False and Misleading Claims of Scientific Misconduct in Early Research into Radiation Dose-response: Part 1. Overlooking Key Historical Text.

In reviewing a video series that they created for the website of the Health Physics Society (HPS), past leaders of the Health Physics Society have treated as authoritative and trustworthy the scientific misconduct theories of University of Massachusetts Professor Edward Calabrese. No mention is made of detailed critiques of Calabrese's work. I show that Calabrese's historical work as presented by HPS's authors is unreliable because it overlooks key historical text and key statistical concepts about the limits of an early atomic bomb genetics study.

False Indications of Dose-Response Nonlinearity in Large Epidemiologic Cancer Radiation Cohort Studies; A Simulation Exercise.

This study explores the likely prevalence of false indications of dose-response nonlinearity in large epidemiologic cancer radiation cohort studies (A-bomb survivors, INWORKS, Techa River). Reasons: Increasing numbers of tests of nonlinearity are being made in studies. Hypothesized nonlinear dose-response models have been justified to policy makers by analyses that rely in part on isolated findings that could be statistical fluctuations.

Implications of Recent Epidemiological Studies for Compensation of Veterans Exposed to Plutonium.

The objective of this paper is to compare post-2007 epidemiological results for plutonium workers to risk predicted by the software program NIOSH-IREP (IREP for short), which is used to determine the lowest dose for a US veteran to obtain cancer compensation. IREP output and methodology were used to predict excess relative risk per Gy (ERR Gy -1 ) for lung cancer at the 99 th credibility percentile, which is used for compensation decisions. Also estimated were relative biological effectiveness factors (RBE) predicted for workers using IREP methodology.

History of Dose, Risk, and Compensation Assessments for US Veterans of the 1966 Plutonium Cleanup in Palomares, Spain.

In 1966, about 1,600 US military men-mostly Air Force-participated in a cleanup of plutonium dispersed from two nuclear bombs in Palomares, Spain. As a base for future analyses, we provide a history of the Palomares incident, including the dosimetry and risk analyses carried out to date and the compensation assessments made for veterans. By law, compensation for illnesses attributed to ionizing radiation is based on maximum estimated doses and standard risk coefficients, with considerable benefit of the doubt given to claimants when there is uncertainty.

Lifetime exposure to ambient air pollution and methylation of tumor suppressor genes in breast tumors.

Background: We previously reported increased risk of breast cancer associated with early life exposure to two measures of air pollution exposure, total suspended particulates (TSP) and traffic emissions (TE), possible proxies for exposure to polycyclic aromatic hydrocarbons (PAHs). Exposure to PAHs has been shown to be associated with aberrant patterns of DNA methylation in peripheral blood of healthy individuals. Exposure to PAHs and methylation in breast tumor tissue has received little attention.

Lessons to be learned from a contentious challenge to mainstream radiobiological science (the linear no-threshold theory of genetic mutations).

There are both statistically valid and invalid reasons why scientists with differing default hypotheses can disagree in high-profile situations. Examples can be found in recent correspondence in this journal, which may offer lessons for resolving challenges to mainstream science, particularly when adherents of a minority view attempt to elevate the status of outlier studies and/or claim that self-interest explains the acceptance of the dominant theory. Edward J.

Polycyclic aromatic hydrocarbons and postmenopausal breast cancer: An evaluation of effect measure modification by body mass index and weight change.

Background: Polycyclic aromatic hydrocarbons (PAHs) have been linked to breast cancer in many, but not all, previous studies. PAHs are lipophilic and stored in fat tissue, which we hypothesized may result in constant low-dose exposure to these carcinogens. No previous studies have evaluated whether obesity modifies associations between multiple measures of PAHs and breast cancer incidence.

Response to, "On the origins of the linear no-threshold (LNT) dogma by means of untruths, artful dodges and blind faith.".

It is not true that successive groups of researchers from academia and research institutions-scientists who served on panels of the US National Academy of Sciences (NAS)-were duped into supporting a linear no-threshold model (LNT) by the opinions expressed in the genetic panel section of the 1956 "BEAR I" report. Successor reports had their own views of the LNT model, relying on mouse and human data, not fruit fly data. Nor was the 1956 report biased and corrupted, as has been charged in an article by Edward J.

Polymorphisms in DNA repair genes, traffic-related polycyclic aromatic hydrocarbon exposure and breast cancer incidence.

Vehicular traffic polycyclic aromatic hydrocarbons (PAHs) have been associated with breast cancer incidence in epidemiologic studies, including our own. Because PAHs damage DNA by forming adducts and oxidative lesions, genetic polymorphisms that alter DNA repair capacity may modify associations between PAH-related exposures and breast cancer risk. Our goal was to examine the association between vehicular traffic exposure and breast cancer incidence within strata of a panel of nine biologically plausible nucleotide excision repair (NER) and base excision repair (BER) genotypes.

Exposure to multiple sources of polycyclic aromatic hydrocarbons and breast cancer incidence.

Background: Despite studies having consistently linked exposure to single-source polycyclic aromatic hydrocarbons (PAHs) to breast cancer, it is unclear whether single sources or specific groups of PAH sources should be targeted for breast cancer risk reduction.

Objectives: This study considers the impact on breast cancer incidence from multiple PAH exposure sources in a single model, which better reflects exposure to these complex mixtures.

Methods: In a population-based case-control study conducted on Long Island, New York (N=1508 breast cancer cases/1556 controls), a Bayesian hierarchical regression approach was used to estimate adjusted posterior means and credible intervals (CrI) for the adjusted odds ratios (ORs) for PAH exposure sources, considered singly and as groups: active smoking; residential environmental tobacco smoke (ETS); indoor and outdoor air pollution; and grilled/smoked meat intake.

Sources of polycyclic aromatic hydrocarbons are associated with gene-specific promoter methylation in women with breast cancer.

Background: Tobacco smoke, diet and indoor/outdoor air pollution, all major sources of polycyclic aromatic hydrocarbons (PAHs), have been associated with breast cancer. Aberrant methylation may be an early event in carcinogenesis, but whether PAHs influence the epigenome is unclear, particularly in breast tissue where methylation may be most relevant. We aimed to evaluate the role of methylation in the association between PAHs and breast cancer.

Vehicular Traffic-Related Polycyclic Aromatic Hydrocarbon Exposure and Breast Cancer Incidence: The Long Island Breast Cancer Study Project (LIBCSP).

Background: Polycyclic aromatic hydrocarbons (PAHs) are widespread environmental pollutants, known human lung carcinogens, and potent mammary carcinogens in laboratory animals. However, the association between PAHs and breast cancer in women is unclear. Vehicular traffic is a major ambient source of PAH exposure.

Indoor air pollution exposure from use of indoor stoves and fireplaces in association with breast cancer: a case-control study.

Background: Previous studies suggest that polycyclic aromatic hydrocarbons (PAHs) may adversely affect breast cancer risk. Indoor air pollution from use of indoor stoves and/or fireplaces is an important source of ambient PAH exposure. However, the association between indoor stove/fireplace use and breast cancer risk is unknown.

Imputation method for lifetime exposure assessment in air pollution epidemiologic studies.

Background: Environmental epidemiology, when focused on the life course of exposure to a specific pollutant, requires historical exposure estimates that are difficult to obtain for the full time period due to gaps in the historical record, especially in earlier years. We show that these gaps can be filled by applying multiple imputation methods to a formal risk equation that incorporates lifetime exposure. We also address challenges that arise, including choice of imputation method, potential bias in regression coefficients, and uncertainty in age-at-exposure sensitivities.

Confidence intervals after multiple imputation: combining profile likelihood information from logistic regressions.

In the logistic regression analysis of a small-sized, case-control study on Alzheimer's disease, some of the risk factors exhibited missing values, motivating the use of multiple imputation. Usually, Rubin's rules (RR) for combining point estimates and variances would then be used to estimate (symmetric) confidence intervals (CIs), on the assumption that the regression coefficients were distributed normally. Yet, rarely is this assumption tested, with or without transformation.

Exposure to traffic emissions: associations with biomarkers of antioxidant status and oxidative damage.

Background: Oxidative stress has been implicated as a possible mechanism for adverse health effects associated with traffic emissions. We examined the association of an estimate of traffic emissions with blood biomarkers of antioxidant capacity (glutathione, glutathione peroxidase, trolox-equivalent antioxidant capacity) and oxidative damage (thiobarbituric acid-reactive substances (TBARS)) among 1810 healthy women, randomly selected from Erie and Niagara Counties in Western New York.

Methods: A geographic traffic emission and meteorological dispersion model was used to estimate annual polycyclic aromatic hydrocarbon (PAH) exposure from traffic emissions for each woman based on her residence at the time of study.

Airborne emissions from 1961 to 2004 of benzo[a]pyrene from U.S. vehicles per km of travel based on tunnel studies.

We identified 13 historical measurements of polycyclic aromatic hydrocarbons (PAHs) in U.S. vehicular traffic tunnels that were either directly presented as tailpipe emission factors in microg per vehicle-kilometer or convertible to such a form.

Exposure to traffic emissions throughout life and risk of breast cancer: the Western New York Exposures and Breast Cancer (WEB) study.

Objective: We previously reported that total suspended particulates exposure (a measure of air pollution) at the time of birth was related to increased postmenopausal breast cancer risk. In this study, we examined breast cancer risk in relation to exposure to air pollution from traffic emissions throughout life.

Methods: We conducted a case-control study of breast cancer.

Validation and calibration of a model used to reconstruct historical exposure to polycyclic aromatic hydrocarbons for use in epidemiologic studies.

Objectives: We previously developed a historical reconstruction model to estimate exposure to airborne polycyclic aromatic hydrocarbons (PAHs) from traffic back to 1960 for use in case-control studies of breast cancer risk. Here we report the results of four exercises to validate and calibrate the model.

Methods: Model predictions of benzo[a]pyrene (BaP) concentration in soil and carpet dust were tested against measurements collected at subjects' homes at interview.

Polycyclic aromatic hydrocarbon-DNA adducts and breast cancer: a pooled analysis.

Polycyclic aromatic hydrocarbon (PAH)-DNA adducts have been associated with breast cancer in several small studies. The authors' pooled analysis included 873 cases and 941 controls from a population-based case-control study. Competitive enzyme-linked immunosorbent assay in peripheral mononuclear cells was conducted in 2 rounds, and results were pooled on the basis of round-specific quantiles.