Environmental Triggers of Atopic Dermatitis & Seasonal Allergies

In this interview, Peter Lio, MD, explores how modern environmental exposures—from pollution to lifestyle shifts—are accelerating type 2 inflammation and fueling atopic dermatitis and seasonal allergies in today’s patients.

Peter Lio, MD is a Clinical Assistant Professor of Dermatology & Pediatrics at Northwestern University Feinberg School of Medicine.

Transcript:

Dr Lio: Hi, I am Peter Lio. I'm a clinical assistant professor of dermatology and pediatrics at Northwestern University Feinberg School of Medicine in Chicago, Illinois. I'm also the founding director of the Chicago Integrative Eczema Center.

From your perspective, what environmental factors today are most significantly accelerating Type 2 inflammation and atopic disease, especially in patients with seasonal allergies or atopic dermatitis?

Dr Lio: This has been such an exciting time because for so long we've noticed that the rate of allergies, the incidences of allergies, keeps seemingly going up and up and up. And this has been very problematic and I don't think we had a great answer until the last couple of years where now it's starting to finally crystallize that there is no doubt there are environmental triggers and causes of this progression.

And I really give a lot of credit to Dr Ian Miles. He's an allergist at the National Institutes of Health. He gave a beautiful lecture several years ago where he used an analogy that sticks with me to this day, and I often invoke him because I think it's so smart. If you live near a lake and you saw a bunch of fish had died, you might first say, well boy, what's wrong with these fish? What's the problem with these particular fish that died? But at some point, if tons of fish are dying in the lake and they're washing up all over the shore, you'd say, wait a minute. What's wrong with this lake? This is not a fish problem. This isn't an individual problem. This is an environmental issue.
And I think we've really crossed over that threshold because we know that the rate of change of allergies in general and type 2 inflammation is way faster than any kind of genetic issue. This is clearly a lifestyle or environmental piece. And I think one of the interesting touch points that we can at least hang our hat on to start with, it may not be the be-all end-all, but it's an important identification.

Again, this is Dr Ian Miles' work is that this class of chemicals called diisocyanates seems to be strongly correlated with the development of atopic dermatitis. And there's some really interesting, as many times we get the initial hints from epidemiology, and one of the really interesting breadcrumbs here was that people who were exposed to wildfire smoke, and it turns out that wildfire smoke has a lot of these isocyanates and diisocyanates. They had a huge uptick in new onset eczema. So this is a big deal. I think finally we're understanding it, and we even have a good possible reason why or a possible mechanism about what's going on under the hood. And part of it is that it's directly damaging to our skin barrier, but also it's disruptive to our microbiome. It kind of poisons the microbiome, and we understand that that also can be a reason for this.
And then once you look at it through that lens, there's another allergist named Cezmi Akdis, and he, I believe, is based in Switzerland. And he writes this beautiful work all about the barrier hypothesis. And it's really sophisticated in that we understand that not just our skin but our gut barrier and our respiratory epithelium, all these epithelial barriers are under constant attack from environmental pollutants and toxins that are damaging the barrier, affecting the microbiome. And voila, this is the story.
So I think finally we have at least something to start with, a reason to give to our patients to say, why is this happening to me? Why is this all over the place? Like, ah, because we're kind of immersed in this toxic lake analogy, if you will, and it's hurting our ability to keep the outside world out and then allowing us to get these allergic reactions and sensitization happening. So we need to think about it from that perspective.

Allergists and immunologists often manage patients with overlapping respiratory allergies and atopic dermatitis. How do you see environmental barrier disruption linking these conditions to day-to-day practice?

Dr Lio: I think for a long time we've known that clearly environmental things can cause they can trigger a flare, right? So if you are in a place where it's very dusty or there are lots of aeroallergens, you might start coughing. I mean clearly or highly fragrance things, your nose starts running, your rhinitis kicks in, irritating things on the skin. So this is very clear, but that is all still true a hundred percent.

But now we're even going one step further that the idea that there are things that maybe aren't directly causing a flare directly, they're not triggering you, but they're contributing to the development of these diseases over time, sort of a lower degree or of chronic inflammation and chronic barrier damage. And I think to me, something that I've talked about with my patients, and I'm very transparent. I say this is probably not the whole story. In fact, I'd be willing to bet anything that's not the whole story, but it's a really important inroad to the story, and it's this idea of transcutaneous sensitization.

So if our barriers are getting damaged and particularly our skin is one of the first ones, then it makes sense that allergens and irritants can get into our skin and into our body in an abnormal way, and that drives this inflammation, which then can manifest in the lungs, in the gut, and in the skin. So we really are beginning to put it all together a little bit more holistically. And I love it because so many of my patients start the discussion with, I think a food is driving my eczema. And that can be true sometimes. It turns out it's pretty rare. In my experience, it's actually almost never really the main driver, but it can be. So I don't want to just dismiss it out of hand. However, what really is important is to understand that if the skin barrier is damaged, you're much more likely to develop food allergies, presumably, at least again, in part through your skin. This trans epidermal or transcutaneous sensitization allows you to develop food allergies over time.

So we have all of these factors. We have things that can directly trigger a flare up. We also have things that are indirectly driving this whole progression towards type 2 inflammation and understanding that it's complicated. I wish it were really easy to just explain, but you take a couple of minutes and explain it. And I've seen so many patients and families go, oh, that makes a lot of sense, right? Suddenly it all starts to fit together. And we realized we were chasing our tail trying to find is it gluten that gives you eczema? Probably not. I mean, certainly inflammatory foods can drive your flareups and stuff to some degree, but this is different than an allergy, right? It's the other way around. It's the fact that you now have severe life-threatening anaphylaxis to peanuts probably because you had broken skin barrier and the peanut allergen entered the skin in an abnormal way.