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

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.

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