Embed Size (px)
Citation preview
AMERICAN JOURNAL OF INDUSTRIAL MEDICINE 43:196–203 (2003)
Symptoms and Lung Function in Health CarePersonnel Exposed to Glutaraldehyde
Andrew Waters, MPH,1 Jeremy Beach, MD,1,2 and Michael Abramson, PhD1�
Background Glutaraldehyde is widely used as a disinfectant for endoscopic equipment.The aim of this study was to investigate work practices and glutaraldehyde exposure inrelation to symptoms and lung function.Methods A questionnaire was administered to 76 nurses. Exposed nurses (n¼ 38) alsocompleted lung function tests and visual analogue scales before and after a work session inwhich glutaraldehyde exposure occurred. Disinfection activities were timed and counted,personal exposures established, and control measures documented.Results Exposure values above the exposure limit (0.10 ppm) were found for all exposurecontrol methods except for the enclosed washing machine. Skin symptoms were 3.6 timesmore likely to be reported by exposed workers. None of the other symptoms weresignificantly associated with glutaraldehyde exposure. There were significant cross-shiftreductions in FVC and FEV1 in the exposed group. No evidence of a dose–responserelationship for symptoms or lung function was found.Conclusions Further exposure controls for both glutaraldehyde and gloves are requiredto improve skin care in glutaraldehyde exposed nurses. Exposure monitoring methods alsoneed review. Am. J. Ind. Med. 43:196–203, 2003. � 2003 Wiley-Liss, Inc.
KEY WORDS: glutaraldehyde; exposure assessment; nurses; lung function;symptoms
INTRODUCTION
Glutaraldehyde (1, 5 pentanedial) has a number of uses,
mostly relating to its biocidal action. These have been
detailed elsewhere [Haley, 1981; Beauchamp et al., 1992]. It
has been estimated that in Australia, 75% of glutaraldehyde is
used in the health industry, of which 73% is used as a cold
disinfectant mainly for flexible endoscopic equipment. Most
of the remainder is used in X-ray film processing. Many
nurses are regularly exposed, as are some technicians and
other skilled professional workers. Exposure may result from
direct accidental contact with the aqueous solution arising
from splashes or droplet formation or from atmospheric
vapor released during disinfection activity.
Glutaraldehyde is a recognized irritant to skin, respira-
tory tract, and eyes, and a skin sensitizer [Haley, 1981].
Glutaraldehyde exposure is also associated with symptoms
such as irritation of the eyes, nose, and throat and headache
[Axon et al., 1981; Jachuck et al., 1984; Corrado et al., 1986;
Norback, 1988; Bullard, 1991; Macnab, 1991; Adam and
Leicester, 1992; Calder et al., 1992; Mwaniki and Guthua,
1992; Waldron, 1992; Leinster et al., 1993; Ellett et al., 1995;
Gannon et al., 1995; Pisaniello et al., 1997].
In Australia the occupational exposure standard for
glutaraldehyde, expressed as a permissible exposure limit—
ceiling value, was reduced from 0.20 to 0.10 ppm in
December 1995 [WorkSafe Australia, 1995]. This compares
with a TLV—ceiling of 0.05 ppm in the USA [American
� 2003Wiley-Liss, Inc.
1Department of Epidemiology and Preventive Medicine, Monash University, Melbourne,Australia
2Institute of Occupational Health, University of Birmingham, United KingdomContract grant sponsor: The Alfred ResearchTrusts; Contract grant number: A-S-Z9733.*Correspondence to: Prof. Michael Abramson, Department of Epidemiology & Preventive
Medicine, Central & Eastern Clinical School,The Alfred, Prahran,Victoria 3181, Australia.E-mail: [email protected]
Accepted 30 September 2002DOI10.1002/ajim.10172. Published online inWiley InterScience
(www.interscience.wiley.com)
Conference of Government Industrial Hygienists, 1998] and
the United Kingdom (short term exposure limit).
Two previous studies [Norback, 1988; Pisaniello et al.,
1997] found a significant association between skin symptoms
and regular use of glutaraldehyde. Evolving work practices
and growing glutaraldehyde use, emerging alternatives [Babb
and Bradley, 1995] and continuing anecdotal reports of
health concerns among users suggested the need for a well
controlled study assessing subjective and objective outcomes
in conjunction with exposure assessments and an evaluation
of work environments and practices.
METHODS
Subject Recruitment
Thirty-eight exposed nurses were recruited from nine
work areas (endoscopy units and operating theaters) in five
health care facilities. The exposed subjects were recruited
when they performed the disinfection role whilst that session
of cold disinfection was monitored. Glutaraldehyde exposure
levels for each exposure event were established for each
exposed subject for the duration of the exposure session (or
patient list) and clinical data collected (see below). Disin-
fection practices could be related to exposure readings and
individual use of protective equipment observed. Essentially,
all regularly exposed nurses in the facilities participating in
the study were recruited.
Random selection on the basis on the job classification of
exposed subjects was used to recruit unexposed subjects.
Unexposed subjects were recruited from two of the part-
icipating health care facilities and only from areas in which
glutaraldehyde was not used. In order to make valid com-
parisons, they were eligible for inclusion if they did not
currently work with and had not worked with glutaral-
dehyde in the previous 12 months. There was no attempt to
control for other potential workplace irritants, however,
glove wearing behavior and associated latex exposure was
investigated. All data collection took place between early
1995 and mid-1998.
Data Collection
All 76 participants completed a symptom questionnaire
(SQ). It collected general health, smoking, medication, glove
wearing, and demographic data. It also collected data on
nine symptoms commonly associated with glutaraldehyde
exposure using a twelve-month recall period. The respiratory
questions were based on the European Community Respira-
tory Health Survey Questionnaire [Burney et al., 1994]. The
symptoms investigated were sneezing, itching, running nose;
burning nasal passages; running itching burning eyes;
headache; burning or irritated throat; cough; wheeze; chest
tightness; and skin problems. Skin problems were defined
as ‘an itchy rash which was coming and going for six months’.
Bodily location of these symptoms was also recorded and
for later analysis categorized as local (hand and forearm) or
remote (distant from hand and forearm) symptoms.
Pulmonary function for exposed subjects was mea-
sured using a dry bellows spirometer (Vitalograph Ltd,
Buckingham, England) in accordance with the minimum
guidelines for spirometry [Pierce and Johns, 1995]. The
measurements were forced vital capacity (FVC) and forced
expiratory volume in one second (FEV1). The ECCS
prediction equations [European Community for Coal and
Steel, 1983] were used.
Exposed subjects also completed a questionnaire of
10-cm visual analogue scales (VASQ) for eight commonly
reported symptoms. This was completed before and after
work in which glutaraldehyde exposure occurred. The
symptoms investigated by this questionnaire were headache,
unpleasant taste, irritation of the nose, eyes, and throat,
cough, wheeze, and breathlessness.
The VASQ was completed prior to the pulmonary
function tests (PFTs) because of the potential for the VASQ
results to be affected by the maximal exhalation for the
pulmonary function tests. Post-exposure visual analogue
scales were completed without reference to the pre-exposure
results. The initial VASQ and PFTs were completed prior to
any workplace exposure to glutaraldehyde on the day of
testing. The final VASQ and PFTs were performed at the end
of disinfection activities for that shift.
Glutaraldehyde exposure for exposed subjects was
determined by a direct reading ‘Glutaraldemeter’ (Lion
Laboratories, South Glamorgan, Wales, UK). Its calibration
was checked prior to each session. Calibration and use were
in accordance with the operating instructions [Anon, 1991].
Data collection included an evaluation of atmospheric ex-
posure during the three main phases of disinfection desig-
nated ‘initial disinfection and immersion,’ ‘removal and
rinsing,’ and ‘drying.’ Air samples were collected from the
breathing zone of exposed subjects. Sampling was repeated
during each phase of disinfection with respect to the exposed
subjects’ work factors.
Control measures such as engineering controls and
personal protective equipment available and used by each
exposed subject were recorded. Engineering controls includ-
ed specific workplace modifications used to control atmo-
spheric release and staff exposures. Methods are summarized
in the legend to Figure 1.
Ethics approval was obtained from two major metropo-
litan health care facilities in Melbourne, Australia. Signed
informed consent was obtained from all participants.
Data was managed and analyzed using SPSS software
(version 6.4.1S). Odds ratios by the exact method were
calculated using Epi-Info (version 6.04b). For all statistical
analysis, P< 0.05 was accepted as the critical level of
significance.
Symptoms, Lung Function, and Glutaraldehyde 197
Power
The study had>80% power of detecting a real difference
between groups for a difference in proportion of symptom
reporting of 22% or greater (assuming a 2-tailed test,
P< 0.05). Given Norback’s [1988] findings, differences in
proportions of greater than 20% for skin problems were
expected. At P< 0.05, this study had a greater than 80%
probability of detecting a 10% change in FEV1. This assumed
a mean FEV1 of 3.34 L (based on, a priori, a female worker
aged 31 and 170 cm tall) taken from the predicted values for
lung function [European Community for Coal and Steel,
1983; Cotes, 1993].
RESULTS
There was a significant difference in response rates
between groups (Fisher’s exact test, P¼ 0.03). None of the
exposed workers declined to participate, whereas six of
the unexposed workers did. The unexposed subjects who
declined to participate came from all classifications exclud-
ing that of nurse manager. A further control was recruited
in this event. Spirometry was missed for one subject, VASQ
for another, and exposure data was missing for a further
two subjects.
There were no significant differences between the ex-
posed and unexposed samples in gender, smoking, age, ‘days
worked per fortnight,’ or ‘time in current position’ (Table I).
Similarly there were no significant differences between the
exposed and unexposed groups, in doctor-diagnosed asthma,
eczema, migraine headache, or hay fever.
Exposure Data
The duration of each designated exposure event ranged
between 5 and 735 seconds (12.25 min). The mean duration
for each of these activities was 57, 142, and 90 s respectively.
Session duration ranged between 95 and 385 min.
All exposed subjects used 2% glutaraldehyde solution
for disinfection. Exposure levels up to 0.15 ppm were de-
tected. Levels above the occupational exposure standard
were detected for all methods of exposure control except
where a washing machine was used, where a peak reading
of 0.08 ppm was obtained (Fig. 1). However, exposure
was only assessed for one subject using a washing machine
and on this occasion, other staff performed concurrent
manual disinfection in the area.
FIGURE1. Plot ofpeakobservedexposure accordingtoprimaryexposure controlmeasure.Legend:DVC,dedicatedvaporcontrol (fume
cupboard); SCAV, splash control with augmented ventilation; EV, dependent on existing ventilation (e.g., operating theaters); STE, sink-top
extraction only (additional personal protective equipment (glasses) used); DWM,dedicatedwashingmachine disinfection.Note:N¼36, two
missingsubjects.
198 Waters et al.
Pulmonary Function
Statistically significant reductions in cross-shift FEV1
and FVC were identified in the exposed group. The mean
reductions were 30 and 50 ml, respectively. There were too
few exposed subjects with asthma diagnosed by a doctor
to analyze their lung function separately. An attempt
was made to identify a dose–response relationship, but
analysis suggested that higher exposure readings were
actually associated with smaller changes in FEV1 (Fig. 2).
An analysis of the duration of exposure session and change
in FEV1 also failed to show evidence of a direct dose–
response relationship (data not shown). Linear regression
modelling indicated that peak exposure was the only signi-
ficant independent predictor, which accounted for 10.3% of
the variance in FEV1. Other variables fitted to the model
included the sum of exposure events, time in current position,
unit in which exposed subject worked, and duration of
exposure session.
Symptoms
The main finding was a significant association of skin
symptoms with glutaraldehyde exposure (OR: 3.59, 95%
CI: 1.15–11.92) (Table II). Logistic regression indicated that
glove wearing was also associated with skin symptoms. No
other symptoms showed a significant association with
glutaraldehyde exposure. Increased exposure to gloves was
both in terms of ‘number of times per shift gloves were worn’
(exposed x¼ 20.7; unexposed x¼ 12.97, P¼ 0.002) and for
‘time per shift spent wearing gloves’ (exposed x¼ 222.1 min;
unexposed x¼ 90.8 min, P< 0.001). All exposed and 36 un-
exposed subjects wore latex gloves. There was, however, a
greater tendency among exposed subjects to wear double
gloves of mixed combinations of gloves, including cotton
gloves under latex gloves and nitrile gloves over latex gloves.
Vinyl gloves were worn by both groups.
Logistic regression indicated that both exposure to
glutaraldehyde (OR: 4.78, 95% CI: 1.3–17.53) and wearing
gloves (OR: 5.70, 95% CI: 1.004–32.26) were independently
associated with skin problems. However, none of the specific
measures of exposure to glutaraldehyde including ‘duration
of exposure,’ ‘number of exposure events,’ and ‘peak observ-
ed exposure’ were associated with skin symptoms.
Subjects who reported skin symptoms were asked to
list the affected areas. These were categorized into local
effects (hand and forearm), and remote effects (skin pro-
blems other than hands and forearms). No significant
association with glutaraldehyde was found for remote skin
symptoms (OR: 1.99, 95% CI: 0.52–8.39, n¼ 75). However,
with an odds ratio of 3.86 (95% CI: 1.23–12.83, n¼ 75),
local symptoms were significantly associated with glutar-
aldehyde exposure (and increased exposure to latex and
glove powder).
Both the exposed and unexposed groups reported a
high prevalence of nose and eye irritation, and headache
TABLE I. Comparison of Exposed and Unexposed Subjects, Statistical Test, and Significance
Demographic data
Sample: Exposed (n¼ 38) Not exposed (n¼ 38) Total (% total)
Gender Fisher’s exact test: two tail P¼ 0.5Male 3 2 5 (6.6)Female 35 36 71 (93.4)
Smoking status Chi-square, df¼ 2,P¼ 0.96Never smoked 24 25 49 (64.5)Former smoker 5 5 10 (13.2)Current smoker 9 8 17 (22.4)
Age of subject Independent samples t¼ 0.61, df¼ 74,P¼ 0.55Mean age 36.7 35.4SD 9.6 10.1
Time in current position (months) Mann^Whitney U¼ 545,P¼ 0.066Mean (median) 35.2 (18.5) months 49 (33)monthsSD 45.5 48.5
Daysworkedper fortnight Mann^Whitney U¼ 718,P¼ 0.96Mean (median) 8.7 (9.5) 8.7 (10)SD 1.7 1.8
A Chi-square analysis of the job title (which formed the basis of matching) of subjects according to exposure status wasalso performed.This was not significant (Chi-squared¼ 0.47, df¼ 3, P¼ 0.93).
Symptoms, Lung Function, and Glutaraldehyde 199
(Table II). Despite the fact that exposed workers in this
study often attributed these symptoms to glutaraldehyde
exposure, there were no statistically significant differences
between groups.
Visual Analogue Scales
Although the mean symptom intensity tended to increase
slightly in most cases, there were no significant cross shift
changes in symptom intensity (Table III). No evidence of a
dose–response relationship was found in relation to any
exposure variable.
DISCUSSION
This study found glutaraldehyde exposure levels up to
0.15 ppm, well above the current Australian occupational
exposure standard of 0.10 ppm. Statistically significant
reductions in FVC and FEV1 were also identified, however,
the mean absolute changes (50 and 30 ml, respectively) were
FIGURE 2. Percent change (reduction) in FEV1 versus the peak exposure event recorded (n¼ 36, two missing subjects. Duplicate
peakexposuresexist).
TABLE II. Comparison Between Exposure Groups of Symptom Prevalence and Odds Ratios for Symptoms Duringthe PreviousTwelveMonths (n¼ 76)
Symptom
Symptomprevalence and odds ratios for symptoms
Symptomprevalence Odds ratios
Unexposed (%) Exposed (%) OR (95%CI) Significance
Skin symptoms 18.4 44.7 3.59 (1.15^11.92) P< 0.05Nasal irritation 76.3 71.1 0.76 (0.24^2.39) NSNasal burning 18.4 31.6 2.04 (0.63^7.05) NSEye irritation 47.4 57.9 1.53 (0.56^4.17) NSHeadache 71.1 86.8 2.69 (0.74^11.00) NSThroat irritation 28.9 31.6 1.13 (0.38^3.39) NSCough 18.4 18.4 1.00 (0.26^3.79) NSWheeze (n¼ 75) 23.7 18.9 0.75 (0.21^2.63) NSChest tightness 15.8 23.7 1.66 (0.46^6.36) NS
200 Waters et al.
quite small. A modest negative correlation coefficient found
for peak exposure and sum of exposure events in association
with FEV1 was an unexpected finding (Table IV, Fig. 2).
Based on anecdotal reports, symptoms measured on the
VASQ would have been anticipated to worsen in association
with exposure. This was not well supported by our results.
Exposed nurses reported skin symptoms significantly more
often. This was confounded by a significant difference in
glove use patterns, as gloves have recognized irritant and
allergic potential. It was beyond the scope of this study to
further investigate skin symptoms.
This research used the Lion Glutaraldemeter for ex-
posure monitoring. It performed reliably during the study.
However for two subjects, no exposure data was collected
due to atmospheric contamination by other compounds to
which the instrument was sensitive. On some 3–5 further
occasions, monitoring was ceased for short periods when
alcohol based compounds were used during endoscopy
procedures. Generally, the exposure values obtained here
appear consistent with other Australian research which used
accepted monitoring methods [Tkaczuk et al., 1993; Naidu
et al., 1995; Pisaniello et al., 1997].
The higher readings, and in particular many of those
above the occupational exposure standard (Fig. 1) could
generally be explained by procedural deficiencies related to
glutaraldehyde use. These included inadvertent glutaralde-
hyde spills detected by monitoring, glutaraldehyde use, or
release outside the capture zone of exposure control equip-
ment and poor practices in areas reliant on existing venti-
lation for exposure minimization. Observed examples of
poor practices included: leaving containers uncovered when
not in use; accumulation of and inappropriate storage, or
disposal of glutaraldehyde contaminated linen and/or paper
towels during the course of the session; ‘excessive’ release of
glutaraldehyde vapor and droplets during vigorous decanting
and disposal; and excessive movement of glutaraldehyde
soaked equipment, waste or linen outside areas of specific air
capture/extraction vents.
Several issues regarding evaluation of atmospheric
glutaraldehyde exposure require exploration. There are two
monitoring methods accepted as being suitable in terms of
specificity, sensitivity, and precision for evaluating glutar-
aldehyde exposure. These are the ‘‘OSHA method 64’’ and
the ‘‘NIOSH method 2532.’’ For each of these methods, a
15 min minimum sampling period is generally used [Wellons
et al., 1998]. Longer sampling times are common and the
exposure values calculated accordingly.
In practical terms, these methods present two signifi-
cant limitations in determination of personal exposure to
glutaraldehyde.
Glutaraldehyde is a recognized irritant. Peak or ceiling
values should be used to determine the exposure to an irritant
[Winder, 1998]. The onset of symptoms in some personnel
can occur rapidly following the onset of exposure. Such
symptoms may be reported as acute and severe.
In the course of this study, the 38 exposed subjects were
subjected to 410 observed exposure events. The longest
observed event was just over 12 min, and the mean duration
of exposure for each phase of disinfection was less than 3 min.
The system of work in endoscopy units was such that in
15 min several exposure events are likely to occur, the
specific value of which cannot be determined by recognized
methods.
These limitations provide support for the use of an alter-
native method enabling the peak exposure to be determined.
The direct reading device used for this study lacks specificity
to glutaraldehyde alone [Anon, 1991; Tkaczuk, 1994].
TABLE III. Change inVisual AnalogScoresFollowingExposure ofNurses toGlutaraldehyde
VAS symptom summary data
SymptomMean change in score(final^ initial) (SD)
Proportionwithworsesymptoms following
exposure (%)
Headache 3.7 (17.7) 45.9Taste in mouth 0 (15.84) 40.5Nasal irritation 0.9 (17.18) 35.1Eye irritation 6.3 (22.55) 29.7Throat irritation 1.0 (18) 18.9Cough �1.3 (9.09) 29.7Wheeze �0.9 (2.87) 18.9Breathlessness 1.4 (6.9) 24.3
N.B. Mean score is in millimetres, n¼ 37.Visual analogue scales were100 mm long.
TABLE IV. Tests of Association Between Glutaraldehyde Exposure Variables and Cross Shift Changein FEV1 (n¼ 36)
Correlation of change in FEV1with exposure variables
Correlation Method Statistic Significance
Peak exposure-FEV1 Pearson’s �0.34 Two tailed, P¼ 0.048Sum of exposure events-FEV1 Spearman’s �0.32 Two tailed, P¼ 0.057Session duration-FEV1 Spearman’s �0.05 Two tailed, P¼ 0.751
Symptoms, Lung Function, and Glutaraldehyde 201
However, it does allow peak exposures to be determined. It is
regarded with some skepticism by occupational hygienists
because of its lack of specificity and questions regarding
its precision [Niven et al., 1997]. While the Glutaraldemeter
is sensitive to other substances commonly used in endos-
copy, an assessor, who remains present during the process,
can readily identify their use. This also enables an observed
exposure to be matched to a specific activity. This data sug-
gests that if glutaraldehyde use as a disinfectant in endoscopy
is to be continued, monitoring equipment and methods need
to be improved.
A significant cross shift reduction in FEV1 and FVC was
identified although the absolute volume change was less than
the error of measurement (5%). Surprisingly, these changes
had a weak inverse correlation with exposure variables, for
which there is no obvious explanation. No exposed subject
had a clinically important (>10%) cross shift change in FEV1
or FVC.
It is unlikely that there was significant selection bias in
subject recruitment, as the prevalence of asthma (13.2%) and
reporting of wheeze in the previous 12 months (21%) were
very similar to an adult asthma prevalence study (13 and 22%
for asthma and 12-month wheeze, respectively) conducted
around the same time in Melbourne [Abramson et al., 1992].
The greater response rate among exposed workers was
expected.
The association between skin symptoms and glutaralde-
hyde was significant, but so was the difference between
groups with regard to glove-wearing behavior. Glove wear-
ing presents a significant confounding variable. However,
latex exposure appears unlikely to explain all our findings
as even after allowing for this, a significant association
remained between glutaraldehyde exposure and skin symp-
toms. Glutaraldehyde exposure probably contributes to skin
symptoms by a local (irritant) effect. On the other hand,
subjects with established dermatitis are more likely to wear
gloves when handling glutaraldehyde. An earlier study
[Norback, 1988] identified an association between glutar-
aldehyde exposure and skin symptoms, but work practices
have altered since then. A more recent study [Pisaniello et al.,
1997] suggested that the skin problems of glutaraldehyde
exposed nurses might be related to frequent hand washing.
That study recruited nearly 78% of exposed subjects from
operating theaters, which could account for this finding. By
comparison, only 13.2% of exposed subjects in the current
study were recruited from operating theaters. Recruiting
theater staff became difficult in the current study, with
disinfection being increasingly done in the sterilizing
department by non-nursing staff. Reduced use of glutaralde-
hyde by theater staff could reflect a continuing trend to better
manage exposure.
Another recent study [Douglas et al., 1997] found that
22% of a similar population of nurses were skin prick positive
to one or more of five latex compounds. More than half the
respondents in that study reported skin symptoms including
local dryness, itch, and erythema in association with wearing
gloves. This compares with 31.6% in the current study (see
Table II). With increases in glove wearing practices
(‘universal precautions’) among hospital nurses and growing
glutaraldehyde use, there is a need for further investigation
into minimizing exposures.
Glutaraldehyde is a cheap and effective disinfectant.
Manual disinfection methods have evolved over many
years. However these work practices are prone to generate
splashes, droplets, and vapor release with the potential to
affect the eye, skin, mucous membranes, and respiratory
tract. Dedicated washing machines are available which
should reduce the potential for exposure. Several accepted
alternative substances exist but they require dedicated
washing machines. Newer technology is emerging (Steris�and Sterrad� processes) which is considerably more
expensive. However, it is the process that is safer rather than
the agent. Some evidence suggests that the efficacy of all these
processes and substances may be dependent on the quality
of the pre-cleaning of the instruments, which essentially
remains a manual process (using water, detergent, brushes,
and visual inspection) [Muscarella, 1996].
In conclusion, it appears that when glutaraldehyde is
used as a disinfectant in the health sector, exposure levels in
excess of the Australian occupational exposure standard
occur with commonly used exposure control methods. Work
practices contribute to this high exposure and this study
identified an excess of skin symptoms in glutaraldehyde
exposed staff. This suggests that there remains some risk at
current Australian exposure levels. Glutaraldehyde exposure
monitoring is difficult in that a peak exposure standard is
defined for this irritant substance, but there is currently no
device or method with sufficient specificity for glutaralde-
hyde able to determine peak exposure. If glutaraldehyde use
as a disinfectant is to continue, it is necessary to improve
exposure control and exposure monitoring. Dedicated
glutaraldehyde based processors, currently available and
similar to those used by alternatives may provide a safer
method, but further research in this area is required. The
confirmed high prevalence of skin symptoms and multiple
risk factors suggest that an exposure reduction strategy
for skin irritants and sensitizers in the health sector is
required.
ACKNOWLEDGMENTS
This research was undertaken with financial support of
the Alfred Research Trusts. Drs. Margaret Ward-Curran and
Rosemary Nixon are acknowledged for their assistance with
the development of elements of the symptom questionnaire
used in this study. The contributions of exposed and unex-
posed staff and hospital administrations are acknowledged as
is Mr. John Wildes, research assistant for this project.
202 Waters et al.
Mr. Frank Mielke Manager Workplace Health and Safety,
The Alfred also provided invaluable assistance.
REFERENCES
Abramson M, Kutin J, Bowes G. 1992. The prevalence of asthma inVictorian adults. Aust NZ J Med 22:358–363.
American Conference of Government Industrial Hygienists. 1998.Threshold limit values and biological exposure indices. Threshold limitvalues for chemical substances and physical agents. 6th Edition.Cincinnati: ACGIH.
Anonymas . 1991. Lion Glutaraldemeter Instruction Manual, version: 7/91–1. South Glamorgan, Wales, UK: Lion Laboratories. 17 p.
Axon ATR, Banks J, Cockel R, Deverill CEA, Newmann C. 1981.Disinfection in upper-digestive-tract endoscopy in Britain. Lancet1(8229):1093–1094.
Babb J, Bradley CR. 1995. A review of glutaraldehyde alternatives. BritJ Theatre Nurs 5(7):20–24.
Beauchamp RO, St. Clair MBG, Fennell TR, Clarke DO, Morgan KT.1992. A critical review of the toxicology of glutaraldehyde. Crit RevToxicol 22(3,4):143–174.
Bullard J. 1991. Use and abuse of glutaraldehyde. Nursing Times87(38):70–71.
Burney PGJ, Luczynska C, Chinn S, Jarvis D. 1994. The EuropeanCommunity Respiratory Health Survey. Eur Respir J 7:954–960.
Calder IM, Wright LP, Grimstone D. 1992. Glutaraldehyde allergy inendoscopy units. Lancet 399:433.
Corrado OJ, Osman J, Davies RJ. 1986. Asthma and rhinitis after ex-posure to glutaraldehyde in endoscopy units. Human Toxicol 5:325–327.
Cotes JE. 1993. Lung function: Assessment and implications inmedicine. Fifth Edition. Oxford: Blackwell Scientific Publications.
Douglas R, Czarny D, Morton J, O’Hehir RE. 1997. Prevalence of IgE-mediated allergy to latex in hospital nursing staff. Aust NZ J Med 27:165–169.
Ellett ML, Mikels CA, Fullhart JW. 1995. SGNA EndoscopicDisinfectant Survey. Gastroenterol Nursing 18(1):2–10.
European Community for Coal and Steel. 1983. Predicted values forlung function. Derived from the working party of the EuropeanCommunity for Coal and Steel. Standardization of lung function tests.Bull Eur Physiopathol Respir 19(Suppl 5):1–95.
Gannon PFG, Bright P, Campbell M, O’Hickey SP, Burge PS. 1995.Occupational asthma due to glutaraldehyde and formaldehyde inendoscopy and X-ray departments. Thorax 50:156–159.
Haley TJ. 1981. A review of the literature of glutaraldehyde. DangerousProperties of Industrial Materials Report 1(7):2–4.
Jachuck SJ, Bound CL, Steel J, Blain PG. 1984. Occupational hazard inhospital staff exposed to 2 percent glutaraldehyde in an endoscopyunit. J Soc Occup Med 39:69–71.
Leinster P, Baum JM, Baxter PJ. 1993. An assessment of exposure toglutaraldehyde in hospitals: Typical exposure levels and recommendedcontrol measures. Brit J Ind Med 50:107–111.
Macnab J. 1991. Glutaraldehyde use in endoscopy: A Canadian Review.Gastroenterol Nursing 14(1):9–13.
McAdam JG, Leicester RJ. 1992. Incidence of aldehyde sensitivity inendoscopy units. Gut 33(Suppl):52.
Muscarella LF. 1996. High-level disinfection or ‘‘Sterilization’’ ofendoscopes? Infection Control Hospital Epidemiol 17:183–187.
Mwaniki DL, Guthua SW. 1992. Occupational exposure to glutaralde-hyde in tropical climates. Lancet 340:1476–1477.
Naidu V, Lam S, O’Donnell G. 1995. Typical glutaraldehyde vapourlevels in endoscope disinfection units in New South Wales Hospitals.J Occup Health Safety Aust NZ 11(1):43–57.
Niven KJM, Cherrie JW, Spencer J. 1997. Estimation of exposure fromspilled glutaraldehyde solutions in a hospital setting. Ann Occup Hyg41(6):691–698.
Norback D. 1988. Skin and respiratory symptoms from exposure toalkaline glutaraldehyde in medical services. Scand J Work EnvironHealth 14:366–371.
Pierce R, Johns DP. 1995. Spirometry: The measurement andinterpretation of ventilatory function in clinical practice. Melbourne,National Asthma Campaign ISBN 0 646 26307 2.
Pisaniello DL, Gun RT, Tkaczuk MN, Nitschke M, Crea J.1997. Glutaraldehyde exposures and symptoms among endoscopynurses in South Australia. Appl Occup Environ Hyg 12(3):171–177.
Tkaczuk M, Pisaniello D, Crea J. 1993. Occupational exposure toglutaraldehyde in South Australia. J Occup Health Safety—Aust NZ9(3):237–243.
Tkaczuk MN, Pisaniello DL, Crea J. 1994. Monitoring of glutaralde-hyde. ACORN J June:31.
Waldron HA. 1992. Glutaraldehyde allergy in hospital workers. Lancet339:880.
Wellons SL, Trawick EG, Stowers MF, Jordan SLP, Wass TL. 1998.Laboratory and hospital evaluation of four personal monitoringmethods for glutaraldehyde in ambient air. Am Ind Hyg Assoc J59(2):96–103.
Winder C. 1998. Misuse of the exposure standard. J Occup HealthSafety Aust NZ 14(2):107–110.
WorkSafe Australia. 1995. Glutaraldehyde: Amendment Advice No. 4.WorkSafe Australia. Sydney.
Symptoms, Lung Function, and Glutaraldehyde 203
