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1.
Toxicol Rep ; 9: 1150-1171, 2022.
Article in English | MEDLINE | ID: mdl-36518393

ABSTRACT

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.

2.
Toxicol Rep ; 9: 316-322, 2022.
Article in English | MEDLINE | ID: mdl-35284240

ABSTRACT

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.

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