TY  - JOUR
AB  - BACKGROUND: Increased lung-cancer risks for low socioeconomic status (SES) groups are only partially attributable to smoking habits. Little effort has been made to investigate the persistent risks related to low SES by quantification of potential biases. METHODS: Based on 12 case-control studies, including 18 centers of the international SYNERGY project (16,550 cases, 20,147 controls), we estimated controlled direct effects (CDE) of SES on lung cancer via multiple logistic regression, adjusted for age, study center, and smoking habits, and stratified by sex. We conducted mediation analysis by inverse odds ratio weighting to estimate natural direct effects (NDE) and natural indirect effects via smoking habits. We considered misclassification of smoking status, selection bias, and unmeasured mediator-outcome confounding by genetic risk, both separately as well as by multiple quantitative bias analysis, using bootstrap to create 95% simulation intervals (SI). RESULTS: Mediation analysis of lung-cancer risks for SES estimated mean proportions of 43% in men and 33% in women attributable to smoking. Bias analyses decreased direct effects of SES on lung cancer, with selection bias showing the strongest reduction in lung-cancer risk in the multiple bias analysis. Lung-cancer risks remained increased for lower SES groups, with higher risks in men [4th versus 1st (highest) SES quartile: CDE 1.50 (SI 1.32-1.69)] than women [CDE 1.20 (SI 1.01-1.45)]. NDE were similar to CDE, particularly in men. CONCLUSIONS: Bias adjustment lowered direct lung-cancer risk estimates of lower SES groups. However, risks for low SES remained elevated, likely attributable to occupational hazards or other environmental exposures.
AU  - Hovanec, J.*
AU  - Kendzia, B.*
AU  - Olsson, A.*
AU  - Schüz, J.*
AU  - Kromhout, H.*
AU  - Vermeulen, R.C.H.*
AU  - Peters, S.*
AU  - Gustavsson, P.*
AU  - Migliore, E.*
AU  - Radoi, L.*
AU  - Barul, C.*
AU  - Consonni, D.*
AU  - Caporaso, N.E.*
AU  - Landi, M.T.*
AU  - Field, J.K.*
AU  - Karrasch, S.
AU  - Wichmann, H.-E.
AU  - Siemiatycki, J.*
AU  - Parent, M.E.*
AU  - Richiardi, L.*
AU  - Simonato, L.*
AU  - Jöckel, K.H.*
AU  - Ahrens, W.*
AU  - Pohlabeln, H.*
AU  - Fernández-Tardón, G.*
AU  - Zaridze, D.*
AU  - McLaughlin, J.R.*
AU  - Demers, P.A.*
AU  - Świątkowska, B.*
AU  - Lissowska, J.*
AU  - Pándics, T.*
AU  - Fabianova, E.*
AU  - Mates, D.*
AU  - Schejbalova, M.*
AU  - Foretova, L.*
AU  - Janout, V.*
AU  - Boffetta, P.*
AU  - Forastiere, F.*
AU  - Straif, K.*
AU  - Brüning, T.*
AU  - Behrens, T.*
C1  - 72113
C2  - 56527
CY  - Two Commerce Sq, 2001 Market St, Philadelphia, Pa 19103 Usa
SP  - 245-252
TI  - Socioeconomic status, smoking, and lung cancer: Mediation and bias analysis in the SYNERGY study.
JO  - Epidemiology
VL  - 36
IS  - 2
PB  - Lippincott Williams & Wilkins
PY  - 2024
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - BACKGROUND: The association between fine particulate matter (PM2.5) and mortality widely differs between as well as within countries. Differences in PM2.5 composition can play a role in modifying the effect estimates, but there is little evidence about which components have higher impacts on mortality. METHODS: We applied a two-stage analysis on data collected from 210 locations in 16 countries. In the first stage, we estimated location-specific relative risks (RR) for mortality associated with daily total PM2.5 through time series regression analysis. We then pooled these estimates in a meta-regression model that included city-specific logratio-transformed proportions of seven PM2.5 components as well as meta-predictors derived from city-specific socio-economic and environmental indicators. RESULTS: We found associations between RR and several PM2.5 components. Increasing the ammonium (NH4+) proportion from 1% to 22%, while keeping a relative average proportion of other components, increased the RR from 1.0063 (95%CI: 1.0030-1.0097) to 1.0102 (95%CI:1.0070-1.0135). Conversely, an increase in nitrate (NO3-) from 1% to 71% resulted in a reduced RR, from 1.0100 (95%CI: 1.0067-1.0133) to 1.0037 (95%CI: 0.9998- 1.0077). Differences in composition explained a substantial part of the heterogeneity in PM2.5 risk. CONCLUSIONS: These findings contribute to the identification of more hazardous emission sources. Further work is needed to understand the health impacts of PM2.5 components and sources given the overlapping sources and correlations among many components.
AU  - Masselot, P.*
AU  - Sera, F.*
AU  - Schneider, R.*
AU  - Kan, H.*
AU  - Lavigne, E.*
AU  - Stafoggia, M.*
AU  - Tobias, A.*
AU  - Chen, H.*
AU  - Burnett, R.T.*
AU  - Schwartz, J.*
AU  - Zanobetti, A.*
AU  - Bell, M.L.*
AU  - Chen, B.Y.*
AU  - Leon Guo, Y.L.*
AU  - Ragettli, M.S.*
AU  - Vicedo-Cabrera, A.M.*
AU  - Åström, C.*
AU  - Forsberg, B.*
AU  - Iñiguez, C.*
AU  - Garland, R.M.*
AU  - Scovronick, N.*
AU  - Madureira, J.*
AU  - Nunes, B.*
AU  - De la Cruz Valencia, C.*
AU  - Hurtado Diaz, M.*
AU  - Honda, Y.*
AU  - Hashizume, M.*
AU  - Fook Cheng Ng, C.*
AU  - Samoli, E.*
AU  - Katsouyanni, K.*
AU  - Schneider, A.E.
AU  - Breitner-Busch, S.
AU  - Ryti, N.R.I.*
AU  - Jaakkola, J.J.K.*
AU  - Maasikmets, M.*
AU  - Orru, H.*
AU  - Guo, Y.*
AU  - Valdés Ortega, N.*
AU  - Matus Correa, P.*
AU  - Tong, S.*
AU  - Gasparrini, A.*
C1  - 63910
C2  - 51788
CY  - Two Commerce Sq, 2001 Market St, Philadelphia, Pa 19103 Usa
SP  - 167-175
TI  - Differential mortality risks associated with PM2.5 components: A multi-country, multi-city study.
JO  - Epidemiology
VL  - 33
IS  - 2
PB  - Lippincott Williams & Wilkins
PY  - 2022
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - BACKGROUND: Due to the non-randomized nature of real-world data, prognostic factors need to be balanced, which is often done by propensity scores (PS). This study aimed to investigate whether autoencoders, which are unsupervised deep learning architectures, might be leveraged to compute PS. METHODS: We selected patient-level data of 128,368 first-line treated cancer patients from the Flatiron Health EHR-derived de-identified database. We trained an autoencoder architecture to learn a lower-dimensional patient representation, which we used to compute PS. To compare the performance of an autoencoder-based PS with established methods, we performed a simulation study. We assessed the balancing and adjustment performance using standardized mean differences (SMD), root-mean-square-errors (RMSE), percent bias and confidence interval (CI) coverage. To illustrate the application of the autoencoder-based PS, we emulated the PRONOUNCE trial by applying the trial's protocol elements within an observational database setting, comparing two chemotherapy regimens. RESULTS: All methods but the manual variable selection approach led to well-balanced cohorts with average SMDs <0.1. LASSO yielded on average the lowest deviation of resulting estimates (RMSE 0.0205) followed by the autoencoder approach (RMSE 0.0248). Altering the hyperparameter setup in sensitivity analysis, the autoencoder approach led to similar results as LASSO (RMSE 0.0203 and 0.0205, respectively). In the case study, all methods provided a similar conclusion with point estimates clustered around the null (e.g. HRautoencoder 1.01 [95% CI 0.80-1.27] vs. HRPRONOUNCE 1.07 [0.83-1.36]). INTERPRETATION: Autoencoder-based PS computation was a feasible approach to control for confounding but did not perform better than some established approaches like LASSO.
AU  - Weberpals, J.*
AU  - Becker, T.*
AU  - Davies, J.*
AU  - Schmich, F.*
AU  - Rüttinger, D.*
AU  - Theis, F.J.
AU  - Bauer-Mehren, A.*
C1  - 61502
C2  - 50320
CY  - Two Commerce Sq, 2001 Market St, Philadelphia, Pa 19103 Usa
SP  - 378-388
TI  - Deep learning-based propensity scores for confounding control in comparative effectiveness research: A large-scale, real-world data study.
JO  - Epidemiology
VL  - 32
IS  - 3
PB  - Lippincott Williams & Wilkins
PY  - 2021
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - BACKGROUND: Exposure to air pollution during pregnancy may increase attention-deficit/hyperactivity disorder (ADHD) symptoms in children, but findings have been inconsistent. We aimed to study this association in a collaborative study of eight European population-based birth/child cohorts, including 29,127 mother-child pairs. METHODS: Air pollution concentrations (nitrogen dioxide [NO2] and particulate matter [PM]) were estimated at the birth address by land-use regression models based on monitoring campaigns performed between 2008 and 2011. We extrapolated concentrations back in time to exact pregnancy periods. Teachers or parents assessed ADHD symptoms at 3-10 years of age. We classified children as having ADHD symptoms within the borderline/clinical range and within the clinical range using validated cutoffs. We combined all adjusted area-specific effect estimates using random-effects meta-analysis and multiple imputations and applied inverse probability-weighting methods to correct for loss to follow-up. RESULTS: We classified a total of 2,801 children as having ADHD symptoms within the borderline/clinical range, and 1,590 within the clinical range. Exposure to air pollution during pregnancy was not associated with a higher odds of ADHD symptoms within the borderline/clinical range (e.g., adjusted odds ratio [OR] for ADHD symptoms of 0.95, 95% confidence interval [CI] = 0.89, 1.01 per 10 µg/m increase in NO2 and 0.98, 95% CI = 0.80, 1.19 per 5 µg/m increase in PM2.5). We observed similar associations for ADHD within the clinical range. CONCLUSIONS: There was no evidence for an increase in risk of ADHD symptoms with increasing prenatal air pollution levels in children aged 3-10 years. See video abstract at, http://links.lww.com/EDE/B379.
AU  - Forns, J.*
AU  - Sunyer, J.*
AU  - García-Esteban, R.*
AU  - Porta, D.*
AU  - Ghassabian, A.*
AU  - Giorgis-Allemand, L.*
AU  - Gong, T.*
AU  - Gehring, U.*
AU  - Sørensen, M.*
AU  - Standl, M.
AU  - Sugiri, D.*
AU  - Almqvist, C.*
AU  - Andiarena, A.*
AU  - Badaloní, C.*
AU  - Beelen, R.*
AU  - Berdel, D.*
AU  - Cesaroni, G.*
AU  - Charles, M.A.*
AU  - Eriksen, K.T.*
AU  - Estarlich, M.*
AU  - Fernández, M.F.*
AU  - Forhan, A.*
AU  - Jaddoe, V.W.V.*
AU  - Korek, M.*
AU  - Lichtenstein, P.*
AU  - Lertxundi, A.*
AU  - Lopez-Espinosa, M.J.*
AU  - Markevych, I.
AU  - de Nazelle, A.*
AU  - Raaschou-Nielsen, O.*
AU  - Nieuwenhuijsen, M.*
AU  - Pérez-Lobato, R.*
AU  - Philippat, C.*
AU  - Slama, R.*
AU  - Tiesler, C.M.
AU  - Verhulst, F.C.*
AU  - von Berg, A.*
AU  - Vrijkotte, T.G.*
AU  - Nybo Andersen, A.M.*
AU  - Heude, B.*
AU  - Krämer, U.*
AU  - Heinrich, J.
AU  - Tiemeier, H.*
AU  - Forastiere, F.*
AU  - Pershagen, G.*
AU  - Brunekreef, B.*
AU  - Guxens, M.*
C1  - 53681
C2  - 44947
CY  - Two Commerce Sq, 2001 Market St, Philadelphia, Pa 19103 Usa
SP  - 618-626
TI  - Air pollution exposure during pregnancy and symptoms of attention deficit and hyperactivity disorder in children in Europe.
JO  - Epidemiology
VL  - 29
IS  - 5
PB  - Lippincott Williams & Wilkins
PY  - 2018
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - BACKGROUND: Although mercury exposure has been associated with several adverse health effects, the association with childhood asthma is under-investigated. Therefore, we explore the association between mercury and childhood asthma in a population with low mercury levels. METHODS: Mercury levels were measured in blood and urine in 1,056 children aged 5-14 years. In addition to including questions about asthma diagnosis and wheezing, the study measured bronchial hyper-responsiveness and allergic sensitization to common aeroallergens. Logistic regression analysis adjusted for major potential confounders. RESULTS: Overall the adjusted odds ratios (aOR) between log blood mercury and the outcomes were 0.8 (95% CI 0.63, 1.11) for asthma, 0.9 (95% CI 0.79, 1.14) for wheeze, 1.1 (95% CI 0.60, 2.03) for bronchial hyperresponsiveness, and 1.0 (95% CI 0.80, 1.17) for allergic sensitization. Urine mercury adjusted for creatinine was also not associated with any of these allergy-related outcomes. CONCLUSIONS: While the results did not support an association between mercury exposure and asthma, studies are needed to assess prenatal and lifetime exposure to mercury and asthma.
AU  - Heinrich, J.
AU  - Feng, G.*
AU  - Trepka, M.J.*
C1  - 49764
C2  - 40938
CY  - Philadelphia
SP  - 116-118
TI  - Low-level mercury exposure and risk of Asthma in school-age children.
JO  - Epidemiology
VL  - 28
IS  - 1
PB  - Lippincott Williams & Wilkins
PY  - 2017
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - BACKGROUND: Evidence is limited regarding risk and the shape of the exposure-response curve at low asbestos exposure levels. We estimated the exposure-response for occupational asbestos exposure and assessed the joint effect of asbestos exposure and smoking by sex and lung cancer subtype in general population studies. METHODS: We pooled 14 case-control studies conducted in 1985-2010 in Europe and Canada, including 17,705 lung cancer cases and 21,813 controls with detailed information on tobacco habits and lifetime occupations. We developed a quantitative job-exposure-matrix to estimate job-, time period-, and region-specific exposure levels. Fiber-years (ff/ml-years) were calculated for each subject by linking the matrix with individual occupational histories. We fit unconditional logistic regression models to estimate odds ratios (ORs), 95% confidence intervals (CIs), and trends. RESULTS: The fully adjusted OR for ever-exposure to asbestos was 1.24 (95% CI, 1.18, 1.31) in men and 1.12 (95% CI, 0.95, 1.31) in women. In men, increasing lung cancer risk was observed with increasing exposure in all smoking categories and for all three major lung cancer subtypes. In women, lung cancer risk for all subtypes was increased in current smokers (ORs ~two-fold). The joint effect of asbestos exposure and smoking did not deviate from multiplicativity among men, and was more than additive among women. CONCLUSIONS: Our results in men showed an excess risk of lung cancer and its subtypes at low cumulative exposure levels, with a steeper exposure-response slope in this exposure range than at higher, previously studied levels. (See video abstract at, http://links.lww.com/EDE/B161.).  
AU  - Olsson, A.C.*
AU  - Vermeulen, R.*
AU  - Schüz, J.*
AU  - Kromhout, H.*
AU  - Pesch, B.*
AU  - Peters, S.*
AU  - Behrens, T.*
AU  - Portengen, L.*
AU  - Mirabelli, D.*
AU  - Gustavsson, P.*
AU  - Kendzia, B.*
AU  - Almansa, J.*
AU  - Luzon, V.*
AU  - Vlaanderen, J.*
AU  - Stücker, I.*
AU  - Guida, F.*
AU  - Consonni, D.*
AU  - Caporaso, N.*
AU  - Landi, M.T.*
AU  - Field, J.*
AU  - Brüske, I.
AU  - Wichmann, H.-E.
AU  - Siemiatycki, J.*
AU  - Parent, M.-E.*
AU  - Richiardi, L.*
AU  - Merletti, F.*
AU  - Jöckel, K.-H.*
AU  - Ahrens, W.*
AU  - Pohlabeln, H.*
AU  - Plato, N.*
AU  - Tardón, A.*
AU  - Zaridze, D.*
AU  - McLaughlin, J.*
AU  - Demers, P.*
AU  - Szeszenia-Dabrowska, N.*
AU  - Lissowska, J.*
AU  - Rudnai, P.*
AU  - Fabianova, E.*
AU  - Stanescu Dumitru, R.*
AU  - Bencko, V.*
AU  - Foretova, L.*
AU  - Janout, V.*
AU  - Boffetta, P.*
AU  - Bueno-de-Mesquita, H.B.*
AU  - Forastiere, F.*
AU  - Brüning, T*
AU  - Straif, K.*
C1  - 50561
C2  - 42359
CY  - Philadelphia
SP  - 288-299
TI  - Exposure-response analyses of asbestos and lung cancer subtypes in a pooled analysis of case-control studies.
JO  - Epidemiology
VL  - 28
IS  - 2
PB  - Lippincott Williams & Wilkins
PY  - 2017
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Epidemiologic evidence on the association between short-term exposure to ultrafine particles and mortality is weak, due to the lack of routine measurements of these particles and standardized multicenter studies. We investigated the relationship between ultrafine particles and particulate matter (PM) and daily mortality in eight European urban areas. METHODS: We collected daily data on nonaccidental and cardiorespiratory mortality, particle number concentrations (as proxy for ultrafine particle number concentration), fine and coarse PM, gases and meteorologic parameters in eight urban areas of Finland, Sweden, Denmark, Germany, Italy, Spain, and Greece, between 1999 and 2013. We applied city-specific time-series Poisson regression models and pooled them with random-effects meta-analysis. RESULTS: We estimated a weak, delayed association between particle number concentration and nonaccidental mortality, with mortality increasing by approximately 0.35% per 10,000 particles/cm increases in particle number concentration occurring 5 to 7 days before death. A similar pattern was found for cause-specific mortality. Estimates decreased after adjustment for fine particles (PM2.5) or nitrogen dioxide (NO2). The stronger association found between particle number concentration and mortality in the warmer season (1.14% increase) became null after adjustment for other pollutants. CONCLUSIONS: We found weak evidence of an association between daily ultrafine particles and mortality. Further studies are required with standardized protocols for ultrafine particle data collection in multiple European cities over extended study periods.
AU  - Stafoggia, M.*
AU  - Schneider, A.E.
AU  - Cyrys, J.
AU  - Samoli, E.*
AU  - Jovanovic, Z.*
AU  - Bedada, G.B.*
AU  - Bellander, T.*
AU  - Cattani, G.*
AU  - Eleftheriadis, K.*
AU  - Faustini, A.*
AU  - Hoffmann, B.*
AU  - Jacquemin, B.*
AU  - Katsouyanni, K.*
AU  - Massling, A.*
AU  - Pekkanen, J.*
AU  - Perez, N.*
AU  - Peters, A.
AU  - Quass, U.*
AU  - Yli-Tuomi, T.*
AU  - Forastiere, F.*
C1  - 50562
C2  - 42360
CY  - Philadelphia
SP  - 172-180
TI  - Association between short-term exposure to ultrafine particles and mortality in Eight European Urban Areas.
JO  - Epidemiology
VL  - 28
IS  - 2
PB  - Lippincott Williams & Wilkins
PY  - 2017
SN  - 1044-3983
ER  - 

TY  - JOUR
AU  - Beyerlein, A.
AU  - Markevych, I.
AU  - Thiering, E.
AU  - Warncke, K.
AU  - Heinrich, J.
AU  - Ziegler, A.-G.
C1  - 48247
C2  - 41012
CY  - Philadelphia
SP  - E26-E28
TI  - Response to: Ambient air pollution is not associated with early manifestation of type 1 diabetes.
JO  - Epidemiology
VL  - 27
IS  - 4
PB  - Lippincott Williams & Wilkins
PY  - 2016
SN  - 1044-3983
ER  - 

TY  - JOUR
AU  - Rosenbauer, J.
AU  - Tamayo, T.*
AU  - Bächle, C.*
AU  - Stahl-Pehe, A.*
AU  - Landwehr, S.*
AU  - Sugiri, D.*
AU  - Krämer, U.*
AU  - Maier, W.
AU  - Hermann, J.M.*
AU  - Holl, R.W.*
AU  - Rathmann, W.*
C1  - 48293
C2  - 41002
CY  - Philadelphia
SP  - E25-E26
TI  - Re: Ambient air pollution and early manifestation of type 1 diabetes.
JO  - Epidemiology
VL  - 27
IS  - 4
PB  - Lippincott Williams & Wilkins
PY  - 2016
SN  - 1044-3983
ER  - 

TY  - JOUR
AU  - Wakeford, R.
AU  - Auvinen, A.*
AU  - Gent, R.N.*
AU  - Jacob, P.
AU  - Kesminiene, A.*
AU  - Laurier, D.*
AU  - Schüz, J.*
AU  - Shore, R.*
AU  - Walsh, L.*
AU  - Zhang, W.*
C1  - 47821
C2  - 39521
CY  - Philadelphia
SP  - E20-E21
TI  - Re: Thyroid cancer among young people in Fukushima.
JO  - Epidemiology
VL  - 27
IS  - 3
PB  - Lippincott Williams & Wilkins
PY  - 2016
SN  - 1044-3983
ER  - 

TY  - JOUR
AU  - Beyerlein, A.
AU  - Krasmann, M.
AU  - Thiering, E.
AU  - Kusian, D.
AU  - Markevych, I.
AU  - D'Orlando, O.
AU  - Warncke, K.*
AU  - Jochner, S.*
AU  - Heinrich, J.
AU  - Ziegler, A.-G.
C1  - 43260
C2  - 36369
CY  - Philadelphia
SP  - e31-e32
TI  - Ambient air pollution and early manifestation of type 1 diabetes.
JO  - Epidemiology
VL  - 26
IS  - 3
PB  - Lippincott Williams & Wilkins
PY  - 2015
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - BACKGROUND: Long-term exposure to particulate matter (PM) has been associated with increased cardiovascular morbidity and mortality but little is known about the role of the chemical composition of PM. This study examined the association of residential long-term exposure to PM components with incident coronary events. METHODS: Eleven cohorts from Finland, Sweden, Denmark, Germany, and Italy participated in this analysis. 5,157 incident coronary events were identified within 100,166 persons followed on average for 11.5 years. Long-term residential concentrations of PM < 10 μm (PM10), PM < 2.5 μm (PM2.5), and a priori selected constituents (copper, iron, nickel, potassium, silicon, sulfur, vanadium, and zinc) were estimated with land-use regression models. We used Cox proportional hazard models adjusted for a common set of confounders to estimate cohort-specific component effects with and without including PM mass, and random effects meta-analyses to pool cohort-specific results. RESULTS: A 100 ng/m³ increase in PM10 K and a 50 ng/m³ increase in PM2.5 K were associated with a 6% (hazard ratio and 95% confidence interval: 1.06 [1.01, 1.12]) and 18% (1.18 [1.06, 1.32]) increase in coronary events. Estimates for PM10 Si and PM2.5 Fe were also elevated. All other PM constituents indicated a positive association with coronary events. When additionally adjusting for PM mass, the estimates decreased except for K. CONCLUSIONS: This multicenter study of 11 European cohorts pointed to an association between long-term exposure to PM constituents and coronary events, especially for indicators of road dust.
AU  - Wolf, K.
AU  - Stafoggia, M.*
AU  - Cesaroni, G.*
AU  - Andersen, Z.J.*
AU  - Beelen, R.*
AU  - Galassi, C.*
AU  - Hennig, F.*
AU  - Migliore, E.*
AU  - Penell, J.*
AU  - Ricceri, F.*
AU  - Sørensen, M.*
AU  - Turunen, A.W.*
AU  - Hampel, R.
AU  - Hoffmann, B.*
AU  - Kälsch, H.*
AU  - Laatikainen, T.*
AU  - Pershagen, G.*
AU  - Raaschou-Nielsen, O.*
AU  - Sacerdote, C.*
AU  - Vineis, P.*
AU  - Badaloni, C.*
AU  - Cyrys, J.
AU  - de Hoogh, K.*
AU  - Eriksen, K.T.*
AU  - Jedynska, A.*
AU  - Keuken, M.*
AU  - Kooter, I.M.*
AU  - Lanki, T.*
AU  - Ranzi, A.*
AU  - Sugiri, D.*
AU  - Tsai, M.Y.*
AU  - Wang, M.*
AU  - Hoek, G.*
AU  - Brunekreef, B.*
AU  - Peters, A.
AU  - Forastiere, F.*
C1  - 44872
C2  - 37072
CY  - Philadelphia
SP  - 565-574
TI  - Long-term exposure to particulate matter constituents and the incidence of coronary events in 11 European cohorts.
JO  - Epidemiology
VL  - 26
IS  - 4
PB  - Lippincott Williams & Wilkins
PY  - 2015
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Background: Heat waves and air pollution are both associated with increased mortality. Their joint effects are less well understood. Methods: We explored the role of air pollution in modifying the effects of heat waves on mortality, within the EuroHEAT project. Daily mortality, meteorologic, and air pollution data from nine European cities for the years 1990-2004 were assembled. We defined heat waves by taking both intensity and duration into account. The city-specific effects of heat wave episodes were estimated using generalized estimating equation models, adjusting for potential confounders with and without inclusion of air pollutants (particles, ozone, nitrogen dioxide, sulphur dioxide, carbon monoxide). To investigate effect modification, we introduced an interaction term between heat waves and each single pollutant in the models. Random effects meta-analysis was used to summarize the city-specific results. Results: The increase in the number of daily deaths during heat wave episodes was 54% higher on high ozone days compared with low, among people age 75-84 years. The heat wave effect on high PM10 days was increased by 36% and 106% in the 75-84 year and 85+ year age groups, respectively. A similar pattern was observed for effects on cardiovascular mortality. Effect modification was less evident for respiratory mortality, although the heat wave effect itself was greater for this cause of death. The heat wave effect was smaller (15-30%) after adjustment for ozone or PM10. Conclusions: The heat wave effect on mortality was larger during high ozone or high PM10 days. When assessing the effect of heat waves on mortality, lack of adjustment for ozone and especially PM10 overestimates effect parameters. This bias has implications for public health policy.
AU  - Analitis, A.*
AU  - Michelozzi, P.*
AU  - D'Ippoliti, D.*
AU  - de'Donato, F.*
AU  - Menne, B.*
AU  - Matthies, F.*
AU  - Atkinson, R.W.*
AU  - Iñiguez, C.*
AU  - Basagana, X.*
AU  - Schneider, A.E.
AU  - Lefranc, A.*
AU  - Paldy, A.*
AU  - Bisanti, L.*
AU  - Katsouyanni, K.*
C1  - 28791
C2  - 30793
SP  - 15-22
TI  - Effects of heat waves on mortality: Effect modification and confounding by air pollutants.
JO  - Epidemiology
VL  - 25
IS  - 1
PB  - Lippincott Williams & Wilkins
PY  - 2014
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - 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.
AU  - Beelen, R.*
AU  - Stafoggia, M.*
AU  - Raaschou-Nielsen, O.*
AU  - Andersen, Z.J.*
AU  - Xun, W.W.*
AU  - Katsouyanni, K.*
AU  - Dimakopoulou, K.*
AU  - Brunekreef, B.*
AU  - Weinmayr, G.*
AU  - Hoffmann, B.*
AU  - Wolf, K.
AU  - Samoli, E.*
AU  - Houthuijs, D.*
AU  - Nieuwenhuijsen, M.*
AU  - Oudin, A.*
AU  - Forsberg, B.*
AU  - Olsson, D.*
AU  - Salomaa, V.*
AU  - Lanki, T.*
AU  - Yli-Tuomi, T.*
AU  - Oftedal, B.*
AU  - Aamodt, G.*
AU  - Nafstad, P.*
AU  - de Faire, U.*
AU  - Pedersen, N.L.*
AU  - Ostenson, C.G.*
AU  - Fratiglioni, L.*
AU  - Penell, J.*
AU  - Korek, M.*
AU  - Pyko, A.*
AU  - Eriksen, K.T.*
AU  - Tjønneland, A.*
AU  - Becker, T.*
AU  - Eeftens, M.*
AU  - Bots, M.L.*
AU  - Meliefste, K.*
AU  - Wang, M.*
AU  - Bueno-de-Mesquita, H.B.*
AU  - Sugiri, D.*
AU  - Krämer, U.*
AU  - Heinrich, J.
AU  - de Hoogh, K.*
AU  - Key, T.*
AU  - Peters, A.
AU  - Cyrys, J.
AU  - Concin, H.*
AU  - Nagel, G.*
AU  - Ineichen, A.*
AU  - Schaffner, E.*
AU  - Probst-Hensch, N.*
AU  - Dratva, J.*
AU  - Ducret-Stich, R.*
AU  - Vilier, A.*
AU  - Clavel-Chapelon, F.*
AU  - Stempfelet, M.*
AU  - Grioni, S.*
AU  - Krogh, V.*
AU  - Tsai, M.Y.*
AU  - Marcon, A.*
AU  - Ricceri, F.*
AU  - Sacerdote, C.*
AU  - Galassi, C.*
AU  - Migliore, E.*
AU  - Ranzi, A.*
AU  - Cesaroni, G.*
AU  - Badaloni, C.*
AU  - Forastiere, F.*
AU  - Tamayo, I.*
AU  - Amiano, P.*
AU  - Dorronsoro, M.*
AU  - Katsoulis, M.*
AU  - Trichopoulou, A.*
AU  - Vineis, P.*
AU  - Hoek, G.*
C1  - 30773
C2  - 33851
CY  - Philadelphia
SP  - 368-378
TI  - Long-term exposure to air pollution and cardiovascular mortality : An analysis of 22 European cohorts.
JO  - Epidemiology
VL  - 25
IS  - 3
PB  - Lippincott Williams & Wilkins
PY  - 2014
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - BACKGROUND:: Previous studies have found relationships between DNA methylation and various environmental contaminant exposures. Associations with weather have not been examined. Because temperature and humidity are related to mortality even on non-extreme days, we hypothesized that temperature and relative humidity may affect methylation. METHODS:: We repeatedly measured methylation on long interspersed nuclear elements (LINE-1), Alu, and 9 candidate genes in blood samples from 777 elderly men participating in the Normative Aging Study (1999-2009). We assessed whether ambient temperature and relative humidity are related to methylation on LINE-1 and Alu, as well as on genes controlling coagulation, inflammation, cortisol, DNA repair, and metabolic pathway. We examined intermediate-term associations of temperature, relative humidity, and their interaction with methylation, using distributed lag models. RESULTS:: Temperature or relative humidity levels were associated with methylation on tissue factor (F3), intercellular adhesion molecule 1 (ICAM-1), toll-like receptor 2 (TRL-2), carnitine O-acetyltransferase (CRAT), interferon gamma (IFN-γ), inducible nitric oxide synthase (iNOS), and glucocorticoid receptor, LINE-1, and Alu. For instance, a 5°C increase in 3-week average temperature in ICAM-1 methylation was associated with a 9% increase (95% confidence interval: 3% to 15%), whereas a 10% increase in 3-week average relative humidity was associated with a 5% decrease (-8% to -1%). The relative humidity association with ICAM-1 methylation was stronger on hot days than mild days. CONCLUSIONS:: DNA methylation in blood cells may reflect biological effects of temperature and relative humidity. Temperature and relative humidity may also interact to produce stronger effects.
AU  - Bind, M.A.*
AU  - Zanobetti, A.*
AU  - Gasparrini, A.*
AU  - Peters, A.
AU  - Coull, B.*
AU  - Baccarelli, A.*
AU  - Tarantini, L.*
AU  - Koutrakis, P.*
AU  - Vokonas, P.*
AU  - Schwartz, J.*
C1  - 31246
C2  - 34253
CY  - Philadelphia
SP  - 561-569
TI  - Effects of temperature and relative humidity on DNA methylation.
JO  - Epidemiology
VL  - 25
IS  - 4
PB  - Lippincott Williams & Wilkins
PY  - 2014
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - BACKGROUND:: Negative effects of long-term exposure to particulate matter (PM) on lung function have been shown repeatedly. Spatial differences in the composition and toxicity of PM may explain differences in observed effect sizes between studies. METHODS:: We conducted a multicenter study in 5 European birth cohorts-BAMSE (Sweden), GINIplus and LISAplus (Germany), MAAS (United Kingdom), and PIAMA (The Netherlands)-for which lung function measurements were available for study subjects at the age of 6 or 8 years. Individual annual average residential exposure to copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc within PM smaller than 2.5 μm (PM2.5) and smaller than 10 μm (PM10) was estimated using land-use regression models. Associations between air pollution and lung function were analyzed by linear regression within cohorts, adjusting for potential confounders, and then combined by random effects meta-analysis. RESULTS:: We observed small reductions in forced expiratory volume in the first second, forced vital capacity, and peak expiratory flow related to exposure to most elemental pollutants, with the most substantial negative associations found for nickel and sulfur. PM10 nickel and PM10 sulfur were associated with decreases in forced expiratory volume in the first second of 1.6% (95% confidence interval = 0.4% to 2.7%) and 2.3% (-0.1% to 4.6%) per increase in exposure of 2 and 200 ng/m, respectively. Associations remained after adjusting for PM mass. However, associations with these elements were not evident in all cohorts, and heterogeneity of associations with exposure to various components was larger than for exposure to PM mass. CONCLUSIONS:: Although we detected small adverse effects on lung function associated with annual average levels of some of the evaluated elements (particularly nickel and sulfur), lower lung function was more consistently associated with increased PM mass.
AU  - Eeftens, M.
AU  - Hoek, G.*
AU  - Gruzieva, O.*
AU  - Mölter, A.*
AU  - Agius, R.M.*
AU  - Beelen, R.*
AU  - Brunekreef, B.*
AU  - Custovic, A.*
AU  - Cyrys, J.
AU  - Fuertes, E.
AU  - Heinrich, J.
AU  - Hoffmann, B.*
AU  - de Hoogh, K.*
AU  - Jedynska, A.*
AU  - Keuken, M.*
AU  - Klümper, C.*
AU  - Kooter, I.M.*
AU  - Krämer, U.*
AU  - Korek, M.*
AU  - Koppelman, G.H.*
AU  - Kuhlbusch, T.A.J.*
AU  - Simpson, A.*
AU  - Smit, H.A.*
AU  - Tsai, M.Y.*
AU  - Wang, M.*
AU  - Wolf, K.
AU  - Pershagen, G.*
AU  - Gehring, U.*
C1  - 31813
C2  - 34780
CY  - Philadelphia
SP  - 648-657
TI  - Elemental composition of particulate matter and the association with lung function.
JO  - Epidemiology
VL  - 25
IS  - 5
PB  - Lippincott Williams & Wilkins
PY  - 2014
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - BACKGROUND:: Accumulating evidence from laboratory animal and human studies suggests that air pollution exposure during pregnancy affects cognitive and psychomotor development in childhood. METHODS:: We analyzed data from 6 European population-based birth cohorts-GENERATION R (The Netherlands), DUISBURG (Germany), EDEN (France), GASPII (Italy), RHEA (Greece), and INMA (Spain)-that recruited mother-infant pairs from 1997 to 2008. Air pollution levels-nitrogen oxides (NO2, NOx) in all regions and particulate matter (PM) with diameters of <2.5, <10, and 2.5-10 μm (PM2.5, PM10, and PMcoarse, respectively) and PM2.5 absorbance in a subgroup-at birth addresses were estimated by land-use regression models, based on monitoring campaigns performed primarily between 2008 and 2011. Levels were back-extrapolated to exact pregnancy periods using background monitoring sites. Cognitive and psychomotor development was assessed between 1 and 6 years of age. Adjusted region-specific effect estimates were combined using random-effects meta-analysis. RESULTS:: A total of 9482 children were included. Air pollution exposure during pregnancy, particularly NO2, was associated with reduced psychomotor development (global psychomotor development score decreased by 0.68 points [95% confidence interval = -1.25 to -0.11] per increase of 10 μg/m in NO2). Similar trends were observed in most regions. No associations were found between any air pollutant and cognitive development. CONCLUSIONS:: Air pollution exposure during pregnancy, particularly NO2 (for which motorized traffic is a major source), was associated with delayed psychomotor development during childhood. Due to the widespread nature of air pollution exposure, the public health impact of the small changes observed at an individual level could be considerable.
AU  - Guxens, M.*
AU  - García-Esteban, R.*
AU  - Giorgis-Allemand, L.*
AU  - Forns, J.*
AU  - Badaloni, C.*
AU  - Ballester, F.*
AU  - Beelen, R.*
AU  - Cesaroni, G.*
AU  - Chatzi, L.*
AU  - de Agostini, M.*
AU  - de Nazelle, A.*
AU  - Eeftens, M.*
AU  - Fernández, M.F.*
AU  - Fernández-Somoano, A.*
AU  - Forastiere, F.*
AU  - Gehring, U.*
AU  - Ghassabian, A.*
AU  - Heude, B.*
AU  - Jaddoe, V.W.*
AU  - Klümper, C.*
AU  - Kogevinas, M.*
AU  - Krämer, U.*
AU  - Larroque, B.*
AU  - Lertxundi, A.*
AU  - Lertxuni, N.*
AU  - Murcia, M.*
AU  - Navel, V.*
AU  - Nieuwenhuijsen, M.*
AU  - Porta, D.*
AU  - Ramos, R.*
AU  - Roumeliotaki, T.*
AU  - Slama, R.*
AU  - Sørensen, M.*
AU  - Stephanou, E.G.*
AU  - Sugiri, D.*
AU  - Tardón, A.*
AU  - Tiemeier, H.*
AU  - Tiesler, C.M.
AU  - Verhulst, F.C.*
AU  - Vrijkotte, T.G.*
AU  - Wilhelm, M.*
AU  - Brunekreef, B.*
AU  - Pershagen, G.*
AU  - Sunyer, J.*
C1  - 31779
C2  - 34769
CY  - Philadelphia
SP  - 636-647
TI  - Air pollution during pregnancy and childhood cognitive and psychomotor development: Six European birth cohorts.
JO  - Epidemiology
VL  - 25
IS  - 5
PB  - Lippincott Williams & Wilkins
PY  - 2014
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Background: Although several studies have examined associations between temperature and cardiovascular-disease-related mortality, fewer have investigated the association between temperature and the development of acute myocardial infarction (MI). Moreover, little is known about who is most susceptible to the effects of temperature. Methods: We analyzed data from the Worcester Heart Attack Study, a community-wide investigation of acute MI in residents of the Worcester (MA) metropolitan area. We used a case-crossover approach to examine the association of apparent temperature with acute MI occurrence and with all-cause in-hospital and postdischarge mortality. We examined effect modification by sociodemographic characteristics, medical history, clinical complications, and physical environment. Results: A decrease in an interquartile range in apparent temperature was associated with an increased risk of acute MI on the same day (hazard ratio = 1.15 [95% confidence interval = 1.01-1.31]). Extreme cold during the 2 days prior was associated with an increased risk of acute MI (1.36 [1.07-1.74]). Extreme heat during the 2 days prior was also associated with an increased risk of mortality (1.44 [1.06-1.96]). Persons living in areas with greater poverty were more susceptible to heat. Conclusions: Exposure to cold increased the risk of acute MI, and exposure to heat increased the risk of dying after an acute MI. Local area vulnerability should be accounted for as cities prepare to adapt to weather fluctuations as a result of climate change.
AU  - Madrigano, J.*
AU  - Mittleman, M.A.*
AU  - Baccarelli, A.*
AU  - Goldberg, R.*
AU  - Melly, S.*
AU  - von Klot, S.
AU  - Schwartz, J.*
C1  - 24270
C2  - 31493
SP  - 439-446
TI  - Temperature, myocardial infarction, and mortality: Effect modification by individual- and area-level characteristics.
JO  - Epidemiology
VL  - 24
IS  - 3
PB  - Lippincott Williams & Wilkins
PY  - 2013
SN  - 1044-3983
ER  - 

TY  - JOUR
AU  - Markevych, I.*
AU  - Wolf, K.
AU  - Hampel, R.
AU  - Breitner-Busch, S.
AU  - Schneider, A.
AU  - von Klot, S.
AU  - Cyrys, J.
AU  - Heinrich, J.
AU  - Döring, A.
AU  - Beelen, R.*
AU  - Koenig, W.*
AU  - Peters, A.
C1  - 27945
C2  - 32871
SP  - 934-935
TI  - Air pollution and liver enzymes.
JO  - Epidemiology
VL  - 24
IS  - 6
PB  - Lippincott Williams & Wilkins
PY  - 2013
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - BACKGROUND: Epidemiologic studies have reported inconsistent findings for the association between air pollution levels and blood pressure (BP), which has been studied mainly in elderly subjects. Short-term air pollution effects on BP have not been investigated in pregnant women, who may constitute a vulnerable population. METHODS: Between 2002 and 2006, 1500 pregnant women from a mother-child cohort study conducted in Nancy and Poitiers, France, underwent 11,220 repeated BP measurements (average, 7.5 measurements/woman). Nitrogen dioxide (NO₂), particulate matter with an aerodynamic diameter below 10 μm (PM₁₀), and meteorologic variables were measured on an hourly basis at permanent monitoring sites. We studied changes of BP in relation to short-term variations of air pollution and temperature with mixed models adjusted for meteorologic and personal characteristics. RESULTS: A 10°C decrease in temperature led to an increase in systolic BP of 0.5% (95% confidence interval = 0.1% to 1.0%). Elevated NO₂-levels 1 day, 5 days and averaged over 7 days before the BP measurement were associated with reduced systolic BP. The strongest decrease was observed for the 7-day NO₂ average (-0.4% [-0.7% to -0.2%] change for an 11 μg/m³ increase in NO₂). PM₁₀ effects on systolic BP differed according to pregnancy trimester: PM₁₀ concentration was associated with systolic BP increases during the first trimester and systolic BP decreases later in pregnancy. CONCLUSIONS: We observed short-term associations of air pollution and of temperature with BP in pregnant women. Whether such changes in BP have clinical implications remains to be investigated.
AU  - Hampel, R.
AU  - Lepeule, J.*
AU  - Schneider, A.E.
AU  - Bottagisi, S.*
AU  - Charles, M.A.*
AU  - Ducimetiere, P.*
AU  - Peters, A.
AU  - Slama, R.*
C1  - 6163
C2  - 28850
SP  - 671-679
TI  - Short-term impact of ambient air pollution and air temperature on blood pressure among pregnant women.
JO  - Epidemiology
VL  - 22
IS  - 5
PB  - Lippincott Williams&Wilkins
PY  - 2011
SN  - 1044-3983
ER  - 

TY  - JOUR
AU  - Hampel, R.
AU  - Wichmann, H.-E.
AU  - Peters, A.
AU  - Breitner-Busch, S.
AU  - Schneider, A.E.
AU  - Zareba, W.*
AU  - Kraus, U.
AU  - Cyrys, J.
AU  - Geruschkat, U.
AU  - Belcredi, P.
AU  - Müller-Nurasyid, M.
C1  - 60086
C2  - 0
CY  - Two Commerce Sq, 2001 Market St, Philadelphia, Pa 19103 Usa
SP  - S134-S134
TI  - Association Between Air Pollution and SDNN is Modified by SNPs Involved in Cardiac Rhythm in Individuals With Diabetes or Impaired Glucose Tolerance.
JO  - Epidemiology
VL  - 22
IS  - 1
PB  - Lippincott Williams & Wilkins
PY  - 2011
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Otitis media is the leading reason young children receive antibiotics or visit a physician. We evaluated the impact of ambient air pollution on outpatient physician visits for otitis media in a population-based birth cohort. All children born in southwestern British Columbia during 1999-2000 were followed until the age of 2 years. Residential air pollution exposures were estimated for the first 24 months of life by inverse-distance weighting of monitor data (CO, NO, NO2, O3, PM2.5, PM10, SO2), temporally adjusted land-use regression models (NO, NO2, PM2.5, black carbon, woodsmoke), and proximity to roads and point sources. We used generalized estimating equations to longitudinally assess the relationship between physician visits for otitis media (ICD-9) and average pollutant exposure in the 2 months prior to the visit, after adjustment for covariates. Complete exposure and risk-factor data were available for 45,513 children (76% of all births). A total of 42% of subjects had 1 or more physician visits for otitis media during follow-up. Adjusted estimates for NO, PM2.5, and woodsmoke were consistently elevated (eg, relative risk of 1.10 [95% confidence interval = 1.07-1.12] per interquartile range [IQR] increase in NO; 1.32 [1.27-1.36] per IQR increase in days of woodsmoke exposure). No increased risks were observed for the remaining pollutants (eg, 1.00 [0.98-1.03] per IQR increase in PM10; 0.99 [0.97-1.01] per IQR increase in black carbon). Modest but consistent associations were found between some measures of air pollution and otitis media in a large birth cohort exposed to relatively low levels of ambient air pollution
AU  - MacIntyre, E.A.
AU  - Karr, C.J.*
AU  - Koehoorn, M.*
AU  - Demers, P.A.*
AU  - Tamburic, L.*
AU  - Lencar, C.*
AU  - Brauer, M.
C1  - 6307
C2  - 28470
CY  - Philadelphia, USA
SP  - 81-89
TI  - Residential air pollution and otitis media during the first two years of life.
JO  - Epidemiology
VL  - 22
IS  - 1
PB  - Lippincott Williams & Wilkins
PY  - 2011
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Background: Certain subgroups in the general population, such as persons with existing cardiovascular or respiratory disease, may be more likely to experience adverse health effects from air pollution. Methods: In this European multicenter study, 25,006 myocardial infarction (MI) survivors in 5 cities were recruited from 1992 to 2002 via registers, and daily mortality was followed for 6 to 12 years in relation to ambient particulate and gaseous air pollution exposure. Daily air pollution levels were obtained from central monitor sites, and particle number concentrations were measured in 2001 and estimated retrospectively based on measured pollutants and meteorology. City-specific effect estimates from time-series analyses with Poisson regression were pooled over all 5 cities. Results: Particle number concentrations and PM, averaged over 2 days (lag 0-1) were associated with increased total nontrauma mortality for patients of age 35 to 74 (5.6% [95% confidence interval, 2.8%-8.5%] per 10,000/cm(3) and 5.1% [1.6%-9.3%] per 10 mu g/m(3), respectively). For longer averaging times (5 and 15 days), carbon monoxide and nitrogen dioxide were also associated with mortality. There were no clear associations with ozone or sulfur dioxide. Conclusion: Exposure to traffic-related air pollution was associated with daily mortality in M1 survivors. Point estimates suggest a stronger effect of air pollution in MI survivors than among the general population.
AU  - Berglind, N.*
AU  - Bellander, T.
AU  - Forastiere, F.*
AU  - von Klot, S.
AU  - Aalto, P.*
AU  - Elosua, R.*
AU  - Kulmala, M.*
AU  - Lanki., T.*
AU  - Löwel, H.
AU  - Peters, A.
AU  - Picciotto, S.*
AU  - Salomaa, V.*
AU  - Stafoggia, M.*
AU  - Sunyer, J.*
AU  - Nyberg, F.*
C1  - 2403
C2  - 26185
SP  - 110-118
TI  - Ambient air pollution and daily mortality among survivors of myocardial infarction.
JO  - Epidemiology
VL  - 20
IS  - 1
PB  - Lippincott Williams & Wilkins
PY  - 2009
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Background: Few studies have investigated new onset of asthma in adults in relation to air pollution. The aim of this study is to investigate the association between modeled background levels of traffic-related air pollution at the subjects' home addresses and self-reported asthma incidence in a European adult population. Methods: Adults from the European Respiratory Health Survey were included (n = 4185 from 17 cities). Subjects' home addresses were geocoded and linked to outdoor nitrogen dioxide (NO,) estimates, as a marker of local traffic-related pollution. We obtained this information from the I-km background NO, surface modeled in APMoSPHERE (Air Pollution Modelling for Support to Policy on Health and Environmental Risk in Europe). Asthma incidence was defined as reporting asthma in the follow-up (1999 to 2001) but not in the baseline (1991 to 1993). Results: A positive association was found between NO, and asthma incidence (odds ratio 1.43; 95% confidence interval = 1.02 to 2.01) per 10 mu g/m(3). Results were homogeneous among centers (P value for heterogeneity = 0.59). Conclusions: We found an association between a marker of traffic-related air pollution and asthma incidence in European adults.
AU  - Jacquemin, B.*
AU  - Sunyer, J.*
AU  - Forsberg, B.*
AU  - Aguilera, I.*
AU  - Briggs, D.*
AU  - García-Esteban, R.*
AU  - Götschi, T.*
AU  - Heinrich, J.
AU  - Järvholm, B.*
AU  - Jarvis, D.*
AU  - Vienneau, D.*
AU  - Künzli, N.*
C1  - 951
C2  - 26113
SP  - 119-126
TI  - Home outdoor NO₂ and new onset of self-reported asthma in adults.
JO  - Epidemiology
VL  - 20
IS  - 1
PB  - Lippincott Williams & Wilkins
PY  - 2009
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Background: Particulate air pollution has been consistently related to cardiovascular mortality. Some evidence Suggests that particulate matter may accelerate the atherosclerotic process. Effects of within-city variations of particulate air pollution on survival after an acute cardiovascular event have been little explored. Methods: We conducted a cohort study of hospital survivors of acute myocardial infarction (MI) from file Worcester, MA, metropolitan area to investigate the long-term effects of within-city variation in traffic-related air pollution on mortality. The study builds on an ongoing community-wide investigation examining changes over time in MI incidence and case-fatality rates. We included confirmed cases of MI in 1995, 1997, 1999, 2001, and 2003. Long-term survival status was ascertained through 2005. A validated spatiotemporal land use regression model for traffic-related air pollution was developed and annual averages of elemental carbon at residence estimated. The effect of estimated elemental carbon on the long-term mortality of patients discharged after MI was analyzed using a Cox proportional hazards model, controlling for a variety of demographic, medical history, and clinical variables. Results: Of the 3895 patients with validated MI, 44% died during follow-up. Exposure to estimated elemental carbon in the year of entry into the study was 0.44 mu g/m(3) on average. All-cause mortality increased by 15% (95% confidence interval = 0.03%-29%) per interquartile range increase in estimated yearly elemental carbon (0.24 mu g/m(3)) after the second year of survival. No association between traffic-related pollution and all-cause mortality was observed during the first 2 years of follow-up. Conclusions: Chronic traffic-related particulate air pollution is associated with increased mortality in hospital survivors of acute MI after the second year of survival.
AU  - von Klot, S.
AU  - Gryparis, A.*
AU  - Tonne, C.*
AU  - Yanosky, J.*
AU  - Coull, B.A.*
AU  - Goldberg, R.J.*
AU  - Lessard, D.*
AU  - Melly, S.J.*
AU  - Suh, H.H.*
AU  - Schwartz, J.*
C1  - 1609
C2  - 26241
SP  - 547-554
TI  - Elemental carbon exposure at residence and survival after acute myocardial infarction.
JO  - Epidemiology
VL  - 20
IS  - 4
PB  - Lippincott Williams & Wilkins
PY  - 2009
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Epidemiological studies have shown that extremes in ambient temperature are associated with short term increases in mortality. To control for seasonality, most previous time series studies used non-parametric functions of time. We conducted a US multi-city study evaluating whether adjustment for influenza epidemics changes the exposure-response function of temperature, and whether controlling for the remaining seasonal pattern could be modeled more simply. Counts of daily cardiovascular deaths and of emergency hospital admissions of the elderly for pneumonia during 1992-2000 were obtained for 48 cities. Applying city-specific Quasi-Poisson regression models we estimated the association between daily cardiovascular mortality and temperature. Models included day-of-the-week indicators and regression splines of temperature, relative humidity, barometric pressure. In the base model a regression spline of date with five degrees of freedom (df) per year captured trend and seasonality. In the alternative model a regression spline of pneumonia admissions, a sinusoidal function of time, and a regression spline of date with ten df were included instead. Temperatures were lower in the north-east compared to the south-west and the range differed greatly. The alternative model fit the data better than the base model based on GSV-scores, capturing well the regular seasonal pattern as well as the irregular pattern of the outcome. The temperature-response function was mostly U- or J-shaped and not greatly affected by adjusting for influenza. The pooled estimated increase in risk for a temperature decrease from 0 to -5°C was 1.6% (95% confidence interval (CI) 0.9-2.4%) in the base and 1.9% (95% CI 1.2-2.6%) in the alternative model. This study on the effect of temperature on mortality shows that including epidemic data explained most of the irregular seasonal pattern, allowing more parsimonious models than when adjusting for seasonality only with smooth functions of time. The effect of cold temperature is not confounded by epidemics.
AU  - von Klot, S.
AU  - Zanobetti, A.*
AU  - Schwartz, J.*
C1  - 5496
C2  - 27917
SP  - S252-S252
TI  - Influenza epidemics, seasonality, and the effects of cold weather on cardiovascular mortality.
JO  - Epidemiology
VL  - 20
IS  - 6
PB  - Lippincott Williams & Wilkins
PY  - 2009
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Lung function is an important measure of respiratory health and a predictor of cardiorespiratory morbidity and mortality. Over the past 2 decades, more than 50 publications have investigated long-term effects of ambient air pollution on lung function with most finding adverse effects. Several studies have also suggested effects from traffic-related air pollution. There is strong support for air pollution effects on the development of lung function in children and adolescents. It remains unclear whether subjects with slower development of lung function compensate by prolonging the growth phase, or whether they end their development at a lower plateau, thus entering the decline phase with a reduced lung function. In adults, the evidence for long-term air pollution effects is mostly based on cross-sectional comparisons. One recent longitudinal study observed that decreasing pollution attenuated the decline of lung function in adults. Earlier inconclusive cohort studies were based on limited data. There is great diversity in study designs, markers of air pollution, approaches to the measurement of exposure, and choices in lung function measures. These limit the comparability of studies and impede quantitative summaries. New studies should use individual-level exposure assessment to clarify the role of traffic and to preclude potential community-level confounding. Further research is needed on the relevance of specific pollution sources, particularly with regard to susceptible populations and relevant exposure periods throughout life.
AU  - Götschi, T.*
AU  - Heinrich, J.
AU  - Sunyer, J.*
AU  - Künzli, N.*
C1  - 2072
C2  - 25728
SP  - 690-701
TI  - Long-term effects of ambient air pollution on lung function: A review.
JO  - Epidemiology
VL  - 19
IS  - 5
PB  - Lippincott Williams & Wilkins
PY  - 2008
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Temperature changes have been associated with increased cardiovascular risk, but the role of inflammatory markers in this relationship is not well understood. The objective of this study was to analyze the association between air temperature and C-reactive protein, interleukin-6 and fibrinogen in postmyocardial infarction patients. METHODS: In a multicenter panel study, the 3 inflammatory blood markers were measured repeatedly. In total, 5813 blood samples in 1003 subjects were collected in 6 European cities representing different climates. Data on patient characteristics and disease history were gathered at the baseline visit. Meteorologic data were obtained from the city-specific network stations. The association was analyzed using a semiparametric model with random patient effects. RESULTS: A 10 degrees C decrease in the 5-day-average of air temperature before the blood withdrawal was associated with a 4% increase in C-reactive protein (4.3% [95% confidence interval = 0.2% to 8.1%]). Correspondingly, an increase of interleukin-6 was observed for the same time window (3.3% [0.1% to 6.3%]) whereas fibrinogen showed an increase of 1.3% (0.2% to 2.4%) with a lag of 3 days. CONCLUSION: A decrease in air temperature, particularly the average temperature of the last 5 days, was associated with an increase in both C-reactive protein and interleukin-6, whereas fibrinogen seemed to react to temperature changes after 3 days. In susceptible patients this might lead to an additional risk for cardiovascular events and suggests a biologic mechanism for the observed seasonal variation in death from ischemic heart disease and stroke in the elderly.
AU  - Schneider, A.E.
AU  - Panagiotakos, D.*
AU  - Picciotto, S.*
AU  - Katsouyanni, K.*
AU  - Löwel, H.
AU  - Jacquemin, B.*
AU  - Lanki, T.*
AU  - Stafoggia, M.*
AU  - Bellander, T.*
AU  - Koenig, W.*
AU  - Peters, A.
AU  - AIRGENE Study Group ()
C1  - 2200
C2  - 25251
SP  - 391-400
TI  - Air temperature and inflammatory responses in myocardial infarction survivors.
JO  - Epidemiology
VL  - 19
IS  - 3
PB  - Lippincott Williams & Wilkins
PY  - 2008
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - A recent analysis indicates that the excess odds ratio for lung cancer by smoking is described by a function that is linear in pack-years and exponential in the logarithm of smoking intensity and its square (Cancer Epidemiol Biomarkers Prev. 2006;15:517-523). The model suggests that below 15-20 cigarettes per day there is a "direct exposure rate" effect, ie, the excess odds ratio per pack-year for higher intensity (and shorter duration) smokers is greater than for lower-intensity (and longer duration) smokers. Above 20 cigarettes per day, there is an "inverse-exposure-rate" effect, ie, the excess odds ratio per pack-year for higher intensity smokers is smaller than for lower-intensity smokers. Using pooled data from 2 large case-control studies of lung cancer (the European Smoking and Health Study and the German Radon Study), we evaluated effect modification of the association between smoking and lung cancer. Interaction effects are very specific. Variations in risk of lung cancer with years since cessation of smoking, age, method of inhalation, and type of cigarette result from interactions with smoking intensity, and not total pack-years. In contrast, risk variations by sex result from the interaction with total pack-years, while intensity effects are homogeneous. Risk variations by age at which smoking started result from interactions with both total pack-years and intensity. All intensity interactions are homogeneous across studies.The specificity of the interactions may provide clues for the molecular basis of the smoking and lung cancer relationship.
AU  - Lubin, J. H.*
AU  - Caporaso, N.*
AU  - Wichmann, H.-E.
AU  - Schaffrath Rosario, A.*
AU  - Alavanja, M.C. R.*
C1  - 2202
C2  - 24588
SP  - 639-648
TI  - Cigarette smoking and lung cancer: Modeling effect modification of total exposure and intensity.
JO  - Epidemiology
VL  - 18
IS  - 5
PB  - Lippincott Williams & Wilkins
PY  - 2007
SN  - 1044-3983
ER  - 

TY  - JOUR
AU  - Gehring, U.
AU  - Heinrich, J.
AU  - Krämer, U.*
AU  - Grote, V.
AU  - Hochadel, M.
AU  - Sugiri, D.*
AU  - Kraft, M.*
AU  - Rauchfuss, K.*
AU  - Eberwein, H.G.*
AU  - Wichmann, H.-E.
C1  - 2932
C2  - 24045
SP  - 545-551
TI  - Long-term exposure to ambient air pollution and cardiopulmonary mortality in woman.
JO  - Epidemiology
VL  - 17
PY  - 2006
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - BACKGROUND: In health surveys, considerable effort and expense are invested to achieve a high response proportion and thereby to reduce selection bias. We investigated the interrelation of recruitment efforts and expense with potential nonresponse bias based on data from a large health survey. METHODS: In a population-based health survey, a stratified sample of 6640 residents of the Augsburg (Germany) region was selected, of whom 4261 attended the main study between October 1999 and April 2001. A short telephone interview yielded additional information on nearly half of the nonparticipants. All recruitment contacts were documented, and expenses were estimated on the basis of unit costs. Different recruitment strategies were modeled retrospectively. We compared their cost savings as well as their influence on the response proportion and on prevalence estimates. RESULTS: The distribution of total contacting cost per individual was highly skewed with 50% of the total sum spent on 17% of the sample. Late responders showed many similarities with nonresponders; both included a higher percentage of people with impaired health and with greater behavioral health risks. We were able to identify recruitment strategies that may save up to 25% of the recruitment costs without significant shift in the parameter estimates. Data collected in the short nonresponder interview proved to be important to correct for possible nonresponse bias. CONCLUSIONS: In general, prolonged recruitment efforts lead to a larger and more representative sample but at increasing marginal costs. Specific cost-saving recruitment strategies that do not enhance response bias can be suggested. Interviews of nonresponders are also useful.  
AU  - Holle, R.
AU  - Hochadel, M.*
AU  - Reitmeir, P.
AU  - Meisinger, C.
AU  - Wichmann, H.-E.
AU  - KORA Study Group (Holle, R.
AU  - John, J.
AU  - Illig, T.
AU  - Peters, A.
AU  - Meisinger, C.
AU  - Wichmann, H.-E.)
C1  - 4300
C2  - 23910
SP  - 639-643
TI  - Prolonged recruitment efforts in health surveys: Effects on response, cost and potential bias.
JO  - Epidemiology
VL  - 17
IS  - 6
PY  - 2006
SN  - 1044-3983
ER  - 

TY  - JOUR
AU  - Slama, R.*
AU  - Morgenstern, V.
AU  - Bouyer, J.*
AU  - Heinrich, J.
C1  - 227
C2  - 24286
SP  - S. 129
TI  - Exposure to traffic-related atmospheric pollutants during pregnancy and term birth weight: A cohort study relying on a stochastic exposure model.
JO  - Epidemiology
VL  - 17
PY  - 2006
SN  - 1044-3983
ER  - 

TY  - JOUR
AU  - Slama, R.*
AU  - Sinno-Tellier, S.*
AU  - Thiebaugeorges, O.*
AU  - Goua, V.*
AU  - Forhan, A.*
AU  - Ducot, B.*
AU  - Annesi-Maesano, I.*
AU  - Heinrich, J.*
AU  - Schweitzer, M.*
AU  - Magnin, G.*
AU  - Bouyer, J.*
AU  - Kaminski, M.*
AU  - Charles, M.A.*
C1  - 2099
C2  - 24287
SP  - 129-130
TI  - Relation between atmospheric pollutants and head circumference in utero and at birth: A cohort study relying on ultrasound imaging during pregnancy.
JO  - Epidemiology
VL  - 17
IS  - 6
PY  - 2006
SN  - 1044-3983
ER  - 

TY  - JOUR
AU  - Wjst, M.
C1  - 1506
C2  - 22574
SP  - 131 S.
TI  - Anonymizing personal identifiers in genetic epidemiologic studies.
JO  - Epidemiology
VL  - 16
IS  - 1
PY  - 2005
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Background: The aim of this article was to investigate the size and possible causes of the reported excess in coronary events on Mondays.
      
      	
      		
      			
      				
      				
      					Methods: We conducted a metaanalysis of data from the World Health Organization (WHO) MONICA Project, which monitored trends and determinants in cardiovascular disease. The MONICA Project was undertaken in 21 countries from 1980 to 1995.
      			
      		
      	
      
      
      	
      		
      			
      				
      				
      					Results: We found a small overall excess rate of coronary events on Mondays. In a population experiencing 100 events per week, we estimate there would be approximately 1 more event on Monday than on any other day. Hierarchical logistic regression showed that the Monday excess was greater in centers with less thorough data collection procedures.
      			
      		
      	
      
      
      	
      
      	Conclusions: The excess of coronary events on Mondays is probably an artifact resulting from events with uncertain dates being coded as taking place on Mondays.
AU  - Barnett, A.G.*
AU  - Dobson, A.J.*
AU  - WHO MONICA Project (Bolte, H.-D.
AU  - Gostomzyk, J.G.
AU  - Hörmann, A.
AU  - Löwel, H.)
C1  - 5161
C2  - 22362
SP  - 583-588
TI  - Is the increase in coronary events on mondays an artifact?
JO  - Epidemiology
VL  - 15
IS  - 5
PY  - 2004
SN  - 1044-3983
ER  - 

TY  - JOUR
AU  - Peters, A.
C1  - 183
C2  - 22016
SP  - 1-2
TI  - Susceptible Subgroups: The Challenge of Studying interactions.
JO  - Epidemiology
VL  - 15
IS  - 2
PY  - 2004
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Background. As part of a multicenter study relating traffic-related air pollution with incidence of asthma in three birth cohort studies (TRAPCA), we used a measurement and modelling procedure to estimate long-term average exposure to traffic-related particulate air pollution in communities throughout the Netherlands; in Munich, Germany; and in Stockholm County, Sweden.
      
      	
      		
      			
      				
      				
      					Methods. In each of the three locations, 40–42 measurement sites were selected to represent rural, urban background and urban traffic locations. At each site and fine particles and filter absorbance (a marker for diesel exhaust particles) were measured for four 2-week periods distributed over approximately 1-year periods between February 1999 and July 2000. We used these measurements to calculate annual average concentrations after adjustment for temporal variation. Traffic-related variables (eg, population density and traffic intensity) were collected using Geographic Information Systems and used in regression models predicting annual average concentrations. From these models we estimated ambient air concentrations at the home addresses of the cohort members.
      			
      		
      	
      
      
      	
      		
      			
      				
      				
      					Results. Regression models using traffic-related variables explained 73%, 56% and 50% of the variability in annual average fine particle concentrations for the Netherlands, Munich and Stockholm County, respectively. For filter absorbance, the regression models explained 81%, 67% and 66% of the variability in the annual average concentrations. Cross-validation to estimate the model prediction errors indicated root mean squared errors of 1.1–1.6 µg/m3 for PM2.5 and 0.22–0.31 *10-5m-1 for absorbance.
      			
      		
      	
      
      
      	
      
      	Conclusions. A substantial fraction of the variability in annual average concentrations for all locations was explained by traffic-related variables. This approach can be used to estimate individual exposures for epidemiologic studies and offers advantages over alternative techniques relying on surrogate variables or traditional approaches that utilize ambient monitoring data alone.
AU  - Brauer, M.*
AU  - Hoek, G.*
AU  - van Vliet, P.*
AU  - Meliefste, K.*
AU  - Fischer, P.*
AU  - Gehring, U.
AU  - Heinrich, J.
AU  - Cyrys, J.
AU  - Bellander, T.*
AU  - Lewne, M.*
AU  - Brunekreef, B.*
C1  - 9537
C2  - 21626
SP  - 228-239
TI  - Estimating Long-Term Average Particulate Air Pollution Concentrations : Application of Traffic Indicators and Geographic Information Systems.
JO  - Epidemiology
VL  - 14
IS  - 2
PY  - 2003
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Background: There is suggestive evidence that residential radon increases lung cancer risk. To elucidate this association further, we conducted a case-control study in Thuringia and Saxony in Eastern Germany during 1990-1997.
      
      	
      		
      			
      				
      				
      					Methods: Histologically confirmed lung cancer patients from hospitals and a random sample of population controls matched on age, sex and geographical area were personally interviewed with respect to residential history, smoking, and other risk factors. One-year radon measurements were performed in houses occupied during the 5-35 years prior to the interview. The final analysis included a total of 1,192 cases and 1,640 controls. Odds ratios (OR) and 95% confidence intervals (CI) were estimated by logistic regression.
      			
      		
      	
      
      
      	
      		
      			
      				
      				
      					Results: Measurements covered on average 72% of the exposure time window, with mean radon concentrations of 76 Bq/m3 among the cases and 74 Bq/m3 among the controls. The smoking- and asbestos-adjusted ORs for categories of radon (50-80, 80-140 and >140 Bq/m*3, compared with 0-50 Bq/m3) were 0.95 (CI = 0.77 to 1.18), 1.13 (CI = 0.86 to1.50) and 1.30 (CI = 0.88 to 1.93). The excess relative risk per 100 Bq/ml was 0.08 (CI = -0.03 to 0.20) for all subjects and 0.09 (CI = -0.06 to 0.27) for subjects with complete measurements for all 30 years.
      			
      		
      	
      
      
      	
      
      	Conclusions: Our data indicate a small increase in lung cancer risk as a result of residential radon that is consistent with the findings of previous indoor radon and miner studies.
AU  - Kreuzer, M.
AU  - Heinrich, J.
AU  - Wölke, G.
AU  - Schaffrath Rosario, A.
AU  - Gerken, M.*
AU  - Wellmann, J.*
AU  - Keller, G.*
AU  - Kreienbrock, L.*
AU  - Wichmann, H.-E.
C1  - 9536
C2  - 21548
SP  - 559-568
TI  - Residential Radon and Risk of Lung Cancer in Eastern Germany.
JO  - Epidemiology
VL  - 14
IS  - 5
PY  - 2003
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Background. Previous research on air pollution effects has found associations with chronic adverse health effects even at the relatively low levels of ambient particulates currently measured in most urban areas.
      
      	
      		
      			
      				
      				
      					Methods. We assessed the impact of declines of total suspended particulates and sulfur dioxide in eastern Germany after reunification on the prevalence of nonallergic respiratory disorders in children. In the 1990s, particle mass (total suspended particulates) and sulfur dioxide declined, whereas number concentrations of nucleation-mode particles (10–30 nm) increased. In three study areas, questionnaires for 7,632 children between 5 and 14 years of age were collected in three phases: 1992–1993, 1995–1996, and 1998–1999.
      			
      		
      	
      
      
      	
      		
      			
      				
      				
      					Results. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for a 50-µg/m3 increment in total suspended particulates were 3.0 (CI = 1.7–5.3) for bronchitis, 2.6 (CI = 1.0–6.6) for sinusitis, and 1.9 (CI = 1.2–3.1) for frequent colds. The effect sizes for a 100-µg/m3 increment in sulfur dioxide were similar. The effect estimates for ambient total suspended particulates and sulfur dioxide were stronger among children not exposed to gas stove emissions, visible molds or dampness, cats, or environmental tobacco smoke.
      			
      		
      	
      
      
      	
      		
      			
      				
      				
      					Conclusions. The decreasing prevalence of nonallergic respiratory symptoms, along with improvements in ambient particle mass and sulfur dioxide (but not in nucleation-mode particles), indicates the reversibility of adverse health effects in children. This adds further evidence of a causal association between combustion-related air pollutants and childhood respiratory symptoms.
      			
      		
      	
      
      
      	
      		
      			
      				
      				
      			
      		
      	
      
      
      	
      		
      			
      				
      				
      					Cross-sectional studies of children in the United States and Europe consistently have shown higher rates of bronchitis and bronchitic symptoms in areas with higher exposure to total suspended particulates (TSP). 1–4 Recently published reviews of air pollution effects 5–7 reported associations with chronic adverse health effects even at the relatively low levels of ambient particulates currently measured in most urban areas.
      			
      		
      	
      
      
      	
      		
      			
      				
      				
      					Since German reunification in 1990, the levels of ambient sulfur dioxide (SO2) and TSP in eastern Germany have declined tremendously. 8 In Erfurt, eastern Germany, the concentrations of accumulation-mode particles (100–500 nm) have decreased, whereas those of nucleation-mode particles (10–30 nm in aerodynamic diameter) have increased. 9,10 In the three areas of this study (all in eastern Germany), we found similar trends in size-specific particle number concentrations between 1993 and 1999. 11 These trends may be related to declining emissions from stationary sources, to increasing emissions from mobile sources, and to clean air regulations that selectively removed larger particles. 9–11
      			
      		
      	
      
      
      	
      
      	If ambient TSP and SO2 levels are associated with bronchitic symptoms in children, a decline in these air pollution concentrations should produce a corresponding decrease in symptom prevalence. We examined this relationship in surveys of children living in eastern Germany.
AU  - Heinrich, J.
AU  - Hoelscher, B.
AU  - Frye, C.
AU  - Meyer, I.
AU  - Pitz, M.
AU  - Cyrys, J.*
AU  - Wjst, M.
AU  - Neas, L.*
AU  - Wichmann, H.-E.
C1  - 22082
C2  - 20734
SP  - 394-401
TI  - Improved Air Quality in Reunified Germany and Decreases in Respiratory Symptoms.
JO  - Epidemiology
VL  - 13
IS  - 4
PY  - 2002
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Air pollution episodes have been associated with increased cardiovascular hospital admissions and mortality in time-series studies. We tested the hypothesis that patients with implanted cardioverter defibrillators experience potentially life-threatening arrhythmias after such air pollution episodes. We compared defibrillator discharge interventions among 100 patients with such devices in eastern Massachusetts, according to variations in concentrations of particulate matter, black carbon, and gaseous air pollutants that were measured daily for the years 1995 through 1997. A 26-ppb increase in nitrogen dioxide was associated with increased defibrillator interventions 2 days later (odds ratio = 1.8; 95% confidence interval = 1.1–2.9). Patients with ten or more interventions experienced increased arrhythmias in association with nitrogen dioxide, carbon monoxide, black carbon, and fine particle mass. These results suggest that elevated levels air pollutants are associated with potentially life-threatening arrhythmia leading to therapeutic interventions by an implanted cardioverter defibrillator.
      
      	
      		
      			
      				
      				
      			
      		
      	
      
      
      	
      		
      			
      				
      				
      					Particulate air pollution episodes have been associated with increased hospital admissions for cardiovascular disease 1–4 and increased cardiovascular mortality 5–11 in epidemiologic studies. Persons with underlying heart disease appear to be at increased risk for the adverse health effects of particulate air pollution. 1–11
      			
      		
      	
      
      
      	
      		
      			
      				
      				
      					Controlled exposure of animals and natural exposures of humans to particulate pollution have shown possible effects of air pollution on the heart. Instillation of 250 micrograms of combustion particles into the lungs of rats with pharmacologically induced pulmonary hypertension produced arrhythmia and doubled their mortality rate. 12 Dogs inhaling concentrated ambient particles showed changes in heart rate variability and electrocardiographic morphology consistent with increased sympathetic nervous system activity. 13,14 Heart rates of elderly subjects in Utah Valley increased in association with elevated concentrations of inhalable particulates (particulate matter less than 10 micrometers in aerodynamic diameter; PM10). 15 In a subset of these subjects, heart rate variability decreased with increasing PM10 concentrations. 15 Increased heart rate and decreased heart rate variability are indicators of altered autonomic control, specifically increased sympathetic stress. Raised sympathetic activity increases the risk of ventricular fibrillation, a severe form of arrhythmia that, without intervention, leads to sudden death. 16
      			
      		
      	
      
      
      	
      
      	We tested the hypothesis that patients with a history of serious arrhythmia requiring implanted cardioverter defibrillators (ICDs) would experience potentially life-threatening arrhythmia associated with air pollution episodes. Traditionally, ventricular arrhythmia is treated with drug therapies. 17 Implantable cardioverter defibrillators monitor electrocardiographic abnormalities and initiate therapeutic interventions. On detection of ventricular fibrillation or ventricular tachycardia, the ICD device will initiate pacing and/or shock therapy to restore a normal cardiac rhythm. Several recent clinical trials have suggested that ICD devices are more effective at preventing death from heart rhythm abnormalities than medications alone. 18,19 The ICD devices provide objective and accurate records of the occurrence and timing of arrhythmic events. We report the results of a pilot study to assess the feasibility of linking cardiac arrhythmias detected by ICD devices with air pollution exposures.
AU  - Peters, A.
AU  - Liu, E.*
AU  - Verrier, R.L.*
AU  - Schwartz, J.*
AU  - Gold, D.R.*
AU  - Mittleman, M.*
AU  - Baliff, J.*
AU  - Oh, A.*
AU  - Allen, G.*
AU  - Monahan, K.*
AU  - Dockery, D.W.*
C1  - 21324
C2  - 19439
SP  - 11-17
TI  - Air Pollution and Incidence of Cardiac Arrhytmia.
JO  - Epidemiology
VL  - 11
IS  - 1
PY  - 2000
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - We conducted a case-control study in 12 European study centers to evaluate the role of occupational risk factors among nonsmokers. We obtained detailed occupational histories from 650 nonsmoking cases (509 females/141 males) and 1,542 nonsmoking controls (1,011 females/531 males). On the basis of an a priori definition of occupations and industries that are known (list A) or suspected (list B) to be associated with lung carcinogenesis, we calculated odds ratios (ORs) for these occupations, using unconditional logistic regression models and adjusting for sex, age, and center effects. Among nonsmoking men, an excess relative risk was observed among those who had worked in list-A occupations [OR = 1.52; 95% confidence interval (CI) = 0.78–2.97] but not in list-B occupations (OR = 1.05; 95% CI = 0.60–1.83). Among nonsmoking women, there was an elevation of risk for list-A occupations (OR = 1.50; 95% CI = 0.49–4.53), although this estimate was imprecise, given that less than 1% of cases and controls were exposed. Exposure to list-B occupations was associated with an increase in relative risk (OR = 1.69; 95% CI = 1.09–2.63) in females, but not in males. Women who had been laundry workers or dry cleaners had an OR of 1.83 (95% CI = 0.98–3.40). Our findings confirm that certain occupational exposures are associated with an increased risk for lung cancer among both female and male nonsmokers; however, knowledge on occupational lung carcinogens is biased toward agents to which mainly men are exposed.
      
      	
      		
      			
      				
      				
      			
      		
      	
      
      
      	
      		
      			
      				
      				
      					Since the early 1950s, it has been well established that smoking is the most important risk factor for lung cancer. 1–3 About 98% of male cases worldwide and 70–90% of European and American female cases report a history of smoking. 4 The population attributable risk percentage for smoking has been estimated to be between 80% and 95% in men 5–7 and about 80% in women. 8 Occupational exposures to carcinogens, indoor radon exposure, dietary habits, industrial air pollution, and environmental tobacco smoke (ETS) are other causes of lung cancer. 9 To examine the separate influence of these risk factors, it is important to control adequately for the impact of smoking. Rough or incomplete recording of the smoking history as well as inadequate consideration of tar contents, inhalation depth, time since smoking cessation, and other smoking behavior patterns have all been discussed as sources of incomplete control of confounding that could be responsible for incorrect risk estimates.
      			
      		
      	
      
      
      	
      
      	Restriction of the analysis to those cases and controls who never smoked should avoid such confounding effects. But, because of the small proportion of lung cancer cases who have never smoked, such restrictions tend to result in imprecise risk estimates. To avoid the problem of low power, an international multicenter case-control study of lung cancer in nonsmokers was initiated in 1988, coordinated by the International Agency for Research on Cancer (IARC). The main objective of the study was to investigate the association between ETS and lung cancer. Results on this exposure have been published elsewhere. 10,11 Here, we investigate the relation between occupational exposures and lung cancer in nonsmokers.
AU  - Pohlabeln, H.*
AU  - Boffetta, P.*
AU  - Ahrens, W.*
AU  - Merletti, F.*
AU  - Agudo, A.*
AU  - Benhamou, E.*
AU  - Brüske, I.
AU  - Ferro, G.*
AU  - Fortes, Ch.*
AU  - Kreuzer, M.
AU  - Wichmann, H.-E.
C1  - 21585
C2  - 19711
SP  - 532-538
TI  - Occupational Risks for Lung Cancer among Nonsmokers.
JO  - Epidemiology
VL  - 11
IS  - 5
PY  - 2000
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Because previous findings have been inconsistent, we explored the association of serum concentrations of uric acid with all-cause and cardiovascular disease mortality and myocardial infarction prospectively. We used data from 1,044 men who are members of the World Health Organization Monitoring Trends and Determinants in Cardiovascular Diseases (MONICA) Augsburg cohort. The men, 45-64 years of age in 1984-1985, were followed through 1992. There were 90 deaths, 44 of which were related to cardiovascular disease; 60 men developed incident nonfatal or fatal myocardial infarction. We estimated hazard rate ratios from Cox proportional hazard models. Uric acid levels > or =373 micromol/liter (fourth quartile) vs < or =319 micromol/liter (first and second quartile) independently predicted all-cause mortality [hazard rate ratio = 2.8; 95% confidence interval (CI) = 1.6-5.0] after adjustment for alcohol, total cholesterol/high-density lipoprotein cholesterol ratio, hypertension, use of diuretic drugs, smoking, body mass index, and education. The adjusted risk of cardiovascular disease mortality was 2.2 (95% CI = 1.0-4.8), and that of myocardial infarction was 1.7 (95% CI = 0.8-3.3). Although residual confounding cannot be excluded, our results are among the few, in men, demonstrating a strong positive association of elevated serum uric acid with all-cause mortality. Future investigations may be able to evaluate whether uric acid contributes independently to the development of cardiovascular disease or is simply a component of the atherogenic metabolic condition known as the insulin resistance syndrome.
AU  - Liese, A.D*
AU  - Hense, H.-W.*
AU  - Löwel, H.
AU  - Döring, A.
AU  - Tietze, M.*
AU  - Keil, U.*
C1  - 21105
C2  - 19138
SP  - 391-397
TI  - Association of serum uric acid with all-cause and cardiovascular disease mortality and incident myocardial infarction in the MONICA Augsburg cohort.
JO  - Epidemiology
VL  - 10
IS  - 4
PY  - 1999
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Hypothetically, blood lead may be involved in blood pressure elevations owing to a facilitation of vascular adrenergic stimulation by extrinsic factors like alcohol. We therefore investigated whether self-reported alcohol consumption was a modifier of the blood lead-blood pressure relation in 3,664 men and women, age 28-67 years, from the MONICA Augsburg study in Germany. In women, only heavy drinkers (40 gm alcohol per day or more) showed a strong relation of blood lead with systolic and diastolic blood pressure, whereas little association was observed for abstaining and for moderately drinking women. In men, we found similar alcohol modifications of the lead-pressure relation only for those with rural, rather than urban, places of residence. We have no explanation for this subgroup divergence. Our results may be taken to indicate a possible role of alcohol consumption in modifying the action of lead on blood pressure.
AU  - Hense, H.W.
AU  - Filipiak, B.
AU  - Keil, U.
C1  - 40063
C2  - 0
SP  - 120-123
TI  - Alcohol consumption as a modifier of the relation between blood lead and blood pressure.
JO  - Epidemiology
VL  - 5
IS  - 1
PY  - 1994
SN  - 1044-3983
ER  - 

TY  - JOUR
AB  - Several reports from large population surveys have indicated that blood lead is positively related to blood pressure. We assessed this relation in 1,703 men (median blood lead = 83μg per liter) and 1,661 women (median blood lead = 60μg per liter), age 28 to 67 years, who participated in the first follow-up examination of the MONICA Augsburg cohort study in 1987-1988. Crude analyses confirmed a strong, positive association of blood lead concentrations with systolic and diastolic blood pressure. We identified age, body mass index, hematocrit, and alcohol consumption as the quantitatively most important confounders of this association. Adjustment for these variables, in particular for hematocrit and alcohol consumption, considerably reduced the magnitude of the blood lead effect on blood pressure. There were no indications for marked nonlinearity or threshold effects. After control of confounders, a difference of 100μg per liter in blood lead levels, corresponding to rather extreme positions in the lower and upper end of the population blood lead distribution, related to estimated blood pressure increases of less than 3mmHg. The appropriateness of treating hematocrit and alcohol consumption as confounders of the blood lead-blood pressure relation is discussed on the basis of current pathophysiologic concepts. We conclude that hematocrit should always be taken into account as a relevant confounder. On the other hand, the interrelation of alcohol consumption, blood lead, and blood pressure is presently not clearly understood; that is, its appropriate analytic handling cannot be determined. The consequences of these considerations on estimates of the blood lead effect on blood pressure may be both over- and underestimations.
AU  - Hense, H.W.
AU  - Filipiak, B.
AU  - Keil, U.
C1  - 20734
C2  - 13954
SP  - 173-179
TI  - The association of blood lead and blood pressure in population surveys.
JO  - Epidemiology
VL  - 4
IS  - 2
PY  - 1993
SN  - 1044-3983
ER  -