Mercury neurotoxicity

Aschner M, Aschner JL. 1990. Mercury neurotoxicity mechanisms of blood-brain barrier transport. Neurosci Biobehav Rev 14 169-176. 

Valcinkas J et al Neurobehavioral assessment of Mohawk Indians for subclinical indications of methyl mercury neurotoxicity. Arch Environ Health 41 269-272, 1986... 

Fish Tuna, shark, sword fish Mercury Neurotoxic, reproductive effects ... 

Tan, KH Winston-Salem State University Winston-Salem, NC Pilot study-astrocyte gene expression and methyl mercury neurotoxicity. NCRR... 

Gallagher PJ, Lee RL. 1980. Role of biotransformation in organic mercury neurotoxicity. Toxicol 15 129-134. 

Sarafian T, Verity MA. 1991. Oxidative mechanisms underlying methyl mercury neurotoxicity. IntJ Dev Neurol 9(2) 147-153. 

A rather insidious form of mercury neurotoxicity can occur when the clement is bound chemically to certain groupings of organic molecules - so called alkylmercury compounds. Such forms of mercury, unlike the inorganic forms, can cross the blood-brain barrier (which is fairly effective at excluding inorganic mercury) and damage... 

Aschner, M., and J.L. Aschner. 1990. Mercury neurotoxicity Mechanisms of hlood-hrain harrier transport. Neurosci. Biobehav. Rev. 14(2) 169-176. 

Uzzell BP, Oler J Chronic low-level mercury exposure and neuropsychological functioning. J Clin Exp Neuropsychol 8 581-593,1986 Valciukas JA, Levin SM, Nicholson WJ, et al Neurobehavioral assessment of Mohawk Indians for subclinical indications of methyl mercury neurotoxicity. Arch Environ Health 41 269-272, 1986... 

Mercury Neurotoxic Electronics, paper pulp manufacture 0.3-2 yr removed by deposition 0.37-0.49 ppb 1.2 ppb... 

Chang, L. W., 1983, Protective effects of selenium against methyl-mercury neurotoxicity A morphological and biochemical study, Exp. Pathol 23 143. 

Organoarsenic compounds have been of importance in human toxicology but have not as yet received much attention in regard to environmental effects. Like methyl mercury compounds, they are both synthesized in the environment from inorganic forms and released into the environment as a consequence of human activity (Environmental Health Criteria 18). They can cause neurotoxicity. 

Brain is a key tissue to analyze for mercury concentration because it is the site of MeHg toxicity. The neurotoxic effects of MeHg in adrrlt mammals inclnde ataxia, difficulty in locomotion neurasthenia, a generalized weakness impairment of hearing... 

Maier WE, Costa LG. 1990. Sodium, potassium-ATPase in rat brain and erythrocytes as a possible target and marker, respectively, for neurotoxicity studies with chlordecone, organotins and mercury compounds. Toxicol Lett 51 175-188. 

Thimerosal is a preservative used in vaccines that has been purported to cause autism in children. The assumption is that thimerosal, also known as ethyl mercury, causes similar effects as methyl mercury, which has neurotoxic and nephrotoxic... 

Methylmercury, which we referred to in the neurotoxicity section, occurs in fish and shellfish found in both the ocean and fresh water systems. The mercury that is the source of methylmercury arises from power plant emissions and industrial processes. Some even comes from... 

The RfDs and TDIs are often used to establish regulatory standards. Such standards usually specify a limit on the allowable concentration of a chemical in an environmental medium. The process is not difficult to understand. The RfD and its related estimates of population thresholds is a dose, typically expressed in mg/(kg b.w. day), that is considered to be without significant risk to human populations exposed daily, for a lifetime. Consider mercury, a metal for which an RfD of 0.0003 mg/(kg b.w. day) has been established by the EPA, based on certain forms of kidney toxicity observed in rats (Table 8.4). These are not the only toxic effects of mercury, but they are the ones seen at the lowest doses. Note also that we are dealing with inorganic mercury, not the methylated form that is neurotoxic. 

The primary human exposure to methyl mercury is from consumption of contaminated fish. The most sensitive population is the developing fetus or infant due to the effects of methyl mercury on the nervous system (neurotoxic) and developmental effects. Exposure limits and fish consumption advisories are directed at pregnant women, women of childbearing age, and children. All agencies also recognize that fish consumption has many nutritional benefits and is an important part of many people s diet. Nevertheless, the widespread distribution of mercury and subsequent bioaccumulation of methyl mercury requires that many agencies have developed recommendation for levels of mercury in fish. Below is a list of some of these recommendations, but it is very important to consult the local fish consumption advisories. 

Mercury Metal - persistent - bioaccumulates - contaminates many species of fish. Widely used in industrial processes. Causes developmental neurotoxicity -children most susceptible... 

There is further analogy with yet "extra concern for toxic chemicals that may also persist in the environment and be transported great distances from their point of entry into the environment. Here the unifying general notion is that unsuspecting individuals are placed at risk, and are thus less able to defend than are the perpetrators. Mercury is a classic example of such a chemical. Mercury is extremely toxic to the CN S. Fetuses, infants, and toddlers are especially sensitive and susceptible to the neurotoxic properties of mercury. Mercury also persists in the environment, and is known to bioaccumulate in the food web and biomagnify up the food chain. 

Pregnant or nursing women exposed to methylmercury through their diet or otherwise also expose their developing fetus or breast-fed infant to the chemical, since methylmercury passes through placental membranes and enters the fetal bloodstream, and also enters breast milk. This is particularly problematic since fetuses and infants (and toddlers) are more susceptible and sensitive to the neurotoxic properties of mercury than are adults. 

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