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.
Chronic hand vibration exposure is now a well-described cause of
Raynaud's phenomenon. According to Palmer et al, it is estimated that
220,000 cases of Raynaud's phenomenon are attributable to vibration
exposure in Great Britain.[1] These epidemiological data, based on a
questionnaire, are considered reasonably accurate.[2] About 4.2 million
workers are exposed to hand transmitted vibration but the real...
Chronic hand vibration exposure is now a well-described cause of
Raynaud's phenomenon. According to Palmer et al, it is estimated that
220,000 cases of Raynaud's phenomenon are attributable to vibration
exposure in Great Britain.[1] These epidemiological data, based on a
questionnaire, are considered reasonably accurate.[2] About 4.2 million
workers are exposed to hand transmitted vibration but the real health and
economic impact is unknown.[3] More precise clinical data are therefore
necessary before implementing a large preventive program.
The hand-arm vibration syndrome encompass a wide range of disorders being
responsible for digital blanching and paresthesias.[4] Different vascular
problems such as a pure vasospastic phenomenon, a digital organic
microangiopathy or an occlusive arterial thrombosis can be observed. A
diffuse vibration neuropathy with mechanical skin receptors involvement or
a carpal tunnel syndrome are also often associated.[5] The relationship
between these neurovascular disorders is not clear but autonomic
dysfunction in carpal tunnel syndrome can induce a Raynaud's phenomenon
which is curable with surgery.[6] The prognosis of these neurovascular
troubles is dependant on the underlying trouble and cannot be evaluated
with a simple questionnaire. As no single test can reliably stage the
vascular and neurological component, the use of a battery of tests is
necessary. Digital capillaroscopy and plethysmography with nerve
conduction studies are recommended as the basic tests. Cold provocation
tests are effective for grading a pure vasospastic Raynaud's phenomenon
but is less reliable in other forms of vibration-induced white finger
explaining why this test is not always well correlated with the vascular
symptoms.[7][8] Doppler and duplex studies are useful to assess the
severity of an occlusive arterial disease.
Workers using hand-held vibrating tools are also exposed to diverse
environmental and occupational factors accounting for the wide clinical
spectra of the disease. Epidemiological studies have pointed out that the
prevalence of vibration-induced white finger is very wide, ranging from 0-
5% in warm climate to 80-100% in northern climate.[9] In the pure
vasospastic Raynaud's phenomenon, cold exposure is probably the most
important triggering factor and cold protection the most effective
preventive measure. In the case of digital blanching associated with
carpal tunnel syndrome, other ergonomic factors such as repetitive
forceful use of the hands are likely to play a dominant role and a
workplace ergonomic modification is indicated.[10] Hypothenar hammer
syndrome is a another frequent cause of digital blanching in mechanics and
carpenters requiring prevention of repetitive hand trauma.[11][12] For the
digital organic microangiopathy and the diffuse vibration neuropathy,
vibration exposure is the only identified factor and suppression of the
exposition is essential. In consequences, a detailed and precise clinical
diagnosis with objective tests is important to determine the real cause of
the vascular symptoms. The impact of vibration exposure on health will be
more precisely evaluated and prevention will be more effective.
1. Palmer KT, Griffin MJ, Syddall H, et al. Prevalence of Raynaud's
phenomenon in Great Britain and its relation to hand transmitted
vibration: a national postal survey. Occup Environ Med 2000;57:448-52.
2. Palmer KT, Haward B, Griffin MJ, et al. Validity of self reported
occupational exposures to hand transmitted and whole body vibration. Occup
Environ Med 2000;57:237-41.
3. Palmer KT, Griffin MJ, Bendall H, et al. Prevalence and pattern of
occupational exposure to hand transmitted vibration in Great Britain:
findings from a national survey. Occup Environ Med 2000;57:218-28.
4. Noel B. Pathophysiology and classification of the vibration white
finger. Int Arch Occup Environ Health 2000;73:150-5.
5. Stromberg T, Dahlin LB, Rosen I, et al. Neurophysiological findings in
vibration-exposed male workers. J Hand Surg [Br] 1999;24:203-9.
6. Verghese J, Galanopoulou AS, Herskovitz S. Autonomic dysfunction in
idiopathic carpal tunnel syndrome. Muscle Nerve 2000;23:1209-13.
7. McLafferty RB, Edwards JM, Ferris BL, et al. Raynaud's syndrome in
workers who use vibrating pneumatic air knives. J Vasc Surg 1999;30:1-7.
8. McGeoch KL, Gilmour WH. Cross sectional study of a workforce exposed to
hand-arm vibration: with objective tests and the Stockholm workshop
scales. Occup Environ Med 2000;57:35-42.
9. Bovenzi M. Exposure-response relationship in the hand-arm vibration
syndrome: an overview of current epidemiology research. Int Arch Occup
Environ Health 1998;71:509-19.
10. Gemne G. Diagnostics of hand-arm system disorders in workers who use
vibrating tools. Occup Environ Med 1997;54:90-5.
11. Little JM, Ferguson DA. The incidence of the hypothenar hammer
syndrome. Arch Surg 1972;105:684-5.
12. Ferris BL, Taylor LM Jr, Oyama K, et al. Hypothenar hammer syndrome:
proposed etiology. J Vasc Surg 2000 Jan;31:104-13.
A meta-analysis that was recently published in this journal[1]
suggested an association between excess pancreatic cancer risk and
exposure to nickel and nickel compounds (meta-risk ratio = 1.9, 95% CI =
1.2 - 3.2, based on 4 studies). Through correspondence with the authors
(Ojaj rvi et al.), I learned that their analysis excluded the many
epidemiological studies that had been conducted on workers in the...
A meta-analysis that was recently published in this journal[1]
suggested an association between excess pancreatic cancer risk and
exposure to nickel and nickel compounds (meta-risk ratio = 1.9, 95% CI =
1.2 - 3.2, based on 4 studies). Through correspondence with the authors
(Ojaj rvi et al.), I learned that their analysis excluded the many
epidemiological studies that had been conducted on workers in the nickel
refining and alloy production industries. While most of these studies
could not contribute to the meta-analysis due to a failure to specifically
examine pancreatic cancer risk, I found two studies of nickel workers that
provide relevant data.
I believe that one of these studies, which examined mortality in
11,500 nickel mining and smelting workers,[2] should have been included in
the Ojaj rvi et al. meta-analysis,[1] based on the criteria used for study
selection. Another study of more than 30,000 workers exposed to nickel
and nickel compounds in the production of nickel alloys[3] was published a
few months after the May, 1998 cutoff that Ojaj rvi and coworkers utilized
to establish the data base for their meta-analysis. The results from
these studies[2][3] add substantially to data used in the Ojaj rvi et al.
analysis[1]:
Table 1 Cancer risks in studies
of workers exposed to nickel and its compounds
Study
Study Type
Included in Ojaj rvi et
al.[1] ?
Pancreatic Cancer Deaths
Relative Risk*
95% Confidence Interval
Thermoelectric
Plant Workers 4]
Cohort
Yes
1
3.6
0.1 -19.9
Cadmium/Nickel
Battery Workers[5]
Cohort
Yes
3
1.7
0.3 4.9
Los Angeles
workplaces[6]
Case-control
Yes
6
1.5
0.4 5.7
Montreal workplaces[7]
Case- Control
Yes
12
2.1
1.1 3.9
Nickel mining
and smelting workers[2]
Cohort
No
12
1.3
0.7 2.3
Nickel alloy
production workers[3]
Cohort
No
131
0.9
0.8 1.1
* SMR/100 for cohort studies.
Combining the data from all of these studies with the meta-analysis
random effects model employed by Ojaj rvi et al.[1] produces a meta-risk
ratio (MRR) of 1.3 (95% CI = 0.9 - 1.9). Interestingly, the two studies
designed specifically to detect excess cancer risks associated with
occupational nickel exposure[2][3] exhibit the lowest relative risks for
pancreatic cancer and differ substantially from the MRR for nickel
exposure calculated by Ojaj rvi et al. (1.9). Moreover, the estimated
relative risk (0.9) from the study of nickel alloy workers[3] is
significantly smaller (p<_0.05 than="than" even="even" the="the" lower="lower" _95="_95" confidence="confidence" limit="limit" for="for" ojaj="ojaj" rvi="ojaj rvi" et="et" al.1="al.1" mrr="mrr" _1.2.="_1.2." p="p"/> The fact that the Ojaj rvi et al.[1] MRR for nickel-related
pancreatic cancer significantly overestimates the risk observed in a large
cohort of nickel workers indicates that the authors' meta-analysis risk
estimates should be viewed with an appropriate degree of caution. These
meta-analysis results may be significantly biased because of limitations
of the studies on which they are based. In studies that relate to nickel,
the potential for misclassification bias is strong because of the complete
confounding of nickel exposure with known carcinogenic hazards such as
cadmium,[5] or asbestos, polycyclic aromatic hydrocarbons, chromium,
beryllium, polychlorinated biphenyls, and hydrazine.[4] Similarly, the
case-control study[7] that contributed the most substantial evidence of a
nickel-related pancreatic cancer risk to the Ojavarvi et al. meta-
analysis[1] provides equally strong statistical evidence of associations
between excess pancreatic cancer and exposures to ten other substances,
some of which are likely be correlated with occupational nickel exposure.
While Ojaj rvi and coworkers are to be congratulated on their
investigation of the aetiology of pancreatic cancer, it is my opinion that
their results are most appropriately viewed as hypotheses that require
further investigation, rather than compelling evidence that links
substances to the induction of pancreatic cancer. As Ojaj rvi et al.[1]
correctly suggest, research to test these hypotheses requires large
studies and more refined measures of exposure. With respect to nickel and
nickel compounds, data from large studies that were not included in the
Ojaj rvi et al. analysis[1] call into question the veracity of a
hypothesis that links nickel exposure to increased pancreatic cancer risk.
References
1 Ojaj rvi IA, Partanen TJ, Ahlbom A, et al. Occupational exposures
and pancreatic cancer: a meta-analysis. Occ Environ Med 2000;97:316-324.
2 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, 1988; 4:277-294.
3 Arena VC, Sussman NB, Redmond CK, et al. Using alternative
comparison populations to assess occupation-related mortality risk. J Occ
Env Med 2000;40:907-916.
4 Cammarano G, Crosignani P, Berrino H, et al. Additional follow-up
of cancer mortality among workers in a thermoelectric power plant. Scand
J Work Environ Health 1986;12:631-2.
5 Andersson K, Elinder CG, Hogstedt C, et al. Mortality among
cadmium and nickel-exposed workers in a Swedish battery factory. Curr Top
Environ Toxicol Chem. 1985;8:399-408.
6 Mack TM, Peters JM, Yu MC, et al. Pancreas cancer is unrelated
to the workplace in Los Angeles. Am J Ind Med 1985;7:253-256.
7 Siemiatycki J, Risk factors for cancer in the workplace, Boca
Raton, FL: CRC Press, 1991.
Dr Loomis draws attention to the potential dangers of the rigid use
of checklists and guidelines to judge occupational and environmental
research. I agree with these sentiments, in particular the concerns about
the increasing number of papers that use compliance with these guidelines
as a justification for conclusions regarding causality. There is, however,
one rapidly expanding area of research that...
Dr Loomis draws attention to the potential dangers of the rigid use
of checklists and guidelines to judge occupational and environmental
research. I agree with these sentiments, in particular the concerns about
the increasing number of papers that use compliance with these guidelines
as a justification for conclusions regarding causality. There is, however,
one rapidly expanding area of research that would benefit from the
development of minimum standards for presentation of results. This is the
field of epidemiological meta-analysis, in which data are generally
abstracted from published papers. Difficulties can arise in deriving a
common set of definitions for variables. For example, in a meta-analysis
of oral contraceptive use and breast cancer risk,[1] 42 different
categorisations of duration of oral contraceptive use were published in
the 24 papers analysed for this variable. Debate within the scientific
community is needed to decide categorisations that are most useful.
Editors could then encourage authors either to use these in their papers
or at least be prepared to make them available on request.
Reference
1. Rushton L, Jones DR. Oral contraceptive use and breast cancer
risk: a meta-analysis of variations with age at diagnosis, parity and
total duration of oral contraceptive use. Br J Obs Gyn 1992;99:239-246.
Editor,
Rushton's recent article on the reporting of occupational and environmental research raises a number of useful points that all researchers would do well to remember when writing up epidemiological findings for publication. Without expressly intending to do so, however, the article also emphasizes the hazards of establishing formal criteria or
checklists for the evaluation of scientific work. Good epi...
Editor,
Rushton's recent article on the reporting of occupational and environmental research raises a number of useful points that all researchers would do well to remember when writing up epidemiological findings for publication. Without expressly intending to do so, however, the article also emphasizes the hazards of establishing formal criteria or
checklists for the evaluation of scientific work. Good epidemiological practices certainly exist, but one of the pitfalls inherent in attempts to codify them is that, by their nature, lists of the features of "good"
research tend to impose a "one size fits all" standard, which - like clothing of the same description - fits nothing particularly well.
The prospect of developing formal guidelines for reporting analyses based on multivariable models illustrates the difficulties. Science involves many kinds of activities, but the significant advances come about through the creative application of human intellect, rather than by rote
repetition of the familiar. Like other aspects of science, epidemiological data analysis blends attention to factual detail with creativity, intuition, judgement and even aesthetics. From the initial choice of model
form to the final specification of covariates and interaction terms, there may be many reasonable ways to model a given data set. Researchers should
be at liberty to analyze their data according to their individual scientific insights. In subsequent evaluations of methods and results, reviewers likewise should be encouraged to apply their scientific judgement, rather than following a recipe.
The opportunity cost involved in demonstrating compliance with guidelines for good practice may also be considerable, as Rushton suggests. Between the growing fear of litigation and mounting demands for accountability, especially in the United States, epidemiologists may
soon spend more time documenting adherence to protocol than doing science.
My particular fear, however, is that guidelines will be used to assail sound research on the grounds that it fails to comply with supposed standards of good science. The misuse of Bradford Hill's ideas about causality illustrates the danger. Hill intended his suggestions as an aid
to researchers, not as evaluative standards for critics; he wrote: "I do not believe...that we can usefully lay down some hard-and-fact rules of evidence that must be obeyed before we accept cause and effect. None of my nine viewpoints ... can be required as a sine qua non. What they can do, with greater or less strength, is help us to make up our minds on the fundamental question." [1] Yet, Hill's ideas are frequently presented as criteria that must be fulfilled for a study's evidence to be accepted.[2]
The involvement of such obviously self-interested groups as the Chemical Manufacturers Association in promoting "good epidemiological practices" makes the potential misuse of guidelines to suppress good research seem all too likely.
I do not mean to suggest that all epidemiological research should be published or accepted at face value, far from it. There will always be a need for review to ensure the quality of published work and to protect the public from policies based on unsound science. I am convinced, however,
that peer review coupled with the opportunity for criticism and debate in the open literature provide the best pathway to this goal. In contrast with standardized criteria, these processes allow multiple, independent readers' perspectives concerning the methodological quality, and the substantive importance of research to be heard. As a result, they reduce
the chances that unconventional but valuable views will be suppressed or that an interested group could gain control over the process for their own purposes.
References
1. Hill AB. The environment and disease: association or causation? Proc R Soc Med 1965;58:295-300.
2. Gamble JF. PM2.5 and mortality in long-term prospective cohort studies: cause-effect or statistical association? Environ Health Perspect 1998;106:535-549.
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...
Editor
Chronic hand vibration exposure is now a well-described cause of Raynaud's phenomenon. According to Palmer et al, it is estimated that 220,000 cases of Raynaud's phenomenon are attributable to vibration exposure in Great Britain.[1] These epidemiological data, based on a questionnaire, are considered reasonably accurate.[2] About 4.2 million workers are exposed to hand transmitted vibration but the real...
Editor
A meta-analysis that was recently published in this journal[1] suggested an association between excess pancreatic cancer risk and exposure to nickel and nickel compounds (meta-risk ratio = 1.9, 95% CI = 1.2 - 3.2, based on 4 studies). Through correspondence with the authors (Ojaj rvi et al.), I learned that their analysis excluded the many epidemiological studies that had been conducted on workers in the...
Dear Editor
Dr Loomis draws attention to the potential dangers of the rigid use of checklists and guidelines to judge occupational and environmental research. I agree with these sentiments, in particular the concerns about the increasing number of papers that use compliance with these guidelines as a justification for conclusions regarding causality. There is, however, one rapidly expanding area of research that...
Editor,
Rushton's recent article on the reporting of occupational and environmental research raises a number of useful points that all researchers would do well to remember when writing up epidemiological findings for publication. Without expressly intending to do so, however, the article also emphasizes the hazards of establishing formal criteria or checklists for the evaluation of scientific work. Good epi...
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