Neurotoxicology 30, — Heyer, N. The association between serotonin transporter gene promoter polymorphism 5-HTTLPR , self-reported symptoms, and dental mercury exposure. Health A 71, — Health A 72, — Julvez, J. Pourcain, B. Prenatal methylmercury exposure and genetic predisposition to cognitive deficit at age 8 years. Epidemiology 24, — Morales, E. Influence of glutathione S-transferase polymorphisms on cognitive functioning effects induced by p,p'-DDT among preschoolers.
Ng, S. Mercury, APOE, and children's neurodevelopment.
- Toxicological Effects of Methylmercury (2000).
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Neurotoxicology 37, 85— National Research Council. Toxicological Effects of Methylmercury. Science and Decisions: Advancing Risk Assessment. Schlawicke Engstrom, K. Genetic variation in glutathione-related genes and body burden of methylmercury. Spulber, S. Effects of maternal smoking and exposure to methylmercury on brain-derived neurotrophic factor concentrations in umbilical cord serum. Toxicol Sci. Stewart, W. ApoE genotype, past adult lead exposure, and neurobehavioral function.
Toxicological Effects of Methylmercury () : Division on Earth and Life Studies
Wang, Y. An investigation of modifying effects of metallothionein single-nucleotide polymorphisms on the association between mercury exposure and biomarker levels. Woods, J. Modification of neurobehavioral effects of mercury by a genetic polymorphism of coproporphyrinogen oxidase in children. Modification of neurobehavioral effects of mercury by genetic polymorphisms of metallothionein in children.
Yokel, R. Blood-brain barrier flux of aluminum, manganese, iron and other metals suspected to contribute to metal-induced neurodegeneration. Pubmed Abstract Pubmed Full Text. Ziv, E. Human population structure and genetic association studies. Pharmacogenomics 4, — Keywords: genetic variation, gene environment interactions, neurodevelopment, methylmercury, developmental toxicity, environmental epidemiology. Citation: Julvez J and Grandjean P Genetic susceptibility to methylmercury developmental neurotoxicity matters. The use, distribution or reproduction in other forums is permitted, provided the original author s or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.
No use, distribution or reproduction is permitted which does not comply with these terms. Toggle navigation. Login Register Login using. You can login by using one of your existing accounts. We will be provided with an authorization token please note: passwords are not shared with us and will sync your accounts for you. Water quality conditions influence mercury toxicity toward aquatic invertebrates, for example, rising water temperature enhances mercury toxicity. Conversely, the toxic effects of mercury may be lessened by increasing water hardness.
Some evidence suggests that mercury exerts behavioral effects on some invertebrates, making them more liable to predation. Median lethal concentration LC 50 values for some terrestrial invertebrates have been developed. For the earthworm Octochaetus pattoni , LC 50 values fall with continued exposure. A day exposure to mercury gives an LC 50 of 2. LC 50 values have been experimentally determined for inorganic mercury for many freshwater fish species.
Saltwater species have higher LC 50 values than freshwater species.
Although inorganic mercury is acutely toxic to freshwater fish it is not as toxic as the organomercurial compounds. As previously noted for invertebrate species, water quality parameters such as dissolved oxygen content, dissolved organic carbon content, temperature, salinity, and water hardness influence the toxicity of mercury in the aquatic environment. However, concentrations of mercury that are not acutely toxic to fish may still adversely impact reproduction, and may also result in physiological, biochemical, and behavioral disturbance. The larval stages of fish are particularly sensitive to mercury toxicity.
Mercury exposure to the larval stages of fish may result in reduced hatching success, deformities, and reduced survival. Most investigations of the toxicity of mercury to amphibians have employed the egg and larval tadpole stages of these animals, and have determined acute toxicity.
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There appears to be considerable species variation in sensitivity of egg and larval stage amphibians to the effects of inorganic mercury. An LC 50 value of 1. Some species appear to be less sensitive and 6 of the 14 have LC 50 values within the range The marbled salamander Ambystoma opacum is at the upper end of the range at No toxicological studies of mercury employing reptiles as test subjects are readily available.
However, there is evidence to suggest that mercury is bioaccumulated by top-tier reptilian predators such as turtles and alligators. Many investigations have addressed the toxicity of organomercurial compounds to birds, and organomercury has proved to be more toxic to birds than inorganic salts. Many laboratory toxicological studies have employed gallinaceous birds, the chicken Gallus gallus domesticus , and other domestic fowl closely related to it.
However, the domestic fowl may not adequately represent wild species, and caution should be taken when interpreting the studies that employ them. Some field reports suggest that wild waterfowl may be more sensitive to the toxic effects of mercury than the domestic waterfowl used in laboratory investigations. Organomercurial compounds cause reproductive impairment in birds, and numerous deleterious effects have variously been reported from the many investigations of this issue. These effects include a reduction in hatchability, reduction of egg production and egg volume, production of soft or thin-shelled eggs, and an increased mortality of young birds.
The use of organomercury seed dressings led to the acute poisoning and death of grain eating birds. The species of birds, raptors hawks, eagles, vultures, falcons, merlins etc. As top-tier predators, the raptors are vulnerable to the effects of bioaccumulated mercury in their prey, and breeding failure has been observed in raptor species in North America and Europe.
Although organochlorine pesticides also compromise the reproductive success of these birds, and pesticide residues may be present in raptors that are the subjects of field studies to determine the magnitude of the effects of dietary mercury, statistical analysis has shown an inverse relationship between mercury content of eggs and brood size.
That is, a higher egg-mercury content was associated with a reduced number of successfully reared birds. The field study that identified an inverse relationship between egg-mercury content and reproductive productivity was conducted in Scotland, on merlins feeding on estuarine birds.
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A similar impact was observed on peregrine falcons, feeding in a coastal area. Loon populations have been adversely impacted by mercury accumulated in the tissues of the fish and aquatic invertebrates that comprise their diet. However, a recent report suggests the effects of bioaccumulated mercury may not be limited to raptors or piscivorous birds, and that elevated mercury levels are observable in insectivorous songbirds. Piscivorous mammals such as the otter and mink, and top-tier predators such as the Florida panther are vulnerable to the acute toxic effects of dietary mercury, and are also at risk from the sub-lethal effects that can impair behavior and reproduction.
A toxicological dietary study of the mink Mustela vison showed organic mercury to be more toxic than mercuric chloride. Ataxia , tremors, and paralysis developed 4 days after the onset of methylmercury related effects. These animals died, despite efforts to arrest the progress of mercury toxicosis by removing methylmercury from their diet and by chelation therapy to remove the metal. Knightes and R. Ambrose Jr. EPA R, 80 pp, Peer-reviewed literature is the primary information source, supplemented by data files provided by various government agencies.
Yoshida, N. Shimizu, M. Elsevier, Oxford. The Encyclopedia of the Anthropocene [ Abstract ]. This synthesis of a comprehensive literature review conducted to identify relevant effect thresholds for wild birds and mammals is based on peer-reviewed publications bird studies and 76 mammal studies that represent much of the literature on the effects of Hg on free-living populations and wild species experimentally dosed in captivity. Molisani, R. Rocha, W. Macado, et al. Brazilian Journal of Biology vol 66 No.
Fish and Wildlife Service, Biological Report 85 1. Ackerman, C. Eagles-Smith, G. Heinz, et al. Irwin, M. Both studies used continuous measures of exposure based on reliable biomarkers, statistical control for a broad range of potential confounders, and measurement of standard, well-respected measures of neuropsychological function.
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Although the 9-year Seychelles follow-up assessed a larger number of developmental end points, adverse effects were seen in the Faroes and New Zealand studies in multiple domains of cognitive and neuromotor function. Nevertheless, not all lead studies have found this association, and substantial variability exists in the magnitudes of the reported effects [ 8 ].
If two studies from this literature were chosen randomly, it is likely that the results would not be entirely concordant. A similar consensus is emerging regarding the effects of low-level PCB exposure on developmental outcomes despite some studies which failed to detect negative effects [ 9 ]. The uncertainties inherent in conducting human studies, which, for ethical reasons, must rely on statistical rather than experimental control for confounders, stem, in part, from unmeasured confounders and effect modifiers that may be idiosyncratic to the sample being studied, but can interfere with our ability to detect true effects and to replicate those found in other studies.
Thus, the failure to detect adverse effects in the Seychelles study could well be due to the substantial sample-to-sample variation expected when trying to identify relatively subtle effects on development in an inherently "noisy" system of complex, multi-determined neurobehavioral end points.
In fact, the NRC analysis noted that comparing the studies with respect to their estimated benchmark doses and associated confidence limits noted much less discrepancy between them.
Methylmercury and brain development: A review of recent literature
Myers et al. It should be noted that the correlation that Myers refers to is between mercury in maternal hair and infant brains.
The same study also examined the correlation between mercury in infant blood and infant brains, and both sets of correlations were in the same range 0. Since cord blood is the gestational surrogate of infant blood, the study cited by Myers et al. Since these metrics each provide information about different periods of development, use of both metrics will increase the likelihood of uncovering a true dose-response relationship.
Both measures were, in fact, employed in the Faroes study and gave strikingly similar results although the cord blood measures generally yielded slightly stronger associations in terms of p-values. An essential point, which Myers et al. Both cord blood and maternal hair and, in fact, all exposure measures result in some degree of exposure misclassification. Thus, any exposure metric including cord blood which yields statistically valid relationships across a range of developmental endpoints provides useful information about the relationship between dose and response.
Another point which continues to be raised in the discussion of the applicability of the Faroes data to exposures in other communities is the notion of "bolus doses" [ 7 ]. It is important to point out that this notion is hypothetical and is supported by few data. Because the largest source of methylmercury exposure in the Faroese is consumption of whale meat that is relatively high in methylmercury concentration, it has been suggested that whale meat dinners might lead to isolated large spikes in methylmercury exposure during pregnancy.
Grandjean has pointed out however, that in addition to whale dinners, stored frozen and dried portions of whale meat are also consumed in small amounts as snacks over extended periods of time [ 11 ]. Dietary assessments in both the Faroes and Seychelles studies were limited and the extent of "bolus" doses cannot be readily determined in either study. However, Grandjean et al. This is comparable to the correlation of 0. Grandjean et al. These comparisons do not speak to the effect of variability in exposure per se on developmental outcomes, but speaks directly to the notion of bolus dose.
The larger the bolus dose, the greater the variability that is expected between the mercury concentration in the segment and the full-length hair sample, which reflects average exposure.