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Objectives: The aim of this study was to determine the association between occupational biomechanical exposures and occurrence of surgically treated ulnar nerve entrapment (UNE). Methods: A cohort of 229 689 male construction workers who participated in a national occupational health surveillance program (1971–1993) were examined prospectively over a 13-year case ascertainment period (2001–2013) for surgically treated UNE. Job title (construction trade), smoking status, height, weight and age were recorded on examination. Job titles were merged into occupational groups of workers performing similar work tasks and having similar training. Occupational biomechanical exposure estimates were assigned to each occupational group with a job exposure matrix (JEM) developed for the study. Negative binomial models were used to assess the relative risks for each biomechanical exposure and the sums of highly correlated biomechanical exposures. Surgical treatment of UNE was determined via a linkage with the Swedish Hospital Outpatient Surgery Register. Results: There were 555 cases of surgically treated UNE within the cohort. Workers exposed to forceful hand-grip factors had a 1.4-fold higher relative risk (95% CI 1.18–1.63) of undergoing surgical treatment for UNE compared to unexposed workers. Occupational groups comprising workers exposed to forceful hand-grip work showed the highest risks for UNE and included concrete workers, floor layers, ground preparatory workers, rock blasters, and sheet-metal workers. Conclusion: Forceful hand-grip work increases the risk for surgically treated ulnar nerve entrapment.

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

Background: The literature on occupational risk factors for ulnar nerve entrapment (UNE), also called cubital tunnel syndrome is sparse. Objectives: The aim was study the association between occupational biomechanical exposures and UNE. Methods: The occurrence of UNE was examined prospectively in a cohort of 229 689 Swedish male construction workers who participated in a nation-wide occupational health surveillance program between 1971 and 1996. UNE case status was defined on the basis of a surgical release of ulnar nerve entrapment; case data were obtained from a national outpatient database for a 13 year observation period (2001-2013). Individual risk factors considered were smoking status, BMI and age. Biomechanical exposure estimates were assigned at the occupational group level using a job exposure matrix developed specifically for the study and included 10 ergonomic (force/posture/repetition) and 2 hand-arm vibration exposure parameters determined a priori to be relevant to UNE. Relative risks (RR) for all biomechanical factors were modelled using negative binomial regression analyses and adjusted for age, smoking habits and BMI. Results: There were 555 cases of surgically treated UNE in the cohort and the average annual incidence was 19.2 cases per 100,000 person-years. Smoking status (ever vs. never smoker RR=1.28, 95% CI=1.07-1.54) and BMI (≥25 kg/m2 vs. < 25 kg/m2 RR=1.60 , 95% CI=1.34-1.91) were associated with increased risk of UNE. Increased grip force (RR=1.54, 95% CI =1.24-1.92), hand-Arm-vibration (RR=1.35, 95% CI=1.07-1.71) upper extremity load (RR=1.63, 95% CI=1.30-1.92), and increased frequency of hand tool use (RR =1.37, 95% CI=1.09-1.71), elbow flexion and extension (RR=1.36, 95% CI=1.10-1.68), and static work (RR=1.36, 95% CI=1.12-1.65) were also associated with increased risk of UNE. Discussion and Conclusions: Our findings demonstrate that multiple biomechanical factors were associated with increased risk of UNE. Many of the identified ris

BACKGROUND: Ambient air pollution contains low concentrations of carcinogens implicated in the etiology of urinary bladder cancer (BC). Little is known about whether exposure to air pollution influences BC in the general population. OBJECTIVE: To evaluate the association between long-term exposure to ambient air pollution and BC incidence. DESIGN, SETTING, AND PARTICIPANTS: We obtained data from 15 population-based cohorts enrolled between 1985 and 2005 in eight European countries (N=303431; mean follow-up 14.1 yr). We estimated exposure to nitrogen oxides (NO2 and NOx), particulate matter (PM) with diameter <10μm (PM10), <2.5μm (PM2.5), between 2.5 and 10μm (PM2.5-10), PM2.5absorbance (soot), elemental constituents of PM, organic carbon, and traffic density at baseline home addresses using standardized land-use regression models from the European Study of Cohorts for Air Pollution Effects project. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: We used Cox proportional-hazards models with adjustment for potential confounders for cohort-specific analyses and meta-analyses to estimate summary hazard ratios (HRs) for BC incidence. RESULTS AND LIMITATIONS: During follow-up, 943 incident BC cases were diagnosed. In the meta-analysis, none of the exposures were associated with BC risk. The summary HRs associated with a 10-μg/m(3) increase in NO2 and 5-μg/m(3) increase in PM2.5 were 0.98 (95% confidence interval [CI] 0.89-1.08) and 0.86 (95% CI 0.63-1.18), respectively. Limitations include the lack of information about lifetime exposure. CONCLUSIONS: There was no evidence of an association between exposure to outdoor air pollution levels at place of residence and risk of BC. PATIENT SUMMARY: We assessed the link between outdoor air pollution at place of residence and bladder cancer using the largest study population to date and extensive assessment of exposure and comprehensive data on personal risk factors such as smoking. We found no association between the levels

Air pollution has been classified as carcinogenic to humans. However, to date little is known about the relevance for cancersof the stomach and upper aerodigestive tract (UADT). We investigated the association of long-term exposure to ambient airpollution with incidence of gastric and UADT cancer in 11 European cohorts. Air pollution exposure was assigned by land-useregression models for particulate matter (PM) below 10mm (PM10), below 2.5mm (PM2.5), between 2.5 and 10mm (PMcoarse),PM2.5absorbance and nitrogen oxides (NO2and NOX) as well as approximated by traffic indicators. Cox regression modelswith adjustment for potential confounders were used for cohort-specific analyses. Combined estimates were determined withrandom effects meta-analyses. During average follow-up of 14.1 years of 305,551 individuals, 744 incident cases of gastriccancer and 933 of UADT cancer occurred. The hazard ratio for an increase of 5mg/m3of PM2.5was 1.38 (95% CI 0.99; 1.92)for gastric and 1.05 (95% CI 0.62; 1.77) for UADT cancers. No associations were found for any of the other exposures consid-ered. Adjustment for additional confounders and restriction to study participants with stable addresses did not influencemarkedly the effect estimate for PM2.5and gastric cancer. Higher estimated risks of gastric cancer associated with PM2.5wasfound in men (HR 1.98 [1.30; 3.01]) as compared to women (HR 0.85 [0.5; 1.45]). This large multicentre cohort study showsan association between long-term exposure to PM2.5and gastric cancer, but not UADT cancers, suggesting that air pollutionmay contribute to gastric cancer risk.

BACKGROUND: Some human and animal studies have recently shown that maternal grandmother's smoking during pregnancy increases the risk of asthma in the grandchildren. We have investigated whether sex of the exposed parent and/or grandchild modifies the association between grandmaternal smoking and grandchild asthma. METHODS: We formed a cohort study based on linkage of national registries with prospectively collected data over three generations. Smoking habits in early pregnancy were registered since 1982 and purchases of prescribed medication since 2005. In all, 10329 children born since 2005 had information on maternal and grandmaternal smoking on both sides and were followed from birth up to 6 years of age. Ages when medication was purchased were used to classify the cohort into never, early transient (0-3 years), early persistent (0-3 and 4-6 years) and late-onset (4-6 years) phenotypes of childhood asthma. RESULTS: Maternal grandmother's smoking was associated with an increased odds of early persistent asthma after adjustment for maternal smoking and other confounders (odds ratio 1.29, 95% confidence interval 1.10-1.51). Grandchild sex did not modify the association. Paternal grandmother's smoking was not associated with any of the asthma phenotypes. CONCLUSION: Maternal but not paternal exposure to nicotine before conception was related to an increased risk of early persistent childhood asthma, but not other asthma phenotypes. Our findings are possibly consistent with a sex specific mode of epigenetic transfer.

BACKGROUND: There is growing interest in exposures prior to conception as possible risk factors for offspring asthma. Although partially supported by evidence from limited human studies, current evidence is inconsistent, and based on recall of exposure status. OBJECTIVE: We aimed to investigate grandmaternal smoking during pregnancy and the risk of asthma in grandchildren using prospectively collected population-based data. METHODS: Information on grandmaternal and maternal smoking during pregnancy and grandchild use of asthma medications was collected from national Swedish registries. Associations between grandmaternal smoking during pregnancy (10-12 weeks), and asthma medication use in grandchildren were investigated using generalized estimating equations. Ages at which asthma medications were prescribed classified childhood asthma into never, early transient (0-3years), late onset (3-6 years) and early persistent (0-3 and 3-6 years) phenotypes. RESULTS: From 1982 to 1986, 44,583 grandmothers gave birth to 46,197 mothers, who gave birth to 66,271 grandchildren (born 1996-2010). Children aged 1-6 years had an increased asthma risk if their grandmothers had smoked during pregnancy, with a higher risk for more exposure (10+ cigs/day; adjusted OR 1·23; 1·17, 1·30). Maternal smoking did not modify this relationship. CONCLUSIONS & CLINICAL RELEVANCE: Children had an increased risk of asthma in the first six years of life if their grandmothers smoked during early pregnancy, independent of maternal smoking. Importantly this exhibited a dose-response relationship and was associated with a persistent childhood asthma phenotype. These findings support possible epigenetic transmission of risk from environmental exposures in previous generations.

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) ≤2.5μm, ≤10μm, and 2.5–10μm 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/m(3)}, PM10 [1.07 (95% CI: 0.89, 1.30) per 10 μg/m(3)], PMcoarse[1.20 (95% CI: 0.96, 1.49 per 5 μg/m(3)], and NO(2) [1.02 (95% CI: 0.98, 1.07 per 10 μg/m(3)], and a statistically significant association with NOx [1.04 (95% CI: 1.00, 1.08) per 20 μg/m(3), p=0.04]. CONCLUSIONS: We found suggestive evidence of an association between ambient air pollution and incidence of postmenopausal breast cancer in European women.

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, Ulna 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 mu g/m(3); 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 n

Recent evidence from studies performed mainly in warm climates suggests an association between exposure to extreme temperatures late in pregnancy and an increased risk of preterm delivery. However, there have been fewer studies on the effect of low temperatures. The aim of this study is to explore the potential association between both heat and cold during late pregnancy and an increased risk of preterm birth in the northern location of Stockholm, Sweden. All singleton spontaneous births that took place in greater Stockholm (1998-2006) were included. Non-linear and delayed effects of mean temperature on the risk of preterm birth were explored through distributed lag non-linear models. Extreme and moderate heat and cold were estimated separately through quasi-Poisson regression analysis in two seasonal periods (heat in warm season, cold in cold season). The risk of preterm birth increased by 4%-5% when the mean temperature reached the 75th percentile (moderate heat) four weeks earlier (reference: the annual median value), with a maximum cumulative risk ratio of 2.50 (95% confidence interval: 1.02-6.15). Inconsistent associations were obtained for cold and extreme heat. Exposure to moderately high temperatures during late pregnancy might be associated with an increase in risk of preterm birth in Stockholm.

BACKGROUND: For the past two decades, several studies have reported associations between elevated levels of ambient air pollution and adverse pregnancy outcomes, although with varying conclusions. OBJECTIVES: To examine possible associations between the traffic pollution situation at the home address, for women who did not change address during pregnancy, and three types of pregnancy outcomes: spontaneous preterm delivery, children born small for gestational age (SGA) and pregnancy-induced hypertensive disorders. METHODS: We used data for the Greater Stockholm Area from the Swedish Medical Birth Register to construct a cohort based on all pregnancies conceived between July 1997 and March 2006, n=100 190. The pregnancy average nitrogen oxide, NOx, levels and annual mean daily vehicles at the home address were used as exposure variables. Mixed-model logistic regression was performed to assess any associations between exposure and outcome. RESULTS: There was an association between elevated traffic pollution exposure during pregnancy and pregnancy-induced hypertensive disorders. A 10 µg/m(3) increase in the pregnancy average NOx level at the home address resulted in an OR of 1.17 (95% CI 1.10 to 1.26). The 2nd to 4th quartiles of NOx were all associated with an increased risk of SGA, but there was no difference in the risk estimate among the higher quartiles. There was a tendency of a higher risk of spontaneous preterm delivery in relation to higher levels of NOx. There was no evidence of an association between vehicle flow, the cruder indicator of traffic pollution, and the studied outcomes in this study. CONCLUSIONS: In this large cohort, there was a fairly strong association between vehicle exhaust levels at the home address and pregnancy-induced hypertensive disorders, after adjustment for important risk factors.

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, Umea and Malmo, as well as a temporal model for Malmo 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 Malmo, hourly ozone data was aggregated into daily means for two measurement stations in Malmo and one in a rural area outside Malmo. Using regression analyses we inserted meteorological variables into different temporal models and the one that performed best for all three stations was chosen. For Malmo the LUR-model had an adjusted model R-2 of 0.40 and cross validation R-2 of 0.17. For Umea the model had an adjusted model R-2 of 0.67 and cross validation adjusted R-2 of 0.48. When restricting the model to only including measuring sites from urban areas, the Malmo model had adjusted model R-2 of 0.51 (cross validation adjusted R-2 0.33) and the Umea model had adjusted model R-2 of 0.81 (validation adjusted R-2 of 0.73). The temporal model had adjusted model R-2 0.54 and 0.61 for the two Malmo sites, the cross validation adjusted R-2 was 0.42. In conclusion, we can with moderate accuracy, at least for Umea, predict the spatial variability, and in Malmo the temporal variability in ozone variation.

Lack of confirmation of symptoms attributed to electromagnetic fields (EMF) and triggered by EMF exposure has highlighted the role of individual factors. Prior observations indicate intolerance to other types of environmental exposures among persons with electromagnetic hypersensitivity (EHS). This study assessed differences in odor and noise intolerance between persons with EHS and healthy controls by use of subscales and global measures of the Chemical Sensitivity Scale (CSS) and the Noise Sensitivity Scale (NSS). The EHS group scored significantly higher than the controls on all CSS and NSS scales. Correlation coefficients between CSS and NSS scores ranged from 0.60 to 0.65 across measures. The findings suggest an association between EHS and odor and noise intolerance, encouraging further investigation of individual factors for understanding EMF-related symptoms.

Background: 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. Methods: We examined whether short-term exposures to ozone (O-3), oxides of nitrogen (NOx), or particulate matter <10 m (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 O-3, NOx, and PM10 with fractions of exhaled NO at 50 and 270 ml/s. Results: An interquartile range increase in 120-hour average O-3 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. Conclusions: Exposure to O-3 was associated with a marker of distal airway inflammation, while the association was less obvious for inflammation of the proximal airways.

BACKGROUND: Land use regression (LUR) models have been developed mostly to explain intraurban variations in air pollution based on often small local monitoring campaigns. Transferability of LUR models from city to city has been investigated, but little is known about the performance of models based on large numbers of monitoring sites covering a large area. OBJECTIVES: We aimed to develop European and regional LUR models and to examine their transferability to areas not used for model development. METHODS: We evaluated LUR models for nitrogen dioxide (NO2) and particulate matter (PM; PM2.5, PM2.5 absorbance) by combining standardized measurement data from 17 (PM) and 23 (NO2) ESCAPE (European Study of Cohorts for Air Pollution Effects) study areas across 14 European countries for PM and NO2. Models were evaluated with cross-validation (CV) and hold-out validation (HV). We investigated the transferability of the models by successively excluding each study area from model building. RESULTS: The European model explained 56% of the concentration variability across all sites for NO2, 86% for PM2.5, and 70% for PM2.5 absorbance. The HV R2s were only slightly lower than the model R2 (NO2, 54%; PM2.5, 80%; PM2.5 absorbance, 70%). The European NO2, PM2.5, and PM2.5 absorbance models explained a median of 59%, 48%, and 70% of within-area variability in individual areas. The transferred models predicted a modest-to-large fraction of variability in areas that were excluded from model building (median R2: NO2, 59%; PM2.5, 42%; PM2.5 absorbance, 67%). CONCLUSIONS: Using a large data set from 23 European study areas, we were able to develop LUR models for NO2 and PM metrics that predicted measurements made at independent sites and areas reasonably well. This finding is useful for assessing exposure in health studies conducted in areas where no measurements were conducted.

BACKGROUND: Air pollution has been associated with cardiovascular mortality, but it remains unclear as to whether specific pollutants are related to specific cardiovascular causes of death. Within the multicenter European Study of Cohorts for Air Pollution Effects (ESCAPE), we investigated the associations of long-term exposure to several air pollutants with all cardiovascular disease (CVD) mortality, as well as with specific cardiovascular causes of death. METHODS: Data from 22 European cohort studies were used. Using a standardized protocol, study area-specific air pollution exposure at the residential address was characterized as annual average concentrations of the following: nitrogen oxides (NO2 and NOx); particles with diameters of less than 2.5 μm (PM2.5), less than 10 μm (PM10), and 10 μm to 2.5 μm (PMcoarse); PM2.5 absorbance estimated by land-use regression models; and traffic indicators. We applied cohort-specific Cox proportional hazards models using a standardized protocol. Random-effects meta-analysis was used to obtain pooled effect estimates. RESULTS: The total study population consisted of 367,383 participants, with 9994 deaths from CVD (including 4,992 from ischemic heart disease, 2264 from myocardial infarction, and 2484 from cerebrovascular disease). All hazard ratios were approximately 1.0, except for particle mass and cerebrovascular disease mortality; for PM2.5, the hazard ratio was 1.21 (95% confidence interval = 0.87-1.69) per 5 μg/m and for PM10, 1.22 (0.91-1.63) per 10 μg/m. CONCLUSION: In a joint analysis of data from 22 European cohorts, most hazard ratios for the association of air pollutants with mortality from overall CVD and with specific CVDs were approximately 1.0, with the exception of particulate mass and cerebrovascular disease mortality for which there was suggestive evidence for an association.

Estimating within-city variability in air pollution concentrations is important. Land use regression (LUR) models are able to explain such small-scale within-city variations. Transparency in LUR model development methods is important to facilitate comparison of methods between different studies. We therefore developed LUR models in a standardized way in 36 study areas in Europe for the ESCAPE (European Study of Cohorts for Air Pollution Effects) project. Nitrogen dioxide (NO2) and nitrogen oxides (NOx) were measured with Ogawa passive samplers at 40 or 80 sites in each of the 36 study areas. The spatial variation in each area was explained by LUR modeling. Centrally and locally available Geographic Information System (GIS) variables were used as potential predictors. A leave-one out cross-validation procedure was used to evaluate the model performance. There was substantial contrast in annual average NO2 and NOx concentrations within the study areas. The model explained variances (R2) of the LUR models ranged from 55% to 92% (median 82%) for NO2 and from 49% to 91% (median 78%) for NOx. For most areas the cross-validation R2 was less than 10% lower than the model R2. Small-scale traffic and population/household density were the most common predictors. The magnitude of the explained variance depended on the contrast in measured concentrations as well as availability of GIS predictors, especially traffic intensity data were important. In an additional evaluation, models in which local traffic intensity was not offered had 10% lower R2 compared to models in the same areas in which these variables were offered. Within the ESCAPE project it was possible to develop LUR models that explained a large fraction of the spatial variance in measured annual average NO2 and NOx concentrations. These LUR models are being used to estimate outdoor concentrations at the home addresses of participants in over 30 cohort studies.

OBJECTIVES: Our aim was to study the possible associations between exposure to elevated levels of air pollution, ozone (O(3)) and vehicle exhaust (NO(x)), during early gestation, and adverse pregnancy outcomes such as pre-eclampsia, preterm birth and small for gestational age. DESIGN: Prospective register-based cohort study. SETTING: The Swedish Medical Birth Register includes data on all deliveries during 1998 to 2006 in Greater Stockholm, Sweden. The national Patient Register and the Prescribed Drug Register were used to collect information on maternal asthma. PARTICIPANTS: All singleton pregnancies, conceived at the earliest in August 1997 and at the latest in February 2006, were included, n=120 755. OUTCOME MEASURES: We studied preterm birth, small for gestational age and pre-eclampsia. RESULTS: 4.4% of pregnancies resulted in a preterm birth. The prevalence of pre-eclampsia was 2.7%. We observed an association between first trimester O(3) and preterm birth (OR 1.04, 95% CI 1.01 to 1.08) as well as an association with pre-eclampsia (OR 1.04, 95% CI 1.01 to 1.08), per 10 µg/m(3) increase in O(3). We observed no association between first trimester NO(x) and adverse pregnancy outcomes. No associations were observed between any of the air pollutants and small for gestational age. CONCLUSIONS: Increased levels of O(3) during the first trimester increased the risk of pre-eclampsia and preterm birth. Air pollutants did not exhibit any effects on fetal growth restriction. We estimated 1 in every 20 cases of pre-eclampsia to be associated with O(3) exposure.

There is growing evidence of adverse birth outcomes due to exposure to air pollution during gestation. However, recent negative studies are also reported. The aim of this study was to assess the effect of ozone and vehicle exhaust exposure (NO2) on the length of the gestational period and risk of preterm delivery. We used data from the Swedish Medical Birth Registry on all vaginally delivered singleton births in the Greater Stockholm area who were conceived during 1987–1995 (n = 115,588). Daily average levels of NO2 (from three measuring stations) and ozone (two stations) were used to estimate trimester and last week of gestation average exposures. Linear regression models were used to assess the association between the two air pollutants and three exposure windows, while logistic regression models were used when analyzing associations with preterm delivery ( < 37 weeks gestation). Five percent were born preterm. The median gestational period was 40 weeks. Higher levels of ozone during the first trimester were associated with shorter gestation as well as with an elevated risk of preterm delivery, the odds ratio from the most complex model was 1.06 (95% CI: 1.00–1.13) per 10 μg/m3 increase in the mean daily 8-h maximum concentration. Higher levels of ozone during the second trimester were associated with shorter gestation but the elevated risk of preterm delivery was not statistically significant. Higher levels of ozone and NO2 during the last week of gestation were associated with a shorter duration of gestation and NO2 also with preterm delivery. There were no significant associations between first and second trimester NO2 exposure estimates and studied outcomes. The effect of first trimester ozone exposure, known to cause oxidative stress, was smallest among women who conceived during autumn when vitamin D status, important for fetal health, in Scandinavian women is the highest.Keywords: pregnancy; preterm birth; vehicle emissions; ozone; nitrogen dioxide

Luftföroreningar är ett känt folkhälsoproblem i tätorter där trafiken oftast är den största enskilda emissionskällan. Det finns dock andra källor som lokalt kan ge upphov till höga luftföroreningshalter och en sådan är småskalig biobränsleeldning. För att begränsa hälsoeffekterna av luftföroreningar finns normvärden reglerade i lagstiftning, och övervakningen av dessa kan ske via mätningar eller olika typer av beräkningar. Syftet med projekt har varit att tillämpa en typ av statistisk beräkningsmodell, ”Land Use Regression (LUR)”, för att predicera halterna av luftföroreningarna bensen och 1,3-butadien i ett antal tätorter med hög andel småskalig biobränsleeldning i och omkring Umeå. Principen för en LUR-modell är att först förklara variationen i luftföroreningshalter mellan ett begränsat antal mätpunkter med skillnader i geografiska variabler, som t.ex. populationsdensitet och trafikflöde inom olika radier runt respektive mätplats. Sedan kan modellen användas för att beräkna halten i många fler punkter. I denna studie har bensen och 1,3-butadien mätts vid tre tillfällen på 39 olika mätpunkter. Geografisk information har samlats in för respektive mätpunkt, och innefattar bland annat trafikvariabler men även uppgifter om biobränsleeldning baserat på uppgifter från sotarregister. LUR-modellen har byggts upp i enlighet med den procedur som finns beskrivet inom ett stort europeiskt forskningsprojekt, ESCAPE. Rapporten visar att det är möjligt utifrån geografiska variabler att predicera halten bensen och 1,3-butadien i en given punkt med acceptabel precision. Resultaten visar också att befolkningstäthet tillsammans med småskalig biobränsleeldning och trafik är de variabler som gemensamt är viktigast för årsmedelhalten bensen och 1,3-butadien. Denna typ av modell är således tillämpbar för att kartlägga och predicera halter av bensen och 1,3-butadien i områden med småskalig biobränsleeldning. Modellen kan även användas för att studera betydelsen av nyetablering av småskali

BACKGROUND: A seasonal effect of month of birth and risk of allergic disease has been suggested by numerous studies. Few studies have directly measured pollen exposures at different points during pregnancy and in early life, and assessed their effects on risk of respiratory disease outcomes. METHODS: Pollen exposure was calculated for the first and last 12 weeks of pregnancy and the first 12 weeks of infancy for all children conceived by women residing in Stockholm, Sweden, between 1988 and 1995. Hospital admission data for respiratory conditions in the first year of life was also collected. RESULTS: Out of 110,381 children, 940 had been hospitalised for asthma by 12-months of age. Pollen levels showed both marked seasonal variations and between year differences. Exposure to high levels of pollen in the last 12 weeks of pregnancy was associated with an increased risk of asthma hospitalisation (aOR = 1.35, 95% CI = 1.07-1.71 for highest quartile versus remaining infants). Exposure to high levels of pollen in the first three months of life was associated with a reduced risk (aOR = 0.76, 95% CI = 0.59-0.98) but only in children of heavy smoking mothers. CONCLUSIONS: High levels of pollen exposure during late pregnancy were somewhat unexpectedly associated with an elevated risk of hospitalisation for asthma within the first year of life.