We have located links that may give you full text access.
Smoking, Systemic Inflammation, and Airflow Limitation: A Mendelian Randomization Analysis of 98 085 Individuals from the General Population.
Nicotine & Tobacco Research 2018 April 25
Introduction: Smoking is associated with systemic and local inflammation in the lungs. Furthermore, in chronic obstructive pulmonary disease (COPD), which is often caused by smoking, there is often systemic inflammation that is linked to lung function impairment. However, the causal pathways linking smoking, systemic inflammation, and airflow limitation are still unknown. We tested whether higher tobacco consumption is associated with higher systemic inflammation, observationally and genetically and whether genetically higher systemic inflammation is associated with airflow limitation.
Methods: We included 98085 individuals aged 20-100 years from the Copenhagen General Population Study; 36589 were former smokers and 16172 were current smokers. CHRNA3 rs1051730 genotype was used as a proxy for higher tobacco consumption and the IL6R rs2228145 genotype was used for higher systemic inflammation. Airflow limitation was defined as forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC)<70%.
Results: Difference in plasma level of C-reactive protein (CRP) was 4.8%(95% CI:4.4-5.2%) per 10 pack-year increase and 1.6%(0.4-2.8%) per T allele. Corresponding differences were 1.2%(1.1-1.3%) and 0.5%(0.3-0.8%) for fibrinogen, 1.2%(1.2-1.3%) and 0.7%(0.5-1.0%) for α1-antitrypsin, 2.0%(1.8-2.1%) and 0.7%(0.4-1.1%)for leukocytes, 1.9%(1.8-2.1%) and 0.8%(0.4-1.2%) for neutrophils, and 0.8%(0.7-1.0%) and 0.4%(0.1-0.7%) for thrombocytes. The differences in these levels were lower for former smokers compared to current smokers. The IL6R rs2228145 genotype was associated with higher plasma acute phase reactants but not with airflow limitation. Compared to the C/C genotype, the odds ratio for airflow limitation was 0.95(95% CI:0.89-1.02) for A/C genotype and 0.94(0.87-1.01) for A/A genotype.
Conclusions: Higher tobacco consumption is associated with higher systemic inflammation both genetically and observationally, while systemic inflammation was not associated with airflow limitation genetically.
Implications: The association between higher tobacco consumption and higher systemic inflammation may be causal, and the association is stronger among current smokers compared to former smokers, indicating that smoking cessation may reduce the effects of smoking on systemic inflammation. Systemic inflammation does not seem to be a causal driver in development of airflow limitation. These findings can help to understand the pathogenic effects of smoking and the interplay between smoking, systemic inflammation, and airflow limitation and hence development and progression of chronic obstructive pulmonary disease (COPD).
Methods: We included 98085 individuals aged 20-100 years from the Copenhagen General Population Study; 36589 were former smokers and 16172 were current smokers. CHRNA3 rs1051730 genotype was used as a proxy for higher tobacco consumption and the IL6R rs2228145 genotype was used for higher systemic inflammation. Airflow limitation was defined as forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC)<70%.
Results: Difference in plasma level of C-reactive protein (CRP) was 4.8%(95% CI:4.4-5.2%) per 10 pack-year increase and 1.6%(0.4-2.8%) per T allele. Corresponding differences were 1.2%(1.1-1.3%) and 0.5%(0.3-0.8%) for fibrinogen, 1.2%(1.2-1.3%) and 0.7%(0.5-1.0%) for α1-antitrypsin, 2.0%(1.8-2.1%) and 0.7%(0.4-1.1%)for leukocytes, 1.9%(1.8-2.1%) and 0.8%(0.4-1.2%) for neutrophils, and 0.8%(0.7-1.0%) and 0.4%(0.1-0.7%) for thrombocytes. The differences in these levels were lower for former smokers compared to current smokers. The IL6R rs2228145 genotype was associated with higher plasma acute phase reactants but not with airflow limitation. Compared to the C/C genotype, the odds ratio for airflow limitation was 0.95(95% CI:0.89-1.02) for A/C genotype and 0.94(0.87-1.01) for A/A genotype.
Conclusions: Higher tobacco consumption is associated with higher systemic inflammation both genetically and observationally, while systemic inflammation was not associated with airflow limitation genetically.
Implications: The association between higher tobacco consumption and higher systemic inflammation may be causal, and the association is stronger among current smokers compared to former smokers, indicating that smoking cessation may reduce the effects of smoking on systemic inflammation. Systemic inflammation does not seem to be a causal driver in development of airflow limitation. These findings can help to understand the pathogenic effects of smoking and the interplay between smoking, systemic inflammation, and airflow limitation and hence development and progression of chronic obstructive pulmonary disease (COPD).
Full text links
Related Resources
Trending Papers
Challenges in Septic Shock: From New Hemodynamics to Blood Purification Therapies.Journal of Personalized Medicine 2024 Februrary 4
Molecular Targets of Novel Therapeutics for Diabetic Kidney Disease: A New Era of Nephroprotection.International Journal of Molecular Sciences 2024 April 4
The 'Ten Commandments' for the 2023 European Society of Cardiology guidelines for the management of endocarditis.European Heart Journal 2024 April 18
A Guide to the Use of Vasopressors and Inotropes for Patients in Shock.Journal of Intensive Care Medicine 2024 April 14
Diagnosis and Management of Cardiac Sarcoidosis: A Scientific Statement From the American Heart Association.Circulation 2024 April 19
Essential thrombocythaemia: A contemporary approach with new drugs on the horizon.British Journal of Haematology 2024 April 9
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app