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.
Rapid urbanization and industrialization in developing areas have resulted in increased vehicle emissions and chemical pollutants, which have been identified as major extrinsic agents correlated to an 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 most impacted by traffic-related air pollutants, and over 30% of schools are located in areas with high exposure to traffic-related air pollutants.
Recently, several systematic reviews concluded 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 an increased risk for transient and persistent wheezing. Still, only long-term exposure to high levels of traffic-related air pollutants is associated with asthma development. Sustained exposure to high levels of traffic-related air pollutants from birth through school age is significantly associated with 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 wheezing.
Apart from asthma and wheezing, exposure to traffic-related air pollutants is also associated with increased 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 an urgent need to develop policies so that the emission of NO2 and other highly pollution gases can be drastically reduced in the next few years. On the other hand, the impact of traffic-related air pollutant exposure on allergic disease is complicated by the presence of additional host (genetic, obesity, comorbidities, and nutritional status) and environmental factors. Avoiding exposure to traffic-related air pollutants is particularly important for individuals with comorbidity of allergic respiratory disease and other chronic conditions.
