• 1 Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA;
  • 2 Department of Hygiene, Kawasaki Medical School, Kurashiki 701-0192, Japan
  • 3 Advanced Molecular Science Research Centre, King George's Medical University, Lucknow, Uttar Pradesh 226003, India
  • 4 Department of Pathology, Kuwait University, Safat 13110, Kuwait
  • 5 Department of Experimental and Clinical Medicine, University of Firenze, Firenze 50134, Italy
  • 6 Center for Environmental Carcinogenesis and Risk Assessment, Environmental Protection and Health Prevention Agency, 40126 Bologna, Italy
  • 7 Institute of Molecular Genetics, National Research Council, Pavia 27100, Italy
  • 8 Toxicology Research Division, Bureau of Chemical Safety, Food Directorate, HPFB, Health Canada, Ottawa, Ontario K1A0K9, Canada
  • 9 Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, Selangor 43400, Malaysia
  • 10 Mediterranean Institute of Oncology, 95029 Viagrande, Italy
  • 11 Molecular Oncology Program, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC 20057, USA
  • 12 Urology Department, Kasr Al-Ainy School of Medicine, Cairo University, El Manial, Cairo 12515, Egypt
  • 13 Department of Environmental and Radiological Health Sciences, Colorado State University/ Colorado School of Public Health, Fort Collins, CO, 80523-1680, USA
  • 14 Environmental and Molecular Toxicology, Environmental Health Sciences Center, Oregon State University, Corvallis, OR 97331, USA,
  • 15 Getting to Know Cancer, Nova Scotia, Canada and
  • 16 Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA; Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA
Carcinogenesis, 2015 Jun;36 Suppl 1:S111-27.
PMID: 26002081 DOI: 10.1093/carcin/bgv033


An increasing number of studies suggest an important role of host immunity as a barrier to tumor formation and progression. Complex mechanisms and multiple pathways are involved in evading innate and adaptive immune responses, with a broad spectrum of chemicals displaying the potential to adversely influence immunosurveillance. The evaluation of the cumulative effects of low-dose exposures from the occupational and natural environment, especially if multiple chemicals target the same gene(s) or pathway(s), is a challenge. We reviewed common environmental chemicals and discussed their potential effects on immunosurveillance. Our overarching objective was to review related signaling pathways influencing immune surveillance such as the pathways involving PI3K/Akt, chemokines, TGF-β, FAK, IGF-1, HIF-1α, IL-6, IL-1α, CTLA-4 and PD-1/PDL-1 could individually or collectively impact immunosurveillance. A number of chemicals that are common in the anthropogenic environment such as fungicides (maneb, fluoxastrobin and pyroclostrobin), herbicides (atrazine), insecticides (pyridaben and azamethiphos), the components of personal care products (triclosan and bisphenol A) and diethylhexylphthalate with pathways critical to tumor immunosurveillance. At this time, these chemicals are not recognized as human carcinogens; however, it is known that they these chemicalscan simultaneously persist in the environment and appear to have some potential interfere with the host immune response, therefore potentially contributing to promotion interacting with of immune evasion mechanisms, and promoting subsequent tumor growth and progression.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.