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.

New Opportunities to Mitigate the Burden of Disease Caused by Traffic Related Air Pollution: Antioxidant-Rich Diets and Supplements.

Air pollution is associated with premature mortality and a wide spectrum of diseases. Traffic-related air pollution (TRAP) is one of the most concerning sources of air pollution for human exposure and health. Until TRAP levels can be significantly reduced on a global scale, there is a need for effective shorter-term strategies to prevent the adverse health effects of TRAP. A growing number of studies suggest that increasing antioxidant intake, through diet or supplementation, may reduce this burden of disease. In this paper, we conducted a non-systematic literature review to assess the available evidence on antioxidant-rich diets and antioxidant supplements as a strategy to mitigate adverse health effects of TRAP in human subjects. We identified 11 studies that fit our inclusion criteria; 3 of which investigated antioxidant-rich diets and 8 of which investigated antioxidant supplements. Overall, we found consistent evidence that dietary intake of antioxidants from adherence to the Mediterranean diet and increased fruit and vegetable consumption is effective in mitigating adverse health effects associated with TRAP. In contrast, antioxidant supplements, including fish oil, olive oil, and vitamin C and E supplements, presented conflicting evidence. Further research is needed to determine why antioxidant supplementation has limited efficacy and whether this relates to effective dose, supplement formulation, timing of administration, or population being studied. There is also a need to better ascertain if susceptible populations, such as children, the elderly, asthmatics and occupational workers consistently exposed to TRAP, should be recommended to increase their antioxidant intake to reduce their burden of disease. Policymakers should consider increasing populations' antioxidant intake, through antioxidant-rich diets, as a relatively cheap and easy preventive measure to lower the burden of disease associated with TRAP.

Inhibition of galectin-3 reduces atherosclerosis in apolipoprotein E-deficient mice.

Atherosclerosis is a major risk factor for cardiovascular disease (CVD) and stroke. Galectin-3 is a carbohydrate-binding lectin implicated in the pathophysiology of CVD and is highly expressed within atherosclerotic lesions in mice and humans. The object of this present study was to use genetic deletion and pharmacological inhibition in a well-characterized mouse model of atherosclerosis to determine the role of galectin-3 in plaque development. Apolipoprotein-E/galectin-3 knockout mice were generated and fed a high-cholesterol "western" diet. Galectin-3 deletion had no consistent effect on the serum lipid profile but halved atherosclerotic lesion formation in the thoracic aorta (57% reduction), the aortic arch (50% reduction) and the brachiocephalic arteries. The aortic plaques were smaller, with reduced lipid core and less collagen. In apolipoprotein E-deficient (ApoE(-/-)) mice, there was a switch from high inducible nitric oxide expression in early lesions (6 weeks) to arginase-1 expression in later lesions (20 weeks), which was reversed in ApoE(-/-)/gal-3(-/-) mice. Administration of modified citrus pectin, an inhibitor of galectin-3, during the latter stage of the disease reduced plaque volume. We conclude that inhibiting galectin-3 causes decreased atherosclerosis. Strategies to inhibit galectin-3 function may reduce plaque progression and potentially represent a novel therapeutic strategy in the treatment of atherosclerotic disease.

NO and sGC-stimulating NO donors.

Our knowledge of nitric oxide (NO) as a crucial endogenous signalling molecule continues to expand. Many, but not all, of the actions of NO are mediated by activation of soluble guanylyl cyclase (sGC) in target tissues. The aim of this chapter is to encapsulate the functions of NO in mammalian biology, tied to the chemistry of this unusual signalling entity. The experimental usefulness and therapeutic potential of the most widely utilised NO donor drugs is reviewed, with special consideration given to the importance of choosing the correct NO donor for any given experiment, in vitro, in vivo or in clinical studies.