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Prenatal air pollution influences neurodevelopment and behavior in autism spectrum disorder by modulating
Richard E Frye1, Janet Cakir2, Shannon Rose3,4
1Barrow Neurological Institute at Phoenix Children's Hospital, Phoenix, AZ, USA. rfrye@phoenixchildrens.com.
Insights
Prenatal exposure to fine particulate matter (PM2.5) impacts children's neurodevelopment and behavior, partly by altering mitochondrial respiration. These findings highlight the role of mitochondria in mediating environmental influences on autism spectrum disorder development.
Area of Science:
- Environmental Health
- Neuroscience
- Mitochondrial Biology
Background:
- Prenatal exposure to air pollution, specifically fine particulate matter (PM2.5), is a growing concern for neurodevelopmental outcomes.
- Mitochondria, crucial for cellular energy, are sensitive to environmental toxins and may play a role in mediating pollution's effects.
- Autism spectrum disorder (ASD) and neurodevelopmental regression (NDR) are complex conditions where environmental factors may contribute.
Purpose of the Study:
- To investigate the association between prenatal PM2.5 exposure and mitochondrial function in children with ASD.
- To determine if mitochondrial respiration mediates the relationship between prenatal PM2.5 exposure and neurodevelopmental and behavioral outcomes in children with ASD.
- To explore the direct and indirect effects of PM2.5 and mitochondrial respiration on neurodevelopment and behavior.
Main Methods:
- Assessed mitochondrial function using Seahorse XFe96 in peripheral blood mononuclear cells from 96 children with ASD.
- Quantified prenatal PM2.5 exposure during the second and third trimesters using EPA Air Quality System data.
- Measured neurodevelopment and behavior using standardized scales (Vineland, Aberrant Behavior Checklist, Social Responsiveness Scale).
Main Results:
- Prenatal PM2.5 exposure was linked to altered mitochondrial respiration in children with ASD, with differing patterns for those with and without NDR.
- Mitochondrial respiration explained 25% and 10% of the effect of average prenatal PM2.5 exposure on neurodevelopment and behavioral symptoms, respectively.
- Structural equation models indicated PM2.5 and mitochondrial respiration significantly influenced neurodevelopment, with behavior indirectly affected by mitochondria via neurodevelopment.
Conclusions:
- Prenatal PM2.5 exposure disrupts neurodevelopment and behavior in children with ASD through mechanisms involving long-term changes in mitochondrial respiration.
- Mitochondrial function is a key pathway through which environmental agents like PM2.5 can impact neurodevelopmental trajectories.
- Considering early developmental patterns is crucial for understanding environmental influences on neurodevelopmental outcomes in ASD.
Abstract:
We investigate the role of the mitochondrion, an organelle highly sensitive to environmental agents, in the influence of prenatal air pollution exposure on neurodevelopment and behavior in 96 children with autism spectrum disorder (ASD) [45 with neurodevelopmental regression (NDR); 76% Male; mean (SD) age 10 y 9 m (3 y 9 m)]. Mitochondrial function was assessed using the Seahorse XFe96 in fresh peripheral blood mononuclear cells. Second and third trimester average and maximal daily exposure to fine air particulate matter of diameter ≤2.5 µm (PM2.5) was obtained from the Environmental Protection Agency's Air Quality System. Neurodevelopment was measured using the Vineland Adaptive Behavior Scale 2nd edition and behavior was assessed using the Aberrant Behavior Checklist and Social Responsiveness Scale. Prenatal PM2.5 exposure influenced mitochondrial respiration during childhood, but this relationship was different for those with (r = 0.25-0.40) and without (r = -0.07 to -0.19) NDR. Mediation analysis found that mitochondrial respiration linked to energy production accounted for 25% (SD = 2%) and 10% (SD = 2%) of the effect of average prenatal PM2.5 exposure on neurodevelopment and behavioral symptoms, respectively. Structural equation models estimated that PM2.5 and mitochondrial respiration accounted for 34% (SD = 4%) and 36% (SD = 3%) of the effect on neurodevelopment, respectively, and that behavior was indirectly influenced by mitochondrial respiration through neurodevelopment but directly influenced by prenatal PM2.5. Our results suggest that prenatal exposure to PM2.5 disrupts neurodevelopment and behavior through complex mechanisms, including long-term changes in mitochondrial respiration and that patterns of early development need to be considered when studying the influence of environmental agents on neurodevelopmental outcomes.
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