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Low-Dose Mixture Hypothesis of Carcinogenesis Workshop: Scientific Underpinnings and Research Recommendations

Environmental health perspectives, 2017-02, Vol.125 (2), p.163-169 [Peer Reviewed Journal]

COPYRIGHT 2017 National Institute of Environmental Health Sciences ;COPYRIGHT 2017 National Institute of Environmental Health Sciences ;Copyright National Institute of Environmental Health Sciences Feb 2017 ;ISSN: 0091-6765 ;EISSN: 1552-9924 ;DOI: 10.1289/EHP411 ;PMID: 27517672

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  • Title:
    Low-Dose Mixture Hypothesis of Carcinogenesis Workshop: Scientific Underpinnings and Research Recommendations
  • Author: Miller, Mark F ; Goodson, William H ; Manjili, Masoud H ; Kleinstreuer, Nicole ; Bisson, William H ; Lowe, Leroy
  • Subjects: Biology ; Breast cancer ; Carcinogenesis ; Carcinogens ; Carcinogens - toxicity ; Chemicals ; Complex Mixtures ; Conferences, meetings and seminars ; Consensus ; Decision making ; Dose-Response Relationship, Drug ; Education ; Environmental Exposure - statistics & numerical data ; Environmental Pollution - statistics & numerical data ; Environmental toxicology ; Hypotheses ; Hypothesis testing ; Medical research ; Models, Animal ; Neoplasms ; NGOs ; Nongovernmental organizations ; Public health ; Researchers ; Review ; Risk Assessment ; Studies ; Task forces ; Toxicology ; Workshops
  • Is Part Of: Environmental health perspectives, 2017-02, Vol.125 (2), p.163-169
  • Description: The current single-chemical-as-carcinogen risk assessment paradigm might underestimate or miss the cumulative effects of exposure to chemical mixtures, as highlighted in recent work from the Halifax Project. This is particularly important for chemical exposures in the low-dose range that may be affecting crucial cancer hallmark mechanisms that serve to enable carcinogenesis. Could ongoing low-dose exposures to a mixture of commonly encountered environmental chemicals produce effects in concert that lead to carcinogenesis? A workshop held at the NIEHS in August 2015 evaluated the scientific support for the low-dose mixture hypothesis of carcinogenesis and developed a research agenda. Here we describe the science that supports this novel theory, identify knowledge gaps, recommend future methodologies, and explore preventative risk assessment and policy decision-making that incorporates cancer biology, environmental health science, translational toxicology, and clinical epidemiology. The theoretical merits of the low-dose carcinogenesis hypothesis are well founded with clear biological relevance, and therefore, the premise warrants further investigation. Expert recommendations include the need for better insights into the ways in which noncarcinogenic constituents might combine to uniquely affect the process of cellular transformation (in vitro) and environmental carcinogenesis (in vivo), including investigations of the role of key defense mechanisms in maintaining transformed cells in a dormant state. The scientific community will need to acknowledge limitations of animal-based models in predicting human responses; evaluate biological events leading to carcinogenesis both spatially and temporally; examine the overlap between measurable cancer hallmarks and characteristics of carcinogens; incorporate epigenetic biomarkers, in silico modelling, high-performance computing and high-resolution imaging, microbiome, metabolomics, and transcriptomics into future research efforts; and build molecular annotations of network perturbations. The restructuring of many existing regulatory frameworks will require adequate testing of relevant environmental mixtures to build a critical mass of evidence on which to base policy decisions. Citation: Miller MF, Goodson WH III, Manjili MH, Kleinstreuer N, Bisson WH, Lowe L. 2017. Low-Dose Mixture Hypothesis of Carcinogenesis Workshop: scientific underpinnings and research recommendations. Environ Health Perspect 125:163-169; http://dx.doi.org/10.1289/EHP411.
  • Publisher: United States: National Institute of Environmental Health Sciences
  • Language: English
  • Identifier: ISSN: 0091-6765
    EISSN: 1552-9924
    DOI: 10.1289/EHP411
    PMID: 27517672
  • Source: U.S. Government Documents
    MEDLINE
    PubMed Central
    ProQuest Central
    DOAJ Directory of Open Access Journals
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