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Most studies investigating the health effects of long-term exposure to air pollution used traditional regression models, although causal inference approaches have been proposed as alternative. However, few studies have applied causal models and comparisons with traditional methods are sparse. We therefore compared the associations between natural-cause mortality and exposure to fine particulate matter (PM(2.5)) and nitrogen dioxide (NO(2)) using traditional Cox and causal models in a large multicenter cohort setting. We analyzed data from eight well-characterized cohorts (pooled cohort) and seven administrative cohorts from eleven European countries. Annual mean PM(2.5) and NO(2) from Europe-wide models were assigned to baseline residential addresses and dichotomized at selected cut-off values (PM(2.5): 10, 12, 15 mug/m(3); NO(2): 20, 40 mug/m(3)). For each pollutant, we estimated the propensity score as the conditional likelihood of exposure given available covariates, and derived corresponding inverse-probability weights (IPW). We applied Cox proportional hazards models i) adjusting for all covariates ("traditional Cox") and ii) weighting by IPW ("causal model"). Of 325,367 and 28,063,809 participants in the pooled and administrative cohorts, 47,131 and 3,580,264 died from natural causes, respectively. For PM(2.5) above vs. below 12 mug/m(3), the hazard ratios (HRs) of natural-cause mortality were 1.17 (95% CI 1.13-1.21) and 1.15 (1.11-1.19) for the traditional and causal models in the pooled cohort, and 1.03 (1.01-1.06) and 1.02 (0.97-1.09) in the administrative cohorts. For NO(2) above vs below 20 mug/m(3), the HRs were 1.12 (1.09-1.14) and 1.07 (1.05-1.09) for the pooled and 1.06 (95% CI 1.03-1.08) and 1.05 (1.02-1.07) for the administrative cohorts. In conclusion, we observed mostly consistent associations between long-term air pollution exposure and natural-cause mortality with both approaches, though estimates partly differed in individual cohorts with no systematic pattern. The application of multiple modelling methods might help to improve causal inference. 299 of 300 words.

Fine particulate matter (PM2.5) is a well-recognized risk factor for premature death. However, evidence on which PM2.5 components are most relevant is unclear.

Epidemiological cohort studies have consistently found associations between long-term exposure to outdoor air pollution and a range of morbidity and mortality endpoints. Recent evaluations by the World Health Organization and the Global Burden of Disease study have suggested that these associations may be nonlinear and may persist at very low concentrations. Studies conducted in North America in particular have suggested that associations with mortality persisted at concentrations of particulate matter with an aerodynamic diameter of less than 2.5 μm (PM2.5) well below current air quality standards and guidelines. The uncertainty about the shape of the concentration-response function at the low end of the concentration distribution, related to the scarcity of observations in the lowest range, was the basis of the current project. Previous studies have focused on PM2.5, but increasingly associations with nitrogen dioxide (NO2) are being reported, particularly in studies that accounted for the fine spatial scale variation of NO2. Very few studies have evaluated the effects of long-term exposure to low concentrations of ozone (O3). Health effects of black carbon (BC), representing primary combustion particles, have not been studied in most large cohort studies of PM2.5. Cohort studies assessing health effects of particle composition, including elements from nontailpipe traffic emissions (iron, copper, and zinc) and secondary aerosol (sulfur) have been few in number and reported inconsistent results.

Background: Ambient air pollution exposure has been associated with higher mortality risk in numerous studies. We assessed potential variability in the magnitude of this association for non-accidental, cardiovascular disease, respiratory disease, and lung cancer mortality in a country-wide administrative cohort by exposure assessment method and by adjustment for geographic subdivisions. Methods: We used the Belgian 2001 census linked to population and mortality register including nearly 5.5 million adults aged >= 30 (mean follow-up: 9.97 years). Annual mean concentrations for fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and ozone (O-3) were assessed at baseline residential address using two exposure methods; Europe-wide hybrid land use regression (LUR) models [100x100m], and Belgium-wide interpolation-dispersion (RIO-IFDM) models [25x25m]. We used Cox proportional hazards models with age as the underlying time scale and adjusted for various individual and area-level covariates. We further adjusted main models for two different area-levels following the European Nomenclature of Territorial Units for Statistics (NUTS); NUTS-1 (n = 3), or NUTS-3 (n = 43). Results: We found no consistent differences between both exposure methods. We observed most robust associations with lung cancer mortality. Hazard Ratios (HRs) per 10 mu g/m(3) increase for NO2 were 1.060 (95%CI 1.0421.078) [hybrid LUR] and 1.040 (95%CI 1.022-1.058) [RIO-IFDM]. Associations with non-accidental, respiratory disease and cardiovascular disease mortality were generally null in main models but were enhanced after further adjustment for NUTS-1 or NUTS-3. HRs for non-accidental mortality per 5 mu g/m(3) increase for PM2.5 for the main model using hybrid LUR exposure were 1.023 (95%CI 1.011-1.035). After including random effects HRs were 1.044 (95%CI 1.033-1.057) [NUTS-1] and 1.076 (95%CI 1.060-1.092) [NUTS-3]. Conclusion: Long-term air pollution exposure was associated with higher lung cancer mortality risk but not consistently with the other studied causes. Magnitude of associations varied by adjustment for geographic subdivisions, area-level socio-economic covariates and less by exposure assessment method. (C) 2021 Published by Elsevier B.V.

BACKGROUND AND AIM: Evidence of the association between long-term exposure to ambient particulate matter components and mortality is inconsistent. We evaluated this association in six large adminis...

BACKGROUND AND AIM: The association between air pollution and mortality from cardiorespiratory disease is well established, yet evidence for other causes is limited. We examined the associations of...

Evidence for the association between long-term exposure to ambient particulate matter components and mortality from natural causes is sparse and inconsistent. We evaluated this association in six large administrative cohorts in the framework of the Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE) project. We analyzed data from country-wide administrative cohorts in Norway, Denmark, the Netherlands, Belgium, Switzerland and in Rome (Italy). Annual 2010 mean concentrations of copper (Cu), iron (Fe), potassium (K), nickel (Ni), sulfur (S), silicon (Si), vanadium (V) and zinc (Zn) in fine particulate matter (PM2.5) were estimated using 100 × 100 m Europe-wide hybrid land use regression models assigned to the participants' residential addresses. We applied cohort-specific Cox proportional hazard models controlling for area- and individual-level covariates to evaluate associations with natural mortality. Two pollutant models adjusting for PM2.5 total mass or nitrogen dioxide (NO2) were also applied. We pooled cohort-specific estimates using a random effects meta-analysis. We included almost 27 million participants contributing more than 240 million person-years. All components except Zn were significantly associated with natural mortality [pooled Hazard Ratios (HRs) (95% CI): 1.037 (1.014, 1.060) per 5 ng/m3 Cu; 1.069 (1.031, 1.108) per 100 ng/m3 Fe; 1.039 (1.018, 1.062) per 50 ng/m3 K; 1.024 (1.006, 1.043) per 1 ng/m3 Ni; 1.036 (1.016, 1.057) per 200 ng/m3 S; 1.152 (1.048, 1.266) per 100 ng/m3 Si; 1.020 (1.006, 1.034) per 2 ng/m3 V]. Only K and Si were robust to PM2.5 or NO2 adjustment [pooled HRs (95% CI) per 50 ng/m3 in K: 1.025 (1.008, 1.044), 1.020 (0.999, 1.042) and per 100 ng/m3 in Si: 1.121 (1.039, 1.209), 1.068 (1.022, 1.117) adjusted for PM2.5 and NO2 correspondingly]. Our findings indicate an association of natural mortality with most components, which was reduced after adjustment for PM2.5 and especially NO2.

BackgroundLong-term exposure to ambient air pollution has been linked to childhood-onset asthma, although evidence is still insufficient. Within the multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we examined the associations of long-term exposures to particulate matter with a diameter 2.5), nitrogen dioxide (NO2) and black carbon (BC) with asthma incidence in adults.MethodsWe pooled data from three cohorts in Denmark and Sweden with information on asthma hospital diagnoses. The average concentrations of air pollutants in 2010 were modelled by hybrid land-use regression models at participants’ baseline residential addresses. Associations of air pollution exposures with asthma incidence were explored with Cox proportional hazard models, adjusting for potential confounders.ResultsOf 98 326 participants, 1965 developed asthma during a mean follow-up of 16.6 years. We observed associations in fully adjusted models with hazard ratios of 1.22 (95% CI 1.04–1.43) per 5 μg·m−3 for PM2.5, 1.17 (95% CI 1.10–1.25) per 10 µg·m−3 for NO2 and 1.15 (95% CI 1.08–1.23) per 0.5×10−5 m−1 for BC. Hazard ratios were larger in cohort subsets with exposure levels below the European Union and US limit values and possibly World Health Organization guidelines for PM2.5 and NO2. NO2 and BC estimates remained unchanged in two-pollutant models with PM2.5, whereas PM2.5 estimates were attenuated to unity. The concentration–response curves showed no evidence of a threshold.ConclusionsLong-term exposure to air pollution, especially from fossil fuel combustion sources such as motorised traffic, was associated with adult-onset asthma, even at levels below the current limit values.

BACKGROUND: Inconsistent associations between long-term exposure to particles with an aerodynamic diameter ≤ 2.5 μ m [fine particulate matter ( PM 2.5 )] components and mortality have been reported, partly related to challenges in exposure assessment. OBJECTIVES: We investigated the associations between long-term exposure to PM 2.5 elemental components and mortality in a large pooled European cohort; to compare health effects of PM 2.5 components estimated with two exposure modeling approaches, namely, supervised linear regression (SLR) and random forest (RF) algorithms. METHODS: We pooled data from eight European cohorts with 323,782 participants, average age 49 y at baseline (1985-2005). Residential exposure to 2010 annual average concentration of eight PM 2.5 components [copper (Cu), iron (Fe), potassium (K), nickel (Ni), sulfur (S), silicon (Si), vanadium (V), and zinc (Zn)] was estimated with Europe-wide SLR and RF models at a 100 × 100 m scale. We applied Cox proportional hazards models to investigate the associations between components and natural and cause-specific mortality. In addition, two-pollutant analyses were conducted by adjusting each component for PM 2.5 mass and nitrogen dioxide ( NO 2 ) separately. RESULTS: We observed 46,640 natural-cause deaths with 6,317,235 person-years and an average follow-up of 19.5 y. All SLR-modeled components were statistically significantly associated with natural-cause mortality in single-pollutant models with hazard ratios (HRs) from 1.05 to 1.27. Similar HRs were observed for RF-modeled Cu, Fe, K, S, V, and Zn with wider confidence intervals (CIs). HRs for SLR-modeled Ni, S, Si, V, and Zn remained above unity and (almost) significant after adjustment for both PM 2.5 and NO 2 . HRs only remained (almost) significant for RF-modeled K and V in two-pollutant models. The HRs for V were 1.03 (95% CI: 1.02, 1.05) and 1.06 (95% CI: 1.02, 1.10) for SLR- and RF-modeled exposures, respectively, per 2 ng / m 3 , adjusting for PM 2.5 mass. Associations with cause-specific mortality were less consistent in two-pollutant models. CONCLUSION: Long-term exposure to V in PM 2.5 was most consistently associated with increased mortality. Associations for the other components were weaker for exposure modeled with RF than SLR in two-pollutant models. https://doi.org/10.1289/EHP8368.

Tinnitus and pain have many similarities. Both are subjective sensations that may turn chronic, they are often accompanied by hypersensitivity in their respective sensory system, and overlapping brain changes have been observed. Since no population study has examined the empirical association between chronic pain and tinnitus, the present study aimed to explore the relationship in a general adult population. We used data from the seventh survey of the Tromsø Study (2015–2016). Participants (aged ≥40) responded to questions about pain and tinnitus. Using multiple logistic regression, we analysed the adjusted relationship between chronic pain and tinnitus in the full sample (n = 19,039), using several tinnitus definitions ranging from tinnitus >5 minutes within the past 12 months (broadest definition) to at least weekly and highly bothersome tinnitus (strictest definition). We also analysed relationships between number of body regions with pain, pain intensity and bothering, and tinnitus >5 minutes, among participants with chronic pain (n = 11,589). We found an association between chronic pain and tinnitus that was present irrespective of tinnitus definition, but was stronger with more bothersome tinnitus. With chronic pain, the odds of tinnitus >5 minutes was 64% higher, while odds of at least weekly, highly bothersome tinnitus was 144% higher than without chronic pain. Among participants with chronic pain, the number of pain regions was the pain variable most strongly associated with tinnitus >5 minutes (OR = 1.17 (95% CI: 1.14–1.20) for an increase of one region), whereas the other pain variables (intensity and bothering) showed weaker associations. All chronic pain variables had significant interactions with age, with the strongest associations for the youngest individuals (40–54 years). Our findings support the existence of an association between chronic pain and tinnitus and emphasises the importance of examining for comorbid pain in tinnitus patients to provide a more comprehensive treatment of tinnitus.

Objective To investigate the associations between air pollution and mortality, focusing on associations below current European Union, United States, and World Health Organization standards and guidelines. Design Pooled analysis of eight cohorts. Setting Multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE) in six European countries. Participants 325 367 adults from the general population recruited mostly in the 1990s or 2000s with detailed lifestyle data. Stratified Cox proportional hazard models were used to analyse the associations between air pollution and mortality. Western Europe-wide land use regression models were used to characterise residential air pollution concentrations of ambient fine particulate matter (PM 2.5 ), nitrogen dioxide, ozone, and black carbon. Main outcome measures Deaths due to natural causes and cause specific mortality. Results Of 325 367 adults followed-up for an average of 19.5 years, 47 131 deaths were observed. Higher exposure to PM 2.5 , nitrogen dioxide, and black carbon was associated with significantly increased risk of almost all outcomes. An increase of 5 µg/m 3 in PM 2.5 was associated with 13% (95% confidence interval 10.6% to 15.5%) increase in natural deaths; the corresponding figure for a 10 µg/m 3 increase in nitrogen dioxide was 8.6% (7% to 10.2%). Associations with PM 2.5 , nitrogen dioxide, and black carbon remained significant at low concentrations. For participants with exposures below the US standard of 12 µg/m 3 an increase of 5 µg/m 3 in PM 2.5 was associated with 29.6% (14% to 47.4%) increase in natural deaths. Conclusions Our study contributes to the evidence that outdoor air pollution is associated with mortality even at low pollution levels below the current European and North American standards and WHO guideline values. These findings are therefore an important contribution to the debate about revision of air quality limits, guidelines, and standards, and future assessments by the Global Burden of Disease.

Introduction: To characterize air pollution exposure at a fine spatial scale, different exposure assessment methods have been applied. Comparison of associations with health from different exposure methods are scarce. The aim of this study was to evaluate associations of air pollution based on hybrid, land-use regression (LUR) and dispersion models with natural cause and cause-specific mortality. Methods: We followed a Dutch national cohort of approximately 10.5 million adults aged 29+ years from 2008 until 2012. We used Cox proportional hazard models with age as underlying time scale and adjusted for several potential individual and area-level socio-economic status confounders to evaluate associations of annual average residential NO2, PM2.5 and BC exposure estimates based on two stochastic models (Dutch LUR, European-wide hybrid) and deterministic Dutch dispersion models. Results: Spatial variability of PM2.5 and BC exposure was smaller for LUR compared to hybrid and dispersion models. NO2 exposure variability was similar for the three methods. Pearson correlations between hybrid, LUR and dispersion modeled NO2 and BC ranged from 0.72 to 0.83; correlations for PM2.5 were slightly lower (0.61–0.72). In general, all three models showed stronger associations of air pollutants with respiratory disease and lung cancer mortality than with natural cause and cardiovascular disease mortality. The strength of the associations differed between the three exposure models. Associations of air pollutants estimated by LUR were generally weaker compared to associations of air pollutants estimated by hybrid and dispersion models. For natural cause mortality, we found a hazard ratio (HR) of 1.030 (95% confidence interval (CI): 1.019, 1.041) per 10 µg/m3 for hybrid modeled NO2, a HR of 1.003 (95% CI: 0.993, 1.013) per 10 µg/m3 for LUR modeled NO2 and a HR of 1.015 (95% CI: 1.005, 1.024) per 10 µg/m3 for dispersion modeled NO2. Conclusion: Air pollution was positively associated with natural cause and cause-specific mortality, but the strength of the associations differed between the three exposure models. Our study documents that the selected exposure model may contribute to heterogeneity in effect estimates of associations between air pollution and health.

Background/aim: Ambient air pollution has been associated with lung cancer, but the shape of the exposure-response function - especially at low exposure levels - is not well described. The aim of this study was to address the relationship between long-term low-level air pollution exposure and lung cancer incidence. Methods: The “Effects of Low-level Air Pollution: a Study in Europe” (ELAPSE) collaboration pools seven cohorts from across Europe. We developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates for nitrogen dioxide (NO2), fine particulate matter (PM2.5), black carbon (BC), and ozone (O3) to assign exposure to cohort participants’ residential addresses in 100 m by 100 m grids. We applied stratified Cox proportional hazards models, adjusting for potential confounders (age, sex, calendar year, marital status, smoking, body mass index, employment status, and neighborhood-level socio-economic status). We fitted linear models, linear models in subsets, Shape-Constrained Health Impact Functions (SCHIF), and natural cubic spline models to assess the shape of the association between air pollution and lung cancer at concentrations below existing standards and guidelines. Results: The analyses included 307,550 cohort participants. During a mean follow-up of 18.1 years, 3956 incident lung cancer cases occurred. Median (Q1, Q3) annual (2010) exposure levels of NO2, PM2.5, BC and O3 (warm season) were 24.2 µg/m3 (19.5, 29.7), 15.4 µg/m3 (12.8, 17.3), 1.6 10−5m−1 (1.3, 1.8), and 86.6 µg/m3 (78.5, 92.9), respectively. We observed a higher risk for lung cancer with higher exposure to PM2.5 (HR: 1.13, 95% CI: 1.05, 1.23 per 5 µg/m3). This association was robust to adjustment for other pollutants. The SCHIF, spline and subset analyses suggested a linear or supra-linear association with no evidence of a threshold. In subset analyses, risk estimates were clearly elevated for the subset of subjects with exposure below the EU limit value of 25 µg/m3. We did not observe associations between NO2, BC or O3 and lung cancer incidence. Conclusions: Long-term ambient PM2.5 exposure is associated with lung cancer incidence even at concentrations below current EU limit values and possibly WHO Air Quality Guidelines.

Introduction: Early onset and high prevalence of allergic diseases result in high individual and socio-economic burdens. Several studies provide evidence for possible effects of environmental factors on allergic diseases, but these are mainly single-exposure studies. The exposome provides a novel holistic approach by simultaneously studying a large set of exposures. The aim of the study was to evaluate the association between a broad range of prenatal and childhood environmental exposures and allergy-related outcomes in children. Material and methods: Analyses of associations between 90 prenatal and 107 childhood exposures and allergy-related outcomes (last 12 months: rhinitis and itchy rash; ever: doctor-diagnosed eczema and food allergy) in 6-11 years old children (n = 1270) from the European Human Early-Life Exposome cohort were performed. Initially, we used an exposome-wide association study (ExWAS) considering the exposures independently, followed by a deletion-substitution-addition selection (DSA) algorithm considering all exposures simultaneously. All the exposure variables selected in the DSA were included in a final multi-exposure model using binomial general linear model (GLM). Results: In ExWAS, no exposures were associated with the outcomes after correction for multiple comparison. In multi-exposure models for prenatal exposures, lower distance of residence to nearest road and higher di-iso-nonyl phthalate level were associated with increased risk of rhinitis, and particulate matter absorbance (PMabs) was associated with a decreased risk. Furthermore, traffic density on nearest road was associated with increased risk of itchy rash and diethyl phthalate with a reduced risk. DSA selected no associations of childhood exposures, or between prenatal exposures and eczema or food allergy. Discussion: This first comprehensive and systematic analysis of many environmental exposures suggests that prenatal exposure to traffic-related variables, PMabs and phthalates are associated with rhinitis and itchy rash. This work was supported by the European Community’s Seventh Framework Programme [grant agreement no 308333—the HELIX project]; Instituto de Salud Carlos III; CIBERESP; Conselleria de Sanitat; Generalitat Valenciana; Department of Health of the Basque Government; Provincial Government of Gipuzkoa; Generalitat de Catalunya-CIRIT; Lithuanian Agency for Science Innovation and Technology [grant number 6-04-2014_31V-66]; Norwegian Ministry of Health and Care Services; Norwegian Ministry of Education and Research; Greek Ministry of Health; Ministerio de Ciencia Innovacion y Universidades [grant number MTM2015-68140-R]; Centro Nacional de Genotipado-CEGEN-PRB2-ISCIII; Fondation de France.

Background Long-term exposure to air pollution has been related to cause-specific mortality. However, results vary across studies because of heterogeneities in exposure assessment and statistical a...

We developed Europe-wide models of long-term exposure to eight elements (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) in particulate matter with diameter

Background: Being overweight constitutes a health risk, and the proportion of overweight and obese children is increasing. It has been argued that road traffic noise could be linked to adiposity through its influence on sleep and stress. Few studies, to our knowledge, have investigated whether noise and adiposity are associated. Most of them were on adults, and we are not aware of any longitudinal study using repeated measures. Objectives: The present longitudinal study investigated whether road traffic noise exposures in pregnancy (N = 6,963; obs = 22,975) or childhood (N = 6,403; obs = 14,585) were associated with body mass index (BMI) trajectories in children. Methods: We obtained information on BMI and covariates from questionnaires used in the Norwegian Mother and Child Cohort Study, Statistics Norway, and Medical Birth Registry of Norway. We modeled road traffic noise for the most exposed façade of children’s present and historical addresses at 6 time points from pregnancy to age 8. We investigated effects on BMI trajectories using repeated measures and linear mixed models. Results: The results indicated that BMI curves depended on road traffic noise exposure during pregnancy, but not on exposure during childhood. Children in the highest decile of traffic noise exposure had increased BMI, with 0.35 kg/m2 more than children in the lowest decile, from birth to age 8 years. Conclusions: The results indicate that exposure to road traffic noise during pregnancy may be associated with children’s BMI trajectories. Future studies should investigate this further, using anthropometric measures such as waist-hip ratio and skinfold thickness, in addition to BMI.

Background We investigated if cancer onset in offspring is related to having short-lived parents for different cancer types and to see if there was a difference in smoking- and non-smoking related cancers. Methods Our study included 524,391 individuals born in Norway 1940–1950. All children were followed up for cancer from the age of 20 until they were between 59 and 69 years. Parental longevity was examined by grouping parental age of death into parents dying before 75 years of age and parents dying at 75 years of age or older. Results An increased risk of 1.14 (95%CI=1.10–1.19) among male offspring and 1.08 (95%CI=1.04–1.12) among female offspring was observed for total cancer when both parents died before the age of 75 compared to offspring with two long-lived parents. The highest increase was found for cancer in the lungs and trachea for both male (HR=1.67, 95%CI=1.50–1.86) and female offspring (HR=1.53, 95%CI=1.33–1.76). For other smoking-related cancers, the risk was lower. No increased risk was observed for non-smoking-related cancers. Conclusion Offspring of long-lived parents have lower risk of developing cancer compared with offspring of short-lived parents. Intergenerational transmission of risk factors from parents to offspring may play an important role, especially for tobacco-related cancers. However, genetic factors cannot be ruled out, since consistent evidence has implicated genetic factors in smoking behaviour.

Several studies have indicated weakly increased risk for kidney cancer among occupational groups exposed to gasoline vapors, engine exhaust, polycyclic aromatic hydrocarbons and other air pollutant ...

Purpose The purpose of the present study was to assess the agreement between self-reported use of sleep medications and tranquilizers and dispensed hypnotics and anxiolytics. Methods Self-reported medication use was obtained from the population-based survey Health and Environment in Oslo (HELMILO) (2009-2010) (n = 13 019). Data on dispensed hypnotics and anxiolytics were obtained from the Norwegian Prescription Database (NorPD). As measures of validity, we calculated sensitivity and specificity using both self-reports and prescription records as the reference standard. Furthermore, we calculated Cohen's kappa. Current self-reported medication use was compared with prescription data in time windows of both 100 and 200 days preceding questionnaire completion. Results The highest sensitivity was observed for current sleep medication use in the 100-day time window (sensitivity = 0.76, 95% confidence interval [CI]: 0.74, 0.79) when using prescription records as the reference standard. Sensitivity was generally lower for tranquilizers compared with sleep medications. Cohen's kappa showed the highest agreement for the 200-day time window with substantial agreement for sleep medications (kappa = 0.64; 95% CI: 0.62, 0.67) and moderate agreement for tranquilizers (kappa = 0.45; 95% CI: 0.41, 0.48). Conclusions The present study suggests moderate to substantial agreement between self-reported use of sleep medications and tranquilizers and dispensed drugs in a general adult population. The magnitude of agreement varied according to drug category and time window. Since self-reported and registry-based use of these drug classes does not match each other accurately, limitations of each data source should be considered when such medications are applied as the exposure or outcome in epidemiologic studies.

Health effects of traffic-related air pollution (TRAP) concentrations in densely populated areas are previously described. However, there is still a lack of knowledge of the health effects of moderate TRAP levels. The aim of the current study, a population-based survey including 16 099 adults (response rate 33%), was to assess the relationship between TRAP estimates and respiratory symptoms in an area with modest levels of traffic; Telemark County, Norway. Respondents reported respiratory symptoms the past 12 months and two TRAP exposure estimates: amount of traffic outside their bedroom window and time spent by foot daily along a moderate to heavy traffic road. Females reported on average more symptoms than males. Significant relationships between traffic outside their bedroom window and number of symptoms were only found among females, with the strongest associations among female occasional smokers (incidence rate ratio [IRR], 1.75, 95% confidence interval (CI) [1.16–2.62] for moderate or heavy traffic compared to no traffic). Significant relationship between time spent daily by foot along a moderate to heavy traffic road and number of symptoms was found among male daily smokers (IRR 1.09, 95% CI [1.04–1.15] per hour increase). Associations between traffic outside bedroom window and each respiratory symptom were found. Significant associations were primarily detected among females, both among smokers and non-smokers. Significant associations between time spent by foot daily along a moderate to heavy traffic road (per hour) and nocturnal dyspnoea (odds ratio (OR) 1.20, 95% CI [1.05–1.38]), nocturnal chest tightness (OR 1.13 [1.00–1.28]) and wheezing (OR 1.14 [1.02–1.29]) were found among daily smokers, primarily men. Overall, we found significant associations between self-reported TRAP exposures and respiratory symptoms. Differences between genders and smoking status were identified. The findings indicate an association between TRAP and respiratory symptoms even in populations exposed to modest levels of TRAP.

Background: An association between long-term exposure to fine particulate matter (PM2.5) and lung cancer has been established in previous studies. PM2.5 is a complex mixture of chemical components from various sources and little is known about whether certain components contribute specifically to the associated lung cancer risk. The present study builds on recent findings from the “Effects of Low-level Air Pollution: A Study in Europe” (ELAPSE) collaboration and addresses the potential association between specific elemental components of PM2.5 and lung cancer incidence. Methods: We pooled seven cohorts from across Europe and assigned exposure estimates for eight components of PM2.5 representing non-tail pipe emissions (copper (Cu), iron (Fe), and zinc (Zn)), long-range transport (sulfur (S)), oil burning/industry emissions (nickel (Ni), vanadium (V)), crustal material (silicon (Si)), and biomass burning (potassium (K)) to cohort participants’ baseline residential address based on 100 m by 100 m grids from newly developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates. We applied stratified Cox proportional hazards models, adjusting for potential confounders (age, sex, calendar year, marital status, smoking, body mass index, employment status, and neighborhood-level socio-economic status). Results: The pooled study population comprised 306,550 individuals with 3916 incident lung cancer events during 5,541,672 person-years of follow-up. We observed a positive association between exposure to all eight components and lung cancer incidence, with adjusted HRs of 1.10 (95% CI 1.05, 1.16) per 50 ng/m3 PM2.5 K, 1.09 (95% CI 1.02, 1.15) per 1 ng/m3 PM2.5 Ni, 1.22 (95% CI 1.11, 1.35) per 200 ng/m3 PM2.5 S, and 1.07 (95% CI 1.02, 1.12) per 200 ng/m3 PM2.5 V. Effect estimates were largely unaffected by adjustment for nitrogen dioxide (NO2). After adjustment for PM2.5 mass, effect estimates of K, Ni, S, and V were slightly attenuated, whereas effect estimates of Cu, Si, Fe, and Zn became null or negative. Conclusions: Our results point towards an increased risk of lung cancer in connection with sources of combustion particles from oil and biomass burning and secondary inorganic aerosols rather than non-exhaust traffic emissions. Specific limit values or guidelines targeting these specific PM2.5 components may prove helpful in future lung cancer prevention strategies.

Background: The Exposome approach allows a holistic view of environmental exposures effects on human health by evaluating multiple exposures simultaneously. Objectives: To evaluate prenatal and postnatal exposures association with lung function in childhood in the large European Human Early-Life Exposome (HELIX) cohort. Methods: We relied on a cohort of 1,301 mother-child pairs for whom the internal (urinary and blood biomarkers and lifestyle characteristics) and external (built environment, air pollution, meteorological factors…) exposome were assessed, totaling 442 exposures (174 prenatal and 268 postnatal). An agnostic environment-wide association study (EWAS) was applied for forced expiratory volume in 1 second in % predicted (FEV1 %), using linear regression models adjusted for confounders for each exposure. Results: The mean age of the children was 8.1 years. FEV1% was available for 1,033 (79.4%) children (mean(sd) = 98.8(13.2)). Without correcting for multiple testing in EWAS, FEV1 was statistically significantly decreased with 1) higher prenatal exposure to perfluorononanoate and perfluorooctanoate; 2) lower prenatal exposure to NO2 (trimester 3) and inverse distance to nearest road; 3) higher postnatal exposure to copper, ethyl-paraben, phthalates (sum of DEHP, MECCP, MEHHP, MEOHP, OXOMINP), house crowding and number of bus public transport mode stops around school, and 4) lower family affluence score. When correcting EWAS results for multiple testing or using variable selection models (DSA), no exposure was selected. Conclusion: This first exposome study on lung function in children confirmed some previously reported associations (e.g. phthalates, PFASs). Funding: Helix (EU H2020 Grant 308333)

Background: The urban exposome is the set of environmental factors that are experienced in the outdoor urban environment and that may influence child development. Objective: The authors’ goal was to describe the urban exposome among European pregnant women and understand its socioeconomic determinants. Methods: Using geographic information systems, remote sensing and spatio-temporal modeling we estimated exposure during pregnancy to 28 environmental indicators in almost 30,000 women from six population-based birth cohorts, in nine urban areas from across Europe. Exposures included meteorological factors, air pollutants, traffic noise, traffic indicators, natural space, the built environment, public transport, facilities, and walkability. Socioeconomic position (SEP), assessed at both the area and individual level, was related to the exposome through an exposome-wide association study and principal component (PC) analysis. Results: Mean±standard deviation (SD) NO2 levels ranged from 13.6±5.1 μg/m3 (in Heraklion, Crete) to 43.2±11 μg/m3 (in Sabadell, Spain), mean±SD walkability score ranged from 0.22±0.04 (Kaunas, Lithuania) to 0.32±0.07 (Valencia, Spain) and mean±SD Normalized Difference Vegetation Index ranged from 0.21±0.05 in Heraklion to 0.51±0.1 in Oslo, Norway. Four PCs explained more than half of variation in the urban exposome. There was considerable heterogeneity in social patterning of the urban exposome across cities. For example, high-SEP (based on family education) women lived in greener, less noisy, and less polluted areas in Bradford, UK (0.39 higher PC1 score, 95% confidence interval (CI): 0.31, 0.47), but the reverse was observed in Oslo (−0.57 PC1 score, 95% CI: −0.73, −0.41). For most cities, effects were stronger when SEP was assessed at the area level: In Bradford, women living in high SEP areas had a 1.34 higher average PC1 score (95% CI: 1.21, 1.48). Conclusions: The urban exposome showed considerable variability across Europe. Pregnant women of low SEP were exposed to higher levels of environmental hazards in some cities, but not others, which may contribute to inequities in child health and development. The research leading to these results received funding from the European Community’s Seventh Framework Programme (FP7/2007-2013) under grant agreement no 308333 – the HELIX project.

Background/Aim: Previous analysis from the large European multicentre ESCAPE study showed an association of particulate matter

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 FÊm 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 282 194 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 106 786 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. © 2018 The Author(s). Chemicals/CAS: nitric oxide, 10102-43-9; nitrogen dioxide, 10102-44-0

BACKGROUND: Epidemiological evidence on the association between ambient air pollution and breast cancer risk is inconsistent. OBJECTIVE: We examined the association between long-term exposure to ambient air pollution and incidence of postmenopausal breast cancer in European women. METHODS: In 15 cohorts from nine European countries, individual estimates of air pollution levels at the residence were estimated by standardized land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE) and Transport related Air Pollution and Health impacts - Integrated Methodologies for Assessing Particulate Matter (TRANSPHORM) projects: particulate matter (PM) ≤2:5 μm, ≤10 μm, and 2:5–10 μm in diameter (PM2:5, PM10, and PMcoarse, respectively); PM2:5 absorbance; nitrogen oxides (NO2 and NOx); traffic intensity; and elemental composition of PM. We estimated cohort-specific associations between breast cancer and air pollutants using Cox regression models, adjusting for major lifestyle risk factors, and pooled cohort-specific estimates using random-effects meta-analyses. RESULTS: Of 74,750 postmenopausal women included in the study, 3,612 developed breast cancer during 991,353 person-years of follow-up. We found positive and statistically insignificant associations between breast cancer and PM2:5 {hazard ratio (HR) =1:08 [95% confidence interval (CI): 0.77, 1.51] per 5 μg/m3 }, PM10 [1.07 (95% CI: 0.89, 1.30) per 10 μg/m3 ], PMcoarse [1.20 (95% CI: 0.96, 1.49 per 5 μg/m3 ], and NO2 [1.02 (95% CI: 0.98, 1.07 per 10 μg/m3 ], and a statistically significant association with NOx [1.04 (95% CI: 1.00, 1.08) per 20 μg/m3, p =0:04]. CONCLUSIONS: We found suggestive evidence of an association between ambient air pollution and incidence of postmenopausal breast cancer in European women. © 2017, Public Health Services, US Dept of Health and Human Services. All rights reserved. Chemicals/CAS: copper, 15158-11-9, 7440-50-8; iron, 14093-02-8, 53858-86-9, 7439-89-6; nickel, 7440-02-0; nitrogen oxide, 11104-93-1; potassium, 7440-09-7; silicon, 7440-21-3; sulfur, 13981-57-2, 7704-34-9; vanadium, 7440-62-2; zinc, 7440-66-6, 14378-32-6

Almost half of the European Union (EU)’s population is exposed to road traffic noise above levels that constitute a health risk. Associations between road traffic noise and impaired sleep in adults have consistently been reported. Less is known about effects of noise on children’s sleep. The aim of this study was to examine the association between nocturnal road traffic noise exposure and children’s parental-reported sleep duration and sleep problems. The present cross-sectional study used data from The Norwegian Mother and Child Cohort Study. Parental report of children’s sleep duration and sleep problems at age 7 was linked to modelled levels of residential night-time road traffic noise. The study population included 2665 children from Oslo, Norway. No association was found between road traffic noise and sleep duration in the total study population (odds ratio (OR): 1.05, 95% confidence interval (CI): [0.94, 1.17]), but a statistically significant association was observed in girls (OR: 1.21, 95% CI: [1.04, 1.41]). For sleep problems, the associations were similar (OR: 1.36, 95% CI: [0.85, 2.16]) in girls. The ORs are presented for an increase of 10 dB. The findings suggest there is an association between road traffic noise and sleep for girls, underlining the importance of protecting children against excessive noise levels. publishedVersion

Background Road traffic noise has been associated with adverse health effects including sleep disturbances. Use of sleep medication as an indicator of sleeping problems has rarely been explored in studies of the effects of traffic noise. Furthermore, using registry data on sleep medications provides an opportunity to study the effects of noise on sleep where attribution of sleep problems to noise is not possible. Methods We used questionnaire data from the population-based study Health and Environment in Oslo (HELMILO) (2009–10) (n = 13,019). Individual data on sleep medications was obtained from the Norwegian Prescription Database (NorPD). Noise levels (L night) were modeled for the most exposed façade of the building at each participant’s home address. Logistic regression models adjusted for potential confounders were used to analyze the association between traffic noise and sleep medication use both for one whole year and for the summer season. The results were reported as changes in the effect estimate per 5 decibel (dB) increase in noise level. Results We observed no association between traffic noise and sleep medication use during one year [odds ratio (OR) = 1.00; 95% confidence interval (CI): 0.96, 1.04]. For sleep medication use in the summer season, there was a positive, however non-significant association (OR = 1.04; 95% CI: 0.99, 1.10). Among individuals sleeping with the bedroom window open, the association increased slightly and was borderline statistically significant (OR = 1.06; 95% CI: 1.00, 1.12). Conclusions We found no evidence of an association between traffic noise and sleep medication use during one year. However, for the summer season, there was some suggestive evidence of an association. These findings indicate that season may play a role in the association between traffic noise and sleep, possibly because indoor traffic noise levels are likely to be higher during summer due to more frequent window opening. More studies are, however, necessary in order to confirm this. © The Author(s). 2017. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

BACKGROUND: Few studies on long-term exposure to air pollution and mortality have been reported from Europe. Within the multicentre European Study of Cohorts for Air Pollution Effects (ESCAPE), we aimed to investigate the association between natural-cause mortality and long-term exposure to several air pollutants. METHODS: We used data from 22 European cohort studies, which created a total study population of 367,251 participants. All cohorts were general population samples, although some were restricted to one sex only. With a strictly standardised protocol, we assessed residential exposure to air pollutants as annual average concentrations of particulate matter (PM) with diameters of less than 2.5 μm (PM2.5), less than 10 μm (PM10), and between 10 μm and 2.5 μm (PMcoarse), PM2.5 absorbance, and annual average concentrations of nitrogen oxides (NO2 and NOx), with land use regression models. We also investigated two traffic intensity variables-traffic intensity on the nearest road (vehicles per day) and total traffic load on all major roads within a 100 m buffer. We did cohort-specific statistical analyses using confounder models with increasing adjustment for confounder variables, and Cox proportional hazards models with a common protocol. We obtained pooled effect estimates through a random-effects meta-analysis. FINDINGS: The total study population consisted of 367,251 participants who contributed 5,118,039 person-years at risk (average follow-up 13.9 years), of whom 29,076 died from a natural cause during follow-up. A significantly increased hazard ratio (HR) for PM2.5 of 1.07 (95% CI 1.02-1.13) per 5 μg/m(3) was recorded. No heterogeneity was noted between individual cohort effect estimates (I(2) p value=0.95). HRs for PM2.5 remained significantly raised even when we included only participants exposed to pollutant concentrations lower than the European annual mean limit value of 25 μg/m(3) (HR 1.06, 95% CI 1.00-1.12) or below 20 μg/m(3) (1.07, 1.01-1.13). INTERPRETATION: Long-term exposure to fine particulate air pollution was associated with natural-cause mortality, even within concentration ranges well below the present European annual mean limit value. FUNDING: European Community's Seventh Framework Program (FP7/2007-2011).