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 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.     

Diesel fumes and the rising prevalence of atopy: An urban legend?

Recently, the incidence of allergic diseases has increased in most industrialized countries of the world. Persistent exposure to particulate air pollution from motor vehicles has been implicated as one of the factors that is responsible for the observed increased prevalence of atopy. Epidemiologic studies conducted in different parts of the world have demonstrated an important association between ambient levels of motor vehicle traffic emissions and increased symptoms of asthma and rhinitis. Additionally, recent human and animal laboratory-based studies have shown that particulate toxic pollutants, and in particular diesel exhaust particles (DEP), can enhance allergic inflammation and induce the development of allergic immune responses. In this article, our current understanding of the mechanisms by which pollutants such as DEPs enhance the underlying allergic inflammatory response is reviewed, and the evidence that supports the causative link between particulate air pollution from motor vehicles and increasing allergic diseases is discussed.     

Air pollution and chronic airway diseases: what should people know and do?

The health effects of air pollution remain a public health concern worldwide. Exposure to air pollution has many substantial adverse effects on human health. Globally, seven million deaths were attributable to the joint effects of household and ambient air pollution. Subjects with chronic respiratory diseases such as chronic obstructive pulmonary disease (COPD) and asthma are especially vulnerable to the detrimental effects of air pollutants. Air pollution can induce the acute exacerbation of COPD and onset of asthma, increase the respiratory morbidity and mortality. The health effects of air pollution depend on the components and sources of pollutants, which varied with countries, seasons, and times. Combustion of solid fuels is a major source of air pollutants in developing countries. To reduce the detrimental effects of air pollution, people especially those with COPD or asthma should be aware of the air quality and take extra measures such as reducing the time outdoor and wearing masks when necessary. For reducing the air pollutants indoor, people should use clean fuels and improve the stoves so as to burn fuel more efficiently and vent emissions to the outside. Air cleaners that can improve the air quality efficiently are recommended.     

Does outdoor air pollution induce new cases of asthma? Biological plausibility and evidence; a review

It is widely accepted that air pollution can exacerbate asthma in those who already have the condition. What is less clear is whether air pollution can contribute to the initiation of new cases of asthma. Mechanistic evidence from toxicological studies, together with recent information on genes that predispose towards the development of asthma, suggests that this is biologically plausible, particularly in the light of the current understanding of asthma as a complex disease with a variety of phenotypes. The epidemiological evidence for associations between ambient levels of air pollutants and asthma prevalence at a whole community level is unconvincing; meta-analysis confirms a lack of association. In contrast, a meta-analysis of cohort studies found an association between asthma incidence and within-community variations in air pollution (largely traffic dominated). Similarly, a systematic review suggests an association of asthma prevalence with exposure to traffic, although only in those living very close to heavily trafficked roads carrying a lot of trucks. Based on this evidence, the U.K.'s Committee on the Medical Effects of Air Pollutants recently concluded that, overall, the evidence is consistent with the possibility that outdoor air pollution might play a role in causing asthma in susceptible individuals living very close to busy roads carrying a lot of truck traffic. Nonetheless, the effect on public health is unlikely to be large: air pollutants are likely to make only a small contribution, compared with other factors, in the development of asthma, and in only a small proportion of the population.     

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.     

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.     

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.     

Pollution de l’air et asthme de l’enfant

The prevalence of asthma and allergic diseases doubled during the last quarter of the 20th century, particularly among children and adolescents. Given this fact, we cannot attribute this increase exclusively to genetic factors. Environmental factors to which it has been attributed include exposure to allergens and to airborne physicochemical pollutants, and changes in the characteristics of respiratory infections in young infants. In this review, we will point out the role of exposure to air pollutants and their interaction with other environmental factors. Whereas concentrations of the ‘classical’ air quality indicators (SO₂, CO) have more or less decreased steadily in developed countries, asthma prevalence has increased during the same period. However, the relation between the increase incidence of asthma and atmospheric pollution should be examined with the knwoledge that there has been an increase in new forms of pollution, in particular, ultrafine particles. There are at present many experimental studies which show that urban pollution (especially that associated with diesel exhaust particles) elicits chronic oxidative stress, bronchial hyperreactivity and allergic inflammation. Several epidemiological studies suggest that there is an association between the density of automobile traffic and the prevalence of respiratory symptoms, especially asthma and allergic rhinitis. Exposure to automobile traffic-related pollutants during early infancy may accelerate or even provoke, among genetically susceptible subjects, bronchial inflammatory processes which could contribute to the increase in the incidence of asthma in industrialized countries.     

Chronic effects of air pollution on respiratory health in Southern California children: findings from the Southern California Children’s Health Study

Outdoor air pollution is one of the leading contributors to adverse respiratory health outcomes in urban areas around the world. Children are highly sensitive to the adverse effects of air pollution due to their rapidly growing lungs, incomplete immune and metabolic functions, patterns of ventilation and high levels of outdoor activity. The Children’s Health Study (CHS) is a continuing series of longitudinal studies that first began in 1993 and has focused on demonstrating the chronic impacts of air pollution on respiratory illnesses from early childhood through adolescence. A large body of evidence from the CHS has documented that exposures to both regional ambient air and traffic-related pollutants are associated with increased asthma prevalence, new-onset asthma, risk of bronchitis and wheezing, deficits of lung function growth, and airway inflammation. These associations may be modulated by key genes involved in oxidative-nitrosative stress pathways via gene-environment interactions. Despite successful efforts to reduce pollution over the past 40 years, air pollution at the current levels still brings many challenges to public health. To further ameliorate adverse health effects attributable to air pollution, many more toxic pollutants may require regulation and control of motor vehicle emissions and other combustion sources may need to be strengthened. Individual interventions based on personal susceptibility may be needed to protect children’s health while control measures are being implemented.     

Contribution of air pollution to COPD and small airway dysfunction

Although in many Western countries levels of ambient air pollution have been improving with the setting of upper limits and better urban planning, air pollution in developing countries and particularly those with rapid industrialization has become a major global problem. Together with increased motor vehicle ownership and traffic congestion, there is a growing issue with airborne particles of respirable size. These particles are thought responsible for respiratory and cardiovascular effects and have also been implicated in cancer pathogenesis. The pathologic effects in the lung are mediated via inflammatory pathways and involve oxidative stress similar to cigarette smoking. These effects are seen in the peripheral airways where the smaller particle fractions are deposited and lead to airway remodelling. However, emphysema and loss of bronchioles seen with cigarette smoking have not been described with ambient air pollution, and there are few studies specifically looking at peripheral airway function. Definitive evidence of air pollution causing COPD is lacking and a different study design is required to link air pollution and COPD.     

Ultrafine particles in urban air and respiratory health among adult asthmatics.

Airborne particles are associated with adverse health effects and contribute to excess mortality in epidemiological studies. A recent hypothesis proposes that the high numbers of ultrafine (<0.1 microm diameter) particles in ambient air might provoke alveolar inflammation and subsequently cause exacerbations in pre-existing cardiopulmonary diseases. To test the hypothesis adult asthmatics were followed with daily peak expiratory flow (PEF) measurements and symptom and medication diaries for six months, while simultaneously monitoring particulate pollution in ambient air. The associations between daily health endpoints of 57 asthmatics and indicators of air pollution were examined by multivariate regression models. Daily mean number concentration of particles, but not particle mass (PM10 (particle mass <10 microm), PM2.5-10, PM2.5, PM1), was negatively associated with daily PEF deviations. The strongest effects were seen for particles in the ultrafine range. However, the effect of ultrafine particles could not definitely be separated from other traffic generated pollutants, namely nitric oxide, nitrogen dioxide and carbon monoxide. No associations were observed with respiratory symptoms or medication use. Particle mass measurements can be strongly influenced by mechanically produced, soil-derived particles, which may not be associated with adverse health effects. Therefore, air quality monitoring should include particle number concentrations, which mainly reflect ultrafine particles.     

Environmental cardiology: studying mechanistic links between pollution and heart disease

Environmental factors are considered key determinants of cardiovascular disease. Although lifestyle choices such as smoking, diet, and exercise are viewed as major environmental influences, the contribution of pollutants and environmental chemicals is less clear. Accumulating evidence suggests that exposure to pollutants and chemicals could elevate the risk of cardiovascular disease. Many epidemiological studies report that exposure to fine particles present in ambient air is associated with an increase in cardiovascular mortality. Statistically significant relationships between particulate air pollution and ischemic heart disease, arrhythmias, and heart failure have been reported. Animal studies show that exposure to ambient air particles increases peripheral thrombosis and atherosclerotic lesion formation. Exposures to arsenic, lead, cadmium, pollutant gases, solvents, and pesticides have also been linked to increased incidence of cardiovascular disease. Mechanistically, these effects have been attributed to changes in the synthesis or reactivity of nitric oxide that may be caused by environmental oxidants or increased endogenous production of reactive oxygen species. Additional studies are urgently needed to: identify the contribution of individual pollutants to specific aspects of cardiovascular disease; establish causality; elucidate the underlying physiological and molecular mechanisms; estimate the relative susceptibility of diseased and healthy individuals and that of specific population groups; and determine whether pollutant exposure are risk correlates, that is, whether they influence major risk factors, such as hypertension, cholesterol, or diabetes, or whether they contribute to the absolute risk of heart disease. Collectively, these investigations could contribute to the emergent field of environmental cardiology.     

Urban asthma

PURPOSE OF REVIEW: To review the possible reasons why the prevalence and morbidity of asthma are greater in those living in an urban setting. RECENT FINDINGS: Urban asthma is associated with exposure to air pollution, urban allergens, and violence. Outdoor air pollution is a particular problem in urban areas and affects children more than adults. Asthma has been shown to be exacerbated by ozone, respirable particulates, and nitrogen dioxide. Exposure to high point sources of pollutants such as heavy traffic is of particular concern. Urban allergens include cockroach, mouse, and rat. Cockroach exposure increases the risk of asthma exacerbations and may increase the risk of developing asthma. Although mouse allergen is also found in suburban homes, the concentration is a log-fold higher in inner-city homes at levels known to elicit symptoms in workers in animal facilities. Rat allergen is found in a third of inner-city homes and is associated with asthma morbidity. A recent interventional study showed that comprehensive environmental control of cockroach allergen reduced asthma morbidity. Finally, stress elicits asthma symptoms and exposure to violence is associated with greater asthma morbidity. SUMMARY: The increase in prevalence and morbidity of asthma associated with urban living is associated with at least three plausible causative factors each of which is amenable to intervention, raising the issue of environmental justice issues: controlling air pollution in general and exposure to point sources in particular; reducing cockroach, mice, and rat infestations; and preventing violence.     

Outdoor air pollution and emergency room visits at a hospital in Delhi

Several reports from large metropolitan cities have indicated significant association between acute morbidity and mortality from cardio-respiratory disorders and daily levels of major pollutants in the ambient air. Despite the wide-spread public concern about the adverse health effects of air pollution, there is substantial uncertainty regarding the effects of these pollutants at a concentration typical of Delhi, which is one of the ten most polluted cities in the world and the most polluted city in India. This study was undertaken to correlate the daily levels of various pollutants with the number of patients visiting the All India Institute of Medical Sciences (AIIMS, New Delhi) casualty for aggravation of certain defined cardiorespiratory disorders. Daily counts of patients visiting the emergency room of the AIIMS for acute asthma, acute exacerbation of chronic obstructive airway disease (COAD) and acute coronary event was obtained in prospective manner from January 1997 to December 1998. Daily mean levels of ambient CO, NOx and SO2 were monitored along with temperature and humidity. Data was analysed using one day time lag for events of interest. Time series analysis was undertaken using Poisson regression and population averaged general estimation equation, correcting for auto-correlation, days of the weak and season. The ambient levels of pollutants exceeded the national air quality standards on most of the days, over the two year period. Further, emergency room visits for asthma, COAD and acute coronary events increased by 21.30%, 24.90% and 24.30% respectively on account of higher than acceptable levels of pollutants. It is concluded that there is considerable burden of cardiorespiratory diseases in Delhi due to high levels of ambient air pollution.     

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.     

Recent evidence for adverse effects of residential proximity to traffic sources on asthma

PURPOSE OF REVIEW: A growing body of evidence indicates that residential proximity to traffic sources increases the risk for asthma and asthma exacerbations. In this review we have considered publications from 2006-2007 that examined the impact of residential traffic-related exposures on asthma occurrence and severity. RECENT FINDINGS: In these studies, exposures were estimated using traffic metrics based on residential distances from major roads and freeways, traffic densities around homes, and models of traffic exposure. Overall, residential proximity to traffic sources was associated with increased asthma occurrence and exacerbations in both children and adults. Land-use regression models were superior to individual traffic metrics in explaining the variability of traffic-related pollutants. Susceptibility may also play a role in variation in the effects of traffic on asthma. SUMMARY: There is consistent evidence that living near traffic sources is associated with asthma occurrence and exacerbations. Future studies have the opportunity to improve exposure estimates by measuring traffic-related pollutants near homes and schools and including time/activity patterns in prediction models. Further research is also warranted to investigate the differential impact of traffic by genetic and other susceptibility factors and to identify specific pollutants that underlie the adverse effect of traffic on asthma.     

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.     

Outdoor air pollution: particulate matter health effects

Numerous investigations studying multiple populations across a variety of environmental settings have demonstrated a strong association between ambient air particulate matter and cardiopulmonary morbidity and mortality. In most studies, the effect size of ambient air particulate pollution on health outcomes is small. However, the exposed population worldwide is very large. Accordingly, particulate air pollution appears to be an important public health hazard that makes an important contribution to the total burden of disease and death in populations across the world. Much of the evidence linking ambient air particulates with adverse health effects is derived from population-based, observational research with potential unidentified confounding exposures, precluding definitive assessments about causation and providing limited mechanistic insights. A growing body of research suggests particulate-associated adverse health effects result from the induction of proinflammatory responses in the lower respiratory tract. Ambient air particulates may increase lung cancer risk.     

Health effects of diesel exhaust emissions.

Epidemiological studies have demonstrated an association between different levels of air pollution and various health outcomes including mortality, exacerbation of asthma, chronic bronchitis, respiratory tract infections, ischaemic heart disease and stroke. Of the motor vehicle generated air pollutants, diesel exhaust particles account for a highly significant percentage of the particles emitted in many towns and cities. This review is therefore focused on the health effects of diesel exhaust, and especially the particular matter components. Acute effects of diesel exhaust exposure include irritation of the nose and eyes, lung function changes, respiratory changes, headache, fatigue and nausea. Chronic exposures are associated with cough, sputum production and lung function decrements. In addition to symptoms, exposure studies in healthy humans have documented a number of profound inflammatory changes in the airways, notably, before changes in pulmonary function can be detected. It is likely that such effects may be even more detrimental in asthmatics and other subjects with compromised pulmonary function. There are also observations supporting the hypothesis that diesel exhaust is one important factor contributing to the allergy pandemic. For example, in many experimental systems, diesel exhaust particles can be shown to act as adjuvants to allergen and hence increase the sensitization response. Much of the research on adverse effects of diesel exhaust, both in vivo and in vitro, has however been conducted in animals. Questions remain concerning the relevance of exposure levels and whether findings in such models can be extrapolated into humans. It is therefore imperative to further assess acute and chronic effects of diesel exhaust in mechanistic studies with careful consideration of exposure levels. Whenever possible and ethically justified, studies should be carried out in humans.