Over the past decades, a substantial increase in the prevalence and incidence of allergic respiratory disease and bronchial asthma has been observed. Epidemiological studies suggest that allergic respiratory diseases are still on the rise, especially in developing countries where the prevalence was previously low.
As a result of rapid urbanization and industrialization in developing areas, increased levels of vehicle emissions and chemical pollutants have been identified as major extrinsic agents that are correlated to the increase in the frequency of allergic respiratory diseases.
Generally, motor vehicles produce a complex mixture of air pollutants including carbon monoxide, nitrogen oxides, particulate matter of varying size, polycyclic aromatic hydrocarbons (e.g., benzopyrene), volatile organic compounds (e.g., benzene), and diesel exhaust particles, which are collectively referred to as traffic-related air pollutants. In North America, up to 45% of the population in cities reside in zones that are most impacted by traffic-related air pollutants, and over 30% of schools are located in the areas highly exposure to traffic-related air pollutants.
Recently, several systematic reviews conclude that there is sufficient evidence to suggest that traffic-related air pollutants can decrease lung function and trigger asthma exacerbation and hospitalizations. For example, a study of a cohort of 11,365 schoolchildren in 16 communities in Southern California indicated that exposure to higher nitrogen dioxide (NO2) concentrations and close residential proximity to a freeway increased asthma prevalence. A study of 5443 Korean children aged 6–14 years also found that children living within 200m of a main road had increased lifetime wheezing, asthma diagnosis, and decreased lung function. Several studies conducted in European countries reported that exposure to higher NO2 increased the incidence of adult-onset asthma.
Scientific studies further suggest that early-life exposure to traffic-related air pollutants is associated with increased risk for transient and persistent wheezing, but only long-term exposure to high levels of traffic-related air pollutants is associated with asthma development. Sustained exposure to high level of traffic-related air pollutants from birth through school age is significantly associated with both transient and persistent asthma and wheezing. Prenatal exposure to traffic-related air pollutants is also associated with an increased risk of asthma and early childhood wheeze.
Apart from asthma and wheezing, exposure to traffic-related air pollutants is also associated with an increase in the prevalence of allergic sensitization, defined as a positive skin prick test to an aeroallergen or food, and eczema. A study of 4907 children aged 9–11 years showed that lifetime eczema was significantly associated with 3-year averaged concentrations of particulate matter (PM10), NO2, and carbon monoxide (CO). A Taiwanese study of 317,926 middle school students demonstrated that flexural eczema was associated with levels of CO and NOX. The study in Southern California suggested that children living less than 75m from the main road were significantly more likely to have lifetime diagnoses and symptoms of allergic rhinitis. The distance to the main road, and the length and proportion of the main road within 200m of the home, were all associated with allergic sensitization.
These findings suggest that there is an urgent need to develop policies so that, in the next few years, the emission of NO2 and other highly pollution gases can be drastically reduced. On the other hand, the impact of traffic-related air pollutants exposure on allergic disease is complicated by the presence of additional host (genetic, obesity, comorbidities, and nutritional status) and environmental factors. To avoid exposure to traffic-related air pollutants is particularly important for individuals with comorbidity of allergic respiratory disease and other chronic conditions.