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Background Previous research suggests an association between road traffic noise and obesity, but current evidence is inconclusive. We aimed to investigate associations between self-reported traffic noise in bedrooms and self-measured obesity markers. 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 linear, and logistic regression models and evaluated effect modifications by sex. Results Women, who reported very high traffic noise levels in bedroom, had 1.35 (95% CI 0.32–2.38) kg/m2 higher BMI and 4.66 (95% CI 1.83–7.48) 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, obese or have abdominal obesity with OR varying from 1.16 to 1.67 compared to women, who reported no traffic noise in the bedroom. Among men we did not find any clear associations between noise pollution and obesity measures. Conclusion Our results suggest that self-reported traffic noise in the bedroom may be associated to being overweight or obese among women, but not among men.

Introduction: Previous studies on the association between abdominal and general obesity and respiratory disease have provided conflicting results. Aims and objectives: We aimed to explore the associations of abdominal obesity with respiratory symptoms, asthma, and chronic obstructive pulmonary disease independently from general obesity in women and men. Methods: This cross-sectional study was based on the Respiratory Health in Northern Europe (RHINE) III questionnaire (n = 12 290) conducted in 2010–2012. Abdominal obesity was self-measured waist circumference using a sex-specific standard cut-off point: ≥102 cm in males and ≥88 cm in females. General obesity was defined as self-reported BMI ≥30.0 kg/m2. Results: There were 4261 subjects (63% women) with abdominal obesity and 1837 subjects (50% women) with general obesity. Both abdominal and general obesity was independent of each other and associated with respiratory symptoms (odds ratio (OR) from 1.25 to 2.00)). Asthma was significantly associated with abdominal and general obesity in women, OR (95% CI) 1.56 (1.30–1.87) and 1.95 (1.56–2.43), respectively, but not in men, OR 1.22 (0.97–3.17) and 1.28 (0.97–1.68) respectively. A similar sex difference was found for self-reported chronic obstructive pulmonary disease. Conclusions: General and abdominal obesity were independent factors associated with respiratory symptoms in adults. Asthma and chronic obstructive pulmonary disease were independently linked to abdominal and general obesity in women but not men.

We studied home environment exposures in relation to asthma, allergic rhinitis and atopic dermatitis among offspring of participants (parents) in the Respiratory Health in Northern Europe (RHINE) study (age ≤ 30 y). Totally 17,881 offspring from Iceland, Norway, Sweden, Denmark and Estonia were included. Home environment exposures, including dampness and mold, type of dwelling, construction year and indoor painting were registered through a questionnaire answered by parents in the first follow up (RHINE II). The parents reported ten years later with in the frame of RHINE III offspring's birth year and offspring's asthma, allergic rhinitis, atopic dermatitis. They also reported dampness and mold at home from RHINE II to RHINE III. The prevalence of offspring's asthma before 10 y, asthma after 10 y, allergic rhinitis at any age and atopic dermatitis at any age were 9.7 %, 4.3 %, 15.6 % and 17.3 %, respectively. Asthma before 10 y was related to any indoor painting at RHINE II (OR = 1.14, 95%CI (1.02, 1.29)). Asthma after 10 y was associated with dampness/mold at home (OR = 1.33–1.62) and living in the newest buildings (constructed in 1986–2001) (OR = 1.30, 95%CI (1.02, 1.66)). Allergic rhinitis was associated with living in newer buildings (constructed in 1961–2001) (OR = 1.16–1.24). Atopic dermatitis was associated with visible mold (OR = 1.35, 95%CI(1.12, 1.62)), dampness/mold at home (OR = 1.18–1.38), living in apartments (OR = 1.22, 95%CI(1.10, 1.35)) and living in newer buildings (constructed in 1961–2001) (OR = 1.14–1.25). There were dose-response effects of dampness and mold on offspring's asthma after 10 y and atopic dermatitis (20 years exposure vs. 10 years exposure). Older offspring had increased risk of developing asthma after 10 y and atopic dermatitis. In conclusion, home dampness and mold, living in apartments, living in newer buildings and indoor painting were associated with offspring's asthma or allergic diseases. Stronger health effects were found among offspring with prolonged exposure of dampness/mold. publishedVersion

Exposure to air pollution is of great concern for public health although studies on the associations between exposure estimates and personal exposure are limited and somewhat inconsistent. The aim of this study was to quantify the associations between personal nitrogen oxides (NOx), ozone (O3) and particulate matter (PM10) exposure levels and ambient levels, and the impact of climate and time spent outdoors in two cities in Sweden. Subjects (n = 65) from two Swedish cities participated in the study. The study protocol included personal exposure measurements at three occasions, or waves. Personal exposure measurements were performed for NOx and O3 for 24 h and PM10 for 24 h, and the participants kept an activity diary. Stationary monitoring stations provided hourly data of NOx, O3 and PM, as well as data on air temperature and relative humidity. Data were analysed using mixed linear models with the subject-id as a random effect and stationary exposure and covariates as fixed effects. Personal exposure levels of NOx, O3 and PM10 were significantly associated with levels measured at air pollution monitoring stations. The associations persisted after adjusting for temperature, relative humidity, city and wave, but the modelled estimates were slightly attenuated from 2.4% (95% CI 1.8–2.9) to 2.0% (0.97–2.94%) for NOx, from 3.7% (95% CI 3.1–4.4) to 2.1% (95% CI 1.1–2.9%) for O3 and from 2.6% (95% 0.9–4.2%) to 1.3% (95% CI − 1.5–4.0) for PM10. After adding covariates, the degree of explanation offered by the model (coefficient of determination, or R2) did not change for NOx (0.64 to 0.63) but increased from 0.46 to 0.63 for O3, and from 0.38 to 0.43 for PM10. Personal exposure to NOx, O3 and PM has moderate to good association with levels measured at urban background sites. The results indicate that stationary measurements are valid as measure of exposure in environmental health risk assessments, especially if they can be refined using activity diaries and meteorological data. Approximately 50–70% of the variation of the personal exposure was explained by the stationary measurement, implying occurrence of misclassification in studies using more crude exposure metrics, potentially leading to underestimates of the effects of exposure to ambient air pollution.

BackgroundExposure to air pollution is of great concern for public health although studies on the associations between exposure estimates and personal exposure are limited and somewhat inconsistent. We aimed to quantify the associations between personal NOx, ozone and PM10 exposure levels to ambient levels, and the impact of climate and time spent outdoors in two cities in Sweden.MethodsSubjects (n=65) from two Swedish cities participated in the study. The study protocol included personal exposure measurements at three occasions, or waves. Personal exposure measurements of NOx, ozone, and PM10, were performed for 10 days and 24 hours respectively, and the participants kept a diary on activities. Stationary monitoring stations provided hourly data of NOx, ozone, and PM, as well as data on air temperature and relative humidity. Data were analysed using mixed linear models with the subject-id as a random effect and stationary exposure and covariates as fixed effects. ResultsPersonal exposure levels of NOx, ozone, and PM10 were significantly associated with levels measured at air-pollution monitoring stations. The associations persisted after adjusting for temperature, relative humidity, city, and wave, but the modelled estimates were slightly attenuated from 2.4% (95% CI 1.8-2.9) to 2.0% (0.97-2.94%) for NOX, from 3.7% (95% CI 3.1-4.4) to 2.1% (95% CI 1.1-2.9%) for O3 and from 2.6% (95% 0.9-4.2%) to 1.3% (95% CI -1.5-4.0) for PM10. After adding covariates, the degree of explanation offered by the model (coefficient of determination, or R2) did not change for NOX (0.64 to 0.63), but increased from 0.46 to 0.63 for O3, and from 0.38 to 0.43 for PM10. ConclusionsPersonal exposure to NOx, ozone and PM have moderate to good association with levels measured at urban background sites. The results indicate that stationary measurements are valid as measure of exposure in environmental health risk assessments, especially if they can be refined using activity diaries and meteorological data. Approximately 50-70% of the variation of the personal exposure was explained by the stationary measurement, implying occurrence of misclassification in studies using more crude exposure metrics, potentially leading to underestimates of the effects of exposure to ambient air pollution

In subjects with asthma and birch-(betula) pollen allergy, exposure is associated with an increase in inflammatory biomarkers, e.g. fraction of exhaled nitric oxide (FENO), a biomarker for type-II airway inflammation. The aim was to examine if airway inflammation is augmented by air pollutant exposure during pollen season. In the study, 40 subjects with physician-diagnosed asthma and birch-pollen allergy and 24 healthy controls without allergy were examined during two pollen seasons (April – June) and out of season (November/December) in two Swedish cities. Personal exposure to birch allergen (24h) and PM10 (24h), NOx (10 days) and O3 (10 days), was measured. Due to skewness, quantile regression was used. FENO50 was higher during pollen season (median 21 ±IQR 15) in asthma v. controls (11 ±13), but not statistically significant (p=0.11). In any season, associations between exposure and FENO was only found in subjects with high FENO (>75th percentile). In asthma, exposure to O3 and PM during pollen-season were associated with substantial increases in FENO (Table 1), and there was a significant interaction between exposure to pollen and O3. NOx was not associated with FENO in any season. O3 and PM exposure was associated with increased airway inflammation during pollen season in subjects with atopic asthma and increased FENO only.

Few studies have investigated associations between self-reported and modelled exposure to traffic pollution. The objective of this study was to examine correlations between self-reported traffic exposure and modelled (a) NOX and (b) traffic proximity in seven different northern European cities; Aarhus (Denmark), Bergen (Norway), Gothenburg, Umeå, and Uppsala (Sweden), Reykjavik (Iceland), and Tartu (Estonia). We analysed data from the RHINE III (Respiratory Health in Northern Europe, www.rhine.nu) cohorts of the seven study cities. Traffic proximity (distance to the nearest road with >10,000 vehicles per day) was calculated and vehicle exhaust (NOX) was modelled using dispersion models and land-use regression (LUR) data from 2011. Participants were asked a question about self-reported traffic intensity near bedroom window and another about traffic noise exposure at the residence. The data were analysed using rank correlation (Kendall's tau) and inter-rater agreement (Cohen's Kappa) between tertiles of modelled NOX and traffic proximity tertile and traffic proximity categories (0–150 metres (m), 150–200 m, >300 m) in each centre. Data on variables of interest were available for 50–99% of study participants per each cohort. Mean modelled NOX levels were between 6.5 and 16.0 μg/m3; median traffic intensity was between 303 and 10,750 m in each centre. In each centre, 7.7–18.7% of respondents reported exposure to high traffic intensity and 3.6–16.3% of respondents reported high exposure to traffic noise. Self-reported residential traffic exposure had low or no correlation with modelled exposure and traffic proximity in all centres, although results were statistically significant (tau = 0.057–0.305). Self-reported residential traffic noise correlated weakly (tau = 0.090–0.255), with modelled exposure in all centres except Reykjavik. Modelled NOX had the highest correlations between self-reported and modelled traffic exposure in five of seven centres, traffic noise exposure had the highest correlation with traffic proximity in tertiles in three centres. Self-reported exposure to high traffic intensity and traffic noise at each participant's residence had low or weak although statistically significant correlations with modelled vehicle exhaust pollution levels and traffic proximity.

To analyze whether living close to a busy road would increase the risk of having cardiac disease and hypertension.Longitudinal cross-sectional study.We used cross-sectional longitudinal questionnaire data from the RHINE study for Tartu in 2000/2001 and 2011/2012. Home addresses of the respondents were geocoded and traffic data obtained from annually conducted traffic counts in Tartu. Relationships between proximity to a busy road and self-reported cardiac disease and hypertension were analyzed with multiple logistic regression.In terms of total traffic (≥10,000 vehicles per day) within a 150-m zone of a busy road, the odds ratio (OR) for prevalence of cardiac disease was significant in 2000/2001 (1.91, 95% CI 1.15-3.16) and 2011/2012 (1.58, 95% CI 1.01-2.47). Prevalence of hypertension was significant only in 2011/2012 (1.61, 95% CI 1.08-2.39). In terms of heavy duty vehicle traffic (≥500 vehicles per day) within a 150-m zone in 2000/2001, the OR was 1.52 (95% CI 1.04-2.24) and 1.49 (95% CI 1.02-2.17) respectively for the prevalence of cardiac disease and hypertension. In 2011/2012 no significant relationship between heavy duty vehicle traffic and cardiac disease or hypertension was found. We also saw a significant relationship between total traffic and the onset of cardiac disease (OR = 2.04, 95% CI 1.07-3.87).This study showed that living closer than 150 m to a busy road can increase the odds of having cardiac disease and hypertension, which should be taken into account in city planning.

Ozone and nitrogen oxides (NO x ) are air pollutants with known associations to adverse health effects on humans. Few studies have simultaneously measured ozone and nitrogen oxides with high spatial resolution. The main aim of this paper was to assess the levels and variation of ground-level ozone, NO2 and NO x in two Swedish cities. An additional aim was to describe the levels of these pollutants within and between three different types of measurement sites (regional background, urban background and traffic sites) and within and between different measurement periods of the year. Three weekly sampling campaigns of NO x and ozone were conducted simultaneously at 20 sites in two Swedish regions using Ogawa badges. Ozone was measured at 20 additional sites in each area. The median ozone concentration for all measurements was statistically significantly higher in Malmö (67 μg/m(3)) compared to Umeå (56 μg/m(3)), and in both cities, ozone levels were highest in April. Measurement period was a more important factor for describing the variation in ozone concentrations than the type of measurement site. The levels of NO2 and NO x were statistically significantly higher in the Malmö area (8.1 and 12 μg/m(3)) compared to the Umeå area (4.5 and 8.9 μg/m(3)). The levels were generally highest at the sites categorized as traffic, while the variability between different seasons was sparse.

Background: Inconsistent associations between socioeconomic position (SEP) and outdoor air pollution have been reported in Europe, but methodological differences prevent any direct between-study comparison. Objectives: Assess and compare the association between SEP and outdoor nitrogen dioxide (NO2) exposure as a marker of traffic exhaust, in 16 cities from eight Western European countries. Methods: Three SEP indicators, two defined at individual-level (education and occupation) and one at neighborhood-level (unemployment rate) were assessed in three European multicenter cohorts. NO2 annual concentration exposure was estimated at participants' addresses with land use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE; http://www.escapeproject.eu/). Pooled and city-specific linear regressions were used to analyze associations between each SEP indicator and NO2. Heterogeneity across cities was assessed using the Higgins' I-squared test (I2). Results: The study population included 5692 participants. Pooled analysis showed that participants with lower individual-SEP were less exposed to NO2. Conversely, participants living in neighborhoods with higher unemployment rate were more exposed. City-specific results exhibited strong heterogeneity (I2 > 76% for the three SEP indicators) resulting in variation of the individual- and neighborhood-SEP patterns of NO2 exposure across cities. The coefficients from a model that included both individual- and neighborhood-SEP indicators were similar to the unadjusted coefficients, suggesting independent associations. Conclusions: Our study showed for the first time using homogenized measures of outcome and exposure across 16 cities the important heterogeneity regarding the association between SEP and NO2 in Western Europe. Importantly, our results showed that individual- and neighborhood-SEP indicators capture different aspects of the association between SEP and exposure to air pollution, stressing the importance of considering both in air pollution health effects studies. The ESCAPE study, funded by the European Community's Seventh Framework Program (FP7/2007-2011) under grant agreement no. 211250 (http://www.escapeproject.eu/).

Ground level ozone [ozone] is considered a harmful air pollutant but there is a knowledge gap regarding its long term health effects. The main aim of this study is to develop local Land Use Regression [LUR] models that can be used to study long term health effects of ozone. The specific aim is to develop spatial LUR models for two Swedish cities, Umeå and Malmö, as well as a temporal model for Malmö in order to assess ozone exposure for long term epidemiological studies. For the spatial model we measured ozone, using Ogawa passive samplers, as weekly averages at 40 sites in each study area, during three seasons. This data was then inserted in the LUR-model with data on traffic, land use, population density and altitude to develop explanatory models of ozone variation. To develop the temporal model for Malmö, hourly ozone data was aggregated into daily means for two measurement stations in Malmö and one in a rural area outside Malmö. Using regression analyses we inserted meteorological variables into different temporal models and the one that performed best for all three stations was chosen. For Malmö the LUR-model had an adjusted model R2 of 0.40 and cross validation R2 of 0.17. For Umeå the model had an adjusted model R2 of 0.67 and cross validation adjusted R2 of 0.48. When restricting the model to only including measuring sites from urban areas, the Malmö model had adjusted model R2 of 0.51 (cross validation adjusted R2 0.33) and the Umeå model had adjusted model R2 of 0.81 (validation adjusted R2 of 0.73). The temporal model had adjusted model R2 0.54 and 0.61 for the two Malmö sites, the cross validation adjusted R2 was 0.42. In conclusion, we can with moderate accuracy, at least for Umeå, predict the spatial variability, and in Malmö the temporal variability in ozone variation.

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).

Adverse effects of air pollution include respiratory inflammation. A few epidemiologic studies have shown elevations in the fraction of exhaled nitric oxide, a marker of airway inflammation, after exposure to traffic-related pollutants.We examined whether short-term exposures to ozone (O3), oxides of nitrogen (NOx), or particulate matter10 μm (PM10) were associated with proximal and distal airway inflammation. The study included 5841 randomly selected Swedish adults from 25 to 75 years of age. Fraction of exhaled nitrogen was measured at two flow rates: 50 ml/s representing the proximal airways and 270 ml/s representing the distal airways. Air pollution data were obtained from an urban monitoring site. We applied linear regression to estimate short-term associations of O3, NOx, and PM10 with fractions of exhaled NO at 50 and 270 ml/s.An interquartile range increase in 120-hour average O3 levels was associated with a 5.1% (95% confidence interval = 1.7% to 8.5%) higher level of fraction of exhaled NO at 270 ml/s and 3.6% (-0.4% to 3.4%) higher level of the fraction of exhaled NO at 50 ml/s. For NOx, a small effect was seen for the 24-hour average on the fraction of exhaled NO at 270 ml/s, while for PM10 no clear effects were seen. There was a tendency for a weaker effect of ozone and a stronger effect of NOx in subjects with asthma.Exposure to O3 was associated with a marker of distal airway inflammation, while the association was less obvious for inflammation of the proximal airways.

BACKGROUND: Whereas it is generally accepted that maternal environment plays a key role in child health, emerging evidence suggests that paternal environment before conception also impacts child health. We aimed to investigate the association between children's asthma risk and parental smoking and welding exposures prior to conception.METHODS: In a longitudinal, multi-country study, parents of 24 168 offspring aged 2-51 years provided information on their life-course smoking habits, occupational exposure to welding and metal fumes, and offspring's asthma before/after age 10 years and hay fever. Logistic regressions investigated the relevant associations controlled for age, study centre, parental characteristics (age, asthma, education) and clustering by family.RESULTS: Non-allergic early-onset asthma (asthma without hay fever, present in 5.8%) was more common in the offspring with fathers who smoked before conception {odds ratio [OR] = 1.68 [95% confidence interval (CI) = 1.18-2.41]}, whereas mothers' smoking before conception did not predict offspring asthma. The risk was highest if father started smoking before age 15 years [3.24 (1.67-6.27)], even if he stopped more than 5 years before conception [2.68 (1.17-6.13)]. Fathers' pre-conception welding was independently associated with non-allergic asthma in his offspring [1.80 (1.29-2.50)]. There was no effect if the father started welding or smoking after birth. The associations were consistent across countries.CONCLUSIONS: Environmental exposures in young men appear to influence the respiratory health of their offspring born many years later. Influences during susceptible stages of spermatocyte development might be important and needs further investigation in humans. We hypothesize that protecting young men from harmful exposures may lead to improved respiratory health in future generations.

Background Exposure to ambient air pollution is suspected to cause cognitive effects, but a prospective cohort is needed to study exposure to air pollution at the home address and the incidence of dementia. Objectives We aimed to assess the association between long-term exposure to traffic-related air pollution and dementia incidence in a major city in northern Sweden. Methods Data on dementia incidence over a 15-year period were obtained from the longitudinal Betula study. Traffic air pollution exposure was assessed using a land-use regression model with a spatial resolution of 50 m × 50 m. Annual mean nitrogen oxide levels at the residential address of the participants at baseline (the start of follow-up) were used as markers for long-term exposure to air pollution. Results Out of 1,806 participants at baseline, 191 were diagnosed with Alzheimer’s disease during follow-up, and 111 were diagnosed with vascular dementia. Participants in the group with the highest exposure were more likely than those in the group with the lowest exposure to be diagnosed with dementia (Alzheimer’s disease or vascular dementia), with a hazard ratio (HR) of 1.43 (95% CI: 0.998, 2.05 for the highest vs. the lowest quartile). The estimates were similar for Alzheimer’s disease (HR 1.38) and vascular dementia (HR 1.47). The HR for dementia associated with the third quartile versus the lowest quartile was 1.48 (95% CI: 1.03, 2.11). A subanalysis that excluded a younger sample that had been retested after only 5 years of follow-up suggested stronger associations with exposure than were present in the full cohort (HR = 1.71; 95% CI: 1.08, 2.73 for the highest vs. the lowest quartile). Conclusions If the associations we observed are causal, then air pollution from traffic might be an important risk factor for vascular dementia and Alzheimer’s disease. Citation Oudin A, Forsberg B, Nordin Adolfsson A, Lind N, Modig L, Nordin M, Nordin S, Adolfsson R, Nilsson LG. 2016. Traffic-related air pollution and dementia incidence in northern Sweden: a longitudinal study. Environ Health Perspect 124:306–312; http://dx.doi.org/10.1289/ehp.1408322

Background Polymorphisms in nitric oxide synthase genes (NOS1, NOS2, and NOS3) have been suggested to have a major impact on fraction of exhaled nitric oxide (FENO), a biomarker of airway inflammation. However, the genetic contribution of NOS polymorphisms to FENO is not fully understood. The aim of this study was to investigate comprehensively the association between single nucleotide polymorphisms (SNPs) in all three NOS genes and FENO in an adult population, and to assess whether such associations are modified by asthma or atopy. Method In 1737 adults from a Swedish general population sample, FENO was measured and genetic variation in the NOS genes was assessed using 49 SNPs. The genetic effect of NOS polymorphisms on FENO, asthma, and atopy was estimated using multiple regression methods. Results In a multi-SNP model based on stepwise regression analysis, two SNPs in NOS2 and one in NOS3 showed independent associations with levels of FENO. For NOS2 SNP rs9901734, subjects had 5.3% (95% CI 1.0% to 9.7%) higher levels of FENO per G allele, and for rs3729508, subjects with CC or CT genotypes had 9.4% (95% CI 3.1% to 15.2%) higher levels compared with TT. For NOS3 SNP rs7830, subjects with GT or TT had 5.6% (95% CI 0.4% to 11.1%) higher levels than GG; the genetic effect of this SNP was stronger in asthmatics (21.9%, 95% CI 4.6% to 42.0%). Conclusion These results suggest that NOS2 is the major NOS gene determining variability in exhaled nitric oxide in the healthy adult population, while NOS3 may play a more important role in asthmatic adults.

Few studies have investigated the relationship between vehicle exhaust and the new onset of asthma among adults. The aim of the present prospective cohort study was to investigate the relationship between the cumulative incidence of asthma and onset of asthma among adults and vehicle exhaust concentrations at home. Participants from three Swedish cities included in the Respiratory Health in Northern Europe cohort constituted the study population. Exposure at each participant's home was calculated using dispersion models. We also used

BACKGROUND AND OBJECTIVE: Cat allergen concentrations higher than 8 μg/g in settled house dust, have been suggested to provoke exacerbation of allergic respiratory symptoms. However, whether the 8μg/g of indoor cat allergen concentration is indeed the minimal exposure required for triggering the asthma related respiratory symptoms or the development of sensitization has not yet been confirmed. We studied the associations between domestic cat allergen concentrations and allergic symptoms in the European Community Respiratory Health Survey II, with the aim of confirming this suggested threshold. METHODS: Cat allergen concentrations were measured in the mattress dust of 3003 participants from 22 study centres. Levels of specific immunoglobulin E to cat allergens were measured in serum samples using an immunoassay. Information on allergic symptoms, medication use, home environment and smoking was obtained from a face-to-face interview. RESULTS: Domestic cat allergen concentrations were not associated with allergic/ asthmatic symptoms in the entire study population, nor in the subset sensitized to cat allergen. We also found no association among individuals exposed to concentrations higher than 8 μg/g. However, exposure to medium cat allergen concentrations (0.24-0.63 μg/g) was positively associated with reported asthmatic respiratory symptoms in subjects who have experienced allergic symptoms when near animals. CONCLUSIONS: The proposed 8 μg/g threshold of cat allergen concentrations for the exacerbation of allergic/ respiratory symptoms was not confirmed in a general European adult population. Potential biases attributable to avoidance behaviours and an imprecise exposure assessment cannot be excluded.

The follow-up of cohorts of adults from more than 20 European centres of the former ECRHS I (1989-1992) investigates long-term effects of exposure to ambient air pollution on respiratory health, in ...

Previous genetic association studies have reported evidence for association of single-nucleotide polymorphisms (SNPs) in the NOS2 gene, encoding inducible nitric oxide synthase (iNOS), to variation in levels of fractional exhaled nitric oxide (FENO) in children and adults. In this study, we evaluated 10 SNPs in the region of chromosome 17 from 26.07 Mb to 26.13 Mb to further understand the contribution of NOS2 to variation in levels of FENO.In a cohort of 5912 adults 25-75 years of age, we investigated the relationship between NOS2 haplotypes and FENO, and effect modification by asthma.Seven common (frequency ≥5%) haplotypes (H1-H7) were inferred from all possible haplotype combinations. One haplotype (H3) was significantly associated with lower levels of FENO: -5.8% (95% CI -9.8 to -1.7; p=0.006) compared with the most common baseline haplotype H1. Two haplotypes (H5 and H6) were significantly associated with higher levels of FENO: +10.7% (95% CI 5.0 to 16.7; p=0.0002) and +14.9% (95% CI 10.6 to 19.3; p=7.8×10(-13)), respectively. The effect of haplotype H3 was mainly seen in subjects with asthma (-21.6% (95% CI -33.5 to -5.9)) and was not significant in subjects without asthma (-4.2% (95% CI -8.4 to 0.2)). The p value for interaction between H3 and asthma status was 0.004.Our findings suggest that several common haplotypes in the NOS2 gene contribute to variation in FENO in adults. We also saw some evidence of effect modification by asthma status on haplotype H3.

Rationale: Prospective cohort studies have shown that chronic exposure to particulate matter and traffic-related air pollution is associated with reduced survival. However, the effects on nonmalignant respiratory mortality are less studied, and the data reported are less consistent. Objectives: We have investigated the relationship of long-term exposure to air pollution and nonmalignant respiratory mortality in 16 cohorts with individual level data within the multicenter European Study of Cohorts for Air Pollution Effects (ESCAPE). Methods: Data from 16 ongoing cohort studies from Europe were used. The total number of subjects was 307,553. There were 1,559 respiratory deaths during follow-up. Measurements and Main Results: Air pollution exposure was estimated by land use regression models at the baseline residential addresses of study participants and traffic-proximity variables were derived from geographical databases following a standardized procedure within, the ESCAPE study. Cohort-specific hazard ratios obtained by Cox proportional hazard models from standardized individual cohort analyses were combined using metaanalyses. We found no significant associations between air pollution exposure and nonmalignant respiratory mortality. Most hazard ratios were slightly below unity, with the exception of the traffic-proximity indicators. Conclusions: In this study of 16 cohorts, there was no-association between air pollution exposure and nonmalignant respiratory mortality.

Background: Ambient air pollution is suspected to cause lung cancer. We aimed to assess the association between long-term exposure to ambient air pollution and lung cancer incidence in European populations. Methods: This prospective analysis of data obtained by the European Study of Cohorts for Air Pollution Effects used data from 17 cohort studies based in nine European countries. Baseline addresses were geocoded and we assessed air pollution by land-use regression models for particulate matter (PM) with diameter of less than 10 μm (PM10), less than 2·5 μm (PM2·5), and between 2·5 and 10 μm (PMcoarse), soot (PM2·5absorbance), nitrogen oxides, and two traffic indicators. We used Cox regression models with adjustment for potential confounders for cohort-specific analyses and random effects models for meta-analyses. Findings: The 312-944 cohort members contributed 4-013-131 person-years at risk. During follow-up (mean 12·8 years), 2095 incident lung cancer cases were diagnosed. The meta-analyses showed a statistically significant association between risk for lung cancer and PM10 (hazard ratio [HR] 1·22 [95% CI 1·03-1·45] per 10 μg/m3). For PM2·5 the HR was 1·18 (0·96-1·46) per 5 μg/m3. The same increments of PM10 and PM2·5 were associated with HRs for adenocarcinomas of the lung of 1·51 (1·10-2·08) and 1·55 (1·05-2·29), respectively. An increase in road traffic of 4000 vehicle-km per day within 100 m of the residence was associated with an HR for lung cancer of 1·09 (0·99-1·21). The results showed no association between lung cancer and nitrogen oxides concentration (HR 1·01 [0·95-1·07] per 20 μg/m3) or traffic intensity on the nearest street (HR 1·00 [0·97-1·04] per 5000 vehicles per day). Interpretation: Particulate matter air pollution contributes to lung cancer incidence in Europe. Funding: European Community's Seventh Framework Programme. © 2013 Elsevier Ltd.

Exposure misclassification in longitudinal studies of air pollution exposure and health effects can occur due to residential mobility in a study population over followup. The aim of this study was to investigate to what extent residential mobility during followup can be expected to cause exposure misclassification in such studies, where exposure at the baseline address is used as the main exposure assessment. The addresses for each participant in a large population-based study (N>25,000) were obtained via national registers. We used a Land Use Regression model to estimate theNOxconcentration for each participant's all addresses during the entire follow-up period (in average 14.6 years) and calculated an average concentration during followup. The Land Use Regression model explained 83% of the variation in measured levels. In summary, theNOxconcentration at the inclusion address was similar to the average concentration over followup with a correlation coefficient of 0.80, indicating that air pollution concentration at study inclusion address could be used as indicator of average air pollution concentrations over followup. The differences between an individual's inclusion and average follow-up mean concentration were small and seemed to be nondifferential with respect to a large range of factors and disease statuses, implying that bias due to residential mobility was small.

The ESCAPE study (European Study of Cohorts for Air Pollution Effects) investigates long-term effects of exposure to air pollution on human health in Europe. This paper documents the spatial variation of measured NO2 and NOx concentrations between and within 36 ESCAPE study areas across Europe. In all study areas NO2 and NOx were measured using standardized methods between October 2008 and April 2011. On average, 41 sites were selected per study area, including regional and urban background as well as street sites. The measurements were conducted in three different seasons, using Ogawa badges. Average concentrations for each site were calculated after adjustment for temporal variation using data obtained from a routine monitor background site. Substantial spatial variability was found in NO2 and NOx concentrations between and within study areas; 40% of the overall NO2 variance was attributable to the variability between study areas and 60% to variability within study areas. The corresponding values for NOx were 30% and 70%. The within-area spatial variability was mostly determined by differences between street and urban background concentrations. The street/urban background concentration ratio for NO2 varied between 1.09 and 3.16 across areas. The highest median concentrations were observed in Southern Europe, the lowest in Northern Europe. In conclusion, we found significant contrasts in annual average NO2 and NOx concentrations between and especially within 36 study areas across Europe. Epidemiological long-term studies should therefore consider different approaches for better characterization of the intra-urban contrasts, either by increasing of the number of monitors or by modelling. (C) 2012 Elsevier Ltd. All rights reserved.

Background An association between traffic air pollution and respiratory symptoms among children has been reported. However, the effects of traffic air pollution on asthma and wheeze have been very sparsely studied in areas with low traffic intensity in cold climate with poor dispersion. We evaluated the impact of vehicle traffic on childhood asthma and wheeze by objective exposure assessment. Methods As a part of the Obstructive Lung Disease in Northern Sweden (OLIN) studies, a questionnaire was sent to the families of all children attending first or second grade in Luleå (72,000 inhabitants) in Northern Sweden in 2006. The age of the children was 7-8 years and the participation rate was 98% (n = 1357). Skin prick tests were performed in 1224 (89%) children. The home addresses were given geographical coordinates and traffic counts were obtained from the local traffic authorities. A proximity model of average daily traffic and average daily heavy vehicle traffic within 200 meters from each participant's home address was used. The associations between traffic exposure and asthma and wheeze, respectively, were analysed in an adjusted multiple logistic regression model. Results Exposure to high traffic flows was uncommon in the study area; only 15% of the children lived within 200 meters from a road with a traffic flow of ≥8000 vehicles per day. Living closer than 200 meters from a road with ≥500 heavy vehicles daily was associated with current wheeze, odds ratio 1.7 (confidence interval 1.0-2.7). A dose-response relation was indicated. An increased risk of asthma was also seen, however not significant, odds ratio 1.5 (confidence interval 0.8-2.9). Stratified analyses revealed that the effect of traffic exposure was restricted to the non-sensitized phenotype of asthma and wheeze. The agreement between self-reported traffic exposure and objective measurements of exposure was moderate. Conclusions This study showed that already at low levels of exposure, vehicle traffic is related to an increased risk of wheeze among children. Thus, the global burden of traffic air pollution may be underestimated.

Objectives: To investigate the association between living near dense traffic and lung function in a cohort of adults from a single urban region. Design: Cross-sectional results from a cohort study. Setting: The adult-onset asthma and exhaled nitric oxide (ADONIX) cohort, sampled during 2001-2008 in Gothenburg, Sweden. Exposure was expressed as the distance from participants' residential address to the nearest road with dense traffic (>10 000 vehicles per day) or very dense traffic (>30 000 vehicles per day). The exposure categories were: low (>500 m; reference), medium (75-500 m) or high (

The objective of this case-control study was to evaluate whether traffic-related air pollution exposure at home increases the risk of asthma in adults and to compare two commonly used exposure variables and differences between urban and rural living. Incident cases of asthma and matched controls of subjects aged 20-60 yrs were recruited in Lulea, Sweden. In total 203 cases and 203 controls were enrolled in the study. Exposure was estimated by traffic flow and measured levels of outdoor nitrogen dioxide (NO2) in the surrounding environment of each home, respectively. The relationship between measured levels of NO2 and traffic flow was studied using linear regression. The results indicated a nonsignificant tendency between living in a home close to a high traffic flow and an increased risk of asthma. The association between asthma and measured NO2 was weak and not significant, but the skin-prick test result acted as an effect modifier with a borderline significant association among positives. The correlation between traffic flow and outdoor NO2 was low. The results suggest that living close to high traffic flows might increase the asthma incidence in adults, while the tendency for nitrogen dioxide was only seen among atopics. Traffic flow and nitrogen dioxide had a lower than expected correlation.

The aim of this study was to investigate the relation between two toxic volatile organic compounds, 1,3-butadiene and benzene, and a commonly used indicator of vehicle exhaust fumes, NO2. This was to see if NO2 can be used to indicate personal exposure to carcinogenic substances or at least estimate ambient levels measured at a stationary point. During the winter of 2001, 40 randomly selected persons living in the City of Umea (in the north of Sweden) were recruited to the study. Personal measurements of 1,3-butadiene, benzene and NO2 were performed for one week, and were repeated for 20 of the 40 participants. Additional information was gathered using a diary kept by each participant. During the same time period weekly stationary measurements were performed at one urban background station and one street station in the city centre. The results from the personal measurements showed a negligible association of NO2 with 1,3-butadiene (r = 0.06) as well as with benzene (r = 0.10), while the correlation coefficient between 1,3-butadiene and benzene was high and significant (r = 0.67). In contrast to the personal measurements, the stationary measurements showed strong relations between 1,3-butadiene, benzene and NO2 both within and in-between the street and urban background station. This study supports NO2 as a potential indicator for 1,3-butadiene and benzene levels in streets or urban background air, while the weak relations found for the personal measurements do not support the use of NO2 as an indicator for personal 1,3-butadiene and benzene exposure.

Background Exhaust emissions from vehicles is a well known problem with both epidemiological and experimental studies showing increasing adverse health effects with elevating levels. Many of the studies concerning vehicle exhausts and health are focused on health outcomes where the proportion attributed to exhaust is low, while there is less information on early and more frequent subjective indicators of adverse effects. Methods The primary aim of this study was to study perceived annoyance in relation to vehicle exhaust concentrations using modelled levels of nitrogen dioxide outside the home as an indicator with high spatial resolution. Almost 2800 persons in a random sample from three Swedish cities (Umea, Uppsala and Gothenburg) responded to our questionnaire. Questions were asked to determine the degree of annoyance related to vehicle exhausts and also the prevalence of irritating and asthmatic symptoms. Exposure was described for each participants home address by meteorological dispersion models with a 50 meter resolution. Results We found a significant increase of peoples' self-assessed annoyance with rising levels of NO2. The odds of being very annoyed by vehicle exhausts increased by 14% per 1 μg/m3 increase of the NO2 level (odds ratio (OR) = 1.14, 95% confidence interval (CI) = 1.11–1.18), and the odds of reporting the air as daily or almost daily irritating increased by 9% (OR = 1.09, 95% CI = 1.05–1.13). Also the odds of reporting asthmatic symptoms increased significantly with elevated NO2 levels (OR = 1.04, 95% CI = 1.01–1.07). Conclusion This study found the degree of annoyance related to vehicle exhaust and irritating and asthmatic symptoms to be significantly dependant on the levels of traffic related pollutants outside the home. The detailed exposure assessment lowers the degree of misclassification as compared to between-city analyses, which makes the results more accurate and applicable on the local scale.