This study adds to the growing

This study adds to the growing body of research showing a link between environmental exposures and LTL (), and suggests that POPs may be able to activate telomerase or other telomere-elongating mechanisms. Activation of telomerase is a critical, early event in carcinogenesis for the majority of cancer types. Once telomere herpes simplex virus infection has been hijacked by cancer cells, they will be able to overcome cellular senescence and apoptosis, and will have better survival. Changes in LTL are believed to be a reflection of these in situ processes (). Questions remain about the exact mechanism by which POPs induce longer telomeres, and the temporal sequence of the relationship, both of which will need to be answered before this observed relationship can be exploited clinically. Other important confounders such as various nutrient intakes and body fat will need to be ruled out as well, and POP-induced LTL changes will need to be evaluated for their effects on human disease. Cross-sectional and prospective studies of telomeres have identified inconsistent relationships between LTL and cancer, with authors identifying both longer and shorter telomeres as predisposing to cancer risk, frequently across different cancers (). This is another question that will need to be answered to assess the relationships between POPs, LTL, and cancer. While NHANES includes self-reported data on prior cancer diagnoses, which was explored in this study, the number of available cancer cases is relatively small, and lacks detailed clinical information (e.g., histology) that would be relevant to this area of research and available through inclusion of formal medical records. Nonetheless finding significant, dose-dependent changes in LTL associated with so many different types of POPs demonstrates that this is a promising area of research. Future prospective, longitudinal studies incorporating detailed data on medical history, lifestyle, and environmental exposures will help completely elucidate the causal mechanisms involved in the complex and dynamic relationship between carcinogens and LTL.
The accumulating epidemiological evidence of elevated cancer risk and mortality in individuals exposed to polychlorinated biphenyls (PCBs) led to their recent classification as human carcinogen by the International Agency for Research on Cancer (IARC) (). However, the mechanisms by which PCBs are linked to cancer are still unclear. In this issue, Scinicariello and Buser () conducted a study of the association between leukocyte telomere length (LTL) and PCB blood levels in a nationally representative sample of the civilian US adult population using data from the National Health and Nutrition Examination Survey (NHANES). The authors showed that higher PCB blood levels were associated with longer LTL, and hypothesized that there could be a link to PCB-related carcinogenesis. A separate study reported similar relationships between LTL and PCB blood levels in a subset of NHANES participants (). However, a small study of healthy Koreans () showed that this relationship was only present at low PCB levels. In contrast, short LTL has been associated with a number of environmental or occupational exposures including particulate matter, black carbon, benzene, toluene, polycyclic aromatic hydrocarbons, N-nitrosamines, pesticides, and lead (reviewed in ), all of which may contribute to PCB blood levels. Telomere shortening in response to chemical exposures may be explained, at least in part, by the induction of an oxidative stress DNA damage response (). Telomeres, the long (TTAGGG) nucleotide repeats and an associated protein complex at chromosome ends, are essential for maintaining chromosomal stability. They shorten with each cell division and therefore are markers for cellular replicative capacity, cellular senescence, and aging. Telomere shortening and chromosomal instability has been described at early stages of carcinogenesis, suggesting a role of telomere dysfunction in cancer initiation ().