Road-traffic noise can induce stress, which may contribute to mental health disorders. Mental health problems have not received much attention in noise research. People perceive noise differently, which may affect the extent to which noise contributes to poor mental health at the individual level. This paper aims to assess the relationships between outdoor traffic noise and noise annoyance and the use of psychotropic medication. We conducted a survey to assess noise annoyance and psychotropic medication among residents of the Helsinki Capital Region of Finland. We also assessed the associations of annoyance and road-traffic noise with sleep disorders, anxiety and depression. Respondents were randomly sampled from the Finnish Population registry, and data was collected using a self-administered questionnaire. Outdoor traffic noise was modelled using the Nordic prediction model. Associations between annoyance and modelled façade-noise levels with mental health outcome indicators were assessed using a binary logistic regression while controlling for socioeconomic, lifestyle and exposure-related factors. A total of 7321 respondents returned completed questionnaires. Among the study respondents, 15%, 7% and 7% used sleep medication, anxiolytic and antidepressant medications, respectively, in the year preceding the study. Noise annoyance was associated with anxiolytic drug use, OR = 1.41 (95% CI: 1.02-1.95), but not with sedative or antidepressant use. There was suggestive association between modelled noise at levels higher than 60 dB and anxiolytic or antidepressant use. In respondents whose bedroom windows faced the street, modelled noise was definitively associated with antidepressant use. Noise sensitivity did not modify the effect of noise but was associated with an increased use of psychotropic medication. We observed suggestive associations between high levels of road-traffic noise and psychotropic medication use. Noise sensitivity was associated with psychotropic medication use.

Extremely low-frequency (ELF) magnetic fields have been classified as possibly carcinogenic, mainly based on rather consistent epidemiological findings suggesting a link between childhood leukaemia and 50–60 Hz magnetic fields from power lines. However, causality is not the only possible explanation for the epidemiological associations, as animal andin vitroexperiments have provided only limited support for carcinogenic effects of ELF magnetic fields. Importantly, there is no generally accepted biophysical mechanism that could explain such effects. In this review, we discuss the possibility that carcinogenic effects are based on the radical pair mechanism (RPM), which seems to be involved in magnetoreception in birds and certain other animals, allowing navigation in the geomagnetic field. We review the current understanding of the RPM in magnetoreception, and discuss cryptochromes as the putative magnetosensitive molecules and their possible links to cancer-relevant biological processes. We then propose a hypothesis for explaining the link between ELF fields and childhood leukaemia, discuss the strengths and weaknesses of the current evidence, and make proposals for further research.

Purpose: In our previous studies, exposure to extremely low frequency (ELF) magnetic fields (MF) altered responses to DNA damage caused by menadione. The aim of this study was to evaluate possible ELF MF induced changes in proteins involved in DNA damage responses and in cell cycle distribution. Materials and methods: Based on our previous studies, the exposure protocol included pre-exposure of human SH-SY5Y neuroblastoma cells to a 50 Hz, 100 μT MF for 24 h prior to a 3-h menadione treatment. As DNA damage responses are relatively fast processes, a 1-h menadione treatment was also included in the experiments. The menadione concentrations used were 1, 10, 15, 20, and 25 μM. Immunoblotting was used to assess the levels of DNA damage response-related proteins (γ-H2AX, Chk1, phospho-Chk1, p21, p27, and p53), while the level of DNA damage was assessed by the alkaline Comet assay. Cell cycle distribution was assayed by SYTOX Green staining followed by flow cytometry analysis. Results: The main findings in MF-exposed cells were decreased p21 protein level after the 1-h menadione treatment, as well as increased proportion of cells in the G1 phase and decreased proportion of S phase cells after the 3-h menadione treatment. These effects were detectable also in the absence of menadione. Conclusions: The results indicate that MF exposure can alter the G1 checkpoint response and that the p21 protein may be involved in early responses to MF exposure.

There is limited understanding of how radiation or chemicals induce genomic instability, and how the instability is epigenetically transmitted to the progeny of exposed cells or organisms. Here we measured the expression of microRNAs (miRNAs) and DNA methyltransferases (DNMTs) in murine embryonal fibroblasts exposed to ionizing radiation or 2,3,7,8 -tetrachlorodibenzo-p-dioxin (TCDD), which were previously shown to induce genomic instability in this cell line. Cadmium was used as a reference agent that does not induce genomic instability in our experimental model. Measurements at 8 and 15 days after exposure did not identify any such persistent changes that could be considered as signals transmitting genomic instability to the progeny of exposed cells. However, measurements at 2 days after exposure revealed findings that may reflect initial stages of genomic instability. Changes that were common to TCDD and two doses of radiation (but not to cadmium) included 5 candidate signature miRNAs and general up-regulation of miRNA expression. Expression of DNMT3a, DNMT3b and DNMT2 were suppressed by cadmium but not by TCDD or radiation, consistently with the hypothesis that sufficient expression of DNMTs is necessary in the initial phase of induced genomic instability.