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: Objective The study was designed to investigate whether beryllium exposure was related to illness diagnosed as sarcoidosis. Chronic beryllium disease (CBD) and sarcoidosis are clinically and pathologically indistinguishable, with only the presence of beryllium-specific T-lymphocytes identifying CBD. Testing for such cells is not feasible in community studies of sarcoidosis but a second characteristic of CBD, its much greater incidence in those with a glutamic acid residue at position 69 of the HLA-DPB1 gene (Glu69), provides an alternative approach to answering this question. Methods Cases of sarcoidosis aged 18–60 years diagnosed in Alberta, Canada, from 1999 to 2005 were approached through their specialist physician, together with age-matched and sex-matched referents with other chronic lung disease. Referents were grouped into chronic obstructive pulmonary disease (COPD), asthma and other lung disease. Participants completed a telephone questionnaire, including industry-specific questionnaires. DNA was extracted from mailed-in mouthwash samples and genotyped for Glu69. Duration of employment in types of work with independently documented beryllium exposure was calculated. Results DNA was extracted for 655 cases (270 Glu69 positive) and 1382 referents (561 positive). No increase in sarcoidosis was seen with either Glu69 or beryllium exposure (none, 〈10, ≥10 years) as main effects: longer duration in possible beryllium jobs was related to COPD. In Glu69 positive men with exposure ≥10 years, the trend towards increasing rate of COPD was reversed, and a significant interaction of duration of exposure and Glu69 was detected (OR=4.51 95% CI 1.17 to 17.48). Conclusions The gene–environment interaction supports the hypothesis that some cases diagnosed as sarcoidosis result from occupational beryllium exposure.

Description: Objectives To investigate inter-reader agreement for the detection of pleural and parenchymal abnormalities using CT in a large cross-sectional study comprising information on individual cumulative exposure to asbestos. Methods The project was approved by the hospital ethics committee, and all patients received information on the study and gave their written informed consent. In 5511 CT scans performed in a cohort of retired workers previously exposed to asbestos and volunteering to participate in a multiregional survey programme (Asbestos Related Diseases Cohort, ARDCO), double randomised standardised readings, triple in case of disagreement, were performed by seven trained expert radiologists specialised in thoracic imaging and blind to the initial interpretation. Inter-reader agreement was evaluated by calculating the -weighted coefficient between pairs of expert readers and results of routine practice and final diagnosis after expert reading. Results -Weighted coefficients between trained experts ranged from 0.28 to 0.52 (fair to good), 0.59 to 0.86 (good to excellent) and 0.11 to 0.66 (poor to good) for the diagnosis of asbestosis, pleural plaques and fibrosis of the visceral pleura, respectively. -Weighted coefficients between results of routine practice and final diagnosis after expert reading were 0.13 (poor), 0.53 (moderate) and 0.11 (poor) for the diagnosis of asbestosis, pleural plaques and fibrosis of the visceral pleura, respectively. Conclusions Interpretation of benign asbestos-related thoracic abnormalities requires standardisation of the reading and trained readers, particularly for participants asking for compensation, and with a view to the longitudinal survey of asbestos-exposed workers.

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.

Description: Objectives To evaluate respiratory related mortality among underground coal miners after 37 years of follow-up. Methods Underlying cause of death for 9033 underground coal miners from 31 US mines enrolled between 1969 and 1971 was evaluated with life table analysis. Cox proportional hazards models were fitted to evaluate the exposure-response relationships between cumulative exposure to coal mine dust and respirable silica and mortality from pneumoconiosis, chronic obstructive pulmonary disease (COPD) and lung cancer. Results Excess mortality was observed for pneumoconiosis (SMR=79.70, 95% CI 72.1 to 87.67), COPD (SMR=1.11, 95% CI 0.99 to 1.24) and lung cancer (SMR=1.08; 95% CI 1.00 to 1.18). Coal mine dust exposure increased risk for mortality from pneumoconiosis and COPD. Mortality from COPD was significantly elevated among ever smokers and former smokers (HR=1.84, 95% CI 1.05 to 3.22; HR K =1.52, 95% CI 0.98 to 2.34, respectively) but not current smokers (HR=0.99, 95% CI 0.76 to 1.28). Respirable silica was positively associated with mortality from pneumoconiosis (HR=1.33, 95% CI 0.94 to 1.33) and COPD (HR=1.04, 95% CI 0.96 to 1.52) in models controlling for coal mine dust. We saw a significant relationship between coal mine dust exposure and lung cancer mortality (HR=1.70; 95% CI 1.02 to 2.83) but not with respirable silica (HR=1.05; 95% CI 0.90 to 1.23). In the most recent follow-up period (2000–2007) both exposures were positively associated with lung cancer mortality, coal mine dust significantly so. Conclusions Our findings support previous studies showing that exposure to coal mine dust and respirable silica leads to increased mortality from malignant and non-malignant respiratory diseases even in the absence of smoking.

Description: Objectives During the 1950s and 1960s, aluminium dust inhalation was used as a potential prophylaxis against silicosis in underground miners, including in Australia. We investigated the association between aluminium dust inhalation and cardiovascular, cerebrovascular and Alzheimer's diseases in a cohort of Australian male underground gold miners. We additionally looked at pneumoconiosis mortality to estimate the effect of the aluminium therapy. Methods SMRs and 95% CI were calculated to compare mortality of the cohort members with that of the Western Australian male population (1961–2009). Internal comparisons on duration of aluminium dust inhalation were examined using Cox regression. Results Aluminium dust inhalation was reported for 647 out of 1894 underground gold miners. During 42 780 person-years of follow-up, 1577 deaths were observed. An indication of increased mortality of Alzheimer's disease among miners ever exposed to aluminium dust was found (SMR=1.38), although it was not statistically significant (95% CI 0.69 to 2.75). Rates for cardiovascular and cerebrovascular death were above population levels, but were similar for subjects with or without a history of aluminium dust inhalation. HRs suggested an increasing risk of cardiovascular disease with duration of aluminium dust inhalation (HR=1.02, 95% CI 1.00 to 1.04, per year of exposure). No difference in the association between duration of work underground and pneumoconiosis was observed between the groups with or without aluminium dust exposure. Conclusions No protective effect against silicosis was observed from aluminium dust inhalation. Conversely, exposure to aluminium dust may possibly increase the risk of cardiovascular disease and dementia of the Alzheimer's type.

Description: Objective To quantify the relationship between death from non-malignant respiratory diseases (NMRD) and exposure to silica dust or radon in a cohort of 58 690 former German uranium miners. Methods In the follow-up period from 1946 to 2008, a total of 2336 underlying deaths from NMRDs occurred, including 715 deaths from chronic obstructive pulmonary diseases (COPD) and 975 deaths from silicosis or other pneumoconiosis. Exposure to respirable crystalline silica and radon was individually assessed by means of a comprehensive job-exposure matrix. Risk analyses were based on a linear Poisson regression model with the baseline stratified by age, calendar year and duration of employment. Results There was no increase in risk of death from COPDs or any other NMRDs in relation to cumulative exposure to silica (mean=5.9, max=56 mg/m 3 -years), except in the group of deaths from silicosis or other pneumoconiosis. Here, a strong non-linear increase in risk was observed. Cumulative radon exposure (mean=280; max=3224 Working Level Months) was not related to death from COPDs or any other NMRDs. Conclusions The present findings do not indicate a relationship between mortality from COPD with silica dust or radon. However, validity of cause of death and lack of control for smoking remain potential sources of bias.

Description: We assessed whether long-term exposure to air pollution is associated with all-cause and cause-specific mortality during a period of declining particulate matter concentrations. Approximately 4800 women aged 55 years from North Rhine-Westphalia, Germany, were followed for up to 18 years. Exposure to air pollution was assessed in two ways: (1) using the distance between the residential address and the nearest major road, as calculated from Geographic Information System data and (2) calculating 1-year average particulate matter concentrations below 10 µm (PM 10 ) and nitrogen dioxide (NO 2 ) levels using data from the nearest air-monitoring station data to the subjects’ residences. Ninety-two per cent of all subjects lived in the same community during the entire follow-up period. Associations between mortality and exposure were assessed using Cox's proportional hazards models, including confounder adjustment. Sixteen per cent of women passed away during the follow-up period. An increase of 7 μg/m 3 PM 10 (IQR) was associated with an increased HR for all-cause (HR 1.15, 95% CI (1.04 to 1.27)), cardiopulmonary (HR 1.39, 95% CI (1.17 to 1.64)), and lung cancer mortality (HR 1.84, 95% CI (1.23 to 2.74)). An increase of 16 μg/m 3 (IQR) NO 2 exposure was associated with all-cause (HR 1.18, 95% CI (1.07 to 1.30)) and cardiopulmonary mortality (HR 1.55, 95% CI (1.30 to 1.84)). The association between cardiopulmonary mortality and PM 10 was reduced for the extended follow-up period, during which PM 10 concentrations (but not NO 2 concentrations) were lower. Living close to a major road was associated with an increased relative risk for all-cause, cardiopulmonary and respiratory mortality. These associations were temporally stable. Long-term exposure to ambient PM 10 and NO 2 was associated with increased mortality rates.