Long-term exposure to transportation noise in relation to global cognitive decline and cognitive impairment: Results from a Swedish longitudinal cohort.

BACKGROUND AND AIMS: Transportation noise is an environmental exposure with mounting evidence of adverse health effects. Besides the increased risk of cardiovascular and metabolic diseases, recent studies suggest that long-term noise exposure might accelerate cognitive decline in older age. We examined the association between transportation noise and cognitive function in a cohort of older adults. METHODS: The present study is based on 2594 dementia-free participants aged 60 + years from the Swedish National study on Aging and Care in Kungsholmen (SNAC-K). Global cognition score and CIND (cognitive impairment, no dementia) were assessed with a comprehensive neuropsychological battery at baseline and up to 16 years. Residential transportation noise resulting from road traffic, railway, and aircraft were estimated at the most exposed façade and the time-weighted average exposure was assessed. Linear mixed-effect models were used to assess the effect of long-term traffic noise exposure on the rate of change in global cognition score. Hazard ratios (HRs) and 95 % confidence intervals (CIs) of CIND by transportation noise exposure were obtained with Cox proportional hazard models. RESULTS: Global cognition score decreased at an average rate of -0.041 (95 %CI -0.043, -0.039) per year. Aircraft noise was associated with a 0.007 (per 10 dB Lden; 95 %CI -0.012, -0.001) faster annual rate of decline. Global cognition score seems to be not affected by road traffic and railway noise. During the follow-up, 422 (21 %) participants developed CIND. A 10-dB Lden difference in exposure to aircraft and railway noise was associated with a 16 % (HR 1.16, 95 %CI 0.91, 1.49) and 26 % (HR 1.26, 95 %CI 1.01, 1.56) increased hazard of CIND in the multi-pollutant model, respectively. No association was found for road traffic (HR 1.00, 95 %CI 0.83, 1.21). CONCLUSIONS: Transportation noise was linked to cognitive impairment and faster cognitive decline among older adults. Future studies are warranted to confirm our results.

Air pollution, social engagement, and depression in older adults: Results from a Swedish population-based cohort study.

Although emerging research has investigated the relationship between outdoor air pollution and depression risk in older adults, the results remain inconclusive. We aimed to determine the relationship between long-term exposure to ambient air pollution and depression among older adults and explore whether active social engagement may modify this association. At baseline (2001-2004), 2812 depression-free older adults from Swedish National Study on Aging and Care in Kungsholmen (SNAC-K) were included. SNAC-K is a longitudinal population-based cohort in Stockholm, Sweden. Incident depression cases occurred during 2004-2013 were ascertained using the Diagnostic and Statistical Manual of Mental Disorders 4th Edition. Air pollution [particulate matter (PM) and nitrogen oxides (NOx)] at the residency were estimated using dispersion models. Social engagement was measured as active participation in social activities (at least twice/week) or inactive (less than twice/week) in the last 12 months. The hazard ratios (HR) and 95% confidence intervals of depression from air pollution exposure of 3-year moving average before diagnosis (1-µg/m3 difference in PM2.5 and PM10, and 10-µg/m3 difference in NOx) were obtained from Cox models considering greenspace and noise. A product term of air pollutant and social activity was added to test the multiplicative interaction and attributable proportion due to interaction was calculated for assessing additive interaction. We identified 137 (4.9%) incident depression cases. Participants exposed to higher concentrations of PM2.5, NOx, and PM10 had 53% (HR:1.53 [1.22, 1.93]), 26% (HR:1.26 [1.01, 1.58]), and 7% (HR:1.07 [0.98, 1.18]) increased hazard of depression, respectively. These associations were largely attenuated in people with active social engagement (HR for PM2.5: 1.04 [0.70, 1.55]; HR for PM10: 0.98 [0.81, 1.18]; and HR for NOx: 1.09 [0.71, 1.66]). Our findings suggest long-term exposure to air pollution may be a risk factor for depression among older adults. An active social engagement might however decrease this risk.

Exposure to long-term source-specific transportation noise and incident breast cancer: A pooled study of eight Nordic cohorts.

BACKGROUND: Environmental noise is an important environmental exposure that can affect health. An association between transportation noise and breast cancer incidence has been suggested, although current evidence is limited. We investigated the pooled association between long-term exposure to transportation noise and breast cancer incidence. METHODS: Pooled data from eight Nordic cohorts provided a study population of 111,492 women. Road, railway, and aircraft noise were modelled at residential addresses. Breast cancer incidence (all, estrogen receptor (ER) positive, and ER negative) was derived from cancer registries. Hazard ratios (HR) were estimated using Cox Proportional Hazards Models, adjusting main models for sociodemographic and lifestyle variables together with long-term exposure to air pollution. RESULTS: A total of 93,859 women were included in the analyses, of whom 5,875 developed breast cancer. The median (5th-95th percentile) 5-year residential road traffic noise was 54.8 (40.0-67.8) dB Lden, and among those exposed, the median railway noise was 51.0 (41.2-65.8) dB Lden. We observed a pooled HR for breast cancer (95 % confidence interval (CI)) of 1.03 (0.99-1.06) per 10 dB increase in 5-year mean exposure to road traffic noise, and 1.03 (95 % CI: 0.96-1.11) for railway noise, after adjustment for lifestyle and sociodemographic covariates. HRs remained unchanged in analyses with further adjustment for PM2.5 and attenuated when adjusted for NO2 (HRs from 1.02 to 1.01), in analyses using the same sample. For aircraft noise, no association was observed. The associations did not vary by ER status for any noise source. In analyses using <60 dB as a cutoff, we found HRs of 1.08 (0.99-1.18) for road traffic and 1.19 (0.95-1.49) for railway noise. CONCLUSIONS: We found weak associations between road and railway noise and breast cancer risk. More high-quality prospective studies are needed, particularly among those exposed to railway and aircraft noise before conclusions regarding noise as a risk factor for breast cancer can be made.

Traffic noise in the bedroom in association with markers of obesity: a cross-sectional study and mediation analysis of the respiratory health in Northern Europe cohort.

BACKGROUND: Previous research suggests an association between road traffic noise and obesity, but current evidence is inconclusive. The aim of this study was to assess the association between nocturnal noise exposure and markers of obesity and to assess whether sleep disturbance might be a mediator in this association. METHODS: We applied data from the Respiratory Health in Northern Europe (RHINE) cohort. We used self-measured waist circumference (WC) and body mass index (BMI) as outcome values. Noise exposure was assessed as perceived traffic noise in the bedroom and/or the bedroom window's location towards the street. We applied adjusted linear, and logistic regression models, evaluated effect modifications and conducted mediation analysis. RESULTS: Based on fully adjusted models we found that women, who reported very high traffic noise levels in bedroom, had 1.30 (95% CI 0.24-2.37) kg/m2 higher BMI and 3.30 (95% CI 0.39-6.20) cm higher WC compared to women, who reported no traffic noise in the bedroom. Women who reported higher exposure to road traffic noise had statistically significant higher odds of being overweight and have abdominal obesity with OR varying from 1.15 to 1.26 compared to women, who reported no traffic noise in the bedroom. For men, the associations were rather opposite, although mostly statistically insignificant. Furthermore, men, who reported much or very much traffic noise in the bedroom, had a statistically significantly lower risk of abdominal obesity. Sleep disturbance fully or partially mediated the association between noise in bedroom and obesity markers among women. CONCLUSION: Our results suggest that self-reported traffic noise in the bedroom may be associated to being overweight or obese trough sleep disturbance among women, but associations were inconclusive among men.

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.

Long-term exposure to traffic noise and risk of incident colon cancer: A pooled study of eleven Nordic cohorts.

Background Colon cancer incidence is rising globally, and factors pertaining to urbanization have been proposed involved in this development. Traffic noise may increase colon cancer risk by causing sleep disturbance and stress, thereby inducing known colon cancer risk-factors, e.g. obesity, diabetes, physical inactivity, and alcohol consumption, but few studies have examined this. Objectives The objective of this study was to investigate the association between traffic noise and colon cancer (all, proximal, distal) in a pooled population of 11 Nordic cohorts, totaling 155,203 persons. Methods We identified residential address history and estimated road, railway, and aircraft noise, as well as air pollution, for all addresses, using similar exposure models across cohorts. Colon cancer cases were identified through national registries. We analyzed data using Cox Proportional Hazards Models, adjusting main models for harmonized sociodemographic and lifestyle data. Results During follow-up (median 18.8 years), 2757 colon cancer cases developed. We found a hazard ratio (HR) of 1.05 (95% confidence interval (CI): 0.99-1.10) per 10-dB higher 5-year mean time-weighted road traffic noise. In sub-type analyses, the association seemed confined to distal colon cancer: HR 1.06 (95% CI: 0.98-1.14). Railway and aircraft noise was not associated with colon cancer, albeit there was some indication in sub-type analyses that railway noise may also be associated with distal colon cancer. In interaction-analyses, the association between road traffic noise and colon cancer was strongest among obese persons and those with high NO2-exposure. Discussion A prominent study strength is the large population with harmonized data across eleven cohorts, and the complete address-history during follow-up. However, each cohort estimated noise independently, and only at the most exposed façade, which may introduce exposure misclassification. Despite this, the results of this pooled study suggest that traffic noise may be a risk factor for colon cancer, especially of distal origin.

Long-Term Exposure to Transportation Noise and Ischemic Heart Disease: A Pooled Analysis of Nine Scandinavian Cohorts.

BACKGROUND: Transportation noise may induce cardiovascular disease, but the public health implications are unclear. OBJECTIVES: The study aimed to assess exposure-response relationships for different transportation noise sources and ischemic heart disease (IHD), including subtypes. METHODS: Pooled analyses were performed of nine cohorts from Denmark and Sweden, together including 132,801 subjects. Time-weighted long-term exposure to road, railway, and aircraft noise, as well as air pollution, was estimated based on residential histories. Hazard ratios (HRs) were calculated using Cox proportional hazards models following adjustment for lifestyle and socioeconomic risk factors. RESULTS: A total of 22,459 incident cases of IHD were identified during follow-up from national patient and mortality registers, including 7,682 cases of myocardial infarction. The adjusted HR for IHD was 1.03 [95% confidence interval (CI) 1.00, 1.05] per 10 dB Lden for both road and railway noise exposure during 5 y prior to the event. Higher risks were indicated for IHD excluding angina pectoris cases, with HRs of 1.06 (95% CI: 1.03, 1.08) and 1.05 (95% CI: 1.01, 1.08) per 10 dB Lden for road and railway noise, respectively. Corresponding HRs for myocardial infarction were 1.02 (95% CI: 0.99, 1.05) and 1.04 (95% CI: 0.99, 1.08). Increased risks were observed for aircraft noise but without clear exposure-response relations. A threshold at around 55 dB Lden was suggested in the exposure-response relation for road traffic noise and IHD. DISCUSSION: Exposure to road, railway, and aircraft noise in the prior 5 y was associated with an increased risk of IHD, particularly after exclusion of angina pectoris cases, which are less well identified in the registries. https://doi.org/10.1289/EHP10745.

Quantitative relationships of perfluoroalkyl acids in drinking water associated with serum concentrations above background in adults living near contamination hotspots in Sweden.

Contaminated drinking water (DW) is a major source of exposure to per- and polyfluoroalkyl substances (PFAS) at locations around PFAS production/use facilities and military airports. This study aimed to investigate quantitative relationships between concentrations in DW and serum of nine perfluoroalkyl acids (PFAAs) in Swedish adult populations living near contamination hotspots. Short-chained (PFPeA, PFHxA, PFHpA, and PFBS) and long-chained PFAAs (PFOA, PFNA, PFDA, PFHxS and PFOS) were measured in DW and serum. We matched DW and serum concentrations for a total of 398 subjects living or working in areas receiving contaminated DW and in one non-contaminated area. Thereafter, linear regression analysis with and without adjustments for co-variates was conducted. This enabled to derive (i) serum concentrations at background exposure (CB) from sources other than local DW exposure (i.e. food, dust and textiles) at 0 ng/L DW concentration, (ii) population-mean PFAA serum:water ratios (SWR) and (iii) PFAA concentrations in DW causing observable elevated serum PFAA concentrations above background variability. Median concentrations of the sum of nine PFAAs ranged between 2.8 and 1790 ng/L in DW and between 7.6 and 96.9 ng/mL in serum. DW concentration was the strongest predictor, resulting in similar unadjusted and adjusted regression coefficients. Mean CB ranged from <0.1 (PFPeA, PFHpA, PFBS) to 5.1 ng/mL (PFOS). Serum concentrations increased significantly with increasing DW concentrations for all PFAAs except for PFPeA with SWRs ranging from <10 (PFHxA, PFHpA and PFBS) to 111 (PFHxS). Observed elevated serum concentrations above background variability were reached at DW concentrations between 24 (PFOA) and 357 ng/L (PFHxA). The unadjusted linear regression predictions agreed well with serum concentrations previously reported in various populations exposed to low and high DW levels of PFOA, PFHxS and PFOS. The quantitative relationships derived herein should be helpful to translate PFAA concentrations in DW to concentrations in serum at the population level.

Occupational noise exposure and risk of incident stroke: a pooled study of five Scandinavian cohorts.

OBJECTIVES: To investigate the association between occupational noise exposure and stroke incidence in a pooled study of five Scandinavian cohorts (NordSOUND). METHODS: We pooled and harmonised data from five Scandinavian cohorts resulting in 78 389 participants. We obtained job data from national registries or questionnaires and recoded these to match a job-exposure matrix developed in Sweden, which specified the annual average daily noise exposure in five exposure classes (LAeq8h): <70, 70-74, 75-79, 80-84, ≥85 dB(A). We identified residential address history and estimated 1-year average road traffic noise at baseline. Using national patient and mortality registers, we identified 7777 stroke cases with a median follow-up of 20.2 years. Analyses were conducted using Cox proportional hazards models adjusting for individual and area-level potential confounders. RESULTS: Exposure to occupational noise at baseline was not associated with overall stroke in the fully adjusted models. For ischaemic stroke, occupational noise was associated with HRs (95% CI) of 1.08 (0.98 to 1.20), 1.09 (0.97 to 1.24) and 1.06 (0.92 to 1.21) in the 75-79, 80-84 and ≥85 dB(A) exposure groups, compared with <70 dB(A), respectively. In subanalyses using time-varying occupational noise exposure, we observed an indication of higher stroke risk among the most exposed (≥85 dB(A)), particularly when restricting analyses to people exposed to occupational noise within the last year (HR: 1.27; 95% CI: 0.99 to 1.63). CONCLUSIONS: We found no association between occupational noise and risk of overall stroke after adjustment for confounders. However, the non-significantly increased risk of ischaemic stroke warrants further investigation.

Long-Term Exposure to Transportation Noise and Risk of Incident Stroke: A Pooled Study of Nine Scandinavian Cohorts.

BACKGROUND: Transportation noise is increasingly acknowledged as a cardiovascular risk factor, but the evidence base for an association with stroke is sparse. OBJECTIVE: We aimed to investigate the association between transportation noise and stroke incidence in a large Scandinavian population. METHODS: We harmonized and pooled data from nine Scandinavian cohorts (seven Swedish, two Danish), totaling 135,951 participants. We identified residential address history and estimated road, railway, and aircraft noise for all addresses. Information on stroke incidence was acquired through linkage to national patient and mortality registries. We analyzed data using Cox proportional hazards models, including socioeconomic and lifestyle confounders, and air pollution. RESULTS: During follow-up (median=19.5y), 11,056 stroke cases were identified. Road traffic noise (Lden) was associated with risk of stroke, with a hazard ratio (HR) of 1.06 [95% confidence interval (CI): 1.03, 1.08] per 10-dB higher 5-y mean time-weighted exposure in analyses adjusted for individual- and area-level socioeconomic covariates. The association was approximately linear and persisted after adjustment for air pollution [particulate matter (PM) with an aerodynamic diameter of ≤2.5µm (PM2.5) and NO2]. Stroke was associated with moderate levels of 5-y aircraft noise exposure (40-50 vs. ≤40 dB) (HR=1.12; 95% CI: 0.99, 1.27), but not with higher exposure (≥50 dB, HR=0.94; 95% CI: 0.79, 1.11). Railway noise was not associated with stroke. DISCUSSION: In this pooled study, road traffic noise was associated with a higher risk of stroke. This finding supports road traffic noise as an important cardiovascular risk factor that should be included when estimating the burden of disease due to traffic noise. https://doi.org/10.1289/EHP8949.

Noise exposure and childhood asthma up to adolescence.

OBJECTIVE: Increasing evidence indicates aggravation of immune-mediated diseases due to physiological and psychological stress. Noise is a stressor, however, little is known about its effects on children's respiratory health. This study investigates the association between pre- or postnatal road traffic or occupational noise exposure and asthma as well as related symptoms from infancy to adolescence. METHODS: The study was conducted in the Swedish birth cohort BAMSE, including over 4000 participants followed with repeated questionnaires and clinical tests until 16 years of age. Pre- and postnatal residential road traffic noise was assessed by estimating time-weighted average noise levels at the most exposed façade. Maternal occupational noise exposure during pregnancy was evaluated using a job-exposure-matrix. The associations between noise exposure and asthma-related outcomes were explored using logistic regression and generalised estimating equations. RESULTS: We observed non-significant associations for asthma ever up to 16 years with residential road traffic noise exposure in infancy ≥55 dBLden (adjusted OR = 1.22; 95% CI 0.90-1.65), as well as prenatal occupational noise exposure ≥80 dBLAeq,8h (1.18, 0.85-1.62). In longitudinal analyses, however, no clear associations between pre- or postnatal exposure to residential road traffic noise, or average exposure to noise since birth, were detected in relation to asthma or wheeze until 16 years. CONCLUSION: We did not find a clear overall association between exposure to noise during different time periods and asthma or wheeze up to adolescence.

Traffic noise and other determinants of blood pressure in adolescence.

BACKGROUND: Exposure to traffic noise has been associated with hypertension in adults but the evidence in adolescents is limited. We investigated long-term road traffic noise exposure, maternal occupational noise during pregnancy and other factors in relation to blood pressure and prehypertension at 16 years of age. METHODS: Systolic and diastolic blood pressure were measured in 2597 adolescents from the Swedish BAMSE birth cohort. Levels of road traffic noise were estimated at home addresses during lifetime and for the mother during pregnancy as well as maternal occupational noise exposure during pregnancy. Exposure to NOx from local sources was also assessed. Associations between noise or NOx exposure and blood pressure or prehypertension were analysed using linear and logistic regression. RESULTS: The prevalence of prehypertension was higher among males and in those with overweight, low physical activity or overweight mothers. No strong or consistent associations were observed between pre- or postnatal exposure to road traffic noise and blood pressure at 16 years of age. However, inverse associations were suggested for systolic or diastolic blood pressure and prehypertension, which reached statistical significance among males (OR 0.80 per 10 dB Lden, 95% CI 0.65-0.99) and those with maternal occupational noise exposure ≥ 70 dB LAeq8h (OR 0.60, 95% CI 0.41-0.87). On the other hand, occupational noise exposure during pregnancy tended to increase systolic blood pressure and prehypertension risk in adolescence. No associations were seen for NOx exposure. CONCLUSION: No conclusive associations were observed between pre- or postnatal noise exposure and blood pressure or prehypertension in adolescents.

Long-term transportation noise exposure and incidence of ischaemic heart disease and stroke: a cohort study.

BACKGROUND: There is limited evidence from longitudinal studies on transportation noise from different sources and development of ischaemic heart disease (IHD) and stroke. OBJECTIVES: This cohort study assessed associations between exposure to noise from road traffic, railway or aircraft and incidence of IHD and stroke. METHODS: In a cohort of 20 012 individuals from Stockholm County, we estimated long-term residential exposure to road traffic, railway and aircraft noise. National Patient and Cause-of-Death Registers were used to identify IHD and stroke events. Information on risk factors was obtained from questionnaires and registers. Adjusted HR for cardiovascular outcomes related to source-specific noise exposure were computed using Cox proportional hazards regression. RESULTS: No clear or consistent associations were observed between transportation noise and incidence of IHD or stroke. However, noise exposure from road traffic and aircraft was related to IHD incidence in women, with HR of 1.11 (95% CI 1.00 to 1.22) and 1.25 (95% CI 1.09 to 1.44) per 10 dB Lden, respectively. For both sexes taken together, we observed a particularly high risk of IHD in those exposed to all three transportation noise sources at≥45 dB Lden, with a HR of 1.57 (95% CI 1.06 to 2.32), and a similar tendency for stroke (HR 1.42; 95% CI 0.87 to 2.32). CONCLUSION: No overall associations were observed between transportation noise exposure and incidence of IHD or stroke. However, there appeared to be an increased risk of IHD in women exposed to road traffic or aircraft noise as well as in those exposed to multiple sources of transportation noise.

Traffic noise exposure in relation to adverse birth outcomes and body mass between birth and adolescence.

BACKGROUND: There is growing evidence that traffic noise exposure is associated with adiposity among adults but data in children are limited. OBJECTIVE: This longitudinal study examined whether pre- and postnatal noise exposure is associated with body mass index (BMI) between birth and adolescence or with adverse birth outcomes. METHODS: The study was conducted using data from the BAMSE birth cohort, which included 4089 children born in Stockholm County, Sweden. Data on BMI from birth to adolescence were collected via questionnaires, clinical examinations and health care records. A national register provided information on birth outcomes. Road traffic noise levels at the most exposed façade were estimated for all residences of the children during follow-up, as well as of their mothers during pregnancy, and time-weighted average exposure was calculated for different time windows. Maternal occupational noise exposure was obtained from a job-exposure-matrix. Logistic- and quantile regression models were used to estimate associations between noise exposure and health outcomes. RESULTS: We found residential road traffic noise exposure to be associated with increases in BMI from school age to adolescence, but not at earlier ages. In the age groups 8-11 years and 12-16 years the BMI increments were 0.11 kg/m2 per 10 dB Lden (95% CI 0.08-0.13) and 0.20 kg/m2 per 10 dB Lden (95% CI 0.17-0.22), respectively. Maternal noise exposure during pregnancy was generally unrelated to adverse birth outcomes and BMI from birth to adolescence in the children, however, traffic noise exposure was associated with a decreased risk of preterm birth CONCLUSION: Residential road traffic noise exposure was associated with BMI increases from school age to adolescence, but not at earlier ages. Maternal occupational noise exposure or exposure from road traffic during pregnancy were not consistently related to birth outcomes or BMI from birth to adolescence.

Transportation noise and incidence of hypertension.

BACKGROUND: The evidence on exposure to transportation noise and development of hypertension is inconclusive, mostly because of a lack of high quality studies of longitudinal design. OBJECTIVES: This cohort study aimed at investigating the association between exposure to road traffic, railway or aircraft noise and incidence of hypertension. We also assessed effects of varying lengths of exposure as well as of multiple sources of exposure. METHODS: Based on the residential histories of a cohort of 4854 men and women from Stockholm County, we estimated the residential exposure to road traffic, railway and aircraft noise in 1, 5 and 10 year time-periods. Hypertension was assessed by blood pressure measurements, information from questionnaires and hospital diagnoses. Extensive information on potential confounders was available from repeated questionnaires and registers. Hazard Ratios (HR) and 95% confidence intervals (CI) of hypertension related to noise exposure was computed from Cox regression models. RESULTS: We observed a positive association between aircraft noise exposure and incidence of hypertension with a HR of 1.16 (95% CI 1.08-1.24) per 10 dB Lden 5 years preceding the event. No clear differences in risk were indicated between the three exposure time windows. Road traffic and railway noise were not associated with incidence of hypertension during any of the exposure periods. There appeared to be a particularly high risk of hypertension among persons exposed to both aircraft and road traffic noise ≥45 dB Lden with an HR of 1.39 (95% CI 1.14-1.70). CONCLUSIONS: Exposure to aircraft noise may result in increased risk of hypertension.

Particulate matter air pollution components and incidence of cancers of the stomach and the upper aerodigestive tract in the European Study of Cohorts of Air Pollution Effects (ESCAPE).

INTRODUCTION: Previous analysis from the large European multicentre ESCAPE study showed an association of ambient particulate matter <2.5 µm (PM2.5) air pollution exposure at residence with the incidence of gastric cancer. It is unclear which components of PM are most relevant for gastric and also upper aerodigestive tract (UADT) cancer and some of them may not be strongly correlated with PM mass. We evaluated the association between long-term exposure to elemental components of PM2.5 and PM10 and gastric and UADT cancer incidence in European adults. METHODS: Baseline addresses of individuals were geocoded and exposure was assessed by land-use regression models for copper (Cu), iron (Fe) and zinc (Zn) representing non-tailpipe traffic emissions; sulphur (S) indicating long-range transport; nickel (Ni) and vanadium (V) for mixed oil-burning and industry; silicon (Si) for crustal material and potassium (K) for biomass burning. Cox regression models with adjustment for potential confounders were used for cohort-specific analyses. Combined estimates were determined with random effects meta-analyses. RESULTS: Ten cohorts in six countries contributed data on 227,044 individuals with an average follow-up of 14.9 years with 633 incident cases of gastric cancer and 763 of UADT cancer. The combined hazard ratio (HR) for an increase of 200 ng/m3 of PM2.5_S was 1.92 (95%-confidence interval (95%-CI) 1.13;3.27) for gastric cancer, with no indication of heterogeneity between cohorts (I2 = 0%), and 1.63 (95%-CI 0.88;3.01) for PM2.5_Zn (I2 = 70%). For the other elements in PM2.5 and all elements in PM10 including PM10_S, non-significant HRs between 0.78 and 1.21 with mostly wide CIs were seen. No association was found between any of the elements and UADT cancer. The HR for PM2.5_S and gastric cancer was robust to adjustment for additional factors, including diet, and restriction to study participants with stable addresses over follow-up resulted in slightly higher effect estimates with a decrease in precision. In a two-pollutant model, the effect estimate for total PM2.5 decreased whereas that for PM2.5_S was robust. CONCLUSION: This large multicentre cohort study shows a robust association between gastric cancer and long-term exposure to PM2.5_S but not PM10_S, suggesting that S in PM2.5 or correlated air pollutants may contribute to the risk of gastric cancer.

Air pollution and incidence of cancers of the stomach and the upper aerodigestive tract in the European Study of Cohorts for Air Pollution Effects (ESCAPE).

Air pollution has been classified as carcinogenic to humans. However, to date little is known about the relevance for cancers of the stomach and upper aerodigestive tract (UADT). We investigated the association of long-term exposure to ambient air pollution with incidence of gastric and UADT cancer in 11 European cohorts. Air pollution exposure was assigned by land-use regression models for particulate matter (PM) below 10 µm (PM10 ), below 2.5 µm (PM2.5 ), between 2.5 and 10 µm (PMcoarse ), PM2.5 absorbance and nitrogen oxides (NO2 and NOX ) as well as approximated by traffic indicators. Cox regression models with adjustment for potential confounders were used for cohort-specific analyses. Combined estimates were determined with random effects meta-analyses. During average follow-up of 14.1 years of 305,551 individuals, 744 incident cases of gastric cancer and 933 of UADT cancer occurred. The hazard ratio for an increase of 5 µg/m3 of PM2.5 was 1.38 (95% CI 0.99; 1.92) for gastric and 1.05 (95% CI 0.62; 1.77) for UADT cancers. No associations were found for any of the other exposures considered. Adjustment for additional confounders and restriction to study participants with stable addresses did not influence markedly the effect estimate for PM2.5 and gastric cancer. Higher estimated risks of gastric cancer associated with PM2.5 was found in men (HR 1.98 [1.30; 3.01]) as compared to women (HR 0.85 [0.5; 1.45]). This large multicentre cohort study shows an association between long-term exposure to PM2.5 and gastric cancer, but not UADT cancers, suggesting that air pollution may contribute to gastric cancer risk.

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 (BC). Little is known about whether exposure to air pollution influences BC in the general population. OBJECTIVE: To evaluate the association between long-term exposure to ambient air pollution and BC incidence. DESIGN, SETTING, AND PARTICIPANTS: We obtained data from 15 population-based cohorts enrolled between 1985 and 2005 in eight European countries (N=303431; mean follow-up 14.1 yr). We estimated exposure to nitrogen oxides (NO2 and NOx), particulate matter (PM) with diameter <10µm (PM10), <2.5µm (PM2.5), between 2.5 and 10µm (PM2.5-10), PM2.5absorbance (soot), elemental constituents of PM, organic carbon, and traffic density at baseline home addresses using standardized land-use regression models from the 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 BC incidence. RESULTS AND LIMITATIONS: During follow-up, 943 incident BC cases were diagnosed. In the meta-analysis, none of the exposures were associated with BC 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 the lack of information about lifetime exposure. CONCLUSIONS: There was no evidence of an association between exposure to outdoor air pollution levels at place of residence and risk of BC. PATIENT SUMMARY: We assessed the link between outdoor air pollution at place of residence and bladder cancer using the largest study population to date and 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 place of residence and bladder cancer risk.

Long-term exposure to ambient air pollution and incidence of brain tumor: the European Study of Cohorts for Air Pollution Effects (ESCAPE).

Background: Epidemiological evidence on the association between ambient air pollution and brain tumor risk is sparse and inconsistent. Methods: In 12 cohorts from 6 European countries, individual estimates of annual mean air pollution levels at the baseline residence were estimated by standardized land-use regression models developed within the ESCAPE and TRANSPHORM projects: particulate matter (PM) ≤2.5, ≤10, and 2.5-10 µm in diameter (PM2.5, PM10, and PMcoarse), PM2.5 absorbance, nitrogen oxides (NO2 and NOx) and elemental composition of PM. We estimated cohort-specific associations of air pollutant concentrations and traffic intensity with total, malignant, and nonmalignant brain tumor, in separate Cox regression models, adjusting for risk factors, and pooled cohort-specific estimates using random-effects meta-analyses. Results: Of 282194 subjects from 12 cohorts, 466 developed malignant brain tumors during 12 years of follow-up. Six of the cohorts also had data on nonmalignant brain tumor, where among 106786 subjects, 366 developed brain tumor: 176 nonmalignant and 190 malignant. We found a positive, statistically nonsignificant association between malignant brain tumor and PM2.5 absorbance (hazard ratio and 95% CI: 1.67; 0.89-3.14 per 10-5/m3), and weak positive or null associations with the other pollutants. Hazard ratio for PM2.5 absorbance (1.01; 0.38-2.71 per 10-5/m3) and all other pollutants were lower for nonmalignant than for malignant brain tumors. Conclusion: We found suggestive evidence of an association between long-term exposure to PM2.5 absorbance indicating traffic-related air pollution and malignant brain tumors, and no association with overall or nonmalignant brain tumors.