Environmental immune disruptors, inflammation and cancer risk
Open accessAbstract
An emerging area in environmental toxicology is the role that chemicals and chemical mixtures have on the cells of the human immune system. This is an important area of research that has been most widely pursued in relation to autoimmune diseases and allergy/asthma as opposed to cancer causation. This is despite the well-recognized role that innate and adaptive immunity play as essential factors in tumorigenesis. Here, we review the role that the innate immune cells of inflammatory responses play in tumorigenesis. Focus is placed on the molecules and pathways that have been mechanistically linked with tumor-associated inflammation. Within the context of chemically induced disturbances in immune function as co-factors in carcinogenesis, the evidence linking environmental toxicant exposures with perturbation in the balance between pro- and anti-inflammatory responses is reviewed. Reported effects of bisphenol A, atrazine, phthalates and other common toxicants on molecular and cellular targets involved in tumor-associated inflammation (e.g. cyclooxygenase/prostaglandin E2, nuclear factor kappa B, nitric oxide synthesis, cytokines and chemokines) are presented as example chemically mediated target molecule perturbations relevant to cancer. Commentary on areas of additional research including the need for innovation and integration of systems biology approaches to the study of environmental exposures and cancer causation are presented.
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These chemicals include bisphenols, flame retardants, phthalates, polycyclic aromatic hydrocarbons, and per- and polyfluoroalkyl substances.
“These chemicals include phthalates, per- and polyfluoroalkyl substances, bisphenols, polycyclic aromatic hydrocarbons and flame retardants165”
From Chronic inflammation in the etiology of disease across the life span (2019) · cites this paper as [165]
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- Authors
- Thompson, P. A., Khatami, M., Baglole, C. J., Sun, J., Harris, S. A., Moon, E.-Y., Al-Mulla, F., Al-Temaimi, R., Brown, D. G., Colacci, A. M., Mondello, C., Raju, J., Ryan, E. P., Woodrick, J., Scovassi, A. I., Singh, N., Vaccari, M., Roy, R., Forte, S., Memeo, L., Salem, H. K., Amedei, A., Hamid, R. A., Lowe, L., Guarnieri, T., & Bisson, W. H.
- Affiliations
- Sejong University (KR)
- National Institutes of Health (US)
- McGill University (CA)
- Rush University (US)
- Cancer Care Ontario (CA)
- Kuwait University (KW)
- Colorado School of Public Health (US)
- Istituto di Genetica Molecolare (IT)
- Health Canada (CA)
- Georgetown University Medical Center (US)
- King George's Medical University (IN)
- Cairo University (EG)
- University of Florence (IT)
- Universiti Putra Malaysia (MY)
- IRCCS Azienda Ospedliero-Universitaria di Bologna Policlinico di Sant'Orsola (IT)
- Oregon State University (US)
- ORCID
- Thompson, Patricia A.
- Khatami, Mahin
- Baglole, Carolyn J.
- Sun, Jun
- Harris, Shelley A.
- Moon, Eun-Yi
- Al-Temaimi, Rabeah
- Brown, Dustin G.
- Mondello, Chiara
- Raju, Jayadev
- Ryan, Elizabeth P.
- Scovassi, A.Ivana
- Singh, Neetu
- Vaccari, Monica
- Roy, Rabindra
- Forte, Stefano
- Memeo, Lorenzo
- Salem, Hosni K.
- Amedei, Amedeo
- Hamid, Roslida A.
- Guarnieri, Tiziana
- Bisson, William H.
- Venue
- Carcinogenesis
- Publisher
- Oxford University Press (OUP)
- Published
- 2015-06
- Volume
- 36
- Issue
- Suppl 1
- Pages
- S232-S253
- ISSN
- 0143-3334 (ISSN-L)
- 1460-2180
- PMC
- PMC4492068
- OpenAlex
- W1959900099
- Cited by
- 227
- References
- 284
- Citations by year
- 2026: 12 · 2025: 17 · 2024: 25 · 2023: 20 · 2022: 13 · 2021: 13 · 2020: 37 · 2019: 18 · 2018: 16 · 2017: 33 · 2016: 18 · 2015: 4 · 2014: 1
- FWCI
- 2.23
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Carcinogenesis (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion, other-oa)
- Florence Research (University of Florence) (submittedVersion)
- eScholarship@McGill (McGill) (submittedVersion, cc-by)
- Funders
- National Cancer Institute (R01CA113447, R01CA092306, T32CA009686)
- National Institute of Diabetes and Digestive and Kidney Diseases (K01DK075386, R03DK089010)
- National Institute of Environmental Health Sciences (R13ES023276, P30ES000210)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- tumor inflammation, innate immunity, bisphenol A, atrazine, phthalates, NF-κB, nitric oxide production, cytokines and chemokines, chemical mixtures, systems biology
- MeSH terms
- Animals, Carcinogens, Environmental, Environmental Exposure, Humans, Immunity, Innate, Inflammation, Neoplasms, Risk, Carcinogenesis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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