Elsevier

The Lancet

Volume 383, Issue 9928, 3–9 May 2014, Pages 1581-1592
The Lancet

Series
Outdoor air pollution and asthma

https://doi.org/10.1016/S0140-6736(14)60617-6Get rights and content

Summary

Traffic and power generation are the main sources of urban air pollution. The idea that outdoor air pollution can cause exacerbations of pre-existing asthma is supported by an evidence base that has been accumulating for several decades, with several studies suggesting a contribution to new-onset asthma as well. In this Series paper, we discuss the effects of particulate matter (PM), gaseous pollutants (ozone, nitrogen dioxide, and sulphur dioxide), and mixed traffic-related air pollution. We focus on clinical studies, both epidemiological and experimental, published in the previous 5 years. From a mechanistic perspective, air pollutants probably cause oxidative injury to the airways, leading to inflammation, remodelling, and increased risk of sensitisation. Although several pollutants have been linked to new-onset asthma, the strength of the evidence is variable. We also discuss clinical implications, policy issues, and research gaps relevant to air pollution and asthma.

Introduction

Outdoor air pollution contributed more than 3% of the annual disability-adjusted life years lost in the 2010 Global Burden of Disease comparative risk assessment, a notable increase since the previous estimate was made in 2000.1 Previous assessments of global disease burden attributed to air pollution were restricted to urban areas or by coarse spatial resolution of concentration estimates.2 In a study of ten European cities, 14% of the cases of incident asthma in children and 15% of all exacerbations of childhood asthma were attributed to exposure to pollutants related to road traffic.3 Urbanisation is an important contributor to asthma and this contribution might be partly attributed to increased outdoor air pollution (figure 1).4, 5, 6 Because many urban centres in the developing world are undergoing rapid population growth accompanied by increased outdoor air pollution, the global burden of asthma is likely to increase. In this context, it is notable that the populations of China, India, and Southeast Asia are equal to the rest of the world combined.

In view of the burden of asthma attributed to outdoor air pollution, a better understanding of why asthmatic individuals are susceptible to this exposure should enable the design of effective preventive strategies. The idea that air pollution can cause exacerbations of pre-existing asthma is supported by an evidence base that has been accumulating for several decades,7, 8, 9, 10 but evidence has emerged that suggests air pollution might cause new-onset asthma as well.11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21 Not all studies support a causal link between air pollution and asthma, and a recent meta-analysis22 of cross-sectional studies that compared communities with different levels of pollution showed no effect of long-term exposure to pollution on asthma prevalence. Although outdoor air pollution almost always occurs as a mixture, air quality is regulated by most jurisdictions in terms of its individual components. Such regulation has meant that experimental studies of humans and animals have been focused on individual pollutants. Because epidemiological studies inherently involve exposure to mixtures of pollutants, substantial efforts are usually made to try to identify the individual effects of pollutants, which often obscures the health effect of the mixture as a whole.

With increasing attention to traffic-related air pollution (TRAP) as the exposure variable of interest, a shift has occurred away from a focus on individual components of the pollution mixture. In this Series paper, we will attempt to discuss the effects of several gaseous pollutants (ozone, nitrogen dioxide, and sulphur dioxide), the independent effects of various forms of PM, and then focus on the effects of TRAP as a mixture. We concentrate on studies published in the past 5 years that report results relevant to both exacerbation and onset of asthma.

We focus primarily, although not exclusively, on epidemiological and experimental clinical studies. Controlled exposure studies in human beings are restricted by small sample size and an inability to study the potentially most susceptible subgroups (eg, children and adults with severe asthma) and the effects of chronic exposure. Epidemiological studies are restricted by imprecise methods of both exposure and asthma outcome assessment and often inadequate data about potentially confounding variables.

Although the potential effect of indoor air pollution on asthma is an important concern, especially in developing countries where much domestic cooking is done with solid fuels, it is outside the scope of this review.

Section snippets

Mechanisms

Why are individuals with asthma so affected by exposure to air pollution? At high concentrations, such as those noted in megacities in India and China, air pollutants might have direct irritant and inflammatory effects on airway neuroreceptors and epithelium, but such levels of exposure rarely occur in North America or Europe. At the lower concentrations that are more typical in high-income countries, other mechanisms are probably in operation. Specific pollutants can induce airway inflammation

Particulate matter

Ambient PM is a ubiquitous atmospheric aerosol with both anthropogenic and natural sources that has been associated with various health effects.50 PM is categorised on the basis of its aerodynamic diameter, with implications for its typical site of deposition when inhaled (figure 3). Coarse PM, with an aerodynamic diameter of 2·5–10 μm, deposits mainly in the head and large conducting airways. Fine PM or PM2·5 deposits throughout the respiratory tract, particularly in small airways and alveoli.

Gases

In view of the central role of oxidative stress in asthma morbidity associated with air pollutants, oxidising gases continue to be an area of substantial research. Ground-level ozone is formed by photochemical reactions between sunlight and pollutant precursors, such as nitrogen oxides and volatile organic compounds, especially in warm conditions and peaks in summer temperatures.66 Nitrogen oxides, including nitrogen dioxide, are formed primarily by the reaction of ozone with nitric oxide

TRAP

TRAP is a complex mixture of PM derived from combustion (including elemental or black carbon) and non-combustion sources (eg, road dust, tyre wear, and brake wear) and primary gaseous emissions including nitrogen oxides. These primary emissions lead to the generation of secondary pollutants such as ozone, nitrates, and organic aerosol. Intense experimental and epidemiological research has greatly advanced our understanding of the role of TRAP in asthma and disease mechanisms underlying this

Risk modifiers

Young children with asthma have long been regarded as a group who are very susceptible to adverse effects from air pollution because of their developing lungs, immature metabolic pathways, high ventilation rates per bodyweight, and increased time exercising outdoors.99, 100 Even exposures in utero might affect postnatal risk of asthma and asthma exacerbations.100, 101 Low birthweight, which might be associated with narrow airways during early childhood, is a risk factor for symptoms of asthma

Clinical implications

One strategy to reduce exacerbations of asthma related to air pollution is for local governments to issue smog alerts on days when ozone or PM2·5 levels are forecast to be high (table 2). Individuals with asthma and other pre-existing cardiopulmonary disorders are urged to stay indoors on such days. Clinicians should encourage patients with asthma (and advise parents of children with asthma), to avoid unnecessary outdoor activity, especially if it entails vigorous exercise that increases minute

Policy issues

Motor vehicle emissions and power plants are the main sources of both primary pollutants (eg, nitrogen oxides, fine PM, and ultrafine PM) and secondary pollutants (eg, ozone, nitrates, sulphates, and organic aerosol) in developed countries. Although improved pollution controls have reduced emissions of pollutants, growing evidence of adverse health effects at levels less than present US, Canadian, and European Union standards suggests that cleaner vehicles and energy production that do not rely

Research gaps

Although much research on air pollution and asthma has been done in the past 5 years, major gaps in our knowledge remain. Perhaps the most critical gap is in our understanding of the mechanisms by which exposure to air pollutants contributes to the onset of asthma, especially in non-atopic children and adults. Gene–environment interaction is an obvious focus of future research. The biological basis for the interactive effects of air pollution and psychological stress is another especially

Conclusions

A substantial body of research on the effects of air pollution on asthma has been published in the past 5 years, adding to the body of knowledge that has accumulated over several decades. Presently, short-term exposures to ozone, nitrogen dioxide, sulphur dioxide, PM2·5, and TRAP is thought to increase the risk of exacerbations of asthma symptoms. Increasing amounts of evidence also suggest that long-term exposures to air pollution, especially TRAP and its surrogate, nitrogen dioxide, can

Search strategy and selection criteria

We searched Pubmed from Jan 1, 2009, to Feb 28, 2014, with the search terms “Asthma” and any of the following specific terms: “Air Pollution”, “Particulate Matter”, “PM2·5”, “PM10”, “Ozone”, “O3”, “Sulfur Dioxide”, “Sulfur Oxides”, “SO2”, “SOx”, “Nitrogen Dioxide”, “Nitrogen Oxides”, “NO2”, “NOx”, “Traffic”, “Diesel”, “Elemental Carbon”, or “Black Carbon”. We searched the reference lists of recent reports and review articles produced with this search strategy to include relevant

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