Tobacco smoke

Summary

Tobacco smoke is a sooty aerosol produced by the incomplete combustion of tobacco during the smoking of cigarettes and other tobacco products. Temperatures in burning cigarettes range from about 400 °C between puffs to about 900 °C during a puff. During the burning of the cigarette tobacco (itself a complex mixture), thousands of chemical substances are generated by combustion, distillation, pyrolysis and pyrosynthesis. Tobacco smoke is used as a fumigant and inhalant. Composition List of additives in cigarettes The particles in tobacco smoke are liquid aerosol droplets (about 20% water), with a mass median aerodynamic diameter (MMAD) that is submicrometer (and thus, fairly "lung-respirable" by humans). The droplets are present in high concentrations (some estimates are as high as 1010 droplets per cm3). Most cigarettes today contain a cigarette filter, which can reduce "tar" and nicotine smoke yields up to 50% by several different mechanisms, with an even greate

Official source

https://en.wikipedia.org/wiki/Tobacco_smoke

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Related publications (2)

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Oxidative stress can contribute to the development of diseases, and may originate from exposures to toxicants commonly found in air pollution and cigarette smoke such as polycyclic aromatic hydrocarbons (PAHs) and volatile organic compounds (VOCs). Yet, associations between these exposures and oxidative stress biomarkers are poorly characterized. We report here novel associations between 14 exposure biomarkers of PAHs and VOCs, and two oxidative stress biomarkers; 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG) and 8-isoprostaglandin F2α (8-isoprostane) in urine obtained from smokers participating in an ongoing clinical study (ESTxENDS, NCT03589989). We also assessed associations between six biomarkers of tobacco smoke exposure (metabolites of nicotine and tobacco-specific nitrosamines (TSNAs)) and both oxidative stress biomarkers. We then quantified the relative importance of each family of the 20 exposure biomarkers on oxidative stress. Participating smokers (153 men and 117 women, median age 44 years) had on average smoked 25 [2–62] years and smoked about 17 [5–40] cigarettes per day at the time of the study. Multiple linear regression results showed an association between 8-oxodG concentrations and the following metabolites in decreasing relative importance: PAHs (beta coefficient β = 0.105, p-value VOCs (β = 0.028, p < 0.001, partial R² = 0.09) > nicotine (β = 0.226, p < 0.001, partial R² = 0.08); and between 8-isoprostane concentrations and metabolites of PAHs (β = 0.117, p < 0.001, partial R² = 0.14) > VOCs (β = 0.040, p < 0.001, partial R² = 0.14) > TSNAs (β = 0.202, p = 0.003, partial R² = 0.09) > nicotine (β = 0.266, p < 0.001, partial R² = 0.08). Behavioral factors known to contribute to oxidative stress, including sleep quality, physical activity, and alcohol consumption, did not play a significant role. Exposures to PAHs and VOCs among smokers were significantly associated with oxidative stress.

Elsevier2022

Increased Myeloid Cell Production and Lung Bacterial Clearance in Mice Exposed to Cigarette Smoke

Alessandra Piersigilli

Pneumonia is a leading cause of hospitalization in patients with chronic obstructive pulmonary disease (COPD). Although most patients with COPD are smokers, the effects of cigarette smoke exposure on clearance of lung bacterial pathogens and on immune and inflammatory responses are incompletely defined. Here, clearance of Streptococcus pneumoniae and Pseudomonas aeruginosa and associated immune responses were examined in mice exposed to cigarette smoke or after smoking cessation. Mice exposed to cigarette smoke for 6 weeks or 4 months demonstrated decreased lung bacterial burden compared with air-exposed mice when infected 16 to 24 hours after exposure. When infection was performed after smoke cessation, bacterial clearance kinetics of mice previously exposed to smoke reversed to levels comparable to those of control mice, suggesting that the observed defects were not dependent on adaptive immunological memory to bacterial determinants found in smoke. Comparing cytokine levels and myeloid cell production before infection in mice exposed to cigarette smoke with mice never exposed or after smoke cessation revealed that reduced bacterial burden was most strongly associated with higher levels of IL-1 beta and granulocyte-macrophage colony-stimulating factor in the lungs and with increased neutrophil reserve and monocyte turnover in the bone marrow. Using Serpinb1a-deficient mice with reduced neutrophil numbers and treatment with granulocyte colony-stimulating factor showed that increased neutrophil numbers contribute only in part to the effect of smoke on infection. Our findings indicate that cigarette smoke induces a temporary and reversible increase in clearance of lung pathogens, which correlates with local inflammation and increased myeloid cell output from the bone marrow.

Amer Thoracic Soc2016

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