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    • Our results on the association between

    2018-10-30

    Our results on the association between PCBs and longer LTL are consistent with the findings reported by Shin and colleagues (Shin et al., 2010) in a cross-sectional study consisting of 84 healthy Korean individuals (33 men and 51 women) with a mean age of 56years (range 42–69years). The authors reported a positive association of several PCBs — PCB99, PCB153, PCB180, PCB183 and PCB187 — with longer LTL (Shin et al., 2010). In their evaluation on polychlorinated dibenzo-para-dioxins and polychlorinated dibenzofurans, the International Agency for Research on Cancer (IARC) classified 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) as carcinogenic to humans (IARC group 1 classification) but other polychlorinated dibenzo-p-dioxins, the nonchlorinated dibenzo-p-dioxin, and polychlorinated dibenzofurans were evaluated as not classifiable as to their carcinogenicity to humans (group 3) (IARC, 1997). PCBs are classified as probable carcinogens by the US Environmental Protection Agency (EPA) (USEPA, 1997). Recently, the IARC concluded that “there is sufficient evidence in humans for the carcinogenicity of polychlorinated biphenyls (PCBs). PCBs cause malignant melanoma. Positive associations have been observed for non-Hodgkin lymphoma and cancer of the breast.” (IARC, 2015). Furthermore, PCB126 and PCB169 were classified by IARC as a human carcinogen (IARC group 1 classification) (IARC, 2015). A recent systematic review and meta-analysis found evidence of a role of PCBs in the development of non-Hodgkin Lymphoma (NHL) (Zani et al., 2013). Freeman and Kohles (Freeman and Kohles, 2012) suggested a causal relationship between NHL and PCB exposure based on the Bradford-Hill criteria. Kramer and colleagues (Kramer et al., 2012), in their analyses of the scientific literature, concluded that the weight of evidence was supportive of a causal role of PCBs in NHL; a biologically plausible explanation of this PU-H71 relationship is the immunosuppressive and inflammatory effects of PCBs. A prospective cohort study with 107 cases reported a dose–response relationship between quartiles of increasing TL and risk of NHL (OR=3.6; 95% CI: 1.4–8.9) (Lan et al., 2009). This association suggested that individuals with longer telomeres have an elevated NHL risk. One may expect that “from a biologic perspective, longer telomere length should allow for longer cellular survival, the accumulation of genetic mutations, and the possibility of accumulating potentially cancer promoting mutations”; (Noy, 2009) therefore, our findings of the association of PCBs with longer LTL may suggest a plausible mechanistic explanation for PCBs role in NHL development. PCBs may act to preserve LTL and possibly act as tumor promoters. Studies in mice and rats demonstrated that PCBs are efficient tumor promoters when administered for extended periods of time following an initiating agent (Faroon et al., 2001; Safe, 1994). Several experimental systems associated activation of the proto-oncogene c-myc with cellular growth and proliferation programs (Dang, 2013) and thus an important feature of cancer initiation and maintenance (Gabay et al., 2014). Moreover, expression of TERT and telomerase activity is induced by c-myc; (Greenberg et al., 1999) therefore, it may be biologically plausible that PCBs may contribute to telomere length maintenance or lessening the loss by attrition by inducing c-myc expression. Gribaldo and colleagues (Gribaldo et al., 1998) showed that PCB138-exposed mouse fibroblast T3-L1 cell lines cultured in serum-free media overexpressed oncogenes that are involved in cell-cycle progression and proliferation, among them c-myc. Exposure of 3T3-L1 cells with PCB169 or PCB126 showed increased expression of c-myc in media containing serum (Gribaldo et al., 1998). Ghosh and colleagues (Ghosh et al., 2007) in an in vitro experiment using human liver (HepG2) cells, showed that chronic exposure of these cells with PCB153 overexpressed c-myc protein compared to short-term exposure. Another underlying mechanism for PCBs contribution to telomere length maintenance may be through activation of the NF-κB which upregulate the human telomerase (Akiyama et al., 2002; Zuo et al., 2011). Kwon and colleagues (Kwon et al., 2002) reported induction of NF-κB of human leukemic mast cell (HLMC) line exposed to PCB153.