The American Journal of Managed Care® (AJMC®) interviewed Elisabet Johansson, PhD, a research fellow at the University of Cincinnati, about how the gene NFE2L2 interacts with secondhand smoke, and increases the risk of asthma.
The American Journal of Managed Care® (AJMC® ) interviewed Elisabet Johansson, PhD, a research fellow at the University of Cincinnati, about how the gene NFE2L2 interacts with scondhand smoke and increases the risk of asthma. Johansson's study entitled, "NFE2L2 Interacts with Second Hand Smoke Exposure to Increase the Risk and Severity of Pediatric Asthma" explored the role of the genotype in this condition. The abstract was released through the American Academy of Allergy, Asthma & Immunology (AAAAI), which canceled its 2020 Annual Meeting due to COVID-19.
AJMC®: This study was conducted on samples taken from children are these results transferable to adults and other age groups with asthma?
Johannson: It's unlikely that they will be because asthma in children is very different. Allergy in general is sort of a progression. We talk about the atopic march, that children tend to first develop atopic dermatitis and then later on they go on to develop asthma and allergic rhinitis. The risk factors for adult astha are different. Most of the interaction studies that have shown the interaction between genotypes and air pollution have been done on children. But it's certainly true that air pollution is a risk factor for asthma on its own. That has been shown many times in both in adults and children.
AJMC®: NFE2L2 genotyping found that 3 SNPs interacted significantly with secondhand smoke exposure to increase asthma risk. Can you explain this link in the context of pulmonary or lung health?
Johannson: Air pollution and secondhand smoke produces reactive oxygen species that in turn produce oxidative stress in cells. This oxidative stress is also involved in inflammatory reactions, and the particular gene in question is involved in the defense against oxidative stress. So when you have several different genotypes of a gene, one may be more effective than the other.
AJMC®: Do these results translate to an observable clinical difference in children's health?
Johannson: What it shows is that we all know that air pollution and secondhand smoke is bad for lung health. But what these studies show, similarly to other interaction studies, is that if you have a certain genotype, you're more vulnerable to certain exposures, for example, secondhand smoke. If those vulnerable populations can be identified early, you can monitor those children and be on the lookout for future development of asthma.
AJMC®: Interactions between secondhand smoke exposure and the genotype are associated with an increased risk of daily asthma symptoms. Should children with asthma be tested for this genotype, and if so, what do parents do with this knowledge?
Johannson: Currently, I think few doctors offices are really set up to do genetic testing. This is not the only gene that that interacts with secondhand smoke and air pollution. There are other genes, for example, glutathione-S transferase. It's a family of genes that are known to similarly create vulnerable populations that have certain risk variants of these genes. Yes, you could in principle. Maybe in the future that is something that could be realized. At this point, it's not a technology that's available in in a regular doctor's office, but it's certainly something that may, in the future, be an option.
AJMC®: Do you have any other aspect of your research we didn't touch on that you would like to highlight?
Johannson: I would stress that we're really talking about identifying vulnerable populations. We talk a lot about genotyping, trying to find a genetic vulnerability for certain diseases. But what we found in our study was that when we looked at all children, and then looked for associations between NFE2L2 to a genotype, and asthma, we didn't see anything. It was only among those children who had been exposed to secondhand smoke that we saw this association between genotype and asthma.
I think that was an important observation, because that explains why you have to take both phenotype and environment into account. That is generally something that's true for a lot of diseases. It's not only geneotype. The take home message that I would like to stress is that you really have to take both phenotype and environmental factors into account to understand how genetics are associated with disease.