Tinnitus: Distinguishing between Subjectively Perceived Loudness and Tinnitus-Related Distress

OBJECTIVES: Overall success of current tinnitus therapies is low, which may be due to the heterogeneity of tinnitus patients. Therefore, subclassification of tinnitus patients is expected to improve therapeutic allocation, which, in turn, is hoped to improve therapeutic success for the individual patient. The present study aims to define factors that differentially influence subjectively perceived tinnitus loudness and tinnitus-related distress. METHODS: In a questionnaire-based cross-sectional survey, the data of 4705 individuals with tinnitus were analyzed. The self-report questionnaire contained items about subjective tinnitus loudness, type of onset, awareness and localization of the tinnitus, hearing impairment, chronic comorbidities, sleep quality, and psychometrically validated questionnaires addressing tinnitus-related distress, depressivity, anxiety, and somatic symptom severity. In a binary step-wise logistic regression model, we tested the predictive power of these variables on subjective tinnitus loudness and tinnitus-related distress. RESULTS: The present data contribute to the distinction between subjective tinnitus loudness and tinnitus-related distress. Whereas subjective loudness was associated with permanent awareness and binaural localization of the tinnitus, tinnitus-related distress was associated with depressivity, anxiety, and somatic symptom severity. CONCLUSIONS: Subjective tinnitus loudness and the potential presence of severe depressivity, anxiety, and somatic symptom severity should be assessed separately from tinnitus-related distress. If loud tinnitus is the major complaint together with mild or moderate tinnitus-related distress, therapies should focus on auditory perception. If levels of depressivity, anxiety or somatic symptom severity are severe, therapies and further diagnosis should focus on these symptoms at first

Exposure to surrounding greenness and natural-cause and cause-specific mortality in the ELAPSE pooled cohort

Background The majority of studies have shown higher greenness exposure associated with reduced mortality risks, but few controlled for spatially correlated air pollution and traffic noise exposures. We aim to address this research gap in the ELAPSE pooled cohort. Methods Mean Normalized Difference Vegetation Index (NDVI) in a 300-m grid cell and 1-km radius were assigned to participants’ baseline home addresses as a measure of surrounding greenness exposure. We used Cox proportional hazards models to estimate the association of NDVI exposure with natural-cause and cause-specific mortality, adjusting for a number of potential confounders including socioeconomic status and lifestyle factors at individual and area-levels. We further assessed the associations between greenness exposure and mortality after adjusting for fine particulate matter (PM2.5), nitrogen dioxide (NO2) and road traffic noise. Results The pooled study population comprised 327,388 individuals who experienced 47,179 natural-cause deaths during 6,374,370 person-years of follow-up. The mean NDVI in the pooled cohort was 0.33 (SD 0.1) and 0.34 (SD 0.1) in the 300-m grid and 1-km buffer. In the main fully adjusted model, 0.1 unit increment of NDVI inside 300-m grid was associated with 5% lower risk of natural-cause mortality (Hazard Ratio (HR) 0.95 (95% CI: 0.94, 0.96)). The associations attenuated after adjustment for air pollution [HR (95% CI): 0.97 (0.96, 0.98) adjusted for PM2.5; 0.98 (0.96, 0.99) adjusted for NO2]. Additional adjustment for traffic noise hardly affected the associations. Consistent results were observed for NDVI within 1-km buffer. After adjustment for air pollution, NDVI was inversely associated with diabetes, respiratory and lung cancer mortality, yet with wider 95% confidence intervals. No association with cardiovascular mortality was found. Conclusions We found a significant inverse association between surrounding greenness and natural-cause mortality, which remained after adjusting for spatially correlated air pollution and traffic noise

Mindfulness-and body-psychotherapy-based group treatment of chronic tinnitus: a randomized controlled pilot study

Background Tinnitus, the perception of sound in absence of an external acoustic source, impairs the quality of life in 2% of the population. Since in most cases causal treatment is not possible, the majority of therapeutic attempts aim at developing and strengthening individual coping and habituation strategies. Therapeutic interventions that incorporate training in mindfulness meditation have become increasingly popular in the treatment of stress-related disorders. Here we conducted a randomized, controlled clinical study to investigate the efficacy of a specific mindfulness- and body-psychotherapy based program in patients suffering from chronic tinnitus. Methods Thirty-six patients were enrolled in this pilot study. The treatment was specifically developed for tinnitus patients and is based on mindfulness and body psychotherapy. Treatment was performed as group therapy at two training weekends that were separated by an interval of 7 weeks (eleven hours/weekend) and in four further two-hour sessions (week 2, 9, 18 and 22). Patients were randomized to receive treatment either immediately or after waiting time, which served as a control condition. The primary study outcome was the change in tinnitus complaints as measured by the German Version of the Tinnitus Questionnaire (TQ). Results ANOVA testing for the primary outcome showed a significant interaction effect time by group (F = 7.4; df = 1,33; p = 0.010). Post hoc t-tests indicated an amelioration of TQ scores from baseline to week 9 in both groups (intervention group: t = 6.2; df = 17; p < 0.001; control group: t = 2.5; df = 16; p = 0.023), but the intervention group improved more than the control group. Groups differed at week 7 and 9, but not at week 24 as far as the TQ score was concerned. Conclusions Our results suggest that this mindfulness- and body-psychotherapy-based approach is feasible in the treatment of tinnitus and merits further evaluation in clinical studies with larger sample sizes. The study is registered with clinicaltrials.gov (NCT01540357)

Early-life environmental exposures and blood pressure in children

Background: Growing evidence exists about the fetal and environmental origins of hypertension, but mainly limited to single-exposure studies. The exposome has been proposed as a more holistic approach by studying many exposures simultaneously. Objectives: This study aims to evaluate the association between a wide range of prenatal and postnatal exposures and blood pressure (BP) in children. Methods: Systolic and diastolic BP were measured among 1,277 children from the European HELIX (Human Early-Life Exposome) cohort aged 6 to 11 years. Prenatal (n = 89) and postnatal (n = 128) exposures include air pollution, built environment, meteorology, natural spaces, traffic, noise, chemicals, and lifestyles. Two methods adjusted for confounders were applied: an exposome-wide association study considering the exposures independently, and the deletion-substitution-addition algorithm considering all the exposures simultaneously. Results: Decreases in systolic BP were observed with facility density (β change for an interquartile-range increase in exposure: −1.7 mm Hg [95% confidence interval (CI): −2.5 to −0.8 mm Hg]), maternal concentrations of polychlorinated biphenyl 118 (−1.4 mm Hg [95% CI: −2.6 to −0.2 mm Hg]) and child concentrations of dichlorodiphenyldichloroethylene (DDE: −1.6 mm Hg [95% CI: −2.4 to −0.7 mm Hg]), hexachlorobenzene (−1.5 mm Hg [95% CI: −2.4 to −0.6 mm Hg]), and mono−benzyl phthalate (−0.7 mm Hg [95% CI: −1.3 to −0.1 mm Hg]), whereas increases in systolic BP were observed with outdoor temperature during pregnancy (1.6 mm Hg [95% CI: 0.2 to 2.9 mm Hg]), high fish intake during pregnancy (2.0 mm Hg [95% CI: 0.4 to 3.5 mm Hg]), maternal cotinine concentrations (1.2 mm Hg [95% CI: -0.3 to 2.8 mm Hg]), and child perfluorooctanoate concentrations (0.9 mm Hg [95% CI: 0.1 to 1.6 mm Hg]). Decreases in diastolic BP were observed with outdoor temperature at examination (−1.4 mm Hg [95% CI: −2.3 to −0.5 mm Hg]) and child DDE concentrations (−1.1 mm Hg [95% CI: −1.9 to −0.3 mm Hg]), whereas increases in diastolic BP were observed with maternal bisphenol-A concentrations (0.7 mm Hg [95% CI: 0.1 to 1.4 mm Hg]), high fish intake during pregnancy (1.2 mm Hg [95% CI: −0.2 to 2.7 mm Hg]), and child copper concentrations (0.9 mm Hg [95% CI: 0.3 to 1.6 mm Hg]). Conclusions: This study suggests that early-life exposure to several chemicals, as well as built environment and meteorological factors, may affect BP in children

Is there an association between ambient air pollution and bladder cancer incidence – Analysis of 15 European cohorts?

Background Ambient air pollution contains low concentrations of carcinogens implicated in the etiology of urinary bladder cancer. Little is known about whether exposure to air pollution influences bladder cancer in the general population. Objective We aimed to evaluate the association between long-term exposure to ambient air pollution and bladder cancer incidence. Design, setting and participants We obtained data from 15 population-based cohorts enrolled between 1985 and 2005 in eight European countries (N=303,431; mean follow-up 14.1 years). We estimated exposure to nitrogen oxides (NO2 and NOX), particulate matter (PM) with diameter &lt;10μm (PM10), &lt;2.5 μm (PM2.5), between 2.5 and 10 μm (PM2.5-10), PM2.5 absorbance (soot), elemental constituents of PM, organic carbon and traffic density at baseline home addresses using standardized land-use regression models from the ESCAPE (European Study of Cohorts for Air Pollution Effects) project. Outcome measurements and statistical analysis We used Cox proportional-hazards models with adjustment for potential confounders for cohort-specific analyses and meta-analyses to estimate summary hazard ratios (HRs) for bladder cancer incidence. Results and Limitations During follow-up, 943 incident bladder cancer cases were diagnosed. In the meta-analysis, none of the exposures were associated with bladder cancer risk. The summary HRs associated with a 10-μg/m3 increase in NO2 and 5-μg/m3 increase in PM2.5 were 0.98 (95% confidence interval (CI): 0.89, 1.08) and 0.86 (95%CI: 0.63, 1.18), respectively. Limitations include lack of information about lifetime exposure. Conclusion There was no evidence of an association between exposure to outdoor air pollution levels at residence and risk of bladder cancer. Patient summary We assessed the link between outdoor air pollution at residence and bladder cancer, using the largest study population to date, extensive assessment of exposure and comprehensive data on personal risk factors such as smoking. We found no association between the levels of outdoor air pollution at residence and bladder cancer risk.1</p