Smokers Have Reduced Nitric Oxide Production by Conducting Airways but Normal Levels in the Alveoli

Pietropaoli, Anthony P.; Perillo, Irene; Perkins, Peter T.; Frasier, Lauren M.; Speers, Donna M.; Frampton, Mark W.; Utell, Mark J.; Hyde, Richard W.

doi:10.1080/08958370701260673

Cited by 11 publications

(12 citation statements)

References 39 publications

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“…In accordance with the present findings, several studies have previously reported reduced FeNO levels in asthmatic smokers 10,26–28 . Reduction in FeNO may be attributed to (i) inhibition of nitric oxide synthase due to high concentrations of exogenous NO in cigarette smoke; (ii) increased levels of carbon monoxide in the airways of smokers, which also inhibits nitric oxide synthase; and (iii) the conversion of NO to peroxynitrite through reaction with other oxygen species or oxygen free radicals 29,30 . FeNO also did not differ significantly between asthmatic smokers and healthy smokers and this is in agreement with two previous studies 26,31 …”

Section: Discussionsupporting

confidence: 92%

Exhaled nitric oxide and exhaled breath condensate pH as predictors of sputum cell counts in optimally treated asthmatic smokers

et al. 2011

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Section: Discussionsupporting

confidence: 92%

Exhaled nitric oxide and exhaled breath condensate pH as predictors of sputum cell counts in optimally treated asthmatic smokers

et al. 2011

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“…This decline may be associated with oxidant injury from the chemical milieu contained in tobacco smoke. Moreover, the persistent upregulation of CBF through an NO pathway may create a rich background for nitration of critical proteins with potentially pathogenic consequences (35). These studies document the immediate physiologic response of the airway epithelium to upregulate CBF upon exposure to tobacco smoke but more importantly suggest that that protracted exposures promote the persistence of this upregulation.…”

Section: Discussionmentioning

confidence: 99%

Increased nasal epithelial ciliary beat frequency associated with lifestyle tobacco smoke exposure

Zhou

Wang²,

Brighton

et al. 2009

Inhalation Toxicology

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The ciliated epithelium of the respiratory airways is one of the first vital systemic surfaces in contact with the ambient air. Ex vivo nasal epithelial ciliary beat frequency (CBF) at room temperature is on the order of 7–8 Hz but may be stimulated by irritant exposure. The upregulation of CBF in response to acute irritant exposure is generally considered to be a transient event with eventual return to baseline. However, studies of CBF dynamics in response to typical lifestyle exposures are limited. This study assessed nasal epithelial CBF among human subjects as a function of quantifiable lifestyle tobacco smoke exposure. Nasal epithelial biopsies were obtained from human subjects with well documented histories of tobacco smoke exposure. CBF was determined using a digital photometric technique and concurrent assays of nasal nitric oxide and urine cotinine and creatinine were performed. Mean CBF among active smokers and non-smokers exposed to environmental tobacco smoke (ETS) was elevated over non-smokers. Although there were dramatic differences in relative levels of tobacco smoke exposure, CBF values among tobacco smoke-exposed groups were comparable. Parallel in vitro studies of cultured nasal epithelium exposed to cigarette smoke condensate further supported these observations. These studies suggest that persistent elevation in nasal epithelial CBF is an early, subtle, physiologic effect associated with lifestyle tobacco smoke exposure. The molecular mechanisms that upregulate CBF may also create a cell molecular milieu capable of provoking the eventual emergence of more overt adverse health effects and the pathogenesis of chronic airway disease.

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“…The inducible NOS (iNOS) is transcriptionally regulated by pro-inflammatory cytokines in epithelial cells and macrophages in the airways (144). FeNO has been shown to be decreased by almost 50% in smokers in several cross-sectional studies (145–148), possibly related to the large amount of NO in cigarette smoke (146). The reduction in FeNO also is thought to be related to nitric oxide synthase inhibition due to cigarette smoke carbon monoxide and/or oxygen free radicals (146, 149).…”

Section: Introductionmentioning

confidence: 99%

“…FeNO has been shown to be decreased by almost 50% in smokers in several cross-sectional studies (145–148), possibly related to the large amount of NO in cigarette smoke (146). The reduction in FeNO also is thought to be related to nitric oxide synthase inhibition due to cigarette smoke carbon monoxide and/or oxygen free radicals (146, 149). Reduced FeNO has been reported to be significantly associated with increased neutrophilic inflammation (150).…”

Section: Introductionmentioning

confidence: 99%

A Review of Pulmonary Toxicity of Electronic Cigarettes in the Context of Smoking: A Focus on Inflammation

Shields

Berman

Brasky

et al. 2017

Cancer Epidemiology, Biomarkers &Amp; Prevention

107

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The use of electronic cigarettes (e-cigs) is increasing rapidly, but their effects on lung toxicity are largely unknown. Smoking is a well-established cause of lung cancer and respiratory disease, in part through inflammation. It is plausible that e-cig use might affect similar inflammatory pathways. E-cigs are used by some smokers as an aid for quitting or smoking reduction, and by never smokers (e.g., adolescents and young adults). The relative effects for impacting disease risk may differ for these groups. Cell culture and experimental animal data indicate that e-cigs have the potential for inducing inflammation, albeit much less than smoking. Human studies show that e-cig use in smokers is associated with substantial reductions in blood or urinary biomarkers of tobacco toxicants when completely switching and somewhat for dual use. However, the extent to which these biomarkers are surrogates for potential lung toxicity remains unclear. The FDA now has regulatory authority over e-cigs and can regulate product and e-liquid design features such as nicotine content and delivery, voltage, e-liquid formulations, and flavors. All of these factors may impact pulmonary toxicity. This review summarizes current data on pulmonary inflammation related to both smoking and e-cig use, with a focus on human lung biomarkers.

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Smokers Have Reduced Nitric Oxide Production by Conducting Airways but Normal Levels in the Alveoli

Cited by 11 publications

References 39 publications

Exhaled nitric oxide and exhaled breath condensate pH as predictors of sputum cell counts in optimally treated asthmatic smokers

Exhaled nitric oxide and exhaled breath condensate pH as predictors of sputum cell counts in optimally treated asthmatic smokers

Increased nasal epithelial ciliary beat frequency associated with lifestyle tobacco smoke exposure

A Review of Pulmonary Toxicity of Electronic Cigarettes in the Context of Smoking: A Focus on Inflammation

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