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A study in linked inflammatory bowel disease (IBD) risk with past exposure to environmental pollutants, mostly pesticides.

In this interview, study author Manasi Agrawal, MD, of the Icahn School of Medicine at Mount Sinai in New York City, discusses the findings.

The following is a transcript of her remarks:

The objective of this pilot study was to measure environmental pollutants in serum samples in our nested case-control study of active military recruits. We have access to serum samples via my mentor Jean-Frederic Colombel -- who is the PI [principal investigator] of the -- up to 10 years before Crohn's disease or ulcerative colitis diagnosis. And so in these serum samples, we wanted to measure environmental pollutants and understand their relationship with inflammatory bowel disease.

In terms of the results, we measured pesticides in serum samples up to 10 years before diagnosis in our nested case-control study using high resolution mass spectrometry alongside our incredible colleagues in environmental health sciences, Lauren Petrick, Vishal Midya, and others. We measured hundreds of different chemicals using this technique, and then we applied mixtures methods to understand how all of these chemicals as a composite linked with inflammatory bowel disease.

We found that prior to diagnosis, this mixture of chemicals was linked with increased risk of both ulcerative colitis and Crohn's disease at 6-10 years before diagnosis, but not at time points closer to diagnosis. This indicates to us that there may be a link between exposure to these chemicals, which primarily consisted of pesticides, and IBD risk when the exposure occurred several years pre-diagnosis.

This study is important because to our knowledge, this is the first study to measure pesticides prior to disease onset, which gives us a temporality, meaning exposure followed by disease diagnosis, and it also helps us understand the relationship with inflammatory bowel disease.

Second, we used this very objective methodology to measure hundreds of different chemicals in serum samples.

And third, we used a very sophisticated mixtures model to understand how as a composite these chemicals may be linked with IBD.

Finally, we also noticed a lag, meaning exposure to these chemicals 6-10 years pre-diagnosis was associated with an increased odds of IBD, but not exposure at closer time points, indicating that there is a lag period, which potentially may have to do with the time taken for the biological effects of these exposures to occur.

I think another very important consideration that this study brings to light is the importance of collaborating across different scientific domains, so environmental health sciences and clinical medicine, and how such collaborations are very important towards understanding how the environment plays a role in our health, the risk of chronic diseases, and various outcomes.

Based on the results that we observed, I think the next steps for the IBD and research community would be validation in external cohorts. I think this would be very important to understand how various pesticides, how various environmental pollutants, link with IBD risk across diverse populations across diverse pollutants.

We also need mechanistic insights. This will be very important to understand how pesticides and other chemicals influence biological processes leading to, potentially, inflammatory bowel disease. And based on all of these data, there may be impacts on regulation as to how these chemicals find their way into our daily lives.

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