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ObjectivesWe aimed to investigate whether there has been a geographic shift in the distribution of mesothelioma deaths in Great Britain given the decline of shipbuilding and progressive exposure regulation.MethodsWe calculated age-adjusted mesothelioma mortality rates and estimated rate ratios for areas with and without a dockyard. We compared spatial autocorrelation statistics (Moran’s I) for age-adjusted rates at local authority district level for 2002–2008 and 2009–2015. We measured the mean distance of the deceased’s postcode to the nearest dockyard at district level and calculated the association of average distance to dockyard and district mesothelioma mortality using simple linear regression for men, for 2002–2008 and 2009–2015.ResultsDistrict age-adjusted male mortality rates fell during 2002–2015 for 80 of 348 districts (23%), rose for 267 (77%) and were unchanged for one district; having one or more dockyards in a district was associated with rates falling (OR=2.43, 95% CI 1.22 to 4.82, p=0.02). The mortality rate ratio for men in districts with a dockyard, compared with those without a dockyard was 1.41 (95% CI 1.35 to 1.48, pConclusionFor most districts age-adjusted mesothelioma mortality rates increased through 2002–2015 but the relative contribution from districts with a dockyard fell. Dockyards remain strongly spatially associated with mesothelioma mortality but the strength of this association appears to be falling and mesothelioma deaths are becoming more dispersed.

ObjectivesTo examine associations between occupational exposures to rubber dust, rubber fumes and N-nitrosamines and non-cancer mortality.MethodsA cohort of 36 441 males aged 35+ years employed in British rubber factories was followed-up to 2015 (94% deceased). Competing risk survival analysis was used to assess risks of dying from non-cancer diseases (respiratory, urinary, cerebrovascular, circulatory and digestive diseases). Occupational exposures to rubber dust, rubber fumes, N-nitrosamines were derived based on a population-specific quantitative job-exposure matrix which in-turn was based on measurements in the EU-EXASRUB database.ResultsExposure–response associations of increased risk with increasing exposure were found for N-nitrosomorpholine with mortality from circulatory diseases (subdistribution hazard ratio (SHR) 1.17; 95% CI 1.12 to 1.23), ischaemic heart disease (IHD) (SHR 1.19; 95% CI 1.13 to 1.26), cerebrovascular disease (SHR 1.19; 95% CI 1.07 to 1.32) and exposures to N-nitrosodimethylamine with respiratory disease mortality (SHR 1.41; 95% CI 1.30 to 1.53). Increased risks for mortality from circulatory disease, IHD and digestive diseases were found with higher levels of exposures to rubber dust, rubber fumes and N-nitrosamines sum, without an exposure-dependent manner. No associations were observed between rubber dust, rubber fumes and N-nitrosamines exposures with mortality from asthma, urinary disease, bronchitis, emphysema, liver disease and some digestive diseases.ConclusionsIn a cohort of rubber factory workers with 49 years of follow-up, increased risk for mortality from circulatory, cerebrovascular, respiratory and digestive diseases were found to be associated with cumulative occupational exposures to specific agents.

In his letter, Professor Sorahan1 poses an important question about our paper,2 namely, whether the results indicate that occupational exposures to agents such as rubber dust, rubber fumes and nitrosamines in the rubber industry are associated with increased risk of mortality from cancers of the bladder, lung, stomach, oesophagus, prostate, larynx, brain, pancreas, liver, and lymphatic and haematopoietic tissue. Sorahan argues that causation does not seem to be warranted since results from …

OBJECTIVES: The standard approach to the assessment of occupational exposures is through the manual collection and coding of job histories. This method is time-consuming and costly and makes it potentially unfeasible to perform high quality analyses on occupational exposures in large population-based studies. Our aim was to develop a novel, efficient web-based tool to collect and code lifetime job histories in the UK Biobank, a population-based cohort of over 500 000 participants. METHODS: We developed OSCAR (occupations self-coding automatic recording) based on the hierarchical structure of the UK Standard Occupational Classification (SOC) 2000, which allows individuals to collect and automatically code their lifetime job histories via a simple decision-tree model. Participants were asked to find each of their jobs by selecting appropriate job categories until they identified their job title, which was linked to a hidden 4-digit SOC code. For each occupation a job title in free text was also collected to estimate Cohen’s kappa (κ) inter-rater agreement between SOC codes assigned by OSCAR and an expert manual coder. RESULTS: OSCAR was administered to 324 653 UK Biobank participants with an existing email address between June and September 2015. Complete 4-digit SOC-coded lifetime job histories were collected for 108 784 participants (response rate: 34%). Agreement between the 4-digit SOC codes assigned by OSCAR and the manual coder for a random sample of 400 job titles was moderately good [κ=0.45, 95% confidence interval (95% CI) 0.42–0.49], and improved when broader job categories were considered (κ=0.64, 95% CI 0.61–0.69 at a 1-digit SOC-code level). CONCLUSIONS: OSCAR is a novel, efficient, and reasonably reliable web-based tool for collecting and automatically coding lifetime job histories in large population-based studies. Further application in other research projects for external validation purposes is warranted.

Occupational exposures are important, preventable causes of chronic obstructive pulmonary disease (COPD). Identification of COPD high-risk jobs is key to focus preventive strategies, but a definitive job-list is unavailable.We addressed this issue by evaluating the association of lifetime job-histories and lung function data in the population-based UK Biobank cohort, whose unprecedented sample size allowed analyses restricted to never-smokers to rule out the most important confounder, tobacco smoking. COPD was spirometrically defined as forced expiratory volume in 1 s/forced vital capacity ratio below the lower limit of normal. Lifetime job-histories were collected via OSCAR (Occupations Self-Coding Automatic Recording), a new validated online tool that automatically codes jobs into the UK Standard Occupational Classification v.2000. Prevalence ratios for COPD by employment duration in each job compared to lifetime office workers were estimated using robust Poisson regression adjusted for age, sex, centre and smoking. Only associations confirmed among never-smokers and never-asthmatics were considered reliable.From the 116 375 participants with complete job-histories, 94 551 had acceptable/repeatable spirometry data and smoking information and were included in the analysis. Six occupations showed an increased COPD risk among never-smokers and never-asthmatics; most of these also with positive exposure-response trends. Interesting new findings included sculptors, gardeners and warehouse workers.COPD patients, especially never-smokers, should be asked about their job-history for better disease management. Focussed preventive strategies in COPD high-risk jobs are warranted.

OBJECTIVES: We examined the mortality of a historic cohort of workers in Great Britain with measured blood lead levels (BLLs). METHODS: SMRs were calculated with the population of Great Britain as the external comparator. Trends in mortality with mean and maximum BLLs and assessed lead exposure were examined using Cox regression. RESULTS: Mean follow-up length among the 9122 study participants was 29.2 years and 3466 deaths occurred. For all causes and all malignant neoplasms, the SMRs were statistically significantly raised. For disease groups of a priori interest, the SMR was significantly raised for lung cancer but not for stomach, brain, kidney, bladder or oesophageal cancers. The SMR was not increased for non-malignant kidney disease but was borderline significantly increased for circulatory diseases, for ischaemic heart disease (IHD) and cerebrovascular disease (CVD). No significant trends with exposure were observed for the cancers of interest, but for circulatory diseases and IHD, there was a statistically significant trend for increasing HR with mean and maximum BLLs. CONCLUSIONS: This study found an excess of lung cancer, although the risk was not clearly associated with increasing BLLs. It also found marginally significant excesses of IHD and CVD, the former being related to mean and maximum BLLs. The finding for IHD may have been due to lead, but could also have been due to other dust exposure associated with lead exposure and possibly tobacco smoking. Further work is required to clarify this and the carcinogenicity of lead.

BackgroundThe International Agency for Research on Cancer (IARC) has determined there is sufficient evidence that working in the rubber manufacturing industry increases the risk of cancers of the stomach, lung, bladder and leukaemia and lymphoma.ObjectivesTo examine mortality patterns of a prospective cohort of men from the rubber and cable manufacturing industries in Great Britain.MethodsSMRs were calculated for males aged 35+ years at start of follow-up in 1967–2015 using the population of England and Wales as the external comparator. Tests for homogeneity and trends in SMRs were also completed.ResultsFor all causes, all malignant neoplasms, non-malignant respiratory diseases and circulatory diseases, SMRs were significantly elevated, and also particularly for cancers of the stomach (SMR=1.26,95% CI 1.18 to 1.36), lung (1.25,95% CI 1.21 to 1.29) and bladder (1.16,95% CI 1.05 to 1.28). However, the observed deaths for leukaemia, non-Hodgkin’s lymphoma (NHL) and multiple myeloma were as expected. Bladder cancer risks were elevated only in workers exposed to antioxidants containing 1-naphthylamine and 2-naphthylamine.ConclusionsThis study provides evidence of excess risks in the rubber industry for some non-cancer diseases and supports IARC’s conclusions in relation to risks for cancers of the bladder, lung and stomach, but not for leukaemia, NHL or multiple myeloma.

Background: Occupational hazards are important, preventable causes of COPD but the high-risk occupations are uncertain. In an analysis of current occupation in the UK Biobank cohort we reported 14 jobs of increased risk (De Matteis, S. et al. OEM 2016). Aims and Objectives: Our aim was to develop these findings using lifetime job-histories to identify occupations at increased COPD risk, taking into account potential confounders. Methods: We used OSCAR, an online tool that automatically codes full job-histories using the UK Standard Occupational Classification (SOC) v.2000 (De Matteis, S. et al. SJWEH 2016). In 2016 we administered OSCAR to all UK Biobank participants with an email address (n=324,653). All paid jobs of >6 months duration, were collated and coded. COPD was spirometry-defined as FEV1/FVC Results: Among 116,375 OSCAR-responders, we analysed the 94,551 with acceptable spirometry data and smoking information. Six occupations showed an increased risk of COPD confirmed by positive exposure-response trends, and in analyses restricted to never-smokers and never-asthmatics. In comparison with our findings for current occupation, some associations were confirmed (e.g. food/drink/tobacco processors: PR 1.70;95%CI:1.17-2.48) while others emerged (e.g. plastics processors: PR 1.86;95%CI:1.09-3.17; agriculture/fishing: PR 1.76;95%CI:1.22-2.55). Conclusions: In order to focus workplace preventive strategies, we are in the process of applying a job-exposure matrix to identify the underlying occupational respiratory hazards.

Background Estimating national burdens of lung cancer from occupational exposure to asbestos is challenging because of the potential for confounding by smoking. Methods To generate a refined estimate, we analysed data on underlying cause of death and last full-time occupation for 3,688,916 deaths among men aged 20–74 years in England and Wales during 1979–2010, calculating proportional mortality ratios (PMRs) standardised for age and social class. We compared observed and expected deaths from lung cancer in 28 occupations with excess mortality from mesothelioma or asbestosis. To reduce the confounding effects of smoking, we adjusted the expected number of lung cancers in each occupation, according to its PMR for chronic obstructive pulmonary disease (COPD) in an analysis that excluded jobs with a known hazard of COPD. Results Adjusted PMRs for lung cancer were elevated in all but one of the 28 asbestos-exposed occupations, but did not correlate with those for cancer of the pleura (Spearman correlation coefficient=−0.3). The total excess of deaths from lung cancer across the 28 occupations over the 31 years of study was 9561 (as compared with 3164 when no adjustment was made). Conclusions Asbestos appeared to account for some 300 excess lung cancer deaths per year in England and Wales, which is approximately 70% of the annual number of deaths from mesothelioma. The lack of correlation between PMRs for the two diseases may reflect different exposure-response relationships.

Background mesothelioma mortality rates in GB have increased tenfold over the last four decades and are currently the highest of any country worldwide. The mesothelioma register contains all deaths mentioning mesothelioma and includes area of residence and occupation of the deceased. Aim to update descriptive analyses of mortality trends by geographical area and last occupation of the deceased to provide evidence about past sources of mesothelioma risk in the GB population. Methods Standardised Mortality Ratios (SMRs) were calculated for local and unitary authority areas; Proportional Mortality Ratios (PMRs) were calculated for categories derived from Standard Occupation Classification coding of job titles from death certificates. Temporal trends in SMRs and PMRs over the period 1981–2014 were examined using Generalised Additive Models (GAMs). Results the influence of geographically-specific sources of past asbestos exposure is still seen in recent mesothelioma mortality rates; areas with the highest SMRs in males tend to be those known to contain large industrial sites that used asbestos such as shipyards. However, the strong effect of asbestos exposures in jobs associated with construction work – which would have been geographically less heterogeneous – is seen in analyses by occupation, and temporal trends suggest that such exposures continued for longer than those associated with specific locations. Conclusions these results reflect the legacy of widespread industrial asbestos use in GB and particularly emphasise the effect of exposures within the building industry which are likely to have continued after those in specific industries such as shipbuilding and manufacturing were substantially reduced.

There exists a great deal of uncertainty as to which specific chemicals present in the rubber products manufacturing industry give rise to the increases in cancer that have been seen to date and which are regarded by the International Agency for Research on Cancer (IARC) as carcinogenic; especially since after this IARC classification, exposures in the rubber industry have decreased considerably and efforts have been made to remove confirmed carcinogens from the production process. We updated a cohort of 40,867 men who were employed in the British rubber industry on 1 February 1967. Follow-up was last updated until 1976 and an excess risk of bladder cancer in men likely exposure to beta-naphthylamine based antioxidants (before these were withdrawn from the process in 1949), excess death from lung cancer across the industry and excess mortality from stomach cancer in the tyre sector were observed. We have extended the mortality follow-up to 45-years and are linking it to a population-specific quantitative job-exposure matrix based on available data previously collected in the EU EXASRUB project. We are currently waiting for tracing outcomes for mortality by the Health & Social Care Information Centre (HSCIC), and so we will present the first results of industry- and job-specific cancer mortality risks as well as quantitative exposure-response associations for rubber dust and fumes and specific n-Nitrosamines. There are only few occupational cohorts of this size with such long follow-up, so the presented analyses will provide an important overview of lifetime exposure-specific cancer mortality risks of specific exposures historically and currently encountered in the industry.

Background Occupational hazards are important, preventable causes of COPD but the high-risk occupations are uncertain. In an analysis of current occupation in the UK Biobank cohort we reported 14 jobs of increased risk (De Matteis, S. et al. OEM 2016). Aims and objectives Our aim was to develop these findings using lifetime job-histories to identify occupations at increased COPD risk, taking into account potential confounders. Methods We used OSCAR, an online tool that automatically codes full job-histories using the UK Standard Occupational Classification (SOC) v.2000 (De Matteis, S. et al. SJWEH 2016). In 2016 we administered OSCAR to all UK Biobank participants with an email address (n=324,653). All paid jobs of >6 months duration, were collated and coded. COPD was spirometry-defined as FEV1/FVC Results Among 116,375 OSCAR-responders, we analysed the 94 551 with acceptable spirometry data and smoking information. Six occupations showed an increased risk of COPD confirmed by positive exposure-response trends, and in analyses restricted to never-smokers and never-asthmatics. In comparison with our findings for current occupation, some associations were confirmed (e.g. food/drink/tobacco processors: PR 1.70;95% CI:1.17–2.48) while others emerged (e.g. plastics processors: PR 1.86;95% CI:1.09–3.17; agriculture/fishing: PR 1.76;95% CI:1.22–2.55). Conclusions In order to focus workplace preventive strategies, we are in the process of applying a job-exposure matrix to identify the underlying occupational respiratory hazards.

Rubber workers in Great Britain were historically exposed to various carcinogenic substances, including β-naphthylamine, which was removed from industrial processes in 1949. The Health and Safety Executive (HSE) initiated in 1967 a prospective occupational cohort study of British rubber industry workers, including men 35 years of age and older, to examine cancer mortality (n=40 867, representing 381 factories). Findings from a 10 year follow-up of that cohort suggested excess mortality from cancers of the bladder, lung, and stomach, which differed by exposure to naphthylamines, as well as by industry sector and job code. The purpose of this analysis is to extend mortality follow-up through to 2015, allowing an assessment of cancers in older ages and with longer latency periods. As well as headline Standardised Mortality Ratios (SMRs) for the cancer subtypes previously investigated, we will present mortality risks for a range of causes including leukaemia, multiple myeloma, circulatory and respiratory diseases. We will use England and Wales reference rates to compare mortality by employment duration and sector in the rubber industry. Preliminary analysis of a majority subset of the cohort (n=34,595) to 2015 identified an elevated all cause SMR of 1.11 (95%CI 1.10–1.12). More detailed results from this multi-decade follow-up of workers from rubber manufacturing will provide valuable insights into cancer mortality risks for exposed occupational populations, both in the UK and elsewhere.

Background Multiple sclerosis (MS) is the most common serious neurological disorder in young people in the UK. In the course of an analysis of trends in occupational mortality in England and Wales over the past thirty years, we observed a striking excess of deaths from MS among men in the Armed Forces, which prompted more detailed investigation. Methods We analysed data on underlying cause of death and last full-time occupation for 3,688,916 deaths among men aged 20–74 years in England and Wales during 1979–2010, calculating proportional mortality ratios (PMRs) standardised for age. We compared PMRs from MS and from motor neurone disease (MND) in the armed forces and in various other occupational groups selected for comparison. Results The overall PMR for MS in the armed forces during 1979–2010 was 242 (95% CI: 202–288). The excess was apparent in each of three separate decades of study (PMRs, ranging from 220 to 255), and across the entire age range. There was no parallel increase in PMRs for MND, and PMRs for MS were not consistently elevated to the same degree in comparator occupations. Conclusions The observed pattern of mortality is unlikely to have arisen by chance or from denominator bias. It may be that some men who leave the Armed Forces because of MS fail to get civilian jobs, and are therefore recorded on their death certificates as last working in the military. Other possible explanations will be discussed.

Dr Egilman and colleagues claim our report1 implies that chrysotile does not cause mesothelioma. So did the International Chrysotile Association, the website of which highlighted our paper with the misleading headline ‘reliable scientific data confirms negligible role of chrysotile in UK patients with asbestos-related lung disease’.2 Our results are consistent with the strong evidence that chrysotile did not cause a large proportion of UK mesotheliomas, but they certainly do not show that the risk is negligible. We said ‘the rapid clearance of chrysotile from the lung with a half-life of a few months explains its virtual absence in our samples, and implies that we cannot estimate its effects except by noting that amphibole lung burdens account very well …

Background: analysis of occupational mortality in England and Wales during 1991–2000 showed no decline in work-attributable deaths from asbestosis. Aims: to explore why there was no decline in mortality from asbestosis despite stricter controls on asbestos exposure over recent decades. Methods: using data from registers of all deaths in Great Britain with mention of mesothelioma or asbestosis on the death certificate, we plotted death rates by 5 year age group within 5 year birth cohorts for(a) mesothelioma and (b) asbestosis without mention of mesothelioma. Results: analysis was based on a total of 33 751 deaths from mesothelioma and 5396 deaths from asbestosis. For both diseases, mortality showed a clear cohort effect; within birth cohorts, death rates increased progressively with age through to 85 years and older. However, highest mortality from mesothelioma was in men born during 1939–43, whereas, mortality from asbestosis peaked in men born during 1924–38. Conclusions: our findings suggest that mortality, in Britain, from asbestosis has been determined mainly by cumulative exposure to asbestos before 45 years of age and that the effect of such exposure continues through to old age. That mortality from asbestosis peaked in earlier birth cohorts than mortality from mesothelioma may reflect a difference in exposure-response relationships for the two diseases. The discrepancy could be explained if risk of asbestosis increased more steeply than that of mesothelioma at higher levels of exposure to asbestos and if the highest prevalence of heavy exposure occurred in earlier birth cohorts than the highest prevalence of less intense exposures

Objectives Asbestos is an inflammatory agent, and there is evidence that inflammatory processes are involved in the development of cardiovascular disease. Whether asbestos is a risk factor for cardiovascular disease has not been established. The objective of this study was to investigate cardiovascular disease mortality in a large cohort of workers occupationally exposed to asbestos. Methods Cardiovascular disease mortality in a cohort of 98912 asbestos workers, with median follow-up of 19 years, was analysed. Unadjusted and smokingadjusted standardised mortality ratios (SMRs) were calculated. The association between indicators of asbestos exposure and mortality was analysed with Poisson regression models, for deaths occurring during the period 1971e2005. Results Altogether 15557 deaths from all causes, 1053 deaths from cerebrovascular disease and 4185 deaths from ischaemic heart disease (IHD) occurred during follow-up. There was statistically significant excess mortality from cerebrovascular disease (SMR: men 1.63, women 2.04) and IHD (SMR: men 1.39, women 1.89). Job and birth cohort were associated with the risk of cerebrovascular and IHD mortality in the Poisson regression model including sex, age, smoking status, job, cohort and duration of exposure. For IHD only, duration of exposure was also statistically significant in this model. Conclusions Cerebrovascular and IHD mortality was significantly higher among these asbestos workers than in the general population and within the cohort mortality was associated with indicators of asbestos exposure. These findings provide some evidence that occupational exposure to asbestos was associated with cardiovascular disease mortality in this group of workers.

Background/objective: Many occupational exposures causing disease cannot feasibly be eliminated entirely, but policies that reduce the exposures may be under consideration. This paper sets out to clarify how to estimate the reduction in occupational disease following a reduction in exposure, and shows a real-data illustration for doing this. Methods: Modest extensions of standard expressions for attributable fractions permit estimation of fractions by which cases would be reduced by policies that do not eliminate exposure but change exposure distributions. However, this requires information on the exposure-response relation and on distribution of exposures. Results: From hypothetical scenarios and a real example this paper explores how attributable cases are distributed by exposure level and, in particular, the proportion by which attributable cancers are reduced by eliminating exposures above a limit (the classic occupational limit regulation). It shows how this depends on the shape of the exposure-response relation and to some extent the shape of the exposure distribution, as well as on the proportion exposed above the limit. For linear no-threshold relations and left-skewed exposure distributions, the majority of the burden may be in a large number of people experiencing small relative risks, and thus may not be tackled by a strategy to reduce exposures above a certain limit. Conclusion: With appropriate data, estimating the disease burden in terms of the distribution of exposure is straightforward and can help to clarify the likely outcome of an intervention.

Background Simian virus 40 (SV40) is a DNA virus that has been shown capable of infecting and transforming cells in various species. Laboratory studies have suggested that inoculation with SV40 is associated with various types of cancer, including mesothelioma. Aims To test the hypothesis, via an ecological analysis, that exposure to SV40 via contaminated polio vaccines is a risk factor for mesothelioma in humans. Methods Mesothelioma mortality rates in Great Britain for two birth cohorts likely to have been exposed to SV40 via poliovirus vaccination were compared with a birth cohort likely to be largely unexposed. Results There was some evidence for both males (P < 0.05) and females (P < 0.05) that the mesothelioma mortality rates were higher in the first exposed cohort: rate ratio (RR) = 2.4 [95% CI (confidence interval) 1.25.0] and RR = 3.7 (95% CI 1.014). However, in the second exposed cohort, mortality rates were elevated in females only, and the evidence was slightly less convincing (P = 0.055). Conclusion Although the results for females show a reduction in the mesothelioma mortality rate coinciding with the introduction of the SV40-free Sabin polio vaccine, the absence of a similar result in males and of a priori biological evidence of a sex-specific SV40 effect, makes chance the most plausible interpretation of these findings.

BACKGROUND: We have conducted a population-based study of pleural mesothelioma patients with occupational histories and measured asbestos lung burdens in occupationally exposed workers and in the general population. The relationship between lung burden and risk, particularly at environmental exposure levels, will enable future mesothelioma rates in people born after 1965 who never installed asbestos to be predicted from their asbestos lung burdens. METHODS: Following personal interview asbestos fibres longer than 5 µm were counted by transmission electron microscopy in lung samples obtained from 133 patients with mesothelioma and 262 patients with lung cancer. ORs for mesothelioma were converted to lifetime risks. RESULTS: Lifetime mesothelioma risk is approximately 0.02% per 1000 amphibole fibres per gram of dry lung tissue over a more than 100-fold range, from 1 to 4 in the most heavily exposed building workers to less than 1 in 500 in most of the population. The asbestos fibres counted were amosite (75%), crocidolite (18%), other amphiboles (5%) and chrysotile (2%). CONCLUSIONS: The approximate linearity of the dose-response together with lung burden measurements in younger people will provide reasonably reliable predictions of future mesothelioma rates in those born since 1965 whose risks cannot yet be seen in national rates. Burdens in those born more recently will indicate the continuing occupational and environmental hazards under current asbestos control regulations. Our results confirm the major contribution of amosite to UK mesothelioma incidence and the substantial contribution of non-occupational exposure, particularly in women.

Objectives: To monitor the impact of health and safety provisions and inform future preventive strategies, we investigated trends in mortality from established occupational hazards in England and Wales.Methods: We analysed data from death certificates on underlying cause of death and last full-time occupation for 3?688?916 deaths among men aged 20–74?years in England and Wales during 1979–2010 (excluding 1981 when records were incomplete). Proportional mortality ratios (PMRs), standardised for age and social class, were calculated for occupations at risk of specified hazards. Observed and expected numbers of deaths for each hazard were summed across occupations, and the differences summarised as average annual excesses.Results: Excess mortality declined substantially for most hazards. For example, the annual excess of deaths from chronic bronchitis and emphysema fell from 170.7 during 1979–1990 to 36.0 in 2001–2010, and that for deaths from injury and poisoning from 237.0 to 87.5. In many cases, the improvements were associated with falling PMRs (suggesting safer working practices), but they also reflected reductions in the numbers of men employed in more hazardous jobs, and declining mortality from some diseases across the whole population. Notable exceptions to the general improvement were diseases caused by asbestos, especially in some construction trades and sinonasal cancer in woodworkers.Conclusions: The highest priority for future prevention of work-related fatalities is the minority of occupational disorders for which excess mortality remains static or is increasing, in particular asbestos-related disease among certain occupations in the construction industry and sinonasal cancer in woodworkers.

Background We became aware of concern about cancer at a Scottish semiconductor manufacturing facility in 1998. Aim To compare cancer experience among current and former workers at the facility, with an appropriate comparison population, making use of any readily available exposure information. Method We obtained personnel and employment episode information from four sources within the company. Workers were flagged for death and cancer registrations at the National Health Service Central Register in Edinburgh. We constructed standardized registration and mortality ratios (SRRs and SMRs), using Scotland as the comparison, with and without an adjustment for deprivation. Results The main mortality analysis included 4388 workers, with a mean length of follow-up of 12.5 years. Overall mortality was substantially below that expected for men, and for women was slightly below expected. Total cancer registrations were close to expected levels for men and women. Four cancers produced noteworthy findings: malignant neoplasm of the trachea, bronchus and lung in women—deprivation adjusted SRR [95% confidence interval (CI), number of cases] 273 (136–488, 11 cases); malignant neoplasm of the stomach in women—adjusted SRR 438 (90–1281, three cases); and malignant neoplasm of the female breast—adjusted SRR 134 (82–206, 20 cases). The unadjusted SMR for male brain cancer was 401 (83–1172, three cases) and there was an additional non-fatal case. Conclusion These findings, particularly those relating to lung cancer, though inconclusive, point to the possibility of a work-related risk of cancer that justifies further investigation.

Objectives An earlier investigation raised concern that some cancer cases might be linked to work at a semiconductor manufacturing plant. The aim of this study was to describe an update of the cancer incidence and mortality of these workers and assess whether workplace exposures contributed to any increased risk of selected cancers. Methods Standardised mortality ratios and standardised incidence ratios were calculated for cancer site groups of a priori interest in a cohort previously flagged against the National Health Service Central Register, with follow-up extended to the 2007 for deaths and 2006 for cancer registrations. Cases of female breast cancer, lung and stomach cancer, and male brain cancer, and a random sample of control subjects individually age-matched to the breast cancer cases, were identified from within the cohort dataset and invited to participate via General Practitioners. Exposures were estimated using a job exposure matrix developed from a historical hygiene assessment and assigned to job histories obtained from personal interview of subjects (or proxies). Results Though the findings were uncertain, there were no excesses of mortality or cancer incidence, either overall or for specific cancer sites, suggestive of a workplace effect. Logistic regression analyses comparing 20 cases of breast cancer with 83 matched controls showed no consistent evidence of any relationship with occupational exposures. Assessment of commonalities of workplace exposures among case sets for other cancer types was limited by the small numbers. Conclusions These results do not support earlier concerns about occupational cancer risks among this cohort.

Much of the current burden of long-latency respiratory disease (LLRD) in Great Britain is attributed to historical asbestos exposure. However, continuing exposure to other agents, notably silica, also contributes to disease burden. The aim of this study was to investigate the incidence of work-related LLRD reported by chest physicians in Great Britain, including variations by age, gender, occupation and suspected agent.LLRD incidence and incidence rate ratios by occupation were estimated (1996–2014). Mesothelioma cases by occupation were compared with proportional mortality ratios.Cases were predominantly in men (95%) and 92% of all cases were attributed to asbestos. Annual average incidence rates (males) per 100 000 were: benign pleural disease, 7.1 (95% CI 6.0–8.2); mesothelioma, 5.4 (4.8–6.0); pneumoconiosis, 1.9 (1.7–2.2); lung cancer, 0.8 (0.6–1.0); chronic obstructive pulmonary disease (COPD), 0.3 (0.2–0.4). Occupations with a particularly high incidence of LLRD were miners and quarrymen (COPD), plumbers and gas fitters (asbestosis), and shipyard and dock workers (all other categories). There was a clear concordance between cases of SWORD mesothelioma and proportional mortality ratios by occupation.Occupationally caused LLRD continues to contribute to a significant disease burden. Many cases are attributable to past exposure to agents such as asbestos and silica, but the potential for occupational exposures persists.Occupational long-latency respiratory disease contributes to a significant disease burden with ongoing exposure risk http://ow.ly/ahyF30gM9DK

Objectives: Workers in the asbestos industry tend to have high smoking rates compared to the general population. Both asbestos exposure and cigarette smoking are recognized risk factors for lung cancer mortality, but the exact nature of the interaction between the two remains uncertain. The aim of this study was to examine the effect of smoking and smoking cessation among asbestos workers in Great Britain (GB) and investigate the interaction between asbestos exposure and smoking. Methods: The study population consisted of 98 912 asbestos workers recruited into the GB Asbestos Survey from 1971, followed-up to December 2005. Poisson regression was used to estimate relative risks of lung cancer mortality associated with smoking habits of the asbestos workers and to assess whether these effects differed within various categories of asbestos exposure. The interaction between asbestos exposure and smoking was examined using the Synergy (S) and Multiplicativity (V) indices, which test the hypotheses of additive and multiplicative interaction, respectively. The proportion of lung cancers among smokers attributable to the interaction of asbestos and smoking was also estimated. Results: During 1 780 233 person-years of follow-up, there were 1878 deaths from lung cancer (12% of all deaths). Risk of lung cancer mortality increased with packs smoked per day, smoking duration, and total smoke exposure (pack-years). Asbestos workers who stopped smoking remained at increased risk of lung cancer mortality up to 40 years after smoking cessation compared to asbestos workers who never smoked. The effects of smoking and stopping smoking did not differ by duration of asbestos exposure, main occupation, age at first asbestos exposure, year of first exposure, or latency period. The interaction between asbestos exposure and smoking for asbestos workers was greater than additive [S 1.4, 95% confidence interval (CI) 1.2–1.6], and the multiplicative hypothesis could not be rejected (V 0.9, 95% CI 0.3–2.4). For those asbestos workers who smoked, an estimated 26% (95% CI 14–38%) of lung cancer deaths were attributable to the interaction of asbestos and smoking. Conclusions: This study emphasizes the importance of smoking prevention and cessation among those who work in the asbestos industry.

Objectives: The Great Britain Asbestos Survey was established to monitor mortality among workers covered by regulations to control occupational exposure to asbestos. This study updates the estimated burden of asbestos-related mortality in the cohort, and identifies risk factors associated with mortality. Methods: From 1971, workers were recruited during initially voluntary and later statutory medical examinations. A brief questionnaire was completed during the medical, and participants were flagged for death registrations. Standardised mortality ratios (SMRs) and proportional mortality ratios (PMRs) were calculated for deaths occurring before 2006. Poisson regression analyses were undertaken for diseases with significant excess mortality. Results: There were 15 496 deaths among 98 117 workers followed-up for 1 779 580 person-years. The SMR for all cause mortality was 141 (95% CI 139 to 143) and for all malignant neoplasms 163 (95% CI 159 to 167). The SMRs for cancers of the stomach (166), lung (187), peritoneum (3730) and pleura (968), mesothelioma (513), cerebrovascular disease (164) and asbestosis (5594) were statistically significantly elevated, as were the corresponding PMRs. In age and sex adjusted analysis, birth cohort, age at first exposure, year of first exposure, duration of exposure, latency and job type were associated with the relative risk of lung, pleural and peritoneal cancers, asbestosis and mesothelioma mortality. Conclusions: Known associations between asbestos exposure and mortality from lung, peritoneal and pleural cancers, mesothelioma and asbestosis were confirmed, and evidence of associations with stroke and stomach cancer mortality was observed. Limited evidence suggested that asbestos-related disease risk may be lower among those first exposed in more recent times.

Objectives Occupational exposure to asbestos is associated with increased morbidity and mortality. The effectiveness of regulations to control exposure is yet to be determined due to the long latency of asbestos-related diseases. The study objectives were to examine mortality trends in a large cohort of asbestos workers in relation to the implementation of the 1983 Asbestos Licensing Regulations (ALR). Methods The study population consisted of British asbestos workers undergoing regular medical examinations between 1971 and 2005. Mesothelioma and asbestosis mortality was defined by presence on the national Mesothelioma or Asbestosis Registers respectively. Mortality trends were examined by comparing mortality to December 2005 in workers attending their first medical before or after the ALR implementation, using Poisson regression models. Results There were 15 557 deaths from all causes among 98 912 men and women to the end of 2005; of these 649 were listed on the Mesothelioma Register and 477 on the Asbestosis Register. In workers first exposed before 1983 and with less than 23 years occupational exposure to asbestos, mesothelioma and asbestosis mortality, adjusted for age, sex, cohort, job, and smoking status, increased with latency; there was no such trend in those first exposed after 1982. The divergence in mortality between the two groups appeared to increase with latency, but limited follow-up time in the post-ALR group means that the findings should be treated with caution. Conclusions This study provides early indications of lower mesothelioma and asbestosis mortality among workers first exposed after implementation of the ALR. © Crown Copyright 2011

Objectives Asbestos is a carcinogen that is the cause of the majority of mesothelioma cases worldwide. Various models have been used to describe the increase and likely future pattern of mesothelioma rates seen in many western countries, a legacy of past heavy industrial asbestos use, but rarely those that estimate mesothelioma risk within a biological framework. Methods We analyse mesothelioma mortality in Great Britain using the two-stage clonal expansion (TSCE) model, a carcinogenesis model that assumes that the development of a malignant cell is the result of two critical and irreversible events. We use asbestos lung burden as the measure of dose that enters the dose-response component of the TSCE model. Within this framework, we relate the probability of mesothelioma to profiles of asbestos lung burden over time for subgroups of the male population derived from British annual asbestos import data and patterns of exposure from a recent population based study on mesothelioma risk in Great Britain. The role of asbestos as an initiator and promoter in carcinogenesis is investigated using Markov Chain Monte Carlo within a Bayesian framework. Results The best-fitting model was found to be one in which both the initiation and promotion rates were dose-dependent. Conclusions Mesothelioma mortality among males in Great Britain is predicted to peak in 2010 with an upper limit of 1854 deaths, however this peak has been found to be particularly sensitive to exposure assumptions. We discuss the impact of these assumptions on the peak and on longer-term projections. ©Crown Copyright (2011)

Objectives Some laboratory studies have suggested that exposure to Simian Virus 40 (SV40) might be a risk factor for mesothelioma. Most human epidemiological studies have not shown an association, though have lacked statistical power because of limited follow-up. We tested the hypothesis of there being an association via an update of an earlier ecological analysis in Britain. Methods National mesothelioma mortality for birth cohorts (1951–55 and 1956–60) with potential for exposure to SV40 via poliovirus vaccination in Britain were compared with those for a birth cohort (1962–66) likely to be unexposed, with consideration given to potential confounding by changes in asbestos exposure. Results There was evidence that mesothelioma rates were higher in the first SV40 potentially exposed cohort than the unexposed in both men (RR=2.4, 95% CI 1.5 to 3.9) and women (RR=2.7, 95% CI 1.1 to 6.1). In the second SV40 potentially exposed cohort, rates in men were no higher than in the unexposed cohort (RR=1.0, 95% CI 0.6 to 1.9) while rates in women were higher but not statistically significantly so (RR=2.0, 95% CI 0.8 to 4.8). Conclusions The reduction in the RR for the second cohort comparison in males may reflect a reduction in asbestos exposure in the second SV40 potentially exposed cohort rather than an effect due to SV40. The suggestion of an increased RR based on both cohort comparisons in females could reflect an SV40 effect confined to females, or more likely, a later reduction in asbestos exposure among women due to a high proportion of their exposures arising from non-occupational sources.

Objectives To describe an update of the cancer incidence and mortality of workers at a Scottish semiconductor manufacturing facility to assess potential workplace cancer risks. Methods Company records had been used to identify a cohort of 4388 workers employed at the facility between 1970 and 1999. Subjects were flagged against National Health Service records for notification of cancer registrations and deaths. Standardised mortality (to end 2007) and cancer registration (to end 2006) ratios (SMRs and SRRs) were calculated for cancer site groups of a priori interest, comparing with Scottish rates adjusted for local deprivation status. Results There was a substantial deficit of mortality overall, particularly among men, compatible, at least in part, with a healthy work effect: SMR% (males) 45, 95% CI 34 to 57; SMR% (females) 73, 95% CI 58 to 90. Total cancer registrations were consistent with expectation for men (SRR% 90, 95% CI 69 to 116) and women (SRR% 102, 95% CI 85 to 122). SRRs for four cancer sites highlighted in an earlier analysis (lung, stomach and breast cancer in women; and brain cancer in men) were not statistically significantly elevated overall; neither were those for any other cancer site group. Analyses of cohort subgroups (including a group more likely to have worked in areas using carcinogens) by time since first employment, and analyses by duration of employment did not reveal any associations suggestive of a workplace effect on cancer rates. Conclusions This analysis does not support earlier concerns about a possible link between working at the facility and increased risks of cancer.

Objectives HSE9s 2001 report on cancer in a Scottish cohort of semiconductor manufacturing workers showed some statistically significant results, suggestive of increased risks. Recently, the follow-up in the cohort was extended. We report on a case-based study to investigate these suggestions. Methods From the extended follow-up, cases of breast, stomach and lung cancer in women, and of brain cancer in men were identified. It was planned that the lung and breast cancer cases would be interviewed and compared with matched controls, and that the rarer stomach and brain cancers would be examined case-only. A questionnaire was designed to collect detailed employment histories within the factory and elsewhere, information relevant to possible asbestos exposure, and lifestyle and environmental factors. A historical hygiene assessment was carried out at the factory, to inform construction of a job-exposure matrix. Results Attempts to recruit cases (or proxy respondents) were only partially successful; as a result, the lung cancers element was converted to a case-only study. Comparison with controls was possible for only 20 breast cancer cases (including 7 proxy respondents). From an extensive programme of conditional logistic analyses, statistical significance was achieved for exposure to arsenic compounds, antimony trioxide and sulphuric acid mist and to gases in general, but only in a few of the analyses. Examination of proxy responses for stomach, lung and brain cancers did not suggest any common workplace factors for any of these outcomes. Conclusions We interpreted this evidence as not supportive of an occupational risk for any of the cancers.

Objectives To explore possible reasons for a continuing increase in asbestosis mortality in Britain by examining age-specific male rates by birth cohort and comparing with those for mesothelioma. Methods Asbestosis and mesothelioma rates were calculated using deaths from the asbestosis and mesothelioma registers and national population data. Age-specific rates by birth cohort were summarised in graphical format. Results There is a strong increase in the asbestosis and mesothelioma rates with increasing age for the majority of birth cohorts. Rates continue to increase rapidly above age 80 for men born between the early 1900s to the mid 1920s particularly for asbestosis. The rate of asbestosis is highest at any given age for men born during the late 1920s. This contrasts with mesothelioma where the highest rate at any given age is for those born in the late 1930s and early 1940s. Asbestos rates at given ages are progressively lower for successive birth cohorts from 1930 onwards, although a strong increase with age is evident within each. Conclusions That the birth cohort with the highest rates occurs earlier for asbestosis than mesothelioma could be consistent with asbestosis being caused by higher exposures than those necessary to cause mesothelioma, and that exposures associated with a risk of mesothelioma continued after those high enough to cause asbestosis had largely ceased. Mortality from asbestosis, even at old ages, appears to be determined mainly by exposures at young ages

Objectives Lead exposure and absorption can lead to many adverse health effects. Statutory monitoring of blood-lead levels in British workers has been undertaken since 1982 in order to prevent the occurrence of lead-related health problems. Our objective was to describe trends in worker blood-lead levels between 1982 and 2010. Methods All British workers with the potential for significant exposure to lead are required to undergo medical surveillance including regular recording of their highest blood-lead level. Doctors supply an annual summary of measurements and numbers of workers suspended from work, categorised by age, sex, industry sector and blood-lead level. Summary statistics based on measurements supplied through 2010 were described and time trends in levels were investigated. Results In 1982, 22 217 workers were under medical surveillance; this fell to 7162 in 2010. The majority of these were male (95%); this remained broadly constant over the period. In 1982, 1.7% of males and 20.3% of females had measurements above the suspension limits (80 μg/100 ml and 40 μg/100 ml). The suspension limit for males was reduced to 70 μg/100 ml in 1986; both were further reduced in 1998 to 60 μg/100 ml and 30 μg/100 ml. Despite these reductions, 0.8% of males and 1.2% of females had measurements above these limits in 2010. The majority of individuals under surveillance were employed in smelting, refining, alloying and casting. Conclusions There was a downward trend in the number of workers under medical surveillance, along with a reduction in the percentage of workers with high blood-lead levels and suspensions from work. © Crown Copyright 2011

We welcome the appearance of the new analysis of asbestos related mortality by Loomis et al ( Occup Environ Med 2009;66:535–42) which constitutes an important addition to the available evidence. We note that the lung cancer risk from these data highlighted by the authors and based on their internal analyses is identical to that suggested as the “best estimate” in our earlier meta-analysis1: a relative risk of 1.102 per 100 f/ml.yr translates almost exactly to an excess over expected of 0.1% per f/ml.yr. The risk of mesothelioma derived from these new data is higher by a factor of 10 than that which emerged from our meta-analysis. The following …