Numerous clinical trials have examined the role of anthocyanins on cardiometabolic health, but their effects have not been quantitatively synthesized and systematically evaluated. The aim of our study was to conduct a systematic review and meta-analysis of randomized controlled trials (RCTs) assessing the effects of anthocyanins on glycemic regulation and lipid profiles in both healthy populations and those with cardiometabolic diseases. The MEDLINE, EMBASE, Cochrane database, OVID EBM Reviews, and clinicaltrials.gov databases were searched until February 2017. RCTs with a duration of ≥2 wk that evaluated the effects of anthocyanins on glycemic control, insulin sensitivity, and lipids as either primary or secondary outcomes were included. The Cochrane Risk of Bias tool was used to assess the study quality. Standardized mean differences (SMDs) were determined by random-effects models. Meta-regression, sensitivity, and subgroup analyses were performed to explore the influence of covariates on the overall effects. Thirty-two RCTs (1491 participants) were eligible for meta-analysis. Anthocyanins significantly reduced fasting glucose (SMD: -0.31; 95% CI: -0.59, -0.04; = 80.7%), 2-h postprandial glucose (SMD: -0.82; 95% CI: -1.49, -0.15; = 77.7), glycated hemoglobin (SMD: -0.65; 95% CI: -1.00, -0.29; = 72.7%), total cholesterol (SMD: -0.33; 95% CI: -0.62, -0.03; = 86.9%), and LDL (SMD: -0.35; 95% CI: -0.66, -0.05; = 85.2%). Sensitivity analyses showed that the overall effects remained similar by excluding the trials with a high or unclear risk of bias. The significant improvements in glycemic control and lipids support the benefits of anthocyanins in the prevention and management of cardiometabolic disease. Further well-designed RCTs are needed to evaluate the long-term effects of anthocyanins on metabolic profiles and to explore the optimal formula and dosage. The protocol for this review was registered at https://www.crd.york.ac.uk/PROSPERO/#index.php as CRD42016033210.

Rising emissions of greenhouse gases in the atmosphere have warmed the planet substantially and are also accompanied by poor air quality. The increased prevalence of allergic airway disease worldwide can be partially attributed to those global environmental changes. Climate change and air pollution pose adverse impacts on respiratory allergies, and that the mechanisms are complex and interactive. Adverse weather conditions, such as extreme temperatures, can act directly on the respiratory tract to induce allergic respiratory illnesses. Thunderstorms and floods can alter the production and distribution of aeroallergens while wildfires and dust storms increase air pollution, and therefore indirectly enhance health risks. Concentrations of particulate matter and ozone in the air have been projected to increase with climate warming and air stagnation, and the rising temperatures and CO 2 increase pollen, molds, and spores, which escalate the risk of allergic respiratory diseases. The synergistic effects of extreme heat and aeroallergens intensify the toxic effect of air pollutants, which in turn augment the allergenicity of aeroallergens. With the Earth's climate change, migration of humans and plants shift the living environments and allergens of susceptible people. Urban residents are exposed to multiple factors while children are sensitive to environmental exposure. Since climate change may pose many unexpected and persistent effects on allergic respiratory diseases, health professionals should advocate for effective mitigation and adaptation strategies to minimize its respiratory health effects.

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ObjectiveTo investigate the association between ambient air pollution and stroke morbidity in different subgroups and seasons.MethodsWe performed a time-series analysis based on generalised linear models to study the short-term exposure–response relationships between air pollution and stroke hospitalisations, and conducted subgroup analyses to identify possible sensitive populations.ResultsFor every 10 µg/m3increase in the concentration of air pollutants, across lag 0–3 days, the relative risk of stroke hospitalisation was 1.029 (95% CI 1.013 to 1.045) for PM2.5, 1.054 (95% CI 1.031 to 1.077) for NO2and 1.012 (95% CI 1.002 to 1.022) for O3. Subgroup analyses showed that statistically significant associations were found in both men and women, middle-aged and older populations, and both cerebral infarction and intracerebral haemorrhage. The seasonal analyses showed that statistically significant associations were found only in the winter.ConclusionsOur study indicates that short-term exposure to PM2.5, NO2and O3may induce stroke morbidity, and the government should take actions to mitigate air pollution and protect sensitive populations.

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