Researchers have worked to clarify the role of genes in prenatal responses to air pollution.
Exposure to air pollution during pregnancy can have many adverse effects in infants and children that can extend into adulthood.
Air pollution exposure is associated with increased risk of low birth weight, preterm birth and risk for developing asthma later in life.
However, the exact way that pollutants have these effects, and the role of genes related to immune function and stress response in this mechanism, is not fully understood.
In a study published in Antioxidants, researchers from Texas A&M University and the University of Florida examined how a gene related to oxidant response affects fetal development in an experimental model.
The researchers exposed animal models to particulate pollution, commonly found in diesel exhaust fumes, with some of the animal models modified to lack the Nrf2 gene, which is known to affect immune function and stress response in adults.
They then evaluated the effects of the particulate matter on litter size, birth weight and immune markers found in the lung and liver tissue of newborn offspring.
The Nrf2-deficient offspring had lower birth weights than the unmodified counterparts, with the greatest difference observed when exposed to pollution.
Exposure to pollution had no notable effects in unmodified animal models, which may indicate that the gene plays some protective role during pregnancy.
The researchers also analyzed lung and liver tissue from the offpsring to measure differences in certain immune markers and expression of genes related to oxidative stress response.
They found significant differences in immune markers in Nrf2-deficient offpsring, indicating a change in immune function in those models. These findings point to the lack of a functioning Nrf2 gene being a main contributor to the differences between the groups.
Although more research is needed, this study demonstrates that the absence of a functioning Nrf2 gene affects prenatal growth of animal models, especially when exposed to ultrafine particulate air pollution in utero.
These findings could point to a possible mechanism through which ultrafine particulate matter can affect placental function and prenatal health.
This highlights a need for further research into the roles of genes on immune and stress response and how those genes interact with environmental factors.
The research also reinforces the importance of establishing health standards for ultrafine particulate matter pollution, which appear to have serious effects on prenatal and neonatal health and development.
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