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1.
Food chemoprevention and air pollution: the health comes with eating.
Visalli, G, Facciolà, A, Laganà, P, Di Pietro, A
Reviews on environmental health. 2020;(4):471-479
Abstract
Ambient air pollution is known to be an important causative agent of many non-communicable diseases, mainly due to fine particulate matter (PM2.5). According to Global Burden Disease study in 2015, the estimated premature deaths caused by PM2.5 were 4.2 million. Besides deaths, airborne pollution's effect on human health also has dramatic economic and social costs, contributing greatly to disability-adjusted life-year (DALY). To reduce the health impact is necessary a double approach, which includes the improvement of air quality and food chemoprevention, aimed at enhancing the homeostatic abilities of exposed subjects. The scavenging, antioxidant, and anti-inflammatory properties of nutraceuticals effectively counteract the pathogenic mechanisms common in almost all non-communicable diseases associated with air pollutants. Moreover, several bioactive compounds of food modulate, by epigenetic mechanisms, the metabolism of xenobiotics, favouring conjugation reactions and promoting excretion. This narrative review summarize the numerous pieces of evidence collected in the last decades by observational and experimental studies which underline the chemopreventive role of flavonoids, contained in several fruits and consumer beverages (wine, tea, etc.), and isothiocyanate sulforaphane, contained in the cruciferous vegetables belonging to the genus Brassica. These bioactive compounds, enhancing the individual homeostatic abilities, reduce the harmful effects of airborne pollution.
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2.
Effects of ambient particulate matter on fasting blood glucose: A systematic review and meta-analysis.
Ma, R, Zhang, Y, Sun, Z, Xu, D, Li, T
Environmental pollution (Barking, Essex : 1987). 2020;:113589
Abstract
Studies have found that ambient particulate matter (PM) affects fasting blood glucose. However, the results are not consistent. We conducted a systematic review and meta-analysis to determine the relationship between PM with an aerodynamic diameter of 10 μm or less (PM10) and PM with an aerodynamic diameter of 2.5 μm or less (PM2.5) and fasting blood glucose. We searched PubMed, Web of Science, the Wanfang Database and the China National Knowledge Infrastructure up to April 1, 2019. A total of 24 papers were included in the review, and 17 studies with complete or convertible quantitative information were included in the meta-analysis. The studies were divided into groups by PM size fractions (PM10 and PM2.5) and length of exposure. Long-term exposures were based on annual average concentrations, and short-term exposures were those lasting less than 28 days. In the long-term exposure group, fasting blood glucose increased 0.10 mmol/L (95% CI: 0.02, 0.17) per 10 μg/m3 of increased PM10 and 0.23 mmol/L (95% CI: 0.01, 0.45) per 10 μg/m3 of increased PM2.5. In the short-term exposure group, fasting blood glucose increased 0.02 mmol/L (95% CI: -0.01, 0.04) per 10 μg/m3 of increased PM10 and 0.08 mmol/L (95% CI: 0.04, 0.11) per 10 μg/m3 of increased PM2.5. Further prospective studies are needed to explore the relationship between ambient PM exposure and fasting blood glucose.
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3.
Air Pollution Neurotoxicity in the Adult Brain: Emerging Concepts from Experimental Findings.
Haghani, A, Morgan, TE, Forman, HJ, Finch, CE
Journal of Alzheimer's disease : JAD. 2020;(3):773-797
Abstract
Epidemiological studies are associating elevated exposure to air pollution with increased risk of Alzheimer's disease and other neurodegenerative disorders. In effect, air pollution accelerates many aging conditions that promote cognitive declines of aging. The underlying mechanisms and scale of effects remain largely unknown due to its chemical and physical complexity. Moreover, individual responses to air pollution are shaped by an intricate interface of pollutant mixture with the biological features of the exposed individual such as age, sex, genetic background, underlying diseases, and nutrition, but also other environmental factors including exposure to cigarette smoke. Resolving this complex manifold requires more detailed environmental and lifestyle data on diverse populations, and a systematic experimental approach. Our review aims to summarize the modest existing literature on experimental studies on air pollution neurotoxicity for adult rodents and identify key gaps and emerging challenges as we go forward. It is timely for experimental biologists to critically understand prior findings and develop innovative approaches to this urgent global problem. We hope to increase recognition of the importance of air pollution on brain aging by our colleagues in the neurosciences and in biomedical gerontology, and to support the immediate translation of the findings into public health guidelines for the regulation of remedial environmental factors that accelerate aging processes.
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4.
The association between short-term exposure to ambient air pollution and fractional exhaled nitric oxide level: A systematic review and meta-analysis of panel studies.
Chen, X, Liu, F, Niu, Z, Mao, S, Tang, H, Li, N, Chen, G, Liu, S, Lu, Y, Xiang, H
Environmental pollution (Barking, Essex : 1987). 2020;(Pt A):114833
Abstract
Several epidemiological studies have evaluated the fractional exhaled nitric oxide (FeNO) of ambient air pollution but the results were controversial. We therefore conducted a systematic review and meta-analysis to investigate the associations between short-term exposure to air pollutants and FeNO level. We searched PubMed and Web of Science and included a total of 27 articles which focused on associations between ambient air pollutants (PM10, PM2.5, black carbon (BC), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3)) exposure and the change of FeNO. Random effect model was used to calculate the percent change of FeNO in association with a 10 or 1 μg/m3 increase in air pollutants exposure concentrations. A 10 μg/m3 increase in short-term PM10, PM2.5, NO2, and SO2 exposure was associated with a 3.20% (95% confidence interval (95%CI): 1.11%, 5.29%), 2.25% (95%CI: 1.51%, 2.99%),4.90% (95%CI: 1.98%, 7.81%), and 8.28% (95%CI: 3.61%, 12.59%) change in FeNO, respectively. A 1 μg/m3 increase in short-term exposure to BC was associated with 3.42% (95%CI: 1.34%, 5.50%) change in FeNO. The association between short-term exposure to O3 and FeNO level was insignificant (P>0.05). Future studies are warranted to investigate the effect of multiple pollutants, different sources and composition of air pollutants on airway inflammation.
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5.
The Relationship Between Air Pollution and Cognitive Functions in Children and Adolescents: A Systematic Review.
Lopuszanska, U, Samardakiewicz, M
Cognitive and behavioral neurology : official journal of the Society for Behavioral and Cognitive Neurology. 2020;(3):157-178
Abstract
Air pollution has a negative impact on one's health and on the central nervous system. We decided to assess studies that evaluated the relationship between air pollution and cognitive functions in children and adolescents by reviewing studies that had been published between January 2009 and May 2019. We searched three major databases for original works (26 studies) and for studies using brain imaging methods based on MRI (six studies). Adverse effects of air pollutants on selected cognitive or psychomotor functions were found in all of the studies. Exposure to nitrogen dioxide, for example, was linked to impaired working memory, general cognitive functions, and psychomotor functions; particulate matter 2.5 was linked to difficulties in working memory, short-term memory, attention, processing speed, and fine motor function; black carbon was linked to poor verbal intelligence, nonverbal intelligence, and working memory; airborne copper was linked to impaired attentiveness and fine motor skills; isophorone was linked to lower mathematical skills; and polycyclic aromatic hydrocarbons in fetal life were linked to lower intelligence scores. The studies using MRI showed that high concentrations of air pollutants were linked to changes in the brain's white matter or lower functional integration and segregation in children's brain networks. In view of the global increase in air pollution, there is a need for further research to elucidate the relationship between air pollution and cognitive and motor development in children. According to some studies, neuroinflammation, the e4 allele of the apolipoprotein E gene, and gutathione-S-transferase gene polymorphism processes may play a role.
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6.
Weather condition, air pollutants, and epidemics as factors that potentially influence the development of Kawasaki disease.
Fujii, F, Egami, N, Inoue, M, Koga, H
The Science of the total environment. 2020;:140469
Abstract
Environmental factors have been suspected to have effects on the development of Kawasaki disease. However, the associations have been conflicting. The aim of this study was to investigate the effects of air pollution, weather conditions, and epidemic infections on the risks for Kawasaki disease in Japan. The concentrations of air pollutants (nitric oxide, nitrogen dioxide, and sulfur dioxide); ambient weather conditions (temperature, atmospheric pressure, relative air humidity, precipitation, sunshine duration, and wind velocity); and the epidemic conditions of 14 infectious diseases in hospitalized patients with Kawasaki disease were monitored from 2011 to 2018 in Beppu, Japan. The overdispersed generalized additive model was used to evaluate the effects, and a combination model with a distributed lag nonlinear model was used to estimate the cumulative effects. The incidence of Kawasaki disease had positive associations with preceding hot temperature and increased concentrations of nitric oxide and sulfur dioxide and a negative association with epidemic herpangina. The cumulative relative risk of Kawasaki disease at 5 lagged days of increased temperature was 1.76 (95% confidence interval: 1.01-3.07). This city-level observational study suggested that the incidence of Kawasaki disease was associated with air pollution and increased temperature and may be indirectly influenced by epidemic herpangina.
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7.
Ambient air pollution and depression: A systematic review with meta-analysis up to 2019.
Fan, SJ, Heinrich, J, Bloom, MS, Zhao, TY, Shi, TX, Feng, WR, Sun, Y, Shen, JC, Yang, ZC, Yang, BY, et al
The Science of the total environment. 2020;:134721
Abstract
Although epidemiological studies have evaluated the associations of ambient air pollution with depression, the results remained mixed. To clarify the nature of the association, we performed a comprehensive systematic review and meta-analysis with the Inverse Variance Heterogeneity (IVhet) model to estimate the effect of ambient air pollution on depression. Three English and four Chinese databases were searched for epidemiologic studies investigating associations of ambient particulate (diameter ≤ 2.5 μm (PM2.5), ≤10 μm (PM10)) and gaseous (nitric oxide (NO), nitrogen dioxide (NO2), carbon monoxide (CO), sulfur dioxide (SO2) and ozone (O3)) air pollutants with depression. Odds ratios (OR) and corresponding 95% confidence intervals (CI) were calculated to evaluate the strength of the associations. We identified 22 eligible studies from 10 countries of the world. Under the IVhet model, per 10 µg/m3 increase in long-term exposure to PM2.5 (OR: 1.12, 95% CI: 0.97-1.29, I2: 51.6), PM10 (OR: 1.04, 95% CI: 0.88-1.25, I2: 85.7), and NO2 (OR: 1.05, 95% CI: 0.83-1.34, I2: 83.6), as well as short-term exposure to PM2.5 (OR: 1.01, 95% CI: 0.99-1.04, I2: 51.6), PM10 (OR: 1.01, 95% CI: 0.98-1.04, I2: 86.7), SO2 (OR: 1.03, 95% CI: 0.99-1.07, I2: 71.2), and O3 (OR: 1.01, 95% CI: 0.99-1.03, I2: 82.2) was not significantly associated with depression. However, we observed significant association between short-term NO2 exposure (per 10 µg/m3 increase) and depression (OR: 1.02, 95% CI: 1.00-1.04, I2: 65.4). However, the heterogeneity was high for all of the pooled estimates, which reduced credibility of the cumulative evidence. Additionally, publication bias was detected for six of eight meta-estimates. In conclusion, short-term exposure to NO2, but not other air pollutants, was significantly associated with depression. Given the limitations, a larger meta-analysis incorporating future well-designed longitudinal studies, and investigations into potential biologic mechanisms, will be necessary for a more definitive result.
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8.
Ambient air pollution and body weight status in adults: A systematic review and meta-analysis.
Huang, S, Zhang, X, Huang, J, Lu, X, Liu, F, Gu, D
Environmental pollution (Barking, Essex : 1987). 2020;(Pt A):114999
Abstract
Overweight and obesity have become a global epidemic and concern, and contributed to at least 4.0 million deaths each year worldwide. However, current evidence regarding the impact of air pollution on body weight status remains inconsistent. We therefore conducted a systematic review and meta-analysis to evaluate the effect of long-term exposure to ambient air pollutants on body weight status in adults. Three databases were searched up to Dec 31, 2019 for articles investigating the association of gaseous (sulfur dioxide, nitrogen dioxide, ozone) and particulate (diameter ≤ 10 μm or ≤ 2.5 μm) air pollutants with body weight status. Random effect models were used to estimate the pooled odds ratios (ORs), regression coefficients (β) and their 95% confidence intervals (95% CIs) associated with air pollution. Among twelve studies that were eligible in the systematic review, ten were used to estimate the pooled effect size, and most of them were cross-sectional studies. We identified that ambient air pollution had adverse effects on body weight status. For example, elevated PM2.5 and O3 were associated with higher level of body mass index, with the pooled β (95% CIs) of 0.34 (0.30-0.38) and 0.21 (0.17-0.24) per 10 μg/m3 increment, respectively. In addition, increased NO2, SO2 and O3 were associated with higher risk of having overweight/obesity, with the corresponding pooled OR (95% CI) of 1.13 (1.01-1.26), 1.04 (1.01-1.06) and 1.07 (1.02-1.13) per 10 μg/m3 increment. Overall, air pollution is a potential risk factor for body weight status in adults, and more high-quality studies, especially prospective studies from severely polluted regions, are warranted for comprehensive understanding of its health effects.
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9.
Exposure to fine particles increases blood pressure of hypertensive outdoor workers: A panel study.
Santos, UP, Ferreira Braga, AL, Bueno Garcia, ML, Amador Pereira, LA, Lin, CA, Chiarelli, PS, Saldiva de André, CD, Afonso de André, P, Singer, JM, Nascimento Saldiva, PH
Environmental research. 2019;:88-94
Abstract
BACKGROUND Hypertension and air pollution are two important risk factors for cardiovascular morbidity and mortality. Although several studies suggest that air pollution has a significant impact on blood pressure, studies on long-term effects are sparse and still controversial. OBJECTIVE To evaluate the effects of exposure of outdoor workers to different levels of traffic-generated PM2.5 on blood pressure. DESIGN This is an observational panel study. PARTICIPANTS 88 non-smoking workers exposed to different concentrations of air pollution were evaluated weekly along four successive weeks. MEASUREMENTS In each week, personal monitoring of 24-h PM2.5 concentration and 24-h ambulatory blood pressure were measured. The association between blood pressure variables and PM2.5, adjusted for age, body mass index, time in job, daily work hours, diabetes, hypertension and cholesterol was assessed by means of multiple linear regression models fitted by least squares. RESULTS Exposure to PM2.5 (ranging from 8.5 to 89.7 μg/m3) is significantly and consistently associated with an increase in average blood pressure. An elevation of 10 μg/m3 in the concentration of PM2.5 is associated with increments of 3.9 mm Hg (CI 95% = [1.5; 6.3]) in average systolic 24-h blood pressure for hypertensive and/or diabetic workers. CONCLUSION Exposure to fine particles, predominantly from vehicular traffic, is associated with elevated blood pressure in hypertensive and/or diabetic workers.
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10.
Association between Outdoor Air Pollution and Childhood Leukemia: A Systematic Review and Dose-Response Meta-Analysis.
Filippini, T, Hatch, EE, Rothman, KJ, Heck, JE, Park, AS, Crippa, A, Orsini, N, Vinceti, M
Environmental health perspectives. 2019;(4):46002
Abstract
BACKGROUND A causal link between outdoor air pollution and childhood leukemia has been proposed, but some older studies suffer from methodological drawbacks. To the best of our knowledge, no systematic reviews have summarized the most recently published evidence and no analyses have examined the dose-response relation. OBJECTIVE We investigated the extent to which outdoor air pollution, especially as resulting from traffic-related contaminants, affects the risk of childhood leukemia. METHODS We searched all case-control and cohort studies that have investigated the risk of childhood leukemia in relation to exposure either to motorized traffic and related contaminants, based on various traffic-related metrics (number of vehicles in the closest roads, road density, and distance from major roads), or to measured or modeled levels of air contaminants such as benzene, nitrogen dioxide, 1,3-butadiene, and particulate matter. We carried out a meta-analysis of all eligible studies, including nine studies published since the last systematic review and, when possible, we fit a dose-response curve using a restricted cubic spline regression model. RESULTS We found 29 studies eligible to be included in our review. In the dose-response analysis, we found little association between disease risk and traffic indicators near the child's residence for most of the exposure range, with an indication of a possible excess risk only at the highest levels. In contrast, benzene exposure was positively and approximately linearly associated with risk of childhood leukemia, particularly for acute myeloid leukemia, among children under 6 y of age, and when exposure assessment at the time of diagnosis was used. Exposure to nitrogen dioxide showed little association with leukemia risk except at the highest levels. DISCUSSION Overall, the epidemiologic literature appears to support an association between benzene and childhood leukemia risk, with no indication of any threshold effect. A role for other measured and unmeasured pollutants from motorized traffic is also possible. https://doi.org/10.1289/EHP4381.