Dear Editor

In response to our study,[1] Kivimäki et al suggested that reported sickness absence frequencies were underestimates of the total sickness absence burden in European Union (EU) member countries.[2] This concern about the veracity of these estimates led Kivimäki et al to caution policy makers to not use this data to inform policy. While we agree that more research is needed to establish potential biases associated with different approaches to ascertain accurate asking sickness absence data, we consider the European Survey on Working Conditions (ESWC) to be useful to inform the cross-national policy debate. Country-specific studies contribute knowledge to the evidence base but cross-national studies such as ours help to provide a stronger basis upon which to make cross-national inferences. Furthermore, cross-national studies become more relevant as data accumulate and the data collection quality improves. We hope that Kivimäki and colleagues are not suggesting the ESWC be discontinued.

We consider the studies by Kivimäki et al to be some of the most relevant epidemiological studies of sickness absence predictors.[3][4][5] Although informative, these studies raise several issues in the context of cross-national comparisons. First, epidemiological cohorts in Finland and the United Kingdom represent very homogenous and specific working populations (ie municipal employees, hospital workers and civil servants) with unknown generalizability to the national representative surveys studied in our paper or the ones referenced by Kivimäki et al.[6][7] Second, a fundamental advantage of national workforce surveys is the ability to capture all workers, whereas registries may lead to an under representation of marginal work groups typically not included in national registries. Indeed, Kivimäki et al are not arguing that the Finnish and British cohorts are representative of the countries’ workforces. Even so, labor market inequalities may cause temporary and less protected workers to be underrepresented in the type of well-designed cohort studies they have referenced.[8] Temporary and less protected workers are important in the EU economy and lack of knowledge about their labor market experiences as related to sickness absence could lead to their further marginalization in the policy debate. Third, Kivimäki et al criticised the data collection method employed in the ESWC. We are not aware of any cross-national study comparing the reliability, validity and performance of different sickness absence data collection methods. Concerns have been raised about who is placed on a sickness absence registry. Registered data are very conditioned by the country’s social security system criteria for sickness absence, which complicates between-countries comparisons.[9] Therefore, whether registries are the gold standard in sickness absence studies remains a point of debate yet to be closed.

In addition, Kivimäki et al compared our results to two survey based studies from Finland and Britain, but differences in sample selection and questionnaire design between these studies may limit comparisons. Our study included people aged 15 years and older who had any paid job during the reference week, or who had a job but were temporarily absent. The recall period for sickness absence was 12 months. The Finnish study was based on employees aged 25 to 64 using a 6 month recall period for sickness absence.[10] The British survey investigated the psychiatric morbidity prevalence among the British adult population. This study sampled workers aged 16-64 years and excluded workers with a psychosis diagnosis. Workers who were currently working or had been working in the last year were asked to report absence days due to their health or feelings.[11] For these reasons, caution is needed if a direct comparison between these three studies is intended.

Finally, we agree with Kivimäki et al that potential bias in the ESWC could be present (see page 868-9 in our article). However, we would argue that the best sources of data to inform policy are derived from systematic efforts to collect sickness absence data in a clear and consistent fashion from a representative sample of the labor force within each country. We consider the evidence presented by Kivimäki et al to support our argument of the difficulty in establishing between-country comparisons due to the fragmented and insufficient sickness absence data available at the European Union level. We consider our results useful. Although the results are preliminary and may be subjected to scientific scrutiny, the comparative findings may provoke researchers to develop standards for sickness absence studies to facilitate between-country comparisons. In addition, we hope the observed differences will promote further investigation into root causes of between-country differences, especially between northern and southern EU members, as well as within-country gender differences. We certainly welcome cross-national collaborative efforts among the EU sickness absence researches to address all these issues.

References

1. Gimeno D, Benavides FG, Benach J, Amick BC III. Distribution of sickness absence in the European Union countries. Occup Environ Med 2004;61:867-9.

2. Kivimäki M, Vahtera J, Head J, Ferrie JE. Are sickness absence frequencies in the study of EU countries underestimates? [electronic response to Gimeno D et al. Distribution of sickness absnce in the European Union countries] occenvmed.com 2004 URL direct link to eLetter.

3. Vahtera J, Pentti J, Kivimäki M. Sickness absence as a predictor of mortality among male and female employees. J Epidemiol Community Health 2004;58:321-6.

4. Kivimäki M, Virtanen M, Vartia M, Elovainio M, Vahtera J, Keltikangas-Järvinen L. Workplace bullying and the risk of cardiovascular disease and depression. Occup Environ Med 2003;60:779-83.

5. Kivimäki 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;327:364-8.

6. Kauppinen T, Hanhela R, Heikkilä P et al. Work and Health in Finland 2003. Finnish Institute of Occupational Health, Helsinki, 2004.

7. Stansfeld SA, Head J, Rasul F, Singleton N, Lee A. Occupation and mental health: Secondary analyses of the ONS Psychiatric Morbidity Survey of Great Britain. Research Report 168, Health and Safety Executive Books, 2003.

8. Moss NE. [Review of the book Why Are Some People Healthy and Others Not? The Determinants of Health of Populations, by Robert G. Evans, Morris L. Barer, and Theodore R. Marmot] Health Affairs 1995;(14) 2:318- 21.

9. Gründemann RWM, van Vuuren CV. Preventing absenteeism at the workplace. Dublin: European Foundation for the Improvement of Living and Working Conditions, 1997

10. Kauppinen T, Hanhela R, Heikkilä P et al. Work and Health in Finland 2003. Finnish Institute of Occupational Health, Helsinki, 2004.

11. Stansfeld SA, Head J, Rasul F, Singleton N, Lee A. Occupation and mental health: Secondary analyses of the ONS Psychiatric Morbidity Survey of Great Britain. Research Report 168, Health and Safety Executive Books, 2003.

Dear Editor

The paper by Chang et al[1] defined a Protective Effectiveness Index (PEI) as a measure of the protection afforded by gloves, whereas in reality it indicates the overall difference in exposure between two groups of workers where other important exposure factors may not be, indeed were not, the same. This raises the possibility that your readers may mistake this index as a reliable guide to glove protection and make inappropriate choices when managing risks from dermal exposure.

Chang et al present results from biological monitoring amongst workers exposed to 2-methoxyethanol (2-ME). The authors use the urinary (and plasma) metabolite levels from workers who wore gloves (cotton and butyl rubber) compared with the levels from other workers who did not wear gloves to assess the protective effectiveness of the protective equipment. They defined the PEI as:

where UMAA is the urinary 2-methoxyacetic acid concentrations, the main metabolite of 2-ME, measured in end of shift samples.

The PEI is zero when the average metabolite levels in both groups are identical and 100% when the UMAA_withglove is zero. If the UMAA_withglove is greater than the levels from the group not wearing gloves then the calculated PEI will be negative.

This approach is quite different from the conventional paradigm for the effectiveness of personal protective equipment. For example, for respiratory protection a Protection Factor (PF) is normally expressed as the ratio of the concentration outside the mask to that inside.[2] Cherrie et al[3] have recently published a proposal for evaluating the effectiveness of gloves against chemicals. They define the PF for gloves analogously to that for respiratory protective equipment:

where U_sk is the mass uptake through the stratum corneum, either with or without gloves being worn.

Using mathematical simulations they showed that the PF_gloves is not constant for a particular glove type but varies depending on the work situation and it decreases as the duration of wearing the gloves increases, even if they are not removed.

One proposal made by Cherrie et al. for measuring the PF_gloves was to use a carefully controlled biological monitoring study. In the Chang et al. study the conditions are not controlled and there is no information about the pattern of wearing the gloves. If the gloves were only worn for a proportion of the working shift then the protection may be seriously compromised by periods when the person works with bare hands. Also, for this type of study to be informative there must be negligible uptake from inhalation exposure.

The authors report that the geometric mean personal inhalation exposure level was 3.3ppm (8h time-weighted average) and the workers refused to wear respiratory protective equipment. From the work of Kezic et al[4] this average exposure might be expected to result in about 5mg of UMMA being excreted in the 48h following exposure, suggesting inhalation exposure may contribute an important part of the UMAA measured in this study and consequently reducing the apparent effectiveness of the gloves.

In the Chang et al study we are not told whether there are differences between the average inhalation exposure levels between those who wore gloves and those that did not. From the tabulated data below (abstracted from Table 1 in Chang et al) it would appear that those wearing gloves may have been exposed to higher inhalation levels. Such differences would further confound the interpretation of the protection offered by gloves by reducing the apparent protection.

Table 1 Inhalation exposure levels and wearing of rubber gloves

If we assume that the UMAA level in urine at the end of the shift is proportional to the dermal uptake then the PF_gloves for the rubber gloves used in the Chang et al study would be about 4 (the PEI was 74%) and for the cotton gloves it would be 1.1 (PEI=11%) for "Special" workers and 0.85 (PEI= -17%) for "Regular" workers. The figure for butyl rubber gloves appear to be particularly low in comparison to what might be expected. For example, Zellers et al[5] have shown that this type of glove material (in fact the same glove manufacturer as the gloves in Chang et al's study) can provide up to 4h protection against 2-ME without any breakthrough. This further suggests that this study does not reliably assess the protection offered by gloves.

Experimental intervention studies using biological monitoring data are probably the best way of estimating PF_gloves. However, it is important to consider and minimise all possible biases and to collect information about usage pattern, particularly the duration of wear and the duration of the tasks.

References

1. Chang, H-Y, Lin, C-C, Shih, T-S, Chan, H, Chou, J-S, and Huang, Y-S, Evaluation of the protective effectiveness of gloves from occupational exposure to 2-methoxyethanol using the biomarkers of 2-methoxyacetic acid levels in the urine and plasma. Occup Environ Med 2004; 61: 697-702.

2. Howie, R, Personal protective equipment, in Occupational Hygiene, J. Harrington and K. Gardiner, Editors. Oxford: Blackwell Science Ltd 1980: 404-416.

3. Cherrie, JW, Semple, S, and Brouwer, D, Gloves and Dermal Exposure to Chemicals: Proposals for Evaluating Workplace Effectiveness. Ann Occup Hyg 2004; 48 (7): 607-615.

4. Kezic, S, Mahieu, K, Monster, AC, and de Wolff, FA, Dermal absorption of vaporous and liquid 2-methoxyethanol and 2-ethoxyethanol in volunteers. Occup Environ Med 1997; 54 (1): 38-43.

5. Zellers, E, Ke, H, D, S, R, S, Patrash, S, Han, M, and Zhang, G, Glove permeation by semiconductor processing mixtures containing glycol-ether derivatives. Am Ind Hyg Assoc J 1992; 53 (2): 105-118.

Dear Editor

As Punnett correctly pointed out in her editorial,[1] we called attention to the need to determine the causes of perceived muscular tension (PMT) in our paper.[2] Unfortunately, the PMT data was only collected at the baseline of the study and not at any of the 10 follow-ups. Due to the lack of longitudinal data we could not explore the cause(s) of PMT in our analyses.

Punnett also raises the issue that any other occupational effects (in this case physical and/or psychosocial exposure) are underestimated in the analyses that are adjusted for PMT. This is a correct observation, though we have presented both univariate and multivariate analyses in the paper and the results in the univariate and the multivariate analyses do not differ that much and the same patterns are observed in both analyses.

Following the above mentioned observations, Punnett comments that the results provide less information than we might wish to have regarding which interventions would decrease muscle tension and resulting neck pain. Although the study did not reveal what factors cause PMT, we believe that the results indicate that PMT can be used both in health surveillance and in health screening. Work places where a high prevalence of PMT is found should be prioritized for interventions (eg health surveillance). These interventions can target both psychosocial and ergonomic work factors. In health screening, individuals with high PMT can be targeted for further examination of possible job and home psychosocial and ergonomic stressors.

Furthermore we suggest that interventions against high PMT conducted by the occupational health services should focus on more than one risk factor. For example, an intervention could comprise optimisation of the workplace layout (modifying the physical demands) in combination with a feedback survey of the psychosocial work environment (modifying the psychosocial factors) and individual training focusing on working and relaxation technique (modifying the individual factors). Although we do not yet have support for this recommendation by data from RCTs of reducing PMT there are interventions studies showing effects on discomfort by multifactor ergonomic actions.[3]

References

1. Punnett L. Work related neck pain: how important is it, and how should we understand its causes? Occup Environ Med 2004; 61: 954-955.

2. Wahlström J, Hagberg M, Toomingas A et al. Perceived muscular tension, job strain, physical exposure, and associations with neck pain among VDU users; a prospective cohort study. Occup Environ Med 2004 61(6): 523-8.

3. Ketola R, Toivonen R, Häkkänen M et al. Effects of ergonomic intervention in work with video display units. Scand J Work Environ Health 2002 28(1): 18-24.

Dear Editor

In a letter, Greenberg,[1] commenting on our paper,[2] raises a number of points with which we disagree.

There is now a broad consensus that amphiboles are vastly more dangerous than chrysotile in their propensity to produce mesothelioma, and even a casual review of the literature indicates that where there is a continuing increase in mesothelioma rates, it is seen in countries that used large amounts of amosite and crocidolite, as we indicated in our paper.

He raises the issue of whether asbestosis must be present to attribute a lung cancer to asbestos exposure. Our paper was not about this issue, we did not say anything about necessary sequence and the phrase he cited was the lone mention of this issue, included in the introduction before focusing on the main subject: mesothelioma. However, since Greenberg raises the subject, the Wilkerson et al paper[3] was in no way a "consensus" by a "group of experts", rather it was the report of a study of hospitalized patients, a study which had a number of serious flaws, as we explained in our published response.[4] Also, even if one assumes that lung cancers can be generated by high exposure to asbestos without the presence of asbestosis, it makes no sense to expect an increased lung cancer risk in the face of declining asbestos usage and increased control of exposure, exactly the factors that are driving the decreased rates of mesothelioma. Greenberg’s own words clearly indicate that he is more interested in the "adversarial spectrum" than the science!

Greenberg complains about the use of national import tonnage as an indicator of potential overall worker exposures to the various asbestos fiber types. There is no other way to do this, and this approach has been used by Peto,[5] and in a previous publication of ours, comparing US and UK mesothelioma trends.[6]

We don’t know exactly what paper Greenberg refers to in his comments about events that occur in test tubes within 4 minutes, but in vitro experimental data must always give way to in vivo experimental data, and the latter to human epidemiology. Greenberg is actually incorrect in stating that all types of fibers are equally potent causes of malignancies in animals. In fact, proper analysis of the original Wagner inhalation experiments in rats indicates that, because the asbestos was delivered on an equal mass and not equal fiber number basis, the number of chrysotile fibers to which the animals were exposed was vastly greater than the number of amphibole fibers but the number of mesotheliomas found was about the same, thus indicating the greater potency of amphiboles in causing mesothelioma. This conclusion has been confirmed for both mesothelioma and lung carcinoma in more modern animal inhalation studies, comprehensively reviewed,[7] and there is in fact considerable evidence that lung cancers in animals exposed to asbestos only develop when asbestosis is present.[8]

Greenberg raises a number of other issues, but the overall thrust of his letter appears to be that declining rates of (readily apparent) asbestos-induced disease should not be viewed as indicating a foreseeable end to the asbestos problem. Yet if declining rates of disease don’t indicate a problem that, with proper control of exposure, will slowly disappear, what will?

Finally, Greenberg closes with kudos for a conference entitled The Third Wave of Asbestos Disease.[9] In the view of most investigators in this field, this conference contributed little to the knowledge base on asbestos-related diseases and served mainly as a political/litigation brief. One wonders if there will ever come a time when any good news about asbestos-related health effects is welcomed by all who profess to have worker health as their primary motivation.

References

(1) Greenberg M. Changing trends in US mesothelioma incidence. Occup Environ Med 2005;62:133–134.

(2) Weill H, Hughes JM, Churg AM. Changing trends in US mesothelioma incidence. Occup Environ Med. 2004 May;61(5):438-41.

(3) Wilkinson P, Hansell DM, Janssens S, et al. Is lung cancer associated with asbestos exposure when there are no small opacities in the chest radiograph? Lancet 1995;345:1074–8.

(4) Weill H, Hughes JM, Jones RN. Asbestos: a risk too far? Lancet 1995; 346:304.

(5) Peto J, Hodgson JT, Matthews FE, Jones JR. Continuing increase in mesothelioma mortality in Britain. Lancet. 1995 Mar 4;345(8949):535-9.

(6) Weill H, Hughes JM. Mesothelioma. Lancet 1995; 345:1234.

(7) Hesterberg TW, Hart GA: Synthetic vitreous fibers: a review of toxicology research and its impact on hazard classification. Crit Rev Toxicol 2001;31:1-53.

(8) Davis JM, Cowie HA. The relationship between fibrosis and cancer in experimental animals exposed to asbestos and other fibers. Environ Health Perspect 1990;88:305-309.

(9) The Third Wave of Asbestos Disease: Exposure to Asbestos in Place --Public Health Control. Conference. New York, New York, June 7-9, 1990. Ann N Y Acad Sci. 1991 Dec 31;643:1-625.