Search

Summary The use of electronic cigarettes (ECs) has grown exponentially over the past few years in China. To obtain the basic information of Chinese EC users, a questionnaire survey was performed to collect the data that describe characteristics of study populations, including daily usage, consumption preference, and risk perception. Volunteers were recruited from Beijing, Shanghai, Guangzhou, and Shenzhen cities of China. In total, among the 511 participants that were included in the analysis, 491 participants (95%) used refillable ECs in the past 3 months. There was a strong association between EC use and traditional cigarette smoking. The majority of participants were dual users and the number of cigarettes smoked decreased with the use of ECs. After using an EC, 20.7% of conventional cigarette smokers attempted to quit smoking. Young people were the primary users across all geographic locations. Specifically, the daily usage for the participants who were 18–39 years old, was higher than those over 40 years old. The majority of participants (59.9%) preferred fruit flavors and 57.8% of them used 1–5 mg/mL nicotine-concentration liquids. Most EC users are motived to quit smoking, and 74.6% claimed that the ECs had no irritant effect on the oral cavity. A total of 50.5% of family members of the study participants reported an improvement of health status while the participants used ECs instead of traditional cigarettes. Overall, the results of this Chinese survey indicate that the per-day cigarette consumption of the dual users decreased whereas their proportion of smokers of low-“tar” cigarettes increased.

Summary With the rapid popularity and increasing numbers of E-cigarette (EC) users, debates on possible health risks and regulation of EC products have attracted attention in public. As a useful means to help assessing the risks of EC consumers, puffing topography studies have come to be an important tool globally. In this paper, a cross-sectional epidemiological study on puffing topography of 511 EC consumers in four cities of China was conducted in January 2018. Data acquisition was based on a questionnaire and a Clinical Research Support System (CReSS) Pocket device for the smoking behavior recording. The results showed that EC consumers in the four cities were mainly young males, most of whom preferred tank systems with zero or low nicotine concentrations (1–5 mg/mL) in the liquid. The average puff volume, puff duration and inter-puff interval (IPI) were 87.2 mL, 1.97 s and 22.0 s, respectively. The factors that may have affected puffing topography such as product type, nicotine concentration, using time, smoking status and battery power were studied. The results suggest that the EC product type and the concentration of nicotine in EC liquids were the main factors that affected the puffing topography of the users. This study was the first study on the puff topography of Chinese EC consumers with a large number of participants. The results may not only help to more deeply understand smoking behavior and to better assess the potential risks for the EC users, but they may also supply useful information for the development of smoking machine regimes for ECs.

Summary Smoking is mainly sustained by nicotine dependence (ND), which varies across ethnic groups principally due to genetic as well as environmental factors. The Fagerström Test for Nicotine Dependence (FTND) and biomarkers of tobacco exposure are two important approaches to assess ND. However, the relationship between ND and FTND of Chinese smokers has not been studied. The aim of this study was to assess the relationship between FTND scores and nicotine, cotinine, 3′-hydroxycotinine (3HC) and nicotine metabolite ratio (NMR, the concentration ratio of 3HC to cotinine) in Chinese smokers. FTND was carried out and general characteristics were collected using a self-administered smoking questionnaire with 289 smokers. Nicotine, cotinine and 3HC in urine were simultaneously determined by liquid chromatography–mass spectrometry/mass spectrometry (LC-MS/MS). The concentrations of nicotine, cotinine and 3HC in the urine of smokers with a high FTND score were higher than in the urine of those with a low FTND score. There were significant correlations between urinary biomarker and FTND scores. Except for FTND item 2 (difficulty to refrain), the other items showed significant associations with the urinary biomarkers. No relationship was found between the nicotine metabolite ratio (NMR, 3′-hydroxycotinine/cotinine) and FTND scores or general characteristics of the participants. In conclusion, biomarkers of tobacco exposure levels are significantly associated with FTND scores. However, FTND Item 2 and NMR were not found to be associated with nicotine dependence in Chinese smokers.

Cigarette smoke significantly induces oxidative stress, resulting in cardiovascular disease. NRF2, a well-known anti-oxidative stress response factor, is generally considered to play protective roles in cardiovascular dysfunction triggered by oxidative stress. Interestingly, recent studies reported adverse effects of NRF2 on the cardiovascular system. These unfavourable pathogenic effects of NRF2 need to be further investigated. Our work shows that cigarette smoke extract (CSE)-induced oxidative stress disturbs fibronectin (FN) assembly during angiogenesis. Furthermore, this effect largely depends on hyperactive NRF2-STAT3 signalling, which consequently promotes abnormal FN deposition. Consistently, disruption of this pathway by inhibiting NRF2 or STAT3 prevents CSE-induced FN disorganization and vasculature disruption in human umbilical vein endothelial cells or zebrafish. Taken together, these findings disclose the cardiovascular dysfunction caused by CSE from a novel perspective that NRF2-dependent signalling engages in FN disorganization.

The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is classified as a Group 1 human carcinogen. It is metabolically activated by P450 enzymes to intermediate methylate and pyridyloxobutylate DNA, resulting in the formation of DNA adduct that is critical for the carcinogenicity of NNK. To directly and objectively examine the DNA adduct formation profiles without the complexity of factors in vivo, in the present study, five kinds of methyl DNA adducts were first identified in the incubation model of NNK established with human lung epithelial cells (BEAS-2B). The level of methyl DNA adducts and metabolites of NNK were quantitatively analyzed, respectively. With the increase of exposure time and dose, the level of methyl DNA adducts and metabolites increased. Furthermore, with the changes of the activity of P450 enzymes, which is the main enzyme regulating the α-hydroxylation of NNK, we found the levels of both methyl adducts and metabolites formed via α-hydroxylation in experimental groups showed the same trend compared with those in control group, while the metabolites formed via other pathways changed in the opposite trend. The result proves that the methyl adducts induced by NNK generate via α-hydroxylation pathway in BEAS-2B cells.

Smokeless tobacco products provide an alternative to cigarettes; however, smokeless tobacco is carcinogenic and harmful to human health. This study evaluated the toxicological effects of snus extracts and cigarette smoke total particulate matter (TPM) on human umbilical vein endothelial cells (HUVECs). Treated cells were examined for cell viability, reactive oxygen species (ROS), apoptosis, and inflammatory cytokines. Moreover, we explored the mechanism of programmed cell death induced by snus. The results showed that snus extracts significantly inhibited cell viability in a dose-dependent manner. ROS was significantly increased in treatment groups, and anti-oxidant treatment could not prevent snus extract-induced cell death. Snus extracts induced apoptosis, DNA damage, activation and cleavage of caspase-3 and caspase-8, pathway-related gene change, and interleukin (IL)-6 and IL-8 release in HUVECs. Snus extracts exposure may induce cytotoxicity, ROS generation, inflammatory cytokines release, and apoptosis or DNA damage through intrinsic and extrinsic pathways in HUVECs.

Rapid risk assessment models for different types of cigarette smoke extract (CSE) exposure are critical to understanding the etiology of chronic obstructive pulmonary disease. The present study investigated inflammation of cultured tracheal tissues with CSE exposure. Rat trachea rings were isolated, cultured, then exposed to various concentrations of CSE from 3R4 F reference cigarettes for 4 h. Tissue/cellular morphology, ultrastructure, viability and damage, inflammatory cell infiltration, and inflammatory protein levels were measured and compared to untreated controls. Human bronchial epithelial cells (BEAS-2B) exposed to 0 or 300 μg/mL CSE were cocultured with macrophages to assess extent of mobilization and phagocytosis. Endotracheal epithelium cilia densities were significantly reduced with increasing CSE concentrations, while mucous membranes became increasingly disordered; both eventually disappeared. Macrophages became larger as the CSE concentration increased, with microvilli and extended pseudopodium covering their surface, and many primary and secondary lysosomes present in the cytoplasm. Inflammatory cell infiltration also increased with increasing CSE dose, as did intracellular adhesion molecule-1(ICAM-1), interleukin-6(IL-6). The method described here may be useful to qualitatively characterized the effects of the compound under study. Then, we use BEAS-2B cell line system to strength the observation made in the cultured tissues. Probably, an approach to integrate results from both experiments will facilitate its application. These results demonstrate that cultured rat tracheal rings have a whole-tissue structure that undergoes inflammatory processes similar to in vivo tissues upon CSE exposure.