Respiratory disease in adults and children
Chronic respiratory disease in children
Children are more active and engage in more outdoor activities than adults. They breathe more rapidly and their metabolic rate is higher. Children’s immune systems are not fully developed, so the incidence of respiratory infections is high. Their lungs are still growing and any deficit in growth will have an impact for the whole of the child’s life. Moreover, possible confounding or modifying factors, such as active smoking, occupational exposure to dust and smoke or medical treatment, are largely absent, making the interpretation of epidemiological results more straightforward. Investigations into the development of lung function in children and the incidence of asthma – the most important chronic disease in children – are particularly relevant and interesting.
As early as the 1980s, several cross-sectional studies from Germany, Switzerland, France and the USA showed that school-age or pre-school children in communities exposed to higher levels of dust, sulfur dioxide (SO2) and NO2 suffered more from cough and acute bronchitis than children in less polluted regions. This phenomenon has been confirmed in recent studies.
Lung function (spirometry)
More recently, many cross-sectional studies have reported lower lung volumes in children living in more polluted areas. Of outstanding importance is the largest and most detailed long-term study ever conducted on air pollution and lung development in children, namely the University of Southern California (USC) Children’s Health Study from the greater Los Angeles area. Several cohorts recruited during elementary or middle school and followed into adulthood confirm that ambient air pollution jeopardises the development of children’s lungs, resulting in lower lung volumes and maximum expiratory flows at 18 years of age.
While exacerbations of asthma clearly correlate with air quality, geographical comparisons of the prevalence of asthma or allergies do not follow differences in urban background levels of pollutants, such as PM2.5 or PM10. Novel approaches now integrate local measurements of traffic-related pollutants, geographic information systems, information about land use and spatial modelling techniques to characterise the local distribution of traffic-related pollutants within communities. People living alongside busy roads experience several-fold higher exposures to traffic-related primary pollutants than people living some 50–100 m further away. Epidemiological studies investigating the prevalence of childhood asthma as a function of proximity to traffic strongly suggest that living close to a busy road increases the risk of developing asthma in childhood, even with confounding factors taken into account. Despite rather different urban structures, traffic patterns and car fleets, this finding has now been confirmed in seminal cohort studies both in the USA (e.g. the USC Children’s Health Study) and Europe. Most importantly, a European birth cohort, with children followed up to 8 years of age, has confirmed a higher incidence of asthma related to ambient air pollution. The results of the USC study are strongly suggestive that there is an interaction between genetic factors and exposure to traffic-related pollutants.
The contrasting lack of association between asthma onset and urban background pollution, and the strong associations between proximity to traffic arteries and asthma incidence – controlling for socioeconomic differences – suggests that those pollutants occurring at very high concentrations along street corridors (e.g. ultrafine particles, black carbon, particle-bound metals) play a key role in the genesis of asthma. Indeed, several recent reviews have concluded that near-road traffic-related air pollutants are causally related to the development of asthma in childhood. Urban planning decisions may therefore have major public health implications. The results place diesel cars, trucks and buses that emit particularly high concentrations of soot and large numbers of very toxic substances loaded on particles from exhaust, abrasion, and suspension, at the centre of the policy debate. While some believe that the impact of traffic-related air pollution on asthma prevalence is small, several health impact assessment studies have now confirmed that the public health burden of living close to a busy road is substantial. This is particularly the case in Europe, where a large proportion of urban citizens live along heavily trafficked street canyons.
Chronic respiratory disease in adults
The most important risk factor for chronic respiratory diseases in adults is smoking, and the health effects of smoking and ambient air pollution have much in common. Studies evaluating the impact of outdoor air pollution on diseases such as COPD and asthma in adults need to take into account the inter-correlation of these factors, in addition to individual traits such as age, sex and genetic factors. Results based on people who have never smoked are particularly valuable.
Chronic cough and phlegm have been associated with long-term ambient PM exposure in several repeated cross-sectional studies in the USA and Europe. The Swiss study on Air Pollution and Lung Disease in Adults (SAPALDIA) confirmed that the prevalence of chronic symptoms declined as individually assigned home outdoor air quality improved. Some studies have shown that respiratory symptoms are more prevalent among participants living close to main streets, independently of background pollutant concentrations. As mentioned in the introduction to this chapter, air pollution is a complex mixture of constituents and such findings may indicate the independent role of some pollutants (or clusters of pollutants) in causing the same or similar health responses. Figure 2 shows the distribution of the prevalence of cough and wheeze among Swiss adults as a function of their residential distance from the highway. This cross-Alpine transit route is the dominant source of primary traffic-related pollutants in this rural valley. In contrast to more homogenously distributed fine particles, the distributions of traffic-related primary pollutants – such as ultrafine particles, diesel soot, CO, NO or metal-rich resuspended particles – follow the very same spatial patterns.
Lung function and COPD
Many studies (mostly cross-sectional, i.e. at a single time-point) have reported associations between lung function and air pollution, and there is a degree of inconsistency in the results, possibly for methodological reasons. Most importantly, reduction in exposure to pollutants has been shown to reduce age-related decline in lung function – a highly relevant finding observed in the SAPALDIA study where exposure to ambient air pollution was estimated at the individual level, taking full account of changes in residence during the 11-year follow-up. While a few studies support the notion that air pollution may also contribute to the development of COPD, further investigations are needed. Major difficulties with this assessment relate to more general challenges and uncertainties in COPD research. While air pollution is clearly associated with impaired development of lung function in children (as discussed previously), the way in which poor lung function in early life relates to later development of COPD is not clearly defined or understood. Moreover, air pollution triggers respiratory symptoms and enhances infections, but it is not known how these findings relate to the development of COPD, though cohort studies confirm that people with chronic symptoms and repeated infections are at higher risk of developing COPD. Last but not least, it is not well established whether COPD in nonsmokers and smokers can be considered as the same phenotype of disease.
Adult asthma incidence
As in children, asthma in adults is not correlated with urban background levels of pollution such as PM2.5. However, the few studies investigating the contribution of local traffic-related air pollution to asthma onset in adults have produced similar findings to those looking at childhood asthma incidence. More research is needed to clarify these results and the interaction with atopy, genetics and other host factors.