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    Polycyclic aromatic hydrocarbons as skin carcinogens: comparison of benzo[a]pyrene, dibenzo[def,p]chrysene and three environmental mixtures in the FVB/N mouse.

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    Authors
    Siddens, Lisbeth K.
    Larkin, Andrew
    Krueger, Sharon K.
    Bradfield, Christopher A.
    Waters, Katrina M.
    Tilton, Susan C.
    Pereira, Cliff B.
    Löhr, Christiane V.
    Arlt, Volker M.
    Phillips, David H.
    Williams, David E.
    Baird, William M.
    Issue Date
    2012-11-01
    
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    Abstract
    The polycyclic aromatic hydrocarbon (PAH), benzo[a]pyrene (BaP), was compared to dibenzo[def,p]chrysene (DBC) and combinations of three environmental PAH mixtures (coal tar, diesel particulate and cigarette smoke condensate) using a two stage, FVB/N mouse skin tumor model. DBC (4nmol) was most potent, reaching 100% tumor incidence with a shorter latency to tumor formation, less than 20 weeks of 12-O-tetradecanoylphorbol-13-acetate (TPA) promotion compared to all other treatments. Multiplicity was 4 times greater than BaP (400 nmol). Both PAHs produced primarily papillomas followed by squamous cell carcinoma and carcinoma in situ. Diesel particulate extract (1 mg SRM 1650b; mix 1) did not differ from toluene controls and failed to elicit a carcinogenic response. Addition of coal tar extract (1 mg SRM 1597a; mix 2) produced a response similar to BaP. Further addition of 2 mg of cigarette smoke condensate (mix 3) did not alter the response with mix 2. PAH-DNA adducts measured in epidermis 12 h post initiation and analyzed by ³²P post-labeling, did not correlate with tumor incidence. PAH-dependent alteration in transcriptome of skin 12 h post initiation was assessed by microarray. Principal component analysis (sum of all treatments) of the 922 significantly altered genes (p<0.05), showed DBC and BaP to cluster distinct from PAH mixtures and each other. BaP and mixtures up-regulated phase 1 and phase 2 metabolizing enzymes while DBC did not. The carcinogenicity with DBC and two of the mixtures was much greater than would be predicted based on published Relative Potency Factors (RPFs).
    Citation
    Toxicol. Appl. Pharmacol. 2012, 264 (3):377-386
    Journal
    Toxicology and Applied Pharmacology
    URI
    http://hdl.handle.net/10146/269635
    DOI
    10.1016/j.taap.2012.08.014
    PubMed ID
    22935520
    Additional Links
    http://www.sciencedirect.com/science/article/pii/S0041008X12003560
    Type
    Article
    Language
    en
    ISSN
    1096-0333
    Sponsors
    This work was supported by the National Institute of Environmental Health (grants P42ES016465 and P42ES016465-S1). Work at King's College London is supported by Cancer Research UK. Volker M. Arlt and David H. Phillips are members of ECNIS2 (Environmental Cancer Risk, Nutrition and Individual Susceptibility 2), a European Union network of excellence.
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.taap.2012.08.014
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