Figure 1. Average concentrations of air pollutants measured in air quality stations across the EU in 2022 according to urbanization level
Traffic stations: located close to a single major road; industrial stations: located close to an industrial area/source; background stations: located where pollution levels are representative of the average exposure of the general population or vegetation. Urban areas: continuously built-up urban areas; suburban areas: largely built-up urban areas; rural areas: all other areas. European air quality information is reported by EEA member countries, including all EU Member States, as well as EEA cooperating and other reporting countries. Data retrieved from Air Quality e-Reporting database (https://www.eea.europa.eu/data-and-maps/data/aqereporting-9).

Traffic-related air pollution and childhood asthma

In December 2020 a court in the United Kingdom made history by ruling acute respiratory failure, severe asthma, and exposure to pollution as one of the causes of the death of a 9-year-old child. The verdict confirmed the need for legislation and proper implementation: it was the illegal levels of air pollution listed amongst failures to reduce levels of NO2 which possibly contributed to her death. Ella Kissi-Debrah’s lived near a busy road in London with her mother and has become the first person in the UK – and potentially the world – for whom air pollution has been listed as a cause of death [22].
The health costs of air pollution are clear: in 2019 about one in 12 new child asthma cases worldwide may be attributable to NO2 pollution [23]. Although these figures have been even worst in the past, with a global decline in the last decade of the NO2-attributable fraction of pediatric asthma incidence from 19.8% in 2000 to 16.0% in 2019, the regional trends remain heterogenous with urban average attributable fractions declining in high-income countries, Latin America and the Caribbean, central and eastern Europe, central, southeast, and east Asia, and Oceania, and escalating in south Asia, sub-Saharan Africa, and North Africa and the Middle East [23].
Vehicle emissions usually mean TRAP, which contains a combination of vehicle exhausts, secondary pollutants, and non-combustion emissions such as road dust (Figure 2 ). Since the difficulty in measuring all the components of TRAP, pollutant surrogates such as measured or modelled concentrations of PM2.5 and PM10 and gases such as NO2, nitric oxide (NO), NOX and ozone (O3), and direct measures of traffic, including proximity/distance of the residence to the main road and traffic volume within the buffer are used. Diesel exhaust particles (DEPs) are generated through the combustion of diesel fuel by vehicles or diesel-powered equipment. Exposure occurs in both environmental and occupational settings and is of particular concern as air quality and engine exhaust control policies are still to produce significant changes in TRAP levels [24]. DEP consists of a carbon nanoparticle core with a complex mixture of metals and organic chemicals that are adsorbed onto their surface and responsible for most of the deleterious effects.
The impact of prenatal exposures to NO2, SO2, and PM10 on subsequent risk of wheezing and asthma development in childhood has been well documented [25]. Recently it was shown that not only do black carbon (BC) particles from environmental exposure reach the fetal side of the human placenta, but further correlate with the mothers’ residential BC exposure averaged over the entire pregnancy [26]. A pooled analysis of two pregnancy cohorts showed that higher exposure to PM2.5 during the sacular phase of fetal lung development was associated with a higher risk of asthma, particularly among those without a maternal history of asthma [27]. Although this is in line with previous observations in two different birth cohorts, where an increase per 2 μg/m3 of PM2.5 exposure during mid-gestation was associated with a 4% increase in the hazard ratio for childhood asthma diagnosis [28, 29], discrepancies exist for PM2.5 windows of exposure based on phases of fetal lung development. Others reported a critical period as early as the 6 weeks including both the pseudoglandular and canalicular phases of lung morphological development suggesting during early pregnancy an impact of pollutants on branching morphogenesis [29]. Yet, as much immune development occurs later in gestation, the critical period for the association between PM2.5 and elevated cord serum total IgE has not surprisingly been suggested to occur between months 6th and 7th of pregnancy [30]. Moreover, children born to mothers reporting elevated stress in pregnancy and with higher PM2.5 exposures between 19 and 23 weeks of gestation were significantly more likely to develop asthma, particularly if they were boys [31].
Although the heterogeneity across studies may limit the ability to draw conclusions, it seems from the overview of meta-analyses that TRAP exposure is associated with both the development and exacerbation of asthma in children (Table 1 ). These findings are limited by diverse definitions in exposure (land-use regression/dispersion models and roadway proximity), outcomes (asthma symptoms, asthma diagnosis, wheeze phenotypes or allergic sensitization), unmeasured confounding of other factors (environmental allergens, climate, diet, physical activity or socioeconomic) and their complex interactions that drive allergic disease and modify the effects of TRAP exposure. A recent overview of systematic reviews and meta-analysis that focused on children’s TRAP exposures as a potential cause for asthma development found an increased risk of 7% for PM2.5, 11% for NO2, 21% for benzene and 6% for TVOCs [32]. Additionally, DEP exposure at age one was positively associated with aeroallergen sensitization at ages two and three [33]. Compared to NO2, PM2.5 has been more strongly associated with outdoor aeroallergen sensitization while exposure to both NO2 and PM2.5 has been significantly associated with food sensitization at the age of 4 and 8 years [34]. There was some evidence that childhood exposure to TRAP may also be associated with increased risks of eczema and hay fever [34].
Table 1. Overview of systematic reviews on the association between Traffic-Related Air Pollution (TRAP) and childhood asthma