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Your Environment. Your Health.

Inflammation

Introduction

inflammation in x-rays of various joints

If a cut on your skin swells up, turns red, and hurts, those symptoms are signs of acute, or short-lived, inflammation. Feeling hot or losing function may be signs of inflammation from other harm to your body. Some inflammation that occurs in your body’s cells or tissues may not have outward symptoms.

Inflammation is a normal part of the body’s defense to injury or infection, and, in this way, it is beneficial. But inflammation is damaging when it occurs in healthy tissues or lasts too long. Known as chronic inflammation, it may persist for months or years.

Inflammation may result from many factors, such as:

  • Environmental chemicals
  • Injuries like scrapes, insect stings, or a splinter in your finger
  • Pathogens (germs) like bacteria, viruses, or fungi
  • Radiation

Inflammation plays a key role in many diseases, some of which are becoming more common and severe. Chronic inflammatory diseases contribute to more than half of deaths worldwide.1 

Inflammation is associated with diseases such as the following:

  • Autoimmune diseases like rheumatoid arthritis
  • Cardiovascular diseases like high blood pressure and heart disease
  • Gastrointestinal disorders like inflammatory bowel disease
  • Lung diseases like asthma
  • Mental illnesses like depression
  • Metabolic diseases like Type 2 diabetes
  • Neurodegenerative diseases like Parkinson’s disease
  • Some types of cancer, like colon cancer

What is NIEHS Doing?

Increasing evidence suggests environmental factors contribute to chronic inflammation. A review2 of scientific literature conducted by NIEHS-funded researchers affiliated with the National Toxicology Program found the environment plays a role in inflammation in both positive and negative ways, such as:

  • Environmental chemicals – The federal Toxicology in the 21st Century, or Tox21, program shows how chemicals we commonly encounter may alter molecular pathways that underlie inflammation.
  • Nutrition – Diets high in refined grains, alcohol, and processed foods can alter gut microbiota and lead to intestinal and immune changes.
  • Microbiome – Studies of various microbiome imbalances and disease states show connections to inflammation.
  • Social and cultural changes – Disrupted sleep patterns, psychosocial stress, artificial light, and other factors influence the immune system.
  • Developmental origins – Childhood obesity, psychological stress, exposure to microbes in infancy, and prenatal conditions are linked to inflammation.
  • Physical activity – When skeletal muscles contract, they release proteins that can reduce inflammation throughout the body.

NIEHS researchers and grantees are exploring ways to predict, prevent, and treat inflammatory diseases. They are studying the underlying causes of inflammatory diseases, developing experiments to examine the inflammatory effects of current and emerging environmental threats, and testing novel strategies to treat environmentally-induced inflammation. Below are examples of recent findings:

  • Chronic liver inflammation and cancer – By suppressing one of the body’s natural mechanisms to fight cancer, chronic liver inflammation can lead to a new tumor-promoting pathway. This discovery may inform liver cancer treatments.3
  • Nanotechnology and lung inflammation – Silver nanowires, which are used in personal care products, food storage boxes, and computers, were taken up by cells in the lungs of rats, leading to lung inflammation.4
  • Ozone and cardiovascular disease – Exposure to ozone, even at levels lower than the current U.S. Environmental Protection Agency (EPA) air quality standard, may lead to cardiovascular disease.5
  • Air pollution and diabetes – The diabetes drug metformin may reduce inflammation triggered by air pollution exposure by preventing immune cells known as macrophages from releasing an inflammatory molecule called interleukin-6.6
  • Inflammation and Parkinson’s disease – Blocking a brain enzyme called soluble epoxide hydrolase in mice helped curb the inflammation associated with the development and progression of Parkinson’s Disease.7
  • Environmental stressors and lifespan – NIEHS scientists demonstrated that inflammatory responses to environmental stressors can reduce lifespan, supporting a theory that longevity depends on a balance between pro- and anti-inflammatory proteins.8
  • B vitamins and air pollution – Taking B vitamins may help lessen the effects of fine particles, a common air pollutant.9
  • Prostate cancer among first responders – Changes in inflammation and immune regulation from exposure to World Trade Center dust may have increased prostate cancer progression among those first responders.10

Future Directions

NIEHS continues to support a wide variety of research projects focused on inflammation and its role in wellness and disease. Questions NIEHS researchers and grantees are addressing include:

  • Which environmental exposures, individually and in combination, affect inflammation?
  • Which genetic and other susceptibility factors influence the inflammatory response?
  • Which biological pathways are involved in environmentally induced inflammation? How do they contribute to different diseases?
  • What biomarkers exist for key events in inflammation?
  • Are there common environmental triggers, pathways, and biomarkers across many diseases? Are there disease-specific triggers, pathways, and biomarkers?
  • Can we prevent chronic inflammation and associated diseases using the above knowledge?

Further Reading

Stories from the Environmental Factor (NIEHS Newsletter)

Additional Resources

Related Health Topics


  1. Furman D, Campisi J, Verdin E, Carrera-Bastos P, Targ S, Franceschi C, Ferrucci L, Gilroy DW, Fasano A, Miller GW, Miller AH, Mantovani A, Weyand CM, Barzilai N, Goronzy JJ, Rando TA, Effros RB, Lucia A, Kleinstreuer N, Slavich GM. 2019. Chronic Inflammation in the Etiology of Disease Across the Life Span. Nature Medicine. 25(12):1822–1832. [Abstract Furman D, Campisi J, Verdin E, Carrera-Bastos P, Targ S, Franceschi C, Ferrucci L, Gilroy DW, Fasano A, Miller GW, Miller AH, Mantovani A, Weyand CM, Barzilai N, Goronzy JJ, Rando TA, Effros RB, Lucia A, Kleinstreuer N, Slavich GM. 2019. Chronic Inflammation in the Etiology of Disease Across the Life Span. Nature Medicine. 25(12):1822–1832.]
  2. Furman D, Campisi J, Verdin E, Carrera-Bastos P, Targ S, Franceschi C, Ferrucci L, Gilroy DW, Fasano A, Miller GW, Miller AH, Mantovani A, Weyand CM, Barzilai N, Goronzy JJ, Rando TA, Effros RB, Lucia A, Kleinstreuer N, Slavich GM. 2019. Chronic Inflammation in the Etiology of Disease Across the Life Span. Nature Medicine. 25(12):1822–1832. [Abstract Furman D, Campisi J, Verdin E, Carrera-Bastos P, Targ S, Franceschi C, Ferrucci L, Gilroy DW, Fasano A, Miller GW, Miller AH, Mantovani A, Weyand CM, Barzilai N, Goronzy JJ, Rando TA, Effros RB, Lucia A, Kleinstreuer N, Slavich GM. 2019. Chronic Inflammation in the Etiology of Disease Across the Life Span. Nature Medicine. 25(12):1822–1832.]
  3. Shalapour S, Lin XJ, Bastian IN, Brain J, Burt AD, Aksenov AA, Vrbanac AF, Li W, Perkins A, Matsutani T, Zhong Z, Dhar D, Navas-Molina JA, Xu J, Loomba R, Downes M, Yu RT, Evans RM, Dorrestein PC, Knight R, Benner C, Anstee QM, Karin M. 2017. Inflammation-induced IgA Plus Cells Dismantle Anti-liver Cancer Immunity. Nature 551(7680):340–345. [Abstract Shalapour S, Lin XJ, Bastian IN, Brain J, Burt AD, Aksenov AA, Vrbanac AF, Li W, Perkins A, Matsutani T, Zhong Z, Dhar D, Navas-Molina JA, Xu J, Loomba R, Downes M, Yu RT, Evans RM, Dorrestein PC, Knight R, Benner C, Anstee QM, Karin M. 2017. Inflammation-induced IgA Plus Cells Dismantle Anti-liver Cancer Immunity. Nature 551(7680):340–345.]
  4. Chung KF, Seiffert J, Chen S, Theodorou IG, Goode AE, Leo BF, McGilvery CM, Hussain F, Wiegman C, Rossios C, Zhu J, Gong J, Tariq F, Yufit V, Monteith AJ, Hashimoto T, Skepper JN, Ryan MP, Zhang J, Tetley TD, Porter AE. 2017. Inactivation, Clearance, and Functional Effects of Lung-instilled Short and Long Silver Nanowires in Rats. ACS Nano 11(3):2652–2664. [Abstract Chung KF, Seiffert J, Chen S, Theodorou IG, Goode AE, Leo BF, McGilvery CM, Hussain F, Wiegman C, Rossios C, Zhu J, Gong J, Tariq F, Yufit V, Monteith AJ, Hashimoto T, Skepper JN, Ryan MP, Zhang J, Tetley TD, Porter AE. 2017. Inactivation, Clearance, and Functional Effects of Lung-instilled Short and Long Silver Nanowires in Rats. ACS Nano 11(3):2652–2664.]
  5. Day DB, Xiang J, Mo J, Li F, Chung M, Gong J, Weschler CJ, Ohman-Strickland PA, Sundell J, Weng W, Zhang Y, Zhang JJ. 2017. Association of Ozone Exposure With Cardiorespiratory Pathophysiologic Mechanisms in Healthy Adults. JAMA Internal Medicine doi: 10.1001/jamainternmed.2017.2842 [Online 17 July 2017]. [Abstract Day DB, Xiang J, Mo J, Li F, Chung M, Gong J, Weschler CJ, Ohman-Strickland PA, Sundell J, Weng W, Zhang Y, Zhang JJ. 2017. Association of Ozone Exposure With Cardiorespiratory Pathophysiologic Mechanisms in Healthy Adults. JAMA Internal Medicine doi: 10.1001/jamainternmed.2017.2842 [Online 17 July 2017].]
  6. Soberanes S, Misharin AV, Jairaman A, Morales-Nebreda L, McQuattie-Pimentel AC, Cho T, Hamanaka RB, Meliton AY, Walter JM, Chen CI, Chi M, Chiu S, Gonzalez-Gonzalez FJ, Antalek M, Adbala-Valencia H, Chiarella SE, Sun KA, Woods PS, Ghio AJ, Jain M, Perlman H, Ridge KM, Morimoto RI, Sznajder JI, Balch WE, Bhorade SM, Bharat A, Prakriya M, Chandel NS, Mutlu GM, Budinger GRS. 2018. Metformin Targets Mitochondrial Electron Transport to Reduce Air Pollution-induced Thrombosis. Cell Metabolism 29:1–13. [Abstract Soberanes S, Misharin AV, Jairaman A, Morales-Nebreda L, McQuattie-Pimentel AC, Cho T, Hamanaka RB, Meliton AY, Walter JM, Chen CI, Chi M, Chiu S, Gonzalez-Gonzalez FJ, Antalek M, Adbala-Valencia H, Chiarella SE, Sun KA, Woods PS, Ghio AJ, Jain M, Perlman H, Ridge KM, Morimoto RI, Sznajder JI, Balch WE, Bhorade SM, Bharat A, Prakriya M, Chandel NS, Mutlu GM, Budinger GRS. 2018. Metformin Targets Mitochondrial Electron Transport to Reduce Air Pollution-induced Thrombosis. Cell Metabolism 29:1–13.]
  7. Ren Q, Ma M, Yang J, Nonaka R, Yamaguchi A, Ishikawa KI, Kobayashi K, Murayama S, Hwang SH, Saiki S, Akamatsu W, Hattori N, Hammock BD, Hashimoto K. 2018. Soluble Epoxide Hydrolase Plays a Key Role in the Pathogenesis of Parkinson's Disease. Proceedings of the National Academy of Sciences of the United States of America 115(25):E5815–E5823. [Abstract Ren Q, Ma M, Yang J, Nonaka R, Yamaguchi A, Ishikawa KI, Kobayashi K, Murayama S, Hwang SH, Saiki S, Akamatsu W, Hattori N, Hammock BD, Hashimoto K. 2018. Soluble Epoxide Hydrolase Plays a Key Role in the Pathogenesis of Parkinson's Disease. Proceedings of the National Academy of Sciences of the United States of America 115(25):E5815–E5823.]
  8. Sung EJ, Ryuda M, Matsumoto H, Uryu O, Ochiai M, Cook ME, Yi NY, Wang H, Putney JW, Bird GS, Shears SB, Hayakawa Y. 2017. Cytokine Signaling Through Drosophila Mthl10 Ties Lifespan to Environmental Stress. Proceedings of the National Academy of Sciences of the United States of America 114(52):13786–13791. [Abstract Sung EJ, Ryuda M, Matsumoto H, Uryu O, Ochiai M, Cook ME, Yi NY, Wang H, Putney JW, Bird GS, Shears SB, Hayakawa Y. 2017. Cytokine Signaling Through Drosophila Mthl10 Ties Lifespan to Environmental Stress. Proceedings of the National Academy of Sciences of the United States of America 114(52):13786–13791.]
  9. Zhong J, Karlsson O, Wang G, Li J, Guo Y, Lin X, Zemplenyi M, Sanchez-Guerra M, Trevisi L, Urch B, Speck M, Liang L, Coull BA, Koutrakis P, Silverman F, Gold DR, Wu T, Baccarelli AA. 2017. B Vitamins Attenuate the Epigenetic Effects of Ambient Fine Particles in a Pilot Human Intervention Trial. Proceedings of the National Academy of Sciences of the United States of America 114(13):3503–3508. [Abstract Zhong J, Karlsson O, Wang G, Li J, Guo Y, Lin X, Zemplenyi M, Sanchez-Guerra M, Trevisi L, Urch B, Speck M, Liang L, Coull BA, Koutrakis P, Silverman F, Gold DR, Wu T, Baccarelli AA. 2017. B Vitamins Attenuate the Epigenetic Effects of Ambient Fine Particles in a Pilot Human Intervention Trial. Proceedings of the National Academy of Sciences of the United States of America 114(13):3503–3508.]
  10. Gong Y, Wang L, Yu H, Alpert N, Cohen MD, Prophete C, Horton L, Sisco M, Park SH, Lee HW, Zelikoff J, Chen LC, Suarez-Farinas M, Donovan MJ, Aaronson SA, Galsky M, Zhu J, Taioli E, Oh WK. 2019. Prostate Cancer in World Trade Center Responders Demonstrates Evidence of an Inflammatory Cascade. Molecular Cancer Research doi: 10.1158/1541-7786.MCR-19-0115 [Online 16 July 2019]. [Abstract Gong Y, Wang L, Yu H, Alpert N, Cohen MD, Prophete C, Horton L, Sisco M, Park SH, Lee HW, Zelikoff J, Chen LC, Suarez-Farinas M, Donovan MJ, Aaronson SA, Galsky M, Zhu J, Taioli E, Oh WK. 2019. Prostate Cancer in World Trade Center Responders Demonstrates Evidence of an Inflammatory Cascade. Molecular Cancer Research doi: 10.1158/1541-7786.MCR-19-0115 [Online 16 July 2019].]
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