Experimental evidence for recovery of mercury-contaminated fish populations.

Anthropogenic releases of mercury (Hg)1-3 are a human health issue4 because the potent toxicant methylmercury (MeHg), formed primarily by microbial methylation of inorganic Hg in aquatic ecosystems, bioaccumulates to high concentrations in fish consumed by humans5,6. Predicting the efficacy of Hg pollution controls on fish MeHg concentrations is complex because many factors influence the production and bioaccumulation of MeHg7-9. Here we conducted a 15-year whole-ecosystem, single-factor experiment to determine the magnitude and timing of reductions in fish MeHg concentrations following reductions in Hg additions to a boreal lake and its watershed. During the seven-year addition phase, we applied enriched Hg isotopes to increase local Hg wet deposition rates fivefold. The Hg isotopes became increasingly incorporated into the food web as MeHg, predominantly from additions to the lake because most of those in the watershed remained there. Thereafter, isotopic additions were stopped, resulting in an approximately 100% reduction in Hg loading to the lake. The concentration of labelled MeHg quickly decreased by up to 91% in lower trophic level organisms, initiating rapid decreases of 38-76% of MeHg concentration in large-bodied fish populations in eight years. Although Hg loading from watersheds may not decline in step with lowering deposition rates, this experiment clearly demonstrates that any reduction in Hg loadings to lakes, whether from direct deposition or runoff, will have immediate benefits to fish consumers.

Determination of Total Mercury and Methylmercury Concentrations in Commercial Canine Diets.

Methylmercury is an organic form of mercury that is well recognized for its bioaccumulation in aquatic species. Consumption of fish contaminated with methylmercury poses a toxicological health risk to both humans and animals. Salmon is an increasingly common ingredient in commercial pet foods because of manufacturers' interest in unconventional protein sources and inclusion of omega-3 polyunsaturated fatty acids. Previous studies have measured total mercury, but not methylmercury, in commercial pet foods. The purpose of this study was to evaluate total mercury and methylmercury concentrations in commercially available salmon-containing and nonsalmon-containing canine diets and to estimate risk of chronic exposure in dogs fed these diets long term. Total mercury was detected in 3 of 24 diets evaluated (12.5%), 2 of which did not contain any ingredients from fish. The single salmon-containing diet that contained total mercury was the lowest of the 3 but was also the only sample positive for methylmercury. None of the 3 mercury-containing diets contained fish oil. Concentrations of total mercury were similar to most data previously reported for pet foods. Using expected calorie intake for dogs of 2 body weights, the mercury concentrations determined in this study were applied to theoretical chronic exposure calculations to assess risk of toxicosis to dogs. Total mercury and methylmercury were uncommonly identified in the commercially available canine diets sampled in this study and were found in concentrations unlikely to pose risk to healthy adult dogs. Common sources of mercury in pet foods remain unknown and are not reliably of seafood origin.

Mercury immune toxicity in harbour seals: links to in vitro toxicity.

BACKGROUND: Mercury is known to bioaccumulate and to magnify in marine mammals, which is a cause of great concern in terms of their general health. In particular, the immune system is known to be susceptible to long-term mercury exposure. The aims of the present study were (1) to determine the mercury level in the blood of free-ranging harbour seals from the North Sea and (2) to examine the link between methylmercury in vitro exposure and immune functions using seal and human mitogen-stimulated peripheral blood mononuclear cells (T-lymphocytes). METHODS: Total mercury was analysed in the blood of 22 harbour seals. Peripheral blood mononuclear cells were isolated from seals (n = 11) and from humans (n = 9). Stimulated lymphocytes of both species were exposed to functional tests (proliferation, metabolic activity, radioactive precursor incorporation) under increasing doses of methylmercury (0.1 to 10 microM). The expression of cytokines (IL-2, IL-4 and TGF-beta) was investigated in seal lymphocytes by RT-PCR and by real time quantitative PCR (n = 5) at methylmercury concentrations of 0.2 and 1 microM. Finally, proteomics analysis was attempted on human lymphocytes (cytoplasmic fraction) in order to identify biochemical pathways of toxicity at concentration of 1 microM (n = 3). RESULTS: The results showed that the number of seal lymphocytes, viability, metabolic activity, DNA and RNA synthesis were reduced in vitro, suggesting deleterious effects of methylmercury concentrations naturally encountered in free-ranging seals. Similar results were found for human lymphocytes. Functional tests showed that a 1 microM concentration was the critical concentration above which lymphocyte activity, proliferation and survival were compromised. The expression of IL-2 and TGF-beta mRNA was weaker in exposed seal lymphocytes compared to control cells (0.2 and 1 microM). Proteomics showed some variation in the protein expression profile (e.g. vimentin). CONCLUSION: Our results suggest that seal and human PBMCs react in a comparable way to MeHg in vitro exposure with, however, larger inter-individual variations. MeHg could be an additional cofactor in the immunosuppressive pollutant cocktail generally described in the blood of seals and this therefore raises the possibility of additional additive effects in the marine mammal immune system.

Lead poisoning and other human-related factors cause significant mortality in white-tailed eagles.

The white-tailed eagle (Haliaeetus albicilla) suffered a severe population decline due to environmental pollutants in the Baltic Sea area ca. 50 years ago but has since been recovering. The main threats for the white-tailed eagle in Finland are now often related to human activities. We examined the human impact on the white-tailed eagle by determining mortality factors of 123 carcasses collected during 2000-2014. Routine necropsy with chemical analyses for lead and mercury were done on all carcasses. We found human-related factors accounting for 60% of the causes of death. The most important of these was lead poisoning (31% of all cases) followed by human-related accidents (e.g. electric power lines and traffic) (24%). The temporal and regional patterns of occurrence of lead poisonings suggested spent lead ammunition as the source. Lead shot was found in the gizzards of some lead-poisoned birds. Scavenging behaviour exposes the white-tailed eagle to lead from spent ammunition.

Toxic effects seen in a herd of beef cattle following exposure to ash residues contaminated by lead and mercury.

Lead poisoning was diagnosed in three cattle along with increased mercury levels in the liver and kidney tissues of two of these animals. The clinical signs were different in each case and included salivation, anorexia, delayed menace response, delayed withdrawal reflex, head pressing, localized muscle fasciculation, reduced tongue tone, ataxia, rumen atony and seizures. Blood lead concentration was increased in all three cases to 0.76, 0.37 and 0.454ppm. Post mortem changes characteristic of lead poisoning were only recognized in one case and included cerebro-cortical oedema, cortical neuronal necrosis and endothelial proliferation, especially at the tips of the cerebral gyri. The animals were poisoned by ingestion of lead-contaminated ash residues from a bonfire. The abnormal levels of mercury in the liver and kidney tissues of two animals may also be at least partly attributable to the intake of the metal in the ash residues. The levels of mercury in the three samples from the ash residue were relatively low (1.31, 0.7 and 2.1ppm).

Mercury exposure and source tracking in distinct marine-caged fish farm in southern China.

Coasts of South China have experienced an unprecedented growth in its marine-caged fish industry. We analyzed mercury concentrations and stable mercury isotope ratios in fourteen fish species from two cage-cultured farms in Southern China. Total mercury concentrations of all species were lower than the human health screening values, but the human exposures through consumption of several carnivorous fish exceeded the USEPA's reference dose. Isotopic compositions in the sediment (δ202Hg: -1.45‰ to -1.23‰; Δ199Hg: -0.04‰ to -0.01‰) suggested that mercury in these farms were from coal combustion and industrial inputs. Commercial food pellets and fresh fish viscera provided the major sources of methylmercury to the farmed fish and dominated their mercury isotopic signatures. Non-carnivorous fish presented lower δ202Hg and Δ199Hg values than the carnivorous fish. Using a mixing model, we demonstrated that the majority of mercury in non-carnivorous species came from pellets and in carnivorous fish came from combined diets of pellets and viscera. Meanwhile, methylmercury concentrations and % methylmercury in the fish were positively correlated with δ202Hg values but not with Δ199Hg values, mainly because fish eating similar feeds maintained similar Δ199Hg values. Environmental influences of cage farming such as fish feces and uneaten viscera that continuously provide organic mercury to the environments need to be considered.

Mercury induced haemocyte alterations in the terrestrial snail Cantareus apertus as novel biomarker.

The aim of the present work was to study the response of a suite of cellular and biochemical markers in the terrestrial snail Cantareus apertus exposed to mercury in view of future use as sensitive tool suitable for mercury polluted soil monitoring and assessment. Besides standardized biomarkers (metallothionein, acetylcholinesterase, and lysosomal membrane stability) novel cellular biomarkers on haemolymph cells were analyzed, including changes in the spread cells/round cells ratio and haemocyte morphometric alterations. The animals were exposed for 14 days to Lactuca sativa soaked for 1h in HgCl2 solutions (0.5 e 1 µM). The temporal dynamics of the responses were assessed by measurements at 3, 7 and 14 days. Following exposure to HgCl2 a significant alteration in the relative frequencies of round cells and spread cells was evident, with a time and dose-dependent increase of the frequencies of round cells with respect to spread cells. These changes were accompanied by cellular morphometric alterations. Concomitantly, a high correspondence between these cellular responses and metallothionein tissutal concentration, lysosomal membrane stability and inhibition of AChE was evident. The study highlights the usefulness of the terrestrial snail C. apertus as bioindicator organism for mercury pollution biomonitoring and, in particular, the use of haemocyte alterations as a suitable biomarker of pollutant effect to be included in a multibiomarker strategy.

Mercury toxicity: biochemical and physiological alterations in nine freshwater teleosts.

Nine fish species subjected to various concentrations (5, 10, 15 and 20 ppm) of mercuric nitrate for 4.5 h. The relationship between the concentrations of mercuric nitrate and the fall in renal glycogen was inverse. There was an elevation in liver and muscle glycogen at 5 ppm mercury. Brain glycogen increased to less than 10 ppm and then decreased. Glucose and lactate levels increased with increasing concentration of mercury, and muscle, liver, kidney and brain glycogen decreased. The effects were more marked in major carp than in the other species.

Intra- and interpopulation variability in maternal transfer of mercury to eggs of walleye (Stizostedion vitreum).

Mercury concentrations were determined for unfertilized eggs from seven walleye populations and for muscle and liver tissue from three of these seven populations in Canada and the United States. Female walleye transferred very little of their body methylmercury burden to their eggs. Methylmercury concentrations in eggs were 1.1-12% of those in muscle, and methylmercury burdens in eggs represented only 0.2-2.1% of the total body burden. Egg methylmercury as a percentage of total mercury increased with maternal length across populations. Percent methylmercury also increased with egg total mercury concentration but the slope of this relationship varied among populations. Egg methylmercury concentration increased with female age, and both muscle and liver methylmercury concentrations. Egg methylmercury concentration was also affected by female length at age but the effect of this relationship varied among populations. Mean predicted egg methylmercury concentrations (ng g(-1) dry) of 8-year-old, 550-mm females for the seven populations were as follows: Clay Lake, 796; Lake Superior, 24.3; Lake Winnipeg, 16.3; Lake Erie, 11.8; Primrose Lake, 8.76; Lake Manitoba, 7.32; Waconda Lake, 6.69.

Relationship between allozyme genotype and sensitivity to stressors in the western mosquitofish Gambusia affinis detected for elevated temperature but not mercury.

Previous studies with Gambusia holbrooki have found associations of allozyme genotype with tolerance to metals, pesticides, heat, and salinity. To examine the generality of these relationships, we looked for similar associations of mercury and heat tolerance with allozyme genotype at the GPI-2, MDH-1 and MDH-2 loci in its sister species Gambusia affinis. This was done to assess if the loci themselves or closely linked loci were associated with mercury tolerance, because weaker linkage associations would be unlikely to persist across species boundaries. Moreover, the use of two very different types of stress allowed us to determine if the higher tolerance of particular allozyme genotypes is specific to a certain stress or reflects a higher tolerance to stress in general. Associations between genotype and tolerance to mercury and heat were determined in laboratory exposures of about 875 fish in each of two exposures where tolerance was measured as time-to-death, followed by electrophoresis on cellulose acetate gels. For none of the three loci did we find an association of genotype with tolerance to mercury. This contrasts with reports of such an association for GPI-2 and MDH-1 in G. holbrooki, so our results do not support the hypothesis that observed associations between allozyme genotypes and mercury tolerance are due to the allozymes or closely linked loci. However, our comparison was weakened by a scarcity of the GPI-2 genotypes reported to be mercury sensitive in G. holbrooki. Furthermore, rapid mortality in our mercury exposure may have affected the ability to detect genotypic differences in survival. The MDH-1 heterozygote showed higher tolerance to heat stress compared to homozygotes, although this difference was only significant for the most common homozygous genotype. No such relationship between MDH-1 and heat stress has been reported in G. holbrooki. We found no evidence that associations between allozyme genotype and tolerance are similar for different types of stresses, which could be an advantage for using allozymes as an indicator of exposure history to a stressor. Our study also showed that G. affinis sex and weight influence tolerance to mercury and heat.

The effect of mercuric chloride intoxication on urinary psi-glutamyl transpeptidase excretion in the sheep.

The activity of the enzyme psi-glutamyl transpeptidase (psi-GT) was measured in the urine of sheep. In clinically normal animals the mean value was 6-3+/-0-6 mU/ml. In sheep with kidney damage induced by the administration of mercuric chloride there were marked increases in urinary concentrations of psi-GT, in some cases values in excess of 1000 mU/ml were recorded. This enzyme may be of value in the diagnosis of certain forms of renal disease.

Pathology of subacute methylmercurialism in cats.

Clinical signs of toxicosis, neurologic lesions, and increased tissue residues of methylmercury (MM)were produced in 9 cats by oral administration of 1.29 and 0.86 mg of Hg/kg of body weight/day as methylmercuric hydroxide. Clinical signs, which began after 15 days of exposure, included anorexia, ataxia, hypermetria, proprioceptive impairment, blindness, vertical nystagmus, and grand mal convulsions. Significant lesions occurred in cerebrum, brainstem, and cerebellum and correlated well with clinical signs. Microscopic central nervous system lesions consisted of neuronal degeneration, necrosis and loss of neurons, swollen axons, demyelination, loss of nerve cell processes, vacuolation of neuropil, gliosis, neuronophagia, perivascular cuffs, endothelial hypertrophy and hyperplasia, leptomeningitis, and infrequent vascular necrosis. Overall distribution of central nervous system lesions was unrelated to daily dose, but more advanced lesions were produced by the smaller daily dose. Mean tissue residues of MM were generally directly related to daily dose, and the average distribution among tissues was constant, with highest concentrations in liver, followed by kidney, spleen, muscle, and brain. In utero exposure of kittens to MM, revealed transplacental accumulation.

Mercury poisoning in a wild mink.

Mercury poisoning was diagnosed in a clinically-ill wild mink (Mustela vison) on the basis of clinical signs, histopathologic lesions and tissue mercury concentrations. The probable source of mercury was through ingestion of fish from the nearby South Saskatchewan River which is known to be contaminated with mercury. This is believed to be the first documented case of mercury intoxication of a wild animal in North America.

Necropsy findings and environmental contaminants in common loons from New York.

Diagnostic and analytical findings are presented for 105 common loons (Gavia immer) found dead or debilitated in New York (USA) from 1972-99. Aspergillosis (23% of cases) and ingestion of lead fishing weights (21%) were the most common pathologies encountered. Stranding on land, shooting, other trauma, gill nets, air sacculitis and peritonitis, and emaciation of uncertain etiology accounted for most of the remaining causes of disease or death. Analysis for total mercury in the liver of 83 loons yielded a geometric mean (gm) of 10.3 mg/kg (wet basis) and range of 0.07 to 371 mg/kg, with emaciated birds generally showing higher levels. Organochlorine contaminant levels in brain were generally low, principally consisting of PCB's (gm = 2.02 mg/kg) and DDE (0.47 mg/kg).

Mercury and persistent organic pollutant concentrations in African fish eagles, marabou storks, and Nile tilapia in Uganda.

The purpose of this research was to evaluate persistent organic pollutant (POP) and mercury concentrations in tissues of African fish eagles (Haliaeetus vocifer) and Nile tilapia (Oreochromis niloticus) from Lake Victoria near Entebbe and Lake Mburo, Uganda. Marabou stork (Leptoptilos crumeniferus) nestlings from urban Kampala (40 km from Entebbe) also were sampled for POPs and mercury. Total mercury was measured in the breast feathers of eight nestling and 10 adult African fish eagles from Lake Mburo, 10 nestling and five adult African fish eagles from Lake Victoria near Entebbe, and 20 nestling marabou storks from Kampala from June 2002 through January 2003. Mercury concentrations in all samples were below levels associated with adverse effects in similar species. Mercury concentrations were significantly higher in eagle adults and nestlings from Entebbe than in adults and nestlings from Lake Mburo (P< or =0.05). No significant differences (P> or =0.05) were found in mercury concentrations between sexes or between the entire fish eagle population sampled at Entebbe and marabou stork nestlings sampled at nearby Kampala. Plasma samples from the same birds were analyzed for 1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane, aldrin, hexachlorocyclohexane (alpha-HCH), dieldrin, endrin, heptachlor and their metabolites, as well as total polychlorinated biphenyls (PCBs). Nile tilapia whole-body cross sections collected from Lake Mburo (n=3) and Lake Victoria near Entebbe (n=8) also were analyzed for these POPs and mercury. No samples contained POPs or PCBs at the limits of detection except for 4,4'-1,1-dichloro-2,2-bis(4-chlorophenyl)ethylene in five adult eagle plasma samples (0.0026+/-0.0015 ppm wet weight) and five Nile tilapia samples (0.002+/-0.001 ppm wet weight) from Entebbe.

Methylmercury accumulation in tissues and its effects on growth and appetite in captive great egrets.

To test the hypothesis that fledging wading birds would be more at risk from mercury toxicosis than younger nestlings, captive great egret nestlings were maintained as controls or were dosed from 1- to 14-wk-old with 0.5 or 5 mg methylmercury chloride/kg wet weight in fish. Birds dosed with 5 mg/kg suffered from subacute toxicosis at wk 10-12. Growing feather concentrations were the most closely correlated with cumulative mercury consumed per weight. Blood concentrations of mercury increased more rapidly after 9 wk in all groups when feathers stopped growing. Total mercury accumulated in tissues in concentrations in the following order: growing scapular feathers > powderdown > mature scapular feathers > liver > kidney > blood > muscle > pancreas > brain > bile > fat > eye. The proportion of total mercury that was methylated depended upon tissue type and dose group. Selenium accumulated in liver in direct proportion to liver mercury concentrations. After wk 9, appetite and weight index (weight/bill length) declined significantly in both dosed groups. At current exposure levels in the Everglades (Florida, USA) mercury deposited in rapidly growing feathers may protect nestlings from adverse effects on growth until feathers cease growing.

Histologic, neurologic, and immunologic effects of methylmercury in captive great egrets.

Captive great egret (Ardea albus) nestlings were maintained as controls or were dosed with methylmercury chloride at low (0.5), and high doses (5 mg/kg, wet weight) in fish. Low dosed birds were given methylmercury at concentrations comparable to current exposure of wild birds in the Everglades (Florida, USA). When compared with controls, low dosed birds had lower packed cell volumes, dingy feathers, increased lymphocytic cuffing in a skin test, increased bone marrow cellularity, decreased bursal wall thickness, decreased thymic lobule size, fewer lymphoid aggregates in lung, increased perivascular edema in lung, and decreased phagocytized carbon in lung. High dosed birds became severely ataxic and had severe hematologic, neurologic, and histologic changes. The most severe lesions were in immune and nervous system tissues. By comparing responses in captive and wild birds, we found that sublethal effects of mercury were detected at lower levels in captive than in wild birds, probably due to the reduced sources of variation characteristic of the highly controlled laboratory study. Conversely, thresholds for more severe changes (death, disease) occurred at lower concentrations in wild birds than in captive birds, probably because wild birds were exposed to multiple stressors. Thus caution should be used in applying lowest observed effect levels between captive and wild studies.

Mercury toxicosis caused by ingestion of a blistering compound in a horse.

Mercury toxicosis by ingestion was diagnosed in a 3-year-old Quarter Horse mare with a history of anorexia and signs of abdominal discomfort. Ten and 9 days prior to admission, an inorganic mercuric blistering agent has been applied for topical treatment of dorsal metacarpal disease. At referral, signs of depression, dependent edema, pollakiuria, nonproductive cough, and oral ulceration were noticed. Laboratory data were consistent with renal dysfunction. Mercury content of blood and urine was high, confirming the diagnosis. The horse responded to intensive care, consisting primarily of IV fluid treatment, and mercury-chelating agents. However, acute laminitis developed, and the owners elected to euthanatize the horse 18 days after mercury exposure. Necropsy findings included renal tubulonephrosis and ulcerative colitis and enteritis. Mercury concentration was highest in kidney and liver tissues. The potential for mercury toxicosis in horses currently exists, and although the prognosis is grave, some horses may recover with appropriate treatment and long-term supportive medical care.

Adrenal function in chickens experiencing mercury toxicity.

Dietary mercury when administered to young chickens via the drinking water depressed growth, increased the rate of mortality and inhibited the normal maturation of the adrenal glands. Additionally, deficiencies of cholesterol and corticosterone were demonstrated in the adrenals. The exogenous administration of 0.5 or 1.5 mg. of corticosterone/100 gm. of body weight alleviated, in part, the toxic effects of mercury as evidenced by a rapid increase in body weight.