Gene-environment interactions with air pollutants may play a critical role in increasing the prevalence of ASD.
Study:Air pollution: an emerging risk factor for autism spectrum disorder. Image credit: Borri_Studio/Shutterstock.com
In a recent review published on Brain Medicinea group of authors examined air pollution as a key environmental risk factor for autism (a neurodevelopmental disorder affecting social skills and behavior), highlighting gene-environment interactions and neurodevelopmental effects.
Background
Air pollution has become a prominent environmental health problem, with recent studies linking exposure to pollutants such as particulate matter (PM), sulfur dioxide (SO2), nitrogen oxide (NO), nitrogen dioxide (NO2) and ozone (O3) with increased risk of autism spectrum disorder (ASD).
These pollutants are thought to contribute to ASD through mechanisms such as neuroinflammation, oxidative stress, and disturbances in neurotransmitter systems.
Vulnerable populations, particularly pregnant women and young children, may face increased risks due to critical stages of brain development. Given the global increase in pollution and the increasing prevalence of ASD, further research is needed to clarify these links and inform prevention strategies.
PM and its neurodevelopmental effects
PM is a well-known class of air pollutants consisting of fine particulate matter PM2.5, which refers to particles less than 2.5 micrometers in diameter, and PM10, which are slightly larger particles, have been extensively studied because of their ability to penetrate deep into the respiratory system. These particles can enter the bloodstream, cross the placental barrier and reach the fetal brain.
Studies have shown that prenatal exposure to PM10 can adversely affect fetal development, and PM2.5, which penetrates even more deeply, has been associated with an increased risk of ASD when exposure occurs during early pregnancy or before arrest. Because of these findings, PM is considered a high-priority pollutant for understanding ASD risk.
NO and NOâ‚‚
NO and NO2 are harmful air pollutants released mainly from vehicle emissions and the burning of industrial fuels. Exposure to these pollutants, particularly during pregnancy and early childhood, can affect normal brain developmental processes such as neuronal migration and myelination.
Recent pioneering research has directly linked NO exposure to ASD, making it one of the first pollutants with a well-defined pathway to ASD risk. The timing of exposure is crucial, as disruptions in brain development during the early prenatal and postnatal periods can lead to long-term neurodevelopmental problems.
O3: A reactive pollutant
O3 is a highly reactive oxygen molecule formed through chemical reactions between volatile organic compounds and nitrogen oxides. Research by McGuinn et al. has established a link between exposure to O3, especially in combination with PM2.5, and an increased risk of ASD.
When exposed during critical developmental windows, such as pregnancy and the first two years of life, ozone can contribute to neurodevelopmental disorders due to its oxidative properties, which can damage brain cells and stunt their growth. This association highlights the need for policies to reduce ground-level ozone, especially in urban and industrial areas.
SO2 and volatile organic compounds
SO2 is another toxic pollutant that comes from burning fossil fuels, vehicle emissions and industrial processes. Studies show that maternal exposure to SO2, particularly during pregnancy and early childhood, is associated with a higher risk of ASD.
In addition, volatile organic compounds such as benzene, which is commonly found in industrial processes, cigarette smoke and emissions are of concern. Exposure to these compounds during pregnancy, particularly in combination with other pollutants such as NO2, may have synergistic effects that further increase the risk of ASD.
Research on SO2 and volatile compounds suggests that the cumulative and mixed effects of air pollution on neurodevelopment are complex and powerful.
Mechanisms linking pollutants to ASD: Neuroinflammation and oxidative stress
The harmful effects of air pollution on the brain can be traced to several biological mechanisms, such as neuroinflammation and oxidative stress. During pregnancy, inhaled pollutants such as PM can lead to an inflammatory response in the fetus and trigger neuroinflammation in the developing brain.
An immature blood-brain barrier allows PMs to reach fetal brain cells, initiating inflammation in cells such as astrocytes and microglia. Pollutants such as NO2 and PM2.5 can activate toll-like receptors (TLRs) and pathways such as nuclear factor kappa-light chain-enhancer of activated B cells (NF-κB), which regulate genes associated with inflammation.
Chronic inflammation in the developing brain can lead to disruption of neural networks, a feature of many people with ASD.
Epigenetic modifications and neurotransmitter imbalances
Air pollution can also cause epigenetic changes, which modify the way genes are expressed without altering the genes themselves Deoxyribonucleic acid (DNA) the sequence itself. DNA methylation and histone modification are two such changes that have been observed in association with air pollution exposure.
These changes can affect genes that control brain development and immune system function, potentially increasing the chance of ASD. In addition, exposure to air pollution disrupts the balance of neurotransmitters such as glutamate and gamma-aminobutyric acid (GABA), both essential for normal brain function.
Imbalances in these neurotransmitters, often seen in people with ASD, can be caused by exposure to pollution and may contribute to the characteristic symptoms of the disorder.
Endocrine disruption and metabolic pathway dysfunction
Some pollutants, particularly fine PM, act as endocrine disruptors, altering hormone levels critical to brain development. This disruption of hormones, such as estrogen and thyroid hormones, at critical developmental stages can lead to neurodevelopmental abnormalities, including ASD.
In addition, air pollution exposure can dysregulate metabolic pathways involving fatty acids, amino acids, and neurotransmitters, which play an important role in neurodevelopment.
Understanding these metabolic effects offers insights into the relationship between pollution and ASD risk, particularly during the vulnerable perinatal period.
conclusions
In summary, the study concludes that air pollution is an important environmental risk factor for ASD, affecting neurodevelopment through multiple mechanisms, including epigenetic modifications, neuroinflammation, oxidative stress, and endocrine disruption.
Exposure to pollutants such as PM, NO2, NO, SO2and O3 during critical developmental windows, particularly in pregnancy and early childhood, increases the risk of ASD.
