Does Methylmercury Have a Role in Causing Developmental Disabilities in Children?

Myers, Gary J.; Davidson, Philip W.

doi:10.2307/3454530

Cited by 30 publications

(19 citation statements)

References 40 publications

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“…Methylmercury poisoning has been clearly associated with severe neurotoxic effects in both animal studies and human poisoning episodes, whereas the evidence for developmental impairments associated with lower level exposures is less clear [Myers and Davidson, 2000].…”

Section: Effects Of Poisoningmentioning

confidence: 99%

Environmental factors associated with a spectrum of neurodevelopmental deficits

Mendola

Selevan

Gutter

et al. 2002

Ment. Retard. Dev. Disabil. Res. Rev.

242

130

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A number of environmental agents have been shown to demonstrate neurotoxic effects either in human or laboratory animal studies. Critical windows of vulnerability to the effects of these agents occur both pre- and postnatally. The nervous system is relatively unique in that different parts are responsible for different functional domains, and these develop at different times (e.g., motor control, sensory, intelligence and attention). In addition, the many cell types in the brain have different windows of vulnerability with varying sensitivities to environmental agents. This review focuses on two environmental agents, lead and methylmercury, to illustrate the neurobehavioral and cognitive effects that can result from early life exposures. Special attention is paid to distinguishing between the effects detected following episodes of poisoning and those detected following lower dose exposures. Perinatal and childhood exposure to high doses of lead results in encephalopathy and convulsions. Lower-dose lead exposures have been associated with impairment in intellectual function and attention. At high levels of prenatal exposure, methylmercury produces mental retardation, cerebral palsy and visual and auditory deficits in children of exposed mothers. At lower levels of methylmercury exposure, the effects in children have been more subtle. Other environmental neurotoxicants that have been shown to produce developmental neurotoxicity include polychlorinated biphenyls (PCBs), dioxins, pesticides, ionizing radiation, environmental tobacco smoke, and maternal use of alcohol, tobacco, marijuana and cocaine. Exposure to environmental agents with neurotoxic effects can result in a spectrum of adverse outcomes from severe mental retardation and disability to more subtle changes in function depending on the timing and dose of the chemical agent.

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Section: Effects Of Poisoningmentioning

confidence: 99%

Environmental factors associated with a spectrum of neurodevelopmental deficits

Mendola

Selevan

Gutter

et al. 2002

Ment. Retard. Dev. Disabil. Res. Rev.

242

130

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“…In summary, the inhibitory effects of MeHg exposure on cell cycle progression and precursor proliferation are relevant to concerns about prenatal and childhood exposure to environmental levels of MeHg on the developing human brain (Myers et al, 2000(Myers et al, ,2003. Our studies build on epidemiological data by identifying a component of neurodevelopment that is susceptible to mercury at levels approaching ambient exposure.…”

Section: Decreased Precursor Proliferation May Reflect Mehg Effects Omentioning

confidence: 99%

Methylmercury elicits rapid inhibition of cell proliferation in the developing brain and decreases cell cycle regulator, cyclin E

Burke

Cheng

et al. 2006

NeuroToxicology

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The developing brain is highly sensitive to methylmercury (MeHg). Still, the initial changes in cell proliferation that may contribute to long-term MeHg effects are largely undefined. Our previous studies with growth factors indicate that acute alterations of G1/S phase transition can permanently affect cell numbers and organ size. Therefore, we determined whether an environmental toxicant could also impact brain development with rapid (6-7h) effects on DNA synthesis and cell cycle machinery in neuronal precursors. In vivo studies in newborn rat hippocampus and cerebellum, two regions of postnatal neurogenesis, were followed by in vitro analysis of two precursor models, cortical and cerebellar cells, focusing on the proteins that regulate G1/S transition. In postnatal day 7 (P7) pups, a single subcutaneous injection of MeHg (3μg/g) acutely (7h) decreased DNA synthesis in the hippocampus by 40% and produced long-term (2 weeks) reductions in total cell number, estimated by DNA quantification. Surprisingly, cerebellar granule cells were resistant to MeHg effects in vivo at comparable tissue concentrations, suggesting region-specific differences in precursor populations. In vitro, MeHg altered proliferation and cell viability, with DNA synthesis selectively inhibited at an early timepoint (6h) corresponding to our in vivo observations. Considering that G1/ S regulators are targets of exogenous signals, we used a well-defined cortical cell model to examine MeHg effects on relevant cyclin dependent kinases (CDK) and CDK inhibitors. At 6h, MeHg decreased by 75% levels of cyclin E, a cell cycle regulator with roles in proliferation and apoptosis, without altering p57, p27, or CDK2 nor levels of activated caspase 3. In aggregate, our observations identify the G1/S transition as an early target of MeHg toxicity and raise the possibility that cyclin E degradation contributes to both decreased proliferation and eventual cell death.

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“…Mercury (Hg) is a major concern due to its potentially adverse impacts on public health (Myers and Davidson 2000;Horvat et al 2003Horvat et al , 2004Cheng et al 2006;Zhang and Wong 2007;Zheng et al 2007). Unfortunately, continuing human activities are exacerbating Hg emissions into the environment.…”

Section: Introductionmentioning

confidence: 99%

Quantification and fractionation of mercury in soils from the Chatian mercury mining deposit, southwestern China

Yang

et al. 2008

Environ Geochem Health

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Contents of total Hg and Hg fraction, organic matter, pH, grain size and chemical composition were measured to investigate the pollution characteristics and binding behavior of Hg in soils collected from the Chatian Hg mining deposit (CMD), southwestern China. The average concentration of Hg concentration in the CMD soils was 155 and 1,315 times higher than that in control soils and Chinese soils, respectively, suggesting that the CMD soils were heavily contaminated by the element. The finding was confirmed by Müller geoaccumulation index assessment with 75% very seriously polluted, 6.25% highly to very highly polluted and 18.75% moderately to highly polluted. Hg sources in the region were natural and anthropogenic: in addition to the pedogenic process and original geochemical situation, human miningrefining activities have also seriously impacted the redistribution of Hg in soils, especially in paddy soils.

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Does Methylmercury Have a Role in Causing Developmental Disabilities in Children?

Cited by 30 publications

References 40 publications

Environmental factors associated with a spectrum of neurodevelopmental deficits

Environmental factors associated with a spectrum of neurodevelopmental deficits

Methylmercury elicits rapid inhibition of cell proliferation in the developing brain and decreases cell cycle regulator, cyclin E

Quantification and fractionation of mercury in soils from the Chatian mercury mining deposit, southwestern China

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