Description: Background MRI has developed into one of the most important medical diagnostic imaging modalities, but it exposes staff to static magnetic fields (SMF) when present in the vicinity of the MR system, and to radiofrequency and switched gradient electromagnetic fields if they are present during image acquisition. We measured exposure to SMF and motion-induced time-varying magnetic fields (TVMF) in MRI staff in clinical practice in the UK to enable extensive assessment of personal exposure levels and variability, which enables comparison to other countries. Methods 8 MRI facilities across National Health Service sites in England, Wales and Scotland were included, and staff randomly selected during the days when measurements were performed were invited to wear a personal MRI-compatible dosimeter and keep a diary to record all procedures and tasks performed during the measured shift. Results 98 participants, primarily radiographers (71%) but also other healthcare staff, anaesthetists and other medical staff were included, resulting in 149 measurements. Average geometric mean peak SMF and TVMF exposures were 448 mT (range 20–2891) and 1083 mT/s (9–12 355 mT/s), and were highest for radiographers (GM=559 mT and GM=734 mT/s). Time-weighted exposures to SMF and TVMF (GM=16 mT (range 5–64) and GM=14 mT/s (range 9–105)) and exposed-time-weighted exposures to SMF and TVMF (GM=27 mT (range 11–89) and GM=17 mT/s (range 9–124)) were overall relative low—primarily because staff were not in the MRI suite for most of their shifts—and did not differ significantly between occupations. Conclusions These results are comparable to the few data available from the UK but they differ from recent data collected in the Netherlands, indicating that UK staff are exposed for shorter periods but to higher levels. These data indicate that exposure to SMF and TVMF from MRI scanners cannot be extrapolated across countries.

Description: Background The current knowledge on respiratory work disability is based on studies that used crude categories of exposure. This may lead to a loss of power, and does not provide sufficient information to allow targeted workplace interventions and follow-up of patients with respiratory symptoms. Objectives The aim of this study was to identify occupations and specific exposures associated with respiratory work disability. Methods In 2013, a self-administered questionnaire was mailed to a random sample of the general population, aged 16–50, in Telemark County, Norway. We defined respiratory work disability as a positive response to the survey question: ‘Have you ever had to change or leave your job because it affected your breathing?’ Occupational exposures were assessed using an asthma-specific job-exposure matrix, and comparison of risks was made for cases and a median of 50 controls per case. Results 247 workers had changed their work because of respiratory symptoms, accounting for 1.7% of the respondents ever employed. The ‘breath-taking jobs’ were cooks/chefs: adjusted OR 3.6 (95% CI 1.6 to 8.0); welders: 5.2 (2.0 to 14); gardeners: 4.5 (1.3 to 15); sheet metal workers: 5.4 (2.0 to 14); cleaners: 5.0 (2.2 to 11); hairdressers: 6.4 (2.5 to 17); and agricultural labourers: 7.4 (2.5 to 22). Job changes were also associated with a variety of occupational exposures, with some differences between men and women. Conclusions Self-report and job-exposure matrix data showed similar findings. For the occupations and exposures associated with job change, preventive measures should be implemented.

Description: Background The association between lung cancer and occupational exposure to organic solvents is discussed. Since different solvents are often used simultaneously , it is difficult to assess the role of individual substances. Objectives The present study is focused on an in-depth investigation of the potential association between lung cancer risk and occupational exposure to a large group of organic solvents, taking into account the well-known risk factors for lung cancer, tobacco smoking and occupational exposure to asbestos. Methods We analysed data from the Investigation of occupational and environmental causes of respiratory cancers (ICARE) study, a large French population-based case–control study, set up between 2001 and 2007. A total of 2276 male cases and 2780 male controls were interviewed, and long-life occupational history was collected. In order to overcome the analytical difficulties created by multiple correlated exposures, we carried out a novel type of analysis based on Bayesian profile regression. Results After analysis with conventional logistic regression methods, none of the 11 solvents examined were associated with lung cancer risk. Through a profile regression approach, we did not observe any significant association between solvent exposure and lung cancer. However, we identified clusters at high risk that are related to occupations known to be at risk of developing lung cancer, such as painters. Conclusions Organic solvents do not appear to be substantial contributors to the occupational risk of lung cancer for the occupations known to be at risk.

Description: Objectives There is evidence of adverse associations between short-term exposure to traffic-related pollution and health, but little is known about the relative contribution of the various sources and particulate constituents. Methods For each day for 2011–2012 in London, UK over 100 air pollutant metrics were assembled using monitors, modelling and chemical analyses. We selected a priori metrics indicative of traffic sources: general traffic, petrol exhaust, diesel exhaust and non-exhaust (mineral dust, brake and tyre wear). Using Poisson regression models, controlling for time-varying confounders, we derived effect estimates for cardiovascular and respiratory hospital admissions at prespecified lags and evaluated the sensitivity of estimates to multipollutant modelling and effect modification by season. Results For single day exposure, we found consistent associations between adult (15–64 years) cardiovascular and paediatric (0–14 years) respiratory admissions with elemental and black carbon (EC/BC), ranging from 0.56% to 1.65% increase per IQR change, and to a lesser degree with carbon monoxide (CO) and aluminium (Al). The average of past 7 days EC/BC exposure was associated with elderly (65+ years) cardiovascular admissions. Indicated associations were higher during the warm period of the year. Although effect estimates were sensitive to the adjustment for other pollutants they remained consistent in direction, indicating independence of associations from different sources, especially between diesel and petrol engines, as well as mineral dust. Conclusions Our results suggest that exhaust related pollutants are associated with increased numbers of adult cardiovascular and paediatric respiratory hospitalisations. More extensive monitoring in urban centres is required to further elucidate the associations.

Description: Background Welders are at risk for cardiovascular disease. Recent studies linked tobacco smoke exposure to hypomethylation of the F2RL3 (coagulation factor II (thrombin) receptor-like 3) gene, a marker for cardiovascular disease prognosis and mortality. However, whether welding fumes cause hypomethylation of F2RL3 remains unknown. Methods We investigated 101 welders (median span of working as a welder: 7 years) and 127 unexposed controls (non-welders with no obvious exposure to respirable dust at work), age range 23–60 years, all currently non-smoking, in Sweden. The participants were interviewed about their work history, lifestyle factors and diseases. Personal sampling of respirable dust was performed for the welders. DNA methylation of F2RL3 in blood was assessed by pyrosequencing of four CpG sites, CpG_2 (corresponds to cg03636183) to CpG_5, in F2RL3 . Multivariable linear regression analysis was used to assess the association between exposure to welding fumes and F2RL3 methylation. Results Welders had 2.6% lower methylation of CpG_5 than controls (p〈0.001). Higher concentrations of measured respirable dust among the welders were associated with hypomethylation of CpG_2, CpG_4 and CpG_5 (β=–0.49 to –1.4, p〈0.012); p〈0.029 adjusted for age, previous smoking, passive smoking, education, current residence and respirator use. Increasing the number of years working as a welder was associated with hypomethylation of CpG_4 (linear regression analysis, β=–0.11, p=0.039, adjusted for previous smoking). Previous tobacco smokers had 1.5–4.7% (p〈0.014) lower methylation of 3 of the 4 CpG sites in F2RL3 (CpG_2, CpG_4 and CpG_5) compared to never-smokers. A non-significant lower risk of cardiovascular disease with more methylation was observed for all CpG sites. Conclusions Welding fumes exposure and previous smoking were associated with F2RL3 hypomethylation. This finding links low-to-moderate exposure to welding fumes to adverse effects on the cardiovascular system, and suggests a potential mechanistic pathway for this link, via epigenetic effects on F2RL3 expression.

Description: Objective To compare short-term effects of fine particles (PM 2.5 ; aerodynamic diameter 〈2.5 µm) from different sources on the blood levels of markers of systemic inflammation. Methods We followed a panel of 52 ischaemic heart disease patients from 15 November 2005 to 21 April 2006 with clinic visits in every second week in the city of Kotka, Finland, and determined nine inflammatory markers from blood samples. In addition, we monitored outdoor air pollution at a fixed site during the study period and conducted a source apportionment of PM 2.5 using the Environmental Protection Agency's model EPA PMF 3.0. We then analysed associations between levels of source-specific PM 2.5 and markers of systemic inflammation using linear mixed models. Results We identified five source categories: regional and long-range transport (LRT), traffic, biomass combustion, sea salt, and pulp industry. We found most evidence for the relation of air pollution and inflammation in LRT, traffic and biomass combustion; the most relevant inflammation markers were C-reactive protein, interleukin-12 and myeloperoxidase. Sea salt was not positively associated with any of the inflammatory markers. Conclusions Results suggest that PM 2.5 from several sources, such as biomass combustion and traffic, are promoters of systemic inflammation, a risk factor for cardiovascular diseases.

Description: Objectives The role of outdoor air pollution in the incidence of chronic obstructive pulmonary disease (COPD) remains unclear. We investigated this question using a large, nationally representative cohort based on primary care records linked to hospital admissions. Methods A cohort of 812 063 patients aged 40–89 years registered with 205 English general practices in 2002 without a COPD diagnosis was followed from 2003 to 2007. First COPD diagnoses recorded either by a general practitioner (GP) or on admission to hospital were identified. Annual average concentrations in 2002 for particulate matter with an aerodynamic diameter 〈10 µm (PM 10 ) and 〈2.5 µm (PM 2.5 ), nitrogen dioxide (NO 2 ), ozone and sulfur dioxide (SO 2 ) at 1 km 2 resolution were estimated from emission-based dispersion models. Hazard ratios (HRs) per interquartile range change were estimated from Cox models adjusting for age, sex, smoking, body mass index and area-level deprivation. Results 16 034 participants (1.92%) received a COPD diagnosis from their GP and 2910 participants (0.35%) were admitted to hospital for COPD. After adjustment, HRs for GP recorded COPD and PM 10 , PM 2.5 and NO 2 were close to unity, positive for SO 2 (HR=1.07 (95% CI 1.03 to 1.11) per 2.2 µg/m 3 ) and negative for ozone (HR=0.94 (0.89 to 1.00) per 3 µg/m 3 ). For admissions HRs for PM 2.5 and NO 2 remained positive (HRs=1.05 (0.98 to 1.13) and 1.06 (0.98 to 1.15) per 1.9 µg/m 3 and 10.7 µg/m 3 , respectively). Conclusions This large population-based cohort study found limited, inconclusive evidence for associations between air pollution and COPD incidence. Further work, utilising improved estimates of air pollution over time and enhanced socioeconomic indicators, is required to clarify the association between air pollution and COPD incidence.

Description: Objectives To estimate the numbers of workers exposed to known and suspected occupational carcinogens in Canada, building on the methods of CARcinogen EXposure (CAREX) projects in the European Union (EU). Methods CAREX Canada consists of estimates of the prevalence and level of exposure to occupational carcinogens. CAREX Canada includes occupational agents evaluated by the International Agency for Research on Cancer as known, probable or possible human carcinogens that were present and feasible to assess in Canadian workplaces. A Canadian Workplace Exposure Database was established to identify the potential for exposure in particular industries and occupations, and to create exposure level estimates among priority agents, where possible. CAREX EU data were reviewed for relevance to the Canadian context and the proportion of workers likely to be exposed by industry and occupation in Canada was assigned using expert assessment and agreement by a minimum of two occupational hygienists. These proportions were used to generate prevalence estimates by linkage with the Census of Population for 2006, and these estimates are available by industry, occupation, sex and province. Results CAREX Canada estimated the number of workers exposed to 44 known, probable and suspected carcinogens. Estimates of levels of exposure were further developed for 18 priority agents. Common exposures included night shift work (1.9 million exposed), solar ultraviolet radiation exposure (1.5 million exposed) and diesel engine exhaust (781 000 exposed). Conclusions A substantial proportion of Canadian workers are exposed to known and suspected carcinogens at work.

Description: Background Ambient air pollution has been consistently associated with exacerbation of respiratory diseases in schoolchildren, but the role of early exposure to traffic-related air pollution in the first occurrence of respiratory symptoms and asthma is not yet clear. Methods We assessed the association between indexes of exposure to traffic-related air pollution during different periods of life and respiratory outcomes in a birth cohort of 672 newborns (Rome, Italy). Direct interviews of the mother were conducted at birth and at 6, 15 months, 4 and 7 years. Exposure to traffic-related air pollution was assessed for each residential address during the follow-up period using a Land-Use Regression model (LUR) for nitrogen dioxide (NO 2 ) and a Geographic Information System (GIS) variable of proximity to high-traffic roads (HTR) (〉10 000vehicles/day). We used age-specific NO 2 levels to develop indices of exposure at birth, current, and lifetime time-weighted average. The association of NO 2 and traffic proximity with respiratory disorders were evaluated using logistic regression in a longitudinal approach (Generalised Estimating Equation). The exposure indexes were used as continuous and categorical variables (cut-off points based on the 75th percentile for NO 2 and the 25th percentile for distance from HTRs). Results The average NO 2 exposure level at birth was 37.2 μg/m 3 (SD 7.2, 10–90th range 29.2–46.1). There were no statistical significant associations between the exposure indices and the respiratory outcomes in the longitudinal model. The odds ratios for a 10-µg/m 3 increase in time-weighted average NO 2 exposure were: asthma incidence OR=1.09; 95 CI% 0.78 to 1.52, wheezing OR=1.07; 95 CI% 0.90 to 1.28, shortness of breath with wheezing OR=1.16; 95 CI% 0.94 to 1.43, cough or phlegm apart from cold OR=1.11; 95 CI% 0.92 to 1.33, and otitis OR=1.08; 95 CI% 0.89 to 1.32. Stronger but not significant associations were found considering the 75th percentile of the NO 2 distribution as a cut-off, especially for incidence of asthma and prevalence of wheeze (OR=1.41; 95 CI% 0.88 to 2.28 and OR=1.27; 95 CI% 0.95 to 1.70, respectively); the highest OR was found for wheezing (OR=2.29; 95 CI% 1.15 to 4.56) at the 7-year follow-up. No association was found with distance from HTRs. Conclusions Exposure to traffic-related air pollution is only weakly associated with respiratory symptoms in young children in the first 7 years of life.

Description: Aims The relation between Dupuytren's contracture and occupational exposure to hand-transmitted vibration (HTV) has frequently been debated. We explored associations in a representative national sample of workers with well-characterised exposure to HTV. Methods We mailed a questionnaire to 21 201 subjects aged 16–64 years, selected at random from the age-sex registers of 34 general practices in Great Britain and to 993 subjects chosen randomly from military pay records, asking about occupational exposure to 39 sources of HTV and about fixed flexion contracture of the little or ring finger. Analysis was restricted to men at work in the previous week. Estimates were made of average daily vibration dose ( A (8) root mean squared velocity (rms)) over that week. Associations with Dupuytren's contracture were estimated by Poisson regression, for lifetime exposure to HTV and for exposures in the past week 〉 A (8) of 2.8 ms –2 rms. Estimates of relative risk (prevalence ratio (PR)) were adjusted for age, smoking status, social class and certain manual activities at work. Results In all 4969 eligible male respondents supplied full information on the study variables. These included 72 men with Dupuytren's contracture, 2287 with occupational exposure to HTV and 409 with A (8)〉2.8 ms –2 in the past week. PRs for occupational exposure to HTV were elevated 1.5-fold. For men with an A (8)〉2.8 ms –2 in the past week, the adjusted PR was 2.85 (95% CI 1.37 to 5.97). Conclusions Our findings suggest that risk of Dupuytren's contracture is more than doubled in men with high levels of weekly exposure to HTV.