Effect of cigarette smoking on smoking biomarkers, blood pressure and blood lipid levels among Sri Lankan male smokers

Herath, Prasanna; Wimalasekera, Savithri; Amarasekara, Thamara; Fernando, Manoj; Turale, Sue

doi:10.1136/postgradmedj-2021-141016

Cited by 20 publications

(26 citation statements)

References 62 publications

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“…Cigarette smoking is classically associated with lipids modifications. Triglycerides level was significantly higher in smokers and thus confirms the literature [28,29]. Interestingly, level of sdLDL which have been associated with an increased risk of CVDs were found lower in smokers than in non-smokers.…”

Section: Discussionsupporting

confidence: 88%

Biological effect of cigarette smoking in endothelial dysfunction: Study of biomarkers of endothelial function, oxidative stress, inflammation, and lipids

Colsoul

Goderniaux

Onorati

et al. 2023

EUR J ENV PUBLIC HLT

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Aims: Tobacco use is involved in endothelial dysfunction, a key marker of cardiovascular diseases. The contribution of tobacco use in their development is assessed by endothelial dysfunction-related biomarkers in smokers and non-smokers. Methods: 138 smokers and 83 non-smokers were recruited. Parameters reflecting the endothelial function, lipid profile and oxidative and inflammatory status, were quantified. Data were used to determine their ability to differentiate smokers and non-smokers. Results: Elevation of inflammation and oxidative stress as well as alteration of endothelial function and lipids profile in smokers were observed. Two biomarkers combinations, including one implying only routine parameters, were identified and allowed to correctly classify >84% of cases. Conclusions: Oxidative status, inflammatory status, and lipids profile were shown altered in smokers, leading to endothelial dysfunction. Endothelial dysfunction-related biomarkers were assessed in terms of their ability to discriminate smokers from non-smokers. The possibility of discrimination based only on classic parameters of blood test appeared conceivable.

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Section: Discussionsupporting

confidence: 88%

Biological effect of cigarette smoking in endothelial dysfunction: Study of biomarkers of endothelial function, oxidative stress, inflammation, and lipids

Colsoul

Goderniaux

Onorati

et al. 2023

EUR J ENV PUBLIC HLT

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“…Apart from epidemiological studies, the pathophysiological mechanisms underlying the association of smoke exposure with headache may be more complex [26] . Chronic smoke exposure can increase nitric oxide levels, desensitizing cerebrovascular endothelial and smooth muscle function, which may reduce vasodilation and limit blood supply to neurons [27] . Furthermore, SE has been shown to inhibit monoamine oxidase activity and levels in the brain.…”

Section: Discussionmentioning

confidence: 99%

Association between smoke exposure and headache among U.S adolescents: a cross-sectional study from the NHANES 1999-2004

Guo,

Wang,

Yan

et al. 2024

Preprint

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Background Headaches are increasingly common among adolescents, with smoking considered a contributing risk factor. Cotinine, a nicotine metabolite, serves as an objective measure of smoke exposure. However, there is limited clinical data on the relationship between serum cotinine levels and headaches in adolescents. Methods A cross-sectional study design was applied, and participants aged 12 to 19 years from the National Health and Nutrition Examination Survey (NHANES) 1999–2004 were included in the analysis. Headache data were obtained through interviews and self-reports. Smoke exposure levels were categorized as unexposed, low secondhand smoke (SHS) exposure, high SHS exposure, and active smoking groups based on serum cotinine levels. The main analyses employed weighted multivariable logistic regression models, accounting for the complex multi-stage sampling design of NHANES. Additionally, a restricted cubic spline model was used to investigate the non-linear relationship between serum cotinine levels and headache. Furthermore, a subgroup analysis was conducted. Results The analysis included 5590 adolescents aged 12 to 19 years, among whom 1442 (24.99%) experienced headaches. After adjusting for all covariates, a positive association was found between log2-transformed serum cotinine and headaches (odds ratio, R=1.04 (1.01, 1.07), P = 0.008). Adolescents with high SHS exposure (serum cotinine levels of 0.316 –10 ng/ml) and those in the active smoking group (serum cotinine≥10 ng/ml) had a higher risk of experiencing headaches compared to the unexposed group (serum cotinine < 0.05 ng/ml) [OR = 1.42 (1.07, 1.90), OR = 1.55 (1.06, 2.27), P for trend = 0.006]. A linear dose-response relationship was observed between log2-transformed serum cotinine and the risk of headaches (P non-linearity > 0.05). Subgroup analysis revealed that the positive associations remained regardless of gender and varied depending on age and central obesity. Conclusion In conclusion, higher smoke exposure, as measured by elevated cotinine levels, was significantly associated with an increased risk of headaches among adolescents. Future research should focus on identifying effective strategies to eliminate smoke exposure and discourage tobacco use in adolescents prevent in adolescents to prevent headaches.

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“…(31)(32)(33). GrimAge incorporates CpGs that capture cigarette smoking pack-years, known as an independent risk factor for unfavorable lipid pro les (32,51). While we adjusted for smoking as a three-category variable, it may not fully eliminate the effects of smoking.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic age acceleration is associated with blood lipid levels in a multi-ancestry sample of older U.S. adults

Lin,

Kiryakos,

Ammous

et al. 2024

Preprint

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Background Dyslipidemia, which is characterized by an unfavorable lipid profile, is a key risk factor for cardiovascular disease (CVD). Understanding the relationships between epigenetic aging and lipid levels may help guide early prevention and treatment efforts for dyslipidemia. Methods We used weighted linear regression to cross-sectionally investigate the associations between five measures of epigenetic age acceleration estimated from whole blood DNA methylation (HorvathAge Acceleration, HannumAge Acceleration, PhenoAge Acceleration, GrimAge Acceleration, and DunedinPACE) and four blood lipid measures (total cholesterol (TC), LDL-C, HDL-C, and triglycerides (TG)) in 3,813 participants (mean age = 70 years) from the Health and Retirement Study (HRS). As a sensitivity analysis, we examined the same associations in participants who fasted prior to the blood draw (n = 2,531) and in participants who did not take lipid-lowering medication (n = 1,869). Using interaction models, we also examined whether the relationships between epigenetic age acceleration and blood lipids differ by demographic factors including age, sex, and educational attainment. Results After adjusting for age, race/ethnicity, sex, fasting status, and lipid-lowering medication use, greater epigenetic age acceleration was associated with lower TC, HDL-C, and LDL-C, and higher TG (p < 0.05). GrimAge acceleration and DunedinPACE associations with all lipids remained significant after further adjusting for body mass index, smoking status, and educational attainment. These associations were stronger in participants who fasted and who did not use lipid-lowering medication, particularly for LDL-C. We observed the largest number of interactions between DunedinPACE and demographic factors, where the associations with lipids were stronger in younger participants, females, and those with higher educational attainment. Conclusion Epigenetic age acceleration, a powerful biomarker of cellular aging, is highly associated with blood lipid levels in older adults. A greater understanding of how these associations differ across demographic groups can help shed light on the relationships between aging and downstream cardiovascular diseases. The inverse associations between epigenetic age and TC and LDL-C could be due to sample limitations or the non-linear relationship between age and these lipids, as both TC and LDL-C decrease faster at older ages. More studies are needed to further understand the temporal relationships between epigenetic age acceleration on blood lipids and other health outcomes.

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Effect of cigarette smoking on smoking biomarkers, blood pressure and blood lipid levels among Sri Lankan male smokers

Cited by 20 publications

References 62 publications

Biological effect of cigarette smoking in endothelial dysfunction: Study of biomarkers of endothelial function, oxidative stress, inflammation, and lipids

Biological effect of cigarette smoking in endothelial dysfunction: Study of biomarkers of endothelial function, oxidative stress, inflammation, and lipids

Association between smoke exposure and headache among U.S adolescents: a cross-sectional study from the NHANES 1999-2004

Epigenetic age acceleration is associated with blood lipid levels in a multi-ancestry sample of older U.S. adults

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