Clin Gastroenterol Hepatol. 2023 Jun;21(6):1617-1626.e9. doi: 10.1016/j.cgh.2022.09.025.Epub 2022 Oct 3.

Philip N Okafor ¹, Alex Dahlen ², Michael Youssef ³, Adegboyega Olayode ⁴, Irene Sonu ⁵, Leila Neshatian ⁵, Linda Nguyen ⁵, Vivek Charu ⁶

Author information

¹Department of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, California. Electronic address: philokafor@post.harvard.edu.

²Quantitative Sciences Unit, Department of Medicine, Stanford University School of Medicine, Stanford, California.

³Department of Internal Medicine, University of Toronto Medical School, Toronto, Ontario, Canada.

⁴Division of Hospital Medicine, Emory University School of Medicine, Atlanta, Georgia.

⁵Department of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, California.

⁶Quantitative Sciences Unit, Department of Medicine, Stanford University School of Medicine, Stanford, California; Department of Pathology, Stanford University School of Medicine, Stanford, California. Electronic address: vcharu@stanford.edu.

Abstract

Background and aims: Prior studies have linked environmental pollutants with gastrointestinal (GI) diseases. Here, we quantify the relationships between 7 pollutants and the zip code-level incidence of irritable bowel syndrome (IBS), functional dyspepsia, inflammatory bowel diseases (IBDs), and eosinophilic esophagitis (EoE) in California.

Methods: Claims in Optum's Clinformatics Data Mart were linked with environmental exposures in California, derived from CalEnviroScreen 3.0. We identified adult patients with new diagnoses of each GI disease, and estimated claims-derived, zip code-level disease incidence rates. Two study periods were considered: 2009-2014 (International Classi?cation of Diseases-Ninth Revision era) and 2016-2019 (International Classi?cation of Diseases-Tenth Revision [ICD-10] era). Multivariable negative binomial regression models were used to test associations between 7 pollutants (ozone, particulate matter <2.5 μm [PM2.5], diesel emissions, drinking water contaminants, pesticides, toxic releases from industrial facilities, traffic density) and zip code-level incidence of the GI diseases along with a negative control outcome, adjusting for numerous potential confounders.

Results: Zip code-level IBS incidence was associated with PM2.5 (P < .001 in both eras) and airborne toxic releases from facilities (P < .001 in both eras). An increase of 1 μg/m³ in PM2.5 or 1% in toxic releases translates to an increase in the IBS incidence rate of about 0.02 cases per 100 person-years. Traffic density and drinking water contaminant exposures were also associated with increasing IBS incidence, but these associations were not significant in both eras. Similarly, exposure to PM2.5, drinking water contaminants and airborne toxic releases from facilities were associated with functional dyspepsia incidence, though not in both eras. No significant associations were noted between pollutants and IBD or EoE incidence.

Conclusion: Exposure to PM2.5 and airborne toxic releases from facilities are associated with higher IBS incidence among a cohort of commercially insured Californians. Environmental pollutant exposure was not associated with the incidence of IBDs and EoE in this cohort.