Author: "Aasvang, Gm" - Searchworks@Jio Institute Digital Library Search Results

Your search keyword '"Aasvang, Gm"' showing total 47 results

Start Over Author "Aasvang, Gm"

47 results on '"Aasvang, Gm"'

1. DNA methylation and body mass index from birth to adolescence: meta-analyses of epigenome-wide association studies

Author: Vehmeijer, Florianne, Küpers, LK, Sharp, GC, Salas, LA, Lent, S, Jima, DD, Tindula, G, Reese, S, Qi, C, Gruzieva, O, Page, C, Rezwan, FI, Melton, PE, Nohr, E, Escaramís, G, Rzehak, P, Heiskala, A, Gong, T, Tuominen, ST, Gao, L, Ross, JP, Starling, AP, Holloway, JW, Yousefi, P, Aasvang, GM, Beilin, LJ, Bergström, A, Binder, E, Chatzi, L, Corpeleijn, E, Czamara, D, Eskenazi, B, Ewart, S, Ferre, N, Grote, V, Gruszfeld, D, Håberg, SE, Hoyo, C, Huen, K, Karlsson, R, Kull, I, Langhendries, J P, Lepeule, J, Magnus, MC, Maguire, RL, Molloy, PL, Monnereau, Claire, Mori, TA, Oken, E, Räikkönen, K, Rifas-Shiman, S, Ruiz-Arenas, C, Sebert, S, Ullemar, V, Verduci, E, Vonk, JM, Xu, CJ, Yang, IV, Zhang, H, Zhang, W, Karmaus, W, Dabelea, D, Muhlhausler, BS, Breton, CV, Lahti, J, Almqvist, C, Jarvelin, M R R, Koletzko, B, Vrijheid, M, Sørensen, TIA, Huang, RC, Arshad, SH, Nystad, W, Melén, E, Koppelman, GH, London, SJ, Holland, N, Bustamante, M, Murphy, SK, Hivert, MF, Baccarelli, A, Relton, CL, Snieder, H, Jaddoe, Vincent, Felix, Janine, Vehmeijer, Florianne, Küpers, LK, Sharp, GC, Salas, LA, Lent, S, Jima, DD, Tindula, G, Reese, S, Qi, C, Gruzieva, O, Page, C, Rezwan, FI, Melton, PE, Nohr, E, Escaramís, G, Rzehak, P, Heiskala, A, Gong, T, Tuominen, ST, Gao, L, Ross, JP, Starling, AP, Holloway, JW, Yousefi, P, Aasvang, GM, Beilin, LJ, Bergström, A, Binder, E, Chatzi, L, Corpeleijn, E, Czamara, D, Eskenazi, B, Ewart, S, Ferre, N, Grote, V, Gruszfeld, D, Håberg, SE, Hoyo, C, Huen, K, Karlsson, R, Kull, I, Langhendries, J P, Lepeule, J, Magnus, MC, Maguire, RL, Molloy, PL, Monnereau, Claire, Mori, TA, Oken, E, Räikkönen, K, Rifas-Shiman, S, Ruiz-Arenas, C, Sebert, S, Ullemar, V, Verduci, E, Vonk, JM, Xu, CJ, Yang, IV, Zhang, H, Zhang, W, Karmaus, W, Dabelea, D, Muhlhausler, BS, Breton, CV, Lahti, J, Almqvist, C, Jarvelin, M R R, Koletzko, B, Vrijheid, M, Sørensen, TIA, Huang, RC, Arshad, SH, Nystad, W, Melén, E, Koppelman, GH, London, SJ, Holland, N, Bustamante, M, Murphy, SK, Hivert, MF, Baccarelli, A, Relton, CL, Snieder, H, Jaddoe, Vincent, and Felix, Janine
Published: 2020

2. DNA methylation and body mass index from birth to adolescence: meta-analyses of epigenome-wide association studies

Author: Universitat Rovira i Virgili, Vehmeijer FOL; Küpers LK; Sharp GC; Salas LA; Lent S; Jima DD; Tindula G; Reese S; Qi C; Gruzieva O; Page C; Rezwan FI; Melton PE; Nohr E; Escaramís G; Rzehak P; Heiskala A; Gong T; Tuominen ST; Gao L; Ross JP; Starling AP; Holloway JW; Yousefi P; Aasvang GM; Beilin LJ; Bergström A; Binder E; Chatzi L; Corpeleijn E; Czamara D; Eskenazi B; Ewart S; Ferre N; Grote V; Gruszfeld D; Håberg SE; Hoyo C; Huen K; Karlsson R, Universitat Rovira i Virgili, and Vehmeijer FOL; Küpers LK; Sharp GC; Salas LA; Lent S; Jima DD; Tindula G; Reese S; Qi C; Gruzieva O; Page C; Rezwan FI; Melton PE; Nohr E; Escaramís G; Rzehak P; Heiskala A; Gong T; Tuominen ST; Gao L; Ross JP; Starling AP; Holloway JW; Yousefi P; Aasvang GM; Beilin LJ; Bergström A; Binder E; Chatzi L; Corpeleijn E; Czamara D; Eskenazi B; Ewart S; Ferre N; Grote V; Gruszfeld D; Håberg SE; Hoyo C; Huen K; Karlsson R
Abstract: © 2020, The Author(s). Background: DNA methylation has been shown to be associated with adiposity in adulthood. However, whether similar DNA methylation patterns are associated with childhood and adolescent body mass index (BMI) is largely unknown. More insight into this relationship at younger ages may have implications for future prevention of obesity and its related traits. Methods: We examined whether DNA methylation in cord blood and whole blood in childhood and adolescence was associated with BMI in the age range from 2 to 18 years using both cross-sectional and longitudinal models. We performed meta-analyses of epigenome-wide association studies including up to 4133 children from 23 studies. We examined the overlap of findings reported in previous studies in children and adults with those in our analyses and calculated enrichment. Results: DNA methylation at three CpGs (cg05937453, cg25212453, and cg10040131), each in a different age range, was associated with BMI at Bonferroni significance, P < 1.06 × 10−7, with a 0.96 standard deviation score (SDS) (standard error (SE) 0.17), 0.32 SDS (SE 0.06), and 0.32 BMI SDS (SE 0.06) higher BMI per 10% increase in methylation, respectively. DNA methylation at nine additional CpGs in the cross-sectional childhood model was associated with BMI at false discovery rate significance. The strength of the associations of DNA methylation at the 187 CpGs previously identified to be associated with adult BMI, increased with advancing age across childhood and adolescence in our analyses. In addition, correlation coefficients between effect estimates for those CpGs in adults and in children and adolescents also increased. Among the top findings for each age range, we observed increasing enrichment for the CpGs that were previously ide
Published: 2020

3. Nocturnal Road Traffic Noise Exposure and Children's Sleep Duration and Sleep Problems

Author: Weyde, KV, Krog, NH, Oftedal, B, Evandt, J, Magnus, P, Øverland, S, Clark, C, Stansfeld, S, and Aasvang, GM
Abstract: Almost half of the European Union (EU)'s population is exposed to road traffic noise above levels that constitute a health risk. Associations between road traffic noise and impaired sleep in adults have consistently been reported. Less is known about effects of noise on children's sleep. The aim of this study was to examine the association between nocturnal road traffic noise exposure and children's parental-reported sleep duration and sleep problems. The present cross-sectional study used data from The Norwegian Mother and Child Cohort Study. Parental report of children's sleep duration and sleep problems at age 7 was linked to modelled levels of residential night-time road traffic noise. The study population included 2665 children from Oslo, Norway. No association was found between road traffic noise and sleep duration in the total study population (odds ratio (OR): 1.05, 95% confidence interval (CI): [0.94, 1.17]), but a statistically significant association was observed in girls (OR: 1.21, 95% CI: [1.04, 1.41]). For sleep problems, the associations were similar (OR: 1.36, 95% CI: [0.85, 2.16]) in girls. The ORs are presented for an increase of 10 dB. The findings suggest there is an association between road traffic noise and sleep for girls, underlining the importance of protecting children against excessive noise levels.
Published: 2017

4. Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013

Author: Vos, T, Barber, Rm, Bell, B, Bertozzi Villa, A, Biryukov, S, Bolliger, I, Charlson, F, Davis, A, Degenhardt, L, Dicker, D, Duan, L, Erskine, H, Feigin, Vl, Ferrari, Aj, Fitzmaurice, C, Fleming, T, Graetz, N, Guinovart, C, Haagsma, J, Hansen, Gm, Hanson, Sw, Heuton, Kr, Higashi, H, Kassebaum, N, Kyu, H, Laurie, E, Liang, X, Lofgren, K, Lozano, R, Macintyre, Mf, Moradi Lakeh, M, Naghavi, M, Nguyen, G, Odell, S, Ortblad, K, Roberts, Da, Roth, Ga, Sandar, L, Serina, Pt, Stanaway, Jd, Steiner, C, Thomas, B, Vollset, Se, Whiteford, H, Wolock, Tm, Ye, P, Zhou, M, Ãvila, Ma, Aasvang, Gm, Abbafati, C, Abbasoglu, Ozgoren, A, Abd Allah, F, Abdel, Aziz, Abera, Sf, Aboyans, V, Abraham, Jp, Abraham, B, Abubakar, I, Abu Raddad, Lj, Abu Rmeileh, Nm, Aburto, Tc, Achoki, T, Ackerman, In, Adelekan, A, Ademi, Z, Adou, Ak, Adsuar, Jc, Arnlov, J, Agardh, Ee, Khabouri, Al, Alam, Ss, Alasfoor, D, Albittar, Mi, Alegretti, Ma, Aleman, Av, Alemu, Za, Alfonso Cristancho, R, Alhabib, S, Ali, R, Alla, F, Allebeck, P, Allen, Pj, Almazroa, Ma, Alsharif, U, Alvarez, E, Alvis, Guzman, Ameli, N, O, Amini, H, Ammar, W, Anderson, Bo, Anderson, Hr, Antonio, Ca, Anwari, P, Apfel, H, Arsenijevic, Vs, Artaman, A, Asghar, Rj, Assadi, R, Atkins, Ls, Atkinson, C, Badawi, A, Bahit, Mc, Bakfalouni, T, Balakrishnan, K, Balalla, S, Banerjee, A, Barker Collo, Sl, Barquera, S, Barregard, L, Barrero, Lh, Basu, S, Basu, A, Baxter, A, Beardsley, J, Bedi, N, Beghi, E, Bekele, T, Bell, Ml, Benjet, C, Bennett, Da, Bensenor, Im, Benzian, H, Bernabe, E, Beyene, Tj, Bhala, N, Bhalla, A, Bhutta, Z, Bienhoff, K, Bikbov, B, Bin, Abdulhak, Blore, Jd, Blyth, Fm, Bohensky, Ma, Bora, Basara, B, Borges, G, Bornstein, Nm, Bose, D, Boufous, S, Bourne, Rr, Boyers, Ln, Brainin, M, Brauer, M, Brayne, Ce, Brazinova, A, Breitborde, Nj, Brenner, H, Briggs, Ad, Brooks, Pm, Brown, J, Brugha, Ts, Buchbinder, R, Buckle, Gc, Bukhman, G, Bulloch, Ag, Burch, M, Burnett, R, Cardenas, R, Cabral, Nl, Campos, Nonato, Campuzano, Ir, Carapetis, Jc, Carpenter, Do, Caso, V, Castaneda Orjuela, Ca, Catala Lopez, F, Chadha, Vk, Chang, Jc, Chen, H, Chen, W, Chiang, Pp, Chimed Ochir, O, Chowdhury, R, Christensen, H, Christophi, Ca, Chugh, Ss, Cirillo, Massimo, Coggeshall, M, Cohen, A, Colistro, V, Colquhoun, Sm, Contreras, Ag, Cooper, Lt, Cooper, C, Cooperrider, K, Coresh, J, Cortinovis, M, Criqui, Mh, Crump, Ja, Cuevas Nasu, L, Dandona, R, Dandona, L, Dansereau, E, Dantes, Hg, Dargan, Pi, Davey, G, Davitoiu, Dv, Dayama, A, La, De, Cruz, Gongora, De, V, Vega, La, De, Sf, Leo, D, Del, Pozo, Cruz, Dellavalle, Rp, Deribe, K, Derrett, S, Des, Jarlais, Dessalegn, M, Deveber, Ga, Dharmaratne, Sd, Diaz Torne, C, Ding, El, Dokova, K, Dorsey, Er, Driscoll, Tr, Duber, H, Durrani, Am, Edmond, Km, Ellenbogen, Rg, Endres, M, Ermakov, Sp, Eshrati, B, Esteghamati, A, Estep, K, Fahimi, S, Farzadfar, F, Fay, Df, Felson, Dt, Fereshtehnejad, Sm, Fernandes, Jg, Ferri, Cp, Flaxman, A, Foigt, N, Foreman, Kj, Fowkes, Fg, Franklin, Rc, Furst, T, Futran, Nd, Gabbe, Bj, Gankpe, Fg, Garcia, Guerra, Geleijnse, Fa, Gessner, Bd, Gibney, Kb, Gillum, Rf, Ginawi, Ia, Giroud, M, Giussani, G, Goenka, S, Goginashvili, K, Gona, P, Gonzalez, De, Cosio, T, Gosselin, Ra, Gotay, Cc, Goto, A, Gouda, Hn, Guerrant, Rl, Gugnani, Hc, Gunnell, D, Gupta, R, Gutierrez, Ra, Hafezi Nejad, N, Hagan, H, Halasa, Y, Hamadeh, Rr, Hamavid, H, Hammami, M, Hankey, Gj, Hao, Y, Harb, Hl, Haro, Jm, Havmoeller, R, Hay, Rj, Hay, S, Hedayati, Mt, Heredia, Pi, Heydarpour, P, Hijar, M, Hoek, Hw, Hoffman, Hj, Hornberger, Jc, Hosgood, Hd, Hossain, M, Hotez, Pj, Hoy, Dg, Hsairi, M, Hu, H, Hu, G, Huang, Jj, Huang, C, Huiart, L, Husseini, A, Iannarone, M, Iburg, Km, Innos, K, Inoue, M, Jacobsen, Kh, Jassal, Sk, Jeemon, P, Jensen, Pn, Jha, V, Jiang, G, Jiang, Y, Jonas, Jb, Joseph, J, Juel, K, Kan, H, Karch, A, Karimkhani, C, Karthikeyan, G, Katz, R, Kaul, A, Kawakami, N, Kazi, Ds, Kemp, Ah, Kengne, Ap, Khader, Ys, Khalifa, Se, Khan, Ea, Khan, G, Khang, Yh, Khonelidze, I, Kieling, C, Kim, D, Kim, S, Kimokoti, Rw, Kinfu, Y, Kinge, Jm, Kissela, Bm, Kivipelto, M, Knibbs, L, Knudsen, Ak, Kokubo, Y, Kosen, S, Kramer, A, Kravchenko, M, Krishnamurthi, Rv, Krishnaswami, S, Kuate, Defo, Kucuk, B, Bicer, B, Kuipers, Ej, Kulkarni, Vs, Kumar, K, Kumar, Ga, Kwan, Gf, Lai, T, Lalloo, R, Lam, H, Lan, Q, Lansingh, Vc, Larson, H, Larsson, A, Lawrynowicz, Ae, Leasher, Jl, Lee, Jt, Leigh, J, Leung, R, Levi, M, Li, B, Li, Y, Liang, J, Lim, S, Lin, Hh, Lind, M, Lindsay, Mp, Lipshultz, Se, Liu, S, Lloyd, Bk, Lockett, Ohno, S, Logroscino, G, Looker, Kj, Lopez, Ad, Lopez Olmedo, N, Lortet Tieulent, J, Lotufo, Pa, Low, N, Lucas, Rm, Lunevicius, R, Lyons, Ra, Ma, J, Ma, S, Mackay, Mt, Majdan, M, Malekzadeh, R, Mapoma, Cc, Marcenes, W, March, Lm, Margono, C, Marks, Gb, Marzan, Mb, Masci, Jr, Mason Jones, Aj, Matzopoulos, Rg, Mayosi, Bm, Mazorodze, Tt, Mcgill, Nw, Mcgrath, Jj, Mckee, M, Mclain, A, Mcmahon, Bj, Meaney, Pa, Mehndiratta, Mm, Mejia Rodriguez, F, Mekonnen, W, Melaku, Ya, Meltzer, M, Memish, Za, Mensah, G, Meretoja, A, Mhimbira, Fa, Micha, R, Miller, Tr, Mills, Ej, Mitchell, Pb, Mock, Cn, Moffitt, Te, Mohamed, Ibrahim, N, Mohammad, Ka, Mokdad, Ah, Mola, Gl, Monasta, L, Montico, M, Montine, Tj, Moore, Ar, Moran, Ae, Morawska, L, Mori, R, Moschandreas, J, Moturi, Wn, Moyer, M, Mozaffarian, D, Mueller, Uo, Mukaigawara, M, Murdoch, Me, Murray, J, Murthy, Ks, Naghavi, P, Nahas, Z, Naheed, A, Naidoo, Ks, Naldi, L, Nand, D, Nangia, V, Narayan, Km, Nash, D, Nejjari, C, Neupane, Sp, Newman, Lm, Newton, Cr, Ng, M, Ngalesoni, Fn, Nhung, Nt, Nisar, Mi, Nolte, S, Norheim, Of, Norman, Re, Norrving, B, Nyakarahuka, L, Ih, Oh, Ohkubo, T, Omer, Sb, Opio, Jn, Ortiz, A, Pandian, Jd, Panelo, Ci, Papachristou, C, Park, Ek, Parry, Cd, Caicedo, Aj, Patten, Sb, Paul, Vk, Pavlin, Bi, Pearce, N, Pedraza, Ls, Pellegrini, Ca, Pereira, Dm, Perez Ruiz, Fp, Perico, N, Pervaiz, A, Pesudovs, K, Peterson, Cb, Petzold, M, Phillips, Mr, Phillips, D, Phillips, B, Piel, Fb, Plass, D, Poenaru, D, Polanczyk, Gv, Polinder, S, Pope, Ca, Popova, S, Poulton, Rg, Pourmalek, F, Prabhakaran, D, Prasad, Nm, Qato, D, Quistberg, Da, Rafay, A, Rahimi, K, Rahimi Movaghar, V, Rahman, Su, Raju, M, Rakovac, I, Rana, Sm, Razavi, H, Refaat, A, Rehm, J, Remuzzi, G, Resnikoff, S, Ribeiro, Al, Riccio, Pm, Richardson, L, Richardus, Jh, Riederer, Am, Robinson, M, Roca, A, Rodriguez, A, Rojas Rueda, D, Ronfani, L, Rothenbacher, D, Roy, N, Ruhago, Gm, Sabin, N, Sacco, Rl, Ksoreide, K, Saha, S, Sahathevan, R, Sahraian, Ma, Sampson, U, Sanabria, Jr, Sanchez Riera, L, Santos, Is, Satpathy, M, Saunders, Je, Sawhney, M, Saylan, Mi, Scarborough, P, Schoettker, B, Schneider, Ij, Schwebel, Dc, Scott, Jg, Seedat, S, Sepanlou, Sg, Serdar, B, Servan Mori, Ee, Shackelford, K, Shaheen, A, Shahraz, S, Shamah, Levy, T, Shangguan, S, She, J, Sheikhbahaei, S, Shepard, Ds, Shi, P, Shibuya, K, Shinohara, Y, Shiri, R, Shishani, K, Shiue, I, Shrime, Mg, Sigfusdottir, Id, Silberberg, Dh, Simard, Ep, Sindi, S, Singh, Ja, Singh, L, Skirbekk, V, Sliwa, K, Soljak, M, Soneji, S, Soshnikov, Ss, Speyer, P, Sposato, La, Sreeramareddy, Ct, Stoeckl, H, Stathopoulou, Vk, Steckling, N, Stein, Mb, Stein, Dj, Steiner, Tj, Stewart, A, Stork, E, Stovner, Lj, Stroumpoulis, K, Sturua, L, Sunguya, Bf, Swaroop, M, Sykes, Bl, Tabb, Km, Takahashi, K, Tan, F, Tandon, N, Tanne, D, Tanner, M, Tavakkoli, M, Taylor, Hr, Ao, Te, Temesgen, Am, Ten, Have, M, Tenkorang, Ey, Terkawi, As, Theadom, Am, Thomas, E, Thorne Lyman, Al, Thrift, Ag, Tleyjeh, Im, Tonelli, M, Topouzis, F, Towbin, Ja, Toyoshima, H, Traebert, J, Tran, Bx, Trasande, L, Trillini, M, Truelsen, T, Trujillo, U, Tsilimbaris, M, Tuzcu, Em, Ukwaja, Kn, Undurraga, Ea, Uzun, Sb, Van, Brakel, Van, Wh, Vijver, De, Van, S, Dingenen, R, Van, Gool, Varakin, Yy, Vasankari, Tj, Vavilala, Ms, Veerman, Lj, Velasquez, Melendez, G, Venketasubramanian, N, Vijayakumar, L, Villalpando, S, Violante, Fs, Vlassov, Vv, Waller, S, Wallin, Mt, Wan, X, Wang, L, Wang, J, Wang, Y, Warouw, Ts, Weichenthal, S, Weiderpass, E, Weintraub, Rg, Werdecker, A, Wessells, Kr, Westerman, R, Wilkinson, Jd, Williams, Hc, Williams, Tn, Woldeyohannes, Sm, Wolfe, Cd, Wong, Jq, Wong, H, Woolf, Ad, Wright, Jl, Wurtz, B, Xu, G, Yang, G, Yano, Y, Yenesew, Ma, Yentur, Gk, Yip, P, Yonemoto, N, Yoon, Sj, Younis, M, Yu, C, Kim, Ky, Zaki, Mel, Zhang, Y, Zhao, Z, Zhao, Y, Zhu, J, Zonies, D, Zunt, Jr, Salomon, Ja, Murray, C. J., Vos, T, Barber, Rm, Bell, B, Bertozzi-Villa, A, Biryukov, S, Bolliger, I, Charlson, F, Davis, A, Degenhardt, L, Dicker, D, Duan, L, Erskine, H, Feigin, Vl, Ferrari, Aj, Fitzmaurice, C, Fleming, T, Graetz, N, Guinovart, C, Haagsma, J, Hansen, Gm, Hanson, Sw, Heuton, Kr, Higashi, H, Kassebaum, N, Kyu, H, Laurie ELiang, X, Lofgren, K, Lozano, R, Macintyre, Mf, Moradi-Lakeh, M, Naghavi, M, Nguyen, G, Odell, S, Ortblad, K, Roberts, Da, Roth, Ga, Sandar, L, Serina, Pt, Stanaway, Jd, Steiner, C, Thomas, B, Vollset, Se, Whiteford, H, Wolock, Tm, Ye, P, Zhou, M, Ãvila, Ma, Aasvang, Gm, Abbafati, C, Abbasoglu Ozgoren, A, Abd-Allah, F, Abdel Aziz MI, Abera, Sf, Aboyans, V, Abraham, Jp, Abraham, B, Abubakar, I, Abu-Raddad, Lj, Abu-Rmeileh, Nm, Aburto, Tc, Achoki TAckerman IN, Adelekan, A, Ademi, Z, Adou, Ak, Adsuar, Jc, Arnlov, J, Agardh, Ee, Al Khabouri MJ, Alam, S, Alasfoor, D, Albittar, Mi, Alegretti MAAleman AV, Alemu, Za, Alfonso-Cristancho, R, Alhabib, S, Ali, R, Alla, F, Allebeck, P, Allen, Pj, Almazroa, Ma, Alsharif, U, Alvarez, E, Alvis-Guzman NAmeli, O, Amini, H, Ammar, W, Anderson, Bo, Anderson, Hr, Antonio, Ca, Anwari, P, Apfel, H, Arsenijevic, V, Artaman, A, Asghar, Rj, Assadi, R, Atkins, L, Atkinson, C, Badawi, A, Bahit, Mc, Bakfalouni, T, Balakrishnan, K, Balalla, S, Banerjee, A, Barker-Collo, Sl, Barquera, S, Barregard, L, Barrero LHBasu, S, Basu, A, Baxter, A, Beardsley, J, Bedi, N, Beghi, E, Bekele, T, Bell, Ml, Benjet, C, Bennett, Da, Bensenor, Im, Benzian, H, Bernabe, E, Beyene TJBhala, N, Bhalla, A, Bhutta, Z, Bienhoff, K, Bikbov, B, Bin Abdulhak, A, Blore, Jd, Blyth, Fm, Bohensky, Ma, Bora Basara, B, Borges, G, Bornstein, Nm, Bose, D, Boufous, S, Bourne, Rr, Boyers, Ln, Brainin, M, Brauer, M, Brayne, Ce, Brazinova, A, Breitborde, Nj, Brenner, H, Briggs, Ad, Brooks, Pm, Brown JBrugha TS, Buchbinder, R, Buckle, Gc, Bukhman, G, Bulloch, Ag, Burch, M, Burnett, R, Cardenas, R, Cabral, Nl, Campos Nonato IR, Campuzano JCCarapetis JR, Carpenter, Do, Caso, V, Castaneda-Orjuela, Ca, Catala-Lopez, F, Chadha, Vk, Chang, Jc, Chen, H, Chen, W, Chiang, Pp, Chimed-Ochir, O, Chowdhury, R, Christensen, H, Christophi, Ca, Chugh, S, Cirillo, M, Coggeshall, M, Cohen, A, Colistro, V, Colquhoun, Sm, Contreras, Ag, Cooper LTCooper, C, Cooperrider, K, Coresh, J, Cortinovis, M, Criqui, Mh, Crump, Ja, Cuevas-Nasu, L, Dandona, R, Dandona, L, Dansereau, E, Dantes, Hg, Dargan, Pi, Davey, G, Davitoiu, Dv, Dayama, A, De la Cruz-Gongora, V, de la Vega SF, De Leo, D, del Pozo-Cruz, B, Dellavalle, Rp, Deribe, K, Derrett, S, Des Jarlais DC, Dessalegn, M, Deveber, Ga, Dharmaratne, Sd, Diaz-Torne, C, Ding, El, Dokova, K, Dorsey, Er, Driscoll, Tr, Duber, H, Durrani, Am, Edmond, Km, Ellenbogen, Rg, Endres, M, Ermakov, Sp, Eshrati, B, Esteghamati, A, Estep, K, Fahimi, S, Farzadfar, F, Fay, Df, Felson, Dt, Fereshtehnejad SMFernandes JG, Ferri, Cp, Flaxman, A, Foigt, N, Foreman, Kj, Fowkes, Fg, Franklin, Rc, Furst, T, Futran, Nd, Gabbe, Bj, Gankpe, Fg, Garcia-Guerra FAGeleijnse JM, Gessner, Bd, Gibney, Kb, Gillum, Rf, Ginawi, Ia, Giroud, M, Giussani, G, Goenka, S, Goginashvili, K, Gona, P, Gonzalez de Cosio TGosselin RA, Gotay, Cc, Goto, A, Gouda, Hn, Guerrant, Rl, Gugnani, Hc, Gunnell, D, Gupta, R, Gutierrez, Ra, Hafezi-Nejad, N, Hagan HHalasa, Y, Hamadeh, Rr, Hamavid, H, Hammami, M, Hankey, Gj, Hao, Y, Harb, Hl, Haro, Jm, Havmoeller, R, Hay, Rj, Hay, S, Hedayati, Mt, Heredia Pi IB, Heydarpour, P, Hijar, M, Hoek, Hw, Hoffman, Hj, Hornberger, Jc, Hosgood, Hd, Hossain, M, Hotez, Pj, Hoy, Dg, Hsairi, M, Hu, H, Hu, G, Huang JJHuang, C, Huiart, L, Husseini, A, Iannarone, M, Iburg, Km, Innos, K, Inoue, M, Jacobsen, Kh, Jassal, Sk, Jeemon, P, Jensen, Pn, Jha, V, Jiang, G, Jiang YJonas JB, Joseph, J, Juel, K, Kan, H, Karch, A, Karimkhani, C, Karthikeyan, G, Katz, R, Kaul, A, Kawakami, N, Kazi, D, Kemp, Ah, Kengne, Ap, Khader, Y, Khalifa, Se, Khan, Ea, Khan, G, Khang, Yh, Khonelidze, I, Kieling, C, Kim, D, Kim, S, Kimokoti, Rw, Kinfu, Y, Kinge, Jm, Kissela, Bm, Kivipelto MKnibbs, L, Knudsen, Ak, Kokubo, Y, Kosen, S, Kramer, A, Kravchenko, M, Krishnamurthi, Rv, Krishnaswami, S, Kuate Defo, B, Kucuk Bicer, B, Kuipers EJKulkarni VS, Kumar, K, Kumar, Ga, Kwan, Gf, Lai, T, Lalloo, R, Lam, H, Lan, Q, Lansingh, Vc, Larson, H, Larsson, A, Lawrynowicz, Ae, Leasher, Jl, Lee, Jt, Leigh, J, Leung, R, Levi, M, Li, B, Li, Y, Liang, J, Lim, S, Lin, Hh, Lind, M, Lindsay, Mp, Lipshultz, Se, Liu, S, Lloyd, Bk, Lockett Ohno, S, Logroscino, G, Looker, Kj, Lopez, Ad, Lopez-Olmedo, N, Lortet-Tieulent, J, Lotufo, Pa, Low, N, Lucas, Rm, Lunevicius, R, Lyons, Ra, Ma, J, Ma, S, Mackay MTMajdan, M, Malekzadeh, R, Mapoma, Cc, Marcenes, W, March, Lm, Margono, C, Marks, Gb, Marzan, Mb, Masci, Jr, Mason-Jones, Aj, Matzopoulos RGMayosi BM, Mazorodze, Tt, Mcgill, Nw, Mcgrath, Jj, Mckee, M, Mclain, A, Mcmahon, Bj, Meaney, Pa, Mehndiratta, Mm, Mejia-Rodriguez, F, Mekonnen, W, Melaku, Ya, Meltzer, M, Memish, Za, Mensah, G, Meretoja, A, Mhimbira, Fa, Micha, R, Miller, Tr, Mills, Ej, Mitchell, Pb, Mock, Cn, Moffitt TEMohamed Ibrahim, N, Mohammad, Ka, Mokdad, Ah, Mola, Gl, Monasta, L, Montico, M, Montine, Tj, Moore, Ar, Moran, Ae, Morawska, L, Mori RMoschandreas, J, Moturi, Wn, Moyer, M, Mozaffarian, D, Mueller, Uo, Mukaigawara, M, Murdoch, Me, Murray, J, Murthy, K, Naghavi, P, Nahas ZNaheed, A, Naidoo, K, Naldi, L, Nand, D, Nangia, V, Narayan, Km, Nash, D, Nejjari, C, Neupane, Sp, Newman, Lm, Newton, Cr, Ng, M, Ngalesoni FNNhung NT, Nisar, Mi, Nolte, S, Norheim, Of, Norman, Re, Norrving, B, Nyakarahuka, L, Oh, Ih, Ohkubo, T, Omer, Sb, Opio, Jn, Ortiz, A, Pandian JDPanelo CI, Papachristou, C, Park, Ek, Parry, Cd, Caicedo, Aj, Patten, Sb, Paul, Vk, Pavlin, Bi, Pearce, N, Pedraza, L, Pellegrini, Ca, Pereira, Dm, Perez-Ruiz, Fp, Perico, N, Pervaiz, A, Pesudovs, K, Peterson, Cb, Petzold, M, Phillips, Mr, Phillips, D, Phillips, B, Piel, Fb, Plass, D, Poenaru, D, Polanczyk GVPolinder, S, Pope, Ca, Popova, S, Poulton, Rg, Pourmalek, F, Prabhakaran, D, Prasad, Nm, Qato, D, Quistberg, Da, Rafay, A, Rahimi, K, Rahimi-Movaghar, V, Rahman, Su, Raju, M, Rakovac, I, Rana, Sm, Razavi, H, Refaat, A, Rehm, J, Remuzzi, G, Resnikoff, S, Ribeiro, Al, Riccio, Pm, Richardson, L, Richardus, Jh, Riederer, Am, Robinson, M, Roca, A, Rodriguez, A, Rojas-Rueda, D, Ronfani, L, Rothenbacher, D, Roy, N, Ruhago, Gm, Sabin, N, Sacco, Rl, Ksoreide, K, Saha, S, Sahathevan, R, Sahraian, Ma, Sampson, U, Sanabria, Jr, Sanchez-Riera, L, Santos, I, Satpathy, M, Saunders, Je, Sawhney, M, Saylan MIScarborough, P, Schoettker, B, Schneider, Ij, Schwebel, Dc, Scott, Jg, Seedat, S, Sepanlou, Sg, Serdar, B, Servan-Mori, Ee, Shackelford, K, Shaheen AShahraz, S, Shamah Levy, T, Shangguan, S, She, J, Sheikhbahaei, S, Shepard, D, Shi, P, Shibuya, K, Shinohara, Y, Shiri, R, Shishani, K, Shiue, I, Shrime, Mg, Sigfusdottir, Id, Silberberg, Dh, Simard, Ep, Sindi, S, Singh, Ja, Singh, L, Skirbekk, V, Sliwa, K, Soljak, M, Soneji, S, Soshnikov, S, Speyer PSposato LA, Sreeramareddy, Ct, Stoeckl, H, Stathopoulou, Vk, Steckling, N, Stein, Mb, Stein, Dj, Steiner, Tj, Stewart, A, Stork, E, Stovner LJStroumpoulis, K, Sturua, L, Sunguya, Bf, Swaroop, M, Sykes, Bl, Tabb, Km, Takahashi, K, Tan, F, Tandon, N, Tanne, D, Tanner, M, Tavakkoli, M, Taylor, Hr, Te Ao BJ, Temesgen, Am, Ten Have, M, Tenkorang, Ey, Terkawi, A, Theadom, Am, Thomas, E, Thorne-Lyman, Al, Thrift, Ag, Tleyjeh, Im, Tonelli, M, Topouzis, F, Towbin, Ja, Toyoshima, H, Traebert, J, Tran, Bx, Trasande, L, Trillini, M, Truelsen, T, Trujillo, U, Tsilimbaris, M, Tuzcu, Em, Ukwaja KNUndurraga EA, Uzun, Sb, van Brakel WH, van de Vijver, S, Van Dingenen, R, van Gool CH, Varakin, Yy, Vasankari, Tj, Vavilala, M, Veerman LJVelasquez-Melendez, G, Venketasubramanian, N, Vijayakumar, L, Villalpando, S, Violante, F, Vlassov, Vv, Waller, S, Wallin, Mt, Wan, X, Wang, L, Wang, J, Wang, Y, Warouw, T, Weichenthal, S, Weiderpass, E, Weintraub, Rg, Werdecker, A, Wessells, Kr, Westerman, R, Wilkinson, Jd, Williams HCWilliams TN, Woldeyohannes, Sm, Wolfe, Cd, Wong, Jq, Wong, H, Woolf, Ad, Wright, Jl, Wurtz, B, Xu, G, Yang, G, Yano, Y, Yenesew, Ma, Yentur GKYip, P, Yonemoto, N, Yoon, Sj, Younis, M, Yu, C, Kim, Ky, Zaki Mel, S, Zhang, Y, Zhao, Z, Zhao, Y, Zhu, J, Zonies, D, Zunt, Jr, Salomon, Ja, Murray, Cj., Vos, Theo, Barber, Ryan M., Bell, Brad, Bertozzi-Villa, Amelia, Biryukov, Stan, Bolliger, Ian, Charlson, Fiona, Davis, Adrian, Degenhardt, Louisa, Dicker, Daniel, Duan, Leilei, Erskine, Holly, Feigin, Valery L., Ferrari, Alize J., Fitzmaurice, Christina, Fleming, Thoma, Graetz, Nichola, Guinovart, Caterina, Haagsma, Juanita, Hansen, Gillian M., Hanson, Sarah Wulf, Heuton, Kyle R., Higashi, Hideki, Kassebaum, Nichola, Kyu, Hmwe, Laurie, Evan, Liang, Xiofeng, Lofgren, Katherine, Lozano, Rafael, Macintyre, Michael F., Moradi-Lakeh, Maziar, Naghavi, Mohsen, Nguyen, Grant, Odell, Shaun, Ortblad, Katrina, Roberts, David Allen, Roth, Gregory A., Sandar, Logan, Serina, Peter T., Stanaway, Jeffrey D., Steiner, Caitlyn, Thomas, Bernadette, Vollset, Stein Emil, Whiteford, Harvey, Wolock, Timothy M., Ye, Pengpeng, Zhou, Maigeng, Ãvila, Marco A., Aasvang, Gunn Marit, Abbafati, Cristiana, Ozgoren, Ayse Abbasoglu, Abd-Allah, Foad, Aziz, Muna I. Abdel, Abera, Semaw F., Aboyans, Victor, Abraham, Jerry P., Abraham, Biju, Abubakar, Ibrahim, Abu-Raddad, Laith J., Abu-Rmeileh, Niveen M.E., Aburto, Tania C., Achoki, Tom, Ackerman, Ilana N., Adelekan, Ademola, Ademi, Zanfina, Adou, Arsène K., Adsuar, Josef C., Arnlov, Johan, Agardh, Emilie E., Al Khabouri, Mazin J., Alam, Sayed Saidul, Alasfoor, Deena, Albittar, Mohammed I., Alegretti, Miguel A., Aleman, Alicia V., Alemu, Zewdie A., Alfonso-Cristancho, Rafael, Alhabib, Samia, Ali, Raghib, Alla, Francoi, Allebeck, Peter, Allen, Peter J., Almazroa, Mohammad Abdulaziz, Alsharif, Ubai, Alvarez, Elena, Alvis-Guzman, Nelson, Ameli, Omid, Amini, Heresh, Ammar, Walid, Anderson, Benjamin O., Anderson, H. Ro, Antonio, Carl Abelardo T., Anwari, Palwasha, Apfel, Henry, Arsenijevic, Valentain S. Arsic, Artaman, Al, Asghar, Rana J., Assadi, Reza, Atkins, Lydia S., Atkinson, Charle, Badawi, Alaa, Bahit, Maria C., Bakfalouni, Talal, Balakrishnan, Kalpana, Balalla, Shivanthi, Banerjee, Amitava, Barker-Collo, Suzanne L., Barquera, Simon, Barregard, Lar, Barrero, Lope H., Basu, Sanjay, Basu, Arindam, Baxter, Amanda, Beardsley, Justin, Bedi, Neeraj, Beghi, Ettore, Bekele, Tolesa, Bell, Michelle L., Benjet, Corina, Bennett, Derrick A., Bensenor, Isabela M., Benzian, Habib, Bernabe, Eduardo, Beyene, Tariku J., Bhala, Neeraj, Bhalla, Ashish, Bhutta, Zulfiqar, Bienhoff, Kelly, Bikbov, Bori, Abdulhak, Aref Bin, Blore, Jed D., Blyth, Fiona M., Bohensky, Megan A., Basara, Berrak Bora, Borges, Guilherme, Bornstein, Natan M., Bose, Dipan, Boufous, Soufiane, Bourne, Rupert R., Boyers, Lindsay N., Brainin, Michael, Brauer, Michael, Brayne, Carol E.G., Brazinova, Alexandra, Breitborde, Nicholas J.K., Brenner, Hermann, Briggs, Adam D.M., Brooks, Peter M., Brown, Jonathan, Brugha, Traolach S., Buchbinder, Rachelle, Buckle, Geoffrey C., Bukhman, Gene, Bulloch, Andrew G., Burch, Michael, Burnett, Richard, Cardenas, Rosario, Cabral, Norberto L., Campos-Nonato, Ismael R., Campuzano, Julio C., Carapetis, Jonathan R., Carpenter, David O., Caso, Valeria, Castaneda-Orjuela, Carlos A., Catala-Lopez, Ferran, Chadha, Vineet K., Chang, Jung-Chen, Chen, Honglei, Chen, Wanqing, Chiang, Peggy P., Chimed-Ochir, Odgerel, Chowdhury, Rajiv, Christensen, Hanne, Christophi, Costas A., Chugh, Sumeet S., Cirillo, Massimo, Coggeshall, Megan, Cohen, Aaron, Colistro, Valentina, Colquhoun, Samantha M., Contreras, Alejandra G., Cooper, Leslie T., Cooper, Cyru, Cooperrider, Kimberly, Coresh, Josef, Cortinovis, Monica, Criqui, Michael H., Crump, John A., Cuevas-Nasu, Lucia, Dandona, Rakhi, Dandona, Lalit, Dansereau, Emily, Dantes, Hector G., Dargan, Paul I., Davey, Gail, Davitoiu, Dragos V., Dayama, Anand, De La Cruz-Gongora, Vanessa, De La Vega, Shelley F., De Leo, Diego, Del Pozo-Cruz, Borja, Dellavalle, Robert P., Deribe, Kebede, Derrett, Sarah, Des Jarlais, Don C., Dessalegn, Muluken, Deveber, Gabrielle A., Dharmaratne, Samath D., Diaz-Torne, Cesar, Ding, Eric L., Dokova, Klara, Dorsey, E.R., Driscoll, Tim R., Duber, Herbert, Durrani, Adnan M., Edmond, Karen M., Ellenbogen, Richard G., Endres, Matthia, Ermakov, Sergey P., Eshrati, Babak, Esteghamati, Alireza, Estep, Kara, Fahimi, Saman, Farzadfar, Farshad, Fay, Derek F.J., Felson, David T., Fereshtehnejad, Seyed-Mohammad, Fernandes, Jefferson G., Ferri, Cluesa P., Flaxman, Abraham, Foigt, Nataliya, Foreman, Kyle J., Fowkes, F Gerry R., Franklin, Richard C., Furst, Thoma, Futran, Neal D., Gabbe, Belinda J., Gankpe, Fortune G., Garcia-Guerra, Francisco A., Geleijnse, Johanna M., Gessner, Bradford D., Gibney, Katherine B., Gillum, Richard F., Ginawi, Ibrahim A., Giroud, Maurice, Giussani, Giorgia, Goenka, Shifalika, Goginashvili, Ketevan, Gona, Philimon, De Cosio, Teresita Gonzalez, Gosselin, Richard A., Gotay, Carolyn C., Goto, Atsushi, Gouda, Hebe N., Guerrant, Richard L., Gugnani, Harish C., Gunnell, David, Gupta, Rajeev, Gupta, Rahul, Gutierrez, Reyna A., Hafezi-Nejad, Nima, Hagan, Holly, Halasa, Yara, Hamadeh, Randah R., Hamavid, Hannah, Hammami, Mouhanad, Hankey, Graeme J., Hao, Yuantao, Harb, Hilda L., Haro, Josep Maria, Havmoeller, Rasmu, Hay, Roderick J., Hay, Simon, Hedayati, Mohammad T., Pi, Ileana B. Heredia, Heydarpour, Pouria, Hijar, Martha, Hoek, Hans W., Hoffman, Howard J., Hornberger, John C., Hosgood, H. Dean, Hossain, Mazeda, Hotez, Peter J., Hoy, Damian G., Hsairi, Mohamed, Hu, Howard, Hu, Guoqing, Huang, John J., Huang, Cheng, Huiart, Laetitia, Husseini, Abdullatif, Iannarone, Marissa, Iburg, Kim M., Innos, Kaire, Inoue, Manami, Jacobsen, Kathryn H., Jassal, Simerjot K., Jeemon, Panniyammakal, Jensen, Paul N., Jha, Vivekanand, Jiang, Guohong, Jiang, Ying, Jonas, Jost B., Joseph, Jonathan, Juel, Knud, Kan, Haidong, Karch, Andre, Karimkhani, Chante, Karthikeyan, Ganesan, Katz, Ronit, Kaul, Anil, Kawakami, Norito, Kazi, Dhruv S., Kemp, Andrew H., Kengne, Andre P., Khader, Yousef S., Khalifa, Shams Eldin A.H., Khan, Ejaz A., Khan, Gulfaraz, Khang, Young-Ho, Khonelidze, Irma, Kieling, Christian, Kim, Daniel, Kim, Sungroul, Kimokoti, Ruth W., Kinfu, Yohanne, Kinge, Jonas M., Kissela, Brett M., Kivipelto, Miia, Knibbs, Luke, Knudsen, Ann Kristin, Kokubo, Yoshihiro, Kosen, Soewarta, Kramer, Alexander, Kravchenko, Michael, Krishnamurthi, Rita V., Krishnaswami, Sanjay, Defo, Barthelemy Kuate, Bicer, Burcu Kucuk, Kuipers, Ernst J., Kulkarni, Veena S., Kumar, Kaushalendra, Kumar, G Anil, Kwan, Gene F., Lai, Taavi, Lalloo, Ratilal, Lam, Hilton, Lan, Qing, Lansingh, Van C., Larson, Heidi, Larsson, Ander, Lawrynowicz, Alicia E.B., Leasher, Janet L., Lee, Jong-Tae, Leigh, Jame, Leung, Ricky, Levi, Miriam, Li, Bin, Li, Yichong, Li, Yongmei, Liang, Juan, Lim, Stephen, Lin, Hsien-Ho, Lind, Margaret, Lindsay, M Patrice, Lipshultz, Steven E., Liu, Shiwei, Lloyd, Belinda K., Ohno, Summer Lockett, Logroscino, Giancarlo, Looker, Katharine J., Lopez, Alan D., Lopez-Olmedo, Nancy, Lortet-Tieulent, Joannie, Lotufo, Paulo A., Low, Nicola, Lucas, Robyn M., Lunevicius, Raimunda, Lyons, Ronan A., Ma, Jixiang, Ma, Stefan, Mackay, Mark T., Majdan, Marek, Malekzadeh, Reza, Mapoma, Christopher C., Marcenes, Wagner, March, Lyn M., Margono, Chri, Marks, Guy B., Marzan, Melvin B., Masci, Joseph R., Mason-Jones, Amanda J., Matzopoulos, Richard G., Mayosi, Bongani M., Mazorodze, Tasara T., Mcgill, Neil W., Mcgrath, John J., Mckee, Martin, Mclain, Abby, Mcmahon, Brian J., Meaney, Peter A., Mehndiratta, Man Mohan, Mejia-Rodriguez, Fabiola, Mekonnen, Wubegzier, Melaku, Yohannes A., Meltzer, Michele, Memish, Ziad A., Mensah, George, Meretoja, Atte, Mhimbira, Francis A., Micha, Renata, Miller, Ted R., Mills, Edward J., Mitchell, Philip B., Mock, Charles N., Moffitt, Terrie E., Ibrahim, Norlinah Mohamed, Mohammad, Karzan A., Mokdad, Ali H., Mola, Glen L., Monasta, Lorenzo, Montico, Marcella, Montine, Thomas J., Moore, Ami R., Moran, Andrew E., Morawska, Lidia, Mori, Rintaro, Moschandreas, Joanna, Moturi, Wilkister N., Moyer, Madeline, Mozaffarian, Dariush, Mueller, Ulrich O., Mukaigawara, Mitsuru, Murdoch, Michele E., Murray, Joseph, Murthy, Kinnari S., Naghavi, Paria, Nahas, Ziad, Naheed, Aliya, Naidoo, Kovin S., Naldi, Luigi, Nand, Devina, Nangia, Vinay, Narayan, K.M. Venkat, Nash, Deni, Nejjari, Chakib, Neupane, Sudan P., Newman, Lori M., Newton, Charles R., Ng, Marie, Ngalesoni, Frida N., Nhung, Nguyen T., Nisar, Muhammad I., Nolte, Sandra, Norheim, Ole F., Norman, Rosana E., Norrving, Bo, Nyakarahuka, Luke, Oh, In Hwan, Ohkubo, Takayoshi, Omer, Saad B., Opio, John Nelson, Ortiz, Alberto, Pandian, Jeyaraj D., Panelo, Carlo Irwin A., Papachristou, Christina, Park, Eun-Kee, Parry, Charles D., Caicedo, Angel J. Paternina, Patten, Scott B., Paul, Vinod K., Pavlin, Boris I., Pearce, Neil, Pedraza, Lilia S., Pellegrini, Carlos A., Pereira, David M., Perez-Ruiz, Fernando P., Perico, Norberto, Pervaiz, Aslam, Pesudovs, Konrad, Peterson, Carrie B., Petzold, Max, Phillips, Michael R., Phillips, David, Phillips, Bryan, Piel, Frederic B., Plass, Dietrich, Poenaru, Dan, Polanczyk, Guilherme V., Polinder, Suzanne, Pope, C.A., Popova, Svetlana, Poulton, Richie G., Pourmalek, Farshad, Prabhakaran, Dorairaj, Prasad, Noela M., Qato, Dima, Quistberg, D.A., Rafay, Anwar, Rahimi, Kazem, Rahimi-Movaghar, Vafa, Rahman, Sajjad Ur, Raju, Murugesan, Rakovac, Ivo, Rana, Saleem M., Razavi, Homie, Refaat, Amany, Rehm, Jurgen, Remuzzi, Giuseppe, Resnikoff, Serge, Ribeiro, Antonio L., Riccio, Patricia M., Richardson, Lee, Richardus, Jan Hendrik, Riederer, Anne M., Robinson, Margot, Roca, Anna, Rodriguez, Alina, Rojas-Rueda, David, Ronfani, Luca, Rothenbacher, Dietrich, Roy, Nobhojit, Ruhago, George M., Sabin, Nsanzimana, Sacco, Ralph L., Ksoreide, Kjetil, Saha, Sukanta, Sahathevan, Ramesh, Sahraian, Mohammad Ali, Sampson, Uchechukwu, Sanabria, Juan R., Sanchez-Riera, Lidia, Santos, Itamar S., Satpathy, Maheswar, Saunders, James E., Sawhney, Monika, Saylan, Mete I., Scarborough, Peter, Schoettker, Ben, Schneider, Ione J.C., Schwebel, David C., Scott, James G., Seedat, Soraya, Sepanlou, Sadaf G., Serdar, Berrin, Servan-Mori, Edson E., Shackelford, Katya, Shaheen, Amira, Shahraz, Saeid, Levy, Teresa Shamah, Shangguan, Siyi, She, Jun, Sheikhbahaei, Sara, Shepard, Donald S., Shi, Peilin, Shibuya, Kenji, Shinohara, Yukito, Shiri, Rahman, Shishani, Kawkab, Shiue, Ivy, Shrime, Mark G., Sigfusdottir, Inga D., Silberberg, Donald H., Simard, Edgar P., Sindi, Shireen, Singh, Jasvinder A., Singh, Lavanya, Skirbekk, Vegard, Sliwa, Karen, Soljak, Michael, Soneji, Samir, Soshnikov, Sergey S., Speyer, Peter, Sposato, Luciano A., Sreeramareddy, Chandrashekhar T., Stoeckl, Heidi, Stathopoulou, Vasiliki Kalliopi, Steckling, Nadine, Stein, Murray B., Stein, Dan J., Steiner, Timothy J., Stewart, Andrea, Stork, Eden, Stovner, Lars J., Stroumpoulis, Konstantino, Sturua, Lela, Sunguya, Bruno F., Swaroop, Mamta, Sykes, Bryan L., Tabb, Karen M., Takahashi, Ken, Tan, Feng, Tandon, Nikhil, Tanne, David, Tanner, Marcel, Tavakkoli, Mohammad, Taylor, Hugh R., Te Ao, Braden J., Temesgen, Awoke Misganaw, Have, Margreet Ten, Tenkorang, Eric Yeboah, Terkawi, Abdullah Sulieman, Theadom, Alice M., Thomas, Elissa, Thorne-Lyman, Andrew L., Thrift, Amanda G., Tleyjeh, Imad M., Tonelli, Marcello, Topouzis, Foti, Towbin, Jeffrey A., Toyoshima, Hideaki, Traebert, Jefferson, Tran, Bach X., Trasande, Leonardo, Trillini, Matia, Truelsen, Thoma, Trujillo, Ulise, Tsilimbaris, Miltiadi, Tuzcu, Emin M., Ukwaja, Kingsley N., Undurraga, Eduardo A., Uzun, Selen B., Van Brakel, Wim H., Van De Vijver, Steven, Dingenen, Rita Van, Van Gool, Coen H., Varakin, Yuri Y., Vasankari, Tommi J., Vavilala, Monica S., Veerman, Lennert J., Velasquez-Melendez, Gustavo, Venketasubramanian, Narayanaswamy, Vijayakumar, Lakshmi, Villalpando, Salvador, Violante, Francesco S., Vlassov, Vasiliy V., Waller, Stephen, Wallin, Mitchell T., Wan, Xia, Wang, Linhong, Wang, Jianli, Wang, Yanping, Warouw, Tati S., Weichenthal, Scott, Weiderpass, Elisabete, Weintraub, Robert G., Werdecker, Andrea, Wessells, K. Ryan, Westerman, Ronny, Wilkinson, James D., Williams, Hywel C., Williams, Thomas N., Woldeyohannes, Solomon M., Wolfe, Charles D.A., Wong, John Q., Wong, Haidong, Woolf, Anthony D., Wright, Jonathan L., Wurtz, Brittany, Xu, Gelin, Yang, Gonghuan, Yano, Yuichiro, Yenesew, Muluken A., Yentur, Gokalp K., Yip, Paul, Yonemoto, Naohiro, Yoon, Seok-Jun, Younis, Mustafa, Yu, Chuanhua, Kim, Kim Yun, Zaki, Maysaa El Sayed, Zhang, Yong, Zhao, Zheng, Zhao, Yong, Zhu, Jun, Zonies, David, Zunt, Joseph R., Salomon, Joshua A., Murray, Christopher J.L., Cell biology, Gastroenterology & Hepatology, Epidemiology, Health Technology Assessment (HTA), and Public Health
Subjects: Male, Gerontology, Nutrition and Disease, Epidemiology, years lived with disability, Global burden of disease, acute and chronic diseases, countries, Prevalence, Disease, Global Health, Medical and Health Sciences, Conduct disorder, Otitis-media, Cost of Illness, Residence Characteristics, Voeding en Ziekte, 80 and over, Global health, 2.2 Factors relating to the physical environment, 2.1 Biological and endogenous factors, countries, Aetiology, Child, Aged, 80 and over, Medicine(all), education.field_of_study, ATTENTION-DEFICIT/HYPERACTIVITY DISORDER, Incidence, Mortality rate, Incidence (epidemiology), Pain Research, Neglected Diseases, Alcohol dependence, General Medicine, Middle Aged, Global burden of disease, Global Burden of Disease Study 2013 Collaborators, Mental Health, Infectious Diseases, Attention deficit/Hyperactivity disorder, Burden of Illness, Child, Preschool, Acute Disease, Female, Life Sciences & Biomedicine, Adult, medicine.medical_specialty, Adolescent, GBD 2013, Population, acute and chronic diseases, Young Adult, Mental-disorders, Age Distribution, Medicine, General & Internal, Weights, General & Internal Medicine, medicine, Humans, Life Science, Disabled Persons, Sex Distribution, Preschool, education, Developing Countries, VLAG, Aged, Science & Technology, business.industry, Developed Countries, Cutaneous Leishmaniasis, Infant, Newborn, Infant, Health outcomes, Newborn, medicine.disease, Comorbidity, Brain Disorders, years lived with disability, Good Health and Well Being, Disease, injury, incidence, prevalence, YLDs, GBD 2010, Chronic Disease, Wounds and Injuries, business, 2.4 Surveillance and distribution, Iron-deficiency, Demography
Abstract: Summary Background Up-to-date evidence about levels and trends in disease and injury incidence, prevalence, and years lived with disability (YLDs) is an essential input into global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013), we estimated these quantities for acute and chronic diseases and injuries for 188 countries between 1990 and 2013. Methods Estimates were calculated for disease and injury incidence, prevalence, and YLDs using GBD 2010 methods with some important refinements. Results for incidence of acute disorders and prevalence of chronic disorders are new additions to the analysis. Key improvements include expansion to the cause and sequelae list, updated systematic reviews, use of detailed injury codes, improvements to the Bayesian meta-regression method (DisMod-MR), and use of severity splits for various causes. An index of data representativeness, showing data availability, was calculated for each cause and impairment during three periods globally and at the country level for 2013. In total, 35 620 distinct sources of data were used and documented to calculated estimates for 301 diseases and injuries and 2337 sequelae. The comorbidity simulation provides estimates for the number of sequelae, concurrently, by individuals by country, year, age, and sex. Disability weights were updated with the addition of new population-based survey data from four countries. Findings Disease and injury were highly prevalent; only a small fraction of individuals had no sequelae. Comorbidity rose substantially with age and in absolute terms from 1990 to 2013. Incidence of acute sequelae were predominantly infectious diseases and short-term injuries, with over 2 billion cases of upper respiratory infections and diarrhoeal disease episodes in 2013, with the notable exception of tooth pain due to permanent caries with more than 200 million incident cases in 2013. Conversely, leading chronic sequelae were largely attributable to non-communicable diseases, with prevalence estimates for asymptomatic permanent caries and tension-type headache of 2·4 billion and 1·6 billion, respectively. The distribution of the number of sequelae in populations varied widely across regions, with an expected relation between age and disease prevalence. YLDs for both sexes increased from 537·6 million in 1990 to 764·8 million in 2013 due to population growth and ageing, whereas the age-standardised rate decreased little from 114·87 per 1000 people to 110·31 per 1000 people between 1990 and 2013. Leading causes of YLDs included low back pain and major depressive disorder among the top ten causes of YLDs in every country. YLD rates per person, by major cause groups, indicated the main drivers of increases were due to musculoskeletal, mental, and substance use disorders, neurological disorders, and chronic respiratory diseases; however HIV/AIDS was a notable driver of increasing YLDs in sub-Saharan Africa. Also, the proportion of disability-adjusted life years due to YLDs increased globally from 21·1% in 1990 to 31·2% in 2013. Interpretation Ageing of the world's population is leading to a substantial increase in the numbers of individuals with sequelae of diseases and injuries. Rates of YLDs are declining much more slowly than mortality rates. The non-fatal dimensions of disease and injury will require more and more attention from health systems. The transition to non-fatal outcomes as the dominant source of burden of disease is occurring rapidly outside of sub-Saharan Africa. Our results can guide future health initiatives through examination of epidemiological trends and a better understanding of variation across countries. Funding Bill & Melinda Gates Foundation. Background Up-to-date evidence about levels and trends in disease and injury incidence, prevalence, and years lived with disability (YLDs) is an essential input into global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013), we estimated these quantities for acute and chronic diseases and injuries for 188 countries between 1990 and 2013. Methods Estimates were calculated for disease and injury incidence, prevalence, and YLDs using GBD 2010 methods with some important refinements. Results for incidence of acute disorders and prevalence of chronic disorders are new additions to the analysis. Key improvements include expansion to the cause and sequelae list, updated systematic reviews, use of detailed injury codes, improvements to the Bayesian meta-regression method (DisMod-MR), and use of severity splits for various causes. An index of data representativeness, showing data availability, was calculated for each cause and impairment during three periods globally and at the country level for 2013. In total, 35 620 distinct sources of data were used and documented to calculated estimates for 301 diseases and injuries and 2337 sequelae. The comorbidity simulation provides estimates for the number of sequelae, concurrently, by individuals by country, year, age, and sex. Disability weights were updated with the addition of new population-based survey data from four countries. Findings Disease and injury were highly prevalent; only a small fraction of individuals had no sequelae. Comorbidity rose substantially with age and in absolute terms from 1990 to 2013. Incidence of acute sequelae were predominantly infectious diseases and short-term injuries, with over 2 billion cases of upper respiratory infections and diarrhoeal disease episodes in 2013, with the notable exception of tooth pain due to permanent caries with more than 200 million incident cases in 2013. Conversely, leading chronic sequelae were largely attributable to non-communicable diseases, with prevalence estimates for asymptomatic permanent caries and tension-type headache of 2·4 billion and 1·6 billion, respectively. The distribution of the number of sequelae in populations varied widely across regions, with an expected relation between age and disease prevalence. YLDs for both sexes increased from 537·6 million in 1990 to 764·8 million in 2013 due to population growth and ageing, whereas the age-standardised rate decreased little from 114·87 per 1000 people to 110·31 per 1000 people between 1990 and 2013. Leading causes of YLDs included low back pain and major depressive disorder among the top ten causes of YLDs in every country. YLD rates per person, by major cause groups, indicated the main drivers of increases were due to musculoskeletal, mental, and substance use disorders, neurological disorders, and chronic respiratory diseases; however HIV/AIDS was a notable driver of increasing YLDs in sub-Saharan Africa. Also, the proportion of disability-adjusted life years due to YLDs increased globally from 21·1% in 1990 to 31·2% in 2013. Interpretation Ageing of the world's population is leading to a substantial increase in the numbers of individuals with sequelae of diseases and injuries. Rates of YLDs are declining much more slowly than mortality rates. The non-fatal dimensions of disease and injury will require more and more attention from health systems. The transition to non-fatal outcomes as the dominant source of burden of disease is occurring rapidly outside of sub-Saharan Africa. Our results can guide future health initiatives through examination of epidemiological trends and a better understanding of variation across countries. Funding Bill & Melinda Gates Foundation.
Published: 2015
Full Text: View/download PDF

5. Occupational noise exposure and maternal pregnancy complications: register-based cohort from urban areas in four Nordic countries.

Author: Pasanen TP, Tiittanen P, Roswall N, Persson Waye K, Selander J, Sanchez Martinez N, Sjöström M, Vincens N, Ögren M, Aasvang GM, Evandt J, Krog NH, Weyde KV, Khan J, Gissler M, Lindstrøm JC, Poulsen AH, Pershagen G, Sorensen M, and Lanki T
Abstract: Objective: To assess the role of occupational noise exposure on pregnancy complications in urban Nordic populations., Methods: A study population covering five metropolitan areas in Denmark, Finland, Norway and Sweden was generated using national birth registries linked with occupational and residential environmental exposures and sociodemographic variables. The data covered all pregnancies during 5-11 year periods in 2004‒2016, resulting in 373 184 pregnancies. Occupational noise exposure was based on a Swedish-developed job-exposure-matrix, containing measured A-weighted annual 8 hour noise levels (L Aeq8h ), and linked with person-specific job-history. Outcomes included diagnosed gestational diabetes, gestational hypertension, mild pre-eclampsia and severe pre-eclampsia. The data were analysed with logistic regression models separately in each country, adjusting for maternal (age, parity, birth year, education and marital status) and residential environmental factors (low neighbourhood income, NO 2 and green and blue space). The results were combined by meta-analysis., Results: Occupational noise exceeding 80 dB, compared with less than 70 dB, was associated with an increased odds of gestational diabetes in all countries, with a combined OR of 1.26 (95% CI 1.04 to 1.51), and mild pre-eclampsia in all countries except Finland, resulting in a combined OR of 1.22 (95% CI 0.99 to 1.51). Further adjustment by maternal body-mass index attenuated these associations. No association with gestational hypertension or severe pre-eclampsia was found., Conclusions: Register data from four nationalities show that gestational diabetes and, tentatively, mild pre-eclampsia was increased among pregnant workers working in occupations where noise levels exceed 80 dB L Aeq8h but not in occupations with lower noise levels., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2025. No commercial re-use. See rights and permissions. Published by BMJ Group.)
Published: 2025
Full Text: View/download PDF

6. Corrigendum to "Residential exposure to transportation noise and risk of incident atrial fibrillation: a pooled study of 11 prospective Nordic cohorts" [The Lancet Regional Health - Europe, Volume 46, November 2024, 101091].

Author: Thacher JD, Roswall N, Ögren M, Pyko A, Åkesson A, Oudin A, Rosengren A, Poulsen AH, Eriksson C, Segersson D, Rizzuto D, Helte E, Andersson EM, Aasvang GM, Engström G, Gudjonsdottir H, Selander J, Christensen JH, Brandt J, Leander K, Overvad K, Mattisson K, Eneroth K, Stucki L, Barregard L, Stockfelt L, Albin M, Simonsen MK, Raaschou-Nielsen O, Jousilahti P, Tiittanen P, Ljungman PLS, Jensen SS, Gustafsson S, Yli-Tuomi T, Cole-Hunter T, Lanki T, Lim YH, Andersen ZJ, Pershagen G, and Sørensen M
Abstract: [This corrects the article DOI: 10.1016/j.lanepe.2024.101091.]., (© 2024 The Author(s).)
Published: 2024
Full Text: View/download PDF

7. Residential exposure to transportation noise and risk of incident atrial fibrillation: a pooled study of 11 prospective Nordic cohorts.

Author: Thacher JD, Roswall N, Ögren M, Pyko A, Åkesson A, Oudin A, Rosengren A, Poulsen AH, Eriksson C, Segersson D, Rizzuto D, Helte E, Andersson EM, Aasvang GM, Engström G, Gudjonsdottir H, Selander J, Christensen JH, Brandt J, Leander K, Overvad K, Mattisson K, Eneroth K, Stucki L, Barregard L, Stockfelt L, Albin M, Simonsen MK, Raaschou-Nielsen O, Jousilahti P, Tiittanen P, Ljungman PLS, Jensen SS, Gustafsson S, Yli-Tuomi T, Cole-Hunter T, Lanki T, Lim YH, Andersen ZJ, Pershagen G, and Sørensen M
Abstract: Background: Transportation noise has been linked with cardiometabolic outcomes, yet whether it is a risk factor for atrial fibrillation (AF) remains inconclusive. We aimed to assess whether transportation noise was associated with AF in a large, pooled Nordic cohort., Methods: We pooled data from 11 Nordic cohorts, totaling 161,115 participants. Based on address history from five years before baseline until end of follow-up, road, railway, and aircraft noise was estimated at a residential level. Incident AF was ascertained via linkage to nationwide patient registries. Cox proportional hazards models were utilized to estimate associations between running 5-year time-weighted mean transportation noise (L den ) and AF after adjusting for sociodemographics, lifestyle, and air pollution., Findings: We identified 18,939 incident AF cases over a median follow-up of 19.6 years. Road traffic noise was associated with AF, with a hazard ratio (HR) and 95% confidence interval (CI) of 1.02 (1.00-1.04) per 10-dB of 5-year mean time-weighted exposure, which changed to 1.03 (1.01-1.06) when implementing a 53-dB cut-off. In effect modification analyses, the association for road traffic noise and AF appeared strongest in women and overweight and obese participants. Compared to exposures ≤40 dB, aircraft noise of 40.1-50 and > 50 dB were associated with HRs of 1.04 (0.93-1.16) and 1.12 (0.98-1.27), respectively. Railway noise was not associated with AF. We found a HR of 1.19 (1.02-1.40) among people exposed to noise from road (≥45 dB), railway (>40 dB), and aircraft (>40 dB) combined., Interpretation: Road traffic noise, and possibly aircraft noise, may be associated with elevated risk of AF., Funding: NordForsk., Competing Interests: All other authors declare no competing interests., (© 2024 The Author(s).)
Published: 2024
Full Text: View/download PDF

8. Long-term exposure to transportation noise and obesity: A pooled analysis of eleven Nordic cohorts.

Author: Persson Å, Pyko A, Stucki L, Ögren M, Åkesson A, Oudin A, Tjønneland A, Rosengren A, Segersson D, Rizzuto D, Helte E, Andersson EM, Aasvang GM, Gudjonsdottir H, Selander J, Christensen JH, Leander K, Mattisson K, Eneroth K, Barregard L, Stockfelt L, Albin M, Simonsen MK, Spanne M, Roswall N, Tiittanen P, Molnár P, Ljungman PLS, Männistö S, Yli-Tuomi T, Cole-Hunter T, Lanki T, Lim YH, Andersen ZJ, Sørensen M, Pershagen G, and Eriksson C
Abstract: Background: Available evidence suggests a link between exposure to transportation noise and an increased risk of obesity. We aimed to assess exposure-response functions for long-term residential exposure to road traffic, railway and aircraft noise, and markers of obesity., Methods: Our cross-sectional study is based on pooled data from 11 Nordic cohorts, including up to 162,639 individuals with either measured (69.2%) or self-reported obesity data. Residential exposure to transportation noise was estimated as a time-weighted average L den 5 years before recruitment. Adjusted linear and logistic regression models were fitted to assess beta coefficients and odds ratios (OR) with 95% confidence intervals (CI) for body mass index, overweight, and obesity, as well as for waist circumference and central obesity. Furthermore, natural splines were fitted to assess the shape of the exposure-response functions., Results: For road traffic noise, the OR for obesity was 1.06 (95% CI = 1.03, 1.08) and for central obesity 1.03 (95% CI = 1.01, 1.05) per 10 dB L den . Thresholds were observed at around 50-55 and 55-60 dB L den , respectively, above which there was an approximate 10% risk increase per 10 dB L den increment for both outcomes. However, linear associations only occurred in participants with measured obesity markers and were strongly influenced by the largest cohort. Similar risk estimates as for road traffic noise were found for railway noise, with no clear thresholds. For aircraft noise, results were uncertain due to the low number of exposed participants., Conclusion: Our results support an association between road traffic and railway noise and obesity., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report., (Copyright © 2024 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)
Published: 2024
Full Text: View/download PDF

9. Childhood exposure to outdoor air pollution in different microenvironments and cognitive and fine motor function in children from six European cohorts.

Author: Domínguez A, Koch S, Marquez S, de Castro M, Urquiza J, Evandt J, Oftedal B, Aasvang GM, Kampouri M, Vafeiadi M, Mon-Williams M, Lewer D, Lepeule J, Andrusaityte S, Vrijheid M, Guxens M, and Nieuwenhuijsen M
Subjects: Child, Humans, Cognition, Cohort Studies, Environmental Exposure analysis, Particulate Matter analysis, Transportation, Air Pollutants toxicity, Air Pollution analysis
Abstract: Background: Exposure to air pollution during childhood has been linked with adverse effects on cognitive development and motor function. However, limited research has been done on the associations of air pollution exposure in different microenvironments such as home, school, or while commuting with these outcomes., Objective: To analyze the association between childhood air pollution exposure in different microenvironments and cognitive and fine motor function from six European birth cohorts., Methods: We included 1301 children from six European birth cohorts aged 6-11 years from the HELIX project. Average outdoor air pollutants concentrations (NO 2 , PM 2.5 ) were estimated using land use regression models for different microenvironments (home, school, and commute), for 1-year before the outcome assessment. Attentional function, cognitive flexibility, non-verbal intelligence, and fine motor function were assessed using the Attention Network Test, Trail Making Test A and B, Raven Colored Progressive Matrices test, and the Finger Tapping test, respectively. Adjusted linear regressions models were run to determine the association between each air pollutant from each microenvironment on each outcome., Results: In pooled analysis we observed high correlation (rs = 0.9) between air pollution exposures levels at home and school. However, the cohort-by-cohort analysis revealed correlations ranging from low to moderate. Air pollution exposure levels while commuting were higher than at home or school. Exposure to air pollution in the different microenvironments was not associated with working memory, attentional function, non-verbal intelligence, and fine motor function. Results remained consistently null in random-effects meta-analysis., Conclusions: No association was observed between outdoor air pollution exposure in different microenvironments (home, school, commute) and cognitive and fine motor function in children from six European birth cohorts. Future research should include a more detailed exposure assessment, considering personal measurements and time spent in different microenvironments., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)
Published: 2024
Full Text: View/download PDF

10. Health position paper and redox perspectives - Disease burden by transportation noise.

Author: Sørensen M, Pershagen G, Thacher JD, Lanki T, Wicki B, Röösli M, Vienneau D, Cantuaria ML, Schmidt JH, Aasvang GM, Al-Kindi S, Osborne MT, Wenzel P, Sastre J, Fleming I, Schulz R, Hahad O, Kuntic M, Zielonka J, Sies H, Grune T, Frenis K, Münzel T, and Daiber A
Subjects: Animals, Humans, Environmental Exposure adverse effects, Cohort Studies, Oxidation-Reduction, Noise, Transportation adverse effects, Myocardial Ischemia
Abstract: Transportation noise is a ubiquitous urban exposure. In 2018, the World Health Organization concluded that chronic exposure to road traffic noise is a risk factor for ischemic heart disease. In contrast, they concluded that the quality of evidence for a link to other diseases was very low to moderate. Since then, several studies on the impact of noise on various diseases have been published. Also, studies investigating the mechanistic pathways underlying noise-induced health effects are emerging. We review the current evidence regarding effects of noise on health and the related disease-mechanisms. Several high-quality cohort studies consistently found road traffic noise to be associated with a higher risk of ischemic heart disease, heart failure, diabetes, and all-cause mortality. Furthermore, recent studies have indicated that road traffic and railway noise may increase the risk of diseases not commonly investigated in an environmental noise context, including breast cancer, dementia, and tinnitus. The harmful effects of noise are related to activation of a physiological stress response and nighttime sleep disturbance. Oxidative stress and inflammation downstream of stress hormone signaling and dysregulated circadian rhythms are identified as major disease-relevant pathomechanistic drivers. We discuss the role of reactive oxygen species and present results from antioxidant interventions. Lastly, we provide an overview of oxidative stress markers and adverse redox processes reported for noise-exposed animals and humans. This position paper summarizes all available epidemiological, clinical, and preclinical evidence of transportation noise as an important environmental risk factor for public health and discusses its implications on the population level., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)
Published: 2024
Full Text: View/download PDF

11. Availability, accessibility, and use of green spaces and cognitive development in primary school children.

Author: Fernandes A, Krog NH, McEachan R, Nieuwenhuijsen M, Julvez J, Márquez S, de Castro M, Urquiza J, Heude B, Vafeiadi M, Gražulevičienė R, Slama R, Dedele A, Aasvang GM, Evandt J, Andrusaityte S, Kampouri M, and Vrijheid M
Subjects: Female, Humans, Child, Regression Analysis, Europe, Schools, Mothers, Cognition
Abstract: Green spaces may have beneficial impacts on children's cognition. However, few studies explored the exposure to green spaces beyond residential areas, and their availability, accessibility and uses at the same time. The aim of the present study was to describe patterns of availability, accessibility, and uses of green spaces among primary school children and to explore how these exposure dimensions are associated with cognitive development. Exposures to green space near home, school, commuting route, and other daily activity locations were assessed for 1607 children aged 6-11 years from six birth cohorts across Europe, and included variables related to: availability (NDVI buffers: 100, 300, 500 m), potential accessibility (proximity to a major green space: linear distance; within 300 m), and use (play time in green spaces: hours/year), and the number of visits to green spaces (times/previous week). Cognition measured as fluid intelligence, inattention, and working memory was assessed by computerized tests. We performed multiple linear regression analyses on pooled and imputed data adjusted for individual and area-level confounders. Availability, accessibility, and uses of green spaces showed a social gradient that was unfavorable in more vulnerable socioeconomic groups. NDVI was associated with more playing time in green spaces, but proximity to a major green space was not. Associations between green space exposures and cognitive function outcomes were not statistically significant in our overall study population. Stratification by socioeconomic variables showed that living within 300 m of a major green space was associated with improved working memory only in children in less deprived residential areas (β = 0.30, CI: 0.09,0.51), and that more time playing in green spaces was associated with better working memory only in children of highly educated mothers (β per IQR increase in hour/year = 0.10; 95% CI: 0.01, 0.19). However, studying within 300 m of a major green space increased inattention scores in children in more deprived areas (β = 15.45, 95% CI: 3.50, 27.40)., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)
Published: 2023
Full Text: View/download PDF

12. Burden of disease due to transportation noise in the Nordic countries.

Author: Aasvang GM, Stockfelt L, Sørensen M, Turunen AW, Roswall N, Yli-Tuomi T, Ögren M, Lanki T, Selander J, Vincens N, Pyko A, Pershagen G, Sulo G, and Bølling AK
Subjects: Humans, Risk Factors, Scandinavian and Nordic Countries epidemiology, Cost of Illness, Environmental Exposure, Noise, Transportation adverse effects, Diabetes Mellitus, Type 2
Abstract: Background: Environmental noise is of increasing concern for public health. Quantification of associated health impacts is important for regulation and preventive strategies., Aim: To estimate the burden of disease (BoD) due to road traffic and railway noise in four Nordic countries and their capitals, in terms of DALYs (Disability-Adjusted Life Years), using comparable input data across countries., Method: Road traffic and railway noise exposure was obtained from the noise mapping conducted according to the Environmental Noise Directive (END) as well as nationwide noise exposure assessments for Denmark and Norway. Noise annoyance, sleep disturbance and ischaemic heart disease were included as the main health outcomes, using exposure-response functions from the WHO, 2018 systematic reviews. Additional analyses included stroke and type 2 diabetes. Country-specific DALY rates from the Global Burden of Disease (GBD) study were used as health input data., Results: Comparable exposure data were not available on a national level for the Nordic countries, only for capital cities. The DALY rates for the capitals ranged from 329 to 485 DALYs/100,000 for road traffic noise and 44 to 146 DALY/100,000 for railway noise. Moreover, the DALY estimates for road traffic noise increased with up to 17% upon inclusion of stroke and diabetes. DALY estimates based on nationwide noise data were 51 and 133% higher than the END-based estimates, for Norway and Denmark, respectively., Conclusion: Further harmonization of noise exposure data is required for between-country comparisons. Moreover, nationwide noise models indicate that DALY estimates based on END considerably underestimate national BoD due to transportation noise. The health-related burden of traffic noise was comparable to that of air pollution, an established risk factor for disease in the GBD framework. Inclusion of environmental noise as a risk factor in the GBD is strongly encouraged., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)
Published: 2023
Full Text: View/download PDF

13. Exposure to long-term source-specific transportation noise and incident breast cancer: A pooled study of eight Nordic cohorts.

Author: Thacher JD, Oudin A, Flanagan E, Mattisson K, Albin M, Roswall N, Pyko A, Aasvang GM, Andersen ZJ, Borgquist S, Brandt J, Broberg K, Cole-Hunter T, Eriksson C, Eneroth K, Gudjonsdottir H, Helte E, Ketzel M, Lanki T, Lim YH, Leander K, Ljungman P, Manjer J, Männistö S, Raaschou-Nielsen O, Pershagen G, Rizzuto D, Sandsveden M, Selander J, Simonsen MK, Stucki L, Spanne M, Stockfelt L, Tjønneland A, Yli-Tuomi T, Tiittanen P, Valencia VH, Ögren M, Åkesson A, and Sørensen M
Subjects: Humans, Female, Cohort Studies, Risk Factors, Prospective Studies, Environmental Exposure adverse effects, Environmental Exposure analysis, Noise, Transportation adverse effects, Breast Neoplasms epidemiology, Breast Neoplasms etiology
Abstract: Background: Environmental noise is an important environmental exposure that can affect health. An association between transportation noise and breast cancer incidence has been suggested, although current evidence is limited. We investigated the pooled association between long-term exposure to transportation noise and breast cancer incidence., Methods: Pooled data from eight Nordic cohorts provided a study population of 111,492 women. Road, railway, and aircraft noise were modelled at residential addresses. Breast cancer incidence (all, estrogen receptor (ER) positive, and ER negative) was derived from cancer registries. Hazard ratios (HR) were estimated using Cox Proportional Hazards Models, adjusting main models for sociodemographic and lifestyle variables together with long-term exposure to air pollution., Results: A total of 93,859 women were included in the analyses, of whom 5,875 developed breast cancer. The median (5th-95th percentile) 5-year residential road traffic noise was 54.8 (40.0-67.8) dB Lden, and among those exposed, the median railway noise was 51.0 (41.2-65.8) dB Lden. We observed a pooled HR for breast cancer (95 % confidence interval (CI)) of 1.03 (0.99-1.06) per 10 dB increase in 5-year mean exposure to road traffic noise, and 1.03 (95 % CI: 0.96-1.11) for railway noise, after adjustment for lifestyle and sociodemographic covariates. HRs remained unchanged in analyses with further adjustment for PM 2.5 and attenuated when adjusted for NO 2 (HRs from 1.02 to 1.01), in analyses using the same sample. For aircraft noise, no association was observed. The associations did not vary by ER status for any noise source. In analyses using <60 dB as a cutoff, we found HRs of 1.08 (0.99-1.18) for road traffic and 1.19 (0.95-1.49) for railway noise., Conclusions: We found weak associations between road and railway noise and breast cancer risk. More high-quality prospective studies are needed, particularly among those exposed to railway and aircraft noise before conclusions regarding noise as a risk factor for breast cancer can be made., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Author(s). Published by Elsevier Ltd.. All rights reserved.)
Published: 2023
Full Text: View/download PDF

14. Long-term exposure to traffic noise and risk of incident colon cancer: A pooled study of eleven Nordic cohorts.

Author: Roswall N, Thacher JD, Ögren M, Pyko A, Åkesson A, Oudin A, Tjønneland A, Rosengren A, Poulsen AH, Eriksson C, Segersson D, Rizzuto D, Helte E, Andersson EM, Aasvang GM, Gudjonsdottir H, Khan J, Selander J, Christensen JH, Brandt J, Leander K, Mattisson K, Eneroth K, Stucki L, Barregard L, Stockfelt L, Albin M, Simonsen MK, Spanne M, Jousilahti P, Tiittanen P, Molnàr P, Ljungman PLS, Yli-Tuomi T, Cole-Hunter T, Lanki T, Hvidtfeldt UA, Lim YH, Andersen ZJ, Pershagen G, and Sørensen M
Subjects: Humans, Cohort Studies, Risk Factors, Environmental Exposure analysis, Denmark epidemiology, Noise, Transportation, Air Pollution, Colonic Neoplasms
Abstract: Background Colon cancer incidence is rising globally, and factors pertaining to urbanization have been proposed involved in this development. Traffic noise may increase colon cancer risk by causing sleep disturbance and stress, thereby inducing known colon cancer risk-factors, e.g. obesity, diabetes, physical inactivity, and alcohol consumption, but few studies have examined this. Objectives The objective of this study was to investigate the association between traffic noise and colon cancer (all, proximal, distal) in a pooled population of 11 Nordic cohorts, totaling 155,203 persons. Methods We identified residential address history and estimated road, railway, and aircraft noise, as well as air pollution, for all addresses, using similar exposure models across cohorts. Colon cancer cases were identified through national registries. We analyzed data using Cox Proportional Hazards Models, adjusting main models for harmonized sociodemographic and lifestyle data. Results During follow-up (median 18.8 years), 2757 colon cancer cases developed. We found a hazard ratio (HR) of 1.05 (95% confidence interval (CI): 0.99-1.10) per 10-dB higher 5-year mean time-weighted road traffic noise. In sub-type analyses, the association seemed confined to distal colon cancer: HR 1.06 (95% CI: 0.98-1.14). Railway and aircraft noise was not associated with colon cancer, albeit there was some indication in sub-type analyses that railway noise may also be associated with distal colon cancer. In interaction-analyses, the association between road traffic noise and colon cancer was strongest among obese persons and those with high NO 2 -exposure. Discussion A prominent study strength is the large population with harmonized data across eleven cohorts, and the complete address-history during follow-up. However, each cohort estimated noise independently, and only at the most exposed façade, which may introduce exposure misclassification. Despite this, the results of this pooled study suggest that traffic noise may be a risk factor for colon cancer, especially of distal origin., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)
Published: 2023
Full Text: View/download PDF

15. Long-Term Exposure to Transportation Noise and Ischemic Heart Disease: A Pooled Analysis of Nine Scandinavian Cohorts.

Author: Pyko A, Roswall N, Ögren M, Oudin A, Rosengren A, Eriksson C, Segersson D, Rizzuto D, Andersson EM, Aasvang GM, Engström G, Gudjonsdottir H, Jørgensen JT, Selander J, Christensen JH, Brandt J, Leander K, Overvad K, Eneroth K, Mattisson K, Barregard L, Stockfelt L, Albin M, Simonsen MK, Tiittanen P, Molnar P, Ljungman P, Solvang Jensen S, Gustafsson S, Lanki T, Lim YH, Andersen ZJ, Sørensen M, and Pershagen G
Subjects: Humans, Environmental Exposure, Angina Pectoris, Noise, Transportation adverse effects, Myocardial Ischemia epidemiology, Myocardial Infarction epidemiology
Abstract: Background: Transportation noise may induce cardiovascular disease, but the public health implications are unclear., Objectives: The study aimed to assess exposure-response relationships for different transportation noise sources and ischemic heart disease (IHD), including subtypes., Methods: Pooled analyses were performed of nine cohorts from Denmark and Sweden, together including 132,801 subjects. Time-weighted long-term exposure to road, railway, and aircraft noise, as well as air pollution, was estimated based on residential histories. Hazard ratios (HRs) were calculated using Cox proportional hazards models following adjustment for lifestyle and socioeconomic risk factors., Results: A total of 22,459 incident cases of IHD were identified during follow-up from national patient and mortality registers, including 7,682 cases of myocardial infarction. The adjusted HR for IHD was 1.03 [95% confidence interval (CI) 1.00, 1.05] per 10 dB L den for both road and railway noise exposure during 5 y prior to the event. Higher risks were indicated for IHD excluding angina pectoris cases, with HRs of 1.06 (95% CI: 1.03, 1.08) and 1.05 (95% CI: 1.01, 1.08) per 10 dB L den for road and railway noise, respectively. Corresponding HRs for myocardial infarction were 1.02 (95% CI: 0.99, 1.05) and 1.04 (95% CI: 0.99, 1.08). Increased risks were observed for aircraft noise but without clear exposure-response relations. A threshold at around 55 dB L den was suggested in the exposure-response relation for road traffic noise and IHD., Discussion: Exposure to road, railway, and aircraft noise in the prior 5 y was associated with an increased risk of IHD, particularly after exclusion of angina pectoris cases, which are less well identified in the registries. https://doi.org/10.1289/EHP10745.
Published: 2023
Full Text: View/download PDF

16. Short- and medium-term air pollution exposure, plasmatic protein levels and blood pressure in children.

Author: de Prado-Bert P, Warembourg C, Dedele A, Heude B, Borràs E, Sabidó E, Aasvang GM, Lepeule J, Wright J, Urquiza J, Gützkow KB, Maitre L, Chatzi L, Casas M, Vafeiadi M, Nieuwenhuijsen MJ, de Castro M, Grazuleviciene R, McEachan RRC, Basagaña X, Vrijheid M, Sunyer J, and Bustamante M
Subjects: Blood Pressure, Child, Environmental Exposure adverse effects, Environmental Exposure analysis, Humans, Nitrogen Dioxide analysis, Particulate Matter analysis, Particulate Matter toxicity, Air Pollutants analysis, Air Pollutants toxicity, Air Pollution adverse effects, Air Pollution analysis
Abstract: Exposure to air pollution influences children's health, however, the biological mechanisms underlying these effects are not completely elucidated. We investigated the association between short- and medium-term outdoor air pollution exposure with protein profiles and their link with blood pressure in 1170 HELIX children aged 6-11 years. Different air pollutants (NO 2 , PM 10 , PM 2.5 , and PM 2.5abs ) were estimated based on residential and school addresses at three different windows of exposure (1-day, 1-week, and 1-year before clinical and molecular assessment). Thirty-six proteins, including adipokines, cytokines, or apolipoproteins, were measured in children's plasma using Luminex. Systolic and diastolic blood pressure (SBP and DBP) were measured following a standardized protocol. We performed an association study for each air pollutant at each location and time window and each outcome, adjusting for potential confounders. After correcting for multiple-testing, hepatocyte growth factor (HGF) and interleukin 8 (IL8) levels were positively associated with 1-week home exposure to some of the pollutants (NO 2 , PM 10 , or PM 2.5 ). NO 2 1-week home exposure was also related to higher SBP. The mediation study suggested that HGF could explain 19% of the short-term effect of NO 2 on blood pressure, but other study designs are needed to prove the causal directionality between HGF and blood pressure., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)
Published: 2022
Full Text: View/download PDF

17. Changes in life expectancy and disease burden in Norway, 1990-2019: an analysis of the Global Burden of Disease Study 2019.

Author: Clarsen B, Nylenna M, Klitkou ST, Vollset SE, Baravelli CM, Bølling AK, Aasvang GM, Sulo G, Naghavi M, Pasovic M, Asaduzzaman M, Bjørge T, Eggen AE, Eikemo TA, Ellingsen CL, Haaland ØA, Hailu A, Hassan S, Hay SI, Juliusson PB, Kisa A, Kisa S, Månsson J, Mekonnen T, Murray CJL, Norheim OF, Ottersen T, Sagoe D, Sripada K, Winkler AS, and Knudsen AKS
Subjects: Cost of Illness, Healthy Life Expectancy, Humans, Norway epidemiology, Global Burden of Disease, Life Expectancy
Abstract: Background: Geographical differences in health outcomes are reported in many countries. Norway has led an active policy aiming for regional balance since the 1970s. Using data from the Global Burden of Disease Study (GBD) 2019, we examined regional differences in development and current state of health across Norwegian counties., Methods: Data for life expectancy, healthy life expectancy (HALE), years of life lost (YLLs), years lived with disability (YLDs), and disability-adjusted life-years (DALYs) in Norway and its 11 counties from 1990 to 2019 were extracted from GBD 2019. County-specific contributors to changes in life expectancy were compared. Inequality in disease burden was examined by use of the Gini coefficient., Findings: Life expectancy and HALE improved in all Norwegian counties from 1990 to 2019. Improvements in life expectancy and HALE were greatest in the two counties with the lowest values in 1990: Oslo, in which life expectancy and HALE increased from 71·9 years (95% uncertainty interval 71·4-72·4) and 63·0 years (60·5-65·4) in 1990 to 81·3 years (80·0-82·7) and 70·6 years (67·4-73·6) in 2019, respectively; and Troms og Finnmark, in which life expectancy and HALE increased from 71·9 years (71·5-72·4) and 63·5 years (60·9-65·6) in 1990 to 80·3 years (79·4-81·2) and 70·0 years (66·8-72·2) in 2019, respectively. Increased life expectancy was mainly due to reductions in cardiovascular disease, neoplasms, and respiratory infections. No significant differences between the national YLD or DALY rates and the corresponding age-standardised rates were reported in any of the counties in 2019; however, Troms og Finnmark had a higher age-standardised YLL rate than the national rate (8394 per 100 000 [95% UI 7801-8944] vs 7536 per 100 000 [7391-7691]). Low inequality between counties was shown for life expectancy, HALE, all level-1 causes of DALYs, and exposure to level-1 risk factors., Interpretation: Over the past 30 years, Norway has reduced inequality in disease burden between counties. However, inequalities still exist at a within-county level and along other sociodemographic gradients. Because of insufficient Norwegian primary data, there remains substantial uncertainty associated with regional estimates for non-fatal disease burden and exposure to risk factors., Funding: Bill & Melinda Gates Foundation, Research Council of Norway, and Norwegian Institute of Public Health., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)
Published: 2022
Full Text: View/download PDF

18. Occupational noise exposure and risk of incident stroke: a pooled study of five Scandinavian cohorts.

Author: Thacher JD, Roswall N, Lissåker C, Aasvang GM, Albin M, Andersson EM, Engström G, Eriksson C, Hvidtfeldt UA, Ketzel M, Khan J, Lanki T, Ljungman PLS, Mattisson K, Molnar P, Raaschou-Nielsen O, Oudin A, Overvad K, Petersen SB, Pershagen G, Poulsen AH, Pyko A, Rizzuto D, Rosengren A, Schioler L, Sjöström M, Stockfelt L, Tiittanen P, Sallsten G, Ögren M, Selander J, and Sorensen M
Abstract: Objectives: To investigate the association between occupational noise exposure and stroke incidence in a pooled study of five Scandinavian cohorts (NordSOUND)., Methods: We pooled and harmonised data from five Scandinavian cohorts resulting in 78 389 participants. We obtained job data from national registries or questionnaires and recoded these to match a job-exposure matrix developed in Sweden, which specified the annual average daily noise exposure in five exposure classes (L Aeq8h ): <70, 70-74, 75-79, 80-84, ≥85 dB(A). We identified residential address history and estimated 1-year average road traffic noise at baseline. Using national patient and mortality registers, we identified 7777 stroke cases with a median follow-up of 20.2 years. Analyses were conducted using Cox proportional hazards models adjusting for individual and area-level potential confounders., Results: Exposure to occupational noise at baseline was not associated with overall stroke in the fully adjusted models. For ischaemic stroke, occupational noise was associated with HRs (95% CI) of 1.08 (0.98 to 1.20), 1.09 (0.97 to 1.24) and 1.06 (0.92 to 1.21) in the 75-79, 80-84 and ≥85 dB(A) exposure groups, compared with <70 dB(A), respectively. In subanalyses using time-varying occupational noise exposure, we observed an indication of higher stroke risk among the most exposed (≥85 dB(A)), particularly when restricting analyses to people exposed to occupational noise within the last year (HR: 1.27; 95% CI: 0.99 to 1.63)., Conclusions: We found no association between occupational noise and risk of overall stroke after adjustment for confounders. However, the non-significantly increased risk of ischaemic stroke warrants further investigation., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)
Published: 2022
Full Text: View/download PDF

19. Green CURIOCITY: a study protocol for a European birth cohort study analysing childhood heat-related health impacts and protective effects of urban natural environments.

Author: van den Bosch M, Basagaña X, Mudu P, Kendrovski V, Maitre L, Hjertager Krog N, Aasvang GM, Grazuleviciene R, McEachan R, Vrijheid M, and Nieuwenhuijsen MJ
Subjects: Air Pollution, Birth Cohort, Child, Child, Preschool, Cities, Cohort Studies, Female, Humans, Pregnancy, Hot Temperature adverse effects, Parks, Recreational
Abstract: Introduction: The European climate is getting warmer and the impact on childhood health and development is insufficiently understood. Equally, how heat-related health risks can be reduced through nature-based solutions, such as exposure to urban natural environments, is unknown. Green CURe In Outdoor CITY spaces (Green CURIOCITY) will analyse how heat exposure during pregnancy affects birth outcomes and how long-term heat exposure may influence children's neurodevelopment. We will also investigate if adverse effects can be mitigated by urban natural environments. A final goal is to visualise intraurban patterns of heat vulnerability and assist planning towards healthier cities., Methods and Analysis: We will use existing data from the Human Early-Life Exposure cohort, which includes information on birth outcomes and neurodevelopment from six European birth cohorts. The cohort is linked to data on prenatal heat exposure and impact on birth outcomes will be analysed with logistic regression models, adjusting for air pollution and noise and sociobehavioural covariates. Similarly, impact of cumulative and immediate heat exposure on neurodevelopmental outcomes at age 5 will be assessed. For both analyses, the potentially moderating impact of natural environments will be quantified. For visualisation, Geographical information systems data will be combined to develop vulnerability maps, demonstrating urban 'hot spots' where the risk of negative impacts of heat is aggravated due to sociodemographic and land use patterns. Finally, geospatial and meteorological data will be used for informing GreenUr, an existing software prototype developed by the WHO Regional Office for Europe to quantify health impacts and augment policy tools for urban green space planning., Ethics and Dissemination: The protocol was approved by the Comité Ético de Investigación Clínica Parc de Salut MAR, Spain. Findings will be published in peer-reviewed journals and presented at policy events. Through stakeholder engagement, the results will also reach user groups and practitioners., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY. Published by BMJ.)
Published: 2022
Full Text: View/download PDF

20. Long-Term Exposure to Transportation Noise and Risk of Incident Stroke: A Pooled Study of Nine Scandinavian Cohorts.

Author: Roswall N, Pyko A, Ögren M, Oudin A, Rosengren A, Lager A, Poulsen AH, Eriksson C, Segersson D, Rizzuto D, Andersson EM, Aasvang GM, Engström G, Jørgensen JT, Selander J, Christensen JH, Thacher J, Leander K, Overvad K, Eneroth K, Mattisson K, Barregård L, Stockfelt L, Albin M, Ketzel M, Simonsen MK, Spanne M, Raaschou-Nielsen O, Magnusson PKE, Tiittanen P, Molnar P, Ljungman P, Lanki T, Lim YH, Andersen ZJ, Pershagen G, and Sørensen M
Subjects: Cohort Studies, Environmental Exposure analysis, Humans, Air Pollutants analysis, Air Pollution analysis, Noise, Transportation adverse effects, Stroke epidemiology
Abstract: Background: Transportation noise is increasingly acknowledged as a cardiovascular risk factor, but the evidence base for an association with stroke is sparse., Objective: We aimed to investigate the association between transportation noise and stroke incidence in a large Scandinavian population., Methods: We harmonized and pooled data from nine Scandinavian cohorts (seven Swedish, two Danish), totaling 135,951 participants. We identified residential address history and estimated road, railway, and aircraft noise for all addresses. Information on stroke incidence was acquired through linkage to national patient and mortality registries. We analyzed data using Cox proportional hazards models, including socioeconomic and lifestyle confounders, and air pollution., Results: During follow-up ( median = 19.5 y ), 11,056 stroke cases were identified. Road traffic noise ( L den ) was associated with risk of stroke, with a hazard ratio (HR) of 1.06 [95% confidence interval (CI): 1.03, 1.08] per 10-dB higher 5-y mean time-weighted exposure in analyses adjusted for individual- and area-level socioeconomic covariates. The association was approximately linear and persisted after adjustment for air pollution [particulate matter (PM) with an aerodynamic diameter of ≤ 2.5 μ m ( PM 2.5 ) and NO 2 ]. Stroke was associated with moderate levels of 5-y aircraft noise exposure (40-50 vs. ≤ 40 dB ) ( HR = 1.12 ; 95% CI: 0.99, 1.27), but not with higher exposure ( ≥ 50 dB , HR = 0.94 ; 95% CI: 0.79, 1.11). Railway noise was not associated with stroke., Discussion: In this pooled study, road traffic noise was associated with a higher risk of stroke. This finding supports road traffic noise as an important cardiovascular risk factor that should be included when estimating the burden of disease due to traffic noise. https://doi.org/10.1289/EHP8949.
Published: 2021
Full Text: View/download PDF

21. Advancing tools for human early lifecourse exposome research and translation (ATHLETE): Project overview.

Author: Vrijheid M, Basagaña X, Gonzalez JR, Jaddoe VWV, Jensen G, Keun HC, McEachan RRC, Porcel J, Siroux V, Swertz MA, Thomsen C, Aasvang GM, Andrušaitytė S, Angeli K, Avraam D, Ballester F, Burton P, Bustamante M, Casas M, Chatzi L, Chevrier C, Cingotti N, Conti D, Crépet A, Dadvand P, Duijts L, van Enckevort E, Esplugues A, Fossati S, Garlantezec R, Gómez Roig MD, Grazuleviciene R, Gützkow KB, Guxens M, Haakma S, Hessel EVS, Hoyles L, Hyde E, Klanova J, van Klaveren JD, Kortenkamp A, Le Brusquet L, Leenen I, Lertxundi A, Lertxundi N, Lionis C, Llop S, Lopez-Espinosa MJ, Lyon-Caen S, Maitre L, Mason D, Mathy S, Mazarico E, Nawrot T, Nieuwenhuijsen M, Ortiz R, Pedersen M, Perelló J, Pérez-Cruz M, Philippat C, Piler P, Pizzi C, Quentin J, Richiardi L, Rodriguez A, Roumeliotaki T, Sabin Capote JM, Santiago L, Santos S, Siskos AP, Strandberg-Larsen K, Stratakis N, Sunyer J, Tenenhaus A, Vafeiadi M, Wilson RC, Wright J, Yang T, and Slama R
Abstract: Early life stages are vulnerable to environmental hazards and present important windows of opportunity for lifelong disease prevention. This makes early life a relevant starting point for exposome studies. The Advancing Tools for Human Early Lifecourse Exposome Research and Translation (ATHLETE) project aims to develop a toolbox of exposome tools and a Europe-wide exposome cohort that will be used to systematically quantify the effects of a wide range of community- and individual-level environmental risk factors on mental, cardiometabolic, and respiratory health outcomes and associated biological pathways, longitudinally from early pregnancy through to adolescence. Exposome tool and data development include as follows: (1) a findable, accessible, interoperable, reusable (FAIR) data infrastructure for early life exposome cohort data, including 16 prospective birth cohorts in 11 European countries; (2) targeted and nontargeted approaches to measure a wide range of environmental exposures (urban, chemical, physical, behavioral, social); (3) advanced statistical and toxicological strategies to analyze complex multidimensional exposome data; (4) estimation of associations between the exposome and early organ development, health trajectories, and biological (metagenomic, metabolomic, epigenetic, aging, and stress) pathways; (5) intervention strategies to improve early life urban and chemical exposomes, co-produced with local communities; and (6) child health impacts and associated costs related to the exposome. Data, tools, and results will be assembled in an openly accessible toolbox, which will provide great opportunities for researchers, policymakers, and other stakeholders, beyond the duration of the project. ATHLETE's results will help to better understand and prevent health damage from environmental exposures and their mixtures from the earliest parts of the life course onward., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report., (Copyright © 2021 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)
Published: 2021
Full Text: View/download PDF

22. Prenatal and childhood exposure to air pollution and traffic and the risk of liver injury in European children.

Author: Garcia E, Stratakis N, Valvi D, Maitre L, Varo N, Aasvang GM, Andrusaityte S, Basagana X, Casas M, de Castro M, Fossati S, Grazuleviciene R, Heude B, Hoek G, Krog NH, McEachan R, Nieuwenhuijsen M, Roumeliotaki T, Slama R, Urquiza J, Vafeiadi M, Vos MB, Wright J, Conti DV, Berhane K, Vrijheid M, McConnell R, and Chatzi L
Abstract: Nonalcoholic fatty liver disease is the most prevalent pediatric chronic liver disease. Experimental studies suggest effects of air pollution and traffic exposure on liver injury. We present the first large-scale human study to evaluate associations of prenatal and childhood air pollution and traffic exposure with liver injury., Methods: Study population included 1,102 children from the Human Early Life Exposome project. Established liver injury biomarkers, including alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, and cytokeratin-18, were measured in serum between ages 6-10 years. Air pollutant exposures included nitrogen dioxide, particulate matter <10 μm (PM 10 ), and <2.5 μm. Traffic measures included traffic density on nearest road, traffic load in 100-m buffer, and inverse distance to nearest road. Exposure assignments were made to residential address during pregnancy (prenatal) and residential and school addresses in year preceding follow-up (childhood). Childhood indoor air pollutant exposures were also examined. Generalized additive models were fitted adjusting for confounders. Interactions by sex and overweight/obese status were examined., Results: Prenatal and childhood exposures to air pollution and traffic were not associated with child liver injury biomarkers. There was a significant interaction between prenatal ambient PM 10 and overweight/obese status for alanine aminotransferase, with stronger associations among children who were overweight/obese. There was no evidence of interaction with sex., Conclusion: This study found no evidence for associations between prenatal or childhood air pollution or traffic exposure with liver injury biomarkers in children. Findings suggest PM 10 associations maybe higher in children who are overweight/obese, consistent with the multiple-hits hypothesis for nonalcoholic fatty liver disease pathogenesis., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report., (Copyright © 2021 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)
Published: 2021
Full Text: View/download PDF

23. DNA methylation and body mass index from birth to adolescence: meta-analyses of epigenome-wide association studies.

Author: Vehmeijer FOL, Küpers LK, Sharp GC, Salas LA, Lent S, Jima DD, Tindula G, Reese S, Qi C, Gruzieva O, Page C, Rezwan FI, Melton PE, Nohr E, Escaramís G, Rzehak P, Heiskala A, Gong T, Tuominen ST, Gao L, Ross JP, Starling AP, Holloway JW, Yousefi P, Aasvang GM, Beilin LJ, Bergström A, Binder E, Chatzi L, Corpeleijn E, Czamara D, Eskenazi B, Ewart S, Ferre N, Grote V, Gruszfeld D, Håberg SE, Hoyo C, Huen K, Karlsson R, Kull I, Langhendries JP, Lepeule J, Magnus MC, Maguire RL, Molloy PL, Monnereau C, Mori TA, Oken E, Räikkönen K, Rifas-Shiman S, Ruiz-Arenas C, Sebert S, Ullemar V, Verduci E, Vonk JM, Xu CJ, Yang IV, Zhang H, Zhang W, Karmaus W, Dabelea D, Muhlhausler BS, Breton CV, Lahti J, Almqvist C, Jarvelin MR, Koletzko B, Vrijheid M, Sørensen TIA, Huang RC, Arshad SH, Nystad W, Melén E, Koppelman GH, London SJ, Holland N, Bustamante M, Murphy SK, Hivert MF, Baccarelli A, Relton CL, Snieder H, Jaddoe VWV, and Felix JF
Subjects: Adolescent, Child, Child, Preschool, CpG Islands, Cross-Sectional Studies, Epigenome, Female, Fetal Blood, Humans, Male, Pediatric Obesity genetics, Pregnancy, Body Mass Index, DNA Methylation, Epigenesis, Genetic, Obesity genetics, Parturition
Abstract: Background: DNA methylation has been shown to be associated with adiposity in adulthood. However, whether similar DNA methylation patterns are associated with childhood and adolescent body mass index (BMI) is largely unknown. More insight into this relationship at younger ages may have implications for future prevention of obesity and its related traits., Methods: We examined whether DNA methylation in cord blood and whole blood in childhood and adolescence was associated with BMI in the age range from 2 to 18 years using both cross-sectional and longitudinal models. We performed meta-analyses of epigenome-wide association studies including up to 4133 children from 23 studies. We examined the overlap of findings reported in previous studies in children and adults with those in our analyses and calculated enrichment., Results: DNA methylation at three CpGs (cg05937453, cg25212453, and cg10040131), each in a different age range, was associated with BMI at Bonferroni significance, P < 1.06 × 10 -7 , with a 0.96 standard deviation score (SDS) (standard error (SE) 0.17), 0.32 SDS (SE 0.06), and 0.32 BMI SDS (SE 0.06) higher BMI per 10% increase in methylation, respectively. DNA methylation at nine additional CpGs in the cross-sectional childhood model was associated with BMI at false discovery rate significance. The strength of the associations of DNA methylation at the 187 CpGs previously identified to be associated with adult BMI, increased with advancing age across childhood and adolescence in our analyses. In addition, correlation coefficients between effect estimates for those CpGs in adults and in children and adolescents also increased. Among the top findings for each age range, we observed increasing enrichment for the CpGs that were previously identified in adults (birth P enrichment = 1; childhood P enrichment = 2.00 × 10 -4 ; adolescence P enrichment = 2.10 × 10 -7 )., Conclusions: There were only minimal associations of DNA methylation with childhood and adolescent BMI. With the advancing age of the participants across childhood and adolescence, we observed increasing overlap with altered DNA methylation loci reported in association with adult BMI. These findings may be compatible with the hypothesis that DNA methylation differences are mostly a consequence rather than a cause of obesity.
Published: 2020
Full Text: View/download PDF

24. Agreement between self-reported and registry-based use of sleep medications and tranquilizers.

Author: Evandt J, Skurtveit S, Oftedal B, Krog NH, Nafstad P, Skovlund E, Schwarze PE, and Aasvang GM
Subjects: Adult, Cross-Sectional Studies, Drug Prescriptions statistics & numerical data, Female, Humans, Male, Norway, Pharmacoepidemiology statistics & numerical data, Prescription Drugs therapeutic use, Sensitivity and Specificity, Pharmacoepidemiology methods, Registries statistics & numerical data, Self Report statistics & numerical data, Sleep Aids, Pharmaceutical therapeutic use, Tranquilizing Agents therapeutic use
Abstract: Purpose: The purpose of the present study was to assess the agreement between self-reported use of sleep medications and tranquilizers and dispensed hypnotics and anxiolytics., Methods: Self-reported medication use was obtained from the population-based survey Health and Environment in Oslo (HELMILO) (2009-2010) (n = 13 019). Data on dispensed hypnotics and anxiolytics were obtained from the Norwegian Prescription Database (NorPD). As measures of validity, we calculated sensitivity and specificity using both self-reports and prescription records as the reference standard. Furthermore, we calculated Cohen's kappa. Current self-reported medication use was compared with prescription data in time windows of both 100 and 200 days preceding questionnaire completion., Results: The highest sensitivity was observed for current sleep medication use in the 100-day time window (sensitivity = 0.76, 95% confidence interval [CI]: 0.74, 0.79) when using prescription records as the reference standard. Sensitivity was generally lower for tranquilizers compared with sleep medications. Cohen's kappa showed the highest agreement for the 200-day time window with substantial agreement for sleep medications (kappa = 0.64; 95% CI: 0.62, 0.67) and moderate agreement for tranquilizers (kappa = 0.45; 95% CI: 0.41, 0.48)., Conclusions: The present study suggests moderate to substantial agreement between self-reported use of sleep medications and tranquilizers and dispensed drugs in a general adult population. The magnitude of agreement varied according to drug category and time window. Since self-reported and registry-based use of these drug classes does not match each other accurately, limitations of each data source should be considered when such medications are applied as the exposure or outcome in epidemiologic studies., (© 2019 John Wiley & Sons, Ltd.)
Published: 2019
Full Text: View/download PDF

25. Early-Life Environmental Exposures and Blood Pressure in Children.

Author: Warembourg C, Maitre L, Tamayo-Uria I, Fossati S, Roumeliotaki T, Aasvang GM, Andrusaityte S, Casas M, Cequier E, Chatzi L, Dedele A, Gonzalez JR, Gražulevičienė R, Haug LS, Hernandez-Ferrer C, Heude B, Karachaliou M, Krog NH, McEachan R, Nieuwenhuijsen M, Petraviciene I, Quentin J, Robinson O, Sakhi AK, Slama R, Thomsen C, Urquiza J, Vafeiadi M, West J, Wright J, Vrijheid M, and Basagaña X
Subjects: Blood Pressure drug effects, Blood Pressure Determination methods, Blood Pressure Determination statistics & numerical data, Built Environment, Child, Dichlorodiphenyl Dichloroethylene analysis, Europe epidemiology, Female, Holistic Health, Humans, Insecticides adverse effects, Insecticides analysis, Male, Meteorological Concepts, Polychlorinated Biphenyls analysis, Pregnancy, Environmental Exposure adverse effects, Environmental Exposure classification, Environmental Exposure prevention & control, Environmental Pollutants adverse effects, Environmental Pollutants analysis, Hypertension diagnosis, Hypertension epidemiology, Hypertension prevention & control, Prenatal Exposure Delayed Effects blood, Prenatal Exposure Delayed Effects diagnosis, Prenatal Exposure Delayed Effects epidemiology
Abstract: Background: Growing evidence exists about the fetal and environmental origins of hypertension, but mainly limited to single-exposure studies. The exposome has been proposed as a more holistic approach by studying many exposures simultaneously., Objectives: This study aims to evaluate the association between a wide range of prenatal and postnatal exposures and blood pressure (BP) in children., Methods: Systolic and diastolic BP were measured among 1,277 children from the European HELIX (Human Early-Life Exposome) cohort aged 6 to 11 years. Prenatal (n = 89) and postnatal (n = 128) exposures include air pollution, built environment, meteorology, natural spaces, traffic, noise, chemicals, and lifestyles. Two methods adjusted for confounders were applied: an exposome-wide association study considering the exposures independently, and the deletion-substitution-addition algorithm considering all the exposures simultaneously., Results: Decreases in systolic BP were observed with facility density (β change for an interquartile-range increase in exposure: -1.7 mm Hg [95% confidence interval (CI): -2.5 to -0.8 mm Hg]), maternal concentrations of polychlorinated biphenyl 118 (-1.4 mm Hg [95% CI: -2.6 to -0.2 mm Hg]) and child concentrations of dichlorodiphenyldichloroethylene (DDE: -1.6 mm Hg [95% CI: -2.4 to -0.7 mm Hg]), hexachlorobenzene (-1.5 mm Hg [95% CI: -2.4 to -0.6 mm Hg]), and mono-benzyl phthalate (-0.7 mm Hg [95% CI: -1.3 to -0.1 mm Hg]), whereas increases in systolic BP were observed with outdoor temperature during pregnancy (1.6 mm Hg [95% CI: 0.2 to 2.9 mm Hg]), high fish intake during pregnancy (2.0 mm Hg [95% CI: 0.4 to 3.5 mm Hg]), maternal cotinine concentrations (1.2 mm Hg [95% CI: -0.3 to 2.8 mm Hg]), and child perfluorooctanoate concentrations (0.9 mm Hg [95% CI: 0.1 to 1.6 mm Hg]). Decreases in diastolic BP were observed with outdoor temperature at examination (-1.4 mm Hg [95% CI: -2.3 to -0.5 mm Hg]) and child DDE concentrations (-1.1 mm Hg [95% CI: -1.9 to -0.3 mm Hg]), whereas increases in diastolic BP were observed with maternal bisphenol-A concentrations (0.7 mm Hg [95% CI: 0.1 to 1.4 mm Hg]), high fish intake during pregnancy (1.2 mm Hg [95% CI: -0.2 to 2.7 mm Hg]), and child copper concentrations (0.9 mm Hg [95% CI: 0.3 to 1.6 mm Hg])., Conclusions: This study suggests that early-life exposure to several chemicals, as well as built environment and meteorological factors, may affect BP in children., (Copyright © 2019 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)
Published: 2019
Full Text: View/download PDF

26. Personal assessment of the external exposome during pregnancy and childhood in Europe.

Author: Donaire-Gonzalez D, Curto A, Valentín A, Andrusaityte S, Basagaña X, Casas M, Chatzi L, de Bont J, de Castro M, Dedele A, Granum B, Grazuleviciene R, Kampouri M, Lyon-Caen S, Manzano-Salgado CB, Aasvang GM, McEachan R, Meinhard-Kjellstad CH, Michalaki E, Pañella P, Petraviciene I, Schwarze PE, Slama R, Robinson O, Tamayo-Uria I, Vafeiadi M, Waiblinger D, Wright J, Vrijheid M, and Nieuwenhuijsen MJ
Subjects: Adult, Child, Cities, Environmental Monitoring, Europe, Exposome, Female, Humans, Particulate Matter, Pregnancy, Air Pollutants, Air Pollution, Environmental Exposure statistics & numerical data
Abstract: The human exposome affects child development and health later in life, but its personal external levels, variability, and correlations are largely unknown. We characterized the personal external exposome of pregnant women and children in eight European cities. Panel studies included 167 pregnant women and 183 children (aged 6-11 years). A personal exposure monitoring kit composed of smartphone, accelerometer, ultraviolet (UV) dosimeter, and two air pollution monitors were used to monitor physical activity (PA), fine particulate matter (PM 2.5 ), black carbon, traffic-related noise, UV-B radiation, and natural outdoor environments (NOE). 77% of women performed the adult recommendation of ≥150 min/week of moderate to vigorous PA (MVPA), while only 3% of children achieved the childhood recommendation of ≥60 min/day MVPA. 11% of women and 17% of children were exposed to daily PM 2.5 levels higher than recommended (≥25μg/m 3 ). Mean exposure to noise ranged from Lden 51.1 dB in Kaunas to Lden 65.2 dB in Barcelona. 4% of women and 23% of children exceeded the recommended maximum of 2 Standard-Erythemal-Dose of UV-B at least once a week. 33% of women and 43% of children never reached the minimum NOE contact recommendation of ≥30 min/week. The variations in air and noise pollution exposure were dominated by between-city variability, while most of the variation observed for NOE contact and PA was between-participants. The correlations between all personal exposures ranged from very low to low (Rho < 0.30). The levels of personal external exposures in both pregnant women and children are above the health recommendations, and there is little correlation between the different exposures. The assessment of the personal external exposome is feasible but sampling requires from one day to more than one year depending on exposure due to high variability between and within cities and participants., (Copyright © 2019 Elsevier Inc. All rights reserved.)
Published: 2019
Full Text: View/download PDF

27. Influence of the Urban Exposome on Birth Weight.

Author: Nieuwenhuijsen MJ, Agier L, Basagaña X, Urquiza J, Tamayo-Uria I, Giorgis-Allemand L, Robinson O, Siroux V, Maitre L, de Castro M, Valentin A, Donaire D, Dadvand P, Aasvang GM, Krog NH, Schwarze PE, Chatzi L, Grazuleviciene R, Andrusaityte S, Dedele A, McEachan R, Wright J, West J, Ibarluzea J, Ballester F, Vrijheid M, and Slama R
Subjects: Cities, Cohort Studies, Environmental Exposure adverse effects, Europe, Female, Humans, Infant, Newborn, Pregnancy, Birth Weight, Environmental Exposure analysis, Exposome
Abstract: Background: The exposome is defined as the totality of environmental exposures from conception onwards. It calls for providing a holistic view of environmental exposures and their effects on human health by evaluating multiple environmental exposures simultaneously during critical periods of life., Objective: We evaluated the association of the urban exposome with birth weight., Methods: We estimated exposure to the urban exposome, including the built environment, air pollution, road traffic noise, meteorology, natural space, and road traffic (corresponding to 24 environmental indicators and 60 exposures) for nearly 32,000 pregnant women from six European birth cohorts. To evaluate associations with either continuous birth weight or term low birth weight (TLBW) risk, we primarily relied on the Deletion-Substitution-Addition (DSA) algorithm, which is an extension of the stepwise variable selection method. Second, we used an exposure-by-exposure exposome-wide association studies (ExWAS) method accounting for multiple hypotheses testing to report associations not adjusted for coexposures., Results: The most consistent statistically significant associations were observed between increasing green space exposure estimated as Normalized Difference Vegetation Index (NDVI) and increased birth weight and decreased TLBW risk. Furthermore, we observed statistically significant associations among presence of public bus line, land use Shannon's Evenness Index, and traffic density and birth weight in our DSA analysis., Conclusion: This investigation is the first large urban exposome study of birth weight that tests many environmental urban exposures. It confirmed previously reported associations for NDVI and generated new hypotheses for a number of built-environment exposures. https://doi.org/10.1289/EHP3971.
Published: 2019
Full Text: View/download PDF

28. The early-life exposome: Description and patterns in six European countries.

Author: Tamayo-Uria I, Maitre L, Thomsen C, Nieuwenhuijsen MJ, Chatzi L, Siroux V, Aasvang GM, Agier L, Andrusaityte S, Casas M, de Castro M, Dedele A, Haug LS, Heude B, Grazuleviciene R, Gutzkow KB, Krog NH, Mason D, McEachan RRC, Meltzer HM, Petraviciene I, Robinson O, Roumeliotaki T, Sakhi AK, Urquiza J, Vafeiadi M, Waiblinger D, Warembourg C, Wright J, Slama R, Vrijheid M, and Basagaña X
Subjects: Air Pollution, Child, Chronic Disease, Cohort Studies, Europe, Female, Humans, Mothers, Pregnancy, Water Purification, Environmental Exposure analysis
Abstract: Characterization of the "exposome", the set of all environmental factors that one is exposed to from conception onwards, has been advocated to better understand the role of environmental factors on chronic diseases. Here, we aimed to describe the early-life exposome. Specifically, we focused on the correlations between multiple environmental exposures, their patterns and their variability across European regions and across time (pregnancy and childhood periods). We relied on the Human Early-Life Exposome (HELIX) project, in which 87 environmental exposures during pregnancy and 122 during the childhood period (grouped in 19 exposure groups) were assessed in 1301 pregnant mothers and their children at 6-11 years in 6 European birth cohorts. Some correlations between exposures in the same exposure group reached high values above 0.8. The median correlation within exposure groups was >0.3 for many exposure groups, reaching 0.69 for water disinfection by products in pregnancy and 0.67 for the meteorological group in childhood. Median correlations between different exposure groups rarely reached 0.3. Some correlations were driven by cohort-level associations (e.g. air pollution and chemicals). Ten principal components explained 45% and 39% of the total variance in the pregnancy and childhood exposome, respectively, while 65 and 90 components were required to explain 95% of the exposome variability. Correlations between maternal (pregnancy) and childhood exposures were high (>0.6) for most exposures modeled at the residential address (e.g. air pollution), but were much lower and even close to zero for some chemical exposures. In conclusion, the early life exposome was high dimensional, meaning that it cannot easily be measured by or reduced to fewer components. Correlations between exposures from different exposure groups were much lower than within exposure groups, which have important implications for co-exposure confounding in multiple exposure studies. Also, we observed the early life exposome to be variable over time and to vary by cohort, so measurements at one time point or one place will not capture its complexities., (Copyright © 2018 The Authors. Published by Elsevier Ltd.. All rights reserved.)
Published: 2019
Full Text: View/download PDF

29. Human Early Life Exposome (HELIX) study: a European population-based exposome cohort.

Author: Maitre L, de Bont J, Casas M, Robinson O, Aasvang GM, Agier L, Andrušaitytė S, Ballester F, Basagaña X, Borràs E, Brochot C, Bustamante M, Carracedo A, de Castro M, Dedele A, Donaire-Gonzalez D, Estivill X, Evandt J, Fossati S, Giorgis-Allemand L, R Gonzalez J, Granum B, Grazuleviciene R, Bjerve Gützkow K, Småstuen Haug L, Hernandez-Ferrer C, Heude B, Ibarluzea J, Julvez J, Karachaliou M, Keun HC, Hjertager Krog N, Lau CE, Leventakou V, Lyon-Caen S, Manzano C, Mason D, McEachan R, Meltzer HM, Petraviciene I, Quentin J, Roumeliotaki T, Sabido E, Saulnier PJ, Siskos AP, Siroux V, Sunyer J, Tamayo I, Urquiza J, Vafeiadi M, van Gent D, Vives-Usano M, Waiblinger D, Warembourg C, Chatzi L, Coen M, van den Hazel P, Nieuwenhuijsen MJ, Slama R, Thomsen C, Wright J, and Vrijheid M
Subjects: Adult, Attention Deficit Disorder with Hyperactivity epidemiology, Biomarkers blood, Biomarkers urine, Blood Pressure, Body Composition, Body Weights and Measures, Child, Preschool, DNA Methylation, Europe epidemiology, Female, Food Hypersensitivity epidemiology, Gene-Environment Interaction, Hazardous Substances, Humans, Infant, Infant, Newborn, Male, Metabolome, Pregnancy, Prenatal Exposure Delayed Effects metabolism, Prospective Studies, Proteome, Psychological Tests, Respiratory Function Tests, Smoking epidemiology, Socioeconomic Factors, Transcriptome, Urban Population, Young Adult, Environmental Exposure analysis, Mothers statistics & numerical data, Prenatal Exposure Delayed Effects epidemiology
Abstract: Purpose: Essential to exposome research is the collection of data on many environmental exposures from different domains in the same subjects. The aim of the Human Early Life Exposome (HELIX) study was to measure and describe multiple environmental exposures during early life (pregnancy and childhood) in a prospective cohort and associate these exposures with molecular omics signatures and child health outcomes. Here, we describe recruitment, measurements available and baseline data of the HELIX study populations., Participants: The HELIX study represents a collaborative project across six established and ongoing longitudinal population-based birth cohort studies in six European countries (France, Greece, Lithuania, Norway, Spain and the UK). HELIX used a multilevel study design with the entire study population totalling 31 472 mother-child pairs, recruited during pregnancy, in the six existing cohorts (first level); a subcohort of 1301 mother-child pairs where biomarkers, omics signatures and child health outcomes were measured at age 6-11 years (second level) and repeat-sampling panel studies with around 150 children and 150 pregnant women aimed at collecting personal exposure data (third level)., Findings to Date: Cohort data include urban environment, hazardous substances and lifestyle-related exposures for women during pregnancy and their offspring from birth until 6-11 years. Common, standardised protocols were used to collect biological samples, measure exposure biomarkers and omics signatures and assess child health across the six cohorts. Baseline data of the cohort show substantial variation in health outcomes and determinants between the six countries, for example, in family affluence levels, tobacco smoking, physical activity, dietary habits and prevalence of childhood obesity, asthma, allergies and attention deficit hyperactivity disorder., Future Plans: HELIX study results will inform on the early life exposome and its association with molecular omics signatures and child health outcomes. Cohort data are accessible for future research involving researchers external to the project., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2018. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)
Published: 2018
Full Text: View/download PDF

30. A Longitudinal Study of Road Traffic Noise and Body Mass Index Trajectories from Birth to 8 Years.

Author: Weyde KV, Krog NH, Oftedal B, Magnus P, White R, Stansfeld S, Øverland S, and Aasvang GM
Subjects: Child, Child Development, Child, Preschool, Female, Humans, Infant, Infant, Newborn, Longitudinal Studies, Male, Noise, Transportation statistics & numerical data, Norway epidemiology, Pediatric Obesity epidemiology, Pediatric Obesity etiology, Pregnancy, Surveys and Questionnaires, Body Mass Index, Noise, Transportation adverse effects, Prenatal Exposure Delayed Effects epidemiology
Abstract: Background: Being overweight constitutes a health risk, and the proportion of overweight and obese children is increasing. It has been argued that road traffic noise could be linked to adiposity through its influence on sleep and stress. Few studies, to our knowledge, have investigated whether noise and adiposity are associated. Most of them were on adults, and we are not aware of any longitudinal study using repeated measures., Objectives: The present longitudinal study investigated whether road traffic noise exposures in pregnancy (N = 6,963; obs = 22,975) or childhood (N = 6,403; obs = 14,585) were associated with body mass index (BMI) trajectories in children., Methods: We obtained information on BMI and covariates from questionnaires used in the Norwegian Mother and Child Cohort Study, Statistics Norway, and Medical Birth Registry of Norway. We modeled road traffic noise for the most exposed façade of children's present and historical addresses at 6 time points from pregnancy to age 8. We investigated effects on BMI trajectories using repeated measures and linear mixed models., Results: The results indicated that BMI curves depended on road traffic noise exposure during pregnancy, but not on exposure during childhood. Children in the highest decile of traffic noise exposure had increased BMI, with 0.35 kg/m more than children in the lowest decile, from birth to age 8 years., Conclusions: The results indicate that exposure to road traffic noise during pregnancy may be associated with children's BMI trajectories. Future studies should investigate this further, using anthropometric measures such as waist-hip ratio and skinfold thickness, in addition to BMI.
Published: 2018
Full Text: View/download PDF

31. Long-term exposure to ambient air pollution and incidence of brain tumor: the European Study of Cohorts for Air Pollution Effects (ESCAPE).

Author: Andersen ZJ, Pedersen M, Weinmayr G, Stafoggia M, Galassi C, Jørgensen JT, Sommar JN, Forsberg B, Olsson D, Oftedal B, Aasvang GM, Schwarze P, Pyko A, Pershagen G, Korek M, Faire U, Östenson CG, Fratiglioni L, Eriksen KT, Poulsen AH, Tjønneland A, Bräuner EV, Peeters PH, Bueno-de-Mesquita B, Jaensch A, Nagel G, Lang A, Wang M, Tsai MY, Grioni S, Marcon A, Krogh V, Ricceri F, Sacerdote C, Migliore E, Vermeulen R, Sokhi R, Keuken M, de Hoogh K, Beelen R, Vineis P, Cesaroni G, Brunekreef B, Hoek G, and Raaschou-Nielsen O
Subjects: Adult, Brain Neoplasms pathology, Cohort Studies, Europe epidemiology, Female, Follow-Up Studies, Humans, Incidence, Male, Middle Aged, Prognosis, Risk Factors, Air Pollution adverse effects, Brain Neoplasms epidemiology, Brain Neoplasms etiology, Environmental Exposure adverse effects, Particulate Matter adverse effects
Abstract: Background: Epidemiological evidence on the association between ambient air pollution and brain tumor risk is sparse and inconsistent., Methods: In 12 cohorts from 6 European countries, individual estimates of annual mean air pollution levels at the baseline residence were estimated by standardized land-use regression models developed within the ESCAPE and TRANSPHORM projects: particulate matter (PM) ≤2.5, ≤10, and 2.5-10 μm in diameter (PM2.5, PM10, and PMcoarse), PM2.5 absorbance, nitrogen oxides (NO2 and NOx) and elemental composition of PM. We estimated cohort-specific associations of air pollutant concentrations and traffic intensity with total, malignant, and nonmalignant brain tumor, in separate Cox regression models, adjusting for risk factors, and pooled cohort-specific estimates using random-effects meta-analyses., Results: Of 282194 subjects from 12 cohorts, 466 developed malignant brain tumors during 12 years of follow-up. Six of the cohorts also had data on nonmalignant brain tumor, where among 106786 subjects, 366 developed brain tumor: 176 nonmalignant and 190 malignant. We found a positive, statistically nonsignificant association between malignant brain tumor and PM2.5 absorbance (hazard ratio and 95% CI: 1.67; 0.89-3.14 per 10-5/m3), and weak positive or null associations with the other pollutants. Hazard ratio for PM2.5 absorbance (1.01; 0.38-2.71 per 10-5/m3) and all other pollutants were lower for nonmalignant than for malignant brain tumors., Conclusion: We found suggestive evidence of an association between long-term exposure to PM2.5 absorbance indicating traffic-related air pollution and malignant brain tumors, and no association with overall or nonmalignant brain tumors., (© The Author(s) 2017. Published by Oxford University Press on behalf of the Society for Neuro-Oncology.)
Published: 2018
Full Text: View/download PDF

32. Road traffic noise and children's inattention.

Author: Weyde KV, Krog NH, Oftedal B, Magnus P, Øverland S, Stansfeld S, Nieuwenhuijsen MJ, Vrijheid M, de Castro Pascual M, and Aasvang GM
Subjects: Child, Child, Preschool, Cities, Cohort Studies, Female, Humans, Logistic Models, Male, Norway, Pregnancy, Sleep, Attention, Environmental Exposure adverse effects, Noise, Transportation adverse effects
Abstract: Background: An increasing number of children are exposed to road traffic noise levels that may lead to adverse effects on health and daily functioning. Childhood is a period of intense growth and brain maturation, and children may therefore be especially vulnerable to road traffic noise. The objective of the present study was to examine whether road traffic noise was associated with reported inattention symptoms in children, and whether this association was mediated by sleep duration., Methods: This study was based on the Norwegian Mother and Child Cohort Study conducted by the Norwegian Institute of Public Health. Parental reports of children's inattention at age 8 were linked to modelled levels of residential road traffic noise. We investigated the association between inattention and noise exposure during pregnancy (n = 1934), noise exposure averaged over 5 years (age 3 to 8 years; n = 1384) and noise exposure at age 8 years (n = 1384), using fractional logit response models. The participants were children from Oslo, Norway., Results: An association with inattention at age 8 years was found for road traffic noise exposure at age 8 years (coef = .0083, CI = [.0012, .0154]; 1.2% point increase in inattention score per 10 dB increase in noise level), road traffic noise exposure average for the last 5 years (coef = .0090, CI = [.0016, .0164]; 1.3% point increase/10 dB), and for pregnancy road traffic noise exposure for boys (coef = .0091, CI = [.0010, .0171]), but not girls (coef = -.0021, CI = [-.0094, .0053]). Criteria for doing mediation analyses were not fulfilled., Conclusion: Results indicate that road traffic noise has a negative impact on children's inattention. We found no mediation by sleep duration.
Published: 2017
Full Text: View/download PDF

33. Road traffic noise and registry based use of sleep medication.

Author: Evandt J, Oftedal B, Krog NH, Skurtveit S, Nafstad P, Schwarze PE, Skovlund E, Houthuijs D, and Aasvang GM
Subjects: Adult, Aged, Aged, 80 and over, Environmental Monitoring, Female, Humans, Male, Middle Aged, Norway, Odds Ratio, Registries, Seasons, Drug Prescriptions statistics & numerical data, Noise, Transportation, Sleep Wake Disorders drug therapy
Abstract: Background: Road traffic noise has been associated with adverse health effects including sleep disturbances. Use of sleep medication as an indicator of sleeping problems has rarely been explored in studies of the effects of traffic noise. Furthermore, using registry data on sleep medications provides an opportunity to study the effects of noise on sleep where attribution of sleep problems to noise is not possible., Methods: We used questionnaire data from the population-based study Health and Environment in Oslo (HELMILO) (2009-10) (n = 13,019). Individual data on sleep medications was obtained from the Norwegian Prescription Database (NorPD). Noise levels (L night ) were modeled for the most exposed façade of the building at each participant's home address. Logistic regression models adjusted for potential confounders were used to analyze the association between traffic noise and sleep medication use both for one whole year and for the summer season. The results were reported as changes in the effect estimate per 5 decibel (dB) increase in noise level., Results: We observed no association between traffic noise and sleep medication use during one year [odds ratio (OR) = 1.00; 95% confidence interval (CI): 0.96, 1.04]. For sleep medication use in the summer season, there was a positive, however non-significant association (OR = 1.04; 95% CI: 0.99, 1.10). Among individuals sleeping with the bedroom window open, the association increased slightly and was borderline statistically significant (OR = 1.06; 95% CI: 1.00, 1.12)., Conclusions: We found no evidence of an association between traffic noise and sleep medication use during one year. However, for the summer season, there was some suggestive evidence of an association. These findings indicate that season may play a role in the association between traffic noise and sleep, possibly because indoor traffic noise levels are likely to be higher during summer due to more frequent window opening. More studies are, however, necessary in order to confirm this.
Published: 2017
Full Text: View/download PDF

34. Long-Term Exposure to Ambient Air Pollution and Incidence of Postmenopausal Breast Cancer in 15 European Cohorts within the ESCAPE Project.

Author: Andersen ZJ, Stafoggia M, Weinmayr G, Pedersen M, Galassi C, Jørgensen JT, Oudin A, Forsberg B, Olsson D, Oftedal B, Aasvang GM, Aamodt G, Pyko A, Pershagen G, Korek M, De Faire U, Pedersen NL, Östenson CG, Fratiglioni L, Eriksen KT, Tjønneland A, Peeters PH, Bueno-de-Mesquita B, Plusquin M, Key TJ, Jaensch A, Nagel G, Lang A, Wang M, Tsai MY, Fournier A, Boutron-Ruault MC, Baglietto L, Grioni S, Marcon A, Krogh V, Ricceri F, Sacerdote C, Migliore E, Tamayo-Uria I, Amiano P, Dorronsoro M, Vermeulen R, Sokhi R, Keuken M, de Hoogh K, Beelen R, Vineis P, Cesaroni G, Brunekreef B, Hoek G, and Raaschou-Nielsen O
Subjects: Aged, Air Pollutants analysis, Cohort Studies, Europe epidemiology, Female, Humans, Incidence, Middle Aged, Air Pollution statistics & numerical data, Breast Neoplasms epidemiology, Environmental Exposure statistics & numerical data, Postmenopause physiology
Abstract: Background: Epidemiological evidence on the association between ambient air pollution and breast cancer risk is inconsistent., Objective: We examined the association between long-term exposure to ambient air pollution and incidence of postmenopausal breast cancer in European women., Methods: In 15 cohorts from nine European countries, individual estimates of air pollution levels at the residence were estimated by standardized land-use regression models developed within the European Study of Cohorts for Air Pollution Effects (ESCAPE) and Transport related Air Pollution and Health impacts – Integrated Methodologies for Assessing Particulate Matter (TRANSPHORM) projects: particulate matter (PM) ≤2.5μm, ≤10μm, and 2.5–10μm in diameter (PM 2.5 , PM 10 , and PM coarse , respectively); PM 2.5 absorbance; nitrogen oxides (NO 2 and NO x ); traffic intensity; and elemental composition of PM. We estimated cohort-specific associations between breast cancer and air pollutants using Cox regression models, adjusting for major lifestyle risk factors, and pooled cohort-specific estimates using random-effects meta-analyses., Results: Of 74,750 postmenopausal women included in the study, 3,612 developed breast cancer during 991,353 person-years of follow-up. We found positive and statistically insignificant associations between breast cancer and PM 2.5 {hazard ratio (HR)=1.08 [95% confidence interval (CI): 0.77, 1.51] per 5 μg/m 3 }, PM 10 [1.07 (95% CI: 0.89, 1.30) per 10 μg/m 3 ], PM coarse [1.20 (95% CI: 0.96, 1.49 per 5 μg/m 3 ], and NO 2 [1.02 (95% CI: 0.98, 1.07 per 10 μg/m 3 ], and a statistically significant association with NO x [1.04 (95% CI: 1.00, 1.08) per 20 μg/m 3 , p =0.04]., Conclusions: We found suggestive evidence of an association between ambient air pollution and incidence of postmenopausal breast cancer in European women. https://doi.org/10.1289/EHP1742.
Published: 2017
Full Text: View/download PDF

35. Nocturnal Road Traffic Noise Exposure and Children's Sleep Duration and Sleep Problems.

Author: Weyde KV, Krog NH, Oftedal B, Evandt J, Magnus P, Øverland S, Clark C, Stansfeld S, and Aasvang GM
Subjects: Child, Cohort Studies, Cross-Sectional Studies, Female, Humans, Norway epidemiology, Sex Factors, Socioeconomic Factors, Environmental Exposure adverse effects, Noise, Transportation adverse effects, Sleep, Sleep Wake Disorders epidemiology
Abstract: Almost half of the European Union (EU)'s population is exposed to road traffic noise above levels that constitute a health risk. Associations between road traffic noise and impaired sleep in adults have consistently been reported. Less is known about effects of noise on children's sleep. The aim of this study was to examine the association between nocturnal road traffic noise exposure and children's parental-reported sleep duration and sleep problems. The present cross-sectional study used data from The Norwegian Mother and Child Cohort Study. Parental report of children's sleep duration and sleep problems at age 7 was linked to modelled levels of residential night-time road traffic noise. The study population included 2665 children from Oslo, Norway. No association was found between road traffic noise and sleep duration in the total study population (odds ratio (OR): 1.05, 95% confidence interval (CI): [0.94, 1.17]), but a statistically significant association was observed in girls (OR: 1.21, 95% CI: [1.04, 1.41]). For sleep problems, the associations were similar (OR: 1.36, 95% CI: [0.85, 2.16]) in girls. The ORs are presented for an increase of 10 dB. The findings suggest there is an association between road traffic noise and sleep for girls, underlining the importance of protecting children against excessive noise levels.
Published: 2017
Full Text: View/download PDF

36. Long-term exposure to ambient air pollution and traffic noise and incident hypertension in seven cohorts of the European study of cohorts for air pollution effects (ESCAPE).

Author: Fuks KB, Weinmayr G, Basagaña X, Gruzieva O, Hampel R, Oftedal B, Sørensen M, Wolf K, Aamodt G, Aasvang GM, Aguilera I, Becker T, Beelen R, Brunekreef B, Caracciolo B, Cyrys J, Elosua R, Eriksen KT, Foraster M, Fratiglioni L, Hilding A, Houthuijs D, Korek M, Künzli N, Marrugat J, Nieuwenhuijsen M, Östenson CG, Penell J, Pershagen G, Raaschou-Nielsen O, Swart WJR, Peters A, and Hoffmann B
Subjects: Aged, Air Pollutants adverse effects, Air Pollutants analysis, Air Pollution analysis, Antihypertensive Agents therapeutic use, Europe epidemiology, Female, Humans, Hypertension drug therapy, Hypertension epidemiology, Incidence, Male, Middle Aged, Particulate Matter adverse effects, Particulate Matter analysis, Prognosis, Prospective Studies, Self Report, Air Pollution adverse effects, Hypertension etiology, Noise, Transportation adverse effects
Abstract: Aims: We investigated whether traffic-related air pollution and noise are associated with incident hypertension in European cohorts., Methods and Results: We included seven cohorts of the European study of cohorts for air pollution effects (ESCAPE). We modelled concentrations of particulate matter with aerodynamic diameter ≤2.5 µm (PM2.5), ≤10 µm (PM10), >2.5, and ≤10 µm (PMcoarse), soot (PM2.5 absorbance), and nitrogen oxides at the addresses of participants with land use regression. Residential exposure to traffic noise was modelled at the facade according to the EU Directive 2002/49/EC. We assessed hypertension as (i) self-reported and (ii) measured (systolic BP ≥ 140 mmHg or diastolic BP ≥ 90 mmHg or intake of BP lowering medication (BPLM). We used Poisson regression with robust variance estimation to analyse associations of traffic-related exposures with incidence of hypertension, controlling for relevant confounders, and combined the results from individual studies with random-effects meta-analysis. Among 41 072 participants free of self-reported hypertension at baseline, 6207 (15.1%) incident cases occurred within 5-9 years of follow-up. Incidence of self-reported hypertension was positively associated with PM2.5 (relative risk (RR) 1.22 [95%-confidence interval (CI):1.08; 1.37] per 5 µg/m³) and PM2.5 absorbance (RR 1.13 [95% CI:1.02; 1.24] per 10 - 5m - 1). These estimates decreased slightly upon adjustment for road traffic noise. Road traffic noise was weakly positively associated with the incidence of self-reported hypertension. Among 10 896 participants at risk, 3549 new cases of measured hypertension occurred. We found no clear associations with measured hypertension., Conclusion: Long-term residential exposures to air pollution and noise are associated with increased incidence of self-reported hypertension., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2016. For Permissions, please email: journals.permissions@oup.com.)
Published: 2017
Full Text: View/download PDF

37. Outdoor air pollution and risk for kidney parenchyma cancer in 14 European cohorts.

Author: Raaschou-Nielsen O, Pedersen M, Stafoggia M, Weinmayr G, Andersen ZJ, Galassi C, Sommar J, Forsberg B, Olsson D, Oftedal B, Krog NH, Aasvang GM, Pyko A, Pershagen G, Korek M, De Faire U, Pedersen NL, Östenson CG, Fratiglioni L, Sørensen M, Eriksen KT, Tjønneland A, Peeters PH, Bueno-de-Mesquita HB, Plusquin M, Key TJ, Jaensch A, Nagel G, Föger B, Wang M, Tsai MY, Grioni S, Marcon A, Krogh V, Ricceri F, Sacerdote C, Migliore E, Tamayo I, Amiano P, Dorronsoro M, Sokhi R, Kooter I, de Hoogh K, Beelen R, Eeftens M, Vermeulen R, Vineis P, Brunekreef B, and Hoek G
Subjects: Adult, Air Pollution adverse effects, Cohort Studies, Environmental Exposure adverse effects, Europe epidemiology, Female, Gasoline, Humans, Lung Neoplasms epidemiology, Male, Middle Aged, Particle Size, Particulate Matter, Risk Factors, Vehicle Emissions, Air Pollutants adverse effects, Kidney Neoplasms diagnosis, Kidney Neoplasms epidemiology
Abstract: Several studies have indicated weakly increased risk for kidney cancer among occupational groups exposed to gasoline vapors, engine exhaust, polycyclic aromatic hydrocarbons and other air pollutants, although not consistently. It was the aim to investigate possible associations between outdoor air pollution at the residence and the incidence of kidney parenchyma cancer in the general population. We used data from 14 European cohorts from the ESCAPE study. We geocoded and assessed air pollution concentrations at baseline addresses by land-use regression models for particulate matter (PM 10 , PM 2.5 , PM coarse , PM 2.5 absorbance (soot)) and nitrogen oxides (NO 2 , NO x ), and collected data on traffic. We used Cox regression models with adjustment for potential confounders for cohort-specific analyses and random effects models for meta-analyses to calculate summary hazard ratios (HRs). The 289,002 cohort members contributed 4,111,908 person-years at risk. During follow-up (mean 14.2 years) 697 incident cancers of the kidney parenchyma were diagnosed. The meta-analyses showed higher HRs in association with higher PM concentration, e.g. HR = 1.57 (95%CI: 0.81-3.01) per 5 μg/m 3 PM 2.5 and HR = 1.36 (95%CI: 0.84-2.19) per 10 -5 m -1 PM 2.5 absorbance, albeit never statistically significant. The HRs in association with nitrogen oxides and traffic density on the nearest street were slightly above one. Sensitivity analyses among participants who did not change residence during follow-up showed stronger associations, but none were statistically significant. Our study provides suggestive evidence that exposure to outdoor PM at the residence may be associated with higher risk for kidney parenchyma cancer; the results should be interpreted cautiously as associations may be due to chance., (© 2016 UICC.)
Published: 2017
Full Text: View/download PDF

38. Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013.

Author: Forouzanfar MH, Alexander L, Anderson HR, Bachman VF, Biryukov S, Brauer M, Burnett R, Casey D, Coates MM, Cohen A, Delwiche K, Estep K, Frostad JJ, Astha KC, Kyu HH, Moradi-Lakeh M, Ng M, Slepak EL, Thomas BA, Wagner J, Aasvang GM, Abbafati C, Abbasoglu Ozgoren A, Abd-Allah F, Abera SF, Aboyans V, Abraham B, Abraham JP, Abubakar I, Abu-Rmeileh NM, Aburto TC, Achoki T, Adelekan A, Adofo K, Adou AK, Adsuar JC, Afshin A, Agardh EE, Al Khabouri MJ, Al Lami FH, Alam SS, Alasfoor D, Albittar MI, Alegretti MA, Aleman AV, Alemu ZA, Alfonso-Cristancho R, Alhabib S, Ali R, Ali MK, Alla F, Allebeck P, Allen PJ, Alsharif U, Alvarez E, Alvis-Guzman N, Amankwaa AA, Amare AT, Ameh EA, Ameli O, Amini H, Ammar W, Anderson BO, Antonio CA, Anwari P, Argeseanu Cunningham S, Arnlöv J, Arsenijevic VS, Artaman A, Asghar RJ, Assadi R, Atkins LS, Atkinson C, Avila MA, Awuah B, Badawi A, Bahit MC, Bakfalouni T, Balakrishnan K, Balalla S, Balu RK, Banerjee A, Barber RM, Barker-Collo SL, Barquera S, Barregard L, Barrero LH, Barrientos-Gutierrez T, Basto-Abreu AC, Basu A, Basu S, Basulaiman MO, Batis Ruvalcaba C, Beardsley J, Bedi N, Bekele T, Bell ML, Benjet C, Bennett DA, Benzian H, Bernabé E, Beyene TJ, Bhala N, Bhalla A, Bhutta ZA, Bikbov B, Bin Abdulhak AA, Blore JD, Blyth FM, Bohensky MA, Bora Başara B, Borges G, Bornstein NM, Bose D, Boufous S, Bourne RR, Brainin M, Brazinova A, Breitborde NJ, Brenner H, Briggs AD, Broday DM, Brooks PM, Bruce NG, Brugha TS, Brunekreef B, Buchbinder R, Bui LN, Bukhman G, Bulloch AG, Burch M, Burney PG, Campos-Nonato IR, Campuzano JC, Cantoral AJ, Caravanos J, Cárdenas R, Cardis E, Carpenter DO, Caso V, Castañeda-Orjuela CA, Castro RE, Catalá-López F, Cavalleri F, Çavlin A, Chadha VK, Chang JC, Charlson FJ, Chen H, Chen W, Chen Z, Chiang PP, Chimed-Ochir O, Chowdhury R, Christophi CA, Chuang TW, Chugh SS, Cirillo M, Claßen TK, Colistro V, Colomar M, Colquhoun SM, Contreras AG, Cooper C, Cooperrider K, Cooper LT, Coresh J, Courville KJ, Criqui MH, Cuevas-Nasu L, Damsere-Derry J, Danawi H, Dandona L, Dandona R, Dargan PI, Davis A, Davitoiu DV, Dayama A, de Castro EF, De la Cruz-Góngora V, De Leo D, de Lima G, Degenhardt L, del Pozo-Cruz B, Dellavalle RP, Deribe K, Derrett S, Des Jarlais DC, Dessalegn M, deVeber GA, Devries KM, Dharmaratne SD, Dherani MK, Dicker D, Ding EL, Dokova K, Dorsey ER, Driscoll TR, Duan L, Durrani AM, Ebel BE, Ellenbogen RG, Elshrek YM, Endres M, Ermakov SP, Erskine HE, Eshrati B, Esteghamati A, Fahimi S, Faraon EJ, Farzadfar F, Fay DF, Feigin VL, Feigl AB, Fereshtehnejad SM, Ferrari AJ, Ferri CP, Flaxman AD, Fleming TD, Foigt N, Foreman KJ, Paleo UF, Franklin RC, Gabbe B, Gaffikin L, Gakidou E, Gamkrelidze A, Gankpé FG, Gansevoort RT, García-Guerra FA, Gasana E, Geleijnse JM, Gessner BD, Gething P, Gibney KB, Gillum RF, Ginawi IA, Giroud M, Giussani G, Goenka S, Goginashvili K, Gomez Dantes H, Gona P, Gonzalez de Cosio T, González-Castell D, Gotay CC, Goto A, Gouda HN, Guerrant RL, Gugnani HC, Guillemin F, Gunnell D, Gupta R, Gupta R, Gutiérrez RA, Hafezi-Nejad N, Hagan H, Hagstromer M, Halasa YA, Hamadeh RR, Hammami M, Hankey GJ, Hao Y, Harb HL, Haregu TN, Haro JM, Havmoeller R, Hay SI, Hedayati MT, Heredia-Pi IB, Hernandez L, Heuton KR, Heydarpour P, Hijar M, Hoek HW, Hoffman HJ, Hornberger JC, Hosgood HD, Hoy DG, Hsairi M, Hu G, Hu H, Huang C, Huang JJ, Hubbell BJ, Huiart L, Husseini A, Iannarone ML, Iburg KM, Idrisov BT, Ikeda N, Innos K, Inoue M, Islami F, Ismayilova S, Jacobsen KH, Jansen HA, Jarvis DL, Jassal SK, Jauregui A, Jayaraman S, Jeemon P, Jensen PN, Jha V, Jiang F, Jiang G, Jiang Y, Jonas JB, Juel K, Kan H, Kany Roseline SS, Karam NE, Karch A, Karema CK, Karthikeyan G, Kaul A, Kawakami N, Kazi DS, Kemp AH, Kengne AP, Keren A, Khader YS, Khalifa SE, Khan EA, Khang YH, Khatibzadeh S, Khonelidze I, Kieling C, Kim D, Kim S, Kim Y, Kimokoti RW, Kinfu Y, Kinge JM, Kissela BM, Kivipelto M, Knibbs LD, Knudsen AK, Kokubo Y, Kose MR, Kosen S, Kraemer A, Kravchenko M, Krishnaswami S, Kromhout H, Ku T, Kuate Defo B, Kucuk Bicer B, Kuipers EJ, Kulkarni C, Kulkarni VS, Kumar GA, Kwan GF, Lai T, Lakshmana Balaji A, Lalloo R, Lallukka T, Lam H, Lan Q, Lansingh VC, Larson HJ, Larsson A, Laryea DO, Lavados PM, Lawrynowicz AE, Leasher JL, Lee JT, Leigh J, Leung R, Levi M, Li Y, Li Y, Liang J, Liang X, Lim SS, Lindsay MP, Lipshultz SE, Liu S, Liu Y, Lloyd BK, Logroscino G, London SJ, Lopez N, Lortet-Tieulent J, Lotufo PA, Lozano R, Lunevicius R, Ma J, Ma S, Machado VM, MacIntyre MF, Magis-Rodriguez C, Mahdi AA, Majdan M, Malekzadeh R, Mangalam S, Mapoma CC, Marape M, Marcenes W, Margolis DJ, Margono C, Marks GB, Martin RV, Marzan MB, Mashal MT, Masiye F, Mason-Jones AJ, Matsushita K, Matzopoulos R, Mayosi BM, Mazorodze TT, McKay AC, McKee M, McLain A, Meaney PA, Medina C, Mehndiratta MM, Mejia-Rodriguez F, Mekonnen W, Melaku YA, Meltzer M, Memish ZA, Mendoza W, Mensah GA, Meretoja A, Mhimbira FA, Micha R, Miller TR, Mills EJ, Misganaw A, Mishra S, Mohamed Ibrahim N, Mohammad KA, Mokdad AH, Mola GL, Monasta L, Montañez Hernandez JC, Montico M, Moore AR, Morawska L, Mori R, Moschandreas J, Moturi WN, Mozaffarian D, Mueller UO, Mukaigawara M, Mullany EC, Murthy KS, Naghavi M, Nahas Z, Naheed A, Naidoo KS, Naldi L, Nand D, Nangia V, Narayan KM, Nash D, Neal B, Nejjari C, Neupane SP, Newton CR, Ngalesoni FN, Ngirabega Jde D, Nguyen G, Nguyen NT, Nieuwenhuijsen MJ, Nisar MI, Nogueira JR, Nolla JM, Nolte S, Norheim OF, Norman RE, Norrving B, Nyakarahuka L, Oh IH, Ohkubo T, Olusanya BO, Omer SB, Opio JN, Orozco R, Pagcatipunan RS Jr, Pain AW, Pandian JD, Panelo CI, Papachristou C, Park EK, Parry CD, Paternina Caicedo AJ, Patten SB, Paul VK, Pavlin BI, Pearce N, Pedraza LS, Pedroza A, Pejin Stokic L, Pekericli A, Pereira DM, Perez-Padilla R, Perez-Ruiz F, Perico N, Perry SA, Pervaiz A, Pesudovs K, Peterson CB, Petzold M, Phillips MR, Phua HP, Plass D, Poenaru D, Polanczyk GV, Polinder S, Pond CD, Pope CA, Pope D, Popova S, Pourmalek F, Powles J, Prabhakaran D, Prasad NM, Qato DM, Quezada AD, Quistberg DA, Racapé L, Rafay A, Rahimi K, Rahimi-Movaghar V, Rahman SU, Raju M, Rakovac I, Rana SM, Rao M, Razavi H, Reddy KS, Refaat AH, Rehm J, Remuzzi G, Ribeiro AL, Riccio PM, Richardson L, Riederer A, Robinson M, Roca A, Rodriguez A, Rojas-Rueda D, Romieu I, Ronfani L, Room R, Roy N, Ruhago GM, Rushton L, Sabin N, Sacco RL, Saha S, Sahathevan R, Sahraian MA, Salomon JA, Salvo D, Sampson UK, Sanabria JR, Sanchez LM, Sánchez-Pimienta TG, Sanchez-Riera L, Sandar L, Santos IS, Sapkota A, Satpathy M, Saunders JE, Sawhney M, Saylan MI, Scarborough P, Schmidt JC, Schneider IJ, Schöttker B, Schwebel DC, Scott JG, Seedat S, Sepanlou SG, Serdar B, Servan-Mori EE, Shaddick G, Shahraz S, Levy TS, Shangguan S, She J, Sheikhbahaei S, Shibuya K, Shin HH, Shinohara Y, Shiri R, Shishani K, Shiue I, Sigfusdottir ID, Silberberg DH, Simard EP, Sindi S, Singh A, Singh GM, Singh JA, Skirbekk V, Sliwa K, Soljak M, Soneji S, Søreide K, Soshnikov S, Sposato LA, Sreeramareddy CT, Stapelberg NJ, Stathopoulou V, Steckling N, Stein DJ, Stein MB, Stephens N, Stöckl H, Straif K, Stroumpoulis K, Sturua L, Sunguya BF, Swaminathan S, Swaroop M, Sykes BL, Tabb KM, Takahashi K, Talongwa RT, Tandon N, Tanne D, Tanner M, Tavakkoli M, Te Ao BJ, Teixeira CM, Téllez Rojo MM, Terkawi AS, Texcalac-Sangrador JL, Thackway SV, Thomson B, Thorne-Lyman AL, Thrift AG, Thurston GD, Tillmann T, Tobollik M, Tonelli M, Topouzis F, Towbin JA, Toyoshima H, Traebert J, Tran BX, Trasande L, Trillini M, Trujillo U, Dimbuene ZT, Tsilimbaris M, Tuzcu EM, Uchendu US, Ukwaja KN, Uzun SB, van de Vijver S, Van Dingenen R, van Gool CH, van Os J, Varakin YY, Vasankari TJ, Vasconcelos AM, Vavilala MS, Veerman LJ, Velasquez-Melendez G, Venketasubramanian N, Vijayakumar L, Villalpando S, Violante FS, Vlassov VV, Vollset SE, Wagner GR, Waller SG, Wallin MT, Wan X, Wang H, Wang J, Wang L, Wang W, Wang Y, Warouw TS, Watts CH, Weichenthal S, Weiderpass E, Weintraub RG, Werdecker A, Wessells KR, Westerman R, Whiteford HA, Wilkinson JD, Williams HC, Williams TN, Woldeyohannes SM, Wolfe CD, Wong JQ, Woolf AD, Wright JL, Wurtz B, Xu G, Yan LL, Yang G, Yano Y, Ye P, Yenesew M, Yentür GK, Yip P, Yonemoto N, Yoon SJ, Younis MZ, Younoussi Z, Yu C, Zaki ME, Zhao Y, Zheng Y, Zhou M, Zhu J, Zhu S, Zou X, Zunt JR, Lopez AD, Vos T, and Murray CJ
Subjects: Female, Global Health statistics & numerical data, Health Behavior, Humans, Male, Nutritional Status, Occupational Exposure adverse effects, Risk Assessment methods, Risk Factors, Sanitation trends, Environmental Exposure adverse effects, Global Health trends, Metabolic Diseases epidemiology, Occupational Diseases epidemiology
Abstract: Background: The Global Burden of Disease, Injuries, and Risk Factor study 2013 (GBD 2013) is the first of a series of annual updates of the GBD. Risk factor quantification, particularly of modifiable risk factors, can help to identify emerging threats to population health and opportunities for prevention. The GBD 2013 provides a timely opportunity to update the comparative risk assessment with new data for exposure, relative risks, and evidence on the appropriate counterfactual risk distribution., Methods: Attributable deaths, years of life lost, years lived with disability, and disability-adjusted life-years (DALYs) have been estimated for 79 risks or clusters of risks using the GBD 2010 methods. Risk-outcome pairs meeting explicit evidence criteria were assessed for 188 countries for the period 1990-2013 by age and sex using three inputs: risk exposure, relative risks, and the theoretical minimum risk exposure level (TMREL). Risks are organised into a hierarchy with blocks of behavioural, environmental and occupational, and metabolic risks at the first level of the hierarchy. The next level in the hierarchy includes nine clusters of related risks and two individual risks, with more detail provided at levels 3 and 4 of the hierarchy. Compared with GBD 2010, six new risk factors have been added: handwashing practices, occupational exposure to trichloroethylene, childhood wasting, childhood stunting, unsafe sex, and low glomerular filtration rate. For most risks, data for exposure were synthesised with a Bayesian meta-regression method, DisMod-MR 2.0, or spatial-temporal Gaussian process regression. Relative risks were based on meta-regressions of published cohort and intervention studies. Attributable burden for clusters of risks and all risks combined took into account evidence on the mediation of some risks such as high body-mass index (BMI) through other risks such as high systolic blood pressure and high cholesterol., Findings: All risks combined account for 57·2% (95% uncertainty interval [UI] 55·8-58·5) of deaths and 41·6% (40·1-43·0) of DALYs. Risks quantified account for 87·9% (86·5-89·3) of cardiovascular disease DALYs, ranging to a low of 0% for neonatal disorders and neglected tropical diseases and malaria. In terms of global DALYs in 2013, six risks or clusters of risks each caused more than 5% of DALYs: dietary risks accounting for 11·3 million deaths and 241·4 million DALYs, high systolic blood pressure for 10·4 million deaths and 208·1 million DALYs, child and maternal malnutrition for 1·7 million deaths and 176·9 million DALYs, tobacco smoke for 6·1 million deaths and 143·5 million DALYs, air pollution for 5·5 million deaths and 141·5 million DALYs, and high BMI for 4·4 million deaths and 134·0 million DALYs. Risk factor patterns vary across regions and countries and with time. In sub-Saharan Africa, the leading risk factors are child and maternal malnutrition, unsafe sex, and unsafe water, sanitation, and handwashing. In women, in nearly all countries in the Americas, north Africa, and the Middle East, and in many other high-income countries, high BMI is the leading risk factor, with high systolic blood pressure as the leading risk in most of Central and Eastern Europe and south and east Asia. For men, high systolic blood pressure or tobacco use are the leading risks in nearly all high-income countries, in north Africa and the Middle East, Europe, and Asia. For men and women, unsafe sex is the leading risk in a corridor from Kenya to South Africa., Interpretation: Behavioural, environmental and occupational, and metabolic risks can explain half of global mortality and more than one-third of global DALYs providing many opportunities for prevention. Of the larger risks, the attributable burden of high BMI has increased in the past 23 years. In view of the prominence of behavioural risk factors, behavioural and social science research on interventions for these risks should be strengthened. Many prevention and primary care policy options are available now to act on key risks., Funding: Bill & Melinda Gates Foundation., (Copyright © 2015 Elsevier Ltd. All rights reserved.)
Published: 2015
Full Text: View/download PDF

39. Exposure to traffic noise and markers of obesity.

Author: Pyko A, Eriksson C, Oftedal B, Hilding A, Östenson CG, Krog NH, Julin B, Aasvang GM, and Pershagen G
Subjects: Adult, Aircraft, Cross-Sectional Studies, Female, Humans, Logistic Models, Male, Middle Aged, Motor Vehicles, Odds Ratio, Railroads, Body Mass Index, Environmental Exposure adverse effects, Noise, Transportation adverse effects, Obesity, Abdominal etiology, Transportation, Waist Circumference, Waist-Hip Ratio
Abstract: Objectives: Limited evidence suggests adverse effects of traffic noise exposure on the metabolic system. This study investigates the association between road traffic noise and obesity markers as well as the role of combined exposure to multiple sources of traffic noise., Methods: In a cross-sectional study performed in 2002-2006, we assessed exposure to noise from road traffic, railways and aircraft at the residences of 5075 Swedish men and women, primarily from suburban and semirural areas of Stockholm County. A detailed questionnaire and medical examination provided information on markers of obesity and potential confounders. Multiple linear and logistic regression models were used to assess associations between traffic noise and body mass index (BMI), waist circumference and waist-hip ratio using WHO definitions of obesity., Results: Road traffic noise was significantly related to waist circumference with a 0.21 cm (95% CI 0.01 to 0.41) increase per 5 dB(A) rise in L(den). The OR for central obesity among those exposed to road traffic noise ≥ 45 dB(A) was 1.18 (95% CI 1.03 to 1.34) in comparison to those exposed below this level. Similar results were seen for waist-hip ratio (OR 1.29; 95% CI 1.14 to 1.45) but not for BMI (OR 0.89; 95% CI 0.76 to 1.04). Central obesity was also associated with exposure to railway and aircraft noise, and a particularly high risk was seen for combined exposure to all three sources of traffic noise (OR 1.95; 95% CI 1.24 to 3.05)., Conclusions: Our results suggest that traffic noise exposure can increase the risk of central obesity. Combined exposure to different sources of traffic noise may convey a particularly high risk., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.)
Published: 2015
Full Text: View/download PDF

40. Road traffic noise and markers of obesity - a population-based study.

Author: Oftedal B, Krog NH, Pyko A, Eriksson C, Graff-Iversen S, Haugen M, Schwarze P, Pershagen G, and Aasvang GM
Subjects: Adult, Aged, Body Mass Index, Female, Follow-Up Studies, Humans, Logistic Models, Male, Middle Aged, Norway epidemiology, Obesity etiology, Obesity, Abdominal epidemiology, Obesity, Abdominal etiology, Sleep Wake Disorders etiology, Waist Circumference, Waist-Height Ratio, Environmental Exposure, Noise, Transportation adverse effects, Obesity diagnosis, Obesity epidemiology, Sleep Wake Disorders epidemiology
Abstract: Background: Noise has been found to be associated with endocrine changes and cardiovascular disease. Increased cortisol levels and chronic sleep problems due to noise may increase the risk of obesity., Objectives: We investigated the relationship between road traffic noise and obesity markers. Furthermore, we explored the modifying role of noise sensitivity, noise annoyance, and sleep disturbances., Methods: We used data from a population-based study, HUBRO (N=15,085), and its follow-up study HELMILO (N=8410) conducted in Oslo, Norway. Measurements were used to define body mass index (BMI), waist circumference (WC), waist-hip ratio (WHR), and these binary outcomes: BMI≥30kg/m(2), WC≥102cm (men)/88cm (women), and WHR≥0.90 (men)/0.85 (women). Modelled levels of road traffic noise (Lden) were assigned to each participant's home address. Linear and logistic regression models were used to examine the associations., Results: The results indicated no significant associations between road traffic noise and obesity markers in the total populations. However, in highly noise sensitive women (n=1106) a 10dB increase in noise level was associated with a slope (=beta) of 1.02 (95% confidence interval (CI): 1.01, 1.03) for BMI, 1.01 (CI: 1.00, 1.02) for WC, and an odds ratio (OR) of 1.24 (CI: 1.01, 1.53) for WHR ≥0.85. The associations appeared weaker in highly noise sensitive men. We found no effect modification of noise annoyance or sleep disturbances. In a sub-population with bedroom facing a road, the associations increased in men (e.g. an OR of 1.25 (CI: 0.88, 1.78) for BMI ≥30kg/m(2)), but not in women. Among long-term residents the associations increased for BMI ≥30kg/m(2) (OR of 1.07 (CI: 0.93, 1.24) in men and 1.10 (CI: 0.97, 1.26) in women), but not for the other outcomes., Conclusion: In an adult urban Scandinavian population, road traffic noise was positively associated with obesity markers among highly noise sensitive women. The associations appeared stronger among men with bedroom facing a street, representing a population with more accurately assigned exposure., (Copyright © 2015 Elsevier Inc. All rights reserved.)
Published: 2015
Full Text: View/download PDF

41. Road traffic noise, sleep and mental health.

Author: Sygna K, Aasvang GM, Aamodt G, Oftedal B, and Krog NH
Subjects: Adult, Aged, Female, Humans, Male, Middle Aged, Regression Analysis, Transportation, Young Adult, Mental Disorders etiology, Mental Health, Noise adverse effects, Sleep
Abstract: This study examines the relationship between road traffic noise, self-reported sleep quality and mental health. The study is cross-sectional and based on data from a survey conducted in Oslo, Norway, in 2000. Psychological distress (Hopkins Symptom Checklist, HSCL-25) was measured along with self-reported somatic health, sleep quality, noise sensitivity and socioeconomic variables. Questionnaire data were combined with modeled estimates of noise exposure. The total study sample consisted of 2898 respondents. After adjustment for potential confounders and stratifying for sleep quality, we found a positive, but not statistically significant association between noise exposure and symptoms of psychological distress among participants with poor sleep quality (slope=0.06, 95% CI: -0.02 to 0.13, per 10 dB increase in noise exposure). In the same sleep quality group, we found a borderline statistically significant association between noise exposure and a symptom level indicating a probable mental disorder (HSCL≥1.55) (odds ratio=1.47, 95% CI: 0.99-1.98, per 10 dB increase in noise exposure). We found no association between road traffic noise and mental health among subjects reporting good and medium sleep quality. The results suggest that road traffic noise may be associated with poorer mental health among subjects with poor sleep. Individuals with poor sleep quality may be more vulnerable to effects of road traffic noise on mental health than individuals with better sleep quality., (Copyright © 2014 Elsevier Inc. All rights reserved.)
Published: 2014
Full Text: View/download PDF

42. Long-term effects of noise reduction measures on noise annoyance and sleep disturbance: the Norwegian facade insulation study.

Author: Amundsen AH, Klæboe R, and Aasvang GM
Subjects: Adult, Consumer Behavior, Female, Follow-Up Studies, Humans, Male, Middle Aged, Norway, Sound Spectrography, Surveys and Questionnaires, Young Adult, Construction Materials, Housing, Noise, Transportation adverse effects, Noise, Transportation prevention & control, Sleep Deprivation etiology, Sleep Deprivation prevention & control, Sleep Wake Disorders etiology, Sleep Wake Disorders prevention & control, Urban Population
Abstract: The Norwegian facade insulation study includes one pre-intervention and two post-intervention surveys. The facade-insulating measures reduced indoor noise levels by 7 dB on average. Before the intervention, 43% of the respondents were highly annoyed by noise. Half a year after the intervention, the proportion of respondents who were highly annoyed by road traffic noise had been significantly reduced to 15%. The second post-intervention study (2 yr after the first post-intervention study) showed that the proportion of highly annoyed respondents had not changed since the first post-intervention study. The reduction in the respondents' self-reported sleep disturbances (due to traffic noise) also remained relatively stable from the first to the second post-intervention study. In the control group, there were no statistically significant differences in annoyance between the pre-intervention and the two post-intervention studies. Previous studies of traffic changes have reported that people "overreact" to noise changes. This study indicated that when considering a receiver measure, such as facade insulation, the effect of reducing indoor noise levels could be predicted from exposure-response curves based on previous studies. Thus no evidence of an "overreaction" was found.
Published: 2013
Full Text: View/download PDF

43. A field study of effects of road traffic and railway noise on polysomnographic sleep parameters.

Author: Aasvang GM, Øverland B, Ursin R, and Moum T
Subjects: Adult, Environmental Exposure, Environmental Monitoring methods, Factor Analysis, Statistical, Female, Humans, Male, Middle Aged, Norway, Risk Assessment, Risk Factors, Sleep Wake Disorders diagnosis, Sleep Wake Disorders physiopathology, Sound Spectrography, Time Factors, Automobiles, Noise, Transportation adverse effects, Polysomnography, Railroads, Sleep Wake Disorders etiology, Sleep, REM
Abstract: The aim of this study was to explore and compare the effect of noise from railway and road traffic on sleep in subjects habitually exposed to nocturnal noise. Forty young and middle aged healthy subjects were studied with polysomnography (PSG) during two consecutive nights in their own bedroom. Noise measurements and recordings were conducted concurrently outside of the bedroom façade as well as inside the bedroom of each participant. Different noise exposure parameters were calculated (L(p,A,eq,night), L(p,A,Fmax,night), and L(AF5,night)) and analyzed in relation to whole-night sleep parameters. The group exposed to railway noise had significantly less Rapid eye movement, (REM) sleep than the group exposed to road traffic noise. A significant association was found between the maximum level (L(p,A,Fmax,night)) of railway noise and time spent in REM sleep. REM sleep was significantly shorter in the group exposed to at least a single railway noise event above 50 dB inside the bedroom. These results, obtained in an ecological valid setting, support previous laboratory findings that railway noise has a stronger impact than road traffic noise on physiological parameters during sleep, and that the maximum noise level is an important predictor of noise effects on sleep assessed by PSG, at least for railway noise., (© 2011 Acoustical Society of America)
Published: 2011
Full Text: View/download PDF

44. The Norwegian Façade Insulation Study: the efficacy of façade insulation in reducing noise annoyance due to road traffic.

Author: Amundsen AH, Klæboe R, and Aasvang GM
Subjects: Case-Control Studies, Environmental Monitoring, Female, Humans, Male, Middle Aged, Norway, Perception, Surveys and Questionnaires, Automobiles, Construction Materials, Emotions, Facility Design and Construction, Noise, Transportation adverse effects
Abstract: The efficacy of façade insulation in providing an improved indoor noise environment and in reducing indoor noise annoyance was examined in a socio-acoustic before-and-after study with a control group. An average equivalent noise reduction inside the dwellings of 7 dB was obtained from the façade insulation. Whereas 42% of the respondents were highly annoyed in the before-situation, this dropped to 16% in the after study. The conclusion is therefore that the façade insulation provided a substantial improvement in the indoor noise environment. The advantage with respect to indoor noise annoyance, of having the bedroom facing the least noise-exposed side of the dwelling corresponded to a 6 dB noise reduction. The changes in annoyance from noise reduction due to the façade insulation were in accordance with what would be expected from the exposure-response curves obtained in the before-situation. A total of 637 respondents participated in the before-study. Of these, 415 also participated in the after study. Indoor and outdoor noise exposure calculations for each of the dwellings were undertaken before and after the façade insulation was implemented., (© 2011 Acoustical Society of America)
Published: 2011
Full Text: View/download PDF

45. Noise, sleep and poor health: Modeling the relationship between road traffic noise and cardiovascular problems.

Author: Fyhri A and Aasvang GM
Subjects: Environmental Exposure statistics & numerical data, Female, Humans, Male, Surveys and Questionnaires, Cardiovascular Diseases epidemiology, Models, Biological, Noise, Transportation statistics & numerical data, Sleep Deprivation epidemiology
Abstract: Several adverse effects have been associated with exposure to traffic noise. Studies supporting a noise-stress-health model have suggested links between noise level and increased noradrenalin concentrations in urine, hypertension and myocardial infarction. Among the more commonly documented effects, sleep disturbances have been regarded as being the most serious. Both noise annoyance and sleep disturbance have been proposed as important mediators of the impact of noise on health. The present paper investigates the relationships among long-term noise exposure, annoyance, sleeping problems and subjective health complaints by the use of a structural equation model. Further, it aims at giving insight into how noise sensitivity is related to sleep disturbances from road traffic noise. Finally, it examines whether any effect of noise exposure or response to noise can be detected on prevalence of cardiovascular problems, when information on sleep disturbances is included in a model. Data from a questionnaire survey conducted among a population sample in Oslo (N=2786) are combined with nighttime noise levels calculated from outside each respondents dwelling, at the bedroom façade. The results of the analysis showed significant relationships between noise annoyance at night and sleeping problems. The model also showed strong links among pseudoneurological complaints, annoyance and sleeping problems, thus pointing to the importance of including information on psychosomatic disorders and mild psychological problems in future studies looking at potential health effects of noise. The analysis showed no relationship between neither noise exposure nor response to noise and cardiovascular problems., (Copyright 2010 Elsevier B.V. All rights reserved.)
Published: 2010
Full Text: View/download PDF

46. Self-reported sleep disturbances due to railway noise: exposure-response relationships for nighttime equivalent and maximum noise levels.

Author: Aasvang GM, Moum T, and Engdahl B
Subjects: Adolescent, Adult, Age Factors, Aged, Aged, 80 and over, Auditory Threshold, Choice Behavior, Female, Humans, Male, Middle Aged, Noise adverse effects, Railroads statistics & numerical data, Sleep Wake Disorders epidemiology, Sleep Wake Disorders etiology
Abstract: The objective of the present survey was to study self-reported sleep disturbances due to railway noise with respect to nighttime equivalent noise level (L(p,A,eq,night)) and maximum noise level (L(p,A,max)). A sample of 1349 people in and around Oslo in Norway exposed to railway noise was studied in a cross-sectional survey to obtain data on sleep disturbances, sleep problems due to noise, and personal characteristics including noise sensitivity. Individual noise exposure levels were determined outside of the bedroom facade, the most-exposed facade, and inside the respondents' bedrooms. The exposure-response relationships were analyzed by using logistic regression models, controlling for possible modifying factors including the number of noise events (train pass-by frequency). L(p,A,eq,night) and L(p,A,max) were significantly correlated, and the proportion of reported noise-induced sleep problems increased as both L(p,A,eq,night) and L(p,A,max) increased. Noise sensitivity, type of bedroom window, and pass-by frequency were significant factors affecting noise-induced sleep disturbances, in addition to the noise exposure level. Because about half of the study population did not use a bedroom at the most-exposed side of the house, the exposure-response curve obtained by using noise levels for the most-exposed facade underestimated noise-induced sleep disturbance for those who actually have their bedroom at the most-exposed facade.
Published: 2008
Full Text: View/download PDF

47. Detection of latex allergens by immunoelectron microscopy in ambient air (PM10) in Oslo, Norway (1997-2003).

Author: Namork E, Kurup VP, Aasvang GM, and Johansen BV
Subjects: Allergens analysis, Automobile Driving, Environmental Monitoring methods, Humans, Microscopy, Immunoelectron methods, Norway, Particle Size, Seasons, Air Pollutants analysis, Latex immunology, Latex Hypersensitivity etiology
Abstract: The authors collected ambient air along two highways in Oslo to investigate the annual variations in particulate matter (PM10) and the presence of latex as an outdoor allergen. PMI, was monitored for a period of five years, during which time the use of studded winter tires was reduced. The presence of latex and of common aeroallergens was examined directly on the collection filters with immunoelectron microscopy visualized in a scanning electron microscope. The annual variation in PM10 was similar over the five years of sampling, with increased mass concentrations in winter. Statistical analysis indicated no major effect from the change to nonstudded tires. The most important factors influencing the PM10 concentration were meteorological parameters like wind and rain. Immnunolabeling of the filters showed latex as an outdoor allergen that adhered to carbon aggregates from vehicle emission. The results also indicated cross-reactive epitopes among the common allergens investigated, which for sensitized subjects may add to the risk of developing latex allergy.
Published: 2004

Catalog

Books, media, physical & digital resources

See catalog results

Searchworks

Select search scope, currently: Articles Catalog books, media & more in Jio Institute collections Articles journal articles & other e-resources

Search

Search Constraints

Refine your results

Search Limiters

Topic

Publication Year Range

Language

Publication Type

Journal

Region

Database

Publisher

47 results on '"Aasvang, Gm"'

Search Results

Catalog

Select search scope, currently: Articles

Catalog

books, media & more in Jio Institute collections

Articles

journal articles & other e-resources