E.J. Calabrese. EPA adopts LNT: New historical perspectives. Chemic-Biological Interactions 308 (2019) 110-112
This paper provides an historical assessment of how the linear non-threshold (LNT) model became adopted as policy by the United States Environmental Protection Agency (US EPA) in 1975  and how prior United States National Academy of Sciences (US NAS) radiation advisory panels may have affected this EPA decision. The paper highlights a generally unrecognized set of recommendations of the 1960 Biological Effect of Atomic Radiation  Genetics and Medical/Pathology Panels that did not support LNT for cancer risk assessment due to their judgements of its scientific limitations and unacceptable uncertainties. These convergent, independent and high profile recommendations were not promoted by the sponsors (i.e., Rockefeller Foundation and the NAS), and were ignored by the media, Congress and the scientific community in contrast to the vast attention directed to the linearity recommendation for germ cell mutation by the BEAR Genetics Panel in 1956 [3,4]. The subsequent Biological Effects of Ionizing Radiation (BEIR) I Committee (1972)  report ignored these BEAR Panel (1960)  recommendations, only commenting on the BEAR 1956 linearity supporting recommendation [3,4]. These actions are documented and assessed for how they influenced why and how EPA adopted linearity for cancer risk assessment based on the BEIR I report.
“The linear no-threshold paradigm, which asserts there are no safe exposure levels, is the product of flawed and corrupted science.” click here
Edward J. Calabrese. The linear No-Threshold (LNT) dose response model: A comprehensive assessment of its historical and scientific foundations. Chemico-Biological Interactions. 301 (2019) 6–25. https://doi.org/10.1016/j.cbi.2018.11.020
The linear no-threshold (LNT) single-hit (SH) dose response model for cancer risk assessment is comprehensively assessed with respect to its historical foundations. This paper also examines how mistakes, ideological biases, and scientific misconduct by key scientists affected the acceptance, validity, and applications of the LNT model for cancer risk assessment. In addition, the analysis demonstrates that the LNT single-hit model was inappropriately adopted for governmental risk assessment, regulatory policy, practices, and for risk communication.
Clewell HH 3rd, Gentry PR, Hack CE, Greene T, Clewell RA. An evaluation of the USEPA Proposed Approaches for applying a biologically based dose-response model in a risk assessment for perchlorate in drinking water. Regulatory toxicology and pharmacology. 2019 Jan 29. pii: S0273-2300(19)30036-4. doi: 10.1016/j.yrtph.2019.01.028.
The United States Environmental Protection Agency’s (USEPA) 2017 report, “Draft Report: Proposed Approaches to Inform the Derivation of a Maximum Contaminant Level Goal for Perchlorate in Drinking Water”, proposes novel approaches for deriving a Maximum Contaminant Level Goal (MCLG) for perchlorate using a biologically-based dose-response (BBDR) model. The USEPA (2017) BBDR model extends previously peer-reviewed perchlorate models to describe the relationship between perchlorate exposure and thyroid hormone levels during early pregnancy. Our evaluation focuses on two key elements of the USEPA (2017) report: the plausibility of BBDR model revisions to describe control of thyroid hormone production in early pregnancy and the basis for linking BBDR model results to neurodevelopmental outcomes. While the USEPA (2017) BBDR model represents a valuable research tool, the lack of supporting data for many of the model assumptions and parameters calls into question the fitness of the extended BBDR model to support quantitative analyses for regulatory decisions on perchlorate in drinking water. Until more data can be developed to address uncertainties in the current BBDR model, USEPA should continue to rely on the RfD recommended by the NAS (USEPA, 2005) when considering further regulatory action.
Yuan T, Zhang H, Chen B, Zhang H, Tao S. Association between lung cancer risk and inorganic arsenic concentration in drinking water: a dose-response meta-analysis. Toxicol Res (Camb). 2018 Sep 18;7(6):1257-1266. doi: 10.1039/c8tx00177d.
High dose arsenic in drinking water (≥100 μg L-1) is known to induce lung cancer, but lung cancer risks at low to moderate arsenic levels and its dose-response relationship remains inconclusive. We conducted a systematic review of cohort and case-control studies that quantitatively reported the association between arsenic concentrations in drinking water and lung cancer risks by searching the PubMed database till June 14, 2018. Pooled relative risks (RRs) of lung cancer associated with full range (10 μg L-1-1000 μg L-1) and low to moderate range (<100 μg L-1) of water arsenic concentrations were calculated using random-effects models. A dose-response meta-analysis was performed to estimate the pooled associations between restricted cubic splines of log-transformed water arsenic and the lung cancer risks. Fifteen studies (9 case-control and 6 cohort studies) involving a total of 218 481 participants met the inclusion criteria. Meta-analysis identified significantly increased risks of lung cancer on exposure to both full range (RR = 1.21; 95% confidence interval [CI] = 1.05-1.37; heterogeneity I 2 = 54.3%) and low to moderate range (RR = 1.18; 95%CI = 1.00-1.35; I 2 = 56.3%) of arsenic-containing water. In the dose-response meta-analysis of eight case-control studies, we found no evidence of non-linearity, although statistical power was limited. The corresponding pooled RRs and their 95%CIs for exposure to 10 μg L-1, 50 μg L-1, and 100 μg L-1 water arsenic were 1.02 (1.00-1.03), 1.10 (1.04-1.15), and 1.20 (1.08-1.32), respectively. We provide evidence on the association between increased lung cancer risks and inorganic arsenic in drinking water across low, moderate and high levels. Minimizing arsenic levels in drinking water may be of public health importance.
Fakour H, Lo SL. Formation and risk assessment of trihalomethanes through different tea brewing habits. Int J Hyg Environ Health. 2018 Sep 1. pii: S1438-4639(18)30193-7. doi: 10.1016/j.ijheh.2018.08.013.
Trihalomethanes (THMs) are suspected carcinogens and reproductive toxicants commonly found in chlorinated drinking water. This study investigates the formation of THMs and their associated risks during different tea brewing habits. Three main categories of tea (black, oolong, and green) under various brewing conditions and drinking water sources were tested. Tea samples prepared in ordinary thermos flask formed significant levels of total THM (TTHM). The highest TTHM formation came from black tea made with tap water, plausibly due to higher concentrations of reactive THM precursors. Compared with tap water, when the background solution is bottled water or distilled water, less TTHM was observed in prepared tea infusions. The results also revealed that unlike the traditional teapot-based tea serving habit, the removal of THMs is significantly reduced when tea infusion is stored in enclosed containers. Risk assessment analysis based on the survey among tea shop costumers also revealed that cancer risks induced by ingestion of THMs through drinking tea infusions prepared in thermos flask exceeded the tolerable level. Data obtained in this research demonstrated that drinking tea infusions directly from enclosed containers can be a significant source of exposure to THMs.
Brenda C. Minatel1, Adam P. Sage1, Christine Anderson, Roland Hubaux, Erin A. Marshall, Wan L. Lam, Victor D. Martinez. Environmental arsenic exposure: From genetic susceptibility to pathogenesis. Environment International Volume 112, March 2018, Pages 183–197
More than 200 million people in 70 countries are exposed to arsenic through drinking water. Chronic exposure to this metalloid has been associated with the onset of many diseases, including cancer. Epidemiological evidence supports its carcinogenic potential, however, detailed molecular mechanisms remain to be elucidated. Despite the global magnitude of this problem, not all individuals face the same risk. Susceptibility to the toxic effects of arsenic is influenced by alterations in genes involved in arsenic metabolism, as well as biological factors, such as age, gender and nutrition. Moreover, chronic arsenic exposure results in several genotoxic and epigenetic alterations tightly associated with the arsenic biotransformation process, resulting in an increased cancer risk. In this review, we: 1) review the roles of inter-individual DNA-level variations influencing the susceptibility to arsenic-induced carcinogenesis; 2) discuss the contribution of arsenic biotransformation to cancer initiation; 3) provide insights into emerging research areas and the challenges in the field; and 4) compile a resource of publicly available arsenic-related DNA-level variations, transcriptome and methylation data. Understanding the molecular mechanisms of arsenic exposure and its subsequent health effects will support efforts to reduce the worldwide health burden and encourage the development of strategies for managing arsenic-related diseases in the era of personalized medicine.