Air pollution induced asthma and alterations in cytokine patterns

In recent decades, clinicians and scientists have witnessed a significant increase in the prevalence of allergic rhinitis and asthma. The factors underlying this phenomenon are clearly complex; however, this rapid increase in the burden of atopic disease has occurred in parallel with rapid industrialization and urbanization in many parts of the world. Consequently, more people are exposed to air pollutants than at any point in human history. Worldwide increases in allergic respiratory disease have mainly been observed in urban communities. Epidemiologic and clinical investigations have suggested a strong link between particulate air pollution and detrimental health effects, including cardiopulmonary morbidity and mortality. The purpose of this review is to provide an evidence-based summary of the effects of air pollutants on asthma, focusing on particulate matter PMs, diesel exhaust particles (DEPs), and ozone as major air pollutants. An overview of observational and experimental studies linking these pollutants with asthma will be provided, followed by consideration of the mechanisms underlying pollutant induced immune response and inflammation. The cytokine response will be viewed in depth and a brief discussion of future research and clinical directions is provided.     

Asthma and air quality

PURPOSE OF REVIEW: There is evidence for an association between asthma and air pollutants, including ozone, NO2 and particulate matter. Since these pollutants are ubiquitous in the urban atmosphere and typically correlated with each other it has been difficult to ascertain the specific sources of air pollution responsible for the observed effects. Similarly, uncertainty in determining a causal agent, or multiple agents, has complicated efforts to identify the mechanisms involved in pollution-mediated asthma events and whether air pollution may cause asthma as well as exacerbate preexisting cases. RECENT FINDINGS: Numerous studies have examined specific sources of air pollution and their relationship to asthma. This review summarizes recent work conducted, specifically, on traffic pollution and presents results that elucidate several plausible biological mechanisms for the observed effects. Of note are studies linking susceptibility to several genetic polymorphisms. Together, these studies suggest that remaining uncertainties in the asthma-air pollution association may be addressed through enhanced assessment of both exposures and outcomes. SUMMARY: Air-pollution research is evolving rapidly; in the near future, clinicians and public health agencies may be able to use this new information to provide recommendations for asthmatics that go beyond only paying attention to the air-pollution forecast.     

Exposure to air pollutants and the gut microbiota: a potential link between exposure,obesity, and type 2 diabetes

ABSTRACT

Work has shown that increased exposure to air pollutants independently contributes to obesity and type 2 diabetes risk, yet the exact mechanisms underlying these associations have not been fully characterized. The current review summarizes recent findings regarding the impact of inhaled and ingested air pollutants on the gut microbiota. Animal and human studies provide evidence that air pollutants, such as particulate matter, nitrogen oxides, and ozone, have the potential to alter the gut microbiota. Further, studies suggest that such exposure-induced alterations to the gut microbiota may contribute to increased risk for obesity and type 2 diabetes through inflammatory pathways. Future work is needed to fully understand the complex interactions between air pollution, the gut microbiome, and human health. Additionally, advanced sequencing methods for gut microbiome research present unique opportunities to study the underlying pathways that link increased air pollution exposure with obesity and type 2 diabetes risk.     

Interaction of matrix metalloproteinases with pulmonary pollutants

An air pollutant consists of any atmospheric substance that may harm humans, animals, vegetation or material. Various air pollutants have been reported, differing in their physicochemical characteristics. They can be grouped into four categories: gaseous pollutants (e.g. ozone, sulfur dioxide, oxides of nitrogen, carbon monoxide and volatile organic compounds), persistent organic pollutants, heavy metals (e.g. cadmium, lead and mercury) and particulate matter (coarse, fine and ultrafine). These pollutants can reach the respiratory system, eliciting pulmonary and/or systemic effects. These effects include inflammation, tissue remodelling and carcinogenesis: all phenomena where matrix metalloproteases (MMPs) play critical roles, given their broad effects on matrix remodelling and modulation of inflammation and cell signalling. Moreover, since expression and activity of MMPs can be induced by such stimuli, the hypothesis has been raised that MMPs could be involved in the health effects of pollutants. Until now, the implication of MMPs in these effects has been studied only for some pollutants and for a restricted selection of MMPs (mainly MMP-1, -2, -9 and -12), while evidence for a link between MMP induction/activation and health effects remains scarce. A larger number of studies is, therefore, needed in order to better understand the implication of MMPs in health effects associated with air pollution.     

Air Pollution and Arrhythmias

Air pollution is commonly defined as the contamination of the air we breathe by any chemical, physical, or biological agent that is potentially threatening to human and ecosystem health. The common pollutants known to be disease-causing are particulate matter, ground-level ozone, sulphur dioxide, nitrogen dioxide, and carbon monoxide. Although the association between increasing concentrations of these pollutants and cardiovascular disease is now accepted, the association of air pollution and arrhythmias is less well established. In this review we provide an in-depth discussion of the association of acute and chronic air pollution exposure and arrhythmia incidence, morbidity, and mortality, and the purported pathophysiological mechanisms. Increases in concentrations of air pollutants have multiple proarrhythmic mechanisms including systemic inflammation (via increases in reactive oxygen species, tumour necrosis factor, and direct effects from translocated particulate matter), structural remodelling (via an increased risk of atherosclerosis and myocardial infarction or by affecting the cell-to-cell coupling and gap junction function), and mitochondrial and autonomic dysfunction. Furthermore, we describe the associations of air pollution and arrhythmias. There is a strong correlation of acute and chronic air pollutant exposure and the incidence of atrial fibrillation. Acute increases in air pollution increase the risk of emergency room visits and hospital admissions for atrial fibrillation and the risk of stroke and mortality in patients with atrial fibrillation. Similarly, there is a strong correlation of increases of air pollutants and the risk of ventricular arrhythmias, out-of-hospital cardiac arrest, and sudden cardiac death.     

Acute effects of air pollution on health: evidence from epidemiological studies

OBJECTIVE: To summarize the evidence of acute health effects from exposure to particulate matter and ozone. MATERIAL AND METHODS: A meta-analysis was performed using random effect models, to summarize the health effects of pollution, published in major international and Mexican journals up to June 2000. RESULTS: Results were given as percent increase in ten units of PM10 (microgram/m3) and ozone (ppb). PM10 was found to have an effect on mortality (0.96%), hospital admissions (1.39%), emergency room visits (3.11%), respiratory symptoms (7.72%), pulmonary forced vital capacity (1.42%), and restricted activity days (7.74%). Ozone effects were equally significant. CONCLUSIONS: These findings show the great impact that air pollutants may have on the health of populations living in large metropolis.     

Environmental risk factors (outdoor air pollution and climatic changes) and increased trend of respiratory allergy.

A wealth of evidence suggests that allergic respiratory diseases such as rhinosinusitis and bronchial asthma have become more common worldwide in recent years and a great deal of etiological and pathogenic research has been carried out to evaluate the possible causes of this increasing trend. There is also some evidence that increased atmospheric concentrations of pollutants such as ozone (O3), nitric oxides (NOx), respirable particulate (PM10) and volatile organic chemicals (VOC5), which result from increased use of liquid petroleum gas or kerosene, may be linked to the increased prevalence of allergic diseases which develop more frequently in urban areas of developed countries. Since bronchial asthma is a syndrome which can be aggravated by inhaled compounds, the effects of air pollutants on health have been the focus of attention. In fact, various studies have demonstrated that inhalation of air pollutants such as O3, nitrogen dioxide (NO2) and sulfur dioxide (SO2), either individually or in combination, can enhance the airway response to inhaled allergens in atopic subjects, thus inducing asthma exacerbations. Moreover, experimental studies have shown that diesel exhaust particulate causes respiratory symptoms and is able also to modulate the immune response by increasing IgE synthesis in predisposed animals and humans. There is also some evidence that air pollutants can interact with aeroallergens in the atmosphere and/or on human airways, potentiating their effects. In fact, by inducing airway inflammation which increases epithelial permeability, some pollutants overcome the mucosal barrier and lead to allergen-induced responses. However, air pollution and climatic changes should also have an indirect effect on allergic response by influencing quantitatively and qualitatively the pollen production by allergenic plants.     

The interaction between particulate air pollution and allergens in enhancing allergic and airway responses

Although the detrimental effects of air pollution on human health have been brought widely to public notice, it appears that less attention has been given to the potential role of toxic air pollutants in the induction of allergic conditions such as asthma, rhinoconjunctivitis, and atopic eczema. A number of large epidemiologic studies have shown that people exposed to intense motor vehicle traffic and its associated emissions are at major risk for allergic symptoms, reduced lung function, and increased sensitization to common airborne allergens. Several laboratory-based studies have demonstrated that particulate air pollutants emitted from motor vehicles can induce allergic inflammation, enhance IgE responses, and increase airway hyperresponsiveness, which could provide an underlying mechanism for the increasing prevalence of allergic diseases. This article reviews the evidence that supports the causative link between particulate air pollution and the sharp increase in the prevalence of type I allergies in developed countries.     

Thrombogenicity and cardiovascular effects of ambient air pollution

Exposure to air pollution is associated with adverse effects on health. In particular, a strong epidemiologic association is observed between acute and chronic exposures to particulate matter and the occurrence of cardiovascular events, coronary artery disease, cerebrovascular disease and venous thromboembolism, especially among older people and people with diabetes and previous cardiovascular conditions. Multiple mechanisms have been postulated to cause the increase in atherothrombotic and thromboembolic events, including the activation by particulate matter of inflammatory pathways and hemostasis factors, production of reactive oxygen species through the oxidative stress pathway, alterations in vascular tone, and decreased heart rate variability (a marker of cardiac autonomic dysfunction and a predictor of sudden cardiac death and arrhythmias). Current knowledge on the biologic mechanisms and the clinical effect of short- and long-term exposure to particulate air pollutants is discussed, emphasizing that life expectancy improved significantly in sites where air pollutants were controlled.     

Prospective study of air pollution and bronchitic symptoms in children with asthma

The relationship of bronchitic symptoms to ambient particulate matter and to particulate elemental and organic carbon (OC), nitrogen dioxide (NO2), and other gaseous pollutants was examined in a cohort of children with asthma in 12 Southern California communities. Symptoms, assessed yearly by questionnaire from 1996 to 1999, were associated with the yearly variability of particulate matter with aerodynamic diameter less than 2.5 microg (odds ratio [OR] 1.09/microg/m3; 95% confidence interval [CI] 1.01-1.17), OC (OR 1.41/microg/m3; 95% CI 1.12-1.78), NO2 (OR 1.07/ppb; 95% CI 1.02-1.13), and ozone (OR 1.06/ppb; 95% CI 1.00-1.12). The ORs associated with yearly within-community variability in air pollution were larger than the effect of the between-community 4-year average concentrations. In two pollutant models, the effects of yearly variation in OC and NO2 were only modestly reduced by adjusting for other pollutants, except in a model containing both OC and NO2; the effects of all other pollutants were reduced after adjusting for OC or NO2. We conclude that OC and NO2 deserve greater attention as potential causes of the chronic symptoms of bronchitis in children with asthma and that previous cross-sectional studies may have underestimated the risks associated with air pollution.     

Air pollution

Despite progress in improving ambient air quality and reducing personal exposures to air pollutants in indoor settings, population exposures to air pollutants remain widespread and are an important public health concern. Many air pollutants are associated with adverse health effects; the most serious include development and exacerbation of asthma, loss of lung function, impaired neurobehavioral development, and death. These outcomes are the focus of current health effects research on environmental tobacco smoke and radon in indoor settings, and lead, ozone, and particulate matter outdoors. Advances in methods to measure exposures to specific pollutants and the identification of markers of individual susceptibility are providing improved data on the relation of exposure and disease, and, in turn, will improve efforts to protect public health.     

Outdoor air pollution and asthma

PURPOSE OF REVIEW: The relation between outdoor air pollution and asthma has always been a major focus of research. The evidence that current levels of air pollution in many countries result in increased morbidity and mortality is fairly consistent. With rapid urbanization in many communities, traffic exhausts have become the major source of pollution, and many recent research studies have attempted to investigate the detrimental effects of this type of pollution. This paper reviews the recent evidence of the possible detrimental effects of ambient air pollution on the inception and morbidity of asthma. RECENT FINDINGS: Traffic related pollution has been confirmed in both cross-sectional and longitudinal studies to be associated with increased asthma morbidity and cardiopulmonary mortality. There is also evidence that pollutants such as ozone and traffic exhausts may be responsible for new incident cases of asthma. Among the particulate pollution, research investigating the ultrafine particles and the bacterial components suggested that these particles may have important role in asthma morbidity. SUMMARY: More research studies are needed to reveal how various air pollutants may interact with the host systems, such as the immune system, leading to increased morbidity in susceptible individuals. Reduction of the current levels of ambient air pollution should be an integral part of the overall effort in minimizing asthma morbidity or mortality in the community.     

Air Pollution and Arrhythmic Risk: The Smog Is Yet to Clear

Epidemiologic evidence has demonstrated that air pollution may impair cardiovascular health, leading to potentially life-threatening arrhythmias. Efforts have been made, with the use of epidemiologic data and controlled exposures in diverse animal and human populations, to verify the relationship between air pollution and arrhythmias. The purpose of this review is to examine and contrast the epidemiologic and toxicologic evidence to date that relates airborne pollutants with cardiac arrhythmia. We have explored the potential biological mechanisms driving this association. Using the PubMed database, we conducted a literature search that included the terms “air pollution” and “arrhythmia” and eventually divergent synonyms such as “particulate matter,” “bradycardia,” and “atrial fibrillation.” We reviewed epidemiologic studies and controlled human and animal exposures independently to determine whether observational conclusions were corroborated by toxicologic results. Numerous pollutants have demonstrated some arrhythmic capacity among healthy and health-compromised populations. However, some exposure studies have shown no significant correlation of air pollutants with arrhythmia, which suggests some uncertainty about the arrhythmogenic potential of air pollution and the mechanisms involved in arrhythmogenesis. While data from an increasing number of controlled exposures with human volunteers suggest a potential mechanistic link between air pollution and altered cardiac electrophysiology, definite conclusions regarding air pollution and arrhythmia are elusive as the direct arrhythmic effects of air pollutants are not entirely consistent across all studies.     

空气污染与心律失常的相关性研究

常见的空气污染物主要包括颗粒物、臭氧、二氧化氮和二氧化硫、一氧化碳等.吸入污染的空气不仅诱发呼吸系统疾病,同时还会诱发心血管疾病.流行病学调查发现人体暴露于污染物中可促进缺血性心脏病、心力衰竭、心律失常和心脏骤停在内的心脏事件的发生,增加心血管病发病率和病死率.现对国内外空气污染与心律失常的相关文献进行综述.     

Adverse effects of outdoor pollution in the elderly

With fewer newborns and people living longer, older people are making up an increasing fraction of the total population. Epidemiological evidence shows that older-age-related health problems affect a wide and expanding proportion of the world population. One of the major epidemiological trends of this century is the rise of chronic diseases that affect more elderly than younger people. A total of 3.7 million premature deaths worldwide in 2012 are attributable to outdoor air pollution; the susceptibility to adverse effects of air pollution is expected to differ widely between people and within the same person, and also over time. Frailty history, a measure of multi-system decline, modifies cumulative associations between air pollution and lung function. Moreover, pre-existing diseases may determine susceptibility. In the elderly, due to comorbidity, exposure to air pollutants may even be fatal. Rapid and not-well-planned urbanization is associated with high level of ambient air pollution, mainly caused by vehicular exhausts. In general, there is sufficient evidence of the adverse effects related to short-term exposure, while fewer studies have addressed the longer-term health effects. Increased pollution exposures have been associated with increased mortality, hospital admissions/emergency-room visits, mainly due to exacerbations of chronic diseases or to respiratory tract infections (e.g., pneumonia). These effects may also be modulated by ambient temperature and many studies show that the elderly are mostly vulnerable to heat waves. The association between heat and mortality in the elderly is well-documented, while less is known regarding the associations with hospital admissions. Chronic exposure to elevated levels of air pollution has been related to the incidence of chronic obstructive pulmonary disease (COPD), chronic bronchitis (CB), asthma, and emphysema. There is also growing evidence suggesting adverse effects on lung function related to long-term exposure to ambient air pollution. Few studies have assessed long-term mortality in the elderly. It is still unclear what are the pollutants most damaging to the health of the elderly. It seems that elderly subjects are more vulnerable to particulate matter (PM) than to other pollutants, with particular effect on daily cardio-respiratory mortality and acute hospital admissions. Not many studies have targeted elderly people specifically, as well as specific respiratory morbidity. Most data have shown higher risks in the elderly compared to the rest of the population. Future epidemiological cohort studies need to keep investigating the health effects of air pollutants (mainly cardiopulmonary diseases) on the elderly.     

Air pollution and allergic disease

Over the past several decades, there has been increased awareness of the health effects of air pollution and much debate regarding the role of global warming. The prevalence of asthma and allergic disease has risen in industrialized countries, and most epidemiologic studies focus on possible causalities between air pollution and these conditions. This review examines salient articles and summarizes findings important to the interaction between allergies and air pollution, specifically volatile organic compounds, global warming, particulate pollutants, atopic risk, indoor air pollution, and prenatal exposure. Further work is necessary to determine whether patients predisposed to developing allergic disease may be more susceptible to the health effects of air pollutants due to the direct interaction between IgE-mediated disease and air pollutants. Until we have more definitive answers, patient education about the importance of good indoor air quality in the home and workplace is essential. Health care providers and the general community should also support public policy designed to improve outdoor air quality by developing programs that provide incentives for industry to comply with controlling pollution emissions.     

The 21st century environment and air quality influences on asthma

"Criteria" air pollutants are federally regulated pollutants that occur widely outdoors and have diverse sources, most often related to combustion. They include ozone (O3), particulate matter, sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and lead. All except lead may interfere with oxygen delivery, and so may be of special concern to asthmatics. In controlled experiments, SO2 causes acute asthma symptoms and bronchoconstriction, preventable by beta-agonist medications. Ozone causes acute irritant symptoms, restrictive lung dysfunction, increased bronchial reactivity, and lower-airway inflammation in healthy people and asthmatics. Exposures to O3, and possibly to other pollutants, appear to exacerbate bronchoconstrictive or inflammatory responses to inhaled aeroallergens (bioaerosols); this may represent an important health risk to asthmatics. Exposure levels known to evoke acute responses to O3 or SO2 are uncommon in community air pollution; however, some asthmatics might be susceptible to lesser, more common exposures. Evidence concerning NO2 is equivocal, but it may have O3-like effects in some asthmatics. Epidemiology has often associated particulate pollution with asthma exacerbations and other cardiorespiratory illnesses, even in cities with relatively mild air pollution. Current laboratory research cannot fully explain this association. Advances in emission controls should further reduce ambient pollution levels, but probably will not reduce asthma morbidity. Better asthma management, with improved anti-inflammatory medications, more careful monitoring by patients and health care providers, and reasonable efforts to reduce pollutant and aeroallergen exposures, offers the best hope to reduce asthma morbidity in the new century.     

Effects of air pollution on respiratory health

Air pollution, which started to become a serious health concern with industrial revolution, has been threatening human health. Epidemiological studies have reported a close relation between air pollution and respiratory morbidity and mortality. Studies investigating the mechanisms underlying respiratory effects of air pollution have reported that pollutants lead to increased respiratory symptoms, decreased respiratory function and induce inflammatory changes in airways. In vitro studies have demonstrated that air pollutants exert their effects by causing cellular injury directly, and indirectly activating intracellular oxidative pathways. Air way epithelial cells, which form the first line of defence against air pollutants, may play an active role in this pathophysiological course.     

The role of outdoor air pollution and climatic changes on the rising trends in respiratory allergy.

Evidence suggests that allergic respiratory diseases such as hay fever and bronchial asthma have become more common world-wide in the last two decades, and the reasons for this increase are still largely unknown. A major responsible factor could be outdoor air pollution, derived from cars and other vehicles. Studies have demonstrated that urbanization and high levels of vehicle emissions and westernized lifestyle is correlated with the increasing frequency of pollen-induced respiratory allergy. People who live in urban areas tend to be more affected by pollen-induced respiratory allergy than those from of rural areas. Pollen allergy has been one of the most frequent models used to study the interrelationship between air pollution and respiratory allergic diseases. Pollen grains or plant-derived paucimicronic components carry allergens that can produce allergic symptoms. They may also interact with air pollution (particulate matter, ozone) in producing these effects. There is evidence that air pollutants may promote airway sensitization by modulating the allergenicity of airborne allergens. Furthermore, airway mucosal damage and impaired mucociliary clearance induced by air pollution may facilitate the access of inhaled allergens to the cells of the immune system. In addition, vegetation reacts with air pollution and environmental conditions and influence the plant allergenicity. Several factors influence this interaction, including type of air pollutants, plant species, nutrient balance, climatic factors, degree of airway sensitization and hyperresponsiveness of exposed subjects.