Environmental Pollutants Are Associated With Irritable Bowel Syndrome in a Commercially Insured Cohort of California Residents

医学 肠易激综合征 入射(几何) 环境卫生 嗜酸性食管炎 混淆 内科学 疾病 光学 物理
作者
Philip N. Okafor,Alex Dahlen,Michael Youssef,Adegboyega Olayode,Irene Sonu,Leila Neshatian,Linda Anh B. Nguyen,Vivek Charu
出处
期刊:Clinical Gastroenterology and Hepatology [Elsevier]
卷期号:21 (6): 1617-1626.e9 被引量:13
标识
DOI:10.1016/j.cgh.2022.09.025
摘要

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 Classification of Diseases–Ninth Revision era) and 2016–2019 (International Classification 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.
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