Secondhand Smoke Exposure, Pulmonary Function, and Cardiovascular Mortality

Eisner, Mark D.; Wang, Yue; Haight, Thaddeus; Balmes, John R.; Hammond, S. Katharine; Tager, Ira B.

doi:10.1016/j.annepidem.2006.10.008

Cited by 85 publications

(70 citation statements)

References 69 publications

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“…The present concentrations of IL-5, IL-6, and IFN-g after SHS exposure were linked with the marked decreases in FEV 1 and FEV 1 /FVC ratio, confirming the association between circulating inflammation markers and FEV 1 (29). In turn, lower FEV 1 and FEV 1 / FVC ratio are associated with a greater prospective risk of cardiovascular mortality among nonsmokers (22). The current finding that inflammatory cytokine levels remain elevated for at least 3 hours after SHS exposure alludes to chronic low-grade systemic inflammation in individuals exposed to SHS on a daily basis and/or at higher smoke concentrations.…”

Section: Table 2 Cotinine Concentrations Cytokine Levels and Time supporting

confidence: 56%

“…Previous epidemiological studies have shown that chronic SHS is associated with a reduction of several lung function measures, yet these findings have not been consistent, and methodological issues have constrained interpretation of the findings (22). The present data show clearly a significant effect of acute SHS on FEV 1 , FEV 1 /FVC ratio, MEF 75% , MEF 50% , and MEF 25% .…”

Section: Discussionsupporting

confidence: 43%

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Acute and Short-term Effects of Secondhand Smoke on Lung Function and Cytokine Production

Flouris

Metsios²,

Carrillo³

et al. 2009

Am J Respir Crit Care Med

108

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Rationale: The acute effect of secondhand smoke (SHS) on lung function and the duration of system disruption remain unknown. Objectives: To assess the SHS effects and their duration on lung function and inflammatory markers. Methods: In a randomized single-blind crossover experiment data were obtained from 16 (8 women) nonsmoking adults at baseline and at 0, 1, and 3 hours after a 1-hour SHS exposure set at bar/ restaurant SHS levels. Measurements and Main Results: Serum and urine cotinine, lung function, and cytokines IL-4, IL-5, IL-6, tumor necrosis factor (TNF)-a, and IFN-g. At 0 hours most lung function parameters were significantly reduced (indicative: FEV 1 , 4.3 6 0.4 vs. 3.8 6 0.3 L; FEV 1 /FVC, 0.9 6 0.1 vs. 0.8 6 0.1; P , 0.05) but at 3 hours they were at baseline levels. In contrast, cotinine (serum, 8.9 6 3.2 vs. 35.5 6 10.2 ngÁml 21 ), IL-4 (41.3 6 5.8 vs. 44.2 6 4.5 pgÁml 21 ), IL-5 (36.1 6 3.2 vs. 60.1 6 7.0 pgÁml 21 ), IL-6 (2.5 6 0.3 vs. 7.6 6 1.4 pgÁml 21 ) and IFN-g (0.3 6 0.2 vs. 0.6 6 0.2 IUÁml 21 ) at 3 hours were higher than at baseline (P , 0.05). IL-4 and TNF-a increased only in men, whereas IL-5, IL-6, and IFN-g were different between sexes after exposure (P , 0.05). Regression analyses revealed inverse associations of FEV 1 and FEV 1 /FVC ratio with IL-5 (P , 0.05) in men and with IL-5 (P 5 0.01), IL-6 (P , 0.001), IFN-g (P 5 0.034) and serum cotinine (P , 0.001) in women. Conclusions: We conclude that 1 hour of SHS exposure at bar/ restaurant levels is accompanied by significant decrements on lung function and marked increases in inflammatory cytokines, particularly in men. More importantly, whereas most smoke-induced effects on lung function appear to recede within 60 minutes, inflammatory cytokines remain elevated for at least 3 hours after exposure to SHS. Keywords: passive smoking; cotinine; respiration; inflammatory markersIn the 10 minutes you will spend reading this article, 111 people will die somewhere in the world from tobacco-induced illnesses.* Fourteen of them have never smoked. † An overwhelming amount of evidence has emerged over the past decades on the adverse health effects of secondhand smoke (SHS) (1-5). Nevertheless, more than 126 million American and 130 million Chinese adult nonsmokers suffer daily SHS exposure, whereas global estimates include 700 million children and 50 million pregnant women (1). Latest reports show that, despite current measures, the prevalence rates of smoking are increasing (2, 3), while the tobacco industry predicts a global expansion of the tobacco epidemic in the near future (3). Moreover, arguments are being expressed that only chronic exposures to SHS represent a health risk and that there is no scientific basis for claims that brief, acute, transient SHS exposures represent a significant acute health hazard in nonsmokers (6). This is, in part, because our knowledge on the effects of SHS is based predominantly on longitudinal epidemiological studies, whereas experimental studies assessing the acute and short-term effects of SHS are sca...

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Section: Table 2 Cotinine Concentrations Cytokine Levels and Time supporting

confidence: 56%

Section: Discussionsupporting

confidence: 43%

Acute and Short-term Effects of Secondhand Smoke on Lung Function and Cytokine Production

Flouris

Metsios²,

Carrillo³

et al. 2009

Am J Respir Crit Care Med

108

View full text Add to dashboard Cite

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“…An increase in inflammatory markers such as L-1β, IL-4, TNF-α, white blood cell count, C-reactive protein, homocysteine, fibrinogen, as well as leukocyte counts accompanied by an immune cell activation has been shown [21,22] . Besides this, a greater decline in lung function, elevated risk of cardiovascular mortality and induction of growth factors (connective tissue growth factor, TGF-β, PDGF-A and B) are also known [23,24] . Whether some reactions to inhalation of environmental tobacco smoke or tobacco smoke in general triggers vascular remodeling, similar to that seen in vasoproliferative PAH, is speculative and should be interpreted with caution.…”

Section: Discussionmentioning

confidence: 99%

Tobacco Smoke Exposure in Pulmonary Arterial and Thromboembolic Pulmonary Hypertension

Keusch¹,

Hildenbrand²,

Bollmann³

et al. 2014

Respiration

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BACKGROUND: Animal studies and data from a single-center study suggest that tobacco smoke exposure may be a risk factor for precapillary pulmonary hypertension (PH). OBJECTIVE: We aimed to survey tobacco smoke exposure in a large PH collective and to compare it with epidemiological data from healthy subjects. METHODS: This is an international, multicenter, case-control study including patients with pulmonary arterial and chronic thromboembolic PH. All patients were asked specific questions about tobacco smoke exposure. Healthy controls were retrieved from the Swiss Health Survey (n = 18,747). RESULTS: Overall (n = 472), 49% of PH patients were smokers and there was a clear sex difference (women 37%, men 71%). Significantly more PH men were smokers compared with healthy controls, whereas less PH women were ever active smokers. However, 50% of the non-smoking PH women were exposed to secondhand smoke, leading to a significantly higher number of tobacco smoke-exposed individuals compared to healthy controls. PH smokers were significantly younger compared to those not exposed. CONCLUSION: Active and environmental tobacco smoke exposure is common in PH. The higher prevalence of male PH smokers, the higher exposure to environmental tobacco smoke in PH women compared to healthy controls and the lower age at PH diagnosis in smokers may indicate a pathogenic role of tobacco smoke exposure in PH. were smokers compared with healthy controls, whereas less PH women were ever active smokers. However, 50% of the non-smoking PH women were exposed to secondhand smoke, leading to a significantly higher number of tobacco smoke-exposed individuals compared to healthy controls. PH smokers were significantly younger compared to those not exposed. Conclusion: Active and environmental tobacco smoke exposure is common in PH. The higher prevalence of male PH smokers, the higher exposure to environmental tobacco smoke in PH women compared to healthy controls and the lower age at PH diagnosis in smokers may indicate a pathogenic role of tobacco smoke exposure in PH.

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“…Despite the potential role of CXCL5 in pulmonary inflammation, the role of CXCL5 in tobacco smoke-induced lung inflammation has not been explored, to the best of our knowledge. Although epidemiological studies indicated an association between SHS exposures and health outcomes for patients with COPD (24,25), only a limited number of studies point to a mechanistic role for SHS in lung inflammation.…”

mentioning

confidence: 99%

Role of CXCL5 in Leukocyte Recruitment to the Lungs during Secondhand Smoke Exposure

Balamayooran¹,

Batra²,

Cai³

et al. 2012

Am J Respir Cell Mol Biol

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Chronic obstructive pulmonary disease (COPD) is the third leading cause of mortality in the United States. The major cause of COPD is cigarette smoking. Extensive leukocyte influx into the lungs, mediated by chemokines, is a critical event leading to COPD. Although both resident and myeloid cells secrete chemokines in response to inflammatory stimuli, little is known about the role of epithelial-derived chemokines, such as CXC chemokine ligand (CXCL)5, in the pathogenesis of cigarette smoke-induced inflammation. To explore the role of CXCL5, we generated CXCL5 genedeficient mice and exposed them to secondhand smoke (SHS) for 5 hours/day for 5 days/week up to 3 weeks (subacute exposure). We observed a reduced recruitment of leukocytes to the lungs of CXCL5 2/2 mice compared with their wild-type (WT) counterparts, and noted that macrophages comprised the predominant leukocytes recruited to the lungs. Irradiation experiments performed on CXCL5 2/2 or WT mice transplanted with WT or CXCL5 2/2 bone marrow revealed that resident but not hematopoietic cell-driven CXCL5 is important for mediating SHS-induced lung inflammation. Interestingly, we observed a significant reduction of monocyte chemotactic protein-1 (MCP-1/CC chemokine ligand 2) concentrations in the lungs of CXCL5 2/2 mice. The instillation of recombinant MCP-1 in CXCL52/2 mice reversed macrophage recruitment. Our results also show the reduced activation of NF-kB/p65 in the lungs, as well as the attenuated activation of C-Jun N-terminal kinase, p42/44, and p38 mitogen-activated protein kinases and the expression of intercellular adhesion molecule-1 in the lungs of SHS-exposed CXCL5 2/2 mice. Our findings suggest an important role for CXCL5 in augmenting leukocyte recruitment in SHS-induced lung inflammation, and provide novel insights into CXCL5-driven pathogenesis.Keywords: smoke; CXCL5/LIX; macrophages; chemokines; cytokines Chronic obstructive pulmonary disease (COPD) is the third leading cause of death in the United States (1-3). According to recent reports, the prevalence of COPD in the United States involves more than 12 million, with an annual mortality of 120,000 (1-3). COPD is an irreversible disease characterized by airway inflammation (chronic bronchitis) and airspace enlargement, along with the destruction of lung parenchyma (emphysema) (4, 5). Although the molecular and cellular mechanisms that contribute to the development of COPD are not well understood, substantial recruitment and activation of inflammatory cells into the airspaces and lung parenchyma has been documented in humans with COPD and implicated in its pathogenesis (4, 5).Cigarette smoking accounts for most of the debilitating effects of COPD, but other environmental risk factors include air pollution and chronic occupational exposure to various dusts (6). Why only a small proportion (10-20%) of smokers develops COPD remains unclear (7). Cigarette smoke (CS) contains more than 4,700 chemicals (8), and is a powerful inducer of inflammatory mediators, including oxidants and proteases,...

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Secondhand Smoke Exposure, Pulmonary Function, and Cardiovascular Mortality

Cited by 85 publications

References 69 publications

Acute and Short-term Effects of Secondhand Smoke on Lung Function and Cytokine Production

Acute and Short-term Effects of Secondhand Smoke on Lung Function and Cytokine Production

Tobacco Smoke Exposure in Pulmonary Arterial and Thromboembolic Pulmonary Hypertension

Role of CXCL5 in Leukocyte Recruitment to the Lungs during Secondhand Smoke Exposure

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