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