Charles Sande: Airway inflammation in early life
Chronic respiratory diseases disproportionately affect young adults in low income settings, particularly when they had been exposed to noxious substances from biomass smoke in early life. Using methods developed to understand airway inflammation caused by viral infections can help us understand the mechanisms underlying this pathology and better devise interventions.
I am Dr Charles Sande, I am a research fellow here at the KEMRI Wellcome Trust Research Programme in Kilifi, Kenya. I work in the general theme of respiratory viruses in children, how they respond to respiratory viruses and other exposures in early life.
My work is to look at how different exposures in early life, in particular respiratory viruses and increasingly environmental exposures such as chronic smoke exposure, affect how children respond in later life to other stimuli. For instance, previous research has shown that children who get infected by respiratory viruses such as RSV, tend to have a greater risk of developing diseases such as asthma. My work is to focus on how those exposures in early life stimulate those responses that then predispose children to those infections later in life.
I focus on specific viral infections; my 'pet' virus is the respiratory syncytial virus (RSV) which predominantly affects children in the first year of life, causing very severe pneumonia. I also work on other things: I am now transitioning from looking specifically at viruses to looking at respiratory exposures more holistically. I am particularly interested in looking at chronic exposure to indoor smoke pollution, and how that predisposes children to respiratory problems later in life.
Indoor smoke pollution in this case refers to exposure to biomass fuels, that people in sub-Saharan Africa and other low-resource settings use predominantly as fuel for cooking, for lighting and other energy uses in the household. Indoor smoke pollution is very noxious to the respiratory tract; therefore when children are chronically exposed they develop a response, which we postulate sets them up for an increased risk of respiratory problems in later life. This is an area of research we are transitioning into, using the tools that we have developed for research on respiratory viruses.
From my point of view, working in airway inflammation, I found really surprising and alarming within our part of the world in sub-Saharan Africa that the disproportionate effect of chronic smoke exposure is having on health in later life. An editorial in the Lancet about 3 or 4 years ago termed it a 'silent epidemic' of chronic respiratory diseases. It is something that is very pervasive in our society that individuals are exposed to these noxious substances from biomass smoke. But no one has really ever looked in any great depth to see how the respiratory tract responds to these exposures. My work for the next couple of years - contingent upon funding - will be to study how those exposures, in effect, remodel the respiratory tract and in so doing, how they elevate the risk of individuals then going on to develop chronic diseases such as asthma or COPD in later life.
When you think about chronic respiratory diseases such as COPD in the West, it is predominantly a disease of old people, it affects those who have smoked all their lives. In places like Africa, the incidence of COPDs is in people in their 30s is really quite striking. It stands to reason that such an early disease burden has to be associated with a shortened life expectancy and increased mortality fairly early in life. Strangely, nobody is looking at this. It is potentially a very serious thing that has gone under the radar, hence the editorial about the 'silent epidemic' of COPDs. It is a very important subject in a very vulnerable population that is completely underappreciated. In a sense, we are trying to invest the science we have developed in other areas and bringing it to bear into this neglected area to better understand the biology of these exposures. The ultimate aim is to develop appropriate interventions to address this problem.
The way we see our research eventually transitioning into clinical translation is by starting from the very basics: understanding the biology of these exposures, understanding how these exposures affect the respiratory tract. Once we understand that, then we can start thinking about areas in which we can prevent the noxious development of those exposures. In effect, looking at what drives the pathology then helps devise mechanisms to intervene against that pathology, and that is the way in which we are looking into it. Therefore, the interventions that we eventually develop will be informed by an understanding of the underlying biology of these exposures.
This interview was recorded in May 2019.