The mediating role of the gut microbiome in the association between ambient air pollution and autistic traits.

This study looked at whether air pollution during pregnancy affects children's autism-related behaviors through changes in gut bacteria. Researchers followed 170 families and found that exposure to air pollution in the first three months of pregnancy was linked to more autism-like traits in 6-year-old children. They also found that these children had different gut bacteria (more Proteobacteria). The study suggests that air pollution might influence autism development partly by changing the gut microbiome, though this accounts for only about 16-23% of the effect.

This cohort study examined 170 mother-child pairs to investigate whether gut microbiome changes mediate the relationship between prenatal air pollution exposure and autistic traits. Researchers measured PM₁₀ and NO₂ exposure during pregnancy and childhood, assessing autistic traits and gut microbiome composition at age 6. First trimester PM₁₀ exposure was associated with increased autistic traits (10.6% increase per IQR) and elevated Proteobacteria abundance (66.9% increase). Similar patterns were observed for NO₂ exposure.

Proteobacteria abundance was independently associated with increased autistic traits (4.4% per 2-fold increase). Mediation analyses revealed that Proteobacteria partially mediated the relationship between first trimester air pollution exposure and later autistic traits (23.2% for PM₁₀, 16.7% for NO₂), suggesting gut microbiome alterations may be one pathway through which early prenatal air pollution exposure influences autism development.

Findings suggest importance of minimizing air pollution exposure during early pregnancy. Gut microbiome assessment may have future diagnostic utility. Results support investigating microbiome-targeted interventions for autism, though replication in larger samples needed. Emphasizes need for environmental protection policies to reduce prenatal pollution exposure as potential autism prevention strategy.

Single cohort study design limits generalizability. Gut microbiome assessed only at age 6, missing developmental trajectory. Air pollution exposure estimated rather than directly measured. Mediation analysis shows partial effect only, indicating other unmeasured pathways exist. Cannot establish definitive causation between pollution, microbiome changes, and autism traits.

Air pollution has been reported to be an environmental risk factor for autism spectrum disorder. However, the gut microbiome's role as a potential mediator has not been investigated. We aimed to clarify whether particulate matter with an aerodynamic diameter ≤10 μm (PM) and nitrogen dioxide (NO) exposure impact autistic traits through the gut microbiome. Using 170 mother-child pairs, PMand NOexposure levels during pregnancy (1st, 2nd, and 3rd trimesters) and annual residential PMlevels at age 2, 4, and 6 years were estimated.

Autistic traits and gut microbiome were assessed at age 6 years. The associations of PMor NOexposure, gut microbiome composition, and autistic traits were explored, and mediation analyses of statistically significant findings were also conducted. Exposure to PMduring the 1st trimester of pregnancy was associated with increased autistic traits (10.6% change per interquartile range (IQR) increase, 95% confidence interval [CI]: 1.1, 21.0) and with Proteobacteria relative abundance at age 6 years (66.9% change per IQR increase, 95% CI: 21.3, 129.8). First trimester NOexposure was associated with autistic traits (12.1% change, 95% CI: 0.1, 25.5) and Proteobacteria relative abundance at age 6 years (48.1% change, 95% CI: -0.1, 119.6).

Proteobacteria relative abundance was related to autistic traits (4.4% change per 2-fold increase, 95% CI: 1.3, 7.5). Relations between PMor NOexposure during the 1st trimester and autistic traits at age 6 years were partially mediated by Proteobacteria (proportion mediated 23.2%, p = 0.01 and 16.7%, p = 0.06; respectively). PMand possibly NOexposure during early pregnancy may affect autistic traits at age 6 years through the alteration of Proteobacteria abundance.