Inflammatory Bowel Disease and the Role of Environmental Toxicants and Triggers

Inflammatory bowel disease, such as ulcerative colitis and Crohn’s disease, is an autoimmune disorder in which the body’s own immune system over-reacts against cells in the gut and causes uncontrolled inflammation. It affects about 2.4 million people in the U.S. and about 4.9 to 6.8 million people worldwide. While research progress continues to provide insights into the inflammatory process underlying inflammatory bowel disease, the exact causes of inflammatory bowel disease in each individual patients remains elusive.

Current limitations of medicine

In a clinical setting, patients diagnosed with ulcerative colitis or Crohn’s disease remain uninformed of what triggered their inflammatory bowel disease in the first place. This is not the fault of the physician or health care professional, because current clinical advances simply do not allow the physician to establish the exact cause of the inflammatory bowel disease in the patient in front of them. And if the cause of the disease cannot be established, of course it cannot be removed for the sake of reversing or curing the disease—or preventing the disease. That is why in the treatment of an autoimmune disease such as inflammatory bowel disease, the pharmacologic intervention is usually directed at suppressing the immune system only, as opposed to the much more precise and intuitively superior approach of targeting the known cause and eliminating it.

Given the current limitations as mentioned above, a prudent and mindful approach in the care of patients with inflammatory bowel disease takes the form of understanding each individual patient’s potential triggers and mediators of the disease, and a meticulous attention to identifying, mitigating, and, when possible, eliminating each factor.

The power of an integrative medicine and functional medicine approach lies in giving patients with inflammatory bowel disease the chance of achieving remission and control of their gut symptoms and happily regaining their quality of life, when concurrently managed by a gastroenterologist and integrative medicine physician. However, before reaching that state, effective immunosuppressive medications may be needed to get the unbridled inflammatory process under control, depending on the severity of disease. After achieving remission, in addition to the care by an integrative and functional medicine physician, it is still important to continue to see the gastroenterologist, as the need for maintenance immunosuppressive treatment is gauged by the severity of disease, and because both ulcerative colitis and Crohn’s disease are associated with an increased risk for colon cancer. (Before we delve even further in this blog, it is crucial to note that a patient who is currently receiving immunosuppressive treatments from a gastroenterologist or another physician should never stop or reduce the dose of their medications on their own. Doing so can result in a flare-up of the inflammatory process and worsening of the disease. Any changes in such potentially life-saving medications, despite known potential adverse effects, should always be done under the guidance of the gastroenterologist or the prescribing physician.)

In this blog, we focus on the potential role that environmental toxicants and triggers play in the origination and development of inflammatory bowel disease.

Environmental toxicants and triggers from industrialization

The emergence of inflammatory bowel disease in developing countries, concurrent with the westernization of lifestyle and industrialization over the last few decades, suggest that environmental triggers may play a role in the development of inflammatory bowel disease. For example, in Japan the incidence of Crohn’s disease and ulcerative colitis increased by more than ten times since the 1970s, and similar data can be observed in China, India, and South Korea. Proposed triggers include dietary change, exposure to environmental pollution by countless compounds, and lifestyle and behavior changes (1).

Research has begun to shed some light on how environmental pollutants, including the chemicals and synthetic materials in daily life (some of which we ingest in our diet), may be connected to inflammatory bowel disease.

“Forever chemicals”

PFAS (which stands for per- and polyfluoroalkyl substances), often called “forever chemicals,” are a large group of man-made chemicals used extensively in industries and consumer products. Their strong carbon-fluoride bonds make them extremely resistant to breaking down, so they can accumulate and persist in the environment for decades to centuries. Over the decades, they have accumulated in water, soil, air, and wildlife all over the world. They can build up in the blood and organs of people over time, and they can remain in the body for many years after exposure is stopped. Harmful health effects of PFAS include high cholesterol levels, hypertension, thyroid dysfunction, immune dysfunction, kidney disease, and cancer (especially kidney and testicular), among others. PFAS are used to make products resistant to water, oil, grease, and stains, so they can be found in nonstick cookware, stain-resistant textiles for furniture and carpeting, water-resistant clothing, personal care products (some dental floss, cosmetics, lotions, sunscreens, shampoos and other hair products), and food packaging (takeout containers, pizza boxes, bakery papers). (The voluntary phase-out of PFAS in food packaging was completed in 2024.) Fish and seafood, eggs, and animal-derived foods such as meat and dairy contain the highest levels of PFAS, with fish and seafood containing the highest.

In a study of 75 military service members that analyzed their blood samples up to ten years prior to the diagnosis of inflammatory bowel disease, along with blood samples from healthy controls, higher concentrations of PFAS in the blood were found to be associated with higher odds of Crohn’s disease and ulcerative colitis (2). In other studies, legacy PFAS, such as PFOA and PFOS, were associated with the risk of ulcerative colitis. However, inconsistent data have been reported as well (3). While the prescription medications cholestyramine and colesevelam, which are bile acid sequestrants, have been shown to significantly speed up the elimination of PFAS from the body in a small clinical trial (4), more research is needed. Results from another small study found that the use of dietary fibers over four weeks was associated with a decrease in PFAS concentration in the blood (5). Reducing exposure is still the most important intervention, including avoidance of PFAS-containing products and the use of certified water filtration systems.

How can PFAS lead to inflammatory bowel disease? The answers to this type of question (“mechanisms of action” question) have been explored in test-tube and animal studies. In mouse studies, exposure to PFAS was associated with disrupted microbiome, loss of gut barrier (“leaky gut”), and reduced production of short-chain fatty acids (which are beneficial biochemicals produced by gut bacteria that nourish the cells lining the colon, strengthen the gut barrier, and reduce inflammation) (3).

Pesticides and herbicides

Pesticides and herbicides, such those used on crops, have been linked to health harms, including cancer, autism, and preterm birth. What about their roles in inflammatory bowel disease? In a study that examined more than 68,000 people who did not have inflammatory bowel disease at the outset, exposure to pesticides was associated with a 20% increased risk of developing new cases of inflammatory bowel disease, and two specific pesticides were associated with a 60% increased risk (6). (The investigators found the association with five organochlorine insecticides, three organophosphate insecticides, one fungicide, and five herbicides). Pesticides are observed to increase oxidative stress, inflammation, and compromise the gut barrier integrity in animal studies (3).

Diet is a primary source of exposure to many pesticides and herbicides, including glyphosate and organophosphates. Studies have shown that switching to an organic diet results in rapid and substantial reductions in urine levels of glyphosate (the most commonly used herbicide) and other pesticides (7, 8). For example, switching to an organic diet led to a 70% decrease in urine glyphosate levels within six days.

Heavy metals

Some metals, such as iron, magnesium, selenium, and zinc, serve important physiologic functions in our body and contribute to our health. On the other hand, heavy metals, such as mercury, lead, arsenic, and cadmium, serve no physiologic roles in the body and are purely toxic. However, even the metals that serve beneficial physiologic purposes in our body can be toxic when present at high levels. A 2025 systematic review found that lead, arsenic, mercury, copper, and iron are associated with inflammatory bowel disease risk (3). Heavy metals can directly induce inflammation and cause oxidative stress, negatively impact the gut microbiome (more accurately, gut microbiota, which is the community of microbes that live in the gut), and increase gut permeability (making the gut more “leaky”).

Air pollution

Some research data have suggested an association between air pollution and inflammatory bowel disease. In a systematic review, four studies were found to report an association between higher levels of PM_2.5 (airborne particulate matter with a diameter of 2.5 micrometers or less) and ulcerative colitis, and one study found a link with inflammatory bowel disease overall (3). However, it should be noted that the data on the association between inflammatory bowel disease and PM_2.5 are inconsistent, with some studies reporting no association or the opposite association. Nitrogen oxides are a group of air pollutants that can come from car exhaust, the burning of fossil fuels in power plants and factories, wildfires, household gas stoves, and dryers. In one study, nitrogen oxides were found to be associated with ulcerative colitis and, in another, with Crohn’s disease (3). In a study of more than 4,700 individuals with inflammatory bowel disease, higher exposures to PM_2.5 were associated with higher risks of surgical removal of portions of small or large bowel, while higher exposures to nitrogen oxides were associated with higher risks of death from all causes (9). Research in mice showed that exposure to airborne particulate matter can result in “leaky gut,” promote gut inflammation, and disrupt the gut microbiome (10).

Food additives

Food additives have become prevalent with industrialization and westernization of diet. Dietary emulsifiers are commonly used in processed foods to stabilize mixtures of fat and water, improve their taste and appearance, and extend shelf life. Common examples include polysorbate 80 (P80), carboxymethylcellulose (CMC), carrageenan, various gums, and lecithin. Mouse experiments showed that relatively low concentrations of two commonly used emulsifiers (P80 and CMC) promoted robust colitis (inflammation of the colon) in mice (11). Using a laboratory model of the human microbiome (rather than doing the experiments directly on humans), researchers examined twenty commonly used dietary emulsifiers and found that many of them (including various carrageenans, gums, P80, and CMC) can directly impact the gut microbiome in a way that promotes gut inflammation, but soy lecithin did not appear to have an impact (12, 13). Currently, research data from human studies on the specific role of emulsifiers in inflammatory bowel disease are still limited, so more clinical research needs to be conducted to better understand the role of dietary emulsifier additives in the development of inflammatory bowel disease in humans. Nevertheless, people who consume more ultra-processed foods, which often contain emulsifiers, are at higher risks of developing inflammatory bowel disease (14). While diet in general is not a focus of this blog, it should be also noted that diets containing high amounts of animal fat and low amounts of fruits and vegetables have been associated with inflammatory bowel disease (15).

NSAIDs

Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen (Advil, Motrin), naproxen (Naprosyn), and indomethacin (Indocin), are well-known for increasing the risk of gastrointestinal tract ulcers and, bleeding, kidney injury, and cardiovascular events. Do they have a role in inflammatory bowel disease? Research has demonstrated that the use of NSAIDs is associated with increased risks of developing new cases of Crohn’s disease and ulcerative colitis. In a study of more than 76,000 female nurses followed over eighteen years (Nurses’ Health Study I), women who used NSAIDs at least 15 days per month had an 87% higher risk for developing ulcerative colitis and a 56% higher risk for Crohn’s disease, compared with nonusers (16). Women who regularly used NSAIDs for more than six years had two times the risk for ulcerative colitis and close to three times the risk for Crohn’s disease than nonusers. However, it should be noted that aspirin, which is also an NSAID but usually used at low doses, was not associated with an increased risk for inflammatory bowel disease. In people with established ulcerative colitis and Crohn’s disease, NSAID use is associated with a slight increase in the rate of relapse (1, 16). How does this happen? The physiologic effects of NSAIDs converge to disrupt gut barrier function and cause “leaky gut,” and these detrimental changes might explain why NSAIDs can play a role in triggering or worsening inflammatory bowel disease (16). Because many NSAIDs are available over-the-counter, patients should be mindful of their potential side effects and discuss with their physicians about their use.

Smoking

Smoking has been well-known to be a risk factor for Crohn’s disease. Current smokers have almost twice the risk of Crohn’s disease compared with never smokers. Patients with Crohn’s disease who continue to smoke have a higher risk of frequent flares, complications, hospitalizations, and multiple surgeries (15). On the other hand, most patients with ulcerative colitis are non-smokers or ex-smokers, rather than current smokers. Nevertheless, ongoing smoking confers no benefit in patients with ulcerative colitis, in terms of frequency of surgical removal of the colon and disease flare, for example. A 2022 consensus statement from a group of international experts in inflammatory bowel disease encourages non-smokers with established inflammatory bowel disease to never start smoking, and encourages current smokers to quit (15). Quitting smoking might have a beneficial effect on the clinical course of Crohn’s disease, and could be associated with overall improved survival in people with ulcerative colitis.

Leaky gut

Intestinal barrier integrity is compromised in patients with inflammatory bowel disease. This compromise is characterized by “leaky gut” and is driven in part by chronic inflammation in the gut. A breakdown of the gut barrier integrity appears to be part of the pathological pathway that links many environmental toxicants and triggers to the final manifestation of inflammatory bowel disease. So, in addition to exposure avoidance, treatment approaches that aim to enhance the gut barrier function could be potential therapeutic strategies for inflammatory bowel disease, as suggested by a review published in the New England Journal of Medicine (17). Many of the strategies in the integrative medicine and functional medicine approach indeed aim to improve the gut barrier function and the gut microbiome. Using food as medicine is a particularly fundamental strategy in this regard.

Integrative and functional medicine approach to inflammatory bowel disease

Mitigation of the potential adverse health effects of these environmental toxicants and triggers starts with reducing or minimizing exposure, and continues with supporting the body so that its innate ability to eliminate these unwanted chemicals from the body is optimized, such as the detoxification capacity of the liver and urinary excretion via the kidneys. These strategies are part of the integrative and functional medicine approach to health, but they should be considered simply part of a prudent and mindful approach to lifelong health and wellbeing.

A good functional medicine and integrative medicine approach to the treatment of inflammatory bowel disease takes into account all of the considerations we have discussed here in this blog, and much more, including the use of food as medicine, optimization of the gut microbiome, and restoration of a dysregulated immune system. This type of good medicine, integrated with the care provided by a gastroenterologist, will offer the individual suffering from inflammatory bowel disease the hope of achieving and maintaining remission and quality of life in order to cherish life to the fullest.

References

1.   Ananthakrishnan AN, Bernstein CN, Iliopoulos D, Macpherson A, Neurath MF, Ali RAR, et al. Environmental triggers in IBD: a review of progress and evidence. Nat Rev Gastroenterol Hepatol. 2018;15(1):39-49.

2.   Agrawal M, Midya V, Maroli A, Magee J, Petrick L, Colombel JF, et al. Per- and Poly-Fluoroalkyl Substances Exposure Is Associated With Later Occurrence of Inflammatory Bowel Disease. Clin Gastroenterol Hepatol. 2024;22(8):1728-30 e8.

3.   Estevinho MM, Midya V, Cohen-Mekelburg S, Allin KH, Fumery M, Pinho SS, et al. Emerging role of environmental pollutants in inflammatory bowel disease risk, outcomes and underlying mechanisms. Gut. 2025;74(3):477-86.

4.   Andersson AG, Xu Y, Karrman A, Cederlund J, Lindh CH, Pineda D, et al. Serum, urinary and fecal concentrations of perfluoroalkyl substances after interventions with cholestyramine/colesevelam and probenecid - cross-over trials in Ronneby, Sweden. Environ Int. 2025;204:109794.

5.   Schlezinger JJ, Bello A, Mangano KM, Biswas K, Patel PP, Pennoyer EH, et al. Per- and poly-fluoroalkyl substances (PFAS) in circulation in a Canadian population: their association with serum-liver enzyme biomarkers and piloting a novel method to reduce serum-PFAS. Environmental health : a global access science source. 2025;24(1):10.

6.   Chen D, Parks CG, Hofmann JN, Beane Freeman LE, Sandler DP. Pesticide use and inflammatory bowel disease in licensed pesticide applicators and spouses in the Agricultural Health Study. Environ Res. 2024;249:118464.

7.   Fagan J, Bohlen L, Patton S, Klein K. Organic diet intervention significantly reduces urinary glyphosate levels in U.S. children and adults. Environ Res. 2020;189:109898.

8.   Gonzalez N, Pamies C, Martinez P, Marti L, Domingo JL, Nadal M, et al. Effects of an organic diet intervention on the levels of organophosphorus metabolites in an adult cohort. Food Res Int. 2023;173(Pt 1):113354.

9.   Chen J, Dan L, Sun Y, Yuan S, Liu W, Chen X, 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(7):77010.

10. Kish L, Hotte N, Kaplan GG, Vincent R, Tso R, Ganzle M, et al. Environmental particulate matter induces murine intestinal inflammatory responses and alters the gut microbiome. PLoS One. 2013;8(4):e62220.

11. Chassaing B, Koren O, Goodrich JK, Poole AC, Srinivasan S, Ley RE, et al. Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome. Nature. 2015;519(7541):92-6.

12. Chassaing B, Van de Wiele T, De Bodt J, Marzorati M, Gewirtz AT. Dietary emulsifiers directly alter human microbiota composition and gene expression ex vivo potentiating intestinal inflammation. Gut. 2017;66(8):1414-27.

13. Naimi S, Viennois E, Gewirtz AT, Chassaing B. Direct impact of commonly used dietary emulsifiers on human gut microbiota. Microbiome. 2021;9(1):66.

14. Narula N, Wong ECL, Dehghan M, Mente A, Rangarajan S, Lanas F, et al. Association of ultra-processed food intake with risk of inflammatory bowel disease: prospective cohort study. Bmj. 2021;374:n1554.

15. Ananthakrishnan AN, Kaplan GG, Bernstein CN, Burke KE, Lochhead PJ, Sasson AN, et al. Lifestyle, behaviour, and environmental modification for the management of patients with inflammatory bowel diseases: an International Organization for Study of Inflammatory Bowel Diseases consensus. Lancet Gastroenterol Hepatol. 2022;7(7):666-78.

16. Ananthakrishnan AN, Higuchi LM, Huang ES, Khalili H, Richter JM, Fuchs CS, et al. Aspirin, nonsteroidal anti-inflammatory drug use, and risk for Crohn disease and ulcerative colitis: a cohort study. Ann Intern Med. 2012;156(5):350-9.

17. Chang JT. Pathophysiology of Inflammatory Bowel Diseases. N Engl J Med. 2020;383(27):2652-64.