Investigating the causal effect of smoking on hay fever and asthma: A Mendelian randomization meta-analysis in the CARTA consortium
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 causa...
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| creator | Skaaby, Tea Taylor, Amy E Jacobsen, Rikke K Paternoster, Lavinia Thuesen, Betina H Ahluwalia, Tarunveer S Larsen, Sofus C Zhou, Ang Wong, Andrew Gabrielsen, Maiken Elvestad Bjørngaard, Johan Håkon Flexeder, Claudia Männistö, Satu Hardy, Rebecca Kuh, Diana Barry, Sarah J Møllehave, Line Tang Cerqueira, Charlotte Friedrich, Nele Bonten, Tobias N Noordam, Raymond Mook-Kanamori, Dennis O Taube, Christian Jessen, Leon E McConnachie, Alex Sattar, Naveed Upton, Mark N McSharry, Charles Bønnelykke, Klaus Bisgaard, Hans Schulz, Holger Strauch, Konstantin Meitinger, Thomas Peters, Annette Grallert, Harald Nohr, Ellen A Kivimäki, Mika Kumari, Meena Völker, Uwe Nauck, Matthias Völzke, Henry Power, Chris Hyppönen, Elina Hansen, Torben Jørgensen, Torben Pedersen, Oluf Salomaa, Veikko Grarup, Niels Langhammer, Arnulf Romundstad, Pål Richard Skorpen, Frank Kaprio, Jaakko Munafò, Marcus R Linneberg, Allan |
| description | 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 |
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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.</description><language>eng</language><publisher>Springer Nature</publisher><creationdate>2017</creationdate><rights>info:eu-repo/semantics/openAccess</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,776,881,26544</link.rule.ids><linktorsrc>$$Uhttp://hdl.handle.net/11250/2502746$$EView_record_in_NORA$$FView_record_in_$$GNORA$$Hfree_for_read</linktorsrc></links><search><creatorcontrib>Skaaby, Tea</creatorcontrib><creatorcontrib>Taylor, Amy E</creatorcontrib><creatorcontrib>Jacobsen, Rikke K</creatorcontrib><creatorcontrib>Paternoster, Lavinia</creatorcontrib><creatorcontrib>Thuesen, Betina H</creatorcontrib><creatorcontrib>Ahluwalia, Tarunveer S</creatorcontrib><creatorcontrib>Larsen, Sofus C</creatorcontrib><creatorcontrib>Zhou, Ang</creatorcontrib><creatorcontrib>Wong, Andrew</creatorcontrib><creatorcontrib>Gabrielsen, Maiken Elvestad</creatorcontrib><creatorcontrib>Bjørngaard, Johan Håkon</creatorcontrib><creatorcontrib>Flexeder, Claudia</creatorcontrib><creatorcontrib>Männistö, Satu</creatorcontrib><creatorcontrib>Hardy, Rebecca</creatorcontrib><creatorcontrib>Kuh, Diana</creatorcontrib><creatorcontrib>Barry, Sarah J</creatorcontrib><creatorcontrib>Møllehave, Line Tang</creatorcontrib><creatorcontrib>Cerqueira, Charlotte</creatorcontrib><creatorcontrib>Friedrich, Nele</creatorcontrib><creatorcontrib>Bonten, Tobias N</creatorcontrib><creatorcontrib>Noordam, Raymond</creatorcontrib><creatorcontrib>Mook-Kanamori, Dennis O</creatorcontrib><creatorcontrib>Taube, Christian</creatorcontrib><creatorcontrib>Jessen, Leon E</creatorcontrib><creatorcontrib>McConnachie, Alex</creatorcontrib><creatorcontrib>Sattar, Naveed</creatorcontrib><creatorcontrib>Upton, Mark N</creatorcontrib><creatorcontrib>McSharry, Charles</creatorcontrib><creatorcontrib>Bønnelykke, Klaus</creatorcontrib><creatorcontrib>Bisgaard, Hans</creatorcontrib><creatorcontrib>Schulz, Holger</creatorcontrib><creatorcontrib>Strauch, Konstantin</creatorcontrib><creatorcontrib>Meitinger, Thomas</creatorcontrib><creatorcontrib>Peters, Annette</creatorcontrib><creatorcontrib>Grallert, Harald</creatorcontrib><creatorcontrib>Nohr, Ellen A</creatorcontrib><creatorcontrib>Kivimäki, Mika</creatorcontrib><creatorcontrib>Kumari, Meena</creatorcontrib><creatorcontrib>Völker, Uwe</creatorcontrib><creatorcontrib>Nauck, Matthias</creatorcontrib><creatorcontrib>Völzke, Henry</creatorcontrib><creatorcontrib>Power, Chris</creatorcontrib><creatorcontrib>Hyppönen, Elina</creatorcontrib><creatorcontrib>Hansen, Torben</creatorcontrib><creatorcontrib>Jørgensen, Torben</creatorcontrib><creatorcontrib>Pedersen, Oluf</creatorcontrib><creatorcontrib>Salomaa, Veikko</creatorcontrib><creatorcontrib>Grarup, Niels</creatorcontrib><creatorcontrib>Langhammer, Arnulf</creatorcontrib><creatorcontrib>Romundstad, Pål Richard</creatorcontrib><creatorcontrib>Skorpen, Frank</creatorcontrib><creatorcontrib>Kaprio, Jaakko</creatorcontrib><creatorcontrib>Munafò, Marcus R</creatorcontrib><creatorcontrib>Linneberg, Allan</creatorcontrib><title>Investigating the causal effect of smoking on hay fever and asthma: A Mendelian randomization meta-analysis in the CARTA consortium</title><description>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. 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S</au><au>Larsen, Sofus C</au><au>Zhou, Ang</au><au>Wong, Andrew</au><au>Gabrielsen, Maiken Elvestad</au><au>Bjørngaard, Johan Håkon</au><au>Flexeder, Claudia</au><au>Männistö, Satu</au><au>Hardy, Rebecca</au><au>Kuh, Diana</au><au>Barry, Sarah J</au><au>Møllehave, Line Tang</au><au>Cerqueira, Charlotte</au><au>Friedrich, Nele</au><au>Bonten, Tobias N</au><au>Noordam, Raymond</au><au>Mook-Kanamori, Dennis O</au><au>Taube, Christian</au><au>Jessen, Leon E</au><au>McConnachie, Alex</au><au>Sattar, Naveed</au><au>Upton, Mark N</au><au>McSharry, Charles</au><au>Bønnelykke, Klaus</au><au>Bisgaard, Hans</au><au>Schulz, Holger</au><au>Strauch, Konstantin</au><au>Meitinger, Thomas</au><au>Peters, Annette</au><au>Grallert, Harald</au><au>Nohr, Ellen A</au><au>Kivimäki, Mika</au><au>Kumari, Meena</au><au>Völker, Uwe</au><au>Nauck, Matthias</au><au>Völzke, Henry</au><au>Power, Chris</au><au>Hyppönen, Elina</au><au>Hansen, Torben</au><au>Jørgensen, Torben</au><au>Pedersen, Oluf</au><au>Salomaa, Veikko</au><au>Grarup, Niels</au><au>Langhammer, Arnulf</au><au>Romundstad, Pål Richard</au><au>Skorpen, Frank</au><au>Kaprio, Jaakko</au><au>Munafò, Marcus R</au><au>Linneberg, Allan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Investigating the causal effect of smoking on hay fever and asthma: A Mendelian randomization meta-analysis in the CARTA consortium</atitle><date>2017</date><risdate>2017</risdate><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.</abstract><pub>Springer Nature</pub><oa>free_for_read</oa></addata></record> |
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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 |
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