@article{discovery1558522,
          volume = {7},
            note = {Open Access: This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.},
           title = {Investigating the causal effect of smoking on hay fever and asthma: a Mendelian randomization meta-analysis in the CARTA consortium},
           month = {May},
            year = {2017},
         journal = {Scientific Reports},
            issn = {2045-2322},
             url = {http://dx.doi.org/10.1038/s41598-017-01977-w},
        keywords = {Asthma;
Risk factors},
        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 {\ensuremath{<}} 0.001) and allergic sensitization (OR = 0.74, 95\% CI: 0.64, 0.86; P {\ensuremath{<}} 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 = {Skaaby, T and Taylor, AE and Jacobsen, RK and Paternoster, L and Thuesen, BH and Ahluwalia, TS and Larsen, SC and Zhou, A and Wong, A and Gabrielsen, ME and Bj{\o}rngaard, JH and Flexeder, C and M{\"a}nnist{\"o}, S and Hardy, R and Kuh, D and Barry, SJ and Tang M{\o}llehave, L and Cerqueira, C and Friedrich, N and Bonten, TN and Noordam, R and Mook-Kanamori, DO and Taube, C and Jessen, LE and McConnachie, A and Sattar, N and Upton, MN and McSharry, C and B{\o}nnelykke, K and Bisgaard, H and Schulz, H and Strauch, K and Meitinger, T and Peters, A and Grallert, H and Nohr, EA and Kivimaki, M and Kumari, M and V{\"o}lker, U and Nauck, M and V{\"o}lzke, H and Power, C and Hypp{\"o}nen, E and Hansen, T and J{\o}rgensen, T and Pedersen, O and Salomaa, V and Grarup, N and Langhammer, A and Romundstad, PR and Skorpen, F and Kaprio, J and R Munaf{\`o}, M and Linneberg, A}
}