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      Combined Toxic Exposures and Human Health: Biomarkers of Exposure and Effect

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          Abstract

          Procedures for risk assessment of chemical mixtures, combined and cumulative exposures are under development, but the scientific database needs considerable expansion. In particular, there is a lack of knowledge on how to monitor effects of complex exposures, and there are few reviews on biomonitoring complex exposures. In this review we summarize articles in which biomonitoring techniques have been developed and used. Most examples describe techniques for biomonitoring effects which may detect early changes induced by many chemical stressors and which have the potential to accelerate data gathering. Some emphasis is put on endocrine disrupters acting via epigenetic mechanisms and on carcinogens. Solid evidence shows that these groups of chemicals can interact and even produce synergistic effects. They may act during sensitive time windows and biomonitoring their effects in epidemiological studies is a challenging task.

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          Obesity, cigarette smoking, and telomere length in women.

          A Valdes, T. Andrew, J. P. Gardner … (2005)
          Obesity and smoking are important risk factors for many age-related diseases. Both are states of heightened oxidative stress, which increases the rate of telomere erosion per replication, and inflammation, which enhances white blood cell turnover. Together, these processes might accelerate telomere erosion with age. We therefore tested the hypothesis that increased body mass and smoking are associated with shortened telomere length in white blood cells. We investigated 1122 white women aged 18-76 years and found that telomere length decreased steadily with age at a mean rate of 27 bp per year. Telomeres of obese women were 240 bp shorter than those of lean women (p=0.026). A dose-dependent relation with smoking was recorded (p=0.017), and each pack-year smoked was equivalent to an additional 5 bp of telomere length lost (18%) compared with the rate in the overall cohort. Our results emphasise the pro-ageing effects of obesity and cigarette smoking.
          Article 0 comments Cited 402 times – based on 0 reviews     Review now
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            Sequence variants at the TERT-CLPTM1L locus associate with many cancer types.

            Thorunn Rafnar, Patrick Sulem, Simon N. Stacey … (2009)
            The common sequence variants that have recently been associated with cancer risk are particular to a single cancer type or at most two. Following up on our genome-wide scan of basal cell carcinoma, we found that rs401681[C] on chromosome 5p15.33 satisfied our threshold for genome-wide significance (OR = 1.25, P = 3.7 x 10(-12)). We tested rs401681 for association with 16 additional cancer types in over 30,000 cancer cases and 45,000 controls and found association with lung cancer (OR = 1.15, P = 7.2 x 10(-8)) and urinary bladder, prostate and cervix cancer (ORs = 1.07-1.31, all P < 4 x 10(-4)). However, rs401681[C] seems to confer protection against cutaneous melanoma (OR = 0.88, P = 8.0 x 10(-4)). Notably, most of these cancer types have a strong environmental component to their risk. Investigation of the region led us to rs2736098[A], which showed stronger association with some cancer types. However, neither variant could fully account for the association of the other. rs2736098 corresponds to A305A in the telomerase reverse transcriptase (TERT) protein and rs401681 is in an intron of the CLPTM1L gene.
            Article 0 comments Cited 184 times – based on 0 reviews     Review now
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              TP53 mutations and hepatocellular carcinoma: insights into the etiology and pathogenesis of liver cancer.

              Xiao Wang, F Staib, Rashid S. Hussain … (2007)
              Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and the major risk factors include chronic infections with the hepatitis B (HBV) or C (HCV) virus, and exposure to dietary aflatoxin B(1) (AFB(1)) or alcohol consumption. Multiple genetic and epigenetic changes are involved in the molecular pathogenesis of HCC, for example, somatic mutations in the p53 tumor suppressor gene (TP53) and the activation of the WNT signal transduction pathway. AFB(1) frequently induces G:C to T:A transversions at the third base in codon 249 of TP53 and cooperates with HBV in causing p53 mutations in HCC. The detection of TP53 mutant DNA in plasma is a biomarker of both AFB(1) exposure and HCC risk. Chronic infection with HBV and HCV viruses, and oxyradical disorders including hemochromatosis, also generate reactive oxygen/nitrogen species that can both damage DNA and mutate cancer-related genes such as TP53. Certain mutant p53 proteins may exhibit a 'gain of oncogenic function'. The p53 biological network is a key responder to this oxidative and nitrosative stress. Depending on the extent of the DNA damage, p53 regulates the transcription of protective antioxidant genes and with extensive DNA damage, transactivates pro-oxidant genes that contribute to apoptosis. The X gene of HBV (HBx) is the most common open reading frame integrated into the host genome in HCC and the integrated HBx is frequently mutated. Mutant HBx proteins still retain their ability to bind to p53, and attenuate DNA repair and p53-mediated apoptosis. In summary, both viruses and chemicals are implicated in the etiology of TP53 mutations during the molecular pathogenesis of HCC.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Environ Res Public Health
                Journal ID (publisher-id): 101238455
                Title: International Journal of Environmental Research and Public Health
                Publisher: Molecular Diversity Preservation International (MDPI)
                ISSN (Print): 1661-7827
                ISSN (Electronic): 1660-4601
                Publication date (Print): March 2011
                Publication date (Electronic): 24 February 2011
                Volume: 8
                Issue: 3
                Pages: 629-647
                Affiliations
                Institute of Environmental Medicine, Karolinska Institutet, Box 210, 171 77 Stockholm, Sweden; E-Mail: ilona.silins@ 123456ki.se
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: johan.hogberg@ 123456ki.se ; Tel.: +46-8-524-87503; Fax: +46-8-343849.
                Article
                Publisher ID: ijerph-08-00629
                DOI: 10.3390/ijerph8030629
                PMC ID: 3083662
                PubMed ID: 21556171
                SO-VID: 35cfc5af-561e-49f7-a7f2-6256964885e5
                Copyright © © 2011 by the authors; licensee MDPI, Basel, Switzerland
                License:

                This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 14 January 2011
                Date accepted : 21 February 2011
                Categories
                Subject: Review

                ScienceOpen disciplines: Public health
                Keywords: biomarkers,combined exposure,chemical mixture,occupational exposure
                Data availability:
                ScienceOpen disciplines: Public health
                Keywords: biomarkers, combined exposure, chemical mixture, occupational exposure

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