The Interactions Between Cigarette Smoking and Reduced Lung Function on Systemic Inflammation

doi:10.1378/chest.127.2.558

Chest

Volume 127, Issue 2, February 2005, Pages 558-564

https://doi.org/10.1378/chest.127.2.558 Get rights and content

Background

Low-grade systemic inflammation is commonly observed in conditions associated with reduced FEV₁. Active cigarette smoking, which is a leading risk factor for decreased FEV₁, can also independently induce systemic inflammation.

Study objectives

To determine the independent contributions of active cigarette smoking and reduced FEV₁ (as well as their potential interactions) on systemic inflammation.

Design

Cross-sectional survey.

Setting

The US general population.

Participants

A total of 7,685 adult participants, ≥ 40 years of age, in the Third National Health and Nutrition Examination Survey, who had acceptable data on spirometry and laboratory measurements such as serum C-reactive protein (CRP).

Measurements

The participants were stratified into four equal groups (quartiles) based on the percent predicted FEV₁ values. Each group was further categorized as active smokers or nonsmokers according to serum cotinine level (ie, ≥ 10 or < 10 ng/mL). Serum levels of CRP, plasma fibrinogen, blood leukocytes, and platelets were compared across the predicted FEV₁ quartile groups and across smoking status using multiple logistic regression models.

Results

We found that active smoking by itself increased the odds of having elevated CRP levels by 63% (adjusted odds ratio [OR], 1.63; 95% confidence interval, 1.28 to 2.09). The adjusted OR for reduced FEV₁ was 2.27 (95% confidence interval, 1.92 to 2.70). Having both risk factors increased the OR to 3.31 (95% confidence interval, 2.73 to 4.02). Similar findings were observed for blood leukocytes and plasma fibrinogen.

Conclusion

These findings suggest an additive effect of active smoking and reduced FEV₁ on markers of systemic inflammation and suggest their potential interactions in the pathogenesis of systemic complications observed in patients with poor lung function.

Section snippets

Study Sample

NHANES 3 was conducted from 1988 to 1994 in the United States by the National Center for Health Statistics of the Centers for Disease Control and Prevention. This was a cross-sectional, multistage, probability representative sample of the civilian noninstitutionalized US population.¹⁸ Once chosen, study participants were asked to complete a questionnaire and a comprehensive physical examination, which included spirometric measurements either in the household or at a specially equipped mobile

Results

The baseline characteristics of the study population are summarized in Table 1. Quartile 1 (lowest FEV₁) contained more whites, more active smokers, and more men than quartile 4 (highest FEV₁). Individuals in quartile 1 tended to be older than those in quartile 4. There were no significant differences in the BMI across the quartiles. Crudely, those in quartile 1 had higher leukocyte, fibrinogen, and CRP levels than those in quartile 4 (Table 1). Adjustments of various factors such as age, sex,

Discussion

The most important and novel finding of this study was that active cigarette smoking and poor FEV₁ had an additive effect on systemic markers of inflammation. Individually, active smoking (as defined by a serum cotinine level of ≥ 10 ng/mL) and reduced FEV₁ (as defined by an FEV₁ of ≤ 83.2% predicted) were associated with 1.6 and 2.3 increased odds of elevated CRP, respectively. For individuals with both of these risk factors, the odds increased by 3.3-fold, indicating an additive response.

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Les études comparant les profils inflammatoires systémiques des fumeurs atteints et indemnes de BPCO présentent des conclusions discordantes.
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Il s’agit d’une étude prospective de type comparative incluant deux groupes de fumeurs actifs de plus de 10 paquets-années et cliniquement stables : 56 BPCO consécutifs (VEMS/CVF postbronchodilatateur < 0,70) et 32 fumeurs consécutifs non BPCO (VEMS/CVF postbronchodilatateur ≥ 0,70). Le tabagisme et les données cliniques, anthropométriques et spirométriques ont été notés. Les marqueurs biologiques sanguins suivants ont été déterminés : leucocytes, hémoglobine, facteur de nécrose tumorale-α (TNF-α), interleukine-6 (IL-6), protéine C réactive (CRP) et vitesse de sédimentation (VS). Selon les taux (normaux/anormaux) de ces marqueurs, deux groupes de fumeurs ont été formés. Les variables quantitatives et qualitatives ont été exprimées, respectivement, en moyennes ± écart-types et en pourcentages.
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Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: [email protected]).

Dr. Sin was supported by a Canada Research Chair and a Michael Smith/St. Paul's Hospital Foundation Professorship. Drs. Sin and Man have received honoraria and research funding from GlaxoSmithKline, AstraZeneca, and Merck Frosst.

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Chest

Clinical Investigations: MiscellaneousThe Interactions Between Cigarette Smoking and Reduced Lung Function on Systemic Inflammation

Background

Study objectives

Design

Setting

Participants

Measurements

Results

Conclusion

Section snippets

Study Sample

Results

Discussion

Chest

Am J Med

Respir Med

Am J Cardiol

Am J Med

Am J Med

Impaired lung function and mortality risk in men and women: findings from the Renfrew and Paisley prospective population study

BMJ

Occurrence and prognostic significance of ventricular arrhythmia is related to pulmonary function: a study from “men born in 1914,”

Circulation

Lung function and risk of myocardial infarction and sudden cardiac death

N Engl J Med

Amplification of inflammation in emphysema and its association with latent adenoviral infection

Am J Respir Crit Care Med

Association of fatigue with an acute phase response in sarcoidosis

Eur Respir J

Increased blood carboxyhaemoglobin concentrations in inflammatory pulmonary diseases

Thorax

Why are patients with chronic obstructive pulmonary disease at increased risk of cardiovascular diseases? The potential role of systemic inflammation in chronic obstructive pulmonary disease

Circulation

Evidence for a relation between metabolic derangements and increased levels of inflammatory mediators in a subgroup of patients with chronic obstructive pulmonary disease

Thorax

Elevated TNF-α production by peripheral blood monocytes of weight-losing COPD patients

Am J Respir Crit Care Med

Inflammatory response and body composition in chronic obstructive pulmonary disease

Am J Respir Crit Care Med

Atherosclerosis: an inflammatory disease

N Engl J Med

Clinical Investigations: Miscellaneous
The Interactions Between Cigarette Smoking and Reduced Lung Function on Systemic Inflammation