Smoking has been known to have negative effects during pregnancy such as asthma and decline in lung function. According to new research, smoking during pregnancy can also lead to defects within the alveoli, tiny air sacs in the lungs where the exchange of oxygen and carbon dioxide takes place, due to a disruption in retinoic acid signaling.
In order to understand the mechanism behind this, researchers from the Brigham and Women's Hospital looked at the effect of maternal smoking on retinoic acid signaling in mice. Retinoic acid (RA) is produced in the body from Vitamin A and is known to be involved in alveolar development as well as lung maintenance throughout life.
At the conclusion of the study, maternal smoking affected the number and birth weight of the mice pups. It also affected the development of their lungs and disrupted retinoic acid signaling within the lungs.
Dr. Kathleen Haley, who led the research, was quoted as saying, "The pups were protected from breathing smoke themselves but were still affected by 'second hand' smoke before birth and through their mother's milk. Smoking affected the regulation of genes, controlled by RA, necessary for lung development, including surfactant Apo protein B. It is known that complete loss of surfactant Apo protein B is linked to severe respiratory failure in infants and down regulation of this, and other genes regulated by RA, can have potentially serious consequences."
The decreases in RA signaling and in the expression of RA controlled genes were most pronounced during the 3-5 days after birth when the lungs are undergoing rapid development. In humans this development stage occurs before birth when the developing fetus receives 'second hand' smoke via the umbilical cord so it seems very likely that the same damaging effects of cigarette smoke on RA signaling are present in humans too.