Hair cortisol as a viable tool for the assessment of an association between environmental noise exposure and chronic stress.

Entrenched in the well-established link between stress and health, noise exposure as a potential contributor to stress-related health effects receives tremendous attention. Indeed, exposure to noise can act as a stressor as evidenced through increased heart rate, blood pressure, adrenaline, epinephrine, and cortisol. Cortisol is secreted from the adrenal glands in response to stressor-induced activation of the hypothalamic-pituitary-adrenal axis. For assessment of environmental noise and stress, repeated sampling in blood, saliva, or urine is necessary to evaluate the association between environmental noise exposure and protracted changes in cortisol. Controlling for the many variables that influence the secretion of cortisol at discrete sampling intervals is challenging. Studies suggest that systemically produced cortisol integrates and remains in hair as it grows, providing a measure that integrates a cortisol response over a longer period, circumventing several limitations associated with multiple sampling. Robust evidence supports the integration of cortisol into hair, yet recent studies call into question the notion that cortisol is retained with growth. The current paper discusses the strengths and limitations of hair cortisol analysis with an emphasis on its utility as a measure of chronic stress in environmental noise studies.

Transcriptional benchmark dose modeling: Exploring how advances in chemical risk assessment may be applied to the radiation field.

Recent advances in "-omics" technologies have simplified capacity to concurrently assess expression profiles of thousands of targets in a cellular system. However, compilation and analysis of "omics" data in support of human health protection remains a challenge. Benchmark dose (BMD) modeling is currently being employed in chemical risk assessment to estimate acceptable levels of exposure. Although typically applied to conventional endpoints, newer software has enabled this application to be extended to transcriptomic datasets. BMD analytical tools now have the capacity to model transcriptional dose-response data to derive meaningful BMD values for genes, pathways and gene ontologies. In this report, radiation data obtained from the Gene Expression Omnibus (GEO) were analyzed to generate BMD values for transcriptional responses. The datasets comprised microarray analyses of human blood gamma-irradiated ex vivo (0-20 Gy) and human-derived cell lines exposed to alpha particle radiation (0.5-1.5 Gy). The distributions of BMDs for statistically significant genes and pathways in response to radiation exposure were examined and compared across studies. BMD modeling could identify pathway/gene sensitivities across wide radiation dose ranges, experimental conditions (time-points, cell types) and radiation qualities. BMD analysis offered a new approach to examine transcriptional data. The results were shown to provide information on transcriptional thresholds of effects to support refined risk assessments for low dose ionizing radiation exposures, derive gene-based values for relative biological effectiveness and identify pathways involved in radiation sensitivities across cell types which may extend to applications a clinical setting. Environ. Mol. Mutagen. 57:589-604, 2016. © 2016 Wiley Periodicals, Inc.

Assessment of genetic damage in peripheral blood of human volunteers exposed (whole-body) to a 200 muT, 60 Hz magnetic field.

AIM: To investigate the extent of damage in nucleated cells in peripheral blood of healthy human volunteers exposed to a whole-body 60 Hz, 200 microT magnetic field. MATERIALS AND METHODS: In this study, 10 male and 10 female healthy human volunteers received a 4 h whole-body exposure to a 200 microT, 60 Hz magnetic field. In addition, five males and five females were treated in a similar fashion, but were exposed to sham conditions. For each subject, a blood sample was obtained prior to the exposure period and aliquots were used as negative- (pre-exposure) and positive- [1.5 Gray (Gy) (60)Cobalt ((60)Co) gamma-irradiation] controls. At the end of the 4 h exposure period, a second blood sample was obtained. The extent of DNA damage was assessed in peripheral human blood leukocytes from all samples using the alkaline comet assay. To detect possible clastogenic effects, the incidence of micronuclei was assessed in phytohemagglutinin (PHA)-stimulated lymphocytes using the cytokinesis-block micronucleus assay. RESULTS: There was no evidence of either increased DNA damage, as indicated by the alkaline comet assay, or increased incidence of micronuclei (MN) in the magnetic field exposed group. However, an in vitro exposure of 1.5 Gy gamma-irradiation caused a significant increase in both DNA damage and MN induction. CONCLUSIONS: This study found no evidence that an acute, whole-body exposure to a 200 microT, 60 Hz magnetic field for 4 hours could cause DNA damage in human blood.