- SNFTAAS
- SUPPORT NETWORK FOR THE ALDEHYDE AND SOLVENT AFFECTED
|
|
Co-ordinator: Phillippa Martin, 48 Martins Rd, Manakau, RD 31, Levin, New Zealand Ph: (0064) 6 362 6826
Fax: (0064) 6 362 6859 martin@levin.pl.net -- http://ncchem.com/snftaas
Treasurer: Lyn Mallia, 14 Tobys Way, Waikanae 6454, NZ Ph/F: (04) 293 6876
APRIL 1999
GLUTARALDEHYDE, ALDEHYDES, SOLVENTS AND OTHER CHEMICALS PRESENT IN X-RAY, THEATRE AND STERILISING ENVIRONMENTS; DARKROOM DISEASE.
Glutaraldehyde (1,5-pentanedial OCH(CH2)CHO ) - GA was synthesised about 1908. Health concerns about formaldehyde in the 1970s led to increasing GA usage. It is widely used as a ;
hardener in X-ray developer solution, (acts on the gelatine in the film);
cold sterilant for endoscopes in hospital theatres; in dentistry and by vets; for farm housing at a 50% solution, eg chicken sheds;
biocide in cooling towers and for inhibition of corrosion-causing bacteria in off-shore oil operations, and in water reservoirs. In mines. It controls bacterial growth in metal working equipment. fixative for tissue in electron microscopy because of its preservation of fine structural detail and localisation of enzymatic activity. Glutaraldehyde inhibits enzyme activity more than formaldehyde, the inhibition increasing with time in the fixative. A fixative also in the tanning industry from the ’60s.
From the early 1970s, glutaraldehyde has been used to treat skin disorders eg (warts, herpes simplex, and hyperhidrosis - excessive sweating of the hands and feet), and used as an adhesive in dentistry. It was also used as a fixative component in the manufacture of tissue transplants (from the late ’80s), in washable wallpaper, sausage casings, cork gaskets, wet strength paper/cardboard (including food packaging) and paper towels, and in textile sizing mixtures made from PVA to waterproof materials;
preservative in pigments and fillers, and even in cosmetics and toiletries (between 1973 and 1984, 74 cosmetics were registered containing GA - hand cream, toner, cleanser, powder, conditioner etc).
inert (unspecified) ingredient of sprays. Also a chemical intermediate in the synthesis of pesticides and pharmaceuticals eg in the development of vaccines for certain allergens.
cleaner/reodorant on some aeroplanes
Commercial names include: Actisan, Aidal (sterilant), Aldecyde 28, Aldesan, Aldespray, Aldetex, Alhydex, Aqucar, Asep, Biomate, Cidex, Coldcide-25 micrpbiocide, Cronex, Derugan, Dioxopentane, DSD, Duraflo, Formula 936N, Gibson’s Formula (aircraft), Gibson’s Actisan (aircraft), Glutaral, Glutaralum, Glutarol, Glutasept, Glutex, Hospex, Ilfotec RT Developer, Industrex, Keymix Glutacide, Microcide, Nalco, Neoquat LA, Parvocide, Pentanedione, Performax, Piror Slimicide, Protectol GDA, Protosan, Relugan GT (tanning), RDIII Developer, RP X-Omat Developer, Safeguard, Sepacid GA 50, Sporicidin, Sonacide, Sterilite, Surflo, Technicide, Tegodor, Totacide 28, Ucarcide, Ucarsan, Uconex, Ultrasan, Veruca-sep, Virasan, Visco, Wavicide (sterilant), Zenicide Plus, Zexocide.
Other nomenclature: Glutardialdehyde; glutaric (di)aldehyde; Glutaral; 1,3-Diformylpropane; pentanedial; 1,5-pentanedione; potentiated acid glutaraldehyde; succin-dialdehyde.
GA is purported to have an "odour threshold" of 0.04 ppm. However, in a series of NIOSH investigations of hospitals, even though most of the air samples indicated that glutaraldehyde concentrations were at or below 0.04 ppm, workers still complained about its irritating odor. This reinforces the general caution that odour is a poor indicator of exposure or predictor of toxicity.
GA is highly soluble in water and hence in the mucous membranes of the respiratory tract, (and blood). NIOSH (USA) became concerned about GA in 1991 when questions were raised about the carcinogenic potential of acetaldehyde, malonaldehyde and formaldehyde and the mutagenicity of other low molecular weight aldehydes.
Glutaraldehyde toxicity. NIOSH data, Dec 1997, "Class: Tumorigen; Mutagen; Reproductive Effector; Primary Irritant." The draft Toxicology and Carcinogenesis Studies of Glutaraldehyde in F344/N Rats and B6C3F1 Mice (Inhalation Studies) NIEHS/NIH presented 30 Oct, 1998, states that under the 2 yr inhalation studies there was no evidence of carcinogenic activity in the mice exposed to up to 250ppb. Incidences of nonneoplastic (non-tumorous) lesions of the nose were significantly increased in rats and mice.
Antec International web site: < http://www.antecint.com/glutaral.htm > "In a Soviet study, repeated oral doses of glutaraldehyde evidently had effects on the heart, kidneys and liver. Repeated oral doses given during pregnancy to rabbits caused foetotoxicity and an increased incidence of malformations was seen at maternally toxic doses. DNA damage, mutations and some evidence of chromosome damage were found in mammalian cells in culture following treatment with glutaraldehyde. It was mutagenic in Ames bacterial assays. DNA damage was not induced in the liver cells of rats treated orally. A dominant lethal mutation assay where female rats were treated orally gave a negative result.
"TheACGIH (USA) TLV ceiling is 0.05ppm. NZ WES-STEL (Workplace Exposure Standard) 0.05ppm; UK short and long-term MEL (Maximum Exposure Limit) 0.05ppm. Both UK limits relate to personal exposure - short term limit is the concentration averaged over a 15 minute sampling time and this should never be exceeded. (Only 60 or so compounds are considered sufficiently hazardous to be given MELs). [From Photosol: "Airborne Glutaraldehyde: legislation and Measurement" May 1999.] "A MEL places a duty on the employer to reduce exposure as low as is reasonably practicable, and in any case below the MEL". They state: The independent committee of occupational health experts "could not identify a safe level of exposure where it could be certain that there would be no risk of serious health effects." (Sept 1997)
A further Chemical Hazard Alert Notice, Feb 98 states: "Because of information now available on the health effects of glutaraldehyde, the committee could no longer identify a level which is both safe and practicably achievable and the OES was withdrawn in Jan 98." [The Occupational Exposure Standard is set at a level at which there are thought to be no adverse effects.] Copies of Gluteraldehyde and You: Guidance for the Healthcare Sector are available from: HSE Books, PO Box 1999, Sudbury, Suffolk, CO10 6FS, England, ph: 01787-881165 f: 01787-313995.
GA is absorbed into the body if the vapour is breathed in. In addition, the vapour and liquid are readily absorbed through the skin. (Chemical Hazard Alert Notice, Sept 1997). For substances assigned a short-term MEL in the UK, the employer MUST:
1) never exceed the MEL
2) keep the exposure as far below it as reasonably practical
3) measure airborne concentrations (unless a formal risk assessment shows the MEL is very unlikely to be breached).
4) keep a record of individuals with work-related symptoms.
"Only about 40 compounds in the UK have been assigned MELs so this reclassification is very significant. So is reducing the limit by a factor of four. MELS are most often allocated to carcinogens and to other substances for which no ‘safe’ health threshold can be identified and for which there is no doubt about the seriousness of the effects of the exposure." (Geof Care, Managing Director, Photosol, London; personal communication, Nov, 1997). Measurement down to a few ppb is straightforward with a high performance liquid chromatograph. The measurement of airborne glutaraldehyde by high-performance liquid chromatography (HPLC) shows 3ppb may be detected with improved eluent and more robust calibration under this system. MBTH measurement of aldehydes detects non-selectively all aldehydes in the environment. The DNPH method (4.4ppb) is more sensitive than MBTH (165 ppb).
Glutaraldehyde is also a sensitiser. A sensitiser notation (SEN) for GA has also just been given.
In the USA 0.2ppm threshold limit was set by OSHA is the 1980s. In 1992, the US Court of Appeals struck down those limits on the grounds that OSHA had not done the degree of investigation that the court thought that the law required. OSHA expects its new standards to be published early 1999. (Letter from Assistant Attorney General to S Sowers and J Kenepp, Oct 1, 1998.)
From < http://www.cdc.gov/niosh/ipcs/0158.html > - International Chemical Safety Cards (WHO/IPC...): "Anyone who has shown symptoms of asthma due to this substance should never again come into contact with this substance"
The proposed WES for Australia is 0.1ppm. OSH NZ has sent out a Chemical Alert Notice for GA, stating that a level below the current 0.2ppm WES is to be considered. Andrea Eng, formerly OSH’s Senior Occupational Health Scientist, says that it is likely that this will be 0.05 ppm for NZ not 0.1ppm as first proposed. The OSH Notice states that "the fact that the WES is likely to be lowered reinforces the need for a review of processes that use glutaraldehyde to ensure that all practicable steps have indeed been taken to prevent or control exposure". If an unsafe environment is suspected, OSH or the equivalent Health and Safety Inspectors should be called in to make accurate readings of chemicals present BEFORE the environment is cleaned up (and preferably without too much warning). This is important if cases for compensation are to succeed.
LEVELS
The problem with glutaraldehyde has continued to be the fact that people have become sensitised at levels well below "safe" limits (and react subsequently to minute quantities). The only glutaraldehyde detected by Scobbie et al (1996) in all of: (a) a survey of 8 typical X-ray locations, (b) the exhaust duct of a Dupont Cronex processor, (c) made-up working strength solutions in a laboratory, (d) a created worst case scenario of a one-time problem area with room ventilation switched off, was "directly above the solution in the developer tank in the problem area where the concentration was about 0.13 ppm.... Other studies of X-ray facilities, although limited, have reported glutaraldehyde concentrations in the range 0.003-0.006 mg/m-³ (0.0009-0.002 ppm) (Leinster et al, 1993)." (OES of the time 0.2ppm).
Higher levels are detected when glutaraldehyde is used as a sterilant or bench wipe. A Scandinavian study recorded glutaraldehyde in air levels: Used as a bench wipe in a 0.5% and 3% solution < 0.04 to 0.7 ppm; During manual procedures <0.01 to 0.2 ppm; With automatic sterilisers < 0.01 to 0.06 ppm; In poorly ventilated rooms 0.04 to 0.06 ppm; In well-ventilated rooms up to 0.01 ppm.
Scobbie and Groves: "An investigation of the atmosphere above an activated sterilising solution suggests that the concentation of up to 2 ppm glutaraldehyde can be formed."
In a 1986 investigation (86-226-1769) of the use of Cidex 7® in a Pennsylvania hospital, NIOSH found breathing zone samples of from 0.1ppm to 0.4 ppm collected over a five to seven minute period. GA use was also investigated at a Denver hospital (85-257). In the radiology department glutaraldehyde solution was applied to the tables using a rag soaked with the solution. Concentrations determined by personal monitoring ranged from 2.0 ppm to about 2.8 ppm (1.98 mg/m3). In the emergency department both personal and area sampling revealed concentrations that ranged from about 1- 2.7 ppm. A West Virginia hospital (90-296-2149) found airborne glutaraldehyde exposures of 0.005 ppm - 0.08 ppm. NIOSH has also conducted investigations in hospitals in Alaska (97-0062-2662) and Montana (87-176-1826). In the Alaskan hospital no GA was detected in any of the samples taken in the X-ray processing dark room. In the Montana hospital GA was used to sterilize sigmoidoscopes; all samples revealed air borne concentrations of glutaraldehyde well below the NIOSH REL of 0.2 ppm (0.03 ppm - 0.07 ppm). The findings from the Montana investigation document the efficacy of local exhaust ventilation in maintaining glutaraldehyde concentrations below those which have been demonstrated in other hospitals.
SILVER RECOVERY - AN UNRECOGNISED SOURCE OF GLUTARALDEHYDE EXPOSURE
One possibly unique case involves a white male radiographer who was in contact with X-ray Chemistry from 1949 until 1993. In the 1950's he developed dermatitis on his hands due to Metol and other constituents in the developer in the days of 'hand processing'. In the late 1980's or early 1990's he started to have breathing problems and this was confirmed as asthma in 1992 by the University Hospital Senior Chest Consultant (who was also his employer). As Radiology Services Manager with limited contact with the clinical departments, his post carried district-wide administrative responsibilities. However, his lifelong interest was in Bulk Silver Recovery in which he was recognised as an authority and it was through this activity that he had contact with chemicals.
When he retired in 1993 he was asked by the University Asthma Research Unit to be a volunteer for the testing of drugs for asthma treatment. They jointly became convinced that he had a work related problem. All the film processors were regularly monitored and there were no problems in that area. So he started to try to establish whether the Silver Recovery facility was the cause of his illness. Ultimately he acquired information from an internal photographic company document that 7-9% of developer containing glutaraldehyde was carried over into the fixer under certain conditions. The Research Unit reluctantly agreed to a glutaraldehyde challenge test. His peak flow (PF) was 49% of predicted value at that time but the challenge was positive. He was assessed at 30% disability. (Personal communication, April 21, 1999.)
NZIMRT - MARJ GORDON MEMORIAL SEMINAR, 15 March, 1997, Palmerston North, NZ:
1) AIRBORNE CONTAMINANTS FROM X-RAY PROCESSING CHEMICALS
Mr Geof Care, Managing director of Photosol, London, questioned why people are sensitised in Xray areas when the highest recorded levels are much lower than in endoscopy units. He demonstrated that pure glutaraldehyde aerosols are formed by condensation of the vapour as it cools. Aerosols are the dispersion of a liquid or a solid in a gas and they have particles 1/1,000 to 1/1,000,000 of a micron. The eye can see the collective properties of an aerosol eg tobacco smoke. Smaller aerosols are invisible and behave as air. He used the Bristol University mass spectrometer to measure the concentration of GA over the developer, then passed fixer vapour over the top. Instantly the GA readout fell. Essex University measured the number of particles generated and showed that when sulphur dioxide was passd over GA vapour, a high number of particles were formed - again good evidence for an aerosol. Most particles were below 1 micron and were highly respirable and capable of reaching the alveoli in the bottom of the lung.
At the AEA, Harwell, GA was heated to 20-35°C to form a saturated vapour concentration, and humidified air and SO² injected in in a controlled manner. The initial concentration of particles increased rapidly whatever the carrier gas used, then the concentration reduced as the carrier gas swept away the GA, the available vapour was reduced and cooling set in - a classic condensation aerosol. (A different pattern would have been produced had SO² been reacting to the GA).
Thus the aerosol contains droplets of pure glutaraldehyde. Sticky deposits were noticed on the walls of the equipment before it reached the counter so the apparatus was made shorter and there was an enormous increase in the number of particles regardless of the carrier gas. SO² gave particles of about 2 microns, and the mixture of humidified air and SO² gave 4 microns. Anything over 1 micron settles out quite rapidly. Significant levels of aerosols were obtained over the whole temperature range therefore these aerosols are viable in a hospital environment. Any of the chemicals may potentially appear as constituents of aerosols formed above the developer for instance acetic acid was demonstrated although it is probably not nearly as significant as the GA aerosol.
In 1988 a mass spectrometer in an Xray dept picked up nothing until a radiographer walked past. For 4 minutes the concentration of GA on the film (and on her hands) was tremendous and that was highest single exposure measured. In 1980/81 Dr Robert Zach and Dr A Fisher in the States, had already confirmed the presence of contact dermatitis and sensitisation to GA from handling film, and suspected asthma was a consequence.
In 1995, Dr Sherwood Burge mentioned a secretary with no previous health problems employed in Birmingham Hospital admin, well away from Xray processing. After 6 months she developed asthma and challenge tests showed GA to be the cause. The culprit? Stacks of freshly processed film placed on the desk beside her. The cooling film with a fairly reactive surface may be acting as a condensing medium (this may be the same concentrating-up process as cigarette smoke on clothing ) so the work environment may be ‘taken home’. Film driers at approx 55°C may make the process even more volatile.
SKIN EXPOSURE LINKED TO RESPIRATORY SENSITISATION -
THE ISOCYANATE CONNECTION:
Photosol’s latest research at AEA Technology in Harwell, is to look at potential unreacted GA on the surface of X-ray film as an unrecognised source of exposure. This may tie in with isocyanate research: "Work on isocyanates is some years ahead but the conundrum of how respiratory sensitisation could occur when measured air concentrations are so low is central also to isocyanate research. Legislators have driven down permissable airborne concentrations to a few parts per billion. (In Britain the MEL for GA is proposed at 50ppb; isocyanates have a MEL of 12 ppb.) But sensitization still occurs." In a paper called
A Holistic Approach to Isocyanate Exposure Monitoring, Tom Klingner links skin exposure to respiratory sensitisation suggesting that by focusing on airborne induced asthmatic response, we have worsened immune sensitisation via dermal exposure and we may be eliminating a natural homeopathic exposure that protects. (Source of paper unknown.)
Several papers have been published which indicate respiratory sensitivity to isocyanates may be related to previous dermal exposure including: *Kimber I. The role of the skin in development of chemical respiratory hypersensitivity. Toxicology Letters. 1996, 86, 89-92.
*Bickis U, Nakatsu K. A single skin dontact with toluene diiocyanate (TDI) causes a one-year persistance of airway sensitisation, demonstrable in vivo and in vitro. Am Hyg Conf and Exposition 1996, No 310.
X-ray chemicals and/or fumes also contain;
-acetic acid, one of the main airborne contaminants at concentrations of about 0.1ppm in typical X-ray film processing environments. In the simulated ‘worst-case conditions’ (see Scobbie et al, 1996 above), acetic acid was detected at 0.46ppm. [The British OES is 10 ppm for an 8hr time-weighted average (HSE, 1995). The NZ TLV is 10ppm. TLV - Threshold Limit Values - refers to airborne concentrations of substances under which it is believed that nearly all workers may be repeatedly exposed day after day without adverse effect. TLV is a ceiling limit which should not be exceeded.] Health effects: irritating vapour to eyes, nose, throat, lungs; inhalation of concentrated vapour may cause chronic inflammation of the lining membranes of the nose, throat and bronchi; contact may cause severe damage to the eyes and skin. Prolonged exposure may cause erosion of the front teeth and darkening (M A Gordon/ACC 1990); experimental, reproductive and mutagenic effects (Sax/Lewis 1989)
-sulphur dioxide, the second main airborne contaminant from Scobbie et al at concentrations of about 0.1ppm. [TLV 2ppm. 0.1 ppm is equivalent to 1/20th of the OES of 2 ppm as an 8 hr time- weighted average (HSE, 1995).] Detected in the simulated worse case conditions at around 0.5 ppm and in the exhaust duct at around 0.8 ppm. Health Effects: Particularly irritating to mucous membranes of URT; chronic effects include rhinitis, dry throat and cough. Conjunctivitis, corneal burns, corneal opacity from direct contact. Systemic effects from moderate exposure include bronchoconstriction with increased pulmonary resistance, high pitched rales, though bronchoconstriction may be asymptomatic. Chronic exposure may result in nasopharyngitis, fatigue, altered sense of smell and chronic bronchitis symptoms. Slight tolerance and general acclimatisation are common. Sensitisation in a few individuals may develop following repeated exposures. The effects on pulmonary function are increased in the presence of respirable particles.
"In guinea pigs, short-term exposure to the ubiquitous air pollutant sulfur dioxide, even at levels below national ambient air quality standards, augments subsequent allergic sensitization of the airways (Reidel 1988). Under the microscope, the bronchi (large airways) in sulphur dioxide exposed guinea pigs appear inflamed and thus may be more permeable, facilitating access of antigens to the immune system..."
Scobbie et al: " Survey in a problem area: Although these concentrations are well within the respective OESs, the investigating team found the conditions in this processing area considerably more uncomfortable ... Concentrations of [sulphur dioxide and acetic acid] in the headspace above the fixer were much higher than in the general room environment. This indicates higher short-term exposures... might occur if operators were directly involved in handling the solutions" (p 429). The concentration of sulphur dioxide and acetic acid in the exhaust duct and problem area "suggests the possibility of localised elevated concentrations in the absence of an exhaust duct" (p 430).
X-Ray chemicals which are involatile in solution (although may be present in fumes/aerosols) include:
- a glycol solvent, type of alcohol. Diethylene glycol (2,2’-Oxydiethanol) - mostly used, poisonous by inhalation, moderately toxic by ingestion, eye and skin irritant or monoethylene glycol (antifreeze). Monopropylene glycol which has much lower toxicity is increasingly used eg by Photosol. Photosol fume surveys occasionally find some glycols. Scobbie et al found <0.05 ppm in the simulated problem location and <0.06ppm in the exhaust duct. UK long term exposure limit (OES) is 23 ppm. Glycols may attack liver, kidneys, central nervous system. Metabolises to oxalic acid in the body. From Terra Nova, 22 Jan, 98: French concerns about ethylene glycols producing malformation of the embryo and foetus during pregnancy and increasing risk of congenital malformation in children whose mothers were exposed to glycol ethers in the workplace during pregnancy, have resulted in a ban on the use of glycol ethers in made-up medicine (eg for acne) and cosmetics. The French consumer magazine has denounced the fact that the dangerous solvents are still on sale in window cleaners, detergents, oven cleaners, glues, pesticides and cosmetics.
-hydroquinone, a benzene derivative; the dust is a skin sensitiser. An active allergen; human poison by ingestion, and suspected carcinogen. "The ingestion of one gram by an adult may induce tinnitus, nausea, dizziness, a sensation of suffocation, an increased rate of respiration, vomiting, pallor, muscular twitchings, headache, dyspnea, cyanosis...." (Irving Sax). Hydroquinone in aqueous solution may take longer to manifest an allergic skin reaction but this is still possible if there is a predisposition to allergies. (Lila C.Albin, Ph.D., Dept. REM, Purdue University). Photosol have developed a hydroquinone-free Xray developer.
-5-nitroindazole, a benzene-derived irritant; irritating to eyes, respiratory system and skin (James Robinson Ltd, MSDS, 1996), and mutagen (National Toxicology Group, 1996), developed by the US Military, present in very small quantities, not much info available.
- potassium/sodium hydroxide, caustic and corrosive.
-potassium/sodium metabisulphite, potential sensitiser.
-phenidone, dust irritating to eyes, skin, respiratory system - (Gordon/ACC). A poison by ingestion - Sax N, Lewis R Dangerous Properties of Industrial Materials 7th Edition, NY, Van Nostrand Reinhold, 1989. Long term effects unknown.
-sulphuric acid
-alumimium sulphate
-ammonium/sodium thiosulphate, heated can give off toxic fumes of sulphurous oxides (interestingly, two Canadian radiographers recently skin tested positive to goldsodium thiosulphate).
Chemicals potentially in Xray fumes/aerososols include:
-toluene. "Freshly prepared developer solutions reveal toluene [a benzene-derived solvent] as a major volatile constituent accompanied by traces of glutaraldehyde and butyraldehyde. As the solutions aged over a period of 13 days, butyraldehyde [a severe irritant] emerged as the most prominent volatile component." Toluene: Acute exposure effects: stomach pains, vomiting, diarrhoea, dizziness and headaches, loss of consciousness. Irritating to eyes and skin, nose and throat, respiratory tract and other mucous membranes. Repeated contact may result in defatting of skin and dermatitis. Long term effects: central nervous system depression, permanent brain damage - reduced memory, blurred vision, loss of concentration, tingling of limbs, irritability, depression, reproductive effects in women eg increased spontaneous abortions, and in men, risk of cancer in all organs. Toluene and benzene probably result from chemical impurities - (G Care, personal communication).
-benzene: - environmental pollutant with a huge range of uses; causes a variety of blood diseases and cancers; genetic mutations in mice; causes leukemia; unavoidable component of tobacco smoke and gasoline (NIEHS, Jan 9, 1997). Benzene was detected as a major component above Type B brand chemicals in the headspace above the developer at one survey location at a similar level to the toluene and butyraldehyde detected (Scobbie, 1996)
-butyraldehyde/butanal: uses - synthetic almond flavouring in food; manufacture of rubber accelerators; synthetic resins; solvents; plasticizers. Some mutagenic data. (NIEHS, 11 Feb, 1998). "Butyraldehyde, a severe irritant, was detected at low concentrations in the exhaust duct and also as a main component above the developer solutions. The laboratory studies showed that butyraldehyde becomes a more significant component of the headspace as the solutions aged and could indicate a higher potential for exposure to this aldehyde when handling waste developer solutions." (Scobbie et al, 1996, p 433). ). "Substantially higher concentrations of sulphur dioxide and acetic acid are present above the chemical solutions themselves and it was only directly above the developer that glutaraldehyde and butyraldehyde were detectable. It is likely that hand-mixing of chemicals, as was frequent in the past, could give rise to relatively high concentrations of these substances during the short time required for dispensing and dilution with water. The spent developer appears to be enriched in butyraldehyde but not enough is known about the health effects of this material to be able to judge its effect." (p 434).
-ammonia (from spill mixes) is intensely irritating to mucous membranes, corrosive burns of skin; systemic effects from mild to moderate exposure are headache, salivation, burning of throat, loss of sense of smell, perspiration, nausea, vomiting. Scobbie et al detected <0.6 ppm in a simulated problem area and up to 1.45ppm in an exhaust duct (OES 25 ppm).
-formaldehyde may be present in the darkroom/radiology suite especially from wood composite particle board, and new furnishings eg carpet, curtains etc. (See pp 12 and 13). Scobbie detected between 0.004 - 0.01ppm in 6 survey locations. "These concentrations are typical of those found in most work environments" (p 428). MEL 2 ppm.
-hydrogen sulphide (highly poisonous, smells like rotten eggs; with long term exposure the nose becomes insensitive. Unusual for it to be present - from decomposing matter in drains, sulphiding silver recovery units or decomposed fixer. (The silver itself is very irritating and can cause chronic bronchitis, kidney damage, and hardening of the arteries over a long period of exposure.)
Scobbie et al also detected trace levels of some phthalates, phenols and alkyl benzenes at survey locations. "...there can be no absolute certainty that film processing was the source" (p 428). Other trace chemicals analysed included propanol, methoxyethanol, ethoxyethanol, butoxyethanol, dihydrofuran, methylpentanone, pyridine etc.
For further chemical information, see Gordon/Laird Guidance Notes, 1990 (ACC) and Photosol’s Fumes from X-Ray Chemistry (Feb 1995) from which much of the above comes. The idea that more glutaraldehyde was added to Xray chemicals during the 1980’s because of the silver crisis may be incorrect.)
GLUTARALDEHYDE IN THEATRE AND STERILISING ENVIRONMENTS
(1) COMPONENTS OF GLUTARALDEHYDE-BASED STERILISING SOLUTIONS
Scobbie and Groves found monomeric glutaraldehyde (ie the basic molecule) as the main component of the vapour above all the brands of activated sterilising solutions and suggested concentrations of up to 2 ppm can be formed. Also found in significant amounts were methanol (SEE UNDER FORMALDEHYDE p 11) and butyraldehyde (SEE X-RAY SECTION p 8). GA is supplied to biocide manufacturers with a small amount of methanol added to prevent polymerisation. Other possible impurities were acrolein, glutaric acid, glutaraldoxime, and polymers of glutaraldehyde.
Analysis of commercial brands of GA at 20ºC indicated methanol as the main constituent of the vapour in the first 10 minutes but GA becomes the main component after this. Cidex Long-Life, Asep and Asep Extra-Life showed no significant difference between the vapour phase of the activated and unactivated forms.
CIDEX: But when the activator was added to Cidex, the proportion of butyraldehyde and GA significantly increased from 0.7ppm to 2ppm. Increasing the temperature from 15ºC to 35ºC increased the methanol given off Cidex, and increased ten-fold the amount of butyraldehyde given off.
OCCUPATIONAL SYMPTOMS IN ENDOSCOPY NURSES EXPOSED TO GLUTARALDEHYDE AND LATEX
NZIMRT - MARJ GORDON MEMORIAL SEMINAR, 15 March, 1997, Palmerston North, NZ:
Dr Aashish Vyas, Research Fellow, North West Lung Centre, Manchester, England:
Seminar presentation 15 March, 1997.
The first half of a rigorous GA study begun by Dr Aashish Vyas, and funded by the European Union and Union Carbide, has been completed and presented to the EU and to the ACGIH. The study attempted to find out if there was a no-effect level for glutaraldehyde. 358 endoscopy nurses in 59 units were studied with: a questionnaire (occular, nasal, and LRT symptoms: cough, wheeze, shortness of breath, tight chestiness, phlegm produced); skin pricks to allergens and latex, respiratory function tests with 2 hourly diaries for 4 weeks; and peak and background levels of GA were sampled using the more selective and sensitive DNPH method (with analysis by high-performance liquid chromatography - HPLC) rather than the usual static head-height levels.
Only nurses whose symptoms worsened during the week and improved at the weekends were included (so those who only improved on holiday were not). 340 nurses were still employed and 310 (91%) had exposure to GA. Almost 70% of the still-employed group had respiratory tract symptoms (whether work or non-work-related). Non-work-related symptoms were greater. Nasal and lower respiratory tract symptoms were most common. Of the 310 GA exposed workers, 20% had work-related nasal symptoms, 13.2% work-related occular symptoms, and 9% work-related lower respiratory symptoms. ppFEVI’s for the GA-exposed were significantly smaller than for the group who had had no GA exposure. Peak flow diaries of those with lower respiratory tract symptoms did not show more than 10% variation therefore formed no evidence of asthma. Only one worker’s blood sample was positive for GA IgE antibodies. There was really no correlation between symptoms and immunological profiles but GA is a low molecular weight compound and should not have its main effect by an IgE mediated pathway. 13 had positive latex skin prick tests. (Latex presents sensitisation risks from the latex itself and from the usually-cornstarch powder lubricant).
18/26 of the ex-employee group were tracked to avoid the problem of dealing with a survivor population. 12/18 had left because of work-related LRT symptoms and were still getting symptoms 3 months later. 10 continued to suffer work-related symptoms even though employed in other parts of the hospital. 9/12 of this group had taken at least 6 months to develop symptoms and many worked for some years before developing symptoms. This was a similar pattern to the current employees and suggested an immunological reaction was taking place, but again there was almost no correlation between symptoms and immunological profiles. An immunological basis for GA induced effects could still be present.
The mean measured peak GA concentration was 0.037 mg/m³ (highest 1.08mg/m³). The mean background concentration was 0.011 mg/m³ (highest 0.15 mg/m³). [The OES was 0.7 mg.m³]. ie most didn’t exceed quarter of the limit. Studies done prior to the 1990s often over- or under-estimate GA levels.
Found 3 spillage sites; one with 0.4 mg/m³ reading - a high degree of unawareness of spillage dangers. 66.5% of units use fully automated units. 33.5% use partially automated units. 87% have decontaminating unit ventilation. 67% have room ventilation. They found a significant association between room ventilation combined with decontaminating unit ventilation, and decreased level of GA exposure. Both ventilations are important. Only nasal symptoms were related to the concentration of GA in the air.
They could not find a level of glutaraldehyde below which symptoms were not encountered. This may be because there are "other symptom-causing chemicals and irritants in the environment" or individuals may have been exposed to spillages and "sensitised by the high exposure to glutaraldehyde [with] on-going symptoms occur[ing] at very low levels and chronic exposure." The ex-employees continue to suffer symptoms despite having been taken out of the environment. They are still in nursing and may have indirect exposure to levels of glutaraldehyde which are quite low and thus their symptoms are recurring, or they may have exposure to other irritants or allergens causing their problems.
Other chemicals could include: latex gloves causing hypersensitivity in 4% (and latex, another major allergen may be involved in cross-reactivity with GA as well as formaldehyde. Sherwood Burge in 1980 postulated this might be the case because GA is a very good cross-linking agent and may cause symptoms which may be augmented by formaldehyde or latex); formalin; and ventilation systems not well-maintained which are extremely prone to Sick Building Syndrome (from formaldehyde and VOCs - volatile organic compounds), especially in new units.
Current employees and others presented to the British Heart/Lung Foundation in London presented with work-related LRT symptoms - cough or chest tightness. Peak flow diaries and methacholine challenges did not find occupational asthma. They have normal spirometry unless they come across GA in the community eg in perfumes. The cough may be related to C-Fibres in the lungs. Challenges with capsaicin (the irritative agent in capsicum) induce cough very similar to GA. The cough occurs after 5 hrs then continues for 24 hrs.
In the ex-employees, 66% had used open baths to clean scopes, and 67% had no ventilation at all, so current nurses would be expected to have fewer symptoms; not so. Perhaps there is increased reporting because of greater awareness. It is felt that glutaraldehyde is a relatively poor respiratory sensitiser probably to high concentrations only, or that aerosol production may cause sensitisation. Personal protection during high exposure procedures is a must. Nurses now use nitrile gloves or low allergen latex gloves, and organic vapour masks. Formalin is made up in pharmacy. Flexible Friends are groups of proactive endoscopy nurses and radiographers working to thrust through changes. The level of absenteeism has fallen dramatically.
***
OTHER CHEMICALS POTENTIALLY IN THEATRE AND STERILISING ENVIRONMENTS
(2) FORMALDEHYDE
(EITHER AS A FIXATIVE, STERILANT, OR COMPONENT OF SICK/TIGHT BUILDINGS)
Called HCHO, (also formalin; formal; methanal; formic aldehyde, methyl aldehyde, methylene glycol, etc. Quaternium indicates that an ingredient releases formaldehyde). Very soluble in water, alcohol and ether. Obtained industrially by oxidation of methyl alcohol in the presence of a catalyst eg copper or silver. Paraformaldehyde is obtained by concentrating aqueous solutions of formaldehyde. Formalin/formal contains 37-50% formaldehyde by weight, plus water and methanol.
LEVELS:
UK: OES 2 ppm NZ: TLV is 2 ppm;
USA: ACGIH: TLV is 1 ppm 8 hours/day, 5 days /wk. TWA 1 ppm, STEL 2 ppm, with a notice of intent to change to a Ceiling Limit of 0.3 ppm. All under review - Canada in 1989 recommended a target level of 0.05 ppm.
Breathing zone samples in a 1983 med student anatomy class found 44% were in excess of 1 ppm. A 1993 study of med students found a mean level of 0.73 ppm. Histology technicians in Finland were exposed to short-term exposures of 0.01-7 ppm, with a mean of 0.45 ppm (1994). [All reported in Weaver. ]
FORMALDEHYDE EFFECTS
Skin reactions: ...chemical can be both irritating and allergy-causing...(EPA). A slight sensation of tiny insects crawling over the eyes, nose and pharynx (formication) is felt at 2-3 ppm. (Zurlo N, via OSH, NZ.) Contact with the vapour or solution causes skin to become white, rough, hard and anaesthetic due to superficial coagulation necrosis. With long exposure, dermatitis and hypersensitivity frequently result. Prolonged exposure may also cause cracking of skin and ulceration, especially around the fingernails.
Inhalation of HCHO vapours produces irritation to the eyes, nose and throat and frequently results in upper respiratory tract irritation, coughing and bronchitis. Asthma may occur in sensitive individuals. Exposure may cause headache, dizziness, difficulty breathing and pulmonary edema. Acute effects include conjunctival and URT irritation from exposure to 0.1 ppm-5 ppm. Severe exposure to fumes may lead to chemical pneumonia. (EPA www.epa.gov/ ). Peak expiratory flow rates in med students decreased slightly over a 10 week anatomy course, a trend which reversed after the course finished. But studies of routinely exposed workers, controls, and asthmatics using controlled chamber challenges have frequently failed to show pulmonary changes. However most patients tested for formaldehyde asthma do not react to specific challenge or have demonstrable antibodies present. Inhalation of 10-20 ppm can lead to lower respiratory tract irritation manifested by cough, chest tightness, and tachycardia. Human systemic effects by inhalation.
After ingestion, degenerative changes may be found in the liver, kidneys, heart and brain. Experimental poison by ingestion, skin contact, inhalation, intravenous, intraperitoneal and subcutaneous routes. Human poison by ingestion. A woman drinking 120 mls of formaldehyde died 28½ hrs later - blood analysis showed that sufficient formaldehyde metabolised rapidly to formic acid (large amounts within half an hour distributing to about 70% of body water) to cause metabolic acidosis.
HCHO is involved in DNA damage and inhibits its repair. HCHO is a suspected human carcinogen and has been shown to produce mutations and abnormal organisms in bacterial studies" - (EPA). Carcinogen - (Dorland’s Medical Dictionary). An experimental carcinogen, tumorigen and teratogen. Experimental reproductive effects. The chemical has been linked to menstrual disorders and pregnancy problems in women exposed to high levels in nail salons (EPA). A study of lab workers in Finland found a significant association between formalin exposure and spontaneous abortion.
Neurotoxin (see also Formaldehyde Neurotoxicity p 29.) A good reference: Lezak M. Neuropsychological Assessment, 1995, Chap 7).
Other symptoms of sensitivity to formaldehyde, including muscle and joint pain, fatigue, and cross reactivity to other chemicals are similar to those listed for glutaraldehyde p 21. Excessive thirst is noted in The Jeremiah Project literature. John Bower, Director, Healthy House Institute, Bloomington, Indiana: In a new study, March 1999: "One of the most insidious problems with formaldehyde is its ability to sensitise people to other pollutants."
FORMALDEHYDE USE
Formaldehyde is a powerful antiseptic, germicide, fungicide, and preservative. The main problem products for formaldehyde emissions are urea-formaldehyde foam insulation in walls and ceilings, and the urea-formaldehyde resins (used as adhesive/glues) to make particle board, medium density fibreboard, and hardboard plywood used in flooring, kitchen/bathroom cabinets, panelling and furniture, melamine decorative laminate and polyacetyl resins. U-F resins are unstable and may release free formaldehyde trapped in the resin and/or formaldehyde from decomposition of the resin polymer itself. Most formaldehyde is released in the first 6 months, but significant release can be expected as the resin undergoes decomposition for a further indefinite period, contributing to sick-building syndrome. Increase in temperature and humidity greatly increases formaldehyde emissions. All exposed surfaces [including edges] must be sealed with paint, polyurethane, or varnish or covered with carpet, vinyl, or tiles etc. "Formaldehyde makes up 50% of the estimated total aldehydes in polluted air". In 1998 formaldehyde ranked tenth in organic chemical production in the USA . Formaldehyde demand is estimated to grow from 9.3 billion pounds to 9.6 billion pounds in 2002 - (Battelle Study, 1999).
"Formaldehyde is probably the top indoor air quality troublemaker" - Thomas J Kelly, chemist, Battelle Memorial Institute, Ohio and author of the new study (Jan, 1999, Envir Science and Technology journal). The study chamber-tested 55 household products, each for 24 hrs. By far the highest omitter was an acid-cured wood floor finish. Fingernail polish and hardener were very high as was new latex paint and floor polish. Among ‘dry’ products, permanent press items eg shirts and linen gave off surprisingly high amounts. The urea-particle board did not meet the voluntary industry standard.
SNFTAAS Network members’ own sensitising exposures to formaldehyde include nursing, lab work, the tanning industry, wood-working jobs, "sick/tight buildings" because of off-gassing from unsealed particle board/composite/ reconstituted/ MDF/ fibreboard/plywood type products, and board-making plants.
ALDEHYDES (mainly formaldehyde) appear/are used in:
Particle/fibreboard (in the resins). Urea-, phenol-, and melamine-formaldehyde resins.
In the manufacture of organic chemicals eg Pentaerythritol, Hexamethylenetetramine and 1,4-Butanediol.
Moulded plastics/thermoplastics. Cellulose esters.
From the incomplete combustion of hydrocarbons: factory emissions (eg triboard mills);
fumes from petrol, diesel, cigarette smoke; asphalt. Burning heating fuels. (Wood smoke emissions also contain particulate matter that contributes to the high rates of asthma in children.)
Pesticides as an inert ingredient (these ingredients do not have to be specified), rodent poison. As a germicide and fungicide for vegetables and other plants; to prevent mildew and spelt in wheat and rot in oats for animal feeds. Maple syrup (from use in tapholes).
Laboratories as a fixative for preservation of specimens/tissue samples.
Photography for hardening gelatin plates and papers, print flatting solution, hypo test solution, hardeners and toners.
Printing - etching materials.for chrome printing and developing.
Paper and cardboard to improve wet strength; carbonless paper, wall paper.
Fabric sizing resins for crease resistant clothes (it makes fibres wrinkle resistant, water resistant, dye fast, flame resistant, shrink proof, moth proof and more elastic); - rayon, rayon-acetate blends, "wash and wear" cotton, shrinkproof wool, polyester blends, artificial silk. Fabric conditioners, softeners. Bed linen.
New carpet, thermal drapes, furnishings, artificial silk, the dye industry for mordanting and improving fastness of dyes.
Perfumes (eg amylcinnamaldehyde, hexylcinnamaldehyde and many others - perfumes are advertised as "If you like the smell of freshly laundered clothes you are sure to enjoy the clean smelling fragrances based on aldehydes. Aldehydes are about sparkle and radiance. ...Check out washing powders...furniture polishes, musk products. Find something familiar in White Linen (Estee Lauder), Chanel No 5, Arpege (Lanvin) or Jovan musk" - [NZ Hair and Beauty]. Fragrances are a major source of poor indoor air quality.
As a preservative/disinfectant in cosmetics - deodorants, toothpaste, anti-septic mouth washes, toothpaste, germicidal soaps, foot powders, shampoos, mousse, conditioner, bubble bath, (Bronopol, Germall 115, Dowicil, Quaternium).
Nail polish, and nail hardener as a resin.
Multiple house cleaning products - detergents, rinse aid, pre-wash stain remover, starch, toilet cleaners; mildew/mould proofing.
Water based paint, paint stripper, finger paints, tempora paint, modelling clay, glues, paste, gum and adhesives eg in footwear; car, floor and shoe polish.
Preserving and coagulating rubber latex. Contraceptives. Vinyl gloves.
Some vaccinations eg pertussis, ’flu vaccination; synthesis of vitamin A, manufacture of antibiotics; chelating agents, wart paint.
Air conditioning units, air fresheners, fumigating to destroy insects etc.
Embalming.
Tanning - especially white or pastel shades.
Slow-release fertilisers, urea, thiourea; for sterilising soils.
The dairy industry for casein, (it is used to render casein, albumin, and gelatin insoluble); farming - as a hoof hardener.
Metal casting (to harden wood to make moulds), cutting oils, corrosion inhibitors in oil drilling muds etc, concrete, plaster, cement, firelighters, match heads, explosives. Glass mirrors.
(From ACGIH 1991, NZ Ministry of Health and miscellaneous others.)
Composite resin replacing amalgam fillings. Root canal fillings, and denture base material release HCHO as do the endodontic [inside the tooth] sealers, AH26 and N2. AH26 has high toxicity after mixing which decreases after several days; N2 releases 1000x more - (Spangberg L et al, J Endo 1993, 19, 596).
Methanol (wood alcohol, methyl alcohol) is a common household solvent used in perfume, windscreen washing liquid, duplicating fluid, antifreeze, shellac, paint remover. It is also added to commercial glutaraldehyde for shipping. Methanol occurs naturally in fruit and vegetables along with ethanol (alcohol). Methanol metabolises in the body to formaldehyde, then to formic acid, and then to substances which can be eliminated - including carbon dioxide and water.
The oxidation products of METHANOL / METHYL ALCOHOL [ie methanol > formaldehyde > formic acid] may induce severe acidosis. The amount causing severe effects varies with the individual especially if ethyl alcohol (ethanol) is consumed at the same time. The two compounds share the same degrading enzyme, alcohol dehydrogenase, and competition from ethanol slows the production of the more toxic products of metabolism - ie formaldehyde and formic acid. Oxidation and excretion of methanol is slow; toxic symptoms do not develop for 12-48 hrs. Symptoms involve the visual apparatus (severe degenerative changes occur within the ganglion cells of the retina; the toxicity of methanol appears to relate directly to formic acid), the CNS, and the gastrointestinal and respiratory tracts. Clinical toxicity relates to acidosis as well as the effects of accumulation of toxic products: nausea, vomiting, generalised weakness, severe abdominal pain, vertigo, headache. Symptoms similar to ethyl alcoholism appear: restlessness, incoordination... confusion and memory defects are common. [Paper available:
CIIN 0024-GOET-85-014]. The half life of HCHO in rabbits etc is estimated to be one minute. Inhaling the fumes of methanol can cause headache, eye irritation, dizziness, visual disturbances and nausea. It damages the liver, heart, kidneys, and lungs.
ASPARTAME artificial sweeteners (Monsanto’s NutraSweet/Equal/Spoonful etc) are highly controversial. Aspartame: L-Aspartyl-l-phenylalanine methyl ester, 98%, aspartame
CAS #22839-47-0
is composed of (at least) three things:
1.) aspartic acid, (around 40%) CAS # 56-84-8
2.) phenylalanine, (around 50%) CAS # 63-91-2
3.) methanol (wood alcohol) (10%) CAS # 67-56-1
A school science report looked at breakdown products of diet coke in different storage conditions: The level of aspartame in a can of Diet Coke was found to be 0.06% by a food testing laboratory. The remaining cans from one case of Diet coke were stored under three different heat conditions for 10 weeks. Seven cans were stored in an incubator (104° F), seven cans were stored at room temperature (68-70°F), others in refrigerator. At the end of 70 days samples were tested for levels of aspartame, formaldehyde and DKP (diketopiperazine).
Refrigerated sample: 0.058% aspartame, 0.00% DKP, 53.5 parts per billion of formaldehyde.
Room temperature sample: 0.05% aspartame, 0.002% DKP, 231 ppb formaldehyde.
Incubator sample: 0.026% aspartame, 0.010% DKP 76.2 ppb formaldehyde.
(Less methanol would result from 1½c of diet soft drink than 1c of fruit juice. However fruit juice does also contain ethanol.)
Individuals with the genetic disease phenylketonuria (PKU) cannot properly utilise the amino acid phenylalanine, hence the warning on the product’s label. Anti-aspartame groups relate symptoms of multiple schlerosis, SLE, fibromyalgia, coma and death etc to aspartame.
The FDA in the USA has just approved aspartame sweeteners for use in heated products - ie that they are able to be subjected to heat without forming breakdown products. The number of products containing aspartame are increasing as the price comes down eg in yoghurts (check the labels) - Chris Wheeler, Soil and Health Association of NZ, P O Box 36170, Northcote, Auckland, NZ. chris@wheeler.pl.net
(Also in NZ: Toxins Awareness Group (NZ) TAG, P O Box 99315, Newmarket, Auckland.)
Links to Aspartame sites: http://www.holisticmed.com/aspartame - http://www.dorway.com
For very good comments on the controversy, see http://urbanlegends.miningco.com
STEVIA is a natural plant-based alternative sweetener.
OTHER NOTES
*Swiss furniture dealers usually sell only furniture that is formaldehyde-free or with very low content. Some manufacturers have prohibited the use of formaldehyde. (Swiss Embassy, 5 Jan 1999)
*Ambient air in downtown Atlanta, Georgia was measured in 1992 with average concentrations of 2.7-3.0 ppb (highest 8.3ppb) for formaldehyde and 2.6-3.2 ppb (highest 8.4 ppb) for acetaldehyde - Grosjean E et al, 1993.
*Recent research has determined that household plants do not substantially reduce formaldehyde form indoor air. (CIIN - Our Toxic Times. February, 1999). [But they look good].
*MTBE (Methyl Tertiary Butyl Ether) was added to gasoline in 1992 to reduce Carbon Monoxide emissions. Evidence is that MTBE is without identifiable benefit. When inhaled it converts to formaldehyde in the body. It also increases exhaust emissions of formaldehyde. (Pollution by Gasoline Containing Hazardous Methyl Tertiary Butyl Ether (MTBE), Archives Envir Health. July/Aug 1998).
*Carbonless paper: MSDS for Mead's NCR paper - latex based adhesive with proplyene glycol, solvents, 68% water, balsam fragance. The solvents include: ethanol, methanol, ethyl acetate, methyl isobutyl ketone, and heptane. The ink is encapsulated in chlorinated paraphenic hydrocarbon product. "Researchers at the University of Florida have recently analyzed CCP (NCR paper) and found small amounts of toluene diisocyanate. Formaldehyde is also in CCP. Phenolic resins, fungicides and dye compunds (phthalide/ fluoran/indole dyes) are listed as non-proprietary ingredients. In nine years of performing building investigations, I have never seen such a high percentage of office workers so severely affected as when CCP was responsible for their many symptoms." (Steven Temes < AirwaysEnv@compuserve.com >1 Apr 1999.)
FORMALDEHYDE - THE CANCER DEBATE: Epidemiological studies suggest formaldehyde causes cancer, especially throat cancer. "In 1980 the Chemical Industry Institute of Toxicology laid out a text-book strategy to counter the negative findings of a study that showed that rats inhaling formaldehyde got cancer. The strategy was as follows:
1) Claim that rats aren’t the right animals to study because they breathe through the nose, never through the mouth.
2) Claim that the exposure levels were unrealistically high (even if they were scientifically too low).
3) Pay for new studies that will produce different results.
4) Hire academic researchers to give ‘independant’ testimonials to the safety of formaldehyde and to put a positive spin on any studies that show cancer in rats.
5 Attack any scientist who says formaldehyde is dangerous.
6) Move aggressively to fund universities and other research institutions to steer research in directions that play down formaldehydes’s dangers.
In A Brief Overview of MCS, Cynthia Wilson of CIIN says: "...in 1981, in response to the poisoning of thousands of people by urea formaldehyde foam insulation, the NRC commissioned a study called Formaldehyde and Other Aldehydes. The report estimated that 10-20% of the population was at risk from low level exposure to aldehydes. Though the report’s major focus was on the cancer risk, it did recommend an extensive study be done on chemical sensitivities. Nothing was done...."
Research at the University of North Carolina, into the carcinogenic effects of aldehydes and the aldehyde precursors, dichloromethane and methyl t-butyl ether is on-going - Henry d’A Heck, Univ of Nth Carolina.
FORMALDEHYDE AND BENZENE IN THE ENVIRONMENT
("CARCINOGENS EVERYWHERE" - Rachel’s Environment and Health Weekly)
U.S. EPA published a report in 1998 saying that 100% of the outdoor air in the continental U.S. is contaminated with eight cancer-causing industrial chemicals at levels that exceed EPA's "benchmark" safety standards. Using 1990 data on toxic industrial emissions, EPA applied mathematical models to estimate year-round average outdoor air concentrations for 148 industrial poisons.
For each of the 148 toxicants, EPA established a "benchmark" level that the agency considers safe. Eight of the 148 industrial poisons exceed EPA's benchmark safety levels all of the time in all the nation's 60,803 census tract areas. All eight are carcinogens; that is, they are known to cause cancer: bis(2-ethylhexyl) phthalate; benzene; carbon tetrachloride; chloroform; ethylene dibromide; ethylene dichloride; formaldehyde; and methyl chloride.
EPA believes that being inside your home or workplace does not protect you from constant exposure to these eight carcinogens. EPA said its mathematical models probably underestimate the true
levels to which the population is exposed. Where actual measurements of toxic contaminants were available, EPA found that the measured levels exceeded the levels estimated by their mathematical models.
In its report, EPA also acknowledged that it may have underestimated the health effects because of multiplier effects since people experience all of them simultaneously. The agency also acknowledged that many of the chemicals have no "benchmark" standards for some effects eg benzene and 1,3-butadiene have both been associated with reproductive and developmental effects but have no benchmarks, so those effects were ignored in this study.
And finally, most (if not all) individuals are exposed to far more than just eight industrial poisons: add in automobile and truck exhaust, second-hand cigarette smoke, prescription drugs, emissions from power plants, smelters, incinerators, and so on.
Ozone in the stratosphere shields the earth from UV light. Ground-level ozone is a harmful pollutant. 80 ppb for 8 hrs is the federal standard being phased in. Ozone is an insoluble-in-water gas which is irritating and toxic and a by-product of the reaction between car exhaust and oxygen. With ozone inhalation, the epithelium of the respiratory tract reacts with unsaturated fatty acids in the plasma membrane to form aldehydes and hydrogen peroxide. This causes the activation of epithelial cells and release of lipids and cytokines which modulate inflammatory responses - Leikauf G D Airway Epithelial Responses to Environmental Oxidative Stress, 1995 and (?)1996. Leikauf, Simpson et al state that there is still controversy over whether formaldehyde can affect the lower respiratory tract. Guinea pigs were exposed to formaldehyde or filtered air for 2 or 8 hrs. At concentrations relevant to environmental exposure (>0.03ppm), formaldehyde alters airway smooth muscle reactivity in guinea pigs through mechanisms that are shared with human airway smooth muscle tested ex vivo. These findings suggest that prolonged low-level exposures may generate abnormal responses in the airways not detectable after acute exposures. This research is on-going.
*Ozone does some damage to nasal tissue but the dose to the underlying tissues increases at the terminal bronchioles - Determinants of gas and vapour uptake in the respiratory tract, CIIT Activities 16, No 3.
*Ozone air purifiers/generators do not reduce indoor pollutants. Health effects: ENT and lung irritation. Causes significant temporary decreases in lung capacity in healthy adults. Short-term exposures can cause increased sensitivity to airborne allergens and irritants; can impair immune system. Long-term exposures to low-level ozone may lead to permanent reduction in lung capacity. (Health Hazards of Ozone -Generating Air Cleaning Devices. California Morbidity, March 1998.)
*From ENVIROS - EPA Research Project; Internet: Ozone is given off by photocopiers at levels which can increase over time [especially if you copy with the lid up and the scanning light hits the air; older and larger machines are more of a problem especially if there is no ventilation] and electrical kitchen appliances.
*From the Health Effects Institute - USA - Internet, March 1998: Diesel engines emit more oxides of nitrogen which contribute to the formation of ground-level ozone (and emit more particulate matter - potentially carcinogenic/mutagenic). The USA EPA (Environmental Protection Agency) has recently released a report which links diesel exhaust emissions to lung cancer even when exposure is too low to cause respiratory problems - concern is because of the hydrocarbons attached to soot particles in a mechanism that is analogous to that of other relatively inert particles in the lung (hs-canada-digest, Nov ’98 and < http://www.dieselnet.com >). Diesel exhaust exposure twice that found in industrialised areas can halve the production of sperm in mice - Science Univ of Tokyo, 1998.
OTHER ALDEHYDES (there are many) include:
Cinnamic aldehyde reported to be a skin irritant, sensitiser and urticariogenic agent; Acetaldehyde results in eye irritation and respiratory discomfort. (Alcohol converts to acetaldehyde via the enzyme alcohol dehydrogenase, in the body);
Acrolein (or acrylaldehyde, acetic aldehyde, acetic ethanol, ethanal, methyl formaldehyde, propenal, ethylene aldehyde, magnacide, biocide, slimicide) causes severe pulmonary irritation, lacrimation (used in WW1 as "Papite" tear gas), and tissue damage, elevated liver alkaline-phosphatase etc. (Pinnas JL, Meinke G C, Hazardous Materials Toxicology...1992, 981-985). Acrolein is very reactive. Human poison by inhalation and through skin. Human mutagenic data. Used as component of military poison gases, herbicide, algicide for water treatment, fungicide, bactericide, to modify food starch, liquid fuel... Produced in large amounts by overheated cooking oils and animal fat. A major contributor to the irritative quality of smoke and petrochemical smog. Metaldehyde is used on slugs and snails. Also a fuel for small heaters. Poisoning in children from eating it results in nausea, vomiting , fever, muscular rigidity, twitching ... convulsions, liver and kidney damage, coma, death from respiratory failure.
Peraldehyde
Aldicarb (2-methyl-2-{methylthio} propionaldehyde O-{methylcarbamoyl} oxime) is one of the most potent pesticides. (EPA)
(3) ANAESTHETICS
"Principal health concerns regarding occupational exposure to anesthetic gases are carcinogenicity, neurobehavioural effects, reproductive effects, interference of nitrous oxide with vitamin B12 metabolism [can cause neurologic abnormalities with chronic heavy exposure], and potential renal and hepatic effects."
These volatile chemicals/drugs inhaled include: ether, chloroform, ethylene, nitrous oxide, cyclopropane, halothane, enflurane, isoflurane, sevoflurane, desflurane. Occupational hazards related to waste anaesthetic gases were recognised in the 1970s and ’80s. Some are readily soluble (ie easily absorbed in solution - blood) eg halothane, enflurane, and isoflurane, or poorly soluble eg nitrous oxide. Only when blood saturation occurs does the drug begin to exert a partial pressure and have an effect; a poorly soluble drug rapidly produces effects. In people with high cardiac output there is rapid delivery of the drug to body tissues where the drug moves out of the blood across tissue membranes. Highly perfused tissues (vessel-rich groups - VRGs) include the brain, heart, kidneys which get 75% of cardiac output. Poorly perfused tissues make up 75% of body mass but get 25% of cardiac output - they have delayed uptakes of anaesthetic agents. Elimination from skeletal muscle and fat will correspondingly be a much slower process. All inhalation agents are respiratory depressants. Current theories suggest that inhalation agents interrupt neuronal activity in the central nervous system and may depress excitatory transmission or may prolong inhibitory transmission.
Professor William Rea, cardiothoracic surgeon, (and subsequently Director of the Brookhaven Environmental Control Unit, Dallas, Texas) attributes his chemical sensitivity to exposure to anaesthetics and fumes from the heart lung machine (motor exhausts and plastics) "in other words, chlorinated hydrocarbons", working in theatre Mon-Sat. He describes his symptoms: headaches gradually getting worse, periods of fatigue, a lot of muscle aches, irritable colon, sore throats all the time, recurrent sinus, flu-like symptoms until his wife said "no-one can have flu 365 days a year."
Anaesthetics used in Nelson Hospital, NZ at the time of maximum glutaraldehyde exposure included nitrous oxide, halothane, isoflurane, sevorane. Anaesthetics at Whangarei Hospital were: nitrous oxide, fluothane (halothane), isoflurane, ethane, cycloprane (very rare), CO2.
Ether, the first general anaesthetic, 1846; excessive use damages the central nervous system. Very flammable (as is cyclopropane).
Nitrous Oxide (used about 1860 on) or laughing gas also used in commercial products eg whipped cream and cooking oil sprays. It "acts to potentiate most volatile anaesthetics". Used without sufficient oxygen can cause irregular heart patterns, brain damage, headache, cerebral edema, death. "Because it is administered in high concentrations, pollution levels are much higher than for the halogenated anaesthetics...". Nitrous Oxide interferes with the formation of one of the essential bases in DNA but there are no clear answers on fetotoxicity or neurological disorders. Exposures in dental operations may be excessive and more difficult to control than in theatre, and dental workers may suffer adverse reproductive effects, decrease in mental performance, audiovisual ability, manual dexterity (NIOSH Alert, 1994). "Memory which is one of the most recently developed functions of the brain, is highly susceptible.....experimental evidence shows nitrous oxide affects the behavioural performance in concentrations as low as 50 ppm".
Chloroform 1831, was the first halogenated hydrocarbon solvent anaesthetic. It depresses respiration and acts directly on the central nervous system. (Halogens are the chemically-similar chlorine, bromine, iodine, fluorine which form salt-like compounds with sodium and most metals.) Its use has been abandoned because of dose-related toxic effects on the liver. Chloroform produces active free radicals during biotransformation by the cytochrome P-450 system. Also causes heartbeat irregularities and damage to the kidneys. Chronic low levels of chloroform may still be found in some municipal water supplies.
Halothane (Fluothane - a bronchodilator.) Used since the 1960s, probably still the most widely used in the world though isoflurane is generally used in UK and USA. Halothane is in essence halogenated ethane (enflurane and isoflurane are halogenated methyl ethyl ethers). Chronic exposure said to lead to nervous system toxicity and behavioural changes. Issues of reproductive toxicity have been more or less discounted. Renal toxicity is dose related and immunological toxicity is less clear. The main danger is hepatotoxicity (liver..). The 1974 survey by the American Society of Anesthetists found increased self-reported liver disease in male and female operating room (OR) nurses, but what was attributable to anesthetics is unknown. (Reported in Suruda, p632).
24 resident doctors were compared at work before (control) and after 3-4 hrs of halothane exposure, and after 3-4 hrs of non-halothane (thio-O²-N²O) exposure. Testing in the non-halothane group showed depression of motor skills by 5.5% and memory by 17%. Testing in the halothane group showed reduction of motor skills up to 27% and memory 45% compared to the control group. Levels of halothane were estimated up to 26ppm. (Another study showed halothane affected motor ability in concentrations as low as 0.2%. Similarly trichloroethylene and cyclopropane). "Memory is a function susceptible to even the lowest concentrations of anaesthetics." (Another study showed enflurane causes no such change.) "Halothane can be traced in the breath of anaesthetists up to 64 h after cessation of exposure." All reported in Malhotra.
Enflurane (Ethrane) is a vasodilator acting directly on smooth muscles. Extremely lipid (fat) soluble; may have prolonged action in obese individuals. Lipid soluble drugs rapidly move across tissue membranes.
Isoflurane (Forane) widely used - has a stabilising effect on the cardiovascular system. Less soluble in blood than halothane therefore recovery more rapid.
Desflurane has lower blood and body tissue solubility therefore its uptake and elimination is faster. It undergoes minimal metabolism and should have low potential for toxic effects.
Exact mechanisms for anaesthesia are not known but volatile anaesthetics have very specific actions at the molecular level with protein receptors rather than surrounding lipid membranes being principal targets. Halogenated anaesthetics depress neuromuscular function and increase the potency of neuromuscular blocking drugs in a dose dependant manner. (1994 information).
(Local anaesthetics are all related to cocaine and no two have the same effect "depending on the person’s physical make-up".)
Potential risks from the use of MMA arise from repeated exposure. Health issues include asthma, dermatitis, eye irritation including possible corneal ulceration, headache and neurological signs. Another of the low molecular weight sensitisers. Monomer fumes may be absorbed by contact lenses increasing eye irritation.
(5) ANOTHER STERILANT - ETHYLENE OXIDE.
"Acute overexposure to EtO causes conjunctival, skin, and respiratory tract irritation, including rhinitis, cough, and shortness of breath. Headache and nausea may also occur. A questionnaire survey found one or more symptoms in most sterilising operators... Reactive airways dysfunction syndrome (RADS) was reported in a railway worker following 4 days exposure from a leaking container... Several target organs may be adversely affected by chronic exposure, including the respiratory, neurologic, dermal, and hematopoietic systems... Chronic exposure resulting in peripheral neuropathy...decreased performance on neuropsychologic testingmemory loss, mild cognitive impairment...atrophy...evidence of axonal degeneration on sural nerve biopsy in one..." A 1982 Finnish study using data from a postal questionnaire and a hospital discharge register showed that in pregnant staff using ethylene oxide for sterilising procedures, frequency of spontaneous abortion was 16.7% compared with 5.6% for non-exposed pregnancies. This increase did not correlate with exposure to gluteraldehyde or formaldehyde, "although glutaraldehyde may not be absolutely safe... Similar increases were seen when one of the two agents was used in combination with other... Exposure to formaldehyde in the sterilisation units may have been minimal particularly when gas chambers are used." The most recent classification of EtO is as a carcinogen - (International Agency for Research on Cancers, 1994). If ethylene oxide is used to sterilise heat sensitive devices, they must be dry as ethylene glycol (see X-ray chemical notes) forms in combination with water. (Kay Ball, Nurse Educator, address to NZ Perioperative Nurses’ Conf, Nov 1998).
SYNERGISTIC EFFECTS - THE COCKTAIL
Many of the Xray and theatre chemicals are individually dangerous and the synergistic effects are unknown. Synergism is the simultaneous action of separate agencies which, together, have greater total effect than the sum of their individual effects, for instance, alcohol significantly increases the effects of lead. The phenomenon is readily seen in the impact of drugs, but never mentioned on Material Safety Data Sheets required for the sale of toxic chemicals in the United States by the Environmental Protection Agency. US lawyer Richard Alexander writes: "Rarely can an MSDS be found that discusses harm from chronic exposures and equally rare is any mention of the synergistic effect of chemicals. Open any of these Material Safety Data Sheet sites to confirm that fact" :
*Material Safety Data Sheets at Oxford University, UK http://physchem.ox.ac.uk:80/MSDS
*Material Safety Data Sheets at Case Western Reserve http://research.nwfsc.noaa.gov/msds.html
Glutaraldehyde and formaldehyde when combined to fix tissue in electron microscopy were much more potent than when used individually. Glutaraldehyde combined with the effects of other sterilants and anaesthetic gases in theatres is uninvestigated. Formaldehyde may be used to preserve specimens and as a sterilant. In radiology and theatre it may also be off-gassing from unsealed particle board shelving etc, carpets and furnishings. Methanol (which metabolises to formaldehyde in the body) was detected in significant quantities in the headspace above GA sterilising solutions. Butyraldehyde was detected above GA solutions in both X-ray and theatre. Theatre nurses may also have had exposure to methylmethacrylate - used to glue bones to new joints. Add in to the radiographers’ cocktail other previously listed X-ray processing chemicals including hydroquinone (phenol), glycols, 5-nitroindazole, and the other corrosive and caustic chemicals (all potentially present in an aerosol), plus the toluene, sulphur dioxide, and acetic acid detected, plus silver, and remember that most radiographers and nurses used no gloves/skin protection let alone respiratory protection. Solvent uptake through skin depends on duration of contact, skin thickness, perfusion and degree of hydration, and the presence of cuts, abrasions or skin diseases. Frequent washing with harsh disinfectants damages the skin barrier. (Goetz, 1985). Many radiographers worked in small rooms which had no ventilation whatsoever. Quite often ventilation was into the ceiling or into unconnected ducts. Many nurses worked in unventilated theatres.
Other VOCs (volatile organic compounds) may be present - these are the components of "sick" or "tight" buildings including solvents from air fresheners (see paper on p. 38) as well as fragrance products - perfumes and strong deodorants; also phenol, bleach and ammonia from cleaning. In X-ray, Scobbie et al also detected benzenes, traces of phthalates (used in making plastics) and trace phenols.
A recent breakthrough in the understanding of Gulf War Syndrome may be changing scientific thinking and promoting further research on chemical synergy. Researchers at the Duke University Medical Center and the Texas Southwestern Medical School reported in April, 1996 that the simultaneous exposure to topical insecticides [DEET and permethrin] and pyrido-stigmine bromide, a drug taken prophylactically to counteract toxic gas warfare agents, causes nervous system damage in chickens. Both teams found that the many symptoms experienced by Gulf War veterans, including headaches, fatigue, aches, decreased attention and rashes, were similar to the symptoms that presented in exposed chickens. Chickens given any two chemicals became lethargic, unable to fly, lost weight and coordination and demonstrated tremors. For those administered all three chemicals, paralysis and death occurred. (May, 1996, Journal of Toxicology and Environmental Health.)
"This observed impact on nerve functioning is significant because survivors of the Gulf War who were exposed to these toxic agents also have demonstrated abnormal nerve function. It proves that hormone-disrupting chemicals, known to cause mild effects, when used in combination produce significantly dramatic hormonal effects".
Hormone-disrupting chemicals known individually to cause mild effects, when used in
combination produced dramatic effects: Synergistic Activation of Estrogen Receptor with Combinations of Environmental Chemicals," 272 Science 1489-1492 (June 7, 1996). Combinations of two or three pesticides, which are commonly found in the environment at low levels, are up to 1600 times more powerful than any of the pesticides individually in their impact on hormones. Some chemicals, which individually do not disrupt hormones, tremendously magnify the ability of other chemicals eg chlordane to disrupt hormones. This study focused on endosulfan, chlordane, toxaphene and dieldrin.
"Chemical Concoctions [Science Times]." New York Times, 30 March, 99, D5.
"The completion of a 5-year study by researchers at the University of Wisconsin reveals that the effects of the "chemical cocktail", made from fertilizer, insecticides and herbicides in agricultural groundwater, can differ from the effects of each chemical individually on the immune, endocrine and nervous systems of humans. A study using mice is reported in the current issue of the journal Toxicology and Industrial Health. Most current agricultural testing methods, according to these researchers, incomprehensively focus on chemicals in isolation and their carcinogenic effects, not their systemic impact."
Occupational Health Physician, Dr Chris Walls (Auckland) states: "[Glutaraldehyde] goes on in common with a number of other chemicals to cause in some people quite bizarre and peculiar symptoms which don’t fit the defined textbook examples". Differences in individual susceptibility play an important role in chemical sensitivity, (for instance a specific gene, CYP2E1, is responsible for the metabolism of benzene in many body tissues. Mice lacking the gene were protected from the toxic effects of benzene exposure. Humans also have this gene and human risk is likely to be a function of CYP2E1 expression. (Medinsky M A et al. CIIT Impact, Sept 1997).
Those with a mutation of CYP2D6 can detoxify the drug debrisoquine at only 0.5%-20% of the normal capacity. In the Korean War, soldiers with G6PD deficiency were hypersensitive to an anti-malarial drug. A genetic predisposition towards MCS and related disorders has long been suspected. There is a 40-fold variation in P450 1A2, one of the P450 enzymes necessary to detoxify various drugs and chemical substances. Many MCS subjects are now known to be P450-compromised. (ACTA update, Dec 98). The debate is that these enzyme level deficiencies are not nearly as marked as in the genetic conditions causing similar symptoms. NIEHS is looking at the enzymes which metabolise substances foreign to the body, to determine the basis for the wide variation in individual responsiveness to environmental toxicants. (CIIT Impact Sept 1997).
PHARMACOGENETICS
From ACTA UPDATE, April 1999: "Mispelled" genes are now known to be at the root of certain adverse reactions to otherwise lifesaving drugs. Ventolin is ineffective for asthmatics with a specific genetic glitch. Another prevents codeine from being converted to its active form... while other glitches prevent ....Prozac from being metabolised. Now the Mayo Clinic is charting genetic profiles before prescribing certain drugs."
SYMPTOMS ASSOCIATED WITH GLUTARALDEHYDE EXPOSURE / DARKROOM DISEASE
Glutaraldehyde-sensitised people will have many of the following symptoms (most common
symptoms from top). The list of symptoms is compiled from: Spicer, Hay, Gordon 1986;
Society of Radiographers - Preventing the Darkroom Disease, 1991; A. Bertino-Clark
- W. Aust HSOA Survey, 1989; Dr A.Vyas’ study, NW Lung Centre, Manchester,
England, 1997; Prof Bill Glass Exposure to Glutaraldehyde Alone or in a Fume Mix Shadows
40, 2, 1997; SNFTAAS Case Histories.
Glutaraldehyde can cause anaphylactic shock - (Kay Ball, Nurse Educator , < KayBall@AOL.COM >).
Kim Crosby has been suffering intense bladder pain with the lining of her bladder fibrosing and scarring - her doctor has said this is an auto-immune response to her chemical injury. (Ontario WSIB -Workplace Safety and Insurance Board - are refusing to say that she has developed occupational asthma from the chemicals though she never had any previous lung problems..they refuse to acknowledge her fibromyalgia and the autoimmune problems...The bladder wall is usually smooth; "mine looks like someone drew mountains along the inside wall. This cause pulling and scarring which in turn causes frequent urination, because my bladder capacity is so small, pain because of the pulling (causes spasms) and pain on urination". Kim says she gets help from DMSO (a medication that is injected into the bladder through a foley catheter). The patient lies on their stomach, back, and both sides for 15 mins each. It seems to resolve the fibrosing. Some patients take 1-2 treatments and others 5-6 once a year. Contact Kim: < crosby.darkroomdisease@sympatico.ca >
Several have Sjögren’s syndrome which includes connective tissue disease, SLE, scleroderma, eye effects - lack of tears, thickening of corneal epithelium, itching and burning of eye, hyperemia (excess blood) of the conjunctiva), and reduced vision. Sjögren’s syndrome usually occurs in middle aged women and is of unknown origin. Two SNFTAAS members have Hashimoto’s disease, a progressive autoimmune disease of the thyroid gland.
One MRT in Canada, Monique Genton, has developed chronic tinnitus, dizziness, and nausea (in addition to asthma and MCS) since her exposure to processor fumes. She was referred to a neuro-auditory specialist, not just an ENT doctor, by her allergist who noted a nystagmus (where the eyes do not track a moving object smoothly). Although her hearing, balance and ENG tests were essentially normal, the neuro ear doctor feels that, based on her clinical history, she has a visual-vestibular disorder that comes from the brainstem, rather than the ear itself. In this disorder, the information from the brain does not match that of the ear due to a brainstem irregularity, and this causes a kind of sea-sickness. Monique often experiences nausea when travelling, even when driving her own car. It is known that people exposed to solvents can develop this disorder, but no one has specifically examined this syndrome in radiographers. (Personal communication, Feb 3, 1999, akimbo@interchange.ubc.ca A number of others are reporting similar symptoms.
Cancers, reproductive effects, chemical sensitivities and health effects in children, diabetes, teeth and gum problems, effects on vision ("toxic agents display a remarkable predilection for the retina" - Recent Advances in Nervous System Toxicology, Golloi, Manzo & Spencer, Plenum), inability to maintain body temperature, lack of interest in sex, focal epilepsy are areas which have been little investigated to do with glutaraldehyde/chemical exposure in radiographers/MRTs/nurses. Hair loss, photophobia, limb numbness, and flushing are extras mentioned by Kathleen Sperrazza in her list of symptoms in the Brigham nurses.
Liver damage (with raised LFT’s and fatty changes in the liver) has been shown on scan in NZ radiographers. Mice exposed for 24 hrs to activated solution showed no kidney or lung damage but the livers showed toxic hepatitis. Dr Adrienne Buffaloe in her paper on the development of asthma in three critical care nurses exposed to glutaraldehyde, ethylene oxide, formaldehyde, butyraldehyde, latex, carbon monoxide, carbon dioxide and other VOCs, describes the role of the liver:
"The liver is the organ primarily responsible for clearing chemicals from the body, with minor percentage of chemical clearance accomplished by the brain, kidneys, lungs and skin. Phase I and Phase H Detoxification Pathways in the liver are comprised of a series of enzymatic reactions that progressively biotransform toxic chemicals which are fat soluble into non-toxic chemicals that are water soluble, so the chemicals can be excreted. This process of biotransformation requires a combination of nutrient co-factors for the enzymes to operate. When these enzymes are saturated , the chemicals can no longer be biotransformed, and are stored. [There seems significant potential for damage from long-term exposure to a chemical like glutaraldehyde which has a predilection for denaturing/cross-linking protein and enzymes. In histology, glutaraldehyde inhibits enzyme activity more than formaldehyde, the inhibition increasing with time in the fixative.] These fat chemical reserves can then serve as a reservoir and an equilibrium between the fat stores and the blood stream and can result in ongoing chemical toxicity long after the initial chemical exposure. Blood levels for toxic chemicals, when positive, demonstrate that there is a circulating quantity that the body has been unable to clear. However the blood level is just a fraction of the total body chemical load, since the concentration in body fat is often 200-300 times the concentration of the chemical found in the blood."
Buffaloe covers the concepts of "Total Allergic Load", "The Spreading Phenomenon" - as the chemical load accumulates, additional organ systems become recruited in the disease process. She also discusses the allergies in a child of one of the nurses.
Her web site: http://www.accessnewage.com/articles/health/chemical.htm"Researchers at UCLA have announced a breakthrough discovery: weight loss releases toxic chemicals absorbed from the environment and hitherto stored in fat reserves, back into the bloodstream. Roy Walford discovered this fact when he was an inhabitant of Biosphere 2. Within the first year of their sojourn in that controlled environment, Biosphereans lost an average of 11 kgs, while their blood levels in DDE and PCB’s initially increased by up to five fold, then subsided as fat reserves were depleted."
(ACTA UPDATE, 47, April, 1999.)
It has been difficult to attribute fatty liver and raised LFTs because so many factors can be involved eg alcohol use, and medication. Some cases accepted for compensation in NZ on this basis from GA exposure have been rescinded.
NETWORKS
Sharon Sowers and Janet Kanepp, 157 Maple Dr, New Holland, PA 17557, USA or email: < SSowers1@aol.com > have a questionnaire investigating some of these health effects. WASTE (Workers Against Senseless Toxic Exposure) is their group in the USA - currently they have 92 medical personnel injured by GA.
WASTE Web site: < http://ncchem.com/waste.htm > .
GASPING (Glutaraldehyde Affected Support Persons) -sub group of Injured Nurses’ Group operates in Victoria, Australia. Contact: Irene Gregory ph: 9470-099 <irenevic@alphalink.com.au> , Gaby Barnewall ph: 9439-9652 or Anne Rutter ph: 9 808-1509, P O Box 49, Burwood, Victoria 3125.
Rick Carlton has set-up the: GLUTARALDEHYDE, ALDEHYDE, AND SOLVENT SENSITIVITY LISTSERVER - GASSLIST!) This list has been established to serve persons interested in these sensitivities (especially Xray personnel and nurses) - to promote internet-wide exchange of research and information. 20 subscribers joined in the first 24 hours.
To subscribe to the list send a normal email message to: listserv@crow.astate.edu with a message of subscribe gasslist
For MCSS Networks see Web site list p. 54.
**Be aware that if you are having surgery with instruments sterilised in GA, there are in the Bibliog several papers reporting reactions from improperly rinsed instruments. (Cidex-induced synovitis, Harner et al, 1989. Endoscope induced colitis, Rozen et al, 1994. Glutaraldehyde Colitis, Birnbaum, 1995).
Because the chemicals have such wide-ranging effects, and because many GPs, who generally make the first contact with the patients, and specialists, lack knowledge of the chemicals, confirmation of these wide-ranging effects is sometimes difficult to obtain. Specialists with excellent knowledge of chemical poisoning must be used. Good taking of work history is very important if chemical damage is suspected. Most research has so far focussed on the skin, eye, nose and respiratory effects of glutaraldehyde, with published and unpublished studies since 1968. Many show that people are affected at levels far below the accepted standards and in unsuspected ways. (See SNFTAAS Bibliography: Axon et al, Collier, Norbach, Jachuk et al, Binding/Wittig, Campbell/Cripps, Carslake, Calder, Trigg et al, Ide, Leinster et al, Tkaczuk et al, Griffiths, Gannon et al, Scobbie et al, Vyas, Care G. ) Neurotoxic effects have been looked at more recently in NZ, Australia and the USA.
GLUTARALDEHYDE-INDUCED NEUROTOXICITY
(See also The Solvent Connection p. 34)
Good information is beginning to emerge in this area of glutaraldehyde damage. Professor Des Gorman states that research conducted in Adelaide, Australia by the Faculty of Medicine and Health Sciences, University of Auckland, shows that glutaraldehyde removes the surfactant lining of cerebral
endothelium and hence damages the blood-brain- barrier. "Any agent that impairs the BBB can cause both direct and secondary (by allowing the ingress of other toxins) brain damage. Hence glutaraldehyde is a plausible cause of neurotoxicity." (Letter to Dr John Monigatti, ACC Workwise, 8 Aug, 1997).
In an Australian paper, three staff cleaning endoscopes in a theatre had been exposed to GA. Testing was by the auditory evoked response potential (AERP) method which measures how long the brain takes to react to stimuli. They showed prolonged response time and a dysfunction related to depression of the brain’s cortical function [the area which controls higher mental functions, perception and behaviour, movement, and the functioning of the main organs]. Dr Teo has subsequently investigated a further 50 nurses; he received his PhD for the development of the AERP test. He has also seen 6 workers in the mining industry affected by glutaraldehyde. [Dr Richard Teo, PO Box 109, Jannali, NSW, 2226, Australia, ph: 041-9268 874, < AERP@intercoast.com.au >.]
Other neuropsychological testing is underway in West Australian health care workers as part of work by Leonie Coxon for a doctorate in forensic psychology.
Of 50 New Zealand SNFTAAS members with glutaraldehyde or formaldehyde exposure, 21 have had neuropsychological testing and all 21 have demonstrated neuropsychological damage classified as mild or moderate. Of these, 13 have been accepted for ACC compensation, 7 are awaiting ACC decisions, 1 is in dispute (with associated epilepsy which post-dates and which she is sure is associated with her chemical exposure). The label is often "chronic glutaraldehyde-induced neurotoxicity with fatigue as a significant feature". [GIN - no tonic!]. Three members have formaldehyde exposure and the rest, 18, are glutaraldehyde-exposed in either X-ray or theatre.
Two papers presented at the Marj Gordon Memorial Seminar, Palmerston North, NZ, March, 1997, examine neuropsychological effects. Dr Bill Glass looked at 13 patients who were mainly nurses using GA as a sterilant or bench wipe (Group A), and 13 who had worked with a chemical cocktail which included GA or, for 2, formaldehyde and benzaldehyde (Group B) in hospital photographic or X-ray departments. 12/13 in Group A, and 7/13 in Group B reported mood, memory, and concentration problems. 10 of Group A were given Hogstedt et al’s ‘Questionnaire 16’ (a recently validated test for early disturbance in CNS function for suspected solvent neurotoxicity). "Evidence of memory, mood and concentration impairment was evident." More detailed short battery neuropsychological tests were completed by 4 patients, and a full clinical evaluation was carried out on 6 patients. "These tests further confirm the neuropsychological damage suffered by patients".
Dr Dorothy Gronwall presented a composite case study, "Jane", based on 3 cases. "Jane’s" pre-morbid ability was in the above average intellectual ability group. In visual perception her copy of the muddly Rey- Osterreith complex figure was not well-organised and was inaccurate and incomplete... This was probably the result of poor frontal lobe function rather than perceptual deficit. Memory for non-verbal material was significantly below average. Attention and concentration: Several tests given including PASAT (Paced Auditory Serial Addition) which showed significantly slowed information processing. Language: significantly below average on controlled word fluency and a faster than normal falloff over time on task which is typical in cases of frontal lobe dysfunction. Executive function: the ability to organise and check what has been done showed impairment consistent with frontal lobe dysfunction. Reaction times: Significantly slower on a computer target test and more so to targets on the right.
Other factors: Intellectual handicap was unlikely; poor motivation unlikely - she did poorly on some tests not on others, and poorly on more interesting tests yet produced excellent scores on more tedious tests; malingering - perhaps she had done some homework and knew the sorts of results she should produce eg low scores on verbal memory, but she scored above average here. Also PASAT is very hard to fake believable scores on. Depression: one would not expect only some scores to be depressed, and only one peripheral vision field to be slower. Closed head injury: no traumatic brain injury - never been knocked out. Substance abuse: "Jane" denied taking alcohol or other mind-altering drugs. Substance abuse is unlikely to have resulted in this pattern of scores.
"It is never possible to produce a definite diagnosis from a neuropsychological assessment. All that can be produced are probabilities, not certainties. So what I can do is to make the statement that these tests are entirely consistent with the history of chemical exposure."
NEUROPSYCHOLOGICAL REASSESSMENT OF THREE N.Z. NURSES
Three cases (theatre nurses from the same hospital) who have been reassessed for on-going neuropsychological damage after long-term exposure to glutaraldehyde. (Reassessed for ACC, NZ by Dr Dorothy Gronwall.)
CASE 1: [Ex-theatre nurse working from the early ‘70s. Unprotected use of glutaraldehyde/formaldehyde until 1991 - open uncovered troughs. Plus the department also had an old-Xray machine off the plaster room. Considered sensitised in 1983 by doctor, with fatigue and ‘flu-like symptoms. 1991-1993 was in a new purpose built theatre with recycled/positive air pressure ventilation system. Multi-system problems developed rapidly. Finished work in December, 1993.]
First assessment: August 1994 (Mr Waddell). Second assessment: August 1995 (Mr Waddell): "Results were broadly similar" to those found in August 1994. "She demonstrated attentional deficits, reduced verbal memory , and slowed visuomotor reaction times."
Third assessment: August 1996. (Dr Louise Smith):
"During the last year it would appear that her physical progress has reached a plateau. She reported that she is coping relatively well in the home setting and can complete tasks e.g. housework if she paces herself and intersperses activity with rest. She experiences bursts of energy which may last 30 mins. Her headaches have markedly reduced and she is sleeping better.
Underlying this improvement is the avoidance of specific food products and environments (e.g. where people are smoking) and close monitoring of fatigue levels. She and her husband have in fact made considerable adjustments to their lifestyle to accommodate her health problems. Exposure will still induce symptoms (eg sweating, loss of sensation in limbs, difficulty with balance) ...
With respect to cognition, confusion in working with numbers has continued as has the inability to identify colours consistently. The attention deficits have also remained (e.g. going into the wrong bank by mistake). The reduced tolerance for frustration continues to be a factor... Socially she has had to restrict her activity...
Her neuropsychological profile remains relatively stable...average to high level of intelligence. ..evidence of attentional deficits, impaired long-term visual memory, and visual-spatial/visuomotor memory. There has been some improvement in short-term memory for information which is verbally presented in that this is now only borderline...The gains which have been made appear to be mainly resultant from lifestyle adjustment ...should she be placed in a less controlled environment (e.g. a workplace) cognitive symptoms would intensify. Neuropsychological testing is no longer appropriate, unless a major change occurs and reassessment takes place in more than 5 years time."
CASE 2 (Ex-theatre nurse): Assessed May 1996 (Dr L Smith): "...Tests indicated a reduction in non-verbal reasoning skills, impaired visuo-spatial skills, impaired verbal memory both short and long term, and mild impairment of long term visual memory."
Assessed July, 1997 (Dr L Smith): "Her report on her functioning was essentially unchanged... She continues to forget to complete tasks, is easily distracted, will forget conversations, and cannot track conversations where several people are talking at once. Writing and word finding are still problematic. As at last assessment she has high fatigue levels and can tolerate approximately half a day of mild activity if she rests or sleeps in the afternoon... For example she knows that doing the groceries is a task which will tire her for the rest of the day, so she plans carefully when she goes. Socially she does make an effort to remain in contact with others...she gives one lecture every six weeks to students to help her feel "normal". Case 2’s frustration with her reduced capacity for work was noted previously. This continues with her stating that she had expected that she would have made more progress. She feels guilty when she is not doing things and tends to compare herself with people her age deciding that she is "useless". Her concern that others do not understand what has happened, has led to a tendency to hide her difficulties from other people. There are indications of the "boom-bust" cycle, whereby she takes any sign of improvement as an indication to increase her activity levels, and then subsequently pushes so hard that symptoms will re-emerge at an even higher level (e.g. will get headaches, perspire, feel somewhat disorientated."
She herself stated that she felt little had changed in the last 14 months and the assessment results support this. Functionally she continues to display cognitive impairment, high levels of fatigue, and reduced tolerance for activity... Her verbal skills are in the normal range but are lower than would be expected given her premorbid history. There is evidence of lowered non-verbal skills, particularly with respect to visuo-motor reaction time. Scores on measures of visuospatial skills and the ability to shift attention between alternatives, remain impaired. Short-term verbal memory is impaired, with long-term verbal memory being borderline to impairment. Short-term visual memory is in the normal range, while long-term visual memory is lowered.
It has now been approximately 2½ years since she finished work, and the neuropsychological test results have been stable for 14 months. It would be fair to say that Case 2 is not ready to consider even part-time work, and that this is most likely to be the situation for some time to come... A repeat neuropsychological assessment is not necessary unless at some point she notices an improvement ...".
CASE 2 and CASE 3 (ex-theatre nurses)
Request by ACC for previous reports to be commented upon, 1 March 1998, of Dr Dorothy Gronwall:
" ...fatigue and not MCS is the main factor in limiting return to work in both cases... Case 2 stopped work... in Dec 1994 after 27 years...
Possible factors: [After head injury, malingering and depression were ruled out]. "Chronic fatigue syndrome (CFS): Fatigue is Case 2’s major limiting factor... A review of the literature on neuro- psychological deficits in CFS shows a very different pattern of subjective and objective scores from those recorded by Case 2. In particular Moss-Morris et al note that there is no clear evidence of sensory or perceptual impairments in CFS, yet there was definite impairment of visual perception in this case. Thus the pattern of her test results and subjective complaints is entirely consistent with the history of many years exposure to glutaraldehyde in her work-place.
There are two issues...The first is that is would be difficult to argue that Case 2 and Case 3 did not have work-related problems which resulted in them having to stop nursing. This was the conclusion made in the two neuropsychological reports in both cases, and obviously a conclusion reached by ACC, since the claims were accepted.
"... why are they still not able to work, in other words why have they not recovered? I found the description of Case 2’s current state [see above] very compelling, because it is almost identical to the accounts I get from older people who have continued to have problems following traumatic brain injury. The "boom and bust" cycle is very common, particularly in high-achieving people who are well-motivated to return to productive employment. Both these ladies are said to find their inability to return to work aversive, and from the reports I would rate them as well-motivated to regain their independence.
As already noted, I was unable to find any definitive information on the time course of recovery from exposure to glutaraldehyde. However I cannot see any logical reason why this would be expected to differ from other kinds of central nervous system injury. There is ample evidence that in most cases fatigue is one of the major limiting factors. Given that they also continue to demonstrate unequivocal impairment on measures of cognitive function, ny conclusion has to be that neither has yet recovered fully from the effects of the exposure."
***
Three critical care nurses in New York were documented by Dr Adrienne Buffaloe: "The patients’ symptoms of neurotoxicity which included a decrease in short-term memory, word retrieval problems, and inability to concentrate improved during the course of their treatment and has continued to improve over the last 18 months. None of the three adults has achieved her baseline neurological functioning. One of the nurses had a brain SPECT scan performed before her arrrival at our centre and the scan showed hypoperfusion in multiple areas consistent with chronic solvent exposure...."
***
To add to the picture, Dr Kaye Kilburn, (Ralph Edgington Professor of Medicine, USC School of Medicine), wrote to a SNFTAAS member: "The toxicity of photographic processing goes up with speed which involves heating. More vapors are produced and escape into the room. The most toxic chemicals are the phenols [for] example hydroquinone... Phenols are particularly toxic to the peripheral nerves and brain when inhaled as aerosols and vapors. These are organic chemicals... A major question is, are you noting nervous system symptoms, diminished recall memory, concentration, forgetting procedures, dizziness, unstable balance, sleep disturbances, somnolence and headaches? If so, then the likelihood of phenol-hydroquinone toxicity increases. I have seen 7 or 8 patients with diminished brain function from working indoors on "rapid processors". I think both glutaraldehyde and hydroquinone are most important candidate chemicals" (15 Jan, 1999). His web site details many of the tests available: <URL: http://www.neuro-test.com >
Geof Care, Managing Director, Photosol, London, replies: "So far as phenols are concerned, three were detected by the HSE: hydroquinone, phenol itself and 2,6-bis(1,1-dimethylethyl)-4-methyl phenol, and all in trace amounts - by inference low ppb's or even ppt's. My paper in the Lancet (Care: Darkroom exposure to hydroquinone, Lancet, 47, 121, 1996) calculates a theoretical HQ saturation vapour concentration of 3ppb which ties in well; even this would be vastly reduced by ventilation. I personally would discount danger from this source unless bad ventilation & other adverse circumstances allowed developer aerosols to be breathed in. Phenol is a gelatin preservative and probably is a faint left-over after film coating that leaches out during processing. The third phenol is unknown to me but again its concentration is minute. In short, I really cannot envisage harm from them unless you were right on top of the solutions and the local exhaust ventilation (nowadays fitted as routine above the tanks) was not working."
***
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)