Evidence on how air pollution impacts brain development has been well documented. The brains of fetuses and infants are susceptible to external stressors during pregnancy and the first year of life because of their weak detoxification mechanisms. Steady exposure to air pollution during the developmental periods of life could lead to permanent alterations in the brain.
Higher exposure to air pollution early in life has been linked to lower cognitive abilities. Air pollutants are responsible for alterations in white matter microstructure and brain morphology. Although many studies have evaluated average exposure to air pollution over a prolonged period, the impact of cumulative exposure has not been determined. Also, these studies have predominantly focused on a specific period, such as the childhood period, without considering exposure during the pregnancy period.
White matter tracts emerge in the fetal brain between 13 and 18 weeks of gestation, and myelination begins around 20 weeks, which advances rapidly throughout the first five years of life and progresses until adulthood.
Average exposure estimates cannot determine which period of life is most susceptible to air pollution. The distributed lag non-linear model (DLNM) considers the entire period of exposure, i.e., from conception to preadolescence, and identifies the crucial period of susceptibility to air pollution. Although few studies have utilized the DLNM method to establish the link between early-life exposure to air pollution and children's cognitive function or behavioral problems, there are no studies that have used this method to understand how brain development is affected by air pollution.
DLNM can identify the underlying pathways representing time-specific associations between air pollution exposure and neural development based on magnetic resonance imaging (MRI) data, which can provide direct insights into brain structures. In a recent Environmental Pollution study, scientists applied DLNM to determine the most crucial period of susceptibility to air pollution exposure between conception and age 8.5 years, which impacts white matter microstructure and brain volumes.
About the study
The study hypothesized that the risk associated with brain outcomes on air pollution exposure is not constant over time, and a specific period of susceptibility may exist. The period of susceptibility was identified after exposure to three commonly present pollutants by determining the alterations in white matter microstructure and brain volumes in preadolescents aged 9-12.
It was proposed that exposure to air pollution during pregnancy and childhood was linked to high mean diffusivity and reduced fractional anisotropy. The operating hypothesis was that exposure to air pollution during pregnancy and childhood was associated with a smaller cerebellum volume, cortical gray matter, cerebral white matter, thalamus, corpus callosum, pallidum, and hippocampus.
Data were obtained from Generation R Study, a population-based birth cohort from Rotterdam, Netherlands. This cohort represented 8879 women recruited during their pregnancy, and 899 were enrolled shortly after delivery between April 2002 and January 2006. When the children were between 9 and 12 years of age, MRIs were performed.
A specific period of susceptibility was observed, from conception to 5 years of age, to air pollution for white matter microstructure. Air pollution exposure in the first two years of life was linked with susceptibility to the putamen. Importantly, the period of susceptibility was determined to be from conception to 5 years of age, concerning NO2 exposure of PM 2.5 for white matter microstructure.
Importantly, the present study did not observe any link between exposure to air pollution at 8–9 years of age and white matter microstructure outcomes. This study indicated susceptibility to air pollutants, especially during the period of rapid myelination of the brain.
This study did not observe the hemisphere-specific effect of air pollution on brain volumes. PM 2.5 exposure in the first year of life was associated with larger putamen volume. No windows of susceptibility to air pollution were found related to the cerebellum and the cortical gray matter. The findings of this study indicated no association between PM 2.5 levels and corpus callosum volume.
Strengths and limitations
The large-sized cohort is a major strength of the current study. Additionally, assessing the effect of air pollution from conception to 8.5 years of age is a prominent time scale. Another strength of this study is its study design related to the adjustment for various socioeconomic and lifestyle variables, which could have confounded the findings.
Some of the limitations of this study include the period of sampling campaigns, i.e., when the participants were between 3.5 and 9 years of age. Additionally, DLNM analysis excluded very preterm children from the analysis. Further, multi-pollutant analyses were not conducted; instead, each air pollutant was separately assessed following brain outcomes. In the current study, white matter microstructure and brain volume in preadolescence were estimated via a single measurement.
Taken together, exposures to air pollutants from pregnancy to age 8.5 years were linked to altered white matter microstructure in preadolescents (9–12 years of age) with specific periods of susceptibility from conception to 5 years. Hence a decrease in air pollutants exposure during pregnancy and childhood is expected to promote normal brain development.