A Breath of Concern: Air Pollution, Pregnancy, and the Developing Brain

Air pollution has long been linked to respiratory and cardiovascular disease, but over the past decade, neuroscience has begun uncovering another, less visible consequence: its effect on the developing brain. Increasing evidence now suggests that maternal exposure to fine particulate matter during pregnancy, particularly PM2.5, may contribute to neurodevelopmental disorders such as autism spectrum disorder (ASD). Across  both human and animal studies, a consistent and biologically plausible pattern emerges: exposure to fine airborne particles during pregnancy is associated with measurable changes in offspring brain development and behaviour.

The Problem with PM2.5

PM2.5 describes particles smaller than 2.5 micrometres, small enough to travel deep into the lungs, enter the bloodstream, and reach the placenta. Their composition is complex and often includes metals such as iron, lead, and zinc, along with organic carbon, nitrates, and sulphates from traffic emissions and industrial combustion. In the UK alone, particulate matter is estimated to contribute to around 10,000 premature deaths each year.

During pregnancy, the placenta acts as a vital barrier between mother and foetus. Yet, research by Wick and colleagues  showed that particles as small as 240 nanometres can cross placental tissue. Once there, they can trigger oxidative stress and inflammation, disrupting nutrient and oxygen exchange and even altering gene expression within placental cells.

What the Evidence Shows

Across a review of twelve core studies the findings were remarkably consistent. Raz et al. found that women exposed to higher concentrations of PM2.5 during the third trimester had a 57% higher likelihood of having a child diagnosed with ASD compared with those in cleaner air environments, even after controlling for socioeconomic and lifestyle factors.

A 2020 study found that increased prenatal exposure to PM2.5 and nitrogen dioxide (NO₂) was linked to poorer neonatal neurobehavioural scores. Male infants appeared more vulnerable, suggesting a potential sex-specific sensitivity to pollution exposure.

In Sweden, researchers analysed data from over 40,000 births and reported that maternal exposure to higher traffic-related PM2.5 levels was significantly associated with increased rates of childhood autism. Meanwhile, work in Taiwan identified heavy metals bound to PM2.5, particularly mercury (Hg), as key neurotoxic components. This study showed that prenatal exposure to mercury containing particulates increased ASD risk by up to 40%, especially when exposure occurred between 10 and 25 weeks post-birth, a critical period for synaptic development.

"Women exposed to higher concentrations of PM2.5 during the third trimester had a 57% higher likelihood of having a child diagnosed with ASD"

Animal studies help explain why. Rodent models exposed to PM2.5 during gestation show microglial activation, elevated inflammatory cytokines (IL-6, IL-1β), and impaired hippocampal synaptic growth. These molecular changes lead to behavioural differences, reduced social interaction and increased repetitive activity, closely resembling some ASD traits observed in humans.

Timing of Exposure

A recurring pattern in both human and animal studies is that timing matters. The first and second trimesters, when the neural tube forms and neurons rapidly differentiate, appear to be the most critical windows of vulnerability. Exposure during these stages was consistently associated with developmental deficits, whereas later exposure produced more variable outcomes. This fits with what we already know about foetal neurodevelopment. Early disruption, whether inflammatory, oxidative, or hormonal, can alter neuronal migration and synaptic patterning in ways that persist long after birth.

Implications for Public Health

Reducing exposure to PM2.5 could have measurable benefits for neurodevelopment at the population level. Cleaner transport systems, stricter air quality regulations, and urban green infrastructure have all been shown to lower particulate concentrations. At the individual level, small actions, such as avoiding exercise near heavy traffic and improving indoor air filtration, can help reduce exposure.

While current data stop short of proving direct causation, the consistency of association across studies, combined with strong mechanistic evidence, needs attention. Future research should focus on longitudinal designs that integrate precise exposure monitoring, placental biomarkers, and neuroimaging in offspring. Understanding sex-specific differences and genetic susceptibility may also help explain why some pregnancies are more affected than others.

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This article was written by Anaxia Uthayakumar and edited by Julia Dabrowska, with graphics produced by Saba Keshan. If you enjoyed this article, be the first to be notified about new posts by signing up to become a WiNUK member (top right of this page)! Interested in writing for WiNUK yourself? Contact us through the blog page and the editors will be in touch.