BC: for black carbon; CO: carbon monoxide; EC: elemental carbon; NOx:
nitrogen oxides: nitrogen dioxide; PM2.5: Particulate Matter <
2.5 μm in diameter; PM10: Particulate Matter < 10 μm in
diameter, PM coarse: Particulate Matter between 2.5 and 10 μm in
diameter; TRAP: traffic-related air pollutants; TVOCs: total volatile
organic pollutants; UFP: Ultra-Fine Particles
Cleaning and consumer products and childhood
asthma
While the development of synthetic chemical compounds has improved our
daily life, the role of exposure to detergents, cleaning and consumer
products in human health has increased in past years with exposure
implicated in the development of several human diseases, such as asthma
[41].
Occupational exposure to cleaning products and disinfectants during
pregnancy may affect the fetus at a critical time window [42].
Maternal exposure starting before conception and continuing is
associated with an approximately two-fold increased risk of childhood
asthma and/or wheeze [42]. This is particularly evident for
phthalate exposure for which even low-level exposure in early life was
associated with up to a fourfold increase in the risk of asthma and
recurrent wheeze at 5 years of age in a dose-dependent manner [43].
Similarly, the use of PVC flooring or wall covering has been reported to
be associated the development of asthma among children and
endocrine-disrupting chemicals exposure in classrooms may not only
impact obesity risk but also the pathogenesis of the obesity and asthma
phenotype through a process mediated by the autonomic nervous system
[44]. Evidence supports that environmental and occupational
exposures may be associated with epigenetic changes that may be
transmissible to offspring, resulting in inherited changes in gene
expression in children of exposed mothers [45], and consequently
affecting the modulation of immune responses and increasing the
susceptibility to develop asthma.
Chlorine bleach or sodium hypochlorite is the most used disinfecting and
cleaning agent, and chlorine disinfection by-products (DBPs), such as
chlorine or trichloramine, are irritants to the respiratory tract and
are also associated with acute lung injury [46]. A recent position
paper on the evidence of the health effects of acute and chronic
exposure to swimming pools suggested that early and chronic exposure to
DBPs may be associated with a higher risk of childhood asthma [47].
Taken together the evidence supports a growing call to mitigation and
prevention actions on the role of cleaning and consumer products on
childhood asthma. Further studies are also needed to evaluate the
longer-term effects of low-to-higher exposure to such products early in
life on asthma at younger ages.
Tobacco and e-cigarettes exposure and childhood
asthma
According to WHO, exposure to second-hand smoke (SHS) kills around 1.2
million people every year and 65 000 of these premature and preventable
deaths are in children under 15 years. A recent meta-analysis of 93
studies examining the effect of SHS exposure reported a significantly
positive association between SHS exposure and doctor-diagnosed asthma in
children [48] (Table 2 ). Although prenatal has a greater
impact than postnatal exposure on childhood asthma, the combined effect
of maternal smoking during and after pregnancy was higher. A pooled
analysis based on data from European birth cohorts suggested a linear
dose-response association between maternal daily cigarette consumption
and increased childhood asthma [49]. Children exposed to
≥10 cigarettes/day during pregnancy had an increased risk of early
transient and persistent asthma [50].
Epidemiological evidence suggests that the effects of maternal smoking
are heritable with further generations continuing to present poor
respiratory outcomes, probably through epigenetic mechanisms [51,
52]. According to these studies, grandmaternal smoking has been shown
to increase the risk of a grandchild’s asthma independently of maternal
smoking. Furthermore, exposure to tobacco smoke is also associated with
more severe asthma symptoms, increased risk of asthma exacerbations as
well as hospitalizations [53]. A systematic review showed an
approximately 2-fold increase in the risk of hospitalization for asthma
among children with asthma and exposed to SHS than children with asthma
but without SHS exposure [53]. Exposure to SHS was also
significantly associated with visits to the emergency department or
urgent care and with an increased risk of wheezing [53].
Since the early 2000s, electronic cigarettes (e-cigarettes) have been
marketed worldwide as a “safer” electronic alternative to combustible
cigarettes and as a device likely to help stop smoking [54]. Unlike
a cigarette, e-cigarettes produce a respirable aerosol without burning
tobacco. Although the number of studies on the short- and long-term
health effects of e-cigarettes is very limited, recent studies suggested
that exposure to e-cigarettes is also a significant factor that has been
shown to increase the incidence of asthma [55]. In 2019, 33% of the
youth with asthma who reported having an asthma attack in the previous
year were exposed to SHS to e-cigarettes [54].
Overall, the evidence contributes to a growing understanding about the
timing of SHS exposure and the development of childhood asthma, showing
that knowledge of critical time windows of exposure is important in
implementing targeted interventions.
Table 2. Overview of the studies on the association between
second-hand smoke (SHS) and childhood asthma