Early-life home environment and risk of asthma among inner-city children - 05/04/18
, Susan V. Lynch, PhD b, Gordon R. Bloomberg, MD c, Meyer Kattan, MD d, Robert A. Wood, MD e, Peter J. Gergen, MD, MPH f, Katy F. Jaffee, MS g, Agustin Calatroni, MS g, Leonard B. Bacharier, MD c, Avrahman Beigelman, MD c, Megan T. Sandel, MD, MPH h, Christine C. Johnson, PhD i, Ali Faruqi, MS b, Clark Santee, BS b, Kei E. Fujimura, PhD b, Douglas Fadrosh, MS b, Homer Boushey, MD b, Cynthia M. Visness, PhD g, James E. Gern, MD jAbstract |
Background |
Environmental exposures in early life appear to play an important role in the pathogenesis of childhood asthma, but the potentially modifiable exposures that lead to asthma remain uncertain.
Objective |
We sought to identify early-life environmental risk factors for childhood asthma in a birth cohort of high-risk inner-city children.
Methods |
We examined the relationship of prenatal and early-life environmental factors to the occurrence of asthma at 7 years of age among 442 children.
Results |
Higher house dust concentrations of cockroach, mouse, and cat allergens in the first 3 years of life were associated with lower risk of asthma (for cockroach allergen: odds ratio per interquartile range increase in concentration, 0.55; 95% CI, 0.36-0.86; P < .01). House dust microbiome analysis using 16S ribosomal RNA sequencing identified 202 and 171 bacterial taxa that were significantly (false discovery rate < 0.05) more or less abundant, respectively, in the homes of children with asthma. A majority of these bacteria were significantly correlated with 1 of more allergen concentrations. Other factors associated significantly positively with asthma included umbilical cord plasma cotinine concentration (odds ratio per geometric SD increase in concentration, 1.76; 95% CI, 1.00-3.09; P = .048) and maternal stress and depression scores.
Conclusion |
Among high-risk inner-city children, higher indoor levels of pet or pest allergens in infancy were associated with lower risk of asthma. The abundance of a number of bacterial taxa in house dust was associated with increased or decreased asthma risk. Prenatal tobacco smoke exposure and higher maternal stress and depression scores in early life were associated with increased asthma risk.
El texto completo de este artículo está disponible en PDF.Key words : Asthma, environment, allergy, allergen, microbiome, stress, depression, smoking
Abbreviations used : FDR, URECA
Esquema
| Supported by federal funds from the National Institute of Allergy and Infectious Diseases/National Institutes of Health (NIH), under contract nos. NO1-AI-25496, NO1-AI-25482, HHSN272200900052C, HHSN272201000052I, 1UM1AI114271-01, and UM2AI117870. Additional support was provided by the National Center for Research Resources/NIH under grants RR00052, M01RR00533, 1UL1RR025771, M01RR00071, 1UL1RR024156, and 5UL1RR024992-02, and the National Center for the Advancement of Translational Research/NIH under grants UL1TR001079 and UL1TR000040. |
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| Disclosure of potential conflict of interest: G. T. O'Connor has received grants from the National Institutes of Health (NIH) and Janssen Pharmaceuticals and has consultant arrangements with AstraZeneca. S. V. Lynch has received grants from the Broad Foundation, the NIH/National Institute of Allergy and Infectious Disease (NIAID; AI113916; AI089473-01), the Sloan Foundation, Pfizer, Gilead Sciences, and Janssen; has received personal fees from Janssen, Boston Consulting Group, Regeneron, and Siolta Therapeutics; has a patent issued for reductive prodrug cancer chemotherapy (Stan449-PRV), and a patent for combination antibiotic and antibody therapy for the treatment of Pseudomonas aeruginosa infection (WO 2010091189 A1) with royalties paid to KaloBios, a patent for therapeutic microbial consortium for induction of immune tolerance licensed to Siolta Therapeutics, a patent for systems and methods for detecting antibiotic resistance (WO 2012027302 A3), a patent for nitroreductase enzymes (US 7687474 B2), a patent for sinusitis diagnostics and treatments (WO 2013155370 A1), and a patent for methods and systems for phylogenetic analysis US 20120264637 A1; and is a cofounder of Siolta Therapeutics, a start-up company that is developing a mixed-species microbial oral therapeutic for induction of immune tolerance. G. R. Bloomberg, K. F. Jaffee, A. Calatroni, A. Faruqi, C. Santee, D. Fadrosh, and C. M. Visness have received grants from the NIH/NIAID. M. Kattan has received grants from the NIH/NIAID and has received personal fees from Novartis Pharma. R. A. Wood has received grants from the NIH, DBV, Aimmune, Astellas, and HAL-Allergy; has consultant arrangements with Stallergenes; is employed by Johns Hopkins University; and receives royalties from UpToDate. L. Bacharier has received a grant from the NIH/NIAID and has received personal fees from Aerocrine, GlaxoSmithKline, Genentech/Novartis, Merck, Cephalon, DBV Technologies, Teva, Boehringer Ingelheim, AstraZeneca, WebMD/Medscape, Sanofi, Vectura, and Circassia. A. Biegelman has received grants from the NIH/NIAID and the NIH/National Heart, Lung, and Blood Institute (NHLBI). M. T. Sandel and C. C. Johnson have received grants from the NIH. K. Fujimura has received a grant from the NIH/NIAID and has a patent pending for microbial consortium. H. Boushey has received grants from the NIH/NIAID and the NIH/NHLBI and serves as an uncompensated member of a Scientific Advisory Committee for Siolta Therapeutics and has no financial interest in, or financial relationship with, the company. J. E. Gern has received a grant from the NIH/NIAID; has received personal fees from Janssen, Regeneron, and PReP Biosciences; and has received travel support from Boehringer Ingelheim. |
Vol 141 - N° 4
P. 1468-1475 - avril 2018 Regresar al número
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