Some Environmental Pollutants Linked to IBS

Certain environmental pollutants were associated with a higher incidence of irritable bowel syndrome (IBS) among a cohort of commercially insured California residents, a large retrospective study showed.

In 1,365 distinct zip codes, exposures to particulate matter <2.5 microns (PM2.5) and airborne toxic releases from facilities were associated with zip code-level IBS incidence during the ICD-9 era from 2009-2014 and the ICD-10 era from 2016-2019 (P<0.001 for both), reported Philip Okafor, MD, MPH, of Stanford University School of Medicine in California, and colleagues.

Specifically, for PM2.5, there was an adjusted incidence rate ratio (aIRR) of 1.032 (95% CI 1.019-1.045) in the ICD-9 era, and an aIRR of 1.025 (95% CI 1.012-1.039) in the ICD-10 era.

For airborne toxic releases, aIRRs were 1.037 (95% CI 1.024-1.050) and 1.027 (95% CI 1.013-1.041), respectively, the group noted in Clinical Gastroenterology and Hepatology.

Every 1 mcg/m³ increase in PM2.5 or 1% increase in airborne toxic releases translated into an increase in IBS incidence of approximately 0.02 cases per 100 person-years — nearly a 3% spike — corresponding to about 7,000 additional annual cases in California, the authors said.

“This is the first study to systematically examine relationships between multiple environmental pollutants and the incidence of several GI diseases in a large population-level cohort,” Okafor and team wrote.

“Pollutant exposure to the gut epithelium can incite local/systemic inflammatory response causing oxidative stress and tissue injury,” they explained. “Pollutants may directly damage the mucosal epithelial barrier causing epithelial cell death, leading to increased intestinal permeability; and pollutants may alter the gut microbiome.”

Drinking water contaminants and traffic density were also linked with increased IBS incidence, but this was only significant during the ICD-9 era, while exposures to airborne toxic releases from facilities, PM2.5, and drinking water contaminants were linked to functional dyspepsia (FD) only during the ICD-10 era.

No significant associations were seen between pollutants and the incidence of inflammatory bowel disease (IBD) or eosinophilic esophagitis (EoE).

The incidence of gastrointestinal diseases has epidemiologically shifted in recent years, Okafor’s group noted. Prior studies have indicated a disproportionate disease burden in recently developed or developing countries, among the elderly, and in new immigrants to the West. While the reasons for this remain largely unknown, researchers have suggested that environmental triggers driving disease development may play a role.

For this ecologic study, Okafor and colleagues examined claims data from Optum’s Clinformatics Data Mart on over 5.3 million California residents during 2009-2014 (n=2,885,171) and 2016-2019 (n=2,491,710). They used a negative control outcome, comparing adults who were diagnosed with a new GI disease, including IBS, IBD, EoE, and FD, with those with shoulder dislocations. Nearly 40% of adults in both eras were 18 to 40 years old, and half were women.

Pollution community vulnerability was evaluated by CalEnviroScreen 3.0 from 2015 to 2018. Okafor and team looked at seven pollutants — pesticides, ozone, PM2.5, diesel emissions, airborne toxic releases from industrial facilities, drinking water contaminants, and traffic density. They adjusted for sociodemographics, county-level fixed effects, and other factors.

The authors acknowledged that they couldn’t assess individual-level exposures, instead using a retrospective study design, which was a limitation. Moreover, other environmental exposures have been linked with the GI diseases assessed in the study, including nitrogen dioxide, sulfur dioxide, heavy metal content, and bacteria prevalence.