Air Pollution Linked to Increased IBS Incidence

Air Pollution Linked to Increased IBS Incidence


Increased levels of air pollution were linked to a slight uptick in new diagnoses of irritable bowel syndrome (IBS) in California residents, according to an ecologic study published in Clinical Gastroenterology and Hepatology.

“These data provide support for the role of environmental pollutants, especially air pollutants, in the development of IBS,” Philip N. Okafor, MD, MPH, of Stanford (Calif.) University, and colleagues wrote. “In contrast, we found no significant relationships between the seven environmental exposures and the zip-code level incidence of functional dyspepsia, ulcerative colitis, Crohn’s disease, and eosinophilic esophagitis.”

The researchers noted that an “epidemiological shift in gastrointestinal diseases is underway,” with increasing incidence of inflammatory bowel disease (IBD), eosinophilic esophagitis, and disorders related to gut-brain interaction.

“While the underlying causes of this shift remain unclear, the association with industrialization suggests that environmental triggers may play a role in disease pathogenesis,” the authors wrote. One potential mechanism to explain such an association could be local or systemic inflammation resulting from pollution exposure and leading to tissue injury. Others could include alterations in the gut microbiome or direct damage to the mucosal epithelial barrier from pollutants, which then results in epithelial cell death and subsequently increased intestinal permeability.

To explore whether any such associations exist, the researchers analyzed the incidence of IBS, functional dyspepsia, ulcerative colitis, Crohn’s disease, and eosinophilic esophagitis in different California zip codes with regards to each area’s levels of seven different pollutant markers. They used claims data for patients with Optum insurance to identify new diagnoses by zip code for nearly 2.9 million adult patients between 2009 and 2014 (ICD-9 era) and nearly 2.5 million patients between 2016 and 2019 (ICD-10 era). Preexisting diagnoses were excluded. The analysis included 1,365 different zip codes.

The measures of pollutants they assessed included the following: ozone, particulate matter less than 2.5 mcm (PM2.5), diesel emissions, drinking water contaminants, pesticides, toxic releases from industrial facilities, and traffic density. They used shoulder dislocations as a negative control in comparing incidence, and they adjusted the analysis to account for socioeconomic markers, patient-level sampling estimates, and county-level fixed effects.

Socioeconomic markers included not only income and race/ethnicity but also health insurance status, educational level, proportion of owner-occupied homes, median house prices, and the proportion of households receiving food stamps or meeting criteria for food insecurity. Given the number of potential confounders, the authors also made statistical adjustment (Bonferroni correction) to account for many multiple comparisons and reduce the likelihood of inflated statistical significance for any one finding.

The researchers found that the incidence of IBS per zip code was associated with the levels of PM2.5 and industrial airborne toxic releases during both time periods. An increase of 1 mcg/m3 of PM2.5 or additional 1% in toxic releases correlated with an additional 0.02 cases of IBS per 100 person-years (adjusted incidence rate ratios approximately 1.03 for IBS associated with both pollutants during both time periods).

“These associations were maintained across extensive adjustment for residual confounding and sensitivity analyses,” the authors added.

Although the researchers also identified an association between IBS incidence and both traffic density and drinking water contaminants, these did not reach statistical significance after adjustment for multiple comparisons. Similarly, diesel particulate matter emissions were associated with functional dyspepsia and IBS until the statistical correction for multiple comparisons. None of the other conditions’ incidence was associated with any pollutant measured included in the study.

The study’s biggest limitation is its ecologic design, which cannot link individual people’s exposures to their specific diagnosis. They also could not consider seasonal changes in pollutant levels or the possible interaction or cumulative effects of different pollutants. The authors also noted a number of other pollution exposures that they did not measure at all in this study, such as nitrogen dioxide, sulfur dioxide, heavy metals, or bacteria.

The authors reported no conflicts of interest. The research was funded by the National Institutes of Health and Stanford University.

This article originally appeared on, part of the Medscape Professional Network.

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