The role of genes in prenatal responses to air pollution

Date:
April 7, 2022
Source:
Texas A&M University
Summary:
Exposure to pollution during pregnancy can have many adverse effects
in infants and children that can even extend into adulthood. For
example, air pollution exposure is associated with increased risk
of low birth weight, preterm birth and risk for developing asthma
later in life. Much of this is due to the fast pace of fetal
growth and development; however, the exact ways pollutants have
these effects and the roles of genes related to immune function
and stress response are not fully understood.



FULL STORY ========================================================================== Exposure to pollution during pregnancy can have many adverse effects in
infants and children that can even extend into adulthood. For example,
air pollution exposure is associated with increased risk of low birth
weight, preterm birth and risk for developing asthma later in life. Much
of this is due to the fast pace of fetal growth and development; however,
the exact ways pollutants have these effects and the roles of genes
related to immune function and stress response are not fully understood.


==========================================================================
In a study published in the journal Antioxidants, researchers from Texas
A&M University and the University of Florida worked to clarify how a gene related to oxidant response known as Nrf2 affects fetal development in
an experimental model. Natalie Johnson, PhD, associate professor at the
Texas A&M School of Public Health, along with Carmen Lau, DVM, Jonathan
Behlen and others exposed animal models modified to lack the Nrf2 gene
and unmodified animal models to particulate pollution like that found
in diesel exhaust. They then evaluated the effects on litter size,
birth weight and immune markers found in the lung and liver tissue of
newborn offspring.

Particulate matter pollution is divided into three categories based
on particle size: coarse particles, fine particles and ultrafine
particles. Fine particles less than 2.5 microns in diameter and ultrafine particles less than one-tenth of a micron across are of greatest
concern. Researchers have found associations between fine particulate
pollution and increased odds of respiratory diseases, but less work has
been done on ultrafine pollutants, and no health standards currently
exist for this smallest category. The tiny size of ultrafine particles
means they can work deeper into airways, possibly making them an even
bigger health risk than fine particles.

The gene Nrf2 is known to affect immune function and stress response
in adults, but research on the effects of this gene in infants and
children has been explored less. To better understand the role of Nrf2
during development and clarify how ultrafine particles affect health, researchers exposed both unmodified animal models and those that have
had the Nrf2 genes knocked out to fresh, filtered air and air containing ultrafine particles like those found in diesel exhaust, a common pollutant
in urban areas. The researchers monitored weight gain in pregnant animal
models in all four groups and recorded litter sizes and birth weights
of the offspring.

There were no statistically significant differences in weight gain in
the animal models in the four groups during pregnancy. Similarly, there
were not notable differences in litter sizes. However, the Nrf2-deficient offspring had lower birth weights than their unmodified counterparts,
with the greatest effects in Nrf2-deficient animal models exposed to
pollution. Exposure to pollution had no notable effects in unmodified
animal models, which may indicate Nrf2 playing 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.

These results are in line with other studies that have found associations between Nrf2 deficiency and some chronic diseases. For example, previous research found that adult Nrf2-deficient animal models were more likely
to develop autoimmune diseases. Although more work lies ahead, 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.


========================================================================== Story Source: Materials provided by Texas_A&M_University. Original written
by Rae Lynn Mitchell. Note: Content may be edited for style and length.


========================================================================== Journal Reference:
1. Carmen H. Lau, Drew Pendleton, Nicholas L. Drury, Jiayun Zhao,
Yixin Li,
Renyi Zhang, Gus A. Wright, Aline Rodrigues Hoffmann, Natalie
M. Johnson.

NRF2 Protects against Altered Pulmonary T Cell Differentiation in
Neonates Following In Utero Ultrafine Particulate Matter Exposure.

Antioxidants, 2022; 11 (2): 202 DOI: 10.3390/antiox11020202 ==========================================================================

Link to news story: https://www.sciencedaily.com/releases/2022/04/220407141922.htm

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