The systematic review of factors associated with the Work Ability
Index raises significant questions about this measure. The paper repeats
the assertion that "the bases for work ability are health and functional
capacity, but work ability is also determined by professional knowledge
and competence (skills), values, attitudes, and motivation, and work
itself." Certainly clinicians are constantly asked to assess the health...
The systematic review of factors associated with the Work Ability
Index raises significant questions about this measure. The paper repeats
the assertion that "the bases for work ability are health and functional
capacity, but work ability is also determined by professional knowledge
and competence (skills), values, attitudes, and motivation, and work
itself." Certainly clinicians are constantly asked to assess the health
and functional components of an individual's work related problems and
help with this aspect of assessment is welcome. However, as table 6
succinctly demonstrates, the WAI shows consistent null associations with
three of the four health and functional capacity constructs -
cardiorespiratory fitness, "mental performance" and poor balance. Whilst
some of these may reflect type 2 errors in the initial studies from the
ORs quoted in the table this is concerning if the WAI is to be used across
a range of health conditions. The results of intervention studies, which
appear to be detected as positive only in those interventions with
physical function components, may reflect a lack of responsiveness of the
instrument to other interventions targetting improvements in, for example,
mental health. In summary this review suggests that the WAI should be used
with caution outside samples of people with musculoskeletal disorders and
that more robust psychometric data be produced in other groups.
The comment by the authors about the computer code IREP used by
NIOSH, namely: “IREP includes a DDREF, which lowers the probability of
causation [PC] for low-dose-rate exposures,” has the potential to be
misinterpreted. IREP contains two discrete DDREF distributions, one for
most solid cancers and another, more restricted, distribution for thyroid
and female breast cancers. The first mentioned, with values of DDREF
rang...
The comment by the authors about the computer code IREP used by
NIOSH, namely: “IREP includes a DDREF, which lowers the probability of
causation [PC] for low-dose-rate exposures,” has the potential to be
misinterpreted. IREP contains two discrete DDREF distributions, one for
most solid cancers and another, more restricted, distribution for thyroid
and female breast cancers. The first mentioned, with values of DDREF
ranging from 0.5 to 5, is most comparable to the inverse of the risk ratio
calculated by Jacob et al.
The IREP-based PC depends on the value selected from this
distribution. To be correct, the PC is never lowered by the DDREF for any
U.S. radiation worker whose claim for compensation is evaluated using
IREP. This is because the 99th percentile of PC is used in making
compensation decisions, unlike the U.K. compensation scheme in which the
50th percentile estimate is used.
In the U.S., values from the lower end of the DDREF distribution
(i.e., <1, which corresponds to a risk ratio >1 in the authors’
parlance) drive PC estimates at the 99th percentile. Thus, the effective
“risk ratio” produced by the DDREF in IREP as it is currently used in
making compensation decisions is influenced by values greater than 1,
which is consistent with current uncertainties in DDREF. This differs from
the approach used in the U.K., which does currently not allow for risk
ratios greater than 1. [jrt@senes.com]
Authors
Craig Steinmaus1, 2
Allan H Smith1
Martyn T Smith1
Authors affiliations
1. School of Public Health, University of California, Berkeley, University
Hall, Berkeley, CA 94720-7360, USA
2. Office of Environmental Health Hazard Assessment, California
Environmental Protection Agency, 1515 Clay St., Oakland, CA 94612
Corresponding author
Craig Steinmaus, School of Publ...
Authors
Craig Steinmaus1, 2
Allan H Smith1
Martyn T Smith1
Authors affiliations
1. School of Public Health, University of California, Berkeley, University
Hall, Berkeley, CA 94720-7360, USA
2. Office of Environmental Health Hazard Assessment, California
Environmental Protection Agency, 1515 Clay St., Oakland, CA 94612
Corresponding author
Craig Steinmaus, School of Public Health, University of California,
Berkeley, University Hall, Berkeley, CA 94720-7360, USA e-mail:
craigs@berkeley.edu
Sir,
The differences in methods between our meta-analysis and that of Swaen et
al. did not “vastly alter” our most important finding or change our
overall conclusion.1,2 Our major conclusion was that evidence of an
association between benzene and non-Hodgkin lymphoma (NHL) could be found
when analyses were focused on results from highly exposed workers and were
appropriately adjusted for the healthy worker effect. In their analysis of
high exposure benzene studies, Swaen et al. implemented a series of
differences in the data used from the studies compared to our own. But
despite the fact that every single one of their major changes resulted in
a lowering of the summary relative risk, Swaen et al. also found a
statistically significant elevated relative risk in the high exposure
studies (RR = 1.33 (95% CI, 1.02-1.74)), just as we did. Even after they
adjusted for heterogeneity, the relative risk remained statistically
significant if correctly estimated. The one-sided p-value after this
adjustment can be estimated from their confidence interval to be 0.03.
Since our a priori hypothesis was that benzene increases, not decreases,
the risk of NHL, a one-tailed p-value is clearly most appropriate here.
The Swaen et al. use of the all-cancer standardized mortality ratio
(SMR) to adjust for the healthy worker effect assumes that benzene or any
of the other agents that the benzene-exposed workers are exposed to will
not cause any other cancer type. However, benzene is a well known cause of
leukemia and risks of this cancer were elevated in many of the studies
used in our meta-analyses. Relative risks of other cancers such as lung
cancer and mesothelioma were also elevated in some of the studies,
probably due to co-exposures like asbestos that can commonly occur with
benzene. Because of these increases in other cancers, the use of the all-
cancer SMR probably biased the Swaen et al. summary relative risks towards
the null. Without this bias, the Swaen et al. summary relative risks would
have been higher than they reported and even more similar to our results
than they already are. In any case, as we noted above, using different
data and different methods, Swaen et al. have produced additional evidence
that benzene increases the overall risk of non-Hodgkin lymphoma in the
available studies to date in a manner which is unlikely to be due to
chance.
References
1. Steinmaus C, Smith AH, Jones RM, Smith MT. Meta-analysis of benzene
exposure and non-Hodgkin lymphoma: biases could mask an important
association. Occup Environ Med 2008; 65:371-8.
2. Swaen GMH, Tsai SP, Burns C. Meta-analysis on benzene exposure and non
Hodgkin lymphoma (Letter to Editor). Occup Environ Med:TBD
Copyright
The Corresponding Author has the right to grant on behalf of all authors
and does grant on behalf of all authors, an exclusive license (or non-
exclusive for government employees) on a worldwide basis to the BMJ
Publishing Group Ltd and its Licensees to permit this article to be
published in Occupational and Environmental Medicine editions and any
other BMJPGL products to exploit all subsidiary rights, as set out in our
license.
Meta-analysis on benzene exposure and non Hodgkin lymphoma
June 30 2009
Gerard M H Swaen1
Shan P. Tsai2
Carol Burns1
1 Department of Epidemiology, The Dow Chemical Company, Midland,
Michigan USA.
2 Shell Health, Shell Oil Company, Houston Texas, USA.
Corresponding Author: Gerard M H Swaen, The Dow Chemical Company,
P.O. Box 444, 4530 AK Terneuzen, The Netherlands 31-(0)43-3626042. E-
mail: gswaen@dow.com
Sir,
A recent meta-analysis on benzene exposure and non Hodgkin lymphoma (NHL)
concluded that the reviewed epidemiological studies provide “new evidence
that benzene causes NHL.” 1 The meta-analysis conducted by Steinmaus et al
differed from the others in several aspects. Firstly, it selected
subgroups with the highest putative exposure to avoid dilution. Secondly,
cohort studies were adjusted for the Healthy Worker Effect (HWE) by
considering the NHL deaths as cases and all other deaths as controls. A
HWE for cancer endpoints is small if any, compared to non cancer
endpoints.2. The results from a meta-analysis of 150 occupational cohort
studies suggest that HWE adjustment may artificially inflate the true RR
for cancer endpoints. 3 Thirdly, outdated cohort study results were used
instead of more recent updates. Fourthly, Steinmaus et al did not
consistently apply their own selection criteria.
We have re-analyzed the Steinmaus et al meta-analysis by precisely
applying their inclusion and exclusion criteria. These include selecting
the highest exposure category relative risk (RR), selecting cancer
incidence versus mortality data and we used the most recent results from
cohort updates whenever available. To maintain consistency, we adjusted
the RR estimates for the HWE by using the all cancer SMR of the selected
sub cohort instead of the all mortality SMR. Herein we present only a
summary table of results. Additional comparative tables are available
upon request.
There were 16 case-control studies included in the Steinmaus et al.
review. We excluded the study by Dryver since it provided no odds ratio
(OR) for benzene exclusively. For the Fabbro-Peray et al. study,
Steinmaus et al selected the OR of those with over 810 days of exposure.
However, we used the subcategory with exposure duration of over 15 years
since it represents the group with longer exposure. For the study by
Schnatter et al the OR for the highest intensity was 0 and Steinmaus et al
selected the OR for the second highest exposure intensity group. We
combined the highest and the second highest exposure intensity groups
(OR=0.49 95% CI: 0.10-2.32). The revised meta-OR for the 15 case-control
studies was 1.17 (95% CI 0.96 – 1.44) (see Table 1).
For the six non refinery cohort studies, we observed inconsistencies
in the authors’ use of the selection sequence. For the Bloemen study, the
longest duration RR was used by Steinmaus et al. although RRs by
cumulative exposure were given. We combined the two cumulative exposure
categories into one category of 28.3+ ppm-years (SMR=0.63 95% CI: 0.08-
2.28). For the Rinsky study, we selected the RR for men (1.00), assuming
that the men were higher exposed, since the jobs with benzene exposure
were generally done by men. Lastly, for Wong et al. the RR for highest
cumulative exposure was replaced with that for highest intensity exposure.
The revised meta-RR for these non-refinery studies was 1.13 (95% CI: 0.80-
1.61) and a meta-RR of 1.05 (95% CI: 0.75-1.47) after adjusting for the
HWE.
In the meta-analysis of the refinery studies, as per the
recommendations of Steinmaus et al., cancer incidence data were selected
if both incidence and mortality were reported. There were two refineries
included in the 1993 study published by Tsai, et al, and the combined
results were used instead of selecting only one of the refineries.
Additionally, we used the combined results from maintenance and process
workers for the study conducted at the Beaumont refinery by Wong since it
is unclear that process workers were more exposed. We selected results
based on the longer duration of work for the study by Pukkala et al,
following the Steinmaus et al. hierarchy. We used the updated data for
the following refinery studies (Sorahan, Thomas and Tsai et al, 1996) 4
5 6. In the update by Tsai and colleagues NHL was listed as one of the
specific disease categories, replacing reticulosarcoma used in the 1996
paper. We selected the updated RR although the longest duration of
employment was shorter. 7 The revised meta-RR for the 21 refinery studies
was 1.00 (95% CI: 0.89-1.12) and 1.06 (95% CI: 0.95-1.18) after adjusting
for the HWE. All the models gave similar results and we only present those
of the fixed model.
All of the meta-RRs calculated in the re-analysis were less than
those reported by Steinmaus et al and most were close to unity. The only
meta-RR that remained statistically significant was that for the high
exposure non refinery studies, consisting of four cohort studies and nine
case-control studies (meta-RR of 1.33, 95% CI: 1.02-1.74), for which
exposure was largely based on self-reported data. The statistical
significance of this meta-RR was lost after adjustment for the
heterogeneity effect (95% CI: 0.99-1.80).
The re-analysis shows that the differences of the applied analytical
methods and relative risks selected can vastly alter the overall meta-
relative risk. The re-analyzed evidence provides little if any support for
an association between benzene exposure and NHL.
Gerard M H Swaen1, Shan P. Tsai2 Carol Burns1. 1 Department of
Epidemiology, The Dow Chemical Company, Midland, Michigan USA.
2 Shell Health, Shell Oil Company, Houston Texas, USA.
Table 1 Summary results of the meta-analysis on benzene exposure and
NHL and for refinery workers and NHL, comparing the results by Steinmaus
et al to our findings (fixed models, other models gave similar results)).
N RR as in Steinmaus RR in the re-analysis
Benzene and NHL
All studies 22 1.22 (1.03-1.46) 1.16 (0.97-1.38)
Case control studies 16 1.23 (1.00-1.50) 1.17 (0.96-1.44)
All high exposure studies 13 1.49 (1.15-1.92) 1.33 (1.02-1.74)1
HWE adjusted cohort studies 6 1.22 (0.89-1.67 1.05 (0.75-1.47)
Refinery work and NHL
All studies 21 1.21 (1.06-1.38) 1.00 (0.89-1.12)
High exposure studies 14 1.30 (1.04-1.62) 1.07 (0.87-1.31)
HWE adjusted all studies 21 1.42 (1.25-1.62) 1.06 (0.95-1.18)
HWE adjusted high exposure studies 14 1.51 (1.22-1.88) 1.20 (0.99-
1.47)
1 statistical significance was lost after adjustment for heterogeneity
(95% CI: 0.99-1.80)
References
1. Steinmaus C, Smith AH, Jones RM, Smith MT. Meta-analysis of
benzene exposure and non-Hodgkin lymphoma: biases could mask an important
association. Occup Environ Med 2008;65(6):371-8.
2. Li CY, Sung FC. A review of the healthy worker effect in
occupational epidemiology. Occup Med (Lond) 1999;49(4):225-9.
3. Greenberg RS, Mandel JS, Pastides H, Britton NL, Rudenko L, Starr
TB. A meta-analysis of cohort studies describing mortality and cancer
incidence among chemical workers in the United States and western Europe.
Epidemiology 2001;12(6):727-40.
4. Sorahan T. Mortality of UK oil refinery and petroleum distribution
workers, 1951-2003. Occup Med (Lond) 2007;57(3):177-85.
5. Dement JM, Hensley L, Kieding S, Lipscomb H. Proportionate
mortality among union members employed at three Texas refineries. Am J Ind
Med 1998;33(4):327-40.>
6. Tsai SP, Ahmed FS, Wendt JK, Foster DE, Donnelly RP, Strawmyer TR.
A 56-year mortality follow-up of Texas petroleum refinery and chemical
employees, 1948-2003. J Occup Environ Med 2007;49(5):557-67.
7. Tsai SP, Chen VW, Fox EE, Wendt JK, Cheng Wu X, Foster DE, et al.
Cancer incidence among refinery and petrochemical employees in Louisiana,
1983-1999. Ann Epidemiol 2004;14(9):722-30.
Licence Statement:
The Corresponding author has the right to grant on behalf of all authors
and does grant on behalf of all authors, an exclusive licence on a
worldwide basis to the BMJ Publishing Group Ltd to permit this article (if
accepted) to be published in OEM and any other BMJPGL products and
sublicences such use and exploit all subsidiary rights, as set out in our
licence
Mortality among British asbestos workers undergoing regular medical examinations (1971-2005). Occup Environ Med 2009; 66: 487-95.
Bengt Sjögren, MD, PhD
Work Environment Toxicology
Institute of Environmental Medicine
Karolinska Institutet
P.O. Box 210
SE-171 77 Stockholm
Sweden
Tel +46 8 524 822 29
Fax +46 8 31 41 24
E-mail Bengt.Sjogren@ki.se
Mortality among British asbestos workers undergoing regular medical examinations (1971-2005). Occup Environ Med 2009; 66: 487-95.
Bengt Sjögren, MD, PhD
Work Environment Toxicology
Institute of Environmental Medicine
Karolinska Institutet
P.O. Box 210
SE-171 77 Stockholm
Sweden
Tel +46 8 524 822 29
Fax +46 8 31 41 24
E-mail Bengt.Sjogren@ki.se
Anne-Helen Harding and coworkers1 presented mortality data from 98117 asbestos-exposed workers and increased mortality due to ischaemic heart disease (IHD), SMR 1.40 (95% CI 1.36-1.44). There are good arguments for further scrutinizing this observation.
Today it is rather established that inhalation of urban air pollutants are associated with increases in mortality and morbidity due to cardiovascular disease. This was observed in short-term, cohort and intervention studies and effects were seen at low concentrations.2
Whether inhalation of asbestos fibers can cause IHD is today an unsolved question. Some studies show a relationship between asbestos exposure and IHD.
A cohort of 3072 white male textile workers exposed to chrysotile was followed through 2001. An increased risk of ischemic heart disease was observed (SMR 1.20, 95%CI 1.10 – 1.32).3
A cohort of about 11000 men employed in the chrysotile mines and mills of Quebec was followed until 1988. IHD was more common among those exposed to 300 or more million particles per cubic foot x years (SMR 1.24) compared with those exposed to less than 30 (SMR 0.92).4
Non-smoking patients with asbestosis were compared with healthy controls. The asbestosis patients had significantly increased serum levels of inflammatory markers.5 During the last decade these markers of inflammation have emerged as risk factors for IHD. A general hypothesis about exposure to inhaled air pollutants and the occurrence of IHD can be expressed in the following way. Inhalation of particles will create a low grade inflammation associated with an increase in plasma fibrinogen and other blood clotting agents. A higher concentration of these agents will increase the likelihood for blood clotting and thereby the risk for myocardial infarction and IHD. 2
I hope these arguments will encourage Harding and coworkers to further explore the relationship between asbestos exposure and the occurrence of IHD in internal analysis.
Literature
1. Harding A-H, Darnton A, Wegerdt J, McElvenny D. Mortality among British asbestos workers undergoing regular medical examinations (1971-2005). Occup Environ Med 2009; 66: 487-95.
2. Sjögren B. Occupational exposure to air pollutants, inflammation and ischemic heart disease, Editorial. Scand J Work Environ Health 2004;30:421-423.
3. Hein MJ, Stayner LT, Lehman E, Dement JM. Follow-up study of chrysotile textile workers: cohort mortality and exposure-response. Occup Environ Med 2007; 64: 616-625.
4. McDonald JC, Liddell FDK, Dufresne A, McDonald AC. The 1891-1920 birth cohort of Quebec chrysotile miners and millers: mortality 1976-88. Br J Ind Med 1993;50:1073-1081.
5. Lehtonen H, Oksa P, Lehtimäki L, et al. Increased alveolar nitric oxide concentration and high levels of leukotriene B4 and 8-isoprostane in exhaled breath condensate in patients with asbestosis. Thorax 2007; 62: 602-607.
Pere Sanz-Gallén, Santiago Nogué, Eva Muñoz and Francisco Sabater*
Clinical Toxicology Unit and *Otorhinolaryngology Service. Hospital Clínic. Barcelona
Sir,
The case-control study by D' Errico et al (1) on occupational risk factors for sinonasal cancer concludes that exposure to arsenic is one such factor and suggests more cases should be reported, as there...
Pere Sanz-Gallén, Santiago Nogué, Eva Muñoz and Francisco Sabater*
Clinical Toxicology Unit and *Otorhinolaryngology Service. Hospital Clínic. Barcelona
Sir,
The case-control study by D' Errico et al (1) on occupational risk factors for sinonasal cancer concludes that exposure to arsenic is one such factor and suggests more cases should be reported, as there are only two studies at present (2,3). We contribute a new case of a worker in the glassware industry, in order to reinforce the relationship between sinonasal cancer and occupational exposure to arsenic.
A middle-aged, non-smoking patient was diagnosed more than a decade previously with squamous cell carcinoma affecting the left maxilla. The initial computed tomography (CT) scan had shown a lesion occupying the space of the left maxillary sinus that had destroyed the bone structure of the left maxilla and invaded the soft facial tissue and the pterygopalatine fossa. A CT scan more than a decade later after surgery and radiotherapy shows changes in the nasal fossa and left maxillary sinus, with a fibrotic mass of scar tissue.
The patient worked in the glassware industry for over twenty years. The main materials forming the mix introduced in the glass furnace were silica, sodium carbonate, potassium carbonate, zinc oxide and lead oxide. The dyes, which represented 0.1% of the mixture, included cadmium sulphide and oxides of cobalt, copper, chromium, manganese and nickel. One per cent of arsenic trioxide was added to the mixture to increase the transparency of the glass. An onsite workplace study showed environmental levels of chromium and nickel <3 µg/m3, but levels of arsenic of 85 µg/m3 (Threshold Limit Value: 10 µg/m3).
Although chromium and nickel oxides, known sinonasal carcinogens, are used in the glassware industry, the environmental levels found were very low. However, the levels of arsenic were very high, in agreement with the study by Battista et al in various glassware companies (3). Therefore, arsenic trioxide should be replaced by other metals and preventive measures should be introduced to minimize the health risks of workers exposed to these substances in the workplace.
References
1. d'Errico A, Pasian S, Baratti A, Zanelli R, Alfonzo S, Gilardi L et al. A case-control study on occupational risk factors for sino-nasal cancer. Occup Environ Med. Publish Ahead of Print, January 19, 2009
2. Roth F. Uber den bronchialkrebs arsengeschadigter winzer. Virchows Arch Pathol Anat 1958;331: 119-137.
3. Battista G, Bartoli D, Iaia TE, Dini F, Fiumalbi C, Ciglioli S et al. Art glassware and sinonasal cancer: report of three cases. Am J Ind Med 1996; 30: 31-35.
This informative article on the occupational wood dust exposure in
Italy requests a monitoring method for received personal doses. Such a
method exists exploiting samples obtained by nasal lavage (1). It is based
on the the chemical analysis for wood polyphenols. Although they are
species specific they are good quantitative indicators of hardwood dust
particles coarse enough to be retained in the na...
This informative article on the occupational wood dust exposure in
Italy requests a monitoring method for received personal doses. Such a
method exists exploiting samples obtained by nasal lavage (1). It is based
on the the chemical analysis for wood polyphenols. Although they are
species specific they are good quantitative indicators of hardwood dust
particles coarse enough to be retained in the nasal passages.
The wood tannins can also be analysed in the suspended dust in the
work room air. This provides the advantage that it gives an idea of
current dusts and previous materials which may not have been properly
cleaned away (2).
References
1 Mämmelä P, Tuomainen A, Vartiainen T, Lindroos L, Kangas J,
Savolainen H. Biological monitoring of wood dust exposure in nasal lavage
by high-performance liquid chromatography. J environ Monit, 2002; 4: 187-
189
2 Bianco M-A, Savolainen H. Woodworkers´ exposure to tannins. J appl
Toxicol, 1994; 14: 293-295
As described in this investigation only a minority workers with an
occupational asthma due to a diisocyanate exposure have specific IgE
antibodies towards the monomers (1).
Therefore, it is likely the host factors play an important role (2).
However, their significance may not be so firm so as to be used as
predictors of a disease. The concept is, however, important in the
workers´ compen...
As described in this investigation only a minority workers with an
occupational asthma due to a diisocyanate exposure have specific IgE
antibodies towards the monomers (1).
Therefore, it is likely the host factors play an important role (2).
However, their significance may not be so firm so as to be used as
predictors of a disease. The concept is, however, important in the
workers´ compensation cases if only those with specific antibodies or
positive provocation test results outside the work place are accepted as
valid cases.
1 Savolainen H. New mechanistic model for organic diisocyanate-
induced respiratory disease. Schweiz Med Wochenschr 1999; 129: 465-7.
2 Berode M, Jost M, Ruegger M, Savolainen H. Host factors in
occupational diisocyanate asthma: a Swiss longitudinal study. Int Arch
Occup Environ Health 2005; 158-163.
Comments on Koppelaar et al, 'Determinants of implementation of
primary preventive interventions on patient handling in healthcare: a
systematic review'. OEM 2009;66:353-360
Koppelaar et al put forward an interesting view on implementation in
their article. They state that the results of interventions will depend
not only on the effectiveness of the intervention itself but also on
appropriate implementation in...
Comments on Koppelaar et al, 'Determinants of implementation of
primary preventive interventions on patient handling in healthcare: a
systematic review'. OEM 2009;66:353-360
Koppelaar et al put forward an interesting view on implementation in
their article. They state that the results of interventions will depend
not only on the effectiveness of the intervention itself but also on
appropriate implementation in the actual work situation. However, the term
implementation and the use of the supportive reference by Groll and
Grimshaw are not used in their proper context here. The idea is that once
an intervention has been shown to be effective, it should be implemented
into health care, meaning that it should be used in 100% of the situations
in which it is appropriate. Koppelaar et al confuse this with the actual
process of the intervention in an evaluative trial. I think that these are
two different processes with different determinants. Since there is no
evidence of effectiveness of interventions that aim at preventing adverse
health effects of handling patients by healthcare workers, these
interventions should not be implemented in practice. If one would like to
improve these types of interventions in research projects, there should be
a clear idea of how the intervention works. Based on these ideas a
maximum powerful intervention can be developed and evaluated. Once proven
effective, the intervention should be implemented in health care. Also in
their review the majority of the studies cited does not have a
statistically significant positive outcome, neither is there a relation
with the outcome of the study and the 'barriers and facilitators' for
implementation.
Moreover, we would like to point out that the review does not deserve
the adjective systematic. The inclusion criteria are unclear because
there is no definition of the study designs to be included. Arbitrarily,
qualitative studies are excluded. The search is limited only to Medline
and Web of Science and it is unclear why important databases such as
Embase, Cinahl and OSHrom are not searched. There is language bias because
only studies written in English are included. Especially for
implementation, one could expect to find studies to be published in
national languages. Even though it is an objective to assess the influence
of barriers and facilitators on the effectiveness of interventions, there
are no methods or results for this objective. The lack of an assessment of
study quality in combination with the inclusion of any study type makes
that the reader has no idea what the validity of the results of the
included studies is. The authors acknowledge this as a limitation of their
study in the discussion section. However, in my view, all these problems
together make it impossible to interpret the results of the review.
"The Corresponding Author has the right to grant on behalf of all
authors and does grant on behalf of all authors, an exclusive license (or
non exclusive for government employees) on a worldwide basis to the BMJ
Publishing Group Ltd and its Licensees to permit this article (if
accepted) to be published in Occupational and Environmental Medicine
editions and any other BMJPG products to exploit all subsidiary rights, as
set out in our licence
Jos Verbeek, MD PhD
Finnish Institute of Occupational Health
Cochrane Occupational Health Field
Kuopio
Finland
1. E Koppelaar, J J Knibbe, H S Miedema, A Burdorf. Determinants of
implementation of primary preventive interventions on patient handling in
healthcare: a systematic review. Occup Environ Med 2009;66:353–360.
2. Grol R, Grimshaw J. From best evidence to best practice: effective
implementation of change in patients’ care. Lancet 2003;362:1225-29.
3. Campbell M, Fitzpatrick R, Haines A, Kinmonth A, Sandercock P,
Spiegelhalter D, Tyrer P. Framework for design and evaluation of complex
interventions to improve health. BMJ 2000;321:694–6
4. Moher D, Tetzlaff J, Tricco AC, Sampson M, Altman DG. Epidemiology and
reporting characteristics of systematic reviews. PLoS Med 4(3);2007:e78.
doi:10.1371/journal.pmed.0040078
We are writing to respond to Dr.Kalman in regard to our article
entitled “Maternal Occupational Exposure and Risk of Spontaneous Abortion
in Veterinary Practice”.
Regarding the risk relating to radiation, we presented data
separately for those with 1-4 x-rays a week in Table 2. Readers are able
to use these analyses rather than those in Table 3 if they prefer. The
results for exposure...
We are writing to respond to Dr.Kalman in regard to our article
entitled “Maternal Occupational Exposure and Risk of Spontaneous Abortion
in Veterinary Practice”.
Regarding the risk relating to radiation, we presented data
separately for those with 1-4 x-rays a week in Table 2. Readers are able
to use these analyses rather than those in Table 3 if they prefer. The
results for exposure to radiation as a continuous variable are also
presented in the text for readers who require more detail (results
section, page 3, column 1, line 16).
In regard to the way data were presented, particularly regarding
exposure to waste anaesthetic gases, we suggest that this is a different
situation to the dose-response variable describing x-rays a week. We
categorized the variable surgery/gas scavenging using both two and three
categories, but in the table we used three categories in order to
disentangle the effects of surgery and waste anaesthetic gases. The
results for the variable surgery/gas scavenger using two categories were
reported in the text (results section, page 3, column 1, line 6).
This study, as documented in the abstract, only reports an increased
risk of spontaneous abortion in veterinarians who performed more than five
radiographic examinations per week. However, we suggest that it would be
wise to advise veterinarians of the possible risk due to radiation even at
low doses, particularly for young females. It has long been established
that x-rays can have harmful effects, including sterility, miscarriage,
mutagenesis and carcinogenesis and, while empirical evidence of harm is
difficult to measure at low doses, the theories of radiation and cancer
biology have to led to widespread adoption of the ALARA principle (as low
as reasonably achievable).
The systematic review of factors associated with the Work Ability Index raises significant questions about this measure. The paper repeats the assertion that "the bases for work ability are health and functional capacity, but work ability is also determined by professional knowledge and competence (skills), values, attitudes, and motivation, and work itself." Certainly clinicians are constantly asked to assess the health...
The comment by the authors about the computer code IREP used by NIOSH, namely: “IREP includes a DDREF, which lowers the probability of causation [PC] for low-dose-rate exposures,” has the potential to be misinterpreted. IREP contains two discrete DDREF distributions, one for most solid cancers and another, more restricted, distribution for thyroid and female breast cancers. The first mentioned, with values of DDREF rang...
Response to Swaen et al.
Authors Craig Steinmaus1, 2 Allan H Smith1 Martyn T Smith1
Authors affiliations 1. School of Public Health, University of California, Berkeley, University Hall, Berkeley, CA 94720-7360, USA 2. Office of Environmental Health Hazard Assessment, California Environmental Protection Agency, 1515 Clay St., Oakland, CA 94612
Corresponding author Craig Steinmaus, School of Publ...
Meta-analysis on benzene exposure and non Hodgkin lymphoma
June 30 2009
Gerard M H Swaen1 Shan P. Tsai2 Carol Burns1
1 Department of Epidemiology, The Dow Chemical Company, Midland, Michigan USA. 2 Shell Health, Shell Oil Company, Houston Texas, USA.
Corresponding Author: Gerard M H Swaen, The Dow Chemical Company, P.O. Box 444, 4530 AK Terneuzen, The Netherlands 31-(0)43-3626042. E-...
Mortality among British asbestos workers undergoing regular medical examinations (1971-2005). Occup Environ Med 2009; 66: 487-95.
Bengt Sjögren, MD, PhD Work Environment Toxicology Institute of Environmental Medicine Karolinska Institutet P.O. Box 210 SE-171 77 Stockholm Sweden Tel +46 8 524 822 29 Fax +46 8 31 41 24 E-mail Bengt.Sjogren@ki.se
Anne-Helen Harding and coworker...
Pere Sanz-Gallén, Santiago Nogué, Eva Muñoz and Francisco Sabater*
Clinical Toxicology Unit and *Otorhinolaryngology Service. Hospital Clínic. Barcelona
Sir,
The case-control study by D' Errico et al (1) on occupational risk factors for sinonasal cancer concludes that exposure to arsenic is one such factor and suggests more cases should be reported, as there...
Dear Editor,
This informative article on the occupational wood dust exposure in Italy requests a monitoring method for received personal doses. Such a method exists exploiting samples obtained by nasal lavage (1). It is based on the the chemical analysis for wood polyphenols. Although they are species specific they are good quantitative indicators of hardwood dust particles coarse enough to be retained in the na...
Dear Editor,
As described in this investigation only a minority workers with an occupational asthma due to a diisocyanate exposure have specific IgE antibodies towards the monomers (1).
Therefore, it is likely the host factors play an important role (2). However, their significance may not be so firm so as to be used as predictors of a disease. The concept is, however, important in the workers´ compen...
Comments on Koppelaar et al, 'Determinants of implementation of primary preventive interventions on patient handling in healthcare: a systematic review'. OEM 2009;66:353-360
Koppelaar et al put forward an interesting view on implementation in their article. They state that the results of interventions will depend not only on the effectiveness of the intervention itself but also on appropriate implementation in...
June 8th 2009
We are writing to respond to Dr.Kalman in regard to our article entitled “Maternal Occupational Exposure and Risk of Spontaneous Abortion in Veterinary Practice”.
Regarding the risk relating to radiation, we presented data separately for those with 1-4 x-rays a week in Table 2. Readers are able to use these analyses rather than those in Table 3 if they prefer. The results for exposure...
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