Investigating the causal effect of smoking on hay fever and asthma: A Mendelian randomization meta-analysis in the CARTA consortium

Tea Skaaby; Amy E. Taylor; Rikke K. Jacobsen; Lavinia Paternoster; Betina H. Thuesen; Tarunveer S. Ahluwalia; Sofus C. Larsen; Ang Zhou; Andrew Wong; Maiken E. Gabrielsen; Johan H. Bjørngaard; Claudia Flexeder; Satu Männistö; Rebecca Hardy; Diana Kuh; Sarah J. Barry; Line Tang Møllehave; Charlotte Cerqueira; Nele Friedrich; Tobias N. Bonten; Raymond Noordam; Dennis O. Mook-Kanamori; Christian Taube; Leon E. Jessen; Alex McConnachie; Naveed Sattar; Mark N. Upton; Charles McSharry; Klaus Bønnelykke; Hans Bisgaard; Holger Schulz; Konstantin Strauch; Thomas Meitinger; Annette Peters; Harald Grallert; Ellen A. Nohr; Mika Kivimaki; Meena Kumari; Uwe Völker; Matthias Nauck; Henry Völzke; Chris Power; Elina Hyppönen; Torben Hansen; Torben Jørgensen; Oluf Pedersen; Veikko Salomaa; Niels Grarup; Arnulf Langhammer; Marcus R. Munafò

doi:10.1038/s41598-017-01977-w

Investigating the causal effect of smoking on hay fever and asthma: A Mendelian randomization meta-analysis in the CARTA consortium

Tea Skaaby
, Amy E. Taylor
, Rikke K. Jacobsen
, Lavinia Paternoster
, Betina H. Thuesen
, Tarunveer S. Ahluwalia
, Sofus C. Larsen
, Ang Zhou
, Andrew Wong
, Maiken E. Gabrielsen
, Johan H. Bjørngaard
, Claudia Flexeder
, Satu Männistö
, Rebecca Hardy
, Diana Kuh
, Sarah J. Barry
, Line Tang Møllehave
, Charlotte Cerqueira
, Nele Friedrich
, Tobias N. Bonten

Raymond Noordam, Dennis O. Mook-Kanamori, Christian Taube, Leon E. Jessen, Alex McConnachie, Naveed Sattar, Mark N. Upton, Charles McSharry, Klaus Bønnelykke, Hans Bisgaard, Holger Schulz, Konstantin Strauch, Thomas Meitinger, Annette Peters, Harald Grallert, Ellen A. Nohr, Mika Kivimaki, Meena Kumari, Uwe Völker, Matthias Nauck, Henry Völzke, Chris Power, Elina Hyppönen, Torben Hansen, Torben Jørgensen, Oluf Pedersen, Veikko Salomaa, Niels Grarup, Arnulf Langhammer, Marcus R. Munafò

Vice Chancellor's Office

University of Bristol
University of Copenhagen
Novo Nordisk Foundation Center for Basic Metabolic Research
Steno Diabetes Center Copenhagen
University of South Australia
University College London
Norwegian University of Science and Technology
Trondheim University Hospital
Helmholtz Center Munich - German Research Center for Environmental Health
National Institute for Health and Welfare (THL)
University of Glasgow
University Medicine and Ernst-Moritz-Arndt University Greifswald
Leiden University Medical Center
King Faisal Specialist Hospital and Research Centre
University of Duisburg
German Center for Lung Research
Ludwig Maximilian University of Munich
Technical University of Munich
Partner Site Munich Heart Alliance
German Center for Diabetes Research (DZD e.V.)
University of Southern Denmark
Institute for Social and Economic Research, University of Essex
South Australian Health and Medical Research Institute
Aalborg University

Research output: Contribution to journal › Article › peer-review

44 Citations (SciVal)

Abstract

Observational studies on smoking and risk of hay fever and asthma have shown inconsistent results. However, observational studies may be biased by confounding and reverse causation. Mendelian randomization uses genetic variants as markers of exposures to examine causal effects. We examined the causal effect of smoking on hay fever and asthma by using the smoking-associated single nucleotide polymorphism (SNP) rs16969968/rs1051730. We included 231,020 participants from 22 population-based studies. Observational analyses showed that current vs never smokers had lower risk of hay fever (odds ratio (OR) = 0·68, 95% confidence interval (CI): 0·61, 0·76; P < 0·001) and allergic sensitization (OR = 0·74, 95% CI: 0·64, 0·86; P < 0·001), but similar asthma risk (OR = 1·00, 95% CI: 0·91, 1·09; P = 0·967). Mendelian randomization analyses in current smokers showed a slightly lower risk of hay fever (OR = 0·958, 95% CI: 0·920, 0·998; P = 0·041), a lower risk of allergic sensitization (OR = 0·92, 95% CI: 0·84, 1·02; P = 0·117), but higher risk of asthma (OR = 1·06, 95% CI: 1·01, 1·11; P = 0·020) per smoking-increasing allele. Our results suggest that smoking may be causally related to a higher risk of asthma and a slightly lower risk of hay fever. However, the adverse events associated with smoking limit its clinical significance.

Original language	English
Article number	2224
Journal	Scientific Reports
Volume	7
Issue number	1
Early online date	22 May 2017
DOIs	https://doi.org/10.1038/s41598-017-01977-w
Publication status	Published - 1 Dec 2017

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Skaaby, T., Taylor, A. E., Jacobsen, R. K., Paternoster, L., Thuesen, B. H., Ahluwalia, T. S., Larsen, S. C., Zhou, A., Wong, A., Gabrielsen, M. E., Bjørngaard, J. H., Flexeder, C., Männistö, S., Hardy, R., Kuh, D., Barry, S. J., Møllehave, L. T., Cerqueira, C., Friedrich, N., ... Munafò, M. R. (2017). Investigating the causal effect of smoking on hay fever and asthma: A Mendelian randomization meta-analysis in the CARTA consortium. Scientific Reports, 7(1), Article 2224. https://doi.org/10.1038/s41598-017-01977-w

Skaaby, T, Taylor, AE, Jacobsen, RK, Paternoster, L, Thuesen, BH, Ahluwalia, TS, Larsen, SC, Zhou, A, Wong, A, Gabrielsen, ME, Bjørngaard, JH, Flexeder, C, Männistö, S, Hardy, R, Kuh, D, Barry, SJ, Møllehave, LT, Cerqueira, C, Friedrich, N, Bonten, TN, Noordam, R, Mook-Kanamori, DO, Taube, C, Jessen, LE, McConnachie, A, Sattar, N, Upton, MN, McSharry, C, Bønnelykke, K, Bisgaard, H, Schulz, H, Strauch, K, Meitinger, T, Peters, A, Grallert, H, Nohr, EA, Kivimaki, M, Kumari, M, Völker, U, Nauck, M, Völzke, H, Power, C, Hyppönen, E, Hansen, T, Jørgensen, T, Pedersen, O, Salomaa, V, Grarup, N, Langhammer, A & Munafò, MR 2017, 'Investigating the causal effect of smoking on hay fever and asthma: A Mendelian randomization meta-analysis in the CARTA consortium', Scientific Reports, vol. 7, no. 1, 2224. https://doi.org/10.1038/s41598-017-01977-w

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title = "Investigating the causal effect of smoking on hay fever and asthma: A Mendelian randomization meta-analysis in the CARTA consortium",

abstract = "Observational studies on smoking and risk of hay fever and asthma have shown inconsistent results. However, observational studies may be biased by confounding and reverse causation. Mendelian randomization uses genetic variants as markers of exposures to examine causal effects. We examined the causal effect of smoking on hay fever and asthma by using the smoking-associated single nucleotide polymorphism (SNP) rs16969968/rs1051730. We included 231,020 participants from 22 population-based studies. Observational analyses showed that current vs never smokers had lower risk of hay fever (odds ratio (OR) = 0·68, 95\% confidence interval (CI): 0·61, 0·76; P < 0·001) and allergic sensitization (OR = 0·74, 95\% CI: 0·64, 0·86; P < 0·001), but similar asthma risk (OR = 1·00, 95\% CI: 0·91, 1·09; P = 0·967). Mendelian randomization analyses in current smokers showed a slightly lower risk of hay fever (OR = 0·958, 95\% CI: 0·920, 0·998; P = 0·041), a lower risk of allergic sensitization (OR = 0·92, 95\% CI: 0·84, 1·02; P = 0·117), but higher risk of asthma (OR = 1·06, 95\% CI: 1·01, 1·11; P = 0·020) per smoking-increasing allele. Our results suggest that smoking may be causally related to a higher risk of asthma and a slightly lower risk of hay fever. However, the adverse events associated with smoking limit its clinical significance.",

author = "Tea Skaaby and Taylor, \{Amy E.\} and Jacobsen, \{Rikke K.\} and Lavinia Paternoster and Thuesen, \{Betina H.\} and Ahluwalia, \{Tarunveer S.\} and Larsen, \{Sofus C.\} and Ang Zhou and Andrew Wong and Gabrielsen, \{Maiken E.\} and Bj{\o}rngaard, \{Johan H.\} and Claudia Flexeder and Satu M{\"a}nnist{\"o} and Rebecca Hardy and Diana Kuh and Barry, \{Sarah J.\} and M{\o}llehave, \{Line Tang\} and Charlotte Cerqueira and Nele Friedrich and Bonten, \{Tobias N.\} and Raymond Noordam and Mook-Kanamori, \{Dennis O.\} and Christian Taube and Jessen, \{Leon E.\} and Alex McConnachie and Naveed Sattar and Upton, \{Mark N.\} and Charles McSharry and Klaus B{\o}nnelykke and Hans Bisgaard and Holger Schulz and Konstantin Strauch and Thomas Meitinger and Annette Peters and Harald Grallert and Nohr, \{Ellen A.\} and Mika Kivimaki and Meena Kumari and Uwe V{\"o}lker and Matthias Nauck and Henry V{\"o}lzke and Chris Power and Elina Hypp{\"o}nen and Torben Hansen and Torben J{\o}rgensen and Oluf Pedersen and Veikko Salomaa and Niels Grarup and Arnulf Langhammer and Munaf{\`o}, \{Marcus R.\}",

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T2 - A Mendelian randomization meta-analysis in the CARTA consortium

AU - Skaaby, Tea

AU - Taylor, Amy E.

AU - Jacobsen, Rikke K.

AU - Paternoster, Lavinia

AU - Thuesen, Betina H.

AU - Ahluwalia, Tarunveer S.

AU - Larsen, Sofus C.

AU - Zhou, Ang

AU - Wong, Andrew

AU - Gabrielsen, Maiken E.

AU - Bjørngaard, Johan H.

AU - Flexeder, Claudia

AU - Männistö, Satu

AU - Hardy, Rebecca

AU - Kuh, Diana

AU - Barry, Sarah J.

AU - Møllehave, Line Tang

AU - Cerqueira, Charlotte

AU - Friedrich, Nele

AU - Bonten, Tobias N.

AU - Noordam, Raymond

AU - Mook-Kanamori, Dennis O.

AU - Taube, Christian

AU - Jessen, Leon E.

AU - McConnachie, Alex

AU - Sattar, Naveed

AU - Upton, Mark N.

AU - McSharry, Charles

AU - Bønnelykke, Klaus

AU - Bisgaard, Hans

AU - Schulz, Holger

AU - Strauch, Konstantin

AU - Meitinger, Thomas

AU - Peters, Annette

AU - Grallert, Harald

AU - Nohr, Ellen A.

AU - Kivimaki, Mika

AU - Kumari, Meena

AU - Völker, Uwe

AU - Nauck, Matthias

AU - Völzke, Henry

AU - Power, Chris

AU - Hyppönen, Elina

AU - Hansen, Torben

AU - Jørgensen, Torben

AU - Pedersen, Oluf

AU - Salomaa, Veikko

AU - Grarup, Niels

AU - Langhammer, Arnulf

AU - Munafò, Marcus R.

PY - 2017/12/1

Y1 - 2017/12/1

N2 - Observational studies on smoking and risk of hay fever and asthma have shown inconsistent results. However, observational studies may be biased by confounding and reverse causation. Mendelian randomization uses genetic variants as markers of exposures to examine causal effects. We examined the causal effect of smoking on hay fever and asthma by using the smoking-associated single nucleotide polymorphism (SNP) rs16969968/rs1051730. We included 231,020 participants from 22 population-based studies. Observational analyses showed that current vs never smokers had lower risk of hay fever (odds ratio (OR) = 0·68, 95% confidence interval (CI): 0·61, 0·76; P < 0·001) and allergic sensitization (OR = 0·74, 95% CI: 0·64, 0·86; P < 0·001), but similar asthma risk (OR = 1·00, 95% CI: 0·91, 1·09; P = 0·967). Mendelian randomization analyses in current smokers showed a slightly lower risk of hay fever (OR = 0·958, 95% CI: 0·920, 0·998; P = 0·041), a lower risk of allergic sensitization (OR = 0·92, 95% CI: 0·84, 1·02; P = 0·117), but higher risk of asthma (OR = 1·06, 95% CI: 1·01, 1·11; P = 0·020) per smoking-increasing allele. Our results suggest that smoking may be causally related to a higher risk of asthma and a slightly lower risk of hay fever. However, the adverse events associated with smoking limit its clinical significance.

AB - Observational studies on smoking and risk of hay fever and asthma have shown inconsistent results. However, observational studies may be biased by confounding and reverse causation. Mendelian randomization uses genetic variants as markers of exposures to examine causal effects. We examined the causal effect of smoking on hay fever and asthma by using the smoking-associated single nucleotide polymorphism (SNP) rs16969968/rs1051730. We included 231,020 participants from 22 population-based studies. Observational analyses showed that current vs never smokers had lower risk of hay fever (odds ratio (OR) = 0·68, 95% confidence interval (CI): 0·61, 0·76; P < 0·001) and allergic sensitization (OR = 0·74, 95% CI: 0·64, 0·86; P < 0·001), but similar asthma risk (OR = 1·00, 95% CI: 0·91, 1·09; P = 0·967). Mendelian randomization analyses in current smokers showed a slightly lower risk of hay fever (OR = 0·958, 95% CI: 0·920, 0·998; P = 0·041), a lower risk of allergic sensitization (OR = 0·92, 95% CI: 0·84, 1·02; P = 0·117), but higher risk of asthma (OR = 1·06, 95% CI: 1·01, 1·11; P = 0·020) per smoking-increasing allele. Our results suggest that smoking may be causally related to a higher risk of asthma and a slightly lower risk of hay fever. However, the adverse events associated with smoking limit its clinical significance.

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ER -

Investigating the causal effect of smoking on hay fever and asthma: A Mendelian randomization meta-analysis in the CARTA consortium

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