Adverse health effects associated with household air pollution: a systematic review, meta-analysis, and burden estimation study.

BACKGROUND: 3 billion people worldwide rely on polluting fuels and technologies for domestic cooking and heating. We estimate the global, regional, and national health burden associated with exposure to household air pollution. METHODS: For the systematic review and meta-analysis, we systematically searched four databases for studies published from database inception to April 2, 2020, that evaluated the risk of adverse cardiorespiratory, paediatric, and maternal outcomes from exposure to household air pollution, compared with no exposure. We used a random-effects model to calculate disease-specific relative risk (RR) meta-estimates. Household air pollution exposure was defined as use of polluting fuels (coal, wood, charcoal, agricultural wastes, animal dung, or kerosene) for household cooking or heating. Temporal trends in mortality and disease burden associated with household air pollution, as measured by disability-adjusted life-years (DALYs), were estimated from 2000 to 2017 using exposure prevalence data from 183 of 193 UN member states. 95% CIs were estimated by propagating uncertainty from the RR meta-estimates, prevalence of household air pollution exposure, and disease-specific mortality and burden estimates using a simulation-based approach. This study is registered with PROSPERO, CRD42019125060. FINDINGS: 476 studies (15·5 million participants) from 123 nations (99 [80%] of which were classified as low-income and middle-income) met the inclusion criteria. Household air pollution was positively associated with asthma (RR 1·23, 95% CI 1·11-1·36), acute respiratory infection in both adults (1·53, 1·22-1·93) and children (1·39, 1·29-1·49), chronic obstructive pulmonary disease (1·70, 1·47-1·97), lung cancer (1·69, 1·44-1·98), and tuberculosis (1·26, 1·08-1·48); cerebrovascular disease (1·09, 1·04-1·14) and ischaemic heart disease (1·10, 1·09-1·11); and low birthweight (1·36, 1·19-1·55) and stillbirth (1·22, 1·06-1·41); as well as with under-5 (1·25, 1·18-1·33), respiratory (1·19, 1·18-1·20), and cardiovascular (1·07, 1·04-1·11) mortality. Household air pollution was associated with 1·8 million (95% CI 1·1-2·7) deaths and 60·9 million (34·6-93·3) DALYs in 2017, with the burden overwhelmingly experienced in low-income and middle-income countries (LMICs; 60·8 million [34·6-92·9] DALYs) compared with high-income countries (0·09 million [0·01-0·40] DALYs). From 2000, mortality associated with household air pollution had reduced by 36% (95% CI 29-43) and disease burden by 30% (25-36), with the greatest reductions observed in higher-income nations. INTERPRETATION: The burden of cardiorespiratory, paediatric, and maternal diseases associated with household air pollution has declined worldwide but remains high in the world's poorest regions. Urgent integrated health and energy strategies are needed to reduce the adverse health impact of household air pollution, especially in LMICs. FUNDING: British Heart Foundation, Wellcome Trust.

Monitoring indirect impact of COVID-19 pandemic on services for cardiovascular diseases in the UK.

OBJECTIVE: To monitor hospital activity for presentation, diagnosis and treatment of cardiovascular diseases during the COVID-19) pandemic to inform on indirect effects. METHODS: Retrospective serial cross-sectional study in nine UK hospitals using hospital activity data from 28 October 2019 (pre-COVID-19) to 10 May 2020 (pre-easing of lockdown) and for the same weeks during 2018-2019. We analysed aggregate data for selected cardiovascular diseases before and during the epidemic. We produced an online visualisation tool to enable near real-time monitoring of trends. RESULTS: Across nine hospitals, total admissions and emergency department (ED) attendances decreased after lockdown (23 March 2020) by 57.9% (57.1%-58.6%) and 52.9% (52.2%-53.5%), respectively, compared with the previous year. Activity for cardiac, cerebrovascular and other vascular conditions started to decline 1-2 weeks before lockdown and fell by 31%-88% after lockdown, with the greatest reductions observed for coronary artery bypass grafts, carotid endarterectomy, aortic aneurysm repair and peripheral arterial disease procedures. Compared with before the first UK COVID-19 (31 January 2020), activity declined across diseases and specialties between the first case and lockdown (total ED attendances relative reduction (RR) 0.94, 0.93-0.95; total hospital admissions RR 0.96, 0.95-0.97) and after lockdown (attendances RR 0.63, 0.62-0.64; admissions RR 0.59, 0.57-0.60). There was limited recovery towards usual levels of some activities from mid-April 2020. CONCLUSIONS: Substantial reductions in total and cardiovascular activities are likely to contribute to a major burden of indirect effects of the pandemic, suggesting they should be monitored and mitigated urgently.

Effects of decontaminated fish oil or a fish and vegetable oil blend on persistent organic pollutant and fatty acid compositions in diet and flesh of Atlantic salmon ( Salmo salar).

The health benefits of seafood are well documented and based on the unique supply of n-3 highly unsaturated fatty acids (HUFA). Aquaculture now contributes about 50 % of food-grade seafood globally and Atlantic salmon (Salmo salar) is a rich source of n-3 HUFA. However, salmon and other oily fish can accumulate lipophilic persistent organic pollutants (POP), including dioxins (PCDD/F), polychlorinated biphenyls (PCB) and polybrominated diphenyl ethers (PBDE), derived largely from feed. In the present study, triplicate groups of salmon, of initial weight 0.78 kg, were fed one of three experimental diets for 11 weeks. The diets were coated with either a northern fish oil (FO) with a high POP content (cNFO), the same oil that had been decontaminated (deNFO) or a blend of southern fish oil, rapeseed and soyabean oils (SFO/RO/SO). Dietary PCDD/F+dioxin-like PCB (DL-PCB) concentrations were 17.36, 0.45 and 0.53 ng toxic equivalents (TEQ)/kg, respectively. After 11 weeks, the flesh concentrations in fish fed the cNFO, deNFO and SFO/RO/SO diets were 6.42, 0.34 and 0.41 ng TEQ/kg, respectively. There were no differences in flesh EPA and DHA between fish fed the cNFO or deNFO diets although EPA and DHA were reduced by 50 and 30 %, respectively, in fish fed the SFO/RO/SO diet. Thus, decontaminated FO can be used to produce salmon high in n-3 HUFA and low in POP. Salmon produced using deNFO would be of high nutritional value and very low in POP and would utilise valuable fish oils that would otherwise be destroyed due to their high pollutant concentrations.

Authenticating production origin of gilthead sea bream (Sparus aurata) by chemical and isotopic fingerprinting.

Recent EU legislation (EC/2065/2001) requires that fish products, of wild and farmed origin, must provide consumer information that describes geographical origin and production method. The aim of the present study was to establish methods that could reliably differentiate between wild and farmed European gilthead sea bream (Sparus aurata). The methods that were chosen were based on chemical and stable isotopic analysis of the readily accessible lipid fraction. This study examined fatty acid profiles by capillary gas chromatography and the isotopic composition of fish oil (delta(13)C, delta(18)O), phospholipid choline nitrogen (delta(15)N) and compound specific analysis of fatty acids (delta(13)C) by isotope ratio mass spectroscopy as parameters that could reliably discriminate samples of wild and farmed sea bream. The sample set comprised of 15 farmed and 15 wild gilthead sea bream (Sparus aurata), obtained from Greece and Spain, respectively. Discrimination was achieved using fatty acid compositions, with linoleic acid (18:2n-6), arachidonic acid (20:4n-6), stearic acid (18:0), vaccenic acid (18:1n-7) and docosapentaenoic acid (22:5n-3) providing the highest contributions for discrimination. Principle components analysis of the data set highlighted good discrimination between wild and farmed fish. Factor 1 and 2 accounted for >70% of the variation in the data. The variables contributing to this discrimination were: the fatty acids 14:0, 16:0, 18:0, 18:1n-9, 18:1n-7, 22:1n-11, 18:2n-6 and 22:5n-3; delta(13)C of the fatty acids 16:0, 18:0, 16:1n-7, 18:1n-9, 20:5n-3 and 22:6n-3; Bulk oil fraction delta(13)C; glycerol/choline fraction bulk delta(13)C; delta(15)N; % N; % lipid.