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
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.
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
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.
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.
This carefully conducted study (1) points at the kidney as a
potential target of toxicity of phenoxy acids in a chronic occupational
exposure.
This is biologically plausible as the phenoxy acids are inhibitors of
chloride channels in renal tubular cells (2) which leads to alterations in
the excretion of urinary electrolytes (3).
Thus, it is entirely possible that the chronic dysfun...
This carefully conducted study (1) points at the kidney as a
potential target of toxicity of phenoxy acids in a chronic occupational
exposure.
This is biologically plausible as the phenoxy acids are inhibitors of
chloride channels in renal tubular cells (2) which leads to alterations in
the excretion of urinary electrolytes (3).
Thus, it is entirely possible that the chronic dysfunction can lead
to renal problems.
1 Boers D, Portengen L,Bas Bueno-de-Mesquita H, et al. Cause-specific
mortality of Dutch chlorophenoxy herbicide manufacturing workers. Occup
Environ Med 2010; 67: 24-31
2 Savolainen H. New uses for old urine tests. Brit J Ind Med 1989;
46: 361-363
3 Manninen A, Kangas J, Klen T, Savolainen H. Exposure of Finnish
farm workers to phenoxy acid herbicides. Arch Environ Contam Toxicol 1986;
15: 107-111
Laney, et al. [1] provide important and compelling insight to
potential causes of the unexpected occurrence of progressive massive
fibrosis among underground coal miners in some areas of the U.S. Based on
the occurrence of “r” opacities in these films, exposure to quartz is the
likely cause. This conclusion is supported by an exposure assessment that
shows elevated exposure to quartz dust in area...
Laney, et al. [1] provide important and compelling insight to
potential causes of the unexpected occurrence of progressive massive
fibrosis among underground coal miners in some areas of the U.S. Based on
the occurrence of “r” opacities in these films, exposure to quartz is the
likely cause. This conclusion is supported by an exposure assessment that
shows elevated exposure to quartz dust in area mines.[2] However, there
is an increase in the prevalence of CWP that extends beyond these areas
and that includes CWP in lower categories [3] and that may have different
causes.
Laney et al.[1] suggest that an increase in hours worked may
contribute to the increase in the prevalence of CWP. I agree. More
important, data to support this suggestion exist. Mine operators report
to MSHA hours worked and average number of workers per quarter [4]. From
these reports, one can easily calculate hours worked per miner. Based on
these data, annual hours worked per underground miner increased from an
average of about 1700 hours per year in 1982 to about 2200 hours per year
in 2006, an increase of nearly 30%. These measures, and measures of dust
concentration, are available for each mine since the early 1970’s. They
could and should be combined to revise estimates of miners’ exposure in
relation to the occurrence of CWP and thereby evaluate this suggestion.
Clearly, a complete understanding of exposure is important for preventing
CWP. Laney et al. [1] have identified an important cause. And as they
suggest, there is more to do.
James L. Weeks, ScD, CIH
Industrial Hygiene Consultant to the United Mine Workers of America
1. Laney AS, Petsonk EL and Attfield MD. Pneumoconiosis among
underground bituminous coal miners in the United States: Is silicosis
becoming more frequent? Occ Enviro Med. Published online 22 Sep 2009.
2. Pollock DE, Potts JD and Joy GJ. Investigation into dust exposure
and mining practices in the Southern Appalachian Region. (ND) (October
28,2009). (http://www.cdc.gov/niosh/mining/pubs/pdfs/iidea.pdf)
3. National Institute for Occupational Safety and Health. Work-
related lung disease surveillance report 2007. (October 28, 2009).
(http://www.cdc.gov/niosh/docs/2008-143/)
We welcome the appearance of this new analysis of asbestos related
mortality which constitutes an important addition to the available
evidence. We note that the lung cancer risk from this data highlighted by
the authors and based on their internal analyses gives an identical risk
factor to the one suggested as the 'best estimate' in our earlier meta-
analysis (1): a relative risk of 1.102 per 100 f/ml.yr translates almost...
We welcome the appearance of this new analysis of asbestos related
mortality which constitutes an important addition to the available
evidence. We note that the lung cancer risk from this data highlighted by
the authors and based on their internal analyses gives an identical risk
factor to the one suggested as the 'best estimate' in our earlier meta-
analysis (1): a relative risk of 1.102 per 100 f/ml.yr translates almost
exactly to an excess over expected of 0.1% per f/ml.yr.
The risk of mesothelioma derived from these new data is higher by a
factor of 10 than that which emerged from our meta-analysis. The following
table shows these new data (labelled N. Carolina) along with the
chrysotile data used in our analysis.
The generally small numbers mean that all the estimates are subject
to substantial statistical error. The largest single set of observations
is that derived from the Canadian mines, and this gives a low and
(statistically) reasonably precise estimate of about 0.001. The remaining
observations are statistically consistent (P=0.075); though mainly due to
their imprecision, rather than to the similarity of the estimates. The
statistical consistency is somewhat improved by also removing the Italian
mines (Balangero) cohort (P=0.10). The mean risk taken across the
remaining cohorts is 0.0070 with a confidence limit running from 0.0038 to
0.013.
Combining the two mining cohorts gives a joint estimate of 0.00096
(95% CI
0.00069, 0.0013).
The estimate from the latest study is based on eight cases. Assuming
Poisson variability the underlying risk could correspond to between 4 and
16 cases. Up to three of the observed cases may be due to amosite
exposure in plant 3, but it could also be argued that some mesothelioma
cases may have been missed during the period prior to the introduction of
ICD 10.
An estimate of 0.007% per f/ml.yr still places the risk of
mesothelioma from chrysotile at least an order of magnitude lower than the
risk we estimate for the amphiboles fibres (0.5 for crocidolite, 0.1 for
amosite). As we argued in our original paper, if the risk from chrysotile
is indeed substantially lower than from the other fibre types then the
level of risk observed in cohorts with mixed exposure provides an upper
limit to the true risk for chrysotile on its own. In our meta-analysis
four of the mixed fibre cohorts had mesothelioma risk estimates around or
below the 0.01 level. In the largest of these (Ferodo) there is a strong
indication that 11 of the 13 mesothelioma deaths were due to crocidolite
exposure. Since the overall risk for this cohort was 0.014, the implied
chrysotile risk in this setting (friction products) would be well below
0.01.
These new results certainly strengthen the case for the proposition
that the per fibre risk of mesothelioma from chrysotile in textile plants
is greater than it is in the mines. Whether this differential also
applies in other settings is not clear from the evidence above: the
absence of mesothelioma deaths in the New Orleans and Connecticut cohorts
is statistically consistent with a risk of 0.01 though, obviously, more
consistent with the mines estimate of 0.001.
John Hodgson
Andrew Darnton
Statistics Branch (Epidemiology Group)
Health and Safety Executive
Redgrave Court (S4.3)
Merton Road
Bootle L20 7HS
United Kingdom
Tel: 0151 951 4566 (fax 4703)
1. JT Hodgson, A Darnton. The quantitative risks of mesothelioma
and lung cancer in relation to asbestos exposure. Ann. occup. Hyg., Vol.
44, No. 8, pp. 565–601
We welcome the comments on our systematic review on factors
associated with the Work Ability Index (WAI) with regard to the practical
implications of the WAI instrument.
After reading the review, the author of the e-letter concludes 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 intended message o...
We welcome the comments on our systematic review on factors
associated with the Work Ability Index (WAI) with regard to the practical
implications of the WAI instrument.
After reading the review, the author of the e-letter concludes 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 intended message of the review is that the
WAI is a useful tool in the field of employability of (older) workers, and
that various work-related and individual factors play a role in someone’s
workability. Our review was restricted to those factors that are not
incorporated in the work ability index itself and, thus, we have not
investigated health complaints, such as musculoskeletal disorders, as
determinants and also refrained from analyzing in which occupational
populations the use of the work ability index may be warranted. We agree
with Nicholas Glozier that the work ability concept is complex and needs
further study. Since the work ability index is a summary score over
different dimensions, caution is required in drawing conclusions on a
decreased WAI score without further diagnosis of reasons for a decreased
WAI and underlying mechanisms. Previous studies have shown that the WAI is
a useful tool among workers in physically demanding professions[1] as well
as among mentally demanding professions[2] to analyze factors at
population level that influence employability of workers and, thus, may be
considered for addressing in interventions.
[1] Alavinia SM, van Duivenbooden C, Burdorf A. Influence of work-
related factors and individual characteristics on work ability among Dutch
construction workers. Scand J Work Environ Health. 2007 Oct;33(5):351-7.
[2] van den Berg TI, Alavinia SM, Bredt FJ, Lindeboom D, Elders LA,
Burdorf A. The influence of psychosocial factors at work and life style on
health and work ability among professional workers. Int Arch Occup Environ
Health. 2008 Aug;81(8):1029-36.
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.
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...
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...
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...
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...
Dear Editor,
This carefully conducted study (1) points at the kidney as a potential target of toxicity of phenoxy acids in a chronic occupational exposure.
This is biologically plausible as the phenoxy acids are inhibitors of chloride channels in renal tubular cells (2) which leads to alterations in the excretion of urinary electrolytes (3).
Thus, it is entirely possible that the chronic dysfun...
To the Editor:
Laney, et al. [1] provide important and compelling insight to potential causes of the unexpected occurrence of progressive massive fibrosis among underground coal miners in some areas of the U.S. Based on the occurrence of “r” opacities in these films, exposure to quartz is the likely cause. This conclusion is supported by an exposure assessment that shows elevated exposure to quartz dust in area...
We welcome the appearance of this new analysis of asbestos related mortality which constitutes an important addition to the available evidence. We note that the lung cancer risk from this data highlighted by the authors and based on their internal analyses gives an identical risk factor to the one suggested as the 'best estimate' in our earlier meta- analysis (1): a relative risk of 1.102 per 100 f/ml.yr translates almost...
We welcome the comments on our systematic review on factors associated with the Work Ability Index (WAI) with regard to the practical implications of the WAI instrument. After reading the review, the author of the e-letter concludes 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 intended message o...
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...
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