121 research outputs found

    Risk of respiratory hospital admission associated with modelled concentrations of Aspergillus fumigatus from composting facilities in England

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    Bioaerosols have been associated with adverse respiratory-related health effects and are emitted in elevated concentrations from composting facilities. We used modelled Aspergillus fumigatus concentrations, a good indicator for bioaerosol emissions, to assess associations with respiratory-related hospital admissions. Mean daily Aspergillus fumigatus concentrations were estimated for each composting site for first full year of permit issue from 2005 onwards to 2014 for Census Output Areas (COAs) within 4 km of 76 composting facilities in England, as previously described (Williams et al., 2019). We fitted a hierarchical generalized mixed model to examine the risk of hospital admission with a primary diagnosis of (i) any respiratory condition, (ii) respiratory infections, (iii) asthma, (iv) COPD, (v) diseases due to organic dust, and (vi) Cystic Fibrosis, in relation to quartiles of Aspergillus fumigatus concentrations. Models included a random intercept for each COA to account for over-dispersion, nested within composting facility, on which a random intercept was fitted to account for clustering of the data, with adjustments for age, sex, ethnicity, deprivation, tobacco sales (smoking proxy) and traffic load (as a proxy for traffic-related air pollution). We included 249,748 respiratory-related and 3163 Cystic Fibrosis hospital admissions in 9606 COAs with a population-weighted centroid within 4 km of the 76 included composting facilities. After adjustment for confounders, no statistically significant effect was observed for any respiratory-related (Relative Risk (RR) = 0.99; 95% Confidence Interval (CI) 0.96–1.01) or for Cystic Fibrosis (RR = 1.01; 95% CI 0.56–1.83) hospital admissions for COAs in the highest quartile of exposure. Similar results were observed across all respiratory disease sub-groups. This study does not provide evidence for increased risks of respiratory-related hospitalisations for those living near composting facilities. However, given the limitations in the dispersion modelling, risks cannot be completely ruled out. Hospital admissions represent severe respiratory episodes, so further study would be needed to investigate whether bioaerosols emitted from composting facilities have impacts on less severe episodes or respiratory symptoms

    Associations of night-time road traffic noise with carotid intima-media thickness and blood pressure : The Whitehall II and SABRE study cohorts

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    Background: Road traffic noise has been linked to increased risk of stroke, for which hypertension and carotid intima-media thickness (cIMT) are risk factors. A link between traffic noise and hypertension has been established, but there are few studies on blood pressure and no studies on cIMT. Objectives: To examine cross-sectional associations for long-term exposure to night-time noise with cIMT, systolic blood pressure (SBP), diastolic blood pressure (DBP) and hypertension. Methods: The study population consisted of 2592 adults from the Whitehall II and SABRE cohort studies living within Greater London who had cIMT, SBP and DBP measured. Exposure to night-time road traffic noise (A-weighted dB, referred to as dBA) was estimated at each participant's residential postcode centroid. Results: Mean night-time road noise levels were 52 dBA (SD=4). In the pooled analysis adjusted for cohort, sex, age, ethnicity, marital status, smoking, area-level deprivation and NOx there was a 9.1 mu m (95% CI: -7.1, 25.2) increase in cIMT in association with 10 dBA increase in night-time noise. Analyses by noise categories of 5560 dBA (16.2 mu m, 95% CI:-8.7, 41.2), and N60 dBA (21.2 mu m, 95% CI:-2.5, 44.9) vs. 60 dBA vs. Conclusions: After adjustments, including for air pollution, the association between night-time road traffic noise and cIMT was only observed among non-medication users but associations with blood pressure and hypertension were largely null. (C) 2016 Elsevier Ltd. All rights reserved.Peer reviewe

    Air pollution and cardiovascular mortality with over 25years follow-up : a combined analysis of two British cohorts

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    Adverse effects of air pollution on cardiovascular disease (CVD) mortality are well established. There are comparatively fewer studies in Europe, and in the UK particularly, than in North America. We examined associations in two British cohorts with >25years of follow-up.; Annual average NO2, SO2 and black smoke (BS) air pollution exposure estimates for 1991 were obtained from land use regression models using contemporaneous monitoring data. From the European Study of Cohorts and Air Pollution (ESCAPE), air pollution estimates in 2010-11 were obtained for NO2, NOx, PM10, PMcoarse and PM2.5. The exposure estimates were assigned to place of residence 1989 for participants in a national birth cohort born in 1946, the MRC National Study of Health and Development (NSHD), and an adult multi-ethnic London cohort, Southall and Brent Revisited (SABRE) recruited 1988-91. The combined median follow-up was 26years. Single-pollutant competing risk models were employed, adjusting for individual risk factors.; Elevated non-significant hazard ratios for CVD mortality were seen with 1991 BS and SO2 and with ESCAPE PM10 and PM2.5 in fully adjusted linear models. Per 10ÎŒg/m(3) increase HRs were 1.11 [95% CI: 0.76-1.61] for BS, 1.05 [95% CI: 0.91-1.22] for SO2, 1.16 [95% CI: 0.70-1.92] for PM10 and 1.30 [95% CI: 0.39-4.34] for PM2.5, with largest effects seen in the fourth quartile of BS and PM2.5 compared to the first with HR 1.24 [95% CI: 0.91-1.61] and 1.21 [95% CI: 0.88-1.66] respectively. There were no consistent associations with other ESCAPE pollutants, or with 1991 NO2. Modelling using Cox regression led to similar results.; Our results support a detrimental long-term effect for air pollutants on cardiovascular mortality

    Restauro, 1-3/1992.

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    Ambient air pollution increases the risk of respiratory mortality, but evidence for impacts on lung function and chronic obstructive pulmonary disease (COPD) is less well established. The aim was to evaluate whether ambient air pollution is associated with lung function and COPD, and explore potential vulnerability factors.We used UK Biobank data on 303 887 individuals aged 40-69 years, with complete covariate data and valid lung function measures. Cross-sectional analyses examined associations of land use regression-based estimates of particulate matter (particles with a 50% cut-off aerodynamic diameter of 2.5 and 10 ”m: PM; 2.5; and PM; 10; , respectively; and coarse particles with diameter between 2.5 Όm and 10 Όm: PM; coarse; ) and nitrogen dioxide (NO; 2; ) concentrations with forced expiratory volume in 1 s (FEV; 1; ), forced vital capacity (FVC), the FEV; 1; /FVC ratio and COPD (FEV; 1; /FVC <lower limit of normal). Effect modification was investigated for sex, age, obesity, smoking status, household income, asthma status and occupations previously linked to COPD.Higher exposures to each pollutant were significantly associated with lower lung function. A 5 ”g·m; -3; increase in PM; 2.5; concentration was associated with lower FEV; 1; (-83.13 mL, 95% CI -92.50- -73.75 mL) and FVC (-62.62 mL, 95% CI -73.91- -51.32 mL). COPD prevalence was associated with higher concentrations of PM; 2.5; (OR 1.52, 95% CI 1.42-1.62, per 5 ”g·m; -3; ), PM; 10; (OR 1.08, 95% CI 1.00-1.16, per 5 ”g·m; -3; ) and NO; 2; (OR 1.12, 95% CI 1.10-1.14, per 10 ”g·m; -3; ), but not with PM; coarse; Stronger lung function associations were seen for males, individuals from lower income households, and "at-risk" occupations, and higher COPD associations were seen for obese, lower income, and non-asthmatic participants.Ambient air pollution was associated with lower lung function and increased COPD prevalence in this large study

    Characterisation of volatile organic compounds in hospital indoor air and exposure health risk determination

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    Several volatile organic compounds (VOCs) have impacts on human health, but little is known about the concentrations of VOCs in the hospital environment. This study characterised VOCs present in clinical assessment rooms. More than 600 samples of air were collected over 31 months (2017–2020) at two hospital sites in Leicester, United Kingdom, and analysed by comprehensive two-dimensional gas chromatography, making this the largest hospital environment database worldwide on VOCs and first such UK study. The most abundant VOCs found were 2-propanol, ethyl chloride, acetone and hexane, with respective mean concentrations of 696.6 ÎŒgm−3, 436.5 ÎŒgm−3, 83.9 ÎŒgm−3 and 58.5 ÎŒgm−3. Acetone, 2-propanol and hexane concentrations were 4, 9 and 30-fold higher respectively compared to similar studies performed in other hospitals. Our results showed that the most frequently detected VOCs, with the highest concentrations, were most likely released by healthcare activities, or related to ingress of vehicle emissions. Hazard quotient (HQ) and cancer risk (CR) were calculated to identify the potential risk of VOCs exposure to the health of healthcare workers. No HQs were measured above 1, compared to inhaled US EPA and OEHHA health guidelines for non-cancer chemicals. For both hospitals, trichloroethylene CR were calculated above 1E-06 by using inhaled US EPA cancer risk values, leading to possible risks to healthcare workers with long-term exposure. More studies of this type, including measurements of VOCs such as formaldehyde that we were unable to include in this study, are needed to better characterise exposures and risks, both to healthcare workers and patients

    Road traffic noise is associated with increased cardiovascular morbidity and mortality and all-cause mortality in London

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    Aims Road traffic noise has been associated with hypertension but evidence for the long-term effects on hospital admissions and mortality is limited. We examined the effects of long-term exposure to road traffic noise on hospital admissions and mortality in the general population. Methods and results The study population consisted of 8.6 million inhabitants of London, one of Europe's largest cities. We assessed smallarea-level associations of day-(7:00-22:59) and nighttime (23:00-06:59) road traffic noise with cardiovascular hospital admissions and all-cause and cardiovascular mortality in all adults (≄25 years) and elderly (≄75 years) through Poisson regression models. We adjusted models for age, sex, area-level socioeconomic deprivation, ethnicity, smoking, air pollution, and neighbourhood spatial structure. Median daytime exposure to road traffic noise was 55.6 dB. Daytime road traffic noise increased the risk of hospital admission for stroke with relative risk (RR) 1.05 [95% confidence interval (CI): 1.02 -1.09] in adults, and 1.09 (95% CI: 1.04-1.14) in the elderly in areas .60 vs. ,55 dB. Nighttime noise was associated with stroke admissions only among the elderly. Daytime noise was significantly associated with all-cause mortality in adults [RR 1.04 (95% CI: 1.00-1.07) in areas .60 vs. ,55 dB]. Positive but non-significant associations were seen with mortality for cardiovascular and ischaemic heart disease, and stroke. Results were similar for the elderly. Conclusions Long-term exposure to road traffic noise was associated with small increased risks of all-cause mortality and cardiovascular mortality and morbidity in the general population, particularly for stroke in the elderly. Translational perspective Road traffic noise has been associated with hypertension but evidence for the long-term effects on hospital admissions and mortality is limited. Our results suggest small increased population risks of all-cause mortality and cardiovascular morbidity and mortality, particularly of stroke in the elderly, at moderate levels of road noise exposure. Findings are consistent with the larger body of evidence linking traffic noise exposure with hypertension

    Prospective study design and data analysis in UK Biobank

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    Population-based prospective studies, such as UK Biobank, are valuable for generating and testing hypotheses about the potential causes of human disease. We describe how UK Biobank's study design, data access policies, and approaches to statistical analysis can help to minimize error and improve the interpretability of research findings, with implications for other population-based prospective studies being established worldwide.</p
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