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1.
The Effects of Air Pollution on the Development of Atopic Disease.
Hassoun, Y, James, C, Bernstein, DI
Clinical reviews in allergy & immunology. 2019;(3):403-414
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Abstract
Air pollution is defined as the presence of noxious substances in the air at levels that impose a health hazard. Thus, there has been long-standing interest in the possible role of indoor and outdoor air pollutants on the development of respiratory disease. In this regard, asthma has been of particular interest but many studies have also been conducted to explore the relationship between air pollution, allergic rhinitis, and atopic dermatitis. Traffic-related air pollutants or TRAP refers to a broad group of pollutants including elemental carbon, black soot, nitrogen dioxide (NO2), nitric oxide (NO), sulfur dioxide (SO2), particulate matter (PM2.5 and PM10), carbon monoxide (CO), and carbon dioxide (CO2). In this review, we aim to examine the current literature regarding the impact of early childhood exposure to TRAP on the development of asthma, allergic rhinitis, and atopic dermatitis. Although there is growing evidence suggesting significant associations, definitive conclusions cannot be made with regard to the effect of TRAP on these diseases. This conundrum may be due to a variety of factors, including different definitions used to define TRAP, case definitions under consideration, a limited number of studies, variation in study designs, and disparities between studies in consideration of confounding factors. Regardless, this review highlights the need for future studies to be conducted, particularly with birth cohorts that explore this relationship further. Such studies may assist in understanding more clearly the pathogenesis of these diseases, as well as other methods by which these diseases could be treated.
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2.
Air pollution and DNA methylation: effects of exposure in humans.
Rider, CF, Carlsten, C
Clinical epigenetics. 2019;(1):131
Abstract
Air pollution exposure is estimated to contribute to approximately seven million early deaths every year worldwide and more than 3% of disability-adjusted life years lost. Air pollution has numerous harmful effects on health and contributes to the development and morbidity of cardiovascular disease, metabolic disorders, and a number of lung pathologies, including asthma and chronic obstructive pulmonary disease (COPD). Emerging data indicate that air pollution exposure modulates the epigenetic mark, DNA methylation (DNAm), and that these changes might in turn influence inflammation, disease development, and exacerbation risk. Several traffic-related air pollution (TRAP) components, including particulate matter (PM), black carbon (BC), ozone (O3), nitrogen oxides (NOx), and polyaromatic hydrocarbons (PAHs), have been associated with changes in DNAm; typically lowering DNAm after exposure. Effects of air pollution on DNAm have been observed across the human lifespan, but it is not yet clear whether early life developmental sensitivity or the accumulation of exposures have the most significant effects on health. Air pollution exposure-associated DNAm patterns are often correlated with long-term negative respiratory health outcomes, including the development of lung diseases, a focus in this review. Recently, interventions such as exercise and B vitamins have been proposed to reduce the impact of air pollution on DNAm and health. Ultimately, improved knowledge of how exposure-induced change in DNAm impacts health, both acutely and chronically, may enable preventative and remedial strategies to reduce morbidity in polluted environments.
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3.
Impacts of atmospheric particulate matter pollution on environmental biogeochemistry of trace metals in soil-plant system: A review.
Luo, X, Bing, H, Luo, Z, Wang, Y, Jin, L
Environmental pollution (Barking, Essex : 1987). 2019;(Pt 1):113138
Abstract
Atmospheric particulate matter (PM) pollution and soil trace metal (TM) contamination are binary environmental issues harming ecosystems and human health, especially in the developing China with rapid urbanization and industrialization. Since PMs contain TMs, the air-soil nexus should be investigated synthetically. Although the PMs and airborne TMs are mainly emitted from urban or industrial areas, they can reach the rural and remote mountain areas owing to the ability of long-range transport. After dry or wet deposition, they will participate in the terrestrial biogeochemical cycles of TMs in various soil-plant systems, including urban soil-greening trees, agricultural soil-food crops, and mountain soil-natural forest systems. Besides the well-known root uptake, the pathway of leaf deposition and foliar absorption contribute significantly to the plant TM accumulation. Moreover, the aerosols can also exert climatic effects by absorption and scattering of solar radiation and by the cloud condensation nuclei activity, thereby indirectly impact plant growth and probably crop TM accumulation through photosynthesis, and then threat health. In particular, this systematic review summarizes the interactions of PMs-TMs in soil-plant systems including the deposition, transfer, accumulation, toxicity, and mechanisms among them. Finally, current knowledge gaps and prospective are proposed for future research agendas. These analyses would be conducive to improving urban air quality and managing the agricultural and ecological risks of airborne metals.
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4.
[Breathing: Ambient Air Pollution and Health - Part II].
Schulz, H, Karrasch, S, Bölke, G, Cyrys, J, Hornberg, C, Pickford, R, Schneider, A, Witt, C, Hoffmann, B
Pneumologie (Stuttgart, Germany). 2019;(6):347-373
Abstract
The second part of the DGP-statement on adverse health effects of ambient air pollution provides an overview of the current ambient air quality in Germany and its development in the past 20 years. Further, effects of air pollution on the cardiovascular system und underlying pathophysiological mechanisms are introduced. Air pollutants form a highly complex and dynamic system of thousands of organic and inorganic components from natural and anthropogenic sources. The pollutants are produced locally or introduced by long-range transport over hundreds of kilometers and are additionally subjected to local meteorological conditions. According to air quality regulations ambient air quality is monitored under uniform standards including immission of particulate matter, up to 2.5 µm (PM2.5) or 10 µm (PM10) in aerodynamic diameter, and of nitrogen dioxide (NO2) or ozone (O3). The clean air measures of recent years led to a continuous decline of air pollution in the past 20 years in Germany. Accordingly, the focus is nowadays directed at population-related health hazards caused by low concentrations of air pollution. Exceeded limits for sulfur dioxide, carbon monoxide, benzene and lead are not detected anymore. Also the number of days with increased ozone concentration declined, although the annual mean concentration is unaltered. Decreasing concentrations of particulate matter and NO2 have been observed, however, about 40 % of the monitoring stations at urban traffic sites still measure values exceeding current limits for NO2. Moreover, the stricter, solely health-based WHO-standards for PM2.5, PM10 and NO2 are still not met so that an optimal protection from air pollution-related health hazards is currently not given for the German population. In recent years, the findings of numerous cross-sectional and longitudinal studies underscored adverse effects of air pollution on the cardiovascular system, especially for particulate matter, although the level of evidence still varies for the different health outcomes. Further, the studies show that cardiovascular health hazards on the population level are of higher relevance than those for the respiratory system. The existing evidence for cardiovascular mortality, hospitalization, ischemic heart diseases, myocardial infarction and stroke can be regarded as strong, while that for heart failure is rather moderate. While the evidence for air pollution-related short-term alteration of the cardiac autonomic balance can be considered as sufficient, long-term effects are still unclear. Likewise, the heterogeneous findings on air pollution-related arrhythmia do currently not allow a distinct conclusion in this regard. A large number of studies support the observation that both, short- and long-term air pollution exposure contribute to increased blood pressure, may impair vascular homeostasis, induce endothelial dysfunction and promote the progression of atherosclerotic lesions. These effects provide reasonable biological explanation for the fatal events associated with exposure to air pollution. Short-term exposure may not pose a significant risk on healthy individuals but may be considered as precursor for fatal events in susceptible populations, while repetitive or long-term exposure may contribute to the development of cardiovascular diseases even in healthy subjects.
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5.
Protective Effect of Breastfeeding on the Adverse Health Effects Induced by Air Pollution: Current Evidence and Possible Mechanisms.
Zielinska, MA, Hamulka, J
International journal of environmental research and public health. 2019;(21)
Abstract
Air pollution is a major social, economic, and health problem around the world. Children are particularly susceptible to the negative effects of air pollution due to their immaturity and excessive growth and development. The aims of this narrative review were to: (1) summarize evidence about the protective effects of breastfeeding on the adverse health effects of air pollution exposure, (2) define and describe the potential mechanisms underlying the protective effects of breastfeeding, and (3) examine the potential effects of air pollution on breastmilk composition and lactation. A literature search was conducted using electronic databases. Existing evidence suggests that breastfeeding has a protective effect on adverse outcomes of indoor and outdoor air pollution exposure in respiratory (infections, lung function, asthma symptoms) and immune (allergic, nervous and cardiovascular) systems, as well as under-five mortality in both developing and developed countries. However, some studies reported no protective effect of breastfeeding or even negative effects of breastfeeding for under-five mortality. Several possible mechanisms of the breastfeeding protective effect were proposed, including the beneficial influence of breastfeeding on immune, respiratory, and nervous systems, which are related to the immunomodulatory, anti-inflammatory, anti-oxidant, and neuroprotective properties of breastmilk. Breastmilk components responsible for its protective effect against air pollutants exposure may be long chain polyunsaturated fatty acids (LC PUFA), antioxidant vitamins, carotenoids, flavonoids, immunoglobins, and cytokines, some of which have concentrations that are diet-dependent. However, maternal exposure to air pollution is related to increased breastmilk concentrations of pollutants (e.g., Polycyclic aromatic hydrocarbons (PAHs) or heavy metals in particulate matter (PM)). Nonetheless, environmental studies have confirmed that breastmilk's protective effects outweigh its potential health risk to the infant. Mothers should be encouraged and supported to breastfeed their infants due to its unique health benefits, as well as its limited ecological footprint, which is associated with decreased waste production and the emission of pollutants.
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Air pollution, environmental chemicals, and smoking may trigger vitamin D deficiency: Evidence and potential mechanisms.
Mousavi, SE, Amini, H, Heydarpour, P, Amini Chermahini, F, Godderis, L
Environment international. 2019;:67-90
Abstract
Beyond vitamin D (VD) effect on bone homeostasis, numerous physiological functions in human health have been described for this versatile prohormone. In 2016, 95% of the world's population lived in areas where annual mean ambient particulate matter (<2.5 μm) levels exceeded the World Health Organization guideline value (Shaddick et al., 2018). On the other hand, industries disperse thousands of chemicals continually into the environment. Further, considerable fraction of populations are exposed to tobacco smoke. All of these may disrupt biochemical pathways and cause detrimental consequences, such as VD deficiency (VDD). In spite of the remarkable number of studies conducted on the role of some of the above mentioned exposures on VDD, the literature suffers from two main shortcomings: (1) an overview of the impacts of environmental exposures on the levels of main VD metabolites, and (2) credible engaged mechanisms in VDD because of those exposures. To summarize explanations for these unclear topics, we conducted the present review, using relevant keywords in the PubMed database, to investigate the adverse effects of exposure to air pollution, some environmental chemicals, and smoking on the VD metabolism, and incorporate relevant potential pathways disrupting VD endocrine system (VDES) leading to VDD. Air pollution may lead to the reduction of VD cutaneous production either directly by blocking ultraviolet B photons or indirectly by decreasing outdoor activity. Heavy metals may reduce VD serum levels by increasing renal tubular dysfunction, as well as downregulating the transcription of cytochrome P450 mixed-function oxidases (CYPs). Endocrine-disrupting chemicals (EDCs) may inhibit the activity and expression of CYPs, and indirectly cause VDD through weight gain and dysregulation of thyroid hormone, parathyroid hormone, and calcium homeostasis. Smoking through several pathways decreases serum 25(OH)D and 1,25(OH)2D levels, VD intake from diet, and the cutaneous production of VD through skin aging. In summary, disturbance in the cutaneous production of cholecalciferol, decreased intestinal intake of VD, the modulation of genes involved in VD homeostasis, and decreased local production of calcitriol in target tissues are the most likely mechanisms that involve in decreasing the serum VD levels.
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Evaluation of a meta-analysis of air quality and heart attacks, a case study.
Stanley Young, S, Kindzierski, WB
Critical reviews in toxicology. 2019;(1):85-94
Abstract
It is generally acknowledged that claims from observational studies often fail to replicate. An exploratory study was undertaken to assess the reliability of base studies used in meta-analysis of short-term air quality-myocardial infarction risk and to judge the reliability of statistical evidence from meta-analysis that uses data from observational studies. A highly cited meta-analysis paper examining whether short-term air quality exposure triggers myocardial infarction was evaluated as a case study. The paper considered six air quality components - carbon monoxide, nitrogen dioxide, sulphur dioxide, particulate matter 10 μm and 2.5 μm in diameter (PM10 and PM2.5), and ozone. The number of possible questions and statistical models at issue in each of 34 base papers used were estimated and p-value plots for each of the air components were constructed to evaluate the effect heterogeneity of p-values used from the base papers. Analysis search spaces (number of statistical tests possible) in the base papers were large, median = 12,288 (interquartile range = 2496 - 58,368), in comparison to actual statistical test results presented. Statistical test results taken from the base papers may not provide unbiased measures of effect for meta-analysis. Shapes of p-value plots for the six air components were consistent with the possibility of analysis manipulation to obtain small p-values in several base papers. Results suggest the appearance of heterogeneous, researcher-generated p-values used in the meta-analysis rather than unbiased evidence of real effects for air quality. We conclude that this meta-analysis does not provide reliable evidence for an association of air quality components with myocardial risk.
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8.
The toxicology of air pollution predicts its epidemiology.
Ghio, AJ, Soukup, JM, Madden, MC
Inhalation toxicology. 2018;(9-10):327-334
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Abstract
The epidemiologic investigation has successively delineated associations of air pollution exposure with non-malignant and malignant lung disease, cardiovascular disease, cerebrovascular disease, pregnancy outcomes, perinatal effects and other extra-pulmonary disease including diabetes. Defining these relationships between air pollution exposure and human health closely parallels results of an earlier epidemiologic investigation into cigarette smoking and environmental tobacco smoke (ETS), two other particle-related exposures. Humic-like substances (HULIS) have been identified as a chemical component common to cigarette smoke and air pollution particles. Toxicology studies provide evidence that a disruption of iron homeostasis with sequestration of host metal by HULIS is a fundamental mechanistic pathway through which biological effects are initiated by cigarette smoke and air pollution particles. As a result of a common chemical component and a shared mechanistic pathway, it should be possible to extrapolate from the epidemiology of cigarette smoking and ETS to predict associations of air pollution exposure with human disease, which are currently unrecognized. Accordingly, it is anticipated that the forthcoming epidemiologic investigation will demonstrate relationships of air pollution with COPD causation, peripheral vascular disease, hypertension, renal disease, digestive disease, loss of bone mass/risk of fractures, dental disease, eye disease, fertility problems, and extrapulmonary malignancies.
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Nonpharmacologic Strategies to Manage Exercise-Induced Bronchoconstriction.
Dickinson, J, Amirav, I, Hostrup, M
Immunology and allergy clinics of North America. 2018;(2):245-258
Abstract
Pharmacologic management of exercise-induced bronchoconstriction (EIB) is the mainstay of preventative therapy. There are some nonpharmacologic interventions, however, that may assist the management of EIB. This review discusses these nonpharmacologic interventions and how they may be applied to patients and athletes with EIB.
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The role of air pollution on ST-elevation myocardial infarction: a narrative mini review.
Shahrbaf, MA, Mahjoob, MP, Khaheshi, I, Akbarzadeh, MA, Barkhordari, E, Naderian, M, Tajrishi, FZ
Future cardiology. 2018;(4):301-306
Abstract
ST-elevation myocardial infarction (STEMI) is one of the potential causes of death worldwide. In spite of substantial advances in its diagnosis and treatment, STEMI is still considered as a major public health dilemma in developed and particularly developing countries. One of the triggering factors of STEMI is supposed to be air pollutants like gaseous pollutants including, sulfur dioxide, nitric dioxide, carbon monoxide, ozone and particulate matters (PM) including, PM under 2.5 µm (PM2.5) and PM under 10 µm (PM10). Air pollution can trigger STEMI with various mechanisms such as increasing inflammatory factors and changing the heart rate or blood viscosity. In this article, we aimed to explore research in the field and discuss the relationship between air pollution and STEMI.