Cigarette

Summary

A cigarette is a narrow cylinder containing a combustible material, typically tobacco, that is rolled into thin paper for smoking. The cigarette is ignited at one end, causing it to smolder; the resulting smoke is orally inhaled via the opposite end. Cigarette smoking is the most common method of tobacco consumption. The term cigarette, as commonly used, refers to a tobacco cigarette, but the word is sometimes used to refer to other substances, such as a cannabis cigarette or an herbal cigarette. A cigarette is distinguished from a cigar by its usually smaller size, use of processed leaf, and paper wrapping, which is typically white. Since the 1920s, cigarettes have been a major source of advertising revenue for the media, of traffic for small stores, and of tax revenue for governments. Since the 1920s, scientists and doctors have been able to link smoking with respiratory illness. Researchers have identified negative health effects from smoking cigarettes such as cancer, chronic o

Official source

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

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Associations between urinary biomarkers of oxidative stress and biomarkers of tobacco smoke exposure in smokers

Florian Frédéric Vincent Breider, Dominique Grandjean, Nicolas Sambiagio

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

Re-assessing the Formation of N-nitrosamines during Chloramination of Various Nitrogenous Compounds using Specific and Total N-nitrosamines Analysis

Florian Frédéric Vincent Breider, Andrea Piazzoli, Urs von Gunten

N-nitrosamines (NOAs) are potent carcinogenic and mutagenic compounds that can be present in water, biological fluids, food, consumer products and cigarette smoke. Several studies have shown that the formation of NOAs in water can arise from the reactions of amine precursors with chemical oxidants such as chloramines, chlorine or ozone.1–3 So far most of the studies published on NOAs in water have focused on only nine specific NOAs selected by the US-Environmental Protection Agency (EPA). However several recent studies have shown that the NOAs selected by the US-EPA might account only for ~5-15% of the total NOAs concentration (TONO) in wastewater.2,4 Therefore, quantifying the TONO is necessary to assess the overall risk associated with the presence of NOAs in water. Many tertiary and quaternary amines present in consumer products (e.g., pharmaceuticals, personal care and household products) are known to be N nitrosodimethylamine (NDMA) precursors during chloramination, but the formation of other NOAs has been rarely studied.5 In this study we have re-evaluated the NOAs formation potential (FP) of various nitrogen-containing micropollutants (chlorhexidine, metformin, benzalkonium chloride and cetyltrimethylammonium chloride) and tertiary and quaternary model amines (trimethyl amine, N,N dimethylbutyl amine, N,N dimethylbenzyl amine and tetramethyl ammonium) using specific NOAs and TONO analysis. All the studied nitrogenous micropollutants displayed quantifiable TONO FP, with molar yields ranging from 0.04 to 11.92%. However, the observed TONO pools constituted mostly of uncharacterized species, not included in US-EPA 8270 NOAs standard mix. Only the benzalkonium chloride showed quantifiable NDMA FP (0.56% molar yield), however, explaining only a minor fraction of the observed TONO FP. The studied model amines showed molar NDMA yields from 0.10% to 5.05%, very similar to the molar TONO yields. LC-qTOF screening of a list of proposed NOAs structures has enabled to identify a novel NOA (N-nitroso-N-methyldodecylamine) from the chloramination of benzalkonium chloride. This finding supports the hypothesis that different functional groups in quaternary amines can act as leaving groups during chloramination and form differing NOA structures at significant yield.

2018

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.