TY - JOUR
T1 - Risk factors for SARS-CoV-2 infection and transmission in households with children with asthma and allergy
T2 - A prospective surveillance study
AU - HEROS study team
AU - Seibold, Max A.
AU - Moore, Camille M.
AU - Everman, Jamie L.
AU - Williams, Blake J.M.
AU - Nolin, James D.
AU - Fairbanks-Mahnke, Ana
AU - Plender, Elizabeth G.
AU - Patel, Bhavika B.
AU - Arbes, Samuel J.
AU - Bacharier, Leonard B.
AU - Bendixsen, Casper G.
AU - Calatroni, Agustin
AU - Camargo, Carlos A.
AU - Dupont, William D.
AU - Furuta, Glenn T.
AU - Gebretsadik, Tebeb
AU - Gruchalla, Rebecca S.
AU - Gupta, Ruchi S.
AU - Khurana Hershey, Gurjit K.
AU - Murrison, Liza Bronner
AU - Jackson, Daniel J.
AU - Johnson, Christine C.
AU - Kattan, Meyer
AU - Liu, Andrew H.
AU - Lussier, Stephanie J.
AU - O'Connor, George T.
AU - Rivera-Spoljaric, Katherine
AU - Phipatanakul, Wanda
AU - Rothenberg, Marc E.
AU - Seroogy, Christine M.
AU - Teach, Stephen J.
AU - Zoratti, Edward M.
AU - Togias, Alkis
AU - Fulkerson, Patricia C.
AU - Hartert, Tina V.
N1 - Funding Information:
We thank the following clinical sites and institutes and investigators and staff thereof: the Childhood Allergy/Asthma Study; Microbes, Allergy, Asthma, and Pets (MAAP); and Wayne County Health, Environment, Allergy, and Asthma Longitudinal Study (WHEALS) cohorts at Henry Ford Health System (investigators Christine Johnson, Edward Zoratti, and Christine Joseph and staff members Ganesa Wegienka, Haejin Kim, Kyra Jones, Amanda Cyrus, Katherine Graham-McNeil, Mark Kolar, Melissa Houston, Verona Ivory, and Callie Knorr); the Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS), Greater Cincinnati Pediatric Clinic Repository (GCPCR), Inner-City Asthma Consortium (ICAC), and Mechanisms of Progression of Atopic Dermatitis to Asthma in Children (MPAACH) cohorts at Cincinnati Children's Hospital Medical Center (investigators Gurjit Khurana Hershey, Carolyn Kercsmar, Liza Bronner Murrison, and Jocelyn Biagini and staff members Kristi Curtsinger, Zachary Flege, David Morgan, Ahmed Ashraf, Jessica Riley, Kristina Keidel, Pamela Groh, Hannah Dixon, Anna-Liisa Vockell, Alexandra Gonzales, Tyler Miles, Angelo Bucci, Asel Baatyrbek Kyzy, Mackenzie Beck, Jeffery Burkle, John Kroner, and Elsie Parmar); the Consortium of Eosinophilic Gastrointestinal Disease Researchers (CEGIR) at Cincinnati Children's Hospital Medical Center (investigator Marc Rothenberg and staff members Kara Kliewer, Heather Foote, and Mike Eby); the Consortium of Eosinophilic Gastrointestinal Disease Researchers (CEGIR) at Children's Hospital Colorado (investigator Glenn Furuta and staff members Kendra Kocher, Rachel Andrews, and Cassandra Burger); the MARC-35 (WIND) and MARC-43 (CHIME) cohorts at Massachusetts General Hospital (investigators Carlos Camargo and Kohei Hasegawa and staff members Ashley Sullivan, Daphne Suzin, Natalie Burke, Vanessa Cardenas, Carson Clay, Lindsay Clinton, Nicole Herrera, Marina Latif, Shelly Qi, Ashley Stone, Lena Volpe, and Janice Espinola); the Childhood Origins of Asthma Study (COAST) at the University of Wisconsin-Madison (investigators Sima Ramratnam, Daniel Jackson, and Robert Lemankse and staff members Gina Crisafi, Liza Salazar, Jessica Fassbender, Jennifer Smith, and Christopher Tisler); the School Inner-City Asthma Intervention Study (SICAS), Environmental Assessment of Sleep in Youth (EASY) and Severe Asthma Research Program cohorts at Boston Children's Hospital (investigator Wanda Phipatanakul and staff members Amparito Cunningham, Giselle Garcia, Sullivan Waskosky, Anna Ramsey, Ethan Ansel-Kelly, Elizabeth Fitzpatrick, and Jesse Fernandez); the Food Allergy Outcomes Related to White and African American Racial Differences (FORWARD) and Improving Technology-Assisted Recording of Asthma Control in Children (iTRACC) cohorts at Ann and Robert H. Lurie Children's Hospital (investigator Ruchi Gupta and staff members Pamela Newmark, Gwen Holtzman, Haley Hultquist, Alexandria Bozen, Kathy Boon, Olivia Negris, Isabel Galic, and Rajeshree Das); the ICAC Leadership Center at the University of Wisconsin-Madison (investigators Daniel Jackson, James Gern, William Busse, and Christine Sorkness and staff member Kellie Hernandez); the ICAC at Boston University School of Medicine (investigators George O'Connor, Robyn Cohen, and Frederic Little and staff members (Nicole Gonzales, Rebecca Mello, Ana Manuelian, Benjamin Ubani, Anastasia Murati, Edlira Gjerasi, and Jessica Gereige); the ICAC at University of Texas Southwestern Medical School (investigator Rebecca Gruchalla and staff members Dolores Santoyo, Deborah Gonzales, Brenda Lewis, Priscilla Arancivia, and Eleazar Valdez); the ICAC at Children's Hospital Colorado (investigator Andrew Liu and staff members Pascuala Pinedo-Estrada, Juana Cerna-Sanchez, Shreya Veera, Sonya Belimezova, and Brooke Tippin); the ICAC at Henry Ford Health System (investigators Edward Zoratti, Haejin Kim, Rachel Kado, and Emily Wang and staff members Gillian Bassirpour, Sherae Hereford, Lauren Mosely, Keara Marks, and Yvette McLaurin); the ICAC at Columbia University Medical Center (investigators Meyer Kattan and Stephanie Lovinsky-Desir) and staff members Rafael Aguilar, Yudy Fernandez-Pau, Claire Jacobs-Sims, Mabel del Orbe, Victoria Piane, Marcela Pierce, Kimberly Sanchez, and Perri Yaniv); the ICAC at Washington University School of Medicine (investigators Leonard Bacharier and Katherine Rivera-Spoljaric and staff members Angela Freie, Kim Ray, Elizabeth Tesson, and Samantha Williams); the ICAC at Children's National Health System (investigators Stephen Teach and William Sheehan and staff members Alicia Mathis, Mahlet Atnafu, Chantel Bennett, Taqwa El-Hussein, Trisha Ibeh, Tiffany Ogundipe, and Pallavi Arasu); the Infant Susceptibility to Pulmonary Infections and Asthma following RSV Exposure (INSPIRE) program at Vanderbilt University Medical Center (investigators Tina Hartert, Tebeb Gebreatsadik, William Dupont, Christian Rosas-Salazar, Steven Brunswasser, and Brittney Snyder) and staff members Alyssa Bednarek, Teresa Chipps, Alexandra Connolly, Roxanne Filardo-Collins, Wais Folad, Kayla Goodman, Karin Han, Rebecca Hollenberg, Kelley Johnston, Jessica Levine, Zhouwen Liu, Christian Lynch, Lisa Martin, Megan McCollum, Kadijah Poleon, Pat Russell, Anisha Satish, Violet Terwilliger, Precious Ukachukwu, Gretchen Walter, Heather White, and Derek Wiggins); National Jewish Health (investigators Max A. Seibold and Camille M. Moore and staff members Jamie L. Everman, Blake J.M. Williams, James D. Nolin, Peter DeFord, Bhavika B. Patel, Elmar Pruesse, Elizabeth Plender, Ana Fairbanks-Mahnke, Michael Montgomery, Cydney Rios, Lucy Johnson, and Caleb Gammon); the National Institute of Allergy and Infectious Disease, Division of Allergy, Immunology, and Transplantation (investigators Patricia Fulkerson and Alkis Togias and staff members Katherine Thompson, Susan Schafer, and Julia Goldstein); Rho (investigators Samuel Arbes, Agustin Calatroni, and Stephanie Lussier and staff members Stephanie Wellford, Sharon Castina, Lasonia Morgan, Joshua Sanders, Rita Slater, Caitlin Suddueth, and Rachel Lisi); the Vanderbilt Coordinating Center (staff members Jessica Marlin, George Tregoning, Yoli Perez-Torres, Jessica Collins, and Krista Vermillion); the Wisconsin Infant Study Cohort (WISC) at Marshfield Clinic Research Institute (investigators Christine Seroogy, James Gern, and Casper Bendixsen and staff members Katherine Barnes, Kyle Koshalek, Terry Foss, and Julie Karl); and the HEROS External Scientific Advisory Group (Collin O'Neil, PhD, at Lehman College; Justin Ortiz, MD, at the University of Maryland; Matthew Altman, MD, at the Benaroya Research Institute; and Michael Sebert, MD, at University of Texas Southwestern Medical Center).
Funding Information:
Please see the Supplementary Appendix in the Online Repository at www.jacionline.org for full cohort and funding information. Grant numbers: AI024156, AI051598, UG3OD023282, 3U19AI070235-14S1, 3U54AI117804-06S1, 3U54AI117804-07S1, R01AI127507, U19 AI104317, PO1HL70381, U01 AI 110397, R01 HL 137192, K24 AI 106822, U10 HL109172, 3R01AI130348-04S1, 1UL1TR001430, 5UM1AI114271, 3UM1AI114271-06S1, 3UM1AI114271-07S1, UM1AI114271, U19 AI 095227-S2, U19 AI 095227-S1, 3PO1AI089473-07S1, AI089473, NIH 3UM1AI151958-01S1, NIH 3UM1AI151958-02S1, 1UM2AI117870, AI050681, and UH3 OD023282.
Publisher Copyright:
© 2022
PY - 2022/8
Y1 - 2022/8
N2 - Background: Whether children and people with asthma and allergic diseases are at increased risk for severe acute respiratory syndrome virus 2 (SARS-CoV-2) infection is unknown. Objective: Our aims were to determine the incidence of SARS-CoV-2 infection in households with children and to also determine whether self-reported asthma and/or other allergic diseases are associated with infection and household transmission. Methods: For 6 months, biweekly nasal swabs and weekly surveys were conducted within 1394 households (N = 4142 participants) to identify incident SARS-CoV-2 infections from May 2020 to February 2021, which was the pandemic period largely before a vaccine and before the emergence of SARS-CoV-2 variants. Participant and household infection and household transmission probabilities were calculated by using time-to-event analyses, and factors associated with infection and transmission risk were determined by using regression analyses. Results: In all, 147 households (261 participants) tested positive for SARS-CoV-2. The household SARS-CoV-2 infection probability was 25.8%; the participant infection probability was similar for children (14.0% [95% CI = 8.0%-19.6%]), teenagers (12.1% [95% CI = 8.2%-15.9%]), and adults (14.0% [95% CI = 9.5%-18.4%]). Infections were symptomatic in 24.5% of children, 41.2% of teenagers, and 62.5% of adults. Self-reported doctor-diagnosed asthma was not a risk factor for infection (adjusted hazard ratio [aHR] = 1.04 [95% CI = 0.73-1.46]), nor was upper respiratory allergy or eczema. Self-reported doctor-diagnosed food allergy was associated with lower infection risk (aHR = 0.50 [95% CI = 0.32-0.81]); higher body mass index was associated with increased infection risk (aHR per 10-point increase = 1.09 [95% CI = 1.03-1.15]). The household secondary attack rate was 57.7%. Asthma was not associated with household transmission, but transmission was lower in households with food allergy (adjusted odds ratio = 0.43 [95% CI = 0.19-0.96]; P =.04). Conclusion: Asthma does not increase the risk of SARS-CoV-2 infection. Food allergy is associated with lower infection risk, whereas body mass index is associated with increased infection risk. Understanding how these factors modify infection risk may offer new avenues for preventing infection.
AB - Background: Whether children and people with asthma and allergic diseases are at increased risk for severe acute respiratory syndrome virus 2 (SARS-CoV-2) infection is unknown. Objective: Our aims were to determine the incidence of SARS-CoV-2 infection in households with children and to also determine whether self-reported asthma and/or other allergic diseases are associated with infection and household transmission. Methods: For 6 months, biweekly nasal swabs and weekly surveys were conducted within 1394 households (N = 4142 participants) to identify incident SARS-CoV-2 infections from May 2020 to February 2021, which was the pandemic period largely before a vaccine and before the emergence of SARS-CoV-2 variants. Participant and household infection and household transmission probabilities were calculated by using time-to-event analyses, and factors associated with infection and transmission risk were determined by using regression analyses. Results: In all, 147 households (261 participants) tested positive for SARS-CoV-2. The household SARS-CoV-2 infection probability was 25.8%; the participant infection probability was similar for children (14.0% [95% CI = 8.0%-19.6%]), teenagers (12.1% [95% CI = 8.2%-15.9%]), and adults (14.0% [95% CI = 9.5%-18.4%]). Infections were symptomatic in 24.5% of children, 41.2% of teenagers, and 62.5% of adults. Self-reported doctor-diagnosed asthma was not a risk factor for infection (adjusted hazard ratio [aHR] = 1.04 [95% CI = 0.73-1.46]), nor was upper respiratory allergy or eczema. Self-reported doctor-diagnosed food allergy was associated with lower infection risk (aHR = 0.50 [95% CI = 0.32-0.81]); higher body mass index was associated with increased infection risk (aHR per 10-point increase = 1.09 [95% CI = 1.03-1.15]). The household secondary attack rate was 57.7%. Asthma was not associated with household transmission, but transmission was lower in households with food allergy (adjusted odds ratio = 0.43 [95% CI = 0.19-0.96]; P =.04). Conclusion: Asthma does not increase the risk of SARS-CoV-2 infection. Food allergy is associated with lower infection risk, whereas body mass index is associated with increased infection risk. Understanding how these factors modify infection risk may offer new avenues for preventing infection.
KW - COVID-19
KW - SARS-CoV-2
KW - asthma
KW - body mass index
KW - food allergy
KW - infection
KW - transmission
UR - http://www.scopus.com/inward/record.url?scp=85135599377&partnerID=8YFLogxK
U2 - 10.1016/j.jaci.2022.05.014
DO - 10.1016/j.jaci.2022.05.014
M3 - Article
C2 - 35660376
AN - SCOPUS:85135599377
SN - 0091-6749
VL - 150
SP - 302
EP - 311
JO - Journal of Allergy and Clinical Immunology
JF - Journal of Allergy and Clinical Immunology
IS - 2
ER -