Background Exposure to black carbon (BC), a tracer of vehicular-traffic-pollution, is associated with increased blood pressure (BP). Identifying biological factors that attenuate BC effects on BP can inform prevention. We evaluated the role of mitochondrial abundance, an adaptive mechanism compensating for cellular-redox-imbalance, in the BC-BP relationship. Methods and Results At one or more visits among 675 older men from the Normative Aging Study (observations=1,252), we assessed daily BP and ambient BC levels from a stationary monitor. To determine blood mitochondrial abundance, we used whole blood to analyze mitochondrial-to-nuclear DNA ratio (mtDNA/nDNA) using quantitative polymerase-chain-reaction. Every standard deviation (SD) increase in 28-day BC moving average (MA) was associated with 1.97 mm Hg (95%CI, 1.23–2.72; P<0.0001) and 3.46 mm Hg (95%CI, 2.06–4.87; P<0.0001) higher diastolic and systolic (SBP) BP, respectively. Positive BC-BP associations existed throughout all time windows. BC MAs (5-day to 28-day) were associated with increased mtDNA/nDNA; every SD increase in 28-day BC MA was associated with 0.12 SD (95%CI, 0.03–0.20; P=0.007) higher mtDNA/nDNA. High mtDNA/nDNA significantly attenuated the BC-SBP association throughout all time windows. The estimated effect of 28-day BC MA on SBP was 1.95-fold larger for individuals at the lowest mtDNA/nDNA quartile midpoint (4.68 mm Hg; 95%CI, 3.03–6.33; P<0.0001), compared to the top quartile midpoint (2.40 mm Hg; 95%CI, 0.81–3.99; P=0.003). Conclusions In older adults, short- to moderate-term ambient BC levels were associated with increased BP and blood mitochondrial abundance. Our findings indicate that increased blood mitochondrial abundance is a compensatory response and attenuates the cardiac effects of BC.

The epitranscriptome comprises more than 100 forms of RNA modifications. Of these, N6methyladenosine (m 6 A) is the most abundantform of RNA methylation, with roles in modulating mRNA transcript processing and regulation. The aims of the study weretoexamine changes inm 6 A RNA methylation in A549 lung epithelial cells in response to environmental toxicants, anddifferential gene expression of m 6 A modulator genes ('readers', 'writers' and 'erasers') in human subjects exposed toparticulate matter (PM) and in lung cancer tissueusing publicly-available microarray datasets.Global m 6 A methylation levelsweremeasured in total RNA after exposuretotwo carcinogens (PM and sodium arsenite) for 24-and 48-hours, and totwo endocrine disruptors (bisphenol A and vinclozolin)for 24-hours.Global m 6 A methylation level significantly decreased with exposure to >62 µg/mlPM, >1 µM sodium arsenite, >1µM bisphenol A (BPA), and0.1µM vinclozolin.In an analysis of a published dataset derived from a population study, we observed that m 6 A writers (METTL3 and WTAP), erasers (FTO and ALKBH5) and readers (HNRPC) showed significantly higher expression among participants in the high-PM 2.5 exposure group compared to those in the low-exposure control group(all p<0.05).Further, the m 6 A writer METTL3shows reduced expression in lung tumors in comparison to normal lung epithelia (p<0.0001).Our findings reveal that m 6 A RNA methylation can be modified by exposure to environmental toxicants, and exposure to particulate matter is associated with differential expression level of m 6 A RNA methylation modification machinery.

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The activity concentrations of 137Cs, 40K, 232Th, 238U and 226Ra were measured in surface soil samples from East and South of Marmara region, Turkey. The physico-chemical parameters (organic matter, CaCO3 contents and pH-value) of the soil samples were determined in the samples collected from 100 sampling stations. The average activity concentrations of 137Cs, 40K, 232Th, 238U and 226Ra were found to be 27.46+/-21.84, 442.51+/-189.85, 26.63+/-15.90, 21.77+/-12.08 and 22.45+/-13.31 Bq kg(-1), respectively. The mean value of total annual external gamma radiation dose equivalent for the natural radionuclides was calculated to be 54.86 microSv. The current data were compared with those found in the other locations of Turkey and different countries.

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Environmental noise exposure is associated with adverse effects on human health including hearing loss, heart disease, and changes in stress-related hormone levels. Alteration in DNA methylation in response to environmental exposures is a well-known phenomenon and it is implicated in many human diseases. Understanding how environmental noise exposures affect DNA methylation patterns may help to elucidate the link between noise and adverse effects on health. In this pilot study we examined the effects of environmental noise exposure on DNA methylation of genes related to brain function and investigated whether these changes are related with metabolic health. We exposed four groups of male Wistar rats to moderate intensity noise (70-75dB with 20-4000Hz) at night for three days as short-term exposure, and for three weeks as long-term exposure. Noise exposure was limited to 45dB during the daytime. Control groups were exposed to only 45dB, day and night. We measured DNA methylation in the Bdnf, Comt, Crhr1, Mc2r, and Snca genes in tissue from four brain regions of the rats (hippocampus, frontal lobe, medulla oblongata, and inferior colliculus). Further, we measured blood pressure and body weight after long-term noise exposure. We found that environmental noise exposure is associated with gene-specific DNA methylation changes in specific regions of the brain. Changes in DNA methylation are significantly associated with changes in body weight (between Bdnf DNA methylation and Δ body weight: r=0.59, p=0.018; and between LINE-1 ORF DNA methylation and Δ body weight: =-0.80, p=0.0004). We also observed that noise exposure decreased blood pressure (p=0.038 for SBP, p=0.017 for DBP and p 0. 017 for MAP) and decreased body weight (β=-26g, p=0.008). In conclusion, environmental noise exposures can induce changes in DNA methylation in the brain, which may be associated with adverse effects upon metabolic health through modulation of response to stress-related hormones.