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In some individuals who have chemical injury increased chemical breakdown products (called free radicals) can be produced by electromagnetic fields.11 The electrical current from EM fields created by human technology is thousands of times stronger then electric messages in brain and nerve cells. This can occur, for example, from mobile/cell phones, cell towers, high voltage power lines, etc.11

Higher EM exposure can cause sensitization in some persons and even commonly used EM-generating technology can increase symptoms.

EM technology can increase “nitric oxide”. When nitric oxide is increased (e.g. as in neural sensitization), this could cause exacerbation by further nitric oxide increase from chemicals or more EM epxosure.11 Excess nitric oxide with excess free radicals can increase damage to essential body lipid cell membranes, brain myelin, mitochondria membranes and other cell structures).11 This damage turns the lipid into a peroxide, called lipid peroxide, obviously undesirable and interfering with function.11



Genetic differences between individuals can make one person up to 100 times more susceptible to effects of a given substance than another person.12 Genetic differences in sulfur and other detoxification contribute greatly to degenerative nerve disease.13,14

Genetic impairment in some kinds of detoxification is very common because it did not affect survival until more recent years. Now workplaces, homes, schools and even public places unknowingly use many toxic chemicals.

Genetic diversity can greatly affect pesticide and other chemical vulnerability.15 Thus chemical products, product use, protection, and “exposure limits” must take genetic diversity into account. One would not install a ceiling fan 6’ from the floor and blame taller people who suffered head injury. The answer is a fan height and a chemical policy that protects everyone.

Certain dietary antioxidants can help reduce this risk.16 People do not know what their genetic susceptibility is nor do they know how to reduce it. Much genetic risk is difficult to test and tests are not available for other risks.



Detoxifying chemicals depletes the ability to detoxify drugs, as discussed above. This increases problems of drug interaction and increases drug intolerance and side effects in chemically injured patients. The following diagram illustrates the percentage of different types of the first detoxification step (called P450 cytochromes) involved in drug interactions.6

Most drugs and chemicals need to be detoxified by similar means before leaving the body. Thus drug usage with chemical injury can further impair ability to detoxify chemicals.



1 S Stohs and D Bagchi , “Oxidative mechanisms in the toxicity of metal ions”, Free Radic Biol Med 18: 321-326.

2 CD Klassen, Editor Casarett and Doulls Toxicology: The Basic Science of Poisons. McGraw Hill, New York, NY, 2001.

For scientific references consult the neural sensitization section on www.chemicalinjury.net.

4 D LeConteur, etal, Age-environment and gene-environment interactions in the pathogens of Parkinson’s disease”, Rev Environ Health 17 51-64, 2002.

5 D Bonneth-Barkay, etal “Toxicity of redox cycling pesticides in primary mesencephalic cultures”, Antiox Redox Signal 7: 649-653, 2005.

6 S Rendic, “Summary of information oh human CYPenzymes: human P450 metabolism data”, Drug Metab Rev.

7 L Brunton, etal, Editors, Goodman and Gilman’s The Physiologic Basis of Therapeutics, McGraw Hill, New York, NY, 2005.

8 G Ziem, “Medical evaluation and treatment of patients with chemical injury and sensitivity”, Invited presentation to Aug 2001 conference sponsored by the National Institute of Environmental Health Sciences. For free download see Website: www.chemicalinjury.net.

9 H Norppa, “Cytogenetic biomarkers and genetic polymorphisms”, Toxicol Lett, 149: 309-334, 2004.

10 AT Proudford etal, “Position paper on urine alkalization”, J Toxicol Clin Toxicol 42:1-26, 2004.

11 F Ozguner, etal, “Mobile phone-induced myocardial oxidative stress: protection by a novel antioxidant agent caffeic acid phenethyl ester:, Toxicol and Indust Health 21: 223-230, 2005.

12 WE Evans, etal, “Pharmacogenomics – Drug disposition, drug targets and side effects”, New Engl J Medicine, 348: 538-549, 2003

13 Drug Metabol Drug Interaction 19:223-40, 2003.

14 Drug Metabol Drug Interaction 18: 79-98, 2001.

15 S Beglev , “Poisons aren’t toxic to everyone equally, Wall Street Journal, Jan 24, 2003.

16 Mol Cell Biol, 24: 5209-5222, 2004.

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