Ambient air pollution and inflammatory bowel disease—a narrative review
Review Article

Ambient air pollution and inflammatory bowel disease—a narrative review

Cyrla Zaltman1 ORCID logo, Paula Arruda do Espírito Santo2 ORCID logo, Marcia Henriques de Magalhães Costa3 ORCID logo

1Department of Internal Medicine, Federal University of Rio de Janeiro (Universidade Federal do Rio de Janeiro/UFRJ), Rio de Janeiro, RJ, Brazil; 2Diagnostic Imaging and Specialized Diagnosis Unit, Federal University of São Carlos, São Carlos, SP, Brazil; 3Department of Clinical Medicine, Fluminense Federal University, Niterói, RJ, Brazil

Contributions: (I) Conception and design: C Zaltman, MH de Magalhães Costa; (II) Administrative support: None; (III) Provision of study materials or patients: None; (IV) Collection and assembly of data: None; (V) Data analysis and interpretation: None; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

Correspondence to: Cyrla Zaltman, MD, PhD. Department of Internal Medicine, Federal University of Rio de Janeiro (Universidade Federal do Rio de Janeiro/UFRJ), rua Uruguaiana 10 sala 1304, centro, Rio de Janeiro, RJ 20050-090, Brazil. Email:

Background and Objective: Environmental factors interact with host cells, primarily during specific vulnerable periods in a genetically predisposed individual. These factors can act as triggers of an exaggerated immune response contributing to the development of inflammatory bowel disease (IBD). The connection between host genome, gut microbiome, and environmental exposures in the development of IBD requires further clarification. The objective of this review is to explore air pollution as a possible risk factor for the development of IBD.

Methods: We searched PubMed, Embase, and Cochrane Library databases to identify studies published up to September 15, 2023. We also analyzed references from relevant original articles and literature reviews to identify additional studies that were not encompassed in the initial database searches. For all eligible studies, we provided a narrative analysis of the findings.

Key Content and Findings: The onset of IBD results from the association of various risk factors including genetic susceptibility, diet, immune dysregulation, and environmental factors that could potentially trigger the disease. Although there are conflicting results regarding the impact of air pollution on IBD pathogenesis, it appears that its role in increasing the expression of pro-inflammatory cytokines, disturbances in microbiota composition and colonic function is associated with a higher risk of incident ulcerative colitis (UC).

Conclusions: Besides conflicting and inconsistent results from previous studies and notable knowledge gaps, there is a plausible chance that the development of IBD can be affected by air pollution. Future prospective studies are required to gain comprehensive insight into this correlation.

Keywords: Inflammatory bowel disease (IBD); ulcerative colitis (UC); Crohn’s disease (CD); air pollution

Received: 27 February 2023; Accepted: 27 March 2024; Published online: 29 May 2024.

doi: 10.21037/dmr-23-12


Inflammatory bowel disease (IBD) is a chronic inflammatory condition that affects the gastrointestinal tract, including Crohn’s disease (CD) and ulcerative colitis (UC) (1). Its etiology remains unknown, but it results from an exaggerated immune response to a trigger in susceptible individuals (2). Long-term or chronic exposure to air pollution has been linked to the development of respiratory diseases and other chronic inflammatory disorders, such as multiple sclerosis and rheumatoid arthritis. These conditions share certain epidemiological and pathogenic characteristics with IBD (3-5).

The incidence of IBD has significantly increased in developing countries over the past few decades, shedding light on the potential role of air pollution as an environmental trigger. Air pollution resulting from industrial progress interacts with susceptible host cells via various mechanisms. It can reversibly alter gene function without modifying the DNA sequence and may play a significant role in the induction or modification of IBD expression. Ambient air pollution exposure, especially during early life stages, may alter the microbiome’s composition and diversity, which could potentially heighten the probability of developing IBD in later stages of life (6).

The objective of this paper is to review air pollution as a potential risk factor for IBD development. We present this article in accordance with the Narrative Review reporting checklist (available at


We searched PubMed, Embase, and Cochrane Library databases to identify studies published up to September 15, 2023. The search strategy was as follows: (pollution) AND (“inflammatory bowel disease” OR IBD OR Crohn OR “ulcerative colitis”).

Two authors conducted an independent screening of all studies identified through the database search, initially based on titles and abstracts. After removing duplicate records and unrelated studies based on the titles and abstracts, full texts of potentially relevant articles were reviewed for inclusion if they met the predefined criteria [(I) observational studies (case series, case reports and cohort studies), reviews, meta-analysis and other studies; (II) reporting data on air pollution and IBD; (III) written in English, Portuguese or Spanish]. We also analyzed references from relevant original articles and literature reviews to identify additional studies that were not encompassed in the initial database searches. Disagreements were resolved through consensus or by a third author. For all eligible studies, we provided a narrative analysis of the findings. The search strategy summary is described in Table 1.

Table 1

The search strategy summary

Items Specification
Date of search July-09-2022, Sep-15-2023
Databases and other sources searched PubMed, Embase and Cochrane Library
Search terms used (pollution) AND (“inflammatory bowel disease” OR IBD OR Crohn OR “ulcerative colitis”)
Timeframe Up to September 2023
Inclusion criteria (I) Observational studies (case series, case reports and cohort studies), reviews, meta-analysis and other studies
(II) Reporting data on air pollution and IBD
(III) Written in English, Portuguese or Spanish
Selection process Two authors conducted an independent screening of all studies, and disagreements were resolved through consensus or by a third author
Additional considerations We also analyzed references from relevant original articles and literature reviews to identify additional studies that were not encompassed in the initial database searches


Air pollution is a complex mixture of heterogeneous substances. The most studied gases in its composition include carbon dioxide (CO2), carbon monoxide (CO), ozone (O3), nitric oxide (NO), nitrogen dioxide (NO2)—often used as a proxy for air pollution related to traffic, nitrogen oxides (NOx), sulfur dioxide (SO2), volatile organic compounds, and par ticulate matter (PM) of varying sizes—for example, PM10 and PM2.5 (7,8).

Studies have demonstrated that inhaled PM pollutants are efficiently cleared from the lungs into the intestine through mucociliary transport (8). These ingested contaminants can have direct and indirect effects on intestinal epithelial cells. Directly, they can alter tight junction proteins, leading to increased production of reactive oxygen species and permeability. Indirectly, these pollutants interact with gut microbiota, resulting in the production of toxins that have further negative effects (9).

Air pollutants can decrease microbes’ diversity and composition, reducing butyrate and short chain fatty acids production and increasing toxic metabolites output (9). This results in a feedback loop, enhancing the deleterious damage of the gut epithelial cells and inducing a pro-inflammatory response with a T cell activation and a Th1, Th17 and Th2 response (9,10). Based on these findings and epidemiological data, researchers conducted studies to explore the association between air pollution and gastrointestinal diseases. The studies assessed not only the pollutant concentration but also the duration of exposure. Despite significant limitations in the results, an association was found between sudden spikes in air pollution and incidents of gastroenteritis (11), non-specific acute abdominal pain (12), and appendicitis (13).

The rising and changing epidemiology of IBD over time and geography, particularly in emerging countries, indicates a potential association of accelerated industrialization and urbanization and IBD expression (14). Industrialization and urbanization can have various consequences that could be considered as triggers for IBD, such as changes in diet, use of antibiotics, hygiene, exposure to microorganisms, and, perhaps most importantly, pollution of water and air (3,14).

Li et al. analyzed the association of various specific air pollutants with the risk of incident IBD, among middle and old aged adults in UK, using a Biobank. Result of their analysis showed that long-term exposure to several air pollutants was associated with the risk of incident UC but not CD (7). A subgroup analysis of the study showed that the connection between all air pollutants and the likelihood of incident UC was significant for non-smokers but not for current smokers (7). The observed outcomes may be accounted for by the impact of nicotine on the production of mucus in the colon, which in turn limits the activity of inflammatory mediators including thromboxane synthetase, cyclooxygenase, and lipoxygenase. Subsequently, there is a plausible link to reduced risk of inflammation and potential mitigation of the negative impact of air pollution on the digestive system (12).

In a case-control study from the UK, Kaplan et al. found that NO2 was associated with a higher risk of UC in young individuals but highlighted the need for further studies in different sub-populations. The same study observed a higher risk of CD among participants aged <23 years who had postnatal NO2 exposure (15). This theory of children being more susceptible to the adverse effects of air pollution than adults were further examined in a study conducted in Canada. The study established a correlation between exposure to Ox during childhood and the development of IBD before the age of 18 (16).

Although a link between air pollutants and CD was not observed, Li et al. discovered an association between the risk of CD and the interaction of PM10 and NO2 in men (7).

In 2022, Adam et al. published a retrospective observational study on 8,136 patients and found a positive association between PM and the risk of autoimmune diseases. In particular, exposure to PM10 was associated with rheumatoid arthritis, while exposure to PM2.5 was associated with rheumatoid arthritis, connective tissue diseases and IBDs. It should be noted that PM2.5 molecules, given their smaller diameter, are less affected by rain and weather conditions than larger PM. In fact, PM2.5 concentrations tend not to fluctuate in response to rain and may represent a more accurate indicator of chronic exposure to air pollution than PM10 (17).

In 2010, Kaplan et al. published a study attempting to link air pollution and IBD. Their analysis revealed that individuals residing in areas with NO2 concentrations in the highest quintile were more likely to develop CD before the age of 23 than those from areas in the lowest quintile. Additionally, the researchers observed a similar association with UC instead of CD when investigating exposure to SO2 (15).

Some air pollutants may worsen the evolution and prognosis of IBD. In 2011, Ananthakrishnan et al. conducted an American ecological analysis, which indicated a significant correlation between countries with higher air pollution emissions and the number of hospitalizations for IBD in adults: for every 1-log increase in the density of total criteria pollutant emissions, there was a 40% increase in the rate of hospitalization (18).

In their study, Ding et al. explored whether daily exposure to PM, O3 and CO was linked to the risk of IBD hospitalizations in two Chinese hospitals. Each increase of 10 mg/m3 of PM, O3 and 0.1 mg/m3 of CO increased the risk of IBD, with the effect being stronger in hot seasons (19).

The most recent paper on this subject is a prospective cohort study published in 2023 by Chen et al., which analyzed the risk of enterotomy, gastrointestinal cancer and all-cause mortality in 4,708 patients with an average follow-up of 12 years. They found that each interquartile range increases in PM2.5 exposure was associated with an increased risk of enterotomy. An increased exposure to NOx and NO2 was also associated with increased all-cause mortality in IBD patients (20).

Several hypotheses have been proposed to explain the link between air pollution and IBD. These include the direct toxic effects of inhaled air pollution on epithelial cells, which can lead to gut microbiome disturbance, increased gut permeability, and immune response induction. Experimental data has shown that chronic exposure to PM can cause high levels of pro-inflammatory cytokines, as well as disruptions in microbiota composition and colon function in mice (3,8,21).

There are notable strengths in this review. We conducted an extensive literature review and could then offer insightful analysis and potential areas for further research on the topic. However, this study is also constrained by certain limitations, particularly those associated with conducting a narrative review, such as potential bias in the assessment of retrieved articles and interpretation of results. Despite all the epidemiological studies published to date on the relationship between air pollution and IBD, conflicting and inconsistent results persist, and significant knowledge gaps remain. Therefore, there is an urgent need for more prospective cohort studies to determine how air pollution affects IBD. The investigation should not only identify environmental factors associated with IBD, but also explore how these exposures are linked in terms of duration, frequency, and temporality, as highlighted by Vieujean et al. in their review about the impact of exposome on the epigenome in IBD (22).


The development of IBD is linked to a range of risk factors, including genetic susceptibility, diet, immune dysregulation, and environmental triggers. Although the effect of air pollution on IBD pathogenesis has yielded contradictory findings, its ability to increase pro-inflammatory cytokine expression, disrupt microbiota composition and colonic function suggests an increased risk of incident IBD. Several gaps still exist, indicating that additional prospective cohort studies are necessary to determine this association.


Funding: None.


Provenance and Peer Review: This article was commissioned by the Guest Editors (Patrick Varga-Weisz and Raquel Franco Leal) for the series “Evidence of Epigenetics in Inflammatory Bowel Diseases” published in Digestive Medicine Research. The article has undergone external peer review.

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at

Peer Review File: Available at

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at The series “Evidence of Epigenetics in Inflammatory Bowel Diseases” was commissioned by the editorial office without any funding or sponsorship. The authors have no other conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See:


  1. Sartor RB. Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis. Nat Clin Pract Gastroenterol Hepatol 2006;3:390-407. [Crossref] [PubMed]
  2. Kuhnen A. Genetic and Environmental Considerations for Inflammatory Bowel Disease. Surg Clin North Am 2019;99:1197-207. [Crossref] [PubMed]
  3. Ananthakrishnan AN, Bernstein CN, Iliopoulos D, et al. Environmental triggers in IBD: a review of progress and evidence. Nat Rev Gastroenterol Hepatol 2018;15:39-49. [Crossref] [PubMed]
  4. Noorimotlagh Z, Azizi M, Pan HF, et al. Association between air pollution and Multiple Sclerosis: A systematic review. Environ Res 2021;196:110386. [Crossref] [PubMed]
  5. Cohen R, Robinson D Jr, Paramore C, et al. Autoimmune disease concomitance among inflammatory bowel disease patients in the United States, 2001-2002. Inflamm Bowel Dis 2008;14:738-43. [Crossref] [PubMed]
  6. Cholapranee A, Ananthakrishnan AN. Environmental Hygiene and Risk of Inflammatory Bowel Diseases: A Systematic Review and Meta-analysis. Inflamm Bowel Dis 2016;22:2191-9. [Crossref] [PubMed]
  7. Li FR, Wu KY, Fan WD, et al. Long-term exposure to air pollution and risk of incident inflammatory bowel disease among middle and old aged adults. Ecotoxicol Environ Saf 2022;242:113835. [Crossref] [PubMed]
  8. Salim SY, Jovel J, Wine E, et al. Exposure to ingested airborne pollutant particulate matter increases mucosal exposure to bacteria and induces early onset of inflammation in neonatal IL-10-deficient mice. Inflamm Bowel Dis 2014;20:1129-38. [Crossref] [PubMed]
  9. Salim SY, Kaplan GG, Madsen KL. Air pollution effects on the gut microbiota: a link between exposure and inflammatory disease. Gut Microbes 2014;5:215-9. [Crossref] [PubMed]
  10. Möller W, Häussinger K, Winkler-Heil R, et al. Mucociliary and long-term particle clearance in the airways of healthy nonsmoker subjects. J Appl Physiol (1985) 2004;97:2200-6. [Crossref] [PubMed]
  11. Orazzo F, Nespoli L, Ito K, et al. Air pollution, aeroallergens, and emergency room visits for acute respiratory diseases and gastroenteric disorders among young children in six Italian cities. Environ Health Perspect 2009;117:1780-5. [Crossref] [PubMed]
  12. Kaplan GG, Szyszkowicz M, Fichna J, et al. Non-specific abdominal pain and air pollution: a novel association. PLoS One 2012;7:e47669. [Crossref] [PubMed]
  13. Kaplan GG, Dixon E, Panaccione R, et al. Effect of ambient air pollution on the incidence of appendicitis. CMAJ 2009;181:591-7. [Crossref] [PubMed]
  14. Cui G, Liu H, Xu G, et al. Exploring Links Between Industrialization, Urbanization, and Chinese Inflammatory Bowel Disease. Front Med (Lausanne) 2021;8:757025. [Crossref] [PubMed]
  15. Kaplan GG, Hubbard J, Korzenik J, et al. The inflammatory bowel diseases and ambient air pollution: a novel association. Am J Gastroenterol 2010;105:2412-9. [Crossref] [PubMed]
  16. Elten M, Benchimol EI, Fell DB, et al. Ambient air pollution and the risk of pediatric-onset inflammatory bowel disease: A population-based cohort study. Environ Int 2020;138:105676. [Crossref] [PubMed]
  17. Adami G, Pontalti M, Cattani G, et al. Association between long-term exposure to air pollution and immune-mediated diseases: a population-based cohort study. RMD Open 2022;8:e002055. [Crossref] [PubMed]
  18. Ananthakrishnan AN, McGinley EL, Binion DG, et al. Ambient air pollution correlates with hospitalizations for inflammatory bowel disease: an ecologic analysis. Inflamm Bowel Dis 2011;17:1138-45. [Crossref] [PubMed]
  19. Ding S, Sun S, Ding R, et al. Association between exposure to air pollutants and the risk of inflammatory bowel diseases visits. Environ Sci Pollut Res Int 2022;29:17645-54. [Crossref] [PubMed]
  20. Chen J, Dan L, Sun Y, et al. Ambient Air Pollution and Risk of Enterotomy, Gastrointestinal Cancer, and All-Cause Mortality among 4,708 Individuals with Inflammatory Bowel Disease: A Prospective Cohort Study. Environ Health Perspect 2023;131:77010. [Crossref] [PubMed]
  21. Kish L, Hotte N, Kaplan GG, et al. Environmental particulate matter induces murine intestinal inflammatory responses and alters the gut microbiome. PLoS One 2013;8:e62220. [Crossref] [PubMed]
  22. Vieujean S, Caron B, Haghnejad V, et al. Impact of the Exposome on the Epigenome in Inflammatory Bowel Disease Patients and Animal Models. Int J Mol Sci 2022;23:7611. [Crossref] [PubMed]
doi: 10.21037/dmr-23-12
Cite this article as: Zaltman C, do Espírito Santo PA, de Magalhães Costa MH. Ambient air pollution and inflammatory bowel disease—a narrative review. Dig Med Res 2024;7:13.

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