Journal of Environmental Science and Health Part C Environmental Carcinogenesis & Ecotoxicology Reviews (J Environ Sci Health C Environ Carcinog Ecotoxicol Rev)

Publisher: Taylor & Francis

Journal description

Environmental Carcinogenesis & Ecotoxicology Reviews is a multidisciplinary journal for the rapid publication of integrative, critical reviews on timely and important subjects in various areas of environmental carcinogenesis. Among the subjects covered are risk assessment of chemical/physical agents and biological factors of environmental significance, basic research and methodology, theoretical modelling, host susceptibility and mechanistic studies, and protection of environment and ecosystems.

Current impact factor: 3.56

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 3.56
2013 Impact Factor 2.5
2012 Impact Factor 3.565
2011 Impact Factor 5.16
2010 Impact Factor 4.84
2009 Impact Factor 3.227
2008 Impact Factor 3.353
2007 Impact Factor 3
2006 Impact Factor 2.154
2005 Impact Factor 1.909
2004 Impact Factor 2.571
2003 Impact Factor 0.565
2002 Impact Factor 0.048

Impact factor over time

Impact factor

Additional details

5-year impact 4.94
Cited half-life 5.80
Immediacy index 0.50
Eigenfactor 0.00
Article influence 1.08
Website Journal of Environmental Science and Health - Part C: Environmental Carcinogenesis & Ecotoxicology Reviews website
Other titles Journal of environmental science and health., Journal of environmental science and health. Part C, Environmental carcinogenesis & ecotoxicology reviews, Environmental carcinogenesis & ecotoxicology reviews, Environmental carcinogenesis and ecotoxicology reviews
ISSN 1532-4095
OCLC 50758183
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Taylor & Francis

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Some individual journals may have policies prohibiting pre-print archiving
    • On author's personal website or departmental website immediately
    • On institutional repository or subject-based repository after either 12 months embargo
    • Publisher's version/PDF cannot be used
    • On a non-profit server
    • Published source must be acknowledged
    • Must link to publisher version
    • Set statements to accompany deposits (see policy)
    • The publisher will deposit in on behalf of authors to a designated institutional repository including PubMed Central, where a deposit agreement exists with the repository
    • STM: Science, Technology and Medicine
    • Publisher last contacted on 25/03/2014
    • This policy is an exception to the default policies of 'Taylor & Francis'
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Pyrrolizidine alkaloids (PAs) require metabolic activation to exert cytotoxicity, genotoxicity, and tumorigenicity. We previously reported that (±)-6,7-dihydro-7-hydroxy-1-hydroxymethyl-5H-pyrrolizine (DHP)-derived DNA adducts are responsible for PA-induced liver tumor formation in rats. In this study, we determined that metabolism of riddelliine and monocrotaline by human or rat liver microsomes produced 7-cysteine-DHP and DHP. The metabolism of 7-glutathionyl-DHP by human and rat liver microsomes also generated 7-cysteine-DHP. Furthermore, reaction of 7-cysteine-DHP with calf thymus DNA in aqueous solution yielded the above-described DHP-derived DNA adducts. This study represents the first report that 7-cysteine-DHP is a new PA metabolite that can lead to DNA adduct formation.
    No preview · Article · Jan 2016 · Journal of Environmental Science and Health Part C Environmental Carcinogenesis & Ecotoxicology Reviews
  • [Show abstract] [Hide abstract]
    ABSTRACT: Pyrrolizidine alkaloids (PAs) induce liver injury (PA-ILI) and are very likely to contribute significantly to drug-induced liver injury (DILI). In this study we used a newly developed UHPLC-MS-based method to detect and quantitate blood pyrrole-protein adducts in DILI patients. Among the 46 suspected DILI patients, 15 were identified as PA-ILI by the identification of PA-containing herbs exposed. Blood pyrrole-protein adducts were detected in all PA-ILI patients (100%). These results confirm that PA-ILI is one of the major causes of DILI and that blood pyrrole-protein adducts quantitated by the newly developed UPLC-MS method can serve as a specific biomarker of PA-ILI.
    No preview · Article · Sep 2015 · Journal of Environmental Science and Health Part C Environmental Carcinogenesis & Ecotoxicology Reviews
  • [Show abstract] [Hide abstract]
    ABSTRACT: Protein termination is an important cellular process. Protein termination relies on the stop-codons in the mRNA interact properly with the releasing factors on the ribosome. One third of inherited diseases, including cancers, are associated with the mutation of the stop-codons. Many pathogens and viruses are able to manipulate their stop codons to express their virulence. The influence of stop-codons is not limited to the primary reading frame of the genes. Stop-codons in the second and third reading frames are referred as premature stop signals (PSC). Stop-codons and PSCs together are collectively referred as stop-signals. The ratios of the stop-signals (referred as translation stop-signals ratio or TSSR) of genetically related bacteria, despite their great differences in gene contents, are much alike. This nearly identical Genomic-TSSR value of genetically related bacteria may suggest that bacterial genome expansion is limited by their unique stop-signals bias. We review the protein termination process and the different types of stop-codon mutation in plants, animals, microbes, and viruses, with special emphasis on the role of PSCs in directing bacterial evolution in their natural environments. Knowing the limit of genomic boundary could facilitate the formulation of new strategies in controlling the spread of diseases and combat antibiotic-resistant bacteria.
    No preview · Article · Jun 2015 · Journal of Environmental Science and Health Part C Environmental Carcinogenesis & Ecotoxicology Reviews
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    ABSTRACT: Synergistic antibacterial activity of combined silver nanoparticles (AgNPs) with tetracycline (polykeptide), neomycin (aminoglycoside), and penicillin (β-lactam) was tested against the multi-drug resistant bacterium Salmonella typhimurium DT104. Dose-dependent inhibition of Salmonella typhimurium DT104 growth is observed for tetracycline-AgNPs and neomycin-AgNPs combination with IC50 of 0.07 μg/mL and 0.43 μg/mL, respectively. There is no inhibition for the bacteria by the penicillin-AgNPs combination. These results suggest that the combination of the ineffective tetracycline or neomycin with AgNPs effectively inhibits the growth of this bacterium. The synergistic antibacterial effect is likely due to enhanced bacterial binding by AgNPs assisted by tetracycline or neomycin, but not by penicillin.
    No preview · Article · Jun 2015 · Journal of Environmental Science and Health Part C Environmental Carcinogenesis & Ecotoxicology Reviews
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    ABSTRACT: Metal nanoclusters (NCs), with dimensions between metal atoms and nanoparticles, have attracted more and more attention due to their unique physical and chemical properties. With their size approaching the Fermi wavelength of electrons, metal NCs possess molecule-like properties and excellent fluorescence emission. Owing to their ultrasmall size, strong fluorescence, and excellent biocompatibility, they have been widely studied in environmental and biological fields concerning their applications. In this review, we will introduce the properties of metal NCs, mainly focusing on the synthesis of metal alloy NCs and the recent progress in their applications in environmental monitoring and cancer therapy.
    No preview · Article · Apr 2015 · Journal of Environmental Science and Health Part C Environmental Carcinogenesis & Ecotoxicology Reviews
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    ABSTRACT: Leukemia is the most frequent malignant disease affecting children. To date, the etiology of childhood leukemia remains largely unknown. Few risk factors (genetic susceptibility, infections, ionizing radiation, etc.) have been clearly identified, but they appear to explain only a small proportion of cases. Considerably more uncertain is the role of other environmental risk factors, such as indoor and outdoor air pollution. We sought to summarize and quantify the association between traffic-related air pollution and risk of childhood leukemia, and further examined results according to method of exposure assessment, study quality, leukemia subtype, time period, and continent where studies took place. After a literature search yielded 6 ecologic and 20 case-control studies, we scored the studies based on the Newcastle-Ottawa Scale. The studies assessed residential exposure to pollutants from motorized traffic by computing traffic density in the neighboring roads or vicinity to petrol stations, or by using measured or modeled nitrogen dioxide and benzene outdoor air levels. Because heterogeneity across studies was observed, random-effects summary odds ratios (OR) and 95% confidence intervals (CI) were reported. Whenever possible we additionally conducted stratified analyses comparing acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). Limiting the analysis to high-quality studies (Newcastle-Ottawa Scale ≥ 7), those using traffic density as the exposure assessment metric showed an increase in childhood leukemia risk in the highest exposure category (OR = 1.07, 95% CI 0.93-1.24). However, we observed evidence of publication bias. Results for NO2 exposure and benzene showed an OR of 1.21 (95% CI 0.97-1.52) and 1.64 (95% CI 0.91-2.95) respectively. When stratifying by leukemia type, the results based upon NO2 were 1.21 (95% CI 1.04-1.41) for ALL and 1.06 (95% CI 0.51-2.21) for AML; based upon benzene were 1.09 (95% CI 0.67-1.77) for ALL and 2.28 (95% CI 1.09-4.75) for AML. Estimates were generally higher for exposures in the postnatal period compared to the prenatal period, and for European studies compared to North American studies. Overall, our results support a link between ambient exposure to traffic pollution and childhood leukemia risk, particularly due to benzene.
    No preview · Article · Jan 2015 · Journal of Environmental Science and Health Part C Environmental Carcinogenesis & Ecotoxicology Reviews
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    ABSTRACT: Transformation assays using cultured cells have been applied to the study of carcinogenesis. Although various cell systems exist, few cell types such as BALB/c 3T3 subclones and Syrian hamster embryo cells have been used to study chemically induced two-stage carcinogenesis. Bhas 42 cells were established as a clone by the transfection with the v-Ha-ras gene into mouse BALB/c 3T3 A31-1-1 cells and their subsequent selection based on their sensitivity to 12-O-tetradecanoylphorbol-13-acetate. Using Bhas 42 cells, transformed foci were induced by the treatment with nongenotoxic carcinogens, most of which act as tumor promoters. Therefore, Bhas 42 cells were considered to be a model of initiated cells. Subsequently, not only nongenotoxic carcinogens but also genotoxic carcinogens, most of which act as tumor initiators, were found to induce transformed foci by the modification of the protocol. Furthermore, transformation of Bhas 42 cells was induced by the transfection with genes of oncogenic potential. We interpret this high sensitivity of Bhas 42 cells to various types of carcinogenic stimuli to be related to the multistage model of carcinogenesis, as the transfection of v-Ha-ras gene further advances the parental BALB/c 3T3 A31-1-1 cells toward higher transforming potential. Thus, we propose that Bhas 42 cells are a novel and sensitive cell line for the analysis of carcinogenesis and can be used for the detection of not only carcinogenic substances but also gene alterations related to oncogenesis. This review will address characteristics of Bhas 42 cells, the transformation assay protocol, validation studies, and the various chemicals tested in this assay.
    No preview · Article · Jan 2015 · Journal of Environmental Science and Health Part C Environmental Carcinogenesis & Ecotoxicology Reviews
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    ABSTRACT: Incretin-based therapies, including the use of incretin mimetics of glucagon-like peptide-1 receptor (GLP-1R) agonists and incretin enhancers of dipeptidyl-peptidase 4 (DPP-4) inhibitors, are widely used by clinicians for glucose lowering in patients with type 2 diabetes mellitus. These agents have benefits of a lower risk of hypoglycemia, being neutral for body weight for DPP-4 inhibitors and having a potential for weight reduction with GLP-1R agonists. They may also have a neutral or beneficial cardiovascular effect. Despite these benefits, an increased risk of cancer (especially pancreatic cancer and thyroid cancer) associated with incretin-based therapies has been reported. In this article, we reviewed related literature of experimental animal and observational human studies, clinical trials, and meta-analyses published until December 15, 2014. Current studies suggested a probable role of GLP-1R activation on the development of pancreatic cancer and thyroid cancer in rodents, but such an effect in humans is not remarkable due to the lower or lack of expression of GLP-1R on human pancreatic ductal cells and thyroid tissues. Findings in human studies are controversial and inconclusive. In the analyses of the US Food and Drug Administration adverse events reporting system, a significantly higher risk of pancreatic cancer was observed for GLP-1R agonists and DPP-4 inhibitors, but a significantly higher risk of thyroid cancer was only observed for GLP-1R agonists. Such a higher risk of pancreatic cancer or thyroid cancer could not be similarly demonstrated in other human observational studies or analyses of data from clinical trials. With regards to cancers other than pancreatic cancer and thyroid cancer, available studies supported a neutral association in humans. Some preliminary studies even suggested a potentially beneficial effect on the development of other cancers with the use of incretins. Based on current evidence, continuous monitoring of the cancer issues related to incretin-based therapies is required, even though the benefits may outweigh the potential cancer risk in the general patients with type 2 diabetes mellitus.
    No preview · Article · Jan 2015 · Journal of Environmental Science and Health Part C Environmental Carcinogenesis & Ecotoxicology Reviews