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://nile1.northland.ac.nz/~Foot/snftaas/snftaas.html>
Treasurer:        Lyn Mallia,   14 Tobys Way, Waikanae 6454,  NZ	 Ph/F: (04)  293 6876						
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APRIL 1999		
GLUTARALDEHYDE, ALDEHYDES,  SOLVENTS  
AND  OTHER  CHEMICALS  
PRESENT IN  X-RAY, THEATRE  
AND  STERILISING  ENVIRONMENTS;
DARKROOM DISEASE.

Glutaraldehyde p1;   Silver Recovery and GA Exposure  p 4;   Marj A Gordon Memorial Seminar: Airborne Contaminants from X-Ray Processing p 5;  Skin Exposure linked to Respiratory Sensitisation  p 6;  X-ray Processing Chemicals and/or Fumes  p 6;   Chemicals Potentially in the X-ray Environment  p 8;  Glutaraldehyde in Theatre and Sterilising Environments  - Components of Glutaraldehyde-Based Sterilising Solutions including Butyraldehyde,  Methanol  p 9;  MAG Mem Seminar: Occupational Symptoms in Endoscopy Nurses Exposed to Glutaraldehyde and Latex  p 9;  Chemicals Potentially in Theatre and Sterilising Environments  -  Formaldehyde:  Levels  p11;  Formaldehyde Effects  p 11;  Formaldehyde Use p 12;  Products Containing Aldehydes  p 13;   Methanol  p 14;  Aspartame  p 14;  Other Notes  p 15;  The Cancer Debate  p 16;  Formaldehyde and Benzene in the Environment  p 16;  Ozone p 17;  Other Aldehydes  p 18;   Anaesthetics  p 18;  Methylmethacrylate  p 20;  Ethylene oxide  p 20;  Synergistic Effects - the Cocktail  p 20;  Research on Synergies  p 21;  Individual Susceptibility  p 22;  Symptoms Associated with Glutaraldehyde/ Darkroom Disease  p22;  Networks  p 25;  Glutaraldehyde-Induced Neurotoxicity  p 25;  Neuropsychological Reassessment of Three NZ Nurses  p 27;  Formaldehyde Neurotoxicity  p 29;   Chemical Assaults on the Brain  p 30;  Rehabilitation  p 31;  The Solvent Connection  p 34;  Parkinson’s  p 37;  Recent Findings - Fragrance Products  p 37,  Air Fresheners  p 38,  
Gasoline  p 38,  Carpets  p 39;   MCSS  p 39;  A Review of  MCS  p 41;   TILT  p 42;   No Cures for MCS  p 42;  CFS  p 43;  Establishing Chemical Sensitivity - Skin Prick Testing  p  44;  Haptens and Challenges  p 45;  Chromosome Testing p 46;   Porphyrins p 47;  Aliphatic Volatile Solvent Testing (2 methyl-pentane, n-hexane)  p 48;  On-going Research  p 49;  Stress!  p 50;  Health and Safety  p 51;    Legal Settlements  p 52;  Conclusion  p 53;  General Bibliography  p 54;   Further Reading  p 54;  Websites  p 54;  It’s All in the Mind!  p 56.

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.

The USA PEL - Permissable Exposure Limit of  0.2 ppm;   NZ WES - Workplace Exposure Standard of  0.2 ppm (10 minute period);   UK  OES  (Occupational Exposure Standard),  measured over a 10 minute period, of  0.2 ppm  [or  0.7 mg/m³]  in air  (conditions under which workers may be exposed day after day without adverse effect) was based on its irritant effects on eyes, nose and throat. These limits are under major revision: 	
The ACGIH (USA) Notice of Intended Change (NIC) is to lower the 
		existing TLV of  0.2 ppm to a TLV ceiling of  0.05 ppm. 

The British Health and Safety Executive (HSE)  has issued a Chemical Hazard Alert Notice.  Their Advisory Committee has recommended that a  Maximum Exposure Limit  (MEL)  of   0.05 ppm,  
expressed as a time weighted average, and 0.05 ppm expressed as a 15-minute reference period,  should be set.  “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 22, 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
	
	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/=AO/=AO  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:  
	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”.) 

(4)    METHYLMETHACRYLATE
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.  

RESEARCH  ON  SYNERGIES
	
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.”

INDIVIDUAL  SUSCEPTIBILITY:  

	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. 	
	-headache
	-sore throat,  constant hhumph,  catarrh   
	-voice change or loss (eg loss of upper register singing mentioned; “my voice goes down” is 		often the first indication of an exposure reaction)  	
	-unexpected fatigue/exhaustion (most of us find the energy to do the things we want to do but 		with this fatigue you can’t.  Constantly falling asleep and sleeping for huge amounts of 		time is common )	
	-sore/watery eyes
	-mood changes:  depression,  anxiety,  irritability,  personality changes,  emotional lability 		(inappropriate talking,  crying,  rapidly changing emotions)
	-concentration difficulties,  reduced ability to learn new things,  memory loss,  (all extremely 		frustrating in intelligent people who have held professional positions and good jobs 		which they like doing),   spaced out feeling
	-tinnitus   	
	-blocked nose  
	-rhinitis
	-bad/metallic taste in mouth, mouth ulcers, lip sores,  
	-chest tightness,  shortness of  breath,  chest  pains,  asthma
	-sinusitis 
	-nasal discharge,  nose bleeds (epistaxis),  ulceration of nasal mucosa 	
	-skin irritation,  itchy burning skin,  rashes,  dermatitis       
	-aching joints and muscles,  uncontrollable twitching,  fibromyalgia
	-cross sensitivity to other chemicals
	-heart arrythmias,   palpitations,  Raynaud’s Syndrome
	-menstrual irregularities            
	-gastrointestinal symptoms incuding  nausea,  diarrhoea,  abdominal pain
	-difficulty urinating/prostatitis
	-earache,  ear infection 
	-pins and needles or numbness in fingers, toes or limbs  			
	-bruising 
	-irritant associated vocal chord dysfunction	

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://www.n-i.com/NCchem/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:  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  NEUROTOXICITY

	Formaldehyde has also been found to have a neurotoxic effect and impairments of attention and memory have been associated with formaldehyde exposure - LEZAK  M D,  Neuropsychological Assessment,  OUP,  1995,  p267.  [Note, significant methanol, which metabolises to formaldehyde  was detected above glutaraldehyde sterilising solutions].  The whole of  Chapter 7 is excellent and gives the following references:  
*p 267: “Because it is so widely used in buildings and furnishings material and in household products, formaldehyde in vapour or derivative form is often present in home environments.”  (Schenker  M.B, et al. Health effects of residence in homes with urea formaldehyde foam insulation.  A pilot study.  Environmental International,   8, 359-363, 1982. 
Singer R.M.  Neurotoxicity Guidebook. 1990. NY. Van Nostrand Reinhold). 	 

*p 267: “Laboratory animals exposed steadily for three months to somewhat higher than normal levels of formaldehyde incurred brain damage particularly involving the parietal cortex”.  (Fel’dman Y.G. and Bonashevskaya T.I.  On the effects of low concentrations of formaldehyde.  Hygiene and Sanitation, 36, 174-180, 1971).   

*p 267:  “ Both acutely and chronically, persons exposed to formaldehyde have complaints implicating the central nervous system, such as headache, dizziness, irritability, memory problems, and sleep disturbances.” (Report on the Consensus Workshop on Formaldehyde.  Environmental Health Perspectives, 58, 323-381, 1984.    Olsen J.H et al,  Formaldehyde induced symptoms in day care centers.  Am Ind Hyg Assoc J.  43, 366-370, 1982.)

*p 267:  “Impairments on tests of attention and short-term memory have been reported for exposed workers” - Bach B, et al.  Human reactions during controlled exposures to low concentrations of formaldehyde - performance tests.  Paper presented at 4th International Conference on Indoor Air Quality and Climate.  Berlin. 1987.    Kaye H. Kilburn, et al.  Formaldehyde Impairs Memory, Equilibrium, and Dexterity in Histology Technicians: effects which persist for days after exposure.  Archives Envir Health, 42, 117-120, 1987.  Paper available CIIN 0024-GOET-85-014.   [305 women technicians, av 17 yrs work. Increasing age was associated with poorer performance on visual memory, block design, trails connecting numbered dots, dexterity, sharpened Romberg (balance), finger writing for peripheral nerve function, as well as longer reaction time.  Increased daily hours of exposure were correlated with reduced performance of story memory, visual memory, digit span (numbers forward and backward), pegboard and sharpened Romberg, and errors on trails. From other studies reported in this paper: “Impaired memory, particularly short-term memory loss is a frequent symptom in histology technicians. Recent observations show that short-term memory does not vary significantly with age”. “Lightheadness, dizziness, and disturbed equilibrium are frequently reported in histology technicians.”  The mechanism of the neurotoxity of formaldehyde has not yet been identified.  However formaldehyde cross-links proteins, DNA, and unsaturated fatty acids. This high affinity for these chemicals suggests a rapid interaction with cells after inhalation or ingestion.  This suggests that little free formaldehyde should reach the nervous system. However the results described decreased neurofunction.] 
LEZAK:
“My experience with a number of persons complaining of memory problems associated with formaldehyde exposure is that many of them displayed attentional deficits which interfered with effective communication and normal information storage and were interpreted by them as “memory” problems. However, using the Halstead-Reitan battery and the Wechsler Memory Scale to examine a small series of persons exposed to low levels of formaldehyde fumes in their homes, Cripe and Dodrill  (Neuropsychological test performances with chronic low-level formaldehyde exposure,  The Clinical Neuropsychologist,  2, 41-48, 1988)  reported no notable differences between them and matched controls.” 

A further formaldehyde neuropsychological reference is:	
C.G. GOETZ,  Organic Solvents  in  Neurotoxins in Clinical Practice,  (Chap 5) 1985. Discusses types of solvents, neuropathy, encephalopathy, myopathy (with reference to fatigue, exercise intolerance, arthralgias, muscle tenderness), and specifically:  methyl alcohol/ formaldehyde, ethylene glycol, amyl/isopropyl alcohol, toluene, n-hexane, aniline, MBK, TCE, carbon tetrachloride. Organs affected by organic solvents in addition to the nervous system include skin, mucous membranes, digestive, hepatic, renal systems.
***

CHEMICAL ASSAULTS ON THE BRAIN.                                                                                       

From Bonnye Matthews’ book  Defining Multiple Chemical Sensitivity,  (McFarland, 1998) Dr Donald Dudley  (retired Professor of Psychiatry and Behavioural Sciences and former Clinical Professor of Neurological Surgery at the University of Washington) describes his theory of how the brain damage is occurring from chemicals with fewer than 6 carbon fragments in their volatile components (such as formaldehyde, MEK, acetone, glutaraldehyde) :
	p 22.  “As indicated in the beginning of this chapter, doctors creating negative bias towards the olfactory system include attitudes expressed in authoritative medical textbooks since at least 1875; the use of technology better suited to other systems (eg the immune system) to study the olfactory system; the lack of adverse effect occurring from ablation of olfactory tracts in the brain (which has been misinterpreted as evidence that the system must have little value); the supposed failure to identify neurotransmitters in the olfactory system; and the supposed failure to identify any essential role this system could have in disease production.  To varying degrees, these factors influence the attitudes of both professional and non- professionals and generate considerable negativity towards MCS patients who point to olfaction as the major source of their medical problens.  Both professionals and nonprofessionals tend to believe that these patients have psychiatric disorders or are simply malingering -  a belief that is inconsistent with the data presented in this study, and a belief that has no business in science.
	An issue of major importance from this author’s point of view, is the fact that neurotransmitters have been found for the olfactory system, and that many are excitatory amino acids such as glutamate and NMDA, or precursors to excitatory amino acids.  These are the same amino acids that are implicated in brain-cell injury and death. They are related to such problems as stroke, pain, depression, and degenerative brain disease.
	Glutamate, NMDA, and other excitatory amino acids injure cells when released.  This injury makes the cell vulnerable to the influx of chloride ions and then to the influx of calcium ions.  A fanciful way of looking at this process is to imagine a balloon being inflated until it bursts. It is postulated that olfactory signals release excitatory amino acids, which lead to cell injury that proceeds to the above process.  If such a mechanism is in operation, it should be possible to procuce the symptoms of MCS by using excitatory amino acid agonists, and to decrease them by using antagonists.  The agonists are the volatile short-chain carbon fragments such as formaldehyde, acetone, and methyl-ethyl ketone.  Molecules such as these, with the same or fewer carbon units than glutamate, can be agonists.  These compounds lead to the release of excitatory amino acids that begin destruction of brain tissue.
	In general, odor thresholds decline with exposure to chemicals having more than six carbon fragments and increase with exposure to chemicals having six or fewer carbon fragments.  The optimal carbon length for producing excitatory amino acid release is six or fewer.  It needs to be emphasized that it is not the carbon chain length of the parent compound that counts.  It is the carbon chain length of the volatile component. In other words, analysing carpet adhesive is of little use; the volatile fragment from carpet adhesive needs to analyzed.
	On the other hand, compounds with greater than six carbon fragments, with a D-configuration and certain other characteristics, can be antagonists of excitatory amino acids.  These compounds, such as MK801 and dextromethorphan hydrobromide, should decrease symptoms of patients with MCS if the hypothesis is correct.  Dextromethorphan hydrobromide, a known excitatory amino acid blocker, does significantly decrease symptoms on olfactory exposure to volatile short-chain carbon compounds in MCS patients.  It has been used by the author in more than 30 of these patients with significant positive efect.  Dextromethorphan hydrobromide has a remarkable track record and has been used in billions of doses as a cough suppressant without significant biologic problems.  To the author’s knowledge MK801, an experimental amino acid blocker, has not been used in patients with MCS.”  

	Madelon Price,  Professor of Neurobiology,  Washington University Medical School writes:  “NMDA antagonists are dangerous agents. Currently there are none that have been approved for use although one may be approved shortly. A very few NMDA antagonists are complex agents that act at multiple sites.  Dextromethorphan is an NMDA antagonist but at the concentration that it is added to cough medicine, it is safe.  Even at high concentration it would probably be safe (but not yet adequately tested) in that it also acts at other receptor sites that block NMDA receptor antagonist toxicity. One should consult with a well informed doctor or scientist before ingesting one of these agents.”

THYROID RELEASING HORMONE

	Bonnye Matthews writes  about another helpful treatment after a chemical exposure:   “That cascade of ill effects (the balloon example with cells) is stopped in its tracks by the use of TRH as a nasal spray.  After Donald Dudley tested me the first time, I called from home the next day and told him the brain fog problem was worse than it had ever been.  He told me if I could get downtown, he'd turn it around.  I thought he was out of his mind, but my mom drove me to his office.  As he so aptly put it, expose me and you've got a person with an IQ of 60 shuffling around.  I was far gone.  In two-and-a-half hours I drove home!  It's amazing stuff!

	Donald Dudley has tried dextromethorphan with success in some cases.  In my case, for example,  DM works following toxic exposure on my lungs but not my brain.  DM puts out the "fire" spots in my lungs within a half hour.  To clear the "brain fog" in my case, I have to use TRH in a nasal spray.  So he's postulating, but also he's seen success in some cases, where DM actually clears the "brain fog."  The postulating is because of the lack of study with agonists.  Without TRH and DM I wouldn't try to do much of what I do.  We actually have pharmacies now (in Seattle) where we can get TRH nasal spray and DM.  I think he's really on to something, but without large numbers of people, I think he's right to stick with postulating.”  An estimate is that it is effective 90% of the cases.  For some it is not effective. Its real value is that it keeps the IQ bites that follow these really bad brain fogs from being so devastating.  (Personal communication).    [Consult your medical professional]

Thyrotropic Releasing Hormone/Thyrotropic Releasing Factor
Injectible (IV)
 - mixing instructions:   1 ampule TRH/TRF + 4 cc bacteriostatic sterile water
 -dosage:   1cc weekly or 1/2 cc weekly if very sensitive intraveinously
Nasal Spray
 -mixing instructions:   1 ampule TRF/TRH + 9cc bacteriostatic sterile water in clean metered nasal spray  -dosage:   1 spray each nostril, twice daily.						bottle
Purchasing Information
 -price ranges from US $106 to $180,  shop around
 -most pharmacies can get it if given enough time - comes in 4-5 ampule containers
Known Responses
 -benefits:  clearer thinking; occasionally brighter vision
 -response time:  anywhere from 2 minutes to 24 hours
 -duration:  1-7 days
 -accumulation:  does accumulate;  less and less is needed over time
 -side effects:  initial response occasionally can include taste of medication, desire to urinate, a sense of nausea momentarily.
[Seek professional medical help.]

GINKGO

Ginkgo  biloba  is one among several herbs worthy of consideration in helping restore brain function.  In mostly German research with more than 50 controlled trials, ginkgo is confirmed good for memory and concentration, confusion, energy loss, tiredness, depression, dizziness, tinnitus.  It reverses poor blood flow seen on EEGs and improves alpha brain activity.  “French experiments show that ginkgo can actually restore the ability of brain cells to transmit and receive signals from neurotransmitters that govern brain activity”.  It is a strong antioxidant and good for cardiovascular function - improves blood flow to extremities.  Also suggested are the antioxidant pycnogenols – pine bark/grape seed extracts – which are reputed to be very good for neuronal damage and many other symptoms of chemical poisoning – there is good research on these also.  Seek help from your health professional.  

REHABILITATION

	Many suffering neuropsychological damage are assessed in the vicinity of being able to cope with perhaps only one or a few hours work per day.  Comments such as: “attempts to return to employment will be unsuccessful if she/he is pressured to return to work too quickly, placed into inappropriate settings, or fatigue levels exacerbating cognitive difficulties are not recognised and taken into account” abound.  Pressure should not be put on these people to undergo rehabilitation  or find a new job earlier than they can manage.  A return to their previous jobs is generally out of the question as exposure to even the slightest trace of chemicals can induce symptoms and further brain damage.  “The weight of evidence point[s] strongly to the conclusion that exposure to solvents over many years can leave workers permanently disabled by impaired memory concentration and mental function, and ... the risk of neurotoxic effects increases as the level of cumulative exposure increases."

Employers and compensation authorities who force people to return to an unsafe-for-them work environment which further damages their health may be liable.  People with past exposure to volatile chemicals have an internal exposure source stored in body fat that can be released gradually into the blood.  Factors that mobilize body fat stores - such as weight loss, exercise - can increase chemical release into the blood. This body burden can aggravate illness in chemically compromised people.  Hard  physical/manual work is usually ruled out because of this and the fatigue factor.

	Finding  “safe”  alternative employment is a huge problem.  On the other hand some people who have worked hard to find alternative work to make themselves useful to society,  upon showing their employers their neuropsychological reports, are faced with such decisions as:  “It is with reluctance that in the light of the report of  31st December 1998 from  [your neuropsychologist], that we are unable to continue your employment as a Teacher Aide.  The safety of yourself and the [autistic] student you are working with is our prime concern.... we feel it is in your best interest to cease working with the student.”  Concerns with OSH were similarly quoted by  IHC   (Peter Lenz,  <lenz@xtra.co.nz> ). 

This is also a further and extremely serious issue for nurses and radiographers involved in the safety/care/ treatment/diagnosis of patients.  Under the NZ Nurses’ Act 1977,  it is mandatory to notify the Health and Disability Committee of a mental or physical disability.  A nurse may be suspended if it is in the public interest to prevent him/her practising or they may be permitted to work under “restricted practice”.  “The committee sees its role as ensuring the safety of the public.”

	“TREATMENT OF PATIENTS EXPOSED TO TOXIC CHEMICALS”.  Kevin Arnold.  The Ohio Psychologist. March 1997.  [Paper available CIIN,  0219-ARNO-97-005].   An excellent article which covers the specific areas of damage - multiple task and simultaneous processing, and certain forms of memory dysfunction which result in disruptions to word recall during verbal expression; headaches, pain, weakness, and fatigue.  CT scans may not clearly show the disorder - PET or SPECT evaluations will help identify localised damage.  The importance of treating the emotional results which often mimic Post Traumatic Stress Disorder (PTSD), and additional emotional problems eg depressive-like symptoms, panic and worry.  Necessity of the psychologist, patient and family understanding the impact of toxins on on the CNS and - the physical aftermath as well as the shattering of the basic assumptions upon which one lives one’s life.  Treatment must combine physical medicine, neuropsychological rehab and psychotherapy.  Importance of all having up-to-date information.  Interventions  can range from development of behaviours to over come poor organisation to working on improvement of memory functions.  Importance of creating reasonable expectations.  Extra effort will be required to help patient complete out-of-therapy exercises.  eg enlisting family, writing out notes and taping sessions....

	Dorothy Gronwall reports a pilot study in Sweden of a rehabilitation programme for the effects of 10 yrs exposure to neurotoxins was positive.  Subjects had no exposure in the 3 months before the study.  Patients took part in group sessions with 4-7 people in each group, and were taken through cognitive rehabilitation and group therapy  sessions.  Neurophysiological measures assessed the effects and patients and families were given questionnaires .  Positive results were found with each type of measure.  The authors conclude the aim should be to improve the patient’s adaptation to the brain dysfunction and the secondary consequences,  and the patient’s self-confidence, self-conception, and everyday functioning.  

	One SNFTAAS member who failed in the High Court v ACC to achieve compensation for MCS from her exposure to photographic chemicals while working for a daily newspaper,  has been working as a postie for 3 years.  She says the almost daily requirement to sort mail and put the letters in the right box has almost completely restored her brain function.  As long as she keeps away from chemical exposures her health is not too bad.  

See also  NO CURES FOR MCS  section,  p 42. 

THE  SOLVENT  CONNECTION	

	NIOSH (USA) stated in 1987 in their Current Intelligence Bulletin that aldehydes are solvents:  “Common  organic  solvents are classified as aliphatic hydrocarbons, cyclic hydrocarbons, aromatic hydrocarbons, halogenated hydrocarbons, ketones, amines, alcohols,  aldehydes, and ethers”. 
In correspondence with New Zealand’s Accident Compensation Corporation (ACC) Professor Gorman, Health Science Centre, University of Auckland,  accepts that glutaraldehyde is a solvent under Axelson and Hogstedt’s definition.  Dr Monigatti  (ACC Workwise, NZ)  states: “We accept glutaraldehyde has solvent-like properties. If chronic solvent exposure can cause these sorts of things then we accept that glutaraldehyde can cause [solvent toxicity] as well....(Safeguard Update, No 96, 20 April, 1998).

NIOSH (1987) states: “ Epidemiologic studies of various groups of solvent-exposed workers have demonstrated statistically significant chronic changes in peripheral nerve function (sensory and motor nerve conduction velocities and electromyographicabnormalities) that persisted for months to years following cessation of exposure.   Epidemiologic studies have also shown statistically significant increases in neurobehavioural effects in workers chronically exposed to organic solvents.  These effects include disorders characterised by reversible subjective symptoms (fatigability, irritability, and memory impairment), sustained changes in personality or mind (emotional instability and diminished impulse control and motivation), and impaired intellectual function (decreased concentration ability, memory, and learning ability).  Among organic solvent abusers, the most severe disorders reported are characterised by irreversible deterioration in intellect and memory... accompanied by structural CNS damage.”  

	Two international workshops have categorised solvent-induced CNS disorders  (NIOSH p 17):
 
	“Type 1 is characterised by fatigue, memory impairment, irritability, difficulty in concentrating, and mild mood disturbance.  Type 2A includes sustained personality or mood changes and Type 2B impairment in intellectual function manifested by diminished concentration, memory and learning capacity.  The boundaries are not necessarily clearcut.”

	Other labels:    Organic Brain Syndrome, OBS    /    Psycho-Organic Syndrome, POS   /
   		          Solvent-Induced Chronic Toxic Encephalopathy,  CTE.

	The diagnosis is usually based on case histories, symptoms and psychometric tests.  Work in Sweden has shown that long-term solvent-exposed workers have disturbances of the equilibrium (vision/sense of balance) system and that an otoneurological test battery (ear nerves/balance) adds worthwhile information about abnormalities within the brainstem-cerebellar complex.  It is the same VIII nerve which carries messages about sound and balance.  

	A second report showed that the long-term solvent exposed  were worse at recognising distorted speech and had significantly longer cortical response audiometry, ie the time taken for the message to reach the brain stem.  There was no difference between the control group and the solvent group in recognising pure tones or single syllable speech.  The findings suggest long-term solvent exposure causes disturbances of the central pathways in the otovestibular complex  (hearing and balance nerves and their connections).  
	Another Swedish study indicates that a 5 year follow-up of workers shows effects on the central nervous system persist after exposure ceases, with reduced activity, leisure, education and training, and more neuropsychiatric symptoms. They did not get worse.  If a worker was removed when he had symptoms without signs of intellectual impairment, recovery was seen in most cases. See also the sections on Glutaldehyde/Formaldehyde Neurotoxicity and Rehabilitation  pp 23-29.

	Dr Keir Howard states:  “It is worth remembering that many organic solvents are related to anaesthetic gases and have the same effects.  Solvents form the base of many paints, laquers, varnishes, thinners, waxes, printing inks and adhesives and are used for degreasing and cleaning purposes as well as forming the base of many therapeutic and pesticide mixtures...  It is always worth being reminded that the commonest organic solvent to which people are exposed is ethyl alcohol in the form of beer, wines and spirits... the effects are essentially identical to over-exposure to the various organic solvents used in the industry... consumption of alcoholic drinks frequently enhances the effects of solvent exposure... tolerance for alcohol is reduced... a worker heavily exposed during a shift may be just as dangerous on the road as someone whose blood alcohol is over the limit.”  Main effects are drying, cracking, reddening skin; dermatitis;  toxic effects on liver, kidneys, and cardiovascular system, on the central and peripheral nervous systems and “general lassitude with tiredness, sleep disturbances and lack of motivation.”

	*From  WHO  (via Toxins Awareness Group):  paint solvents are carcinogenic, painters having a 40% higher chance of  lung cancer and 20% higher of stomach, bladder, larynx, etc cancers,  while their children are at increased risk of leukaemia and brain tumours.

	*From the  NZEPMU  printers’ seminar 1998,  on solvent neurotoxicity:  50% of solvent neurotoxicity comes from the printing industy.  From Prof  Bill Glass’s introduction: solvents cause abortions and affect sperm.  Measured air levels don’t include skin absorption. For toluene, hippuric acid is tested in urine - the levels rise and fall depending on work exposure. [Toluene and benzene were discovered in the headspace above X-ray processing solutions.]  Solvents accumulate in fats and are excreted more slowly.  One story:  that of the bloke whose wife made him sleep facing a new tallboy (because he breathed fumes on her all night - many solvents are excreted through the respiratory system) and stripped the finish off part of it by the end of the year.  Those affected often become aggressive both at work and at home.  It is common to find marriages and relationships falling apart.

	*From  David Appleby,  OSH, NZ:  Many  WES  (Worker Exposure Stds) are still set too high for solvents and anaesthetic gases to prevent solvent neurotoxicity and adverse pregnancy outcomes.  These limits are political.  The lower the WES the more toxic the chemical. A chemical with a WES of 25 is four times more toxic than a WES of 100. Also WES are based on studies of healthy males. He suggested his experience is that women are more sensitive to, and experience more harmful effects from solvents than men.  Women can consume only 2/3 the alcohol of men.  [Like Asians, women have less alcohol dehydrogenase enzyme]  ?similar for solvents.  There is some evidence that solvents not soluble in water cause more harm  and more readily enter the bloodstream.  [See Anaesthetics p 18].  Benzene is an example - see the SNFTAAS’ Bibliography on our web page:  Medinsky MA, Determinants of gas and vapour uptake in the respiratory tract,  CIIT, 16, 2, 1996, or    www.ciit.org/ACT96/ACTIVITIESMAR96/mar96.html]  
Also the metabolites of benzene (eg 2,5-hexanedione) are more neurotoxic than the parent compound.

	*From NIOSH - Organic Solvent Neurotoxicity 1987:  Exercise increases breathing and heart rate and can lead to increased solvent uptake through the lungs, eg one study showed a 28% increase in zylene uptake.   Ethanol modifies solvent metabolism:  7 volunteers who drank ethanol (alcohol) and inhaled toluene had a higher blood concentration of toluene than when no alcohol was drunk.  It was thought this was because of competition for alcohol dehydrogenase necessary for the metabolism of both.  
	But in another study, 33 workers who regularly drank alcohol had significantly lower blood toluene concentrations than other workers who seldom drank.  This suggests chronic ethanol ingestion induces solvent metabolising enzymes in the liver and thereby lowers blood solvent concentrations. 

	*Significant associations with spontaneous abortion were found for exposure to formalin, toluene and zylene in women working in pathology and histology laboratories 3 or more days a week.  This agreed with some earlier studies but because of the multi-exposure to chemicals the results have to be interpreted cautiously.   Toluene is certainly implicated here. 	

	*Birth Defects Found In Babies of Women Exposed to Solvents. Wall Street Journal, 24 March 1999, A6.  A study published in the Journal of the American Medical Association found that pregnant women exposed to organic solvents at work are 13 times more likely to have a baby with major birth defects, and are at increased risk for miscarriages, low birth weight, fetal distress, and prematurity.  Organic solvents are found in paints, pesticides, adhesives, lacquers, and cleaning agents, and the study found more problems in women employed in factories, laboratories, graphic design or printing businesses, and as chemists.  Dr. Richard Schwarz, an obstetrics consultant to the March of Dimes, warned that the study group was too small to reach definitive conclusions at this point.

	*The aromatics which have replaced lead in petrol are toluene, zylene, benzene, mesitylene and dimethyl-benzene.  “The data leaves no doubt that additives are thoroughgoing  highly potent carcingogens”.  It’s much safer to fill your mower, outboard, chainsaw... with leaded petrol.

	*MEK or 2-Butanone (an organic solvent - also called methyl ethyl ketone, methyl acetone)  is  found in vehicle exhaust; off-gasses naturally from trees; off-gasses formaldehyde when burned.  Used in/for adhesives,  foil,  cleaning products,  dental adhesive,  film,  vinyl,  food flavouring,  glue,  gums,  laquer, synthetic leather, lube oils, paint stripper, transparent paper,  paraffin wax,  perfume,  pesticide inert, plastic, printing ink,  resin,  rosin,  synthetic rubber,  varnish.  (Our Toxic Times, p 9, Dec, 1998).

	*ACTA Update, No 37, Oct 1997:  Neurotoxicity - An Overview  E G Hilary:  “...Since WW2 there have been 600 million synthetic chemicals unleashed on the world... The human nervous system is designed to be extremely sensitive. It registers the slightest sound, the touch of a feather over skin, the subtlety of conceptual thinking .... stress is a hackneyed diagnosis... rare brain cancer glioma is increasing astonishingly.... neurobehavioural testing in populations chronically exposed to neurotoxins is vital... ”  

	Inerts: the secret pesticides.   Inerts are the ingredients in pesticides which do not have to be specified. EPA lists over 1400 of these including solvents, stabilisers, and preservatives.  Linguistic gymnastics allow tricky manouvres. Inerts include glycol ether, xylene, toluene, formaldehyde and glutaraldehyde. (NCAP - Internet:   http://www.efn.org/~ncap/ActiveInertsRel.htm).  71 different solvents were identified in 8,000 pesticides in 1993, (particularly xylene).  The solvent may explain the increases in the risks for leukemia and non-Hodgkins lymphoma in farmers. 

PARKINSON'S  and  SOLVENTS
	Parkinson's is a progressive brain disorder that is almost always fatal, but the suffering can go on for years. The disease usually strikes people over age 60, but a few people get it before they reach 40.  More than a million Americans are living with the disease at any one time.
	Parkinson's begins when the brain cells which produce dopamine begin to die. Dopamine serves as a chemical messenger helping to control muscle activities. Loss of dopamine gives rise to stiffness, tremor, slow movement, difficulty with balance, difficulty walking, a stooped-over, shuffling gait. As the disease progresses, the patient may develop difficulty speaking, symptoms of senility (dementia) similar to Alzheimer's, and severe depression.
	Causes have been debated for 150 years.  A breakthrough occurred in the early 1980s when a group of young people developed the symptoms of Parkinson's disease after taking an illegal drug called MPTP, which is similar to the narcotic pain killer meperidine (which is sold under the trade name Demerol). MPTP is also similar in chemical structure to several pesticides and herbicides.  Subsequently, symptoms of Parkinson's were induced in monkeys by feeding them MPTP. Early studies began to show a pattern: many people with Parkinson's have a history of exposure to pesticides, especially insecticides and herbicides.
	Jan 28, 1999, a genetic cause for most Parkinson's disease was effectively ruled out by the publication of a study of nearly 20,000 identical twins who did not get Parkinson's any more often than two unrelated individuals.  The researchers reported that, “genetic factors appear to be important when [Parkinson's] disease begins at or before age 50.”  Fewer than 10% come into this category.
	That leaves environmental chemicals as the culprit for the vast majority of Parkinson's. Since the late 1980s, a steady stream of studies from around the world has shown again and again that a common thread among victims of Parkinson's is a history of exposure to insecticides and herbicides. 
	 Most recently a study showed that exposure to industrial solvents is linked to Parkinson's. 

***

RECENT FINDINGS  -   Fragrances,  Air Fresheners,  Gasoline,  Carpets. 

	*Anderson R.C. and Anderson J.H.  Acute Toxic Effects of Fragrance Products.  Anderson Laboratories, West Harford, Vermont, USA.  Archives of Envir Health.  53(2): 138-146, 1998.  
Assessed ability of fragrance products to cause acute toxic effects in mammals using std ASTM-E-981 toxicological method to determine lung and sensory irritation.  Mice are much less sensitive than most humans so little chance of false positives. FOB neurobehavioural screening tool also used.  Confounding factors like viral or bacterial infections ruled out.  Five fragrance products were tested on 186 groups of mice, with 21 sham tests on unexposed control groups.  Zero grade medical air blown in to establish baseline control.  Then a small vial of cotton-tipped fragrance-sprayed applicators opened.  15 minutes recovery given after 1 hour exposure.  Testing over 3 yrs in 2 different labs.  Found “statistically significant acute toxic effects for sensory and pulmonary irritation, airflow limitation, and/or neurotoxicity for each product,  often at lowest dose tested.  As opposed to the shams, breathing immediately became abnormal - breathing gradually returned to normal when exposure ceased.  Neurological effects evaluated 15 mins after exposure ceased -  83 shams scored 4.6; some fragrance mice scored in excess of 100.  Abnormal responses included: altered posture, gait, muscle tone, tremors, abnormal repetitive movements, severe lip smacking, eye, ear, tail twitching, rapid circling oblivious to other mice, increased response to stimuli, abnormal reflexes and grip, balance problems.  Many statistically significant.  Some developed facial swelling, hair erection, localised cyanosis (dark discolouration of skin from reduced haemoglobin)  - might be significant for possible disruption of porphyrin metabolism/ disrupted heme leading to reduced haemoglobin, severe lacrimation, protruding eyeballs, paralysis of 1-2 limbs, coma, convulsions, death.  Five fragrance mice died  (mechanism unclear), no sham-exposed died.  Repeat exposures (2/day for 2 days) produced no increase in shams’ symptoms  but increased neurotoxicity in the fragrance mice - perhaps some “increasing sensitivity to the fragrance product emissions, perhaps even time-dependant sensitization.”  “We believe that these behavioural changes reflected toxicity in selected areas of the nervous system, rather than nonspecific effects (eg general anesthesia)...because some functions were unchanged”.  Inhalation excitotoxicity, or excess excitatory neurotransmitter firing from chemical stimulation of the olfactory nerves can cause specific neurologic effects, and even convulsions.  Other studies have shown induced airflow limitation in asthmatic humans exposed to spray colognes, scent-strips and perfumed magazines.  Highly irritant limolene was found on analysis.

AIR FRESHENERS

	*Anderson R C, Anderson J H. Toxic Effects of Air Freshener Emissions.  Archives of Environmental Health 52(6): 433-441 (1997).  Reported in Our Toxic Times  July 1998  by Cindy Duehring.  Air “fresheners” do much the opposite by releasing volatile organic compounds (VOCs) and adding to the indoor air pollution. This study used the ASTM-E-981 and FOB to assess sensory, pulmonary and neurological function changes in mice.  Used a brand often complained of.  One hour exposure to common air freshener  levels caused increases in sensory and pulmonary irritation, airflow velocity decreases (bronchoconstriction, asthma-like), and behavioural abnormalities consistent with neurologic impairment.  Some mice died.  The adverse effects were not found in the sham exposure (control) mice and none of these died.  After air freshener fumes were introduced, the respiratory rate changed and dropped as much as 50% within 10 minutes.  It returned rapidly towards baseline when exposure ceased and pure zero grade air was reintroduced.  Other tests involved air from a ‘room with a small air quality problem’, and a small amount of fresh latex paint.  In both tests they greatly increased the total VOCs.  The neurotoxicity was especially increased to severe levels in the ‘room’ test which would approximate exposure in a small kitchen.  The mouse to human applicability for sensory and pulmonary irritation is well-established.  Analysis of the VOCs in the test air found toluene,  limonene (can cause symptoms affecting the eye, skin, stomach, lung, and brain including dizziness, inco-ordination, convulsions, and death), pinene, sabinene, phellandrene, methoxybenzaldehyde, dihydrobenzofuran, terpinolene, ocimene, terpinene, butanoic acid, thujene, and methyl formamide.  The MSDS lists its health hazards: 2 on a scale of 1-4  (4 worst),  and recommends a NIOSH approved respirator  “if the vapour concentration is high due to heat”.  High vapour “may cause headache, nervousness, dizziness, tremours, fatigue, nausea, narcosis”.  Use of air fresheners in confined spaces like elevators could well give possible high vapour concentrations. 
	Note:  Formaldehyde and phenol are also components of air fresheners most of which “interfere with your ability to smell by coating your nasal passages with an oil film or by releasing a deadening nerve agent”. (Richard Alexander,  Top “10” Hazardous Household Chemicals,  <http://wwwconsumerlawpage.com/article/household-chemicals.shtml>  

GASOLINE

	*Davidoff A L, Keyl P M, Meggs W.  Development of Multiple Chemical Sensitivities in Laborers after Acute Gasoline Fume Exposure in an Underground Tunnelling Operation.  Arch Envir Health  53(3): 183-189  (1998).  Reported by Cindy Duerhing in OTT,  Nov 1998,  pp13-14.  
Seventy-seven tunnel workers were chronically exposed for 2 mnths to gasoline fumes including benzene while excavating.  30 workers were randomly chosen and compared with a random sample of 30 from the general population and a reference group of others with MCSS.  Initial symptoms: nausea, headache, throat irritation, eye irritation, cough consistent with exposure levels between 150ppm and 500ppm.  10-13 mnths after the incident, chronic health complaints were still present for some - 26.7% reported the new onset of chemical hypersensitivities and other characteristics that fit the conservative criteria for MCSS. Relatively naive, low socioeconomic non-litigious laborers reported: CNS system, musculoskeletal symptoms, lower respiratory and gastrointestinal problems. All groups reported some chemical sensitivities including 33% of the general population group.  60.7% of the gasoline group had sensitivities before the exposure but an additional 33% reported new or intensified sensitivities.  This was not a group of disgruntled workers or housewives with mass hysteria.  In this well-documented exposure none of the workers (all males) had previously complained of MCSS;  none had been seen by clinical ecologists or were members of support groups.  When interviewed, all the workers were seeking work or were gainfully employed.  Routine assays showed no differentiating abnormalities.

CARPETS

	*Cindy Duehring.  Carpet Toxicity Associated with MCS and Chronic Illness in Humans.  EARN  Profile. Vol  9, No 1.  (Reported in Our Toxic Times, Feb 1999. From JA Anderson’s Reactions to Carpet Emissions in Journal of Nutritional and Envir Med 7, 177-185, 1997.)  
Synthetic carpets emit more than 200 chemicals.  Anderson Lab researchers questioned 110 families with a carpet which showed positive test results for toxicity.  Their symptoms were diverse and overlapped  MCS.  Fatigue 85%;  pain in trunk or limbs 73%;  CNS - concentration/memory 72%;  skin rash/hair loss 45%;  tremors 40%;  irregular heartbeat 37%;  swollen glands 21%;  diarrhoea 29%;  blurred vision 47%;  
paralysis 9%;  convulsions 3%;   respiratory 65%;  headache 60%;  weakness 51%;  ENT 85%....
82% had developed symptoms within 3 mnths.  “The mechanism appears to involve acute toxicity (rather than allergic mediators) because they can be demonstrated within 60 minutes of the first exposure of naive mice to these carpet emissions”  in the lab.  The lab testing involved computer analysis and observation of mice behaviour. On video, showed many cases of abnormal movements eg rapid continuous circling, twitching, paralysis, coma/convulsions.  Some carpets killed none, some killed all four mice.  The sensory and pulmonary irritation, nervous system effects, and muscle weakness  correlated well with corresponding effects in humans.  In general, symptoms clearly decreased away from the exposure.  Odour is not a reliable guide to presence of toxins.  
Another study found similar symptoms in Swedish teachers in schools with wall-to-wall carpet compared with hardwood floors, including increased conjunctival irritation, swollen eyelids, facial rash, headache, and unusual fatigue.  When teachers moved to non-carpeted schools symptoms decreased.  Other studies have linked carpet exposure with oral pharyngeal cancers and lymphocytic leukemia in carpet installers/workers. 

MCSS  and  TILT	

	The first overview of environmental illness was written in Italy in 1700.  Bernardino Ramazzini, the father of industrial medicine, examined 42 occupations in a Treatise on the Diseases of Tradesmen, (including painters).  More extensive knowledge of the effects of solvents picked up in the 1970s.  Several papers in the 1960’s noted the relatively strong irritant and/or toxic properties of glutaraldehyde used as a sterilant with concern gradually increasing.  Research on the effects of chemicals in X-ray  goes back to work on glutaraldehyde begun by Dr Robert Zach in the USA in the late 1970s and the wider campaign about all the X-ray chemicals begun by Marjorie Gordon,  (who gave the name Darkroom Disease in 1984), and The Society of Radiographers  (UK)  subsequently.  See also the SNFTAAS  Bibliography:  http://nile1.northland.ac.nz/~Foot/snftaas/snftaas.html            or at            http://ncchem.com 

	Many of the effects of  glutaraldehyde,  formaldehyde and  solvents on sensitised individuals are the same,  and with the finding of  the solvents toluene and benzene in Xray chemistry, and the presence of the anaesthetic solvents in theatres,  the  SNFTAAS  network aims to support anyone exposed to any of these chemicals. Once sensitised,  many  glutaraldehyde /formaldehyde /solvent sensitised  people cross-react to an enormous range of chemicals and products used in modern living and based hugely on the petro-chemical industry.
	With solvent exposure, it is apparent that  "people are being affected ...  at levels below the WES"..  The same applies to glutaraldehyde  and formaldehyde:  “..some especially sensitive people are likely to be affected by volatile organic compounds  [VOCs]  below the threshold of discomfort for the general population......Many of these volatiles are known irritants and intoxicants and include xylene and toluene from paint, formaldehyde from particle board and ketones from lacquers  and adhesives.” A clue that an ingredient may be a petro-chemical is the “prop” prefix. 

OTHER “FLATTENERS”:  Organic solvents: new copiers, computers and printers which off-gas organics from plastic casings and other construction components (hydrocarbons and VOCs - these emissions are believed to decrease over time to negligible levels), ‘Twink’, spirit pens, printing inks eg photocopier ink with benzene/toluene, new magazines, fresh newspaper; dry cleaning  - anything with these solvents  including  pesticides;  alcohol  (the first stage of the metabolism of alcohol in the liver is into an aldehyde - acetaldehyde; perfumes are mainly alcohol);  chlorine;  some  food preservatives,  are some of the other things which  “flatten” sensitised people.  Wines and many other foods eg sausages, may contain  sulphur dioxide as a preservative.  Similarly  many manufactured foods contain  additives eg  TBHA (tert-butylhydroquinone),  BHT (butylated hydroxytoluene), and acetic acid.  Minute quantities of such substances may affect those already  'primed'.  (See also the list of  aldehyde-containing products  p 13.)	

“THE COLLATED EVIDENCE SUGGESTS MCS DOES EXIST”

	Independent, London, 14 March 1999:  “A report commissioned by the British Health and Safety Executive has concluded that [MCS]  does exist and could be caused by chemicals affecting part of the brain. The study, carried out by the Institute of Occupational Medicine and endorsed by the Department of Health, also links MCS with other unexplained 20th-century illnesses, such as chronic fatigue syndrome and ME.”  
	Thousands of victims of a syndrome known as “Chemical Aids” are set to claim millions of pounds in compensation after winning a long battle for their condition to be officially recognised. Until now, successive governments have refused to acknowledge the existence of multiple chemical sensitivity (MCS), caused by chemical poisoning, which experts claim is experienced by as many as one person in 10. 
	Sufferers develop allergic reactions after being exposed to products including pesticides and wood treatments. The chemicals can cause blackouts, memory loss and vomiting when those affected subsequently come into contact with ordinary domestic products, such as hairsprays or washing powder. Several studies have dismissed the disorder as psychological and have linked it with child abuse. Campaigners say victims now plan to sue companies including Monsanto and Zeneca, which they blame for not giving adequate warning of possible side-effects from the toxic chemicals they use to produce pesticides and insecticides. They believe that manufacturers should be forced to seek safer alternatives to substances such as lindane, which has been blamed for many cases of MCS.
	Margaret Anderson, a victim, says lindane is responsible for ruining her life. The retired civil servant has suffered from an irregular heartbeat and muscle spasms since her neighbours in Ludlow, Shropshire, had their house treated with the chemical nearly eight years ago.  Miss Anderson now suffers an allergic reaction if she drinks coffee or smells diesel fumes. “When they treated the house I was gasping and choking and my doctor referred me to the Birmingham Poisons Unit. Then I found out that I reacted if I had a glass of wine or touched washing powder,” she said. “My social life has been reduced by half and I have to avoid  hospitals like the plague because of the chemicals that they use. Doctors are not trained to deal with this and most women just get shunted on to hormone replacement therapy. This report is a step forward because it recognises there is a problem for the first time.”

MCS  -  COMMONLY ACCEPTED CRITERIA

“1.  There are usually multiple symptoms involving multiple body systems, such as the nervous, respiratory, gastrointestinal, and the musculo-skeletal systems.
2.  Typically, symptoms occur after initial exposures which can be identified by the person (such as the chemical off-gassing during the installation of new carpeting), or repeated low-levels of chronic exposures  (such as pesticide spraying, working over a dry cleaning shop, or with solvents).
3.  Symptoms occur and subside in response to an ever-increasing number of substances and products at lower and lower levels.  Reactions are triggered by petrochemicals, combustion sources and by-products and coal tar derivatives.
4.  Symptoms are brought on by very low levels of exposures - below the permissable exposure levels for various chemicals established by the government, and usually below exposure levels tolerated by most people.
5.  Symptoms are triggered by exposures to a wider range of substances found in the workplace and at home.  Solvents (paint, varnishes, adhesives, pesticides, and cleaning solutions) are most frequently implicated.  Some other substances include new building materials and furnishings, formaldehyde in new clothes, perfumes and colognes, detergents, air exhaust, books, and copying machines and laser printer toners.
6.  Other explanations for the symptoms can be ruled out. 
 (A compilation from various sources by Nancy Day:  Hazards at the Brigham.  Revolution, Spring 1995.)

A REVIEW OF MULTIPLE CHEMICAL SENSITIVITY.   
R A Graveling, A Pilkington, J P K George, M P Butler, S N Tannahill.   Institute of Occupational Medicine, Edinburgh, UK.  1999.

A critical review of several hundred references on MCS.  “Despite extensive literature on the existence of MCS, there is no unequivocal epidemiological evidence;  quantitative exposure data are singularly lacking; and qualitative exposure data are, at best, patchy.  There is also some evidence to suggest that MCS is sometimes used as an indiscriminate diagnosis for undiagnosed disorders.  Despite this, the collated evidence suggests that MCS does exist  although its prevalence generally seems to be exaggerated.  Many causal mechanisms have been proposed, some suggesting a physical origin - such as MCS reflecting an immunological overload (total body load) - others favouring a psychological basis - such as MCS symptoms being evoked as part of a conditioned response to previous trauma.  The available evidence seems most strongly to support a physical mechanism involving senstisation of  part of the midbrain known as the limbic system.  However, it is increasingly being recognised that the psychological milieu of a person can considerably influence physical illness, either through generating a predisposition to disease or in the subsequent prognosis.  Work is needed to establish the prevalence of MCS and to confirm or refute selected causal mechanisms.”  
	“The concepts of masking and TILT both merit consideration ... it seems there is a range of individual susceptibility to the effects of chemicals... It is plausible that components of unrelated chemicals could share certain carbon links with similar surface activity able to trigger a response in a previously sensitised person.... As yet limbic kindling... is purely hypothetical.  It seems to fit most, if not all, the facts concerning MCS and can be supported by knowledge of the neurophysiology of the brain... However this... has to explain why MCS is not more prevalent among groups with higher exposures...”  

***

Perhaps the use of a controversial MCS diagnosis in a work-related injury (eg solvent,  glutaral- dehyde or formaldehyde exposure) has kept physicians and patients away from an MCS diagnosis for fear of having the claim for compensation rejected upon  psychosomatic/it’s all the the head/they have PMT etc  grounds.  There is no doubt about the MCS symptoms of some of the glutaraldehyde, formaldehyde, and solvent members of this network.  There is also no doubt about the general policy of rejection of MCS claims upon psychological grounds by the ACC of New Zealand, until the recent acceptance in the High Court  of three claims for solvent and pesticide exposures resulting in MCSS.  (One claim for MCS from exposure to photographic chemicals was accepted by ACC in 1992  (Marriot  ACA 249/91).  Some MCS claims were accepted in the early 1980s.)  Several claims for MCSS in nurses and radiographers are currently at ACC review.

From ACTA UPDATE,  April 1999.  “One of Australia’s most promising young show horses has tested hyper-sensitive to more than 3 dozen foods and natural stubstances... it is obvious the horse also reacts to numerous synthetic chemicals with reactions which have both behavioural and physical manifestations. Surely not even the most skeptical can accuse an animal of holding “an inappropriate belief system... ”

TOXICANT INDUCED LOSS OF TOLERANCE:  (TILT)

	Dr Claudia Miller,   Assistant Professor in Allergy and Immunology at the University of Texas Health Science Centre, San Antonio, and  Nicholas Ashford,  Professor of Technology and Policy at the MITposits that their new, testable  TILT  theory of  chemically induced disease shows how in certain susceptible persons,  a single high level or repeated low-level exposure to chemicals may cause some people to lose their natural tolerance for various chemicals,  foods and drugs.  Subsequently, ultra-low levels of the same and chemically-unrelated  substances trigger symptoms,  thus perpetuating illness.  
	Converging lines of evidence support this theory:  (1) The fact that similar multisystem symptoms and new-onset intolerances have been reported by different investigators among  different demographic groups following exposure to many different types of chemicals;  (2) the internal consistency of these patients’ complaints of intolerances for not only tiny doses of inhaled chemicals but also various foods, caffeine, alcohol, and medications;  (3) the degree to which the illness mimics addiction;  (4) the identification of an anatomical substate whose malfunction might explain these problems (the limbic system); and  (5)  recent animal models that replicate key features of   TILT.
	Ultimately, human challenges conducted in an environmentally-controlled hospital unit may be essential for resolving questions of etiology (psychogenic, toxicogenic) in a definitive manner.  A set of postulates for etiological verification is offered.

TILT Website:   http://www.med.vc.edu/htdocs/medicine/ceg/oxstress/Leikauf.htm

***
TIME DEPENDANT SENSITIZATION
At the American Chemical Society Symposium, Aug 1998,  Barbara Sorg, University of Washington, described attempts to use time-dependent sensitisation to model MCS.  Low doses of formaldehyde were administered daily for 7 or 20 days to rats which were, 2 weeks later, tested for response to cocaine.  The F-treated rats showed more cocaine reaction (rearing and moving about) than did the controls.  She then blocked this activity with tranquiliser injected into the portion of the limbic system of the brain which influences emotional/endocrine etc processes.  The results demonstrated how the sensitivity to an endogenous (from outside the body) chemical can be changed.  (Our Toxic Times, Dec 1998).  

NO CURES  FOR  MCS:
	Cynthia Wilson, CIIN, in Our Toxic Times, March 1999, quotes the adage: “An illness for which there are many treatments has no cure”.  Several surveys of MCS have shown the only point of agreement is that there is no cure.  MCS is progressive.  The more you are exposed the more damage can be done.  Four categories of treatment:  (1). No harm.  (2).  Benefit unlikely or patient made worse.  (3). Treating the illnesses and conditions which appear concurrently.  Other medical causes need to be ruled out. The longer an MCS person is on a drug the more likely they are to develop an adverse reaction to it.  (4).  The treatment universally beneficial and hated:  AVOIDANCE.  It wrecks havoc on families.  Tracking chemical triggers can be long and painful - on average 3 yrs to work  out and successfully manage.  “No exposure, no symptoms, no need for medication.”  Avoidance builds tolerance but sufferers begin to to feel so good many mistake the feeling for being cured.  But people in this stage are on very dangerous ground and are devastated when they forget avoidance and get an exposure that may undo years of avoidance.
	Join CIIN  to get the full article.

CHRONIC  FATIGUE  SYNDROME 

	CFS forms part of the diagnosis in some chemical injuries.  Research by the Collaborative Pain Research Unit  (including Prof Tim Roberts and Dr Hugh Dunstan, Dept Biological Sciences of the University of Newcastle;  Dr Neil McGregor, clinical scientist;  Dr Henry Butt, of John Hunter Hospital) and duplicated in Sweden, has  (Aug 1997) linked a common bacterial infection, mycoplasma,  to CFS.  One SNFTAAS member whose doctor is involved in this research writes: “My food absorption and gut function is poor.  Consequently I am on digestive enzymes, amino acid supplements, massive doses of vitamin C (1200mg), calcium and vitamin D (not absorbing), acidophilus plus a bowel flora food, all in excessively large doses with no side effects.  He also performed a new test for mycoplasma infections using DNA - positive (as were 4 other glutaraldehyde-affected).  Consequently, I have been on double strength antibiotics for 8 months with some interesting results.  I was told all my symptoms would come back if it was going to work and then I would get better.  I had a range of symptoms that I had not even connected to my exposure and, yes, I have not felt this well for a long long time.”  
	This mycoplasma test is also available at Waikato Hospital, NZ - cost c. $150.  The haematologist involved is Kevin Barratt who works with the blood bank.  
	
The Challenge of Chronic illness;  A Report on the Recent International CFS Conference,  Sydney,  1999.    Peter Evans,  ACTA.  (Report in  UPDATE, No 47, April, 1999)
	Predominant theme was evidence of the role of bacterial and viral infections in CFS - such as mycoplasma fermentans, rickettsia, chlamydia, and stealth viruses with their experimental treatments.   Other research subjects are serum potassium and hormone dysregulation following exercise; biochemical and urinary metabolite abnormalities; the disruption of ion exchange mechanisms across the cell wall (channelopathy) and the presence of an interferon enzyme of low molecular weight, called RNase L which may have potential  as a diagnostic marker.  Although the treatment of CFS with multiple combinations of antibiotics does have some promise, many of the organisms are not proven pathological or thought necessarily to be a cause of CFS.  However the increased presence of mycobacterium and other organisms may be a result of immune dysfunction through a process similar to HIV/AIDS where opportunistic infections contribute to the disease process.  A legal warning was given on the potential for litigation relating to institutional negligence in the care of people with CFS.   Conference transcripts from Alsion Hunter Memorial Foundation  ph (02) 9418 2465.
Web sites:  http://www.immed.org     (mycoplasma, antibiotics, nutritional support)
	     http://www.ccid.org         (stealth viruses)
	
	NOTE:  ACTA Update Oct 98:  Such a positive response [to antibiotics] may only happen in an atypical subset, as antibiotics can trigger an acute reaction in MCS sufferers.  Mycoplasmas, the smallest bacterial organisms with the capacity to invade cells, tissues and blood, are aeons old and were not previously considered human pathogens, however the organism may have mutated. 

Hedrick T.  The Royal Colleges report on CFS.  CFIDS Chronicle, 1997, 10, 1, 8-13.  This is an  “insidiously biased and potentially harmful” report on Chronic Fatigue Syndrome....with a pervasive psychiatric bias... Neuroimaging studies were largely dismissed....No credibility was given to the ‘reverse causation’ hypothesis that the reactive depression or anxiety may develop because of the experience of having a debilitating illness for which cause and treatment are not known, and that may result in loss of career and lead many patients to have negative health experiences with health professionals.  Is a self-reported physical symptom psychiatric or physical?  Dr Leonard Jason (Monitor, Nov 1996):  “People with CFS can make you a list of all the things they want to do tomorrow, but a person with depression cannot...Also CFS patients tend to suffer from exercise intolerance - they find exercising particularly difficult and tiring - whereas exercise usually makes depressed people feel better”.  A 1994  US study found no significant reduction in depression, self-reported stress, or fatigue scores in CFS patients under-going cognitive-behavioural intervention (CBT), whereas positive results were found for persons with depression.  This report may trivialise the illness - “just being tired”. And a lot more.

***

Professor Brian Goble brings together the effects of chemicals in two reasonably specialised but very interesting papers on the following Australian Chemical Trauma Alliance (ACTA) web page:   http://www-mugc.cc.monash.edu.au/~deg  
		Implications of toxic substances exposure to humans and animals.	
		Enzymatic influences causation of brain cell damage.
He was exposed to Agent Orange and other chemicals in Vietnam and appears as an expert witness in many different chemical cases with very good success.  (Fees reasonable and will do a report).  <goble@kin.on.net>                                         <http://www-mugc.cc.monash.edu.au/~degob1/goble>
	Another good ACTA article is “Don't Fight The Healing Process”.  ACTA’s address is:  
c/o Tracy Brown,  178 Chapel St,  Armidale,  NSW,  2350,  Australia.   <acespade@northnet.com.au>
ACTA’s website:  http://www.ozemail.com.au/~actuall                                         

ESTABLISHING  CHEMICAL  SENSITIVITY   

THE  SKIN  PATCH  TEST  (SPT).  
	Allergies affect over 20% of the population in the UK and  “recent epidemiological studies have indicated that many chemical pollutants are allergenic ...and the incidence of atopic allergy is increasing with pollution”.  Allergies are difficult to diagnose and it is hard to get a clear indication of all the allergens implicated.  One of the oldest tests is Skin Prick Testing  involving the introduction of allergen extract into the upper layer of skin - gives immediate results.  However disadvantages include poor quality, unstable, non-standard solutions that may also contain irritants. Also, the assessment is subjective and skin response variable and may be influenced by medication.  The test carries the risk of serious adverse reactions. 

Betty Bridges   bcb56 <bcb56@IX.NETCOM.COM>  writes:  	

	Skin Patch testing is diagnostic for skin allergies. It is not diagnostic for inhaled allergens. I am most familar with fragrance materials. Many fragrance materials are also skin irritants. The concentrations are formulated to provide enough exposure to trigger a reaction if the person is allergic to the material, but not high enough for concentration to cause an irritant reaction or cause sensitization if the allergy did not exist. Patch tests that covered larger areas (so there was more exposure) had greater positive results. (Gefeller O, et al. The association between size of test chamber and patch test reaction: A statistical reanalysis. Contact Dermatitis. 1999 Jan, 4, 1, 14-8.)
	....The size of the reaction is the gauge of how allergic a person is to the substance. The larger the area of reaction, the more sensitive. There are a few people that are so highly sensitive to an allergen that an anaphalactic reaction is a real possibility from a scratch test. For this reason scratch tests are not usually used if a person is suspected of having very severe allergies to a particular substance. RAST tests are done on the blood instead. 
	All allergy tests have limits. There are false positives and false negatives. A person can have respiratory sensitisation to a substance and the tests be negative. In the case of isocyanates
only about a third have positive antibodies to the substance, but have positive respiratory challenge tests. Results of allergy testing are manifested as a local reaction in the case of skin testing and as elevated antibodies in blood testing  (IgE, IgG).”

	Some SNFTAAS members show a reaction to glutaraldehyde with skin testing but many do not;  many have wider, delayed testing responses.   
	Nethercott et al looked at contact dermatitis due to GA in health care workers.  Allergic contact dermatitis due to GA was found in 13.  Concomitant sensitivity to other chemicals was noted in 10.  The positive patch test was only evident for every 2 in 4.  In 5, the skin disease forced the worker to leave his occupation.  Garcia, 1972  described a prosecutor’s assistant who showed glutaraldehyde/formaldehyde cross-reactivity on SPT but had apparently had no contact with glutaraldehyde.

	From Glasgow, Scotland:  Skin testing done in 1987/8 by Dr Forsythe, Dermatologist, at Glasgow Royal Infirmary, of 12 radiographers and technicians with darkroom disease.  
Reactions:
	6 cinnamon						glutaraldehyde 1
	8 E210-219 (Benzoates) 					formaldehyde 2
	nickel 5							cetramide 1
	sorbic acid 1						mint 1
	cobalt 2							oil of Peru 1
	neomycin 1

A control group of OTs was done at the same time but this weren't followed up at the time.  Recently one of the Glasgow  technicians who was retested now patch tests positive to almost all perfumes and a large variety of household cleaners.  She also has mucous membrane reactions (swelling) to plastics which didn't show up on the skin test of her back. 

HAPTENS and CHALLENGES

Betty Bridges  (see above): “Challenge testing is different from allergy testing. The person is exposed to the substance in question, then observed and tested to see what happens. This has definite risks and is sometimes difficult to do. If the substance being tested has an odor, it is difficult to do a blinded test. A blinded test is necessary to determine that it is not the odor that triggers the response.  In general in a challenge test, the least amount of the substance needed to cause a reaction is used.”

From  Our Toxic Times,  (April 1999, Vol 10, No 4).  Dr Patrick  Williams  (Benchmark Genetics,  USA  
ph 507- 645-2378)  has a good explanation of how the immune system reacts with chemicals following the traditional toxicological model: “CHEMICALLY  INDUCED  IMMUNE  RESPONSE  EXPLAINED”.   It covers Innate Immunity  (the body’s physical and chemical barriers;  blood proteins; phagocytic macrophages, neutrophils, and natural killer cells) and Acquired Immunity - a specific immune response to each foreign agent.  Also  Chemical Irritants, Toxicants and Allergens.  “Toxic effects sre not produced by a chemical agent unless that agent or its metabolites reach susceptible cells tissues, or organs within the body.  In addition, the concentration and longevity of the chemical in the body are critically important to the production of a toxic effect...and the susceptibility of the body. As in the case of chemical irritants, cellular and tissue toxicity results in an inflmmatory response.  If this occurs on the external surface, redness, swelling, heat, and pain will be observed.  These same indications of inflammation occur inside the body as well.”
	“Chemical allergy is an immunologically mediated adverse reaction resulting from previous exposure (sensitisation) to a specific chemical or structurally similar one  (hypersensitivity).  Most chemicals and their metabolic products are not large enough to be recognized by the immune system as a foreign substance.”  However, when a chemical binds with a “self” protein  (called a hapten)  it forms an antigen and can now be recognized by the immune system ... “This hapten-protein complex (antigen) is then capable of stimulating the formation of antibodies, which occurs over a 7-14 day period.  This process is called sensitization.”  

	Hypersensitivity can be classified into four types on the basis of immune mechanisms and mediator molecules (this is a simplification):   TYPE 1  Immediate Hypersensitivity - typically mediated by IgE  (eg isocyanates).   TYPE 2   Antibody-Mediated Cytotoxic Hypersensitivity - antibodies against haptens bound to cell surfaces (eg heavy metals).   TYPE 3  Immune Complex Mediated Hypersenstivity  - deposition of antigen-antibody complexes in various tissues (blood vessels and joints).   TYPE 4  Cell Mediated Hypersensitivity  - sensitized T cells (typically in skin) release cytokines in response to a secondary exposure  (eg allergic contact dermatitis which represents a true allergy with minute amounts of chemical causing reactions.  This is distinct from irritant contact dermatitis where the severity of the reaction is related to the dose applied.)  50% of chemically sensitive patients display Type 4  (Rea, 1992.) 

Dr Sherwood Burge,  Birmingham Heartlands Hospital, Bordesley Green East, Birmingham  B9 5SS, England (ph 0121 766 6611, fax  0121 685 5558) has done a great deal of work on glutaraldehyde and occupational asthma.  He has developed the hapten for GA.  He can do specific allergy testing to GA. It must be done fairly quickly after exposure - at least within the first 6 months. He has set up booth challenges for X-ray chemistry and GA. 

CHROMOSOME TESTING 
	is available in Adelaide, Australia through Dr Judy Ford.  She writes: “There are positive findings in more than 70% with glutaraldehyde exposure, with no limit to the time between exposure and blood-testing. The test looks at the rate of “sporadic” chromosome abnormalities.  The rate found per cell is about 1 cell per 1,000 analysed.  This is elevated 30 times in people who have been chemically exposed, so so there are usually 1 or more abnormal cells in 50.  This is like a fingerprint left at the scene of the crime.  It is damage that we can observe but obviously indicates a far greater level of damage to the mitochondrial DNA (the energy system for the cell).  The DNA in mitochondria cannot be repaired and so damage is permanent. 

	The test takes about 10 days -2 wks. We have recently analysed our data on (a) past exposures - analysed by chromosome analysis and (b) current exposures - measured by the micronucleus test.  Most of the people with legal claims belong to the first group.  Whilst I write reports, legal cases usually require an extra report which explains the particular relevance of the findings to the particular case.  I charge $150 per hour for the writing of these reports but they are well recieved by the lawyers. There can be a delay with Customs/Quarantine so if you wish to go ahead with testing  I will send you some labels to attach to the outside of packages.  Please send a specimen of heparinised blood (never clotted - about 10 mls in a lithium heparin tube) with some sealant around the top - we usually use Parafilm.  This stops problems with pressure changes in the plane.  The blood tube then needs to be packaged appropriately for international air transport (we can return packaging).  Hopefully one of your Pathology Companies can assist.  On the outside of the package put  “Human blood, pathogen-free, for genetic testing” and mark it URGENT.  Just send a letter (or Pathology Form) of referral with patient's name and address, doctor's name and address/fax number for the report plus date of birth.  If the details of the exposure, when, for how long, how much are known, please include them.
Contact: DOVE Australia.   Email:   <info@mtx.net.au>   or search for   <http://www.mtx.net.au>    or:  
Dr Judy Ford,  Genetic Consulting and Testing, 8 Butler Dr,  Hendon,  Adelaide,  Australia. 
 ph:  08 8244 3402. 

	

PORPHYRINS  
	In  A Brief Overview of MCS,  Cynthia Wilson, CIIN, says: “One key element that is emerging is that chemical sensitivity is probably not an immune system dysfunction or related to allergies.  The latest research strongly suggests that chemical sensitivity is most probably some combination of CNS damage and enzyme deficiencies that can cause problems with the endocrine and immune systems....”
	
	“While most MCS research has focused on an immune system mechanism, MCS critics have repeatedly pointed out that much of what MCS sufferers claim simply cannot be immune system mediated. Especially controversial have been reactions which begin immediately upon exposure to chemicals or immediately upon the cessation of an exposure.  With the exception of a histamine response and some IgE-mediated responses such as anaphylactic shock,  the immune system is not generally capable of reacting as fast as the symptoms appear.  This has led some researchers to look at the central nervous system because it can and does have the capacity to respond within the time-frame most patients experience.  For example, if your immediate reaction is nausea or vomiting, these reactions are most probably being neurologically mediated.  Neurologic testing is finally proving subtle nervous system dysfunction and damage...” 

	“The neurological phenomenon known as time-dependent sensitisation (TDS),...has an amazing and uncanny similarity to MCS and not only helps to explain how the brain becomes sensitized to low-level chemical exposures in the first place, but the role that stress plays in adverse reactions.  It also provides a mechanism for cross sensitization to unrelated chemicals... thought to be impossible by MCS adversaries because no immune system mechanism has ever been established for it.  Because classical toxicology makes no allowances for cross sensitization either, the impossibility of cross sensitisation became a critical element in most theories of why MCS had to be a psychological rather a physiological disorder...”  (For TDS, see also  Cross Sensitisation p40.)
	
	“...in 1994, testing showed that over 90% of MCS sufferers have developed ..Disorders of Porphyrinopathy...The porphyrias are a group of rare metabolic, enzyme deficiency disorders involving the production of heme (for producing haemoglobin and  cytochrome P-450), and liver and/or bone marrow damage. They have many symptoms in common with MCS, the most significant being chemical intolerance/sensitivity and the fact that any estrogen mimicking chemical or drug can trigger an attack...this estrogen connection may be one reason females are more susceptible... A recent study of Gulf War veterans discovered that plasma butyrylcholonesterase enzyme deficiencies were playing a significant role in how people get poisoned.  A Danish study found that women in their 30s and 40s are at an all time low for the production of this enzyme.  Plasma butyr..s are scavenger enzymes for removing toxins from the body...I believe that these metabolic problems will provide the tie that binds all of the chemically injured communities together.  ...Autoimmune disorders are ...suspected as a consequence of being poisoned...”.  

	From Our Toxic Times, Aug 1998: Clinical  similarities of MCS to porphyria  include: “Apparent neurological basis for many of the symptoms, familial pattern of susceptibility thought to relate to probable genetic enzyme deficiency, and symptoms exacerbated by many medications.”  For a good explanation of porphyria, see Defining Multiple Chemical Sensitivity, Bonnye L. Matthews, McFarland 1998.  (This book also contains chapters by Dr Donald Dudley on Evoked Potential Testing, and  Dr Gunnar Heuser on SPECT brain scanning.)  Blood testing for chemically-induced porphyria needs to be done through the Mayo Clinic, Rochester, Minnesota,  when a person is “normal” and after an exposure. Articles on porphyrins appear in CIIN’s Our Toxic Times, April, August, October 1998. 

The Chemical Information Injury Network (CIIN) has a marvellous Resource Directory and  EARN provides computer literature searches etc at very reasonable cost.  CIIN, P.O. Box 301, White Sulphur Springs, Montana  59645-0301.  Ph: (406) 547-2255  F: -2455.   Web:  http://biz-comm.com/CIIN

ALIPHATIC VOLATILE SOLVENT TESTING    
	Abnormal body levels of  2 and 3 methylpentane and n-hexane have been detected in radiographers/MRTs/nurses.  The mechanism for their presence is not explained.
 	From the WASTE web page:  “Last summer (mid ’97) a member of WASTE had a two inch yellow staining with a wicking line across her bra and at both armpits.  This was followed by  sleepness night and then a horrible two weeks of toxic illness.  The lab felt this indicated the chemicals could still be active and recommended a blood analysis.  Methyl pentane showed 4x higher than normal.  Testing for methyl pentane and hexane in a further 10 USA nurses and MRTs affected by GA has shown all with  abnormal levels of  methyl pentane ranging from 7 to 102 (with normal being 4.5), some with and n-hexane, from 20 to 152 (with normal being 2).  Methanol is added to gluteraldehyde (pentanedione).  [See also p14  for methanol.]  They suspect that is where glut  metabolises to methylpentane.”  

Explanations/theories are currently being sought. Geof Care (Photosol) writes:  “N-hexane and methylpentane are not constituents of water-based photographic processing chemicals. Both are immiscible with water and so would be useless for any purpose including the removal of water after fixation. The UK HSE found no trace of either in their exhaustive study of fume components above fresh and used X-ray chemicals which identified over 50 other compounds, often impurities in raw materials or incompletely removed solvents etc from the manufacture of film base (Scobbie & Groves: Chemical pollutants in X-ray film processing departments, Ann.Occup.Hyg., 40, 423-435, 1996.) 

		Sample 1:  Away from the chemical since 1992;  methylpentane was 17. 
		Sample 2:  Ditto since 1992;  methylpentane 31. Also showed elevated n-hexane.
		Sample 3:  Methylpentane 7  -  she has recently left her job.
		Sample 4:  Anne W: methyl pentane 29.4,  n-hexane 21.1;  she has not been 			  	   working for a year.			
		Sample 5:  Methylpentane  7.  She never worked with the chemical but was a floor above 			  an X-ray dept with linking air conditioning.  She is still working.  The Xray 			  facility is gone.
		Sample 6:  Rose S’s tests were done 10 mnths after she was terminated from work;  			   methylpentane 7.4,    n-hexane 1.8
		Sample  7:  X-ray tech had the highest levels - 102 for methylpentane and n-hexane 152.  			   She is currently working in an x-ray dept.
		Sample 8:  Had only a slight elevation, 3 methyl pentane - 4.7, working part time,  20 			   yrsin dept with unventilated processor. (Also male).
		Sample 9:  Just stopped work with dermatitis and asthma.  3-Methylpentane 17 and 			   n-hexane 41.6.		
		Sample 10: Ramragee M.  Lab Report  7/28/98   Panel # 6.                                                 
                                   Compound           	                 Results	        		 Population Average          
		    n-Pentane              		     1.0                         		   1.0                     
		    2,2-Dimethylbutane		     1.0        	               	   1.0                                                        
                                    2-Methylpentane     		     7.9 		                                   1.0             
		    3-Methylpentane      		     21.1                                          	   4.5                                            
                                    n-Hexane                 		     19.5                                        	   2.0
                                    n-Heptane     	           		     1.0                                           	   1.0                               
								(Personal communications)

2-METHYLPENTANE    C6-H14   [Information from ChemWatch]  
	Synonyms:  Also called pentane,  2-methyl-iso-hexane,  1,2-dimethylbutane.  May be shipped as Hexane.  Used as solvent for paints, adhesives.  Reduced health hazard replacement for n-hexane.  
	Acute health Effects:  In general, the branched hexanes are much less toxic than n-hexane.  Based on structural and physicochemical similarities, hexane isomers are expected to be adsorbed, distributed and excreted like n-hexane.  Adipose (fatty) tissue has a high affinity for all C6 alkanes.  Solubility of hexane isomers in adipose, brain, liver, kidney, heart and muscle tissues was found to be higher than in blood.
	Inhaled:  Acute effects from inhalation of high concentrations of vapour are pulmonary irritation,  including coughing, with nausea; central nervous depression - characterised by headache and dizziness; increased reaction time, fatigue and loss of co-ordination....Symptoms of moderate poisoning may include giddiness, headache, dizziness and nausea...

HEXANE  AND  RELATED  HYDROCARBONS   [National Academy of  Sciences, 1995]
Hexane and related aliphatic hydrocarbons exhibit only slight acute toxicity by all routes of exposure... inhalation at high concentrations may result in light-headedness, giddiness, nausea and headache... Chronic exposure may cause central nervous system toxicity...

N-HEXANE   [Source: Shell Co.]
Shipping Name:  Hexanes,  Methylpentanes
	Use:  An incidental component of many aliphatic solvent mixes used as lacquer, paint and enamel thinners;  also in ink reducers and cleaning solvents.  Also used for solvent extraction of oil seeds [eg soya]and in pesticide residue analysis and gas chromatography.  
	Chronic Health Effects:  Principal routes of exposure are usually by inhalation of vapour and skin contact with the material.  Chronic inhalation or skin exposure to n-hexane may cause peripheral neuropathy, (eg damage to nerve ends in extremities with loss of sensation); and characteristic thickening.  Nerve damage has been documented with chronic exposures of greater than 500ppm.  Improvement in condition does not immediately follow removal from exposure and symptoms may progress for two or three months.  Recovery may take a year or more depending on severity of exposure, and may not always be complete.  Exposure to n-hexane with MEK will accelerate the appearance of damage.  Other isomers of hexane do not cause nerve damage. 

Dr William L. Marcus, Ph.D., D.A.B.T.  EPA.  Test interpretation:  toxdoc@crosslink.net  Aug 15, 1998                   
“There is no simple answer to your questions. The methyl pentanes appear to adversely affect the kidneys by forming branched chain aldehydes and or keytones that block the descending tubules, so it is important to monitor your kidney function.  N-Hexane is extremely dangerous. It attacks the nervous system causing various peripheral nervous system problems. It also attacks the central nervous system causing many different subtle problems ranging from changes in personality to loss of recent memory. Many of these symptoms are peripheral neuropathies (stocking glove syndrome) and motor problems [which] appear to most practising physicians unrelated. There are also problems with vision.  Headache and sleep disorders are also not uncommon. They are all related. The mechanism is well described.  N-hexane’s metabolite, hexane dione causes an interruption in axion-plasmic flow causing a condition known as die-back syndrome.  Since none of these materials are normal, any level in the blood is upsetting.  However, I am surprised to see that they can be measured at all. They are readily metabolized into far more toxic metabolites. They are stored in fat in large amounts especially if exposure has taken place over long periods of time. That portends worsening problems that are difficult to ameliorate.”

Contact    Accu Chem Labs, Richardson, Texas - Ph  0168 1800 747 2878   (Jerry Laporte, Ext 12).    Cost - US $155.    The samples need to arrive in 3 days - phone first for the Aliphatic Volatile Solvent Test Kit.

Urine testing of  3 SNFTAAS members in NZ for the metabolite of n-hexane (hexanedione) was negative.

SOME OF THE ON-GOING RESEARCH

	Many of the symptoms of glutaraldehyde/Xray chemical exposure from p 22 are not well- researched and it is the sheer weight of numbers which has shown that these symptoms are common to cases of chemical injury.  The study on respiratory effects begun by  Dr Aashish Vyas, was  funded by Union Carbide  for a further  two years to the tune of  £120,000 to look at the possible more wide-ranging effects of this chemical.  Dr Nair Raza will run this study from the NW Lung Centre, Manchester, England.  
	*Professor Claudia Miller, of the University of Texas Health  Science Centre, San Antonio, has gathered data for a comparitive study of  Gulf War veterans, breast implant patients,  MCS patients, and the glutaraldehyde affected, to follow up the TILT theory.  She is currently looking allergy, CFS, auto-immune disease, cancer, drug reactivity etc in the next generation as well, in families with more than one MCS sufferer (Update Oct 98). 
	*The Environmental  Hypersensitivity  Research Unit at the University of Toronto is also studying the etiology, diagnosis and treatment of environmental sensitivity in the hope of developing a rigorous methology for these. 
	*From ACTA UPDATE, No 38, Dec 1997:  The Canadian Govt has funded another environmental health centre, allied with Dalhousie University... smokeless, scent free, electric heating etc... for research, diagnosis, treatment.  Clinic “inundated”.  The Ontario Govt began its MCS work in 1985.  The Canadian govt has underway 14 research initiatives on housing for the chemically sensitive. 
	*Dr Les Simpson continues to look at blood samples using an electron microscope.  He has a major interest in pathogenesis (the cause of the disease process). He has found that chronic disorders such as ME/CFS,  MS,  AIDS, arachnoiditis,  SLE, OOS, fibromyalgia, Gulf War Syndrome, have increased numbers of red blood cells which are not the normal disc shape ie “Flat cells”.  The altered echinocytes are stiff, move more slowly through the capillaries and have low oxygen carrying capacity, hence insufficient oxygen is delivered to various organs and feelings of tiredness.  Viral infections also give rise to altered red blood cell shapes but in non-susceptible individuals these changes disappear in under two weeks.  Symptomatic individuals show changes for years.  About 50% of cases with ME with increased cup forms respond to injections of Vitamin B; others to evening primose oil and/or Trental.  (from an  OSH NZ handout and the ASAMS newsletter,  Oct 1998).  
	At the Perioperative Nurses’ Conference, NZ, Nov 1998, Dr Tim Ewer spoke of how the red cell cup forms seen in live blood samples become chronated and link to form rouleau or “caterpiller-like” piles of coins, with longer chains in more chemically sensitised  individuals. As the same time the white cells become paralysed and lose their clean-up “hoovering”-round- the-red-cells function.  

THE ROLE OF STRESS

The Less Stress Book   (A Consumers’ Institute Guide, NZ, 1997)  does provide some understanding of why many health professionals describe ill-health from chemical exposure as stress .  From p29:				
PHYSICAL SIGNS OF STRESS
	“Tiredness, fatigue. Difficulty catching breath, frequent deep sighing, shallow, rapid breaths
	Cold hands.  Muscular tension. Clenched jaw.. stiff neck,  frequent fidgety movement, difficulty 	keeping still. Grinding teeth, sore muscles, tight stomach. Frequent urge to urinate. Diarrhoea and 	stomach upsets, heartburn.  Increased illness - especially colds that won’t go, small rashes.
	Headaches, migraines, tinnitus.  Easily startled, jumpy, nervous, anxious. Trembling or shaking
	Significant weight change (without dieting). 

BEHAVIOURAL AND PERFORMANCE SIGNS OF STRESS
	Difficulty sleeping; sleep not restorative.  Changes in appearance; slippage in personal standards
	Routines break down; apathy and indifference.  Reduced activity levels’; a tendency to ‘cruise’ or 	‘blob out’. Mental disorganisation, difficulty concentrating, forgetting things. Multi-tasking 	inefficiently... Missing deadlines, meetings, appointments (not just very occasionally).  Work piles 	up; quality breaks down.  Avoidance of certain situations or people.  Calls not returned.  	Absences; increased sick days.  Increased use of alcohol, drugs, partying, overeating.

RELATIONSHIP AND EMOTIONAL SIGNS OF STRESS
	Cynical, hostile or rigid attitudes to work or other circumstances.  Hardening of stances on touchy 	issues.  Reduced tolerance; inability to see both sides of an issue; grumpy with children or partner
	Marked mood swings or changes.  Unhappiness with life; finding fault, irrational blaming.
	Powerful emotions - distress, anger, fear - closer to the surface. Withdrawal from friends, lovers
	Avoidance of social situations and commitments.  Sexual appetite falls away.  Able to talk only 	about ‘problems’.” 

HEALTH AND SAFETY
	As chemical illnesses resulting from workplace exposures are preventable illnesses,  it is scandalous that with the knowledge of the dangers of these chemicals,  people have continued to have been, and are still being made  ill.  In X-ray, if the chemical can’t be eliminated or substituted for,  the process should be  enclosed and ventilated.  In theatre, glutaraldehyde remains an outstanding cheap sterilant as long as excellent ventilation/handling is present.  This means dedicated local exhaust ventilation eg behind/below the developer or decontamination unit  (GA is heavier than air) and sufficient general room ventilation  ensuring  the recommended number of air changes per hour,  (between 10-20 air changes are suggested in various sources) with  good directional air flow to avoid fumes being drawn into the breathed-air flow.  Fume adsorbers don’t replace good ventilation.  New research has shown that the absorbstar filters are not as effective because of the increased humidity levels needed in the darkrooms.  
	Centralise use of chemicals. Pouring GA disturbs the surface tension and releases GA into the air.  Note that health problems are being reported from products replacing glutaraldehyde  (eg peracetic acid as a sterilant)  despite calculated levels in the atmosphere being almost negligible.  Note also, if using GA, thorough cleaning of scopes before soaking is critical as glutaraldehyde bonds protein in place inside the scopes. Put dried scopes in to soak so as not to dilute the GA. The FDA requires scopes to be soaked 45 mins @ 25º.  
                Monitor the level of chemicals.  Minimise the number of people exposed.  Reduce the period of exposure. Clean regularly.  Store and dispose safely so fumes cannot escape. 
               
                   Check out  environmental requirements. It is not acceptable to tip the waste untreated down the drain. Union Carbide, manufacturers of glutaraldehyde, Ucarsan®, state the product “should not be disposed of by draining into a sewer system or natural waterways. They could be toxic to the biomass of biological waste treatment systems or to aquatic life in natural waters.  The situation is complicated by the inclusion of quaternary ammonium compounds in glutaraldehyde formulations which can be toxic to fish.”  
              
             ‘Neutralin’, manufactured by National Diagnostics, neutralises all aldehydes by converting them into nonhazardous, non-toxic, non-corrosive, polymer and water.  You buy a 5 gallon pail which is ready to receive 5 gallons of  4% formaldehyde (10% formalin) . 
                   
                 Under 1996 regulations in the UK (and in Europe), likely in force end of 1998, most photographic solutions  must be labelled “Special (Hazardous) Waste” because of the ammonium thiosulphate and each consignment will incur a £15 fee.  

	Use low-allergy latex  gloves for short term use (GA penetrates latex) or nitrile gloves for longer periods and suitable  masks/respirators eg organic vapour masks, for short term possible high exposure (eg changing chemicals).  Filters in activated carbon filter masks must be changed according to a regular programme - once the filter is saturated there is no barrier to any further contaminant passing through to the wearer’s lungs.  High humidity affects their life. In some situations one solvent may displace another releasing the first substance into the lungs.  The respirator should be stored in a clean sealed container.  Goggles are compulsory; an eyewash station should be near.  Rinse the eye for 15 mins.  Contact lenses may bond to the eye. Do not smoke, eat, drink in the area. Small spills can be neutralised with ammonia.  Larger spills require a special clean-up team. A personal health surveillance system is essential.  Glutaraldehyde-free Xray chemicals are available.  Equipment has to be regularly inspected and maintained and procedures developed.  A good publication detailing all of the above in  X-Ray is  Photosol’s  Safety with Chemicals and Fumes  (1997).  Note that problems can still arise from air conditioning, building materials, photocopiers etc.

SOME  RECENT  LEGAL  SETTLEMENTS

	*Jan 1999,  £150,000 out-of-court settlement for a Glasgow radiographer who worked in a Medical Centre and had to retire 9 years ago at the age of 46 on medical grounds. Case taken by the MSF Union.	
	*In Glasgow, Scotland, the MSF Union also won a £180,000 out-of-court settlement with the Greater Glasgow Health Board for darkroom disease in 5 radiographers and technicians. For 15 years, claims of ill-health were fobbed off as “mass hysteria” and “women’s troubles”.  Anne Clarkson has a huge list of things she must avoid including  “disinfectants, most fabrics, felt pens and petrol fumes.  She can’t drink tea out of a plastic cup because fumes triggered by the heat hurt her throat. ‘It started with a tingling inside my lip then my nose got pins and needles.  Skin was peeling off like perished rubber.  My face burned and my eyes were sore and by the time I got home I was physically sick’.” She received £50,000.  Rose Paterson received £80,000.  She cannot even use a telephone without losing her voice because of her sensitivity to plastic. More than a hundred other claims in Scotland are expected. Daily Record, Oct 24, 1998.

	*Court of Appeals of Arkansas.  Case for Workers’ Compensation allowed against her employer.  The appellant worked as a GI lab assistant for 8 yrs disinfecting GI equipment.  Diagnosed with thrombocytosis (abnormal increase in blood platelets), reactive airways disease etc.  May 27, 1998.

	*Southern Crown Health Enterprise, NZ, pleaded guilty to exposing 2 nurses to glutaraldehyde - fined $8,000.  Safeguard, May/June 1997. A proportion of the settlement went to the nurses.
	*The British HSE  prosecuted a farmer for exposing a worker to disinfectant after the worker entered a mushroom shed being fumigated and suffered ill-health.  The farmer was fined £4,000 and costs of £1,500. (Nov 1997.)

	*In Ogden v Airedale Health Authority, 1995 a hospital radiographer won £77,000 in the first case to reach the English High Court, after developing occupational asthma caused by exposure to darkroom chemicals.  Occ Health Review, March/April, 1996.  Professor Peter Hewitt and Dr Sherwood Burge were expert witnesses in this case.  (Professor P J Hewitt, University of Bradford, Bradford, West Yorkshire, England.  Ph: 01274 383202   Fax: 01274 307951.  email: vcb@bradford.ac.uk )
	
*1990,  Bath Hospital paid £62,500 compensation to radiographers.  1992, David Wilcox, radiographer, settled out-of court with Colchester General Hospital,  England.  There have been a number of other settlements involving radiographers.

	*Cases for workers’ compensation from exposure to Xray processing chemicals have been accepted by ACC in New Zealand since 1983.

Multiple Chemical Sensitivity Syndrome (MCSS) Cases in NZ

	*One case for multiple chemical sensitivities won at ACC Appeal, Oct 1992.  John Robert Marriott, from exposure to chemicals from his work as a photo engraver, and  diagnosed as  “darkroom diseases”  by  Dr John Gillies,  Respiratory Physician,  and  Multiple Chemical Sensitivity  by  Professor Glass.  Judge Blackwood stated:  “There has not been a precise clinical diagnosis of a reaction to any specific chemical, but in the light of the reports from Dr Turner and Professor Glass, I am bound to accept that long-term exposure to a chemical mix can give rise to multiple chemical sensitivities”.  (ACA 249/91  Decision No 402/92.)
	*Derrick John Burston; exposure to many  solvents.  Neurotoxicity and multiple other health effects.  Judge Cartwright:  “...the appellant became very ill following exposure to chemicals in the course of his employment... That the evidence is not entirely conclusive as to the precise diagnosis of the appellant’s ailment, is not a necessary prerequisite...it is most unfortunate that the real cogency of the appellant’s case came to be dismissed in the slipstream of the debate on MCS.”  July 1998.  (ACA360/94.    Decision  No 58/98.)
 	*Craig McPherson for 2,4,5-T etc in his job as a sharemilker.  Itching skin, skin loss, violent stomach pains, diarrhoea, muscular aches and pains, lethargy, headaches.  Judge Cartwright:  “The contest over the labelling of the condition, whether MCS or herbicide poisoning with a subsequent persisting chronicity, creates a digression or focus on the wrong issue...MCS is a diagnosis which ACC is able to accept, and which it has accepted previously.  McPherson still suffered sensitivity to a variety of chemicals, including fresh ink  fumes, some soaps and toothpastes, some food and drinks, flysprays and antibiotics...”  October 1998.  (ACA 066/88   Decision No 86/98.)
	*Mark Wardle for Paraquat and Roundup after clearing a section (piece of land) - won at ACC appeal.  Dizziness, rashes, sweats, fatigue, mental confusion, headaches.  Became sensitive to other chemicals including paint and petrol fumes.  The judgement stated:  “...multiple chemical sensitivity does indeed exist”.  (NZ Herald Dec 21, 1998).  Decision No  100/98.  Reference ACA 517/93 
	*John Trembath for chemical poisoning from being drenched with 245-T and 24D in 1981. (Dominion, Jan 4, 1999).

CONCLUDING

	In Alberta, Canada, use of glutaraldehyde falls under legislation which controls pesticides, herbicides and fungicides. In order to use GA you have to be a certified pesticide applicator.  Nurses and radiographers have been allowed to to paddle in it for years. 
	 An American X-ray facility in Nebraska  has inadequate ventilation - a SNFTAAS member relieved there and managed to achieve a visit by an OSHA representative.  His response was, "You have air coming in and air going out.  The Environmental Protection Agency is more powerful politically than we are.  They say it is too  DANGEROUS  to vent outside,  so I really can't recommend to anyone that it be vented outside."  
	Only with safe workplaces will the number with debilitating chemical illnesses remain static. The true cost of inaction by managers in the health industry and in any industries using dangerous chemicals must be placed with the manufacturers/managers/owners.  
	Cross-sensitivity makes  vocational retraining extremely difficult  because there are few jobs/training that do not require exposure to some chemicals even in getting to work.  But even retraining in computer work, which can be undertaken in the relative safety of a non-sensitising home environment,  is hard because of short term memory loss and difficulty in concentration which makes new learning very difficult, (plus the off-gassing effects of the VOC chemicals used in the making of a new computer).  
	A 27 November, 1998  UK  NHS  Health Service Circular  to all Chief Executives, Directors of Public Health, Advisors in General Practice etc says:   “Glutaraldehyde  -  Status:  Action.    A new, legally enforceable MEL is expected to be introduced in early 1999... Trusts should:
	i    put revised procedures in place ...
	ii   plan to complete modification of current control systems eg ventilation...
	iii  replace current arrangements with an effective washer/disinfector by early 1999 where the MEL cannot be met in either of the above ways.  Glutaraldehyde is a volatile disinfecting and sterilising agent... exposure has been known to cause a range of problems from irritation of the eyes, nose and throat to skin sensitisation and asthma....   The HSE does not consider current hand-held equipment adequate for measuring airborne glutaraldehyde levels down to the requirements of the new MEL.  A number of laboratories have the capacity to carry out these measurements.”  AT LAST.  (Even if many of the other symptoms are not yet acknowledged.)

	It is imperative that health and safety organisations in every country take a much tougher line to provide the incentive for proper handling of the chemicals and good ventilation and personal protection - in NZ it is good that increased levies on employers, based on injury records, are starting to bite.  Whether this trend will continue with the privatisation and dismantling of ACC’s workplace injury insurance scheme has yet to be seen.  It is not good enough  that in other instances, knowledge of cases which have succeeded in court  and  the threat of legal action are the real incentives to cleaning up the work environment.
***

GENERAL BIBLIOGRAPHY:
	1.  Gordon M and Laird I.  Guidance Notes for the Provision  of a Safe Work Environment,   published by the Accident Compensation Corporation, P.O. Box 242, Wellington, New Zealand,  1990 ISBN 0-477-04616-9.  (Now only available in photocopy)
	2.  Spicer J, Hay and Gordon M A  Workplace exposure and reported health in New Zealand diagnostic radiographers.   Australasian Radiology.  30,.3 281-6 1986 
	3.  Safety with Chemicals and Fumes.  Photosol.  15 Bakers Court, Paycocke Rd,  Basildon,  Essex  SS14 3EH,  England.    Ph: (01268)  293612      Fax:   (01268) 523111         
	4.  Beauchamp Robert O et al .   A Critical Review of the Toxicology of Glutaraldehyde.  Critical Reviews in Toxicology,  22(3,4):143-174 (1992)
	5.  Documentation of the Threshold Limit Values and Biological Exposure Indices.  Sixth Edition, 1991.  American  Conference of  Governmental  Industrial  Hygienists.  
	6.  Clinical and immunologic evaluation of workers exposed to glutaraldehyde.  Curran AD, Burge PS,  Wiley K.  Allergy,  1996: 51, 826-832.
	7.   Norbach  Dan.   Skin and Respiratory symptoms from workers exposure to alkaline glutaraldehyde in medical services.  Scand J Work Environ Health  1988, 14,  366-371

FURTHER READING:

Chemical Exposures - Low Levels and High Stakes  by  Nicholas Ashford and Claudia Miller.  Second Edition, 1998. Van Nostrand Reinhold.  ISBN 0-442-02524-6

Defining Multiple Chemical Sensitivity.  Bonnye L Matthews.  McFarland, 1998.  ISBN 0-7864-0413-2

Chemical Exposure and Disease - the Layperson’s Guide to Understanding Cause and Effect.  Janette D. Sherman, M.D., PO Box 4605, Alexandria, VA 22303, USA
ISBN No. 0-0911131-31-0       $35.00 + $4.00 for shipping.

Theo Colborn, et al.  Our Stolen Future: Are We Threatening Our Fertility,  Intelligence and Survival?

Chemical Exposure and Human Health:  A Reference to 314 Chemicals with a Guide to Symptoms.   Cynthia Wilson.  McFarland and Co.  1993.

And many more good books.  CIIN has an excellent list.

SOME WEB SITES:

*http://www.clt.astate.edu/RadSci/PDark.htm   (Educational site with glutaraldehyde-specific information.,     from Rick Carlton,  Arkansas State University.)  To subscribe to ‘gasslist’ send a normal email message to:   listserv@crow.astate.edu     with a message of    <subscribe gasslist>  
*TILT Website:   http://www.med.vc.edu/htdocs/medicine/ceg/oxstress/Leikauf.htm  *http://www.ehcd.com/index.html  Dr William Rea’s Environmental Health Centre, Dallas, Web Bulletin Board.  Vols  1-4 of William Rea’s book Chemical Sensitivity, based on experience of 28,000 patients, are available.   
*http://www.neuro-test.com   Dr Kaye Kilburn’s web site on neurotoxicity. 
*ACTA’s website:  http://www.ozemail.com.au/~actuall                                         
*http://consumerlawpage.com/article/bookchems.html   (The Alexander Law Firm represents the injured, consumers, small business owners, and industrial workers in cases involving accidents, defective products, toxic chemical poisoning and pollution, and corporate fraud involving stocks and products. The firm holds Martindale-Hubbell's highest rating, is recognized in the List of Preeminent Law Firms in the U. S. and has been elected to the International Society of Primerus Law Firms. 
*http://occ-env-med.mc.duke.edu/oem/  Duke Occupational & Environmental Medicine - (Covers ATSDR, 	OSHA,  IRIS,  NIOSH,  Medline and more)
*http://www.worksafe.gov.au/worksafe/FULLTEXT/toc/h3-40.htm   Glutaraldehyde Full Public Report  
*http://chemfinder.camsoft.com/  ChemFinder Searching
*http://ntp-server.niehs.nih.gov/  National Toxicology Program (NTP) Home Page</A>
*http://www.antecint.com/glutaral.htm  Antec International Ltd. - Aldehyde, Glutaraldehyde, etc issues.  
*http://www.cea.purdue.edu/iahcsmm/  (Basic principles of sterilisation)
*http://steele.ohsu.edu/croet/research.html   Center for Research on Occupational and Environmental Toxicology  (CROET) Listed below are the main themes in CROET's basic and applied research projects for each of the major issues:
	Investigating the effects of low-level chemical exposures
	Preventing and repairing damage to the nervous system
	Identifying gene-environment interactions
*http://www.ameliaww.com/fpin/fpin.htm  (For information on health effects of fragrances)  or
http://www.users.globalnet.co.uk/~aair/
*http://www.ccohs.ca/search.html    The Canadian Centre for Occupational Health and Safety (CCOHS).  
A search for glutaraldehyde yields 9 articles:  (1) Health Effects of GA.  (2)  Basic Information on GA.   (3) GA.   (4) Working Safely with GA.   (5) First Aid for Exposure to GA.  (6) Personal Protective Equipment.  (7) International Hazard Classifications for GA.   (8) Source Info on GA.   (9)  Site Map.
*http://www.med.ed.ac.uk/hew/qsar/astchem.html   Low molecular weight chemicals that cause asthma/ 	University of Edinburgh.

INTERNATIONAL MCSS RESOURCES.

*The Internet Family Support Group for members of families with MCS, CFIDS, Environmental Illness etc can be found  via email at:	familysupport-mcs@groups.com         
*Read and post messages on the web:	http://eGroups.com/list/familysupport-mcs
*Web site of  MCS  Referral and Resources - set up by Dr Grace Ziem:  http://www.mcsrr.org/
*Dr Mark Donohoe, Australian specialist:  http://www.planet.ark.org/new/drmark1.html.
*International Directory on MCS:  http://www.w3-mediator.de/mcs/index.htm
*CIIN  (Chemical Injury Information Network),  PO Box 301, White Sulphur Springs, Montana 59645-0301, USA.  Ph: (406) 547-2455.  F:  (406) 547-2455.
*NCEHS  (National Centre for Environmental Health Strategies), 1100 Rural Avenue, Voorhees, New Jersey  08043, USA.  Ph:  (609) 429-5353  

The Jeremiah Project is an outreach ministry run by Rev Linda Reinhardt (herself disabled from pesticide poisoning) and sponsored by the Presbyterian Church.  It provides a chemical-free open air worship centre, resource library, etc plus services to homebound individuals.  Address:  HC-1   222 Soft Wind,  Canyon Lake, Texas 78133,  USA.   Ph: 830-935-4618.  

THE WRITER AND SNFTAAS HAVE DONE EVERYTHING THEY CAN TO ENSURE THE ACCURACY 
OF THIS INFORMATION BUT TAKE NO RESPONSIBILITY FOR THIS INFORMATION 
OR CONSEQUENCES RESULTING FROM THE PROVISION OF THIS INFORMATION.
THE WRITER DOES NOT HAVE A SCIENTIFIC BACKGROUND AND CAN ONLY REPORT INFORMATION!  
	       PLEASE SEEK ANY TREATMENT FROM A QUALIFIED MEDICAL PRACTITIONER

ALL IN THE MIND			 When I was young and full of rhymes
and all my days were salady,
Almost I could enjoy the times 
I caught some current malady.
Then, cheerful, knocked upon my door
The jocular physician,
With tonics and with comfort for
my innocent condition
Then friends would fetch me flowers 
and nurses rub my back,
and I could talk for hours
concerning my attack.
But now when vapours dog me,
what solace do I find?
My cronies can’t endure me;
The doctors scorn to cure me,
And, though I ail, assure me
It’s all a state of mind.

It’s psychosomatic now, psychosomatic,
Whatever you suffer is psychosomatic.
Your liver’s aquiver?  You’re feeling infirm?
Dispose of the notion you harbour a germ.
				Angina,
				          Arthritis,
					     Abdominal pain......
They’re nothing but symptoms of marital strain,
They’re nothing but proof that your love life is minus,
The ego is aching
Instead of the sinus.
So face up and brace up and stifle that sneeze,
It’s psychosomatic.  And ten dollars please.

There was a time that I recall
If one grew pale and thinnish
The pundits loved to lay it all an foods unvitaminish,
Or else, dogmatic, would maintain
Infection somewhere acted.
And when they’d shorn the tonsils twain,
They pulled the tooth impacted.
But now that orgies dental
Have made a modish halt,
Your ills today are mental
 and likely your own fault.
Now specialists inform you,
while knitting of their brows,
Your pain though sharp and shooting, 
is caused beyond disputing 
because you hate commuting or can’t abide your spouse.

It’s psychosomatic now, psychosomatic.
You breathed in some diesel, it’s psychosomatic.
That asthmatic attack while washing the floor --
You did it on purpose to get out of chores.
M C S,   I E I,   End-of-centuryitis?
The medics they still continue to fight us.
On days when we cannot get up off the bed
We’re told to remember  “It’s all in the head”. 
But if they are right then why so much pain
   When truly, yes truly, in this there’s no gain!

Phyllis McGinley  - a long time ago  (with a few alterations).                                             (Courtesy ASAMS, Dec 1998)