David Savitz (Brown University, USA) answers some of the questions from the participants in the webinar “COVID19: The Day Before”.
When we mention that more research is needed, how important are children in this research? Noting their suppressed vaccine response if they have a larger PFAS exposure and in general being more susceptible to change. Rebecka Jonsson
DAVID SAVITZ (Brown University): It is true that the evidence of PFAS adversely affecting immune response is greater than that for adults, so it is reasonable to speculate that children’s susceptibility to infectious disease would be impaired. As I noted, the direct evidence that it does so is very limited and it would be helpful to conduct sufficiently large, rigorous studies to detect adverse effects on those infections children are most susceptible to. This would not necessarily apply to COVID-19 where children seem to be less vulnerable but would apply to a wide range of other pathogens that affect children.
I suggest these presentations underscore the fact that the very basics of exposure assessment in the context of environmental epidemiology and/or infectious disease epidemiology are necessary. Do you agree? If so, can you share examples of collaboration between exposure scientists and epidemiologists in applying this formula to the Covid19 pandemic? J.R. Nuckols, PhD
DAVID SAVITZ: As always in environmental epidemiology, the quality of exposure assessment is often the limiting factor in determining study quality. In assessing the connection between environmental pollutants and infectious disease, both must be assessed carefully particularly because we expect effects, if present, to be modest in magnitude. This is an important point in that environmental epidemiologists may assess pollutant exposure with rigor but be less familiar with how to assess exposure to infectious agents and vice versa. The study team clearly needs to include both realms of expertise in exposure assessment.
What do you think might be the role of environmental impacts (pollution, chemicals, warming, urbanization) on gut microbiome in our responses to infectious diseases? Denise Naniche
DAVID SAVITZ: That would constitute another pathway for environmental agents to influence infectious disease
risk, also with limited data to the best of my knowledge. It is quite reasonable to consider the potential for environmental pollutants to alter the microbiome in multiple sites including but not limited to gut microbiome. In fact, this could be a more sensitive endpoint than the presence of clinical infection to consider as a potential consequence of environmental pollution.