The study will be electronically published on June 1, 2012 in BioMed Central’s open access journal, Respiratory Research.
It is known that the effects of smoking on the developing lung have long-term consequences for the child’s health. Children of mothers who smoke have an increased risk of asthma and lung infections and have a more rapid decline of lung function if they begin to smoke as adults.
In order to understand the mechanism behind this, BWH researchers looked at the effect of maternal smoking on retinoic acid signaling in mice. Retinoic acid is made in the body from vitamin A and is known to be involved in lung development and maintenance throughout life.
Maternal smoking affected the number and birth weight of their pups. It also affected the development of the pups’ lungs and disrupted retinoic acid signaling in their lungs. Reduction of retinoic acid signaling was also seen in lung cells treated with cigarette smoke in the lab.
“The pups were protected from breathing smoke themselves but were still affected by ‘second hand’ smoke before birth and through their mother’s milk,” said Kathleen Haley, MD, BWH Pulmonary Division, Department of Medicine, who led the research. “Smoking affected the regulation of genes, controlled by retinoic acid, necessary for lung development, including surfactant apoprotein B. It is known that complete loss of surfactant apoprotein B is linked to severe respiratory failure in infants and down regulation of this, and other genes regulated by retinoic acid, can have potentially serious consequences.”
The decreases in retinoic acid signaling and in the expression of retinoic acid-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 retinoic acid signaling are present in humans too.
This press release was adapted from an original version provided by BioMed Central.
This research was supported by Flight Attendants Medical Research Institute, National Institutes of Health (NIH K08 HL7910, NIH R01 HL097144 and NIH R03 ES16399), and Lovelace Respiratory Research Institute/ Brigham and Women’s Hospital consortium for lung research.