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Recent eLetters

Displaying 1-10 letters out of 205 published

  1. Analyses of cadmium and kidney function in lead workers were adjusted for lead

    We thank Dr. Kawada for his interest in our manuscript entitled "Associations of low-level urine cadmium with kidney function in lead workers."[1] As discussed in the methods and shown in the footnotes to Tables 3 and 4 in the manuscript, we adjusted for blood and tibia lead. We have presented lead analyses in this cohort in multiple past publications[2-8] so, in order to focus on the unique cadmium associations and comply with space considerations, we did not show the lead regression coefficients. Multiple linear regression was used in the analysis.

    References:

    1 Weaver VM, Kim NS, Jaar BG et al. Associations of low-level urine cadmium with kidney function in lead workers. Occup Environ Med 2011;68:250-256. doi:oem.2010.056077 [pii] 10.1136/oem.2010.056077 [doi] [published Online First 2010/10/27].

    2 Weaver VM, Lee BK, Ahn KD et al. Associations of lead biomarkers with renal function in Korean lead workers. Occup Environ Med 2003;60:551- 62. 2003/07/29].

    3 Weaver VM, Schwartz BS, Ahn KD et al. Associations of renal function with polymorphisms in the delta-aminolevulinic acid dehydratase, vitamin D receptor, and nitric oxide synthase genes in Korean lead workers. Environ Health Perspect 2003;111:1613-9. 2003/10/07].

    4 Weaver VM, Jaar BG, Schwartz BS et al. Associations among lead dose biomarkers, uric acid, and renal function in Korean lead workers. Environ Health Perspect 2005;113:36-42. 2005/01/01].

    5 Weaver VM, Lee BK, Todd AC et al. Associations of patella lead and other lead biomarkers with renal function in lead workers. J Occup Environ Med 2005;47:235-43. doi:00043764-200503000-00005 [pii] [published Online First 2005/03/12].

    6 Weaver VM, Schwartz BS, Jaar BG et al. Associations of uric acid with polymorphisms in the delta-aminolevulinic acid dehydratase, vitamin D receptor, and nitric oxide synthase genes in Korean lead workers. Environ Health Perspect 2005;113:1509-15. 2005/11/03].

    7 Weaver VM, Lee BK, Todd AC et al. Effect modification by delta- aminolevulinic acid dehydratase, vitamin D receptor, and nitric oxide synthase gene polymorphisms on associations between patella lead and renal function in lead workers. Environ Res 2006;102:61-9. doi:S0013- 9351(06)00002-8 [pii] 10.1016/j.envres.2006.01.001 [doi] [published Online First 2006/02/21].

    8 Weaver VM, Griswold M, Todd AC et al. Longitudinal associations between lead dose and renal function in lead workers. Environ Res 2009;109:101-7. doi:S0013-9351(08)00215-6 [pii] 10.1016/j.envres.2008.09.005 [doi] [published Online First 2008/11/29].

    Conflict of Interest:

    None declared

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  2. Response to "Does self-reported computer work add biologically relevant information beyond that of objectively recorded computer work?"

    We appreciate the careful reading of our editorial [1] by Drs. Mikkelsen and Andersen. We regret our omission of the one published NUDATA study available at the time our editorial was submitted [2]. That study reported significant associations between mouse usage time collected with memory resident software and both, acute neck pain and acute shoulder pain, among 2146 technical assistants. However, because i) median mouse usage time was 5.2 hours/week and median keyboard usage time was 0.9 hours/week, and ii) rates of moderate or greater musculoskeletal pain were very low among the participating computer users, we are concerned about the generalizability of the observed associations to workers with greater mouse and keyboard use.

    Regarding differences in associations with musculoskeletal disorders (MSDs) observed across studies using self-reported estimates of computer use versus memory resident software documentation of computer use, we made no argument that one was correct and the other was incorrect. Rather, we raised the concern that these two exposure assessment methods capture different (but not totally unrelated) aspects of computer use relevant to MSD risk. The absence of perfect correlation between self-reported estimates of computer use and memory resident software documentation of computer use may be due to error in self report, differences in the kind of exposure information captured, or both. The claims of methodological objectivity and validity presented by Mikkelsen and Andersen do not address this fundamental question. We continue to believe, as noted in our editorial, that a better understanding of the attributes of work captured by self report and by computer registration software will clarify what appear to be inconsistent results reported by studies using them.

    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. 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

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  3. Does self-reported computer work add biologically relevant information beyond that of objectively recorded computer work?

    In a recent editorial Gerr et al.[1] discuss computer work and musculoskeletal outcomes based on self-reported exposure versus objective recordings using computer software. They state that only one small study (n=27) using objective recordings was published before a large study by Ijmker et al.[2], published in the same issue as the editorial. They failed to consider the results of two NUDATA papers based on more than 2000 study participants, one of them published in the OEM[3]. The results of the study of Ijmker et al. and the NUDATA studies consistently indicate that sustained or severe pain outcomes were not related to objective computer work recordings. The editorial argues that the results of the study of Ijmker et al does not invalidate the much larger literature in which self-reported computer use was associated with musculoskeletal symptoms. The main argument seems to be that objective recordings do not capture the relevant exposures, e.g. holding the hands over the keyboard without keying and that different cut points for such non-activity periods may invalidate the objective recordings. However, objective software-based computer work recordings are in very good accordance with other objective measures like video- recordings, and much better than self-reported exposure. Furthermore, within reasonable limits, different cut-off values for non-activity periods do not change these relations or computer times very much. This is consistent evidence from several studies and not from "preliminary investigations", as stated in the editorial. Finally, exposure times based on different cut off's are highly correlated, and their relation to musculoskeletal outcomes will not vary much with different cut-offs [4]. Contrary to the editorial, we find it very unlikely that retrospective self-reports about computer use during several months should capture biologically important aspects of computer work which are not captured by a validated objective method, which prospectively collects exact computer use data on a daily basis.

    References

    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. IJmker S, Huysmans MA, van der Beek AJ, et al. Software-recorded and self-reported duration of computer use in relation to the onset of severe arm-wrist-hand pain and neck-shoulder pain. Occup Environ Med 2011; 68: 502-9

    3. 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.

    4. 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 2011 May 24 [Epub ahead of print]

    Conflict of Interest:

    None declared

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  4. Re:Analysis of job strain effects

    We thank Dr. Mikkelsen and colleagues for their constructive comments on our paper. Our responses to their three major questions are listed below.

    1) Why did we present various formulations of job strain?

    The five formulations of job strain have been commonly reported in the literature. Often, authors chose one or two formulations and thus would not know if their results were consistent across different formulations. In our study, with the encouragement of an OEM peer reviewer, we presented results for all five formulations so that readers can compare the results both across different formulations and with previous job strain studies. We agree with Mikkelsen et al. that four of the five formulations of job strain we examined could be the result of the effect of job control only. As shown in Table 3, job demands was not significantly associated with IMT whereas job control was.

    2) Why did we not show the main effect coefficients for job demands and control as we showed the coefficient for the multiplicative term in Table 4?

    When a multiplicative term is included in a regression model, the main effects of the interacted variables have a more complex interpretation;1 that is, the coefficients represent the magnitude of effect for each variable when the other is 0. We showed the main effects of the two variables in Table 3, which represent the magnitude of each variable's effect when the other is controlled for. For the sake of brevity, we did not show the coefficients for demands and control after the multiplicative term was included in the model. This was explained in the footnote for Table 4.

    3) Why did we illustrate the interaction in dichotomous terms (Figure 1) and ignored that high job demands were protective?

    Figure 1 is an illustration of the interaction, which could have been constructed using the mean+1SD as "high" and the mean-1SD as "low" or other ways. We used the median split again for the sake of simplicity and also because it is a commonly used approach in the job strain literature. We do recognize that the demand-control model was only partially supported in our study; that is, job control was protective only for those who reported high job demands. Overall, job demands did not have a significant association with IMT, as shown in Table 3. The following paragraph is our discussion on this finding from an earlier draft. Unfortunately, this paragraph was excluded from the final version because of the word limit.

    Contrary to the demand-control model's prediction,2 we did not find significant associations between IMT and job demands. The Cardiovascular Risk in Young Finns Study also failed to find the same significant association.3 The majority of CVD studies have found positive associations between job demands and CVD,4 but Belki? et al.4 identified five studies that reported an inverse association between psychological job demands and CVD.5-9 In the MESA cohort, of which about 30% were immigrants, the job demands scale had acceptable scale reliability among U.S.-born participants but not among immigrants (Cronbach's alpha = 0.75 for U.S.-born, ranged from 0.45 to 0.65 for immigrants, depending on the language used in data collection10). Limitations in the measure of job demands used in heterogeneous samples like ours may have limited our ability to detect associations of job demands with IMT.

    References:

    1. Cohen J, Cohen P. Applied Multiple Regression: Correlation Analysis for the Behavioral Sciences. 2nd ed. Hillsdale, NJ: Lawrence Erlbaum, 1983.

    2. Karasek RA. Job demands, job decision latitude, and mental strain: Implications for job redesign. Administrative Science Quarterly 1979;24:285-308.

    3. Hinsta T, Kivim?ki M, Elovainio M, Vahtera J, Hintsanen M, Viikari JSA, et al. Is the association between job strain and carotid intima-media thickness attributable to pre-employment environmental and dispositional factors? The Cardiovascular Risk in Young Finns Study. Occupational and Environmental Medicine 2008;65:676-82.

    4. Belki? KL, Landsbergis PA, Schnall P, Baker D. Is job strain a major source of cardiovascular disease risk? Scand. J. Work Environ. Health 2004;30(2):81-128.

    5. Alterman T, Shekelle RB, Vernon SW, Burau KD. Decision latitude, psychologic demand, job strain and coronary heart disease in the Western Electric Study. American Journal of Epidemiology 1994;139:620-27.

    6. Bobak M, Hertzman C, Skovoda Z, Marmot MG. Association between psychosocial factors at work and non-fatal myocardial infarction in a population based case-control study in Czech men. Epidemiology 1998;9:43- 47.

    7. Hall EM, Johnson JV, Tsou TS. Women, occupation, and risk of cardiovascular morbidity and mortality. Occupational Medicine 1993;8:709- 19.

    8. Johnson JV, Stewart W, Hall EM, Fredlund P, Theorell T. Long-term psychosocial work environment and cardiovascular mortality among Swedish men. American Journal of Public Health 1996;86:324-31.

    9. Steenland K, Johnson JV, Nowlin S. A follow-up study of job strain and heart disease among males in the NHANES1 population. American Journal of Industrial Medicine 1997;31:256-59.

    10. Fujishiro K, Landsbergis P, Diez Roux AV, Hinckley Stukovsky K, Shrager S, Baron S. Factorial invariance, scale reliability, and validity of the decision latitude and psychological demands scales for immigrant workers: The Multi-Ethnic Study of Atherosclerosis (MESA). Journal of Immigrant and Minority Health 2010;13:533-40.

    Conflict of Interest:

    None declared

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  5. Exposure to keyboard/mouse use = keystrokes + mouse clicks + POSTURE - a missing variable that cannot be overstated

    Self-report of duration of computer use is usually overestimated. The search for a valid measure of exposure to keyboard/mouse use resulted in the development of a computer registration software. The use of this new software generated unexpected results when IJmker et al.1 found software- recorded computer use was not significantly associated with upper extremity/neck symptom onset while self-reported computer use was signficantly associated with symptoms in the neck/shoulder and arm/hand. What is captured in the self-report that is missing in the software- recorded duration of computer use? In the editorial by Gerr and Fethke2 reference is made to work by Homan and Armstrong3 that noted the potential negative effect of time spent with hands held over the keyboard but without keying. In our Medical-Ergonomic Program4 we refer to this position as the 'action ready' posture when the forearm(s) is in full pronation over the keyboard or mouse causing muscle activation of the forearm extensor muscles. This may lead to the development of painful trigger points in the forearm extensor muscles, a common area of complaints by computer users.4 Activities such as reading, talking, thinking etc. while using the computer are frequently accompanied by this 'action ready' posture. Time spent in these activities is included when self-reporting duration of computer use but would not be captured in computer registration software.

    Other posture issues without keystrokes or mouse clicks involve the neck/shoulder area. Computer users have a habit of not sitting up straight against the back of the chair and carry their shoulders forward. This posture activates the muscles involved with scapulae stabilization and shortens the pectoralis minor4 resulting in painful trigger points in the overused muscles . Neck/shoulder muscles are also activated when mouse use is with the arm extended away from the body, when the monitor is too far away and the chin juts forward or when the keyboard is too high and the shoulders remain hiked to compensate. Maintenance of these postures with or without keystrokes and mouse clicks are an etiology for upper extremity symptoms that needs to be added to the exposure equation for computer use.

    1. IJmker S, Huysmans MA, van der Beek AJ, et al. Software-recorder and self-reported duration of computer use in relation to the onset of severe arm-wrist-hand pain and neck-shoulder pain. Occup Environ Med 2011;68:502-209.

    2. Gerr F and 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- 466.

    3. Homan MM and Armstrong TJ. Evaluation of three methodologies for assessing work activity during computer use. AIHA J (Fairfax, VA) 2003;64:48-55.

    4. Bleecker ML, Celio MA, Barnes SK. A medical-ergonomic program for symptomatic keyboard/mouse users. JOEM 2011;53:561-567.

    Conflict of Interest:

    None declared

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  6. Analysis of job strain effects

    Fujishiro et al.1 recently published data on the association of job demands and control with carotid artery intima-media thickness (IMT). The joined effect of demands and control (strain) was analyzed by five different strain definitions: 1. a quadrant term (median splits of demands and control), 2. combinations of tertiles of demands and control, 3. an additive term (demands minus control) , 4. a quotient term (the ratio) and 5. a multiplicative term (the product).

    The first three terms are linear combinations of demands and control, which are less informative than the corresponding linear combination based on regression analyses of the mutually adjusted effects of demands and control. The quotient term implies interaction between demands and control but does not examine if there is one, its size, form or statistical significance. An effect of any of the first four strain terms may be due to an effect of only one of the two factors. Why introduce a strain measure of the joined effect of demands and control, if it may only reflect the effect of one of these variables? A parsimonious and informative way to examine the joined effect of demands and control is regression analyses with demands, control and their multiplicative term included as covariates. The authors published the effects of the multiplicative term but not the main effects. These are needed to evaluate the form of any interaction. The authors only illustrate the form of the interaction by dichotomous combinations of demands and control. The authors interpret the interaction as confirmation of the job strain theory because high job control protected against thick IMT, especially among persons with high job demands. However, they overlook that high job demands also protected against thick IMT. The interaction effect as a whole was not in accordance with the job strain model.

    References 1. Fujishiro K, Diez Roux AV, Landsbergis P, et al. Associations of occupation, job control and job demands with intima-media thickness: The Multi-Ethnic Study of Atherosclerosis (MESA). Occup Environ Med 2011;68:319-326.

    Conflict of Interest:

    None declared

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  7. A dose-response for asbestos

    The article by Clin et al. (1) provides additional information for a dose-response relationship with asbestos and cancer. Information where a response curve changes effect as observed from background is critical in establishing a safe exposure limit (threshold -exposure/concentration- dose). Some investigators have reported this threshold is around 25 fiber/ml-years (2); although for some members of an exposed group this may be lower (3). However, a cumulative no-effect value does not provide information applicable for practical every day use when monitoring worker exposure.

    Recent studies (4,5,6) have suggested levels of exposure where there was no excess increase in cancer, notably lung cancer and mesothelioma. This is especially noted for non-smokers where risk does not exceed unity (lung cancer), even for high asbestos exposure, while there is a significant increased risk for smokers and former smokers (6,7). Thus, it appears smoking is the primary contributor and confounder of disease for historical and current asbestos workers (6). Compounding this issue is the high number of smokers performing asbestos abatement work (approximately 60% or greater depending on the population observed even at the present time) (8,9). The high rate of smoking makes it difficult to estimate a threshold and subsequently establish an exposure value from this type of information. Certainly, for today's asbestos workers smoking constitutes their greatest risk (6,9,10). Recent studies with direct (4,5) and indirect (e.g. Job Exposure Matrix and Job Specific Modules) (6,11) exposure information do allow an estimate of a threshold exposure dose. Although, exposure can greatly vary over time (4), it appears even with mixed fiber exposure (chrysotile and amphibole) (5) a threshold of 1.0 f/ml-year is applicable, but at the upper range. If chrysotile alone is used in this estimate, it appears a higher value would be warranted (5). Taken together, with a safety margin to include a lower reported value in causation of asbestosis (about 23 f//ml - years) (11), a threshold of 0.8 f/ml-year would appear applicable (20 f/ml - years). From this, using a work time period of 25 years, which is not likely for asbestos workers in the United States, due to physical demands of the occupation and actual length of the "industry", allows suggestion for a threshold of 0.8 f/ml-Time Weighted Average. When present exposure levels are included in this evaluation (12), it is unlikely workers in developed nations will exceed a cumulative exposure of 20 or 25 fiber/ml-years. Comparison of this proposed threshold with data reported by Clin et al., for lung cancer and mesothelioma, with 25 years or less of exposure (table 1 in Clin et al.), provides support for this threshold value. However, any value will be controversial, especially in establishing a threshold.

    References

    1. Clin B, Morlais F, Launoy G, Guizard AV, Dubois B, Bouvier V, Desoubeaux N, Marquignon MF, Raffaelli C, Paris C, Galateau-Salle F, Guittet L, Letourneux M. Environ Occup Med 2011; First online March 15, 2011.

    2. Lange JH. Emergence of a New Policy for Asbestos: A Result of the World Trade Center Tragedy. Indoor and Built Environment 2004; 12:21-33.

    3. Pierce JS, McKinley MA, Paustenbach DJ, Finley BL. An evaluation of reported no-effect chrysotile asbestos exposures for lung cancer and mesothelioma. Crit Rev Toxicol. 2008;38:191-214.

    4. Sichletidis L, Chloros D, Spyratos D, Haidich AB, Fourkiotou I, Kakoura M, Patakas D. Mortality from occupational exposure to relatively pure chrysotile: a 39-year study. Respiration. 2009;78:63-8.

    5. Dodic Fikfak M, Kriebel D, Quinn MM, Eisen EA, Wegman DH. A case control study of lung cancer and exposure to chrysotile and amphibole at a slovenian asbestos-cement plant. Ann Occup Hyg. 2007 51:261-8.

    6. Frost G. The joint effect of asbestos exposure and smoking on the risk of lung cancer mortality for asbestos workers (1971-2005). 2011; Health & Safety Executive (HSE); (http://www.hse.gov.uk/research/rrhtm/rr730.htm)

    7. Frost G, Darnton A, Harding AH. The effect of smoking on the risk of lung cancer mortality for asbestos workers in Great Britain (1971- 2005). Ann Occup Hyg. 2011 55:239-47.

    8. Frost G, Harding AH, Darnton A, McElvenny D, Morgan D. Occupational exposure to asbestos and mortality among asbestos removal workers: a Poisson regression analysis. Br J Cancer. 2008 99:822-9.

    9. Lange JH, Mastrangelo G, Buja A. Smoking and alcohol use in asbestos abatement workers. Bull Environ Contam Toxicol 2006 77:338-42.

    10. Harding A-H, Darnton A, Wegerdt J, McElvenny D. Mortality among British asbestos workers undergoing regular medical examinations (1971- 2005). Occup Environ Med 2009;66487-495.

    11. Mastrangelo G, Ballarin MN, Bellini E, Bicciato F, Zannol F, Gioffr? F, Zedde A, Tessadri G, Fedeli U, Valentini F, Scoizzato L, Marangi G, Lange JH. Asbestos exposure and benign asbestos diseases in 772 formerly exposed workers: dose-response relationships. Am J Ind Med 2009 52:596-602.

    12. Lange JH, Sites SL, Mastrangelo G, Thomulka KW. Exposure to airborne asbestos during abatement of ceiling material, window caulking, floor tile, and roofing material. Bull Environ Contam Toxicol 2006 77:718- 22.

    Conflict of Interest:

    None declared

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  8. Renal effects of cadmium exposure

    Dear Editor,

    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.

    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

    Conflict of Interest:

    None declared

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  9. Response to: Exposure to occupational noise and cardiovascular disease in the United States: the National Health and Nutrition Examination Survey 1999-2004. Gan et al. 68:183-190 doi:10.1136/oem.2010.055269

    Gan et al, 2011 [1] concluded that long-term, occupational noise exposure was associated with increased prevalence of coronary heart disease (CHD), for which the authors report a clear exposure-response relationship that was particularly strong for participants aged < 50 years, men and current smokers. We do not believe the results support these conclusions, particularly in light of notable study limitations.

    The cross-sectional design is a significant drawback. Self-reported exposure and outcome data created uncertainty, regarding time ordering of events. Additionally, exposed subjects had many well-known risk factors - representing strong confounders - for cardiovascular disease (CVD)/CHD, the effects of which cannot be entirely removed by statistical adjustment. Moreover, unrecognized bias was likely introduced by including potential causal intermediates and over-adjusting logistic models,[2] for which a mechanistic basis is not well established. Although the authors dismissed the presence of misclassification as non-differential, simulations have shown this argument to be less persuasive.[3]

    We raise additional concerns. First, heterogeneity of effect (Figure 2) precluded reporting summary estimates. It was incorrect to state, for example, that an increased odds of CHD were observed particularly for men when they were observed only for them. Second, the authors misapplied the test for trend of a monotonic exposure-response relationship.[4] Finally, potentially important effect patterns were obscured by aggregating outcomes to ascertain CVD/CHD prevalence. CVD, the primary endpoint of interest and the aggregate of six variables, was not discussed. The significant association reported for CHD was largely driven by the relatively strong association observed only for angina pectoris.

    Given the prevalence of occupational noise exposure, even a modest association would represent an important contributor to the development of CVD/CHD. Unfortunately, Gan et al [1] does little to advance our understanding of whether such an association exists, particularly because the mechanism of action is so poorly understood. We agree with the authors that cohort studies are warranted. These studies should use objective exposure and outcome measurements.

    References

    1 Gan WQ, Davies HW, Demers PA. Exposure to occupational noise exposure and cardiovascular disease in the United States: the National Health and Nutrition Examination Survey 1999-2004. Occup Environ Med 2010;68:183-190

    2 Schisterman EF, Cole SR, Platt RW. Overadjustment bias and unnecessary adjustment in epidemiologic studies. Epidemiology 2009;20:488 -495

    3 Jurek AM, Greenland S, Maldonado G. How far from non-differential does exposure or disease misclassification have to be to bias measures of association away from the null? Int J Epidemiol 2008; 37:382-5

    4 Maclure M, Greenland S. Tests for trend and dose response: misinterpretations and alternatives. Am J Epidemiol 1992;135:96-104

    Conflict of Interest:

    None declared

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  10. Observational Studies - Workforce Perspective?

    The publication of an editorial(1) and opposing commentaries(2,3) underlines the profile OEM believes should be given to debate of the proposal for observational epidemiologic studies and their protocols to be registered in advance(4). I would however express my surprise that none of these 3 offerings make mention of the workforce perspective in their analyses of the issues. The editorial itself(1) and the commentary opposing the protocol(3) do not make mention of workers at all, while the pro-commentary(2) simply includes employees in a list of those involved in collaboration to reduce difficulties in accessing data.

    It may be possible to identify both pros and cons for the registration proposal based on workforce issues, but to do so in this letter would detract from its principal purpose in registering the observation that these aspects have not been considered to date. Research is a vital element of Occupational Health. OEM is the adopted official Journal of the Faculty of Occupational Medicine of the Royal College of Physicians (London). The Faculty first introduced a section dealing with research in its ethical guidelines in 1999(5) identifying workers as key customers of research, as well as identifying the need for clear and detailed protocols, as well as worker consultation. As an Occupational Physician, I am convinced that workers are owed a very real duty of care in relation to research, whether there are clinical elements of the study or not. The trauma and distress that research results publication and the media response to such publication can cause a workforce, should not be underestimated.

    References 1 Loomis D. Journal Requirements to Register Observational Studies: OEM's Policy. OEM 2011;68:83/4. 2 Rushton L. Should Protocols for Observational Research be Registered? OEM 2011; 68:84-86. 3 Pearce N. Registration of Protocols for Observational Research is Unnecessary and Would Do More Harm Than Good. OEM 2011; 68:86-88. 4 European Centre for Ecotoxicology and Toxicology of Chemicals. Workshop Report, number 18: Enhancement of the Scientific Process and Transparency of Observational Studies, 2009. 5 The Faculty of Occupational Medicine Guidance on Ethics for Occupational Physicians, 5th Edition, May 1999.

    Conflict of Interest:

    None declared

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