Pesticide neurotoxicity - Health Risks and Environmental Issues

Townsend Letter for Doctors and Patients,  July, 2002  by Rose Marie Williams

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During WWII nerve poisons were developed as chemical warfare to be used against the enemy. When peace was restored, the government helped the chemical companies find other uses for their products. Formulas that were designed to kill humans were reconfigured in lower doses to kill insects. The toxicity to humans never ceased, it just became more difficult to associate symptoms with exposure and clearly establish cause and effect.

Thousands of chemicals in myriad combinations pervade our lives. In the past half century each successive generation has been exposed to ever more toxins than the previous generation. Coincidentally, the variety and number of individuals afflicted with neurological disorders is outpacing medicine's ability to correctly identify, and successfully treat these illnesses.

The companies that make pharmaceutical drugs play a dominant role in the health care industry. They control grant money and research projects, influence university studies, serve on boards of governmental health organizations, as well as research hospitals. Often they are the same companies that manufacture pesticides and spend billions of dollars to influence legislation, designing laws that are more protective of their fiscal well-being than the public's physical well-being.

Pesticide poisoning is commonly under-diagnosed since health care providers generally receive very little training in occupational and environmental health, or particularly in pesticide-related illnesses. Childhood poisonings are complicated by the greater vulnerability of the very young. The neurological development of children involves an additional level of risk not present in adults. Transplacental absorption and breast milk may pose additional routes of exposure. It is important to know about pesticides used and stored in the home, daycare facility, school, play areas, and athletic fields. (1)

Organophosphate insecticides have replaced organochlorine insecticides, and are now the most widely available products used in homes, gardens, veterinary medicine and agriculture. Organophosphates share a common mechanism of cholinesterase inhibition and can cause similar symptoms. Exposure to the same organophosphate by multiple routes, or to multiple organophosphates by multiple routes can lead to serious toxicity and heightened sensitivity. (2)

"Organophosphates poison insects and mammals by phosphorylation of the acetyl cholinesterase enzyme (AChE) at nerve endings, resulting in a loss of AChE. The effector organ then becomes over-stimulated by the excess acetylcholine in the nerve ending." (3)

At cholinergic nerve junctions with smooth muscle and gland cells, high AChE concentration causes muscle contraction and secretion. Excess AChE at skeletal muscle junctions may cause muscle twitching, or weaken and paralyze the cell by depolarizing the end plate. In the central nervous system high AChE concentrations may cause sensory and behavior disturbances, incoordination, depressed motor function, and respiratory depression. Death from organophosphate poisoning results from increased pulmonary secretions combined with respiratory failure. (4)

Organophosphates are easily absorbed by inhalation, ingestion, and skin penetration. Breakdown occurs chiefly by hydrolysis in the liver and can vary widely from one compound to the next. Products that breakdown slowly are stored in body fat. Diazinon and methyl parathion are two organophosphates with significant lipid solubility, allowing fat storage with delayed slow-release toxicity. (5)

In some cases organophosphates have caused a different kind of neurotoxicity consisting of damage to the afferent fibers of peripheral and central nerves associated with inhibition of "neuropathy target esterase" (NTE). This delayed syndrome is characterized by weakness or paralysis and parathesia of the extremities. (6)

Three epidemiological studies suggest that some patients acutely poisoned by organophosphates can experience long-term neuropsychiatric sequelae. Findings show decreased performance on neurobehavioral tests, including memory, concentration, mood, and compound-specific peripheral neuropathy in some cases. Some individuals report persistent headaches, blurred vision, muscle weakness, depression, memory and concentration problems, irritability, and/or development of intolerance to specific chemical odors. (7)

One reason organophosphates replaced organochlorine products is because they break down faster and are not as persistent in the environment. However, they produce additional chemicals (metabolites) in the breakdown process, some of which can be more toxic than the original chemical and longer lasting in the environment.

In March 2001 the Centers for Disease Control & Prevention (CDC) conducted a study on US residents for five chemicals that are breakdown products of organophosphate insecticides. The CDC survey found that three of the five breakdown products were found in over 90% of the people tested. Since the monitoring study looked at people from the ages of six to 59, this suggests that exposure of children and pregnant women to pesticides may be surprisingly more common than assumed. (8)