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GLUTARALDEHYDE IN THEATRE

AND STERILISING ENVIRONMENTS

(1)   COMPONENTS OF  GLUTARALDEHYDE-BASED  STERILISING  SOLUTIONS

Scobbie and Groves

[1] found monomeric glutaraldehyde  (ie the basic molecule) as the main component of the vapour above all the brands of activated sterilising solutions and suggested concentrations of up to 2 ppm can be formed.  Also found in significant amounts were methanol  (SEE   UNDER  FORMALDEHYDE  p 11)   and butyraldehyde  (SEE X-RAY SECTION  p 8).  GA is supplied to biocide manufacturers with a small amount of methanol added to prevent polymerisation.  Other possible impurities were acrolein, glutaric acid, glutaraldoxime, and polymers of glutaraldehyde.

                Analysis of commercial brands of GA at 20ºC indicated methanol as the main constituent of the vapour in the first 10 minutes but GA becomes the main component after this. Cidex Long-Life, Asep and Asep Extra-Life showed no significant difference between the vapour phase of the activated and unactivated forms.

                CIDEX:  But when the activator was added to Cidex, the proportion of butyraldehyde and GA significantly increased from 0.7ppm to 2ppm.  Increasing the temperature from 15ºC to 35ºC increased the methanol given off Cidex, and increased ten-fold the amount of butyraldehyde given off.  

 OCCUPATIONAL SYMPTOMS IN ENDOSCOPY NURSES

EXPOSED TO GLUTARALDEHYDE AND LATEX 

NZIMRT  -  MARJ GORDON MEMORIAL SEMINAR,  15 March, 1997,  Palmerston North,  NZ:

Dr Aashish Vyas,   Research Fellow,   North West Lung Centre,  Manchester, England:

Seminar presentation 15 March, 1997.

The first half of a rigorous GA study  begun by  Dr Aashish Vyas, and funded by the European Union and Union Carbide, has been completed and presented to the EU and to the ACGIH. The study attempted to find out if there was a no-effect level for glutaraldehyde.  358 endoscopy nurses in 59 units were studied  with: a questionnaire  (occular, nasal, and LRT symptoms: cough, wheeze, shortness of breath, tight chestiness, phlegm produced); skin pricks to allergens and latex,  respiratory function tests with 2 hourly diaries for 4 weeks; and  peak and background levels of GA were sampled using the more selective and sensitive DNPH method (with analysis by high-performance liquid chromatography - HPLC) rather than the usual static head-height levels.

                Only nurses whose symptoms worsened during the week and improved at the weekends were included (so those who only improved on holiday were not).  340 nurses were still employed and 310  (91%) had exposure to GA.  Almost  70%  of the still-employed group had respiratory tract symptoms (whether work or non-work-related).   Non-work-related symptoms were greater.  Nasal and lower respiratory tract symptoms were most common.  Of  the  310  GA exposed workers,  20% had work-related nasal symptoms,  13.2% work-related occular symptoms,  and 9% work-related lower respiratory symptoms.   ppFEVI's for  the GA-exposed were significantly smaller than for the group who had had no GA exposure.  Peak flow diaries of those with lower respiratory tract symptoms did not show more than 10% variation therefore formed no evidence of asthma.  Only one worker's blood sample was positive for GA IgE antibodies. There was really no correlation between symptoms and immunological profiles but GA is a low molecular weight compound and should not have its main effect by an IgE mediated pathway.  13 had positive latex skin prick tests.  (Latex presents sensitisation risks from the latex itself and from the usually-cornstarch powder lubricant). 

                18/26 of the ex-employee group were tracked to avoid the problem of dealing with a survivor population.  12/18  had left because of work-related  LRT symptoms and were still getting symptoms 3 months later.  10 continued to suffer work-related symptoms even though employed in other parts of the hospital.  9/12 of this group had  taken at least 6 months to develop symptoms and many worked for some years before developing symptoms.  This was a similar pattern to the current employees and suggested an immunological reaction was taking place, but again there was almost no correlation between symptoms and immunological profiles.  An immunological basis for GA induced effects could still be present. 

                The mean measured peak GA concentration  was 0.037 mg/m³ (highest 1.08mg/m³).  The mean background concentration was 0.011 mg/m³ (highest 0.15 mg/m³).  [The  OES was 0.7 mg.m³].  ie most didn't exceed quarter of the limit.  Studies done prior to the 1990s often over- or under-estimate GA levels. 

Found 3 spillage sites; one with  0.4  mg/m³ reading - a high degree of unawareness of spillage dangers.  66.5% of units use fully automated units.  33.5% use partially automated units.  87% have decontaminating unit ventilation.  67%  have room ventilation.  They found a significant association between room ventilation combined with decontaminating unit ventilation, and decreased level of GA exposure.  Both ventilations are important.  Only nasal symptoms were related to the concentration of GA in the air.

 They could not find a level of glutaraldehyde below which symptoms were not encountered.  This may be because there are "other symptom-causing chemicals and irritants in the environment" or individuals may have been exposed to spillages and "sensitised by the high exposure to glutaraldehyde [with] on-going symptoms occur[ing] at very low levels and chronic exposure."  The ex-employees continue to suffer symptoms despite having been taken out of the environment.  They are still in nursing and may have indirect exposure to levels of glutaraldehyde which are quite low and thus their symptoms are recurring, or they may have exposure to other irritants or allergens causing their problems.

                Other chemicals could include: latex gloves causing hypersensitivity in 4%  (and latex, another major allergen may be involved in cross-reactivity with GA as well as formaldehyde.  Sherwood Burge in 1980 postulated this might be the case because GA is a very good cross-linking agent and may cause symptoms which may be augmented by formaldehyde or latex); formalin; and ventilation systems not well-maintained which are extremely prone to Sick Building Syndrome (from formaldehyde and VOCs - volatile organic compounds), especially in new units.

                Current employees and others presented to the British Heart/Lung Foundation in London  presented with work-related LRT symptoms - cough or chest tightness.  Peak flow diaries and methacholine challenges did not find occupational asthma.  They have normal spirometry unless they come across GA in the community eg in perfumes.  The cough may be related to C-Fibres in the lungs.  Challenges with capsaicin  (the irritative agent in capsicum) induce cough very similar to GA. The cough occurs after 5 hrs  then continues for  24 hrs.

                In the ex-employees, 66% had used open baths to clean scopes, and  67% had no ventilation at all, so current nurses would be expected to have fewer symptoms; not so.  Perhaps there is increased reporting because of greater awareness.  It is felt  that glutaraldehyde is a relatively poor respiratory sensitiser probably to high concentrations only, or that aerosol production may cause sensitisation.  Personal protection during high exposure procedures is a must.  Nurses now use nitrile gloves or low allergen latex gloves, and organic vapour masks.  Formalin is made up in pharmacy.  Flexible Friends are groups of proactive endoscopy nurses and radiographers working to thrust through changes.  The level of absenteeism has fallen dramatically.

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