TY  - JOUR
AB  - Mathematical models are able to reflect biological processes and to capture epidemiological data. Thus, they may help elucidating roles of risk factors in disease progression. We propose to account for smoking, hypertension and dyslipidemia in a previously published process-oriented model that de- scribes the development of atherosclerotic lesions resulting in myocardial infarction (MI). The model is sex-specific and incorporates individual heterogeneity. It was applied to population-based individual risk factors and MI rates (KORA study) together with subclinical atherosclerotic le-sion data (PDAY Study). Different model variants were evaluated testing the association of risk factors with different disease processes. Best fits were obtained for smoking affecting a late stage disease process, suggesting a thrombo-genic role. Hypertension was mainly related to complicated, vulnerable lesions. Dyslipidemia was con-sistent with increasing the number of initial lesions. By accounting for heterogeneity, individual hazard ratios differ from the population average. The mean individual hazard ratio for smoking was twice the population based hazard ratio for men, and even more for women. Atherosclerotic lesion progression and MI incidence data can be related in a mathematical model to illuminate how risk factors affect different phases of this pathological process.
AU  - Simonetto, C.
AU  - Heier, M.
AU  - Peters, A.
AU  - Kaiser, J.C.
AU  - Rospleszcz, S.
C1  - 64529
C2  - 52255
SP  - 1766–1775
TI  - From atherosclerosis to myocardial infarction - a process-oriented model investigating the role of risk factors.
JO  - Am. J. Epidemiol.
VL  - 191
IS  - 10
PY  - 2022
SN  - 0002-9262
ER  - 

TY  - JOUR
AU  - Simonetto, C.
AU  - Heier, M.
AU  - Peters, A.
AU  - Kaiser, J.C.
AU  - Rospleszcz, S.
C1  - 65471
C2  - 52698
SP  - 1781–1782
TI  - Response to AJE-00301-2022 Invited Commentary "Mechanistic and biologically based models in epidemiology; A powerful underutilized tool" by Rafael Meza & Jihyoun Jeon.
JO  - Am. J. Epidemiol.
VL  - 191
IS  - 10
PY  - 2022
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - Women with a history of breast cancer among family members are at increased risk for breast cancer. However, it is unknown whether a familial breast cancer history (FBCH) also increases individual susceptibility to breast cancer from radiation exposure. In this cohort study, 17,200 female Swedish hemangioma patients with 1,079 breast cancer cases diagnosed between 1958 and 2013, exposed to ionizing radiation in infancy, were linked to their first-degree relatives. The association between FBCH and radiation-induced breast cancer risk was assessed. Further, the relevance for breast cancer radiotherapy and mammography screening was evaluated. On average, the radiation-induced excess relative risk and excess absolute risk of breast cancer at age 50 years were 0.51 Gy(-1) (95% confidence interval (CI): 0.33, 0.71) and 10.8 cases/10,000 person-years/Gy (95% CI: 7.0, 14.6), respectively. Radiation risk was higher by a factor of 2.7 (95% CI: 1.0, 4.8; P = 0.05) if 1 first-degree relative was affected by breast cancer. For whole-breast standard radiotherapy at age 40 years with a contralateral breast dose of 0.72 Gy, the 20-year radiation-related excess risk of contralateral breast cancer was estimated to increase from 0.6% for women without FBCH to 1.7% for women with FBCH. In a biennial mammography screening program at ages 40-74 years, radiation risk up to age 80 years would increase from 0.11% for women without FBCH to 0.29% for women with FBCH.
AU  - Eidemüller, M.
AU  - Holmberg, E.*
AU  - Lundell, M.*
AU  - Karlsson, P.*
C1  - 61293
C2  - 49792
CY  - Journals Dept, 2001 Evans Rd, Cary, Nc 27513 Usa
SP  - 76-84
TI  - Evidence for increased susceptibility to breast cancer from exposure to ionizing radiation due to a familial history of breast cancer: Results from the Swedish hemangioma cohort.
JO  - Am. J. Epidemiol.
VL  - 190
IS  - 1
PB  - Oxford Univ Press Inc
PY  - 2021
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - The numbers of international collaborations among birth cohort studies designed to better understand asthma and allergies have increased in the last several years. However, differences in definitions and methods preclude direct pooling of original data on individual participants. As part of the Mechanisms of the Development of Allergy (MeDALL) Project, we harmonized data from 14 birth cohort studies (each with 3-20 follow-up periods) carried out in 9 European countries during 1990-1998 or 2003-2009. The harmonization process followed 6 steps: 1) organization of the harmonization panel; 2) identification of variables relevant to MeDALL objectives (candidate variables); 3) proposal of a definition for each candidate variable (reference definition); 4) assessment of the compatibility of each cohort variable with its reference definition (inferential equivalence) and classification of this inferential equivalence as complete, partial, or impossible; 5) convocation of a workshop to agree on the reference definitions and classifications of inferential equivalence; and 6) preparation and delivery of data through a knowledge management portal. We agreed on 137 reference definitions. The inferential equivalence of 3,551 cohort variables to their corresponding reference definitions was classified as complete, partial, and impossible for 70%, 15%, and 15% of the variables, respectively. A harmonized database was delivered to MeDALL investigators. In asthma and allergy birth cohorts, the harmonization of data for pooled analyses is feasible, and high inferential comparability may be achieved. The MeDALL harmonization approach can be used in other collaborative projects.
AU  - Benet, M.*
AU  - Albang, R.*
AU  - Pinart, M.*
AU  - Hohmann, C.*
AU  - Tischer, C.G.*
AU  - Annesi-Maesano, I.*
AU  - Baïz, N.*
AU  - Bindslev-Jensen, C.*
AU  - Lødrup Carlsen, K.C.*
AU  - Carlsen, K.H.*
AU  - Cirugeda, L.*
AU  - Eller, E.*
AU  - Fantini, M.P.*
AU  - Gehring, U.*
AU  - Gerhard, B.*
AU  - Gori, D.*
AU  - Hallner, E.*
AU  - Kull, I.*
AU  - Lenzi, J.*
AU  - McEachan, R.*
AU  - Minina, E.*
AU  - Momas, I.*
AU  - Narduzzi, S.*
AU  - Petherick, E.S*
AU  - Porta, D.*
AU  - Rancière, F.*
AU  - Standl, M.
AU  - Torrent, M.*
AU  - Wijga, A.H.*
AU  - Wright, J.*
AU  - Kogevinas, M*
AU  - Guerra, S.*
AU  - Sunyer, J.*
AU  - Keil, T.O.*
AU  - Bousquet, J.*
AU  - Maier, D.*
AU  - Antò, J.M.*
AU  - Garcia-Aymerich, J.*
C1  - 54575
C2  - 45686
CY  - Journals Dept, 2001 Evans Rd, Cary, Nc 27513 Usa
SP  - 408-417
TI  - Integrating clinical and epidemiologic data on allergic diseases across birth cohorts: A harmonization study in the mechanisms of the development of allergy project.
JO  - Am. J. Epidemiol.
VL  - 188
IS  - 2
PB  - Oxford Univ Press Inc
PY  - 2019
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - A person's lipid profile is influenced by genetic variants and alcohol consumption, but the contribution of interactions between these exposures has not been studied. We therefore incorporated gene-alcohol interactions into a multiancestry genome-wide association study of levels of high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglycerides. We included 45 studies in stage 1 (genome-wide discovery) and 66 studies in stage 2 (focused follow-up), for a total of 394,584 individuals from 5 ancestry groups. Analyses covered the period July 2014-November 2017. Genetic main effects and interaction effects were jointly assessed by means of a 2-degrees-of-freedom (df) test, and a 1-df test was used to assess the interaction effects alone. Variants at 495 loci were at least suggestively associated (P < 1 x 10(-6)) with lipid levels in stage 1 and were evaluated in stage 2, followed by combined analyses of stage 1 and stage 2. In the combined analysis of stages 1 and 2, a total of 147 independent loci were associated with lipid levels at P < 5 x 10(-8) using 2-df tests, of which 18 were novel. No genome-wide-significant associations were found testing the interaction effect alone. The novel loci included several genes (proprotein convertase subtilisin/kexin type 5 (PCSK5), vascular endothelial growth factor B (VEGFB), and apolipoprotein B mRNA editing enzyme, catalytic polypeptide 1 (APOBEC1) complementation factor (A1CF)) that have a putative role in lipid metabolism on the basis of existing evidence from cellular and experimental models.
AU  - de Vries, P.S.*
AU  - Brown, M.R.*
AU  - Bentley, A.R.*
AU  - Sung, Y.J.*
AU  - Winkler, T.W.*
AU  - Ntalla, I.*
AU  - Schwander, K.*
AU  - Kraja, A.T.*
AU  - Guo, X.*
AU  - Franceschini, N.*
AU  - Cheng, C.Y.*
AU  - Sim, X.*
AU  - Vojinovic, D.*
AU  - Huffman, J.E.*
AU  - Musani, S.K.*
AU  - Li, C.*
AU  - Feitosa, M.F.*
AU  - Richard, M.A.*
AU  - Noordam, R.*
AU  - Aschard, H.*
AU  - Bartz, T.M.*
AU  - Bielak, L.F.*
AU  - Deng, X.*
AU  - Dorajoo, R.*
AU  - Lohman, K.K.*
AU  - Manning, A.K.*
AU  - Rankinen, T.*
AU  - Smith, A.V.*
AU  - Tajuddin, S.M.*
AU  - Evangelou, E.*
AU  - Graff, M.*
AU  - Alver, M.*
AU  - Boissel, M.*
AU  - Chai, J.F.*
AU  - Chen, X.*
AU  - Divers, J.*
AU  - Gandin, I.*
AU  - Gao, C.*
AU  - Goel, A.*
AU  - Hagemeijer, Y.*
AU  - Harris, S.E.*
AU  - Hartwig, F.P.*
AU  - He, M.*
AU  - Horimoto, A.R.V.R.*
AU  - Hsu, F.C.*
AU  - Jackson, A.U.*
AU  - Kasturiratne, A.*
AU  - Komulainen, P.*
AU  - Kühnel, B.
AU  - Laguzzi, F.*
AU  - Lee, J.H.*
AU  - Luan, J.*
AU  - Lyytikäinen, L.P.*
AU  - Matoba, N.*
AU  - Nolte, I.M.*
AU  - Pietzner, M.*
AU  - Riaz, M.*
AU  - Said, M.A.*
AU  - Scott, R.A.*
AU  - Sofer, T.*
AU  - Stancáková, A.*
AU  - Takeuchi, F.*
AU  - Tayo, B.O.*
AU  - van der Most, P.J.*
AU  - Varga, T.V.*
AU  - Wang, Y.*
AU  - Ware, E.B.*
AU  - Wen, W.*
AU  - Yanek, L.R.*
AU  - Zhang, W.*
AU  - Zhao, J.H.*
AU  - Afaq, S.*
AU  - Amin, N.*
AU  - Amini, M.*
AU  - Arking, D.E.*
AU  - Aung, T.*
AU  - Ballantyne, C.*
AU  - Boerwinkle, E.*
AU  - Broeckel, U.*
AU  - Campbell, A.*
AU  - Canouil, M.*
AU  - Charumathi, S.*
AU  - Chen, Y.I.*
AU  - Connell, J.M.*
AU  - de Faire, U.*
AU  - de Las Fuentes, L.*
AU  - de Mutsert, R.*
AU  - de Silva, H.J.*
AU  - Ding, J.*
AU  - Dominiczak, A.F.*
AU  - Duan, Q.*
AU  - Eaton, C.B.*
AU  - Eppinga, R.N.*
AU  - Faul, J.D.*
AU  - Fisher, V.*
AU  - Forrester, T.*
AU  - Franco, O.H.*
AU  - Friedlander, Y.*
AU  - Ghanbari, M.*
AU  - Giulianini, F.*
AU  - Grabe, H.J.*
AU  - Grove, M.L.*
AU  - Gu, C.C.*
AU  - Harris, T.B.*
AU  - Heikkinen, S.*
AU  - Heng, C.K.*
AU  - Hirata, M.*
AU  - Hixson, J.E.*
AU  - Howard, B.V.*
AU  - Ikram, M.A.*
AU  - Jacobs, D.R.*
AU  - Johnson, C.*
AU  - Jonas, J.B.*
AU  - Kammerer, C.M.*
AU  - Katsuya, T.*
AU  - Khor, C.C.*
AU  - Kilpeläinen, T.O.*
AU  - Koh, W.P.*
AU  - Koistinen, H.A.*
AU  - Kolcic, I.*
AU  - Kooperberg, C.*
AU  - Krieger, J.E.*
AU  - Kritchevsky, S.B.*
AU  - Kubo, M.*
AU  - Kuusisto, J.*
AU  - Lakka, T.A.*
AU  - Langefeld, C.D.*
AU  - Langenberg, C.*
AU  - Launer, L.J.*
AU  - Lehne, B.*
AU  - Lemaitre, R.N.*
AU  - Li, Y.*
AU  - Liang, J.*
AU  - Liu, J.*
AU  - Liu, K.*
AU  - Loh, M.*
AU  - Louie, T.*
AU  - Mägi, R.*
AU  - Manichaikul, A.W.*
AU  - McKenzie, C.A.*
AU  - Meitinger, T.
AU  - Metspalu, A.*
AU  - Milaneschi, Y.*
AU  - Milani, L.*
AU  - Mohlke, K.L.*
AU  - Mosley, T.H.*
AU  - Mukamal, K.J.*
AU  - Nalls, M.A.*
AU  - Nauck, M.*
AU  - Nelson, C.P.*
AU  - Sotoodehnia, N.*
AU  - O'Connell, J.R.*
AU  - Palmer, N.D.*
AU  - Pazoki, R.*
AU  - Pedersen, N.L.*
AU  - Peters, A.
AU  - Peyser, P.A.*
AU  - Polasek, O.*
AU  - Poulter, N.*
AU  - Raffel, L.J.*
AU  - Raitakari, O.T.*
AU  - Reiner, A.P.*
AU  - Rice, T.K.*
AU  - Rich, S.S.*
AU  - Robino, A.*
AU  - Robinson, J.G.*
AU  - Rose, L.M.*
AU  - Rudan, I.*
AU  - Schmidt, C.O.*
AU  - Schreiner, P.J.*
AU  - Scott, W.R.*
AU  - Sever, P.*
AU  - Shi, Y.*
AU  - Sidney, S.*
AU  - Sims, M.*
AU  - Smith, B.H.*
AU  - Smith, J.A.*
AU  - Snieder, H.*
AU  - Starr, J.M.*
AU  - Strauch, K.
AU  - Tan, N.*
AU  - Taylor, K.D.*
AU  - Teo, Y.Y.*
AU  - Tham, Y.C.*
AU  - Uitterlinden, A.G.*
AU  - van Heemst, D.*
AU  - Vuckovic, D.*
AU  - Waldenberger, M.
AU  - Wang, L.*
AU  - Wang, Z.*
AU  - Wei, W.B.*
AU  - Williams, C.*
AU  - Wilson, G.*
AU  - Wojczynski, M.K.*
AU  - Yao, J.*
AU  - Yu, B.*
AU  - Yu, C.*
AU  - Yuan, J.M.*
AU  - Zhao, W.*
AU  - Zonderman, A.B.*
AU  - Becker, D.M.*
AU  - Boehnke, M.*
AU  - Bowden, D.W.*
AU  - Chambers, J.C.*
AU  - Deary, I.J.*
AU  - Esko, T.*
AU  - Farrall, M.*
AU  - Franks, P.W.*
AU  - Freedman, B.I.*
AU  - Froguel, P.*
AU  - Gasparini, P.*
AU  - Gieger, C.
AU  - Horta, B.L.*
AU  - Kamatani, Y.*
AU  - Kato, N.*
AU  - Kooner, J.S.*
AU  - Laakso, M.*
AU  - Leander, K.*
AU  - Lehtimäki, T.*
AU  - Magnusson, P.K.E.*
AU  - Penninx, B.*
AU  - Pereira, A.C.*
AU  - Rauramaa, R.*
AU  - Samani, N.J.*
AU  - Scott, J.*
AU  - Shu, X.O.*
AU  - van der Harst, P.*
AU  - Wagenknecht, L.E.*
AU  - Wang, Y.X.*
AU  - Wareham, N.J.*
AU  - Watkins, H.*
AU  - Weir, D.R.*
AU  - Wickremasinghe, A.R.*
AU  - Zheng, W.*
AU  - Elliott, P.*
AU  - North, K.E.*
AU  - Bouchard, C.*
AU  - Evans, M.K.*
AU  - Gudnason, V.*
AU  - Liu, C.T.*
AU  - Liu, Y.*
AU  - Psaty, B.M.*
AU  - Ridker, P.M.*
AU  - van Dam, R.M.*
AU  - Kardia, S.L.R.*
AU  - Zhu, X.*
AU  - Rotimi, C.N.*
AU  - Mook-Kanamori, D.O.*
AU  - Fornage, M.*
AU  - Kelly, T.N.*
AU  - Fox, E.R.*
AU  - Hayward, C.*
AU  - van Duijn, C.M.*
AU  - Tai, E.S.*
AU  - Wong, T.Y.*
AU  - Rotter, J.I.*
AU  - Gauderman, W.J.*
AU  - Province, M.A.*
AU  - Munroe, P.B.*
AU  - Rice, K.*
AU  - Chasman, D.I.*
AU  - Cupples, L.A.*
AU  - Rao, D.C.*
AU  - Morrison, A.C.*
C1  - 56053
C2  - 46763
CY  - Journals Dept, 2001 Evans Rd, Cary, Nc 27513 Usa
SP  - 1033-1054
TI  - Multiancestry genome-wide association study of lipid levels incorporating gene-alcohol interactions.
JO  - Am. J. Epidemiol.
VL  - 188
IS  - 6
PB  - Oxford Univ Press Inc
PY  - 2019
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - To investigate the risk of lung cancer after exposure to welding fumes, hexavalent chromium (Cr(VI)), and nickel, we analyzed 3,418 lung cancer cases and 3,488 controls among men from 2 German case-control studies (1988-1996). We developed a welding-process exposure matrix from measurements of these agents, and this was linked with welding histories from a job-specific questionnaire to calculate cumulative exposure variables. Logistic regression models were fitted to estimate odds ratios with confidence intervals conditional on study, and they adjusted for age, smoking, and working in other at-risk occupations. Additionally, we mutually adjusted for the other exposure variables under study. Overall, 800 cases and 645 controls ever worked as regular or occasional welders. Odds ratios for lung cancer with high exposure were 1.55 (95% confidence interval (CI): 1.17, 2.05; median, 1.8 mg/m(3) x years) for welding fumes, 1.85 (95% CI: 1.35, 2.54; median, 1.4 mu g/m(3) x years) for Cr(VI), and 1.60 (95% CI: 1.21, 2.12; median, 9 mu g/m(3) x years) for nickel. Risk estimates increased with increasing cumulative exposure to welding fumes and with increasing exposure duration for Cr(VI) and nickel. Our results showed that welding fumes, Cr(VI), and nickel might contribute independently to the excess lung cancer risk associated with welding. However, quantitative exposure assessment remains challenging.
AU  - Pesch, B.*
AU  - Kendzia, B.*
AU  - Pohlabeln, H.*
AU  - Ahrens, W.*
AU  - Wichmann, H.-E.
AU  - Siemiatycki, J.*
AU  - Taeger, D.*
AU  - Zschiesche, W.*
AU  - Behrens, T.*
AU  - Jöckel, K.H.*
AU  - Brüning, T.*
C1  - 57433
C2  - 47765
CY  - Journals Dept, 2001 Evans Rd, Cary, Nc 27513 Usa
SP  - 1984-1993
TI  - Exposure to welding fumes, hexavalent chromium, or nickel and risk of lung cancer.
JO  - Am. J. Epidemiol.
VL  - 188
IS  - 11
PB  - Oxford Univ Press Inc
PY  - 2019
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - The Consortium of Metabolomics Studies (COMETS) was established in 2014 to facilitate large-scale collaborative research on the human metabolome and its relationship with disease etiology, diagnosis, and prognosis. COMETS comprises 47 cohorts from Asia, Europe, North America, and South America that together include more than 136,000 participants with blood metabolomics data on samples collected from 1985 to 2017. Metabolomics data were provided by 17 different platforms, with the most frequently used labs being Metabolon, Inc. (14 cohorts), the Broad Institute (15 cohorts), and Nightingale Health (11 cohorts). Participants have been followed for a median of 23 years for health outcomes including death, cancer, cardiovascular disease, diabetes, and others; many of the studies are ongoing. Available exposure-related data include common clinical measurements and behavioral factors, as well as genome-wide genotype data. Two feasibility studies were conducted to evaluate the comparability of metabolomics platforms used by COMETS cohorts. The first study showed that the overlap between any 2 different laboratories ranged from 6 to 121 metabolites at 5 leading laboratories. The second study showed that the median Spearman correlation comparing 111 overlapping metabolites captured by Metabolon and the Broad Institute was 0.79 (interquartile range, 0.56-0.89).
AU  - Yu, B.*
AU  - Zanetti, K.A.*
AU  - Temprosa, M.*
AU  - Albanes, D.*
AU  - Appel, N.*
AU  - Barrera, C.B.*
AU  - Ben-Shlomo, Y.*
AU  - Boerwinkle, E.*
AU  - Casas, J.P.*
AU  - Clish, C.*
AU  - Dale, C.E.*
AU  - Dehghan, A.*
AU  - Derkach, A.*
AU  - Eliassen, A.H.*
AU  - Elliott, P.*
AU  - Fahy, E.*
AU  - Gieger, C.
AU  - Gunter, M.J.*
AU  - Harada, S.*
AU  - Harris, T.*
AU  - Herr, D.R.*
AU  - Herrington, D.*
AU  - Hirschhorn, J.N.*
AU  - Hoover, E.*
AU  - Hsing, A.W.*
AU  - Johansson, M.*
AU  - Kelly, R.S.*
AU  - Khoo, C.M.*
AU  - Kivimäki, M.*
AU  - Kristal, B.S.*
AU  - Langenberg, C.*
AU  - Lasky-Su, J.*
AU  - Lawlor, D.A.*
AU  - Lotta, L.A.*
AU  - Mangino, M.*
AU  - Le Marchand, L.*
AU  - Mathé, E.*
AU  - Matthews, C.E.*
AU  - Menni, C.*
AU  - Mucci, L.A.*
AU  - Murphy, R.*
AU  - Oresič, M.*
AU  - Orwoll, E.S.*
AU  - Ose, J.*
AU  - Pereira, A.C.*
AU  - Playdon, M.C.*
AU  - Poston, L.*
AU  - Price, J.*
AU  - Qi, Q.*
AU  - Rexrode, K.*
AU  - Risch, A.*
AU  - Sampson, J.*
AU  - Seow, W.J.*
AU  - Sesso, H.D.*
AU  - Shah, S.H.*
AU  - Shu, X.O.*
AU  - Smith, G.C.S.*
AU  - Sovio, U.*
AU  - Stevens, V.L.*
AU  - Stolzenberg-Solomon, R.S.*
AU  - Takebayashi, T.*
AU  - Tillin, T.*
AU  - Travis, R.*
AU  - Tzoulaki, I.*
AU  - Ulrich, C.M.*
AU  - Vasan, R.S.*
AU  - Verma, M.*
AU  - Wang, Y.*
AU  - Wareham, N.J.*
AU  - Wong, A.*
AU  - Younes, N.*
AU  - Zhao, H.*
AU  - Zheng, W.*
AU  - Moore, S.C.*
C1  - 56201
C2  - 46899
CY  - Journals Dept, 2001 Evans Rd, Cary, Nc 27513 Usa
SP  - 991-1012
TI  - The consortium of metabolomics studies (COMETS): Metabolomics in 47 prospective cohort studies.
JO  - Am. J. Epidemiol.
VL  - 188
IS  - 6
PB  - Oxford Univ Press Inc
PY  - 2019
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - Early infections have been suggested to be associated with increased risk for later celiac disease (CD). We analyzed prospective claims data of n = 295,420 infants from Bavaria, Germany, born between 2005 and 2007 containing information on medically attended infectious diseases according to ICD-10 code on a quarterly basis to calculate hazard ratios and 95% confidence intervals of time to CD diagnosis by infection exposure, adjusting for sex, calendar month of birth and number of previous healthcare visits. CD risk was increased in children who had a gastrointestinal infection during the first year of life (hazard ratio = 1.32, 95% confidence interval: 1.12, 1.55) and to a lesser extent also in children with a respiratory infection during the first year (hazard ratio = 1.22, 95% confidence interval: 1.04, 1.43). Repeated gastrointestinal infections during the first year of life were associated with particularly increased CD risk in later life. These findings indicate that early gastrointestinal infections may be relevant for CD development.
AU  - Beyerlein, A.
AU  - Donnachie, E.*
AU  - Ziegler, A.-G.
C1  - 51761
C2  - 43330
CY  - Cary
SP  - 1277-1280
TI  - Infections in early Life and development of celiac disease.
JO  - Am. J. Epidemiol.
VL  - 186
IS  - 11
PB  - Oxford Univ Press Inc
PY  - 2017
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - The added value of incorporating information from repeated blood pressure and cholesterol measurements to predict cardiovascular disease (CVD) risk has not been rigorously assessed. We used data on 191,445 adults from the Emerging Risk Factors Collaboration (38 cohorts from 17 countries with data encompassing 1962-2014) with more than 1 million measurements of systolic blood pressure, total cholesterol, and high-density lipoprotein cholesterol. Over a median 12 years of follow-up, 21,170 CVD events occurred. Risk prediction models using cumulative mean values of repeated measurements and summary measures from longitudinal modeling of the repeated measurements were compared with models using measurements from a single time point. Risk discrimination (C-index) and net reclassification were calculated, and changes in C-indices were meta-analyzed across studies. Compared with the single-time-point model, the cumulative means and longitudinal models increased the C-index by 0.0040 (95% confidence interval (CI): 0.0023, 0.0057) and 0.0023 (95% CI: 0.0005, 0.0042), respectively. Reclassification was also improved in both models; compared with the single-time-point model, overall net reclassification improvements were 0.0369 (95% CI: 0.0303, 0.0436) for the cumulative-means model and 0.0177 (95% CI: 0.0110, 0.0243) for the longitudinal model. In conclusion, incorporating repeated measurements of blood pressure and cholesterol into CVD risk prediction models slightly improves risk prediction.
AU  - Paige, E.*
AU  - Barrett, J.*
AU  - Pennells, L.*
AU  - Sweeting, M.*
AU  - Willeit, P.*
AU  - di Angelantonio, E.*
AU  - Gudnason, V.*
AU  - Nørdestgaard, B.G.*
AU  - Psaty, B.M.*
AU  - Goldbourt, U.*
AU  - Best, L.G.*
AU  - Assmann, G.*
AU  - Salonen, J.T.*
AU  - Nietert, P.J.*
AU  - Verschuren, W.M.M.*
AU  - Brunner, E.J.*
AU  - Kronmal, R.A.*
AU  - Salomaa, V.*
AU  - Bakker, S.J.L.*
AU  - Dagenais, G.R.*
AU  - Sato, S.*
AU  - Jansson, J.*
AU  - Willeit, J.*
AU  - Onat, A.*
AU  - de la Camara, A.G.*
AU  - Roussel, R.*
AU  - Völzke, H.*
AU  - Dankner, R.*
AU  - Tipping, R.W.*
AU  - Meade, T.W.*
AU  - Donfrancesco, C.*
AU  - Kuller, L.H.*
AU  - Peters, A.
AU  - Gallacher, J.*
AU  - Kromhout, D.*
AU  - Iso, H.*
AU  - Knuiman, M.*
AU  - Casiglia, E.*
AU  - Kavousi, M.*
AU  - Palmieri, L.*
AU  - Sundström, J.*
AU  - Davis, B.R.*
AU  - Njolstad, I.*
AU  - Couper, D.*
AU  - Danesh, J.*
AU  - Thompson, S.G.*
AU  - Wood, A.*
C1  - 52206
C2  - 43763
CY  - Cary
SP  - 899-907
TI  - Use of repeated blood pressure and cholesterol measurements to improve cardiovascular disease risk prediction: An individual-participant-data meta-analysis.
JO  - Am. J. Epidemiol.
VL  - 186
IS  - 8
PB  - Oxford Univ Press Inc
PY  - 2017
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - Occupational exposure to aerosolized particles of oil-based metalworking fluid was recently linked to deaths from ischemic heart disease. The current recommended exposure limits might be insufficient. Studying cardiovascular mortality is challenging because symptoms can induce sicker workers to reduce their exposure, causing healthy-worker survivor bias. G-estimation of accelerated failure time models reduces this bias and permits comparison of multiple exposure interventions. Michigan autoworkers from the United AutoWorkers-General Motors cohort (n = 38,666) were followed from 1941 through 1994. Separate binary variables indicated whether annual exposure exceeded a series of potential limits. Separate g-estimation analyses for each limit yielded the total number of life-years that could have been saved among persons who died from specific cardiovascular causes by enforcing that exposure limit. Banning oil-based fluids would have saved an estimated 4,003 (95% confidence interval: 2,200, 5,807) life-years among those who died of ischemic heart disease. Estimates for cardiovascular disease overall, acute myocardial infarction, and cerebrovascular disease were 3,500 (95% confidence interval: 1,350, 5,651), 2,932 (95% confidence interval: 1,587, 4,277), and 917 (95% confidence interval: -80, 1,913) life-years, respectively. A limit of 0.01 mg/m(3) would have had a similar impact on cerebrovascular disease but one only half as great on ischemic heart disease. Analyses suggest that limiting exposure to metalworking fluids could have saved many life-years lost to cardiovascular diseases in this cohort.
AU  - Picciotto, S.*
AU  - Peters, A.
AU  - Eisen, E.A.*
C1  - 44379
C2  - 36808
CY  - Cary
SP  - 563-570
TI  - Hypothetical exposure limits for oil-based metalworking fluids and cardiovascular mortality in a cohort of autoworkers: Structural accelerated failure time models in a public health framework.
JO  - Am. J. Epidemiol.
VL  - 181
IS  - 8
PB  - Oxford Univ Press Inc
PY  - 2015
SN  - 0002-9262
ER  - 

TY  - JOUR
AU  - Beyerlein, A.
C1  - 31732
C2  - 36286
CY  - Cary
SP  - 330-331
TI  - Quantile regression-opportunities and challenges from a user's perspective.
JO  - Am. J. Epidemiol.
VL  - 180
IS  - 3
PB  - Oxford Univ Press Inc
PY  - 2014
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - Individual participant time-to-event data from multiple prospective epidemiologic studies enable detailed investigation into the predictive ability of risk models. Here we address the challenges in appropriately combining such information across studies. Methods are exemplified by analyses of log C-reactive protein and conventional risk factors for coronary heart disease in the Emerging Risk Factors Collaboration, a collation of individual data from multiple prospective studies with an average follow-up duration of 9.8 years (dates varied). We derive risk prediction models using Cox proportional hazards regression analysis stratified by study and obtain estimates of risk discrimination, Harrell's concordance index, and Royston's discrimination measure within each study; we then combine the estimates across studies using a weighted meta-analysis. Various weighting approaches are compared and lead us to recommend using the number of events in each study. We also discuss the calculation of measures of reclassification for multiple studies. We further show that comparison of differences in predictive ability across subgroups should be based only on within-study information and that combining measures of risk discrimination from case-control studies and prospective studies is problematic. The concordance index and discrimination measure gave qualitatively similar results throughout. While the concordance index was very heterogeneous between studies, principally because of differing age ranges, the increments in the concordance index from adding log C-reactive protein to conventional risk factors were more homogeneous.
AU  - Pennells, L.*
AU  - Kaptoge, S.*
AU  - White, I.R.*
AU  - Thompson, S.G.*
AU  - Wood, A.M.*
AU  - Emerging Risk Factors Collaboration (Meisinger, C.)
C1  - 29083
C2  - 33626
CY  - Cary
SP  - 621-632
TI  - Assessing risk prediction models using individual participant data from multiple studies.
JO  - Am. J. Epidemiol.
VL  - 179
IS  - 5
PB  - Oxford Univ Press Inc
PY  - 2014
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - The indiscriminate use of the cumulative exposure metric (the product of intensity and duration of exposure) might bias reported associations between exposure to hazardous agents and cancer risk. To assess the independent effects of duration and intensity of exposure on cancer risk, we explored effect modification of the association of cumulative exposure and cancer risk by intensity of exposure. We applied a flexible excess odds ratio model that is linear in cumulative exposure but potentially nonlinear in intensity of exposure to 15 case-control studies of cigarette smoking and lung cancer (19852009). Our model accommodated modification of the excess odds ratio per pack-year of cigarette smoking by time since smoking cessation among former smokers. We observed negative effect modification of the association of pack-years of cigarette smoking and lung cancer by intensity of cigarette smoke for persons who smoked more than 2030 cigarettes per day. Patterns of effect modification were similar across individual studies and across major lung cancer subtypes. We observed strong negative effect modification by time since smoking cessation. Application of our method in this example of cigarette smoking and lung cancer demonstrated that reducing a complex exposure history to a metric such as cumulative exposure is too restrictive.
AU  - Vlaanderen, J.*
AU  - Portengen, L.*
AU  - Schüz, J.*
AU  - Olsson, A.*
AU  - Pesch, B.*
AU  - Kendzia, B.*
AU  - Stücker, I.*
AU  - Guida, F.*
AU  - Brüske, I.
AU  - Wichmann, H.-E.
AU  - Consonni, D.*
AU  - Landi, M.T.*
AU  - Caporaso, N.*
AU  - Siemiatycki, J.*
AU  - Merletti, F.*
AU  - Mirabelli, D.*
AU  - Richiardi, L.*
AU  - Gustavsson, P.*
AU  - Plato, N.*
AU  - Jöckel, K.-H.*
AU  - Ahrens, W.*
AU  - Pohlabeln, H.*
AU  - Tardón, A.*
AU  - Zaridze, D.*
AU  - Field, J.K.*
AU  - 't Mannetje, A.*
AU  - Pearce, N.*
AU  - McLaughlin, J.*
AU  - Demers, P.*
AU  - Szeszenia-Dabrowska, N.*
AU  - Lissowska, J.*
AU  - Rudnai, P.*
AU  - Fabianova, E.*
AU  - Dumitru, R.S.*
AU  - Bencko, V.*
AU  - Foretova, L.*
AU  - Janout, V.*
AU  - Boffetta, P.*
AU  - Forastiere, F.*
AU  - Bueno-de-Mesquita, H.B.*
AU  - Peters, S.*
AU  - Brüning, T*
AU  - Kromhout, H.*
AU  - Straif, K.*
AU  - Vermeulen, R.*
C1  - 30633
C2  - 33754
CY  - Cary
SP  - 290-298
TI  - Effect modification of the association of cumulative exposure and cancer risk by intensity of exposure and time since exposure cessation: A flexible method applied to cigarette smoking and lung cancer in the SYNERGY study.
JO  - Am. J. Epidemiol.
VL  - 179
IS  - 3
PB  - Oxford Univ Press Inc
PY  - 2014
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - Obesity is of global health concern. There are well-described inverse relationships between female pubertal timing and obesity. Recent genome-wide association studies of age at menarche identified several obesity-related variants. Using data from the ReproGen Consortium, we employed meta-analytical techniques to estimate the associations of 95 a priori and recently identified obesity-related (body mass index (weight (kg)/height (m)(2)), waist circumference, and waist:hip ratio) single-nucleotide polymorphisms (SNPs) with age at menarche in 92,116 women of European descent from 38 studies (1970-2010), in order to estimate associations between genetic variants associated with central or overall adiposity and pubertal timing in girls. Investigators in each study performed a separate analysis of associations between the selected SNPs and age at menarche (ages 9-17 years) using linear regression models and adjusting for birth year, site (as appropriate), and population stratification. Heterogeneity of effect-measure estimates was investigated using meta-regression. Six novel associations of body mass index loci with age at menarche were identified, and 11 adiposity loci previously reported to be associated with age at menarche were confirmed, but none of the central adiposity variants individually showed significant associations. These findings suggest complex genetic relationships between menarche and overall obesity, and to a lesser extent central obesity, in normal processes of growth and development.
AU  - Fernández-Rhodes, L.*
AU  - Demerath, E.W.*
AU  - Cousminer, D.L.*
AU  - Tao, R.*
AU  - Dreyfus, J.G.*
AU  - Esko, T.*
AU  - Smith, A.V.*
AU  - Gudnason, V.*
AU  - Harris, T.B.*
AU  - Launer, L.*
AU  - McArdle, P.F.*
AU  - Yerges-Armstrong, L.M.*
AU  - Elks, C.E.*
AU  - Strachan, D.P.*
AU  - Kutalik, Z.*
AU  - Vollenweider, P.*
AU  - Feenstra, B.*
AU  - Boyd, H.A.*
AU  - Metspalu, A.*
AU  - Mihailov, E.*
AU  - Broer, L.*
AU  - Zillikens, M.C.*
AU  - Oostra, B.*
AU  - van Duijn, C.M.*
AU  - Lunetta, K.L.*
AU  - Perry, J.R.*
AU  - Murray, A.*
AU  - Koller, D.L.*
AU  - Lai, D.*
AU  - Corre, T.*
AU  - Toniolo, D.*
AU  - Albrecht, E.
AU  - Stöckl, D.
AU  - Grallert, H.
AU  - Gieger, C.
AU  - Hayward, C.*
AU  - Polasek, O.*
AU  - Rudan, I.*
AU  - Wilson, J.F.*
AU  - He, C.*
AU  - Kraft, P.*
AU  - Hu, F.B.*
AU  - Hunter, D.J.*
AU  - Hottenga, J.J.*
AU  - Willemsen, G.*
AU  - Boomsma, D.I.*
AU  - Byrne, E.M.*
AU  - Martin, N.G.*
AU  - Montgomery, G.W.*
AU  - Warrington, N.M.*
AU  - Pennell, C.E.*
AU  - Stolk, L.*
AU  - Visser, J.A.*
AU  - Hofman, A.*
AU  - Uitterlinden, A.G.*
AU  - Rivadeneira, F.*
AU  - Lin, P.*
AU  - Fisher, S.L.*
AU  - Bierut, L.J.*
AU  - Crisponi, L.*
AU  - Porcu, E.*
AU  - Mangino, M.*
AU  - Zhai, G.*
AU  - Spector, T.D.*
AU  - Buring, J.E.*
AU  - Rose, L.M.*
AU  - Ridker, P.M.*
AU  - Poole, C.*
AU  - Hirschhorn, J.N.*
AU  - Murabito, J.M.*
AU  - Chasman, D.I.*
AU  - Widen, E.*
AU  - North, K.E.*
AU  - Ong, K.K.*
AU  - Franceschini, N.*
C1  - 26741
C2  - 32363
SP  - 451-460
TI  - Association of adiposity genetic variants with menarche timing in 92,105 women of European descent.
JO  - Am. J. Epidemiol.
VL  - 178
IS  - 3
PB  - Oxford Univ. Press
PY  - 2013
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - Several epidemiologic studies have indicated an increased risk of lung cancer among welders. We used the SYNERGY project database to assess welding as a risk factor for developing lung cancer. The database includes data on 15,483 male lung cancer cases and 18,388 male controls from 16 studies in Europe, Canada, China, and New Zealand conducted between 1985 and 2010. Odds ratios and 95% confidence intervals between regular or occasional welding and lung cancer were estimated, with adjustment for smoking, age, study center, and employment in other occupations associated with lung cancer risk. Overall, 568 cases and 427 controls had ever worked as welders and had an odds ratio of developing lung cancer of 1.44 (95% confidence interval: 1.25, 1.67) with the odds ratio increasing for longer duration of welding. In never and light smokers, the odds ratio was 1.96 (95% confidence interval: 1.37, 2.79). The odds ratios were somewhat higher for squamous and small cell lung cancers than for adenocarcinoma. Another 1,994 cases and 1,930 controls had ever worked in occupations with occasional welding. Work in any of these occupations was associated with some elevation of risk, though not as much as observed in regular welders. Our findings lend further support to the hypothesis that welding is associated with an increased risk of lung cancer.
AU  - Kendzia, B.*
AU  - Behrens, T.*
AU  - Jöckel, K.-H.*
AU  - Siemiatycki, J.*
AU  - Kromhout, H.*
AU  - Vermeulen, R.*
AU  - Peters, S.*
AU  - van Gelder, R.*
AU  - Olsson, A.*
AU  - Brüske, I.
AU  - Wichmann, H.-E.
AU  - Stücker, I.*
AU  - Guida, F.*
AU  - Tardón, A.*
AU  - Merletti, F.*
AU  - Mirabelli, D.*
AU  - Richiardi, L.*
AU  - Pohlabeln, H.*
AU  - Ahrens, W.*
AU  - Landi, M.T.*
AU  - Caporaso, N.*
AU  - Consonni, D.*
AU  - Zaridze, D.*
AU  - Szeszenia-Dabrowska, N.*
AU  - Lissowska, J.*
AU  - Gustavsson, P.*
AU  - Marcus, M.W.*
AU  - Fabianova, E.*
AU  - 't Mannetje, A.*
AU  - Pearce, N.*
AU  - Tse, L.A.*
AU  - Yu, I.T.*
AU  - Rudnai, P.*
AU  - Bencko, V.*
AU  - Janout, V.*
AU  - Mates, D.*
AU  - Foretova, L.*
AU  - Forastiere, F.*
AU  - McLaughlin, J.*
AU  - Demers, P.*
AU  - Bueno-de-Mesquita, H.B.*
AU  - Boffetta, P.*
AU  - Schüz, J.*
AU  - Straif, K.*
AU  - Pesch, B.*
AU  - Brüning, T*
C1  - 28559
C2  - 33449
SP  - 1513-1525
TI  - Welding and lung cancer in a pooled analysis of case-control studies.
JO  - Am. J. Epidemiol.
VL  - 178
IS  - 10
PB  - Oxford Univ. Press
PY  - 2013
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - The objective of this study was to investigate the association between residential environment and type 2 diabetes. We pooled cross-sectional data from 5 population-based German studies (1997-2006): the Cardiovascular Disease, Living and Ageing in Halle Study, the Dortmund Health Study, the Heinz Nixdorf Recall Study, the Cooperative Health Research in the Region of Augsburg Study, and the Study of Health in Pomerania. The outcome of interest was the presence of self-reported type 2 diabetes. We conducted mixed logistic regression models in a hierarchical data set with 8,879 individuals aged 45-74 years on level 1; 226 neighborhoods on level 2; and 5 study regions on level 3. The analyses were adjusted for age, sex, social class, and employment status. The odds ratio for type 2 diabetes was highest in eastern Germany (odds ratio = 1.98, 95% confidence interval: 1.81, 2.14) and northeastern Germany (odds ratio = 1.58, 95% confidence interval: 1.40, 1.77) and lowest in southern Germany (reference) after adjustment for individual variables. Neighborhood unemployment rates explained a large proportion of regional differences. Individuals residing in neighborhoods with high unemployment rates had elevated odds of type 2 diabetes (odds ratio = 1.62, 95% confidence interval: 1.25, 2.09). The diverging levels of unemployment in neighborhoods and regions are an independent source of disparities in type 2 diabetes.
AU  - Müller, G.*
AU  - Kluttig, A.*
AU  - Greiser, K.H.*
AU  - Moebus, S.*
AU  - Slomiany, U.*
AU  - Schipf, S.*
AU  - Völzke, H.*
AU  - Maier, W.
AU  - Meisinger, C.
AU  - Tamayo, T.*
AU  - Rathmann, W.*
AU  - Berger, K.*
C1  - 24553
C2  - 31571
SP  - 221-230
TI  - Regional and neighborhood disparities in the odds of type 2 diabetes: Results from 5 population-based studies in Germany (DIAB-CORE Consortium).
JO  - Am. J. Epidemiol.
VL  - 178
IS  - 2
PB  - Oxford Univ. Press
PY  - 2013
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - Increased lung cancer risks among hairdressers were observed in large registry-based cohort studies from Scandinavia, but these studies could not adjust for smoking. Our objective was to evaluate the lung cancer risk among hairdressers while adjusting for smoking and other confounders in a pooled database of 16 case-control studies conducted in Europe, Canada, China, and New Zealand between 1985 and 2010 (the Pooled Analysis of Case-Control Studies on the Joint Effects of Occupational Carcinogens in the Development of Lung Cancer). Lifetime occupational and smoking information was collected through interviews with 19,369 cases of lung cancer and 23,674 matched population or hospital controls. Overall, 170 cases and 167 controls had ever worked as hairdresser or barber. The odds ratios for lung cancer in women were 1.65 (95% confidence interval (CI): 1.16, 2.35) without adjustment for smoking and 1.12 (95% CI: 0.75, 1.68) with adjustment for smoking; however, women employed before 1954 also experienced an increased lung cancer risk after adjustment for smoking (odds ratio = 2.66, 95% CI: 1.09, 6.47). The odds ratios in male hairdressers/barbers were generally not elevated, except for an increased odds ratio for adenocarcinoma in long-term barbers (odds ratio = 2.20, 95% CI: 1.02, 4.77). Our results suggest that the increased lung cancer risks among hairdressers are due to their smoking behavior; single elevated risk estimates should be interpreted with caution and need replication in other studies.
AU  - Olsson, A.C.*
AU  - Xu, Y.*
AU  - Schüz, J.*
AU  - Vlaanderen, J.*
AU  - Kromhout, H.*
AU  - Vermeulen, R.*
AU  - Peters, S.*
AU  - Stücker, I.*
AU  - Guida, F.*
AU  - Brüske, I.
AU  - Wichmann, H.-E.
AU  - Consonni, D.*
AU  - Landi, M.T.*
AU  - Caporaso, N.*
AU  - Tse, L.A.*
AU  - Yu, I.T.*
AU  - Siemiatycki, J.*
AU  - Richardson, L.*
AU  - Mirabelli, D.*
AU  - Richiardi, L.*
AU  - Simonato, L.*
AU  - Gustavsson, P.*
AU  - Plato, N.*
AU  - Jöckel, K.-H.*
AU  - Ahrens, W.*
AU  - Pohlabeln, H.*
AU  - Tardón, A.*
AU  - Zaridze, D.*
AU  - Marcus, M.W.*
AU  - 't Mannetje, A.*
AU  - Pearce, N.*
AU  - McLaughlin, J.*
AU  - Demers, P.*
AU  - Szeszenia-Dabrowska, N.*
AU  - Lissowska, J.*
AU  - Rudnai, P.*
AU  - Fabianova, E.*
AU  - Dumitru, R.S.*
AU  - Bencko, V.*
AU  - Foretova, L.*
AU  - Janout, V.*
AU  - Boffetta, P.*
AU  - Fortes, C.*
AU  - Bueno-de-Mesquita, H.B.*
AU  - Kendzia, B.*
AU  - Behrens, T.*
AU  - Pesch, B.*
AU  - Brüning, T*
AU  - Straif, K.*
C1  - 28558
C2  - 33448
SP  - 1355-1365
TI  - Lung cancer risk among hairdressers: A pooled analysis of case-control studies conducted between 1985 and 2010.
JO  - Am. J. Epidemiol.
VL  - 178
IS  - 9
PB  - Oxford Univ. Press
PY  - 2013
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - To clarify the role of previous lung diseases (chronic bronchitis, emphysema, pneumonia, and tuberculosis) in the development of lung cancer, the authors conducted a pooled analysis of studies in the International Lung Cancer Consortium. Seventeen studies including 24,607 cases and 81,829 controls (noncases), mainly conducted in Europe and North America, were included (19842011). Using self-reported data on previous diagnoses of lung diseases, the authors derived study-specific effect estimates by means of logistic regression models or Cox proportional hazards models adjusted for age, sex, and cumulative tobacco smoking. Estimates were pooled using random-effects models. Analyses stratified by smoking status and histology were also conducted. A history of emphysema conferred a 2.44-fold increased risk of lung cancer (95 confidence interval (CI): 1.64, 3.62 (16 studies)). A history of chronic bronchitis conferred a relative risk of 1.47 (95 CI: 1.29, 1.68 (13 studies)). Tuberculosis (relative risk 1.48, 95 CI: 1.17, 1.87 (16 studies)) and pneumonia (relative risk 1.57, 95 CI: 1.22, 2.01 (12 studies)) were also associated with lung cancer risk. Among never smokers, elevated risks were observed for emphysema, pneumonia, and tuberculosis. These results suggest that previous lung diseases influence lung cancer risk independently of tobacco use and that these diseases are important for assessing individual risk.
AU  - Brenner, D.R.*
AU  - Boffetta, P.*
AU  - Duell, E.J.*
AU  - Bickeböller, H.*
AU  - Rosenberger, A.*
AU  - McCormack, V.*
AU  - Muscat, J.E.*
AU  - Yang, P.*
AU  - Wichmann, H.-E.
AU  - Brüske, I.
AU  - Schwartz, A.G.*
AU  - Cote, M.L.*
AU  - Tjonneland, A.*
AU  - Friis, S.*
AU  - Le Marchand, L.*
AU  - Zhang, Z.-F.*
AU  - Morgenstern, H.*
AU  - Szeszenia-Dabrowska, N.*
AU  - Lissowska, J.*
AU  - Zaridze, D.*
AU  - Rudnai, P.*
AU  - Fabianova, E.*
AU  - Foretova, L.*
AU  - Janout, V.*
AU  - Bencko, V.*
AU  - Schejbalova, M.*
AU  - Brennan, P.*
AU  - Mates, I.N.*
AU  - Lazarus, P.*
AU  - Field, J.K.*
AU  - Raji, O.*
AU  - McLaughlin, J.R.*
AU  - Liu, G.*
AU  - Wiencke, J.*
AU  - Neri, M.*
AU  - Ugolini, D.*
AU  - Andrew, A.S.*
AU  - Lan, Q.*
AU  - Hu, W.*
AU  - Orlow, I.*
AU  - Park, B.J.*
AU  - Hung, R.J.*
C1  - 10707
C2  - 30417
SP  - 573-585
TI  - Previous lung diseases and lung cancer risk: A pooled analysis from the International Lung Cancer Consortium.
JO  - Am. J. Epidemiol.
VL  - 176
IS  - 7
PB  - Oxford Univ. Press
PY  - 2012
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - For most associations of common single nucleotide polymorphisms (SNPs) with common diseases, the genetic model of inheritance is unknown. The authors extended and applied a Bayesian meta-analysis approach to data from 19 studies on 17 replicated associations with type 2 diabetes. For 13 SNPs, the data fitted very well to an additive model of inheritance for the diabetes risk allele; for 4 SNPs, the data were consistent with either an additive model or a dominant model; and for 2 SNPs, the data were consistent with an additive or recessive model. Results were robust to the use of different priors and after exclusion of data for which index SNPs had been examined indirectly through proxy markers. The Bayesian meta-analysis model yielded point estimates for the genetic effects that were very similar to those previously reported based on fixed- or random-effects models, but uncertainty about several of the effects was substantially larger. The authors also examined the extent of between-study heterogeneity in the genetic model and found generally small between-study deviation values for the genetic model parameter. Heterosis could not be excluded for 4 SNPs. Information on the genetic model of robustly replicated association signals derived from genome-wide association studies may be useful for predictive modeling and for designing biologic and functional experiments.
AU  - Salanti, G.*
AU  - Southam, L.*
AU  - Altshuler, D.*
AU  - Ardlie, K.*
AU  - Barroso, I.*
AU  - Boehnke, M.*
AU  - Cornelis, M.C.*
AU  - Frayling, T.M.*
AU  - Grallert, H.
AU  - Grarup, N.*
AU  - Groop, L.*
AU  - Hansen, T.*
AU  - Hattersley, A.T.*
AU  - Hu, F.B.*
AU  - Hveem, K.*
AU  - Illig, T.
AU  - Kuusisto, J.*
AU  - Laakso, M.*
AU  - Langenberg, C.*
AU  - Lyssenko, V.*
AU  - McCarthy, M.I.*
AU  - Morris, A.*
AU  - Morris, A.D.*
AU  - Palmer, C.N.A.*
AU  - Payne, F.*
AU  - Platou, C.G.P.*
AU  - Scott, L.J.*
AU  - Voight, B.F.*
AU  - Wareham, N.J.*
AU  - Zeggini, E.*
AU  - Ioannidis, J.P.A.*
C1  - 91
C2  - 26590
CY  - Oxford
SP  - 537-545
TI  - Underlying genetic models of inheritance in established type 2 diabetes associations.
JO  - Am. J. Epidemiol.
VL  - 170
IS  - 5
PB  - Oxford Univ Press
PY  - 2009
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - Previously, estimation of genotype misclassification of single nucleotide polymorphisms (SNPs) as encountered in epidemiologic practice and involving thousands of subjects was lacking. The authors collected representative data on approximately 14,000 subjects from 8 studies and 646,558 genotypes assessed in 2005 by means of matrix-assisted laser desorption ionization time-of-flight mass spectrometry. Overall discordance among 57,805 double genotypes from routine quality control was 0.36%. Fitting different misclassification models by maximum likelihood assuming identical misclassification for all SNPs, the estimated misclassification probabilities ranged from 0.0000 to 0.0035. When applying the misclassification simulation and extrapolation (MC-SIMEX) method for the first time to genetic data to account for the misclassification in a reanalysis of adiponectin-encoding (APM1) gene SNP associations with plasma adiponectin in 1,770 subjects, the authors found no impact of this small error on association estimates but increased estimates for a more substantial error. This study is the first to provide large-scale epidemiologic data on SNP genotype misclassification. The estimated misclassification in this example was small and negligible for association estimates, which is reassuring and essential for detecting SNP associations. In situations with more substantial error, the presented approach using duplicate genotyping and the MC-SIMEX method is practical and helpful for quantifying the genotyping error and its impact.
AU  - Heid, I.M.
AU  - Lamina, C.
AU  - Küchenhoff, H.*
AU  - Fischer, G.
AU  - Klopp, N.
AU  - Kolz, M.
AU  - Grallert, H.
AU  - Vollmert, C.
AU  - Wagner, S.
AU  - Huth, C.
AU  - Müller, J.*
AU  - Müller, M.
AU  - Hunt, S.C.*
AU  - Peters, A.
AU  - Paulweber, B.*
AU  - Wichmann, H.-E.
AU  - Kronenberg, F.*
AU  - Illig, T.
C1  - 239
C2  - 25817
SP  - 878-889
TI  - Estimating the Single Nucleotide Polymorphism Genotype Misclassification From Routine Double Measurements in a Large Epidemiologic Sample.
JO  - Am. J. Epidemiol.
VL  - 168
IS  - 8
PB  - Oxford Univ. Press
PY  - 2008
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - A recent analysis showed that the excess odds ratio (EOR) for lung cancer due to smoking can be modeled by a function which is linear in total pack-years and exponential in the logarithm of smoking intensity and its square. Below 15-20 cigarettes per day, the EOR/pack-year increased with intensity (direct exposure rate or enhanced potency effect), suggesting greater risk for a total exposure delivered at higher intensity (for a shorter duration) than for an equivalent exposure delivered at lower intensity. Above 20 cigarettes per day, the EOR/pack-year decreased with increasing intensity (inverse exposure rate or reduced potency effect), suggesting greater risk for a total exposure delivered at lower intensity (for a longer duration) than for an equivalent exposure delivered at higher intensity. The authors applied this model to data from 10 case-control studies of cancer, including cancers of the lung, bladder, oral cavity, pancreas, and esophagus. At lower intensities, there was enhanced potency for several cancer sites, but narrow ranges for pack-years increased uncertainty, precluding definitive conclusions. At higher intensities, there was a consistent reduced potency effect across studies. The intensity effects were statistically homogeneous, indicating that after accounting for risk from total pack-years, intensity patterns were comparable across the diverse cancer sites.
AU  - Lubin, J.H.*
AU  - Alavanja, M.C. R.*
AU  - Caporaso, N.*
AU  - Brown, L.M.*
AU  - Brownson, R.C.*
AU  - Field, R.W.*
AU  - Garcia-Closas, M.*
AU  - Hartge, P.*
AU  - Hauptmann, M.*
AU  - Hayes, R.B.*
AU  - Kleinerman, R.*
AU  - Kogevinas, M.*
AU  - Krewski, D.*
AU  - Langholz, B.*
AU  - Letourneau, E.G.*
AU  - Lynch, C.F.*
AU  - Malats, N.*
AU  - Sandler, D.P.*
AU  - Schaffrath Rosario, A.*
AU  - Schoenberg, J.B.*
AU  - Silverman, D.T.*
AU  - Wang, Z.Y.*
AU  - Wichmann, H.-E.
AU  - Wilcox, H.B.*
AU  - Zielinski, J.M.*
C1  - 3881
C2  - 25016
SP  - 479-489
TI  - Cigarette smoking and cancer risk: Modeling total exposure and intensity.
JO  - Am. J. Epidemiol.
VL  - 166
IS  - 4
PB  - Oxford Univ. Press
PY  - 2007
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - Individuals from the same population share a number of contextual circumstances that may condition a common level of blood pressure over and above individual characteristics. Understanding this population effect is relevant for both etiologic research and prevention strategies. Using multilevel regression analyses, the authors quantified the extent to which individual differences in systolic blood pressure (SBP) could be attributed to the population level. They also investigated possible cross-level interactions between the population in which a person lived and pharmacological (antihypertensive medication) and nonpharmacological (body mass index) effects on individual SBP. They analyzed data on 23,796 men and 24,986 women aged 35–64 years from 39 worldwide Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) study populations participating in the final survey of this World Health Organization project (1989–1997). SBP was positively associated with low educational achievement, high body mass index, and use of antihypertensive medication and, for women, was negatively associated with smoking. About 7–8% of all SBP differences between subjects were attributed to the population level. However, this population effect was particularly strong (i.e., 20%) in antihypertensive medication users and overweight women. This empirical evidence of a population effect on individual SBP emphasizes the importance of developing population-wide strategies to reduce individual risk of hypertension.
AU  - Merlo, J.*
AU  - Asplund, K.*
AU  - Lynch, J.*
AU  - Råstam, L.*
AU  - Dobson, A.*
AU  - World Health Organization MONICA Project
C1  - 2184
C2  - 22197
SP  - 1168-1179
TI  - Population effects on individual systolic blood pressure: A multilevel analysis of the world health organization MONICA project.
JO  - Am. J. Epidemiol.
VL  - 159
IS  - 12
PY  - 2004
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - The ULTRA Study, a study investigating the association between fine and ultrafine particulate air pollution and cardiorespiratory health, was conducted during the winter of 1998–1999 in Amsterdam, the Netherlands; Erfurt, Germany; and Helsinki, Finland. At each study center, a panel of elderly subjects with coronary heart disease recorded cardiac and respiratory symptoms in a diary. Exposure to ambient air pollution was characterized by measuring daily mass concentrations of particles smaller than 10 µm (PM10) and 2.5 µm (PM2.5), number concentrations of ultrafine particles (NC0.01–0.1), and gases. Odds ratios for the relation of symptoms to air pollution, adjusted for time trend, respiratory infections, and meteorologic variables, were mostly homogeneous across the centers. No association was found between air pollution and chest pain. A 10-µg/m3 increase in PM2.5 was positively associated with the incidence of shortness of breath (odds ratio (OR) = 1.12, 95% confidence interval (CI): 1.02, 1.24) and with avoidance of activities (OR = 1.09, 95% CI: 0.97, 1.22). NC0.01–0.1 was only associated with the prevalence of avoidance of activities (OR = 1.10, 95% CI: 1.01, 1.19). In conclusion, PM2.5 was associated with some cardiac symptoms in three panels of elderly subjects. PM2.5 was more strongly related to cardiorespiratory symptoms than ultrafine particles were.
AU  - de Hartog, J.J.*
AU  - Hoek, G.*
AU  - Peters, A.
AU  - Timonen, K.L.*
AU  - Ibald-Mulli, A.
AU  - Brunekreef, B.*
AU  - Heinrich, J.
AU  - Tiittanen, P.*
AU  - van Wijnen, J.H.*
AU  - Kreyling, W.G.
AU  - Kulmala, M.*
AU  - Pekkanen, J.*
C1  - 10382
C2  - 21250
SP  - 613-623
TI  - Effects of Fine and Ultrafine Particles on Cardiorespiratory Symptoms in Elderly Subjects with Coronary Heart Disease. The ULTRA Study.
JO  - Am. J. Epidemiol.
VL  - 157
IS  - 7
PY  - 2003
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - The authors sought to assess the repeatability of
      
      	measurements of C-reactive protein, an independent
      
      	predictor of coronary heart disease, in a large cohort of apparently healthy men and to correct earlier estimates
      
      	of the association of C-reactive protein and coronary heart disease for the measurement error in this protein. They
      
      	measured C-reactive protein by a high-sensitivity assay in 936 men aged 45–64 years in the MONICA (Monitoring
      
      	of Trends and Determinants in Cardiovascular Disease) Augsburg cohort in 1984–1985 and remeasured it 3
      
      	years later. All men were subjected to an 8-year follow-up of their cardiovascular status. The analytical variation
      
      	of the assay was small, with the analytical variance component at 1 percent of the within-subject variance
      
      	component, a repeatability coefficient of 25 percent, and a reliability coefficient of 1.00. In contrast, the within-
      
      	subject variation of C-reactive protein corresponded to a repeatability coefficient of 740 percent and a reliability
      
      	coefficient of 0.54, indicating considerable within-subject variation. Based on the authors’ estimates, three serial
      
      	determinations of C-reactive protein should be done to achieve a reliability of 0.75, the value they found for total
      
      	cholesterol. Correcting the hazard ratios in their original analysis of the association of coronary heart disease and
      
      	high-sensitivity-assay C-reactive protein for the measurement error in C-reactive protein and covariables leads
      
      	to a considerably larger estimate. The results suggest that the true association between C-reactive protein and
      
      	cardiovascular risk is underestimated by a single C-reactive protein determination, and that several serial C-
      
      	reactive protein measurements should be taken.
AU  - Koenig, W.*
AU  - Sund, M.
AU  - Fröhlich, M.*
AU  - Löwel, H.
AU  - Hutchinson, W.L.*
AU  - Pepys, M.B.*
C1  - 10383
C2  - 21553
SP  - 357-364
TI  - Refinement of the Association of Serum C-reactive Protein Concentration and Coronary Heart Disease Risk by Correction for Within-Subject Variation over Time : The MONICA Augsburg Studies,1984-1987.
JO  - Am. J. Epidemiol.
VL  - 158
IS  - 4
PY  - 2003
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - In a 1990-1996 case-control study in western Germany, the authors investigated lung cancer risk due to exposure to residential radon. Confirmed lung cancer cases from hospitals and a random sample of community controls were interviewed by trained interviewers regarding different risk factors. For 1 year, alpha track detectors were placed in dwellings to measure radon gas concentrations. The evaluation included 1,449 cases and 2,297 controls recruited from the entire study area and a subsample of 365 cases and 595 controls from radon-prone areas of the basic study region. Rate ratios were estimated by using conditional logistic regression adjusted for smoking and for asbestos exposure. In the entire study area, no rate ratios different from 1.0 were found; in the radon-prone areas, the adjusted rate ratios for exposure in the present dwelling were 1.59 (95% confidence interval (Cl): 1.08, 2.27), 1.93 (95% Cl: 1.19, 3.13), and 1.93 (95% Cl: 0.99, 3.77) for 50-80, 80-140, and >140 Bq/m(3), respectively, compared with 0-50 Bq/m(3). The excess rate ratio for an increase of 100 Bq/m(3) was 0.13 (-0.12 to 0.46). An analysis based on cumulative exposure produced similar results. The results provide additional evidence that residential radon is a risk factor for lung cancer, although a risk was detected in radon-prone areas only, not in the entire study area.
AU  - Kreienbrock, L.
AU  - Kreuzer, M.
AU  - Gerken, M.
AU  - Dingerkus, G.*
AU  - Wellmann, J.
AU  - Keller, G.*
AU  - Wichmann, H.-E.
C1  - 10381
C2  - 19874
SP  - 42-52
TI  - Case-Control Study on Lung Cancer and Residential Radon in Western Germany.
JO  - Am. J. Epidemiol.
VL  - 153 
IS  - 1
PB  - Oxford Univ. Press
PY  - 2001
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - Occupational exposures such as crystalline silica, diesel engine exhaust, polycyclic aromatic hydrocarbons, and man-made mineral fibers are strongly suspected to increase lung cancer risk. Two case-control studies in Germany conducted between 1988 and 1996 were pooled for a joint analysis. A total of 3,498 male cases and 3,541 male population controls, frequency matched for age and region, were included in the study. The lifelong history of all jobs and industries was coded and occupational exposures were evaluated by expert rating. Odds ratios, crude and adjusted for smoking and asbestos exposure, were calculated by conditional logistic regression. Job-related evaluation showed a statistically significant increased odds ratio adjusted for smoking among farmers; forestry workers, fishermen, and livestock workers; miners and quarrymen; chemical processors; cabinet makers and related wood workers; metal producers and processors; bricklayers and carpenters; road construction workers, pipelayers and well diggers; plasterers, insulators, and upholsterers; painters and lacquerers; stationary engine and heavy equipment operators; transport workers and freight handlers; and service workers. With regard to specific occupational exposures, elevated odds ratios (OR) (95% confidence intervals (CI) for lung cancer risk adjusted for smoking and asbestos exposure were observed for man-made mineral fibers (OR = 1.48, 95% CI 1.17, 1.88); crystalline silica (OR = 1.41, 95% CI 1.22, 1.62); diesel engine exhaust (OR = 1.43, 95% CI 1.23, 1.67); and polycyclic aromatic hydrocarbons (OR = 1.53, 95% CI 1.14, 2.04). The risk of asbestos exposure, adjusted for smoking was also increased (OR = 1.41, 95% CI 1.24, 1.60).
AU  - Brüske, I.
AU  - Möhner, M.*
AU  - Pohlabeln, H.*
AU  - Ahrens, W.*
AU  - Bolm-Audorff, U.*
AU  - Kreienbrock, L.
AU  - Kreuzer, M.
AU  - Jahn, I.*
AU  - Wichmann, H.-E.
AU  - Jöckel, K.-H.*
C1  - 21303
C2  - 19418
SP  - 384-395
TI  - Occupational Lung Cancer Risk for Men in Germany: Results from a Pooled Case-Control Study.
JO  - Am. J. Epidemiol.
VL  - 151
IS  - 4
PY  - 2000
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - To assess the association between exposure to environmental tobacco smoke (ETS) and lung cancer, the authors personally interviewed 292 lifelong nonsmoking lung cancer cases (recruited from 15 hospitals in the study area) and 1,338 nonsmoking controls (randomly selected by population registries) between 1990 and 1996 in Germany. Subjects were asked by a standardized questionnaire about exposure to ETS in childhood, by spouse, at work, and in transportation and social settings. Several indicators of these different sources of exposure were investigated, using not or low exposed subjects as the reference category. The most informative quantification index was weighted duration of exposure (hours x level of smokiness). No effect of ETS exposure during childhood and no clear effect of spousal ETS were observed. However, for the highest category of exposure, clear effects of ETS at the workplace (odds ratio (OR) = 1.93; 95% confidence interval (CI): 1.04, 3.58), in vehicles (OR = 2.64; 95% CI: 1.30, 5.36), and from all sources combined (OR = 1.39; 95% CI: 0.96, 2.01) were found. Adjustment for occupational carcinogens, radon, and diet did not appreciably change the results. These findings suggest that exposures to high levels of ETS at the workplace and in other public indoor settings appear to be important risk factors for lung cancer risk in nonsmokers.
AU  - Kreuzer, M.
AU  - Krauss, M.
AU  - Kreienbrock, L.
AU  - Jöckel, K.-H.*
AU  - Wichmann, H.-E.
C1  - 21314
C2  - 19429
SP  - 241-250
TI  - Environmental Tobacco Smoke and Lung Cancer: A Case-Control Study in Germany.
JO  - Am. J. Epidemiol.
VL  - 151
IS  - 3
PY  - 2000
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - The risk or rate advancement period (RAP) proposed by Brenner et al. (Epidemiology 1993;4:229–36) conveys information on the impact of a risk factor on the age dimension of chronic disease occurrence and may thus facilitate communication of epidemiologic findings. The RAP expresses how much sooner a given risk or rate of disease occurrence is reached among exposed than among unexposed individuals. The purpose of the present analysis was to derive estimates of RAPs for cardiovascular risk factors in relation to incident nonfatal and fatal myocardial infarction in middle-aged men of the Monitoring Trends and Determinants in Cardiovascular Diseases (MONICA) Augsburg cohort, Germany, between 1984 and 1995. RAPs were estimated based on Cox proportional hazards models. After multivariate adjustment, hypertension, smoking, and dyslipidemia were associated with RAPs of 8, 11, and 11 years, respectively, conditional on infarction-free survival to baseline and absence of competing risks. The RAP may be interpreted as that, on average, smokers are expected to advance their risk of myocardial infarction approximately 11 years compared with never/former smokers; for example, 50-year-old smokers are expected to carry the same risk of infarction as 61-year-old nonsmokers. The authors encourage the use and evaluation of the RAP as an effective risk communication tool in actual counseling situations.
AU  - Liese, A.D.*
AU  - Hense, H.-W.*
AU  - Brenner, H.*
AU  - Löwel, H.
AU  - Keil, U.
C1  - 21587
C2  - 19713
SP  - 884-888
TI  - Assessing the Impact of Classical Risk Factors on Myocardial Infarction by Rate Advancement Periods.
JO  - Am. J. Epidemiol.
VL  - 152
IS  - 9
PY  - 2000
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - This paper assesses whether air pollution increases resting heart rates in 2,681 men and women aged 25-64 years who participated in the MONICA (monitoring of trends and determinants in cardiovascular disease) Augsburg cohort. Increases in heart rate were observed during the air pollution episode in January 1985 compared with non-episode days adjusted for cardiovascular risk factors and meteorologic parameters. Consistently, heart rates were also elevated at high concentrations of sulfur dioxide, total suspended particulates, or carbon monoxide. Acceleration in heart rates indicates an altered autonomic control of the heart in association with air pollution, which may contribute to the observed health effects in association with air pollution.
AU  - Peters, A.
AU  - Perz, S.
AU  - Döring, A.
AU  - Stieber, J.
AU  - Koenig, W.*
AU  - Wichmann, H.-E.
C1  - 21086
C2  - 19119
SP  - 1094-1098
TI  - Increases in heart rate during an air pollution episode.
JO  - Am. J. Epidemiol.
VL  - 150
IS  - 10
PY  - 1999
SN  - 0002-9262
ER  - 

TY  - JOUR
AU  - Hense, H.W.
AU  - Filipiak, B.
AU  - Keil, U.
C1  - 40053
C2  - 38075
SP  - 543
TI  - Re: "blood lead as a cardiovascular risk factor".
JO  - Am. J. Epidemiol.
VL  - 139
IS  - 5
PY  - 1994
SN  - 0002-9262
ER  - 

TY  - JOUR
AB  - This study examined the association between women's employment and high density lipoprotein (HDL) cholesterol. Subjects were 1,998 women aged 25-64 years who were sampled by the first MONICA Augsburg Survey (Monitoring of Trends and Determinants in Cardiovascular Disease). The women were sampled from the population of Augsburg, Federal Republic of Germany, in 1984-1985, were followed up for 3 years, and were reexamined in 1987-1988. In cross- sectional analysis (1984-1985), the mean HDL cholesterol level of employed women was 3.4 mg/dl higher than that of full-time homemakers (p < 0.001). After adjustment for age, body mass, cigarette smoking, consumption of coffee and alcohol, use of sex hormones, leisure-time physical activity, and reproductive history, this difference decreased to 2.1 mg/dl and remained statistically significant (p < 0.01). As was predicted from the cross- sectional findings, the mean HDL cholesterol levels of women who gave up employment and became full-time homemakers during the follow-up period decreased by 3.04 mg/dl (p < 0.01), whereas homemakers who became employed showed no significant change in HDL cholesterol levels. The change in mean HDL cholesterol of employed women who had become homemakers could be explained in part by changes in alcohol consumption and in number of pregnancies. The authors conclude that giving up employment is related to life-style changes that are associated with a decrease in HDL cholesterol levels. Furthermore, the findings suggest that employment may exert a beneficial influence on coronary risk in women that is consistent with a positive association between employment and HDL cholesterol.
AU  - Haertel, U.
AU  - Heiss, G.M.
AU  - Filipiak, B.
AU  - Doering, A.
C1  - 40624
C2  - 38753
SP  - 68-78
TI  - Cross-sectional and longitudinal associations between high density lipoprotein cholesterol and women's employment.
JO  - Am. J. Epidemiol.
VL  - 135
IS  - 1
PY  - 1992
SN  - 0002-9262
ER  -