Burden of disease due to transportation noise in the Nordic countries.

BACKGROUND: Environmental noise is of increasing concern for public health. Quantification of associated health impacts is important for regulation and preventive strategies. AIM: To estimate the burden of disease (BoD) due to road traffic and railway noise in four Nordic countries and their capitals, in terms of DALYs (Disability-Adjusted Life Years), using comparable input data across countries. METHOD: Road traffic and railway noise exposure was obtained from the noise mapping conducted according to the Environmental Noise Directive (END) as well as nationwide noise exposure assessments for Denmark and Norway. Noise annoyance, sleep disturbance and ischaemic heart disease were included as the main health outcomes, using exposure-response functions from the WHO, 2018 systematic reviews. Additional analyses included stroke and type 2 diabetes. Country-specific DALY rates from the Global Burden of Disease (GBD) study were used as health input data. RESULTS: Comparable exposure data were not available on a national level for the Nordic countries, only for capital cities. The DALY rates for the capitals ranged from 329 to 485 DALYs/100,000 for road traffic noise and 44 to 146 DALY/100,000 for railway noise. Moreover, the DALY estimates for road traffic noise increased with up to 17% upon inclusion of stroke and diabetes. DALY estimates based on nationwide noise data were 51 and 133% higher than the END-based estimates, for Norway and Denmark, respectively. CONCLUSION: Further harmonization of noise exposure data is required for between-country comparisons. Moreover, nationwide noise models indicate that DALY estimates based on END considerably underestimate national BoD due to transportation noise. The health-related burden of traffic noise was comparable to that of air pollution, an established risk factor for disease in the GBD framework. Inclusion of environmental noise as a risk factor in the GBD is strongly encouraged.

Assessment of chronic bronchitis and risk factors in young adults: results from BAMSE.

BACKGROUND: Chronic bronchitis is associated with substantial morbidity among elderly adults, but little is known about its prevalence and risk factors in young adults. Our aim was to assess the prevalence and early-life risk factors for chronic bronchitis in young adults. METHODS: Questionnaire data and clinical measures from the 24-year follow-up of the Swedish BAMSE (Child (Barn), Allergy, Milieu, Stockholm, Epidemiological) cohort were used. We assessed chronic bronchitis (CB) as the combination of cough and mucus production in the morning during winter. Environmental and clinical data from birth and onwards were used for analyses of risk factors. RESULTS: At the 24-year follow-up, 75% (n=3064) participants completed the questionnaire and 2030 performed spirometry. The overall prevalence of CB was 5.5% (n=158) with similar estimates in males and females. 49% of CB cases experienced more than three self-reported respiratory infections in the past year compared to 18% in non-CB subjects (p<0.001), and 37% of cases were current smokers (versus 19% of non-CB cases). Statistically significant lower post-bronchodilator forced expiratory volume in 1 s/forced vital capacity were observed in CB compared to non-CB subjects (mean z-score -0.06 versus 0.13, p=0.027). Daily smoking (adjusted (a)OR 3.85, p<0.001), air pollution exposure (black carbon at ages 1-4 years aOR 1.71 per 1 µg·m-3 increase, p=0.009) and exclusive breastfeeding for ≤4 months (aOR 0.66, p=0.044) were associated with CB. CONCLUSION: Chronic bronchitis in young adults is associated with recurrent respiratory infections. Besides smoking, our results support the role of early-life exposures, such as air pollution and exclusive breastfeeding, for respiratory health later in life.

Residential traffic noise exposure assessment: application and evaluation of European Environmental Noise Directive maps.

Digital noise maps produced according to the European Environmental Noise Directive (END) could provide valuable exposure information in noise and health research. However, their usefulness in epidemiological studies has not been evaluated. The objective of this study was to apply and evaluate Swedish END maps for assessments of residential traffic noise exposure. END maps from three Swedish cities were used to assess residential traffic noise exposure for a population sample of 2496 men and women included in a national Environmental Health Survey. For each subject, we assessed noise levels manually and automatically at three geographical points, using survey data to locate dwellings within buildings. Cohen's kappa coefficient (κ) was used to assess agreement between the noise estimates. To evaluate the maps, we compared the observed and predicted proportions of annoyed residents as a function of noise exposure using survey data and already established exposure-response relationships. The root mean square deviation (r.m.s.) was used to assess the precision of observed estimates. The agreement between the noise estimates ranged from κ=0.4 to 0.8. Generally, there was a high correspondence between observed and predicted exposure-response relationships for noise annoyance, regardless of method and if data on dwelling location within building were used. The best precision was, however, found when we manually corrected the noise level according to the location of the dwelling within buildings (r.m.s.=0.029). Noise maps based on the END appear useful for assessing residential traffic noise exposure, particularly if combined with survey data on dwelling location.

Assessment of the neuropeptide S system in anxiety disorders.

BACKGROUND: The G protein-coupled receptor neuropeptide S receptor 1 (NPSR1) and its ligand neuropeptide S (NPS) form a signaling system mainly implicated in susceptibility to asthma and inflammatory disorders in humans and regulation of anxiety and arousal in rodents. We addressed here the role of NPS and NPSR1 as susceptibility genes for human anxiety disorders. METHODS: We performed comprehensive association analysis of genetic variants in NPS and NPSR1 in three independent study samples. We first studied a population-based sample (Health 2000, Finland) of 321 anxiety disorder patients and 1317 control subjects and subsequently a Spanish clinical panic disorder sample consisting of 188 cases and 315 control subjects. In addition, we examined a birth cohort of 2020 children (Barn Allergi Miljö Stockholm Epidemiologi [BAMSE], Sweden). We then tested whether alleles of the most significantly associated single nucleotide polymorphisms alter DNA-protein complex formation in electrophoretic mobility shift assays. Finally, we compared acute stress responses on the gene expression level in wild-type and Npsr1(-/-) mice. RESULTS: We confirmed previously observed epidemiological association between anxiety and asthma in two population-based cohorts. Single nucleotide polymorphisms within NPS and NPSR1 associated with panic disorder diagnosis in the Finnish and Spanish samples and with parent-reported anxiety/depression in the BAMSE sample. Moreover, some of the implicated single nucleotide polymorphisms potentially affect transcription factor binding. Expression of neurotrophin-3, a neurotrophic factor connected to stress and panic reaction, was significantly downregulated in brain regions of stressed Npsr1(-/-) mice, whereas interleukin-1 beta, an active stress-related immunotransmitter, was upregulated. CONCLUSIONS: Our results suggest that NPS-NPSR1 signaling is likely involved in anxiety.

Hypertension and Exposure to Noise near Airports (HYENA): study design and noise exposure assessment.

An increasing number of people live near airports with considerable noise and air pollution. The Hypertension and Exposure to Noise near Airports (HYENA) project aims to assess the impact of airport-related noise exposure on blood pressure (BP) and cardiovascular disease using a cross-sectional study design. We selected 6,000 persons (45-70 years of age) who had lived at least 5 years near one of six major European airports. We used modeled aircraft noise contours, aiming to maximize exposure contrast. Automated BP instruments are used to reduce observer error. We designed a standardized questionnaire to collect data on annoyance, noise disturbance, and major confounders. Cortisol in saliva was collected in a subsample of the study population (n = 500) stratified by noise exposure level. To investigate short-term noise effects on BP and possible effects on nighttime BP dipping, we measured 24-hr BP and assessed continuous night noise in another subsample (n = 200). To ensure comparability between countries, we used common noise models to assess individual noise exposure, with a resolution of 1 dB(A). Modifiers of individual exposure, such as the orientation of living and bedroom toward roads, window-opening habits, and sound insulation, were assessed by the questionnaire. For four airports, we estimated exposure to air pollution to explore modifying effects of air pollution on cardiovascular disease. The project assesses exposure to traffic-related air pollutants, primarily using data from another project funded by the European Union (APMoSPHERE, Air Pollution Modelling for Support to Policy on Health and Environmental Risks in Europe).

Glass-based radon-exposure assessment and lung cancer risk.

Lung cancer risk estimation in relation to residential radon exposure remains uncertain, partly as a result of imprecision in air-based retrospective radon-exposure assessment in epidemiological studies. A recently developed methodology provides estimates for past radon concentrations and involves measurement of the surface activity of a glass object that has been in a subject's dwellings through the period for exposure assessment. Such glass measurements were performed for 110 lung cancer subjects, diagnosed 1985 to 1995, and for 231 control subjects, recruited in a case-control study of residential radon and lung cancer among never-smokers in Sweden. The relative risks (with 95% confidence intervals) of lung cancer in relation to categories of surface-based average domestic radon concentration during three decades, delimited by cutpoints at 50, 80, and 140 Bq m(-3), were 1.60 (0.8 to 3.4), 1.96 (0.9 to 4.2), and 2.20 (0.9 to 5.6), respectively, with average radon concentrations below 50 Bq m(-3) used as reference category, and with adjustment for other risk factors. These relative risks, and the excess relative risk (ERR) of 75% (-4% to 430%) per 100 Bq m(-3) obtained when using a continuous variable for surface-based average radon concentration estimates, were about twice the size of the corresponding relative risks obtained among these subjects when using air-based average radon concentration estimates. This suggests that surface-based estimates may provide a more relevant exposure proxy than air-based estimates for relating past radon exposure to lung cancer risk.