With interest we read the article by Gustavsson and colleagues [1] on the breast cancer risk in a cohort with night work. The authors started from two facts: First, “night shift work” [2] was classified as “probably carcinogenic to humans” (Group 2A) by the International Agency for Research on Cancer [IARC]; second, the evidence in humans was considered limited because of variable results and potential bias. Since prior studies had problems regarding exposure assessment, Gustavsson et al. emphasized their very detailed registry-based data on night work. Yet, as key result the authors noted that “conclusions are limited due to a short period of follow-up and lack of information of night work before 2008”. Thus, this study perpetuates limited epidemiological evidence for the carcinogenicity of night work. Although the limited data on shift work is a drawback of this study, it is not the only limitation. We would like to discuss a conceptual problem that may have contributed to the limited conclusions and that the authors did not address.
The IARC monograph mentions chronotype and sleep 73 and 199 times, respectively [2]. Chronotype tells us when persons prefer sleep or work and activity. Potentially harmful circadian disruption (CD) [3] can occur at any time over 24 hours when activities or sleep are misaligned with the chronotype-associated biological nights [3 4] or biological days. This leads to occupational and non-occupational CD [5]. Possible effects of not c...
With interest we read the article by Gustavsson and colleagues [1] on the breast cancer risk in a cohort with night work. The authors started from two facts: First, “night shift work” [2] was classified as “probably carcinogenic to humans” (Group 2A) by the International Agency for Research on Cancer [IARC]; second, the evidence in humans was considered limited because of variable results and potential bias. Since prior studies had problems regarding exposure assessment, Gustavsson et al. emphasized their very detailed registry-based data on night work. Yet, as key result the authors noted that “conclusions are limited due to a short period of follow-up and lack of information of night work before 2008”. Thus, this study perpetuates limited epidemiological evidence for the carcinogenicity of night work. Although the limited data on shift work is a drawback of this study, it is not the only limitation. We would like to discuss a conceptual problem that may have contributed to the limited conclusions and that the authors did not address.
The IARC monograph mentions chronotype and sleep 73 and 199 times, respectively [2]. Chronotype tells us when persons prefer sleep or work and activity. Potentially harmful circadian disruption (CD) [3] can occur at any time over 24 hours when activities or sleep are misaligned with the chronotype-associated biological nights [3 4] or biological days. This leads to occupational and non-occupational CD [5]. Possible effects of not considering all contributions from such ubiquitous exposures have been exemplified: 1950 landmark data “scenarios” with workplace- and non-workplace smoking evinced that neither the magnitude nor the direction (!) of estimated cancer risks would have been correct if exposures off work had been ignored [6].
Thus, why not use a comprehensive dose concept to capture CD, as we regularly do in occupational epidemiology? We can assess cumulative CD as time-dependent long-term dose [7 8] by determining how much of each study participants’ biological night does not overlap with individual sleep time, and this would capture exposures to CD both at and off work. Scandinavian countries with their excellent databases may provide the data for time-related analytical procedures [9 10] needed for this integrated dose epidemiology.
Overall, such circadian epidemiology may help to avoid conclusions such as “Most exposure metrics showed no association with breast cancer risk” [1]. Combining the methodological rigor of occupational epidemiology with insights from chronobiology may shed light on plausible relationships between ubiquitous sources of CD and disease, including cancer.
REFERENCES
1 Gustavsson P, Bigert C, Andersson T, et al. Night work and breast cancer risk in a cohort of female healthcare employees in Stockholm, Sweden. Occup Environ Med 2023;80(7):372-76. doi: 10.1136/oemed-2022-108673
2 IARC. Carcinogenicity of night shift work. Lancet Oncol 2019;20(8):1058-59. doi: 10.1016/S1470-2045(19)30455-3
3 IARC. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Volume 98. Painting, Firefighting and Shiftwork. Lyon, France., 2010.
4 Erren TC, Gross JV, Fritschi L. Focusing on the biological night: towards an epidemiological measure of circadian disruption. Occup Environ Med 2017;74(3):159-60. doi: 10.1136/oemed-2016-104056
5 Erren TC, Lewis P. Hypothesis: ubiquitous circadian disruption can cause cancer. Eur J Epidemiol 2019;34(1):1-4. doi: 10.1007/s10654-018-0469-6
6 Erren TC, Lewis P, Morfeld P. The riddle of shiftwork and disturbed chronobiology: a case study of landmark smoking data demonstrates fallacies of not considering the ubiquity of an exposure. J Occup Med Toxicol 2020;15:10. doi: 10.1186/s12995-020-00263-2
7 Erren TC, Morfeld P. Shift work and cancer research: a thought experiment into a potential chronobiological fallacy of past and perspectives for future epidemiological studies. Neuro Endocrinol Lett 2013;34(4):282-6.
8 Morfeld P, Erren, T.C. Shift Work, Chronotype, and Cancer Risk-Letter. Cancer Epidemiology, Biomarkers & Prevention 2019
9 Rothman KJ, Greenland, S., Lash, T.L. Modern epidemiology 3rd ed.: Philadelphia: Lippincott Williams & Wilkins 2008.
10 Robins J. The control of confounding by intermediate variables. Statistics in medicine 1989;8(6):679-701. doi: 10.1002/sim.4780080608
The paper by Go et al (Occup Environ Med 2023;80425-30) is an important reminder of the problem of quartz in coal mine dusts and of its association with early development of pneumoconiosis, often associated with unusual radiological patterns. The UK work which they kindly cite brought to light a problem for regulation of the quartz in coal mine dust – that in many cases quartz concentrations greater than 0.1mg/m3 in mine environments seemed not to be associated with development of silicosis. Experimentally, the toxicity of quartz is reduced when it is associated, as is usual in coal mines, with a high concentration of other silicates, which occlude the crystal surface. This led to the pragmatic solution of ignoring quartz if it constituted less than 10% of the total mine dust concentration (which then was regulated as less than 5mg/m3).
These difficulties in setting and monitoring compliance with a quartz standard in coal mines are obsolete in UK as long as mines remain closed. However, while mining continues elsewhere it is important to recognise that miners know when they are cutting rock and so do their employers. When this is happening it should be recognised that they are at risk of silicosis and, as the authors show, the implications are far more serious for their health than those from coal alone; any early radiological evidence is usually too late for the miners and extra action to increase their safety needs to be required of the employer in these circumstan...
The paper by Go et al (Occup Environ Med 2023;80425-30) is an important reminder of the problem of quartz in coal mine dusts and of its association with early development of pneumoconiosis, often associated with unusual radiological patterns. The UK work which they kindly cite brought to light a problem for regulation of the quartz in coal mine dust – that in many cases quartz concentrations greater than 0.1mg/m3 in mine environments seemed not to be associated with development of silicosis. Experimentally, the toxicity of quartz is reduced when it is associated, as is usual in coal mines, with a high concentration of other silicates, which occlude the crystal surface. This led to the pragmatic solution of ignoring quartz if it constituted less than 10% of the total mine dust concentration (which then was regulated as less than 5mg/m3).
These difficulties in setting and monitoring compliance with a quartz standard in coal mines are obsolete in UK as long as mines remain closed. However, while mining continues elsewhere it is important to recognise that miners know when they are cutting rock and so do their employers. When this is happening it should be recognised that they are at risk of silicosis and, as the authors show, the implications are far more serious for their health than those from coal alone; any early radiological evidence is usually too late for the miners and extra action to increase their safety needs to be required of the employer in these circumstances.
Anthony Seaton
This study reports an alarming prevalence of silicosis in Victoria, Australia at 28.2% among workers in the stone benchtop industry (SBI). [1] That prevalence is higher than reported in SBI workers in another Australian state of Queensland (22.7%). [4] The Victorian silicosis screening program reported respiratory function tests and chest x-rays to be of limited value in screening this high-risk population which has significant implications for health and safety policy. It also calls into question the adequacy of current screening programs in other Australian States and Territories.
In the adjoining state of New South Wales (NSW), Australia, there has been an obligation on the health and safety regulator (SafeWork NSW) to maintain a Dust Diseases Register and to provide a report on the Register at the end of each financial year since October 2020. This information is provided and published in the NSW Dust Disease Register Annual Report. However, no information is provided on the total number of workers screened (or the denominator) to enable understanding of the incidence and prevalence of silicosis in NSW.
A desk-based “case finding” study from May 2021 in NSW estimated the average incidence (new cases) of silicosis among engineered stone workers in NSW at between 4% and 9% for the three-year reporting period, and suggested that incidence values may also be considered as the estimated prevalence within SBI workers. [3] This prevalence estimate is significant...
This study reports an alarming prevalence of silicosis in Victoria, Australia at 28.2% among workers in the stone benchtop industry (SBI). [1] That prevalence is higher than reported in SBI workers in another Australian state of Queensland (22.7%). [4] The Victorian silicosis screening program reported respiratory function tests and chest x-rays to be of limited value in screening this high-risk population which has significant implications for health and safety policy. It also calls into question the adequacy of current screening programs in other Australian States and Territories.
In the adjoining state of New South Wales (NSW), Australia, there has been an obligation on the health and safety regulator (SafeWork NSW) to maintain a Dust Diseases Register and to provide a report on the Register at the end of each financial year since October 2020. This information is provided and published in the NSW Dust Disease Register Annual Report. However, no information is provided on the total number of workers screened (or the denominator) to enable understanding of the incidence and prevalence of silicosis in NSW.
A desk-based “case finding” study from May 2021 in NSW estimated the average incidence (new cases) of silicosis among engineered stone workers in NSW at between 4% and 9% for the three-year reporting period, and suggested that incidence values may also be considered as the estimated prevalence within SBI workers. [3] This prevalence estimate is significantly lower than that reported in the neighbouring states.
In late 2022, a member of the NSW Parliament requested documents relating to information held by Insurance and Care NSW (icare) for its silicosis screening program under Standing Order 52 (SO52). [5] This resulted in information becoming publicly available, including the documents created since 1 January 2020 relating to the NSW silicosis screening program. [6] Contained in these documents was data on the number of people screened from specific industries (including engineered stone), the number of cases reported, and information on screening methods used. That information was reviewed with regard to silicosis prevalence in the NSW SBI and compared the figures with the findings of that reported in the neighbouring states of Victoria and Queensland.
The SO52 information confirmed a prevalence of silica related diseases (SRD) of only 7% in NSW SBI workers. This prevalence represents approximately 25% of that reported by adjoining states for the same period. [1] This low reported prevalence in NSW is more likely to reflect differences in respiratory surveillance methods between NSW and neighbouring states rather than a difference in SRD statistics and health protection. For example, CT scans were offered to workers as part of the NSW icare health screening program, but were only used for 18.8% of NSW workers. [6] CT scans are more sensitive in comparison to chest x rays in detecting early disease, and reliance of x-ray may have influenced the NSW results. It should also be noted that in NSW, although it is mandatory for workers in the SBI to be screened, it is not mandatory for employers to use icare services, and private contractors can be employed. This can result in a statistical bias because there is no mandatory reporting for results to the NSW silicosis registry in the absence of diagnosed disease. This is despite recommendations having been made by the Thoracic Society of Australia and New Zealand (TSANZ) in 2020; [7] and as part of the review into the Dust Diseases Scheme in 2019 to include this data, along with the standardisation of health assessment method. [8]
The findings of the Victorian screening program confirmed that relying on symptoms, spirometry screening or chest X-ray will miss many cases of silicosis and silica-related disorders, and that the prevalence of silicosis and SRDIs in the SBI in Australia is shockingly high. [1] If the prevalence in NSW is truly closer to that reported in Queensland and Victoria (between 22 and 28%), then more than 400 cases of SRDIs are expected based on the numbers of workers screened by icare. This would represent a shortfall of over 200 undiagnosed workers in NSW that may not be receiving essential care and support. It seems likely that cases in NSW are being underestimated.
Existing systems for the discovery and reporting of SRDI cases need urgent updating. More comprehensive and accurate data is urgently needed on the prevalence of SRDI’s in NSW to better inform health policy and prevention efforts; and to reduce the burden of preventable disease on these workers and their families.
References
1. Hoy, R.F., et al., Prevalence and risk factors for silicosis among a large cohort of stone benchtop industry workers. Occupational and Environmental Medicine, 2023: p. oemed-2023-108892.
2. SafeWork NSW, NSW Dust Disease Register Annual Report 2020-21. 2021.
3. Golder Associates Pty Ltd, Case Finding Study - Respirable crystalline silica exposure in the NSW manufactured stone industry. 2021.
4. WorkSafe Queensland. Silicosis - Workcover Screening Outcomes. . 2022 [cited 2023 23 June]; Available from: https://www.worksafe.qld.gov.au/claims-and-insurance/work-related-injuri....
5. Parliament of New South Wales, Legislative Council Minutes No. 149. 2022. Available from: https://www.parliament.nsw.gov.au/tp/files/83469/Resolution - SafeWork NSW and Insurance and Care NSW (icare) - 16 November 2022.pdf
6. Department of Premier and Cabinet, Order for Papers - Supplementary Return - SafeWork NSW and Insurance and Care NSW (icare). 2023.Available from: https://www.parliament.nsw.gov.au/tp/files/83926/SO52%20Index%20-%20Supp...(icare)%20-%2012.01.2023.pdf
7. Perret, J.L., et al., Respiratory surveillance for coal mine dust and artificial stone exposed workers in Australia and New Zealand: A position statement from the Thoracic Society of Australia and New Zealand*. Respirology, 2020. 25(11): p. 1193-1202.
8. Justice, S.C.o.L.a., 2019 Review of the Dust Diseases Scheme Silicosis in the manufactured stone industry. 2020. Available from: https://www.parliament.nsw.gov.au/lcdocs/inquiries/2538/Report%2073%20%E...
Dose-dependent diagnostic efficiency and self-reporting related to a longer work history and hence to cumulative dose could explain the above-average risk of cataracts in radiologic technologists [1]. Of concern was the discrepancy between the findings for cataract history and cataract surgery, where risks for the latter were somewhat lower and generally not significant [1]. A similar pattern of significant excess relative risk (ERR) for cataract and non-significant ERR for cataract surgery has also been reported in the Mayak nuclear workers. [2,3]. This agrees with the concept of dose-dependent diagnostic efficiency with detection of mild cases not requiring surgery. Among the various groups that have been studied for radiation-associated cataract, a significant ERR for cataract surgery has been reported only in the Japanese atomic bomb survivors [4-6], where the effect of the acute exposure could indeed have taken place. More details [7].
1. Little MP, Cahoon EK, Kitahara CM, Simon SL, Hamada N, Linet MS. Occupational radiation exposure and excess additive risk of cataract incidence in a cohort of US radiologic technologists. Occup Environ Med. 2020 Jan;77(1):1-8. doi: 10.1136/oemed-2019-105902.
2. Azizova TV , Hamada N , Grigoryeva ES , et al. . Risk of various types of cataracts in a cohort of Mayak workers following chronic occupational exposure to ionizing radiation. Eur J Epidemiol2018;33:1193–204.doi:10.1007/s10654-018-0450-4
3. Azizova TV , Hamad...
Dose-dependent diagnostic efficiency and self-reporting related to a longer work history and hence to cumulative dose could explain the above-average risk of cataracts in radiologic technologists [1]. Of concern was the discrepancy between the findings for cataract history and cataract surgery, where risks for the latter were somewhat lower and generally not significant [1]. A similar pattern of significant excess relative risk (ERR) for cataract and non-significant ERR for cataract surgery has also been reported in the Mayak nuclear workers. [2,3]. This agrees with the concept of dose-dependent diagnostic efficiency with detection of mild cases not requiring surgery. Among the various groups that have been studied for radiation-associated cataract, a significant ERR for cataract surgery has been reported only in the Japanese atomic bomb survivors [4-6], where the effect of the acute exposure could indeed have taken place. More details [7].
1. Little MP, Cahoon EK, Kitahara CM, Simon SL, Hamada N, Linet MS. Occupational radiation exposure and excess additive risk of cataract incidence in a cohort of US radiologic technologists. Occup Environ Med. 2020 Jan;77(1):1-8. doi: 10.1136/oemed-2019-105902.
2. Azizova TV , Hamada N , Grigoryeva ES , et al. . Risk of various types of cataracts in a cohort of Mayak workers following chronic occupational exposure to ionizing radiation. Eur J Epidemiol2018;33:1193–204.doi:10.1007/s10654-018-0450-4
3. Azizova TV , Hamada N , Bragin EV , et al . Risk of cataract removal surgery in Mayak PA workers occupationally exposed to ionizing radiation over prolonged periods. Radiat Environ Biophys2019;58:139–49.doi:10.1007/s00411-019-00787-0
4. Neriishi K , Nakashima E , Akahoshi M , et al . Radiation dose and cataract surgery incidence in atomic bomb survivors, 1986–2005. Radiology2012;265:167–74.doi:10.1148/radiol.12111947 CrossRefPubMedWeb of ScienceGoogle Scholar
5. Little MP. A review of non-cancer effects, especially circulatory and ocular diseases. Radiat Environ Biophys 2013;52:435–49. doi:10.1007/s00411-013-0484-7
6. Shore RE . Radiation and cataract risk: impact of recent epidemiologic studies on ICRP judgments. Mutation Research/Reviews in Mutation Research 2016;770:231–7.doi:10.1016/j.mrrev.2016.06.006
7. Jargin SV. Chapter 3. Overestimation of Medical Consequences of Radioactive Contaminations in the Former Soviet Union. Advances in Environmental Research. Vol. 83. Nova Science Publishers, Inc., 2021. DOI: https://doi.org/10.52305/BPZX5742
We thank Dr. Nicholson and Prof. Cullinan for their interest in our
paper,[1] and welcome the opportunity to respond to their comments and
provide clarification.
We did review the most up-to-date version of all guidelines,
including the 2010 version of the BOHRF guidelines. In the "Results"
section of our paper, the first column of Table 1 cites the most recent
guideline versions published in the peer-reviewed...
We thank Dr. Nicholson and Prof. Cullinan for their interest in our
paper,[1] and welcome the opportunity to respond to their comments and
provide clarification.
We did review the most up-to-date version of all guidelines,
including the 2010 version of the BOHRF guidelines. In the "Results"
section of our paper, the first column of Table 1 cites the most recent
guideline versions published in the peer-reviewed literature; for the
BOHRF guidelines that was a summary of the 2004 version, published in
2005.[2] Unsurprisingly, our focus was indeed on the 2010 evidence review
and recommendations document,[3] which we appropriately cite in the second
column of Table 1 and not only in the "Introduction" section, as
suggested. It is not clear to us why Nicholson and Cullinan thought that
we appraised the older version and not the latest one.
As explained in the "Methods" section of our paper, for every
guideline reviewed "we thoroughly searched for any accompanying technical
and supporting documents in order to better inform our assessments".
Accordingly, we did of course visit the BOHRF website and were very much
aware of the documents that Nicholson and Cullinan make reference to.
However, these are short informational brochures based on the BOHRF
guidelines, whereas the ERS document is much more comprehensive; it
summarizes all key questions and recommendations along with the associated
evidence grades, and is suitably titled as "pocket guidelines".[4]
Consequently, the statement in our paper that "ERS was the only guideline
that provided a pocket version" cannot, in our opinion, be reasonably
described as "factually incorrect".
In the AGREE II, the existence of summary documents represents only
one criterion of a single item (out of four) in the "Applicability"
domain. In any event though, since all appraisers were indeed aware and
took account of the BOHRF brochures, neither the score for "Applicability"
nor the overall score of the BOHRF guidelines is "incorrect and
unreliable" as suggested.
Having said that, it should be pointed out that the AGREE II does not
claim to be a perfectly objective and repeatable instrument, even though
the high number of appraisers in our review ensures improved reliability.
The AGREE II does require a measure of personal judgement, and as its
authors note, "the criteria and considerations [outlined] are there to
guide, not replace, these judgements".[5] It assesses a strictly defined
aspect of guideline quality, and does not evaluate, for example, the
clinical appropriateness or validity of the recommendations themselves.[6]
Therefore, appraisals using the AGREE II should not be perceived as
passing judgement on the work of guideline developers, and are best used
as tools to identify areas for further improvement.
We do acknowledge the mistaken URL in reference 9 of our paper, and
thank Nicholson and Cullinan for pointing this out. The correct URL is
http://www.bohrf.org.uk/downloads/OccupationalAsthmaEvidenceReview-
Mar2010.pdf.
1 Lytras T, Bonovas S, Chronis C, et al. Occupational Asthma
guidelines: a systematic quality appraisal using the AGREE II instrument.
Occup Environ Med 2014;71:81-6. doi:10.1136/oemed-2013-101656
2 Nicholson PJ, Cullinan P, Taylor AJN, et al. Evidence based
guidelines for the prevention, identification, and management of
occupational asthma. Occup Environ Med 2005;62:290-9.
doi:10.1136/oem.2004.016287
3 Nicholson PJ, Cullinan P, Burge PS, et al. Occupational asthma:
Prevention, identification & management: Systematic review &
recommendations. London: : British Occupational Health Research Foundation
2010. http://www.bohrf.org.uk/downloads/OccupationalAsthmaEvidenceReview-
Mar2010.pdf
4 European Respiratory Society. ERS Pocket Guidelines. Work-related
Asthma: Guidelines for the Management of Work-related Asthma. European
Respiratory Society 2012. http://www.ers-
education.org/Media/Media.aspx?idMedia=208120
5 AGREE Next Steps Consortium. The AGREE II instrument. 2009.
http://www.agreetrust.org/index.aspx?o=1397
6 Brouwers MC, Kho ME, Browman GP, et al. AGREE II: advancing
guideline development, reporting and evaluation in health care. CMAJ
2010;182:E839-842. doi:10.1503/cmaj.090449
We write to correct errors in the paper Occupational asthma
guidelines: a systematic quality appraisal using the AGREE II instrument
1.
The methodology for this study states that the authors reviewed the
most up to date versions of guidelines. While in their Introduction the
authors cite (their reference 9) a statement from the 2010 BOHRF
systematic review 2; within the Results section it is clear that they
a...
We write to correct errors in the paper Occupational asthma
guidelines: a systematic quality appraisal using the AGREE II instrument
1.
The methodology for this study states that the authors reviewed the
most up to date versions of guidelines. While in their Introduction the
authors cite (their reference 9) a statement from the 2010 BOHRF
systematic review 2; within the Results section it is clear that they
appraised their reference 35 which is a short version of the 2004 BOHRF
systematic review 3 published in Occup Environ Med in 2005 4.
The authors state that only the European Respiratory Society
guidelines produced pocket sized versions. This is factually incorrect.
Both the 2004 and 2010 BORF reviews published a series of concise
summaries for: a) employers, workers and their representatives, b) general
practitioners (GPs) and practice-based nurses, c) occupational health
professionals; and d) an algorithm for GPs. All are freely accessible at
http://www.bohrf.org.uk/projects/asthma.html. Consequently the authors
scored the BOHRF guidelines incorrectly low for domain 5 (applicability);
as a result the overall quality score is incorrect and unreliable.
Within the reference section the authors' hyperlink to the 2010 BOHRF
occupational asthma review is incorrect; it actually being a link to a
review of occupational contact dermatitis.
1. Lytras T, Bonovas S, Chronis C, et al. Occupational Asthma
guidelines: a systematic quality appraisal using the AGREE II instrument.
Occup Environ Med. 2014;71:81-6.
2. Nicholson PJ, Cullinan P, Burge PS, et al. Occupational asthma:
Prevention, identification & management: Systematic review &
recommendations. London: British Occupational Health Research Foundation,
2010.
3. Nicholson PJ, Cullinan P, Newman Taylor AJ, et al. Evidence based
guidelines for the prevention, identification, and management of
occupational asthma. Occup Environ Med 2005;62:290-9.
4. Newman Taylor AJ, Nicholson PJ, Cullinan P, et al. Occupational
asthma: Prevention, identification & management: Systematic review
& recommendations. London: British Occupational Health Research
Foundation, 2004.
Conflict of Interest:
Authors of BOHRF guidelines reviewed in this paper.
We thank Dr. Morfeld for his comments on our updated mortality study
of the U.S. coal miners study.[1] However, we disagree with his assertion
that the excess of lung cancer we observed must be attributed to smoking
alone. Firstly, despite the smoking prevalence being higher in our cohort
than in the U.S. population in 1970, smokers in our population were
significantly less likely to be heavy smokers (> 24 cigarettes...
We thank Dr. Morfeld for his comments on our updated mortality study
of the U.S. coal miners study.[1] However, we disagree with his assertion
that the excess of lung cancer we observed must be attributed to smoking
alone. Firstly, despite the smoking prevalence being higher in our cohort
than in the U.S. population in 1970, smokers in our population were
significantly less likely to be heavy smokers (> 24 cigarettes daily)
than men in the general US population (12.4% vs. 28.0%). Secondly, greater
weight should be given to the findings from the internal analysis, which
controlled for smoking, than to the SMR analysis. Here, as Dr. Morfeld
acknowledges, there was a clear dose-response relationship between coal-
mine dust exposure and lung cancer. Of note, there was an inverse
relationship between radiographic CWP status and lung cancer mortality,
implying that CWP and lung cancer were competing causes of death, and
leading to weakening of the relationship between dust exposure and lung
cancer for the older miners (i.e., those exposed to the high levels of
dust existing prior to the 1969 Federal dust regulations).
Table 1 shows the mean cumulative coal dust exposures by year, as
requested by Dr. Morfeld. These levels were lower in the last eight years
of follow-up and were higher among lung cancer cases than among all
subjects in that decade. This is probably explained by the fact that
subjects with higher cumulative exposures were more likely to die during
the earlier years of follow-up due to the effects of exposure and their
age.
Dr. Morfeld correctly stated that we lacked work histories on our
miners after enrolment (1969 to 1971), but incorrectly asserted that work
histories were absent before enrolment. The lack of work histories in the
post-enrolment period may have introduced some misclassification of
exposures. However, as we and others have emphasized,[2,3] and as
demonstrated by our sensitivity analysis, any such misclassification is
likely minimal as most participants accumulated the bulk of their exposure
before enrolment.
We agree with Dr. Morfeld, and stated in our article, that the
British study of coal miners [4] had better exposure data than our study.
While both studies show an excess of lung cancer in their most recent
period of follow-up, [1,4] the British findings suggest that the excess is
most strongly associated with silica, rather than with coal dust exposure
as seen in our study. However, from both studies it is clear that there
is an excess of lung cancer among coal miners which is unlikely explained
by smoking alone.
Finally, we are confused by Dr. Morfeld's reference to the healthy
worker survivor effect as a reason for dismissing our findings. As has
been shown [3] the study was subject to a strong healthy worker survivor
effect, causing a reduction in mortality in the early years of follow-up.
We remain firm in our conclusion that "Our findings and those from
the British coal-miners cohort strongly suggest the need for continued
investigation of lung cancer mortality and incidence among coal
miners."[1]
Table I: Coal mine dust by year of death among all cohort members and
among those for whom the underlying cause of death was lung cancer
Mean Cumulative Exposure
Coal Mine Dust
(mg/m3-yrs)
All Lung Cancer
(n= 8,829) (n= 568)
Calendar
year of death
1970-1989 89.7 86.9
1980-1999 82.0 75.5
2000-2007 42.8 51.5
Literature
1. Graber, J.M., Stayner, L.T., Cohen,R.A., Conroy, L.M., Attfield,
M. D., Respiratory disease mortality among US coal miners; results after
37 years of follow-up. Occup Environ Med, 2014. 71: p. 30-39.
2. Kuempel, E.D., et al., Exposure-response analysis of mortality among
coal miners in the United States. Am J Ind Med, 1995. 28(2): p. 167-84.
3. Attfield, M.D. and E.D. Kuempel, Mortality among U.S. underground coal
miners: a 23-year follow-up. Am J Ind Med, 2008. 51(4): p. 231-45
4. Miller, B.G. and L. MacCalman, Cause-specific mortality in British coal
workers and exposure to respirable dust and quartz. Occup Environ Med,
2010. 67(4): p. 270-6
I read with interest about the updated US coalminer mortality
study[1]. The lung cancer SMR was slightly elevated (SMR=1.08, 95% CI:
1.00-1.18). This excess is unexceptionable because of a higher proportion
of smokers at the start of follow-up in 1969/1971 (current smokers: 54%)
in comparison to the US male population in 1970 (44.1%). Internal analyses
showed an association of lung cancer mortality...
I read with interest about the updated US coalminer mortality
study[1]. The lung cancer SMR was slightly elevated (SMR=1.08, 95% CI:
1.00-1.18). This excess is unexceptionable because of a higher proportion
of smokers at the start of follow-up in 1969/1971 (current smokers: 54%)
in comparison to the US male population in 1970 (44.1%). Internal analyses
showed an association of lung cancer mortality with coalmine dust exposure
but only during the last follow-up interval from 2000 to 2007. Thus, it is
of interest to see the distribution of the cumulative exposures across the
different calendar time periods. It remains unclear why this information
was not given in Table 2 (why does Table 2 report on 568 lung cancer cases
but Table 4 on 583 cases?)
This US study suffers from an incomplete assessment of occupational
histories in coalminers: no start and end date of jobs held before
1969/1971 available, no information on jobs held after 1969/1971, and no
end date of working as a coalminer for 16.2% of cohort members. Thus, only
a crude assessment of exposure to coalmine dust up to the start of follow-
up was possible: no time-dependent exposure analysis or lagging of
exposures could be done. Crystalline silica concentration data suffered
from additional limitations because measurements were available only after
1981 but had to be allocated to jobs held before 1969/1971.
The largest study to date with better assessment of exposures in a
time-dependent manner was performed in the UK[2]: the overall evidence
does not support a lung cancer excess risk due to coalmine dust exposure.
The findings of the US study do not seem to change this view despite
obvious limitations due to the Healthy Worker Survivor Effect (models that
adjust for time since last employment do not solve this problem)[3].
References
1 Graber JM, Stayner LT, Cohen RA, et al. Respiratory disease
mortality among US coal miners; results after 37 years of follow-up. Occup
Environ Med 2014;71:30-39.
2 Miller BG, MacCalman L. Cause-specific mortality in British coal
workers and exposure to respirable dust and quartz. Occup Environ Med
2010; 67:270-276.
3 Naimi AI, Richardson DB, Cole SR. Causal Inference in Occupational
Epidemiology: Accounting for the Healthy Worker Effect by Using Structural
Nested Models. Am J Epidemiol. 2013;178:1681-1686.
Conflict of Interest:
Yes, I have a competing interest.
The author performed epidemiological studies on German coalminers and gives scientific advice to the German coalmining industry.
We thank Dr Idrovo for his thoughts on our paper (1) regarding
multilevel approaches to ecological studies (2). We agree with Dr Idrovo
that incorporating different levels of aggregation to explore the impact
of macro-determinants, or "cultural determinants", would be useful and
could, in theory, illuminate important factors beyond causal hypothecation
at the individual-level.
In our study, however, we were unable to ful...
We thank Dr Idrovo for his thoughts on our paper (1) regarding
multilevel approaches to ecological studies (2). We agree with Dr Idrovo
that incorporating different levels of aggregation to explore the impact
of macro-determinants, or "cultural determinants", would be useful and
could, in theory, illuminate important factors beyond causal hypothecation
at the individual-level.
In our study, however, we were unable to fully explore the effects of
different levels of aggregation for the following reasons:
(1) a priori it is difficult to define levels of aggregation based on
(expected) homogeneity of ecological, social, cultural or economical macro
-determinants that could be of importance in investigating associations
between cancer incidence and population proxies of this exposure, other
than solely based on geographical location or on arbitrarily defined cut-
offs in indices like the Human Development Index.
(2) Our study included only 165 nations, which limits statistical power on
aggregation. Hopefully, national data will become available for more
countries with time, but even then the total number of countries in the
world is insufficient for exhaustive aggregation.
In fact, we carried out a multilevel analysis during the development
of the methodology in (1) using geographical location (defined as
"Continent") as the highest level of aggregation. The results were not
described in (1), but a comparison between our final logistic model (using
1995 as the base year for the exposure proxy) and a multi-level logistic
alternative showed similar results for the fixed-effects parameters (gross
national income per capita, human development index, and 1995 mobile
cellular subscriptions [per 100 people]). Aggregation did not provide any
additional information, other than an indication that the between-
continent variance is relatively small and only about 50% of the variance
between countries within a continent. The effect size of the association
between mobile cellular subscriptions (per 100 people) and brain cancer
(national age-adjusted incidence rates) was similar for both methods but
with reduced statistical power. Furthermore, the Bayesian Information
Criterion (BIC) indicates that the single level logistic model had a
better fit.
Although we broadly agree with Dr Idrovo's approach to analysing
ecological studies we believe the concept of "diseases of civilization" as
used by Milham (3) should not be used as an illustration of these macro-
determinants. In fact, one of us has published a critique of Milham's
paper (4), which we think is an example of the "ecological fallacy" (5) to
which Dr Idrovo alludes (2).
References
1. de Vocht F, Hannam K, Buchan I. Environmental risk factors for cancers
of the brain and nervous system: the use of ecological data to generate
hypotheses. Occup Environ Med 2013; 70(5): 349-56.
2. Idrovo AJ. Three interpretations of an ecological study. Occup Environ
Med 2013; in press.
3. Milham S. Historical evidence that electrification caused the 20th
century epidemic of "diseases of civilization". Med Hypotheses
2010;74(2):337-45.
4. de Vocht F and Burstyn I. Historical "evidence" that electrification
caused the 20th century epidemic of diseases of civilization and the
ecological fallacy. Med Hyptheses 2010; 74(5): 957-8.
5. Morgenstern H. Ecological studies in epidemiology: concepts,
principles, and methods. Annu Rev Pub Health 1995; 16: 61-81.
Cullilinan et al [1] reported six obliterative bronchiolitis (OB)
cases with plausible correlation with fiberglass-reinforced plastics (FRP)
fabrication. Five of them were boat builders and one worked for a cooling-
tower manufacturer. Due to the complexity of the FRP-related boat building
processes, the exact agent(s) and process causing OB were difficult to
determine. The cooling-tower manufacturing had a simpler manufact...
Cullilinan et al [1] reported six obliterative bronchiolitis (OB)
cases with plausible correlation with fiberglass-reinforced plastics (FRP)
fabrication. Five of them were boat builders and one worked for a cooling-
tower manufacturer. Due to the complexity of the FRP-related boat building
processes, the exact agent(s) and process causing OB were difficult to
determine. The cooling-tower manufacturing had a simpler manufacturing
process, and may help narrow down the actual processes leading to OB. Both
industries involved gel coating and manual lamination of FRP.
Recently, we identified additional two patients with OB and exposure
to FRP lamination. The first is a 35 year-old man who has worked in a FRP
yacht manufacturing factory for 4 years. He develops persistent dyspnea
one year after starting FRP lamination. Lung function shows severe airway
obstruction with forced vital capacity (FVC) and forced expiratory volume
in 1 second (FEV1) 2.72 and 1.28 liters, respectively. Work exposure
included various resins, mainly polyester resin with MEKPO (as catalyst)
and styrene (as active diluents).
The second patient, a 28 year-old man, was a water storage tank
repairer for 8 years. His work involved mainly leakage-proof FRP
lamination. Dyspnea developed two years after starting job; and progressed
badly that he had to quit this year. Chest CT scan revealed air-trapping.
Lung function showed severe irreversible obstructive ventilatory defect,
with FVC 3.56 liters and FEV1 1.55 liters, respectively.
Two points are noteworthy in our second patient. He has never been
involved in gel coating processes; and he only used polyester resin (with
MEKPO and styrene) as glue at work. These imply that the actual process
causing OB was likely FRP lamination, not gel coating. Besides, polyester
resin containing MEKPO and styrene could be the responsible agent.
Nevertheless, these are indirect evidences. The conclusive identification
of the actual causal agent(s) warrants further investigation.
Reference
1. Paul Cullinan, Clive R McGavin, Kathleen Kreiss, et al. Obliterative
bronchiolitis in fibreglass workers: a new occupational disease? Occup
Environ Med 2013;70:357-9.
With interest we read the article by Gustavsson and colleagues [1] on the breast cancer risk in a cohort with night work. The authors started from two facts: First, “night shift work” [2] was classified as “probably carcinogenic to humans” (Group 2A) by the International Agency for Research on Cancer [IARC]; second, the evidence in humans was considered limited because of variable results and potential bias. Since prior studies had problems regarding exposure assessment, Gustavsson et al. emphasized their very detailed registry-based data on night work. Yet, as key result the authors noted that “conclusions are limited due to a short period of follow-up and lack of information of night work before 2008”. Thus, this study perpetuates limited epidemiological evidence for the carcinogenicity of night work. Although the limited data on shift work is a drawback of this study, it is not the only limitation. We would like to discuss a conceptual problem that may have contributed to the limited conclusions and that the authors did not address.
Show MoreThe IARC monograph mentions chronotype and sleep 73 and 199 times, respectively [2]. Chronotype tells us when persons prefer sleep or work and activity. Potentially harmful circadian disruption (CD) [3] can occur at any time over 24 hours when activities or sleep are misaligned with the chronotype-associated biological nights [3 4] or biological days. This leads to occupational and non-occupational CD [5]. Possible effects of not c...
The paper by Go et al (Occup Environ Med 2023;80425-30) is an important reminder of the problem of quartz in coal mine dusts and of its association with early development of pneumoconiosis, often associated with unusual radiological patterns. The UK work which they kindly cite brought to light a problem for regulation of the quartz in coal mine dust – that in many cases quartz concentrations greater than 0.1mg/m3 in mine environments seemed not to be associated with development of silicosis. Experimentally, the toxicity of quartz is reduced when it is associated, as is usual in coal mines, with a high concentration of other silicates, which occlude the crystal surface. This led to the pragmatic solution of ignoring quartz if it constituted less than 10% of the total mine dust concentration (which then was regulated as less than 5mg/m3).
Show MoreThese difficulties in setting and monitoring compliance with a quartz standard in coal mines are obsolete in UK as long as mines remain closed. However, while mining continues elsewhere it is important to recognise that miners know when they are cutting rock and so do their employers. When this is happening it should be recognised that they are at risk of silicosis and, as the authors show, the implications are far more serious for their health than those from coal alone; any early radiological evidence is usually too late for the miners and extra action to increase their safety needs to be required of the employer in these circumstan...
This study reports an alarming prevalence of silicosis in Victoria, Australia at 28.2% among workers in the stone benchtop industry (SBI). [1] That prevalence is higher than reported in SBI workers in another Australian state of Queensland (22.7%). [4] The Victorian silicosis screening program reported respiratory function tests and chest x-rays to be of limited value in screening this high-risk population which has significant implications for health and safety policy. It also calls into question the adequacy of current screening programs in other Australian States and Territories.
In the adjoining state of New South Wales (NSW), Australia, there has been an obligation on the health and safety regulator (SafeWork NSW) to maintain a Dust Diseases Register and to provide a report on the Register at the end of each financial year since October 2020. This information is provided and published in the NSW Dust Disease Register Annual Report. However, no information is provided on the total number of workers screened (or the denominator) to enable understanding of the incidence and prevalence of silicosis in NSW.
A desk-based “case finding” study from May 2021 in NSW estimated the average incidence (new cases) of silicosis among engineered stone workers in NSW at between 4% and 9% for the three-year reporting period, and suggested that incidence values may also be considered as the estimated prevalence within SBI workers. [3] This prevalence estimate is significant...
Show MoreDose-dependent diagnostic efficiency and self-reporting related to a longer work history and hence to cumulative dose could explain the above-average risk of cataracts in radiologic technologists [1]. Of concern was the discrepancy between the findings for cataract history and cataract surgery, where risks for the latter were somewhat lower and generally not significant [1]. A similar pattern of significant excess relative risk (ERR) for cataract and non-significant ERR for cataract surgery has also been reported in the Mayak nuclear workers. [2,3]. This agrees with the concept of dose-dependent diagnostic efficiency with detection of mild cases not requiring surgery. Among the various groups that have been studied for radiation-associated cataract, a significant ERR for cataract surgery has been reported only in the Japanese atomic bomb survivors [4-6], where the effect of the acute exposure could indeed have taken place. More details [7].
Show More1. Little MP, Cahoon EK, Kitahara CM, Simon SL, Hamada N, Linet MS. Occupational radiation exposure and excess additive risk of cataract incidence in a cohort of US radiologic technologists. Occup Environ Med. 2020 Jan;77(1):1-8. doi: 10.1136/oemed-2019-105902.
2. Azizova TV , Hamada N , Grigoryeva ES , et al. . Risk of various types of cataracts in a cohort of Mayak workers following chronic occupational exposure to ionizing radiation. Eur J Epidemiol2018;33:1193–204.doi:10.1007/s10654-018-0450-4
3. Azizova TV , Hamad...
We thank Dr. Nicholson and Prof. Cullinan for their interest in our paper,[1] and welcome the opportunity to respond to their comments and provide clarification.
We did review the most up-to-date version of all guidelines, including the 2010 version of the BOHRF guidelines. In the "Results" section of our paper, the first column of Table 1 cites the most recent guideline versions published in the peer-reviewed...
We write to correct errors in the paper Occupational asthma guidelines: a systematic quality appraisal using the AGREE II instrument 1.
The methodology for this study states that the authors reviewed the most up to date versions of guidelines. While in their Introduction the authors cite (their reference 9) a statement from the 2010 BOHRF systematic review 2; within the Results section it is clear that they a...
We thank Dr. Morfeld for his comments on our updated mortality study of the U.S. coal miners study.[1] However, we disagree with his assertion that the excess of lung cancer we observed must be attributed to smoking alone. Firstly, despite the smoking prevalence being higher in our cohort than in the U.S. population in 1970, smokers in our population were significantly less likely to be heavy smokers (> 24 cigarettes...
Dear Editor,
I read with interest about the updated US coalminer mortality study[1]. The lung cancer SMR was slightly elevated (SMR=1.08, 95% CI: 1.00-1.18). This excess is unexceptionable because of a higher proportion of smokers at the start of follow-up in 1969/1971 (current smokers: 54%) in comparison to the US male population in 1970 (44.1%). Internal analyses showed an association of lung cancer mortality...
We thank Dr Idrovo for his thoughts on our paper (1) regarding multilevel approaches to ecological studies (2). We agree with Dr Idrovo that incorporating different levels of aggregation to explore the impact of macro-determinants, or "cultural determinants", would be useful and could, in theory, illuminate important factors beyond causal hypothecation at the individual-level. In our study, however, we were unable to ful...
Cullilinan et al [1] reported six obliterative bronchiolitis (OB) cases with plausible correlation with fiberglass-reinforced plastics (FRP) fabrication. Five of them were boat builders and one worked for a cooling- tower manufacturer. Due to the complexity of the FRP-related boat building processes, the exact agent(s) and process causing OB were difficult to determine. The cooling-tower manufacturing had a simpler manufact...
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