Description: Objectives Several respirable hazards, including smoking and indoor air pollution from biomass, were suggested to increase the risk of tuberculosis. Few studies have been conducted on ambient air pollution and tuberculosis. We investigated the association between exposure to ambient air pollution and incidence of active tuberculosis. Methods We conducted a cohort study using 106 678 participants of a community-based screening service in Taiwan, 2005–2012. We estimated individual exposure to air pollution using data from the nearest air quality monitoring station and the road intensity within a 500 m buffer zone. The incidence of tuberculosis was ascertained from the national tuberculosis registry. Results After a median follow-up of 6.7 years, 418 cases of tuberculosis occurred. Exposure to fine particulate matter (PM 2.5 ) was associated with increased risk of active tuberculosis (adjusted HR: 1.39/10 μg/m 3 (95% CI 0.95 to 2.03)). In addition, traffic-related air pollution including nitrogen dioxide (adjusted HR: 1.33/10 ppb; 95% CI 1.04 to 1.70), nitrogen oxides (adjusted HR: 1.21/10 ppb; 95% CI 1.04 to 1.41) and carbon monoxide (adjusted HR: 1.89/ppm; 95% CI 0.78 to 4.58) was associated with tuberculosis risk. There was a non-significant trend between the length of major roads in the neighbourhood and culture-confirmed tuberculosis (adjusted HR: 1.04/km; 95% CI 0.995 to 1.09). Conclusions Our study revealed a possible link between ambient air pollution and risk of active tuberculosis. Since people from developing countries continue to be exposed to high levels of ambient air pollution and to experience high rates of tuberculosis, the impact of worsening air pollution on global tuberculosis control warrants further investigation.

Description: Objectives Policies have been introduced to reduce sickness absence, but their effectiveness is largely unknown. In a natural experiment, we examined effects of legislative changes on return to work and work participation. Methods The source population consisted of up to 72 164 Finnish public sector employees with a permanent job contract in 2008–2011 (before) and in 2013–2014 (after). We used employees with a continuous sickness absence of at least 30 calendar-days (n=5708–6393), 60 compensated days (n=1481–1655) and 90 compensated days (n=766–932). We examined sustainable return to work (a minimum of 28 consecutive working days) with survival analysis as well as monthly work participation after a sickness absence, and annual gain in work participation after the intervention, using trajectory analyses. Results Sustainable return to work after 60 days of sickness absence occurred earlier after the legislative changes (p value 0.017), although the effect reduced towards the end of the follow-up. There were no differences in return to work after a 30 or 90 days of sickness absence. The largest annual gain, postintervention versus preintervention, in monthly work participation was observed among employees with 60 days of sickness absence and was 230.9 person-years/10 000 employees. The corresponding annual gains among those with 30 days and 90 days of sickness absence were 51.8 and 39.6, respectively. Conclusions Our findings suggest that the legislative changes, obligating early notification of prolonged sickness absences as well as assessment of remaining work ability and possibilities to continue working, may enhance sustainable return to work in the short term. Other measures will be needed to enhance work participation, especially in the long term.

Description: The burden of disabling musculoskeletal pain and injuries (musculoskeletal disorders, MSDs) arising from work-related causes in many workplaces remains substantial. There is little consensus on the most appropriate interventions for MSDs. Our objective was to update a systematic review of workplace-based interventions for preventing and managing upper extremity MSD (UEMSD). We followed a systematic review process developed by the Institute for Work & Health and an adapted best evidence synthesis. 6 electronic databases were searched (January 2008 until April 2013 inclusive) yielding 9909 non-duplicate references. 26 high-quality and medium-quality studies relevant to our research question were combined with 35 from the original review to synthesise the evidence on 30 different intervention categories. There was strong evidence for one intervention category, resistance training, leading to the recommendation: Implementing a workplace-based resistance training exercise programme can help prevent and manage UEMSD and symptoms . The synthesis also revealed moderate evidence for stretching programmes, mouse use feedback and forearm supports in preventing UEMSD or symptoms. There was also moderate evidence for no benefit for EMG biofeedback, job stress management training, and office workstation adjustment for UEMSD and symptoms. Messages are proposed for both these and other intervention categories.

Description: The aim of this study was to estimate the prevalence of viral hepatitis C (HCV) infection among healthcare workers (HCWs) compared to the general population. A systematic search for the years 1989–2014 was conducted in the Medline, Embase and Cochrane databases. Studies on hepatitis C in HCWs were included if they incorporated either a control group or reference data for the general population. The study quality was classified as high, moderate or low. Pooled effect estimates were calculated to determine the odds of occupational infection. Heterogeneity between studies was analysed using the 2 test (p〈0.10) and quantified using the I 2 test. 57 studies met our criteria for inclusion and 44 were included in the meta-analysis. Analysis of high and moderate quality studies showed a significantly increased OR for HCV infection in HCWs relative to control populations, with a value of 1.6 (95% CI 1.03 to 2.42). Stratification by study region gave an OR of 2.1 in low prevalence countries; while stratification by occupational groups gave an increased prevalence for medical (OR 2.2) and for laboratory staff (OR 2.2). The OR for professionals at high risk of blood contact was 2.7. The pooled analysis indicates that the prevalence of infection is significantly higher in HCWs than in the general population. The highest prevalence was observed among medical and laboratory staff. Prospective studies that focus on HCW-specific activity and personal risk factors for HCV infection are needed.

Description: Background Asthma prevalence and acute exacerbations have been associated with endotoxin exposure. However, there are limited data on relations between acute asthma outcomes in children and personal exposure to endotoxin or whether this relation is modified by personal air pollution exposures. Methods We made repeated measurements of the fractional concentration of exhaled NO (F e NO ), forced expiratory volume in 1 s (FEV 1 ) and personal endotoxin exposures in patients with persistent asthma aged 9–18 years, each of whom was followed for 10 consecutive days in Riverside and Whittier, California. Endotoxin was measured in PM 2.5 , and simultaneously we measured personal exposure to air pollutants: NO 2 and PM 2.5 mass, elemental carbon and organic carbon. Endotoxin exposure–response relations and interactions between endotoxin and air pollutants were analysed with mixed models controlling for personal temperature, humidity and the 10-day period. Results Neither percent-predicted FEV 1 nor F e NO was associated with personal endotoxin overall; however, endotoxin was associated with FEV 1 among patients with average percent-predicted FEV 1 〈80%. When NO 2 was above its median, F e NO increased by 2.2% (95% CI –0.8% to 5.2%) for an interquartile increase in personal endotoxin, whereas F e NO was lower by –1.8% (95% CI –4% to 0.5%) when NO 2 was≤its median. However, this is out of 12 interaction tests between personal endotoxin and a binary air pollutant for each outcome (FEV 1 and F e NO ), and there were no interactions with any continuous-scaled pollutant. Conclusions Personal endotoxin exposure was not associated with acute daily changes in F e NO or FEV 1 in a cohort panel of schoolchildren with asthma, except for decreased FEV 1 among patients with more severe asthma (percent-predicted FEV 1 〈80%). There was limited evidence of effect modification of endotoxin by personal exposure to air pollution.

Description: Objectives Non-communicable diseases (NCDs) constitute an increasing slice of the global burden of disease, with the South-East Asia region projected to see the highest increase in NCD-related deaths over the next decade. Mining industry employees may be exposed to various factors potentially elevating their NCD risk. This study aimed to assess the distribution and 5-year longitudinal trends of key metabolic NCD risk factors in a cohort of copper–gold mining company workers in Papua, Indonesia. Methods Metabolic indicators of NCD risk were assessed among employees (15 580 at baseline, 6496 prospectively) of a large copper–gold mining operation in Papua, Indonesia, using routinely collected 5-year medical surveillance data. The study cohort comprised individuals aged 18–68 years employed for ≥1 year during 2008–2013. Assessed risk factors were based on repeat measures of cholesterol, blood glucose, blood pressure and body weight, using WHO criteria. Results Metabolic risk indicator rates were markedly high and increased significantly from baseline through 5-year follow-up (p〈0.001). Adjusting for gender and age, longer duration of employment (≥10 years) predicted raised cholesterol (adjusted OR (AOR)=1.13, p=0.003), raised blood pressure (AOR=1.16, p=0.009) and overweight/obesity (AOR=1.14, p=0.001) at baseline; and persistent raised cholesterol (AOR=1.26, p=0.003), and both incident (AOR=1.33, p=0.014) and persistent raised blood glucose (AOR=1.62, p=0.044) at 3-year follow-up. Conclusions Individuals employed for longer periods in a mining operations setting in Papua, Indonesia, may face elevated NCD risk through various routes. Workplace health promotion interventions and policies targeting modifiable lifestyle patterns and environmental exposures present an important opportunity to reduce such susceptibilities and mitigate associated health risks.

Description: Objectives Common mental disorders (CMDs) are a major cause of rising disability benefit expenditures. We urgently need evidence on programmes that can increase work participation in CMDs. The aim of this study was to evaluate the effectiveness of work-focused cognitive–behavioural therapy (CBT) and individual job support for people struggling with work participation due to CMDs. Methods A randomised controlled multicentre trial (RCT) including 1193 participants was conducted. Participants were on sick leave, at risk of going on sick leave or on long-term benefits. The intervention integrated work-focused CBT with individual job support. The control group received usual care. The main outcome was objectively ascertained work participation at 12 months follow-up, with changes in mental health and health-related quality of life as secondary outcomes. Results A larger proportion of participants in the intervention group had increased or maintained their work participation at follow-up compared to the control group (44.2% vs 37.2%, p=0.015). The difference remained significant after 18 months (difference 7.8%, p=0.018), and was even stronger for those on long-term benefits (difference 12.2%, p=0.007). The intervention also reduced depression (t=3.23, p≤0.001) and anxiety symptoms (t=2.52, p=0.012) and increased health-related quality of life (t=2.24, p=0.026) more than usual care. Conclusions A work-focused CBT and individual job support was more effective than usual care in increasing or maintaining work participation for people with CMDs. The effects were profound for people on long-term benefits. This is the first large-scale RCT to demonstrate an effect of a behavioural intervention on work participation for the large group of workers with CMDs. Trial registration number ClinicalTrials.gov, registration number: NCT01146730.

Description: Background In several studies, exposure to fine particulate matter (PM) has been associated with inflammation, with inconsistent results. We used repeated measurements to examine the association of long-term fine and ultrafine particle exposure with several blood markers of inflammation and coagulation. Methods We used baseline (2000–2003) and follow-up (2006–2008) data from the Heinz Nixdorf Recall Study, a German population-based prospective cohort of 4814 participants. A chemistry transport model was applied to model daily surface concentrations of PM air pollutants (PM 10 , PM 2.5 ) and particle number on a grid of 1 km 2 . Applying mixed regression models, we analysed associations of long-term (mean of 365 days prior to blood draw) particle exposure at each participant's residence with the level of high-sensitivity C reactive protein (hs-CRP), fibrinogen, platelet and white cell count (WCC), adjusting for short-term PM exposure (moving averages of 1–7 days), personal characteristics, season, ambient temperature (1–5 days), ozone and time trend. Results We analysed 6488 observations: 3275 participants with baseline data and 3213 with follow-up data. An increase of 2.4 µg/m 3 in long-term PM 2.5 was associated with an adjusted increase of 5.4% (95% CI 0.6% to 10.5%) in hs-CRP and of 2.3% (95% CI 1.4% to 3.3%) in the platelet count. Fibrinogen and WCC were not associated with long-term particle exposure. Conclusions In this population-based cohort, we found associations of long-term exposure to PM with markers of inflammation (hs-CRP) and coagulation (platelets). This finding supports the hypothesis that inflammatory processes might contribute to chronic effects of air pollution on cardiovascular disease.

Description: Introduction Italy produced and imported a large amount of raw asbestos, up to the ban in 1992, with a peak in the period between 1976 and 1980 at about 160 000 tons/year. The National Register of Mesotheliomas (ReNaM, "Registro Nazionale dei Mesoteliomi" in Italian), a surveillance system of mesothelioma incidence, has been active since 2002, operating through a regional structure. Methods The Operating Regional Center (COR) actively researches cases and defines asbestos exposure on the basis of national guidelines. Diagnostic, demographic and exposure characteristics of non-occupationally exposed cases are analysed and described with respect to occupationally exposed cases. Results Standardised incidence rates for pleural mesothelioma in 2008 were 3.84 (per 100 000) for men and 1.45 for women, respectively. Among the 15 845 mesothelioma cases registered between 1993 and 2008, exposure to asbestos fibres was investigated for 12 065 individuals (76.1%), identifying 530 (4.4%) with familial exposure (they lived with an occupationally exposed cohabitant), 514 (4.3%) with environmental exposure to asbestos (they lived near sources of asbestos pollution and were never occupationally exposed) and 188 (1.6%) exposed through hobby-related or other leisure activities. Clusters of cases due to environmental exposure are mainly related to the presence of asbestos-cement industry plants (Casale Monferrato, Broni, Bari), to shipbuilding and repair activities (Monfalcone, Trieste, La Spezia, Genova) and soil contamination (Biancavilla in Sicily). Conclusions Asbestos pollution outside the workplace contributes significantly to the burden of asbestos-related diseases, suggesting the need to prevent exposures and to discuss how to deal with compensation rights for malignant mesothelioma cases induced by non-occupational exposure to asbestos.

Description: We welcome the opportunity to respond to Goodman et al , 1 and to correct their misperceptions about our paper. 2 As noted in their letter, Kerper et al 3 also recently analysed lung function decrements associated with pleural plaques. While the methodological details of our publications differed somewhat, the identified literature and the conclusions regarding magnitude of effect on lung function were well aligned. We found statistically significant 2–4% decrements in lung function in people exposed to asbestos with pleural plaques relative to asbestos-exposed people without abnormalities. Kerper et al 3 reported 3–5% decrements. It is not clear why Kerper et al 3 chose to ignore differences in study size: all studies were considered equally in their analysis, despite sample sizes ranging from tens to thousands, and a summary estimate was not calculated. With respect to the specific points raised, 1 although we...