Scientists at the University of Pittsburgh Graduate School of Public Health and the German Research Center for Environmental Health have identified certain genetic mutations that may lead to poor lung development in children.
Poor lung development makes kids more vulnerable to diseases such as chronic obstructive pulmonary disease (COPD) later in life.
For the study, lead researchers Dr George Leikauf, and Dr Holger Schulz looked at a gene called superoxide dismutase 3 (SOD3), previously shown to protect the lungs from the effects of asbestos and oxidative stress.
They found that the presence of single nucleotide polymorphisms, or SNPs, variations in DNA sequences, in SOD3 that were linked to lung function in mice.
For further analysis, the researchers went on to assess SOD3 mutations in children ages 9 to 11 by testing for SNPs linked to lung function.
The researchers discovered two common SNPs associated with poorer lung function. One of these SNPs likely alters the expression levels of SOD3.
Lung function was tested with spirometry, which measures the amount and speed of exhaled air.
Previously, genetic variants in SOD3 have been associated with loss of lung function in COPD, which is mainly caused by cigarette smoking.
"We know SOD3 protects the lung against injury caused by chemicals in cigarette smoke, and it could be a link between childhood exposure to environmental tobacco smoke and poor lung development," said Leikaf.
He said one day it might be possible to identify at-risk children and develop a medication that would foster optimal lung development.
The study appears online in Physiological Genomics.