4. Discussions
In this study, we included 5819 children from the Jinan birth cohort who
completed two years of follow-up, with a cumulative eczema incidence of
19.8%. We found that O3 exposure in the early life was
positively associated with the risk of eczema at 0-2 years of age,
particularly O3 exposure during pregnancy (OR1.12, 95% CI 1.06-1.19). A Canadian study found that exposure to
oxidant air pollutants before the age of 3 was associated with an
increased risk of eczema(Teresa To et al., 2020). Another Belarusian
study found that higher average annual ground-level ozone was associated
with a high incidence of eczema in infants(Belugina, Yagovdik, Belugina,
& Belugin, 2018). Consistent with the results of our study. The DLM
model was used to find sensitive windows for O3 exposure
and found that 32-42 weeks of gestation, 0-10 and 91-105 weeks of
postnatal life were critical risk windows. The joint effect of
pollutants on eczema risk at different periods was analyzed by the WQS
model, O3 exposure during pregnancy played a dominant
role in this joint effect (weighting >0.3). The same result
was found in the PCA, with PC1 (the largest coefficient for
O3) positively associated with the risk of eczema
(aOR 1.011, 95% CI 1.007-1.015. It has been shown that
O3 exposure increased both transcript and protein levels
of the main inflammasome complex, such as ASC and caspase-1, and
O3 can activate cutaneous inflammasome in a redox
dependent manner(Ferrara et al., 2020). This pathway may play a role in
the increased risk of eczema from O3 exposure.
In our study, PM exposure was also found to increase the risk of eczema.
When PM10 was divided into PM2.5 and
PM2.5-10 by particle size, only large
PM2.5-10 particles had an effect during pregnancy, while
small PM2.5 particles had no significant effect,
however, both PM2.5 and PM2.5-10 had a
significant effect during the first year of life. It is speculated that
the mother may provide some protection against PM-induced fetal harm. A
study in Guangzhou, China, reported that high three-day exposure to
PM10 and PM2.5 was positively associated
with the number of eczema outpatient visits in children under 12 years
of age(J. Zhang et al., 2022). Another study found that
PM2.5 exposure during pregnancy combined with postnatal
tobacco exposure increased the risk of eczema(Jedrychowski et al.,
2011). A Korean study found that PM10 exposure increased
the risk of eczema, while PM2.5 had no significant
effect(Min et al., 2020). The different findings on the effects of
PM10 and PM2.5 on childhood eczema may
be due to the differences in chemical composition and emission sources.
The DLM was used to find the critical window of PM exposure during
pregnancy and postnatal period respectively and found that the risk
window for PM10 was 0-23 weeks postnatal and for
PM2.5-10 was 3-13 weeks postnatal. This may reveal that
newborns are more vulnerable in the first six months of life when PM
exposure is more likely to increase the risk of eczema.
A 2018 review mentioned that the atopic march begins with eczema(Hill &
Spergel, 2018). It is noteworthy that, we found the sensitivity window
for eczema also appeared early, during the third trimester
(O3) and the first 6 months of life (O3and PM). A Mexican study found that the window of sensitivity for
PM2.5 exposure to recurrent wheeze was 6 to 39 weeks
after birth(Rivera Rivera et al., 2021). A Chinese study found that the
critical window of O3 exposure for asthma and wheezing
was 31-37 weeks of gestation and 1-105 weeks after birth(Bai et al.,
2023). Eczema has an earlier window of sensitivity to air pollutants
than other allergic diseases. Therefore, prevention of eczema is also
important for the prevention of other allergic diseases.
The study population was divided into four groups based on eczema at 1
year of age and eczema at 2 years of age. Air pollutant exposure during
pregnancy and the first year after birth increased the risk of eczema
only at age 1 and eczema only at age 2 compared to the no eczema group,
but had no significant effect on persistent eczema. The risk of eczema
is influenced by a combination of environmental and genetic factors(Shi
et al., 2021), and we speculate that genetic factors may play a key role
in the development of persistent eczema.
The incidence of eczema in this study was 19.8% and the pollutants
positively associated with the risk of eczema were O3and PM. The cumulative eczema incidence in children aged 3-6 years was
26.8% in a 2019 study from Hubei(Deng et al., 2019), which showed that
PM2.5 and PM10 during pregnancy
increased the risk of eczema, and this study had a PM2.5concentration of 72.11 ± 5.12μg/m3, higher than 54.9 ±
7.0μg/m3 in our study, meanwhile, PM10concentrations of 114.65 ± 9.63μg/m3, close to our
study. A 2016 study in Shanghai reported a cumulative eczema incidence
of 21.1% in children aged 4-6 years (Liu et al., 2016), which found
that pregnancy NO2 exposure increased the risk of
eczema, while PM10 had no significant effect, the
NO2 concentration during pregnancy in that study was
54.9 ± 10.5μg/m3, in our study was 45.37 ±
5.5μg/m3, the PM10 concentration was
82.7 ± 7.7μg/m3, and in our study was 113.4 ±
11.6μg/m3. Differences in pollutant concentrations
between regions may be one reason why the types of pollutants affecting
the risk of eczema vary between studies.
The main strength and novelty of our study lies in its prospective birth
cohort design, to explore the impact of long-term exposure to air
pollutants in the early life on eczema at 0-2 years of age. Secondly, we
found effects of O3 and PM exposure on eczema risk and
identified critical risk windows. Thirdly, we explored the combined
effect of air pollutants on eczema by WQS and PCA, and the dominant role
of O3 exposure during pregnancy was found. The
limitation of this study is that eczema before one year of age is a
mother-reported symptom of eczema and there is no specific date of
onset. Secondly, the pregnancy information was obtained from the
mother’s recollection after the birth of the child, which may lead to
recall bias. Finally, our study only considered outdoor exposure to air
pollutants and lacked an assessment of indoor exposure.