Environmental research
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Environmental research · Jul 2017
Long-term residential road traffic noise and NO2 exposure in relation to risk of incident myocardial infarction - A Danish cohort study.
Road traffic is a source of both air pollution and noise; two environmental hazards both found to increase the risk of ischemic heart disease. Given the high correlation between these pollutants, it is important to investigate combined effects, in relation to myocardial infarction (MI). ⋯ Both road traffic noise and NO2 were associated with a higher risk of MI in single-pollutant models. In two-pollutant models, mainly noise was associated with MI. Combined exposure to both pollutants was associated with the highest risk.
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Environmental research · May 2017
Allergic disease associations with regional and localized estimates of air pollution.
Exposure to multiple types of air pollution may contribute to and exacerbate allergic diseases including asthma and wheezing. However, few studies have examined chronic air pollution exposure and allergic disease outcomes among an adult population. Associations between potential estimates of annual average fine particulate matter (PM2.5), traffic related air pollution, and industrial source air emissions and three allergic disease outcomes (asthma, allergies and wheezing) were examined in a state-wide general population of adults. ⋯ Within this population exposed to overall annual average levels of estimated low level chronic exposure to fine particulate matter (PM2.5) at or near 12μg/m3, the USEPA standard for air quality, significant association between both modeled PM2.5 exposure and proximity to roadways with asthma and allergies but not wheezing were found. Industrial source emissions were not associated with any allergic disease outcomes.
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Considerable recent findings have revealed that the linear dose response for cancer risk assessment has not only outlived its utility in predicting risk but is based on a flawed scientific foundation. The present article characterizes this demise of a key concept of environmental risk assessment, in the framework of a figurative obituary of a long-lived concept that has poorly served society. This obituary is intended to illustrate an integrated mix of poignant and improper historical judgments that led to both the acceptance and ultimately the demise of this once intellectually facile and nearly universally accepted concept.
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Environmental research · Apr 2017
Review Historical ArticleThe threshold vs LNT showdown: Dose rate findings exposed flaws in the LNT model part 2. How a mistake led BEIR I to adopt LNT.
This paper reveals that nearly 25 years after the National Academy of Sciences (NAS), Biological Effects of Ionizing Radiation (BEIR) I Committee (1972) used Russell's dose-rate data to support the adoption of the linear-no-threshold (LNT) dose response model for genetic and cancer risk assessment, Russell acknowledged a significant under-reporting of the mutation rate of the historical control group. This error, which was unknown to BEIR I, had profound implications, leading it to incorrectly adopt the LNT model, which was a decision that profoundly changed the course of risk assessment for radiation and chemicals to the present.
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Environmental research · Apr 2017
Review Historical ArticleThe threshold vs LNT showdown: Dose rate findings exposed flaws in the LNT model part 1. The Russell-Muller debate.
This paper assesses the discovery of the dose-rate effect in radiation genetics and how it challenged fundamental tenets of the linear non-threshold (LNT) dose response model, including the assumptions that all mutational damage is cumulative and irreversible and that the dose-response is linear at low doses. Newly uncovered historical information also describes how a key 1964 report by the International Commission for Radiological Protection (ICRP) addressed the effects of dose rate in the assessment of genetic risk. This unique story involves assessments by two leading radiation geneticists, Hermann J. ⋯ Russell, who independently argued that the report's Genetic Summary Section on dose rate was incorrect while simultaneously offering vastly different views as to what the report's summary should have contained. This paper reveals occurrences of scientific disagreements, how conflicts were resolved, which view(s) prevailed and why. During this process the Nobel Laureate, Muller, provided incorrect information to the ICRP in what appears to have been an attempt to manipulate the decision-making process and to prevent the dose-rate concept from being adopted into risk assessment practices.