Meta-analysis of the effects of smoking and smoking cessation on triglyceride levels.

Smoking increases lipid levels, including triglycerides, leading to increased cardiovascular disease risk. We performed a meta-analysis to quantify the effects of smoking and smoking cessation on triglyceride levels. The PubMed and Scopus databases were searched to identify studies reporting either triglyceride levels in smokers and non-smokers or the effects of smoking cessation on triglyceride levels. Fixed- and random-effects models were used to perform the analyses when three or more studies/comparisons were available. We identified 169 and 21 studies evaluating the effects of smoking and smoking cessation, respectively, on triglyceride levels. Triglyceride levels were 0.50 mmol/L (95% confidence interval: 0.49-0.50 mmol/L) higher in smokers than non-smokers, but the effect differed widely across studies. No statistically significant effect was observed on triglyceride levels between baseline and 6 weeks (mean difference [MD] = 0.02 [-0.09, 0.12] mmol/L), 2 months (MD = 0.03 [-0.21, 0.27] mmol/L), 3 months (MD = 0.08 [-0.03, 0.21] mmol/L), or 1 year (MD = 0.04 [-0.06, 0.14] mmol/L) after quitting. However, a slightly significant decrease in triglyceride levels was observed at 1 month after cessation (MD = -0.15 [-0.15, -0.01] mmol/L). The results of this meta-analysis provide a basis for understanding the effects of smoking and smoking cessation on triglyceride levels, which could have important implications for public health.

Smoking and apolipoprotein levels: A meta-analysis of published data.

Background: Apolipoproteins are major components of lipoproteins such as high-density lipoprotein (HDL) and very-low-density lipoprotein and are considered nontraditional markers in the risk assessment for cardiovascular disease. The goal of this review was to quantify the effects of smoking and smoking cessation on serum levels of apolipoproteins AI, AII, and B and the ratio of apolipoproteins B and AI. Methods: PubMed and Scopus were searched up to June 2021 to identify publications that reported the levels of apolipoproteins AI, AII, and B and the apolipoprotein B/AI ratio in smokers and nonsmokers as well as articles reporting the effect of smoking cessation on the same endpoints. Meta-analyses were performed when a sufficient number (n ≥ 3) of articles evaluating the same outcome were available. Results: Forty-nine studies had assessed apolipoprotein levels in smokers and nonsmokers. The meta-analyses comparing the levels of apolipoproteins AI and AII showed decreased levels in smokers relative to nonsmokers. On the other hand, the apolipoprotein B levels and apolipoprotein B/AI ratio were increased in smokers relative to nonsmokers. Insufficient publications were available on which to perform meta-analyses on the effects of smoking cessation on apolipoprotein levels. Conclusions: Smoking is associated with reduced levels of apolipoproteins AI and AII (in line with reduced levels of HLD-cholesterol) and increased apolipoprotein B levels and apolipoprotein B/AI ratio, thereby confirming the negative impact of smoking on lipid metabolism, which contributes to increased cardiovascular risk. More data are needed to elucidate the effects of smoking cessation on these cardiovascular risk endpoints.

Ischemic Heart Disease and Chronic Obstructive Pulmonary Disease Hospitalizations in Japan Before and After the Introduction of a Heated Tobacco Product.

To substantiate the beneficial effects of switching from cigarette smoking to heated tobacco products (HTP), this study conducted a time-trend analysis using data from the Japanese Medical Data Center (JMDC) database. Specifically, we assessed hospitalization numbers for chronic obstructive pulmonary disease (COPD) exacerbations and acute ischemic heart disease (IHD) before and after the introduction of HTPs in the Japanese market. This study replicated a previous study using a different Japanese real-world data source (Medical Data Vision). We retrieved the number of hospitalizations associated with the International Classification of Diseases-10 codes for COPD and IHD from 2010 to 2019-5 years before to 4 years after introducing HTPs in the Japanese market-from the JMDC database. Then, we used interrupted time-series analyses to test the hypothesis that the introduction of HTPs is associated with a reduction in hospitalizations for COPD (all codes), COPD exacerbation, COPD exacerbation plus lower respiratory tract infections (LRTI), and IHD, adjusting for age, sex, seasonality, and flu vaccination rates. Analysis of all available data from the JMDC database revealed a significant reduction in the number of hospitalizations for COPD (all codes; P = 0.0001) and IHD using Diagnosis Procedure Combination data on causative disease flags (P < 0.00001). We also observed a non-significant reduction in hospitalizations for COPD plus LRTI as well as IHD after HTP introduction in Japan. This study confirmed the findings of our previous study where a decrease in hospitalizations due to COPD exacerbation after the introduction of HTPs in Japan was also shown. Nevertheless, these findings warrant further research to evaluate the impact of HTPs on the health of populations in other countries where these products have been introduced.

Influence of tobacco smoking on the development of halitosis.

Background: Halitosis is the general term used to describe any disagreeable odor in exhaled air, regardless of whether the odorous substances originate from oral or non-oral sources. Previous research has strongly associated tobacco smoking in the development of halitosis, as it increases the synthesis of toxic volatile sulfur compounds in diseased periodontal pockets. In this review, we summarize the etiopathology and epidemiology of halitosis as well as the current evidence on the impact of smoking by means of a meta-analysis. Methods: PubMed and Embase were searched to identify publications that reported halitosis in smokers and nonsmokers. Meta-analyses were performed if a sufficient number (n ≥ 3) of articles were available that evaluated the same outcome. Results: The meta-analyses showed that there was an increased risk of halitosis in current smokers versus nonsmokers (odds ratios). These results were consistent both in fixed and random effects models. Even though the interstudy heterogeneity was high (I2 = 91%), sensitivity analysis by limiting the number of studies yielded similar results, with no-to-moderate heterogeneity (I2 = 0-65%). The analysis comparing ever smokers with never smokers showed no significant difference in the risk of halitosis in ever smokers. The same effect was observed when upon stratifying the analyses on the basis of ascertainment of halitosis (self-reported or measured by a Halimeter). Conclusions: Halitosis is a common condition which can affect the quality of life of those affected. The results from this literature review and meta-analysis show that current smokers are more likely to suffer from halitosis, even if they are less likely to report it.