In-utero exposure to noxious gasses adversely affects the respiratory health of the developing child. Epidemiological studies have found clear associations between in-uteroexposure to inhaled oxidants such as cigarette smoke or pollution and the subsequent development of asthma and COPD, however the reason why this occurs is largely unknown. We discovered that in-utero exposure to cigarette smoke resulted in oxidative stress driven pulmonary inflammation in the offspring at birth which persisted into adulthood. 

In our second forerunner study, we were the first to show that in-uteroexposure to e-cigarette aerosols with or without nicotine results in increased oxidative stress and chronic lung inflammation in offspring. This is likely caused by altered epigenetic imprinting (DNA methylation), as we found maternal e-cigarette exposure increased DNA methylation in the offspring.  DNA methylation is an epigenetic control mechanism which represses gene transcription. 

These findings lead us to hypothesise that in-utero exposure to inhaled oxidants epigenetically reprograms DNA, including specific changes in lung cells, resulting in chronic inflammation and heightened allergic and inflammatory responses. 

In your PhD, you will discover which genes are epigenetically reprogrammed in-utero following exposure to inhaled oxidants. 

please contact brian.oliver@uts.edu.au for more information.