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Prenatal air pollution exposure may slow newborn brain development


In an evolving health landscape, emerging research continues to highlight concerns that could impact everyday wellbeing. Here’s the key update you should know about:

A new study from Spain reveals that babies born to mothers exposed to higher air pollution levels in pregnancy show signs of slower brain myelination, a subtle but telling shift in how early brain wiring unfolds.

Study: Unraveling the impact of prenatal air pollution for neonatal brain maturation. Image credit: PeopleImages/Shutterstock.com

A recent study published in Environment International suggests that prenatal exposure to air pollution is linked to delayed maturation in the newborn, likely associated with a slowing of the rate of myelination.

Introduction

The developing brain is highly vulnerable to injury by environmental factors, including air pollution. This can cause neuropsychiatric disorders, which are among the significant causes of disability worldwide.

Particulate matter with a diameter of 2.5 µm or less (PM2.5) is often used as a pollution indicator because it originates in so many different sources of pollution and contains a spectrum of pollutants, including potentially toxic elements and essential trace metals such as iron, copper, and zinc. It is easily inhaled, and the particles can penetrate the blood-brain barrier, causing adverse effects on the brain.

Prenatal PM2.5 exposure impacts fetal development. Conversely, it exposes the fetus to essential micronutrients like copper, iron, and zinc, all of which promote gestational white matter myelination. Little is known about the outcome of these opposing exposures on the brain, mirroring the complex fetal response to pollution.

For instance, offspring of women exposed to particulate matter of the PM10 variety had larger brain ventricles and cerebelli. The opposite was true of NO2 exposure, though both are pollutants. Opposite effects have been reported with other brain areas.

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Myelination is an important marker of brain maturation. It involves the formation of myelin sheaths around the axons of the neurons. The myelin sheath speeds up nerve conduction and shapes brain circuitry. Myelination begins from the basic pathways of the brain and progresses to higher circuits, which is reflected in the individual’s behavioral development.

Air pollution exposure before birth causes changes in the brain’s white matter, including its myelin content and structure. This led to the current study, which examined PM2.5 exposure during pregnancy as a predictor of newborn brain myelination.

About the study

The study sample comprised 93 newborns born at three hospitals in Barcelona, Spain, between 2018 and 2021. Their prenatal PM2.5 exposure was modeled, separately for the embryonic and late fetal phases. The newborn brain was imaged by magnetic resonance imaging (MRI) at 29 days of postnatal life.

Study findings

The infant’s age at the time of the MRI was linked to brain volume and overall myelination, indicating the ability to record short-term neonatal brain development. However, this association was not found for cortical myelination.

Increasing prenatal PM2.5 exposure in early pregnancy was associated with a lower cortical myelinated white matter content. In late pregnancy, it was linked to lower overall myelination. There were no associations with brain volume. This suggests that the brain cortex and deep white matter may respond differently to chemical pollution in early developmental stages.  

This pattern was also observed with trace element exposure, though the associations weakened or disappeared when adjusted for confounding factors.

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The findings suggest a delay in early myelination following exposure to air pollution in the prenatal period. However, since myelination is a dynamic process whose rate varies with age, brain region, and the availability of nutrition, this observation does not necessarily indicate a harmful or permanent effect on the fetus.

In fact, one prior study indicates that slower but more sustained white matter myelination is found in children with higher cognitive skills. The apparently slower maturation occurred during the first year of life, while a catch-up phase occurred over the next year.

Again, the placenta may protect the fetus from certain pollutants, which simultaneously allows essential elements to pass through.

Conclusions

Women exposed to air pollution in pregnancy had babies with lower white matter myelination in the newborn period. Reduced cortical myelination was specifically associated with higher PM2.5 exposure in early pregnancy, but global myelination declined with later exposure. These findings suggest a potential delay in neonatal brain maturation.

Significant associations were not found for iron, copper, or zinc in PM2.5, though the observed trends were in the same direction.

The authors noted that:

This study underscores the impact of environmental factors on neonatal brain development and the importance of stringent air quality policies.

The cognitive outcome of delayed neonatal white matter myelination remains unknown. Thus, the study also underlines the importance of longitudinal research to understand how prenatal air pollution affects long-term behavior and intellectual development.

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