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2. Global burden of 87 risk factors in 204 countries and territories, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019
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Soufiane Boufous, Yousef Veisani, Mehran Asadi-Aliabadi, Sharath Burugina Nagaraja, Maziar Moradi-Lakeh, Getachew Mullu Kassa, Edward J Mills, Dimas Ria Angga Pribadi, William James Dangel, Mohamad-Hani Temsah, Catherine O. Johnson, Gregory A. Roth, Giuseppe Gorini, Fariborz Mansour-Ghanaei, Alberto Ortiz, Samad Azari, Assefa Ayalew Ayalew Ayalew Gebreslassie, Salime Goharinezhad, Stephanie R. M. Zimsen, Peng Zheng, Michael Assmus, Elisabetta Pupillo, Bach Xuan Tran, Lal B. Rawal, Narayanaswamy Venketasubramanian, Noushin Mohammadifard, Stephen S Lim, Ata Rafiee, Maria Inês Schmidt, Vincent C. Iannucci, Suzanne Lyn Barker-Collo, Leah E. Cahill, Tauseef Ahmad, Platon D. Lopukhov, Kazumasa Yamagishi, Abdullah Al Mamun, Iqbal R. F. Elyazar, Giovanni Damiani, Mohammad Hossein Bakhshaei, Mehdi Fazlzadeh, Virginia Núñez-Samudio, Alyssa Pennini, Dietrich Plass, Atkilt Esaiyas Etisso, Gebre Teklemariam Demoz, Alexandrea Watson, Arvin Haj-Mirzaian, Paul S Briant, Frank B. Osei, Blair R. Bumgarner, Maciej Banach, Ravensara S. Travillian, Kai-Lan Chang, Shirin Djalalinia, Hasan Yusefzadeh, Silvano Gallus, Seyyed Meysam Mousavi, Bernhard T. Baune, Aaron van Donkelaar, Azeem Majeed, Hans Kromhout, Robert Ancuceanu, Blessing J. Akombi, Pushpendra Singh, Nayu Ikeda, William M. Gardner, Zahid A Butt, Mohammad Abdollahi, Temesgen Yihunie Akalu, Rahman Shiri, Benn Sartorius, Ai-Min Wu, Bing Fang Hwang, Flavia M. Cicuttini, Hiroyasu Iso, Luis Camera, Amin Soheili, Félix Carvalho, Yun Jin Kim, Caleb Mackay Salpeter Irvine, Mehdi Mirzaei-Alavijeh, Iman Halvaei, Saqib Ali, Giulio Castelpietra, Catalina Liliana Andrei, Ali Kazemi Karyani, Parkes J Kendrick, Hamidreza Haririan, Lucas Guimarães Abreu, Mukhammad David Naimzada, Jeff T. Zhao, Samiah Alam, Sorin Hostiuc, Shaun Wen Huey Lee, João Mauricio Castaldelli-Maia, Behzad Karami Matin, Cyrus Alinia, Takahiro Tabuchi, Manu Raj Mathur, Søren Thorgaard Skou, Thomas Khaled Dwayne Classen, Reza Heidari-Soureshjani, Massimo Cirillo, Nikita Otstavnov, Mehdi Bohluli, Ruth W. Kimokoti, Animut Tagele Tamiru, Masoumeh Sadeghi, Mohammad Ali Jahani, Itamar S. Santos, Mekdes Tigistu Yilma, Lars Johansson, Arielle Wilder Eagan, Nevine El Nahas, Silvia Schiavolin, Kevin D. Shield, Dinh-Toi Chu, Shiva Borzouei, Paul S. F. Yip, Beatrix Haddock, Gianfranco Alicandro, Vasily Vlassov, Deanna Anderlini, Giuseppe Remuzzi, Khalid A Altirkawi, Farahnaz Joukar, Aso Mohammad Darwesh, Ratilal Lalloo, Panniyammakal Jeemon, Rohollah Kalhor, Daniel Youngwhan Cho, Weijia Fu, João Pedro Silva, Rodrigo Sarmiento-Suarez, Seth Christopher Yaw Appiah, Mehdi Ahmadi, Jacob Olusegun Olusanya, José Neves, Gaorui Guo, Tomas Y. Yeheyis, John S. Ji, Charles D. H. Parry, Maryam Ghadimi, Seyed-Mohammad Fereshtehnejad, Serge Resnikoff, Anna E. Torre, Vinod C Nayak, Jamileh Shadid, Susanne Breitner, Mohammad Khammarnia, Mathilde Touvier, Ensiyeh Jenabi, Hosna Janjani, Floriane Ausloos, Irmina Maria Michalek, Alexandra S. Boon-Dooley, Jessica A. Cruz, Syed Mohamed Aljunid, Abiodun M. Adeoye, André Faro, Bartosz Miazgowski, Jobert Richie Nansseu, Erin C Mullany, Giannina Ferrara, Martin McKee, Emmanuel Peprah, Oommen John, Reza Saeedi, Yasser Vasseghian, Dragos Virgil Davitoiu, Sarah Wulf Hanson, Yingxi Zhao, Omid Shafaat, Ali Rajabpour-Sanati, Farid Najafi, Ana Maria Mantilla Herrera, Fatemeh Rajati, Tarun Gupta, Łukasz Szumowski, Mohammed Ibrahim Mohialdeen Gubari, Peter Njenga Keiyoro, Dharmesh Kumar Lal, Zhi Jiang Zhang, Osayomwanbo Osarenotor, Tanvir M. Huda, Perminder S. Sachdev, Farhad Ghamari, Era Upadhyay, Vivek Kumar, Guoqing Hu, Vinay Nangia, Vladimir Andreevich Korshunov, Saeed Shahabi, Golnaz Heidari, Ashraf Nabhan, Robert C. Reiner, Aziz Rezapour, Justin J. Lang, Rakhi Dandona, Josephine W. Ngunjiri, Anna-Karin Danielsson, André Karch, Filippo Ariani, Ahmed Abdelalim, Masih Tajdini, Stefanos Tyrovolas, Mohamed Hsairi, Jae Il Shin, Jasvinder A. Singh, Meghan D. Mooney, Fiona B. Bennitt, Hesam Alizade, Segun Emmanuel Ibitoye, Pradhum Ram, Soraya Siabani, Evanson Z. Sambala, Reza Malekzadeh, Falk Schwendicke, Lalit Dandona, Masoud Moradi, Molly R Nixon, Roya Mirzaei, Rachel Feldman, Hosni Salem, Alberto L. García-Basteiro, Lorainne Tudor Car, Sharareh Eskandarieh, Ramesh Holla, Ritesh G. Menezes, Taraneh Yousefinezhadi, Hai Quang Pham, Hamideh Salimzadeh, Luisa Sorio Flor, Priya Rathi, Ali Bijani, Harvey Whiteford, Shanshan Li, Aleksandr Y. Aravkin, Joshua A. Salomon, Franz Castro, Lisa M. Force, Abdilahi Yousuf Yousuf, Mina Anjomshoa, Ken Takahashi, Maigeng Zhou, Telma Zahirian Moghadam, Maseer Khan, Irina Filip, Santi Martini, Randah R. Hamadeh, Somayeh Bohlouli, Joana Morgado-da-Costa, Tim Driscoll, Jingkai Wei, Hermann Brenner, Reza Rawassizadeh, Radoslaw Sierpinski, Saman Esmaeilnejad, Emmanuel Wandera Okunga, Marisa Freitas, Srikanta Banerjee, Feleke Mekonnen Demeke, Shahin Soltani, Naser Mohammad Gholi Mezerji, Reed J D Sorensen, Elena V. Gnedovskaya, Johan Ärnlöv, Ivo Rakovac, Reza Mohammadpourhodki, Hussain Jafari, Atte Meretoja, Yasir Waheed, Fahad Alanezi, Arya Haj-Mirzaian, Sezer Kisa, Jaifred Christian F. Lopez, Khalid F. Alhabib, Basema Saddik, Michael R. Phillips, Vishnu Renjith, Yafeng Wang, Kevan R. Polkinghorne, Liliana G Ciobanu, Jacek Jerzy Jozwiak, Gelin Xu, Richard C. Franklin, Junjie Wu, Thomas R. Hird, Mohammad Zamani, Diana Silva, Fotis Topouzis, Irena Ilic, Jeffrey D. Stanaway, Hadi Pourjafar, Huong Lan Thi Nguyen, Khaled Khatab, Ammas Siraj Mohammed, Ziyad Al-Aly, A. A. Fomenkov, Charlie Ashbaugh, Mowafa Househ, Paul I. Dargan, Endalkachew Worku Mengesha, Shaimaa I. El-Jaafary, Ernoiz Antriyandarti, Iffat Elbarazi, Dara K. Mohammad, Naznin Hossain, Reza Shirkoohi, João M. Furtado, Arash Ziapour, Morteza Jafarinia, M. Mofizul Islam, Anamika Pandey, Ahmed I. Hasaballah, Tanuj Kanchan, Lee Ling Lim, Muktar Omer Omer, Charles D.A. Wolfe, Ulrich O Mueller, Helen Bitew, V. Prakash, Fereshteh Mehri, Randall V. Martin, Claudiu Herteliu, Constance D. Pond, Min Jeong Shin, Morteza Oladnabi, Antonio Maria Borzì, Yousef Mohammad, Yuichiro Yano, Luke D. Knibbs, Kevin S Ikuta, Maryam Mirzaei, Andreea Mirica, Sofia Boston Redford, Siamak Sabour, Mariya Vladimirovna Titova, Davood Anvari, Ghobad Moradi, Jordi Alonso, Shiwei Liu, Theo Vos, Tuomo J. Meretoja, Ireneous N. Soyiri, Owen R. Cooper, Seyed Sina Naghibi Irvani, Kejia Hu, Hannah J. Henrikson, Sanni Yaya, Robert P. Dellavalle, Chidozie Declan Iwu, Sergey Soshnikov, Jee-Young Jasmine Choi, Satinath Mukhopadhyay, Zabihollah Yousefi, Iman El Sayed, Biresaw Wassihun Alemu, Neeti Kapoor, Ahmad Daryani, Cathleen Keller, Ibrahim Abdollahpour, Nuno Taveira, Masoud Foroutan, Fatemeh Amiri, Mariam Molokhia, Songhomitra Panda-Jonas, Amy E. Peden, Rufus Akinyemi, Ejaz Ahmad Khan, Mostafa Amini-Rarani, J. Becker, Hamidreza Pazoki Toroudi, Ben Lacey, Kidanemaryam Berhe, Simon Yadgir, Spencer L. James, Cory N. Spencer, Aletta E. Schutte, Mu'awiyyah Babale Sufiyan, Arash Tehrani-Banihashemi, Govinda Prasad Dhungana, Fereshteh Ansari, Rixing Xu, Jonathan F. Mosser, Josep Maria Haro, Enrico Rubagotti, Anurag Agrawal, Zahiruddin Quazi Syed, Hoa Thi Do, Ettore Beghi, Seyed Mohammad Kazem Aghamir, Abraham Geremew, Alireza Esteghamati, Paramjit Gill, Farzad Jalilian, J. Jason West, Mikhail Sergeevich Zastrozhin, Albertino Damasceno, Bruce Bartholow Duncan, Nazir Fattahi, Daniel Cury Ribeiro, Michael Brauer, Mark A. Stokes, Veincent Christian Filipino Pepito, Lidia Morawska, Fiona J Charlson, Babak Moazen, Dejana Braithwaite, Jonathan M. Kocarnik, Sergio I. Prada, Andrea Farioli, Zahra Atafar, Heather Orpana, Daniela Balzi, Marco Vacante, Rahmatollah Moradzadeh, Jacek A. Kopec, Iván Landires, Robert G. Weintraub, Leonardo Roever, Yannick Béjot, Markus P. Schlaich, Hamed Zandian, Subramanian Senthilkumaran, Klara Dokova, Vahid Alipour, Sowmya J. Rao, Rakesh Ghosh, Omar Mukhtar Salman, Faris Lami, Marcos Roberto Tovani-Palone, Hamid Reza Tohidinik, Seyed Mohammad Riahi, Adnan Kisa, Ghasem Azarian, Caroline Stein, Zulfiqar A. Bhutta, Sinead Langan, Kunihiro Matsushita, Lauren E. Schaeffer, Kathryn H. Jacobsen, Mehdi Naderi, Mehdi Hosseinzadeh, Nizal Sarrafzadegan, Bahram Armoon, Dan J. Stein, Jessica Fanzo, Morenike Oluwatoyin Folayan, Luca Ronfani, Phetole Walter Mahasha, Nicholas J K Breitborde, Adrian Oţoiu, Arash Sarveazad, Marc L. Serre, Mostafa Hosseini, Nicolas Cherbuin, George D. Thurston, Jalal Arabloo, Mokhtar Mahdavi, Andre Rodrigues Duraes, Ana Laura Manda, Ahmed Abualhasan, Nima Rezaei, Yuan-Pang Wang, Theodore Patrick Younker, Alireza Ansari-Moghaddam, Borhan Mansouri, Adam E. Berman, Khezar Hayat, Rosario Cárdenas, Bolajoko O. Olusanya, Tommi Vasankari, Simon I. Hay, Fatemeh Ghaffarifar, Leo Stockfelt, Ai Koyanagi, Giorgia Giussani, Yuming Guo, Sonia Saxena, Deborah Carvalho Malta, Mehedi Hasan, Negar Rezaei, Maja Pasovic, Jukka Takala, Bogdan Oancea, Sare Safi, A. Werdecker, Florian Fischer, Beatriz Paulina Ayala Quintanilla, Muhammad Shahdaat Bin Sayeed, Takeshi Fukumoto, Maha Atout, Brijesh Sathian, Cristina Bosetti, Mitchell T. Wallin, Agegnehu Bante, Helen Ippolito, Anthony Masaka, Chantal Huynh, Justin Lo, Jordan Weiss, Joemer C. Maravilla, Alberto Raggi, Peter W. Gething, Cristiana Abbafati, Daniela Ribeiro, Mohammad Farahmand, Yetunde O. John-Akinola, Isabela M. Benseñor, Emilie R Maddison, John J. McGrath, Salman Khazaei, Scott B. Patten, Jean Jacques Noubiap, Emmanuela Gakidou, Celine M. Barthelemy, Ashish Badiye, George C. Patton, Obinna Onwujekwe, Peter Allebeck, Victor Aboyans, Olayinka Stephen Ilesanmi, Mousa Yaminfirooz, Neeraj Bedi, Nicholas L S Roberts, Joht Singh Chandan, Hans W. Hoek, Usman Iqbal, Nima Hafezi-Nejad, Haley Lescinsky, Naohiro Yonemoto, Ahmad Ghashghaee, Anders Larsson, David C. Schwebel, Milena Ilic, Richard T. Burnett, Yang Liu, Carlo La Vecchia, Felix Akpojene Ogbo, Morteza Naserbakht, Sangram Kishor Patel, Melanie S. Hammer, Prasanna Mithra, Mohammad Amin Bahrami, Kanyin L. Ong, Mona Pathak, Afshin Maleki, Saeid Safiri, Masood Ali Shaikh, Kate Causey, Michael R.M. Abrigo, Jost B. Jonas, Dian Kusuma, Jagadish Rao Padubidri, Mihajlo Jakovljevic, Ali S. Shalash, Abdiwahab Hashi, Ionut Negoi, Nataliya A. Foigt, Andrey Nikolaevich Briko, François Alla, Giuseppe Grosso, Houman Goudarzi, Di H. Cross, Vera Marisa Costa, Eduarda Fernandes, Chandrashekhar T Sreeramareddy, Odgerel Chimed-Ochir, Sonia Rodríguez-Ramírez, Bo Norrving, Kerem Shuval, Jacob L. Stubbs, Muhammad Ali, Shuhei Nomura, Man Mohan Mehndiratta, Chisom Joyqueenet Akunna, Abdollah Mohammadian-Hafshejani, Navid Rabiee, Dana Bryazka, Hussen Mohammed, Asadollah Gholamian, Ashley Marks, Rizwan Kalani, Molly E. Herbert, Islam Y. Elgendy, Moritz U. G. Kraemer, Chuanhua Yu, Suzanne Polinder, Pascual R. Valdez, Jennifer Rickard, Kylie Ball, Turki Alanzi, Mohsen Bayati, Hamed Mirzaei, Christopher M Odell, Amira Shaheen, Ziad A. Memish, Thirunavukkarasu Sathish, Michael A. Piradov, Hamed Kalani, Lorenzo Monasta, Christopher S Yilgwan, Desalegn Getnet Demsie, Riaz Uddin, Rizwan Suliankatchi Abdulkader, Vinay Srinivasan, Hamid Ahmadieh, Claudio Alberto Dávila-Cervantes, Raffaele Palladino, Chukwudi A Nnaji, Mika Shigematsu, Stein Emil Vollset, Abbas Sheikhtaheri, Paulo A. Lotufo, Nasir Salam, Binyam Minuye Birihane, Mohammad Ali Mansournia, Tomislav Mestrovic, Samer Hamidi, Rajesh Sagar, Mayowa O. Owolabi, Kara Estep, Ester Cerin, Michael T. Chung, Simon Øverland, Amir Taherkhani, Sheng Chia Chung, Martin Amogre Ayanore, Nikolaos Dervenis, Joan B. Soriano, Tahereh Javaheri, Victor Adekanmbi, Seid Tiku Mereta, Gbenga A. Kayode, Christopher R. Cederroth, Razique Anwer, Rajan Nikbakhsh, Kaja Abbas, Fatemeh Heydarpour, Louisa Degenhardt, Tahiya Alam, Mohammad Miri, Alibek Mereke, David Laith Rawaf, Ippazio Cosimo Antonazzo, Erkin M. Mirrakhimov, Seyed Hossein Yahyazadeh Jabbari, Desta Debalkie Atnafu, Davide Sattin, Moslem Soofi, Edris Hasanpoor, Krittika Bhattacharyya, Mika Kivimäki, Nikolay Ivanovich Briko, Joanna L Whisnant, Christopher J L Murray, Simin Mouodi, Alize J. Ferrari, Damian Santomauro, Katrin Burkart, Tudorel Andrei, Alberto Baldasseroni, Hafiz Ansar Rasul Suleria, Valery L. Feigin, Nauman Khalid, Ewerton Cousin, S. Mohammad Sajadi, Francisco Rogerlândio Martins-Melo, Shankar M Bakkannavar, Themba G.G. Ginindza, Sadaf G. Sepanlou, Sheikh Mohammed Shariful Islam, Sanjay Basu, Getinet Ayano, Paula Moraga, Soheil Hassanipour, Jason A. Anderson, Catherine Bisignano, Iyad Sultan, Deepak Kumar Pasupula, Keivan Ahmadi, Fariba Dorostkar, Rajeev Gupta, David M. Pereira, Mustafa Z. Younis, Adel Spotin, Rasmus Havmoeller, Yeshambel T. Nigatu, Barthelemy Kuate Defo, Mithila Faruque, Alan D. Lopez, Shailesh Advani, Behshad Naghshtabrizi, Shane D. Morrison, Inga Dora Sigfusdottir, Konrad Pesudovs, Anna Gershberg Hayoon, Raaj Kishore Biswas, Reshmi Bhageerathy, H. Dean Hosgood, Giulia Carreras, Sarika Chaturvedi, James L. Fisher, In-Hwan Oh, G Anil Kumar, Christoph Nowak, Vijay Kumar Chattu, Puja C Rao, Marcel Ausloos, Ali Kabir, Rannveig Sigurvinsdottir, Leeberk Raja Inbaraj, Edgar Denova-Gutiérrez, Rafael Tabarés-Seisdedos, Minh Nguyen, Ashkan Afshin, Payman Salamati, Colin Angus, Mona M. Khater, Ehsan Sadeghi, Mahalaqua Nazli Khatib, Antonio Biondi, Valentin Yurievich Skryabin, Mohsen Abbasi-Kangevari, Andrew T Olagunju, Amir Radfar, Laith J. Abu-Raddad, Marcello Tonelli, Hesam Ghiasvand, Hanne Christensen, Juan Jesus Carrero, Maryam Adabi, Saravanan Muthupandian, Kurt Straif, Hossein Samadi Kafil, Lope H Barrero, Harish Chander Gugnani, Mohammad Fareed, Morteza Shamsizadeh, Jemal Abdu Mohammed, Juan A Rivera, Shai Linn, Saad M.A. Dahlawi, Janni Leung, Shokofeh Maleki, Mohd Anisul Karim, Kamarul Imran Musa, Farshad Pourmalek, Dietrich Rothenbacher, Kiomars Sharafi, Alessandra C. Goulart, Leila Doshmangir, Gabriele Nagel, Helena Manguerra, Olatunji O. Adetokunboh, Srinivasa Vittal Katikireddi, Nermin Ghith, Maha El Tantawi, Awoke Misganaw, Yunquan Zhang, Carl Abelardo T. Antonio, Vahid Rashedi, Mehran Shams-Beyranvand, Bhaskaran Unnikrishnan, Holly E. Erskine, Ann Kristin Knudsen, Marissa B Reitsma, Getayeneh Antehunegn Tesema, Javad Javidnia, Ismael R. Campos-Nonato, Biniyam Sahiledengle Geberemariyam, Godfrey Mutashambara Rwegerera, Alaa Badawi, James Leigh, Morteza Arab-Zozani, Kyle E. Simpson, Muluken Bekele Sorrie, Roghiyeh Faridnia, Vivekanand Jha, Tomasz Miazgowski, Aaron J Cohen, Chukwuma David Umeokonkwo, Alessandra Lugo, Adhanom Gebreegziabher Baraki, Akshaya Srikanth Bhagavathula, Caitlyn Steiner, Gholamreza Roshandel, Cuong Tat Nguyen, Tania G Sánchez-Pimienta, Ahamarshan Jayaraman Nagarajan, Laura Kemmer, Ihoghosa Osamuyi Iyamu, Seyedeh Zahra Masoumi, Vivian Chia-Rong Hsieh, Kris J. Krohn, Phoebe Anne Rhinehart, Sarah Wozniak, Sahar Saeedi Moghaddam, Kate E. LeGrand, Christian Kieling, Vahid Yazdi-Feyzabadi, Robin Room, Zelalem Nigussie Azene, Kelly Cercy, Paul H. Lee, Stanislav S. Otstavnov, Dinesh Bhandari, Rafael Alves Guimarães, Zemenu Tadesse Tessema, Aziz Sheikh, Michellr L. Bell, Marwa Rashad Salem, Kirsten E. Wiens, Emma U.R. Smith, Hassan Abolhassani, Cristiano Piccinelli, Kedir Hussein Abegaz, G.K. Mini, Christian Razo, Manuela L. Ferreira, Diego De Leo, Francesco Saverio Violante, Aristidis Tsatsakis, Zahra Sadat Dibaji Forooshani, Tea Lallukka, Dickson A. Amugsi, Anna Poznańska, Graeme J. Hankey, Kewal Krishan, Maryam Zamanian, Eirini Skiadaresi, Jai K Das, Felix Greaves, Tessa M. Pilz, Sameer Vali Gopalani, Mansour Ghafourifard, M. DeLang, Morteza Mahmoudi, Alton Lu, Brian J. Hall, Ravi Prakash Jha, David Edvardsson, Xiu Ju George Zhao, Farshad Farzadfar, Hadi Hassankhani, Samuel M. Ostroff, Gerhard Sulo, Keyghobad Ghadiri, Neeraj Bhala, Stefan Lorkowski, Mohammad Rabiee, Sivan Yegnanarayana Iyer Saraswathy, Amirhossein Sahebkar, Rashid Abdi Guled, Abdallah M. Samy, Roman Topor-Madry, Michal Grivna, Afsaneh Arzani, Ayesha Humayun, Simin Liu, Maryam Khayamzadeh, Davoud Adham, Ahad Bakhtiari, Shafiu Mohammed, Paolo Lauriola, Abbas Mosapour, Sophia Emmons-Bell, Khurshid Alam, Rajat Das Gupta, Matilde Leonardi, Muktar Beshir Ahmed, Jeffrey V. Lazarus, Mohamed M. Gad, Kelly Compton, Leila R Kalankesh, Abdelrahman Ibrahim Abushouk, Mikk Jürisson, Catherine M. Antony, Ali A. Asadi-Pooya, Daniel Diaz, Salman Rawaf, Gina Agarwal, Ted R. Miller, Rebecca Ivers, João Vasco Santos, Savita Lasrado, Abdul Moiz Hafiz, Amir Almasi-Hashiani, Praveen Hoogar, Fares Alahdab, Om P Kurmi, Anbissa Muleta Senbeta, Tomi Akinyemiju, Boris Bikbov, Muhammad Aziz Rahman, Amin Mousavi Khaneghah, Yahya Safari, Guilherme Borges, Carlos A Castañeda-Orjuela, Kenji Shibuya, Bahman Yousefi, Berrin Serdar, Karen M. Tabb, Sonali Kochhar, Till Bärnighausen, Kala M. Mehta, Mostafa Dianatinasab, Arash Etemadi, Melissa Y. Wei, Kiana Ramezanzadeh, Lingkan Barua, Zubair Kabir, Rade Vukovic, Hesham M. Al-Mekhlafi, Shoshana H. Ballew, Miriam Levi, Zainab Samad, Florentino Luciano Caetano dos Santos, Juan Sanabria, Ramu Rawat, Chinwe Juliana Iwu, Gabrielle B. Britton, Colm McAlinden, Mohsen Naghavi, Maarten J. Postma, Chhabi Lal Ranabhat, Jalil Jaafari, Walter Mendoza, Mahesh P A, Pallab K. Maulik, Ali H. Mokdad, Andre M. N. Renzaho, Milena Santric-Milicevic, Parvaiz A Koul, Foad Abd-Allah, Mihaela Hostiuc, Richard G. Cowden, Ronny Westerman, Meghdad Pirsaheb, Department of Earth Observation Science, UT-I-ITC-ACQUAL, Faculty of Geo-Information Science and Earth Observation, Real World Studies in PharmacoEpidemiology, -Genetics, -Economics and -Therapy (PEGET), Value, Affordability and Sustainability (VALUE), Microbes in Health and Disease (MHD), Tampere University, Tays Research Services, Health Sciences, Murray, C. J. L., Aravkin, A. Y., Zheng, P., Abbafati, C., Abbas, K. M., Abbasi-Kangevari, M., Abd-Allah, F., Abdelalim, A., Abdollahi, M., Abdollahpour, I., Abegaz, K. H., Abolhassani, H., Aboyans, V., Abreu, L. G., Abrigo, M. R. M., Abualhasan, A., Abu-Raddad, L. J., Abushouk, A. I., Adabi, M., Adekanmbi, V., Adeoye, A. M., Adetokunboh, O. O., Adham, D., Advani, S. 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W., Ausloos, F., Ausloos, M., Ayala Quintanilla, B. P., Ayano, G., Ayanore, M. A., Azari, S., Azarian, G., Azene, Z. N., Badawi, A., Badiye, A. D., Bahrami, M. A., Bakhshaei, M. H., Bakhtiari, A., Bakkannavar, S. M., Baldasseroni, A., Ball, K., Ballew, S. H., Balzi, D., Banach, M., Banerjee, S. K., Bante, A. B., Baraki, A. G., Barker-Collo, S. L., Barnighausen, T. W., Barrero, L. H., Barthelemy, C. M., Barua, L., Basu, S., Baune, B. T., Bayati, M., Becker, J. S., Bedi, N., Beghi, E., Bejot, Y., Bell, M. L., Bennitt, F. B., Bensenor, I. M., Berhe, K., Berman, A. E., Bhagavathula, A. S., Bhageerathy, R., Bhala, N., Bhandari, D., Bhattacharyya, K., Bhutta, Z. A., Bijani, A., Bikbov, B., Bin Sayeed, M. S., Biondi, A., Birihane, B. M., Bisignano, C., Biswas, R. K., Bitew, H., Bohlouli, S., Bohluli, M., Boon-Dooley, A. S., Borges, G., Borzi, A. M., Borzouei, S., Bosetti, C., Boufous, S., Braithwaite, D., Breitborde, N. J. K., Breitner, S., Brenner, H., Briant, P. S., Briko, A. N., Briko, N. 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G, Bryazka, D, Bumgarner, B, Burkart, K, Burnett, R, Burugina Nagaraja, S, Butt, Z, Caetano Dos Santos, F, Cahill, L, Camera, L, Campos-Nonato, I, Cardenas, R, Carreras, G, Carrero, J, Carvalho, F, Castaldelli-Maia, J, Castaneda-Orjuela, C, Castelpietra, G, Castro, F, Causey, K, Cederroth, C, Cercy, K, Cerin, E, Chandan, J, Chang, K, Charlson, F, Chattu, V, Chaturvedi, S, Cherbuin, N, Chimed-Ochir, O, Cho, D, Choi, J, Christensen, H, Chu, D, Chung, M, Chung, S, Cicuttini, F, Ciobanu, L, Cirillo, M, Classen, T, Cohen, A, Compton, K, Cooper, O, Costa, V, Cousin, E, Cowden, R, Cross, D, Cruz, J, Dahlawi, S, Damasceno, A, Damiani, G, Dandona, L, Dandona, R, Dangel, W, Danielsson, A, Dargan, P, Darwesh, A, Daryani, A, Das, J, Das Gupta, R, das Neves, J, Davila-Cervantes, C, Davitoiu, D, De Leo, D, Degenhardt, L, Delang, M, Dellavalle, R, Demeke, F, Demoz, G, Demsie, D, Denova-Gutierrez, E, Dervenis, N, Dhungana, G, Dianatinasab, M, Dias da Silva, D, Diaz, D, Dibaji Forooshani, Z, Djalalinia, S, Do, H, Dokova, K, Dorostkar, F, Doshmangir, L, Driscoll, T, Duncan, B, Duraes, A, Eagan, A, Edvardsson, D, El Nahas, N, El Sayed, I, El Tantawi, M, Elbarazi, I, Elgendy, I, El-Jaafary, S, Elyazar, I, Emmons-Bell, S, Erskine, H, Eskandarieh, S, Esmaeilnejad, S, Esteghamati, A, Estep, K, Etemadi, A, Etisso, A, Fanzo, J, Farahmand, M, Fareed, M, Faridnia, R, Farioli, A, Faro, A, Faruque, M, Farzadfar, F, Fattahi, N, Fazlzadeh, M, Feigin, V, Feldman, R, Fereshtehnejad, S, Fernandes, E, Ferrara, G, Ferrari, A, Ferreira, M, Filip, I, Fischer, F, Fisher, J, Flor, L, Foigt, N, Folayan, M, Fomenkov, A, Force, L, Foroutan, M, Franklin, R, Freitas, M, Fu, W, Fukumoto, T, Furtado, J, Gad, M, Gakidou, E, Gallus, S, Garcia-Basteiro, A, Gardner, W, Geberemariyam, B, Ayalew Gebreslassie, A, Geremew, A, Gershberg Hayoon, A, Gething, P, Ghadimi, M, Ghadiri, K, Ghaffarifar, F, Ghafourifard, M, Ghamari, F, Ghashghaee, A, Ghiasvand, H, Ghith, N, Gholamian, A, Ghosh, R, Gill, P, Ginindza, T, Giussani, G, Gnedovskaya, E, Goharinezhad, S, Gopalani, S, Gorini, G, Goudarzi, H, Goulart, A, Greaves, F, Grivna, M, Grosso, G, Gubari, M, Gugnani, H, Guimaraes, R, Guled, R, Guo, G, Guo, Y, Gupta, R, Gupta, T, Haddock, B, Hafezi-Nejad, N, Hafiz, A, Haj-Mirzaian, A, Hall, B, Halvaei, I, Hamadeh, R, Hamidi, S, Hammer, M, Hankey, G, Haririan, H, Haro, J, Hasaballah, A, Hasan, M, Hasanpoor, E, Hashi, A, Hassanipour, S, Hassankhani, H, Havmoeller, R, Hay, S, Hayat, K, Heidari, G, Heidari-Soureshjani, R, Henrikson, H, Herbert, M, Herteliu, C, Heydarpour, F, Hird, T, Hoek, H, Holla, R, Hoogar, P, Hosgood, H, Hossain, N, Hosseini, M, Hosseinzadeh, M, Hostiuc, M, Hostiuc, S, Househ, M, Hsairi, M, Hsieh, V, Hu, G, Hu, K, Huda, T, Humayun, A, Huynh, C, Hwang, B, Iannucci, V, Ibitoye, S, Ikeda, N, Ikuta, K, Ilesanmi, O, Ilic, I, Ilic, M, Inbaraj, L, Ippolito, H, Iqbal, U, Irvani, S, Irvine, C, Islam, M, Islam, S, Iso, H, Ivers, R, Iwu, C, Iyamu, I, Jaafari, J, Jacobsen, K, Jafari, H, Jafarinia, M, Jahani, M, Jakovljevic, M, Jalilian, F, James, S, Janjani, H, Javaheri, T, Javidnia, J, Jeemon, P, Jenabi, E, Jha, R, Jha, V, Ji, J, Johansson, L, John, O, John-Akinola, Y, Johnson, C, Jonas, J, Joukar, F, Jozwiak, J, Jurisson, M, Kabir, A, Kabir, Z, Kalani, H, Kalani, R, Kalankesh, L, Kalhor, R, Kanchan, T, Kapoor, N, Matin, B, Karch, A, Karim, M, Kassa, G, Katikireddi, S, Kayode, G, Kazemi Karyani, A, Keiyoro, P, Keller, C, Kemmer, L, Kendrick, P, Khalid, N, Khammarnia, M, Khan, E, Khan, M, Khatab, K, Khater, M, Khatib, M, Khayamzadeh, M, Khazaei, S, Kieling, C, Kim, Y, Kimokoti, R, Kisa, A, Kisa, S, Kivimaki, M, Knibbs, L, Knudsen, A, Kocarnik, J, Kochhar, S, Kopec, J, Korshunov, V, Koul, P, Koyanagi, A, Kraemer, M, Krishan, K, Krohn, K, Kromhout, H, Kuate Defo, B, Kumar, G, Kumar, V, Kurmi, O, Kusuma, D, La Vecchia, C, Lal, D, Lalloo, R, Lallukka, T, Lami, F, Landires, I, Lang, J, Langan, S, Larsson, A, Lasrado, S, Lauriola, P, Lazarus, J, Lee, P, Lee, S, Legrand, K, Leigh, J, Leonardi, M, Lescinsky, H, Leung, J, Levi, M, Li, S, Lim, L, Linn, S, Liu, S, Liu, Y, Lo, J, Lopez, A, Lopez, J, Lopukhov, P, Lorkowski, S, Lotufo, P, Lu, A, Lugo, A, Maddison, E, Mahasha, P, Mahdavi, M, Mahmoudi, M, Majeed, A, Maleki, A, Maleki, S, Malekzadeh, R, Malta, D, Mamun, A, Manda, A, Manguerra, H, Mansour-Ghanaei, F, Mansouri, B, Mansournia, M, Mantilla Herrera, A, Maravilla, J, Marks, A, Martin, R, Martini, S, Martins-Melo, F, Masaka, A, Masoumi, S, Mathur, M, Matsushita, K, Maulik, P, Mcalinden, C, Mcgrath, J, Mckee, M, Mehndiratta, M, Mehri, F, Mehta, K, Memish, Z, Mendoza, W, Menezes, R, Mengesha, E, Mereke, A, Mereta, S, Meretoja, A, Meretoja, T, Mestrovic, T, Miazgowski, B, Miazgowski, T, Michalek, I, Miller, T, Mills, E, Mini, G, Miri, M, Mirica, A, Mirrakhimov, E, Mirzaei, H, Mirzaei, M, Mirzaei, R, Mirzaei-Alavijeh, M, Misganaw, A, Mithra, P, Moazen, B, Mohammad, D, Mohammad, Y, Mohammad Gholi Mezerji, N, Mohammadian-Hafshejani, A, Mohammadifard, N, Mohammadpourhodki, R, Mohammed, A, Mohammed, H, Mohammed, J, Mohammed, S, Mokdad, A, Molokhia, M, Monasta, L, Mooney, M, Moradi, G, Moradi, M, Moradi-Lakeh, M, Moradzadeh, R, Moraga, P, Morawska, L, Morgado-Da-Costa, J, Morrison, S, Mosapour, A, Mosser, J, Mouodi, S, Mousavi, S, Khaneghah, A, Mueller, U, Mukhopadhyay, S, Mullany, E, Musa, K, Muthupandian, S, Nabhan, A, Naderi, M, Nagarajan, A, Nagel, G, Naghavi, M, Naghshtabrizi, B, Naimzada, M, Najafi, F, Nangia, V, Nansseu, J, Naserbakht, M, Nayak, V, Negoi, I, Ngunjiri, J, Nguyen, C, Nguyen, H, Nguyen, M, Nigatu, Y, Nikbakhsh, R, Nixon, M, Nnaji, C, Nomura, S, Norrving, B, Noubiap, J, Nowak, C, Nunez-Samudio, V, Oancea, B, Odell, C, Ogbo, F, Oh, I, Okunga, E, Oladnabi, M, Olagunju, A, Olusanya, B, Olusanya, J, Omer, M, Ong, K, Onwujekwe, O, Orpana, H, Ortiz, A, Osarenotor, O, Osei, F, Ostroff, S, Otoiu, A, Otstavnov, N, Otstavnov, S, Overland, S, Owolabi, M, Mahesh, P, Padubidri, J, Palladino, R, Panda-Jonas, S, Pandey, A, Parry, C, Pasovic, M, Pasupula, D, Patel, S, Pathak, M, Patten, S, Patton, G, Toroudi, H, Peden, A, Pennini, A, Pepito, V, Peprah, E, Pereira, D, Pesudovs, K, Pham, H, Phillips, M, Piccinelli, C, Pilz, T, Piradov, M, Pirsaheb, M, Plass, D, Polinder, S, Polkinghorne, K, Pond, C, Postma, M, Pourjafar, H, Pourmalek, F, Poznanska, A, Prada, S, Prakash, V, Pribadi, D, Pupillo, E, Syed, Z, Rabiee, M, Rabiee, N, Radfar, A, Rafiee, A, Raggi, A, Rahman, M, Rajabpour-Sanati, A, Rajati, F, Rakovac, I, Ram, P, Ramezanzadeh, K, Ranabhat, C, Rao, P, Rao, S, Rashedi, V, Rathi, P, Rawaf, D, Rawaf, S, Rawal, L, Rawassizadeh, R, Rawat, R, Razo, C, Redford, S, Reiner, R, Reitsma, M, Remuzzi, G, Renjith, V, Renzaho, A, Resnikoff, S, Rezaei, N, Rezapour, A, Rhinehart, P, Riahi, S, Ribeiro, D, Rickard, J, Rivera, J, Roberts, N, Rodriguez-Ramirez, S, Roever, L, Ronfani, L, Room, R, Roshandel, G, Roth, G, Rothenbacher, D, Rubagotti, E, Rwegerera, G, Sabour, S, Sachdev, P, Saddik, B, Sadeghi, E, Sadeghi, M, Saeedi, R, Saeedi Moghaddam, S, Safari, Y, Safi, S, Safiri, S, Sagar, R, Sahebkar, A, Sajadi, S, Salam, N, Salamati, P, Salem, H, Salem, M, Salimzadeh, H, Salman, O, Salomon, J, Samad, Z, Samadi Kafil, H, Sambala, E, Samy, A, Sanabria, J, Sanchez-Pimienta, T, Santomauro, D, Santos, I, Santos, J, Santric-Milicevic, M, Saraswathy, S, Sarmiento-Suarez, R, Sarrafzadegan, N, Sarveazad, A, Sathian, B, Sathish, T, Sattin, D, Saxena, S, Schaeffer, L, Schiavolin, S, Schlaich, M, Schmidt, M, Schutte, A, Schwebel, D, Schwendicke, F, Senbeta, A, Senthilkumaran, S, Sepanlou, S, Serdar, B, Serre, M, Shadid, J, Shafaat, O, Shahabi, S, Shaheen, A, Shaikh, M, Shalash, A, Shams-Beyranvand, M, Shamsizadeh, M, Sharafi, K, Sheikh, A, Sheikhtaheri, A, Shibuya, K, Shield, K, Shigematsu, M, Shin, J, Shin, M, Shiri, R, Shirkoohi, R, Shuval, K, Siabani, S, Sierpinski, R, Sigfusdottir, I, Sigurvinsdottir, R, Silva, J, Simpson, K, Singh, J, Singh, P, Skiadaresi, E, Skou, S, Skryabin, V, Smith, E, Soheili, A, Soltani, S, Soofi, M, Sorensen, R, Soriano, J, Sorrie, M, Soshnikov, S, Soyiri, I, Spencer, C, Spotin, A, Sreeramareddy, C, Srinivasan, V, Stanaway, J, Stein, C, Stein, D, Steiner, C, Stockfelt, L, Stokes, M, Straif, K, Stubbs, J, Sufiyan, M, Suleria, H, Suliankatchi Abdulkader, R, Sulo, G, Sultan, I, Tabares-Seisdedos, R, Tabb, K, Tabuchi, T, Taherkhani, A, Tajdini, M, Takahashi, K, Takala, J, Tamiru, A, Taveira, N, Tehrani-Banihashemi, A, Temsah, M, Tesema, G, Tessema, Z, Thurston, G, Titova, M, Tohidinik, H, Tonelli, M, Topor-Madry, R, Topouzis, F, Torre, A, Touvier, M, Tovani-Palone, M, Tran, B, Travillian, R, Tsatsakis, A, Tudor Car, L, Tyrovolas, S, Uddin, R, Umeokonkwo, C, Unnikrishnan, B, Upadhyay, E, Vacante, M, Valdez, P, van Donkelaar, A, Vasankari, T, Vasseghian, Y, Veisani, Y, Venketasubramanian, N, Violante, F, Vlassov, V, Vollset, S, Vos, T, Vukovic, R, Waheed, Y, Wallin, M, Wang, Y, Watson, A, Wei, J, Wei, M, Weintraub, R, Weiss, J, Werdecker, A, West, J, Westerman, R, Whisnant, J, Whiteford, H, Wiens, K, Wolfe, C, Wozniak, S, Wu, A, Wu, J, Wulf Hanson, S, Xu, G, Xu, R, Yadgir, S, Yahyazadeh Jabbari, S, Yamagishi, K, Yaminfirooz, M, Yano, Y, Yaya, S, Yazdi-Feyzabadi, V, Yeheyis, T, Yilgwan, C, Yilma, M, Yip, P, Yonemoto, N, Younis, M, Younker, T, Yousefi, B, Yousefi, Z, Yousefinezhadi, T, Yousuf, A, Yu, C, Yusefzadeh, H, Moghadam, T, Zamani, M, Zamanian, M, Zandian, H, Zastrozhin, M, Zhang, Y, Zhang, Z, Zhao, J, Zhao, X, Zhao, Y, Zheng, P, Zhou, M, Ziapour, A, Zimsen, S, Lim, S, Murray, C, GBD 2019 Risk Factors Collaborator, Violante FS, Biosciences, Department of Public Health, Clinicum, Department of Neurosciences, HUS Comprehensive Cancer Center, Environmental Sciences, Sub Foundations&PhilosophyofNaturSc begr, IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Public Health, Bin Sayeed, M. S. B., Caetano Dos Santos, F. L., Camera, L. A., Elyazar, I. R. F., Ayalew Gebreslassie, A. A. A., Ginindza, T. G., Matin, B. K., Morgado-Da-Costa, J., Khaneghah, A. M., Mahesh, P. A., Toroudi, H. P., Syed, Z. Q., Salem, M. R., Skou, S. T., Tovani-Palone, M. R., Tudor Car, L. T., and Moghadam, T. Z.
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Male ,Nutritional Sciences ,Specific risk ,Contaminación del Aire Interior ,030204 cardiovascular system & hematology ,Socioeconomic Factor ,systematic analysis ,Global Health ,Body Mass Index ,Global Burden of Disease ,Health Risk Behavior ,Health Risk Behaviors ,Disease studies ,0302 clinical medicine ,Risk Factors ,METABOLIC RISKS ,030212 general & internal medicine ,11 Medical and Health Sciences ,Factores de Riesgo ,2. Zero hunger ,education.field_of_study ,Public health ,Injuries ,Public Health, Global Health, Social Medicine and Epidemiology ,General Medicine ,GBD ,risck factors ,attributable burden of disease ,3142 Public health care science, environmental and occupational health ,3. Good health ,Relative risk ,Environmental health ,Health ,Hypertension ,Global Burden of Diseases, Injuries, Risk Factors ,A990 Medicine and Dentistry not elsewhere classified ,Female ,Leading risk factors ,Global Health Metrics ,Cohort study ,Human ,medicine.medical_specialty ,Substance-Related Disorders ,Population ,UNITED-STATES ,Risk Assessment ,DIET ,ITC-HYBRID ,03 medical and health sciences ,Life Expectancy ,MORTALITY ,DISABILITY ,POLLUTION ,CLUSTERS ,SDG 3 - Good Health and Well-being ,General & Internal Medicine ,medicine ,Humans ,Global Burden of Disease Study ,Risk factor ,education ,Global burden ,business.industry ,Risk Factor ,Malnutrition ,Klinisk medicin ,Global Burden of Diseases ,Environmental Exposure ,medicine.disease ,Enfermedades ,purl.org/pe-repo/ocde/ford#3.02.00 [https] ,Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi ,Years of potential life lost ,Socioeconomic Factors ,Risk factors ,Disease study ,Hyperglycemia ,ITC-ISI-JOURNAL-ARTICLE ,NA ,Clinical Medicine ,business ,RA - Abstract
Background Rigorous analysis of levels and trends in exposure to leading risk factors and quantification of their effect on human health are important to identify where public health is making progress and in which cases current efforts are inadequate. The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 provides a standardised and comprehensive assessment of the magnitude of risk factor exposure, relative risk, and attributable burden of disease. Methods GBD 2019 estimated attributable mortality, years of life lost (YLLs), years of life lived with disability (YLDs), and disability-adjusted life-years (DALYs) for 87 risk factors and combinations of risk factors, at the global level, regionally, and for 204 countries and territories. GBD uses a hierarchical list of risk factors so that specific risk factors (eg, sodium intake), and related aggregates (eg, diet quality), are both evaluated. This method has six analytical steps. (1) We included 560 risk-outcome pairs that met criteria for convincing or probable evidence on the basis of research studies. 12 risk-outcome pairs included in GBD 2017 no longer met inclusion criteria and 47 risk-outcome pairs for risks already included in GBD 2017 were added based on new evidence. (2) Relative risks were estimated as a function of exposure based on published systematic reviews, 81 systematic reviews done for GBD 2019, and meta-regression. (3) Levels of exposure in each age-sex-location-year included in the study were estimated based on all available data sources using spatiotemporal Gaussian process regression, DisMod-MR 2.1, a Bayesian meta-regression method, or alternative methods. (4) We determined, from published trials or cohort studies, the level of exposure associated with minimum risk, called the theoretical minimum risk exposure level. (5) Attributable deaths, YLLs, YLDs, and DALYs were computed by multiplying population attributable fractions (PAFs) by the relevant outcome quantity for each age-sex-location-year. (6) PAFs and attributable burden for combinations of risk factors were estimated taking into account mediation of different risk factors through other risk factors. Across all six analytical steps, 30 652 distinct data sources were used in the analysis. Uncertainty in each step of the analysis was propagated into the final estimates of attributable burden. Exposure levels for dichotomous, polytomous, and continuous risk factors were summarised with use of the summary exposure value to facilitate comparisons over time, across location, and across risks. Because the entire time series from 1990 to 2019 has been re-estimated with use of consistent data and methods, these results supersede previously published GBD estimates of attributable burden. Findings The largest declines in risk exposure from 2010 to 2019 were among a set of risks that are strongly linked to social and economic development, including household air pollution; unsafe water, sanitation, and handwashing; and child growth failure. Global declines also occurred for tobacco smoking and lead exposure. The largest increases in risk exposure were for ambient particulate matter pollution, drug use, high fasting plasma glucose, and high body-mass index. In 2019, the leading Level 2 risk factor globally for attributable deaths was high systolic blood pressure, which accounted for 10.8 million (95% uncertainty interval [UI] 9.51-12.1) deaths (19.2% [16.9-21.3] of all deaths in 2019), followed by tobacco (smoked, second-hand, and chewing), which accounted for 8.71 million (8.12-9.31) deaths (15.4% [14.6-16.2] of all deaths in 2019). The leading Level 2 risk factor for attributable DALYs globally in 2019 was child and maternal malnutrition, which largely affects health in the youngest age groups and accounted for 295 million (253-350) DALYs (11.6% [10.3-13.1] of all global DALYs that year). The risk factor burden varied considerably in 2019 between age groups and locations. Among children aged 0-9 years, the three leading detailed risk factors for attributable DALYs were all related to malnutrition. Iron deficiency was the leading risk factor for those aged 10-24 years, alcohol use for those aged 25-49 years, and high systolic blood pressure for those aged 50-74 years and 75 years and older. Interpretation Overall, the record for reducing exposure to harmful risks over the past three decades is poor. Success with reducing smoking and lead exposure through regulatory policy might point the way for a stronger role for public policy on other risks in addition to continued efforts to provide information on risk factor harm to the general public. Copyright (C) 2020 The Author(s). Published by Elsevier Ltd.
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- 2020
3. Long-term exposure to several constituents and sources of PM 2.5 is associated with incidence of upper aerodigestive tract cancers but not gastric cancer: Results from the large pooled European cohort of the ELAPSE project.
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Weinmayr G, Chen J, Jaensch A, Skodda L, Rodopoulou S, Strak M, de Hoogh K, Andersen ZJ, Bellander T, Brandt J, Fecht D, Forastiere F, Gulliver J, Hertel O, Hoffmann B, Hvidtfeldt UA, Katsouyanni K, Ketzel M, Leander K, Magnusson PKE, Pershagen G, Rizzuto D, Samoli E, Severi G, Stafoggia M, Tjønneland A, Vermeulen R, Wolf K, Zitt E, Brunekreef B, Thurston G, Hoek G, Raaschou-Nielsen O, and Nagel G
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- Humans, Particulate Matter analysis, Incidence, Environmental Exposure analysis, Stomach Neoplasms chemically induced, Stomach Neoplasms epidemiology, Air Pollution analysis, Air Pollutants analysis
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It is unclear whether cancers of the upper aerodigestive tract (UADT) and gastric cancer are related to air pollution, due to few studies with inconsistent results. The effects of particulate matter (PM) may vary across locations due to different source contributions and related PM compositions, and it is not clear which PM constituents/sources are most relevant from a consideration of overall mass concentration alone. We therefore investigated the association of UADT and gastric cancers with PM
2.5 elemental constituents and sources components indicative of different sources within a large multicentre population based epidemiological study. Cohorts with at least 10 cases per cohort led to ten and eight cohorts from five countries contributing to UADT- and gastric cancer analysis, respectively. Outcome ascertainment was based on cancer registry data or data of comparable quality. We assigned home address exposure to eight elemental constituents (Cu, Fe, K, Ni, S, Si, V and Zn) estimated from Europe-wide exposure models, and five source components identified by absolute principal component analysis (APCA). Cox regression models were run with age as time scale, stratified for sex and cohort and adjusted for relevant individual and neighbourhood level confounders. We observed 1139 UADT and 872 gastric cancer cases during a mean follow-up of 18.3 and 18.5 years, respectively. UADT cancer incidence was associated with all constituents except K in single element analyses. After adjustment for NO2 , only Ni and V remained associated with UADT. Residual oil combustion and traffic source components were associated with UADT cancer persisting in the multiple source model. No associations were found for any of the elements or source components and gastric cancer incidence. Our results indicate an association of several PM constituents indicative of different sources with UADT but not gastric cancer incidence with the most robust evidence for traffic and residual oil combustion., 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
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4. Portable air cleaner use and biomarkers of inflammation: A systematic review and meta-analysis.
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Wittkopp S, Walzer D, Thorpe L, Roberts T, Xia Y, Gordon T, Thurston G, Brook R, and Newman JD
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Fine particulate matter air pollution (PM
2.5 ) is a major contributor to cardiovascular morbidity and mortality, potentially via increased inflammation. PM2.5 exposure increases inflammatory biomarkers linked to cardiovascular disease, including CRP, IL-6 and TNFα. Portable air cleaners (PACs) reduce individual PM2.5 exposure but evidence is limited regarding whether PACs also reduce inflammatory biomarkers. We performed a systematic review and meta-analysis of trials evaluating the use of PACs to reduce PM2.5 exposure and inflammatory biomarker concentrations. We identified English-language articles of randomized sham-controlled trials evaluating high efficiency particulate air filters in non-smoking, residential settings measuring serum CRP, IL-6 and TNFα before and after active versus sham filtration, and performed meta-analysis on the extracted modeled percent change in biomarker concentration across studies. Of 487 articles identified, we analyzed 14 studies enrolling 778 participants that met inclusion criteria. These studies showed PACs reduced PM2.5 by 61.5 % on average. Of the 14 included studies, 10 reported CRP concentrations in 570 participants; these showed active PAC use was associated with 7 % lower CRP (95 % CI: -14 % to 0.0 %, p = 0.05). Nine studies of IL-6, with 379 participants, showed active PAC use was associated with 13 % lower IL-6 (95 % CI: [-23 %, -3 %], p = 0.009). Six studies, with 269 participants, reported TNF-α and demonstrated no statistical evidence of difference between active and sham PAC use. Portable air cleaners that reduce PM2.5 exposure can decrease concentrations of inflammatory biomarkers associated with cardiovascular disease. Additional studies are needed to evaluate clinical outcomes and other biomarkers., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Jonathan D. Newman reports financial support was provided by National Heart Lung and Blood Institute.- Published
- 2022
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5. Application of data science methods to identify school and home risk factors for asthma and allergy-related symptoms among children in New York.
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Deng X, Thurston G, Zhang W, Ryan I, Jiang C, Khwaja H, Romeiko X, Marks T, Ye B, Qu Y, and Lin S
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- Child, Data Science, Environmental Exposure, Humans, New York epidemiology, Risk Factors, Schools, Air Pollution, Indoor, Asthma epidemiology
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Objectives: Few studies have comprehensively assessed multiple environmental exposures affecting children's health. This study applied machine-learning methods to evaluate how indoor environmental conditions at home and school contribute to asthma and allergy-related symptoms., Methods: We randomly selected 10 public schools representing different socioeconomic statuses in New York State (2017-2019) and distributed questionnaires to students to collect health status and home-and school-environmental exposures. Indoor air quality was measured at school, and ambient particle exposures (PM
2.5 and components) were measured using real-time personal monitors for 48 h. We used random forest model to identify the most important risk factors for asthma and allergy-related symptoms, and decision tree for visualizing the inter-relationships among the multiple risk factors with the health outcomes., Results: The top contributing factors identified for asthma were family rhinitis history (relative importance: 10.40%), plant pollen trigger (5.48%); bedroom carpet (3.58%); environmental tobacco smoke (ETS) trigger symptom (2.98%); and ETS exposure (2.56%). For allergy-related symptoms, plant pollen trigger (10.88%), higher paternal education (7.33%), bedroom carpet (5.28%), family rhinitis history (4.78%), and higher maternal education (4.25%) were the strongest contributing factors. Conversely, primary heating with hot water radiator was negatively (-6.86%) associated with asthma symptoms. Younger children (<9 years old) with family history of rhinitis and carpeting in the bedroom were the prominent combined risk factors for asthma. Children jointly exposed to pollen, solvents, and carpeting in their home tended to have greater risks of allergy-related symptoms, even without family history of rhinitis., Conclusion: Family rhinitis history, bedroom carpet, and pollen triggers were the most important risk factors for both asthma and allergy-related symptoms. Our new findings included that hot-water radiator was related to reduced asthma symptoms, and the combination of young age, rhinitis history, and bedroom carpeting was related to increased asthma symptoms. Further studies are needed to confirm our findings., Competing Interests: Declaration of competing interest The authors declare that they have no competing interests regarding the publication of this manuscript., (Copyright © 2021 Elsevier B.V. All rights reserved.)- Published
- 2021
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6. A land use regression model of nitrogen dioxide and fine particulate matter in a complex urban core in Lanzhou, China.
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Jin L, Berman JD, Warren JL, Levy JI, Thurston G, Zhang Y, Xu X, Wang S, Zhang Y, and Bell ML
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- China, Cities, Environmental Monitoring, Air Pollutants, Air Pollution statistics & numerical data, Nitrogen Dioxide analysis, Particulate Matter analysis
- Abstract
Background: Land use regression (LUR) models have been widely used to estimate air pollution exposures at high spatial resolution. However, few LUR models were developed for rapidly developing urban cores, which have substantially higher densities of population and built-up areas than the surrounding areas within a city's administrative boundary. Further, few studies incorporated vertical variations of air pollution in exposure assessment, which might be important to estimate exposures for people living in high-rise buildings., Objective: A LUR model was developed for the urban core of Lanzhou, China, along with a model of vertical concentration gradients in high-rise buildings., Methods: In each of four seasons in 2016-2017, NO
2 was measured using Ogawa badges for 2 weeks at 75 ground-level sites. PM2.5 was measured using DataRAM for shorter time intervals at a subset (N = 38) of the 75 sites. Vertical profile measurements were conducted on 9 stories at 2 high-rise buildings (N = 18), with one building facing traffic and another facing away from traffic. The average seasonal concentrations of NO2 and PM2.5 at ground level were regressed against spatial predictors, including elevation, population, road network, land cover, and land use. The vertical variations were investigated and linked to ground-level predictions with exponential models., Results: We developed robust LUR models at the ground level for estimated annual averages of NO2 (R2 : 0.71, adjusted R2 : 0.67, and Leave-One-Out Cross Validation (LOOCV) R2 : 0.64) and PM2.5 (R2 : 0.77, adjusted R2 : of 0.73, and LOOCV R2 : 0.67) in the urban core of Lanzhou, China. The LUR models for the estimated seasonal averages of NO2 showed similar patterns. Vertical variation of NO2 and PM2.5 differed by windows orientation with respect to traffic, by season or by time of a day. Vertical variation functions incorporated the ground-level LUR predictions, in a form that could allow for exposure assessment in future epidemiological investigations., Conclusions: Ground-level NO2 and PM2.5 showed substantial spatial variations, explained by traffic and land use patterns. Further, vertical variation of air pollution levels is significant under certain conditions, suggesting that exposure misclassification could occur with traditional LUR that ignores vertical variation. More studies are needed to fully characterize three-dimensional concentration patterns to accurately estimate air pollution exposures for residents in high-rise buildings, but our LUR models reinforce that concentration heterogeneity is not captured by the limited government monitors in the Lanzhou urban area., (Copyright © 2019 Elsevier Inc. All rights reserved.)- Published
- 2019
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7. Deliberating performance targets workshop: Potential paths for emerging PM 2.5 and O 3 air sensor progress.
- Author
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Williams R, Duvall R, Kilaru V, Hagler G, Hassinger L, Benedict K, Rice J, Kaufman A, Judge R, Pierce G, Allen G, Bergin M, Cohen RC, Fransioli P, Gerboles M, Habre R, Hannigan M, Jack D, Louie P, Martin NA, Penza M, Polidori A, Subramanian R, Ray K, Schauer J, Seto E, Thurston G, Turner J, Wexler AS, and Ning Z
- Abstract
The United States Environmental Protection Agency held an international two-day workshop in June 2018 to deliberate possible performance targets for non-regulatory fine particulate matter (PM
2.5 ) and ozone (O3 ) air sensors. The need for a workshop arose from the lack of any market-wide manufacturer requirement for Ozone documented sensor performance evaluations, the lack of any independent third party or government-based sensor performance certification program, and uncertainty among all users as to the general usability of air sensor data. A multi-sector subject matter expert panel was assembled to facilitate an open discussion on these issues with multiple stakeholders. This summary provides an overview of the workshop purpose, key findings from the deliberations, and considerations for future actions specific to sensors. Important findings concerning PM2.5 and O3 sensors included the lack of consistent performance indicators and statistical metrics as well as highly variable data quality requirements depending on the intended use. While the workshop did not attempt to yield consensus on any topic, a key message was that a number of possible future actions would be beneficial to all stakeholders regarding sensor technologies. These included documentation of best practices, sharing quality assurance results along with sensor data, and the development of a common performance target lexicon, performance targets, and test protocols.- Published
- 2019
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8. Angiopoietin-2-driven vascular remodeling in airway inflammation.
- Author
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Tabruyn SP, Colton K, Morisada T, Fuxe J, Wiegand SJ, Thurston G, Coyle AJ, Connor J, and McDonald DM
- Subjects
- Angiopoietin-2 genetics, Angiopoietin-2 immunology, Angiopoietin-2 metabolism, Animals, Blood Vessels metabolism, Inflammation genetics, Inflammation metabolism, Male, Mice, Mice, Inbred C57BL, Mycoplasma Infections complications, Mycoplasma Infections genetics, Mycoplasma Infections metabolism, Mycoplasma pulmonis physiology, Neovascularization, Physiologic physiology, Pneumonia etiology, Pneumonia genetics, Pneumonia metabolism, Pneumonia pathology, Receptor Protein-Tyrosine Kinases antagonists & inhibitors, Receptor Protein-Tyrosine Kinases metabolism, Receptor Protein-Tyrosine Kinases physiology, Receptor, TIE-2, Respiratory System metabolism, Respiratory System pathology, Respiratory Tract Diseases metabolism, Respiratory Tract Diseases pathology, Angiopoietin-2 physiology, Blood Vessels physiology, Neovascularization, Physiologic genetics, Respiratory System blood supply, Respiratory Tract Diseases genetics
- Abstract
Vascular remodeling is a feature of chronic inflammation during which capillaries transform into venules that expand the region of the vasculature in which leakage and leukocyte emigration both occur. Recently, we found that angiopoietin/Tie2 receptor signaling drives the transformation of capillaries into venules at an early stage of the sustained inflammatory response in the airways of mice infected with Mycoplasma pulmonis. However, the precise contributions of both angiopoietin-1 (Ang1) and angiopoietin-2 (Ang2) are not clear. In this study, we sought to determine the contribution of Ang2 to this vascular remodeling. Ang2 mRNA expression levels increased and phosphorylated Tie2 immunoreactivity in mucosal blood vessels decreased, indicative of diminished receptor signaling after infection. Selective inhibition of Ang2 throughout the infection by administration of either of two distinct function-blocking antibodies reduced the suppression of Tie2 phosphorylation and decreased the remodeling of mucosal capillaries into venules, the amount of leukocyte influx, and disease severity. These findings are consistent with Ang2 acting as an antagonist of Tie2 receptors and the reduction of Tie2 phosphorylation in endothelial cells rendering the vasculature more responsive to cytokines that promote both vascular remodeling and the consequences of inflammation after M. pulmonis infection. By blocking such changes, Ang2 inhibitors may prove beneficial in the treatment of sustained inflammation in which vascular remodeling, leakage, and leukocyte influx contribute to its pathophysiology.
- Published
- 2010
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9. Angiopoietin/Tie2 signaling transforms capillaries into venules primed for leukocyte trafficking in airway inflammation.
- Author
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Fuxe J, Lashnits E, O'Brien S, Baluk P, Tabruyn SP, Kuhnert F, Kuo C, Thurston G, and McDonald DM
- Subjects
- Adenoviridae metabolism, Animals, Biological Transport, Intercellular Adhesion Molecule-1 biosynthesis, Mice, Mice, Inbred C57BL, Mycoplasma pulmonis metabolism, Venules metabolism, Angiopoietin-1 metabolism, Capillaries metabolism, Inflammation, Leukocytes cytology, Receptor, TIE-2 metabolism, Signal Transduction, Vascular Endothelial Growth Factor A metabolism
- Abstract
Vascular endothelial growth factor (VEGF) is a key angiogenic factor in tumors, but less is known about what drives vascular remodeling in inflammation, where plasma leakage and leukocyte influx are prominent features. In chronic airway inflammation in mice infected by the bacterium Mycoplasma pulmonis (M. pulmonis), the segment of the microvasculature that supports leukocyte adhesion and migration expands through remodeling of capillaries into vessels with features of venules. Here, we report that the angiopoietin/Tie2 pathway is an essential driving force for capillary remodeling into venules in M. pulmonis-infected mouse airways. Similar to M. pulmonis infection, systemic overexpression of angiopoietin-1 (Ang1) resulted in remodeling of airway capillaries into venular-like vessels that expressed venous markers like P-selectin, ICAM-1, and EphB4 and were sites of leukocyte adhesion during lipopolysaccharide-induced acute inflammation. Ang1 and Ang2 protein increased in M. pulmonis-infected mouse airways but came from different cellular sources: Ang1 was expressed in infiltrating neutrophils and Ang2 in endothelial cells. Indeed, systemic administration of soluble Tie2 inhibited capillary remodeling, induction of venous markers, and leukocyte influx in M. pulmonis-infected mouse airways. Together, these findings suggest that blockade of the Ang/Tie2 pathway may represent a therapeutic approach in airway inflammation.
- Published
- 2010
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10. Expression of vascular notch ligand delta-like 4 and inflammatory markers in breast cancer.
- Author
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Jubb AM, Soilleux EJ, Turley H, Steers G, Parker A, Low I, Blades J, Li JL, Allen P, Leek R, Noguera-Troise I, Gatter KC, Thurston G, and Harris AL
- Subjects
- Adaptor Proteins, Signal Transducing, Aged, Calcium-Binding Proteins, Cell Line, Tumor, Disease-Free Survival, Endothelium pathology, Female, Humans, Immunohistochemistry, In Situ Hybridization, Inflammation, Middle Aged, Prognosis, Breast pathology, Breast Neoplasms pathology, Hemangiosarcoma pathology, Intercellular Signaling Peptides and Proteins biosynthesis, Intercellular Signaling Peptides and Proteins physiology
- Abstract
Delta-like ligand 4 (Dll4) is a Notch ligand that is predominantly expressed in the endothelium. Evidence from xenografts suggests that inhibiting Dll4 may overcome resistance to antivascular endothelial growth factor therapy. The aims of this study were to characterize the expression of Dll4 in breast cancer and assess whether it is associated with inflammatory markers and prognosis. We examined 296 breast adenocarcinomas and 38 ductal carcinoma in situ tissues that were represented in tissue microarrays. Additional whole sections representing 10 breast adenocarcinomas, 10 normal breast tissues, and 16 angiosarcomas were included. Immunohistochemistry was then performed by using validated antibodies against Dll4, CD68, CD14, Dendritic Cell-Specific Intercellular adhesion molecule-3-Grabbing Non-integrin (DC-SIGN), CD123, neutrophil elastase, CD31, and carbonic anhydrase 9. Dll4 was selectively expressed by intratumoral endothelial cells in 73% to 100% of breast adenocarcinomas, 18% of in situ ductal carcinomas, and all lactating breast cases, but not normal nonlactating breast. High intensity of endothelial Dll4 expression was a statistically significant adverse prognostic factor in univariate (P = 0.002 and P = 0.01) and multivariate analyses (P = 0.03 and P = 0.04) of overall survival and relapse-free survival, respectively. Among the inflammatory markers, only CD68 and DC-SIGN were significant prognostic factors in univariate (but not multivariate) analyses of overall survival (P = 0.01 and 0.002, respectively). In summary, Dll4 was expressed by endothelium associated with breast cancer cells. In these retrospective subset analyses, endothelial Dll4 expression was a statistically significant multivariate prognostic factor.
- Published
- 2010
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11. Public health benefits of strategies to reduce greenhouse-gas emissions: health implications of short-lived greenhouse pollutants.
- Author
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Smith KR, Jerrett M, Anderson HR, Burnett RT, Stone V, Derwent R, Atkinson RW, Cohen A, Shonkoff SB, Krewski D, Pope CA 3rd, Thun MJ, and Thurston G
- Subjects
- Global Warming, United States, Carbon toxicity, Environmental Pollutants toxicity, Greenhouse Effect prevention & control, Ozone toxicity, Public Health, Sulfates toxicity
- Abstract
In this report we review the health effects of three short-lived greenhouse pollutants-black carbon, ozone, and sulphates. We undertook new meta-analyses of existing time-series studies and an analysis of a cohort of 352,000 people in 66 US cities during 18 years of follow-up. This cohort study provides estimates of mortality effects from long-term exposure to elemental carbon, an indicator of black carbon mass, and evidence that ozone exerts an independent risk of mortality. Associations among these pollutants make drawing conclusions about their individual health effects difficult at present, but sulphate seems to have the most robust effects in multiple-pollutant models. Generally, the toxicology of the pure compounds and their epidemiology diverge because atmospheric black carbon, ozone, and sulphate are associated and could interact with related toxic species. Although sulphate is a cooling agent, black carbon and ozone could together exert nearly half as much global warming as carbon dioxide. The complexity of these health and climate effects needs to be recognised in mitigation policies., (Copyright 2009 Elsevier Ltd. All rights reserved.)
- Published
- 2009
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12. VEGF-mediated cross-talk within the neonatal murine thymus.
- Author
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Cuddihy AR, Ge S, Zhu J, Jang J, Chidgey A, Thurston G, Boyd R, and Crooks GM
- Subjects
- Animals, Capillaries growth & development, Cell Count, Endothelium, Vascular drug effects, Epithelial Cells drug effects, Gene Expression Regulation, Developmental, Lymphocytes, Null immunology, Mice, Mice, Inbred C57BL, Neovascularization, Physiologic physiology, Pericytes ultrastructure, Reverse Transcriptase Polymerase Chain Reaction, Specific Pathogen-Free Organisms, Thymus Gland blood supply, Thymus Gland cytology, Thymus Gland growth & development, Vascular Endothelial Growth Factor A biosynthesis, Vascular Endothelial Growth Factor A genetics, Vascular Endothelial Growth Factor Receptor-2 biosynthesis, Vascular Endothelial Growth Factor Receptor-2 genetics, Animals, Newborn physiology, Endothelium, Vascular metabolism, Epithelial Cells metabolism, Thymus Gland physiology, Vascular Endothelial Growth Factor A physiology, Vascular Endothelial Growth Factor Receptor-2 physiology
- Abstract
Although the mechanisms of cross-talk that regulate the hematopoietic and epithelial compartments of the thymus are well established, the interactions of these compartments with the thymic endothelium have been largely ignored. Current understanding of the thymic vasculature is based on studies of adult thymus. We show that the neonatal period represents a unique phase of thymic growth and differentiation, marked by endothelium that is organized as primitive, dense networks of capillaries dependent on vascular endothelial growth factor (VEGF). VEGF dependence in neonates is mediated by significantly higher levels of both VEGF production and endothelial VEGF receptor 2 (VEGF-R2) expression than in the adult thymus. VEGF is expressed locally in the neonatal thymus by immature, CD4(-)CD8(-) "double negative" (DN) thymocytes and thymic epithelium. Relative to adult thymus, the neonatal thymus has greater thymocyte proliferation, and a predominance of immature thymocytes and cortical thymic epithelial cells (cTECs). Inhibition of VEGF signaling during the neonatal period results in rapid loss of the dense capillaries in the thymus and a marked reduction in the number of thymocytes. These data demonstrate that, during the early postnatal period, VEGF mediates cross-talk between the thymocyte and endothelial compartments of the thymus.
- Published
- 2009
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13. Angiopoietin-1 promotes lymphatic sprouting and hyperplasia.
- Author
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Tammela T, Saaristo A, Lohela M, Morisada T, Tornberg J, Norrmén C, Oike Y, Pajusola K, Thurston G, Suda T, Yla-Herttuala S, and Alitalo K
- Subjects
- Adenoviridae genetics, Animals, Blotting, Northern, Cell Proliferation, Cells, Cultured, Cloning, Molecular, Dermis metabolism, Edema, Endothelium cytology, Epidermal Cells, Genetic Vectors, Humans, Immunohistochemistry, Mice, Mice, Transgenic, Microscopy, Fluorescence, Protein Structure, Tertiary, Receptor, TIE-2 metabolism, Recombinant Fusion Proteins metabolism, Signal Transduction, Up-Regulation, Vascular Endothelial Growth Factor Receptor-3 metabolism, Angiopoietin-1 physiology, Endothelium, Vascular cytology, Hyperplasia pathology, Lymphatic System physiology, Neovascularization, Physiologic
- Abstract
Angiopoietin 1 (Ang1), a ligand for the receptor tyrosine kinase Tie2, regulates the formation and stabilization of the blood vessel network during embryogenesis. In adults, Ang1 is associated with blood vessel stabilization and recruitment of perivascular cells, whereas Ang2 acts to counter these actions. Recent results from gene-targeted mice have shown that Ang2 is also essential for the proper patterning of lymphatic vessels and that Ang1 can be substituted for this function. In order to characterize the effects of the angiopoietins on lymphatic vessels, we employed viral vectors for overexpression of Ang1 in adult mouse tissues. We found that Ang1 activated lymphatic vessel endothelial proliferation, vessel enlargement, and generation of long endothelial cell filopodia that eventually fused, leading to new sprouts and vessel development. Cutaneous lymphatic hyperplasia was also detected in transgenic mice expressing Ang1 in the basal epidermal cells. Tie2 was expressed in the lymphatic endothelial cells and Ang1 stimulation of these cells resulted in up-regulation of vascular endothelial growth factor receptor 3 (VEGFR-3). Furthermore, a soluble form of VEGFR-3 inhibited the observed lymphatic sprouting. Our results reinforce the concept that Ang1 therapy may be useful in settings of tissue edema.
- Published
- 2005
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14. Inhibition of vascular endothelial growth factor (VEGF) signaling in cancer causes loss of endothelial fenestrations, regression of tumor vessels, and appearance of basement membrane ghosts.
- Author
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Inai T, Mancuso M, Hashizume H, Baffert F, Haskell A, Baluk P, Hu-Lowe DD, Shalinsky DR, Thurston G, Yancopoulos GD, and McDonald DM
- Subjects
- Animals, Basement Membrane pathology, Basement Membrane ultrastructure, Endothelium, Vascular pathology, Endothelium, Vascular ultrastructure, Fluorescein-5-isothiocyanate, Fluorescent Dyes, Immunohistochemistry, Lectins metabolism, Lung Neoplasms blood supply, Lung Neoplasms pathology, Lung Neoplasms ultrastructure, Mice, Mice, Inbred C57BL, Mice, Transgenic, Microscopy, Confocal, Microscopy, Electron, Microscopy, Electron, Scanning, Neoplasms pathology, Neoplasms ultrastructure, Vascular Endothelial Growth Factor A pharmacology, Basement Membrane drug effects, Endothelium, Vascular drug effects, Neoplasms blood supply, Neovascularization, Pathologic drug therapy, Signal Transduction drug effects, Vascular Endothelial Growth Factor A antagonists & inhibitors
- Abstract
Angiogenesis inhibitors are receiving increased attention as cancer therapeutics, but little is known of the cellular effects of these inhibitors on tumor vessels. We sought to determine whether two agents, AG013736 and VEGF-Trap, that inhibit vascular endothelial growth factor (VEGF) signaling, merely stop angiogenesis or cause regression of existing tumor vessels. Here, we report that treatment with these inhibitors caused robust and early changes in endothelial cells, pericytes, and basement membrane of vessels in spontaneous islet-cell tumors of RIP-Tag2 transgenic mice and in subcutaneously implanted Lewis lung carcinomas. Strikingly, within 24 hours, endothelial fenestrations in RIP-Tag2 tumors disappeared, vascular sprouting was suppressed, and patency and blood flow ceased in some vessels. By 7 days, vascular density decreased more than 70%, and VEGFR-2 and VEGFR-3 expression was reduced in surviving endothelial cells. Vessels in Lewis lung tumors, which lacked endothelial fenestrations, showed less regression. In both tumors, pericytes did not degenerate to the same extent as endothelial cells, and those on surviving tumor vessels acquired a more normal phenotype. Vascular basement membrane persisted after endothelial cells degenerated, providing a ghost-like record of pretreatment vessel number and location and a potential scaffold for vessel regrowth. The potent anti-vascular action observed is evidence that VEGF signaling inhibitors do more than stop angiogenesis. Early loss of endothelial fenestrations in RIP-Tag2 tumors is a clue that vessel phenotype may be predictive of exceptional sensitivity to these inhibitors.
- Published
- 2004
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15. The Tie-2 ligand angiopoietin-2 is stored in and rapidly released upon stimulation from endothelial cell Weibel-Palade bodies.
- Author
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Fiedler U, Scharpfenecker M, Koidl S, Hegen A, Grunow V, Schmidt JM, Kriz W, Thurston G, and Augustin HG
- Subjects
- Angiopoietin-2 genetics, Carcinogens pharmacology, Cells, Cultured, Endothelium, Vascular cytology, Endothelium, Vascular drug effects, Gene Expression, Humans, Ligands, Muscle, Smooth, Vascular cytology, P-Selectin metabolism, Tetradecanoylphorbol Acetate pharmacology, Umbilical Arteries cytology, Umbilical Veins cytology, Angiopoietin-2 metabolism, Endothelium, Vascular metabolism, Receptor, TIE-2 metabolism, Weibel-Palade Bodies metabolism
- Abstract
The angiopoietins Ang-1 and Ang-2 have been identified as ligands with opposing functions of the receptor tyrosine kinase Tie-2 regulating endothelial cell survival and vascular maturation. Ang-1 acts in a paracrine agonistic manner, whereas Ang-2 appears to act primarily as an autocrine antagonistic regulator. To shed further light on the complexity of autocrine/paracrine agonistic/antagonistic functions of the angiopoietin/Tie-2 system, we have studied Ang-2 synthesis and secretion in different populations of wild-type and retrovirally Ang-2-transduced endothelial cells. Endogenous and overexpressed endothelial cell Ang-2 is expressed in a characteristic granular pattern indicative of a cytoplasmic storage granule. Light and electron microscopic double staining revealed Ang-2 colocalization with von Willebrand factor, identifying Ang-2 as a Weibel-Palade body molecule. Costaining with P-selectin showed that storage of Ang-2 and P-selectin in Weibel-Palade bodies is mutually exclusive. Stored Ang-2 has a long half-life of more than 18 hours and can be secreted within minutes of stimulation (eg, by phorbol 12-myristate 13-acetate [PMA], thrombin, and histamine). Collectively, the identification of Ang-2 as a stored, rapidly available molecule in endothelial cells strongly suggests functions of the angiopoietin/Tie-2 system beyond the established roles during angiogenesis likely to be involved in rapid vascular homeostatic reactions such as inflammation and coagulation.
- Published
- 2004
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16. World Trade Center cough.
- Author
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Chen LC and Thurston G
- Subjects
- Humans, New York City, Air Pollutants adverse effects, Cough etiology, Dust, Rescue Work, Terrorism
- Published
- 2002
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17. Time course of endothelial cell proliferation and microvascular remodeling in chronic inflammation.
- Author
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Ezaki T, Baluk P, Thurston G, La Barbara A, Woo C, and McDonald DM
- Subjects
- Animals, Body Weight, Capillary Permeability, Cell Adhesion, Cell Division, Chronic Disease, DNA biosynthesis, Inflammation immunology, Inflammation microbiology, Kinetics, Leukocytes immunology, Lung blood supply, Male, Mice, Mice, Inbred C3H, Mycoplasma Infections immunology, Neovascularization, Pathologic immunology, Neovascularization, Pathologic microbiology, Phenotype, Respiratory Tract Infections immunology, Endothelium, Vascular pathology, Inflammation pathology, Microcirculation pathology, Mycoplasma Infections pathology, Neovascularization, Pathologic pathology, Respiratory Tract Infections pathology
- Abstract
Angiogenesis and vascular remodeling are features of many chronic inflammatory diseases. When diseases evolve slowly, the accompanying changes in the microvasculature would seem to be similarly gradual. Here we report that the rate of endothelial cell proliferation and the size of blood vessels increases rapidly after the onset of an infection that leads to chronic inflammatory airway disease. In C3H mice inoculated with Mycoplasma pulmonis, the tracheal microvasculature, made visible by perfusion of Lycopersicon esculentum lectin, rapidly enlarged from 4 to 7 days after infection and then plateaued. Diameters of arterioles, capillaries, and venules increased on average 148, 214, and 74%, respectively. Endothelial cell proliferation, measured by bromodeoxyuridine (BrdU) labeling, peaked at 5 days (18 times the pathogen-free value), declined sharply until day 9, but remained at approximately 3 times the pathogen-free value for at least 28 days. Remodeled capillaries and venules were sites of focal plasma leakage and extensive leukocyte adherence. Most systemic manifestations of the infection occurred well after the peak of endothelial proliferation, and the humoral immune response to M. pulmonis was among the latest, increasing after 14 days. These data show that endothelial cell proliferation and microvascular remodeling occur at an early stage of chronic airway disease and suggest that the vascular changes precede widespread tissue remodeling.
- Published
- 2001
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18. Openings between defective endothelial cells explain tumor vessel leakiness.
- Author
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Hashizume H, Baluk P, Morikawa S, McLean JW, Thurston G, Roberge S, Jain RK, and McDonald DM
- Subjects
- Animals, Blood Vessels metabolism, Blood Vessels pathology, Female, Male, Mammary Neoplasms, Animal pathology, Mammary Neoplasms, Animal physiopathology, Mice, Microscopy, Electron, Microscopy, Electron, Scanning, Microscopy, Fluorescence, Neoplasm Transplantation, Capillary Permeability, Endothelium, Vascular pathology, Extracellular Space physiology, Mammary Neoplasms, Animal blood supply, Mammary Neoplasms, Animal metabolism
- Abstract
Leakiness of blood vessels in tumors may contribute to disease progression and is key to certain forms of cancer therapy, but the structural basis of the leakiness is unclear. We sought to determine whether endothelial gaps or transcellular holes, similar to those found in leaky vessels in inflammation, could explain the leakiness of tumor vessels. Blood vessels in MCa-IV mouse mammary carcinomas, which are known to be unusually leaky (functional pore size 1.2-2 microm), were compared to vessels in three less leaky tumors and normal mammary glands. Vessels were identified by their binding of intravascularly injected fluorescent cationic liposomes and Lycopersicon esculentum lectin and by CD31 (PECAM) immunoreactivity. The luminal surface of vessels in all four tumors had a defective endothelial monolayer as revealed by scanning electron microscopy. In MCa-IV tumors, 14% of the vessel surface was lined by poorly connected, overlapping cells. The most superficial lining cells, like endothelial cells, had CD31 immunoreactivity and fenestrae with diaphragms, but they had a branched phenotype with cytoplasmic projections as long as 50 microm. Some branched cells were separated by intercellular openings (mean diameter 1.7 microm; range, 0.3-4.7 microm). Transcellular holes (mean diameter 0.6 microm) were also present but were only 8% as numerous as intercellular openings. Some CD31-positive cells protruded into the vessel lumen; others sprouted into perivascular tumor tissue. Tumors in RIP-Tag2 mice had, in addition, tumor cell-lined lakes of extravasated erythrocytes. We conclude that some tumor vessels have a defective cellular lining composed of disorganized, loosely connected, branched, overlapping or sprouting endothelial cells. Openings between these cells contribute to tumor vessel leakiness and may permit access of macromolecular therapeutic agents to tumor cells.
- Published
- 2000
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19. Endothelial cell heterogeneity in venules of mouse airways induced by polarized inflammatory stimulus.
- Author
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Murphy TJ, Thurston G, Ezaki T, and McDonald DM
- Subjects
- Animals, Cell Adhesion physiology, Cell Adhesion Molecules metabolism, Cell Division physiology, Chronic Disease, Endothelium, Vascular metabolism, Endothelium, Vascular microbiology, Leukocytes physiology, Male, Mice, Mice, Inbred C3H, Microscopy, Electron, Mycoplasma Infections metabolism, Trachea microbiology, Vasculitis metabolism, Vasculitis pathology, Venules metabolism, Venules microbiology, Venules pathology, Endothelium, Vascular pathology, Mycoplasma Infections pathology, Trachea blood supply, Vasculitis microbiology
- Abstract
We sought to determine whether the changes in microvascular endothelial cells (EC) caused by a polarized chronic inflammatory stimulus depend on proximity to the stimulus. C3H mice were infected with Mycoplasma pulmonis, which attaches to the airway epithelium and creates a polarized inflammatory stimulus across the airway wall. At 1, 2, or 4 weeks, the tracheal vasculature was stained by perfusion of silver nitrate to mark EC borders or biotinylated Lycopersicon esculentum lectin to label the EC surface and adherent leukocytes. E-selectin immunoreactivity and EC proliferation were also localized. We found that the size, shape, and immunoreactivity for adhesion molecules on EC nearest the airway lumen (subepithelial EC) were different from those on the opposite surface of the same vessels. Subepithelial EC were smaller, more irregular in shape, had greater E-selectin immunoreactivity, and had twice as many adherent leukocytes. In contrast, proliferating EC were uniformly distributed around the vessel circumference. We conclude that the polarized stimulus created by M. pulmonis infection differentially changes the size, shape, and function of EC nearest the airway epithelium. This heterogeneity may result from a gradient of inflammatory mediators that triggers the influx of leukocytes into the airway lumen.
- Published
- 1999
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20. Angiogenesis in mice with chronic airway inflammation: strain-dependent differences.
- Author
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Thurston G, Murphy TJ, Baluk P, Lindsey JR, and McDonald DM
- Subjects
- Animals, Capillary Permeability drug effects, Cell Count, Chronic Disease, Endothelium, Vascular metabolism, Endothelium, Vascular pathology, Evans Blue metabolism, Female, Male, Mice, Mice, Inbred C3H, Mice, Inbred C57BL, Neovascularization, Pathologic genetics, Neovascularization, Pathologic metabolism, Pneumonia, Mycoplasma genetics, Pneumonia, Mycoplasma metabolism, Pneumonia, Mycoplasma pathology, Silver Staining, Species Specificity, Specific Pathogen-Free Organisms, Substance P pharmacology, Trachea metabolism, Trachea pathology, Tracheitis genetics, Tracheitis microbiology, Wheat Germ Agglutinins metabolism, Neovascularization, Pathologic pathology, Trachea blood supply, Tracheitis pathology
- Abstract
Chronic inflammation is associated with blood vessel proliferation and enlargement and changes in vessel phenotype. We sought to determine whether these changes represent different types of angiogenesis and whether they are stimulus dependent. Chronic airway inflammation, produced by infection with Mycoplasma pulmonis, was compared in strains of mice known to be resistant (C57BL/6) or susceptible (C3H). Tracheal vascularity, assessed in whole mounts after Lycopersicon esculentum lectin staining, increased in both strains at 1, 2, 4, and 8 weeks after infection, but the type of vascular remodeling was different. The number of vessels doubled in tracheas of C57BL/6 mice, with corresponding increases of capillaries and venules. In contrast, neither the number nor the length of vessels changed in C3H mice. Instead, vessel diameter and endothelial cell number doubled, and the proportion of venules doubled with a corresponding decrease of capillaries. Although the infection had no effect on baseline plasma leakage, in both strains it potentiated the leakage produced by substance P. We conclude that the same stimulus can result in blood vessel proliferation or enlargement, depending on the host response. Endothelial cells proliferate in both cases, but in one case new capillaries form whereas in the other capillaries convert to venules.
- Published
- 1998
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21. Endothelial gaps and adherent leukocytes in allergen-induced early- and late-phase plasma leakage in rat airways.
- Author
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Baluk P, Bolton P, Hirata A, Thurston G, and McDonald DM
- Subjects
- Animals, Capillary Permeability drug effects, Cell Movement drug effects, Endothelium, Vascular ultrastructure, Indicators and Reagents, Indoles, Leukocytes ultrastructure, Male, Organometallic Compounds, Ovalbumin pharmacology, Rats, Rats, Inbred F344, Rats, Inbred Lew, Rats, Wistar, Silver Staining, Time Factors, Trachea blood supply, Trachea drug effects, Trachea pathology, Trachea ultrastructure, Allergens physiology, Capillary Permeability physiology, Endothelium, Vascular pathology, Hypersensitivity pathology, Leukocytes cytology
- Abstract
Exposure of sensitized individuals to antigen can induce allergic responses in the respiratory tract, manifested by early and late phases of vasodilatation, plasma leakage, leukocyte influx, and bronchoconstriction. Similar responses can occur in the skin, eye, and gastrointestinal tract. The early-phase response involves mast cell mediators and the late-phase response is leukocyte dependent, but the mechanism of leakage is not understood. We sought to identify the leaky blood vessels, to determine whether these vessels contained endothelial gaps, and to analyze the relationship of the gaps to adherent leukocytes, using biotinylated lectins or silver nitrate to stain the cells in situ and Monastral blue as a tracer to quantify plasma leakage. Most of the leakage occurred in postcapillary venules (< 40-microns diameter), whereas most of the leukocyte migration (predominantly neutrophils) occurred in collecting venules. Capillaries and arterioles did not leak. Endothelial gaps were found in the leaky venules, both by silver nitrate staining and by scanning electron microscopy, and 94% of the gaps were distinct from sites of leukocyte adhesion or migration. We conclude that endothelial gaps contribute to both early and late phases of plasma leakage induced by antigen, but most leakage occurs upstream to sites of leukocyte adhesion.
- Published
- 1998
22. The nature and origins of acid summer haze air pollution in metropolitan Toronto, Ontario.
- Author
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Thurston GD, Gorczynski JE Jr, Currie JH, He D, Ito K, Hipfner J, Waldman J, Lioy PJ, and Lippmann M
- Subjects
- Aerosols, Humans, Hydrogen-Ion Concentration, Ontario, Regression Analysis, Seasons, Sulfates analysis, Sulfuric Acids analysis, Acids analysis, Air Pollution analysis, Environmental Monitoring, Urban Health
- Abstract
During July and August of 1986, 1987, and 1988, a field study was conducted of ambient acidic aerosol levels in Toronto, Ontario. Fine particle mass (da < 2.5 microns) samples were collected twice daily at a central-city site for the determination of particulate-phase strong acidity (H+) and sulfate (SO4 =). Two additional H(+)-monitoring sites were concurrently operated during the summers of 1986 and 1987 to examine the spatial variability of H+ within the metropolitan area. During the summer of 1986, a quasi-continuous total sulfate/sulfuric acid analyzer was also deployed to allow a determination of the chemical form of H+. Results indicate that acid aerosol episodes (H+ > or = 100 nmole/m3) did occur in this city during the summer months, and that H+ peaks were well correlated with sulfate peaks. Virtually all of the H+ was found to be present as ammonium bisulfate (NH4HSO4). While H+ concentrations were highly correlated among the three monitoring sites (r = 0.9), the highest H+/SO4 = ratios prevailed during SO4 = episode periods and at the least urbanized site. This latter trend was apparently due to greater neutralization of H+ by local ammonia at the more urbanized sites. Comparisons of day vs night H+/SO4 = ratios, an examination of air mass back-trajectories, and contemporaneous H+ measurements at surrounding sites collectively indicated that transported regional haze air pollution from the United States is a major contributor to the H+ events recorded within Toronto.
- Published
- 1994
- Full Text
- View/download PDF
23. Respiratory hospital admissions and summertime haze air pollution in Toronto, Ontario: consideration of the role of acid aerosols.
- Author
-
Thurston GD, Ito K, Hayes CG, Bates DV, and Lippmann M
- Subjects
- Acids analysis, Aerosols, Air Pollution analysis, Humans, Hydrogen-Ion Concentration, Ontario epidemiology, Ozone adverse effects, Ozone analysis, Regression Analysis, Respiratory Tract Diseases epidemiology, Seasons, Sulfates adverse effects, Sulfates analysis, Temperature, Acids adverse effects, Air Pollution adverse effects, Hospitalization statistics & numerical data, Respiratory Tract Diseases etiology
- Abstract
A study of air pollution and daily hospital admissions for respiratory causes was conducted in Toronto, Ontario. Fine aerosol (da < 2.5 microns) samples were collected daily at a central city site during July and August 1986, 1987, and 1988 and were subsequently extracted and analyzed for daily particulate phase aerosol strong acidity (H+) and sulfates (SO4 =). Daily counts of respiratory admissions to 22 acute care hospitals and daily meteorological and environmental data (e.g. ozone [O3], total suspended particulate matter [TSP], and thoracic particle mass [PM10] were also obtained. Regression analyses indicated that only the O3, H+, and SO4 = associations with respiratory and asthma admissions remained consistently significant after controlling for temperature. Even after excluding days with maximum 1-hr O3 > 120 ppb, O3 was still strongly significant. In the various model specifications considered, the relative particle metric strengths of association with admissions were generally H+ > SO4 = > FP > PM10 > TSP, indicating that particle size and composition are of central importance in defining the adverse human health effects of particulate matter. On average, summertime haze air pollution was associated with 24% of all respiratory admissions (21% with O3, 3% with H+). On peak pollution days, however, aerosol acidity yielded the highest relative risk estimates (e.g., RR = 1.5 at 391 nmole/m3 H+), and summertime haze was associated with roughly half of all respiratory admissions.
- Published
- 1994
- Full Text
- View/download PDF
24. Effects of single- and multiday ozone exposures on respiratory function in active normal children.
- Author
-
Spektor DM, Thurston GD, Mao J, He D, Hayes C, and Lippmann M
- Subjects
- Adolescent, Air Pollutants analysis, Child, Dose-Response Relationship, Drug, Female, Forced Expiratory Flow Rates drug effects, Forced Expiratory Flow Rates physiology, Forced Expiratory Volume drug effects, Forced Expiratory Volume physiology, Humans, Male, Regression Analysis, Respiration drug effects, Spirometry, Time Factors, Vital Capacity drug effects, Vital Capacity physiology, Environmental Exposure, Ozone pharmacology, Respiration physiology
- Abstract
Ventilatory function was measured twice daily on 46 healthy children aged 8-14 years on at least 7 days for each child during a 4-week period at a northwestern New Jersey residential summer camp in 1988. The highest 1-hr O3 concentration was 150 ppb, while the highest 12-hr H+ concentration (as H2SO4) was 18.6 micrograms/m3. The highest temperature-humidity index was 81 degrees F. The regressions of FVC, FEV1, FEF25-75, and PEFR on O3 in the hour preceding the afternoon function measurements yielded slopes essentially the same as those measured on other children at the same camp in 1984. Regressions of the changes in function between the late morning and late afternoon function measurements on average O3 concentration between them produced significant, but somewhat smaller effects, while regressions of morning function on O3 during the previous day indicated small but still significant effects. There were no significant correlations with other measured environmental variables including H+. Based on the results of this study and similar previous studies, we conclude that O3 exposures in ambient air produce greater lung function deficits in active young people in natural settings then does pure O3 in controlled chamber exposure studies because of: (1) longer exposures; (2) potentiation by other factors in the ambient exposures; (3) the persistence of effects from prior day's exposures; and (4) the persistence of a transient response associated with the daily peak of exposure. It follows that projections of likely effects in the real world from controlled chamber exposure studies should either have a large margin of safety, or the judgment of the extent of effects likely to occur among populations should be based directly on the effects observed in field studies.
- Published
- 1991
- Full Text
- View/download PDF
25. Rheology of pharmaceutical systems: oscillatory and steady shear of non-Newtonian viscoelastic liquids.
- Author
-
Thurston GB and Martin A
- Subjects
- Carboxymethylcellulose Sodium, Chemical Phenomena, Chemistry, Pharmaceutical, Chemistry, Physical, Elasticity, Models, Chemical, Viscosity, Rheology
- Abstract
A comparative analysis of oscillatory and steady shear rate measurements was made on carboxymethylcellulose solutions of two concentrations and two viscosity grades. In the oscillatory methods, the material is examined under nearly quiescent equilibrium conditions. Steady shear, conversely, produces large deformations and may yield false results, often interpreted as thixotropy, if the shear rate experiment is not conducted properly. Solutions of carboxymethylcellulose at concentrations ordinarily used in drug product formulations were examined by oscillatory and steady shear methods at low shear. Viscoelastic properties of pharmaceutical materials were measured using a newly developed oscillometric instrument. Mathematical expressions, formulated on the basis of a generalized Maxwell model for viscoelasticity and viscosity in steady shear, were correlated using these two rheological test methods. The results showed large increases in viscosity and relaxation time with increasing carboxymethylcellulose concentrations as well as with increasing molecular weights of the polymeric solute. The behavior of carboxymethylcellulose under both oscillatory and steady shear agreed with theory, linking the two methods of testing. Applications in pharmacy to this rheological analysis are presented. The present investigation attempted to bridge the gap between oscillatory and steady shear methods, demonstrating how both can find appropriate use in the analysis of non-Newtonian materials of pharmaceutical importance.
- Published
- 1978
- Full Text
- View/download PDF
26. Cramp and salt balance.
- Author
-
THURSTON G
- Subjects
- Humans, Muscle Cramp
- Published
- 1947
- Full Text
- View/download PDF
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