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Traffic-generated pollution contains particles and gases (eg, oxides of nitrogen) that are known to have health effects.1 Concentrations of pollutants emitted by motor vehicles are highest within 150 m of roadways and remain raised up to 300 m from roadways, but fall off markedly beyond that range.2 3 Exposure to the mixture of traffic-generated pollutants may be more relevant to human health than exposure to any single ambient air pollutant, making epidemiological investigations of traffic effects a key component of research into the public health impact of air pollution. However, assessment of exposure to traffic-related air pollution can be problematic. Exposure to traffic can be estimated with complex dispersion models of pollutants from local freeway and non-freeway sources, but the data inputs required for such modelling are not always available. A frequently used simpler approach has been to estimate residential distance to roadways.
A number of studies have found an increased prevalence of asthma or asthma symptoms in children who live near roadways with high traffic counts.4–8 One large British study that focused on traffic within 150 m of children’s homes found a gradient in risk that increased markedly with decreasing residential distance to a main road.7 A large study in southern California showed an increased prevalence of asthma and wheeze in children living within 75 m of a major roadway.9 Another study by Jerrett et al that analysed data from the same southern California cohort was able to demonstrate an association between the incidence of asthma and exposure to traffic-related pollution.10 A recent review summarised the evidence for traffic pollution as a risk factor for both asthma exacerbation and onset as strong.11
In contrast to the relatively rich literature for children, little has been published on the effects of traffic-related pollution on asthma in adults. Although several previous studies in adults with asthma have found that exposure to traffic—as measured by distance of residence from nearest major roadway—was associated with asthma symptoms, health care utilisation or decreased lung function,12–14 the study by Künzli and colleagues15 reported in this issue of Thorax is the first to show convincing evidence that exposure to traffic-related particulate matter increases the risk of adult-onset asthma (see page 664). When the paper by Künzli et al is taken together with the study by Jerrett et al,10 we now have evidence in both children and adults that traffic-related pollution can cause as well as exacerbate asthma.
Given the robust effects observed on asthma outcomes in other studies of both children and adults, it is somewhat surprising that distance to roadway was not associated with the risk of new-onset asthma in over 2700 non-smoking Swiss adults in the analysis by Künzli et al.15 The authors speculate that they did not find an effect of distance to roadway because their study design was longitudinal, and this variable did not change over time for most subjects. Moreover, they contend that the modelled traffic-related particulate matter exposures which they assigned to their subjects captured the spatial and temporal heterogeneity of individual exposures better than can be achieved with distance to roadway metrics. They suggest that this greater heterogeneity of exposure allowed their analysis to achieve statistical significance despite the relatively small number of new cases of asthma in the SAPALDIA cohort. Similar reasoning can be applied to the study by Jerrett et al which captured spatial heterogeneity in traffic exposures by using nitrogen dioxide concentrations measured immediately outside the children’s homes as a proxy for the traffic-related pollution mixture.10
Perhaps the greatest research challenge regarding the impact of traffic-related pollution on asthma is to determine what specific constituents of the mixture are responsible for the observed effects. While diesel exhaust particles have clearly been shown to induce both cytotoxic and immune adjuvant responses in toxicological studies16 as well as acute lung function decrements in subjects with asthma,17 it has been difficult to distinguish diesel effects from those of other components of the traffic mixture in epidemiological studies, largely due to an inability to assess exposure properly. Until we develop better exposure assessment methods, we will be unable to meet this challenge. Without good data about the causative agents in the traffic pollution mixture, our ability to control exposures to protect the health of people with asthma will continue to be handicapped.
Competing interests: None.
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