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We read with interest the paper on glutaraldehyde and symptoms in endoscopy nursing staff.1 It is reported that there was an absence of objective evidence of the physiological changes associated with asthma. Peak expiratory flow (PEF) records from 17 cases were analysed by the OASYS-2 computer program, and three of these had OASYS-2 scores less than 2.5. These cases were thought not to show asthma because PEF diurnal variability was less than 15%. We have recently shown that increased diurnal variability is not found in most workers with occupational asthma.2 Part of the explanation may be that the acrophase (time of maximum PEF in a 24 hour period) in normal and asthmatic people occurs at around 1600 with a trough about 12 hours later. Any deterioration in lung function due to exposure in the workplace is superimposed on the normal circadian rhythm. Thus, if a worker starting work in the morning has a fall in PEF that continued throughout the day while at work, the maximum PEF occurring at the time of the acrophase might be reduced. This would tend to reduce the diurnal variability. Even in non-occupational asthma there is considerable overlap of PEF variability with that occurring in normal people.3 Use of non-linear PEF meters significantly underestimates variability in PEF4 but even when PEF readings are linearised, an absence of an increase in diurnal variability does not exclude asthma. An OASYS-2 score greater than 2.5 has a specificity of 94% for diagnosing occupational asthma.5 We suspect that, provided peak flow records were of adequate quality, the three cases with OASYS-2 scores greater than 2.5 did indeed have occupational asthma.
Since 1995, 29 cases of occupational asthma due to glutaraldehyde have been reported to SHIELD, the West Midlands reporting scheme for occupational asthma. A study of 24 workers referred to the Occupational Lung Disease Clinic in Birmingham with respiratory symptoms temporally related to glutaraldehyde exposure found that 16 had a definite occupational effect evident on their PEF records.6 Five of eight workers with equivocal PEF records underwent specific bronchial provocation tests to 2% glutaraldehyde, all of which were positive as were three challenge tests in workers with suggestive PEF records. The challenge subjects included two in whom PEF diurnal variability was less than 10%. Of the subjects, seven out of 24 also had positive specific IgE to glutaraldehyde.
The sensitivity of serial PEF records in showing occupational asthma drops dramatically if less than three to four weeks of recordings are performed or if they are of inadequate quality—for example, less than four readings a day. We have found that objective evidence of asthma induced by glutaraldehyde can be obtained in a large proportion of workers with respiratory tractsymptoms temporally related to exposure to glutaraldehyde when adequately sought after.
Vyas et al reply
Anees et al raise a very important issue in terms of the physiological criteria on which a diagnosis of occupational asthma should be based and in particular the clinical significance of small work related declines in peak expiratory flow. We fully accept that a lack of an increase in diurnal variation does not exclude a diagnosis of occupational asthma. The pattern of peak flow measurements in occupational asthma quite often shows a marked difference in the mean peak flow on working days compared with days away from work without any increase in diurnal variation. Burgeet al refer to the phenomenon of small work related changes in their publication1-1 and raise the question as to whether this represents asthma or other lung pathology. Their opinion at that time was that it was unclear what was the importance of these small changes. The example that they give in their article showed, taking the lowest peak flow recording during the working week and the highest on days away from work, a variation in peak flow in excess of 20% which we would accept as compatible with asthma and from the pattern illustrated probable occupational asthma. The small group of workers that we studied had diurnal variations in peak flow ranging between 5.7% and 9.8% and taking the worst working day peak flow and the best day off work peak flows, a variation between 11% and 13.5% (our peak flow recordings were linearised). This degree of variation does not satisfy the British Thoracic Society criteria for a diagnosis of bronchial asthma, neither do they satisfy a positive challenge response in bronchial challenge study. We have seen similar patterns of peak flow recordings in textile workers exposed to dust, both with and without notable contamination with endotoxin. We took the view that the small peak flow changes were due to an irritant effect and postulate the same mechanism in this group exposed to glutaraldehyde. The clinical histories provided by these workers does not suggest increasing respiratory symptoms with continued exposure. Although it is possible that the changes that we have reported may represent a very mild form of occupational asthma, the clinical picture and the small physiological variation in peak flow, in our opinion is more consistent with an irritant airway response than the development of occupational asthma. Our paper is not intended to suggest that glutaraldehyde is not capable of inducing occupational asthma, for which there is convincing published evidence, in addition to our own personal experience. Our paper reports the findings of an epidemiological survey of a large population of currently exposed endoscopy nurses and has shown that while respiratory symptoms occur in this group, the lung physiology and the immunology have not supported a suggestion of a high prevalence of occupational asthma at current exposure levels.
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