What
could aluminum pollution of a mudflat do to Stockton Harbor's biota?
Stockton Harbor southwestern shore has expanded into the harbor with significant amounts of spent acidified bauxite and phosphate waste from historic alum and superphosphate fertilizer production dumped onto wooden cribs that expanded the shoreline bluff at the southwest end of the Harbor over top of part of the beach. Does it matter?
Researchers have been looking for some time into the effect on the survival of fish and shellfish and even plankton role of acidified seawater in the uptake of toxic metals by fish and shellfish and their larvae.
Dissolved aluminium in acidic seawater has drawn concern. For either pollutant is relatively low impact until combined
Verdict?
"Larvae subjected to
* a single 24-hour, acid-only pulse of pH 4.5: No mortality
* a single 24 hour acid pulse and a monomeric aluminum pulse: 96% mortality
Significant effects have been noted low pH including pulses of acidity. Below are excerpts of some of those studies, with important points boldfaced for convenience.
Egg and larval pH and aluminum associations
Klauda et al. (1991) suggest that a range of pH 5.0 to 8.5 for both the alewife egg and prolarva life stage is optimal. Klauda et al. (1987) suggested that during an acidic pulse between pH 5.5 and 6.2, critical conditions associated with more than 50% direct mortality could occur.
Klauda et al. (1991) found that larvae subjected to a single 24-hour, acid-only pulse of pH 4.5 experienced no mortality, while
those subjected to a 24-hour single acid pulse and 446 µg/L inorganic monomeric aluminum pulse suffered a 96% mortality rate. A single 12-hour acid-only pulse of 4.0 resulted in 38% mortality (Klauda et al. 1991).
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The effects of aluminum and acid on the gill morphology in rainbow trout, Salmo gairdneii Robert E. Evans, Scott B. Brown and Toshiaki J. Hara
http://www.springerlink.com/content/n4863154757800t0/
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Homeostasis and Toxicology of Non-Essential Metals ALUMINUM.
Fish Physiology July 2, 2011, Volume 31, Part B, Pages 67–123
Excerpt: "Toxic mechanisms include impairment of gill ionoregulation (acceleration of passive ion losses and inhibition of their active uptake) by cationic Al species (especially Al3+), and/or respiratory dysfunction due to
precipitation of Al(OH)3 or polymerization of aluminum hydroxides on the gill surface during alkalinization of water passing over the gills."
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Low concentrations of inorganic monomeric aluminum impair physiological status and marine survival of Atlantic salmon
Two strains of Atlantic salmon (Salmo salar) presmolts were exposed for 3 months to moderately acidic water (pH 5.8; 6 2 mug aluminum (Ali) l(-1) inorganic monomeric aluminum-acid exposure group) or non-acid water (pH > 6.5 -6.9; < 5 mug Ali l(-1)-Good/control group) at NINA Research Station, Ims, Southern Norway. Exposure to low concentrations of Ali raised the gill-aluminum (gill-Al) concentration by 20-30 mug At g(-1)
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Effects of acidic water and aluminum exposure on gill Na(+), K(+)-ATPase alpha-subunit isoforms, enzyme activity, physiology and return rates in Atlantic salmon
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Salmon lice or suboptimal water quality — Reasons for reduced postsmolt survival? Norwegian Institute for Water Quality
1. Introduction
High levels of H+ and aluminium (Al) are lethal to Atlantic salmon (Salmo salar L.) smolts (Rosseland and Staurnes, 1994; Gensemer and Playle, 1999). Water toxicity is related to increased concentrations of H+ (reduced pH) and inorganic monomeric aluminum (Ali) in freshwater. At lethal concentrations, H+ acts primarily on the permeability of the cell membrane disrupting ionoregulation, whereas aluminum exerts its toxic properties by accumulation on and in the gill tissue, disrupting ionoregulation and impairing respiration. At lower concentrations, Al can still affect population traits by affecting growth, swimming performance, immune defence, behaviour and seawater tolerance (Rosseland and Staurnes, 1994; Staurnes et al., 1995, 1996; Kroglund and Staurnes, 1999; Ytrestøyl et al., 2001; Kroglund and Finstad, 2003).
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Environment Canada Aluminum Salts and fish and plankton
2.4.1.1 Aquatic Organisms
Most of the research on the impact of aluminum on aquatic life has been related to the impacts of acid rain. In this report, emphasis was placed on the potential toxic impacts of aluminum in waters of neutral or near-neutral
pH as the available information suggests that releases associated with the three aluminum salts being assessed occur primarily into waters of circumneutral pH (Roy 1999b; Germain et al., 2000). As described below, because of this consideration, the most relevant effects data identified were for fish. This assessment report does not provide a detailed examination of potential effects from exposure to polymeric aluminum, as polymeric aluminum is most likely to form, and to cause toxicity, during the neutralization of acidic aluminum-rich waters and this is unlikely to occur in the release scenarios considered in this assessment (Roy 1999b).
The gills are the primary target organ for aluminum in fish (Dussault et al. 2001). Aluminum binds to the gill surface, causing swelling and fusion of the lamellae and increased diffusion distance for gas exchange (Karlsson-Norrgren et al. 1986; Tietge et al. 1988). The resulting damage leads to loss of membrane permeability, reduced ion uptake, loss of plasma ions, and changes in blood parameters relating to respiration. Fish death may result from ionoregulatory or respiratory failure, or a combination of both, depending upon the pH of the water and concentration of waterborne aluminum (Neville 1985; Booth et al. 1988; Gensemer and Playle 1999). Ionoregulatory disturbances prevail at lower pH (e.g., below 4.5) and relate to decreased levels of plasma Na+ and Cl¯ ions (Neville 1985; Gensemer and Playle 1999). At pH levels above 5.5, binding of the positively charged aluminum species to negatively charged sites on the gill surface, with subsequent aluminum polymerization, leads to mucous secretion, clogging of the interlamellar spaces and hypoxia (Neville 1985; Poléo 1995; Poléo et al. 1995; Gensemer and Playle 1999).
Aluminum exposure may also disrupt ionic balance and osmoregulation in aquatic invertebrates (Otto and Svensson 1983). Reduced Na+ and/or Ca2+ uptake in response to aluminum exposure have been documented in crayfish (Appleberg 1985; Malley and Chang 1985), mayfly nymphs (Herrmann 1987) and the water boatman, Corixa sp. (Witters et al. 1984). Aluminum reduced Na+ influx and, to a lesser extent, increased outflux, in Daphnia magna, thereby impairing osmoregulation (Havas and Likens 1985).
Aluminum may disrupt the respiratory organs of some invertebrates, such as the anal papillae of the phantom midge, Chaoborus sp. (Havas 1986). Respiratory effects can occur when acidic waters are rapidly neutralized, such as when an acidic tributary enters a larger, neutral receiving stream, leading to the formation of mononuclear and polynuclear aluminum species from the dissolved ion (Gensemer and Playle 1999). These species may bind to or precipitate onto the bodies of invertebrates, creating a physical barrier to respiration. Aluminum has been reported to impair reproduction in Daphnia magna (Beisinger and Christensen 1972), although recent work with Daphnia pulexsuggests that adaptive strategies which heighten survivorship and fecundity may occur following long-term exposure to sublethal levels (Wold et al. 2005). Hall et al. (1985) reported that aluminum may reduce the surface tension of water, affecting egg deposition, emergence, feeding and mating behaviour of some stream invertebrates.
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Literature Review and Analysis of the Chronic and Acute Toxicity of Aluminum in Aquatic Environments FINAL REPORT - March 27,1998
Robert W. Gensemer, Ph.D. Department of Biology, Boston University, and Richard C. Playle, Ph.D. Department of Biology, Wilfrid Laurier University Canada
"Investigating the biological effects of aluminum has become a major focus of
aquatic research. Much of this interest stems from recent work on the biological effects of acidic precipitation, because Al becomes more soluble and, hence, potentially more toxic to aquatic biota at acidic pH. Starting around 1980, it became widely accepted that Al was a major factor affecting the success of aquatic organisms and communities in acidic habitats (Cronan and Schofield 1979, Drablos and Tollan 1980, Muniz and Levistad 1980, Schofield and Trojnar 1980).
Since then, research on the biological effects of acidification often has supported the contention that Al can be a major factor responsible for the demise of biotic communities (Dillon et al. 1984, Campbell and Stokes 1985, Schindler 1988, Charles 1991, Last and Watling 1991, Scheuhammer 1991)"
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Episodic acidification of small streams in the northeastern United States: Fish mortality in field bioassays.
Van Sickle J(a); Baker J P; Simonin H A; Baldigo B P; Kretser W A; Sharpe W E
Excerpt Ecological Application 6 (2):p408-421 1996
In situ bioassays were performed as part of the Episodic Response Project, to evaluate the effects of episodic stream acidification on mortality of brook trout (Salvelinus fontinalis) and forage fish species. We report the results of 122 bioassays in 13 streams of the three study regions: the Adirondack mountains of New York, the Catskill mountains of New York, and the Northern Appalachian Plateau of Pennsylvania.
Bioassays during acidic episodes had significantly higher mortality than did bioassays conducted under nonacidic conditions, but there was little difference in mortality rates in bioassays experiencing acidic episodes and those experiencing acidic conditions throughout the test period. Multiple logistic regression models were used to relate bioassay mortality rates to summary statistics of time-varying stream chemistry (inorganic monomeric aluminum, calcium, pH, and dissolved organic carbon) estimated for the 20-d bioassay periods.
The large suite of candidate regressors also included biological, regional, and seasonal factors, as well as severa
l statistics summarizing various features of aluminum exposure duration and magnitude. Regressor variable selection and model assessment were complicated by multicollinearity and overdispersion.
For the target fish species, brook trout, bioassay mortality was most closely related to time-weighted median inorganic aluminum. Median Ca and minimum pH offered additional explanatory power, as did stream-specific aluminum responses. Due to high multicollinearity, the relative importance of different aluminum exposure duration and magnitude variables was difficult to assess, but these variables taken together added no significant explanatory power to models already containing median aluminum.
Between 59 and 79% of the variation in brook trout mortality was explained by models employing between one and five regressors. Simpler models were developed for smaller sets of bioassays that tested slimy and mottled sculpin (Cottus cognatus and C. bairdi) as well as blacknose dace (Rhinichthys atratulus).
For these forage species a single inorganic aluminum exposure variable successfully accounted for 86-98% of the observed mortality. Even though field bioassays showed evidence of multiple toxicity factors, model results suggest that
adequate mortality predictions can be obtained from a single index of inorganic Al concentrations during exposure periods.
