Medical Journal Papers and Magazine/Newspaper Articles

 Updated; August, 1998

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YEAR's 1968-80 | 1981 | 1982 | 1983 | 1984 | 1985 | 1986 | 1987 | 1988 | 1989 |

1990 | 1991 | 1992 |1993 | 1994 | 1995 | 1996 | 1997 | 1998

Glutaraldehyde/Aldehyde Toxicity Data 36
Glutaraldehyde and Formaldehyde in Electron Microscopy
Reports and Safety Manuals
Photography Papers
Sulphur Dioxide


Sanderson K V, Cronin E. Glutaraldehyde and contact dermatitis. British Medical Journal. 28 Sept, 1968. (2 theatre sisters; one devel. cracking and hardening of skin in 3 wks and 3 mnths later rash on hands, arms and R chin, with papules. Improved on holiday. Second had sore nail bed then rash on hands. Both had handled formalin. Both patch-tested positive to GA but neg to fomalin. Withdrawing GA from the theatre.)

Jordan W P , Dahl M V, Albert H L. Contact dermatitis from glutaraldehyde. Arch Derm 1972, 105, 94-95. (5 patients with allergic contact dermatitis to pure GA - 3 dental assistants; one male with excessive perspiration of the feet treated with 10% glut; one male with fingernail tinea. Positive patch tests to GA and GA-tanned leather, both the wool and the skin. Thus enough GA is free or dissociates from the collagen of the leather to cause a reaction.)

Maibach H. Glutaraldehyde: cross reactions to formaldehyde? Contact Dermatitis 1975, 1:326-327. (21 patients who patch-tested positive to GA at 96 hrs had no patch-test reaction to formaldehyde. 6 had neg reaction to 25% GA on soles but severe dermat to 2.5% on inside elbow test.)

Belanii K G & Priedkalns M D. An epidemic of pseudomembranous laryngotracheitis. Anesthesiology 1977 47: 530-531.

(7 patients who were intubated devel either sore throats, hoarseness or dypsnea [difficulty breathing] - 4 had to have tracheostomies. Larynxes were edematous and swollen; not bacterial or fungal. Trace GA was found inside the endotracheal tubes. One still had hoaresness 14 mnths later. GA is the suspected cause - no problems since, after using disposable tubes.)

Martin H. Connective tissue reactions to acid glutaraldehyde. Oral Surg, 1978, 46,433-440.

Osterberg B. Residual glutaraldehyde in plastics and rubbers after exposure to alkalinized glutaraldehyde solution and its importance on blood cell toxicity. Arch Pharm Chem Sci Ed. 1978, 6, 241-248.

Rea William J. Environmentally triggered cardiac disease. Annals of Allergy 1978, 40, 243-251, April. (12 highly selected patients with non-arteriosclerotic cardiac arrhythmias and/or chest pain refractory to medication and having symptoms related to smooth muscle sensitizaion were studied in a rigidly controlled relatively fume- and particle-free environment. The majority of signs and symptoms cleared in 10 patients without medication while under environmental control and in 10 of the 12 patients all arrhythmias were reproduced with controlled repeated individual-blind and double-blind incitant challenges. Blood abnormalities occurred in the complement and T-lymphocyte systems. One patient, a 38 year old physician devel symptoms related to smooth muscle sensitisation incl. gastrointestinal bloating, belching, gas, cramping; also urinary urgency, chest tightness, and peripheral arterial spasm when exposed to X-Ray developer fumes. When forced to stay in developing area, symptoms progressed to shortness of breath and frequent premature ventricular contractions. Withdrawal resulted in cessation. Same over at least 20 exposures.)

Reed Charles R, Allergy/Immunology, Introduction Post Graduate Medicine 65, 4, April, 1979. (Allergic syndromes eg rhinitis can follow exposure to antigens or to chemical or physical stimuli. GA in photographic or radiographic chemicals is suspected of causing non-IgE mediated occ asthma.)

Zach Robert .J. How prevalent is glutaraldehyde sensitivity? Consultant May, 1980, 116. (Zach asks "Can inhalation produce membrane sensitisation resulting in allergic contact dermatitis and allergic nasal, bronchial, laryngeal or vocal chord edema?" and how to test for sensitisation - any danger, what form of GA to use? Response: 1. Don Brown, Envir H&S, Univ of Michigan - Varpela et al (1971) studies indicate proposed TLV 0.03ppm adequate - few toxic effects on animals with 10x exposure. GA can be acute sensitiser - the manufs of Cidex report small amount of contact allergic dermatitis and once sensitised, some individuals manifested allergic reactions when exposed to even the vapours of GA. Manufacturer unaware of any sensitation. by inhalation. 2. Marshall Guthrie: Contact sensitisation and edema of mucous membranes, and other symptoms suggestive of allergic response are possible following repeat exposure.)

Axon A T R et al. Disinfection in upper-digestive-tract endoscopy in Britain. Lancet 1981; i: 1093-94. (British Society of Gastroenterologists’ Survey. 37% of staff (36 members) in 16 units performing more than 500 endoscopies/month reported symptoms including skin, conjunctivitis, and nasal symptoms, even when working below GA limits.)

Fisher A.A. Reactions to glutaraldehyde with particular reference to radiologists and technicians. Cutis 1981, 28, 113-12. (First report of radiologist and x-ray tech with allergic contact dermatitis. Zack’s suspicions of contact dermatitis of the fingers from handling freshly processed film confirmed by Fisher - in a radiologist. and a technician both with positive patch test to 1% GA. Zack’s question as above in Cutis. Zack suspects several radiologists and techs have developed asthma and laryngeal edema. Special study planned by Zack. GA used for sterilising scopes etc and artificial kidneys. 2% water solution for sterilising. Stable for long periods if stored cool but once sodium bicarb is added the new alkaline solution undergoes polymerisation and loses antimicrobial properties within 2-3 wks.

Other reports of allergic GA dermatitis in nurses from handling sterilised instruments:

a)Sanderson and Cronin 1968.

b) Skog E, Sensitivity to glutaraldehyde, Contact Derm Newsletter 1968, 4: 79.

c) Harman R O’Grady K J, Contact dermatitis due to sensitivity to Cidex (activated glutaraldehyde), Contact Derm Newsletter, 1972, 11: 279.

d) Lyon T C, Allergic contact dermatitis due to Cidex, Oral Surg, 1971, 32:895.

e) Neering 1974. f) Gordon H H, GA contact dermatitis. Contact Derm Newsletter. 1974, 15:442 - inhalation therapy assistant with acquired allergic contact dermatitis from GA cold sterilant.

Does GA cross react with formaldehyde?

a) Neering H and van Ketel W G, Glutaraldehyde and formaldehyde allergy, Contact Derm Newsletter 1974, 16:518 - one renal dialysis assistant who had been in contact with both GA and formald had positive patch tests to both.

b) Garcia R L Delayed hypersensitivity reaction to to glutaraldehyde and formaldehyde, Bull Assoc Military 1972, 21:11 - one positive to both who had formaldehyde contact as a prosecutor’s assistant but no apparent GA contact. c) Fisher’s 6 formaldehyde cases did not react to GA..

Comaish S, Glutaraldehyde lowers skin friction and enhances skin resistance to acute friction injury, Acta Derm Venereol 1973, 53: 455 recommended that GA made skin tougher to prevent blisters - a single application lasted up to 3 days. GA has known antiperspirant action.

Gordon H H, Herpes zoster and simplex, Cutis 12: 918, 1973, recommended GA treatment for herpes zoster and simplex, and for Pseudomonas infections, Arch Dermatol, 1974,:106:261.)

1981 1981

Family practioners may develop contact dermatitis from handling dry X-Rays. Family Practice News. Approx 1981, Vol 12, 2, p7. (Zack warning. GA vapour may also cause nose, throat and resp symptoms in those with dermatitis as with Zack himself. GA used because partially replaces the need for expensive silver. [Accuracy of this is questionned.] Dr Fisher confirmed chronic dermatologist in a radiologist and tech. Fisher says GA sensitisation develops in about 1% who handle X-Rays, but about 5% of radiologists and techs develop sensitivity to GA.. Zach conducting survey of radiologists to correlate asthma, sinus and respiratory problems.)

Hansen K S. Glutaraldehyde occupational dermatitis. Short Communications. 1981, 81-82. (Case report 1: 50 yr old cleaning woman using Korsolin for 6 mnths with rubber gloves devel dermatatis on hands and arms. Improved weekends. Positive patch GA test. Korsolin contains glut/formald/glycol/urea/solvents/boric acid. Case 2: 42 yr old nurse working on same ward as case 1 developed eczema after 3 mnths of disinfecting respirators - also used rubber gloves. Patch posiive to GA and rubber.)

Lind T, McDonald J A, Avioli L V. Adult Respiratory Distress Syndrome Arch. Intern. Med 1981, 141, 1749-1753, Dec. (Inhaled toxins (plus shock, infection, trauma, liquid aspiration, drug overdose, hematologic and metabolic disorders etc) can cause acute local lung injury. Whatever the cause, grossly similar patholological changes occur in the alveoli and capillaries. Injury to the alveolar-capillary unit causes injury to pulmonary capillary and epithelial cell permeability which allows flooding of alveoli. Four hallmarks: 1. hypoxemia, (lack of oxygen in the blood) 2. decreased lung compliance, 3. decreased functional residual capacity, 4. diffuse alveolar infiltrates on chest roentgenogram.)

Reed Charles E . (Mayo Clinic). Occupational asthma Postgraduate Medicine 1981, 70, 2. (Occupational asthma does not include non-specific aggravation of chronic asthma by irritating fumes or dusts at work. Workers with pre-existing IgE-mediated allergy are predisposed to asthma in occupations where the offending agent is a protein antigen eg baking, but in industries involving chemicals, allergic patients are not predisposed to asthma. Reaction may be prompt or delayed for several hrs or recur night after night for a week or so after a single exposure, depending on dose inhaled and more so on individual reactivity. The pattern of remission away from work is a valuable diagnostic tool. Remission may take days or weeks especially for instance from toluene diisocyanate, probably because of greatly increased airway irritability which renders the airways highly reactive to nonspecific irritants, exercise and cold air. A positive skin test may only reflect exposure to an antigen, not prove the antigen is causing symptoms. Skin testing may be highly dangerous in highly sensitised persons. With agents like toluene which seem to act as pharmacologic agents, skin tests or RASTS (estimation of antigen-specific IgE antibodies) are of no value. )

ACGIH C Glutaraldehyde 1981 (Properties. Toxicity data. Summary of literature. GA in water is stable but when sodium bicarbonate is added, the glut is activated and its sporicidal, bacterial, viricidal, fungicidal, activity lasts for 14 days. GA has two active carbonyl (CO=) groups which react with tissue proteins by cross-linking. The irritant effect is also increased with activated glutaraldehyde.

Varpela E et al, Liberation of alkalinized glutaraldehyde by respirators after cold sterilization, Acta Anasth Scand, 1971, 15, 291. Mice exposed to 8% and 33% glut for 24 hrs reacted with nervous behaviour, panting, face washing; symptoms disappearing after a few hours. Livers of mice exposed to the 33ppm showed definite toxic hepatitis, possibly reversible as the mice sacrificed 24 hrs later showed less liver damage. OSH, California detected 0.38ppm in the breathing zone from a 2% activated solution in a simulated sterilising procedure. At the end of the procedure when equipment was being air-hose dried, the operator and investigators all experienced eye, nose, throat irritation and sudden headaches. C E Colwell at Union Carbide, New York, questioned MBTH testing and found by gas chromatography that exposures above 0.5ppm are intolerably irritating. This method could detect 0.1ppm. An odour panel judged odour threshold recog to be 0.04ppm by volume and irritation response to be 0.3ppm. Therefore TLV ceiling for GA vapour set at 0.2ppm)

1982 1982

Ballantyne B. Glutaraldehyde: Bibliography on health-related studies. Union Carbide Corpn., 1982.

Zach Robert. Cidex. Reader Tip. American Family Physician, January 1982. (Warning of dermatitis, rhinitis, occupational asthma from GA vapour, and residuals on endotracheal tubes causing laryngotracheitis.)

Zach Robert. Diagnostic Tips. Primary Cardiology April, 1982 (Warning of edema of larynx, bronchospasm, chemical rhinitis after lung function testing or respiratory therapy, if GA used to sterilise mouthpieces and tubing. Report in Am J Hosp Pharmacy (20:465,1963) said that GA levels of 6 ppm persisted in rubber tubing after as many as 5 washings.)

1983 1983

Field G B. Assessment of Occupational Asthma Patient Management. 12, 9, 35-44, Sept 1983. (Work envir may cause asthma by sensitising the worker to a specific substance, or aggravate asthma by non-specific irritation of the bronchial tree. Detailed occupational and clinical history is the best guide and diagnosis can often be made on history alone. Patient will usually have worked in the environment for mnths or yrs. Most cases progress relentlessly but when exposure is mild or intermittent, symptoms may fluctuate. Symptoms appearing towards end of shift and reaching a peak in the evening after work are typical. Symptoms occurring within a few minutes are more often the result of non-specific irritation. There is periodicity over the working week with symptoms more severe in latter part of week and remitting over weekend, but this may become blurred. Remission over holidays is a striking feature but this may not begin for a week or more. On return to work, attacks may take a week to regain their former severity (cf non-specific bronchial irritation which will occur first day back). Bronchial hyper-reactivity of occ asthma usually, but not always remits over mnths or yrs. Dyspnoea with exercise is a consistent feature - may be last feature to resolve. Conventional allergic mechnisms appear to be involved in only a minority, and atopic indiidual no more likely than non-atopic to devel occ asthma. Antibodies are inconsistent and bear no close relationship to severity of symptoms therefore skin testing and RAST testing (the estimation of antigen-specific IgE antibodies) are rarely indicated. Bronchial challenge is the most definitive test but should only be ttempted under a specialist thoracic physician. Requires patient in hospital for 48 hrs, baseline meas of forced expiratory function in one second (FEV1), or peak expiratory flow fate (PEFR). After challenge, measurements taken at intervals for 24 hrs and repeated with stronger dose if no reaction. BRONCHIAL CHALLENGE SHOULD NOT BE ATTEMPTED WITH POTENT SENSITISING AGENTS eg toluene di-isocyanate, NOR IF MEASUREMENTS REVEAL CONSIDERABLE IMPAIRMENT OF BREATHING. No weight should be attached to a neg. reaction if the patient has left the job (this is rather like the absence of symptoms on Mondays and after hols). A useful assessment is to give the patient a mini peak flow meter and diary, recording 4-5 times daily.)

Gordon M.A. ARE RADIOGRAPHERS AT RISK? Shadows 1983; 26:4; 8-12. (NZ Silver Jubilee Conference paper. Marjorie Aline Gordon history - had spent last 9 mnths investigating the problem of hypersensitivity to X-ray chems. Qualified 1950, worked Wgtn Hosp 5 yrs, married, 4 children, returned to work 1967 setting up small private Xray dept in Otaki Med Centre under Dr John Weston, Radiologist. Small darkroom, hand processor, no outside ventn, sole charge for 11yrs, 2,500 patients/yr. 1979 moved to new Med Centre with auto processor plus hand processor for non-screen film. From 1971 had nocturnal arrthmia and tachycardia, dyspnoea after exercise. Sore throat/husky voice cleared in weekend. Developed severe arrthythmia and tachycardia and worsening ENT symptoms with increasing frequency. June 1982, very severe heart smptoms and onset of tinnitus, inc mucosal exudate and excessive fatigue. Medication unsuccessful. ECG taken duting 23 hr cardiac attack showed reaction typical of thyrotoxicosis - but thyroid tests normal. ENT specialist Oct ‘82 confirmed no sinus infection and no explanation of the tinnitus - stated the mucous membranes had all the appearance of a hypersensitivity, not an allergy. Returned to Rhythmadon med but worsening of nausea, tremor, weakness, excessive tiredness, blurred vision, and tinnitus. All except tinnitus improved at wknds. Nov ‘82 realisation that had to withdraw from work situation. Employer contacted Agfa-Gavaert, NZ, who denied any problems. Symptoms subsided over 3 wks sick leave. Returned to work December and symptoms all returned in a few days. Cardiologist stated condition pointed to a toxic chem reaction. Jan ‘83 cleaners spilt waste fixer - caused such severe symptoms that Agfa suggested a darkroom fan and ducting waste fixer to outside. Left on visit to UK and J Weston paid airfare to AGFA in Belgium. GP had previously contacted Agfa’s Dr De Wever who stated if the prob was respiratory only non-contact would prevent further occurrences. Agfa gave product info usually only available to senior sales staff. Agfa’s chem containers only warn of danger of skin contact but this info contained inhalation and toxic warnings. Attended July British Radiographers’ Conference. Question at the AGM - others affected? The Society had had other complaints they were beginning to look at. Warren Town, Society’s Industrial Relations Officer sending 316 quest to 82 H&S Reps - result: 494 identified physical discomfort. Home to NZ and 25 letters from radiographers all around the world: 13 with heart probs, 41 ENT, 40 chest, 41 excessive tiredness, 6 eye symptoms, 6 nausea, 3 painful joints. eg Coby, Sth Africa doing quality control in primitive conditions: "...attacks similar to anxiety neurosis. High pulse, perspiration, exudate in larynx, tinnitus, gross fatigue, often painful joints. During inspections in summer, admitted to hosp with ?rheumatic fever, ?viral myocarditis. All haematology/ endocrinology tests neg". Linda, UK: "...chest uncomfortable and tight, and palpitations I assumed to be from anxiety". Mr MC, UK: "...referred to consultant for ?cardiac arrhythmia, chest pains, tinnitus and excessive tiredness...on holiday my tinnitus was much improved. We know of 5 radiogs who have had serious URII heart probs...". From Wales: "...the dkrm is very small and problems started in 1982 when second processor installed. 12 on staff. ...furry mouth, catarrh, sneezing, headaches, sinusitis, chest pains, coughs, conjunctivitis... only stop on hol...I think they believe we are a bunch of neurotic women.". Mr H, Germany, "...suffering for 3 yrs.. We spend 1 hrs/day in darkroom.. My general stuffiness has been described as hay fever but I have never suffered from this..". Maire, Ireland: "I did not suffer sinus or respiratory infections until 1st yr as a student... sinus, nasal stuffiness, headaches, 4 virus infections, 2 pneumonias, sinuses washed out 4x.. NO RELIEF sore throats, gums, fatigue.". Patricia, S Africa, "...laryngitis for 9 yrs...radiol gave me a talking to and asked if I would have any voice left in 5 yrs...gave up full-time radiog...". Graham, Scotland: " suffers headaches, nausea, vomiting, tinnitus only when working in one small poorly ventilated darkroom.". John, England: "..doing 5,000 exams/yr. Began with feeling of burned sore mouth, white deposit on tongue, difficulty in swallowing, intense dryness, catarrh...Jan ‘82 found breathing blood pressure much below normal...felt as though I would faint. ECG and barium meal neg....told either a worn-out workaholic or had a phobia about work or off my chump, or going thru the vapours at 95F for many hrs/wk...I admire your nerve in writing as there is a risk you could make a fool of yourself and look like some sort of nutter" . T F Chitty from May and Baker made contact; concerned - had written article on sulphur dioxide. MAG’s AIMS: Education, ventilation, need to work with the chem companies. Questionnaire planned. Returned to work - a week back and even with change to door position and an assistant, could no longer work.)

Hansen K S. Occupational Dermatoses in Hospital Cleaning Women. Contact Dermatis. 1983, 5, 81-82, Sept 9.

Hansen K S. Glutaraldehyde Occupational Dermatitis. Contact Dermatitis 1983, 1, 81-82

1984 1984

Benson W G Case report - Exposure to Glutaraldehyde J Soc Occup Med 1984, 34, 63-64. (Endoscopy sister with constantly irritating eyes /conjunctivitis and increased breathlessness. Did peak flow meas. 2 hrly: 300 Litres/min at work. Peak flows improved at weekends to 410 L/min. In the week with an alternative sterilant, the only day with a fall was when another nurse was disinfecting with glut in the room next door. Support for GA being strong irritant and sensitiser)

Goncalo, S. et al. Occupational Contact Dermatitis to Glutaraldehyde. Contact Dermatitis. 1984, 10, 183-4. (Five cases of allergic contact dermatitis to glutaraldehyde from occupatonal exposure to Cidex. All reacted to several concentrations of activated Cidex and glut. Two reacted to formaldehyde. None of the 42 controls reacted (18 worked with Cidex manipulators, 24 no Cidex contact.....the precocious occurence of sensitization in all patients (4 to 6 mnths) suggests, as in Hansen's cases, that it is a strong allergen, and that the use of rubber gloves does not seem to afford complete protection.)

Tolerton J. Toxic Fumes - Marjorie fights for others at risk. NZ Women's Weekly, Sept 24, 1984, 4-6 (MAG's story from 1982, travel to UK, Aust, USA, then UK again to prove that radiographers are at risk. Her job in private practice, and health - falling asleep eating dinner, cardiac attacks, tinnitus, throat like heavy smoker, chronic laryngitis, tested for toxic thyroid, bad reaction to cleaning out a tank and the penny dropped. 3 wks off - better, cardiologist suggested looked like a toxic reaction. Visit to Agfa, Belgium, then Wales Conference, "Radiography News" article, 25 replies. Tried work again - immediately affected. Accepted by ACC (Workers’ Compensation). NZ survey with Spicer and Hay, Massey University. Medline search revealed Dr Zach's theory that glut was cause. Visit to Zach but NZ "the only place to really bring it into the open". Chemical companies willing to give info/help.)

"Occupational Asthma: Help is on the Way." June 19, 1984. Monroe Evening Times. (Dr Robert Zach/MAG meeting: asthmatic reactions in 5% of radiologists, skin plus eye, ear, nose and throat reactions, sensitisation to glut., ventilation the key, employees should be pre-screened, 1978 Univ of Oregon/Zach GA survey (aborted).)

Gordon M.A. The effects on health of inhaling toxic chemical fumes given off during the processing of x-ray films. Shadows 1984, 27, 4, 28-33, Dec. (Letter from photog company [Agfa] "We believe you have highlighted an area in  radiography which obviously needs more attention and research....size and ventilation of the darkroom is a factor of almost equal importance...". One page quest. (compiled from symptoms described in letters from all over the world and from symptoms described by NZ control sample group) devised. This went to radiogs with symptoms in the UK (21 sent, 60 ret), Aust (16 sent, 48 ret), S Africa, NZ; total 130 returned. Results: Headaches 103 / 79%, Sore throat/hoarseness 102 / 78.5%, Unexpected fatigue 93 / 71.5%, Bad taste in mouth 84 / 64%, Sore eyes 80 / 61.5%, Sinus probs 73 / 56%, Catarrh 73 / 56%, Nasal discharge 66 / 51%, Nausea 62 / 48%, Tight chest 60 / 46%, Painful joints 52 / 40%, Chest pains 50 / 38%, Shortness of breath 50 / 38%, Skin rash 44 / 38%, Mouth ulcers 43 / 33%, Lip sores 34 / 26%, Unusual heart rhythms 32 / 25%, Tinnitus 27 / 21%, Loss of feeling in extremities 22 / 17%.

Brit Soc. of Radiogs questionnaire of 82 Xray depts: 61 depts reported sore throats, 49 bad taste in mouth, 42 tight chest, 40 nausea, 31 mouth ulcers, 29 nasal discharge, plus eye, sinus probs, headaches, drowsiness. MAG’s work - Medline search had revealed Zack’s observations on GA. Contacted and met Zack who had begun research with the Univ of Oregon, 13,000 postcard quests to USA Xray personnel at cost of $20,000. Zack only received back 600 of the many which were returned as the university was not prepared to continue the investigation for fear of losing philanthropic support [from a photog co]. Dr Charles Reed lists GA as suspected of causing non-IgE mediated occ asthma (1979).

Meetings: on to the UK and discussions with Dr Cronin - had seen no contact dermatiits in radiogs. Dr Sanderson suggested skin patch tests. Dr Anthony Newman-Taylor (Brampton Hosp) agreed research must continue with a medical team. Prof C Rossiter (London Sch Hygiene and Occ Med) stated he was convinced there was a problem and suggested morbidity study (agreed this already achieved) and personal aldehyde monitoring devices. He could do air monitoring study if funding available. He discussed the problem with Kodak who are looking to safer processors and better labelling.

ISRRT/Brit Soc Radiogs Conference, Eastbourne, June, met G Care (Photosol), T Chitty (May and Baker) and discussed prob of measuring 0.2ppm accurately. Dr Conix ( AGFA-Gavaert) working on new hardener. Meeting with H&S Exec in Bristol - now testing for GA/formald/acetic acid/SO. Serious health probs at the Royal United Hosp, Bath. Further meetings: Dr Hughes, Immunologist (Royal Postgrad. Med School, Hammersmith); Dr C Bishop, H&S Exec re thesis on formald; Dr Bernard Hogben re formald case similar to MAG’s; Dr F Chandra (Sen Med Officer, DHSS); Dr M Greenberg, (toxicologist, DHSS) who referred to the lethal cocktail; Dr Ward (DHSS) re cover as an occ disease; M Jordan, Secretary, Coll of Radiogs - MAG to write for"Radiography"; Warren Town/Dr Audrey Jacobs, Society of Rads.

GA Usage; no warnings on chem containers, nothing on inhalation dangers. TLV - Threshold Limit Values - these are airborne concentrations of substances to which it is believed nearly all workers may be exposed day after day; some people react below the TLVs; danger from aldehydes as well as the recognised SO and acetic acid. Hazard control must include processor exhaust and extra room ventilation etc, plus checks on those who have worked with aldehydes before or have allergy history. Grants received: ISRRT WRETF $460, NZ Rouse Educ Trust $350, AGFA-Gavaert $200 travel. $24,000 of her own money. Dr W J Weston, her employer, "There is no doubt that this will be the most important contribution you will make to radiography and radiology in your lifetime".)

von Wartburg J P, Buhler R. Biology of Disease. Alcoholism and aldehydism: new biomedical concepts. Laboratory Investigation 1984, 50, 1, 5-15. (New research in alcoholism shows great variability with respect to metabolism of alcohol and its first oxidation product, acetaldehyde. Hypothesis that individual and racial differencess in alcohol metabolism are based on genetically determined variability of the enzymes alcohol dehydrogenase(ADH), and aldehyde dehydrogenase (ALDH). As a toxic intermediate of alcohol metabolism, acetaldehyde plays a central role. Three positive ranges of acetaldehyde levels can be defined: a) normal b) the "acute aldehyde syndrome" with extremely high levels of acetaldehyde, c) "chronic aldehydism" with aldehyde levels elevated 2-5 times. In Orientals lacking mitochondrial isoenzymes of the liver (the enzyme is present but inactive) , acetaldehyde accumulates and produces symptoms of intoxication: facial flushing, dilation of blood vessels, tachycardia, hypotension (abnormally low blood pressure), headache, nausea, vomiting, muscle weakness, sleeplessness after ethanol ingestion. This syndrome is highly aversive and thus prevents individuals from drinking. Alcoholics have slightly elevated levels of blood acetaldehyde. In alcoholic liver disease the mitochondria suffer severe damage, thus aldehyde oxidation is disturbed producing an accumulation of acetaldehyde which leads to a further disturbance of mitochondria. Acetaldehyde is also oxidised in the cytoplasm of the liver by cytosolic liver ALDH - this activity is reduced with alcoholic liver disease and could explain the disturbed acetaldehyde metabolism. Alcohol toxicity leads to the devel of fatty liver. One study suggested that test subjects with alcoholism in their families had higher blood acetaldehyde levels after a test dose of ethanol (alcohol). High concentrations of ADH were found in just a few cells of the kidney, gastrointesinal tract, liver, brain (cerebral cortex, cerebellum, hypothalamus), testes, pancreas (acetaldehyde also has a marked effect on insulin and glucogen release). "Therefore many of the organs could be direct targets of acetaldehyde ... even at low blood acetaldehyde levels".)

1985 1985

Bardazzi F, Malino M et al. Glutaraldehyde dermatitis in nurses. Contact dermatitis. 1985, 14, 5, 319. (541 hospital cleaning women showed a very low prevalence (0.2%) of sensitisation to GA but several cases of dermatitis in hospital staff.)

Brooks S M, Weiss M A, Bernstein I L Reactive Airways Dysfunction Syndrome (RADS). Persistant Asthma Syndrome after High Level Irritant Exposures Chest, 1985, 88, 376-384 (10 individuals developed asthma-like illness after a single exposure to high levels of a highly irritating fume, vapour, or smoke, most the result of a workplace accident. (One was a fumigating fog aerosol containing aldehyde and glycol etc - 6 mnths later she had sensitisn to cat/dog/house dust/ragweed/spores. One was bookstore fire smoke [? formaldehyde]; her symptoms began to develop the next day - had had a past history of allergic rhinitis). The illness simulated bronchial asthma and was associated with airways hyperreactivity but differed from typical occ asthma because of its rapid onset, specific relationship to a single environmental exposure and no apparent exposure presenstitisation with an apparent lack of allergic or immunologic etiology. None had any apparent respiratory complaints at the time of the accident, although two had allergic rhinitis. Mean duration of RADS was 3 years, one case was evaluated 12 yrs after the event. In some, an apparent delayed response from time of exposure was noted. Methacholine challenge method. "While our definition of RADS is restrictive ... it is conceivable that a low-level chronic exposure could cause a similar type process in some individuals."

Other long-term reactions reported:

Harkonen et al (1983): 3 miners had persistant airways hyperreactivity 4 yrs after SO exposure in an explosion.

Charon (1979): SO exposure, 3 severe/1 mild airways obstruction.

Flury et al (1983): concentrated ammonia fumes exposure; developed documented airways obstruction over 5 yrs.

Axford et al (1976); single severe toluene exposure. 4 yrs later 20 men with persistent respiratory symptoms.)

Denning J, The hazards of women's work New Scientist 17 Jan, 1985 (Body strength, shape/size issues. Women have proportionately less muscle but more fat (20-25% compared with 10-15%) which may make women more sensitive to chem pollutants eg organic solvents which are stored in body fat. The more rapid detoxifying liver metabolism in men may make them more susceptible if the metabolites are more toxic than the original chemical. Hirokawa, 1955 noticed women took longer to eliminate benzene from tissues and were more sensitive to toxic effects such as decreases in number of white blood cells. Female and castrated rabbits more sensitive than males to benzene. Men and women suffer greater toxic effects if fat rather than lean. Much of testing of safe chemical limits has been done on males. In a sex hormone factory, 12/30 f. employees had symptoms of excess oestrogen (4.3 x the rate of a matched group) from breathing, swallowing, skin absorbtion. Nurses at risk from cytostatic cancer drugs. A long list of chemicals including solvents can upset the menstrual cycle. Chemical pollutants pass through the placenta - most dangerous time is when babies develop their organ systems. Significant risks from halothane and nitrous oxide - high rates of infertlity and spontaneous abortions in these workers. Pregnant lab workers susceptible to viruses inhaled from aerosols - lost more pregnancies.)

Gordon M.A. A review of the toxicological effects of inhalation of fumes from photographic and radiographic chemicals during processing. Shadows 1985; 28:4; 8-9. (From Honolulu presentation. Some chemical companies now giving warnings on products. Damage:1. irritability or contact symptoms 2. systemic and toxic illnesses. Results of NZ survey showed most symptoms positively correlated to length of time spent in darkroom. Formaldehyde detected in Xray rooms indicates it is given off during processing [this is incorrect - comes from other things in the envir.]. Formald and SO are sensitisers. 1. Pre-sensitisation: small amount of the chemical absorbed and slowly builds up a reaction which may be rapid or take years. 2. Senstisation: when the immune system is triggered. 3. Reaction can happen within hours causing inflammation of respiratory tract and susceptible tissues in the individual. (Case1) 43, f, 18 yrs without problems. New job 1980, unventilated darkroom in which used fixer/devel stored. Spillages frequent and "blow-back" from processor into waste fixer. Exhaust from rapid processor not connected. Painful joints, rash, ulcers, loss of feeling in extremities, laryngitis. SLE diag. Withdrawn from work - dramatic improvement. Returned to work - within 4 days painful joints, rash, ulcers, laryngitis returned. 5 radiogs diag SLE. (Case 2) 33, m, no problems until 1981 sole-charge in darkroom with small fan and leaking auto processor ducting fumes into the ceiling. Nasal pain, tinnitus, catarrh, nasal discharge leading to tight chest, shortness of breath, unexplained. pneumonia. More bronchitis, pneumonia; by 1984 all the above plus painful joints and arrythmias. ECG showed typical toxic reaction. [This is Case 2 in 1987 paper.] (Case 3) MAG’s. Case (4): 42, f. New processor, 1978, sore eyes, ulcers, sore throat, voice loss, painful stiff joints, marked tiredness leading to 1981 with L facial weakness (L motor neurone facial palsy). New processor with leaking exhaust. Another new processor1983 - palsy subsided but respiratory symptoms debilitating. Case (5): 64, m, radiologist. Used auto processor from 1970 and did silver recovery. Following inflammatory reaction to fumes, infection seemed to travel down bronchial tubes to cause alveolitis with resultant pneumonia. SO mask - no further pneumonia. Permanent damage to mucous membranes of nares which became thickened and elevated - it was thought this might be a collagen prob. [Same person, Case No 4 in MAG’s 1987 paper].

Gordon M.A. Danger-toxic fumes! Radiography News April 1985. (Hazardous chems: Hydroquinone symptoms reported from 1945 - tinnitus, nausea, dizziness, increased respiration, headache, dyspnoea. Diethylene Glycol ingestion causes vomiting, cyanosis, headache, tachypnoea, pulmonary oedema. Acetic acid - ingestion causes burning of mucous membranes of mouth, throat, stomach, nausea. Glutaraldehyde. Sodium sulphite. Potassium hydroxide. Ammonium thiosulphate. Sodium sulphite. Acetic acid. Aluminium chloride. Breathing rather than swallowing can deliver the chemicals straight into the bloodstream, bypassing the detoxifying liver and damaging delicate membranes en route. In the ‘60s glutaraldehyde was added, and ammonium thiosulphate replaced sodium. Now have a mixture of chemicals (synergism), minimal washing of film and heated chemicals!!

NZ workplace survey results/tables. 72% response rate. Analysis, Dr J Spicer: most symptoms correlated positively with length of time in darkoom. Those with symptoms in the last 12 mnths: headache 76%; sore throat/hoarseness 69%; nasal discharge 61%; soreness of eyes 57%; unexpected fatigue 56%; sinus problems 50%; nausea 47%; painful joints 46%; bad taste in mouth 44%; mouth ulcers 35%; catarrh 29%; ringing in ears (tinnitus) 27%; tight chest 25%; skin rash 25%; lip sores 23%; shortness of breath 22%; unusual heart rhthms 19%; chest pains 18%; loss of feeling in extemities 15%.

British Society of Radiographers H &S survey of 82 Xray depts: sore throats 61 depts; bad taste 49; tight chest 42; nausea 40; mouth ulcers 31; nasal discharge 29 [plus eye, sinus, drowsiness, headache - MAG 1984 paper]. Zack’s, and Belani and Priedkalns (1977) work on GA. Zach left with paralysed vocal chord and severe sensitisation - insurance paid compensation but wouldn’t admit liability. Epidemiological survey urgently needed.)

1986 1986

Cold disinfectants led to closure. Occupational Health. 1987 , p102.

Collier S. Hazards in the darkroom. Health and Safety at Work. May 1986. (Carole Sewell, senior hospital radiographer, London, England; acute sinus pains, sore eyes, aching and ringing ears, infections, exhaustion, lost voice, bad taste, skin dry and split. Has to wear respirator to work. Warren Town of Society of Radiographers believes 30% of technicians could be in trouble. Survey by Society of Radiographers showed 500 radiogs in 82 British Hospitals experienced health problems. HSE say chems detected below limits, no obvious agent responsible, only very very few had reported problems. MSDS (Material Safety Data Sheets) are completely inadequate. Carole S says poor machine design a problem. The chems are agitated and heated, hot humid air rises, exhaust air from film drying compartment can blow back over the chemical tank and vice versa. In one double strength processor the dryer fans were activated as the film entered the drying section causing a gust to blow back into the eyes and nose of the operator. An extractor fan in her dept created more problems by drawing fumes out of the processor - these then blown into the room.).

Corrado O J et al. Asthma and rhinitis after exposure to glutaraldehyde in endoscopy units. Human Toxicology. 1986, 5, 325-327. (The first report to use provocation testing to confirm, in two out of four endoscopy nurses, a relation between exposure to alkaline glutaraldehyde and respiratory disease. 1) Nurse, 33, with hay fever and pollen asthma, 2 wks after starting work in endoscopy unit developed severe nasal symptoms. FEV in 1 sec was 2.7 litres - in normal range. No improvement with salbutamol inhalant. 2) Nurse, 30, with rhinitis and asthma noticed marked deterioration. Better using Dettox. Normal FEV 1.9. 3) Nurse, 43, devel asthma and rhinitis 2 wks after starting in endoscopy. Had history of both but never so severe and only in May-Aug. FEV normal. 4) Nurse, 37, 5 yrs in endoscopy, had chest tightness. Improved with Dettox. No improvement on salbutamol. Lung FT normal.

Conducted provocation testing. Blind testing impossible because of glut’s odour. Patient 1 had both an immediate (within 20 mins) rhinorrhoea and sneezing response and late, (2h), nasal airways resistance, (NAR), response after 20 min of exposure to open trough. Patient 2 had 22% fall in FEV1 after 80 min. NAR levels too high to measure. 1 and 2 had no change with saline control. 3 and 4 had no change with either. The development of the late reactions after provocation suggests that the underlying mechanism is allergic in nature and not simply an irritant effect on the airways. Findings have far wider implications as glutaraldehyde is used in several hospital departments as a histological fixative, a hardener for X-ray film and in the treatment of certain skin conditions.)

Gordon M A. Occupational stress and the radiographer, Letter to the editor. Radiography May/June 1986, 52, 603 (Fatigue, headaches, gastro-intestinal upsets, irritability etc far more likely to result from unhealthy work environment.) Shim C and Williams M.H. Effect of odors in asthma. American Journal of Medicine. 1986, 80, 18-22, Jan. (Many patients complain that some odors worsen their asthma. Perfume amd cologne are two of the most frequently mentioned offenders....A survey of 60 asthmatic patients revealed a history of repiratory symptoms in 57 on exposure to one or more common odours. Four patients with a history of worsening of asthma on exposure to cologne underwent challenge with a cologne, and their pulmonary function was tested before, during and after the exposure. Forced expiratory volume, FEV, in one second declined 18 to 58 percent below the baseline period during the 10 minute exposure and gradually increased in the next 20 minutes.... Odours are an important cause of worsening of asthma.)

Spicer J, Hay D M, Gordon M A. Workplace exposure and reported health in New Zealand diagnostic radiographers. Australasian Radiology 1986, 30, 3, 281-286. (Postal survey of 349 practising radiogs correlating length of time in the darkroom with symptoms. Results suggested to be underestimates of exposure-symptom relationships. Headache, sore eyes, tight chest, unusual heart rhythms appeared to be uncorrelated with length of exposure. All other symptoms showed a correlation. Tables given. The inhalation or ingestion or absorbtion pathways are implicated in the bad taste, sinus, nasal discharge, catarrh and lip sores. Lip sores, fatigue, painful joints, and numb extremities correlate with greatest exposure to the workplace; the latter three raise the possibility of systemic disorders. Other symptoms: sore throat/ hoarseness, nausea, mouth ulcers, ringing ears, rash, chest pains. Further more focussed studies now needed especially on URT disorders.

Gordon M A, Laird I. Guidance Notes for the Provision of a Safe Work Environment and Safe Work Practice for Radiographers and Darkroom Technicians. 1986. ACC, NZ. (Revised 1990) (See under "Reports".)

1987 1987

Gordon M.A. Reactions to chemical fumes in radiology departments. Radiography 1987, 52, 607, 85- 89. (Four case reports. No 1. Exhaust to processor not connected; puffy hands/feet, blurred vision, May ‘83 collapsed, loss of feeling in left foot and rt side of face. Spots over whole body. Bad taste. May ‘85, collapsed - loss of feeling left side of body, weakness, cold; atropine injection. No evidence of heart disease. After that, severe chest pain, nausea, pins and needles in lip, palate and tongue, numb R face, left arm and leg, pain left scapular, weakness, speech slurring. Most symptoms improved 2 wks away.All recurred within hours back. Still sensitive to traffic fumes, red wine, hair spray, cigarette smoke, aint,newsprint

No 2. Processor fumes vented into ceiling; small fan. 1981, nasal pain, earache, tinnitus. 1982 catarrh, rhinitis, shortness of breath, chest tightness, sore throats, lack of energy. 1983, unexplained pneumonia, wouldn’t clear. Still URT symptoms, tinnitus, fatigue, plus prostatitis which improved on hol. Continual chest infections not respondong to antibiotics. By 1984 arrythmias, prostatitis, tinnitus, catarrh, rhinitis, fatigue, sinuses blocked, wheeziness; 1985 medically unfit for radiography. New job but particle board walls with formaldehyde forced him to give up. Now sensitive to paint, petrol, cigarette smoke. [Case 2 in 1985 paper]. Case No 3. MAG. 1970-1979 - manual processor - cardiac arrthmias, tachycardia began. 1979 auto processor, worse cardiac, tinnitus, headache, URT, lip sores, severe sore throats, hoarseness. 1982 tachycardia: weakness, tremor, nausea, blurred vision. Aug: increased fibrillation, severe retrosternal burning pain, irritability, shakiness. Sept, cardiologist. (Xrays pictured.) Normal thyroid. Oct, ENT surgeon: suggestive of hypersensitivity and systemic illness. May 1983, left work, symptoms subsided. Sept returned to work and suffered atrial fibrillation. Left work. Intermittent tinnitus, headaches, lip sores went, recurrent laryngeal/tracheal infections. Reactions to petrol, cig smoke, hot dry air, cold winds, paint, red wine, radiographic chems. ENT assessment; permanent damage to vocal chords. No 4. Radiologist who did silver recovery in unventilated area. 1970-83 had 9 bouts of unexplained pneumonia following URT infection. Leaky tap nose stopped once on holiday. Nostrils became fissured, thickened. 1981 - area of consolidation about the R hilum - not a lesion. Final pneumonia 1983 - used full face mask from then on. 1986 lymphoid lymphoma. [Case 5 in 1985 paper])

Gordon M.A. Darkroom diseases and how to combat them. Journal of the Royal Society of Health 1987, 107, 3, 102-103. (The chemicals, synergism, symptoms, pulmonary transfer of toxic substances by-passes the detoxifying liver. Sensitisation. Prevention: Engineering/ventilation/ safe practice/ personal protection/ training/darkroom finish.)

Jaworski C et al. Allergic contact dermatitis to glutaraldehyde in a hair conditioner. Cleve Clin J Med. 1987, 54, 443-444. (22 yr old, f , with scalp eczema and secondary infection, hair loss. 90% improvement after 2 wks non-contact with the 1% glut conditioner. Pos patch test after 72 hrs to 0.1% glut. 74 cosmetics with GA were US registered between 1973-1984).

Laverton Sue. Letter to Ed. Shadows, 1988. (Wanganui Hospital. After new automatic processor, one radiographer began to complain of nausea/vomiting/headache after a session. Ineffectual expelair. 42. Extra expelair useless - despite frequent requests for better ventilation, told nothing could be done. ?change of recipe - smell became stronger - difficulty with speech then total voice loss for 5 mths. ENT surgeon stated hypertrophy of false vocal chords consistent with toxic chemical inhalation over long period. Left with husky voice and severe sensitivity to wind, smoke, paint fumes etc.)

Menne Torkil Regional variations in contact sensitization. Cleveden Clinic J of Med 1987, 54, 5, 377-8, Sept/Oct. (Main prerequisites for allergic contact sensitization are (a) a genetically susceptible individual, (b) a hapten [absorbed through the skin in an appropriate conc, (c) normally functioning Langerhans cells [probable antigen-presenting cells involved in immune responses] in the epidermis. Great variation on absorption depending on site. Skin response on back more pronounced than on arms. 25% GA popular for treating plantar warts etc. Contact dermatitis on soles rare - low density of Langerhans cells and probably also because of strong binding of GA to keratin. "GA must be regarded as one of the ubiquitous allergens".)

Straughn J. Avoiding glutaraldehyde irritation of the mucous membranes. Gastrointestinal Endoscopy 1987, 33, 5, 396-7. (Some staff found GA irritating but a modification to the Scope Guard system eliminated this with a system of long tube holders for dirty and clean endoscopes sunk into the bench).

Cold disinfectants led to closure. Occupational Health. April 1987. (2 hospital endoscopy units forced to close after staff sensitised to GA. Recent survey of 200 members of British Society for Gastroenterology showed up to 1/3 in endoscopy were affected by fumes or contact with Cidex, Asep, Gigasept, Tutacide etc. Christianne Newman, nurse advisor to BSH, sensitised after 2 yrs - says fume cupboards and special gloves impractical for routine cleaning of endoscopes. Do 15 in 3 hrs - would need many new ones (at 10,000 each) if to observe full precautions. RCN reluctant to take up nurses’ cause because of lack of nurses willing to put details in writing.

1988 1988

Gordon M.A. Darkroom diseases. Shadows 1988; 31:4; 18-20. (Radiographerss at risk are those using daylight/tabletop processors without adequate ventilation - ultrasound, radiotherapy, theatre and sole charge. Sensitisation after cumulative low-level, or eg a single spillage. Symptoms. Minute quantities prod non-IgE mediated response - asthma-like reaction is not a histamine release (unless it’s to sulphur dioxide). Blood tests by immunologist on 2 sick radiographers from different hospitals showed similar blood abnormalities even though different symptoms. 32 radiogs with no reported symptoms filled in brief personal questionnaire on age, sex, number of yrs exposure, allergies etc. Random blood tests showed blood abnormalities in 13/32 [41%] and evidence of immune stimulation in 31.2%: 5 positive ANA titres, 3 elevated antibodies to single-stranded DNA, positive auto-antibody readings in 2; minor deviation in peripheral blood mononuclear cell types were seen in another 3. A variety of minor blood screen abnormalities probably attributable to upper resp or other infections noted."Sufficient cause for concern to look at the matter in a ...controlled study". [Note, this never took place because of ethical concerns in NZ at the time.] )

Gordon M A. Chemical hazards in film processing. An update on research. Shadows, 1988, 31, 2, 28-29. (Publication achieved of Guidance Notes by ACC with 2,500 distributed and 2nd edition planned plus poster for the ISRRT.

3 months in the UK helping sick radiographers obtain compensation. ISRRT Teachers’ Seminar in Canada to persuade Schools of Radiography to incorporate the Guidance Notes into syllabus. One firm working on GA free developer. Blood testing for evidence of immune stimulation planned.)

Gordon M A. Chemical hazards in film processing. ISRRT Newsletter: The Control of Hazards in Radiographic Practice. 1988, 24, 1, 9-12. (Changes in processing, chemicals used, symptoms, control of hazards, health and safety in the work environment, health questionnaires, instruction in schools of radiography, wall charts.)

Nethercott J R, Holness D L, Page E. Occupational contact dermatitis due to glutaraldehyde in health care workers. Contact Dermatitis 1988, 18, 193-196. (Hand dermatitis in 13 healthcare workers, 4 yrs plus exposure. GA patch test strips in place for 48 hrs. Best reading at 96 hrs; only every two in four had a positive skin patch test. Hand eczema persisted even after subjects left their jobs. Sensitisation in 10 to formald and latex probably took place at the same time from the work envionment.)

Norback D. Skin and respiratory symptoms from exposure to alkaline glutaraldehyde in medical services. Scand. J Wk.Environ.Hlth. 1988, 14, 366-371 (Eye, skin, airway, headache, nausea, fatigue studied re cold sterilisation. Measurements revealed that GA exposure was intermittent and well below Swedish OES, but the exposed group showed significantly increased frequency of rashes, nasal and throat symptoms, headache and nausea. Results of patch testing were negative in those with rashes, suggesting that GA has its effect through direct irritation rather than allergy. Those who used GA most had 3x as many symptoms as those who used it least.)

Prima T, Pasquale R de, et al. Contact dermatitis from glutaraldehyde. Contact Dermatatis 1988, 19, 3 (Cleaner developed eczematous dermatitis after using Cidex for disinfection of instruments. Patch testing showed positive reaction to GA - should be considered a potent allergen.)

1989 1989

Bakke JV. Photochemicals and their effects on health. Tidsskr Nor Laegeforen 1989, 109, 3, 361-362. Jan.

[Article in Norwegian] PMID: 2916222, UI: 89130514. (Health hazards related to chemicals used in X-ray

departments and photographic laboratories need looking at. The chemicals which pollute the environment in such premises may cause symptoms related to the skin, mucous membranes, eyes and airways. Teratogenic, mutagenic and neurotoxic effects cannot be excluded).

Bakke J V, Bjerkvik P S, Pedersen I L, Eldoen G, Seim H. Occupational diseases among personnel at a radiology department. Tidsskr Nor Laegeforen. 1989, 109, 3, 345-349, Jan 30. [Article in Norwegian]. (Little attention hitherto paid to health injuries to personnel in X-ray departments after exposure to photochemicals. 24/30 employees at the X-ray department in Molde were shown to have health problems related to their work, including symptoms relating to the eyes, the upper and lower respiratory tract, and headache and lassitude. Analysis of the work environment showed constant extensive exposure of the employees to chemicals over a long period. After improvements to the environment, health problems were reduced appreciably, but not nullified. Some personnel had acquired permanent impairments. Bronchial hyperreactivity was discovered in 19 of the personnel, 13 of whom had subjective symptoms of obstruction and asthma but no manifestation of allergy. Relation between the work environment and impaired health; advice on how to avoid similar problems in the future.)

Burge P S Occupational risks of glutaraldehyde. Brit. Med.J. 1989, 299, 342. Aug. (Review of glut lit with the conclusion that some hospital workers developed symptoms under current limits. GA is the best sterilant therefore better to reduce exposure with appropriate measures).

CCH International. Hazard Alerts: gluteraldehyde and chemicals used in Xray processing. 1989, 90-102. (Two hazard alerts issued in the UK: 1) Glutaraldehyde - Occ Asthma documented plus respiratory, skin, and mucous membrane problems at levels below limits of 0.2ppm ceiling. Health authority fined 1000 plus 984 costs for causing occupational asthma. 2) Xray film processing chems - two out-of-court settlements for 62,000 centred around SO, hydroquinone, glut etc.

Cotes J E, Steel J, Leathart G L. Work Related Lung Disorders. Blackwell Scientific Publications. 1989. (Chap 16. Occ Asthma. Asthma is a disease which is characterised by wide variations over short periods of time in resistance to flow in intrapulmonary airways. the common feature is airflow limitation which varies in intensity from hour to hour. Types of work-related asthma: a) extrinsic atopic asthma where bronchoconstriction is mediated by IgE immunoglobulins; recognised by immediate reaction to inhalation allergen or allergy skin tests. b) extrinsic non-atopic asthma: asthma caused by an external agent i.e. mediated by some mechanism other than IgE. May show an immediate or delayed response, or both. (Isocyanates can cause both a) and b) types). [Atopic: genetic predisposition to allergens.]

Lung function in asthma (readily meas by FEV or PEF). Basic immunology: Immediate (Type 1) reactions; the mechanism of a) whole antigens (eg pollens) and, b) antigenic substances of low molecular weight chems (haptens).

Skin testing. RAST test (for detecting the presence in serum of IgE antibody which is specific for a particular antigen. Inhalation challenge testing at work or in the hospital lab. (Should "not be undertaken in the lab for medico-legal purposes and where occ asthma is a recognised hazard - monitoring at work should be used instead."). Testing for non-specific bronchial hyperreactivity by methacholine or histamine; sensitivity to non-specific bronchoconstrictor agents is increased in people recovering from occ asthma particularly those with delayed onset type; reactivity can be increased by inhalation challenge or the ingestion of the sensitizing substance in a dosage too small to cause bronchoconstriction. Diagnosis of occ asthma, often not clear-cut, prevalence - usually affects about 5%. Management and prevention. Examples of asthma: from drugs - aspirin, antibiotics; birds and animal residues; crustacea, insects, mites; tree dust/bark/sap, veg products including grains, gum, etc; spores - mouldy hay, grain, compost, mushroom; enzymes - eg in detergents and papain from pawpaw; dyes including tartrazine; metal salts; chemicals - isocyanates used to make polyurethanes (foams for upholstery, packaging; paints, sealants, plastics); colophony (pine resin) used in soldering, sticking plaster adhesive; epoxy compounds for making PVC, resins, paints, dyes, laquers esp if heated; formaldehyde - the starting point for the resins phenol-, melamine-, para-formaldehyde for glue and plastic foams. Formaldehyde liberated when these are heated. Also formald used as disinfectant, fungicide, hardener. Can cause immediate or delayed-onset asthma.)

Fowler J. F. Allergic contact dermatitis from glutaraldehyde exposure. J of Occ Med. 1989, 31, 10. (Hospital maintenance employee developed airborne contact dermatitis cleaning respiratory therapy equipment. Patch tested allergic to GA.)

Gordon M.A. Dangers in the darkroom. The Radiographer 1989, 36, 3, 114-115. (Summary of chems; pulmonary transfer of toxic substances means material is delivered directly into the bloodstream - access to the liver with its detoxifying enzymes is delayed. Delicate membranes of respiratory passages are irritated and damaged en route. Symptoms.

Sensitisn process. Hydroquinone, a benzene derivative, ?found in urine of darkroom technicians as a sulphate ester or malondialdehyde. GA a known sensitiser. Detection in atmosphere - mass spectograph necessary. Gas chromograph or dreger tubes not sensitive enough. Prevention.)

Harner, C.D. et al. Cidex-Induced synovitis. The American Journal of Sports Medicine. 1989, 17, 1, 96-102. (Microscopic evidence of inflammation was observed in the synovium of rabbit knees that had been injected with 10ppm of Cidex (2% glutaraldehyde). Stronger soln produced greater synovial inflammation. No evidence of delayed allergic component. Rinse solutions between operations had signif. levels of Cidex at several hospitals: 1,000 ppm by 5th rinse. Arthroscopic (endoscopes used for examining joints) complications could be linked to Cidex-induced synovitis, although this has not been proven clinically. Previous lab studies on toxic effects of 2% glut on epithelial lined tissues of gastro-intestinal, urological, pulmonary, skin, occular tissues have concluded GA only mildly toxic to living tissue.)

Jachuck S J, Bound C L, Steel J, Blain P G. Occupational Hazard in Hospital Staff exposed to 2 per cent glutaraldehyde

1989 in an endoscopy unit. Soc.Occup.Med 1989 39, 69-71. (Studied 8/9 wrkrs in endosc unit, 2 of whom had presented with symptoms. One worker had airways obstruction (breathlessness), 6 eye irritation, 6 rhinitis, 3 dermatitis, 1 nausea, 1 headache. GA below limit. MBTH testing used measures all aldehydes. 60 min TWA of 0.42 mg/m found.)

Parish N, "Darkroom disease expert interviewed." The Chronicle, NZ. Aug 14. 1989. (Report of BBC interview with MAG: Glasgow radiog dept closed because staff refuse to work there, first test case coming before court, Valerie Hughes' case featured on BBC’s "You and Yours", bill before English Parliament calling for Health Dept enquiry into toxic fumes.)

Pollard J. 'Dread of darkroom disease’, and 'Half X-ray staff have symptoms.' Pollard J. (Western Australia - Adrian Bertino-Clarke/Health Dept's survey in 1989 showed 64% of respondants reported symptoms. Rural hosps especially lacking ventilation.)

Tam M, Freeman S. Occupational allergic contact dermatitis due to glutaraldehyde: a study of 6 cases due to Wavicide and Aldecyde. J Occ Health and Safety 1989, 5, 6, 487-491. (6 non-atopic patients. Contact derm. on hands, (also face and forearms of 3). Strong positive patch tests. Two had positive only on the 4th day reading. Also positive to formalin,...thiuram (rubber), ...fragrance mix.)

Watson J. "Hospital staff claim chemicals poisonous." Scotland on Sunday. June 4 1989.(Rose Paterson, one of 17 out of 25 sick technicians at Southern General Hosp, Glasow, taking legal action. 20 yrs as MRT, mouth ulcers, frightening breathing probs, voice lost, eyelids swelled, skin came off top lip. Tried 5 times to go back to work.)

Wiggans P, McCurdy S A, Zeidenberg W. Epistaxis due to gluteraldehyde exposure. J Occ Med 3,10, 854-856. (Hosp employee with recurrent nosebleed and other URT irritation symptoms plus skin rash. Poor ventn and uncovered containers.)

1990 1990

'Bath pays 62,500 compensation for radiographers in toxic fumes case.' Radiography Today 1990, January, p 1. (Exposure to SO, hydroquinone, GA etc in poorly ventilated rooms.)

Linda's darkroom disease. Woman. 7 April 1990. (13 yrs exposure at Avon Hosp, sore throats, stuffy nose, husky voice, cough progressed to violent chest pains, lethargy, numb arm, palpitations, asthma, excruciating earache and severe headache; settled out-of-court).

Aw T.C., Barnes A. Occupational health and the use of chemical disinfectants: what is needed under COSHH regulations. ISSM Journal July/Aug, 1990, 7-8. (GA asthma resulted in 1,000 fine and equiv costs against district health authority in case taken by endosc nurse - The Independent, 22/2/89. Sterilants: GA, formald - causes irritant and allergic dermatitis, urticaria, irritn of respiratory tract, asthma and ?carcinogenic; phenols - skin and eye irritn; hydrogen peroxide, iodine and chlorine all irritant to resp tract and skin; alcohols - defatting can result in irritant derm.)

Babb J R. Chemical Disinfection and COSSH - safe and effective work practices. ISSM Journal July/Aug, 1990, 9-12. (West Midlands RHA survey of GA usage. 377 replies. 9% had no formal ventn, 76% no local exhaust ventn, 26% made no attempt to dilute discharge, 10% used a fume cupboard. Most GA use was for endosc. What sterilant should be used where - auto claving preferable but GA use in lab as a wide-spectrum non-corrosive disinfectant appears justified. GA

GA not rec for respiratory equipment. Table of properties of disinfectants. Fume cupboards are the most effective, over the whole work station for GA fumes. Need for dentists to use glut fast diminishing (Glenwright & Shovelton, 1989). Glut introd in 1963. Axon et al, 1981 - 37% of units performing more than 500 endoscs/mnth reported staff became sensitive. Study of theatre users, Trigg, 1984 - 55% reported reactions to GA. In Neumann (unpublished), 75% endosc nurses complained of reactions to glut. None of these studies included a control group. Safe practices - incl. do not use as bench wipe; rinse well and change water freq; tight fitting lids; dilute discharge; activated charcoal filter etc.)

Binding N, Wittig K. Exposure to formaldehyde and glutaraldehyde in operating theatres. Int Arch Occup Envir Health. 1990, 62, 233-8. (Meas 5 min TWA exposures up to 2.0 mg/m when a 3% soln was used to wipe down theatre benches;

0.53 mg/m detected over the duration of the cleanup. OES is 0.7mg/m for a 10 min TWA.)

Fisher A A. Allergic contact dermatitis of the hands fom Sporicidin (GA phenate) used to disinfect endoscopes. Cutis. 1990, 455, 4, 193-196.

Gibbs J. Glutaraldehyde: handle with care Nursing Times 1990, Vol 86, 21, May 23. (Survey of depts using GA in Middlesex Hospital. - Used only for delicate/expensive equip. Some proper soaking baths but also open bucket, washing up bowl 1990 1990 and other uncovered trays. Undated activated glut. Only one area with special ventn. In one room GA vapour so overpowering everyone’s eyes watered. Little knowledge of dangers or safety equip. Extra money for fume cabinets and ventn to meet COSHH regulations will be required.)

Gordon M.A. Radiographers at risk. Shadows Dec, 1990, 38-39. (MAG’s story of the 7 years of research. Survey results published in ‘Australasian Radiology’ took 2 yrs and much watered down. No matter what evidence, the ‘experts’ will never agree. "One has to drive on and leave everyone else to catch up with you." At the 1984 ISRRT conference enthusiasm for MAG’s findings had evaporated and the impression was that the authorities wished she would go back to NZ and forget the whole thing. Advised the London Hazards Centre and the UK COHSE Union. Details of grants/help received - ISRRT World Educ Trust Fund (3 grants), ACC published the Guidance Notes; NZ Health Dept paid (reluctantly) for 2nd printing of Guidance Notes; WRETF and AGFA for poster. Improvements being made in exhausts by processor manufacturers. Chemical company guidelines; Photosol’s glut-free devel. Six cases acepted by ACC, NZ.

UK compensations for 2 radiographers and one tech. Court cases pending. Sensitisation - one radiog collapsed at wheel of car at the lights, from petol fumes. University of Bristol detected high levels of GA on radiographer’s hands.)

Gordon M A, Laird I. Guidance Notes for the Provision of a Safe Work Environment and Safe Work Practice for Radiographers and Darkroom Technicians. 1990. ACC, NZ (See under "Reports".)

Morning Star "Safety fine for health authority." Aug 22. 199? (Bristol and Western Health Authority fined 1000, costs 963 for exposing Patricia McCormack to chemical fumes from glut - acute breathing difficulties. Proper fume cupboard now installed.)

1991 1991

Barry M. "Danger in the Dark". Evening Times, Nov 11, 1991 (Seminar in Glasgow attended by 100 sufferers, to press for mandatory Code of Practice and Darkroom Disease to be officially recognised. Glasgow University Occ Health says Darkroom Disease: "not been subject to thorough epidemiological analysis..... There is not a huge occupational hazard". Rose Paterson, technician, caught in blowback from the machine - couldn't breathe. Told symptoms were mass hysteria. Allergic to suede, leather, benzoate preservatives in food, cig smoke in a few seconds, alcohol. Shopping in town takes a week to recover. Given job in pay office - reacted to the ink on payslips. Marlene Barrie, radiographer - reacts to passport photo machines, some plastic chairs, new photocopying (can't breathe); certain chems cause mouth to burn and blister. Anne Clarkson, technician for 25 yrs, loses voice reacting to plastic chemicals in phone, allergic to polycotton especially in washing machine, nail polish, bubble bath, glue in shoes, cellophane, diesel (little bus travel), limited sense of taste and smell. Finger-nails went black and teeth discoloured, aches/pains, bloodspots in mouth.)

Ballard J, Nursing Times (UK) Use and abuse of glutaraldehyde. 1991, 87, 38, 70-71. (1989-90, 11 hosp theatre and out-patient depts studied . Some smaller hospitals using salad bowls/buckets etc with/without lids to sterilise endoscopes. Some had had COSHH assessments. 8/307 staff were identified with work-related problems especially the units using open systems. Theatre staff aware of high level of irritant symptoms but occ connection not always made. Surgeons more reluctant to admit to health probs. Recommendations made. Revisited in 6 mnths - many improvements. Older hospitals most problems.

Campbell M, Cripps N F. Environmental control of glutaraldehyde. Health Estate Jnl . Nov 1991. (New COSHH regs 1988, new limit - 0 .7mg/m (2ppm) over 10 mins not 8 hrs; short term exposure must be limited. GA readily vaporises at room temp.

W. Midlands RHA survey: 377 responses, 10% used fume cabinet, 76% no local exhaust, 10% relied on natural ventn, 15% did not clean equip before sterilisation. A glut alternative could be used in 50% of uses. Measurements were well below GA std.. Higher readings: decanting/filling/drainage. Air readings 30 mins after spill gave 0.18mg/m. Control strategies include discharge direct to drain and dilute, ventilation systems, fume cabinet design, charcoal filters, required tests.) 

Carslake P. "Sad tale that ended a twenty year career" Radiography Today. Sept 1991, 37 (Joyce Davis, 20 yrs in radiography at Royal Liverpool Children's Hosp. Had symptoms from 1982, saw allergy and ENT specialists - terrible sinus problems, totally lost sense of smell, palpitations (given beta blockers), cortisone for rhinitis - became allergic to that. Headaches and nausea at work. Thickening of sinuses - ENT said "nothing could be done". 1990 chem poisoning diagnosed; sacked on grounds of incapacity. Forced into clerical job sending ambulance invoices. Reacts to paints etc. Scared friends suffering in silence.)

Carslake P. Poison in the Air Radiography Today Sept 1991, 36-37. (10 radiographers in UK claiming compensation from employers. Many others remain silent in fear of losing jobs. 1991, Society of Radiographers’ survey of 3,000 members showed 1/3 had pre-sensitisation symptoms. Only 5% of depts were adequately ventilated. Tests of fumes show nothing above limits. Society of Radiographers prefers to work with employers to find people alternative employment and pay compensation rather than face more expensive legal action for loss of job.)

Response: Alan Budge, British Photographic Assoc. Letter, Radiography Today, Nov 1991. (May and Baker’s low sulphur dioxide fixer early ‘80s; mid-’80s - reduction of GA concentration and complexed with bisulphite; recent introd of safer glycols eg diethylene/propylene glycol; chemical mixers; funds must be available for proper installation of processors.)

Carslake P. Preventing darkroom disease - Editorial Radiography Today Sept 1991. (Co-operative approach needed from govt, unions and employers.)

Lange L. "Radiographers at risk from darkroom disease", Medical Imaging May 1991, pp1,8,9. (Report of MAG's address to Australian Institute of Radiographers. Story of her research; Aust NHMRC release of "Guidelines for lab personnel working with carcinogenic or highly toxic chemicals".)

Middleton J. Under the COSHH. Technic. February, 1991. (COSHH, UK - Control of Substances Hazardous to Health - 1989, required employers to assess risks to employees’ health at work and prevent exposure to hazardous substances where possible, introduce and maintain controls, and monitor the controls.`... COSHH Advisory Code of Practice: total enclosure - partial enclosure with local exhaust - local exhaust alone - general ventn for small amounts - reduce no. of people exposed - personal protective equipment - proper cleaning - safe storage/disposal - prohibition of eating/drinking/smoking - spillages - maintenance. Monitoring of levels yearly. Health surveillance is no substitute for the above. COSHH surveillance records must be kept for 30 yrs.)

Naughton M. "Danger lurking in the darkroom". Morning Star, 7 Sept, 1991. (MSF Seminar, inadequate British COSHH Regulations.)

Poteet M. "Darkroom Disease Plagues RTs". R.S. Wavelength USA, Aug/Sept 1991 (Symptoms, MAG's story.’Guidance Notes’

Tibbotts Audrey. Letter, Radiography Today. Nov, 1991. (One of Bath radiogs; tribute to MAG. Disheartening that radiographers still being affected. Compensation does not make up for loss of one’s job and health. NZIMRT awarded MAG an honorary fellowship.)

Tilke B 7 "New Zealand Technologist tells of Chemical Risk". Advance July 8, 1991. Conference of Americas - Report: MAG's work: summary of hazards. Kodak response: - use gloves and other safety precautions for skin irritation; "extremely rare" for sensitations to occur.

1992 1992

Alexander R. Proving chemically induced asthma symptoms; Reactive Airways Dysfunction Syndrome, a new medical development. 1992 (Internet). (RADS is identical to asthma but induced by chemical exposure. Occurs after one exposure to a lung irritant and respiratory symptoms occur within 24 hrs. Many resolve in 6 mnths but some continue for 5 yrs. Methacholine testing confirms airway hyperresponsiveness. PEFR documents a greater than 20% drop in PF over 24 hrs. Case study: RADS from acetic acid. RADS from glutaraldehyde exposure now a provable claim.) [Richard Alexander is a Californian attorney and founding member of the National Association of Consumer Advocates. The Alexander law firm specialises in negligence, chemical ...consumer fraud cases.]

Beauchamp R .O, St Clair M.B.G, Fennell T.R, Clarke D.O, Morgan K.T. A Critical Review of the Toxicology of Glutaraldehyde. Critical Reviews in Toxicology 1992, 22, 3, 4 143-174. (Substantial review of the GA toxicity literature to this date. Properties, uses, human effects, regulations, studies on animals, metabolism of GA in the body by enzymes, etc. Further studies needed on irritation of respiratory tract, potential neurotoxiciy, developmental effects and mechanism of action.)

Calder, I.M. et al. Glutaraldehyde Allergy in Endoscopy Units, The Lancet. 1992, 339, 433, Feb 15. (65% of 167 survey respondents from 17 hospitals reported symptoms and 38% had two or more, including: eye irritation, skin discolouration or irritation, headache, cough or shortness of breath. At two hospitals, environmental measurements of glutaraldehyde were below the UK occupational exposure standard).

Cullinan P., Hayes J., Cannon J., Madan I., Heap D, Newman Taylor A. Occupational asthma in radiographers. Lancet 1992, 340, 12 Dec. (Case No 1. 28, f, radiog for 5 yrs. GA challenge with 11% solution. Had hay-fever since adolescence and immediate reaction to skin test allergens - late asthmatic response at 3 hrs to GA. Case No 2. 24, f. Radiographer for 5

yrs.Hay-fever/bronchitis during childhood. New job - poor ventilation - developed wheezing at work, severe reaction after fixer spillage. Immediate reaction to skin test allergens. Single blind testing to 2 part fixer provoked fall in FEV (max 35%). Did not react to 2% or 1% GA.)

Ferriman A. Sterilising chemical ‘is harming NHS staff’. ?Sunday Times. 25 Oct, 1992. (Increased day surgery with rocketing use of endoscopes means damage to health of National Health Service staff from glutaraldehyde sterilant. Royal College of Nursing and Cohse are fighting cases for their members. Almost 1,000 radiographers are affected. Kathleen Garland, 47, ended up in one day as a respiratory cripple. 12 mnths later, lung capacity still down 25%.)

Glass B. Glutaraldehyde: Why Now? Safeguard, 1992, 16, 10-11. (Increase in worker consciousness; increase in exposure with existing workers being requiredd to work longer hours. M: can no longer work in radiography; mood and memory effects, sore eyes, nasal sores, headaches, tinnitus and severe respiratory tract sensitivity. With 6 mnths off work, symptoms became localised to respiratory tract with hoarseness and chest tightness. S: radiog, illness developed after spills on unsealed floor. Unexplained excessive tiredness, mood changes, skin tingling, repeated sore throats. Cross sensitivity to petrol fumes and solvents. P: tech exposed to formald, then GA. Developed migraines, tinnitus and joint pains. 3 mnths since exposure stopped - migraines less severe. R: tech who worked with GA for 15-20 hrs/wk for 12 yrs. Sore throats and occasional chest infection became more severe with a new cleaning room with fumes from sink full of GA exhausted straight upwards into his face. Repeated chest infections, memory problems, hoarse voice, blotchy facial skin, chest tightness. M: X-ray tech in small unventilated workplace with exposed containers of GA. Frequent spills of GA onto R calf - developed thickening of skin and joint pains - schleroderma diagnosis. GP Nurse: End-of-day exhaustion and blocked nose. Moods became unpredictable and sleep disturbed, short-term memory deteriorated. Unventilated 8x6 workspace; 2 open containers of GA.. Colleague in a better ventilated room, but not wearing gloves developed dermatitis on fingers and elbow flexures and became short of breath as an aerobics instructor. 4 hospital endoscopy staff: chest tightness, shortness of breath, sneezing, dermatitis of eyelids. Hospital nurse: working in X-ray in small, hot, unventilated room, developed U/LRT sensitivity and a multi-organ sensitivity. "GA is not a simple chemical in terms of its reported effects...It has irritant and allergic health consequences as well as those of immunotoxicity".)

Kuntz L. "Darkroom Disease." R.T. Image Aug 31, 1992 4-10, 59. (Beth Moore, Sth Carolina; exhaustion, loss of voice after 15 yrs. Took 1 yrs to diagnose DD and discover venilation ducts weren't working. Terrible smell in room - Beth couldn't smell it. Took $10,000 pay cut but got out in time. Susan C: 17 yrs developing Xrays, mixing chems - eyes would burn, gagging. Then seisures; medication made superviser complain about her bad attitude. Now, all joints ache, 3 different arthritis medications didn't work, numb fingertips, ears hurt - no infection, constant stomach pains - no ulcer, tired, weak and confused. Offered hospital cafeteria job - refused. Seizures stopped, other ailments continued. MCS/chemical aids/DD debate; Mary Lamielle, President, National Centre for Environmental Health Strategies (NCEHS) describes MCS symptoms: sore throats, skin rashes, constant headaches, nausea, achy joints, fatigue, confusion and heart irregularities. MCS reactions: pre-sensitisation, sensitisation, reaction. Environmental physicians called "pseudoscientists". American Med Assoc: neutral. Am Coll of Physicians and Am Acad of Allergy and Immunology doubt MCS existence. National Academy of Science acknowledge need for more study: not enough evidence. Waddell: Professor of Pharmacology and Toxicology, University of Louisville, "It’s just a growing mass hysteria in the country". Fink, allergist:"Many MCS patients have psychiatric problems". Kodak toxicologist says "We are not aware of anything in photographic chemicals that would cause what has been called MCS...we’re not aware of any substantiated information that they cause asthma or bronchitis or any other respiratory problems". MAG's story. Theodore Simon: SPECT imaging showed significant reaction to a range of chems including formald, compared to control group. Patients reacted to diethylene glycol, 1-phenol, nitroindazole, and ammonium compounds. Earon Davis, lawyer - thousands of social security claims involving MCS settled and some workers compensation. Davidoff study of MCS planned. 3 Canadian CT techs were seated next to a processor and believe their miscarriages were linked to the clearly-smelled fumes.)

Kuntz L. "Help for darkroom disease." R.T. Image USA 28 Sept, 1992. p11, p28. (MAG's MCS; 140 USA MRTs have written to MAG for help. How to diagnose/avoid DD/MCS. OSHA requirements: written company policy for handling, proper labelling of chems, employee training, MSDS.). (Letter: M Highsmith. Headache, sinus, earache, pupil dilation of 1cm; good after vacation: chronic sinusitis with with possible mucosal reaction to noxious chems.)

3M NZ Ltd Gluteraldehyde - controlling the hazard October 1992. (Skin and respiratory symptoms, safe practices, eg do not use for routine cleaning, exhausts should operate 24 hrs/day, suitable respirators etc.)

Mulligan M. The Dunstan experience. Shadows 1992, 35,4, 28-29. (Her senstisation to many every day chems. Denial by radiographers because of fear of loss of jobs. Symptoms put down to lack of interest in work, obscure malaise , neurosis, pre/post menstrual/menopausal etc. Use now of Photosol’s glut-free devel, CD 77 and Rhone-Poulenc low SO fixer in Dunstan Hosp. Helen Walker forced to stop work. Author thought she could keep going - a month later couldn’t breathe 1992 1992 in the X-ray dept. Applied for ACC)

Newman M A and Kachuba J B. Glutaraldehyde: A Potential Health Risk to Nurses, Gastroenterol Nurs. 1992, 14, 6, 296-300, June, discussion pp. 300-1. (Potential toxicity to GA, health effects, sampling methodology re OSH, air monitoring necessary, and recommendations for reducing exposure to glutaraldehyde).

Ryle G. "Nurse wins payout for chemical exposure at work." The Age. 19 November 1992. (June Grinter, Nurse, Bendigo, Victoria, Aust; headaches, exhaustion, gritty eyes, ...out-of-court settlement).

"Rush of Claims tipped." Sydney Morning Herald, 19, Nov, 1992. (June Grinter; took 20 mnths to get doctors to confirm her illness - no-one would listen, could hardly walk. Turned into a ‘zombie’. A supermarket trip causes severe reaction and exhaustion.)

Stodart K. Poisoned at work. NZ Nursing Journal, March 1992, 12-13 (40 yr old radiology nurse, from 1988 developed Raynaud's syndrome, cramps, bloating, wind and pain, bladder problemss, upset menstrual cycle, weight loss, bruising, vulnerability to infection, joint pain, headaches, inability to perspire, ankle oedema, rashes, mood swings, lack of concentration, short-term memory loss. [See Anne’s story also, Dec 1992]. Improved on holiday. Applied for ACC - ACC consultants were unhelpful, even abusive. CTU advised Prof Bill Glass who recognised chem poisoning; accepted for ACC. Tried to work 10 hrs and developed Bell's palsy and shingles. Had to sell house; used to forget where car was parked. Reacts to aldehydes in fungi, dairy and wheat foods, fruit sugars, paint, cig smoke, solvents etc.)

Townsend Sue. Glutaraldehyde - should it have a place in general practice? NZ Practice Nurse Dec 1992, 50-53. "Anne’s" story. Radiology nurse - puzzling bruising and abdominal pain. Put down to emotional component. Other symptoms worsened [see above story also] - plus circulation, hypotension, jaundice, gritty eyes, sore throat, breathlessness, sinusitis, mouth ulcers, herpes, joint pain, headache, palpitations, fatigue. ACC 1991. Sold home. Reaction to paint, chlorine, cig smoke, petrol fumes. Dr Chris Walls: "It goes on in common with a number of other chems to cause in some people quite bizarre and peculiar symptoms which don’t fit the defined textbook examples." Nelson Hospital "clean-up" after nurse splashed in the eye. Sydney in-vitro fertilisation low success rate - ?glut fumes from exposed tray. Worksafe Aust Hazard Alert. 1981 Brit survey of 16 units found 37% of staff had sensitisation problems. 1989 Bristol Health Authority fined 1,000. GPs’ unintentional ignorance. Alternatives for sterilising.

Trigg C.J., Heap D.C., Herdman M.J., Davies R.J. A radiographer's asthma. Resp. Med., 1992, 86, 167-169. (Occ asthma diagnosed in 39 yr m. radiographer, headache, ulcers. Hole in processor ventilation tube. 3 mnths later during maintenance developed chest tightness, itchy eyes, acute sinusitis, earache, conjunctivitis, dyspnoea. Had hay fever and atypical pneumonia 4 yrs previously. Positive skin pricks to pollen, cat, Aspergillus f. Positive specific challenge - PEFR declined during week. 16% fall in FEV1 on active challenge day. Minimum chemical emissions from processing room but continued to experience symptoms when near. Unable to continue working as a radiographer - retrained.)

Waldron, H.A. Glutaraldehyde Allergy in Hospital Workers. Lancet. [letter] 1992, 339, 880. Apr 4. (A survey of 150 staff from 18 departments at St Mary’s and Middlesex Hosps who were exposed to glutaraldehyde . Although over 9% of all subjects complained of a wheezy chest when they were exposed to glutaraldehyde, none had abnormal lung function tests, not even those who smoked. Although a single test of lung function has limitations, these data do not provide any evidence for chronic airways disease in this group of hospital workers)

Warneminde Martin. Hazard in our hospitals. The Bulletin ? Aug 1992.

1993 1993


Blondell Jerome. Gluteraldehyde Bibliography. EPA, Washington DC. (Includes 40 papers/letters not referenced in the SNFTAAS Bibliog - many from anaesthetic, gastroenterology and dental journals.)

Godard Ph, Chanez P. Epithelium and Asthma. ?1993/4 (Epithelial cells were thought to have simple barrier role of mucous secretion and removal of noxious agents by their cilia. Changes in the bronchial epithelium almost always found in asthmatics - a fragile appearance. In patients who died bronchial epithelium almost always shed. Epithelial cells now found to release pro-inflammatory mediators, to participate in regeneration of cilia, and initiate repair of epithelial cells. Epithelial cells of asthmatics can be directly activated by anti-IgE, therefore possible that cells can be directly triggered by allergens. Pollutants eg ozone can activate bronchial epithelial cells [from Davies RJ, Devalia Jl. Air pollution and airway epithelial cells. Agents Actions Suppl 43:87-96, 1993]. Asthmatic patients with an intact epithelium have inc number of inflammatory cells among epithelial cells - these are target cells easily accessible to allergens or non-specific irritants. Inhaled corticosteroids are able to repair bronchial epithelium.)

Single Photon Emission Computerized Tomography (SPECT) Scan of MCS Patient's Brain Before and After Challenge with Perfume Inhalation. Doctor's Report. Dec 1993. Internet. (With pictures. 30 minutes after inhalation of perfume. Findings: 1) Diminished cerebral blood flow 2) Bilateral frontal, temporal and parietal hypofusion 3) Marked scalloping pattern of perfusion in frontal and parietal lobes. 4) Vasculitis v exposure to neurotoxic substances.)

Chan-Yeung M, McMurren T, Catonio-Begley F, Lam S. Clinical Aspects of Allergic Disease. J Allergy Clin Immunol, May, 1993, 91, 974-8. (Sterilising agents eg formald and GA have given rise to Occ Asthma. 33 yr old respiratory tech: mild asthma since childhood. At 26 yrs attacks only returned after a cold. For 4 years job was to clean bronchoscopes with Sporicidin (3.6% glut) and assist physicians. Normal chest X-Ray. Positive skin test to feathers and fur. Gold standard lab challenge performed: preshift and postshift spirometry showed postshift drop of 23% in FEV1 even though taking high dose beclomethasone. Serial measurement of peak expiratory flow rate (PEFR) done over one week at work and 2 wks on vacation showed progressive improvement first 4 days; FEV1 1.8L before, 2.4L on ret. from hol. Nonspecific bronchial hyperresponsiveness measured, and workplace challenge test which showed a progressive fall in FEV1 as she progressively cleaned three bronchscopes. Lung function tests did not return to normal 24 hrs after challenge indicating late asthmatic reaction in line with an allergic rather than irritant reaction. Unusual for occ asthma caused by low molecular weight compounds to develop in subjects with a pre-existing asthma. History of asthma should not exclude the diagnosis of occ asthma caused by a workplace agent).

Connaughton, Peter. "Occupational Exposure to glutaraldehyde Associated With Tachycardia and Palpatations," The Medical Journal of Australia. [letter]. 1993, 159, 567, 18 Oct. (7 patients, occupationally exposed to glutaraldehyde, presented with either palpitations or tachycardia, temporally related to exposure. No other causes were identified from their history, physical examination or ECGs. Symptoms ceased with change of job or workplace modification. Patients also had other recognised GA symptoms which also resolved. ECG details. Monitoring during exposure documented

these symptoms. Further investigation warranted.)

Dailey J, Parnes R, Aminlari A. Glutaraldehyde Keratopathy. Am J of Opthalmology. 1993, 115, 2, 256-8, Feb.

Gordon M.A. Prevention of darkroom disease. Shadows 1993, 36,3, 29-30. Presented at 1993 NZIMRT Conference. (Recent publication of Safe Occupational Use of Glutaraldehyde in the Health Industries, 1992, reinforces‘Guidance Notes’. Don’t stand around the processor. Dr Alan Broughton, Antibody Assay Lab, California, attempting to develop a test for GA to demonstrate antibodies in human serum albumen - "It is not surprising that hypersensitivity problems occur with it because as a chemical with two carbonyl groups it will be very reactive and probably adducts to albumen pretty much like formaldehyde." Work in Whangarei for 2 yrs by occ nurse, Eunice Nutman, on ANA levels in Xray staff. H &S Committee of NZIMRT has written asking about setting up GA register. Photosol’s work on airborne interaction between SO reacting with GA. New European Code of Practice 1991, for labelling photographic chemicals allows companies at their discretion to omit mention of GA in their H &S data sheets. By complexing GA with bisulphate, they can claim the developer is non-hazardous. When the developer is mixed to working strength, the free aldehyde concentration is below 1% and also escapes the need for warning. Some companies still deny GA in their products.)

Hewitt P.J. Occupational health problems in processing of x-ray photographic films. Ann. Occup Hyg, 1993, 37, 3, 287-295. (Holistic approach to this complex microclimate is stressed; a single cause is unlikely. Design of rooms, surfaces, directional air flow, sealed drains, reduction of SO and GA emissions, leakages, foil-covered bottles, sealed pipework, air-changes 10-15/hr (OK with attention to all other factors), temps 20-24C, humidity 40-70%, specialist routine maintenance, PPE - personal protective equipment, (Respiratory Protective Equip (RPE) should only be necessary as an emergency), training, air monitoring of limited value - low readings need expert interpretation; health surveillance.)

Hopkinson G, "Glutaraldehyde may be asbestos of the '90s". ?Evening Standard, 16 Jan, 1993. (MAG's story. NZ/Australian govt warnings. Uses of GA in farming, timber, tanning, piggeries, chicken farms, dental and vet, clinics, embalming, liquid fabric softener, air-care products... Margaret Desborough, Palmerston North, NZ, 12 yrs radiography A & E, had to leave job with lupus and has damage to connective tissues, swollen hands, rashes, ulcers. Photosol’s

GA-free developer being trialled in Dunstan. 3M has sold 100 respirators to hospitals. World’s leading gastro-enterology teaching hospital, Middlesex in London, only uses GA in enclosed machines to sterilise instruments in contact with Aids or hep B. NZ nurses often told they have depression. GA is imported by Union Chems from Union Carbide, USA; BASF from Germany for leather, tanning and cleaners. J&J imports Cidex from the UK; Medic Corp imports Aidal plus and Wavicide from Aust; Douglas Pharmaceuticals mixes GA in NZ into Zenicide (lab instrument steriliser). Union Chemical says GA a lot safer than formald because not carcinogenic - problems are "isolated cases". BASF says a lot of hype is generated about ....chemical products. Kodak is trialling a GA free alternative.)

Ide W. Developments in the darkroom: a cross-sectional study of sickness absence, work-related symptoms and environmental monitoring of darkroom technicians in a hospital in Glasgow. Health and Safety Exec. Glasgow. 1993. (9 f. radiographic techs matched with OTs for age, sex, smoking. Symptom questionnaire including respiratory plus wider symptoms eg palpitations, unusual tiredness, nausea, sore joints etc. Sickness absence data for one year: techs had 204 days off, OTs 41 days. Respiratory symptoms: 1/3 of problems not statistically signif. Occ hygiene results within normal limits.)

Kaczuk M N, Crea J. Gluteraldehyde exposure of encoscopy nurses. Proceedings of 14th Annual Conference, Aust. Inst. Occ. Hygienists. Dec 1993.

Leinster P, Baum J M, Baxter P J. An sssessment of exposure to glutaraldehyde in hospitals; typical exposure levels and recommended control measures. British Journal of Industrial Medicine. 1993, 50, 107-111. (HPLC analysis of 77 samples at 14 locations in six SW England Hospitals. In personal monitoring, levels between 0.003-0.17mg/m measured (10 min TWA limit is 0.7mg/m). X-Ray only recorded 0.003 to 0.006mg/m. Acetic acid and diethylene glycol are likely to present a greater inhalation risk than GA. Static monitoring was between 0.002-0.23 mg/m. Little ventilation and no openable windows. The greatest exposure risk was the 5 minutes every half hour as endoscopes put in or removed from solution. Two people commented they had rhinitis they attributed to GA. Non-essential uses like wiping walls and cleaning bedpans should be discontinued. Recommendations for safe use...)

Mulligan M. The Dunstan experience part II - ventilation. Shadows, 1993, 36, 3, 28-29. (Use at Dunstan Hospital of Photosol’s CD77 GA-free developer, plus low SO fixer, plus ventn: exhaust fan installed inadequate. Argument with experts - the engineer designed cowling, venting to outside chimney. Air supply via light-tight grilles included diesel fumes and lunch! and probably recycled some of the fumes. Local glazier built perspex enclosure for the processor which has its own extraction system - $500-$600.)

Stevens A. B. (The Royal Hospitals, Belfast) Letter re Cowan R E, Harrison J. Aldehyde disinfectants and health in endoscopy units. Report of Working Party of the BSG Endoscopy Committee. ?1993 p717. (If an employee devels occ asthma, the employee should not be permitted to make the decision re continued exposure. Redeployment and retraining may be the best outcome which can be expected. Whether subjects with pre-existing asthma should be employed in jobs with GA exposure is a difficult issue. Response, Cowan/Harrison: Report states further exposure to GA should be avoided but sometimes this is not possible or desirable.)

Tkaczuk M, Pisaniello D, Crea J, Occupational exposure to glutaraldehyde in South Australia Occup Health & Safety 1993 9, 3, 237-243. (Testing by OSHA Method 64 (HPLC). Site 1): Operating theatre. 1% GA used. Lid buckled, good personal protection, 16 air changes/hr. Headaches reported on busy days. 2): Endosc prep room. 1% glut. 27 air changes/hr. Headaches and tingling of face when lid off. Dermatitis of feet probably from dripping endoscopes.

3): Dental surgery. 2% glut. Severe dermatitis when no gloves used. 4). Embalmer: 1.4 % formald/0.6% GA. Highest formaldehyde detected was 1.83ppm when the embalmer got between the body and the vent. 5). Darkroom large hosp:

0 .4% GA used. Reading 0.001 ppm during cleaning. No other GA detected. 6): Hosp darkrm. 0.001ppm detected. 7): Egg storage room at chicken farm. Eggs collected from floor and sprayed with 0.1-0.3% activated kill any bacteria on shells, minimising chick mortality. 0.007ppm in the area. Collectors complained of face and resp irritation. No gloves etc worn. GA sprayed onto unprotected skin. Recommended: - minimise dripping from endoscopes - do not rinse with spray rosette. Workers did not read MSDS or understand risk. Review exposure std of 0.02ppm.

Darkroom Hazards. Safetyline Magazine, Worksafe Western Australia. No. 20 Nov, 1993. (Many chemicals used give off hazardous vapours or harmful gases such as formaldehyde,glutaraldehyde, hydroquinone, ammonia, sulphur dioxide, and hydrogen sulphide. "Exposure to these can affect the liver, lungs, kidneys, reproductive system, gastro-intestinal tract or CNS"...)

1994 1994

Chandler G. "The Unidentified Debilitating Disease." R.S. Wavelength, Aug 1994. (Opening a processor after a film jam caused her eyes to water and nose and throat feel as though on fire. Violent coughing and throat began to constrict - couldn't breathe, Emergency Room to restore breathing... Diagnosis: MCS - multiple chemical sensitivity. MAG’s work. Fighting to petition OSHA for protective regulations.)

Dewitte J-D, Chan-Yeung M, Malo J-L. Medicolegal and compensation aspects of occupational asthma. European Respiratory Journal. 1994, 7, 969-980. (Due to the significant medical, medicolegal, social and financial consequences, it is of the utmost importance that the diagnosis of occupational asthma be proved by objective means. Two types of occ asthma: 1) appearing after latency period 2) that without latency, or RADS. How to confirm? Questionnaires good but lack specificity. Immunological testing does not prove the bronchi have been affected and is only suitable for protein-derived high molecular weight agents. Documenting airway changes at work or with PEFR require an honest, co-operative subject and are less sensitive than FEV1. Also there are no objective criteria for assessing recordings and there may be false negs and positives. Specific inhalation challenge is still the gold standard though false positives and negatives do occur. Provision for compensation for temporary impairment and permanent disability/impairment (2 yrs after removal from exposure) should be considered. Subject should not be further exposed; threshold for symptoms/ hyper- responsiveness is much lower; subjects react to minute amount of causative agent. 60-90% fail to recover several years after exposure. American Thoracic Society chart for assessing impairment - score 0-11 pts. Compensation systems chart for different countries. eg Quebec. Causal agents lists should be regularly updated. Atopy only relevant in one in three lab animal handlers. Early detection very important in preventing permanent asthma. Skin testing cannot be performed for low molecular weight chems eg GA as the mechanism is not IgE-mediated. A combination of questionnaires and bronchial tests have to be relied on.)

Hotchkiss S. How thin is your skin? New Scientist, Jan 1994, No 1910, 24-27. (Research at St Mary’s, London into rates of absorption of different chems by the skin. Pieces of skin put into nutrient bath. Skin contains enzymes to breakdown toxic chemicals. Some enzymes may make chemicals more toxic or carcinogenic eg those that break down hydrocarbons. Structure of skin. Around 10% pesticides absorbed. Some rapidly absorbed can’t be washed off eg the phthallic acid esthers used as fragrances. Some barrier creams enhance absorbtion eg of phenol used in perfume manufacture. Up to 24% of fragrance chems may be absorbed through skin. This is increased if ethanol is added as in perfumes because ethanol temporarily alters the skin lipids. Cinnamaldehyde absorption may reach 50%. "Cinnamaldehyde may cause an 1994 1994 allergic response". Many aromatherapy oils are potent concentrated chems. Chemicals which damage the skin eg formaldehyde are thought to be too small to be recognised by the immune system and must be bound together with skin protein to stimulate an immune response. If the chemical is reactive enough it may combine directly with skin protein, or may be metabolised by enzymes into a compound which is sufficiently reactive to bind to skin protein.)

Griffiths R. The Presence of sulphur dioxide and other toxic fumes within processing environments, and associated health problems. Radiography Today Nov. 1994 60, 690, 13-16. (Summary of UK progress to date; COSHH regulations; survey of 100 radiogs on awareness of work dangers, testing by Drager tube for SO - well below safe levels of 2ppm. Photosol XF2 and Kodak X-Omatic RA lowest SO fumes. Traditional fixer solutions gave off most fumes (above EH40 limits). Few radiographerrs used masks; most hazardous place to stand is round the processor; monitoring had been covert; still a prevalence of darkroom disease symptoms probably because staff had been pre-sensitised or had past history of allergies (these people most susceptible); 18% identified menstrual disorders associated with work (J Tell, National Press Photographers’ Health Survey Art’s Hazard News, 12,5,12, 1989 had found a correlation between menstrual disorders, miscarriages, and potential darkroom fumes).

Hayes J P and Fitzgerald M X. Occupational asthma among hospital health care personnel: a cause for concern? Thorax. 1994, 49, 198-200. (A general review addressing the increase in individual case reports of health care workers, including radiographers, developing asthma as a result of substances encountered in the work place. Glutaraldehyde and ammonium thiosulphate (in fixer) classified as low molecular weight chemicals, which often makes the diagnosis of asthma less clear. "Similarly, an association between symptoms and exposure to a sensitising agent may not be apparent because asthma caused by low molecular weight chemicals may induce atypical non-specific symptoms such as cough or chest discomfort. More classic symptoms such as wheeze and chest tightness may not occur until late in the evening or during the night after exposure. "Furthermore, because the nature of health care involves working a variety of shifts and days, workers may be less readily able to correlate delayed symptoms with workplace exposure. Peak flow measurements are recommended. There is no accurate means of quantifying occupational asthma. Meanwhile carefully conducted studies would very like reveal a greater prevalence of work related asthma than is currently realized.)

Le Goaster A, Deschamps F, Kalis B. Four cases of contact dermatitis in hospital employees handling disinfectants. Semaine des Hospitaux. 1994, 70, 88-90.

McLaughlin D. Crying in the Dark. North & South, NZ. Nov 1994; 128-136. (MAG's story, Sept ‘82 so weak couldn’t pick up new grandchild, heart arrhythmia at 170 beats/min. Cardiologist said "nervous tension". Off work 3 days - went back, massive tinnitus/and racing heartbeats. One of the GPs said her throat had the inflamed membranes of a heavy smoker - but didn’t smoke. He said: "You work with some very toxic chemicals". Cardiologist diagnosed toxic reaction. The Medical Centre had got new state of art developer in 1980 which blew straight into her face.... at AGFA in Belgium the head chemist said anyone who developed problems was transferred away from the chemicals....back in NZ, ACC accepted case in 6 wks. Glut’s uses; some react; women’s health issues not taken seriously; 1984 she and the Massey researchers took 1 hrs to convince the Health Dept to issue a warning; Health Dept asked her to write guidelines with Ian Laird, Massey occ health lecturer - took 13 mnths to write and became international reference work. Workers still being exposed eg Northland Hosp. Marjan Creusan-Foot suing for exemplary damages. [Decision currently awaited.] - new CT suite 1991 - staff complained about the temperature and fumes. C-F developed memory loss, vocal chord ganuloma, crippling joint pains, hoarseness, general weakness. Improved on hol. Ill within hours on return. Told to stop work - hospital immediately took out the air conditioning; fumes were not measured. 6 mnths leave - quickly fell ill on return. ACC accepted. Problems of retraining and re-employment at 44. Health slowly improving but medication for joint pains... photographer husband can’t have darkroom in the house. Increasing use of GA as a sterilant with HIV, AIDS, laparascopes. Margaret Mulligan - Chief Radiog; sensitised; like having a heart attack; couldn’t breathe; management wanted proof so surveyed 12 other hospitals - similar problems; GA-free CD77 used. Pene Clifford, Helen Walker, MM underwent detox programme - exercise/ vitamins/ sauna. Dunedin Hospital using Kodak Rapid Access because two staff had to quit. Bill Glass, Assoc Professor Occ Health, Otago Univ, 20+ cases. Problems are well-known internationally. Sceptics are ostriches. Not everyone gets the flu and not everyone using GA has a problem. "The real problems begin with the one or two people who move from the more general response to sensitivity." A lot of doctors don’t take work histories but people spend 8 or 10 hrs a day at work. Eunice Nutman, Northland - blood tests found elevated antibodies in 19/38 staff - usually only 20% of the population. MAG did not want it to take the 50 yrs it took to get stronger controls on radiation.

Pickford Alison. The hhumph of the chemical djinn. Shadows 1994. (Disconnected processor exhaust caused her problems - headache, sore throat, tight chest, reduced peak flow, tiredness, poor recall, depressed over things which usually don’t matter. Could not return even after ventilation fixed. Sort help from Clinical Ecologist, vegan diet and vitamins etc.

Very low levels of GA were measured.)

Rosalski S B, Dooley J S. Liver function profiles and their interpretation. Btitish J of Hosp Med. 1994 51,1, 181-186

Rozen P, Somjen G J et al. Endoscope-induced colitis: description, probable cause by glutaraldehyde, and prevention.

Gastrointestinal Endoscopy. 1994, 40, 5, 547-553. (6 cases of acute colitis after sigmoidoscopy probably caused by GA residues. Residues in the rinse water contained the equiv of 0.2% GA..)

Stenton S C, et al. Glutaraldehyde, asthma and work - a cautionary tale. Occ Med (Oxf), 44, 2, 95-8, May. (Endoscopy nurse, 46, had symptoms suggestive of occ asthma. Inhalation challenge in endoscopy caused FEV1 fall 3.6 to 1.5 litres. Double blind inhalation challenges (up to 0.32ppm for 10 min) gave no obvious asthmatic reactions. Slight increase in airway responsiveness, PD20FEV1 from >6400 to 1850 micrograms. Even with sophisticated techniques clear-cut result may be elusive.)

Stump Fred D et al. Influence of oxygenated fuels on the emmissions from three pre-1985 light duty passenger vehicles. J of the Air and Waste Management Assoc. June, 1994, p781...(Car exhausts tested using regular gasoline and an ozygenated fuel containing 9.5% MTBE, more olefins and fewer aromatics [benzene, toluene, and xylene are the principal aromatics] than the base fuel. No reduction in emissions from oxygenated fuel. Total hydrocarbons (THCs), speciated hydrocarbons, speciated aldehydes, CO, oxides of nitrogen (NOx), benzene, and 1,3-butanedione emissions were measured. THC, CO, benzene, and 1,3-butanedial, formaldehyde, acetaldehyde, total aldehydes, decreased with increasing air temps. NOx increased with incr temp. More formaldehyde was emitted when MBTE fuel used.)

Teo R K C, Naidu V A. The effects of glutaraldehyde exposure on human brain function. Worksafe Australia paper presented to the 13 Annual Conference Australian Inst.itute Occ. Hygienists, 4/12/94. (3 staff exposed to GA in a theatre while cleaning endoscopes were tested by the auditory evoked potential method. They showed prolongation of the response time (p3 latency) a dysfunction related to the depression of the cortical function of the brain.)

Use and Management of Glutaraldehyde Solutions Safety Action Bulletin 1994, No 108 (Action reqd. GA is a respiratory sensitising agent and exposure to the vapour may cause occ asthma).

1995 1995

Barry M MSF Seminar Dangers of glutaraldehyde & other chemicals used in x-ray film processing. Glasgow, Sept 1995. (Speakers: Sherwood Burge, M Gordon, Geof Care, Photosol -[transient high exposures, aerosol theory], Warren Town - Soc of Radiog -(problems in getting Dept Health to lower OES and give a MEL), Glenn Johnson MSF Union.)

Batchelor Gerald L. Glutaraldehyde toxicity. Shadows 38 , 4, 20-21, Dec 1995. (Occ Health Advisor, Northland Health. Cases from radiology and theatre. Individuals can have any or all 4 different types of immune response (hypersensitivity). 1) IgE (?IgG4) mediated eg hayfever, anaphylaxis, extrinsic asthma, acute contact dermatitis, urticaria. 2) A chemical may affect certain cells which react with IgG or IgM antibodies and may cause cell destuction - ie auto-antibodies which may cause auto-immune diseases eg SLE (lupus) or following certain drugs or chems. Needs careful history taking. 3) From precipitation of antigen-antibody complexes in tissues which have tortuous arterioles eg kidneys, eyes. 4) Immune responses mediated by T-cells eg delayed contact dermatitis (several days later). Chems can trigger a similar response. Auto-immune diseases occur in ratio of 8 female to 1 male so high chance of seeing these in radiology and theatre. Those sensitised to GA may develop cross-sensitivities especially to aldehydes (in diesel/petrol exhaust) , and organic solvents. Also to perfumes, carpets, new clothes, cigarette smoke, new chipboard [these contain aldehydes] and some food preservatives. Some people complain of similar symptoms from agricultural chems, mercury, and silicone implants. GA symptoms - plus include difficulty concentrating and sleep disorder. Depression is common but is this a primary effect of the GA or secondary effect following continual fatigue, frustration etc? Those with long-term problems slowly improve but contact with, for instance, diesel fumes causes recurrence of symptoms. If sensitised, must be totally removed.)

Birnbaum, B.A. et al. "Glutaraldehyde colitis: radiologic findings," Radiology. 1995, 195, 1, 131-4, Apr. (Two percent GA on colonic mucosa may result in toxic colitis, and the clinical features may mimic those of colonic ischemia. A retropective review of four patients with GA-induced colitis who developed a self-limited syndrome of cramps and abdominable pains, tenesmus (straining) and rectal bleeding within 48 hours of uncomplicated sigmoidoscopy or colonoscopy. CT showed circumferential thickening of the left side of the colonic wall in all. From Hospital of University of Pennsylvania.)

Care G Feb, 1995, Photosol Ltd, 15 Bakers Court, Basildon, Essex, SS14 3EH, England. :

Fumes from X-Ray Chemistry (Sources, exposure limits, action to be taken.)

Ultimate Waste Disposal (Landfill, Incineration, Trade Efflent, Recycling)

X-Ray Chemistry and the Environment June 1995 (Overview of green issues, COSHH regs, fume measurements, fume prevention and control, environmental protection act, waste disposal via contractor, disposal to drain, new technologies for pollution control.)

Sick Building Syndrome (How does it relate to Darkroom Disease?)

Cuthbert J, Groves J. The Measurement of Airborne Glutaraldehyde by High-performance Liquid Chromotography. 1995, 39, 223-233. Ann.Occup.Hyg. (Evaluation of GA personal exposure measuring methods. MBTH method measures all aldehydes and it has to operate close to its detection limits. NIOSH uses gas chromotographic analysis, with 165 ppb detection. The OSHA method uses DNPH with analysis by HPLC. A change to the eluent used in HPLC is suggested along with more robust calibration. Tests show sampling efficiency is unaffected by humidity changes of 20-70%. Samples can be stored at room temperature up to 4 wks. Detection limit is about 3 ppb for a 2 litre sample (about 1/65th of the current OES).

Ellett M L, Mikels C A, Fullhart J W. SGNA endoscopic disinfectant survey. Gastroenterology Nursing. 1995, 18, 1, 2-10. Jan/Feb. (Study to describe prevalence of health problems and safe practices. 37.8% reported at least one symptom/illness before exposure to GA. Nearly 60% reported symptoms after GA exposure. Healthcare workers employed 5 yrs or more tended to report fewer health problems preexposure and slightly more problems postexposure compared with total. Smokers: nearly equal number of problems pre- and post-exposure. 95% always wore gloves; 52% moisture-proof outerwear; 28% masks; 55% eye protection. Those who always used protective attire reported as many symptoms/illness as those who did not.)

Flett Malcolm. Glutaraldehyde misery. North and South. March, 1995. Letter. (A large number of people in NZ who have had contact with glutaraldehyde (Relugan GTA), in the light tanning industry - lamb and sheep skins for garments, belts, shoe leather... MF worked 13 yrs, up to 14 hrs/day, 6 days/wk. Used 50% solution, capable of tanning human skin golden brown. (Skin then dries and flakes off). Mid-1980 ACC claim refused. After 3 mnths off with migraine and anorexia (1.9m tall/64 kg) learnt to avoid trigger foods - beer, chocolate, wine. By 1985 had to leave work and found had developed multiple chemical sensitivity. ACC claim relodged.)

Gannon P.F.G., Bright P., Campbell M., O'Hickey S.P., Sherwood Burge P. Occupational asthma due to glutaraldehyde and formaldehyde in endoscopy and x-ray departments. Thorax, 1995, 50, 156-159 (7 cases of occ asthma in 5 nurses, 1 radiographer, and 1 X-ray secretary who reacted to newly-developed X-ray film placed beside her for 6 mnths. PEF records suggestive of occ. asthma; positive specific bronchial challenges to GA with mostly late reactions and falls of 15% FEV1 or more. Unlikely that the effect of GA on the airway was solely as an irritant. 5/7 had no history of asthma, rhinitis or eczema and were non-atopic on common allergens. The results of breathing zone samples collected during 3 of the simulated specific bronchial challenge tests ranged from 0.064mg/m to 0.081 mg/m (short term occ exp standard is 0.07mg/m). Median for personal short term exposure samples in endoscopy was 0.16mg/m. 19 X-ray darkroom samples had less than 0.009mg/m. 3 subjects also positive to formaldehyde suggesting cross-reactivity.)

Gordon M. A. A history of X-ray chemical developers. Shadows, Rntgen Centenary Journal, Nov 1995, 58-60 (Includes photographic chemical developments from 1837 to present, plus one case history of liver damage in 34 yr old male radiographer with raised LFTs and a liver biopsy which showed an hepatic process in keeping with a toxic reaction. [See David Wilcox, 1995] ).

Kumar P et al. Inhalation challenge effects of perfume scent strips in patients with asthma. Ann Allergy Asthma Immunol. 1995, 75, 429-33, Nov. (Inhalation challenges using perfume produced significant declines in FEVI in 29 asthmatic patients when compared with 13 control subjects. Perfume-scented strips in magazines can cause exacerbations of symptoms and airway obstruction in asthmatic patients. Severe and atopic asthma increases risk of adverse repiratory reactions to perfumes.)

Loats G. Glutaraldehyde is not okay. Aust Nursing J. 1995, 3, 1, p6, July

Tighter controls on glutaraldehyde proposed. Aust Nursing J. 1995, 3, 1, p25, July.

Menzies D. Glutaraldehyde - controlling the risk to health British Jnl of Theatre Nursing 1995, 4, 11, 13-15. (Lack of risk control measures in place in National Health Service theatres. COSHH Regulations 1988 require that the exposure to all hazardous agents be reviewed and measures put in place to control the risk to health. Systemic effects have not been described as occurring in the workplace - GA recognised to be irritant and allergenic to the site of contact. SWORD project - collates nationally reports of occ asthma - 30 cases ‘89-’91 due to GA (19 were nurses.) Occ rhinitis more likely to be under-reported. The author compared 204 GA exposed health care workers with unexposed workers in the same hospitals. Questionnaire/skin inspection/lung function/measure of exposure to GA (all measurements were below OES). The wheeze and nasal irritation reported by the exposed workers too small to be statistically significant. Dermatitis and lung function the same in both groups. 2 probable occ asthma, 5 respiratory irritant, 3 with existing asthma  xacerbated. Safe practices. Envir monitoring still necessary with ventilation or fume cabinet. Pre-employment screening to identify employees who may be more susceptible. Civil claim for damages: Cooper v South West Durham Health Authority, 1994, because of inadequate training and PPE; 32,500 compensation.)

Nowak A.K., Shilkin K.B., Jeffrey G.P. Darkroom hepatitis after exposure to hydroquinone. (Letter) The Lancet, May 6, 1995, 345, 1187. (URT symptoms, fatigue, nausea, anorexia in 34 yr old male W. Australian radiographer. The authors believed the abnormal Liver Function Tests were probably caused by exposure to hydroquinone. Liver biopsy showed prominent Kupffer cells and collections of lymphocytes, histiocyted, and some eosinophils. Hepatocyte nuclear pleomorphism and occasional necrotic hepatocytes.)

Response: Care G.L. Darkroom exposure to hydroquinone. (Letter) Lancet, 1996, 347, 121. (Quinone - more toxic than, and oxidised from, hydroquinone may be present in aerosols above the developer with droplets small enough to reach the lungs.)

Pennel Di. Chemical Caution. Nursing N Z. Nov. 1995 (Safe handling , attitude warnings).

Photosol. X-ray Processing Chemical Components: Health Related Bibliography. Nov, 1995.

Scobbie E, Groves J.A. An Investigation of the Composition of the Vapour Evolved from Aqueous Glutaraldehyde Solutions Ann Occup Hyg. 1995, 39, 1, 63-78 (Only 0.7 ppm of GA was detected above unactivated Cidex but approx 2ppm of GA can be formed above activated 2% Cidex sterilising solution - the equivalent of lifting the lid on a closed container of activated solution. GA vapour showed a tendency to adsorb reversibly onto stainless steel. Small concentrations of methanol (sometimes added as a stabiliser to prevent polymerisation) and butyraldehyde were detected. Methanol increased with temp above all samples but butyraldehyde increased 10 fold above activated Cidex with temperature increase from 15-35C. There was little difference in the vapour composition of 3 other unactivated and activated sterilants. Impurities may include acrolein and glutaric acid. Fourier transform infrared (FTIR) spectrometry lacked sensitivity for some measurements so gas chromatography was used and also high performance liquid chromatography.)

West, A.B. et al. Glutaraldeyde colitis following endoscopy: clinical and pathological features and investigation of an outbreak. Gastroenterology. 1995, 108, 4, 1250-5, Apr. (Describes the clinical features of glutaraldehyde-induced colitis and the pathology of the mucosal injury in 4 patients due to its inadvertant introduction to the gastrointestinal tract via endoscopes or tubing connecting water bottles. Within 3 mnths, 3 patients experienced severe acute proctocolitis. It seems similar to ischemic (lack of blood getting to a part) colitis in biopsy specimens. From Pathology Lab, Yale Univ.)

David Wilcox - Case study Synergy. September 1995, p23. (1989 tired - thought stress. Moved to Colchester General Hospital with more darkrom work. Tiredness and lethargy hit like a brick wall. To G.P. - blood tests - Gamma GT raised to such a point normally assoc with alcohol - but was teetotal. Had to write safety procedures: found hollow floor like a chemical sewer under the tiles. Better at weekends, much better on hol. Occ health began to monitor liver enzymes which went up within a week of being back at work. Had to look after a number of machines Feb ‘91. Told to take 3 days off and slept for 50 hrs - woke tired, like bad flu and needed all his energy to put one foot in front of the other. Chronically ill for two yrs. Back to GP. Gamma GT highest they had ever been (equiv to 8-9 pints beer in one sitting). Medical opinion from Barts - not allowed to work anymore. "Hospital didn’t know what to do with me". March ‘93 - offered ultrasound work. Gamma GTs well down. Concurrently with this had been having tests which showed peak flow reduced by 18% . Legal claim was based on this. Case just completed with 22,000 out-of-court settlement. Warren Town and Society of Radoigraphers a huge help.)

1996 1996

Anderson R. "Darkroom Disease: A Matter of Debate". ASRT Scanner 1996, 28, 10, July, p1, p8. (OSHA 1968 PEL stds may be out-dated. MCS debate - chemical sensitivity: physiological or psychological?

Asthma and Allergy Foundation of America: ph: 800-727-8462. American Academy of Envir Med: ph 913-341-0765.

Chemical Injury Information Network: ph: 406-547-2255)

"ASRT responds to dangers of DD." p3 (ASRT to petition OSHA for guidelines to include safe darkroom practices that address MCS via engineering controls and personal protective equipment.)

Bateman P. Workplace Wheezing Safeguard, NZ. Oct, 1996. (Dr Chris Walls: occ asthma widely underdiagnosed. Dr Evan Dryson: occupational asthma rare. 20-50% will continue to suffer long-term despite being removed from workplace. Sensitisers list including urea-formaldehyde, diisocyanates, enzymes etc. Aluminium smelter (potroom) asthma in 1% per year; pre-employment questionnaire and lung finction test, and 6 mnthly checks necessary; those with asthma re-employed in transport depot. Radiography asthma controversial - one NZ expert says GA is not proven to be a sensitiser, another that radiographers blame alleged chem sensitivity on Xray chems and conclude they have the contentious MCS. Prof Bill Glass: there is no argument about GA and occ asthma - radiographers get occ asthma. Early diagnosis the key. Dr Dryson: any adult-onset asthma should be considered occupational in origin until proven otherwise. Dr Andrew Veale: Occ asthma is grossly under-recognised - many doctors do not take good occ history. Case study 1: Qualified as a radiog 1982, scared to take GA sensitivity test in case of very bad reaction - no response to pollens, grains, etc. Only way to stop symptoms is complete avoidance. Tries to avoid chemicals around home. Can't go to hairdresser- gets bleeding nose, itchy skin, and asthma. Couldn't go with child to dentist after accident. When really sick couldn't speak on phone or eat dinner - just cough. Case Study 2: Got new unvented auto processor in 1993 - respiratory symptoms from then. Confirmed this year occ asthma. Wanted to keep working but compromised her health. April: massive asthma attack after working 9 days, peak flow down from 450 to 150. 4 days on, PF dec; 3 days off, PF inc. Took 9 wks off - lasted back hr. Carbon mask to use household cleaners, ....cigarette smoke, perfume, diesel cause probs... Having to retrain and relocate. OK if away from chems.

Care G. ' Is Your Job Making You Ill?' Photosol Ltd. 1996, 19, 4-06.

Cullen J. Avoiding Chemical Poisoning. Kai Tiaki: Nursing New Zealand. Aug, 96. (5 theatre nurses from Whangarei Hosp won their battle with ACC for glut poisoning. Carol Gilmour, NZNO: nurses unlikely to work again in hosp setting. Sens to glut and some other chems. Short-term memory loss, poor concentration, resp probs, low physical energy. Glut no longer used in any Northland public hosp. JC: sens to some foods, perfume, cig smoke... Aldehyde uses, how to use safely (contact lenses can absorb), probs with recycling air conditioning system - under positive pressure the air will be forced into your body. Suspect: rhinitis, fatigue, menstrual disturbance, dermatitis, headaches, sleep disturbance, gastric or bowel probs. Use since 60s and 70s may result in high levels stored in the body. Union Carbide in April halved the rec airborne exp level to 0.1ppm. GP will know little.)

Curran A D, Burge P S, Wiley K. Clinical and immunologic evaluation of workers exposed to glutaraldehyde Allergy 1996, 51, 826-832. (The first evidence of immunologic sensitisation in some workers exposed to GA. 31% of exposed workers with occupational asthma had antibody levels greater than the unexposed population. GA may behave like other low-molecular weight chems [eg isocyanates] in that specific antibodies can be detected in only a small percentage of exposed workers with work-related respiratory symptoms.)

Heck Henry d’A. Curriculum in Toxicology, Univ of Nth Carolina. Internet. (Theme of research is the dose of chemical delivered to target tissues, and the pharmacokinetics and metabolism of endogenous chemicals. Main areas: 1) chemical carcinogenesis induced by aldehydes and aldehyde precursors (such as dichloromethane and methyl t-butyl ether). 2) enocrine toxicology (such chemicals as bis-phenol A and endosulfan). Refs include: Casanova M, Conolly R B, Heck H d’A, DNA-protein cross-links (DPX) and cell proliferation in B6C3F1 mice but not Syrian golden hamsters exposed to dichloromethane: pharmacokinetics and risk assessment with DPX as dosimeter. Fundamental and Applied Tox., accepted for publication (1996).) 

Hewitt P. Industrial Photography - controlling substances hazardous to health. The Safety and Health Practitioner. 1996, Sept, 22-24. (How photographic film works. Chemicals used, design and operational deficiencies, use of low hazard chemicals, ventilation, couplings, surfaces, drains, PPE.)

Juberg R et al. "Kodak tests air contaminants." ASRT Scanner 1996, 28, 9. (3 hospitals tested with exhausts turned off in processor room plus tests in chemical mixing room. Acetic acid, sulfur dioxide, ammonia below OSHA PEL's and ACGIH TLV's. GA below detection limit. Independant study confirmed these findings. Individuals not expected to be exposed to hazardous levels during routine mixing.)

Kiec-Swiercynska, M. Occupational Allergic Contact Dermatitis (OACD) in Lodz. 1990-1994 Occupational Medicine, 1996, 46, 3, 205-208. (Among health care workers there has been a notable increase in OACD; sensitivity to formaldehyde and glutaraldehyde has become frequent. Occ skin diseases are 9% of occ disease. Av of 66.4 cases/yr 1990-94 (cf 34/yr 1972-87 , 8.6%). OACD most frequent in health care workers (25.6%) = 85 cases. 18.1% (60) showed allergy to formaldehyde, 33 f, 27 m (cf 7.9% 1972-87). 12 f showed allergy to glut. In females with OACD, 18.9% were nurses (30), lab assistants 17% (27).

Of 60 with formald allergy: fitters 12, lab assistant 5, nurses 10, turners 4, physicians 6, other 23. The second most frequent cause of occupational sensitivity in Poland after metals was disinfecting agents, including formaldehyde.

The reduction in allergies in the building /textile/clothing industries reflects the fall in these industries. The health care industries have in the meantime started using large nos of various disinfectants including formald and GA. Allergy to fragrances was in most cases accompanied by allergy to other allergen groups.)

Martin Yvonne. Workers may be allergic to their jobs. Sunday Star Times. 20 Oct, 1996. (OSH estimates 10% new adult asthma cases are workplace related. Dr John Gillies, Christchurch, NZ - the tip of the iceberg - people scared of losing jobs - end up with irreversible asthma. 20-50% suffer long term effects. Mussel openers’ asthma; aluminium potroom asthma.)

Medinsky Michelle A. Determinants of gas and vapor uptake in the respiratory tract. Chemical Industry Institute of Toxicology, CIIT Activities 16, 2, March Activities, 1996. (Water solubility and reactivity are used determine gas and vapor uptake to predict where and how inhaled gases and vapours will react with respiratory tract tissue. Water soluble gas dissolves in the mucus lining most of the URT. Mucus is 90-95% water and acts as a sink. After dissolving, the gas molecules can diffuse into the underlying epithelial cells. Eventually, some gas molecules diffuse into the blood capillaries for transport o other tissues. But the aqueous mucus lining is not a natural home for water insoluble gases. These tend to be highly soluble in lipids or organic solvents. A few molecules may diffuse to the epithelial cells but most fail to dissolve and reenter the airspace, or lumen, and move down toward the lower portions of the RT, where large surfaces and short distances between the airspace and blood facilitate absorbtion.

Chemical reactivity controls the molecular interactions with respiratory tissues. A reactive gas interacts with the mucus tissue or blood. The concentration of the reactive gas drops very rapidly across the distance from the airway lumen to the blood. Some gases react so rapidly, very little reaches the blood. But an inert gas can ultimately diffuse through the RT layers; higher concentrations may eventually reach the blood which carries these to other parts of the body where they may produce toxicity.

Water-soluble and reactive vapour eg formaldehyde. This produced nasal tumors in rats at high concentrations. Dr Henry Heck (CIIT 1983) determined nasal mucosa the target site for inhaled HCHO. He found the highest concentrations of formaldehyde-derived material in the nasal mucosa. 1990, models of nasal cavities showed that high airflow moves HCHO to certain parts of the nasal passages. Once it contacts the mucosal surface, it dissolves and because it is reactive gas, its reactive products stay in that region of deposition. At high doses, HCHO can kill cells, react with DNA, and eventually cause tumors.

Water-soluble, non-reactive vapors and gases: Taken up by the mucosal lining of the nasal cavities. Some may diffuse into blood cpaillaries because concentration of vapor is highestin the airway lumen and molecules mov from high concentration to low concentration. During exhalation, air coming from deep in the lungs has very low concentrations of the water soluble vapors so gases move back into the airway lumen. Vapors desorb and are exhaled - the wash-in, wash-out effect. Ethanol and methanol are almost entirely scrubbed by the nose on inhalation but on exhalation up to 30% is desorbed and exhaled. Methanol absorbed in the URT is transported to other parts of the body where it exerts its toxic effects. It is metabolised in the live to formate.

Water-insoluble, reactive: Greater uptake occurs in regions of greater surface area eg alveoli rather than trachea. Uptake and diffusion depends on rate of reaction with resp tract tissues and fluids eg ozone which is a by-product between car exhaust and oxygen - it is irritating and toxic. About 50% is removed by the large surface area of the nasal cavity as it reacts with mucus; very little reaches the underlying tissues. Does some damage to nasal tissue. Greatest ozone dose is in the terminal bronchioles where the mucus coating is thin enough that some ozone can avoid reaction and penetrate the tissues. As it moves further into the alveoli (the gas exchange units of the lungs), the large increase in surface area reduces the concentration of ozone able to reach any one of the alveoli.

Water-insoluble, non-reactive: eg benzene. Causes toxicity to blood cells and leukemia. Absorbtion primarily in the alveoli - the region where oxygen is absorbed into the blood. The alveoli region has air, tissues, blood. Vapours can be brought to the alveoli by the blood or taken away from the alveoli by the blood. This concentration ratio is equal to a constant called the blood:air coefficient. The larger this coefficient, the better the movement of vapor from air into the alveoli.

Other insoluble vapors may be transformed by lung cells to toxic metabolites eg butadiene, a plastics monomer, produces tumors in the lung of mice but not rats. Mice form the largest amounts of butadiene monoepoxide. Model predictions suggest humans would form monoepoxide much more like rats.)

Metso T, et al. Can early asthma be confirmed by laboratory tests? Allergy. 1996, 51, 4. (Tests on 23 patients who had had symptoms suggesting asthma for less than a year. The best test, histamine challenge, had sensitivity of only 48%. With PEF added, 65%. With sputum eosinophil cationic protein (ECP) 74%. With serum ECP 78%. It appears that detection can be increased further through the development of improved sputum tests.)

Molloy J. Posthumous award recognises work. The Chronicle. Wed, Dec 18, 1996. (Marjorie Gordon awarded posthumous silver medal for her work on the dangers of Xray chemicals, by the Society and College of Radigraphers in the UK, following her death in February after a car accident.)

O’Donnell D. Important announcement affecting occupational health safety. Circular from Medic Corp Ltd. April 1996. ("...Union Carbide are to halve the recommended airborne exposure level of GA from 0.2ppm (ceiling) to 0.1ppm (ceiling). The decision comes from careful consideration of the results of recent animal studies and reports of eye and respiratory irritation among medical workers.")

Pickford A. Report from Survey of Work-Related Chemical Injury - October 1996 (Unpublished NZ questionnaire. 41 replies from people ACC accepted, 76 sent out. 30 MRTs; 14 nurses; 7 others . 6 claims accepted 1980-1989, 7 in 1990-1992, 17 in 1993-4, 7 in 1995. Age of withdrawal from the workplace: 5 30-39yrs , 19 40-49yrs, 8 50-65yrs. 10  identified specific high exposure incidents. Symptoms upon ceasing work: respiratory 35, skin 34, head 33, memory 32, eyes 32, sinuses 31, below average energy levels 31, depression 25, heart 23, ears 22, throat 22, health problems from other chemicals 22, liver 5, other (eg erratic menstruation, joint/muscle pains, sweating, nausea) 24. No active management 13 - health does slowly improve with time. Orthodox treatment 10 (2 found it beneficial). Alternative treatment 10 (8 found it beneficial). Orthodox and alternative treatment 8 (3 said beneficial). No re-exposure 18. Re-exposure 22 (eg part-time or trying again back at work) - symptoms increased on re-exposure 22. Re-exposure or a general anaesthetic put recovery back in those who were improving. Significant illness/psychological stress prior to sensitivity: nil 32, yes 9. Warning symptoms over years: bad/metallic taste, bad breath, numb/tingling lips, sore throat, cold sores, sinus congestion, post-nasal drip, gradual loss of singing voice, irregular headaches, migraine, chestiness, excessive fatigue, exercise intolerance, food intolerances. Common late symptoms: reduced PFV, very marked excess fatigue, dark circles under eyes, sore eyes, difficulty focussing; increasing depression, mood swings, anxiety, memory loss, concentration, dizziness, spaced out feeling, allergic reaction to other chems.)

Smedley J, Coggon D. Health surveillance for hospital employees exposed to respiratory sensitizers. Occupational Medicine. 1996, 46, 1, 33-6, Feb. ( 78 National Health Service occ health departments invited to take part in an audit of health surveillance for employees exposed to respiratory sensitising agents. Most had responsibility for workers using glutaraldehyde, formaldehyde, methyl methacrylate and X-ray processing chemicals, but many departments had no written policies for surveillance and the methods used were often labour intensive. Only a minority had communicated the results of screening to employees, failure to do so a breach of statutory duty. Major discrepancies between departments in criteria for excluding employees from work with respiratory sensitising agents. Occupational physicians caring for hospital staff should establish guidelines for surveillance of people working with the sensitisers.) 

Smedley J., Inskip H., Wield G., Coggan D. Work related respiratory symptoms in radiographers. Occup. Envir.Med. 1996, 53 450-454. (Postal questionnaire of 2,354 radiogs and 3,048 physiotherapists. Findings suggest that symptoms may arise from genuine toxicity. Radiogs were more likely to complain of symptoms that were worse at work: mouth soreness (1.9% v 0.5% Prevalence Ratio 3.6, Confidence Interval 95% ), sore itchy or runny eyes (15.1% v 6.2% PR 2.46), sore throat (16.2% v 6.8% PR 2.42), mouth ulcers (1.4% v 0.6% PR 2.18), persistant blocked nose (10.6% v 5.3% PR 1.98), headache (28.8% v 15.2%, PR 1.94), persistent itchy nose or sneezing (12.6% v 6 .6% PR 1.93), . Other significant symptoms were: persistant runny nose (7.9% v 5.4% PR 1.46), dizziness (3.2% v 2.3% PR 1.42), excessive fatigue (20.5% v 14.4% PR 1.41), blurred vision (1.2% v 0.9% PR 1.29), skin rash (6.1% v 4.8% PR 1.26). Small and non-significant differences were found with: abdominal pain (1.9% v 1.7% PR 1.12), nausea (3.1% v 3.1% PR 1.04), numbness hands/face/feet (0.6 v 0.5% PR 1.04), dysuria (0.8% v 0.8% PR 0.96), joint pain/ stiffness (7.4% v 9.2%, PR 0.82). The work-related symptoms seemed to be associated with working at least 20 hrs/wk with automatic processing machines (especially leaking machines). Unblocking a processor drain was significantly assoc with sore eyes, itchy nose/sneezing and headache. Symptoms reported have been described in association with sick building syndrome and Xray depts are particularly likely to have the small rooms, lack of external windows, poor lighting, excessive heat, low humidity to predispose to this syndrome. This study found a slightly higher one year prevalence of probable asthma in radiographers than controls. The survey found 235 radiogs with wheeze or chest tightness that was worse at work.)

Scobbie Emma, Dabill David W, Groves John A. Chemical pollutants in x-ray film processing departments. Annals Occ. Hyg. 1996, 40, 4, 423-435. (Chemicals used:- Developer: glutaraldehyde (or bisulphate complex), hydroquinone, a glycol, acetic acid, sodium sulphite, potassium hydroxide, phenidone. Fixer: ammonium thiosulphate, acetic acid, aluminium sulphate, sodium sulphite, sulphuric acid, a glycol ether.

Main airborne contaminants in X-ray depts were sulphur dioxide and acetic acid at concentrations less than 0.1 ppm. A previous problem area revealed acetic acid and sulphur dioxide at about 0.5ppm and conditions were distinctly uncomfortable. Samples of sulphur dioxide and acetic acid from the processor exhaust duct were around 0.8 ppm .GA not detected in ambient air of the typical locations or in the problem area or the exhaust duct. GA was only found in the developer tank in the problem area at 0.13ppm. Butyraldehyde, a severe irritant, was found at low concentrations in the processor exhaust duct and was a main component above the developer solutions. Lab studies show that butyraldehyde increases as the developer ages - could indicate higher potential for exposure when handling waste fixer. Freshly prepared developer revealed toluene as a major volatile constituent with traces of GA and butyraldehyde. Benzene was detected as a major constituent in the headspace of a survey location. [Photosol believes toluene and benzene are likely to be impurities in some of the chemical constituents - personal communication]. Shutting off the ventilation to recreate a problem area simply resulted in increased concentrations of sulphur dioxide and acetic acid which seems to indicate that if darkroom disease arose from day-to-day activities, then these two chemicals must have been involved. Only directly above the chemical solutions were GA and butyraldehyde detected - hand mixing in the past may have given rise to relatively high concentrations of the chemicals detected.)

Taylor AE. Cardiovascular effects of environmental chemicals. Otolaryngology - Head and Neck Surgery. 114, 2, 209-211, 1996. (Recent data on the environmental toxins lead, carbondisulfide, asbestos, arsenic, ozone, cadmium, fluorocarbons, freon and pesticides. These toxins produce hypertension and cardiac arrthymias in most studies and are not necessarily related to primary lung disease and secondary heart disease. Possible mechanisms include: (1) damage to the endothelial barrier in the vascular sustem, (2) activation of leukocytes and platelets, (3) initiation of plaque formation, (4) stimulation of the inflammatory response, (5) kidney-related hyertension, and (6) direct damage to cardiac and blood vessel tissue. Needs lots more studies.

Terry Keith X-ray film processor chemicals. The how, why and where of their effects on the medical diagnostic technicians that work with them. NDMDI Study Project. 30 Aug, 1996. {(a). Background. (b) Toxicology. (c) Treating Chemical Sensitisation - the Environmental Health Centre, Texas, has developed and tested programmes for 15 yrs - people improved significantly proven by intradermal and inhaled challenge - no re-exposure problems. This programme of 1) Avoidance 2) Nutritional supplementation 3) Sauna/physical therapy has been adapted by Ted Pearson, a Christchurch doctor. This detoxification programme aims at ridding the body of fat soluble toxic residues by mobilising then from their storage sites in fatty tissue and eliminating by hyperstimulation of normal excretory pathways. (Not for heavy metals.) 4 hrs /day for 2 wks. Two with X-ray chemical contact said they had good improvements (Margaret Mulligan one). About $900 for the basic course, non-ACC funded. (d) Processor Chemicals -incl 5 Nitroindazole info. (e) Routes into the body - Aerosols.

(f) MRT health survey comparison with teachers who have: close contact with public, institutional work environment, similar professional standing, similar stress levels, BUT little chemical contact.

85% of 105 radiographers answered "Yes" to one or more symptoms attributable to fume exposure. 65% of radiographers and 42% of teachers believed their symptoms resolved/lessened away from work. Most common symptom for teachers and radiogs was burning sensation in throat. Most common for radiogs were also need to keep clearing throat and dry flaking skin. Radiology group symptoms: eye, nose, throat irritation incl cough, hoarseness; URT, LRT, poor concentration, memory, skin. Lethargy and fatigue the most common "other" symptom overall; 3 reported cross- sensitisation The number of MRTs with no symptoms was greatest in the oldest and longest-serving groups with the youngest group next. No difference in symptoms between premises using glutaraldehyde-free chemistry. None of centres had all of: H&S committee, protocols for safe handling, environmental management plan for spills, and a spill kit. Most of centres (11) had venting through the ceiling; one had low-level venting. Two had taken chemical related sick leave in past 2 yrs = 105 lost work days; one employee on ACC for 3 yrs; 4 depts had had staff leave with chemical exposure problems.

Overwhelming theme of teachers’ comments was stress - tiredness, irritability, altered sleep patterns, reduced concentration, high blood pressure, tension, peptic ulcers, emotional problems of depression, crying, resentment or panic attacks.

APPENDICES: Chart of chemicals used in AGFA and KODAK chemistry and their mutagenicity, plus the toxicology on each. Contents of GA spill kit: incl sodium metabisulphite - available from Clean Room Garments Pty Ltd.
Ventilation: X-ray vntn in NZ governed by NZ Std 4303:1990 Air Supply. Regulates for acceptable indoor air - "... no known contaminants at harmful concentrations... > 80% of people do not express dissatisfaction", p3.

Australian Std 1688.2 1991 Air Extraction. Processor fumes are in "effluent" category requiring local exhaust: "Toxic, irritant, asphyxiant, offensive... dust fumes or vapours." Clause requires extraction to be as close as possible to source using special surrounds or hoods to ensure positive capture. Air velocity entry to be not less than 0.5 m/sec.

Clause 2,4 prohibits recycling of air from health care facilities. GA and diethylene glycol are heavier than air yet only one dept had low-level extraction. 11/14 had celing extraction - could be drawing fumes across breathing zone. Air pressure in the darkroom should be slightly positive relative to the processor. These stds were enacted in 1991/2 (after many processors installed). Complete enclosure of the processor can be done for $500-$600.}

Whitaker K. Darkroom Disease : Multiple chemical sensitivity continues to be debated in medical field. R.T.Image 1996, 9, 12, June 3, 10-15. (Dr Grace Ziem and Dr Albert Donnay on MCS symptoms and debate, need for a definition. Opponents believe symptoms are psychogenic and psychosomatic. Jackie Jones, (and Leslie Alder) - Salt Lake City, headaches, runny noses, sore throats, chest pains, voice change through the day, in 2 yrs voice disappeared. Ventilation installed but symptoms of headache, chest pain, hoarseness returned. Told "in their heads". Ziem - significant political and economic implications eg in petrochem industry, if MCS accepted. Legislation to accommodate MCS victims could include nontoxic pest control, and the removal of petrochemical air fresheners. 7% of Californian pop claim to have been diagnosed with MCS. Renovated US govt EPA building caused sick building symptoms. Dr Linda Davidoff evaluated 10 studies which purport the psychological position of MCS. 9/10 had seven methodological flaws and the tenth had three. Statements from the American College of Physicians, American Academy Allied Immunology, American Medical Association don’t reflect new additions to MCS literature. Dept Housing and Urban Devel recognises MCS. NCEHS - first congressional funding. MCS follows basic principle of toxicology - the greater the exposure the greater the dose. Ziem: the psychological approach prescribing psychotropic drugs can make a patient worse. Kodak ‘...X-ray developers can cause skin and eye irritation...and potential..allergic skin reaction"; impt of prevention.)

Macfie Rebecca. Solvent-Induced Neurotoxicity - the New Asbestos? Safeguard. Jan/Feb 1996, 29-36. (Aucklander David Duke would leave work in a state of bliss - stoned. 14 yrs screen printer, now with crippling headaches - takes 20 mins to lift head off pillow - wicked mood swings - affectionate one minute then threatening to pack his bags. Comes off phone and can't remember who he was talking to... clumsy and inco-ordinate, dropping things... Had no idea about the chems. Little or no ventilation or PPE - the rubber gloves disintegrating with chem contact.

Est 100,000 NZers regularly exposed to solvents at work. Used for thinning, dissolving and cleaning oils, fats, resins, paints. Present in paint and stripper, glues, inks, dyes, textiles, agric products, pharmaceuticals. Many highly volatile - evap readily at room temp. epidemic predicted. OSH NODS register has 222 suspected SIN. Av exposure 18 yrs. 4 have less than 10 yrs. 42 confirmed with Type 2B neurotoxicity (mood swings, fatigue AND impaired brain functioning with difficulty learning new material). Stress and malingering is a cynical conclusion. Dr Evan Dryson: "Insidious symptoms...initially disappear over weekends... but over the years become chronic..a fundamental change in personality...inability to work , participate socially eg in playing cards, music, hobby... inability also to manage relationships and function sexually. Marriage break-up appears more common. Dr Jenni Ogden: Many are prescribed anti-depressants or sleeping pills. Put together13 case studies: Men with stable work histories...10 with nausea, vomiting, diarrhoea, tingling fingers, dizziness, dermatitis. One withdrawal-type symptoms on holiday. 13 excessive fatigue, 3 debilitating anxiety, 9 depression, 3 on anti-depressants. One, Type 3 dementia. 2 uncontrollably violent towards their families. All 13 debilitating memory etc probs. One pesticide exposed forgot he'd taken apart a piece of equipment and did it again. Diaries not much help - forget where they put it. Dryson: NODS cases are the tip of the iceberg. 19/42 (see above) were spray painters in typical NZ workshops - "not excessive" levels of exposure - people are being affected at levels below the WES [Worker Exposure Std]. OSH view - to aim for absolute elimination, isolation, and minimisation. Proof for prosecution difficult - the WES would be taken as std. Dr Bill Glass: moodiness etc...intolerance to alcohol... like alcoholism "except solvents are more toxic". Often radical improvement in tempers once person retires. Printing

Packaging Media Union: management of H&S in many workplaces is "fragile". NZEPMU: Workers have a notion chems endanger their health but don't know specifics plus the macho "wuss" attitude. Motor Body Builders Assoc attributes problem largely to back-yarders. Manders Ink: a move away from toluene, methylene chloride, zylene, benzene, MEK, and glycol ether solvents to the alternative vegetable oil and citrus based products but they are more expensive and less efficient.

A-L Dalpech: Mid 1800s Paris workers exposed to carbon disulphide in rubber vulcanisation showed nervous excitement/collapse, or mood fluctuations, insomnia, memory probs, loss of sensation and impotence. Not until Scandinavian research in 1970s that neuropsych disorders highlighted.
Details of Type 1, Type 2A, 2B, Type 3 neurotoxicity. Other suggested health efects: MS, focal epilepsy, motor 8hrs/day, 5 days/wk over 40 yrs may incr risk of leukemia by c.70%. Finnish women with solvnet exposure have incr liver cancer. Hodgkins and non-Hodgkins lymphoma assoc with solvent exposure. Other solvents linked with liver and kidney damage.

Threshold limit Values (TLVs, developed by the USA ACGIH) are NZ WES. OSH says they help define limits but employers see them as 'line in the sand'. Bill Glass: "At best scientific guesses" - only account for fumes, not skin absorption or a mixture of solvents. Some TLVs influenced by vested corporate interests.

1997 1997

American Conference of Governmental Industrial Hygienists (ACGIH) Notice of Intended Change (NIC) to lower the Threshold Limit Value from TLV-Ceiling of 0.2ppm to a TLV-Ceiling of 0.05ppm for glutaraldehyde. (draft) avail from:

ACHIH, Kemper Woods Business Center, 1330f Kemper Meadow Drive, Cincinnati, OH 45440-1634, USA. Fax: 513-742-2020

ALERT Backgrounder on Occupational Asthma (Internet) Allied Lawyers Response Team . (Statistics: 1 in 20 asthmatic adults (2 million) in UK. 1 in 5 in adult asthma in certain industrial areas is occ. SWORD estimates 1400 new cases a year. True frequency of acute occupational respiratory diseases in the UK may have been 3x that reported, 1994. 1994 Report estimated 70 million lost in sickness benefit and 400 million in productivity. Occ asthma can be reversed if stopped early enough. "Few GPs have time or medical school training to determine whether a condition is work-related" - Asthma at Work p112.

What is asthma..... Treatment: bronchodilators to relax the muscles that tighten around the bronchioles. If doesn’t work, corticosteroids may be prescribed - potential side effects. Untreated asthma is serious and potentially disabling from stretching of alveoli by accumulations of stale air which can damage delicate tissues to the point where they lose elasticity and cease to function. Sensitisers: recognised by the immune system as foreign. At first reactions only occur at time of exposure however constant exposure can result in permanent sensitisation and the person will become ill when in contact with a variety of allergens which act as triggers, notwithstanding that previously the person never suffered any allergic reaction to such items. Sensitisers: isocyanates, glutaraldehyde, formaldehyde, adhesives/plastics/moulding resins.....latex... Irritants do not provoke an immune or allergenic reaction - they simply narrow the airways.

Requirements for claims in the UK: >14% disabled; client must not stay in work or could damage claim through contributory negligence, COSSH Regs 1995 - onus on employers to eradicate/minimise/monitor risk.)

Ashford Nicholas A, Miller Claudia S. Chemical Exposures - Low Levels and High Stakes. Second Edition. 1997. Van Nostrand Reinhold, NY. (Chap 1: Chemical Exposures and Sensitive Populations. 2: Key Terms and Concepts. 3: Origins of Multiple Chemical Sensitivity and Effects on Health. 4: Mechanisms of Multiple Chemical Sensitivities. 5: Diagnosis and Treatment. 6: Needs, Concerns and Recommendations. 7: Recent Developments - government interest, European perspectives. 8: Key Research Findings Since the First Edition - biomarkers, overlaps with other illnesses. (pp237-8: TILT hypothesis an umbrella for glutaraldehyde in X-ray chemicals reported to initiate sensitivities), magnitude of the problem, origins, mechanisms. 9: Reviews, Commentaries, and Polemics. 10: Research and Medical Needs .)Levi Vic. Bug Link to Fatigue. Sydney Sun-Herald 17/8/97. (Newcastle (Australia) and Swedish scientists have independently linked a common bacterial infection to chronic fatigue syndrome (CFS). Hope to collaborate on diagnostic and treatment strategies. The Collaborative Pain Research Unit has been investigating chronic fatigue and pain (myalgia) for 7 yrs. Patent lodged. Swedes treated some patients using the organism as a vaccine.)

Baskett Pat. The Hidden Pervader. NZ Herald, Nov 22, pp G1-G3, 1997 (Story of nurses, Jennifer Cullen and Jean Firman.

JC loved work for 30 yrs in theatre. Now 52, off work 3 yrs. Anything energetic gives severe headaches, dizziness, joint pains, prolonged tiredness, and nose bleeds; used to play hockey in forwards but ended up in goal - tiredness worst; 9 mths on ACC (80% of salary) but ACC has revised its decision and stopped payment. One of 5 at Whangarei Hosp. GA is considered less toxic than the probable carcinogen, formaldehyde. Whangarei introduced GA 1978 - had no smell - dipped hands in it like soap and water. Symptoms similar to CFS and depression and MCS. Prof Glass OSH audit: Whangarei Hosp "dilatory". The air-conditioning up-grade recycled the fumes. JF rated 100% disabled by ACC. 10 yrs exposure appears largely irreversible - can’t remember characters in a book, can’t count embroidery stitches, take a pulse because can’t look at clock and count. Ostracism the worst - everybody thought her mad. MAG’s work. SNFTAA set up. NZ phone survey [Pickford] in 1996 of 45 public and 26 private radiology clinics showed 2 private and 7 public clinics either had no ventilation or air-conditioning only. Proposed NZ WES for glut: 0.1ppm. OSH Med Officer, Dr Evan Dryson: "It’s ..impossible to check that the guidelines are being adhered to..." Dr Chris Walls: Are guidelines a red herring? ... people can have symptoms within those levels.

Formaldehyde is in cleaners, polishes, shampoo, but more in unsealed particle board eg furniture, flooring, thermal backed furnishings, unflued LPG heaters/cookers, cigarette smoke.)

Bateman P. First Glutaraldehyde Case. Safeguard (NZ) May/June 1997. (Southern Crown Health Enterprise pleaded guilty to exposing 2 nurses to glut - fined $8,000. In old part of hospital due for replacement.. Headaches and respiratory irritation from open troughs. Protective equipment provided. No ventilation.)

BOHS. COSHH Guidance on Glutaraldehyde. 13/6/97. Internet. (ACGIH TLV Committee Notice of Intended Change = 0.05ppm ceiling. MEL of 0.05ppm being considered by UK Advisory Committee on Toxic Substances. Problem areas: open troughs, residual contamination of surgeons’ eyepieces, down the sink, rinsing for longer than two minutes, cleaning X-Ray developer rollers etc. Precautions... Email: ).

Crosby Kim. Darkroom Disease. Filter. (Ontario AMRT) 32 ,5, 3, Sept 1997. (Regular column to run. Kim’s lectures, darkroom inspections cause her voice loss, asthma probs - inhaled medications 21x/day. Now an NZ support network. Ventilation 1997 1997 single most important factor - 12-15 air changes/hr, LOCAL exhaust plus general room ventilation with an average processor needing 500 CFM (cubic ft/min) is a minimum requirement. A bathroom fan venting into the ceiling is unacceptable!! Temps 20-22C. Keep darkrooms clean from spills. Put up an Adsorbstar filter in the darkroom - if used up in less than 6 mnths there are problems. Try White Mountain products. Still waiting for claim decision - Kim refused to take the WCB "quick decision" offer.)

Filter 32, 7, 6, Nov, 1997. (DD is a wide-ranging set of reactions including respiratory problems and heart arrhythmias. May be mild irritation to career threatening disability. Sensitisation is an allergic response which triggers an immune system response. Once sensitised, an individual may react to even minute re-exposure. DD may come from years of low exposure or one major spill. Factors: 1. Wide variety of reactions - each individual’s immune response. 2. many chems used in devel and finishing films. 3. site variables.

Kim awaiting open hearing date with mediator on her claim.)

Filter 33, 1 Jan, 1998. (From Southfield, Michigan conference: medical testing for chemical injury. Medical testing, dietary changes, nutritional supplements should only be on advice of physician. Technology to prove chemical injuries just beginning to catch up with the technology that ceated them. Neurospect Brain Scan Studies are the most promising; also metabolic tests. The following are tests you may discuss with a physician:

Chemicals, metabolites, heavy metals in the body: 1. Blood tests. 2. Urine tests. 3. Fat biopsies.

Immune system testing: 1. Antibody Assay testing for chem antibody formation. 2. Activated Lymphocyte Profiles. 3. Autoimmune Disease Profiles plus cardiolopin antibody. 4. Autoimmune Profiles for nervous system disorders. 5. Allergy testing for foods, moulds, pollens and chems.

Metabolic testing: (see next issue) 1. 24 hr urine and stool porphyrins. 2. RBC porphyrins. 3. Porphyrin enzymes.

Neuropsychological testing: 1. Complete neurological examination. 2. Positron Emission Tomography (PET) scans. 3. MRI scans. 4. Quantified Electroencephalogram (qEEC) with evoked potentials. 5. SPECT scans.

6. Neurobehavioural testing a) Halstead-Reitan b) Wide-range Achievement Test Revised c) Occ exposure tests.

d) Tests for concentration eg digit span/digit symbol e) Verbal learning test.

Other: 1. Enzyme testing for cholinesterases, antioxidants, liver etc. 2. Amino acids profiles: Standard panel and neuro-psychiatric panel. 3. Rhinolaryngoscopic examn to check for nasal passage damage. 4. Conditions and disorders associated with specific chem exposure such as aplastic anaemia, pulmonary function tests, heart monitoring, detailed and sensitive testing for various organ and/or system damage. 5. Acetonitrile Bio-uptake survey: Blood acetonitrile, cyanide, acetone, ecataldehyde, urine-acetaldehyde, formic acid, thiocyanate. NMS #0093 6. Aniline exposure bioprofile: Urine- total P-aminophenol, NMS#0390 7. Phthalate bio-uptake profile: Urine-benzylbutyl, dimethyloxyethyl.Anyone having testing please send history and results to: Kim Crosby, MRT(R), 36 Cherrywood Ave, Leamington, Ontario, N8H 4Z9, Canada, for research and legislation purposes.)

Chemical Sensitivity at Work in Medicine - Programme, Marj Gordon Memorial Seminar: Chemical Sensitivity at Work in Medicine with Special Reference to Glutaraldehyde and Xray Processing Chemicals. (New Zealand Institute of Medical Radiation Technologists - NZIMRT), Palmerston North, NZ, March, 1997. (Speakers’ abstracts)

Safeguard Update 70, 24 March, 1997. Aerosol glutaraldehyde theory. (Report of Geof Care, Photosol, presentation to MAG Memorial Seminar, March 8, 1998: evidence presented for GA-based aerosols in darkrooms. Puzzle: radiographers are sensitised to GA yet levels are so low. 4 possible mechanisms - 1. That some people are sensitive to minute concentrations. 2. Wrong measurement (discounted). 3. There are transient high exposures eg mixing, cleaning, spillage, handling film. 4. Aerosol formation. Aerosols are formed from GA vapour. SO and humidified air both scavenge GA so it is no longer detectable by standard analytical instruments. Also, an unexpected source of GA was from processed film leaving a large amount of GA on hands of a radiog.; a secretary became asthmatic from GA exposure from stacks of film).

Safeguard Update 71: 7 April 1997. Tilting at chemical sensitivity. (Report of Keynote speaker, MAG Mem Sem, Dr Claudia Miller. Misunderstandings with the term MCS - sensitisation is not necessarily occurring; intolerance not solely due to chemical exposures; ‘sensitivity’ does not convey the potentally disabling nature of the condition nor its origins in toxic exposure. MCS is controversial but something is going on. Studied 80 Gulf War vets with new on-set intolerance - one said "the perfect perfume used to be WD40" , another used to bathe in solvents and loved exhaust - now can’t bear it and cannot remember part numbers he had once committed to memory. 2/3 of vets who were alcohol users could no longer tolerate it. She proposes TILT as an emerging theory of disease, like germ and immune theories, though far more research is required to rigorously test TILT. [See Miller Claudia, 1997, below.] The problem of ‘masking‘ where people are exposed to multiple stimulants must be avoided in a four step challenge process: 1. Avoidance of all incitants so remission occurs. 2. Reintroduction of specific incitant causes specific set of symptoms. 3. Withdrawal of incitant causes symptoms to disappear. 4. Re-exposure (4-7 days) causes same set of symptoms. Rigorous testing again required. Many aspects of TILT parallel addiction and disruption of the limbic system could be the tolerance lowering mechanism.

Batchelor G. Glutaraldehyde - One example of a range of problems. Presented to the MAG Mem Seminar and reprinted in Shadows 40, 2, 1997. (Other situations provoke similar problems to the Darkroom Disease chem cocktail; role of individual susceptibility. 1. Agricultural chems eg 2-4 ; one 80 yr old sprayed himself regularly to cool off, another has fatigue and nausea whenever there is spray. 2. Fibromyalgia - diffuse musculo-skeletal pain and tenderness especially on acupuncture points. Relies on history. 3. Sick building syndrome (SBS) affecting some in new or remodelled buildings. 4. Mercury amalgam 5. Silicone breast implants - some showed neg or low ANA titres and pos Western Blot technique. Some of his GA exposed patients showed strong correlation between exposure and ANAs. Would be interesting to do W Blot on GA exposed. 6. Chronic Fatigue Syndrome (CFS). Also Myalgic Encephalitis (ME) and Tapanui Flu - primarily diagnosed by history. 7. Multiple Chemical Sensitivity (MCS) - has a hugely long definition. In SBS - formaldehyde a main culprit - daily formaldehyde at med school but few seemed to have problems so perhaps there was no synergistic effect. Fatigue is common to all these -"You can’t even do the things you really enjoy.")

Glass B. Exposure to glutaraldehyde alone or in a fume mix. MAG Mem Sem and Shadows 1997, 40, No.2 (Tribute to MAG.

26 referred patients over 6 yr period. Group A worked with glut as a sterilant or bench wipe. Group B photographic or Xray chem mix. Low levels measured in Scandinavia and UK, but NIOSH in Colorado measured 6/10 higher than .2ppm Darkrooms in UK in 1993 small, often open drains, poor local exhaust ventilation, inadequate general ventn. Few measurements in NZ. Little difference in symptoms between Gp A and Gp B except for skin symptoms (10/4). Most common symptoms were those irritative to eye, nose, throat, LRT, skin, plus headache and fatigue, as well as cross sensitivity, and neuropsychological - mood, memory, concentration. 5 confirmed asthma, 4 dermatitis, 1 schleroderma.

Neuropsych symptoms more common in Gp A: 12. Gp B: 7. 10/13 from Gp A were given ‘Questionnaire 16’. This tests memory, understanding, concentration, mood. More detailed psychological testing as well confirmed neuropsychological damage. These symptoms were not asked about in Spicer, Hay, Gordon, 1986. Q 16 tests for early disturbance in CNS function (recently validated for testing occ. solvent neurotoxicity).

Cross sensitivity: 7 cases in Gp A, 8 in Gp B; included reactions to petrol fumes, cigarette smoke, deodorants, hairsprays, paper and household cleaners. Many of these contain formaldehyde, (a chemical relative of GA). Tachycardia and palpitations: 7 in Gp A, 3 in Gp B. Connaughton (1993) noted 7 cases; Spicer, Hay, Gordon 17/367.

GA alone or the chem mix? Occ medicine premise: "Toxic effects of a chemical are more severe when the dose is high and dose is a consequence of concentration and exposure time...". "Energy and money spent on providing good working conditions. and better technical systems is more effective than fruitless research on trying to find a single causative agent".)

Gronwall D. Neuropsychological Assessment: A Case Study. MAG Mem Sem and Shadows 1997, 40, No.2. (Chronic exposure to neurotoxins can result in poor memory, concentration problems, excessive fatigue, reduced impulse control and decreased initiative etc. This case is a composite of several chem injury patients - "Jane". Important to establish pre-injury ability. Widely used is New Adult Reading Test (NART). Should be able to say words such as ache, quadruped if known before injury. Correlates highly with verbal and full-scale IQ. Jane above av. On general intelligence assessment, Jane didn’t do well on abstract reasoning, and digit symbol which is most sensitive to brain damage and involves memory, visuo-motor co-ordination, ability to work under stress and time. Visual perception - significantly below av probably because of poor frontal lobe function. Verbal memory above av on immediate and delayed recall of prose, but non-verbal significantly below av. Attention and concentration - PASAT (Paced Auditory Serial Addition Test) - Jane coped at first but scored signif below av for her age; became distressed on the third trial - a significantly slowed info processing rate. No evidence of impairment on naming or word-finding but scored significantly below av on controlled word fluency (giving as many words as possible from a given letter in 60 sec) - typical of frontal lobe dysfunction. Executive function - ability to plan, organise and check - was impaired -again frontal lobe. With reaction times Jane was much slower esp responding to targets on the R visual field. In most areas Jane scored at good av level consistent with her expected pre-morbid ability but was significantly impaired in non-verbal memory, concentration, info processing, planning , organising, monitoring.

Reasons: 1. Intellectual handicap - unlikely. 2. Poor motivation - unlikely as did well on some tests and produced excellent scores on the tedious tests. 3. Malingering - she would be likely to fake low scores on verbal memory. Also impossible to fake PASAT. 4. Depression - some difficult tasks were above av - would expect all scores to be affected. R and L peripheral vision scores were significantly different. 5. Closed head injury - excluded - Jane never knocked out. 6. Substance abuse - denied; would not expect this pattern. 7. CFS/ME - expect impaired verbal memory. No cases of impaired frontal lobe function are found in CFS. The probabilities are that the results are consistent with chemical exposure. Some neuropsychological rehabilation seems possible.)

Hedrick T. The Royal Colleges report on CFS. CFIDS Chronicle, Internet. 1997, 10, 1, 8-13. (A paper criticising 1996 The Royal Colleges Report on CFS. Terry Hedrick, PhD, makes the point that the report has a pervasive bias that the problem is psychiatric. It recognised that CFS is a substantial problem. They endorsed the use of the label CFS not ME "which erroneously endorses the existence of a specific pathological process for which in the context there is no evidence". 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. The data presented by the Royal Colleges shows that CFS patients have higher rates of psychological disorders than for defined illnesses such as rheumatoid arthritis. 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". The report constantly speculates how the psychological can infuence the development, severity or persistance of CFS. The report simplifies the literature that psychological stress worsens CFS. Bias occurred in the assessment of CFS immunological information with criticism of the different methodologies, definitions, measurements but there were no problems with these issues from the psychological literature. 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" - this has significant implications in disability insurance, home schooling for children and stress. A child who unsuccessfully under goes poor CBT or graduated exercise feels a failure. US researchers are exploring why past studies have found widely varying rates of psychological morbidity in CFS populations).

Leikauf, George D et al. Airway epithelial responses to environmental oxidative stress. CIIR. Internet. ?1997 :

1) With ozone inhalation, the epithelium of the respiratory tract reacts by forming aldehydes and hydrogen peroxide "The ozone reacts at the airway luminal surface with unsaturated fatty acids contained in the extracellular fluid and plasma membrane to form aldehydes and hydroxyhydroperoxides... ozone can augment eicosanoid release [eg leukotrienes which are rather similar to histamine but 1,000x worse] ..the major metabolites detected were prostaglandins E2, F2_, and 15-hydroxyeicosatetraenoic acid. The 9-carbon aldehyde in contrast to the 3-, and 6- carbon aldehyde, stimulated release suggesting that this effect increases with increasing chain length."

2) Exposure of humans to ozone results in increased lung neutrophils [a type of leucocyte or bacteria micro- organism killer] and elastase [enzyme for protein digestion]. Ozone inhalation induces inflammation and increases chemokine expression in mouse lung. The neutrophil chemotactic factor, macrophage inflammatory protein 2 (MIP-2) may be responsible for ozone-induced increases in lung neutrophils and the findings indicate that direct exposure of alveolar macrophages [phagocytes or cells which ingest dusts] to an oxidant [like ozone] is sufficient to induce MIP-2 expression [inflammation].

3) Corticosteroid use: The literature indicates that many inhaled environmental agents produce pulmonary cell injury that can be amplified by inflammation. Airway inflammation is often associated with the infiltration of activated neutrophils and subsequent protease release. Although aiding in the digestion and phagocytosis of foreign proteins and microorganisms, neutrophil proteases can indiscriminately damage healthy lung tissue. To limit tissue damage, airways possess several antiproteases eg SLPI. Fluticasone was much more effective than hydrocortisone at exerting anti-inflammatory effects. Corticosteroids work in part by increasing SLPI [an antiprotease] levels and their effects augment the response to elastase.

4) It is still controversial whether formaldehyde can affect the lower respiratory tract. Guinea pigs were exposed to formaldehyde or filtered air for 2 or 8 hrs. Airway smooth muscle was evaluated in vivo and ex vivo. Specific pulmonary resistance and airway reactivity to acetylcholine increased with formaldehyde exposure. Formaldehyde exposure caused bronchoconstriction and hyperreactivity at lower concentrations when exposure duration was extended from 2 to 8 hrs. Exposure to >0.3ppm for 8 hrs was sufficient to produce a significant increase in airway reactivity , while similar effects only occurred after >9ppm for 2 hrs. Formaldehyde exposure also heightens airway smooth muscle responsiveness to acetylcholine ex vivo. Results with human airway smooth muscle also suggest that formaldehyde alters reactivity to cholinergic stimulation, and recent studies suggest that reactivity to neuropeptidergic stimulation is also altered by formaldehyde. Thus at concentrations relevant to environmental exposure, 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.

Future Directions: With the demonstration that ozonolysis products important to the toxicology of ozone and that these compounds are more potent than hydrogen peroxide, they plan to examine the effects of the compunds on chemokine the effects of aldehydes on human epithelial cell functions and smooth muscle functions...

Martin Peter. .Investigating a case of possible glutaraldehyde sensitivity. MAG Mem Sem and Shadows , Sept, 1997, 40, 3, 22 . (Physicians should have a low threshold for considering the possibility of workplace illness in cases of late-onset asthma or if a time relationship in symptoms is suggested. Peak flow and symptom diaries, LFTs, tests for atopy all useful, plus workplace challenge with patient recording PFs. Case: 34 yr radiog, 9 yrs of headache and other systemic systems, 6 wks of coughing /wheezing much better at weekends. Prednisone helpful but inhaled steroids did not maintain the improvement. No history of asthma or atopic disorders but mother and one child asthmatic. First examination - spirometry and chest Xray normal. PFs recorded during long weekend normal but very unstable within few hrs of return to work. Made ACC claim; one mnth off, could do sport etc with few symptoms. Became wheezy during visit to work (in outpatients adjacent to radiology with same ventilation). Tried to return to work; rapid return of symptoms. Probable sensitivity to GA. Advised further work as a radiographer was unlikely to be possible. Except in very severe cases it is useful to provide hard evidence for compensation by returning the patient to work but remove quickly if problems recur. Few NZ hosps have lab challenge facilities - can be very severe reactions.)

Medinsky M A et al. Specific gene found to play a key role in the toxicity of benzene. CIIT Impact. Internet. Sept 1997. (Benzene which occurs in car emissions, cigarette smoke, industrial solvents, [and headspace of processing chemicals] can cause leukemia. The enzyme CYP2E1 is responsible for the metabolism of benzene in many tissues of the body. Mice which lacked this enzyme were protected from the toxic effects of benzene. Humans similarly. Other genes may result in increased toxicity. NIEHS is looking at the enzymes including CYP2E1, which metabolise substances foreign to the body, to determine the basis for the wide variation in individual responsiveness to environmental toxicants).

Miller Claudia. Toxicant-induced Loss of Tolerance. Environmental Health Perspectives, 1997, 105, Supplement 2, March, 445-453. (Also presented to MAG Mem Sem, 1997. Reprinted in part in Shadows 1997, 40, 2, 4-9 and Shadows 1997, 40, 3, 23-28) (Proposes a new verifiable theory of disease, TILT, to explain chem sensitivity. This posits that a single high-level or repeated lower-levels of chem exposure can cause susceptible people to lose their normal tolerance for various chems, foods and drugs. Subsequent very minor exposures to these substances trigger symptoms and perpetuate illness. Patients and doctors may not recognise these triggers because of overlapping effects of multiple exposures, and habituation, phenomena that may mask the effects.).

[ See also Safeguard Update 71:7 April, 1997; Montague, 1998; Ashford/Miller’s book Chemical Exposures..1997; D Blank, 1998 (in "Formaldehyde" section).]

Miller Claudia, Ashford N, Doty R, Lamielle M, Otto D, Rahill A, Wallace L. Empirical Approaches for the Imvestigation of Toxicant-induced Loss of Tolerance. Envir Health Perspectives. 1997, 105, 2, 515-519. (Hypothesis: sensitivity to low-level chem exposures develops in two steps... The Working Gp on TILT has formulated a series of research questions to test this: Q1. Do some individuals experience chem sensitivity at low levels unexplained by classical toxicological thresholds and dose-response relationships, and outside normally expected variation in the population? Q2. Do chem sensitive subjects exhibit masking that may interfere with the reproducibility of their responses to chem challenges? Q3. Does chem sensitivity develop because of acute, intermittent, or continuous exposure to certain substances? Q4. If so, what substances are most likely to initiate this? An experimental aproach for testing directly the relationship between patients’ reported symptoms and specific exposures was outlined in response to Q1, a key question. Double-blind, placebo-controlled challenges performed in an environmentally controlled hospital facility (environmental medical unit) coupled with rigorous documentation of both obective and subjective responses are necessary to answer this question and to help elucidate the nature and origins of chem sensitivity.)

Nellis Robert. Human liver cells can predict the metabolism of toxic chemicals in people. CIIT Impact. Aug 1997. (Isolated human liver cells can be used directly in cancer risk assessments.. Studies using isolated rat liver cells accurately described the metabolism and toxicity of several toxic chemicals in whole animals. In a study with the solvent furan (furan produces liver cancer in mice and rats and is a solvent present in many foods eg coffee and tinned meats) which does not directly modify DNA but which is rapidly metabolised by liver cells, the internal dose of furan was 3x more in whole rats and 10x more in whole mice than in humans. The human liver receives a much lower dose than the livers of rats and mice exposed to the same concentration of some chemical air pollutants. Furan delivery to the liver by blood flow was much slower than the rate of furan metabolism in the liver. This indicates variations due to genetics, diet etc "do not affect the metabolism of furan". Similar expected for other rapidly metabolised air pollutants).

Thompson I. Actions, Inactions & Reactions MAG Mem Sem , and Shadows 1997, 40, No 2, 22-24. (Proctor and Gamble withdrew suspect tampons. Johns Manville for 30 yrs allowed hundreds of asbestos-related deaths by not responding to evidence. Photographic manufacturers’ sales pitch said the new chemistry was quicker and cleaner. Cine film brought in rollers to move the film. Chem shortage in the war devel a ‘safe’ happy solution which only turned fingernails brown. Retail domestic film worked on dip and dunk. Kodak and others worked to move film through solution faster and with thinner gelatine emulsion. Ingredients were added to make developer and fixer more active and to harden the emulsion.

Plus premixed chems. Times reduced from 1hr to 20 mins to 90 secs. No-one questioned, no data on boxes, perfume added and flowers were printed on the boxes. 10 yrs ago in PN Hospital, chems were mixed in open tanks in the viewing room, the tank gauge lid had to be lifted to see how full the tank was, the solutions were paddled up and down to mix, mixing units gave an illusion of safety but their limited capacity meant more frequent mixing. Now staff have clear plastic hoods, tyvek gowns over uniforms, nitrile gloves and tyvek shoe protection. All processors encased. Solutions are drained before rollers removed; cleaning sinks have ventn, total air conditioning upgraded, air pollution monitoring devices sent to USA. Work situations in the States and Denmark have the latest tech but not even attempts at ventn. In 20 yrs the writer has not been contacted by any company about product safety or staff ill-health. One Australasian manager ridiculed a query. Contrast the NZ Dairy Board who withdrew condensed milk because of possible processing fault, Air NZ who grounded aircraft to check a possible fault picked up elsewhere in the world.)

Vyas A. Occupational symptoms in endoscopy nurses exposed to glutaraldehyde and latex.. North West Lung Centre, Manchester Hospital, England. MAG Mem Sem. March 1997. (Endoscopy nurses were surveyed in 59 endoscopy units. A total of 340 currently employed nurses, 310 of whom were exposed to glutaraldehyde, and 18 former endoscopy nurses took part in the study. The survey included a symptom questionnaire, skin pricks to common allergens and latex, measurements of glutaraldehyde and latex specific IgE, respiratory function tests, and personal sampling for measurements of peak and background glutaraldehyde concentrations. 31.8% of all current workers were asymptomatic. The most common symptoms in the remaining current employees were related to the nose and lower respiratory tract. For all symptoms the presence of non-work related was higher than for work related. The prevalence of work-related occular, nasal and lower respiratory tract symptoms for glutaraldehyde exposed current employees was 13.2, 20.0 and 9.0% respectively. Only nasal symptoms were statistically related to glutaraldehyde (peak) airborne concentrations. The ppFEV1 for work-related lower respiratory tract symptoms in glutaraldehyde exposed workers was statistically significantly smaller than for the corresponding non-work related group. Peak flow diaries completed by current workers having lower respiratory tract symptoms did not show more than 10% variation, and hence formed no evidence of asthma. Only one blood sample showed a positive IgE result for glutaraldehyde, 13 were positive for latex specific IgE. There were 20 positive latex skin prick tests. The mean measured glutaraldehyde concentrations, as mean (and range), were 0.037 (0-1.08) mg/m peak, and 0.011 (0-0.15) mg/m background. Twelve of the 18 former employees stated that they left because of lower respiratory tract symptoms, with a latency of 3 months or greater. Ten still complain of lower respiratory tract symptoms despite the fact that 9 are no longer in direct contact with glutaraldehyde. The findings provide no objective proof of occupational asthma in the currently working group of nurses. Specific bronchial provocation testing in ex-employees with occupational lower respiratory symptoms may provide further information. However this information may not be totally reliable due to the absence of continuing occupational exposure in most of this group).

Chemical Hazard Alert Notice - Glutaraldehyde. British Health and Safety Executive Sept 1997. (GA OES 0.2ppm (0.83mg.m), 15 min ref period. GA has been reviewed by an independent committee of experts in occ health. (The Health and Safety Commission’s Working Group on Assessment of Toxic Chemicals) "..the committee could not identify a safe level of exposure where it could be certain that there would be no risk of serious health effects...The Advisory Committee on Toxic Substances has recommended that a Maximum Exposure Limit (MEL) of 0.05ppm, expressed as an 8 hr TWA and 0.05 ppm expressed as a 15 min reference period should be set. A MEL places a duty on the employer to reduce exposure to as low as is reasonably procticable, and in any case below the MEL."

HSE Press Release: HSE issues warning to farmers and growers on use of disinfectants. Nov 1997. (Incident where employee entered mushroom growing shed while fumigation in process. HSE investigated - prosecuted - fine 4,000, costs 1,500. GA widely used on farms; linked to occ asthma, eye and throat irritation, and may cause allergic dermatitis.) 

Chamberlain Jenny. Something nasty in the boatyard. North and South. Sept 1997. (Boatbuilders at risk from: occ asthma, dermatitis, work-related deafness, solvent-induced neurotoxicity, chemical poisoning, and insecticide poisoning (from antifouling paint). A sophisticated high-tech activity based on wooden boat, backyard traditions done "sloppily by grubby males who expect everyone to clean up after them" - Dr Chris Walls, OSH. Hamish Lourie's ACETONE (ketone), two-pot ISOCYANIDE MIXES, ANTIFOUL, TREATED TIMBER, STYRENE, FIBREGLASSING , EPOXY RESINS, and AMINE HARDENER exposure - and STRESS diagnosis - OSH did nothing. Neil Williamson's post-cure epoxy resin. Robert Wallace's epoxy resin and acetone. Harmen Hielkema's foggy mist of carbon fibre, fibreglass, overspray, and antifoul. Boating Industries Assoc role - minimal. UNITEC courses cover the hazards but no control over students once in the workplace. OSH ineffectual but waking up.)

From web page
Des Jardins Andrea. Sweet poison: what your nose can't tell you about the dangers of perfume. 1997. (One fragrance can have 600 chem ingredients. At least 5,000 chems used in manuf of fragrance products (FPs). Many of the only 16% tested are regulated as hazardous materials. The FDA really knows very little of the health effects of FP. FPs can cross the blood brain barrier. Linalool, the most abundant chem in perfume, can cause lethargy, depression and life-threatening respiratory effects. Critics say people sensitive to fragrances are experiencing an anxiety attack brought on by memory of one bad fragrance. But many find different fragrances cause different effects and some cause no effects. Children more susceptible. Fragrance chems can show in breast milk.)
Kendall Julia. Making Sense of Scents. (Perfumes may produce toxic and more often allergic resp disorders (asthma) as well as neurological and cutaneous disorders. (Ann Dermatol Vernereal, 113, 31-41, 1686). In 1986 Nat Acad Science targeted insecticides, heavy metals, solvents, food additives, some air pollutants and fragrances as high priority for neurotoxic testing....95% fragrance chems (FCs) are synthetic from petroleum, incl benzene derivatives, aldehydes... t-Butyl Toluene. FCs caused testicular atrophy and myelin disease (the myelin sheath protects the nerves and does not regenerate (TOXLINE). Some FCs eg toluene, MEK, ethanol known to cause birth defects and cancer and are designated hazardous waste chems. Toluene was found in every fragrance sample collected by the EPA in 1991. Toluene causes asthma. Perfumes are now also in furniture wax, tyres, plastic garbage bags, inks, hair gel, hairspray, kitty litter.)

Kendall Julia. The health risks of twenty most common chemicals found in thirty one fragrance products by a 1991 EPA study. (From MSDS.) (Incl: Acetone, Benzaldehyde (in perfume, cologne, hairspray, laundry bleach, deod, detergent, vaseline lotion, shvaing cream, shampoo, bar soap, DW detergent. Narcotic. Sensitizer. "Local anaesthetic, CNS depressant...irritation to mouth, throat, eyes, skin, lungs, and GI tract, causing nausea and abdominal pain. May cause kidney damage. Do not use with contact lenses.") Benzyl alcohol, Camphor, Ethanol etc.)

Purdue/IAHCSMM. Glutaraldehyde Safety Action Plan 1997
(A programme demonstrating how to: 1) Monitor exposure levels. OSHA Ceiling Value Limit of 0.2 ppm must not be exceeded at any time. ACGIH has proposed reduction to 0.05 ppm CVL. One study (Notarianni GL, Glutaraldehyde overexposure: myth or reality? One hospital-wide study. J of Healthcare Materiel Management, 10, 6, 20-34, 1992) found the glutaraldemeter identified overexposures not detected by 15 min TWA method and the TWA system greatly understated ceiling value exposure levels. OSHA recommends CVL monitoring should be for the shortest time poss - GAmeter can take virtually instant samples. Monitoring badges req min sampling time of 15 mins - will tend to greatly understate CVL [OSH, NZ says GA-meters suffer from interference from other aldehdes and are not very accurate below 0.1ppm]. 2) Develop a Safety Action Programme 3) Evaluate and select PPE eg eyecare - need splash goggles with side protection; eyeshield/face masks for bloodborne pathogen protection not approp for GA; face shields should wrap round the face and extend past the chin... Gloves: disposable latex gloves not adequate - too thin and too short - need to be 11-13" long. OSHA has fined hosps $1800 for allowing latex gloves. Initrile and butyl rubber most impervious. Polye-thylene OK for several hours. Employer should request documentation on gloves. Clothing - must all be made of material impervious to GA - liquid-resistant not enough. 4) Implement programmes for disposal and clean-up... OSHA requires eye-wash units which provide 0.4 gallon/minute continuously for 15 mins, within 10 seconds or 100m of all GA usage locations... Minimise agitation of the soln. Min of 10 air changes/hr plus local exhaust fume hoods with a minimum face velocity of 80 feet/minute. Neutralise solns before disposal - pouring can cause signif vapours. Some sewage facilities prohibit disposal through the drain because of residual antimicrobial activity. GA should end up at 10 ppm or less...Spills cleaned up immed. Response team. If levels 2.0 ppm or less can wear half-face respirator. If more than 10ppm, must have SCBA unit.
Survey: May 1994, 4001 questionnaires were returned by Society of Gastroenterology Nurses and Associates (SGNA). 60% reported symptoms started since glut contact. Those with previous ENT symptoms found they seemed to worsen. (Ellet M, presented at 1994 Annual Convention). GA is by far the cheapest sterilant. 1995, Working Group of the Association for the Advancement of Medical Instrumentation finished new std for control of exposure to GA: Safe Use and Handling of GA-based Products in Health Care Facilities. (AAMI, 1996).)

1998 1998

Care Alan. Clean Sweep. Occupational Health, July 1998. (GA can irritate and sensitise. Message not getting through to those in charge. British Soc of Gastroenterologists' special report: Aldehyde disinfectants and health in endoscopy units, sets out recommendations.mirroring COSHH. One nurse had worked in hosp since 1975; exposed to chem fumes in ENT 1992-3. Classic pattern of glut poisoning - summer 94 - stuffed-up nose, watery eyes, headache. Following summer worse. HSE inspector noticed a no. of others with skin rashes and other symptoms. Nu-Cidex (hydrogen perroxide and peracetic acid) introduced - no occ exposure std for this - nurse's symptoms returned on contact with this new product. The nurse was sensitised to GA and many other substances. Had to be found other work - loss of a valuable asset and court proceedings for damages underway. HSE further Chemical hazard Alert Notice, Feb 98: "Because of info now available ...the committee could no longer identify a level which is both safe and practicably achievable and the OES was withdrawn in Jan 98.")

Clangor Tom. A Holistic Approach to Isocyanate Monitoring. ??? (Despite ever lower detection methods (50 parts per trillion) and lower worker exposures, isocyanate sensitisation and asthma remain problems (NIOSH, 1996). Recent toxicological studies have shown that the role of the skin in the development of chemical respiratory hyper-sensitivity may be the most significant route leading to immune sensitization. Reliance on air stds as a measure of workplace safety is a failed policy. As airborne exposures dropped, it was accepted that short-term high-level peak exposures were responsible though these never documented. US consumption of polyurethanes est at 4.6 billion pounds, 1996. In 1982, shown that initial inhalation exposure to toluene diisocyanate (TDI) inhibited subsequent skin reaction in guinea pigs. 1990, inhalation exposure to MDI was proposed to result in T-cell mediated suppression of IgE response thereby playing a protective role in preventing allergen sensitisation in the lung. But skin exposure elicited persistent high-titre IgE response which was boosted by further systemic exposure. Subsequent studies confirmed the inability to induce respiratory sensitisation via inhalation exposure in guinea pigs. But a single dermal exposure induced resp response in the majority of animals upon subsequent inhalation. By focusing on airborne induced asthmatic response, we have worsened immune sensitisation via dermal exposure. - may be eliminating a natural homeopathic exposure that protects. Urine anal can document the contribution of dermal exposures to total isocyanate exposure - sometimes as much as 10x the inhalation dose. Orthopaedic nurses sensitised to MDI from a new composite cast - no airborne exposure detected. Limited recognition of residual isocyanate in cured urethane especially in polyurethane foam products - eg food packages, shoe soles, foundry sandcastings. Healthcare workers reqd to wash hands frequently with harsh disinfectants damage the skin barrier. Latex allergy is a hapten type allergy that may induce pulmonary hypersensitivity similar to isocy. Latex protein absorption through the skin may sensitise the glove wearer to foreign protein.)

Perkner JJ et al. Irritant-Associated Vocal Chord Dysfunction. JOEM. 40, 2, 136-143. (VCD is a disorder of the larynx in which the vocal chords adduct (come together) inappropriately. Often assoc with psychiatric dysfunction, being female, employment in health care. Freq misdiagnosed as asthma - can occur together. 11 cases reported in which there was a temporal association between VCD onset and a single exposure to occ or envir irritants (33 controls). Irritant exposure causes new, rapid (within 24 hrs) onset of respiratory symptoms due to VCD alone. The IVCD cases showed typical findings of adduction of the anterior 2/3 of the vocal chords with a "posterior chink". IVCD is assoc with much higher rates of chronic rhinosinusitis and gastroesophageal reflux disease (GERD). Essential to consider IVCD in patients with acute respiratory complaints after irritant exposures in order to distinguish it from RADS. Direct laryngoscopy when symptoms present is the gold std diagnosis. Important to provide appropriate treatment - VCD benefits from speech therapy not corticosteroids etc.)

Anderson RC, Anderson JH. First research study proves acute toxic effects of fragrance products. Our Toxic Times 9, 4, 1-7, 1998. (From March/April Archives of Envir Health, 1998). (Fragrance products (FPs) produce a pleasant odour via effects on the olfactory apparatus (first cranial nerve), however some people report unpleasant reactions to FPs. In most mammals, another chemical sense mediated by the 5th cranial nerve, results in perception of irritancy or pungency. This sensory irritation (SI) results in local neurogenic inflammation (NI). This toxic event can be predicted by the makeup of the molecules. FPs are a complex mix of volatile organic chems so could affect the 5th cranial nerve endings and produce SI and NI. 186 groups of mice were exposed to 5 different commercial FPs. Statistically signif acute toxic effects obtained for SI, pulmonary irritation (PI), airflow limitation (AFL), and systemic neurotoxicity (NT), in many cases at the lowest dose. Repeat exposures incr the NT scores. Behavioural abnormalities were seen in posture, gait, muscle tone, tremors, abnormal repetitive movements (eg severe lip smacking, eye, ear, tail twitching, rapid circling regardless of other mice), and incr response to stimuli. Some died after exposure to high samples. Authors believed behaviour reflected toxicity in selected areas of the nervous system as some functions were unaffected eg reach, righting and grip. Some of chemical components are known toxins. Limonene, 4-hydroxy-3-methoxy benzaldehyde, linalool, terpinolene, benzene dicarboxylic acid etc were found. The results predict some humans might experience some irritation, respiratory difficulty, and CNS reactions - dizziness, incoordination, confusion, fatigue.)

Genton Monique Shedding Light on Darkroom Disease, The Canadian Journal of MRT, 29, 2, 60-65, 1998. (Excellent review of 20 yrs of literature pertaining to radiology workers. Spicer, Hay, Gordon; Rea; Fisher; Zack; Friedlander; Kipen; Ide; Norback; Bakke; Sherwood Burge; Cullinan; Calder; Waldron; Trigg; Connaughton; Gordon; Leinster et al; Kodak; Hewitt; Gannonet al; Curran et al; Scobbie et al; Smedley and Coggan. Dilemma of illness devel at air levels below limits. Theory of greater exposure from skin absorption - NH Pearce, Bristol Univ (unpublished), detected glut vapour arising from radiog's hands after handling freshly processed film. Beauchamp 1992 reported animal studies showing 3.3-13.8% of topically applied glut penetrated the skin. Approx 3% glut in cotton pellets was absorbed systemically after embedding in animal tissue for only 5 mins.
Chessor/Svirchev 1997 suggest manufs, who often do not include air-flow info from the processor exhaust , should post this on the internet. Problems of quantifying DD through resp test, skin tests not necessarily reliable. Cross-reactivity an important issue esp to other aldehydes: in diesel exhaust (which contins more aldehydes than gasoline exhaust), organic solvents, perfumes, formaldehyde in new carpets, clothes, chipboard; cig smoke, some food preservatives, particle board. Female dominated staff may influence how symptoms are perceived. The biomedical field is not exempt from gender bias: Harding/O'Barr, Sex and Scientific Inquiry (1987); Kirdup/Smith Keller, Inventing Women: Science Technology and Gender in the Making of modern Science (1993); Schiebinger L. Nature's Body: Gender in the Making of Modern Science (1993). Importance of education and prevention.)

Chandler Ginger. Absence of Proof is Not Proof of Absence. RT Image, March 30, 1998, pp6-7.
(Summary of the highlights of the 'Marj Gordon Memorial Seminar'- papers by G Care, Dr A Vyas, Prof Bill Glass, Dr Dorothy Gronwall, Professor Claudia Miller, Dr Peter Martin. Ginger's current diagnosis (resulting from the jamming of the mammography processor and her lifting the lid): "vocal chord dysfunction, upper airway dysfunction, reactive airway dysjunction, gastrointestinal reflux and chronic rhinosinusitis".)

Krakowiak A et al. Airway response to formaldehyde Inhalation in Asthmatic Subjects with Suspected Respiratory Formaldehyde Sensitization. Am J Ind Med. 33, 274-281, 1998. (Inhaled formaldehyde at a level as low as 0.5 mg/m did not induce a specific allergic response in either the upper or in the lower part of the respiratory tract. Moreover, there was no difference in nasal response to FM in asthmatic subjects occupationally exposed to FM and healthy subjects.)

ENVIROS - Photocopier, Laser printer toner dust linked to lung disease. EPA Research Project to investigate further; ?1998 Internet: (Report of Lancet, Letter, Sept 1996. Case of non-smoking 39 yr old newspaper worker with dry cough and shortness of breath - employed to retrieve computer information for 18 mnths, had a lung and lymph node biopsy which showed tissue lumps - granulomas - of silicon, iron, copper, and aluminium - all used in toner dust. With prolonged exposure, these can grow together causing lung fibrosis.

Limited published data on emissions from office equipment - copiers, computers, printers, off-gas organics from plastic casings and other construction components...these are believed to decrease over time to negligible levels. Photocopiers emit hydrocarbons, ozone, and VOCs [eg xylene, toluene, ketones] at levels which can increase over time. EPA is designing a test method for measuring indoor emissions fom office machines and testing mid-range mchines - findings to be presented in July. Rec: proper ventilation, mask filtration, enclosure of dusty areas.)

Stress May Affect Breast Cancer. Reuters - The NZ Herald, 9 Jan, 1998. (The stress of a breast cancer diagnosis and treatment can affect a woman’s immune system. Ohio State Univ questionnaire found a clear link. Chronic/traumatic stress possibly reduces ability to resist the spread of cancer. Those with highest stress had lower levels of natural killer (NK) cell lysis - less activity by cells that ferret out malignant tumour cells attach to them, poke holes and kill them. The patients’ immune cells also did not react properly in other tests.)

Gorman Des, Dryson Evan. Diagnosis of chemical poisoning: report of a working party established by the Australasian Faculty of Occupational Medicine, Royal Australasian College of Physicians, Auckland, 9 May 1997. NZMJ. 13 Feb, 1998. (Controversial nature of some poisonings eg MCS - most physicians cannot find a biologically plausible explanation for such patients’ symptoms... usually considered to be in same mysterious category as CFS. Cannot use the diagnostic approaches of pharmacology (dechallenge/ rechallenge) because:

1) Adverse effect of many toxins including carcinogenesis etc
2) H&S legislation constrains the challenge process
3) Type of information on new pharmaceuticals not available for these toxins eg comprehensive risk data exist for 0.1% of 10,000 chemicals in common use in California.
4) Actual formulation and degree and nature of contamination is often not known.
5) Few reliable environmental and biological assays exist
6) There are many confounders eg alcohol and unrelated personality and mood disorders, for problems attributed to occupational and environmental poisons especially for chronic [on-going] effects and putative [so-called] neurotoxic agents. To give the patient the benefit of the doubt for compensation purposes often results in large increases in morbidity [prevalence for that disease]. Objectivity in the absence of good toxico-

logical and biological markers is difficult therefore cumulative probability estimates are preferred. Notes are given for each category including - B1, Note 7: "Consideration should be given to cross-sensitisation after exposure to a very similar compound". If A2 is met, B2 cannot be considered. If B3 is met, C3 cannot be considered. Case study: Registered nurse, complains of short-term memory problems, loss of higher mental functions, depression and chemical intolerances. Used a lot of GA - she was ‘soaked’, plus operating theatre had very high levels of nitrous oxide. Has significant psychometric abnormalities typical of "recent" brain injury. Normal lung function, no reactivity to exercise or histamine. Normal immune.

Scoring forglutaraldehyde-induced

encephalopathy (degenerative disease of the brain): A1=0, B2=0 (exposure is past and there are no biological markers for GA). "This does not invalidate the scoring as it is not necessary to be able to assess each criterion to accumulate a probablity score". A2=0 (encephalopathy is not typical and no provocative/relieving tests). B1=5, C1=2. B3=0, C3=2 (neural damage is biologiclly plausible). TOTAL = 9.

No active treatment, should receive memory enhancement strategies. Some compensation is appropriate and she should be discouraged from further GA contact. Scoring for MCS: A1=0, A2=0, B2=0, C2=0 (alcohol/psychosocial stressors are factors), C1=2 (severe reactions to very dissimilar chemicals not present in her workplace rules out B1=0. This reaction to novel agents is not characteristic of GA nor biologically plausible B3=0, C3=0. TOTAL=2. The nurse may benefit from some counselling aimed at reducing her illness beliefs and mobilising her socially and in the workforce.)

Stellman Jeanne Mager. Chemical Hazards in Health Care. ILO, CH-1211, Geneva. Feb: 1998. (Health care institutions are heavy users of chemicals; these institutions are complex environments which must undertake inventory of identity and location of all chemicals. "Right to Know" laws seek to assure that workers be informed of the name and nature of chemicals workers exposed to on-the-job. Workers are often lower priority in "getting the best for the patient". Care in avoiding spreading and treating infection in patients (disinfectants/antibiotics etc) can be detrimental to worker. Risks from cumulative exposure even though doses low. Aerosols from chemotherapeutic drugs caused mutagenic activity in urine. Used to be common to leave steriliser door open a crack to get rid of excess ethylene oxide or accumulate freshly sterilised materials until enough to fill aerator. Glutaraldehyde. Inadequate knowledge of long-term exposures to disinfecting agents to minimise bacterial count on skin. Long-term consequences of anaesthetic gases not well-understood eg on nervous and reproductive system. Acrylic resins/cements used in surgical implants and dentistry - appear inert when cured but monomers etc are released during the reaction. These associated with chronic effects in animals. Cutting poyester resin impregnated bandages/reinforced plaster results in toxic polyurethane fumes. Laser surgery/electrocauterisation results in fumes. Asbestos in building. Plumbers - lead fumes. Food - sensitising ingredients; frying - ?carcinogenic substances, natural gas contaminants eg oxides of nitrogen. Hospital wastes. Ionising radiation from implants. High energy sources in theatre can transform anaesthetic gases to free radicals. Latex gloves. Mercury - manometers (blood pressure) and dental. Formaldehyde - autopsy/pathology. Cyanide - post-mortem fumes. Drugs: Antineoplastic agents, Chlorhexidine, Colbalt compounds, Hydralazine, Penicillin, Pentamidine, Waste Anaesthetic, Psyllium, Ribivarin.)

O’Connor Teresa. Poisoned careers. Kai Tiaki. Dec/Jan, 1998. (Pauline Hamson and Angela Newman’s TILT after exposure to GA . PH: working since 1974 at Nelson Hosp, from 1977 in theatre. Probably short-term memory loss and vomiting started from late ‘80s. Early ‘96 in theatre, got 3 full-face blasts of GA - violently sick, with "damson red eyes, tingling face and tongue, tight skin, pounding headache and nasal conjestion" - and "tipped into TILT". Jan ‘97 - violent reaction to hip operation cement - nursing career over. Accepted for ACC. Employers paid $2,500 for detox with a local doctor. New real estate career had to be abandoned because of chems in new homes. AN worked at Nelson Hosp from 1976; in theatre from 1989 - both PH and AN used to immerse hands in GA. By 1990 AN had headaches, tingling mouth, sore throat, tickly cough, gritty, burning eyes - eventually steroid drops every half hour. Explosive headaches. 1994 - worked all day in theatre, can’t remember driving home, shaking, couldn’t open the door or eat. 6 wk break but chems in envir and home affecting health. Left work July ‘97. ACC accepted. Neither can shop in supermarkets, banks, furniture stores [formald], chemists [perfumes], read magazines/newspapers (ink solvents). Exposure to perfume or diesel fumes causes PH a night of vomiting. In May other nurses refused to work and Steris system introduced. Taking legal action against Nelson/Marlborough Health Services for compensation for loss of health, career, pension. 1992 OSH recommendations especially on ventilation never carried out. CHEs underfunded - $40-100,000 peanuts compared with nurses’ suffering.)

O’Connor Teresa. Glutaraldehyde Dangers. Kai Tiaki Dec 1997 /Jan 1998. ( H &S Exec: Chemical Hazard Alert Notice - GA, recommending an MEL of 0.05ppm. Proposed Aust/NZ level of 0.1ppm disappointing - P Martin. Dr Aashish Vyas’s GA research highlights dangers. SNFTAA growing - 51 sick NZers plus overseas. Martin: ACC’s unfair-on-the-GA- affected "Test of Poisoning". ACC position: "Glutaraldehyde is an irritant which can result in occ asthma and there is no evidence to suggest that glutaraldehyde has any other effect. Some conditions such as MCS or CFS are claimed for it. But there is no evidence to suggest that any of these are linked to GA." ACC is revisiting claims to ensure claimants are still suffering the condition for which cover was granted.)

Montague Peter. A New Mechanism of Disease? Rachel’s Environmental and Health Weekly #585. Feb 12, 1998. (Summary of MCS - history/background/symptoms/controversy because it does not fit any of three currently accepted mechanisms of disease - infectious, immune system, or cancer. Often labelled psychogenic. 1987 EPA (Environmental Protection Agency) installed 27,000 sq yds carpet and remodelled. 200 developed SBS symptoms and several dozen reported later developing MCS. The National Research Council now accepts SBS. Two new populations with MCS symptoms: Gulf War vets and women with silicone breast implants. New Ashford/Miller book suggests a hypothesis (which could be tested) about the origins of the disease(s). The chem companies know how much is at stake - have labelled MCS research "junk science" and fund a new research arm - the Environmental Sensitivities Research Institute (ESRI). DowElanco, Monsanto, Procter and Gamble, the Cosmetic Toiletries and Fragrances Association, and others in pharmaceuticals, pesticides etc each pay $10,000/yr to fund ESRI. Dr Ronald Gots, head of ESRI, runs the National Medical Advisory Group which provides expert witnesses to defend the chem companies in lawsuits. Dr Gots has published no original peer-reviewed research on MCS yet specialises in saying MCS is a mental disorder. This claim has staying power because it can’t be tested scientifically and controversial topics have trouble attracting funding. ESRI advertorial: "...many established scientists and physicians doubt MCS actually does exist; it exists only because a patient believes it does and because a doctor validates that belief...for info write..."(1996).

Ashford/Miller both highly qualified, have won prestigious Macedo award. Clear, intelligent new book suggests how MCS occurs: 1) initiated by high exposure or repeated exposure 2) triggering by extremely low exposure to many different chems. Not everyone gets MCS; not everyone who gets a beesting goes into anaphylactic shock. Recent evidence suggests the nervous system (or nervous and immune systems together) somehow become sensitised. TILT a better name. Just as different infectious diseases cause fever, different initiating events may give rise to somewhat different ailments, all of which cause sensitivity to chems. To test, special environmental medical unit needs to be built, in a hospital, to expose patients under controlled conditions; NO FUNDING. Ashford/Miller do not name those who lobby to promote untested psychogenic theories, but they have contributed to widespread government inertia. Many at govt-sponsored/scientific meetings or on official boards or grant proposal panels are paid corporate spokespersons/ consultants who do not reveal their conflict of interest. "Is criminal too strong a word for those being paid by the chem corporations to stand in the way of this research?")


Folls Laurence. Health warning over 'dangerous solvent'. Terra Nova, Jan 22, 1998. (Toxic risks of glycol ethers (E series) used in water paints, inks, household products eg window-cleaners, detergents, oven cleaners; glues, pesticides, photographic developers, cosmetics "a new public health scandal". Also in steel, engineering, electronics. Derivatives of propylene glycol (P series) much safer. E series potentially produce malformation of embryo/foetus in animals during pregnancy. Teams of British, French, Italian, Dutch scientists found signif incr in risk of congenital malformation in children of mothers exposed to glycol ethers in workplace during pregnancy).

Small Businesses with Big Risks. Janus. No 26. ?1998 (By 1856 toxic effects of solvents known. Dutch Govt labour inspectors have found too little effort to reduce exposure to solvents esp in smaller businesses - danger of Organic Brain Syndrome (OBS). 515 companies in The Netherlands use 13,303,000 kg and 7,378,000 litres of solvents. Most is in petroleum and chem industry. Next are printers/labels/stickers, then painters/floor covering, then motor vehicle, then leather goods. Most used: thinners, turps/white spirit, toluene, xylene, acetone, and SBP. Poor stats kept - 30 Type 2 and 3 new cases each year. 'Solvent Teams' being set up to diagnose OBS - the EC is collecting stats. Criteria: 1] At least 5 yrs exposure or exposure to high conc over shorter periods. 2] Two or more of: forgetfulness or conc probs, and at least 2 of changes in behav, headaches, tiredness, emotional disturbance. 3] Must not be alcoholic etc. Screening questionnaire for painters with 102 questions.)



(See also 1996 Glutaraldehyde Full Public Report

1992 Beauchamp et al. Critical review of the toxicology of glutaraldehyde.

1981 ACGIH C glutaraldehyde)

Varpela, E. et al. Liberation of Alkalinised Glutaraldehyde by Respirators After Cold Sterilisation, Acta Anasth. Scand. 1971, 15, 291. (Activated aldehyde is more effective than pure glutaraldehyde. Mice exposed for 24 hours showed no lung or kidney damage but livers showed toxic hepatitis.) See also in ACGIH, 1981

Spencer P, Bischoff M, Schaumburg H. On the the specific molecular configuration of neurotoxic aliphatic hexacarbon compounds causing central peripheral distal axonopathy. Toxicology and Applied Pharmacology 1978, 44, 17-28. (Rats were fed ad lib 0.01% GA for 14 wks - rats did not develop the central peripheral distal axonopathy (neurotoxic "dying back", hindlimb weakness, giant axonal swelling and myelin changes) which rats fed on hexanedione or hexanediol did.)

Roland C, Grafstrom et al. Aldehyde induced inhibition of DNA repair. Genetic Toxicology of Environmental Chemicals 1986, 255-264. Alan R Liss. (The aldehydes acrolein (acrylaldehyde), formaldehyde and acetaldehyde cause pathological effects in cultured bronchial cells. DNA was damaged, mutated and DNA repair inhibited with formaldehyde. Acrolein worst. Formaldehyde may be cytotoxic, carcinogenic in the lung.)

Pinnas J L, Meinke G C. Hazardous Materials Toxicology, Clinical Principles of Environmental Health. 1992, 981-985. (Acetaldehyde used in wide variety of industries and occurs naturally in humans and higher plants. 50-200 ppm has resulted in eye irritation and respiratory discomfort. High blood concentration caused dyspnea (difficult breathing) and CNS damage.

Acrolein is a component of wood, cotton, polyethlene, cigarette smoke, fuel exhausts, and photochemical smog. Has caused severe pulmonary irritation, lacrimation (tears), tissue damage, elevated liver alkaline phosphatase, inhibition of protein synthesis, weight loss, enzymatic inhibition, and death. Suspected carcinogen and immunotoxicant.

Cinnamic-aldehyde common in household products and foods; reported to be skin irritant, sensitiser, and urticariogenic agent.

Glutaraldehyde is a microbiocidal, therapeutic, and tanning agent, and preservative, plus used in preparation of microcapsules and implantable collagen, and manufacture of resins and dyes. Occ asthma reported, and occ skin dermatitis and skin sensitisation.

Chloroacetaldehyde, crotonaldehyde, furfural, benzaldehyde [artificial essential oil of almond; a flavourer in medication].

Frantz S W. Glutaraldehyde: species comparisons of in-vitro skin penetration. J of Toxicology, 1993 12, 4, 349-361. (Skin from women, rats, mice, guinea pigs, rabbits compared. GA did not penetrate any of the skin specimens to a significant degree. Suggests that only minimal amounts of GA may be available for systemic uptake and distribution after skin exposure. Potential for human absorption may be less than other lab animals.

Kari F W. Technical report on toxicity studies of glutaraldehyde. National Toxicology Program (NTP), US Dept Health and Human Services, Research Triangle Park, North Carolina. 1993. (Rats and mice given GA by whole body inhalation at concentration of 0-16ppm for 6 hrs/day, 5 days/week. GA exposure associated with numerous necrotic, inflammatory, regenerative lesions confined to the respiratory tract, including squamous metaplasia, hyperplasia, and inflammation or necrosis of the larynx and/or nasal passages. The no-observed-adverse-effect level for respiratory lesions in rats was 125ppb; in mice it was as low as 62.5ppb. No significant signs of systemic toxicity. Respiratory tract appears to be the major target for GA toxicity.)

Zissu D et al. Nasal and pulmonary toxicity of glutaraldehyde in mice. Toxicology Letters. 1994, 71, 1, 53-62. (Mice exposed oronasally up to 4.5ppm for 1 hr. Decreased respiratory rate monitored up to 30 min post-exposure. GA caused rapid decrease in respiratory rate, usually in 2 min. Other mice exposed up to 2.6ppm for 6 hrs daily for up to 14 days. 1ppm -2.6ppm exposure gave respiratory difficulty with gasping, lung rales, mouth breathing. All exposures caused concentration- dependant increase in lesions in the respiratory epithelium of the septum, nasoturbinates and maxilloturbinates. Lesions consisted of areas of decilation (loss of cilia), squamous metaplaplasia, and focal exfoliation and necrosis (cell death). Variable infiltrate (seen by staining) was scattered throughout the epithelium and and connective tissues of the septum and turbinates. Lesions induced by 1ppm still there after 2 wks, but less severe after 4 wks. No lesions seen in lungs or trachea. Exposure to GA as low as 0.1ppm of the RD 50 causes upper respiratory tract damage in mice.)


NIOSH (Internet) Dec 1997. RTECS (Registry of Toxic Effects of Chemical Substances) database - Glutaraldehyde. (The RTECS record contains research data on GA as a Tumorigen, Mutagen, Reproductive Effector, Primary Irritant". Contains a summary of ?most world literature on GA toxicology including Sept/Oct 1997 EPA and NTP reports with sources. Lots of tests on mice, rats, hamsters, chickens, human cells, salmonella. Mentions severe skin/eye irritation, mutation, DNA human lymphocyte damage, DNA hamster fibroblast damage, sister chromatid exchange hamster ovary, DNA damage chicken leucocyte. Rat: testes, epididymis, sperm duct, prostate, seminal vessicle, Cowper’s gland, accessory glands, uterus, cervix, vagina, fetotoxicity. Mouse: developmental abnormalities - CNS , craniofacial, musculoskeletal, fetotoxicity. Rat/mouse: dermatitis after systemic exposure. Mouse: altered sleep time, somnolence (general depressed activity), excitement, food intake. Rat/mouse: changes in urine composition, bladder weight, weight loss, decreased weight gain, fatty liver degeneration, true cholinesterase, lungs, thorax, respiration, death in the "U" date type field. Rat: changes in liver/spleen weight, normocytic anemia.)

NIOSH: Current Intelligence Bulletin on Aldehydes.


Bowes J.H. and Cater C.W. The reaction of glutaraldehyde with proteins and other biological materials. Journal of Royal Microscopial Society, 1966, 85, 2 April. (Glutaraldehyde is used for the stabilisation of proteins especially collagens. Glutaraldehyde used for tanning to make material more resistant to enzymes. Glutaraldehyde reacts at much lower pH and binds more than formaldehyde and is more stable. Binding is with amino groups. pH is optimal for glutaraldehyde.)

Anderson Paul J. Purification and quantification of glutaraldehyde and its effect on several enzyme activities in skeletal muscle. J of Histochem and Cytochem 1967, 15, 11, 652-661. (The purest glutaraldehyde extracted the largest sample of enzyme for analysis (from rat muscle).)

Wesselink P.R, Thoden van Velsen S.K, van den Hoofff A. Tissue reaction to implantation of unfixed and glutaraldehyde- fixed heterologous tissue. Journal of Endontics: 1977, 3, 6, June. (Glutaraldehyde fixed transplanted foreign protein seems to elicit prolonged emission of immunogens.)

Gorman S.P, Scott E.M. The state of glutaraldehyde molecule in relation to its biocidal activity. J Pharm, Pharmacol. 1980, 32, 131. (Increasing alkalinity and temperature makes glutaraldehyde more biocidal.)

D. Hopwood: Some Aspects of Fixation wih Glutaraldehyde. J. Anat. 1967, 101, 1, 82-92. (In the tanning industry, GA is a powerful cross-linking substance. Glutaraldehyde rapidly denatures protein far more efficiently than formaldehyde (1965). Fixation for electron microscope slides - fixation is a form of denaturation associated with unmasking of various groups from within protein molecules. With glutaraldehyde protein denaturation, loss of enzyme activity is far greater than with formaldehyde, the loss increasing with time in the fixative.)

Kirkeby S. and Moe D: Studies on the actions of glutaraldehyde, formaldehyde, and mixtures of glutaraldehyde and formaldehyde on tissue proteins. Acta histochem. 1968, 79, 115-121. (Glutaraldehyde and formaldehyde together are much more effective fixatives)

1973 D. Hopwood. Aldehyde treatment involves artefactual tissue morphology especially on a molecular level.

Enzyme activities are depressed . GA is very good at immobilising enzymes - papers from 1951, 1964, 1970, 1973, 1980.

Aldehydes denature antigen determinants and cause antigen masking (1984)

Aldehydes crosslink with proteins (1978, 1980).

Nei Tokio. Roles of Fixatives and Cryoprotectants in cryotechniques for Electron Microscopy: Effects of Gluteraldehyde and Glycerol on structures and functions of platelets J Electron Microsc. 1981, 30, 1, 69-71. (GA caused cell shrinkage. ADP-induced aggregation of platelets was inibited even with 0.05% GA, enhanced with increase in concentration.)

E. Gendler, S. Gendler, and M. E. Nimni: Toxic reactions evoked by glutaraldehyde-fixed pericardium and cardiac valve tissue bioprosthesis. J. of Biomed. Mat. Research, 1984, 18, 727-736. (Porcine heart valves were treated with glutaraldehyde to enhance stability and remove antigenicity; washed for 24 hrs, still showed local toxic reaction at site. Residual effects still detectable 6 months later.)

Puchtler H, Meloan S.N. On the chenistry of formaldehyde fixation and its effects on immunohistochemical reactions, Histochemistry 1985, 82:201-04 (Formaldehyde can't be washed out once it fixes tissue - proteins. Formaldehyde

irreversibly alters prekeratin, myosin, collagen, laminen, fibronectin. Plus contains very good summary of the history of formalin fixation - formalin causes considerable shrinkage of muscle and connective tissue. "Extensive cross-linking impairs antigens by direct chemical effects and by structural distortions" (Sterenberger L A. 1979, Immunochemistry, 2nd ED John Willey and Sons, NY.)

Kuykendall JR, Bogdanffy MS. Efficiency of DNA-Histone crosslinking induced by saturated and unsaturated aldehydes in vitro. Mutation Research. 1992, 283, 2, 131-136. (Calf thymus DNA was incubated with aldehydes. In the saturated aldehydes, formaldehyde was the most potent cross-linker, followed by acetaldehyde [or acetic aldehyde or ethanal, pungent liquid used in manufacture of perfumes and flavours, and an intermediate in the metabolism of alcohol. Causes irritation of mucous membranes, lacrimation, photophobia, conjunctivitis, corneal injury, rhinitis, anosmia, bronchitis, pneumonia, pleurisy, headache, and unconsciousness], propionaldehyde [propionic acid is a fatty acid fermented by several bacteria found in humans, animals, silage and dairy products eg cheese] and butyraldehyde [or butanal. Uses: synthetic flavouring in foods; manufacture of rubber accelerators; synthetic resins; solvents; plasticisers. In vitro genetic toxicology - positive, sister chromatid exchanges.]

Among the unsaturated aldehydes acrolein [highly toxic liquid from the decomposition of glycerin] was most potent, then crotonaldehyde and trans-2-pentenal. The cross-linking efficiency of the difunctional aldehyde, glutaraldehyde, is probably related to its bifunctional nature. The ability of aldehydes to form DNA-protein crosslinks decreases with increasing length of the carbon chain.. The absence of saturation enhances cross-linking activity.


ASHRAE Health Facilities-Air Conditioning Applications Handbook 1982

Atmospheric Conditions in the Workplace Dept of Labour 1983

Guidance Notes for Testing Ventilation ASHRAE/Labour Dept/Health Dept 1985

McLellan DM. Hospital Hazards NZ Hospital 1986

ASHRAE Industrial Air Conditioning & Exhaust Systems ASRAE Handbook 198?

Bace Eduard. A healthy environment for radiographers and darkroom technicians. Shadows. 1991, 34, 3, 30-34..

( Proven ventilation system installed at Wellington Hospital plus costing)

Babb J Evaluation of the keymed DFE-20 Glutaraldehyde Extraction System Institute Occ.Health Birmingham 1990

Mulligan M. The Dunstan experience part II. - ventilation. Shadows, 1993, 36,3,28-29. (Use of Photosol’s CD77 glut free fixer, plus low SO fixer, plus ventn: exhaust fan installed inadequate. Argument with experts. Engineer designed cowling, venting to outside chimney. Air supply via light-tight grilles included diesel fumes and lunch! and probably recycles some of the fumes. Local glazier built perspex enclosure for the processor which has its own extraction system - $500-$600.)

Chessor E., Svirchev L. Ventilation of X-ray Film Processors British Columbia Workers Compensation Board 1997 and in Appl Occ Environ Hyg 12(8) Aug 97. (Background - M Gordon; symptoms - from Soc of Radiog survey; tell-tale routes of exposure - recurrent odour, leaking chems, deposits of crystals, aerosols. Lack of manufacturers’ specifications for direct exhaust airflow rate. Prince George Regional Hospital - calculations done for exhaust system airflow and there should have been no problem - except a 2ft section of duct was missing in the ceiling! Asthma, sinusitis and migraine headaches largely disappeared when fixed. Two other X-ray ventilation solutions, with measurements etc given. One processor was venting 350 ft/minute velocities. Almost all processors have a duct to which direct venting can be attached. - they should. None of three manufacturers’ manuals specified useful static pressure or air-flow. It’s time they did. Suggested airflow: 30’/min at a static pressure of 0.25 inches WG. Until manufacturers establish and publish these, individuals could put this info on a web site. Ideal processor exhaust system figures given.)


Design Guidelines for Environmental Conditions in Operating Theatres. Burgess O R A. Jan, 1989. WORKS NZ. (General requirements, temperature, humidiaty, air quantity and quality, air movement and pressure. Air conditioning and ventilation systems, air filters, sealing of airways, air cond system controls, air control, air extraction. System management, commissioning, operation and maintenance, management responsibilities, quality assurance. Environmental testing, testing of filters, bacteriological testing, particle measurement and counting, air cond component testing. Medical factors related to environmental testing.)

Stoke John Dr. Radiographic Processing Rooms, Wellington Hospital: an Occupational Health Opinion. 16 Jan, 1989. (Ventilation in the darkrooms should be improved in line with the "Guidance Notes for the Provision of a Safe Work Environment...")

Bertino-Clarke A. Report to HSO Australia Occ Health and Safety Committee. July, 1989. (20 page report on potential chem hazards of X-ray film processing, plus effects and case reports. Details of chemicals.)

August, 1989. Attachment. (Details for assessment of hazards, air sampling, proper ventilation, darkrm design, hygiene.)

Langley Jeff. Assessment Report, Royal Perth Hospital, W Australia. Nov, 1989. (29 recommendations to improve extremely poor handling practices, open drains, inad ventilation etc - detailed)

Gordon M.A. and Laird Ian. Guidance Notes for the Provision of a Safe Work Environment and Safe Work practice for Radiiographers and Darkroom Technicians. Accident Compensation Corpn., P. O. Box 242, Wellington, New Zealand. Second Edition, 1990. (Available in photocopy.) (Responsbility for safe working envir. Potential hazards in Xray film processing. Effects on health. Assessment of hazards. Safe work practice. Emergency procedures. Health surveillance. Appendices: Ventn, temp, humidity. Darkroom design, air sampling methods. Toxicological survey. Data sheets.)

Gluteraldehyde Survey In Hospitals - NSW Health Dept. June 1991. (Includes review of health hazards, list of chemical components of Du Pont, Kodak and Agfa Xray chemicals, and extensive photographic record of safe/unsafe GA containers and leaking developers etc)

Smith R J , Clark R T R & al. British Columbia AMRT Chemical Hazards in Film Processing. 199?

A Report on the Fumes in Radiology and the use of Glutaraldehyde at Whangarei Hospital. Bill Glass - Oct. 1992.

The Safe Occupational Use of Glutaraldehyde in the Health Industries. Health and Technical Services, OSH, Department of Labour, Wellington, New Zealand, August 1992.

Health Status of Western Australian Radiography Employees. Health Dept of WA. Jan, 1992. (177 questionnaires; 75% complained about uncomfortable chems fumes, 64% had some symptoms.)

Worker Health in the Indoor Environment of Palmerston North Hospital - Ngaire Smidt. Nov 1994.

Report of the Enquiry into the Procedures of the Accident Compensation Corporation, NZ - Judge Peter Trapski. Nov 1994.

McMahon Barry. Monitoring a Dangerous Chemical in the Hospital Environment. Spectrum - Biomed Engineering Assoc, Ireland. (Engineer’s responsibility. Monitoring - the meter which supposedly gave a GA reading did not give reproducible results and was sensitive to other aldehydes.)

Occupational Exposure Limits EH 40/95. British Health and Safety Executive. 1995

Guidelines for the Safe Use of Glutaraldehyde in Health Care Facilities. NSW Health. 28 November 1996

Issues concerning the use of glutaraldehyde as a disinfectant. Antec International [UK]. Internet. (Re disinfection in livestock housing with vastly greater exposure levels - estimates a level of 452 ppm from a 2% solution is easily possible. [10 min threshold value is 0.2ppm.] Envir hazard: minimal published data. "Taking this lack of data into account and the fact that it is bacteriostatic, a discharge to watercourse would be unacceptable". Union Carbide on Ucarsan: "..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." BIBRA Toxicity data: "...glut was of moderate to high acute oral toxicity in rats and caused lung damage in rats and mice. In a Soviet study, repeated oral doses given during pregnancy to rabbits caused foetotoxicity and an increased incidence of malformations were seen at maternally toxic doses. DNA damage, mutations and some evidence of chromosome damage were found in mammalian cells in culture following treatment with glut. 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 rats were treated orally gave a negative result". Efficacy: Temperature: Cidex is 100x less active against TB mycobacterium at 20C than at 25C. There are reports of micro-organisms, Bacillus subtilis and Mycobacterium chelonae resistance to GA noted in the literature. From Union Carbide MSDS: "Vapour is irritating to the respiratory tract, causing stinging sensations in the nose and throat, discharge from the nose, possibly bleeding from the nose, coughing, chest discomfort and tightness, difficulty with breathing, and headache." ).

Glutaraldehyde Full Public Report Worksafe Australia. 1996.

(Extremely extensive report on every aspect of the use, chemical identity, detection, kinetics, production, metabolism, experiments, toxicity, health effects, hazard classification, current practices (photos), OSH assessment, environmental effects, etc...)

Care Geof. Safety with Chemicals and Fumes. Photosol. 1997. 34 pages (1. Introduction; 2. Responsibility; 3. Hazard Identification - Chemicals, Exposure Routes, Nature of hazards; 4. Risk Assessment - Identify personnel entering , Summarise activities taking place, Identify activities creating risk; 5. Risk Control - Legal req, Exposure prevention, Engineering controls, Admin controls - (Good housekeeping , Maintenance, Inspection, Procedures, Personal Protective Equipment, Improvements required); 6. Training; 7. References. Safety Check List. Table 1: Symptoms reported among radiographers. Table 2: Dangerous Substances Associated with Rapid Processing Radiographic Chemicals, - Notes. Table 3: Sick Building Syndrome - Symptoms, Building Features, Sources of Indoor Air Contaminants.


Table 4: Heirarchy of Measures for preventing or controlling exposure.


Miller B A, Blair A. Mortality patterns among press photographers. J Occ Med 1983, 9, 349-54. ( Mortality survey among white male press photographers - statistically significant increase in pancreatic cancer.)

Liden Carola. Occupational dermatoses at a film laboratory. Contact Dermatitis. 1984, 10, 77-87 (Contact allergies)

Hodgson M J, Parkinson D K. Respiratory disease in a photographer. Am J Ind Med 9, 349-354 1986 (Sore throat, eye, nose irritation, chest tightness, headache. From SO, acetic acid.)

Kipen H., Lerman Y. Respiratory abnormalities among photographic developers: a report of three cases. Am .J .Ind.Med. 1986, 9, 341-7. (Black and white developing. Skin lesions from 1930s with allergic/nonallergic dermatitis, and lichen planus. Corneal opacities described after exposure to hydroquinone, 1958. Acetic acid and sulfur dioxide as respiratory irritants, 1982, 1983, 1983. Only one paper reporting chronic respiratory effects, 1982. The following alert to potential respiratory manifestations. No 1:URT, LRT symptoms; No 2: tiredness, runny nose, sore throat, nausea, chest pain;

No 3: headache, dizziness, nose, throat, eye irritation, shortness of breath, nausea, pruritis, chem taste in mouth, burning in chest.)

Chemical Hazards. NZ Photo Lithographers and Artists Union.

Clement J. Are photographic chemicals potential killers? Br.J.Photography 1988, 135, 12-13. (Death from aplastic anaemia - chem basis).

Making Darkrooms Safer - A National Report on Occ Health and Safety. National Press Photographers Association. 1988 (USA)

Throwing Light on Darkrooms. Worksafe Australia ?1992 (Hazards, info on the chemicals, questionnaire etc)


- a great deal more info is available.

. Chitty T.F. Sulphur Dioxide - review of its effects and tolerance. Radiography 1979, 45, 77-80. (History of, acute exposure, toxic dose, individual susceptability.)

Witek T.J.Jr., Schachter E.N., Beck G.J., Cain W.S., Colice G, Leaderer B.P. Respiratory symptoms associated with sulfur dioxide exposure. Int.Arch.Occup.Envir.Health 1985, 55, 179-183.

Schachter E.N., Witek T.J. Jr., Beck G.J., Hosein H.R., Colice G., Leaderer B.P., Cain W. Airway effects of low concentrations of sulfur dioxide: Dose-response characteristics. Arch.Envir.Health. Jan/Feb, 1984, 39, 1, 34-42.


(This is a tiny fraction of the huge amount of information on formaldehyde.)

Morris D L . Formaldehyde sensitivity and toxicity. (Letter) JAMA, 1981, 246, 4, 329. (The writer, an allergist who had noticed since 1968, sensitivity to formaldehyde in insulation products. Symptoms of dyspnea, headache, eye irritation, rhinitis, cough and rash all common and correlate well with degree of exposure and intradermal testing. With the Univ of Wisconsin, he measured 0.13ppm in clothing stores, (these rose after new clothes unpacked), 0.6ppm in fabric stores, 1.7ppm in biology wet lab. patients with strong sensitivity cannot tolerate the fabric stores. The mildly sensitive can’t tolerate the lab. All the patients with strong sensitivies that he had seen exhibied allergies to other chemicals, inhalants and food. Response: Rocky Mt Poison Centre: Toxic problem exists also from workers doing "foaming" - mostly problems disappear after a few days, but some homes continue to cause problems eg some people can’t tolerate permanent-press clothes not previously a problem.)

Main D M., Hogan T J., Health effects of low level exposure to formaldehyde. Jnl. Occ. Med. 1983, 25, 896-900

Bernstein R S, Stayner L T, Elliott L J, Kimbrough R, Falk H, Blade L. Inhalation exposure to formaldehyde: an overview of its toxicology, epidemiology, monitoring and control. Am.Ind.Hyg. Assn Jnl. Nov 1984, 45, 778-785.

Beall J.R., Ulsamer A.G. Response to "Formaldehyde and hepatotoxicity : a review". Jnl. Tox & Env.Hlth, 1984, 14, 468-470.

Burge P S, et al. Occupational asthma due to formaldehyde. Thorax 1985, 40, 255-60.

Edling C., Hellquest H., Odkvist L. Occupational exposure to formaldehyde and histopathological changes in the nasal mucosa. Brit.J. Ind. Med. 1988, 45, 761-765.

Thrasher J.D., Broughton A., Micevich P. Antibodies and immune profiles of individuals occupationally exposed to formaldehyde: six case reports. Am.J.Ind.Med. 1988, 14, 479-488.

Annabell Ross. A chemical that cripples. Wairarapa Times Age. April 10, 1989. (Clarry Jensen, 49, Napier. Laminating factory - itchy skin and blisters from the formaldehyde in the glue and released by the heat from high speed saws. 2 yrs after first syptoms, had to leave. Skin bled even at touch of clothing. 6 yrs later his skin still erupts into dermatitis if he goes into joinery factory. Liver damage may improve with time. Had had no problems as a farmer. Boss showing symptoms of blistered fingers and sore eyelids. For 7 yrs "John", 37, used formalin at sea to "poach" all the marine animals in the sample; then transferred to MAF’s photographic section. Off work a lot, always tired, night sweats, palpitations. Transferred to mussell research farm; better. Joined Hanimex operating 24 hr processing lab. All symptoms returned. Various jobs gave reactions - computing gave migraines [?solvents in computer component manuf], ill woodworking, garden centre OK. Given clean bill of health. Off ACC. Joined cleaning firm, - old symptoms; salvage department at General Motors - cough and dizzy spells. Now any minute contact with formaldehyde gives severe headache, debilitating tiredness, deep cough, tinnitus, and asthma-like breathing difficulties. "Bill" - symptoms began with introduction of particle board 1970s. Eye, skin, asthma-like symptoms. Then sores all over. Better off work. Gave up 1985. The masks used caused more irritation.)

Godish Thad. Indoor Air Quality Notes: Formaldehyde - Our Homes and Health. Dept Natural Resources, Ball State Univ. 1989, 1, 2nd Ed, Summer. (Increasing evidence that formald may be responsible for variety of irritating symptoms especially from urea-formaldehyde foam insulation. Govts adopting indoor air quality standards. Formald a potent eye, URT and skin irritant and may cause asthma. Evidence also indicates central nervous system damage includes fatigue, headaches, and depression. Potential cancer risk. Presumptive evidence for a cause/effect relationship between reported health problems and indoor home envir:- more than one family member affected; individuals most at home most affected; symptoms diminish on absence; symptoms diminish with ventilation; seasonal pattern related to beginning of heating season; symptom onset associated with time eg moving into new house, renovations, etc; symptoms reported by visitors. Presumptive evidence for cause/effect between building related illness symptoms and contamination of own home: symptoms similar to those reported by workers occupationally exposed; short-term exposure studies show symptoms at concentrations as low as 0 .10ppm; symptoms diminish at less than 35% humidity; symptoms onset occurs in other environments where elevated formaldehyde levels common eg furniture/clothing stores; presence of sources such as particle board, urea-f foam...; formaldehyde levels of 0.06ppm or higher; symptoms increase with formaldehyde concentration; symptoms most severe in new/mobile homes.

At formaldehyde levels typical of modular homes (0.35 ppm) Danish workers report eye, nose, throat, headache, abnormal tiredness, menstrual irregularities, unnatural thirst. Canadians with UFFI (urea-formald foam insul - av 0.045ppm): dose response dizziness, diarrhoea, eye, nosebleed, cough, sputum, nasal airway resistance and auquamous metaplasmia of nasal epitheliel cells. Ball State studies:- dose response relationship in mobile homes and homes with particle board average concentrations 0.09 ppm) - eye irritation, dry/sore throat, runny nose, cough, sinus irritation, headaches, unusual fatigue , depression, difficulty sleeping, rashes, bloody nose, nausea, diarrhoea, chest pain, and abdominal pain. Gynaecologists should seriously evaluate formald link with menstrual problems.

U-F resins are chemically unstable - may release free formaldehyde from unreacted formaldehyde trapped in the resin. This casuses most of the formald found in the first 6 mths. 50% decline is common. But significant continuous release can be expected from hydrolytic decomposition of the resin polymer itself - indefinitely. Cabinetry and furniture are overlooked sources especially when new, from the particleboard and fiberboard, and from the acid catalyzed wood finish. At temperatures between 65-85F an increase of 10F will approx double F levels. Increase in relative humidity from 30-70% will give 40% increase in formaldehyde levels. Similar indoor and outdoor temperatures also give higher rates of emission.)

Thrasher J D, Broughton Alan, Madison R. Immune activation and autoantibodies in humans with long-term inhalation exposure to formaldehyde. Arch.Envir. Health. July/Aug 1990 45, 40, 217-223 (1. Controls: chiropractic students exposed to HCHO 13hrs/wk for 28 wks during anatomy - 0.43ppm. 2. 19 mobile home residents. 3. 21 new office building workers. 4. 21 patients removed from original HCHO exposure for at least 1yr. 5. 8 who had exposure to HCHO at work eg mortuary, particle board, carbonless copy paper. All patients had sought treatment for CNS symptoms (headache, memory loss, difficulty completing tasks, dizziness), URT, LRT, skeletal-muscle complaints, gastroenteritis. In common: initial flu-like illness from which not fully recovered, chronic fatigue, sensitivity to low concentrations of chems. Controls had fewest positive anti-HCHO-HSA antibodies; positive titers signiicantly greater for patient groups. Controls had lowest frequency of autoantibodies; mobile homes highest. Immune activation, autoantibodies, and anti-HCHO-HSO antibodies are associated with long-term formaldehyde inhalation.)

Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th Edtion. ACGIH. 1991, pp 664-688. (Extensive review of all aspects of formaldehyde.)

Grosjean E et al. Ambient levels of formaldehyde and acetaldehyde in Atlanta, Georgia. J of the Air and Waste Management Assoc. April, 1993, p 469- (Formaldehyde and acetaldehyde are the two most abundant carbonyls in ambient air; from many mobile and stationary sources and formed in situ by oxidation of virtually all hydrocarbons plus they are substantial sources of free radicals. Formaldehyde has received attention for possible carcinogenic properties and acetald and its oxidation products for mutagenic properties. Formaldehyde and acetaldehyde are emitted by vehicles that use the oxygenated [additives containing oxygen, hydrogen, carbon in the molecular structure] fuels methanol and ethanol respectively. Ambient levels measured in Atlanta, July- Aug 1992. Av 2.7-3ppb for formaldehyde; 2.6-3.2ppb for acetaldehyde. Highest 8.3ppb and 8.4ppb respectively)

Miller Claudia S, Mitzel Howard C. Chemical Sensitivity Attributed to Pesticide Exposure Versus Remodeling. Archives of Envir Health. 1995, 50, 2, 119-129. (112 who reported onset of MCS after well-documented exposure to organophosphate or carbamate pesticide, or to remodelled building, completed questionnaire. Both groups reported similar patterns of symptoms and identified similar inhalants and ingestants as triggers which suggested a common mechanism for their conditions. Significantly greater severity for the pesticide group especially for neuromuscular, affective, airway, gastrointestinal and cardiac symptoms. Evidence for posssible biological pathway for MCS and a final common pathway for the condition. Features of this sample were inconsistent with somatoform disorder ie onset after 30 yrs of age in 83%, predominance of severe cognitive symptoms, environmental causes. 81% had been working full-time, now 12.5% full-time (av 7.7yrs post exposure). Approx 40% had consulted 10+ med practioners. Disabling neuropsychological symptoms reported by MCS groups strikingly similar to those exposed to pesticides and solvents.)

Riedel F et al. Formaldehyde (FA) exposure enhances inhalative allergic sensitization in the guinea pig. Allergy. Munksgaard. Vol 51, 2, Feb 1996. (3 groups of guinea pigs exposed over 5 days to different concentrations of FA, then to sensitising agent, ovalbumin (OA). Given bronchial provocation 3 wks later. In the group exposed to 0.25ppm, 10/12 were sensitive to OA c.f. 3/12 in control group. Serum anti-OA-antibodies were significantly higher. Short term exposure to low concentrations of formalddehyde can significantly enhance sensitisation to inhaled allergens in the guinea pig).

Barnett Antony. The deadly secret of DIY’s dream material. The Observer, UK. 21 Sept, 1997. (Medium density fibreboard (MDF) versatile wonder product of the ‘90s - users sick from it call it the asbestos of the ‘90s. MDF is compound of wood dust and scrap (80%), bonded with formaldehyde resin (13%); water (7%). When cut, sanded etc releases clouds of dust-coated formaldehyde particles much smaller than normal woods. Californian building Ind Assoc puts up stickers saying "This house contains a chemical known to cause cancer, birth defects or other reproductive hazards". 1994 USA reduced limit to 0.3ppm (7x lower than British limit of 2ppm). Director of Centre for Occ and Envir Health, Leicester: "I believe we have significantly underestimated the potential risk of MDF in Britain. There is evidence that FA exposed workers have higher rates of lung cancer and [nose and throat] cancer." Gas emissions from new MDF furniture can also cause ill-health. Wood Panel Industries Federation says claims are "based on ...unsubstantiated rumours..... tomatoes and kippers contain considerably more FA than MDF" ; cancer link questioned. Editor of Hazards: "Dusk masks won’t filter super-fine particles; vacuum cleaners won’t pick them up" Estimated world consumption by 2,000 will be 1 million cu metres.)

Blank Dennis M. A Growing Sensitivity to What’s in the Air. New York Times. Feb 22, 1998. Defining MCS objectively or agreeing that it exists is a big headache for legal and medical professions. Symptoms: dizziness, memory loss, rashes, chronic fatigue, food allergies, breathing difficulties, eye and sinus irritation, and headaches. Once afflicted, victims exposure to certain chems or products can prompt a relapse even if not previously sensitive. Many cases linked to SBS in poorly ventilated buildings where formaldehyde gas is trapped after being released from new carpeting, glues or furniture. SBS also caused by mould and mildew in air-conditioning. Ashford/Miller: indoor air pollution costs tens of billions of dollars annually. J Woods, consultant, estimates $60 billion lost from employee sickness etc. - 20-30% of US commercial buildings affected plus 10-15% undetected. OSH est $8.1 billion to get all commercial buildings complying with IAQ proposed stds. Dr Albert Robbins: "silent epidemic". Only Alaska, Connecticut, Delaware, Maryland, Massachusetts, New Mexico, NY and Ohio officially recog MCS. Dr Grace Ziem: 19 federal/ 22 state agencies recognise MCS. W est Virginia Workers’ Comp endorsed no recognition of MCS in Nov.‘97. Ohio Industrial Commission awarded J Taylor $400,000 for fumes from new carpet in an office; asthma, vomiting, chest pains - hospitalised and required to continue working. Now highly sensitive to fragrances, even the smell of foods cooking. Doesn’t remember well and depressed. Others, eg Levi Strauss set up special office - no carpet etc. New research -Univ of Cincinnati - workplace conditions cited in 15% of all asthma cases and employees exposed to more than 240 offending chems - led by latex gloves. 1996 survey of 4,000 Californians said 6.3% diagnosed with MCS; 15.9% were chemically sensitive. Equal Employment Opportunities Commission data: 386 complaints in last 4 yrs for unfair dismissal or not being provided with adequate environment. 1,542 complaints since 1992 for discrimination over asthma. H Creamer, Mass., won Social Security after being exposed to urethane fumes during office remodelling - first federal court case in which MCS accepted as a "medically determinable impairment. The Public Health and Science Office of the NIH is spending $800,000 to study possible links between MCS and Persian Gulf War Illness.)



NIOSH. Organic Solvent Neurotoxicity. Current Intelligence Bulletin #-48, March 1987. (Acute neurotoxic effects: narcosis, anesthesia, CNS depression, respiratory arrest, unconsciousness, death. Epidemiologic studies have demonstrated statistically significant chronic changes in a) peripheral nerve function (sensory and motor nerve conduction velocities and electromyographic abnormalities) that persisted for months to years following cessation of exposure b) neurobehavioural effects which 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."... "Common organic solvents are classified as aliphatic hydrocarbons, cyclic hydrocarbons, aromatic hydrocarbons, halogenated hydrocarbons, ketones, amines, alcohols, aldehydes, and ethers". Review of acute and chronic toxicity literature: neurophysiologic effects, neurobehavioural effects, metabolism, distribution and transformation in the body, excretion. Research needs.)

Montague Peter. Organic Solvents Damage Brain and Central Nervous System. Internet. Effects on CNS quoted from Am J of Psychiatry, Nov, 1988: (forgetfulness, difficulties concentrating, depressed affect [feelings], heightened irritablility, dizziness, motor inco-ordination, weakness in extremities. Objective evidence: more fatigue, tension, irritability, mood changes, diff with memory and conc. Poorer reaction time, memory, abstract reasoning, visuospatial ability, manual dexterity, perceptuomotor speed. Parosmia: sense of smell altered - and some odours become exceedingly disagreeable eg airspray, perfume. Cacosmia - heightened sensitivity to odours often with headaches, dizziness, nausea. Reports a study by C Ryan et al "Cascosmia and Neurobehavioural Dysfunction Asoc with Occ Exp to Mixtures of Organic Solvents", Am J of Psychiatry, Vol 145,1442-1445, 1988: Two matched gps blue-collar workers, solvent/non-solvent exposed, tested for hand-eye co-ord, learning and memory, attention span etc. The solvent-exposed gp performed poorly on many of the tests. The members of the solvent-exp gp experiencing nausea after contact with some odours performed most poorly. The results are consistent with a diagnosis of actual brain damage.)

1994 1994

After Simon. OS&H, January 1994. (Letter: June Freeman - Simon Freeman, 17, came home from work staggering and fell into a deep sleep...had worked on degreasing tank containing trichloroethylene...took quinine tabs and died next morning... Not old enough to buy a tube of glue. Attempts at deregulation could leave the small business workers with fewer safeguards - big businesses usually have strategies.
"Water is a solvent... but most organic solvents are anaesthetic at high concentrations. Some solvents also exaggerate the effect of naturally occurring adrenaline in the heart. They are heavier than air and hazardous accumulations can occur in confined spaces". Pregnant boot and shoemakers in the 1980s had signif no. of spontaneous abortions - glue thought to be fetotoxic. 1985 H&SE review on 10 glycol ethers - indicated impairment of male fertility and developmental toxicity in animals. 1993 revised limits for glycol ethers known to be teratogenic (damaging to unborn child). Women in semi-conductor factories had a miscarriage rate of 12-14% cf normal 10%. Why do Danish steel workers have low sperm count? The Civil Service Occ Health Service: evidence for fetal damage ... is not substantiated. Volatility (capaciy to vaporise) makes organic solvents dangerous. The EC phase out for CFCs and carbontetrachloride was 1 Jan, 1995. Businesses should ask "Do I need to clean?" 62% employers have poor awareness of COSSH Regulations.

Baker E L. A review of recent research on health effects of human occupational exposure to organic solvents. JOM. 36, 10, 1079-1092, October 1994. (Extensive review of research performed since 1985 with particular attention to issues of reversibility of neurotoxicity following cessation of exposure - the weight of evidence points strongly to the concl that exposure over many years can leave workers permanently disabled by impaired memory, concentration and mental function; the risk incr as the level of cumulative exposure increases . Health effects involving other organ systems especially reproductive, renal, and hepatic disorders discussed. Also future research, practical implications, prevention programs.)

1995 1995 Measurement and prediction of solvent neurotoxicity. ?1995. (Many organic solvents eg alcohols, ketones, ethers, alkanes also have general anaesthetic properties. Work to understand mechanism of anaesthesia/narcosis may also be relevant for toxicity studies of organic solvents, especially as such anaestheitcs are toxic at high conc. General anaesthesia can be induced by a wide variety of structurally dissimilar molecules, therefore the the mechansm must involve some rather non-specific interactions at the target site. Membrane expansion due to organic solvents and general anaesthetics is well documented. Much evidence which lends support to the general view that proteins not lipids are the major site of action of narcotics comes form the enzyme luciferase which is extremely sensitive to the action of these molecules. Concentrations of a diverse range of anaesthetic agents (eg halothane, methoxyflurane, chloroform, diethylether, aliphatic and aromatic alcohols, ketones and alkanes) which were needed to inhibit luciferase activity by 50% were essentially identical to those needed to induce anaesthesia. We may see a shift in our view of the importance of proteins as targets of organic solvents in intact cells. )

Glass Bill. Solvent Neurotoxicity. Patient Management. August, 1995, 15-21. (Widespread use in paint, lino laying, boot making, lab work, fibreglassing. Difficulties of diagnosis esp with many new organic solvents and mixtures. Neurotoxic responses to long-term solvent exposure are vigorously dabated. (1) Can long-term inhalation lead to permanent damage of the CNS? (2) Are there sufficiently reliable and objective diagnostic procedures? (3) What is the likelihood of recovery? The Clinical Response - Mild: end-of-day dizziness, nausea, headache, drunkeness, negative breathalyser. Moderate: end of week moodiness, carelessness about work quality, irritability, sleep and concentration difficulties, unpleasant smelling sweating at night in bed, solvent smell on breath esp in bed. Recovery over the weekend but over time the symptoms will persist. Patient should bring a spouse etc - often contradict "I'm fine" statements about moods. Relationships often deteriorated - girlfriends ditching, couples separating. Aggressive behaviour, verbal and physicl abuse. Severe: Focal epilepsy. MS. Motor neurone disease. Hearing. Colour vision - may be that loss reflects neural damage. Smell - benzene, formaldehyde, trichloroethylene, cyclohexanone implicated - hyposmia and anosmia [diminished and no sense of smell]. Cacosmia [usually pleasant smell perceived as unpleasant] also noted where hairspray, petrol, perfumes give headache, dizziness and nausea. Chronic fatigue. Sleep apnoea. Neuropsychiatric disorders. Peripheral neuropathy esp from n-hexane, carbon disulphide, methyl-n-butyl ketone, styrene, trichloroethylene. Chronic toxic encephalopathy - studied in the 70s in Denmark, in painters and varnishers: long-term low-level exposure; neuropsychiatric symptoms eg fatigue, memory impairment, and concentration difficulties; defects in perceptual and psychomotor functions tests; also brain atrophy, changes in regional cerebral bood flow, changes in cerebrospinal fluid proteins. Edward Baker's 1994 Review: a consistency of findings. Diagnosing Chronic Solvent Toxic Encephalopathy: 1) Careful occ history incl workplace visit, 2) Careful clinical history noting any temporal relationship between exposure and symptoms and using 1985 International Workshop Classification
(Type 1, Type 2A, 2B etc) 3) Objective easurement of CNS impairment by a clinical psychologist with solvent experience. Possible tests. 4) Other eg EEG, evoked potentials, electro-neuromyography, computed CT, MRI... 5) Exclusion of other causes. Acute exposure with long term sequel: Possible - labourer spray painted truck - still impairments 3 yrs on. Long-Term? If removed with no intellectual impairment, good. If symptoms with impaired intellectual function, effects on CNS persist. No apparent progressive disease. Case Study 1: Leather garment worker (glues). 2. Boat builder (solvent mixtures) 3. Shoe manufacturing (glue incl MEK).)

1996 1996

Macfie Rebecca. Solvent-Induced Neurotoxicity - the New Asbestos? Safeguard. Jan/Feb 1996, 29-36. (Aucklander David Duke would leave work in a state of bliss - stoned. 14 yrs screen printer, now with crippling headaches - takes 20 mins to lift head off pillow - wicked mood swings - affectionate one minute then threatening to pack his bags. Comes off phone and can't remember who he was talking to... clumsy and inco-ordinate, dropping things... Had no idea about the chems. Little or no ventilation or PPE - the rubber gloves disintegrating with chem contact.
Est 100,000 NZers regularly exposed to solvents at work. Used for thinning, dissolving and cleaning oils, fats, resins, paints. Present in paint and stripper, glues, inks, dyes, textiles, agric products, pharmaceuticals. Many highly volatile - evap readily at room temp. epidemic predicted. OSH NODS register has 222 suspected SIN. Av exposure 18 yrs. 4 have less than 10 yrs. 42 confirmed with Type 2B neurotoxicity (mood swings, fatigue AND impaired brain functioning with difficulty learning new material). Stress and malingering is a cynical conclusion. Dr Evan Dryson: "Insidious symptoms...initially disappear over weekends... but over the years become chronic..a fundamental change in personality...inability to work , participate socially eg in playing cards, music, hobby... inability also to manage relationships and function sexually. Marriage break-up appears more common. Dr Jenni Ogden: Many are prescribed anti-depressants or sleeping pills. Put together13 case studies: Men with stable work histories...10 with nausea, vomiting, diarrhoea, tingling fingers, dizziness, dermatitis. One withdrawal-type symptoms on holiday. 13 excessive fatigue, 3 debilitating anxiety, 9 depression, 3 on anti-depressants. One, Type 3 dementia. 2 uncontrollably violent towards their families. All 13 debilitating memory etc probs. One pesticide exposed forgot he'd taken apart a piece of equipment and did it again. Diaries not much help - forget where they put it. Dryson: NODS cases are the tip of the iceberg. 19/42 (see above) were spray painters in typical NZ workshops - "not excessive" levels of exposure - people are being affected at levels below the WES [Worker Exposure Std]. OSH view - to aim for absolute elimination, isolation, and minimisation. Proof for prosecution difficult - the WES would be taken as std. Dr Bill Glass: moodiness etc...intolerance to alcohol... like alcoholism "except solvents are more toxic". Often radical improvement in tempers once person retires. Printing

Packaging Media Union: management of H&S in many workplaces is "fragile". NZEPMU: Workers have a notion chems endanger their health but don't know specifics plus the macho "wuss" attitude. Motor Body Builders Assoc attributes problem largely to back-yarders. Manders Ink: a move away from toluene, methylene chloride, zylene, benzene, MEK, and glycol ether solvents to the alternative vegetable oil and citrus based products but they are more expensive and less efficient.
A-L Dalpech: Mid 1800s Paris workers exposed to carbon disulphide in rubber vulcanisation showed nervous excitement/collapse, or mood fluctuations, insomnia, memory probs, loss of sensation and impotence. Not until Scandinavian research in 1970s that neuropsych disorders highlighted.
Details of Type 1, Type 2A, 2B, Type 3 neurotoxicity. Other suggested health efects: MS, focal epilepsy, motor 8hrs/day, 5 days/wk over 40 yrs may incr risk of leukemia by c.70%. Finnish women with solvnet exposure have incr liver cancer. Hodgkins and non-Hodgkins lymphoma assoc with solvent exposure. Other solvents linked with liver and kidney damage.
Threshold limit Values (TLVs, developed by the USA ACGIH) are NZ WES. OSH says they help define limits but employers see them as 'line in the sand'. Bill Glass: "At best scientific guesses" - only account for fumes, not skin absorption or a mixture of solvents. Some TLVs influenced by vested corporate interests.

1997 1997

Chamberlain Jenny. Something nasty in the boatyard. North and South. Sept 1997. (Boatbuilders at risk from: occ asthma, dermatitis, work-related deafness, solvent-induced neurotoxicity, chemical poisoning, and insecticide poisoning (from antifouling paint). A sophisticated high-tech activity based on wooden boat, backyard traditions done "sloppily by grubby males who expect everyone to clean up after them" - Dr Chris Walls, OSH. Hamish Lourie's ACETONE (ketone), two-pot ISOCYANIDE MIXES, ANTIFOUL, TREATED TIMBER, STYRENE, FIBREGLASSING , EPOXY RESINS, and AMINE HARDENER exposure - and STRESS diagnosis - OSH did nothing. Neil Williamson's post-cure epoxy resin. Robert Wallace's epoxy resin and acetone. Harmen Hielkema's foggy mist of carbon fibre, fibreglass, overspray, and antifoul. Boating Industries Assoc role - minimal. UNITEC courses cover the hazards but no control over students once in the workplace. OSH ineffectual but waking up.)

1998 1998

Folls Laurence. Health warning over 'dangerous solvent'. Terra Nova, Jan 22, 1998. (Toxic risks of glycol ethers (E series) used in water paints, inks, household products eg window-cleaners, detergents, oven cleaners; glues, pesticides, photographic developers, cosmetics "a new public health scandal". Also in steel, engineering, electronics. Derivatives of propylene glycol (P series) much safer. E series potentially produce malformation of embryo/foetus in animals during pregnancy. Teams of British, French, Italian, Dutch scientists found signif incr in risk of congenital malformation in children of mothers exposed to glycol ethers in workplace during pregnancy).

Small Businesses with Big Risks. Janus. No 26. ?1998 (By 1856 toxic effects of solvents known. Dutch Govt labour inspectors have found too little effort to reduce exposure to solvents esp in smaller businesses - danger of Organic Brain Syndrome (OBS). 515 companies in The Netherlands use 13,303,000 kg and 7,378,000 litres of solvents. Most is in petroleum and chem industry. Next are printers/labels/stickers, then painters/floor covering, then motor vehicle, then leather goods. Most used: thinners, turps/white spirit, toluene, xylene, acetone, and SBP. Poor stats kept - 30 Type 2 and 3 new cases each year. 'Solvent Teams' being set up to diagnose OBS - the EC is collecting stats. Criteria: 1] At least 5 yrs exposure or exposure to high conc over shorter periods. 2] Two or more of: forgetfulness or conc probs, and at least 2 of changes in behav, headaches, tiredness, emotional disturbance. 3] Must not be alcoholic etc. Screening questionnaire for painters with 102 questions.)


Supplementary information may one day follow on other chemicals used or detected in X-ray processing environments including: acetic acid, diethylene/monopropylene glycol, hydroquinone, 5-nitroindazole, potassium/sodium hydroxide, potassium sodium metabisulphite, phenidone, sulphuric acid, aluminium sulphate, ammonium/sodium thiosulphate, ammonia, hydrogen sulphide, butyraldehyde, toluene, benzene. The role of theatre anaesthetic gases in conjunction with glutaraldehyde exposure needs investigation.