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 Previous research has indicated that occupational exposure to pesticides and possibly airborne endotoxin may increase the risk of developing Parkinson disease (PD). We studied the associations of PD with occupational exposure to pesticides, specifically to the functional subclasses insecticides, herbicides and fungicides, and to airborne endotoxin. In addition we evaluated specific pesticides (active ingredients) previously associated with PD. Methods We used data from a hospital-based case–control study, including 444 patients with PD and 876 age and sex matched controls. Exposures to pesticides from application and re-entry work were estimated with the ALOHA+job-exposure matrix and with an exposure algorithm based on self-reported information on pesticide use. To assess exposure to specific active ingredients a crop-exposure matrix was developed. Endotoxin exposure was estimated with the DOM job-exposure matrix. Results The results showed almost no significant associations. However, ORs were elevated in the higher exposure categories for pesticides in general, insecticides, herbicides and fungicides, and below unity for endotoxin exposure. The analyses on specific active ingredients showed a significant association of PD risk with the fungicide benomyl. Conclusions This study did not provide evidence for a relation between pesticide exposure and PD. However, the consistently elevated ORs in the higher exposure categories suggest that a positive association may exist. The possible association with the active ingredient benomyl requires follow-up in other studies. This study did not provide support for a possible association between endotoxin exposure and PD.

Description: Objective To investigate the role of occupational exposure to chlorinated solvents in lung cancer aetiology. Methods ICARE (Investigation of occupational and environmental CAuses of REspiratory cancers) is a French, multicentre, population-based, case–control study. Information on the lifelong work history of 2926 cases and 3555 controls was collected using standardised questionnaires. Occupational exposures were assessed using job-exposure matrices for five chlorinated solvents. Solvents were studied separately and in combinations. ORs were computed using unconditional logistic regression models adjusted for classic risk factors, including a history of cigarette smoking and exposure to asbestos. Adjustment for socioeconomic status (SES) was also made. Results After adjustment for exposure to asbestos, we observed a positive, statistically significant association with lung cancer for men and women exposed to a combination of perchloroethylene (PCE), trichloroethylene and dichloromethane (DCM). Further adjustment for SES slightly decreased this association. In contrast, no statistically significant associations were found for other solvent combinations. Conclusions These results suggest that exposure to PCE may constitute a risk factor for lung cancer, especially among women, who seem to have a higher prevalence of exposure than men.

Description: Objectives To examine vascular endothelial growth factor (VEGF) and PGE2 levels in urine from the copper smelting workers exposed to arsenic and analyse the relationships between urinary VEGF or PGE2 level and arsenical metabolites. Methods The study was conducted in a group of 106 copper-smelting male workers. Information about each subject was obtained by questionnaire, inorganic As (iAs), monomethylarsonic acid (MMA), dimethylarsinic acid (DMA), VEGF and prostaglandin E2 (PGE2) in urine were determined. Standing height, body weight, and blood pressure were measured. Results According to the urine arsenic levels, participants were separated into three groups: Group 1: urine total arsenic 〈35 mg/L, Group 2: 35–100 mg/L, and Group 3: 〉100 mg/L. The median levels of urinary VEGF and PGE2 in Groups 1, 2 and 3 were 10.57 and 1032.0 pg/mL, 24.39 and 1060.9 pg/mL, and 49.0 and 1330.4 pg/mL, respectively. Urinary VEGF levels were positive associated with arsenical metabolites (iAs, MMA, DMA and TAs). Additionally, urinary VEGF and PGE2 levels were all correlated positively with the urinary MMA% (r=0.221, p=0.026 and r=0.206, p=0.037). While urinary VEGF was negatively with DMA% and secondary methylation index (r=–0.242, p=0.014 and r=–0.214, p=0.030, respectively). Conclusions Urinary VEGF and PGE2 levels increased in arsenic exposure copper smelting workers, and urinary VEGF levels are well associated with the urinary arsenicals. This finding may provide useful information for developing measurement, prevention and treatment of damage induced by arsenic in the future.

Description: Objective To develop a job-exposure matrix (JEM) that estimates exposure to eight variables representing different aspects of shiftwork among female workers. Methods Occupational history and shiftwork exposure data were obtained from a population-based breast cancer case–control study. Exposure to light at night, phase shift, sleep disturbances, poor diet, lack of physical activity, lack of vitamin D, and graveyard and early morning shifts, was calculated by occupational code. Three threshold values based on the frequency of exposure were considered (10%, 30% and 50%) for use as cut-offs in determining exposure for each occupational code. JEM-based exposure classification was compared with that from the OccIDEAS application (job-specific questionnaires and assessment by rules) by assessing the effect on the OR for phase shift and breast cancer. Using data from the Australian Workplace Exposure Study, the specificity and sensitivity of the threshold values were calculated for each exposure variable. Results 127 of 413 occupational codes involved exposure to one or more shiftwork variables. Occupations with the highest probability of exposure shiftwork included nurses and midwives. Using the 30% threshold, the OR for the association between phase shift exposure and breast cancer was decreased and no longer statistically significant (OR=1.14, 95% CI 0.92 to 1.42). The 30% cut-off point demonstrated best specificity and sensitivity, although results varied between exposure variables. Conclusions This JEM provides a set of indicators reflecting biologically plausible mechanisms for the potential impact of shiftwork on health and may provide an alternative method of exposure assessment in the absence of detailed job history and exposure data.

Description: Objective We examined occupational exposures and sperm morphology to establish whether exposures implicated differed from those affecting motile sperm concentration. Methods Computer aided sperm morphometric assessment was undertaken on morphology slides obtained as part of a multi-centre study in 1999–2002 of occupational factors in male infertility. Men attending 14 fertility clinics across the UK were recruited and gave a semen sample. Before results of the semen analysis were known, the men completed detailed questionnaires about their employment and lifestyle. Occupational exposures were assessed by occupational hygienists. Data were analysed using an unmatched case-referent design, allowing for clustering and for confounders. Three case definitions were used: poor morphology (normal morphology 〈4%), low motile sperm count (MSC) (〈4.8 x 10 6 ) and either condition. Results Morphology results were available for 1861/2011 men employed at the time of recruitment. Of these 1861, 296 (15.9%) had poor morphology; of the 2011with sperm count, 453 (22.5%) had low MSC; 654/1981 (33.0%) had either condition. Poor morphology, adjusted for confounding, was related to self-reported lifetime exposure to lead (OR=1.33; 95% CI 1.00 to 1.75). Low MSC was also related to self-reported lead and to hygienist-assessed glycol ether exposure. Self-reported use of paint stripper (OR=1.47; 95% CI 1.07 to 2.03) and lead, but not glycol ether, were significantly related to the combined case definition. Conclusions While this study did not identify any occupational exposure uniquely related to sperm morphology, the capacity of the study to detect risk was increased by including morphology with sperm concentration and motility.

Description: Globally, neurological disorders account for about 4% of all deaths and about 5% of disability-adjusted life-years from non-communicable disease. 1 Diagnosis of a neurological disease can be devastating, and in most instances there is no cure. A recent editorial in the Lancet 2 commented that neurological diseases remain neglected and ignored: ‘unlike cancer, stroke, and diabetes, which all have strategies and clinical champions, degenerative disorders are heterogeneous and complex’. Neurological disease includes a broad spectrum of conditions, several of which have occupational causes. The motor neurone diseases (MND) are a spectrum of neurodegenerative disorders characterised by progressive muscular paralysis due to degeneration of motor neurones in the primary motor cortex, brainstem and spinal cord. 3 Although the vast majority of cases of (MND) are ‘sporadic’ (ie, non-genetic), most current research into the causes of MND involves primarily or solely genetic factors and few studies of occupational...

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 Chronic mucus hypersecretion (CMH) is highly prevalent in smokers and associated with an accelerated lung function decline and chronic obstructive pulmonary disease (COPD). Several risk factors contribute to CMH and to COPD. It is, however, unknown if risk factors for CMH are similar in persons with and without COPD. Methods 1479 persons with and 8529 without COPD, participating in the general population-based LifeLines cohort, completed questionnaires and underwent spirometry. Occupational exposure was assessed using the ALOHA+ job exposure matrix. Analyses were performed using multiple logistic regression models. Results In COPD, a significantly higher risk for CMH was associated with higher pack-years smoking (per 10 pack-years) (OR=1.28; 1.12 to 1.46) and environmental tobacco smoke (ETS) (OR=2.06; 1.33 to 3.19). In non-COPD; male gender (OR=1.91; 1.51 to 2.41), higher Body Mass Index (OR=1.04; 1.01 to 1.06), higher pack-years smoking (OR=1.28; 1.14 to 1.44), current smoking (OR=1.50; 1.04 to 2.18), low and high exposure to mineral dust (OR=1.39; 1.04 to 1.87 and OR=1.60; 1.02 to 2.52), high exposure to gases & fumes (OR=2.19; 1.49 to 3.22). Significant interactions were found between COPD and exposure to gases & fumes (p=0.018) and aromatic solvents (p=0.038). Conclusions A higher risk for CMH was associated with higher pack-years smoking regardless of COPD status. However, a higher risk for CMH was associated with high occupational exposure to gases & fumes in individuals without COPD only.

Description: Background People in sedentary occupations are at increased risk of hip fracture. Hip fracture is significantly associated with low bone mineral density (BMD) measured at the hip. Physical activity is important in the development and maintenance of BMD, but the effects of occupational physical activity on bone health are unclear. We investigated the influence of lifetime physical activity on BMD at the hip. Methods This was a cross-sectional epidemiological study of the associations between total hip BMD measured by dual-energy X-ray absorptiometry at retirement age and lifetime exposure to occupational physical workload (standing/walking ≥4 h/day; lifting ≥25 kg; energetic work sufficient to induce sweating and manual work). Results Complete data on occupational exposures were available for 860 adults (488 men and 372 women) who had worked ≥20 years. Their mean age was 65 years, and many reported heavy physical workplace activities over prolonged durations. There were no statistically significant associations between total hip BMD and any of these measures of lifetime occupational physical activity in men or women. Conclusions Lifetime cumulative occupational activity was not associated with hip BMD at retirement age. Our findings suggest that, if sedentary work conveys an increased risk of hip fracture, it is unlikely that the mechanism is through reductions in BMD at the hip and may relate to other physical effects, such as falls risk. Further studies will be needed to test this hypothesis.