 1986).
  • Larmoyeux and Piper (1973 in Hicks 2000) tested hatchery water and found that ammonia levels greater than 0.5 mg/L and DO concentrations of less than 5.0 mg/L caused a reduction in fish length and damage to gill tissue.

3. How important is this driver?

Contaminants, such as ammonia, enter the lower San Joaquin River from non-point sources and wastewater treatment plants upstream of the DWSC (Lehman et al. 2004). The importance of this driver is unclear because of limited understanding of the effects of toxicants on Chinook salmon and the effect of multiple stressors on fish in their natural environment.

4. How well is this driver understood?

While some laboratory studies define contaminant levels that are toxic to fish, little is known about the acute and chronic effects of toxic substances on Chinook salmon.

Jump to "Chinook Salmon" discussion under other Secondary Drivers:
Low DO Tolerance | Alternative Habitats | Occurrence of Sensitive Life Stages | Food Web | Parasites and Pathogens | Activity Levels | High Water Temperatures

Delta Smelt (Hypomesus transpacificus)

Hypothesis:

Exposure of delta smelt to toxic substances raises the incipient limiting threshold for DO compared to the threshold for unexposed delta smelt.

1. How does this driver operate?

Delta smelt may be negatively affected by toxic substances, such as urban or agricultural runoff (Kuivila and Foe 1995; Werner et al. 2000; Kuivila and Moon 2004). One of the leading hypotheses for the recent (since 2000) rapid decline of delta smelt is that they are negatively affected by agricultural pesticides or urban runoff (Bennett 2005) (General Effects).

2. Are there critical thresholds associated with this driver?

Presumably, there are critical thresholds for exposure to toxic substances, beyond which the ability of delta smelt to extract DO from water is compromised. No studies of the effects of different toxic substances on delta smelt DO tolerances have been published.

3. How important is this driver?

The existence and extent of a synergistic interaction between toxic substance exposure and low-DO exposure have not been documented.

4. How well is this driver understood?

No specific information is available to determine:

  • the immediate (acute) or developmental (chronic) effects toxic substances have on delta smelt,
  • the effect low DO conditions have on the toxicity of these substances, or
  • the effect these substances have on delta smelt DO thresholds.

Jump to "Delta Smelt" discussion under other Secondary Drivers:
Low DO Tolerance | Alternative Habitats | Occurrence of Sensitive Life Stages | Food Web | Parasites and Pathogens | Activity Levels | High Water Temperatures

Longfin Smelt (Spirinchus thaleichthys)

Hypothesis:

Exposure of longfin smelt to toxic substances raises the incipient limiting threshold for DO compared to the threshold for unexposed longfin smelt.

1. How does this driver operate?

Longfin smelt may be negatively affected by chemical pollution such as urban or agricultural runoff (Kuivila and Foe 1995; Werner et al. 2000; Kuivila and Moon 2004). One of the leading hypotheses for the recent (post-2000) rapid decline of fish native to the Delta is that they are negatively affected by agricultural pesticides or urban runoff (Bennett 2005) (General Effects). No specific information is available regarding the effects of toxic substances on longfin smelt, or on the interaction of toxic substances with sensitivity to low DO concentrations.

2. Are there critical thresholds associated with this driver?

Presumably, there are critical thresholds for exposure to toxic substances beyond which the ability of longfin smelt to extract oxygen from water is compromised. At this time, no studies of the effects of different toxic substances on longfin smelt DO tolerances have been published.

3. How important is this driver?

The existence and extent of a synergistic interaction between toxic substance exposure and exposure to low DO have not been documented for longfin smelt at this time.

4. How well is this driver understood?

No information is currently available to determine either the immediate (acute) or developmental (chronic) effects of toxic substances on longfin smelt, the effect low DO can have on the toxicity of these substances, or the effect these substances have on longfin smelt DO thresholds.

Jump to "Longfin Smelt" discussion under other Secondary Drivers:
Low DO Tolerance | Alternative Habitats | Occurrence of Sensitive Life Stages | Food Web | Parasites and Pathogens | Activity Levels | High Water Temperatures

Sacramento Splittail (Pogonichthys macrolepidotus)

Hypothesis:

Exposure of Sacramento splittail to toxic substances raises the incipient limiting threshold for DO compared to the threshold for unexposed splittail.

1. How does this driver operate?

Sacramento splittail may be negatively affected by chemical pollution, such as runoff or sediments contaminated with pesticides (Kuivila and Foe 1995; Kuivila and Moon 2004). Teh et al. (2004) found that exposure to the pesticide diazinon caused adverse impacts in young Sacramento splittail. Sommer et al. (unpublished) speculated that the benthic foraging habits of Sacramento splittail exposed them to potentially deleterious levels of selenium. This exposure could, in turn, affect the ability of Sacramento splittail to access DO.

2. Are there critical thresholds associated with this driver?

Presumably, there are critical thresholds for exposure to toxic substances, beyond which the ability of Sacramento splittail to extract oxygen from water is compromised. No studies of the effects of different toxic substances on Sacramento splittail DO tolerances have been published.

3. How important is this driver?

The existence and extent of a synergistic interaction between toxic substance exposure and exposure to low DO concentrations have not been documented for Sacramento splittail.

4. How well is this driver understood?

Little is known about the immediate (acute) or developmental (chronic) effects of toxic substances on Sacramento splittail. No studies have examined the effects of exposure to toxic substances on Sacramento splittail or the effects low DO concentrations can have on the toxicity of these substances.

Jump to "Sacramento Splittail" discussion under other Secondary Drivers:
Low DO Tolerance | Alternative Habitats | Occurrence of Sensitive Life Stages | Food Web | Parasites and Pathogens | Activity Levels | High Water Temperatures

White Sturgeon (Acipenser transmontanus)

Hypothesis:

As exposure of white sturgeon to toxic substances increases, the DO concentration required to avoid adverse effects also increases.

1. How does this driver operate?

White sturgeon may be negatively affected by chemical pollution such as urban or agricultural runoff (Kuivila and Foe 1995; Werner et al. 2000; Kuivila and Moon 2004). One of the leading hypotheses for the recent (post-2000) rapid decline of fish native to the Delta is that they are negatively affected by agricultural pesticides or urban runoff (Bennett 2005). Because, like all Acipenser sp., white sturgeon are bottom-feeders, they may be particularly sensitive to toxins that accumulate in bottom sediments or benthic organisms. Sommer et al. (unpublished) speculated that the benthic foraging habits of splittail exposed them to potentially deleterious levels of selenium and that this exposure could, in turn, affect the ability of splittail to access DO. White sturgeon are also benthic foragers and, like splittail, they eat clams, crabs, and other benthic organisms (Moyle 2002); thus, Sommer et al.ís speculation may apply to white sturgeon as well.

2. Are there critical thresholds associated with this driver?

Presumably, there are critical thresholds for exposure to toxic substances, beyond which the ability of white sturgeon to extract oxygen from water is compromised. No studies of the effects of different toxic substances on white sturgeon DO tolerances have been published.

3. How important is this driver?

The existence and extent of a synergistic interaction between toxic substance exposure and exposure to low DO have not been documented for white sturgeon.

4. How well is this driver understood?

No information is currently available to determine either the immediate (acute) or developmental (chronic) effects of toxic substances on white sturgeon, the effect low DO can have on the toxicity of these substances, or the effect these substances have on white sturgeon DO thresholds.

Jump to "White Sturgeon" discussion under other Secondary Drivers:
Low DO Tolerance | Alternative Habitats | Occurrence of Sensitive Life Stages | Food Web | Parasites and Pathogens | Activity Levels | High Water Temperatures

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 Secondary Drivers:
Low DO Tolerance | Alternative Habitats | Occurrence of Sensitive Life Stages | Food Web | Parasites and Pathogens | Activity Levels | High Water Temperatures

Striped Bass (Morone saxatilis)

Hypothesis:

Exposure of striped bass to toxic substances increases the incipient limiting threshold concentration for DO compared to the threshold for unexposed striped bass.

1. How does this driver operate?

The toxicity of particular chemicals to fish varies depending on water quality conditions, including DO, pH, salinity, and hardness (Meehan 1991; Palawski et al. 1985; Richards and Rago 1999). Striped bass are known to be vulnerable to metal toxins, particularly aluminum, with larval stages being more sensitive (Richards and Rago 1999). Toxic substances and reduced oxygen concentrations change the physiology and behavior of striped bass in the field (Cox and Coutant 1981). When striped bass are already stressed from low DO concentrations, other stressors can be expected to intensify the effects (Coutant 1985). In general, organisms living near their environmental tolerance limits (such as low DO concentrations) are more susceptible to additional chemical stress, especially when exacerbated by increased temperatures or low food supplies (Heugens et al. 2002). Additionally, striped bass may be predisposed to the adverse effects of low DO concentrations after having previously experienced suboptimal conditions, such as exposure to toxicants (Coutant 1985).

2. Are there critical thresholds associated with this driver?

Specific thresholds of lethal exposure for striped bass in the wild are difficult to determine. The EPA has set water quality maximum limits to protect aquatic life, but it becomes difficult to identify specific lethal limits when exposure is combined with other environmental stresses, such as low DO concentrations or elevated temperatures. Lethal exposure concentrations depend not only on exposure dose but also on duration. In addition, it is difficult to separate out the individual effects of multiple stressors acting simultaneously to produce a negative impact. Saiki et al. (1992) concluded that agricultural subsurface drainwater entering the San Joaquin River was 100% lethal to juvenile striped bass within 23 days without dilution. High concentrations of major ions present in atypical ratios were largely responsible for mortality, but the effects of selenium and boron could not be clearly described. In combination with reduced DO concentrations, it is reasonable to assume that the lethal exposure duration would have been reduced.

3. How important is this driver?

This driver may be significant because large volumes of saline subsurface agricultural drainwater enter the San Joaquin River each year. This drainwater includes ions of sodium and sulfate in addition to chromium, mercury, selenium, and other trace elements in concentrations near or exceeding maximum limits established by the EPA for protecting aquatic life (Saiki et al. 1992). Stevens et al. (1985) hypothesized that one of the reasons behind striped bass declines in the Delta was stress induced by toxic substances such as petrochemicals and pesticides. They suggested that larval striped bass may suffer from chronic exposure to sublethal levels of these substances, but that it was not possible to determine the contribution of chemicals to striped bass population declines. Bailey et al. (1994) found similar results, indicating that Colusa Basin Drain discharges were acutely toxic to striped bass embryos and larvae and that a model based on pesticide use better predicted abundance during declines than one based on historical river flows and Delta diversions. The impacts of other chemicals such as mercury, cadmium, copper, zinc, nickel, and other agricultural chemicals are unknown.

4. How well is this driver understood?

The specific impacts of toxic substances on striped bass populations in combination with low DO concentrations in the DWSC are not clear.

Jump to "Striped Bass" discussion under other Secondary Drivers:
Low DO Tolerance | Alternative Habitats | Occurrence of Sensitive Life Stages | Food Web | Parasites and Pathogens | Activity Levels | High Water Temperatures