A new study just published on Feb 2011 in the journal of cancer makes a strong argument for applying hyperbaric oxygenation therapy (HBOT) for those patients who have had either surgery or radiation therapy for brain tumors. The study followed patients who had been treated with HBOT and there was a marked improvement in cognitive [...]
» Click Here to Read the full ArticleA Brief Review Of The Neurotoxic Effects
Of Environmental Chemicals.
By Walter J Crinnion N.D.
Abstract
The neurotoxic effect of chemicals are reviewed. For many years studies have been published showing that acute and chronic exposure to organic solvents cause both short term and lasting neurobehavioral problems. More physically destructive neurological problems such as Amyotrophic Lateral Sclerosis have also been linked to toxins. Recently, evidence has come to light linking Parkinson’s disease to a chemical-induced injury. Since then the theory of toxin-induced central nervous system deficits which are revealed by normal aging has been advanced.
Introduction
The neurologic effect of chemicals has been observed since 1856, when Delpech published his observation on the neurotoxicity of carbon Disulphide.(1) The journals now abound with such articles, yet the average clinician is unaware of the possible chemical etiology of neurological diseases.
The majority of published data shows that chemicals cause neuropsychological and behavioral problem. Recently the list of Parkinsonism and other Motoneurone diseases could be caused by environmental toxins. Calne postulated that exposure to environmental chemicals could cause subclinical damage in specific regions of the central nervous system.(2) With aging, certain individuals could then exhibit the symptoms of this damage as normal age-related neuronal attrition occurs. Parkinson’s, Alzheimer’s and Motoneurone diseases are all due to selective neuronal degeneration to the substantia nigra, medial basal forebrain and the motor neurons respectively. The location of initial chemical damage in the CNS would determine which disease was manifested in later years. Recently, evidence of just such chemical damage leading to Parkinsonism has come to light.
Parkinson’s Disease (PD)
In 1979, Davis and colleagues described a 23-year-old chemistry graduate who had been using a synthetic heroin he had manufactured.(3) He had done it successfully for several months until he changed the temperature and reaction time. When he did that he was hospitalized within a few days. Langstrom then showed the same occurrence in several drug users.(4) All of these individuals demonstrated the classical signs for PD. Langstrom obtained samples of the heroin analogue and found the contaminate 1-methl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Since then both mice(5) and monkeys(6) have been found to react to MPTP with PD as well. In the mice study, Gupta found that aged mice responded with PD more then young mice. This finding tends to support Calne’s theory about subclinical damage being manifested with age-related neuron death. The younger mice presumably were able to compensate for the damage because they had more functional neurons in the substantia nigra than older mice.
Calne(7) took further steps to prove his theory by using positron emission tomography (PET). PET is able to visualize dopamine and its metabolites in nigrostriatal nerve endings when using the dopa analogue 6-flourodopa. Calne used this method on four people who had used MPTP but had no symptoms of PD. All of these four individuals exhibited the damage to the nigrostriatal pathway that was exhibited in persons with clinical PD, but not in normal healthy subjects. This gave evidence that MPTP causes subclinical damage without causing signs of PD.
MPTP is not the only chemical found to cause PD. Davis(8) reported on a 53-year-old cropduster who had worked with organophosphate pesticides for 13 years. He had experienced several episodes of acute symptoms of PD, whereupon he quit his job. Also, Melamed and Lavy reported on a 40-year-old chemist who had been exposed to 20 kg of carbon tetrachloride over a 3 month period of time.(9) He developed treatment with levodopa. Bocchetta and Corsini reported two others who developed PD after working with pesticides for several years, the other was a 38-year-old chemist who had worked in a chemical plant making petroleum derivatives and pesticides.
Many of the symptoms of PD–cerebellar ataxia, resting and intention tremor, cogwheel rigidity, etc.,–were widely found in a population of patients exposed to a combination of carbon tetrachloride and carbon disulfide.(11) In the study, the researchers attributed these neurotoxic symptoms to the CS2 rather than CC14. Their subjects were grain storage workers or processors and were exposed to this chemical that was used as a fumigant. However, carbon disulfide had long been known to be neurotoxic and is used commercially in the manufacture of rayon, rubber, cellophane, flotation agents and pesticides as well as the extraction of oil from olives and palm stones.
Alzheimers
A chronic deficiency of central cholinergic function has been implicated in Alzheimers disease(12), as well as a number of other neurological problems. Recently, Mistry reported on a cholinotoxin which will allow the development of an animal model for neurotoxin-induced Alzheimers.(13)
The organophosphate pesticides are a group of compounds that are powerful inhibitors of cholinesterase. Their action leads to an accumulation of acetylcholine at the nerve synapses resulting in overstimulation and then paralysis of neural transmission. The present effect by organophosphate will supply a cholinergic function deficit which may be associated with such neurologic problems as Alzheimers(12), tartive dyskinesia(14),and Huntington’s chorea(15).
Muscle Paralysis
Senanayake and Karalliedde presented 10 patients with acute organophosphate poisoning(16). All of them exhibited paralysis of their proximal limb muscles, neck flexors, motor cranial nerves, and respiratory muscles as acute symptoms. After 96 hours several of the symptoms persisted including weaknesses of neck flexion (none of the patients were able to raise their head from the pillow) and Proximal limb weakness. Some of them developed transient dystonic movement of the limbs and some developed persistent polyneuropathy.
Deceased Sensory and Motor Nerve Coordination
In 1979, over 2000 people were poisoned in Taiwan by cooking ail contaminated with polychlorinated biphenyls (PCB). Rong-Chi Chen studied 110 such individuals within one year of the exposure(17). He said his colleagues reported that abnormal slowing of sensory nerve conduction and motor nerve conduction was present in up to 44% of their patients. He noticed that the higher the serum level of PCB metabolite, polychlorinated quarter phenyls, the slower the conduction rate.
Amyotrophic Lateral Sclerosis
Lou Gehrigs Disease (ALS) normally occurs at the rate of 1 in 50000 Americans per year. However, a complex picture including ALS along with some symptoms of PD and Alzheimers type dementia (ALS-PD Complex) used to be very common in Guam. The rate of this complex was at lease fifty times higher than in either Europe or North America. This Complex also occurs in southern New Guinea, and the Kii Peninsula in Japan. A deficiency of calcium and magnesium leading to an accumulation of aluminum has been proposed as one cause (18). Another theory is the consumption of a cycad seed that contains beta-N-methylamino-L-alanine (BMAA), a potent neurotoxin. In the US there have been certain clusters of ALS cases, some of the most interesting center around the fertilizer Milorganite, which at one time was found to be high in Cadmium(19).
Neurobehavioral Problem
Several neurobehavioral problems have been linked to certain chemicals. In a study of 305 histology technicians, Kilburn (20) found that exposure to formaldehyde correlated with disturbances of memory, equilibrium and dexterity. These symptoms increased with increased exposure to formaldehyde as well as increased age. While it is possible to dismiss the symptom amplification associated with increased age to the natural age-related attrition of brain function, it may well relate back to Calne’s theory.
In addition to formaldehyde-induced problems, there is abundant evidence pointing to the role that solvents play in similar neurobehavioral problems. In 1984 Gregerson (21) and colleagues published their study showing definite neurotoxic effects of organic solvents. His group found significant changes in emotional behavior and cerebral astheopia in exposed groups. They also found that exposed individuals performed poorer in learning and memory concentration ability, and attention. As with the other studies, the affected performances were poorer with increased exposure and increased age.
Similar results have been reported by Cherry, 1985 (22); Ekberg, 1986 (23) and Fidler, 1987 (24). (The reader should be aware that a Medline search will reveal many more references than these, and each of the above mentioned articles have long bibliographies as well.)
In 1987 Dager and colleagues published a study (25) giving three case histories of individuals who experienced panic attacks after being exposed to organic solvents. The solvent exposure in these individuals included toluene and Methylethylketone (MEK), both of which are quite common as are panic problems. Two of the three individuals had the attacks re-created with lactate infusion indicating that they would be likely to have panic problems anyway.
Summary
At the present time it has become next to impossible to avoid exposure to chemicals in our daily lives. It is equally as impossible to ignore the staggering number of neurological illnesses. These illnesses can have minor to major impact on the quality of life for the affected individual as well as their friends, relative and the society. It is quite possible that one of the major causes of neurologic morbidity may be found right under our very noses, actually passing through them, if you will.
Environmental toxins have been clearly linked to Parkinson’s disease, ALS, Motoneuron disease, decreased nerve conductivity and numerous neurobehavioral problems. With the staggering amount of information concerning this it is obvious that the term “Better Living Through Chemistry” is patently false. It behooves us to use proper avoidance and prophylactic measures both for ourselves as well as for our patients. The neural function that is saved may be your own.
