In a recent interesting research report published in your journal,
Andersen et al. [1] performed a 4-year prospective COHORT study with
yearly assessments trying to develop variables that could predict the
development of new onset neck/shoulder pain. They determined that
repetitive movements of the shoulder/arm, jobs with high demands and low
control were variables which were all independently a...
In a recent interesting research report published in your journal,
Andersen et al. [1] performed a 4-year prospective COHORT study with
yearly assessments trying to develop variables that could predict the
development of new onset neck/shoulder pain. They determined that
repetitive movements of the shoulder/arm, jobs with high demands and low
control were variables which were all independently associated with
development of neck/shoulder pain.
It is to be noted that Nahit et al.[2]
have also previously noted an association between high job demands and low
job control and development of musculoskeletal pain. Nahit et al.[2] also noted that those who perceived their work as stressful most of the
time, were more likely to report pain.[2]
From another standpoint, Fishbain et al. [3,5,6] and Rosomoff et al. [4] have examined if pre-injury job satisfaction impacts on “intent” to
return to work after pain facility treatment. In the first reports
Fishbain et al. [3] demonstrated that chronic pain patients not intending
to return to work after pain facility treatment were more likely to
complain of job dissatisfaction. In the second report from this group,
Rosomoff et al. [4] demonstrated that an association between non-intent to
return to work after pain facility treatment and pre-injury job
dissatisfaction was similarly found across Workers’ Compensation and non-
Workers’ Compensation chronic pain patients. In the third reports,
Fishbain et al. [5] looked at actual return to work after pain facility
treatment in relation to these variables. They found that actual return
to work was predicted at one month ”by intent”, perceived job stress and
job like (job dissatisfaction) plus other variables. At 36 months, return
to work was predicted by “intent” and by perceived job stress plus other
variables. In the final study, Fishbain et al. [6] attempted to predict
“intent” to return to work after pain facility treatment in relation to
actual return to work. “Intent” was predicted by perceived pre-injury job
stress plus other variables. In addition, those chronic pain patients who
intended to return and did not were predicted by whether there was a job
to go back to. Also chronic pain patients not intending to go back to work
to the pre-injury job initially, but doing so later, were predicted by
having a job to go back. Overall, this series of studies points to a
strong relationship between pre-injury work variables such as job
dissatisfaction and “intent” to return to that job after treatment. In
addition, these studies indirectly support the findings of Nahit et al.[2]
It seems that in trying to understand the low back pain injury/neck
pain injury and recovery process, it is important to take into account
work related perceptions such as those of perceived job dissatisfaction
and job stress. It is likely that some of the patients identified in
Anderson’s et al. study [1] as developing neck/shoulder pain would have
gone on to develop chronic pain. It is also likely that a significant
percentage of the patients developing chronic pain would have perceived
their pre-injury job as stressful. Thus, rehabilitation efforts with these
patients would have been difficult at best. As such, there is communality
between Anderson’s et al. findings [1] and that of Fishbain [3,5,6] and
colleagues.[4] As pointed out by Anderson et al. [1] workplace
interventions should be geared toward preventing the development of
chronic pain.
References
1. Andersen JH, Kaergaard A, Mikkelsen S, Jensen UF, Frost P, Bonde
JP, Fallentin N, Thomsen JF. Risk factors in the onsets of neck/shoulder
pain in a prospective study of workers in industrial and service
companies. Occup J Env. Med 2003;60(9):649-5.
2. Nahit ES, Pritchard CM, Cherry NM et al. The influence of work related
psychosocial factors and psychological distress on regional
musculoskeletal pain: a study of newly employed workers. J Rheumatology
2001;28:6:1378-1384.
3. Fishbain DA, Rosomoff HL, Cutler R et al. Do chronic pain patients’
perceptions about their preinjury jobs determine their intent to return to
the same type of job post-pain facility treatment? Clin J Pain 1995;11:267
-278.
4. Rosomoff HL, Fishbain DA, Cutler R et al. Do chronic pain patients’
perceptions about their preinjury jobs differ as a function of worker
compensation and non-worker compensation status? Clin J Pain 1997;12:2997-
306.
5. Fishbain DA, Cutler B, Rosomoff HL et al. The prediction of chronic
pain patient “intents,” and “discrepancy with non-intent” for return to
work post pain facility treatment. Clin J Pain 1999;15:141-150.
6. Fishbain DA, Cutler RB, Rosomoff HL, Khalil T, Steele-Rosomoff R.
Impact of chronic pain patient’s job perception variables on actual return
to work. Clin J Pain 1997;13(3):197-205.
We read with great interest the recent publication by Boers et al
(2010), in which they presented updated mortality results from an
occupational cohort of Dutch chlorophenoxy herbicide manufacturing
workers. The previous follow-up from this cohort (Hooiveld et al, 1998)
reported a statistically significant dose-related increase in mortality
from ischemic heart disease (IHD) with increasing levels of modeled TCDD
exposur...
We read with great interest the recent publication by Boers et al
(2010), in which they presented updated mortality results from an
occupational cohort of Dutch chlorophenoxy herbicide manufacturing
workers. The previous follow-up from this cohort (Hooiveld et al, 1998)
reported a statistically significant dose-related increase in mortality
from ischemic heart disease (IHD) with increasing levels of modeled TCDD
exposure. The relative risks in the medium and high TCDD exposure
categories compared to the low category were 1.5 (95% CI 0.7-3.6) and 2.3
(95% CI 1.0-5.0), respectively (Hooiveld et al, 1998). The earlier study
was cited in our recent literature review of cardiovascular disease
mortality in relation to dioxin exposure (Humblet et al, 2008).
In the present publication (Boers et al, 2010) the authors concluded
that the observed associations between occupational exposure and IHD were
attenuated compared with those found in their previous analysis. However,
in their recent paper they did not present the updated results for IHD
from the analysis of modeled TCDD. The authors explained that they did not
use the earlier TCDD model approach because it was available only for one
of the two factories in the study, and furthermore was based on a small
number of blood samples. These considerations notwithstanding, we believe
that it would be important to provide the updated modeled TCDD results
both for IHD and all circulatory disease. At a minimum it would provide
comparability with the previous findings from their study. Furthermore,
future literature reviews on cardiovascular disease and TCDD would then be
able to include this information, providing guidance for future dioxin
risk assessments. This is especially important since the suggestion of an
increased IHD risk persisted in the updated results that were presented,
i.e. a statistically non-significant increased IHD relative risk of 1.6
(95% CI 0.72-3.55) among the workers exposed to a 1963 accidental release
of dioxins. These workers would be expected to be among the highest
exposed of all the workers.
O Humblet, R Hauser
Correspondence to: Mr. O Humblet, Department of Environmental Health,
Harvard School of Public Health, Boston, Massachusetts, USA;
ohumblet@hsph.harvard.edu
References
Boers D, Portengen L, Bueno-de-Mesquita HB, Heederik D, Vermeulen R.
Cause-specific mortality of Dutch chlorophenoxy herbicide manufacturing
workers. Occup Environ Med. 2010 Jan;67(1):24-31.
Hooiveld M, Heederik DJ, Kogevinas M, Boffetta P, Needham LL,
Patterson DG Jr, Bueno-de-Mesquita HB. Second follow-up of a Dutch cohort
occupationally exposed to phenoxy herbicides, chlorophenols, and
contaminants. Am J Epidemiol. 1998 May 1;147(9):891-901.
Humblet O, Birnbaum L, Rimm E, Mittleman MA, Hauser R. Dioxins and
cardiovascular disease mortality. Environ Health Perspect. 2008
Nov;116(11):1443-8.
Within the Introduction the authors wrongly state that 4-chloro-ortho
-toluidine is present in cigarette smoke. Whereas ortho-toluidine has been
repeatedly reported to be present in cigarette smoke, this has never been
reported for 4-chloro-ortho-toluidine. ortho-Toluidine has also been
implicated in bladder cancer in the rubber industry (Baan et al. Lancet
Oncol. 9:322-323, 2008) and this was corroborated by results of a...
Within the Introduction the authors wrongly state that 4-chloro-ortho
-toluidine is present in cigarette smoke. Whereas ortho-toluidine has been
repeatedly reported to be present in cigarette smoke, this has never been
reported for 4-chloro-ortho-toluidine. ortho-Toluidine has also been
implicated in bladder cancer in the rubber industry (Baan et al. Lancet
Oncol. 9:322-323, 2008) and this was corroborated by results of a
biomonitoring study (Ward et al. J.Natl.Cancer Inst. 88:1046-1052, 1996).
In the Discussion/Conclusion a comment on the possibility to pinpoint
possibly relevant exposure to known bladder carcinogens by biomonitoring
is missing.
A recent article by Daniels [1] in this journal presented
occupational stress data from the 15 European Union (EU) countries.
Cross-
national comparisons contribute to our scientific understanding of how and
why health-related indicators (i.e. stress) are unequally distributed
across countries and provide clues and guidelines for researchers, policy
makers and trade unions at the EU level. Howeve...
A recent article by Daniels [1] in this journal presented
occupational stress data from the 15 European Union (EU) countries.
Cross-
national comparisons contribute to our scientific understanding of how and
why health-related indicators (i.e. stress) are unequally distributed
across countries and provide clues and guidelines for researchers, policy
makers and trade unions at the EU level. However, we are concerned the
data’s strengths and limitations are not explained appropriately to inform
the policy debate. Specifically we have four concerns.
Our first concern is related to sample selection. The data were drawn
from the Third European Survey on Working Conditions (ESWC) conducted in
2000.[2] The sampling strategy was designed to obtain nationally
representative samples of the total active population, including non-
Europeans if they could be interviewed in the national language of the
country where they worked. Daniels asserted occupational stress is
socially constructed and thus used nationality to obtain a more
homogeneous sample. However, removing workers who may be experiencing the
greatest stress and hazardous working conditions from the sample may
represent a severe selection bias.[3]
The inflow of foreign workers (especially the so called low-skilled
immigrants) to the EU advanced industrial countries is increasing.[4]
Immigrant workers are becoming a significant part of the active EU
population and are likely to rise sharply with the addition of the ten new
EU countries.[5,6] Compared to native workers, non-EU nationals have
greater problems obtaining jobs.[7] They may obtain employment in
contractual jobs where exposure to work-related stressors is high.[8] It
is plausible foreign workers are more frequently employed in ‘bad’ jobs
exposed to more hazardous work environments.[9]
Furthermore, because of the ambiguity of the statement "individuals
who were working in a different country as their nationality" (i.e.
immigrants) – it is unclear who is being excluded and whether the issue of
the social construction of stress can be redressed through the exclusion.
The ESWC does not identify whether a person was born in the country of
present nationality, lived in the same country since birth with or without
the nationality of that country, or lived, or was born, elsewhere before
coming to the country of present nationality. Neither does the ESWC
provide data on when, in a life course perspective, the arrival of a
person to a country occurred which may be relevant for assimilating social
constructs by an individual. All these factors can influence health
variability and without such detailed data deductions based only on a
person’s nationality seems uncertain.
Second, information bias can affect the results.[3] By means of
principal component analyses, Daniels grouped a number of items (stress,
anxiety, irritability, sleeping problems, stomach ache, headache, or
overall fatigue) to create an "index of perceived risk from occupational
stress". However, two methodological issues have to be considered. First,
if, as Daniels argues, stress is socially constructed and thereby biased
by nationality, how can be the occupational stress index be created using
the total sample instead of only those workers who were working in the
same country as their nationality. We would agree this was the appropriate
approach if Daniels would not have argued for a social construction of
stress. Second, in the ESWC questionnaire, a filter question existed
before the selection of the symptoms that the author did not mention. Only
after replying that their work affected their health, which some 60% of
the workers did, could participants endorse any of 22 symptoms.[2] In
analyses using the same data set,[8,10,11] we found differences in
various health-related outcomes (stress, overall fatigue, job
dissatisfaction and sickness absence) by country, type of employment, and
gender.[12] So, grouping items without exploring individual symptom
variation might hide important differences.
Third, in the discussion section, Daniels stated that according to
his findings, compared to workers in higher ranked countries, British
workers and workers in other lower ranked countries may be less likely to
attribute minor or non-specific psychosomatic symptoms to work (or might
attribute them erroneously to other life domains) when consulting with
health practitioners. We are aware of no data to support such an
assertion. Hence, the findings do not support this conclusion, so we
suggest prudence in the application of these results to policy and
practice decisions.
Fourth, Daniels ranked the EU countries investigated according to the
number of stress related symptoms attributed to work. From these
differences Daniels’s made inferences about how sociocultural factors and
the role of the media can affect health perceptions. Given the concerns
expressed above abut selection and information bias we wonder how the
results led to these inferences. Furthermore, although Daniels recognised
that these processes may not apply to other EU countries, he focused
almost the entire discussion section on the UK, building an idiosyncratic
and ad hoc explanation for the UK that seems unsupported by the research.
A way to facilitate more systematic analyses could be by classifying the
countries according to certain common characteristics. In social and
policy research, different typologies have been proposed. For instance,
Esping-Andersen’s typology has proven to be useful in comparing welfare
states and may be helpful in the present study’s context.[13]
Moreover, the Daniels’ ranking is very different, and in some cases
completely inverse, than the one obtained by us when analyzing sickness
absence data from the same survey.[14] Among other factors that could
explain this divergence, it has to be considered that different outcomes
could present different between-countries distributions. Compared to
Daniels’ occupational stress index, sickness absence is recognised as a
public health surveillance measure indicating countries economic
performance.[15] Rankings are an important tool scientists can use to
communicate with policy makers. The ESWC provides a unique data source for
scientists. Differences between our work and Daniels illustrates the need
to develop mechanisms to enable researchers using the ESWC to share
results prior to publication.
Finally, we do understand that the space available for short papers
limits the author’s possibility to explain in detail all relevant issues.
However, we think that authors should give the reader as much information
as needed to judge the results validity.
References
1.Daniels K. Perceived risk from occupational stress: a survey of 15
European countries. Occup Environ Med 2004; 61: 467-70.
2.Paoli P, Merllié D. Third European Survey on Working Conditions
2000. Dublin: European Foundation for the Improvement of Living and
Working Conditions Luxembourg: Office for Official Publication of the
European Communities, 2001.
3.Szklo M, Nieto FJ. Understanding lack of validity: Bias. In: Szklo
M, Nieto FJ. Epidemiology. Beyond the Basics. Gaithersburg: Aspen
Publishers, Inc., 2000; 125-76.
4.Lowell BL, Kemper Y. Transatlantic Roundtable on Low-skilled
Migration in the Twenty-first Century: Prospects and Policies.
International Migration 2004;42(1):117-40.
5.Hilderink H, van der Gaag N, van Wissen L, Jennissen R, Román A,
Salt J, Clarke J, Pinkerton C. Analysis and forecasting of international
migration by major groups - Part III. Luxembourg: Office for Official
Publication of the European Communities, 2003.
6.Angrist JD, Kugler AD. Protective or counter-productive? Labour
market institutions and the effect of immigration on EU natives. Economic
Journal 2003; 113(488): F302-F331.
7.Thorogood D, Winqvist K. Women and men migrating to and from the
European Union. Statistics in focus 2/2003. European Communities, 2003.
8.Wrench J. Preventing Racism at the Workplace. A summary. European
Foundation for the Improvement of Living and Working Conditions.
Luxembourg: Office for Official Publications of the European Communities,
1996.
9.Benach J, Gimeno D, Benavides FG. Employment status and health.
Dublin: European Foundation for the Improvement of Living and Working
Conditions. Luxembourg: Office for Official Publication of the European
Communities, 2002.
10.Benach J, Gimeno D, Benavides FG, Martínez JM, Torné MM. Types of
employment and health in the European Union: changes from 1995 to 2000.
Eur J Public Health (in press).
11.Gimeno D, Benavides FG, Amick III BC, Benach J, Martínez JM.
Psychosocial factors and work-related sickness absence among permanent and
non-permanent employment. J Epidemiol Community Health (in press).
12.Karjalainen A (Coordinator). Work and health in the EU. A
statistical portrait. Data 1994–2002. Luxembourg: Office for Official
Publication of the European Communities, 2004.
13.Esping-Andersen G. The three worlds of welfare capitalism.
Princeton (NJ): Princeton University Press, 1990.
14.Gimeno D, Benavides FG, Benach J, Amick III BC. Distribution of
sickness absence in the European Union countries Occup Environ Med (in
press).
15.Kivimaki M, Head J, Ferrie JE, Shipley MJ, Vahtera J, Marmot MG.
Sickness absence as a global measure of health: evidence from mortality in
the Whitehall II prospective cohort study. BMJ 2003 16;327:364-9.
Considering the temporal association between exposure to benzene and
the later development of leukaemia it is questionable if this phenomena is
also true for NHL.1 From several independent epidemiologic studies with
consistent findings it can be concluded, that 10 to 15 years after
exposure to benzene has been stopped, the risk of leukaemia is
significantly less or even absent.2,3,4
Considering the temporal association between exposure to benzene and
the later development of leukaemia it is questionable if this phenomena is
also true for NHL.1 From several independent epidemiologic studies with
consistent findings it can be concluded, that 10 to 15 years after
exposure to benzene has been stopped, the risk of leukaemia is
significantly less or even absent.2,3,4
Assuming that the underlying mechanism for leukaemia and NHL is the
same, it would be important to use the large database of the "Epilymph
study" to analyze the temporal pattern between exposure and disease.
The study found increased risks for chronic lymphocytic leukaemia
after exposure to toluene and xylene. A benzene exposure was excluded.
These statistical associations must be discussed with respect to the
genotoxicologic evidence of these aromatic hydro-carbons. Compared to
benzene, toluene and xylene have not been proven as human carcinogens. The
IARC Working Group concluded in 1999, that there is inadequate evidence in
humans for the carcinogenicity of toluene and xylenes.5 Therefore the
associations must be interpreted with caution and do not support
causality.
Literature:
1. Triebig G. Implications of latency period between benzene exposure and
development of leukemia - a synopis of literature. Chem Biol Interact
2010; 184: 26-29.
2. Hayes RB, Song-Nian Yin, Dosemeci M. Benzene and the dose related
incidence of hematologic neoplasm in China. J Natl Cancer Inst 1997; 89:
1065-1071.
3. Finkelstein MM. Leukemia after exposure to benzene: temporal trends and
implications for standards. Am J Ind Med 2000; 38: 1-7.
4. Glass DC, Sim MR, Fritschi L, Gray CN, Jolley DJ, Gibbons CG. Letter to
the editor. Leukemia risk and relvant benzene exposure period. Am J Ind
Med 2002; 42:481-489
5. IARC Monographs on the evaluation of carcinogenic risks to humans. Re-
evaluation of Some Organic Chemicals, Hydrazine and Hydrogen Peroxide.
Volume 71, Part two (Toluene) and Part three (Xylene). World Health
Organization International Agency for Research on Cancer, 1999
Correspondence to:
Prof. Dr. G. Triebig, M.D., M.Sc.
Institute and Outpatient Clinic for
Occupational and Social Medicine
University of Heidelberg
Vossstr. 2
D-69115 Heidelberg
Germany
Tel.: ( 49) 6221 56 51 01
Fax: ( 49) 6221 56 29 91
Email: GTriebig@med.uni-heidelberg.de
In a recent short report, a summary of the results of a
workplace based colorectal tumour-screening programme in UK was given.[1]
During 2001-02 we organised a similar programme within BASF's – the
world's largest chemical company – Ludwigshafen/Germany site. Our findings
were published in a German language paper.[2] Our target group included all
13 265 actively working employees aged 45 years or above. Those exp...
In a recent short report, a summary of the results of a
workplace based colorectal tumour-screening programme in UK was given.[1]
During 2001-02 we organised a similar programme within BASF's – the
world's largest chemical company – Ludwigshafen/Germany site. Our findings
were published in a German language paper.[2] Our target group included all
13 265 actively working employees aged 45 years or above. Those expressing
interest were given a standardised questionnaire concerning risk factors
for colorectal cancer and a test for occult faecal blood (FOBT). If the
test was positive and/or a positive answer was given to the question on
blood in the stool or on a positive family history, colonoscopy – to be
arranged via the general practitioner – was advised, in line with the
recommendations of the German Society of Digestive and Metabolic Diseases.
Finally, 3732 employees (337 women, 3395 men; mean age 52 years) had
completed the questionnaire and the FOBT results were available (28 % of
the target group). Colonoscopy was recommended to 688 employees, 323 of
whom (47 %) underwent the investigation. Nine of the subjects already had
manifest cancer, six of them in the early stage T1 or T2. Adenomatous
polyps were found in an additional 61 and subsequently excised.
Cost-benefit calculations were done in a twofold manner: at company
level and at public-health system level. The financial cost of screening
at company level was € 108 000 (testing kits plus office materials € 6000,
staff costs € 102 000). Based on the employer's obligation in Germany to
compensate disease-related lost work time during the first six weeks a
benefit due to avoided lost work time was calculated to be 1 110 000 (cost
-benefit ratio 1:10). The financial cost of the programme at public-health
system level was € 50 000 (specialist visit, colonoscopy plus removal of
adenoma). The benefit was calculated to be € 700 000 by avoided hospital
stay and surgery (cost-benefit ratio 1:14). In the future our workplace
based programme will be offered routinely.
References
(1) ECHO: Workplace based faecal occult blood screening. Occup Environ
Med 2004; 61,413
(2) Webendörfer S, Messerer P, Eberle F et al. Darmkrebs-Vorsorge im
Betrieb. Dtsch Med Wochenschr 2004; 129: 239-243
In his letter, Predicting chemicals causing cancer in animals as
human carcinogens (Occup Environ Med 2010;67:720), Huff surprisingly finds
opportunity to promote long-term carcinogenesis bioassays using animals in
response to an editorial by Suarthana et al (Occup Environ Med
2009;66:713e14), Predicting occupational diseases. In their editorial,
Suarthana et al generalize from the development of diagnostic models to
pred...
In his letter, Predicting chemicals causing cancer in animals as
human carcinogens (Occup Environ Med 2010;67:720), Huff surprisingly finds
opportunity to promote long-term carcinogenesis bioassays using animals in
response to an editorial by Suarthana et al (Occup Environ Med
2009;66:713e14), Predicting occupational diseases. In their editorial,
Suarthana et al generalize from the development of diagnostic models to
predict sensitisation to occupational allergens. Suarthana et al mention
no animal studies and conclude that "[t]here is now an opportunity to
develop prediction models for diverse occupational diseases, especially
given the existing large epidemiological studies."
Huff asserts that "findings from independently conducted bioassays on
the same chemicals are consistent[.]" In fact, a comparison of 121
bioassays from the U.S. National Toxicology Program (NTP) database with
those in the published scientific literature found that the studies
produced consistent results only 57 percent of the time.[1] Huff also
claims that "less than10% of all chemicals if evaluated in bioassays would
be predicted to be carcinogenic." In our analysis of more than 500 NTP
bioassays, we show that more than half of the substances evaluated
produced evidence of carcinogenicity in at least one group of animals.[2]
The high false positive rate is thought to be an indirect effect of
increased cell proliferation in response to cell injury and death caused
by the near toxic doses of test substances used.[3] Huff observes that
there are more similarities than differences between rodents and humans.
However, well-characterized species-specific modes of action not operating
in humans also contribute to the high rate of false positives.[4]
The time has come for antiquated animal tests like the bioassay to be
abandoned in favor of modern, human-relevant methods such as the
epidemiological studies recommended in Suarthana et al's editorial, high-
throughput in vitro methods, and computational toxicology.
[1] Gottmann E, Kramer S, Pfahringer B, et al. Data quality in
predictive toxicology: reproducibility of rodent carcinogenicity
experiments. Environ Health Perspect 2001;109:509-14.
[2] PETA. Wasted money, wasted lives: A layperson's guide to the
problems with rodent cancer studies and the National Toxicology Program.
Norfolk, VA: People for the Ethical Treatment of Animals. 2006.
http://www.mediapeta.com/peta/pdf/Wasted-money-PDF.pdf (accessed 17 Sept
2010).
[3] Gaylor DW. Are tumor incidence rates from chronic bioassays
telling us what we need to know about carcinogens? Regul Toxicol Pharmacol
2005;41:128-33.
[4] Cohen SM. Human carcinogenic risk evaluation: an alternative
approach to the two-year rodent bioassay. Toxicol Sci 2004;80:225-9.
Conflict of Interest:
Conflict of Interest:
The author is employed by People for the Ethical Treatment of Animals.
Atkinson et al,[1] reported “particularly among those monitored for
plutonium exposure there was a significant excess mortality from cancer of
the pleura”.
However, they also note the lack of a trend for radiation
dose. The authors’ suggest that these cancers are mostly mesothelioma and
that asbestos is the likely causative agent. There is no mention of other
agents that can cause mesothe...
Atkinson et al,[1] reported “particularly among those monitored for
plutonium exposure there was a significant excess mortality from cancer of
the pleura”.
However, they also note the lack of a trend for radiation
dose. The authors’ suggest that these cancers are mostly mesothelioma and
that asbestos is the likely causative agent. There is no mention of other
agents that can cause mesothelioma; although they elude to other causes
(“…are strongly related to exposure to asbestos.”). I would like to point
out that others [2-4] reported ionizing radiation as a possible aetiological
agent for mesothelioma. This appears to include a case4 involving short-
term ionizing radiation exposure. In addition, mesothelioma appears to be
caused by a number of other agents (e.g. sugar cane, viruses)[5,6] besides
asbestos and radiation. It has been suggested that non-asbestos causes of
mesothelioma may be as high as 87%,[7] although a lower percent has been
reported (around 13%).[8] Readers need to be aware that there appears to be
many agents, including spontaneous events5, which may be responsible for
cases of pleural cancer (mesothelioma).
References
1. Atkinson WD., Law DV., Bromley KJ., Inskip HM. Mortality of
employees of the United Kingdom atomic energy authority, 1946-87. Occup
Environ Med. 2004; 61:577-85.
2. Lerman Y, Learman Y, Schachter P, Herceg B, Lieberman Y, Yellin A.
Radiation associated malignant pleural mesothelioma. Thorax. 1991;46:463-
4.
3. Hoffman J, Mintzer D, Warhol MJ. Malignant mesothelioma following
radiation therapy. Am J Med. 1994;94:379-92.
4. Mizuki M, Yukishige K, Abe Y, Tsuda T. A case of malignant pleural
mesothelioma following exposure to atomic radiation in Nagasaki.
Respirology. 1997;2:201-5.
5. Hubbard R. The aethiology of mesothelioma: are risk factors other
than asbestos exposure important? Thorax 1997;52:406-7.
6. Lange JH. Other non asbestos causes of mesothelioma besides the
SV40 virus. (eletter) Thorax. 2004;
http://thorax.bmjjournals.com/cgi/eletters/57/4/353#161
7. Peterson JT, Greenberg SD, Buffler PA. (1984) Non-asbestos-related
malignant mesothelioma: a review. Cancer 54:951-60.
8. Yates DH, Corrin B, Stidolph PN, Browne K. Malignant mesothelioma
in south east England: clincopathological experience of 272 cases. Thorax
1997:52:507-12.
We thank Dr Triebig for his interesting comments on our article ââ¬ÅOccupational exposure to solvents and risk of lymphoma subtypes: results from the Epilymph case-control studyââ¬ï¿½.1,2 Epidemiological evidence is growing about the various etiological factors of specific lymphoma subtypes, and perhaps the different mechanisms involved.3 In our paper, we referred to previous reports suggesting an interaction o...
We thank Dr Triebig for his interesting comments on our article “Occupational exposure to solvents and risk of lymphoma subtypes: results from the Epilymph case-control study�.1,2 Epidemiological evidence is growing about the various etiological factors of specific lymphoma subtypes, and perhaps the different mechanisms involved.3 In our paper, we referred to previous reports suggesting an interaction of occupational benzene exposure with familial history of haematological diseases and history of immune system diseases,4 apparently indicating an immune system disruption as a mechanism of lymphomagenesis among benzene-exposed workers. However, while those hypotheses apply to NHL in general, we did find a positive link with CLL and dubious findings for follicular lymphoma, but not with DLBCL. It is worth commenting that immune dysfunction is reportedly more relevant for DLBCL and marginal zone lymphoma than for CLL and follicular lymphoma.3 We also referred to benzene genotoxicity as a plausible mechanism, as several genotoxic effects of benzene, and particularly, long-arm deletion of chromosome 6 and trisomy of chromosomes 2, 4, 6, 11, 12, 14 and 18, also occur among lymphoma patients.5,6
The etiologic role of benzene is well established for non-lymphocytic leukaemia, and the recent IARC re-evaluation of human carcinogens in the Monographs N. 1-99 has raised the attention for future research on other neoplasms of the lymphohaemopoietic tissue.7 A variety of combinations of multifactorial factors might plausibly intervene in the chain of events leading to each individual subtype of lymphohaemopoietic malignancies. Whether this variety of aetiological patterns is reflected by excess risk in specific time windows since exposure onset is a question perhaps too early to answer. Nonetheless, we followed Dr Triebig suggestion and explored risk of B-cell lymphoma and CLL by year of initiating exposure, whether up to 1970, between 1971 and 1980, or from 1981 onwards. As the Epilymph study started at different times in the participating countries from 1996 onwards, the 10-15 years interval indicated by Dr Triebig would fit into the last time window. While no substantial changes in risk of B-cell lymphoma were observed by time window in all exposed and in those classified with the highest confidence of exposure to benzene, risk of CLL was highest among subjects who started exposure in 1971-1980 (all exposed: OR = 2.24, 95% CI 0.98 - 5.12; high confidence: OR = 3.33, 95% CI 1.01- 11.0), it was still elevated among those whose exposure started before 1970 (all exposed: OR = 1.53, 95% CI 1.08 - 2.17; high confidence: OR = 1.52, 95% CI 0.97- 2.39), and it was not elevated among those who started exposure from 1981 onwards(all exposed: OR = 2.20, 95% CI 0.72 - 6.76; high confidence: OR = 1.27, 95% CI 0.16- 10.2). It is worth mentioning that this last group included only a tiny fraction of the exposed, mainly because of the regulatory restrictions introduced in the ‘70s. Also, subjects exposed to benzene from 1981 onwards might have been exposed to lower concentrations and for a shorter period; therefore, if cumulative dose over time were to be the correct indicator, the absence of effects might be accounted for by lower cumulative doses.
As it concerns risk associated with toluene and xylene exposure, Table 5 in our paper shows that the excess risk associated with toluene was mostly accounted for by co-occurrent exposure to benzene.2 On the other hand, the elevated risk associated with xylene exposure was generated by extremely small numbers with isolated exposure to xylene. We don’t feel confident to infer about toluene and xylene risk related to their genotoxicity, based on such poor epidemiological evidence.
Further time-related modelling of CLL risk as a function of dose of exposure to benzene, and proper stratification of overlapping exposures, would require pooled analyses of studies with high quality exposure data, an opportunity currently provided only by the Interlymph Consortium.
References
1. Triebig G. “Occupational exposure to solvents and risk of lymphoma subtypes: results from the Epilymph case-control study�. Occup Environ Med 2010; e-letter (published 7 September 2010)
2. Cocco P, t’Mannetje A, Fadda D, Melis M, Becker N, de Sanjose´ S, Foretova L, Mareckova J, Staines A, Kleefeld S, Maynadie´ M, Nieters A, Brennan P, Boffetta P. exposure to solvents and risk of lymphoma subtypes: results from the Epilymph case-control study. Occup Environ Med 2010;67:341-347.
3. Morton LM, Wang SS, Cozen W, Chatterjee N, Davis S, Severson RK, Colt JS, Vasf MA, Rothman N, Blair A, Bernstein L, Croos AJ, DeRoos AJ, Engels EA, Hein DW, Hill DA, Kelemen LE, Lim U, Lynch CF, Schenk M, Wacholder S, Ward MH, Hoar Zahm S, Chanock SJ, Cerhan JR, Hartge P. Etiologic heterogeneity among non-Hodgkin lymphoma subtypes. Blood 2008;112:5150-60.
4. Vineis P, Miligi L, Seniori Costantini A. Exposure to solvents and risk of non-Hodgkin lymphoma: clues on putative mechanisms. Cancer Epidemiol Biomarkers Prev 2007;16:381-4.
5. Zhang L, Rothman N, Li G, Guo W, Yang W, Hubbard AE, Hayes RB, Yin S, Lu W, Smith MT. Aberrations in chromosomes associated with lymphoma and therapy-related leukemia in benzene-exposed workers. Environ Mol Mutagen 2007;48:467-74.
6. McHale CM, Lan Q, Corso C, Li G, Zhang L, Vermeulen R, Curry JD, Shen M, Turakulov R, Higuchi R, Germer S, Yin S, Rothman N, Smith MT.. Chromosome translocations in workers exposed to benzene. J Natl Cancer Inst Monogr 2008;39:74-7.
7. Baan R, Grosse Y, Straif K, Secretan B, El Ghissassi F, Bouvard V, Benbrahimm-Tallaa L, Guha N, Freeman C, Galichet L. A review of human carcinogens – Part F: Chemical agents and related occupations. Lancet Oncology 2009;10:1143-4.
Conflict of Interest: None Declared
Gimeno, Amick, Benavides and Benach [1] raise a number of issues with
a paper recently published in Occupational and Environmental Medicine.[2]
It is important that researchers cross-examine others’ findings and
conclusions, as well as explain and defend their own findings and
conclusions, so that debate can proceed that is both informed and useful
for policy and practice.
Gimeno, Amick, Benavides and Benach [1] raise a number of issues with
a paper recently published in Occupational and Environmental Medicine.[2]
It is important that researchers cross-examine others’ findings and
conclusions, as well as explain and defend their own findings and
conclusions, so that debate can proceed that is both informed and useful
for policy and practice.
In the original paper, I present findings that suggest the perceived
risk from occupational stress varied across countries in the EU. I
interpreted the findings as suggesting an element of social construction
is present in such perceived risk, and that this element of social
construction could have implications for policy, in respect of risk
communication, for example.
There are two important things to note about these conclusions.
First, I analysed perceived risk from occupational stress, and not
objective risk. These are recognised as two separate entities.[3] Whilst
they are arguably intertwined closely in occupational stress and emotional
health,[4] these data do not speak to this issue, and I drew no
conclusions concerning objective risk. However, perceived risk is an
important issue that can have practical implications, as noted.[2]
Second, it is uncontroversial in many areas concerned with risks to
health (e.g. nuclear power, food) that risk is partially socially
constructed, at this social construction has important practical
implications.[5] There is no reason I know of why there should be
controversy concerning the practical implications of a socially
constructed element to risk from occupational stress.
Gimeno et al. raise four concerns.
1. The first issue is related to sample selection. The data were drawn from
the Third European Survey on Working Conditions (ESWC), and then a more
homogenous sample selected of people working in the same country as their
nationality. Albeit imperfect (as noted by Gimeno et al), this procedure
excludes workers who are more likely to have recent extensive experience
of different working cultures. As noted in the paper, then, ‘variation
within individuals due to multiple influences of work cultures was
minimized’. Note I use the term minimized, rather than excluded.
Notwithstanding, this procedure provides a more accurate means of
assessing socio-cultural influences on perceived risk of occupational
stress than was possible just by comparing responses across country of
data collection or by comparing people of different nationalities.
Gimeno et al. explain that there is an influx of foreign workers into
the EU, and that these workers may be exposed to more hazardous working
conditions. Gimeno et al. make the argument that ‘removing workers who may
be experiencing the greatest stress and hazardous working conditions from
the sample may represent a severe selection bias’. I would agree with
Gimeno et al.had the purpose of the paper been to determine objective risk
in all areas of the labour market in the countries surveyed. Further, I
agree that such workers are an important section of EU labour markets
deserving of research in their own right with a view to informed
intervention to enhance their working conditions – and such research
should include assessment of perceived and objective risk in due course.
However, the purpose of the paper was to determine whether there is a
socially constructed element in the perceptions of stress that can be
attributed to socio-cultural variables at the national level. Including
such workers may well have skewed the data by introducing a level of bias
related to the nationality of immigrant workers in a country.
Gimeno note ambiguity with the statement "individuals who were
working in a different country as their nationality". As well as re-
reading the paper, I have conducted an electronic search of the paper, and
cannot find this quote. Therefore I am unsure of the context of the quote,
and so cannot be sure of the source of the perceived ambiguity. However,
Gimeno et al. do raise issues not covered in the ESWC data concerning
assimilation of social constructs and life-course data, all of which are
relevant to propagation of cultural values at an individual level [6] and
possibly also risk perception. However, by including only those people who
list their nationality as being the same as the country they work in, it
is a reasonable assumption that they will be familiar with the dominant
cultural values of that country (even if they do not subscribe to those
values themselves). Other data would be desirable of course, but
unfortunately, they are not available.
2. The second concern raised by Gimeno et al concerns the use index of
perceived risk of occupational stress. They raise an issue concerned with
principal components analysis (PCA) conducted on the whole sample, rather
than the sub-set used to compare the EU countries. It seems that the
implication of this argument is that a different cluster of symptoms would
be uncovered by PCA conducted on the sub-sample. I re-analysed the data,
using only those people that worked in the same country as their
nationality. PCA indicated the same pattern of relationships between
perceived risk of symptoms.
What does this analysis mean though? It seems that a cluster of
symptoms – which may be labelled stress – are commonly perceived as co-
occurring. This might be because when such symptoms occur, they commonly
occur together. This could reflect a physiological process, or heightened
cognitive processing of physical sensations during emotional episodes.[7]
However, as other analyses in [2] show, the extent to which the risk of
experiencing these symptoms is attributed to work has a socially
constructed component.
Gimeno et al. do raise the point that important differences might
exist between individual health-related outcomes, and that these health-
related outcomes might vary between factors such as type of employment,
gender etc. First, in [2], I did control for industry, demographic
factors, job dissatisfaction and perceived working conditions. In this
way, factors that might represent cross-national variations in working
practices (such as working hours) and individual level factors (such as
job dissatisfaction) could not be said to account for the pattern of
findings. Second, the ESWC contains many individual level questions
assessed by single item indicators. By looking at health outcomes
assessed by single indicators, there is danger that any findings reflect
the error of measurement embedded in single item indicators of
indeterminate reliability - rather than the true variable of interest.
This threat is magnified in analyses involving large samples, where even
small differences due to error can be labelled statistically reliable. By
producing a scale – with an acceptable reliability coefficient (a=0.73),
this possibility is lessened.[2]
Gimeno et al. also bring attention to the nature of the questions in
the ESWC that I used to examine cross-national differences. It is
important to note that the question I used asked participants to attribute
various symptoms to work, not whether those symptoms were currently being
experienced. Therefore, the question reflects a perception of the impact
of work on symptoms – and not symptoms themselves or any underlying
pathology. Therefore, any conclusions drawn from the data cannot reflect
anything other than factors influencing the perceived influence of work on
various symptoms.
3. The third concern raised by Gimeno et al regards the empirical status of
my conclusion that workers in lower ranked countries might be less likely
to attribute minor or non-specific psychosomatic symptoms to work when
consulting with health practitioners. Whilst Gimeno et al are aware of no
data that support such a conclusion, this conclusion – however conditional
the language within which it is phrased - cannot be dismissed without
further work. There is evidence that indicates emotional displays and
discussion of life stress during consultation might cause misdiagnosis.[8] This potential for misdiagnosis arguably warrants further
investigation.
4. The fourth concern raised by Gimeno et al. concerns the discussion section,
especially in relation to conclusions with respect to the UK. I conclude
that the media and socio-cultural factors – specifically cultural
attitudes – might influence perceptions of risk from occupational stress.
There is an extensive literature relating to these issues in relation to
other risks – and some of the more prominent examples were referenced in
[2]. There is also discussion elsewhere of socio-cultural factors and the
media in influencing perceptions of risk from occupational stress [9] and
in politicising stress as a social issue that subsequently influences
reporting of stress.[10]
Gimeno et al. suggest that classifying countries according to common
characteristics could provide an a priori basis for explaining the pattern
of findings. The cultural approach to risk perception [11] provides one
such approach. In this framework, countries with an individualist
orientation (Ireland and Great Britain in this sample) would be expected
to be ranked lower than other countries. This was indeed the case in [2].
However, countries with a more egalitarian orientation, such as the Nordic
countries and Germanic countries, would be predicted to be ranked near the
top, and countries with more hierarchical work cultures – such as France –
would be expected to be ranked lower than the Nordic and Germanic
countries. The results clearly do not bear such predictions out (see 12
for a cultural typology of European countries).
Therefore, the ranking of countries may reflect more complex
processes than simple categorisation of countries on cultural or other
factors. This conclusion is supported by some of the literature cited in
[2] that has been used to discuss the British case [9,13-15]. In
this literature, a number of suggestions have been made, in which, factors
such as the media, socio-cultural factors and cognitive processes in the
perception of risk have been advocated as explanations or partial
explanations for perceived risk from occupational stress. I do not know
the extent to which the scientific and policy literature in other
countries covers such issues, but the fact there is open debate in the
scientific community concerning such issues in Britain makes Britain a
useful focus for analysis. Moreover, the British case with respect to
monitoring stress and intervention is now more interesting, given the
introduction of Stress Management Standards by the UK Health and Safety
Executive. In due course, the British case will provide a useful focus for
analysis of how advisory rather than coercive processes influence
reporting and perception of occupational stress. It was for these reasons
that the discussion section had some focus on the British case.
So rather than further cross-national comparisons on perceptions of
stress – now we know they exist but not why - researchers might find it
useful to examine individual countries on a case-by-case basis, so as to
build rich pictures of the factors that influence perceived risk from
stress in any one societal context and explain in more detail the pattern
of findings in [2]. Once such exploratory work has been completed,
research can move to hypothesis testing.
Finally, Gimeno et al. note that different rankings are apparent if
different dependent variables are used. This should not be surprising – I
can think of no reason why sickness absence has to necessarily mirror
findings with attributions of stress-related symptoms to work – although
there might be several reasons why they could be loosely coupled. Stress
is not the only reason for absence from work.
Whether the ranking in [2] is more or less accurate and the reasons
for the rankings, only further research can tell. However, the socially
constructed elements of stress have real policy implications. They are
worthy of further debate and research. To ignore them or deny them
ultimately will be to the detriment of policy, intervention and
occupational health.
2. Daniels, K. Perceived risk from occupational stress: a survey of
15 European countries. Occup Environ Med, 2004; 61: 467-70.
3. Royal Society. Risk: Analysis, Perception and Management. London:
Royal Society, 1992.
4. Daniels K, Harris C, Briner R. Understanding the Risks of Stress:
A Cognitive Approach. Sudbury: HSE Books, 2002.
5. Kasperson RE, Kasperson JX, Renn O. The social amplification of
risk: progress in developing an integrative framework. In S Krimsky, D
Golding (eds) Social theories of risk. London: Praeger, 1992.
6. Berry JW. Immigration, acculturation, and adaptation. Applied
Psychology: An International Review, 1997; 46: 5-34.
7. Kirmayer LJ, Robbins JM, Paris J. Somatoform disorders:
personality and the social matrix of somatic distress. Journal of Abnormal
Psychology, 1994; 103: 125-136.
8. Ellington L, Wiebe D. Neuroticism, symptom presentation, and
medical decision making. Health Psychology, 1999; 18: 634-643.
9. Daniels, K. Why aren’t managers concerned about occupational
stress? Work & Stress, 1996; 10: 352-366.
10. Barley SR, Knight DB. Toward a cultural theory of stress
complaints. In B.M.Staw & L.L. Cummings (Eds.), Research in
organizational behavior, 1992; 14: 1-48.
11. Thompson M, Ellis R, Wildavsky A. Cultural Theory. Boulder:
Westview, 1990.
12. Ronen S, Shenkar, D. Clustering countries on attitudinal
dimensions: a review and synthesis. Academy of Management Review, 1985;
10: 435-454.
13. Wesseley S, Hotopf M. Are some public health issues better
neglected? Lancet 2001; 357: 976-7.
14. Newton T. ‘Managing stress’ emotion and power at work. London:
Sage, 1995.
15. Rick J, Hillage J, Honey S, Perryman S. Stress: big issue, but
what are the problems? Brighton: The Institute for Employment Studies,
1997.
16. Gimeno D, Benavides FG, Benach J, Amick III BC. Distribution of
sickness absence in the European Union Countries. Occup Environ Med (in
press).
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Dear Editor
Gimeno, Amick, Benavides and Benach [1] raise a number of issues with a paper recently published in Occupational and Environmental Medicine.[2] It is important that researchers cross-examine others’ findings and conclusions, as well as explain and defend their own findings and conclusions, so that debate can proceed that is both informed and useful for policy and practice.
In the original...
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