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Papers on diesel exhaust released for publication

9 Mar, 12 | by Dana Loomis

I wrote recently about attempts by an industry group to prevent publication of key papers on the risk of cancer among workers exposed to diesel exhaust. A mining industry coalition had obtained an order from a court in Louisiana, USA that restrained the study’s authors, most of whom are US government scientists, from publishing the study results for 90 days while the industry and a congressional committee reviewed the papers and the raw data. An industry lawyer also sent letters to several journals, including OEM, advising the editors not to publish papers from the diesel study. An editorial on these events and their implications for scientific communication has been published online and will appear in the April issue of OEM (1).

The situation changed this week with respect to the delayed papers. The US government agencies that sponsored the study had appealed the court’s order, and on 29 February a higher court stayed the original ruling, opening the way for the papers to be published (2, 3). More details of these events have been reported in Nature news (4). The public interest in knowing the results of this important study will be served and the IARC monograph meeting on the carcinogenicity of diesel exhaust scheduled for June will presumably go forward as planned.

While this is good news for these papers and the evaluation of diesel exhaust, there are still reasons to be concerned about the larger implications of the case. A lawsuit was used to delay the open publication of important scientific findings while parties with a financial interest were given time to go through the data. While the industry is entitled to draw their own conclusions from the data, there is no scientific or ethical reason that they should be able to do so before workers, the public and the scientific community.


1. Loomis D, Sim MR. Suppressing publication threatens scientific progress. Occup Environ Med 2012;69:229 doi:10.1136/oemed-2012-100740.

2. Attfield MD, Schlieff PL, Lubin JH et al. The diesel exhaust in miners study: a cohort mortality study with emphasis on lung cancer. J Natl Cancer Inst 2012;104:1-15. DOI: 10.1093/jnci/djs035.

3. Silverman DT, Sarmanic CM, Lubin JH, et al. The diesel exhaust in miners study: a nested case-control study of lung cancer and diesel exhaust. J Natl Cancer Inst 2012;104:1-14. doi: 10.1093/jnci/djs034.

4. Tollefson J. Embattled scientists publish study linking (surprise) diesel exhaust and cancer. Nature News Blog. 2012.

Industry attorney warns against publishing papers on diesel exhaust

18 Feb, 12 | by Dana Loomis

OEM recently received a letter from an attorney in the United States referring to an order of a US district court and warning us not to publish papers from a NIOSH/NCI study on the effects of diesel exhaust in a cohort of miners.  The letter’s author, Henry Chajet, is a Washington, DC, lawyer and lobbyist who has represented industry in challenging occupational health and safety regulations, and we have learned that he has sent similar letters to other journals in the UK and the US.

For OEM, the actual impact of the letter and the court’s order is minimal at this stage.  The papers in question have been submitted to other journals and it is questionable whether a US judge’s order would apply to the Journal as an entity based in the UK.  However, the broader implications of the court order and the industry’s tactics are cause for concern.

The judge’s order is a highly unusual instance of prior restraint of scientific publication.  It was issued in a lawsuit filed by the mining industry against the US government agencies that conducted the diesel study, which alleges that the study results are “inaccurate and faulty.”  The order requires the study’s authors to turn over materials related to the research to the industry and a committee of the US Congress and gives those groups 90 days to review them before the papers can be published.  The judge’s order is being appealed, but it’s likely that the papers will be held up for some time with further court filings and motions.   A substantial delay in publication of key results from the study could affect IARC’s planned re-evaluation of the carcinogenicity of diesel exhaust scheduled for June.

Ironically, Mr. Chajet has said that the purpose of challenging the diesel study was “to get the information and open the door and let the participants and the public see what the conclusions are based on the science ” (1), but the industry’s action may have exactly the opposite effect.  The public have a compelling interest in knowing the findings of this important study, which is not served by using the legal system to restrain publication of the key papers and the open discussion and debate that is sure to follow.



Re: Response to “Does self-reported computer work add biologically relevant information beyond that of objectively recorded computer work?”

18 Feb, 12 | by lelliott

We thank Gerr and Fethke for their response to our remarks on their editorial on self-reported versus objectively recorded computer times [1]. Gerr and Fethke continue to disregard the consistent evidence that objectively recorded computer times are much more accurate and valid than self-reported computer times when compared to external “gold” standards [2,3]. They suggest that self-reported computer times may be superior to objectively recorded computer times in capturing biologically relevant risk factors for musculoskeletal disorders. Their basic argument is that musculoskeletal disorders seem to be related to self-reported but not to objectively recorded computer times. According to Gerr and Fethke this discrepancy could be due to error in self report, differences in the kind of exposure information captured, or both. They blame us that our “claims of methodological objectivity and validity … do not address this fundamental question”.

However, we did address this question [3]. We studied if the differences between self-reported and objectively recorded computer times depended on the level of computer times, variation in computer times, level of arm pain, psychosocial work characteristics, age, gender, and personality characteristics. Concerning work characteristics, self-reported computer times increased with a high degree of variation between weeks; and a one hour increase in weekly computer time was overestimated, especially at low levels of computer time. In our opinion these findings reflect self-report biases, rather than self-report “captures” of biologically relevant information. We found no musculoskeletal health effects of computer work speed, sustained activity or micropauses or their interactions with computer times [2,4]. Of course, other factors may also be considered and our findings should be replicated.

Gerr and Fethke are concerned about the generalisability of the NUDATA results with reference to our objective median exposure times [2,4]. However, these are without any relevance to generalisabilty. The NUDATA cohort was designed to include persons with low as well as high computer work hours in order to examine internal exposure-response relations. Therefore, it is the representation of variation in computer work hours that counts, not means or medians. These problems have been thoroughly discussed in our previous publications [2,4].

Sigurd Mikkelsen
Johan Hviid Andersen


1. Gerr F, Fethke N. Ascertaining computer use in studies of musculoskeletal outcomes among computer workers: differences between self-report and computer registration software. Occup Environ Med 2011; 68: 465-66.

2. Mikkelsen S, Lassen CF, Vilstrup I, et al. Does computer use affect the incidence of distal arm pain? A one-year prospective study using objective measures of computer use. Int Arch Occup Environ Health 2012;85:139-52.

3. Mikkelsen S, Vilstrup I, Lassen CF, et al. Validity of questionnaire self-reports on computer, mouse and keyboard usage during a four-week period. Occup Environ Med 2007; 64:541-7.

4. Andersen JH, Harhoff M, Grimstrup S, et al. Computer mouse use predicts acute pain but not prolonged or chronic pain in the neck and shoulder. Occup Environ Med 2008;65 :126-31.

Conflict of Interest: None declared

Renal Effects of Cadmium Exposure

19 Apr, 11 | by lelliott

I have read with the greatest interest the convincing study on the dose-response of cadmium ions in kidneys (1). Cadmium compounds also harm the proteoglycan metabolism (2), and by using the urinary proteoglycan excretion as an indicator of cadmium effects the threshold would be at 5 microg/g creatinine (3). This agrees very well with the threshold found in
the current investigation.

Heikki Savolainen

1 Chaumont A, De Winter F, Dumont X, et al. The threshold level of urinary cadmium associated with increased urinary excretion of retinol-binding protein and beta-2-microglobulin: a reassessment in a large cohort of nickel cadmium battery workers. Occup Environ Med 2011; 68:257-264.

2 Savolainen H. Cadmium-associated renal disease. Renal Failure 1995;17:483-487.

3 Savolainen H. Studies on urinary proteoglycan excretion in occupational cadmium exposure. Pharmacol Toxicol 1994; 75:113-114.

Termination: Education Research Centers

24 Mar, 11 | by lelliott

The Fiscal Year 2012 Budget released recently by the U.S. Office of Management and Budget (OMB) proposes termination of funding for the Educational and Research Centers (ERCs) Program within the National Institute of Occupational Safety and Health (NIOSH), stating that the “intended goals of the program have been met.” The goals, according to the OMB, were to provide seed money for academic institutions to develop or expand occupational health and safety training programs for specialists practicing in the field, with the intention that the programs would become self-sustaining after 5 years.

The American College of Occupational and Environmental Medicine (ACOEM) has posted on their website ( a letter to members of the Appropriations Committee about the proposed cuts. The “Terminations, Reductions, and Savings” Report is located on the White House website (


26 Jan, 11 | by lelliott

The 22nd International Conference on Epidemiology in Occupational Health (EPICOH) will be held in Oxford, 7-9 September, 2011. The website, with details, may be viewed here:

RE: The ghost of methods past: exposure assessment versus job-exposure matrix studies

26 Jan, 11 | by lelliott

Dr. Burstyn, in his commentary [1], underscores the critical importance of using the best exposure assessment methods possible to minimize misclassification. We agree about the value of expert formulated models for systematically and transparently documenting exposure assessment, but caution that many existing studies may not be readily adapted to such model building. For such studies, the best alternative exposure assessment methodology should be employed, such as job-exposure matrices (JEMs) or expert assessments of self-reported work histories. Even though the relationships between the true exposure and estimates by expert assessment and a JEM are unknown (which is the case for most exposure assessments) we believe that understanding the differences between the two methods is informative, especially given the considerable time and resources necessary to carry out an expert assessment.

As Dr. Burstyn indicates [1], neither assessment approach used in our study [2] allows us to claim that lead definitely causes brain tumors. However, if this is the standard for judging the success of an exposure assessment method, most methods are failures. Although only suggestive, we do see some evidence of an association and indicate that future studies would benefit from the most accurate exposure assessment method available. The intent of our analysis was to compare two widely used approaches and to encourage epidemiologists to pursue the best exposure assessment methods possible. We acknowledge limitations with the expert assessment approach and strongly support the development and use of new exposure assessment methods. However, expert assessment may be the best approach available to an existing study and could reveal important associations that future studies can explore in greater detail using more refined exposure assessment techniques.

Parveen Bhatti
Patricia Stewart
Martha S. Linet
Peter D. Inskip
Aaron Blair
Preetha Rajaraman

1. Burstyn I. The ghost of methods past: exposure assessment versus
job-exposure matrix studies. Occup Environ Med 2011;68:2-3 doi:10.1136/oem.2009.054585. (Available at

2. Bhatti P, Stewart PA, Linet MS, Blair A, Inskip PD, Rajaraman P.
Comparison of occupational exposure assessment methods in a case-control study of lead, genetic susceptibility and risk of adult brain tumours. Occup Environ Med 2011;68:4-9 doi:10.1136/ oem.2009.048132. (Available at

Registration of Observational Epidemiological Studies

2 Dec, 10 | by lelliott

Two papers commenting on a recent proposal to require registration of observational epidemiological studies have just been published electronically on OEM’s web site. These commentaries offer differing views as to what should be done, but neither is a statement of this journal’s policy.

We currently do not require observational research submitted to OEM to be registered and we have no plans to do so. This position is based primarily on the belief that observational studies are fundamentally different from clinical trials in both objectives and scientific approach.

I will explain the Journal’s policy and the reasons behind it in a future issue of the printed journal. Readers are also invited to give their opinions on whether observational studies should be registered in contributions to the OEM blog.

Dana Loomis

Further Corroboration of the Asthmagenicity of 5-Aminosalicylic Acid

17 Nov, 10 | by lelliott

Sastre et al described a case of occupational asthma caused by a novel low molecular weight (LMW) respiratory sensitiser, 5-aminosalicylic acid (5-ASA) [1]. They concluded that the mechanism was probably not IgE-mediated because of a negative skin prick test and a late response to bronchial challenge testing with 5-ASA. They remarked, as is the case with several other LMW asthmagens, that the mechanism by which 5-ASA caused asthma is unknown.

Such uncertainty, and likely heterogeneity in the pathophysiological mechanisms of asthma due to LMW chemicals, is one of the reasons why no single in vitro or in vivo testing method has been developed for the prediction of asthmagenic potential. One way round this problem has been to utilise an ‘in silico’ approach that makes no a priori assumptions about pathophysiological mechanism. The development of such a quantitative structure activity relationship (QSAR) model and its initial validation was published in a previous edition of Occupational and Environmental Medicine [2]. This assigns an asthma hazard index, which is a value between zero and one, and the most recent validation [3] has demonstrated that it has good global predictive value.

By entering the chemical structure of 5-ASA (fig 1) into this model, an ‘asthma hazard index’ of 0.82 was obtained indicating a high probability of asthmagenicity.

Novel LMW chemical causes of occupational asthma such as the one reported by Sastre et al appear only intermittently in the literature but respiratory physicians have used this QSAR model to provide corroborating evidence in the identification of a novel asthmagen [4]. This model may also be of use when a clinician has diagnosed occupational asthma where the cause could be one of several LMW (organic) chemicals none of which are recognized respiratory sensitisers. By ranking the possible causes according to the QSAR-generated asthma hazard index, it may be possible to prioritise the agent(s) with which to perform bronchial challenge testing. Further evaluation of the QSAR model for this purpose is planned and we would encourage respiratory and occupational physicians to utilise the model, which is freely available on the internet [5] for such purposes, and register their interest and observations by email with the undersigned.

Dr. Martin Seed, University of Manchester

Professor Raymond Agius, University of Manchester


1. Sastre J, del Potro MG, Aguado E, et al. Occupational asthma due to 5- aminosalicylic acid. Occup Environ Med 2010;67:798-9.

2. Jarvis J, Seed MJ, Elton RA, et al. Relationship between chemical structure and the occupational asthma hazard of low molecular weight organic compounds. Occup Environ Med 2005;62:243-50.

3. Seed MJ, Agius RM. Further validation of computer-based prediction of chemical asthma hazard. Occup Med 2010;60:115–20.

4. Moore VC, Manney S, Vellore AD, et al. Occupational asthma to gel flux containing dodecanedioic acid. Allergy 2009;64:1099-1107.

5. The University of Manchester. Centre for Occupational and Environmental Health. Mechanisms of Occupational Asthma; Occupational asthma hazard prediction programme. (accessed November 2010).

Nightshift Work and Breast Cancer: Response

17 Nov, 10 | by lelliott

17 November 2010

The statement by IARC that “Shiftwork that involves circadian disruption is probably carcinogenic to humans” [1] raises the issue of evidence-based measures for prevention, which was the focus of our letter. Assuming that nightshift work is indeed causally related to breast cancer one option for prevention would be to set limits for the individual cumulated amount of night work [2]. Such an approach would, however, only prevent cancer cases if there is a multiplicative exposure-response relation or a threshold. If this is not the case, only setting an upper limit for years of nightshifts for the individual workers would distribute the risk among more workers but not reduce the total number of cases.

Therefore, we analyzed the 9 epidemiological studies in order to examine the exposure-response relation. We agree with Hansen and Stevens that the study by Kjaer et al [3] lacks individual information on night-shift work but only proxy measures. We therefore reanalysed the data excluding this study and 3 other studies relying on proxy measures of nightshift work [4],[5],[6] and included a study recently published with relevant exposure information [7]. We obtained a meta-odds ratio of 1.004, 95% CI 1.001-1.008 by year of nightshift work. There was no indication of neither a threshold nor a meaningful exposure-response relation and thus the available limited epidemiological data do not provide evidence to warn against long-term nightshift work for the individual worker. On the other hand, there are plenty arguments for reducing the total population burden of nightshift work, among others the suspicion raised about increased breast cancer risk.

Henrik A Kolstad & Jens Peter Bonde


1.      International Agency for Research on Cancer. IARC Monographs on the evaluation of carcinogenic risks to humans. Painting, firefighting, and shiftwork. Lyon: International Agency for Research on Cancer; 2010. 563-766.

2.      Fritschi L. Shift work and cancer. bmj 2009;339:b2653.

3.      Kjaer TK, Hansen J. Cancer incidence among large cohort of female Danish registered nurses. Scand J Work Environ Health 2009;35(6):446-53.

4.      Tynes T, Hannevik M, Andersen A et al. Incidence of breast cancer in Norwegian female radio and telegraph operators. Cancer Causes Control 1996;7(2):197-204.

5.      Hansen J. Increased breast cancer risk among women who work predominantly at night. Epidemiol 2001;12(1):74-7.

6.      Lie JA, Roessink J, Kjaerheim K. Breast cancer and night work among Norwegian nurses. Cancer Causes Control 2006;17(1):39-44.

7.      Pronk A, Ji BT, Shu XO et al. Night-shift work and breast cancer risk in a cohort of Chinese women. Am J Epidemiol 2010;171(9):953-9.

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