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.

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.

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.

A Literature Review and Framework Proposal for Halitosis Assessment in Cigarette Smokers and Alternative Nicotine-Delivery Products Users.

Halitosis is a health condition which counts cigarette smoking (CS) among its major risk factors. Cigarette smoke can cause an imbalance in the oral bacterial community, leading to several oral diseases and conditions, including intraoral halitosis. Although the best approach to decrease smoking-related health risks is quitting smoking, this is not feasible for many smokers. Switching to potentially reduced-risk products, like electronic vapor products (EVP) or heated tobacco products (HTP), may help improve the conditions associated with CS. To date, there have been few systematic studies on the effects of CS on halitosis and none have assessed the effects of EVP and HTP use. Self-assessment studies have shown large limitations owing to the lack of reliability in the participants' judgment. This has compelled the scientific community to develop a strategy for meaningful assessment of these new products in comparison with cigarettes. Here, we compiled a review of the existing literature on CS and halitosis and propose a 3-layer approach that combines the use of the most advanced breath analysis techniques and multi-omics analysis to define the interactions between oral bacterial species and their role in halitosis both in vitro and in vivo. Such an approach will allow us to compare the effects of different nicotine-delivery products on oral bacteria and quantify their impact on halitosis. Defining the impact of alternative nicotine-delivery products on intraoral halitosis and its associated bacteria will help the scientific community advance a step further toward understanding the safety of these products and their potentiall risks for consumers.

Impact of switching to a heat-not-burn tobacco product on CYP1A2 activity.

BACKGROUND: Cigarette smoking induces cytochrome P450 1A2 (CYP1A2) expression and activity, while smoking cessation normalizes the levels of this enzyme. The aim of this publication is to summarize the data on CYP1A2 gene expression and activity in preclinical and clinical studies on the Tobacco Heating System (THS), currently marketed as IQOS® with HEETs®, and to summarize the potential effects on CYP1A2 to be expected upon switching to reduced-risk products (RRPs). METHODS: We summarized PMI's preclinical and clinical data on the effects of switching from cigarette smoking to THS. RESULTS: Data from four preclinical mouse and rat studies showed that, upon either cessation of cigarette smoke exposure or switching to THS exposure, the upregulation of CYP1A2 observed with exposure to cigarette smoke reverted close to fresh-air levels. Data from four clinical studies yielded similar results on CYP1A2 activity within a time frame of five days. Furthermore, the effects of switching to THS were similar to those seen after smoking cessation. CONCLUSIONS: Because smoking cessation and switching to either electronic cigarettes or THS seem to have similar effects on CYP1A2 activity, the same measures taken for patients treated with narrow therapeutic index drugs that are metabolized by CYP1A2 and who quit smoking should be recommended for those switching to RRPs.

Influence of smoking on levels of urinary 8-iso Prostaglandin F2α.

BACKGROUND: To evaluate the reduced-risk potential of alternative tobacco products, biomarkers that are involved in the biological pathways affected by cigarette smoking and smoking cessation are needed. Isoprostanes, a measure of oxidative stress, appear to be influenced by smoking and reversible upon smoking cessation and therefore could be a good biomarker. This review aims at quantifying the effect of smoking and smoking cessation on levels of urinary 8-iso prostaglandin F2α (8-epi-PGF2α), an isoprostane. METHODS: PubMed and Scopus databases were searched for publications that reported 8-epi-PGF2α levels in smokers and nonsmokers as well as articles reporting the effect of smoking cessation on 8-epi-PGF2α levels. RESULTS: Eighteen studies assessing 8-epi-PGF2α levels by smoking status were identified. Five of the papers reported the results as quantity excreted in 24-hour urine (µg/24 h), and 15 reported creatinine adjusted values. The meta-analyses show increased levels of 8-epi-PGF2α in current smokers compared with nonsmokers (mean difference = 0.16, 95% confidence interval [95%CI]: 0.14-0.19 µg/24 h with inconsistency statistic [I2] = 98%; mean difference = 172.38, 95%CI: 152.75-192.01 pg/mg creatinine with I2 = 89%, respectively). There were too few publications to perform a meta-analysis assessing the effects of smoking cessation on 8-epi-PGF2α levels. CONCLUSIONS: Due to the high heterogeneity among the studies included in these meta-analyses, it is difficult to generalize the results; however, our study indicates increased levels of 8-epi-PGF2α and therefore increased oxidative stress in smokers compared with nonsmokers. More studies are still needed to assess if 8-epi-PGF2α levels are reversible after cessation.

Influence of smoking and smoking cessation on levels of urinary 11-dehydro thromboxane B2.

BACKGROUND: Thromboxane is a key clinical risk endpoint of smoking-induced inflammation which has been associated in the pathogenesis of cardiovascular disease. The goal of this review is to quantify the effect of smoking and smoking cessation on one of its urinary metabolites, 11-dehydrothromboxaneB2. METHODS: PubMed and SCOPUS were searched to identify publications which report urinary 11-dehydrothromboxaneB2 levels in smokers and non-smokers, as well as articles reporting the effect of smoking cessation on urinary 11-dehydrothromboxaneB2 excretion. RESULTS: We found ten studies assessing urinary 11-dehydrothroboxaneB2 levels in smokers and non-smokers. Four papers reported the amount of urinary 11-dehydrothromboxaneB2 excreted in 24 h while six reported the amount excreted adjusted for creatinine. The meta-analyses comparing the excretion of urinary 11-dehydrothromboxane in current smokers to non-smokers report increased levels in current smokers (mean difference = 0.31 µg/24-h [95%CI: 0.27-0.34] and 166.45 pg/mg creatinine [95%CI: 120.51-212.40]). There were not enough publications to perform meta-analyses on the effects of smoking cessation on urinary 11-dehydrothromboxaneB2 excretion. CONCLUSIONS: Urinary 11-dehydrothromboxaneB2 levels are increased in cigarette smokers, however, more data are needed to elucidate the effects of smoking cessation on urinary 11-dehydrothromboxaneB2 excretion.