FORMALDEHYDE NEUROTOXICITY
Formaldehyde has also been found to have a neurotoxic effect and impairments of attention and memory have been associated with formaldehyde exposure - LEZAK M D, Neuropsychological Assessment, OUP, 1995, p267. [Note, significant methanol, which metabolises to formaldehyde was detected above glutaraldehyde sterilising solutions]. The whole of Chapter 7 is excellent and gives the following references:
*p 267: “Because it is so widely used in buildings and furnishings material and in household products, formaldehyde in vapour or derivative form is often present in home environments.” (Schenker M.B, et al. Health effects of residence in homes with urea formaldehyde foam insulation. A pilot study. Environmental International, 8, 359-363, 1982.
Singer R.M. Neurotoxicity Guidebook. 1990. NY. Van Nostrand Reinhold).
*p 267: “Laboratory animals exposed steadily for three months to somewhat higher than normal levels of formaldehyde incurred brain damage particularly involving the parietal cortex”. (Fel’dman Y.G. and Bonashevskaya T.I. On the effects of low concentrations of formaldehyde. Hygiene and Sanitation, 36, 174-180, 1971).
*p 267: “ Both acutely and chronically, persons exposed to formaldehyde have complaints implicating the central nervous system, such as headache, dizziness, irritability, memory problems, and sleep disturbances.” (Report on the Consensus Workshop on Formaldehyde. Environmental Health Perspectives, 58, 323-381, 1984. Olsen J.H et al, Formaldehyde induced symptoms in day care centers. Am Ind Hyg Assoc J. 43, 366-370, 1982.)
*p 267: “Impairments on tests of attention and short-term memory have been reported for exposed workers” - Bach B, et al. Human reactions during controlled exposures to low concentrations of formaldehyde - performance tests. Paper presented at 4th International Conference on Indoor Air Quality and Climate. Berlin. 1987. Kaye H. Kilburn, et al. Formaldehyde Impairs Memory, Equilibrium, and Dexterity in Histology Technicians: effects which persist for days after exposure. Archives Envir Health, 42, 117-120, 1987. Paper available CIIN 0024-GOET-85-014. [305 women technicians, av 17 yrs work. Increasing age was associated with poorer performance on visual memory, block design, trails connecting numbered dots, dexterity, sharpened Romberg (balance), finger writing for peripheral nerve function, as well as longer reaction time. Increased daily hours of exposure were correlated with reduced performance of story memory, visual memory, digit span (numbers forward and backward), pegboard and sharpened Romberg, and errors on trails. From other studies reported in this paper: “Impaired memory, particularly short-term memory loss is a frequent symptom in histology technicians. Recent observations show that short-term memory does not vary significantly with age”. “Lightheadness, dizziness, and disturbed equilibrium are frequently reported in histology technicians.” The mechanism of the neurotoxity of formaldehyde has not yet been identified. However formaldehyde cross-links proteins, DNA, and unsaturated fatty acids. This high affinity for these chemicals suggests a rapid interaction with cells after inhalation or ingestion. This suggests that little free formaldehyde should reach the nervous system. However the results described decreased neurofunction.]
LEZAK:
“My experience with a number of persons complaining of memory problems associated with formaldehyde exposure is that many of them displayed attentional deficits which interfered with effective communication and normal information storage and were interpreted by them as “memory” problems. However, using the Halstead-Reitan battery and the Wechsler Memory Scale to examine a small series of persons exposed to low levels of formaldehyde fumes in their homes, Cripe and Dodrill (Neuropsychological test performances with chronic low-level formaldehyde exposure, The Clinical Neuropsychologist, 2, 41-48, 1988) reported no notable differences between them and matched controls.”
A further formaldehyde neuropsychological reference is:
C.G. GOETZ, Organic Solvents in Neurotoxins in Clinical Practice, (Chap 5) 1985. Discusses types of solvents, neuropathy, encephalopathy, myopathy (with reference to fatigue, exercise intolerance, arthralgias, muscle tenderness), and specifically: methyl alcohol/ formaldehyde, ethylene glycol, amyl/isopropyl alcohol, toluene, n-hexane, aniline, MBK, TCE, carbon tetrachloride. Organs affected by organic solvents in addition to the nervous system include skin, mucous membranes, digestive, hepatic, renal systems.
***
CHEMICAL ASSAULTS ON THE BRAIN.
From Bonnye Matthews’ book Defining Multiple Chemical Sensitivity, (McFarland, 1998) Dr Donald Dudley (retired Professor of Psychiatry and Behavioural Sciences and former Clinical Professor of Neurological Surgery at the University of Washington) describes his theory of how the brain damage is occurring from chemicals with fewer than 6 carbon fragments in their volatile components (such as formaldehyde, MEK, acetone, glutaraldehyde) :
p 22. “As indicated in the beginning of this chapter, doctors creating negative bias towards the olfactory system include attitudes expressed in authoritative medical textbooks since at least 1875; the use of technology better suited to other systems (eg the immune system) to study the olfactory system; the lack of adverse effect occurring from ablation of olfactory tracts in the brain (which has been misinterpreted as evidence that the system must have little value); the supposed failure to identify neurotransmitters in the olfactory system; and the supposed failure to identify any essential role this system could have in disease production. To varying degrees, these factors influence the attitudes of both professional and non- professionals and generate considerable negativity towards MCS patients who point to olfaction as the major source of their medical problens. Both professionals and nonprofessionals tend to believe that these patients have psychiatric disorders or are simply malingering - a belief that is inconsistent with the data presented in this study, and a belief that has no business in science.
An issue of major importance from this author’s point of view, is the fact that neurotransmitters have been found for the olfactory system, and that many are excitatory amino acids such as glutamate and NMDA, or precursors to excitatory amino acids. These are the same amino acids that are implicated in brain-cell injury and death. They are related to such problems as stroke, pain, depression, and degenerative brain disease.
Glutamate, NMDA, and other excitatory amino acids injure cells when released. This injury makes the cell vulnerable to the influx of chloride ions and then to the influx of calcium ions. A fanciful way of looking at this process is to imagine a balloon being inflated until it bursts. It is postulated that olfactory signals release excitatory amino acids, which lead to cell injury that proceeds to the above process. If such a mechanism is in operation, it should be possible to procuce the symptoms of MCS by using excitatory amino acid agonists, and to decrease them by using antagonists. The agonists are the volatile short-chain carbon fragments such as formaldehyde, acetone, and methyl-ethyl ketone. Molecules such as these, with the same or fewer carbon units than glutamate, can be agonists. These compounds lead to the release of excitatory amino acids that begin destruction of brain tissue.
In general, odor thresholds decline with exposure to chemicals having more than six carbon fragments and increase with exposure to chemicals having six or fewer carbon fragments. The optimal carbon length for producing excitatory amino acid release is six or fewer. It needs to be emphasized that it is not the carbon chain length of the parent compound that counts. It is the carbon chain length of the volatile component. In other words, analysing carpet adhesive is of little use; the volatile fragment from carpet adhesive needs to analyzed.
On the other hand, compounds with greater than six carbon fragments, with a D-configuration and certain other characteristics, can be antagonists of excitatory amino acids. These compounds, such as MK801 and dextromethorphan hydrobromide, should decrease symptoms of patients with MCS if the hypothesis is correct. Dextromethorphan hydrobromide, a known excitatory amino acid blocker, does significantly decrease symptoms on olfactory exposure to volatile short-chain carbon compounds in MCS patients. It has been used by the author in more than 30 of these patients with significant positive efect. Dextromethorphan hydrobromide has a remarkable track record and has been used in billions of doses as a cough suppressant without significant biologic problems. To the author’s knowledge MK801, an experimental amino acid blocker, has not been used in patients with MCS.”
Madelon Price, Professor of Neurobiology, Washington University Medical School writes: “NMDA antagonists are dangerous agents. Currently there are none that have been approved for use although one may be approved shortly. A very few NMDA antagonists are complex agents that act at multiple sites. Dextromethorphan is an NMDA antagonist but at the concentration that it is added to cough medicine, it is safe. Even at high concentration it would probably be safe (but not yet adequately tested) in that it also acts at other receptor sites that block NMDA receptor antagonist toxicity. One should consult with a well informed doctor or scientist before ingesting one of these agents.”
THYROID RELEASING HORMONE
Bonnye Matthews writes about another helpful treatment after a chemical exposure: “That cascade of ill effects (the balloon example with cells) is stopped in its tracks by the use of TRH as a nasal spray. After Donald Dudley tested me the first time, I called from home the next day and told him the brain fog problem was worse than it had ever been. He told me if I could get downtown, he'd turn it around. I thought he was out of his mind, but my mom drove me to his office. As he so aptly put it, expose me and you've got a person with an IQ of 60 shuffling around. I was far gone. In two-and-a-half hours I drove home! It's amazing stuff!
Donald Dudley has tried dextromethorphan with success in some cases. In my case, for example, DM works following toxic exposure on my lungs but not my brain. DM puts out the "fire" spots in my lungs within a half hour. To clear the "brain fog" in my case, I have to use TRH in a nasal spray. So he's postulating, but also he's seen success in some cases, where DM actually clears the "brain fog." The postulating is because of the lack of study with agonists. Without TRH and DM I wouldn't try to do much of what I do. We actually have pharmacies now (in Seattle) where we can get TRH nasal spray and DM. I think he's really on to something, but without large numbers of people, I think he's right to stick with postulating.” An estimate is that it is effective 90% of the cases. For some it is not effective. Its real value is that it keeps the IQ bites that follow these really bad brain fogs from being so devastating. (Personal communication). [Consult your medical professional]
Thyrotropic Releasing Hormone/Thyrotropic Releasing Factor
Injectible (IV)
- mixing instructions: 1 ampule TRH/TRF + 4 cc bacteriostatic sterile water
-dosage: 1cc weekly or 1/2 cc weekly if very sensitive intraveinously
Nasal Spray
-mixing instructions: 1 ampule TRF/TRH + 9cc bacteriostatic sterile water in clean metered nasal spray -dosage: 1 spray each nostril, twice daily. bottle
Purchasing Information
-price ranges from US $106 to $180, shop around
-most pharmacies can get it if given enough time - comes in 4-5 ampule containers
Known Responses
-benefits: clearer thinking; occasionally brighter vision
-response time: anywhere from 2 minutes to 24 hours
-duration: 1-7 days
-accumulation: does accumulate; less and less is needed over time
-side effects: initial response occasionally can include taste of medication, desire to urinate, a sense of nausea momentarily.
[Seek professional medical help.]
GINKGO
Ginkgo biloba is one among several herbs worthy of consideration in helping restore brain function. In mostly German research with more than 50 controlled trials, ginkgo is confirmed good for memory and concentration, confusion, energy loss, tiredness, depression, dizziness, tinnitus. It reverses poor blood flow seen on EEGs and improves alpha brain activity. “French experiments show that ginkgo can actually restore the ability of brain cells to transmit and receive signals from neurotransmitters that govern brain activity”.[1] It is a strong antioxidant and good for cardiovascular function - improves blood flow to extremities. Also suggested are the antioxidant pycnogenols – pine bark/grape seed extracts – which are reputed to be very good for neuronal damage and many other symptoms of chemical poisoning – there is good research on these also. Seek help from your health professional.
