Neurotoxins are a special class of metabolic poison that attack nerve cells. Disruption of the nervous system as a result of exposure to neurotoxins usually is quick and destructive.
Neurotoxins are categorized according to the nature of their impact on the nervous system. Anesthetics (e.g., ether, chloroform, halothane), chlorinated hydrocarbons (e.g., dichlorodiphenyltrichloroethane [DDT], Dieldrin, Aldrin), and heavy metals (e.g., lead, mercury) disrupt the ion transport across cell membranes essential for nerve action. Common pesticides, including carbamates such as Sevin, Zeneb, and Maneb, and the organophosphates such as Malathion and Parathion, inhibit acetylcholinesterase, an enzyme that regulates nerve signal transmission between nerve cells and the organs and tissues they innervate.
Neurotoxins are common in living organisms, including bacteria, fungi, plants, arachnids (e.g., spiders), marine life, and vertebrates. Botulinum neurotoxin, the cause of botulism, is produced by the bacterium Clostridium botulinum. Venomous snakes, spiders, and scorpions all paralyze their prey by injecting a neurotoxin. Parts of the Japanese puffer fish contain neurotoxins that can be fatal if eaten. Anesthetics are neurotoxins with beneficial medical uses. Botox, a form of botulinum toxin, has been approved by the U.S. Food and Drug Administration (FDA) for cosmetic and limited medical use.
Cell damage associated with the introduction of neurotoxins occurs through direct contact with the chemical or a loss of oxygen to the cell. This results in damage to cellular components, especially in those required for the synthesis of protein and other cell components.
The symptoms associated with pesticide poisoning include eye and skin irritation, blurred vision, headache, anorexia, nausea, vomiting, increased sweating, increased salivation, diarrhea, abdominal pain, slight bradycardia, ataxia, muscle weakness and twitching, and generalized weakness of respiratory muscles.
Symptoms associated with poisoning of the central nervous system include giddiness, anxiety, insomnia, drowsiness, difficulty concentrating, poor recall, confusion, slurred speech, convulsions, coma with the absence of reflexes, depression of respiratory and circulatory centers, paralysis, fall in blood pressure, and death.
Some links between environmental neurotoxin exposure and neuromuscular and brain dysfunction have been identified. Physiological symptoms of Alzheimer's disease, amyotrophic lateral sclerosis (ALS) or Lou Gehrig's disease, and lathyrism have been identified in populations exposed to substances containing known neurotoxins. For example, studies have shown that heroin addicts who used synthetic heroin contaminated with methylphenyltetrahydropyridine developed a condition that manifests symptoms identical to those associated with Parkinson's disease. On the island of Guam, the natives who incorporate the seeds of the false sago plant (cycas circinalis) into their diet develop a condition very similar to ALS. The development of this condition has been associated with the specific nonprotein amino acid, B methylamino-1-alanine, present in the seeds.
Diagnosis is made, usually by a neurologist, based on the patient's history and a variety of neurological and toxicology tests. Tests will vary depending on the type of neurotoxin suspected.
Initial treatment consists of eliminating continued exposure to the neurotoxin. Beyond that, treatment varies depending on the type of neurotoxin to which the individual has been exposed. In many cases, supportive care is the only available treatment. Chelation therapy may be used as part of a comprehensive treatment for some heavy metal neurotoxins (e.g., lead). For a few neurotoxins such as rattlesnake venom, an antivenin can be administered. In many cases, neurological damage is irreversible.
Prevention involves educating individuals about the potential neurotoxicity of chemicals used in the workplace and in hobbies. Organizations such as the U.S. Environmental Protection Agency (EPA) and the Occupational Health and Safety Administration (OSHA) set limits on the amount of many toxins, including neurotoxins, permitted in the environment and in the workplace.
See also Food and Drug Administration ; Lead ; Mercury ; Toxicology .
Satoh, Tetsuo, ed. Anticholinesterase Pesticides: Metabolism, Neurotoxicity, and Epidemiology. Hoboken, NJ: Wiley, 2010.
Spaeth, Kenneth R. et al. Heavy metals: A Rapid Clinical Guide to Neurotoxicity and Other Common Concerns. New York: Nova Science, 2010.
Camp, Allison. “Neurotoxins.” Toxipedia.com . http://toxipedia.org/display/toxipedia/Neurotoxins (accessed October 17, 2012).
Centers for Disease Control and Prevention (CDC). “Organic Solvents.” http://www.cdc.gov/niosh/topics/organsolv (accessed October 17, 2012).
National Center for Biotechnology Information. “Resources for Neurotoxins.” http://www.ncbi.nlm.nih.gov/sites/ga?disorder=neurotoxins (accessed October 17, 2012).
National Geographic Society. “Pick Your Poison—12 Toxic Tales.” http://science.nationalgeographic.com/science/health-and-human-body/human-body/poison-toxictales.html (accessed October 17, 2012).
Agency for Toxic Substances and Disease Registry, 4770 Buford Hwy. NE, Atlanta, GA, 30341, (800) 232-4636; TTY: (888) 232-6348, email@example.com, http://www.atsdr.cdc.gov/ .
Centers for Disease Control and Prevention, 1600 Clifton Rd., Atlanta, GA, 30333, (404) 639-3534, (800) CDCINFO (800-232-4636); TTY: (888) 232-6348, firstname.lastname@example.org, http://www.cdc.gov .
Environmental Protection Agency (EPA), Ariel Rios Bldg., 1200 Pennsylvania Ave. NW, Washington, DC, 20460, (202) 272-0167; TTY (202) 272-0165, http://www.epa.gov .
Brian R. Barthel
Revised by Tish Davidson, AM