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: 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: Background Asbestos is a known carcinogen. However, little is known about the differential effects of size-specific asbestos fibres. Previous research has examined the relationship with lung cancer of each fibre group in the absence of others. Attempts to model all fibre groups within a single regression model have failed due to high correlations across fibre size groups. Methods We compare results from frequentist models for individual fibre size groups, and a hierarchical Bayesian model that included all fibre groups to estimate the relationship of size-specific asbestos fibre groups to lung cancer mortality. The hierarchical model assumes partial exchangeability of the effects of size-specific asbestos fibre groups to lung cancer, and is capable of handling the strong correlation of the exposure data. Results When fibre groups are modelled independently with a frequentist model, there appears to be an increase in the dose-response with increasing fibre size. However, when subject to a hierarchical structure, this trend vanishes, and the effects of distinct fibre groups appear largely similar. Conclusions This is the first occasion where distinct asbestos fibre groups have been assessed in a single regression model; however, even the use of a hierarchical modelling structure does not appear to overcome all the statistical fluctuations arising from the high correlations across fibre groups. We believe these results should be compared with other occupational cohorts with similar fibre group information. Finally, results for the smallest fibre group may be suggestive of a carcinogenic potential for nanofibres.

Description: Objectives In attempts to overcome the limitations of self-reported data in occupational health research, job-exposure matrices, which assign exposure by occupation, have emerged as an objective approach for assessing occupational exposures. On the basis of a lung cancer case–control study conducted in the Greater Toronto Area, 1997–2002, assessment of occupational exposure to asbestos was compared using self-reports and a general population job-exposure matrix (DOM-JEM). Methods Cases and frequency matched controls provided life-time job histories and self-reported exposures to potential lung carcinogens including asbestos through a detailed questionnaire. Exposure to asbestos was also assigned to each job by linking occupational histories with DOM-JEM. Agreement in classification of exposed and unexposed jobs according to self-reports and DOM-JEM was evaluated using Cohen's . Risks for lung cancer were estimated using unconditional logistic regression for each exposure assessment approach. Results The prevalence of occupational asbestos exposure was greater when based on DOM-JEM than when based on self-reports. Agreement in classifying exposure to jobs between the two assessment approaches was poor. The risk of lung cancer was not elevated among workers who self-reported asbestos exposure, whereas workers considered exposed on the basis of DOM-JEM were almost twice as likely as unexposed workers to be diagnosed with lung cancer (OR 1.9, 95% CI 1.3 to 2.7). Conclusions It is generally assumed by epidemiologists that self-reported exposure assessments result in inflated risk estimates. In this study, self-reports found no association with a well-established risk factor, whereas a high-quality job-exposure matrix revealed relative risk estimates that are more consistent with previous findings.

Description: Objectives An ‘information gap’ has been identified regarding the effects of chronic disease on occupational injury risk. We investigated the association of ischaemic heart disease, hypertension, diabetes, depression and asthma with acute occupational injury in a cohort of manufacturing workers from 1 January 1997 through 31 December 2007. Methods We used administrative data on real-time injury, medical claims, workplace characteristics and demographics to examine this association. We employed a piecewise exponential model within an Andersen–Gill framework with a frailty term at the employee level to account for inclusion of multiple injuries for each employee, random effects at the employee level due to correlation among jobs held by an employee, and experience on the job as a covariate. Results One-third of employees had at least one of the diseases during the study period. After adjusting for potential confounders, presence of these diseases was associated with increased hazard of injury: heart disease (HR 1.23, 95% CI 1.11 to 1.36), diabetes (HR 1.17, 95% CI 1.08 to 1.27), depression (HR 1.25, 95% CI 1.12 to 1.38) and asthma (HR 1.14, 95% CI 1.02 to 1.287). Hypertension was not significantly associated with hazard of injury. Associations of chronic disease with injury risk were less evident for more serious reportable injuries; only depression and a summary health metric derived from claims remained significantly positive in this subset. Conclusions Our results suggest that chronic heart disease, diabetes and depression confer an increased risk for acute occupational injury.

Description: Objectives Asbestos is the name given to a group of naturally occurring silicate mineral fibres that were widely used in industry during the 20th century due to their desirable physical properties. Although use in the USA has fallen over the last three decades, significant exposure in the developing world continues and the burden of disease is considerable. Asbestos is a known risk factor for several malignant diseases, including lung cancer and mesothelioma, and has more recently been implicated in pharyngeal and laryngeal cancer. However, studies of asbestos and cancers of the larynx or pharynx with adequate sample size that control for major head and neck squamous cell carcinoma (HNSCC) risk factors remain relatively sparse. Methods We report findings from a case–control study of 674 incident male HNSCC cases from the greater Boston region and 857 population-based male controls, matched on age (±3 years), sex, and town or neighbourhood of residence. Multivariable logistic regression was used to assess the association between occupational asbestos exposure and HNSCC by primary tumour site. Results 190 cases (28.2%) and 203 controls (23.7%) reported occupational exposure to asbestos. Occupational asbestos exposure was associated with elevated risk of pharyngeal carcinoma in men (OR 1.41, 95% CI 1.01 to 1.97), adjusted for age, race, smoking, alcohol consumption, education, income and HPV16 serology, with borderline increasing risk for each decade in the exposed occupation (OR 1.10, 95% CI 0.99 to 1.23). Conclusions These observations are consistent with mounting evidence that asbestos is a risk factor for pharyngeal cancer.

Description: Objectives The healthy worker effect usually leads to underestimation of the association between occupational exposure and asthma. The role of irritants in work-related asthma is disputed. We estimated the effect of occupational exposure on asthma expression in a longitudinal study, using marginal structural modelling to control for the healthy worker effect. Methods Analyses included 1284 participants (17–79 years, 48% men) from the follow-up (2003–2007) of the French Epidemiological study on the Genetics and Environment of Asthma (case-control study). Age at asthma onset, periods with/without attacks over lifetime and occupational history were recorded retrospectively. Exposures to known asthmagens, irritants or low level of chemicals/allergens were evaluated through a job-exposure matrix. The job history was reconstructed into 5-year intervals. Results Thirty-one per cent of subjects had ever been exposed to occupational asthmagens. Among the 38% of subjects who had asthma (ever), presence of attacks was reported in 52% of all time periods. Using standard analyses, no association was observed between exposure to known asthmagens (OR (95% CI): 0.99 (0.72 to 1.36)) or to irritants/low level of chemicals/allergens (0.82 (0.56 to 1.20)) and asthma attacks. Using a marginal structural model, all associations increased with suggestive evidence for known asthmagens (1.26 (0.90 to 1.76)), and reaching statistical significance for irritants/low level of chemicals/allergens (1.56 (1.02 to 2.40)). Conclusions The healthy worker effect has an important impact in risk assessment in work-related asthma studies. Marginal structural models are useful to eliminate imbalances in exposure due to disease-driven selection. Results support the role of irritants in work-related asthma.

Description: Objectives To quantify the variation in rates of absence due to musculoskeletal pain across 47 occupational groups (mostly nurses and office workers) from 18 countries, and to explore personal and group-level risk factors that might explain observed differences. Methods A standardised questionnaire was used to obtain information about musculoskeletal pain, sickness absence and possible risk factors in a cross-sectional survey of 12 416 workers (92–1017 per occupational group). Additionally, group-level data on socioeconomic variables, such as sick pay and unemployment rates, were assembled by members of the study team in each country. Associations of sickness absence with risk factors were examined by Poisson regression. Results Overall, there were more than 30-fold differences between occupational groups in the 12-month prevalence of prolonged musculoskeletal sickness absence, and even among office workers carrying out similar occupational tasks, the variation was more than tenfold. Personal risk factors included older age, lower educational level, tendency to somatise, physical loading at work and prolonged absence for non-musculoskeletal illness. However, these explained little of the variation between occupational groups. After adjustment for individual characteristics, prolonged musculoskeletal sickness absence was more frequent in groups with greater time pressure at work, lower job control and more adverse beliefs about the work-relatedness of musculoskeletal disorders. Conclusions Musculoskeletal sickness absence might be reduced by eliminating excessive time pressures in work, maximising employees’ responsibility and control and providing flexibility of duties for those with disabling symptoms. Care should be taken not to overstate work as a cause of musculoskeletal injury.

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.

Description: Objectives Environmental tobacco smoke (ETS) has a range of adverse health effects, but its association with dementia remains unclear and with dementia syndromes unknown. We examined the dose–response relationship between ETS exposure and dementia syndromes. Methods Using a standard method of GMS, we interviewed 5921 people aged ≥60 years in five provinces in China in 2007–2009 and characterised their ETS exposure. Five levels of dementia syndrome were diagnosed using the Automated Geriatric Examination for Computer Assisted Taxonomy instrument. The relative risk (RR) of moderate (levels 1–2) and severe (levels 3–5) dementia syndromes among participants exposed to ETS was calculated in multivariate adjusted regression models. Results 626 participants (10.6%) had severe dementia syndromes and 869 (14.7%) moderate syndromes. Participants exposed to ETS had a significantly increased risk of severe syndromes (adjusted RR 1.29, 95% CI 1.05 to 1.59). This was dose-dependently related to exposure level and duration. The cumulative exposure dose data showed an adjusted RR of 0.99 (95% CI 0.76 to 1.28) for 〉0–24 level years of exposure, 1.15 (95% CI 0.93 to 1.42) for 25–49 level years, 1.18 (95% CI 0.87 to 1.59) for 59–74 level years, 1.39 (95% CI 1.03 to 1.84) for 75–99 level years and 1.95 (95% CI 1.34 to 2.83) for ≥100 level years. Significant associations with severe syndromes were found in never smokers and in former/current smokers. There were no positive associations between ETS and moderate dementia syndromes. Conclusions ETS should be considered an important risk factor for severe dementia syndromes. Avoidance of ETS may reduce the rates of severe dementia syndromes worldwide.