Burns et al.[1] report a significant excess of deaths due to amyotrophic lateral sclerosis (ALS) in a cohort of Dow employees potentially exposed to the herbicide 2,4-Dichlorophenoxyacetic (2,4-D), but then argue against the plausibility of a causal association, concluding that the association "is not consistent with previous human or animal studies".
This conclusion and the authors' characterisatio...
Burns et al.[1] report a significant excess of deaths due to amyotrophic lateral sclerosis (ALS) in a cohort of Dow employees potentially exposed to the herbicide 2,4-Dichlorophenoxyacetic (2,4-D), but then argue against the plausibility of a causal association, concluding that the association "is not consistent with previous human or animal studies".
This conclusion and the authors' characterisation of the relevant epidemiologic studies appear to rely entirely upon statistical significance, which downplays the importance of their finding. Firstly, the authors state that "cohort studies of people with exposure to 2,4-D (have not) reported
increased rates of ALS," citing two studies,[2] [3] both of which have limited power to detect the risk of ALS. One of the two studies assessed risk in a cohort that was quite young with a relatively short follow up,[2] and would therefore be unlikely to detect an increased risk for a
disease such as ALS, which has a much older median age at onset. Burns et al then go on to state that "exposure to pesticides and agricultural chemicals have shown no significant association in several studies"(emphasis added).[1]
In each of the three case-control studies cited, however, ALS was positively associated with pesticides or agricultural chemicals, with reported ORs of 1.4,[4] 2.0,[5]
and 3.0,[6] although the associations do not reach statistical significance. Finally, Burns et al refer to a case-control study,[7] which found a significant association between ALS and pesticides, but, they emphasise, "did not find a significant association of exposure to
herbicides".[1] The association between ALS and herbicide exposure was increased, however, and the lack of statistical significance reflected, at least in part, small numbers.
None of this is meant to say that the finding of a significant association between ALS and 2,4-D is conclusive.
The finding is, however, consistent with several previous studies and, instead of being played down, warrants serious attention in future studies.
D M Freedman
National Cancer Institute
Division of Cancer Epidemiology and Genetics
USA
1. Burns CJ, Beard KK, Cartmill JB. Mortality in chemical workers potentially exposed to 2,4-dichlorophenoxyacetic acid (2,4-D) 1945-94: an update. Occup Environ Med 2001;58:24-30.
2. Zahm SH. Mortality study of pesticide applicators and other employees of a lawn care service company. J Occup Environ Med 1997;39:1055-67.
3. Coggon D, Pannett B, Winter P. Mortality and incidence of cancer at four factories making phenoxy herbicides. Br J Ind Med 1991;48:173-8.
4. Chancellor AM, Slattery JM, Fraser H, et al. Risk factors for motor neuron disease: a case-control study based on patients from the Scottish Motor Neuron Disease Register. J Neurol Neurosurg Psychiatry 1993;56:1200-6.
5. Deapen DM, Henderson BE. A case-control study of amyotrophic lateral sclerosis. Am J Epidemiol 1986;123:790-9.
6. Saviettieri G, Salemi G, Arcara A, et al. A case-control study of amyotrophic lateral sclerosis. Neuroepidemiology 1991;10:242-5.
7.McGuire V, Longstreth WT Jr, Nelson LM, et al. Occupational exposures and amyotrophic lateral sclerosis.
Am J Epidem 1997;145:1076-88.
Granath and colleagues take issue with our update of a cohort of
acrylamide (AMD) workers from three U.S. plants[1] claiming that "it
exemplifies the shortcomings of studies of this type to detect moderate
influences of specific causative factors on cancer mortality or
incidence." To support their contention that we overlooked a small but
"unacceptable" increase in cancer risk, they performed a crude
q...
Granath and colleagues take issue with our update of a cohort of
acrylamide (AMD) workers from three U.S. plants[1] claiming that "it
exemplifies the shortcomings of studies of this type to detect moderate
influences of specific causative factors on cancer mortality or
incidence." To support their contention that we overlooked a small but
"unacceptable" increase in cancer risk, they performed a crude
quantitative risk assessment. Granath et al. suggested that we perform a
within cohort dose-response analysis with all malignant neoplasms as the
endpoint as a means of attaining greater statistical power. They further
contend that a priori focus on specific cancer sites implicated in
previous experimental animal studies is mostly a consequence of the
pattern of background incidences in the animal strain used. While choosing
a generic health outcome such as all cancer sites combined will certainly
increase statistical power, it also greatly reduces the ability to
evaluate the all important specificity of an exposure-response
relationship. It is unlikely that even the most potent carcinogenic agent
will increase the risks of all cancer sites to a level that can be
detected with epidemiological methods.
We were fully justified in using cancer site-specific findings as the
focus of our epidemiological investigation. The use of cancer site-
specific findings from experimental animal studies to formulate a priori
testable etiologic hypotheses for human studies is an effective, accepted
method commonly employed in occupational epidemiological research. Animal
studies can be particularly helpful when investigators are faced with a
paucity of extant epidemiological evidence such as in the case of AMD.
This practice does not preclude, however, the exploratory investigation of
other non-implicated sites as long as the related findings are interpreted
in light of their hypothesis generating nature.
We agree that for many of the a priori cancer sites examined in our
study, the statistical power to detect a moderate mortality excess (1.5 to
twofold or greater) was low, a point addressed in the discussion section
of our paper. However, the power of our study to detect a twofold or
greater excess in lung cancer, the endpoint of primary concern, at the one
-sided 5% significance level was in the excellent range (0.87), as would
be the power to detect a similar excess of pancreatic cancer in a future
update of this cohort.
Granath et al. overlook a fundamental point - occupational cohort
studies of the type we used to evaluate cancer mortality risks among AMD
exposed workers are neither designed nor necessarily well suited for
quantitative risk assessment purposes. Occupational cohort studies are
purposely not designed to detect small excesses in the range of 5-15%
deemed by Granath et al. as unacceptable. The primary reason for this is
that excesses of this magnitude could easily be due, at least in part, to
one or more confounding factors. Observational epidemiological studies
usually cannot discriminate among such small mixed effects, and are
generally most useful for detecting increases in risk that exceed 50-100%
as these are unlikely to be due to uncontrolled confounding. Statistical
power considerations notwithstanding, the fact remains that our study is
the largest and most comprehensive study of AMD exposure conducted to
date, and will continue to provide useful epidemiological Information
through future updates and analysis.
Gary M. Marsh
Ada O. Youk
Lorraine J. Lucas
Laura C. Schall
1. Marsh GM, Lucas L, Youk AO, Schall LC: Mortality Patterns among
Workers
Exposed to Acrylamide: 1994 Follow-Up. Occup Environ Med 1999;56:181-190.
Recently the results of a comprehensive epidemiological follow up
study of cancer mortality in cohorts with occupational exposure to
acrylamide was published.[1] With the exception of a weak significance for
a raised incidence of pancreas cancer the study arrived by and large at
the conclusion that there is "little evidence for a causal relationship
between exposure to acrylamide and mortality from any c...
Recently the results of a comprehensive epidemiological follow up
study of cancer mortality in cohorts with occupational exposure to
acrylamide was published.[1] With the exception of a weak significance for
a raised incidence of pancreas cancer the study arrived by and large at
the conclusion that there is "little evidence for a causal relationship
between exposure to acrylamide and mortality from any cancer sites". The
study updates and confirms an investigation 10 years earlier of the same
cohorts.[2] The analysis was based on standardised mortality ratios (SMR)
in comparison with US national or relevant county mortality statistics. It
exemplifies the shortcomings of epidemiological studies of this kind to
detect moderate influences of specific causative factors on cancer
mortality or incidence. The investigators praise themselves of having
carried out "the most definitive study of the human carcinogenic potential
of exposure to acrylamide conducted to date". The results, however, pose
questions. Could unacceptable risks be detected? Which risks would have
been expected?
For the US workers the average cumulative exposure is given to 0.25 mg/m3
y. (We assume this to correspond to exposure of the whole factory staff to
0.25 mg/m3 for 365 eight-hour working days). At an alveolar ventilation
rate of 0.2 L/kg min this exposure would mean a cumulative uptake of
about 9 mg acrylamide per kg body weight. This dose corresponds to a
lifetime (70 years) uptake of 0.35 µg/kg d. According to the estimate of
U.S. EPA[3] this would correspond to a cancer risk of 1.6 10-3. An
estimate based on the multiplicative model[4] would arrive at a ca 3 times
higher risk, 5 10-3. With a cancer mortality in the Western World
countries of 0.18, these figures correspond to an 1-3% increase of the
cancer mortality risk, i.e. a RR of 1.01-1.03. Since about one fifth of
the workers were defined as exposed (with greater than or equal to 10-3 mg/m3 years) the relative
risk in the exposed group due to inhalation of acrylamide may have been
about 1.05-1.15.
Although it is doubtful that these risk increments could be considered
negligible, they would not be detectable in a study of the present kind.
Since uptake via the skin often occurs in work leading to inhalation of
acrylamide it is possible that the true risk increments are considerably
higher. If we assume the total relative risk (from inhalation plus dermal
uptake) to be in the range of 1.1-1.2, it is a pertinent question whether
this risk increment is detectable within the large material studied by
Marsh et al.[1]
Like many other materials of similar kinds the data are far from ideal for
epidemiological analyses. The main reasons for this are the skew
distribution of duration of employment, the incompleteness of data for
smoking, and the healthy worker effect. The healthy worker effect leads to
a deficit in death rates from all causes, in the present study by about
20% for all causes except cancers. Deficits in SMR for all malignant
neoplasms and for certain tumour types are also often significant,
although with a disturbing influence of a significantly increased SMR for
lung cancer in an earlier period. (The significant decrease in lung cancer
deaths as well as deaths in diseases of the circulatory system from 1925-
83 to 1984-94 would be compatible with a drastic reduction, before 1984,
of smoking.) It is expected that the healthy worker effect comprises
cancer, at least to some extent, as well as other causes of death.
A straightforward way of overcoming the healthy worker effect is a within cohort analysis of the regression of mortalities or incidences on the
estimated dose. Marsh et al.,[1] have done this for each of a few selected
tumour sites. Due to too few observed deaths in each dose interval the
statistical power of this material is, however, too small to show
anything.
This analysis of individual sites, avoiding a pooling of data that would
increase the statistical power, illustrates the widespread dogma that
different cancer types are affected specifically by carcinogens. It has
been shown for a few mutagenic carcinogens including acrylamide that a
linear multiplicative model, Pj = P0j (1+ ß D), can be fitted to
experimental cancer incidence data and, for radiation, to human data.[5]
Pj and P0j are the total and background risks of tumour at site j, D the
dose and ß a relative risk coefficient that is (at least approximately)
the same for all tumour sites j. ß is thus applicable to pooled data for
groups of sites or for all (responding) sites. Although analysis of death
risks associated with specific tumours has its indisputable value, a
restriction of significance estimation to individual sites leads as a main
effect to a loss of statistical power. For related reasons the
identification of certain sites as "interesting", with reference to
response to acrylamide in animal experiments, is mostly a consequence of
the pattern of background incidences P0j in the animal strain used.
The authors of the paper,[1] possess a material of extreme value in
further efforts to clarify the carcinogenic potency of acrylamide. In view
of the importance of this question we urge the authors of the paper to
continue their work, particularly with analyses of regression on pooled
data, primarily for all cancer, with and without exclusion of smoking related sites.
Fredrik Granath
Dept of Medical Epidemiology,
Karolinka Institute
Lars Ehrenberg
Dept of Genetic and Cellular Toxicology,
Stockholm University
Birgit Paulsson
Margareta Törnqvist
Department of Environmental Chemistry,
Stockholm University,
S-106 91 Stockholm,
Sweden
1. Marsh, GM, Lorraine, JL, Youk AO, Schall LC. Environ Med
1999;56:181-190.
2. Collins JJ, Swaen GMH, Marsh GM, Utidjian HMD, Caporossi JC, Lucas
LJ. J Occup Med 1989;31:614-617.
3. U.S. EPA, United States Environmental Protection Agency.
Assessment of Health Risks from Exposure to Acrylamide. 1990 U.S.
Environmental Protection Agency: Washington, DC.
4. Törnqvist M, Bergmark E, Ehrenberg L, Granath F. [Risk Assessment
of Acrylamide] (in Swedish) National Chemicals Inspectorate, Solna,
Sweden. 1998 PM 7-98.
In their 1999 study of workers exposed to acrylamide, Marsh et al
conducted an SMR analysis and fit several relative risk regression models
to the data.[1] In each analysis, they found risk of pancreatic cancer
elevated by about twofold for workers in the highest cumulative exposure
group, but risk of pancreatic cancer did not increase monotonically with
cumulative exposure in any of their analyses. Dur...
In their 1999 study of workers exposed to acrylamide, Marsh et al
conducted an SMR analysis and fit several relative risk regression models
to the data.[1] In each analysis, they found risk of pancreatic cancer
elevated by about twofold for workers in the highest cumulative exposure
group, but risk of pancreatic cancer did not increase monotonically with
cumulative exposure in any of their analyses. Duration of exposure was
monotonically related and mean intensity showed a nearly monotonic
relationship with pancreatic cancer risk.
The cut points Marsh et al chose for the cumulative exposure groups
are based on multiples of current and proposed regulated levels of
exposure intensity.[1] [2] Because these cut points resulted in small
numbers of expected deaths in the low and intermediate exposure groups,
1.08 and 2.74 respectively, we have regrouped the data to attempt to
obtain more stable SMRs. These results are presented in Table 1 and
indicate a monotonic dose-response pattern with the SMRs increasing from
0.80 to 1.31 to 2.26.
Table 1. Observed deaths, expected deaths, and SMRs for cancer of
the
pancreas, all US workers, 1950-94, local county comparisons, two
lowest exposure groups combined.
Cumulative Exposure (mg/m3.y)
Obs
Exp
SMR
95% CI
30
37.50
0.80
0.54-1.14
0.001-0.29
5
3.82
1.31
0.35-3.05
>0.30
9
3.98
2.26
1.03-4.29
In part based on the absence of a pattern of monotonically increasing
risk with increased cumulative exposure, Marsh et al. argue that, "our
findings for cancer of the pancreas should be interpreted with caution, in
the context of an exploratory analysis to generate hypotheses."[1]
Nevertheless, given the sufficient evidence in experimental animals for
the carcinogenicity of acrylamide.[3] this study plays an important role
in the evaluation of safety for occupational exposures to acrylamide.
When data are sparse, it is not always clear how best to choose cut
points; the grouping we have shown results in a finding that is more
compatible with the findings for duration and for intensity of exposure.
It would be interesting to see if a regrouping of the exposure categories
alters the results of the analyses based on internal comparisons.
MR. Schulz
I Hertz-Picciotto
E van Wijngaarden
J Calderon Hernandez
Department of Epidemiology,
University of North Carolina at Chapel Hill
LM. Ball
Department of Environmental Sciences and Engineering,
University of North Carolina at Chapel Hill
1. Marsh GM, Lucas LJ, Youk AO, et al. Mortality patterns among
workers exposed to acrylamide: 1994 follow up. Occup Environ Med
1999;56:181-90.
2. Collins JJ, Swaen GH, Marsh GM, et al. Mortality patterns among workers
exposed to acrylamide. J Occup Med 1989;31:614-17.
3. International Agency for Research on Cancer. Acrylamide In IARC
Monographs on the Evaluation of Carcinogenic Risks to Humans; Some
Industrial Chemicals Volume 60. Lyon, France 1994.
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 >2.5.
These cases were felt not to show asthma because PEF d...
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 >2.5.
These cases were felt not to show asthma because PEF diurnal variability
was less than 15%. We have recently shown that increased diurnal
variability is not found in the majority of 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 individuals
occurs at around 16:00 hours 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
whilst 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 individuals.[3] Use of non-
linear PEF meters significantly underestimates PEF variability [4] but
even when PEF readings are linearised, an absence of an increase in
diurnal variability does not exclude asthma. An Oasys-2 score of >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 >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, 7 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 per day. We have found that objective evidence of glutaraldehyde
induced asthma can be obtained in a large proportion of workers with
respiratory tract symptoms temporally related to glutaraldehyde exposure
when adequately sought after.
W Anees
A S Robertson
P S Burge
Occupational Lung Disease Unit
Birmingham Heartlands Hospital
Birmingham B9 5SS
1. Vyas A, Pickering CAC, Oldham LA, et al. Survey of symptoms,
respiratory function, and immunology and their relation to glutaraldehyde
and other occupational exposures among endoscopy nursing staff. Occup
Environ Med 2000;7:752-9.
2. Anees W, Burge PS. Diurnal variability of peak expiratory flow and non
-specific bronchial reactivity in workers with occupational asthma. Eur
Respir J 2000;16:520s
3. Higgins BG, Britton JR, Chinn S, et al: The distribution of peak
expiratory flow variability in a population sample. Am Rev Respir Dis
1989;140:1368-72.
4. Miles JF, Miller MR: Influence of peak flow meter non-linearity on
recorded PEF variability. Thorax 1992;47:891
5. Burge PS, Pantin CF, Newton DT, et al. Development of an expert system
for the interpretation of serial peak expiratory flow measurements in the
diagnosis of occupational asthma. Occup Environ Med 1999;56:758-64.
6. Di Stefano F, Siriruttanapruk S, McCoach JS, Burge PS. Glutaraldehyde:
an occupational hazard in the hospital setting. Allergy 1999;54:1105-9.
We read with interest a recently published study on personal exposure
of asthmatic children to nitrogen dioxide (NO2), relative to
concentrations in outdoor air.[1]
In their results, authors didn't find:
1. "…significant correlation… between each child's weekly mean personal
exposures and mean outdoor concentrations for the corresponding periods";
2. "…marked evidence of seasonality" on personal exposure...
We read with interest a recently published study on personal exposure
of asthmatic children to nitrogen dioxide (NO2), relative to
concentrations in outdoor air.[1]
In their results, authors didn't find:
1. "…significant correlation… between each child's weekly mean personal
exposures and mean outdoor concentrations for the corresponding periods";
2. "…marked evidence of seasonality" on personal exposure .
They concluded: "…at low concentrations, changes in NO2 in outdoor
air…contribute little to variations in personal exposure to the
pollutant."
We think that these conclusions cannot be drawn from the method used to
evaluate outdoor concentrations. Besides, we report different findings on
seasonal trend at higher levels of personal exposure.
We performed a study to evaluate the annual distribution of personal
exposure to NO2 in school children of Novara, a small city in north west
Italy (about 110.000 inhabitants) and to study determinants of this
exposure.
NO2 exposure was measured using passive samplers (Palme's tubes) in 310
school children aged 5-14 years. The children wore the tubes 5 days a
week, in each season of the year.
The possible differences in personal measurements were assessed by ANOVA
and Tuckey tests. Information about the sources of potential exposure was
collected by a questionnaire. The relative risk for these variables was
estimated with a multiple regression model (Logit). The annual average of
6,200 measurements was 42.7 mg/m3 with a significant difference between
seasons, and higher values in winter. The only factor associated with
increased personal exposure was to live along busy streets, only for
children of maternal school.
Even if designs of two studies are different, at this point it is possible
to make some considerations.
Firstly, at higher levels of NO2 exposure respect to those reported by
Linaker et al,[1] the seasonal changes of concentration in outdoor air
contribute significantly to variations in intra-individual exposure.
Besides, the role of risk factors present at home, respect to child-child
differences, is not clear. We suppose that our result depends on actual
habit of children to spend, everyday, a lot of hours in many different
occupations away from home, reducing the individual differences caused by
domestic sources of NO2.
Secondly, we think that only one measurement station used by Linaker et
al.[1] is inappropriate to evaluate the real impact of outdoor
concentrations on personal exposure, because outdoor levels of pollutants
are, in our and in other studies,[2] [3] related to traffic density in
each street.
1. Catherine H Linaker, Anoop J Chauhan, Hazel M Inskip, Stephen T
Holgate. Personal exposure of children to nitrogen dioxide relative to
concentrations in outdoor air; Occup Environ Med 2000;57:472-6.
2. Shima M, Adachi M. Indoor nitrogen dioxide in homes along trunk roads
with heavy traffic; Occup Environ Med 1998;55:428-33.
3. Kramer U, Koch T, Ranft U, Ring J, Behrendt II. Traffic related air
pollution is associated with atopy in children living in urban areas;
Epidemiology 2000;11:64-70.
Editor,
I was interested to read the excellent COPE Report Paper[1] and note
Occupational and Environmental Medicine's intention to follow these
guidelines.
In particular, from the occupational health point of view, I welcome
the inclusion of involvement of the study participants in consideration
and agreement of the research protocol, though I am a little sad that the
COPE Committee...
Editor,
I was interested to read the excellent COPE Report Paper[1] and note
Occupational and Environmental Medicine's intention to follow these
guidelines.
In particular, from the occupational health point of view, I welcome
the inclusion of involvement of the study participants in consideration
and agreement of the research protocol, though I am a little sad that the
COPE Committee have restricted their consideration of pre-publication
information of the results to "patients, especially if there are clinical
implications."[1]
As you are aware, the Professional Guidance on Ethics for
Occupational Physicians[2] now includes a specific section on occupational
health research which highlights the need to consider release of results,
including pre-publication briefings to workforces who are the subjects of
such research. I know that the BMJ Publishing Group have long been in
support of this sort of ethical stance, and would hope that in the future
COPE might expand their consideration of pre-publication information
beyond patients and clinical medicine into workers in the occupational
setting.
Another area of ethics of research relevant to occupational health
not considered by COPE is the field of data access and shared data.
Research in the work place can be consented to by the workforce for a
specific purpose, specific protocol, and even on occasion for a specific
researcher's use. There remains the question whether this data once
obtained is, or should be, available for others to use in other protocols
for other purposes. Certainly in the nuclear industry, we have taken the
view that it should not without revisiting the consent of the workforce.
Perhaps this too is an area that COPE might address in the future.
References
1. Committee on Publication Ethics. Occup Environ Med 2000;57:506-9.
2. Faculty of Occupational Medicine. Section 6. Guidance on Ethics for Occupational Physicians. 5th ed. London: Faculty of Occupational Medicine, 1999.
As victims of bullying and proponents of emotional intelligence in
the health profession we read with interest your article on workplace
bullying.[1]
Kavimaki et al[1] did not mentioned whether the responses were
anonymous. Identified responses may underestimate the incidence of
bullying in the cohort. Given that previous studies (mentioned by the
authors in the discussion) have shown a consid...
As victims of bullying and proponents of emotional intelligence in
the health profession we read with interest your article on workplace
bullying.[1]
Kavimaki et al[1] did not mentioned whether the responses were
anonymous. Identified responses may underestimate the incidence of
bullying in the cohort. Given that previous studies (mentioned by the
authors in the discussion) have shown a considerable percentage of victims
deciding to resign as a result of bullying, it is a pity that the article
by Kivimaki et al did not contain similar data. The other two issues that should have been included were the duration of being bullied, and how many
bullies are actually are aware that they are bullies. These can be addressed by asking
the question: Have you subjected your colleagues to such bullying
behaviour?
With doctors and nurses constituting 58% of the victims, we wonder
whether the authors could reanalyse their data to see whether there is a
higher incidence of bullying in the high stress specialities such as adult
intensive care and neonatal intensive care.[2] We would also like to
know whether the victims in their study were offered any counselling by
their institutions, and if so, the nature and impact of the counselling.
Emotional intelligence is defined by the five emotional quotients of
self awareness of feelings, emotional self regulation, self monitoring and
goal setting, empathy, and social and communication skills.[3] According
to Goleman, “The rules for work are changing, we’re being judged by a new
yardstick: not just how smart we are, or our expertise, but also how well
we handle ourselves and each other.”[4] Emotional intelligence is
considered more important than IQ in enabling people to function well in
society.[5] We would like to suggest that emotional intelligence, which
can be taught, can be an important solution to reducing the incidence of
bullying in the workplace.[6]
References:
1. Kivimaki M, Elovainio M, Vahtera J Workplace bullying and sickness absence in hospital staff. Occup Environ Med 2000;57:656-60
2. Rosenthal SL, Schmid KD, Black MM. Stress and coping in a NICU.
Res Nurs Health 1989;12:257-65
3. Goleman D. Emotional intelligence. Why it can matter more than IQ. London: Bloomsbury Publishing Plc, 1995
4. Goleman D. Working with Emotional Intelligence. London: Bloomsbury Publishing Plc, 1998
5. Goleman D. What makes a leader? Harv Bus Rev 1998;76:93-102
6. Koh TS, Koh THHG. Disruptive doctors: emotion based medicine is as important as evidence based medicine. MJA (in press)
The recent article by Vyas, et al.[1] raises some concerns to which I
would be grateful if they could respond.
1) In the abstract one of the objectives is stated as finding the
nature and incidence of symptoms experienced by a large sample of hospital
endoscopy nurses. The study design is cross-sectional and used an adapted
version of the MRC questionnaire for respiratory symptoms. This study
design normally re...
The recent article by Vyas, et al.[1] raises some concerns to which I
would be grateful if they could respond.
1) In the abstract one of the objectives is stated as finding the
nature and incidence of symptoms experienced by a large sample of hospital
endoscopy nurses. The study design is cross-sectional and used an adapted
version of the MRC questionnaire for respiratory symptoms. This study
design normally records disease prevalence rather than incidence.[2] It
would be helpful to know if the questionnaire sought information on new
symptoms in a given time period in the past, or the presence of symptoms.
2) For the purposes of the study, work related symptoms (WRSs) of
contact dermatitis were defined as contact skin rash, which occurred when
working on the endoscopy unit and could not be attributed to known non-occupational agents. It is not clear what validation process was performed
prior to using this section of the questionnaire in the study. The authors
have indicated that 8 of the 13 subjects with a positive test to IgE
specific to latex had WRSs of dermatitis, and indicate this is non-significant. The authors definition of contact dermatitis would have
resulted in staff with contact urticaria answering positively to this
section. As such, the presence of IgE specific to latex could well be of
significance as staff would have used latex gloves.
3) Cross-sectional studies are enhanced by the inclusion of ex-employees. In this study only 18 of 68 ex-employees participated in this
study. All 18 were among 26 staff who had left within the past five years
for health reasons. As such a selection bias exists and the interpretation
of the frequency of WRSs in ex-employees should be cautious. In addition, it is noted that 8 of the 18 ex-employees continue to work as
nurses and may experience WRSs from circumstances related to current
workplaces rather than endoscopy suites. The absence of a control group of
nurses working in areas without exposure to glutaraldehyde would have been
of help in interpreting the results obtained.
References
1. A Vyas, C A C Pickering, L A Oldham, H C Francis, A M Fletcher, T Merrett, and R McL Niven.
Survey of symptoms, respiratory function, and immunology and their relation to glutaraldehyde and other
occupational exposures among endoscopy nursing staff
Occup Environ Med 2000;57:752-759
2. Last JM. A Dictionary of Epidemiology. Oxford: Oxford
University Press, 1995
We thank Dr. Seilkop for his comment and have, in essence, not much
to
add to it. The study by Shannon et al.[1] had obviously been overlooked
and the study by Arena et al.[2] was published after our deadline
for the inclusion of studies.
Dr. Seilkop´s Table has errors for the study by Andersson et al.[3]
The number of
pacreatic cancer deaths should be 2; relative risk should be 1.2; and
95% conf...
We thank Dr. Seilkop for his comment and have, in essence, not much
to
add to it. The study by Shannon et al.[1] had obviously been overlooked
and the study by Arena et al.[2] was published after our deadline
for the inclusion of studies.
Dr. Seilkop´s Table has errors for the study by Andersson et al.[3]
The number of
pacreatic cancer deaths should be 2; relative risk should be 1.2; and
95% confidence interval should be 0.1 - 4.5.
References
1. Shannon HS, Walsh C, Jadon N, et al. Mortality of 11,500 nickel
workers - extended follow up and relationship to environmental
conditions. Toxicol Ind Health 1991;7:277-94.
2. Arena VC, Sussman NB, Redmond CK, et al. Using alternative
comparison populations to assess occupation-related mortality risk. J
Occup Environ Med 1998;40:907-16.
3.Andersson VC, Elinder CG, Hogstedt C, et al. Mortality among
cadmium
and nickel-exposed workers in a Swedish battery factory. Current Topics
in Environmental and Toxicological Chemmistry 1985;399-408.
Editor
Burns et al.[1] report a significant excess of deaths due to amyotrophic lateral sclerosis (ALS) in a cohort of Dow employees potentially exposed to the herbicide 2,4-Dichlorophenoxyacetic (2,4-D), but then argue against the plausibility of a causal association, concluding that the association "is not consistent with previous human or animal studies".
This conclusion and the authors' characterisatio...
Editor,
Granath and colleagues take issue with our update of a cohort of acrylamide (AMD) workers from three U.S. plants[1] claiming that "it exemplifies the shortcomings of studies of this type to detect moderate influences of specific causative factors on cancer mortality or incidence." To support their contention that we overlooked a small but "unacceptable" increase in cancer risk, they performed a crude q...
Editor,
Recently the results of a comprehensive epidemiological follow up study of cancer mortality in cohorts with occupational exposure to acrylamide was published.[1] With the exception of a weak significance for a raised incidence of pancreas cancer the study arrived by and large at the conclusion that there is "little evidence for a causal relationship between exposure to acrylamide and mortality from any c...
Editor,
In their 1999 study of workers exposed to acrylamide, Marsh et al conducted an SMR analysis and fit several relative risk regression models to the data.[1] In each analysis, they found risk of pancreatic cancer elevated by about twofold for workers in the highest cumulative exposure group, but risk of pancreatic cancer did not increase monotonically with cumulative exposure in any of their analyses. Dur...
Editor
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 >2.5. These cases were felt not to show asthma because PEF d...
Editor,
We read with interest a recently published study on personal exposure of asthmatic children to nitrogen dioxide (NO2), relative to concentrations in outdoor air.[1] In their results, authors didn't find: 1. "…significant correlation… between each child's weekly mean personal exposures and mean outdoor concentrations for the corresponding periods"; 2. "…marked evidence of seasonality" on personal exposure...
Editor,
I was interested to read the excellent COPE Report Paper[1] and note Occupational and Environmental Medicine's intention to follow these guidelines.
In particular, from the occupational health point of view, I welcome the inclusion of involvement of the study participants in consideration and agreement of the research protocol, though I am a little sad that the COPE Committee...
Editor
As victims of bullying and proponents of emotional intelligence in the health profession we read with interest your article on workplace bullying.[1]
Kavimaki et al[1] did not mentioned whether the responses were anonymous. Identified responses may underestimate the incidence of bullying in the cohort. Given that previous studies (mentioned by the authors in the discussion) have shown a consid...
The recent article by Vyas, et al.[1] raises some concerns to which I would be grateful if they could respond.
1) In the abstract one of the objectives is stated as finding the nature and incidence of symptoms experienced by a large sample of hospital endoscopy nurses. The study design is cross-sectional and used an adapted version of the MRC questionnaire for respiratory symptoms. This study design normally re...
Editor
We thank Dr. Seilkop for his comment and have, in essence, not much to add to it. The study by Shannon et al.[1] had obviously been overlooked and the study by Arena et al.[2] was published after our deadline for the inclusion of studies.
Dr. Seilkop´s Table has errors for the study by Andersson et al.[3] The number of pacreatic cancer deaths should be 2; relative risk should be 1.2; and 95% conf...
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