Lake Ontario Salmon Research Articles

The history of the Atlantic Salmon in Lake Ontario

The history of the Atlantic Salmon (Salmo salar), also referred to as Salmon below, in Lake Ontario is an accumulation of authentic published accounts, which were almost completed by J. R. Dymond before his death. H. H. MacKay completed the work on Dymond’s behalf (Dymond and MacKay, unpublished, 1966), but it remained largely unknown. The present authors (MEB, EH, PWB) have sought to present an updated subset of Dymond and MacKay’s work as the history of Lake Ontario Salmon is a crucial story in the history of the Great Lakes and its fisheries. The information provided should add materially to the knowledge of the causes that led to the decline and ultimate extirpation of a fascinating and valuable fish, notwithstanding all the efforts that were made to restore it by artificial means.

Lake Ontario salmon (Salmo salar) were not migratory: A long-standing historical debate solved through stable isotope analysis.

Lake Ontario once supported a large complex of Atlantic Salmon (Salmo salar) populations that became extinct prior to scientific study. Since the 1860s, research efforts to conserve and reintroduce a sustainable population of Atlantic Salmon have focused on determining whether Lake Ontario’s original salmon populations had migrated to the Atlantic Ocean as part of their lifecycle (anadromy), stayed in the lake year-round (potamodromy), or both. We used stable carbon, nitrogen, and sulfur isotope analyses of archaeological bones and historical museum-archived salmon scales to show that the original salmon populations from Lake Ontario completed their entire lifecycle without migrating to the Atlantic Ocean. With a time depth of more than 500 years, our findings provide a unique baseline with significant potential for informing modern restocking and conservation efforts.

Long‐term changes in legacy trace organic contaminants and mercury in Lake Ontario salmon in relation to source controls, trophodynamics, and climatic variability

We used long‐term (20+ yr) datasets to determine how the sum of 209 polychlorinated biphenyl congeners ([ΣPCB]), dodecachloropentacyclodecane ([mirex]), para‐para dichlorodiphenyltrichloroethane ([ p,p'‐DDT]), and total mercury ([Tot‐Hg]) concentrations have changed in Lake Ontario chinook salmon (Oncorhynchus tshawytscha, 1983‐2003) and coho salmon (Oncorhynchus kisutch, 1976‐2003). Exponential decay models best describe temporal reductions of persistent organic pollutant concentrations [POPs], including [ΣPCB], [mirex], and [p,p'‐DDT], in chinook (r2 = 0.68‐0.77, p < 0.001) and coho (r2 = 0.68‐0.87, p < 0.001) salmon over the record. In comparison, declines in [Tot‐Hg] were slight, with linear models best describing trends (r2 = 0.49‐0.50, p = <0.001‐0.001). Rapid declines of [POPs] from the mid‐1970s through the early 1980s were attributed mostly to Canada‐United States bans on usage and sedimentation; subsequent concentration oscillations were linked to salmonine stocking and nutrient abatement programs, climatic cycles, and alewife (Alosa pseudoharengus) population dynamics.

Effects of Great Lakes Fish Consumption on Brain PCB Pattern, Concentration, and Progressive-Ratio Performance

This study investigated the effects of consumption of Great Lakes fish on progressive ratio performance, and on the pattern and concentrations of brain polychlorinated biphenyls (PCBs), dichlorodiphenyldichloroethene (DDE), and mirex in the rat. Adult, male Sprague–Dawley rats were fed a 30% diet of either Lake Ontario salmon (LAKE), Pacific Ocean salmon, or lab chow control for 20 or 65 days. Following the treatment regimen, half the rats from each group were sacrificed immediately for gas chromatographic analysis of organochlorine contaminants, and the other half were tested on a multiple fixed-ratio–progressive–ratio reinforcement schedule and then sacrificed for analysis. Consumption of Lake Ontario fish resulted in significantly higher levels of brain PCBs, DDE, and mirex relative to controls, but still well within human exposure ranges (<1 μg/g fat). Consumption of Lake Ontario fish for 20 or 65 days produced an average brain PCB concentration of 457 and 934 ng/g fat, respectively. Consumption of laboratory rat chow or Pacific Ocean salmon for 20 or 65 days produced an average brain PCB concentration of 240, 464, and 441 ng/g fat, respectively. Moreover, both LAKE-fed groups showed a much more heavily chlorinated pattern of brain PCBs than all control groups, as evidenced by both significant increases in the most heavily chlorinated PCB congeners and significant increases in the average chlorine biphenyl. All LAKE brains contained significant concentrations of DDE and mirex, whereas no control brains contained any detectable quantities. Analysis of progressive-ratio performance indicated that LAKE rats responded normally during fixed-ratio schedules but quit significantly sooner than control rats on a progressive-ratio 5 (PR5) schedule, indicating reduced persistence on progressively leaner reinforcement schedules. Analysis of brain PCBs indicated that total PCBs were most strongly related to PR5 performance. These data indicate that consumption by rats of contaminated Lake Ontario fish produces (1) increased concentrations of PCBs, DDE, and mirex in the brain, (2) a more heavily chlorinated distribution of PCBs in the brain, and (3) reduced persistence of progressive-ratio reinforcement schedules. While these behavioral changes are related to brain PCB level, more work is necessary before the effects can be directly attributed to PCBs.

The Toxicological Effects Following the Ingestion of Chinook Salmon from the Great Lakes by Sprague–Dawley Rats during a Two-Generation Feeding-Reproduction Study

A two-generation reproduction–feeding study was undertaken with Sprague–Dawley rats to ascertain the effects of ingesting chinook salmon fillets caught in the Credit River, which empties into Lake Ontario (LO), or in the Owen Sound region of Lake Huron (LH). Rats (30/sex/group) were randomly assigned to groups whose dietary protein consisted of casein and/or lyophilized salmon [Group 1: 20% casein (controls); Group 2: 15% casein + 5% LO salmon (LO-5%); Group 3: 20% LO salmon (LO-20%); Group 4: 15% casein + 5% LH salmon (LH-5%); Group 5: 20% LH salmon (LH-20%)]. After 70 days on test, the males and females were mated on a 1:1 basis within diet groups. Approximately 70 days postweaning, one F1male and one F1female from 24 litters were mated within diet groups, avoiding sibling matings. At weaning, the F0and F1adults and the F1and F2neonates not randomly selected for further testing were necropsied. Evaluated parameters included growth, feed consumption, organ weights, reproduction indices, serum chemistry, hematology, and coagulation times. The only statistically significant effects which were present in both generations were increased relative liver and kidney weights of both sexes in the LO-20% and LH-20% groups; the LH-20% females had lower alanine transaminase activity than the controls; the controls had lower creatinine levels than the fish groups and the LO-20% females; the LH-20% and LO-20% males had a lower blood urea nitrogen than the controls; and the LH-20% females had a heavier terminal body weight than the controls and a lower number of red blood cells, hematocrit, hemoglobin values, and mean platelet volume. There was a tendency for the fish-fed groups to grow faster, eat more feed, and have larger litters with heavier pups. Overall, there was little to suggest that the myriad of contaminants in chinook salmon from the Great Lakes presented an appreciable toxicological risk to Sprague–Dawley growth and reproduction.

Neurochemical Effects of Consumption of Great Lakes Salmon by Rats

This study, part of a larger project to determine the health consequences of both perinatal and adult exposure to contaminated salmon from the Great Lakes, determined the neurochemical effects of exposure of rats to chow adulterated with lyophilized salmon fillets. Concentrations of biogenic amines, their metabolites, and choline acetyltransferase (ChAT) were determined in the frontal cortex (FC), nucleus accumbens, caudate nucleus (CN), hippocampus (HC), and substantia nigra (SN) of adult rats who had been exposed, both perinatally and as adults, to standard rat chow adulterated with either 5 or 20% (w/w) lyophilized fillets from either Lake Huron (LH) or Lake Ontario (LO) salmon. Dopamine (DA) concentrations in the FC were significantly decreased following exposure to both 20% fish diets. CN DA concentrations were significantly reduced in rats exposed to all diets, while SN DA was decreased only in the LO20-fed animals. SN norepinephrine concentrations were reduced in all groups except for the LO5-fed rats. 3,4-Dihydroxyphenylacetic acid (DOPAC) concentrations in the FC were significantly increased in the LH20 and LO5 groups, while CN DOPAC concentrations were reduced in LH20, LO5, and LO20 animals. 5-Hydroxyindoleacetic acid concentrations were reduced in the FC and CN of all animals exposed to diets adulterated with Great Lakes salmon. ChAT concentrations were unaffected in rats exposed to any of the adulterated diets. The significant reductions in DA, particularly in the FC and CN, suggest that either fish-borne contaminants or consumption of fish, per se, may affect behaviors that require inhibition of normal responding. We conclude that consumption of contaminated fish from the Great Lakes may result in sufficient reductions in biogenic amine function to result in significant deficits in important behavioral functions in the rat and, by inference, in the perinatally exposed human.

Neurobehavioral Effects of Chronic Ingestion of Great Lakes Chinook Salmon

Cross-generational chronic feeding of either a 5 or a 20% lyophilized Lake Huron (LH) or Lake Ontario (LO) chinook salmon diet to rats caused no observable effects on many behavioral dimensions including activity, exploration, sensorimotor function, and stereotypy. As assessed by the Morris water maze and the radial arm maze, there was no diet-induced impairment of spatial learning or long-term memory. There was no evidence that the fish diets caused an exaggerated response to food reward reduction as had been observed previously for rats fed Oswego area Lake Ontario salmon. Effects of the fish diets with the exception of one statistically significant but probably meaningless effect on the Morris water maze for females were found only for male rats and only for males who ate the 20% diet. F1male rats were reluctant to traverse a runway for a single pellet reward. Performance of the reference/working memory version of the radial arm maze was affected for the F1LO-20 rats and for the F2LH-20 rats. Until further research is conducted it would be unwise to ignore indications that male rats may show some effect of chronic consumption of the highest concentration of these diets, particularly on tasks that require intact frontocortical dopamine function.

Maternal consumption of Lake Ontario salmon in rats produces behavioral changes in the offspring.

The current study assessed the effects of maternal, paternal, or combined parental consumption of Lake Ontario salmon in rats on the behavior of their offspring. Adult female Sprague-Dawley rats were put on a 30 day diet of either ground rat chow containing 30% Lake Ontario salmon (LAKE) or 30% Pacific Ocean salmon (OCEAN). These females were then mated with adult male rats similarly exposed (LAKE or OCEAN). An additional control group of males and females who were fed ground rat chow (MASH) only were also mated. These pairing combinations resulted in five offspring groups: LAKE-LAKE, LAKE-OCEAN, OCEAN-LAKE, OCEAN-OCEAN, MASH-MASH. When the offspring reached 80 days of age, they were tested for reactivity to frustrative nonreward using runway successive negative contrast, which has been repeatedly shown to be increased in adult rats fed Ontario salmon. Consistent with previous work, results showed that the behavior of the OCEAN-OCEAN rats did not differ from the MASH-MASH group, indicating that a salmon diet per se does not cause behavioral change. However, the offspring of dams who consumed Lake Ontario salmon (LAKE-LAKE and OCEAN-LAKE) showed an increased depression effect relative to controls. There was little evidence of a paternal effect. A follow-up experiment employed cross-fostering to determine the relative contribution of pre- and/or postnatal exposure to Lake Ontario salmon consumption on offspring behavior. Rat pups were cross-fostered to or from dams who consumed Lake Ontario salmon during gestation and parturition. Results from two separate replications indicated that prenatal (LAKE to OCEAN) exposure alone or postnatal (OCEAN to LAKE) exposure alone produced a large increase in successive negative contrast relative to controls (OCEAN to OCEAN). These data are strong evidence of behavioral changes produced by maternal consumption of Lake Ontario salmon in the offspring rat. Further, they indicate that either prenatal or postnatal exposure alone is sufficient to produce behavioral changes in the offspring.

Behavioral effects of prenatal and adult exposure to toxic chemicals found in Lake Ontario fish: two methodological approaches.

Two research approaches are described that were used to determine behavioral changes following a diet of Lake Ontario fish. Approach 1 involved the correlational method, in which human subjects voluntarily ate contaminated Lake Ontario fish. Demographic information, data on the amount of Lake Ontario fish consumed, and control variables were obtained during an interview. Respondents' behavior, as well as the behavior of their children, then was measured. Because subjects were not assigned randomly to eat or not eat Lake Ontario fish, other variables that might have influenced both consumption of fish and behavior had to be considered. Therefore, confounding variables were measured and their influence controlled for using statistical techniques. Approach 2 involved the experimental method using laboratory rats, where subjects were assigned randomly to receive a diet of environmentally contaminated Lake Ontario salmon, relatively uncontaminated Pacific Ocean salmon, or no salmon. Since the rats fed Lake Ontario salmon behaved differently than the other two groups on nine tasks, it was concluded that the contaminants in Lake Ontario salmon caused behavioral changes. Random assignment of subjects to groups eliminated competing explanations. If similar behavioral (e.g., emotional or cognitive) results were obtained using the two approaches, then the results utilizing rats probably could be generalized to humans, and the correlational results found in humans probably were due to a cause and effect relationship.

Salmonine Consumption as a Source of Mirex in Human Breast Milk near Rochester, New York

Fifty-seven pre-natal classes were attended to recruit 30 donors of human milk samples in the vicinity of Rochester, NY. Donors were categorized into two groups of 15 Lake Ontario fish eaters (LOFE) and non-Lake Ontario fish eaters (NLOFE). A comparison of mirex concentrations in breast milk of Lake Ontario fish eaters with non-Lake Ontario fish eaters indicated no significant difference in median mirex concentrations (0.09 vs 0.06 ng/g milk). When the Lake Ontario fish eaters were divided into panfish and salmonine consumers, significant differences in mirex concentration in breast milk were observed. Women eating Lake Ontario salmonines have significantly higher concentrations of mirex (median = 0.21 ng/g milk) in their breast milk than Lake Ontario panfish consumers (median = 0.03 ng/g milk) and the NLOFE group (median = 0.06 ng/g milk). Photomirex concentrations were consistently higher in both donor groups than mirex and were significantly higher in the breast milk of salmonine consumers than in both the panfish consumers and the NLOFE group. The relatively high concentrations of photomirex in the breast milk of all donors (LOFE and NLOFE) suggest volatilization and an atmospheric transport of this contaminant. The child of a woman salmonine consumer, breast feeding daily at the median concentration level observed for a month, has a loading of mirex (816 ng mirex/kg) that is equivalent to consuming three Lake Ontario salmon meals at the FDA action level and that represents 2.9 times more mirex than an adult male should consume per month according to the NYS Department of Health advisory.

Laboratory Rat Experiments Show Consumption of Lake Ontario Salmon Causes Behavioral Changes: Support for Wildlife and Human Research Results

As part of the Cause-Effect Linkages II Conference, research was reviewed that showed behavioral changes in laboratory rats fed for 20 days a 30% diet of Lake Ontario salmon. Results from nine behavioral tests indicate that when testing involved a negative experience rather than only a positive experience the experimental group fed Lake Ontario salmon differed from the control groups fed Pacific Ocean salmon or no salmon. Behavioral differences between the two control groups have never been found. Offspring of rats fed the Lake Ontario salmon diet showed similar behavioral changes, even when tested in adulthood and never fed Lake Ontario salmon. These results, using the experimental method, can be viewed as providing the “ missing link” between the results observed in wildlife living in the Great Lakes region and children whose mothers had eaten Lake Michigan fish (see other papers in this journal issue). Since the adult rats fed Lake Ontario salmon and their offspring showed no signs of illness and had equal weight gain when compared with the two control groups, it appears as if changes in behavior may occur at doses lower than those needed to produce physical illness.

Reward reductions found more aversive by rats fed environmentally contaminated salmon

Pacific salmon stocked in Lake Ontario concentrate persistent toxic chemicals such as PCBs, DDT, DDE, mercury and dioxin. The present experiments support earlier findings that consumption of these salmon by laboratory rats increases their behavioral reactions to negative events. For 20 days rats were fed a diet consisting of 30% Lake Ontario salmon or a control diet of Pacific Ocean salmon or no salmon. They were then trained to run down an alley to receive a large 15-pellet or small 1-pellet food reward (6 trials/day). Following 72 trials the 15-pellet groups were shifted to 1 pellet for 90 trials, and showed a contrast (depression) effect: they ran more slowly than the groups always given 1 pellet. Rats previously fed Lake Ontario salmon showed a much larger contrast effect than the two control groups. These results were replicated in a second experiment, and a group fed a 10% diet of Lake Ontario salmon for 60 days showed the same size contrast effect as the group fed a 30% diet for 20 days.

Neurotoxic behavioral effects of Lake Ontario salmon diets in rats

Six experiments were conducted to examine possible neurotoxic effects of the exposure to contaminants in Lake Ontario salmon administered through the diets of rats. Rats were fed different concentrations of fish (8%, 15% or 30%) in one of three diet conditions: Lake Ontario salmon, Pacific Ocean salmon, or laboratory rat chow only. Following 20 days on the diets, rats were tested for five minutes per day in a modified open field for one or three days. Lake Ontario salmon diets consistently produced significantly lower activity, rearing, and nosepoke behaviors in comparison with ocean salmon or rat chow diet conditions. A dose-response effect for concentration of lake salmon was obtained, and the attenuation effect occurred in males, females, adult or young animals, and postweaning females, with fish sampled over a five-year period. While only two of several potential contaminants were tested, both fish and brain analyses of mirex and PCBs relate to the behavioral effects.

Immunomodulation in C57BI/6 mice following consumption of halogenated aromatic hydrocarbon‐contaminated coho salmon(Oncorhynchus kisutch)from lake Ontario

This report describes studies designed to assess the immunomodulatory effects associated with the consumption of coho salmon containing halogenated aromatic hydrocarbons (HAHs) and other compounds naturally bioaccumulated from Lake Ontario. Diets containing 33% coho salmon from Lake Ontario or the Pacific Ocean were fed to juvenile C57Bl/6 mice for 2-4 mo. Following 60 d, the mice that consumed Lake Ontario salmon had reduced IgM, IgG, and IgA plaque-forming cell responses to sheep erythrocytes. No changes were observed in total numbers of spleen lymphocytes, total T-lymphocytes or T-lymphocyte subsets as determined by flow cytometry. Cellular immunity, assessed by the cytotoxic T-lymphocyte response to allogeneic tumor target cells, was not altered following dietary exposure to Lake Ontario coho salmon for 4 mo. The observed humoral immunomodulation correlated with elevated PCB levels in the Lake Ontario salmon diets. The levels of pollutants such as mercury, tin compounds and other metals, PCDDs, and PCDFs were not examined.

Ingestion of environmentally contaminated Lake Ontario salmon by laboratory rats increases avoidance of unpredictable aversive nonreward and mild electric shock.

To determine what behavioral changes are caused by consumption of Lake Ontario salmon, a 30% diet of Lake Ontario or control Pacific Ocean salmon was fed to rats for 20 days. In Experiments 1 and 2 (preference-for-predictability E-maze test), rats fed Lake Ontario salmon developed a preference for predictable food rewards more quickly than did the control rats. In Experiments 3 (passive avoidance) and 4 (conditioned suppression), rats fed Lake Ontario salmon suppressed responding to food far more after the introduction of mild electric shocks than did control rats. All results supported the hypothesis that ingestion of Lake Ontario salmon, contaminated with polychlorinated biphenyls, mercury, lead, etc., increases the reactivity of rats to aversive events. The results were successfully simulated by DMOD, a mathematical model of learning, using the assumption that rats fed Lake Ontario salmon find unpredictable nonreward and mild shock more aversive.

Ingestion of environmentally contaminated Lake Ontario salmon by laboratory rats increases avoidance of unpredictable aversive nonreward and mild electric shock.

Ingestion of environmentally contaminated Lake Ontario salmon by laboratory rats increases avoidance of unpredictable aversive nonreward and mild electric shock.

Content and Chemical Form of Mercury and Selenium in Lake Ontario Salmon and Trout

The content and chemical form of mercury and selenium were determined in the edible tissue of salmon (coho, chinook) and trout (lake, brown) taken offshore from Lake Ontario near Rochester, New York. For all fish species, total mercury content ranged from 0.3 to 0.8 μg/g (fresh-weight), which is similar to concentrations commonly found in canned tuna. Most of the total mercury (63 to 79 percent) was present as methylmercury, the remainder being divalent inorganic mercury. For all species, 6 to 45 percent of the total selenium content was present as selenate (SeVI), the remainder being selenite (SeIV) and selenide (Se-11). On a molar basis, total selenium content usually exceeded that of total mercury. Samples of smoked and unsmoked brown trout fillets were also examined. Based on the results of this study there is no immediate human health hazard from mercury and selenium. However, there is a need to report specific chemical forms of these metals in Lake Ontario salmonid fishes so that elevated concentrations can be better evaluated.

Toxicological response and its reversibility in rats fed Lake Ontario or Pacific coho salmon for 13 weeks.

Lake Ontario coho salmon were known to contain a mixture of chemical contaminants. A previous study demonstrated that rats fed the Lake Ontario fish-supplemented diet for 28 days exhibited mild biochemical and histological changes. The purpose of the present study was to determine the effects due to a longer term of exposure and the reversibility of these effects. Growth rate and food consumption were not affected by feeding the animals with Lake Ontario or Pacific fish-supplemented diets for 13 weeks. No deaths were observed. Decreased spleen weights were observed in groups of males fed 1.45%, 5.8% Lake Ontario and 2.9% Pacific diet. After a 13 week recovery the spleen weights returned to normal. Decreased serum potassium was observed in male rats fed 2.9% Lake Ontario diet, and all levels of Pacific diet for 13 weeks, and was not evident following maintenance on normal diet. Serum glucose was not affected by the 13-week period of treatment, however; a reduction in this parameter occurred in male rats fed the two highest doses of Lake Ontario diet and all doses of Pacific diet following the 13-week recovery period. Minor hematological changes occurred only in the male rats fed either Lake Ontario or Pacific diet following a 13 week recovery period and included reduced marrow myeloid cells and myeloid/erythroid ratio. Hepatic microsomal ethoxyresorufin deethylase activity was significantly increased in rats ingesting Lake Ontario diet. Mild histological changes occurred in the liver and thyroid of the treated males, and in the liver and kidney of the treated females. These changes were attributed to the chemical residues and/or the fish diet. Data presented here indicated that the Lake Ontario fish-supplemented diet can cause mild biochemical, hematological and histological changes but most of these were reversible when exposure was terminated.

Contaminant Accumulation and Physiological Response in Rainbow Trout (Salmo gairdneri) Reared on Naturally Contaminated Diets

Juvenile rainbow trout were reared for 24 wk on practical-type diets formulated with fish meals derived from coho salmon (Oncorhynchus kisutch) taken from Lake Michigan, Lake Ontario, and the Pacific Ocean. Levels of contaminants (DDT, chlordane, dieldrin, mirex, and PCBs) increased 10-fold from control and Pacific Ocean salmon-based diets to Lake Ontario salmon-based diets. Rainbow trout accumulated contaminants in direct proportion to dietary levels. However, there were no significant differences in the final body weights, feed to gain ratios, or mortality rates of the trout reared on the different test diets. No signs of abnormal behavior or any indication of histopathological abnormalities were observed in any of the fish. There were no signs of thyroid hyperplasia or any significant decline in serum T3 or T4 levels with increasing dietary contaminant levels. Therefore, rainbow trout do not appear to have been affected by the uptake and accumulation of contaminants. However, the trout did not appear to regulate their body burden of contaminants; this ultimately could prove to be toxic and may adversely affect the ability of these fish to reproduce and survive. The final concentrations of mirex and PCBs in the Lake Ontario-fed fish exceeded the allowed limits to protect human health; therefore, fish meals produced from Lake Ontario salmon are unsuitable as a source of feed for aquaculture of rainbow trout intended for human consumption.

The Influence of Sex, Size, and Season on Mirex Levels within Selected Tissues of Lake Ontario Salmon

Statistical comparisons were made for mirex concentration in whole fillet, red muscle, belly flap, skin, dorsal loin, and caudal peduncle between sexes in coho (Oncorhynchus kisutch) and chinook ( O. tschawytscha) salmon collected from Lake Ontario during the spring and autumn. These data were also correlated with season, sex, and weight. Comparisons of mirex concentrations between skin, belly flap, and whole fillet and between dorsal loin and caudal peduncle were not statistically different. Significant differences in mirex concentrations were found between groups for (A) belly flap/skin/whole fillet tissue group, (B) red muscle tissue, and (C) the dorsal loin/caudal peduncle tissue group with concentrations decreasing from group A to group C. In general, mirex concentrations (mg/kg) increase with individual fish weight and appear to parallel reported lipid concentrations for similar tissues. Although no discernable pattern was evident, concentrations of mirex were observed to be significantly different between sexes or seasons in some tissues.