Exposure to environmental pollutants during pregnancy may boost the risk of asthma in offspring for up to three consecutive generations, a study found.
The mouse study, “Transgenerational transmission of asthma risk after exposure to environmental particles during pregnancy,” appeared in the American Journal of Physiology – Lung Cellular and Molecular Physiology.
Researchers followed three generations of mice across three groups. Mothers in the first group were exposed to diesel exhaust particles during pregnancy, while pregnant mothers in the second were exposed to urban air particle concentrates. The third group consisted of healthy controls not exposed to any pollutants.
After comparing cells from the lungs of the first, second and third generations of offspring from the three groups, researchers found that all generations descended from mice exposed to diesel exhaust particles during pregnancy had much higher levels of eosinophils, a type of immune cell commonly found in the presence of allergies.
Moreover, third-generation offspring showed higher levels of interleukin proteins (namely IL-5 and IL-3), known to be involved in regulating the immune system, and also a marker of asthma risk. The more prominent results, however, were found among the first and second generations.
The team hypothesized that epigenetic mechanisms caused the transmission of these features across generations.
Epigenetics refers to the study of potentially heritable changes in gene activity that do not involve changes in the DNA sequence. These changes can be induced by external or environmental factors. Epigenetic changes are a natural occurrence, and they can also be influenced by age, lifestyle or disease.
DNA methylation is one type of epigenetic mechanism in which a chemical methyl group is added to the DNA molecule. Methylation can change the activity of genes.
Researchers found that exposure to environmental pollutants led to distinct DNA methylation changes in the three offspring generations, namely in immune cells called dendritic cells, which are known to play a key role in the development of asthma in early life.
These findings suggested that such DNA changes could be the cause for the increased risk of asthma to pass from generation to generation.
Environmental factors like air pollutants or cigarette smoking can influence epigenetic modifications, and may also be involved in skewing the immune system towards a particular type of feature associated with a higher susceptibility to asthma. They may also modulate the immune and inflammatory processes that affect treatment responsiveness.
The study may help doctors and researchers begin to recognize that asthma may not be merely an inflammatory disease but “to a large extent, an epigenetic disease,” Alexey Fedulov, its senior author, said in a press release. He noted that “this approach may allow entirely new therapeutic strategies.”