Women who smoke during pregnancy may be putting their unborn children at increased risk for a DNA change, a new study suggests.
The change, called DNA methylation, can change a gene's usual function. The researchers argue that the altered genes, which can be passed from parent to child, may explain why some children are more likely than others to develop certain diseases, such as childhood asthma.
The study, which was to be presented at an American Thoracic Society conference in Denver, analysed questionnaires completed by the mothers and grandmothers of 173 children that assessed their smoking habits during pregnancy. DNA samples from cheek cells of mothers and children were also collected and evaluated.
The researchers found that DNA methylation of the AXL gene, a gene that plays an important role in many human cancers and immune response, occurred more than twice as often in children whose mothers had smoked while carrying them in the womb.
Smoking in pregnancy and asthma in children
They noted a stronger association in girls than in boys, and they found no significant tie between a grandmother's smoking and DNA methylation of AXL in either the mother or her child.
"Imprinted genes appear to be particularly susceptible to these exposures since they come from one parent and only a single copy from one chromosome in DNA is active," study author Carrie Breton, an assistant professor of preventive medicine at the University of Southern California said in a American Thoracic Society news release.
"Any environmentally induced epigenetic changes will have greater impact on gene expression and function. In-utero and early life exposures are likely to be important, given what we know about timing during development when epigenetic marks are established."
Investigating the effects of environmental exposures on epigenetics, or changes in gene function or expression that occur as the result of mechanisms other than changes to the underlying DNA sequence, is a largely unexplored area of research that holds great promise for understanding the biological mechanisms that underlie exposure-disease associations, Breton added.
"We are interested in further characterising the pattern of epigenetic marks across this gene and whether there is a widespread response to both maternal smoking exposure and air pollution exposure in utero," she said. "We hope to also evaluate timing of effects of exposure during trimester by increasing the number of samples we evaluated in a manner that will let us compare trimester-specific exposures."
Experts note that research presented at meetings should be considered preliminary because it has not been subjected to the rigorous scrutiny given to research published in medical journals.
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