Electronic cigarettes (e-cigarettes) have rapidly increased in popularity within the last 2 years in Malaysia. The study aims to understand the association between e-cigarette use behaviors and salivary cotinine (a CYP2AA metabolite of nicotine) concentration to inform the development of future e-cigarette control policies. A convenience sample of saliva from 144 e-cigarette users was obtained between November and December 2015. The study participants used refill liquid containing between 0 and 12 mg/ml of nicotine. The overall median cotinine concentration of the study participants was 81.1 ng/ml (interquartile range = 8.5-195.8). Among the zero-nicotine and single e-cigarette users, the median cotinine level was 51.1 (interquartile range = 8.20-125.35) ng/ml. Factors significantly associated with a higher salivary cotinine concentration were dual use of e-cigarettes and tobacco cigarettes, regular and daily e-cigarette use, a longer duration of e-cigarette use, using a higher amount of e-liquid, and a shorter duration to finish a refill. Multivariate analysis revealed that e-cigarette use of 1-6 and 6-12 months (but not 1 month and below) was significantly associated with a higher cotinine concentration. Cotinine found in zero-nicotine e-liquids implies the importance of stringent regulatory governance for the consistency of labeled nicotine content of e-cigarette liquid in the market. Zero-nicotine e-cigarette users should also be informed of the likelihood of environmental exposure to tobacco smoke. Future studies conducted on larger samples are warranted to validate the association between duration of e-cigarette use and salivary cotinine concentration as well as to investigate underlying mechanisms.
Background: Consistency and accuracy of results in assessing health risks due to vaping or e-cigarette use are difficult to achieve without established consumption data. The present report covers baseline data on vaping topography and reasons for use among local users in Klang Valley, Malaysia.
Methods: An 80-item survey regarding socio-demographic characteristics, smoking topography and reasons for e-cigarette use was employed to assess e-cigarette users recruited from several public universities and private organisations. The survey questionnaire was self-administered. Data were analysed using statistical software.
Results: Eighty-six current e-cigarette users participated with more than half (51.2%) of them aged ≥ 25 years old. Significant proportions of the sample were single (51.2%), had a tertiary education level (63.5%) and a household income of less than USD1000 per month (65.2%). Median duration of e-cigarette use was less than a year; users drew approximately 50 puffs per day and refilled twice a day. The majority (74%) used e-liquids containing nicotine with a concentration of 6 μg/mL. Daily users spent USD18-23 per month. Reasons for using the e-cigarette included enjoyment of the products (85.9%), perception of lower toxicity than tobacco (87%), and the fact that it was a cheaper smoking alternative (61%).
Conclusion: The data on e-cigarette smoking topography obtained in this study are novel. The reasons of usage were mainly users’ enjoyment of e-cigarettes, preparation for quitting smoking, perception of low toxicity and a healthier smoking substitute and cheapness in the long run. The results establish basic knowledge for the local vaping topography and reference material for future e-cigarette-related research.
Nicotine is a major alkaloid of tobacco, which can increase free radical formation, leading to osteoporosis. The effects of nicotine administration and cessation on bone histomorphometry and biomarkers were studied in 28 Sprague-Dawley male rats. Rats aged 3 months and weighing 250-300 g were divided into four groups: control (C, normal saline for 4 months), nicotine for 2 months (N2), nicotine for 4 months (N4), and nicotine cessation (NC). The NC group was given nicotine for the first 2 months and then allowed to recover for the following 2 months without nicotine. Histomorphometric analysis was done using an image analyzer. ELISA kits were used to measure serum osteocalcin (bone formation marker) and pyridinoline (PYD, bone resorption marker) levels at month 0, month 2, and month 4. All test groups showed a significant decrease in BV/TV, Ob.S/BS, dLS/BS, MAR, BFR/BS, and osteocalcin levels and an increase in sLS/BS and PYD levels compared to group C. No significant differences were observed in all parameters measured among the test groups, except for MAR and BFR/BS. In conclusion, nicotine administration at a dose of 7 mg/kg for 2 and 4 months has detrimental effects on bone metabolism. Nicotine administration at 7 mg/kg for 2 months is sufficient to produce significant effects on bone histomorphometric parameters and biomarkers. In addition, prolonging the treatment for another 2 months did not show any significant differences. Cessation of nicotine for 2 months did not reverse the effects.
Vascular endothelial dysfunction (VED) plays an important role in the initiation of cardiovascular diseases. Roselle, enriched with antioxidants, demonstrates high potential in alleviating hypertension. This study was undertaken to investigate the effects of roselle supplementation of VED and remodelling in a rodent model with prolonged nicotine administration. Male Sprague-Dawley rats (n = 6 per group) were administered with 0.6 mg/kg nicotine for 28 days to induce VED. The rats were given either aqueous roselle (100 mg/kg) or normal saline orally 30 min prior to nicotine injection daily. One additional group of rats served as control. Thoracic aorta was isolated from rats to measure vascular reactivity, vascular remodelling and oxidative stress. Roselle significantly lowered aortic sensitivity to phenylephrine-induced vasoconstriction (Endo-(+) Cmax = 234.5 ± 3.9%, Endo-(-) Cmax = 247.6 ± 5.2%) compared with untreated nicotine group (Endo-(+) Cmax = 264.5 ± 6.9%, Endo-(-) Cmax = 276.5 ± 6.8%). Roselle also improved aortic response to endothelium-dependent vasodilator, acetylcholine (Endo-(+) Rmax = 73.2 ± 2.1%, Endo-(-) Rmax = 26.2 ± 0.8%) compared to nicotine group (Endo-(+) Rmax = 57.8 ± 1.7%, Endo-(-) Rmax = 20.9 ± 0.8%). In addition, roselle prevented an increase in intimal media thickness and elastic lamellae proliferation to preserve vascular architecture. Moreover, we also observed a significantly lowered degree of oxidative stress in parallel with increased antioxidant enzymes in aortic tissues of the roselle-treated group. This study demonstrated that roselle prevents VED and remodelling, and as such it has high nutraceutical value as supplement to prevent cardiovascular diseases.
This study investigated the impact of prolonged nicotine administration on myocardial susceptibility to ischaemia-reperfusion (I/R) injury in a rat model and determined whether nicotine affects mitochondrial reactive oxygen species (ROS) production and permeability transition in rat hearts. Sprague-Dawley rats were administered 0.6 or 1.2 mg/kg nicotine for 28 days, and their hearts were isolated at end-point for assessment of myocardial susceptibility to I/R injury ex vivo. Rat heart mitochondria were also isolated from a subset of rats for analysis of mitochondrial ROS production and permeability transition. Compared to the vehicle controls, rat hearts isolated from nicotine-administered rats exhibited poorer left ventricular function that worsened over the course of I/R. Coronary flow rate was also severely impaired in the nicotine groups at baseline and this worsened after I/R. Nicotine administration significantly increased mitochondrial ROS production and permeability transition relative to the vehicle controls. Interestingly, pre-incubation of isolated mitochondria with ROS scavengers (superoxide dismutase and mitoTEMPO) significantly abolished nicotine-induced increase in mitochondria permeability transition in isolated rat heart mitochondria. Overall, our data showed that prolonged nicotine administration enhances myocardial susceptibility to I/R injury in rats and this is associated with mitochondrial ROS-driven increase in mitochondrial permeability transition.
Previous studies have shown that nicotine enhances oxidative DNA damage and leads to increased lipid peroxidation, which affects embryo development. The present study investigated the effect of daily supplementation of gamma-tocotrienol on oocytes of nicotine-treated mice.