Forskning
Udskriv Udskriv
Switch language
Region Hovedstaden - en del af Københavns Universitetshospital
Udgivet

Smoking and Increased White and Red Blood Cells: A Mendelian Randomization Approach in the Copenhagen General Population Study

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

DOI

  1. Apolipoprotein M and Sphingosine-1-Phosphate Receptor 1 promote the transendothelial transport of High-Density Lipoprotein

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Low High-Density Lipoprotein Cholesterol and High White Blood Cell Counts: A Mendelian Randomization Study

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Plasma Albumin and Incident Cardiovascular Disease: Results From the CGPS and an Updated Meta-Analysis

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  1. Lipoprotein(a) levels at birth and in early childhood: The COMPARE Study

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Triglyceride-rich Lipoprotein Cholesterol (Remnant Cholesterol) as a Therapeutic Target for Cardiovascular Disease Risk

    Publikation: Bidrag til bog/antologi/rapportBidrag til bog/antologiFormidling

  3. A possible explanation for the contrasting results of REDUCE-IT vs. STRENGTH: cohort study mimicking trial designs

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Vis graf over relationer

Objective- Whether tobacco smoking causally affects white and red blood cells and thrombocyte counts is unknown. Using a Mendelian randomization approach, we tested the hypothesis that smoking causes increases in these blood cell indices. Approach and Results- We included 104 607 white Danes aged 20 to 100 years from the Copenhagen General Population Study with information on blood cell indices, smoking habits, and CHRNA3 (alpha 3 nicotinic cholinergic receptor) rs1051730 genotype, where the T allele causes higher tobacco consumption; 41 759 were former smokers and 17 852 current smokers. In multivariable adjusted observational analyses and compared with never smokers, white blood cells were associated with up to 19% increases, thrombocytes with up to 4.7% increases, and red blood cell indices with up to 2.3% increases in former and current smokers. All associations were dose dependent, with tobacco consumption but for white blood cells and thrombocytes also dependent on smoking cessation time in former smokers; highest increases were for <1-year smoking cessation and lowest increases for >10-year smoking cessation. In age- and sex-adjusted genetic analyses, percent differences per T allele increase in current smokers were 1.15% (95% CI, 0.61%-1.68%) for leukocytes, 1.07% (0.38%-1.76%) for neutrophils, 1.34% (0.66%-2.02%) for lymphocytes, 1.50% (0.83%-2.18%) for monocytes, -0.60% (-1.91% to 0.74%) for eosinophils, 0.17% (-0.94% to 1.29%) for basophils, 0.38% (-0.17% to 0.93%) for thrombocytes, 0.04% (-0.14% to 0.23%) for erythrocytes, 0.34% (0.17% to 0.50%) for hematocrit, 0.26% (0.09% to 0.43%) for hemoglobin, and 0.29% (0.18% to 0.41%) for mean corpuscular volume. Conclusions- Smoking causes increased blood leukocytes, neutrophils, lymphocytes, and monocytes, as well as increased hematocrit, hemoglobin, and mean corpuscular volume. The observational smoking relationships were long term for white blood cells and short term for red blood cell indices.

OriginalsprogEngelsk
TidsskriftArteriosclerosis, Thrombosis, and Vascular Biology
Vol/bind39
Udgave nummer5
Sider (fra-til)965-977
Antal sider13
ISSN1079-5642
DOI
StatusUdgivet - maj 2019

ID: 57033945