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Environmental Paper Series
The Effects of Neurotoxins on Human Health:
Mercury, Lead, and, Pesticides
by Waterose
The word "neurotoxic" literally translates as "nerve poison". Broadly described, a neurotoxicant is any chemical substance which adversely acts on the structure or function of the nervous system. It is important to understand not only the effects and types of neurotoxicants, but also the sources and pathways by which these substances enter the environment. Neurotoxicants are ubiquitous in the environment and they have a serious impact on human health (Isaacson,1992). Neurotoxicants affect the nervous system in different ways; this depends on the molecular structure of the neurotoxic chemical substance and the specific function and structure of the nervous system tissue (Isaacson, 1992). In order to understand the effects and classes of neurotoxicants, it is important to understand the functions and structures of the nervous system.
The nervous system has three overlapping functions: sensory input, integration, and motor output (Campbell, 1993). The peripheral nervous system (PNS) carries signals from the sensory input organs to the brain and carries output instructions from the brain to the motor controls. The integration of the input/output signals is controlled by the central nervous system (CNS) which includes the brain and the spinal cord. The nervous system has two types of cells; transmitting neuron cells which conduct electrical impulses or signals, and supporting glial cells which provide structural integrity for the nervous system (Campbell, 1993). The neuron cells, from receiving end to transmitting end, are comprised of several components. The branched dendrites receive the incoming signal. The cell body houses the nucleus and other organelles. The axon and the axon hillock conduct signals away from the cell body. The axon is wrapped by the Myelin sheath which is made of a series of Schwann cells which grow around the axon. Schwann cells are high in lipids and are therefore poor electrical conductors, they serve to focus the electrical impulses inside the axon. The axon is terminated by the branched synaptic terminal where the signal is passed onto another neuron via the neuron pathway. The flow of electrical impulses is controlled by the ion gradient across the membrane wall. The interaction between the sending neuron, or the presynaptic cell, and the receiving cell, or the postsynaptic cell, is controlled by both electrical synapses and chemical synapses.
Neurotoxicants are chemical substances that injure the neurotransmission of signals. There are three basic types of damage that can occur (Internet, Neurotoxicity Scorecard). Neuronopathy refers to general damage to the neuron cell body. Axonopathy refers to damage to the neuron axon. Myelinopathy refers to damage to the Myelin sheath. The symptoms of neurotoxic poisoning in the CNS and the PNS differ because each of these nervous systems have different functions. Neurotoxins that act on the CNS impair neurotransmission in the brain and the spinal cord causing confusion, irritability, fatigue, and other behavioural changes. Metals, such as mercury and lead, affect the CNS. Neurotoxins that act on the PNS impair neurotransmission in the other biological systems causing weakness, prickling or tingling in the limbs and loss of motor control. Organic pesticides, such as organophosphates, affect the PNS. Neurotoxicants, whether in the form of metals, organics, or pesticides, are omnifarious and pose a serious threat to human health.
Mercury (Hg) is recognised as a serious threat to human health because of the way it acts on the CNS (Aschner, 1992). The effects of Hg on the CNS include neurological damage, irritability, paralysis, blindness, insanity, chromosome damage, and birth defects (Manahan, 1994). The most infamous case of mercury poisoning was the Minamata Bay area of Japan in the 1950’s when 111 cases of mercury poisoning were reported and 43 deaths occurred (Manahan, 1994). This event was attributed to the consumption of seafood contaminated with mercury waste from a chemical manufacturing plant.
The sources of Hg can either be naturally weathered from the Earth’s crust or from anthropogenic activities (Aschner, 1992). Examples of anthropogenic point sources include wastes from industrial processes, mining, and, coal processes (Manahan, 1994). Mercury exists in several forms. These forms include: the metallic form (Hg0), the mercurous form (Hg+) and the mercuric form (Hg2+) (Aschner, 1992). The pathways of human exposure to Hg occur through long range transport in the atmosphere, concentrations in fresh water, and through biomagnification in the food chain. The inorganic metallic and mercurous forms are transformed into organic compounds, called methylmercury forms (MeHg) by aquatic organisms. MeHg biomagnifies in the food chain and consumption of contaminated fish is the major pathway of introduction to human populations (Weiner, 1996).
Methylmercury and alkyl mercury species are lipid soluble and can penetrate the "Blood-Brain Barrier" and attack the CNS (Aschner, 1992). The blood-brain barrier is a special continuous layer of endothelial cells with tight junctions that prevent the blood from entering the brain parenchyma. Once in the brain, MeHg causes degeneration of the cortex and the cerebellum by altering the translational mechanism of transfer RNA. MeHg significantly impairs the functions of neurons in the following ways: inhibits enzymes, changes electrical properties of axons, disrupts axonal transport, creates Hg radicals by homolytic cleavage of MeHg, and disrupts the neuronal cytoskeleton. Mercury species can spread throughout the entire body bioaccumulating in lipids and organs such as the liver. Mercury poisoning causes birth defects and mercury poisoning has long been recognised as a serious threat to human health.
Equally serious, the neurotoxic properties of lead (Pb) affect both the CNS and the PNS (Castellino, 1995). The serious effects of lead include acute encephalopathy, which is a disease of the brain in children (Castellino, 1995); peripheral motor neuropathy, which is impaired control of the limbs; and pica, which is an eating disorder that causes people to crave toxicants (Donovick, 1992). Children are at serious risk from lead poisoning from the placental stage of development because lead in the bloodstream passes through the placenta and directly into the brain of the foetus where it begins neurological degradation (Riess, 1992).
The sources of Pb can be either naturally weathered from the Earth’s crust or from anthropogenic activities. Lead was used for centuries because of its’ soft malleable properties and lead poisoning from food containers or jewellery was not uncommon (Riess, 1992). Anthropogenic sources of lead include industrial wastes, mines, solders in household water pipes, paints, and formerly, in leaded gasoline. Lead exists in several states but the most toxic state is Pb2+ (Minnema, 1992). The pathways of human exposure to Pb occur through the inhalation of lead particles in the atmosphere, the consumption of lead in contaminated drinking water, and the consumption of lead in the food chain. Lead is non-biodegradable and can remain in the soil indefinitely. There is constant uptake by plants and soil fauna which transfers lead through the food chain and into the human body (Riess, 1992).
Lead has direct neurotoxicological effects on the CNS. These effects include decreased synapse growth and density, impaired neuron growth, impaired neuronal differentiation, induced glial cell development, and altered neurochemical signals (Minnema, 1992). Lead alters every aspect of the functions of the nervous system. The high risk element of concern is that lead permeates all of the major components of the ecosystem that are used by humans.
Another broad category of neurotoxins ubiquitous in the environment and harmful to humans, are organic pesticides (Overstreet, 1992). The most widely used pesticides are the organophosphates (OP) which consist of carbon-hydrogen skeletons with phosphate groups attached. The effects of OP’s on the PNS include peripheral muscarinic actions such as salivation, diarrhoea, and urination, and peripheral nicotinic actions such as paralysis. The source of these neurotoxins is exclusively anthropogenic. The pathways of exposure to humans are through direct contact by agricultural workers, airborne OP’s in the atmosphere, residuals on crops, and runoff into groundwater. Human intake is through inhalation, absorption through the skin, and ingestion.
The primary neurological effect of OP’s is to act as an inhibitor to pathway functions by blocking the cholinergic neurotransmitter system (Overstreet, 1992). Cholinergic neurons use the enzyme, acetylcholinesterase (A Ch E), for transmission at the synapse. These neurons are essential to the CNS, PNS, and in particular, the motor output functions of the nervous system. The effects of OP’s are irreversible and cause permanent damage to the neurons. Furthermore, the effects on the nervous system magnify with increased exposure dosage and frequency of exposure, thus increasing the risk to humans.
The underlying concern about neurotoxins and their harm to human health is that they are omnifarious in the environment and exposure is inescapable. Mercury, lead, and organophosphates are just a few examples of the multitude of neurotoxins that act on the human nervous system. This is cause for grave concern and action to mitigate the damage to the ecosystem and ultimately, human health is needed.
References:
Campbell, N.A. 1993. Biology. Third Edition. Benjamin Cummings, Redwood City, Ca. 1190 pp.
Castellino, P. et al. 1995. Inorganic Lead Exposure: Metabolism and Intoxication. Lewis Publishers, Boca Raton, Florida. 516 pp.
Donovick, J., Burright, R. 1992. "Lead Poisoning, Toxocariasis, and Pica: Links to Neurobehavioral Disorders." in The Vulnerable Brain and Environmental Risks. Volume 2. Toxins in Food. Plenum Press, NY, NY. pp. 127-146.
Internet. 1998. Neurotixicity Definition.
Available at URL: http://www.scorecard.org/health-effects/ explanation.tcl?short_hazard_name=neuro
Isaacson, R. and Jensen K. 1992. The Vulnerable Brain and Environmental Risks. Volume 2. Toxins in Food. Plenum Press, NY, NY. 332 pp.
Manahan, S.E. 1994. Environmental Chemistry. Sixth Edition. Lewis Publishers, Boca Raton, Florida. 811 pp.
Minnema, D. 1992. "Neurotoxic Metals and Neuronal Signalling Processes." in The Vulnerable Brain and Environmental Risks. Volume 2. Toxins in Food. Plenum Press, NY, NY. pp. 83-109.
Overstreet, D., Schiller, G. 1992. "Central Nervous System Pasticity and Pathology Induced by Exposure to Organophosphate Pesticides." in The Vulnerable Brain and Environmental Risks.Volume 2. Toxins in Food. Plenum Press, NY, NY. pp. 197-214.
Riess, J., Needleman, H. 1992. "Cognitive, Neural, and Behavioural Effects of Low-Level Lead Exposure." in The Vulnerable Brain and Environmental Risks.Volume 2. Toxins in Food. Plenum Press, NY, NY. pp. 111-126.
Weiner, G., Spry, J. 1996. Edited by Beyer, W.N. et al. "Toxicological Significance of Mercury in Freshwater Fish" in Environmental Contaminants in Wildlife: Interpreting Tissue Concentrations. SETAC Special Publication Series. CRC Press, Boca Raton, Florida. pp. 297-339.
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