This study examined the acute effects of smoking electronic cigarettes (EC) and tobacco cigarettes (TC) on sympathetic nerve activity and blood pressure in healthy male smokers. 12 male smokers underwent measurements of muscle sympathetic nerve activity, skin sympathetic nerve activity, heart rate, and blood pressure at baseline and after smoking either 2 TC cigarettes, an EC, or sham smoking. Both TC and EC smoking significantly increased blood pressure and heart rate compared to baseline. Both also significantly decreased muscle sympathetic nerve activity and increased skin sympathetic nerve activity, with similar effects between TC and EC smoking. The responses to smoking were greater than those from sham smoking. The results suggest that the acute effects of EC smoking on the autonomic nervous system and hemodynamics are similar to
Abstract— Cigarette smoking is one of the major causes of cancer and cardiovascular diseases leading to millions of premature deaths each year all over the world. Scientists have identified about 4,000 different substances in tobacco all of which have certain degree of toxic effects. At least 43 of them known carcinogens.
Objective: The aim of this study is to assess the extent of adverse effect of cigarette and shisha on haematological parameters in male population of Khartoum State – Sudan.
Subject and Methods: One hundred and fifty male subjects participated in this study, cigarette smoker (n= 50), shisha smoker (n= 50) and non-smoker (n= 50). The smokers were regularly smoking at least for 10 years. Fresh peripheral blood samples from healthy adult non-smokers and smokers (males) were collected and analysed for Red Blood Cells (RBC) count, haemoglobin (Hb) content, packed cell volume (PCV), MCV, MCH and MCHC, total and differential leucocytes (WBC) counts and total platelets count by using fully automatic haematological analyser.
Results: The smokers of cigarette and shisha had significantly higher level of Hb, HCT, RBCs, TWBC count and MCHC. However, platelets counts were significantly lower in cigarette smokers than that of non-smokers. Study shows that the duration of smoking had no significant effect on haematological parameters except Hb.
Conclusion: It concluded that smoking alters haematological parameter that is injurious to health.
This document summarizes several studies investigating the relationship between smoking and venous thromboembolism (VTE) risk. The studies found:
1) Current smoking was associated with a higher risk of VTE compared to never smokers, with a positive dose-response relationship. Former smokers had the same risk as never smokers.
2) Heavier smokers (>20 pack-years) had higher risks of total and provoked VTE compared to never smokers. The risk of provoked VTE increased with more pack-years of smoking.
3) The modestly increased risks of VTE in current or former women smokers were attenuated after adjusting for smoking-related diseases and decreased physical activity, suggesting an indirect relationship between smoking
Smoking may potentially interact with warfarin therapy by increasing its clearance and reducing its anticoagulant effects. A systematic review found smoking was associated with a 12.13% increase in warfarin dose requirements and an additional 2.26 mg per week compared to non-smokers. While earlier studies did not find a relationship between smoking and INR levels, recent evidence suggests smoking can significantly impact warfarin therapy through enzyme-inducing effects.
The document discusses a study on smoking patterns in tuberculosis patients in Bangladesh, finding that 61% were smokers before their TB diagnosis, with 50.8% continuing to smoke after diagnosis despite treatment. Younger age groups between 21-50 were most likely to smoke, with over 68% smoking less than 10 cigarettes per day, and the most common reason for continuing smoking was to reduce stress. The study recommends that evaluating smoking status in TB patients and encouraging smoking cessation could help improve treatment outcomes.
Wet cupping therapy was applied to 5 points on the back of 40 healthy participants. Electrocardiography recordings were taken before and after to analyze heart rate variability (HRV), a measure of sympathovagal balance. All HRV parameters, including SDNN, SDANN, RMSSD, pNN50, LF, and HF, increased after cupping therapy compared to before, indicating cupping restored sympathovagal balance. This is the first study to show in humans that cupping therapy may have cardioprotective effects by stimulating the peripheral nervous system.
MD16510A - ISPOR US poster Medtronic v2.0Goran Medic
Cluster headache is a severe primary headache disorder characterized by recurring unilateral headaches. Chronic cluster headache (CCH) involves attacks occurring more than once daily without remission. A literature review found limited evidence on the burden and outcomes of recommended treatments for CCH. CCH was reported to have a substantial impact on work productivity and quality of life. Treatments like zolmitriptan nasal spray showed some efficacy compared to placebo, but outcomes were inconsistently reported. Overall, the review found an evidence gap in understanding the disease burden and treatment efficacy due to heterogeneity in reporting. More well-designed studies are needed.
This document discusses electronic cigarettes (ECs) and whether they are safer than combustible cigarettes. It summarizes that while ECs may expose users to fewer harmful chemicals than smoking, the long-term safety of ECs is still unknown. Studies have found potentially harmful chemicals in EC vapor, but in much lower amounts than in cigarette smoke. The regulation of ECs is also debated, as stricter rules may discourage innovation but make the products less appealing to youth and non-smokers. The evidence that ECs help smokers quit is also limited and inconclusive. More research is still needed to understand the public health impact of ECs.
Abstract— Cigarette smoking is one of the major causes of cancer and cardiovascular diseases leading to millions of premature deaths each year all over the world. Scientists have identified about 4,000 different substances in tobacco all of which have certain degree of toxic effects. At least 43 of them known carcinogens.
Objective: The aim of this study is to assess the extent of adverse effect of cigarette and shisha on haematological parameters in male population of Khartoum State – Sudan.
Subject and Methods: One hundred and fifty male subjects participated in this study, cigarette smoker (n= 50), shisha smoker (n= 50) and non-smoker (n= 50). The smokers were regularly smoking at least for 10 years. Fresh peripheral blood samples from healthy adult non-smokers and smokers (males) were collected and analysed for Red Blood Cells (RBC) count, haemoglobin (Hb) content, packed cell volume (PCV), MCV, MCH and MCHC, total and differential leucocytes (WBC) counts and total platelets count by using fully automatic haematological analyser.
Results: The smokers of cigarette and shisha had significantly higher level of Hb, HCT, RBCs, TWBC count and MCHC. However, platelets counts were significantly lower in cigarette smokers than that of non-smokers. Study shows that the duration of smoking had no significant effect on haematological parameters except Hb.
Conclusion: It concluded that smoking alters haematological parameter that is injurious to health.
This document summarizes several studies investigating the relationship between smoking and venous thromboembolism (VTE) risk. The studies found:
1) Current smoking was associated with a higher risk of VTE compared to never smokers, with a positive dose-response relationship. Former smokers had the same risk as never smokers.
2) Heavier smokers (>20 pack-years) had higher risks of total and provoked VTE compared to never smokers. The risk of provoked VTE increased with more pack-years of smoking.
3) The modestly increased risks of VTE in current or former women smokers were attenuated after adjusting for smoking-related diseases and decreased physical activity, suggesting an indirect relationship between smoking
Smoking may potentially interact with warfarin therapy by increasing its clearance and reducing its anticoagulant effects. A systematic review found smoking was associated with a 12.13% increase in warfarin dose requirements and an additional 2.26 mg per week compared to non-smokers. While earlier studies did not find a relationship between smoking and INR levels, recent evidence suggests smoking can significantly impact warfarin therapy through enzyme-inducing effects.
The document discusses a study on smoking patterns in tuberculosis patients in Bangladesh, finding that 61% were smokers before their TB diagnosis, with 50.8% continuing to smoke after diagnosis despite treatment. Younger age groups between 21-50 were most likely to smoke, with over 68% smoking less than 10 cigarettes per day, and the most common reason for continuing smoking was to reduce stress. The study recommends that evaluating smoking status in TB patients and encouraging smoking cessation could help improve treatment outcomes.
Wet cupping therapy was applied to 5 points on the back of 40 healthy participants. Electrocardiography recordings were taken before and after to analyze heart rate variability (HRV), a measure of sympathovagal balance. All HRV parameters, including SDNN, SDANN, RMSSD, pNN50, LF, and HF, increased after cupping therapy compared to before, indicating cupping restored sympathovagal balance. This is the first study to show in humans that cupping therapy may have cardioprotective effects by stimulating the peripheral nervous system.
MD16510A - ISPOR US poster Medtronic v2.0Goran Medic
Cluster headache is a severe primary headache disorder characterized by recurring unilateral headaches. Chronic cluster headache (CCH) involves attacks occurring more than once daily without remission. A literature review found limited evidence on the burden and outcomes of recommended treatments for CCH. CCH was reported to have a substantial impact on work productivity and quality of life. Treatments like zolmitriptan nasal spray showed some efficacy compared to placebo, but outcomes were inconsistently reported. Overall, the review found an evidence gap in understanding the disease burden and treatment efficacy due to heterogeneity in reporting. More well-designed studies are needed.
This document discusses electronic cigarettes (ECs) and whether they are safer than combustible cigarettes. It summarizes that while ECs may expose users to fewer harmful chemicals than smoking, the long-term safety of ECs is still unknown. Studies have found potentially harmful chemicals in EC vapor, but in much lower amounts than in cigarette smoke. The regulation of ECs is also debated, as stricter rules may discourage innovation but make the products less appealing to youth and non-smokers. The evidence that ECs help smokers quit is also limited and inconclusive. More research is still needed to understand the public health impact of ECs.
This study examined oral mucosal lesions in 45 former smokers and 45 electronic cigarette consumers. Oral examinations found lesions in 55 total patients, with 36 lesions in electronic cigarette consumers and 19 in former smokers. Nicotine stomatitis, hairy tongue, and hyperplastic candidiasis were significantly more common among electronic cigarette consumers. The study aims to evaluate differences in oral mucosal lesions between the groups but found no statistically significant difference in total prevalence of lesions.
This document summarizes a study that examined the effects of cigarette smoking on various inflammatory and hemostatic biomarkers. The study found that the pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha were significantly higher in the plasma of smoker subjects compared to non-smokers. However, the study found no significant differences in other markers like interleukin-10, C-reactive protein, D-dimer, and ferritin between smoker and non-smoker groups. Additionally, the study found no association between smoking intensity and biomarker levels among smoker subjects. The findings suggest cigarette smoking may elevate interleukin-6 and tumor necrosis factor-alpha levels in a dose-dependent manner.
This study examined biomarkers of exposure to carcinogens in smokers who switched between regular and light cigarettes for short periods. Sixteen smokers smoked their regular cigarettes for one week, then a light cigarette with half the machine-measured nicotine for one week, then back to their regular. Biomarkers were measured weekly and showed high levels of compensation - smokers adjusted their smoking behavior to take in similar levels of carcinogens despite the cigarette change. Compensation occurred through both smoking more cigarettes per day and smoking more intensely. Exposure levels to various carcinogens remained similar, suggesting short-term switching to light cigarettes is unlikely to reduce health risks from smoking.
This study examined the acute effects of cigarette smoking on coronary blood vessels. Twenty-four long-term smokers underwent cardiac catheterization. Smoking one cigarette caused immediate constriction of both proximal and distal epicardial arteries of 5-8%, returning to baseline within 30 minutes. Coronary blood flow velocity decreased by 7% and resistance increased by 21% despite increased heart rate and blood pressure. The control group showed no vascular changes. Smoking acutely constricts epicardial arteries and increases coronary resistance, potentially contributing to cardiovascular harm.
This study compared the effects of cigarette smoke, e-cigarette vapor, and pure nicotine on cell viability using HeLa cells. Various concentrations of smoke and vapor condensates collected from a mechanical smoking system were applied to cells for 24 hours. An MTT assay then measured cell viability. Cigarette smoke exposure resulted in lower viability than e-cigarette vapor, but higher than pure nicotine. The results provide insight into the acute toxicity of these substances and whether e-cigarettes may be less harmful than cigarettes.
Tabaquismo factor de riesgo cardiovascular y disfuncion endotelial Ricardo Mora MD
Tabaquismo como factor de riesgo endotelial y disfuncion endotelial; Dr. Ricardo Mora Moreno R2C; IMSS UMAE T1; León, Guanajuato, Mexico; 09 de Noviembre del 2017
An Experimental Method to Determine the Concentration of Nicotine in Exhaled ...Fontem Ventures
- An experimental method was presented to determine the concentration of nicotine in exhaled breath after using e-cigarettes and the nicotine retention rate.
- Three experienced e-cigarette users vaped e-cigarettes containing different nicotine concentrations while a smoking topography analyzer recorded puff volume and duration. This allowed determining the nicotine concentration inhaled per puff.
- A PTR-MS instrument then measured nicotine in exhaled breath, allowing calculation of the retention rate by comparing to the inhaled nicotine concentration. Over 99% of nicotine was retained when inhaled and 86% when held in the mouth. Exhaled nicotine concentrations were low (1.8-1786 ppb
This study compared the effects of levosimendan, dobutamine, and vasodilator therapy on ongoing myocardial injury in patients with acute decompensated heart failure. The study found that while all treatments were associated with decreases in cardiac troponin I levels and improvements in hemodynamic and functional indicators, levosimendan treatment showed the most pronounced improvements, especially in left ventricular ejection fraction and systolic pulmonary artery pressure. However, none of the treatments significantly reduced cardiac troponin I levels compared to each other. The study demonstrated beneficial effects of short-term use of levosimendan, dobutamine, and nitroglycerin on ongoing myocardial injury in acute decompensated heart failure.
These are the slides for my talk delivered at the Lisbon Addictions conference October 2019 as part of the FuturiZe round table on safer drugs.
A recording of the presentation can be found on my YouTube channel 'Lynne Talks Vape': https://youtu.be/8jTQvoWu1Pk
Psychological studies involving humans suggested that addiction is a form of learning and that relapse is a persistent memory of the drug experiences [1,2]. It is the gene transcription factor Cyclic AMP Response-Element-Binding protein (CREB) acting as a switch, converting short-term memory to long-term memory, referred to as the acetylation of chromatin structures [3].
Harvard University Public Health Problem Paper.docxwrite4
This document summarizes a large prospective study conducted by the American Cancer Society from 1959 to 1972 that investigated mortality risks from tobacco use. Over 1 million men and women were enrolled in the study and followed for 12 years. Detailed tables in the appendices present mortality data by smoking status, level of cigarette consumption, and other factors. The results provide strong evidence of the causal link between smoking and several diseases, most notably lung cancer, coronary heart disease, cerebrovascular disease, and chronic obstructive pulmonary disease.
Harvard University Public Health Problem Paper.docxwrite31
This document summarizes a large prospective study conducted by the American Cancer Society from 1959 to 1972 that investigated mortality risks from tobacco use. Over 1 million men and women were enrolled in the study and followed for 12 years. Detailed tables in the appendices present mortality data by smoking status, level of cigarette consumption, and other factors. The results provide strong evidence of the causal link between smoking and several diseases, most notably lung cancer, coronary heart disease, cerebrovascular disease, and chronic obstructive pulmonary disease.
Cardiac Enzyme Responses among Marijuana Smokersasclepiuspdfs
Aim: This study was carried out to determine the activity of aspartate aminotransferase (AST) and creatine kinase (CK) in marijuana smokers. Materials and Methods: Twenty confirmed marijuana smokers and 20 apparently non-smokers (control) between the ages of 20 and 40 years were selected for this study. The level of AST and CK were carried out by standard methods. Results: The level of AST (44.49 ± 5.18IU/L) in marijuana smokers was significantly increased when compared with the control (28.28 ± 6.12IU/L) (P ˂ 0.05). Furthermore, the level of CK (295.84 ± 6.58 IU/L) in marijuana smokers was significantly increased when compared with the control (110.03 ± 11.80 IU/L) (P ˂ 0.05)). Conclusion: The results obtained probably indicate that marijuana smokers are more likely to develop a cardiac problem. Hence, smoking of marijuana is not beneficial to health as it may be linked with myocardial infarction.
Evaluation of Biomarkers of Exposure and Cardiovascular & Pulmonary Function Endpoints in Adult Smokers Following Partial or Complete Substitution of Cigarettes with Electronic Cigarettes
Smoking Cessation: Barriers and Available Methods Dr R R Kasliwal
Tobacco use is the leading global cause of avoidable death worldwide and a key modifiable risk factor for the development of a range of diseases, including cardiovascular disease, chronic obstructive pulmonary disease and some cancers (1-3). In the 1960s, the US Surgeon General and American Heart Association issued reports warning of the dangers of smoking on fatal coronary artery disease (4-6). Since those early publications, 32 US Surgeon General reports have been released exposing the harmful effects of cigarette smoking on cardiovascular health (7,8). The 1983 Surgeon General’s Report (9) was devoted entirely to cardiovascular disease. It concluded that cigarette smoking is one of the three major independent risk factors for heart disease.
E-Cigarettes: Promise, Peril, and Probabilistic Population PredictionCertara
E-cigarettes, which deliver nicotine without carcinogenic tar, hold the promise to save the lives of many smokers who switch to them, but risks include failure to quit cigarettes (dual use), increased initiation to nicotine products among youth, relapse of former smokers to e-cigarettes, and e-cigarettes becoming a “gateway to smoking.” To capture these uncertainties and weigh benefits vs. risks, prediction of e-cigarette health impacts must use a broad range of probability-weighted scenarios.
Tobacco smoking is a major public health threat for both
smokers and nonsmokers. There is accumulating evidence
demonstrating that smoking causes several human
diseases, including those affecting the cardiovascular system.
Indeed, tobacco smoking is responsible for up to 30% of heart
disease–related deaths in the United States each year.1 This
is the single most preventable risk factor related to the
development of cardiovascular disease, bringing about a trend
toward tobacco harm reduction that started years ago.2 As
tobacco usage declined over time in the United States,
industries introduced an alternative known as electronic
cigarettes (e-cigarettes) claiming they were a healthier
alternative to tobacco smoking.3
Since then, the number of e-cigarette users has increased
significantly because of the perception that they serve as a
healthy substitute to tobacco consumption with minimal or no
harm, a lack of usage regulations (although that has now
changed), and the appealing nature of these devices, among
other reasons.4 Consequently, e-cigarettes became the most
commonly used smoking products, especially among youth,
with more than a 9-fold increase in usage from 2011 to
2015.5 Based on these considerations, it is clear that there
are many unanswered questions regarding the overall safety,
efficacy of harm reduction, and the long-term health impact of
these devices.
Besides their potential negative health effects on users,
there is increasing evidence that e-cigarettes emit considerable
levels of toxicants, such as nicotine, volatile organic
compounds, and carbonyls, in addition to releasing particulate
matter (PM).6,7 Thus, they possess a potential harm to
nonusers either through secondhand or thirdhand exposure.
This is especially the case in vulnerable populations, such as
children, elderly, pregnant females, and those with a history of
Effects of substituting cigarettes with e-cigarettes in adult smokers Fontem Ventures
Measurement of cardiovascular and pulmonary function endpoints
and other physiological effects following partial or complete
substitution of cigarettes with electronic cigarettes in adult smokers
This research provides evidence that cravings are associated with individual patterns of arousal and are expressed differently in smokers and non-smokers. Patterns of physiologic arousal were identified for craving and tobacco use. This research supports the development of individual algorithms to predict tobacco use for tobacco cessation treatment.
This study examined oral mucosal lesions in 45 former smokers and 45 electronic cigarette consumers. Oral examinations found lesions in 55 total patients, with 36 lesions in electronic cigarette consumers and 19 in former smokers. Nicotine stomatitis, hairy tongue, and hyperplastic candidiasis were significantly more common among electronic cigarette consumers. The study aims to evaluate differences in oral mucosal lesions between the groups but found no statistically significant difference in total prevalence of lesions.
This document summarizes a study that examined the effects of cigarette smoking on various inflammatory and hemostatic biomarkers. The study found that the pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha were significantly higher in the plasma of smoker subjects compared to non-smokers. However, the study found no significant differences in other markers like interleukin-10, C-reactive protein, D-dimer, and ferritin between smoker and non-smoker groups. Additionally, the study found no association between smoking intensity and biomarker levels among smoker subjects. The findings suggest cigarette smoking may elevate interleukin-6 and tumor necrosis factor-alpha levels in a dose-dependent manner.
This study examined biomarkers of exposure to carcinogens in smokers who switched between regular and light cigarettes for short periods. Sixteen smokers smoked their regular cigarettes for one week, then a light cigarette with half the machine-measured nicotine for one week, then back to their regular. Biomarkers were measured weekly and showed high levels of compensation - smokers adjusted their smoking behavior to take in similar levels of carcinogens despite the cigarette change. Compensation occurred through both smoking more cigarettes per day and smoking more intensely. Exposure levels to various carcinogens remained similar, suggesting short-term switching to light cigarettes is unlikely to reduce health risks from smoking.
This study examined the acute effects of cigarette smoking on coronary blood vessels. Twenty-four long-term smokers underwent cardiac catheterization. Smoking one cigarette caused immediate constriction of both proximal and distal epicardial arteries of 5-8%, returning to baseline within 30 minutes. Coronary blood flow velocity decreased by 7% and resistance increased by 21% despite increased heart rate and blood pressure. The control group showed no vascular changes. Smoking acutely constricts epicardial arteries and increases coronary resistance, potentially contributing to cardiovascular harm.
This study compared the effects of cigarette smoke, e-cigarette vapor, and pure nicotine on cell viability using HeLa cells. Various concentrations of smoke and vapor condensates collected from a mechanical smoking system were applied to cells for 24 hours. An MTT assay then measured cell viability. Cigarette smoke exposure resulted in lower viability than e-cigarette vapor, but higher than pure nicotine. The results provide insight into the acute toxicity of these substances and whether e-cigarettes may be less harmful than cigarettes.
Tabaquismo factor de riesgo cardiovascular y disfuncion endotelial Ricardo Mora MD
Tabaquismo como factor de riesgo endotelial y disfuncion endotelial; Dr. Ricardo Mora Moreno R2C; IMSS UMAE T1; León, Guanajuato, Mexico; 09 de Noviembre del 2017
An Experimental Method to Determine the Concentration of Nicotine in Exhaled ...Fontem Ventures
- An experimental method was presented to determine the concentration of nicotine in exhaled breath after using e-cigarettes and the nicotine retention rate.
- Three experienced e-cigarette users vaped e-cigarettes containing different nicotine concentrations while a smoking topography analyzer recorded puff volume and duration. This allowed determining the nicotine concentration inhaled per puff.
- A PTR-MS instrument then measured nicotine in exhaled breath, allowing calculation of the retention rate by comparing to the inhaled nicotine concentration. Over 99% of nicotine was retained when inhaled and 86% when held in the mouth. Exhaled nicotine concentrations were low (1.8-1786 ppb
This study compared the effects of levosimendan, dobutamine, and vasodilator therapy on ongoing myocardial injury in patients with acute decompensated heart failure. The study found that while all treatments were associated with decreases in cardiac troponin I levels and improvements in hemodynamic and functional indicators, levosimendan treatment showed the most pronounced improvements, especially in left ventricular ejection fraction and systolic pulmonary artery pressure. However, none of the treatments significantly reduced cardiac troponin I levels compared to each other. The study demonstrated beneficial effects of short-term use of levosimendan, dobutamine, and nitroglycerin on ongoing myocardial injury in acute decompensated heart failure.
These are the slides for my talk delivered at the Lisbon Addictions conference October 2019 as part of the FuturiZe round table on safer drugs.
A recording of the presentation can be found on my YouTube channel 'Lynne Talks Vape': https://youtu.be/8jTQvoWu1Pk
Psychological studies involving humans suggested that addiction is a form of learning and that relapse is a persistent memory of the drug experiences [1,2]. It is the gene transcription factor Cyclic AMP Response-Element-Binding protein (CREB) acting as a switch, converting short-term memory to long-term memory, referred to as the acetylation of chromatin structures [3].
Harvard University Public Health Problem Paper.docxwrite4
This document summarizes a large prospective study conducted by the American Cancer Society from 1959 to 1972 that investigated mortality risks from tobacco use. Over 1 million men and women were enrolled in the study and followed for 12 years. Detailed tables in the appendices present mortality data by smoking status, level of cigarette consumption, and other factors. The results provide strong evidence of the causal link between smoking and several diseases, most notably lung cancer, coronary heart disease, cerebrovascular disease, and chronic obstructive pulmonary disease.
Harvard University Public Health Problem Paper.docxwrite31
This document summarizes a large prospective study conducted by the American Cancer Society from 1959 to 1972 that investigated mortality risks from tobacco use. Over 1 million men and women were enrolled in the study and followed for 12 years. Detailed tables in the appendices present mortality data by smoking status, level of cigarette consumption, and other factors. The results provide strong evidence of the causal link between smoking and several diseases, most notably lung cancer, coronary heart disease, cerebrovascular disease, and chronic obstructive pulmonary disease.
Cardiac Enzyme Responses among Marijuana Smokersasclepiuspdfs
Aim: This study was carried out to determine the activity of aspartate aminotransferase (AST) and creatine kinase (CK) in marijuana smokers. Materials and Methods: Twenty confirmed marijuana smokers and 20 apparently non-smokers (control) between the ages of 20 and 40 years were selected for this study. The level of AST and CK were carried out by standard methods. Results: The level of AST (44.49 ± 5.18IU/L) in marijuana smokers was significantly increased when compared with the control (28.28 ± 6.12IU/L) (P ˂ 0.05). Furthermore, the level of CK (295.84 ± 6.58 IU/L) in marijuana smokers was significantly increased when compared with the control (110.03 ± 11.80 IU/L) (P ˂ 0.05)). Conclusion: The results obtained probably indicate that marijuana smokers are more likely to develop a cardiac problem. Hence, smoking of marijuana is not beneficial to health as it may be linked with myocardial infarction.
Evaluation of Biomarkers of Exposure and Cardiovascular & Pulmonary Function Endpoints in Adult Smokers Following Partial or Complete Substitution of Cigarettes with Electronic Cigarettes
Smoking Cessation: Barriers and Available Methods Dr R R Kasliwal
Tobacco use is the leading global cause of avoidable death worldwide and a key modifiable risk factor for the development of a range of diseases, including cardiovascular disease, chronic obstructive pulmonary disease and some cancers (1-3). In the 1960s, the US Surgeon General and American Heart Association issued reports warning of the dangers of smoking on fatal coronary artery disease (4-6). Since those early publications, 32 US Surgeon General reports have been released exposing the harmful effects of cigarette smoking on cardiovascular health (7,8). The 1983 Surgeon General’s Report (9) was devoted entirely to cardiovascular disease. It concluded that cigarette smoking is one of the three major independent risk factors for heart disease.
E-Cigarettes: Promise, Peril, and Probabilistic Population PredictionCertara
E-cigarettes, which deliver nicotine without carcinogenic tar, hold the promise to save the lives of many smokers who switch to them, but risks include failure to quit cigarettes (dual use), increased initiation to nicotine products among youth, relapse of former smokers to e-cigarettes, and e-cigarettes becoming a “gateway to smoking.” To capture these uncertainties and weigh benefits vs. risks, prediction of e-cigarette health impacts must use a broad range of probability-weighted scenarios.
Tobacco smoking is a major public health threat for both
smokers and nonsmokers. There is accumulating evidence
demonstrating that smoking causes several human
diseases, including those affecting the cardiovascular system.
Indeed, tobacco smoking is responsible for up to 30% of heart
disease–related deaths in the United States each year.1 This
is the single most preventable risk factor related to the
development of cardiovascular disease, bringing about a trend
toward tobacco harm reduction that started years ago.2 As
tobacco usage declined over time in the United States,
industries introduced an alternative known as electronic
cigarettes (e-cigarettes) claiming they were a healthier
alternative to tobacco smoking.3
Since then, the number of e-cigarette users has increased
significantly because of the perception that they serve as a
healthy substitute to tobacco consumption with minimal or no
harm, a lack of usage regulations (although that has now
changed), and the appealing nature of these devices, among
other reasons.4 Consequently, e-cigarettes became the most
commonly used smoking products, especially among youth,
with more than a 9-fold increase in usage from 2011 to
2015.5 Based on these considerations, it is clear that there
are many unanswered questions regarding the overall safety,
efficacy of harm reduction, and the long-term health impact of
these devices.
Besides their potential negative health effects on users,
there is increasing evidence that e-cigarettes emit considerable
levels of toxicants, such as nicotine, volatile organic
compounds, and carbonyls, in addition to releasing particulate
matter (PM).6,7 Thus, they possess a potential harm to
nonusers either through secondhand or thirdhand exposure.
This is especially the case in vulnerable populations, such as
children, elderly, pregnant females, and those with a history of
Effects of substituting cigarettes with e-cigarettes in adult smokers Fontem Ventures
Measurement of cardiovascular and pulmonary function endpoints
and other physiological effects following partial or complete
substitution of cigarettes with electronic cigarettes in adult smokers
This research provides evidence that cravings are associated with individual patterns of arousal and are expressed differently in smokers and non-smokers. Patterns of physiologic arousal were identified for craving and tobacco use. This research supports the development of individual algorithms to predict tobacco use for tobacco cessation treatment.
Andreas Schleicher presents PISA 2022 Volume III - Creative Thinking - 18 Jun...EduSkills OECD
Andreas Schleicher, Director of Education and Skills at the OECD presents at the launch of PISA 2022 Volume III - Creative Minds, Creative Schools on 18 June 2024.
A Visual Guide to 1 Samuel | A Tale of Two HeartsSteve Thomason
These slides walk through the story of 1 Samuel. Samuel is the last judge of Israel. The people reject God and want a king. Saul is anointed as the first king, but he is not a good king. David, the shepherd boy is anointed and Saul is envious of him. David shows honor while Saul continues to self destruct.
Philippine Edukasyong Pantahanan at Pangkabuhayan (EPP) CurriculumMJDuyan
(𝐓𝐋𝐄 𝟏𝟎𝟎) (𝐋𝐞𝐬𝐬𝐨𝐧 𝟏)-𝐏𝐫𝐞𝐥𝐢𝐦𝐬
𝐃𝐢𝐬𝐜𝐮𝐬𝐬 𝐭𝐡𝐞 𝐄𝐏𝐏 𝐂𝐮𝐫𝐫𝐢𝐜𝐮𝐥𝐮𝐦 𝐢𝐧 𝐭𝐡𝐞 𝐏𝐡𝐢𝐥𝐢𝐩𝐩𝐢𝐧𝐞𝐬:
- Understand the goals and objectives of the Edukasyong Pantahanan at Pangkabuhayan (EPP) curriculum, recognizing its importance in fostering practical life skills and values among students. Students will also be able to identify the key components and subjects covered, such as agriculture, home economics, industrial arts, and information and communication technology.
𝐄𝐱𝐩𝐥𝐚𝐢𝐧 𝐭𝐡𝐞 𝐍𝐚𝐭𝐮𝐫𝐞 𝐚𝐧𝐝 𝐒𝐜𝐨𝐩𝐞 𝐨𝐟 𝐚𝐧 𝐄𝐧𝐭𝐫𝐞𝐩𝐫𝐞𝐧𝐞𝐮𝐫:
-Define entrepreneurship, distinguishing it from general business activities by emphasizing its focus on innovation, risk-taking, and value creation. Students will describe the characteristics and traits of successful entrepreneurs, including their roles and responsibilities, and discuss the broader economic and social impacts of entrepreneurial activities on both local and global scales.
This presentation was provided by Rebecca Benner, Ph.D., of the American Society of Anesthesiologists, for the second session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session Two: 'Expanding Pathways to Publishing Careers,' was held June 13, 2024.
Elevate Your Nonprofit's Online Presence_ A Guide to Effective SEO Strategies...TechSoup
Whether you're new to SEO or looking to refine your existing strategies, this webinar will provide you with actionable insights and practical tips to elevate your nonprofit's online presence.
2. Int. J. Environ. Res. Public Health 2022, 19, 3237 2 of 11
heart rate variability [12,13] and unfavorable changes in muscle sympathetic nerve activity
(MSNA) and skin sympathetic nerve activity (SSNA) [4,14–19]. However, the link of EC
consumption with sympathetic modulation has not been adequately explored with most
evidence coming from studies assessing the changes in heart rate variability [1,20–23].
There is only one recent study showing the link of vaping with acute increases in arterial
pressure and unfavorable autonomic regulation in healthy non-smokers [23].
Based on the above, to explore the potential mechanisms of the adverse effects of EC
smoking on the cardiovascular and autonomic system, it would be helpful to compare the
impact of EC and TC smoking on sympathetic activity by the means of microneurography
and on hemodynamic parameters. Thus, we assessed the acute effects of TC and EC
exposures on MSNA and SSNA as well as on arterial pressure in healthy habitual TC
smokers.
2. Material and Methods
2.1. Subjects
Healthy male volunteers between the ages of 25 and 45 years were eligible for en-
rollment if they met the following criteria: reference [1] no current (within 1-year) EC
smoking, [2] body mass index ≤30 kg/m2; reference [3] no known health problems; refer-
ence [4] alcoholic intake ≤2 drinks per day and no illicit drug use (determined through
screening questionnaire); reference [5] lack of exposure to secondhand smoke, or using
licensed nicotine replacement therapies; reference [6] current TC smoking (10 cigarettes
daily).
A total of 15 participants meeting the above criteria were enrolled in this study. Three
subjects completed only part of the protocol procedures and were excluded. Thus, we
evaluated the effects of smoking in 12 healthy normotensive habitual male TC smokers
(mean age: 34 ± 4 years and body mass index: 24 ± 3 kg/m2), free of diabetes melli-
tus, hyperlipidemia, or any other systemic disease, after detailed clinic and laboratory
examinations, who were taking no medication.
2.2. Measurements
Subjects abstained from caffeine, ethanol and nicotine for at least 12 h before each
session and were tested in the supine position in a temperature-controlled (23 ◦C) room.
After instrumentation, the subjects were asked to remain quiet for an acclimation period of
5 min or until the hemodynamic variables and MSNA and SSNA recordings were stable.
Heart rate was measured continuously by an ECG, and blood pressure was measured
beat-to-beat by an automatic plethysmograph (Finometer MIDI, Finapres Medical Systems
BV, Institutenweg 25, 7521 PH Enschede The Netherlands). In more detail, MSNA was
obtained through a tungsten microelectrode inserted into the right or left peroneal nerve
posterior to the fibular head. The microelectrode is made of tungsten with a diameter of
200 mm in the shaft, tapering to an uninsulated tip of 1–5 mm. A reference electrode is
positioned subcutaneously 1–3 cm from the recording electrode and serves as a ground. The
nerve signal was amplified according to prespecified algorithms, fed through a bandpass
filter (700–2000 Hz) and integrated with a nerve traffic analyzer (ML 185 NeuroAmpEx;
ADInstruments Ltd., Oxford, UK). Integrated nerve activity was monitored and the MSNA
and SSNA were assessed according to established methodology [24–26]. Neurograms
were accepted only if they did not show simultaneous skin and muscle sympathetic nerve
traffic and if the signal-to-noise ratio was more than 3 [3,8,9]. The MSNA and SSNA were
identified by their characteristic morphology and relationship to the R waves on the ECG
and quantified as bursts’ frequency (bursts per minute). The measurement has been shown
to be highly reproducible with an intra-observer reproducibility of around 3.8–4.5% [24–26].
Plasma norepinephrine levels were measured by high-performance liquid chromatog-
raphy with electrochemical detection as previously reported. Inter-assay and intra-assay
coefficients are 3.86% and 3.64%, respectively. Blood samples were obtained at baseline and
3. Int. J. Environ. Res. Public Health 2022, 19, 3237 3 of 11
after completion of each phase of TC and EC smoking sessions. No blood samples were
collected for sham smoking.
2.3. Experimental Session
The study design was randomized and sham controlled with 3 experimental sessions
(sham smoking, TC smoking and EC smoking). The sessions were performed in random
order, each session on a separate day. Randomization was performed with means of closed
envelopes for each subject and session (Figure 1). After baseline measurements at rest,
the subjects were then asked to smoke (puffing habits left uncontrolled) 2 TC cigarettes
containing 1.1 mg nicotine, smoke an EC or simulate smoking with a drinking straw with a
filter (sham smoking), in line with previous methodology [16,17,27]. The first TC cigarette
or sham smoking (Phase 1 of TC or sham smoking) was separated by 5 min from the second
TC cigarette or sham smoking (Phase 2 of TC or sham smoking). Regarding EC smoking,
participants were advised every 30 s to place the EC in mouth, inhale for 3 s, hold aerosol
in for 3 s and then exhale. The time points for measurements in EC smoking were the
period of 5 min (Phase 1) and 30 min (Phase 2) as previously suggested [20–22]. The EC
used in the study was one with tobacco-flavored liquid, vegetable glycerin/propylene
glycol solvents with 1.2% nicotine. Changes in MSNA, SSNA, blood pressure and heart
rate were calculated for the last 2 min of each smoking phase, when the effects of smoking
are especially marked [15,16]. The present study complies with the Declaration of Helsinki
and the locally appointed ethics committee has approved the research protocol. Informed
consent has been obtained from all subjects.
has been shown to be highly reproducible with an intra‐observer reproducibility of
around 3.8–4.5% [24–26].
Plasma norepinephrine levels were measured by high‐performance liquid chroma‐
tography with electrochemical detection as previously reported. Inter‐assay and intra‐as‐
say coefficients are 3.86% and 3.64%, respectively. Blood samples were obtained at base‐
line and after completion of each phase of TC and EC smoking sessions. No blood samples
were collected for sham smoking.
2.3. Experimental Session
The study design was randomized and sham controlled with 3 experimental sessions
(sham smoking, TC smoking and EC smoking). The sessions were performed in random
order, each session on a separate day. Randomization was performed with means of
closed envelopes for each subject and session (Figure 1). After baseline measurements at
rest, the subjects were then asked to smoke (puffing habits left uncontrolled) 2 TC ciga‐
rettes containing 1.1 mg nicotine, smoke an EC or simulate smoking with a drinking straw
with a filter (sham smoking), in line with previous methodology [16,17,27]. The first TC
cigarette or sham smoking (Phase 1 of TC or sham smoking) was separated by 5 min from
the second TC cigarette or sham smoking (Phase 2 of TC or sham smoking). Regarding
EC smoking, participants were advised every 30 s to place the EC in mouth, inhale for 3
s, hold aerosol in for 3 s and then exhale. The time points for measurements in EC smoking
were the period of 5 min (Phase 1) and 30 min (Phase 2) as previously suggested [20–22].
The EC used in the study was one with tobacco‐flavored liquid, vegetable glycerin/pro‐
pylene glycol solvents with 1.2% nicotine. Changes in MSNA, SSNA, blood pressure and
heart rate were calculated for the last 2 min of each smoking phase, when the effects of
smoking are especially marked [15,16]. The present study complies with the Declaration
of Helsinki and the locally appointed ethics committee has approved the research proto‐
col. Informed consent has been obtained from all subjects.
Figure 1. The study design illustrating the randomization to TC, EC and sham smoking sessions in
random order, each session on a separate day. EC, electronic cigarette; MSNA, muscle sympathetic
nerve activity; SSNA, skin sympathetic nerve activity; TC, tobacco cigarette.
2.4. Statistical Analysis
Sample size was based on end points of MSNA and SSNA. Because there were no
data regarding the acute effects of EC on sympathetic nervous system components, we
used the reported pooled SD of MSNA and SSNA after TC smoking [16,17]. Assuming
similar SDs with EC use, a sample size of 10 subjects was required in order to achieve a
statistical power of 80% power with a two‐sided alpha = 0.05. Our final analysis included
12 subjects. Data were analyzed by repeated‐measures analysis of variance (ANOVA)
Figure 1. The study design illustrating the randomization to TC, EC and sham smoking sessions in
random order, each session on a separate day. EC, electronic cigarette; MSNA, muscle sympathetic
nerve activity; SSNA, skin sympathetic nerve activity; TC, tobacco cigarette.
2.4. Statistical Analysis
Sample size was based on end points of MSNA and SSNA. Because there were no data
regarding the acute effects of EC on sympathetic nervous system components, we used
the reported pooled SD of MSNA and SSNA after TC smoking [16,17]. Assuming similar
SDs with EC use, a sample size of 10 subjects was required in order to achieve a statistical
power of 80% power with a two-sided alpha = 0.05. Our final analysis included 12 subjects.
Data were analyzed by repeated-measures analysis of variance (ANOVA) using Box’s
conservative epsilon, considering time (before versus during smoking) as the within factor
and session (sham smoking, TC smoking alone and EC smoking) as the between factor. The
p-values for differences within a session were obtained by post hoc tests (planned contrasts).
Results are expressed as mean ± standard deviation (SD). All tests were two-sided and
p 0.002 was considered significant after Bonferroni adjustment for multiple comparisons.
4. Int. J. Environ. Res. Public Health 2022, 19, 3237 4 of 11
STATA® v.16.0 (StataCorp, College Station, TX 77845, USA) statistical software was used
for the analysis.
3. Results
At the start of the TC, EC and sham smoking sessions there were no differences
regarding baseline MAP, heart rate, MSNA and SSNA (p = NS for all, Tables 1 and 2).
Table 1. Effects of TC and EC smoking on hemodynamic parameters and on sympathetic activity.
Parameter Baseline TC Phase 1 TC Phase 2 p Baseline EC Phase 1 EC Phase 2 p
Systolic BP
(mmHg)
117 ± 5 126 ± 6 129 ± 5 0.001 119 ± 5 127 ± 6 133 ± 5 0.001
Diastolic BP
(mmHg)
67 ± 3 71 ± 3 73 ± 3 0.001 68 ± 4 72 ± 4 75 ± 5 0.001
Heart rate
(bpm)
64 ± 5 72 ± 6 76 ± 5 0.001 66 ± 6 71 ± 6 75 ± 8 0.001
MAP (mmHg) 84 ± 3 90 ± 3 92 ± 3 0.001 84 ± 3 90 ± 3 94 ± 4 0.001
MSNA
(bursts/min)
23 ± 3 17 ± 3 17 ± 4 0.001 24 ± 3 16 ± 4 16 ± 3 0.001
SSNA
(bursts/min)
13 ± 2 22 ± 3 23 ± 3 0.001 13 ± 2 20 ± 2 22 ± 2 0.001
Plasma NE
(pg/mL)
168 ± 19 170 ± 22 182 ± 27 0.002 173 ± 22 185 ± 17 231 ± 30 0.003
BP, blood pressure; EC, electronic cigarette; MAP, mean arterial pressure; MSNA, muscle sympathetic nerve
activity; NE, norepinephrine; SSNA, skin sympathetic nerve activity; TC, tobacco cigarette. p-values for differences
within a session were obtained by post hoc tests (planned contrasts). Results are expressed as mean ± standard
deviation (SD). All tests were two-sided and p 0.002 was considered significant after Bonferroni adjustment for
multiple comparisons.
Table 2. Effects of sham smoking on hemodynamic parameters and on sympathetic activity.
Parameter Baseline Sham Smoking Phase 1 Sham Smoking Phase 2 p
Systolic BP
(mmHg)
114 ± 5 113 ± 4 112 ± 5 0.135
Diastolic BP
(mmHg)
65 ± 3 66 ± 3 64 ± 3 0.094
Heart rate
(bpm)
63 ± 4 64 ± 5 64 ± 5 0.041
MAP (mmHg) 84 ± 3 82 ± 3 80 ± 3 0.001
MSNA
(bursts/min)
24 ± 2 23 ± 2 23 ± 3 0.023
SSNA
(bursts/min)
15 ± 2 14 ± 2 15 ± 3 0.076
BP, blood pressure; MAP, mean arterial pressure; MSNA, muscle sympathetic nerve activity; SSNA, skin sympa-
thetic nerve activity. p-values for differences within a session were obtained by post hoc tests (planned contrasts).
Results are expressed as mean ± standard deviation (SD). All tests were two-sided and p 0.002 was considered
significant after Bonferroni adjustment for multiple comparisons.
3.1. Effects of Smoking on Hemodynamic Parameters
After the first and second phases of tobacco cigarette smoking, there was a significant
increase in mean arterial pressure (by 6 and 8 mmHg, respectively, overall p 0.001) and
heart rate (by 8 and 12 beats/minute, respectively, overall p 0.001) (Table 1, Figure 2),
compared to baseline. Similarly, EC smoking at 5 and 30 min compared to baseline was
accompanied by augmentation in mean arterial pressure (by 6 and 10 mmHg, respectively,
overall p 0.001) and heart rate (by 5 and 9 beats/minute, respectively, overall p 0.001)
5. Int. J. Environ. Res. Public Health 2022, 19, 3237 5 of 11
(Table 1, Figure 2). Regarding sham smoking, it was accompanied by a reduction in mean
arterial pressure (by 2 and 4 mmHg, respectively, p = 0.001) after the first and second
cigarette compared to baseline, whereas there was no significant difference in heart rate
(p = 0.041) (Table 2, Figure 2).
3.1. Effects of Smoking on Hemodynamic Parameters
After the first and second phases of tobacco cigarette smoking, there was a significant
increase in mean arterial pressure (by 6 and 8 mmHg, respectively, overall p 0.001) and
heart rate (by 8 and 12 beats/minute, respectively, overall p 0.001) (Table 1, Figure 2),
compared to baseline. Similarly, EC smoking at 5 and 30 min compared to baseline was
accompanied by augmentation in mean arterial pressure (by 6 and 10 mmHg, respec‐
tively, overall p 0.001) and heart rate (by 5 and 9 beats/minute, respectively, overall p
0.001) (Table 1, Figure 2). Regarding sham smoking, it was accompanied by a reduction
in mean arterial pressure (by 2 and 4 mmHg, respectively, p = 0.001) after the first and
second cigarette compared to baseline, whereas there was no significant difference in
heart rate (p = 0.041) (Table 2, Figure 2).
Figure 2. MAP at baseline and phases 1 and 2 of TC, EC and sham smoking. EC, electronic cigarette;
MAP, mean arterial pressure; TC, tobacco cigarette., SS=sham smoking
3.2. Effects of Smoking on Sympathetic Nervous System
The first and second TC smoking phases were accompanied by lower MSNA (by 6
and 6 bursts/minute, respectively, overall p 0.001) compared to baseline, whereas SSNA
was increased (by 9 and 10 bursts/minute respectively, overall p 0.001) (Table 1, Figures
3 and 4).
Additionally, EC smoking at 5 and 30 min compared to baseline caused a decrease in
MSNA (by 8 and 8 bursts/minute, respectively, overall p 0.001) and an augmentation in
SSNA (by 7 and 9 bursts per minute, respectively, overall p 0.001) (Table 1, and Figures
3 and 4). Plasma norepinephrine levels were significantly increased after TC but not after
EC smoking (Table 1).
Sham smoking had no significant effect on MSNA (p = 0.023) and SSNA (p = 0.076)
(Table 2 and Figures 3 and 4].
Figure 2. MAP at baseline and phases 1 and 2 of TC, EC and sham smoking. EC, electronic cigarette;
MAP, mean arterial pressure; TC, tobacco cigarette, SS, sham smoking.
3.2. Effects of Smoking on Sympathetic Nervous System
The first and second TC smoking phases were accompanied by lower MSNA (by
6 and 6 bursts/minute, respectively, overall p 0.001) compared to baseline, whereas
SSNA was increased (by 9 and 10 bursts/minute respectively, overall p 0.001) (Table 1,
Figures 3 and 4).
Additionally, EC smoking at 5 and 30 min compared to baseline caused a decrease in
MSNA (by 8 and 8 bursts/minute, respectively, overall p 0.001) and an augmentation
in SSNA (by 7 and 9 bursts per minute, respectively, overall p 0.001) (Table 1, and
Figures 3 and 4). Plasma norepinephrine levels were significantly increased after TC but
not after EC smoking (Table 1).
Sham smoking had no significant effect on MSNA (p = 0.023) and SSNA (p = 0.076)
(Table 2 and Figures 3 and 4].
The MSNA decrease was significant during both TC and EC sessions (p 0.001 for
both comparisons) and was similar between them (−25.1% ± 9.8% vs. −34.4% ± 8.3%,
respectively, p = 0.018). Both decreases were significantly higher (p 0.001 for both com-
parisons) than that elicited by sham smoking (−4.4% ± 4.8%), although this was not
significant by itself (p = 0.012) (Figure 5). SSNA increase was significant in both TC and
EC groups (p 0.001 for both comparisons) and similar between them (73.4% ± 17.9% and
71.9% ± 7%, respectively, p = 0.829). In addition, this difference was significantly higher
(p 0.001 for both comparisons) than that during sham smoking where a slight but not
statistically significant mean reduction was found (−1.3% ± 17.9%, p = 0.698) (Figure 5).
6. Int. J. Environ. Res. Public Health 2022, 19, 3237 6 of 11
Int. J. Environ. Res. Public Health 2022, 19, x FOR PEER REVIEW 6 of 11
Figure 3. MSNA at baseline and phases 1 and 2 of TC, EC and sham smoking. EC, electronic ciga‐
rette; MSNA, muscle sympathetic nerve activity; TC, tobacco cigarette.
Figure 4. SSNA at baseline and phases 1 and 2 EC and sham smoking. EC, electronic cigarette; SSNA,
skin sympathetic nerve activity; TC, tobacco cigarette.
The MSNA decrease was significant during both TC and EC sessions (p 0.001 for
both comparisons) and was similar between them (−25.1% ± 9.8% vs. −34.4% ± 8.3%, re‐
spectively, p = 0.018). Both decreases were significantly higher (p 0.001 for both
Figure 3. MSNA at baseline and phases 1 and 2 of TC, EC and sham smoking. EC, electronic cigarette;
MSNA, muscle sympathetic nerve activity; TC, tobacco cigarette, SS, sham smoking.
Int. J. Environ. Res. Public Health 2022, 19, x FOR PEER REVIEW 6 of 11
Figure 3. MSNA at baseline and phases 1 and 2 of TC, EC and sham smoking. EC, electronic ciga‐
rette; MSNA, muscle sympathetic nerve activity; TC, tobacco cigarette.
Figure 4. SSNA at baseline and phases 1 and 2 EC and sham smoking. EC, electronic cigarette; SSNA,
skin sympathetic nerve activity; TC, tobacco cigarette.
The MSNA decrease was significant during both TC and EC sessions (p 0.001 for
both comparisons) and was similar between them (−25.1% ± 9.8% vs. −34.4% ± 8.3%, re‐
spectively, p = 0.018). Both decreases were significantly higher (p 0.001 for both
Figure 4. SSNA at baseline and phases 1 and 2 EC and sham smoking. EC, electronic cigarette; SSNA,
skin sympathetic nerve activity; TC, tobacco cigarette, SS, sham smoking.
7. Int. J. Environ. Res. Public Health 2022, 19, 3237 7 of 11
comparisons) than that elicited by sham smoking (−4.4% ± 4.8%), although this was not
significant by itself (p = 0.012) (Figure 5). SSNA increase was significant in both TC and
EC groups (p 0.001 for both comparisons) and similar between them (73.4% ± 17.9% and
71.9% ± 7%, respectively, p = 0.829). In addition, this difference was significantly higher (p
0.001 for both comparisons) than that during sham smoking where a slight but not sta‐
tistically significant mean reduction was found (−1.3% ± 17.9%, p = 0.698) (Figure 5).
Figure 5. Changes in MSNA and SSNA by TC, EC and sham smoking. EC, electronic cigarette;
MSNA, muscle sympathetic nerve activity; SSNA, skin sympathetic nerve activity; TC, tobacco cig‐
arette.
There was no association of the change in MAP with the alterations in MSNA and
SSNA during sessions of TC, EC and sham smoking (data not shown). Moreover, norepi‐
nephrine levels were not related to MSNA and SSNA changes (data not shown).
4. Discussion
To the best of our knowledge, this is the first study to have assessed the effect of both
TC and EC smoking on MSNA and SSNA in healthy smokers. Our findings indicate that
ECs have a powerful sympathetic excitatory effect, similar to that elicited by TCs. EC
smoking may act at a central level to cause a uniform increase in sympathetic nerve traffic
to blood vessels, skin and the heart. Alterations in sympathetic drive are paralleled by an
increase in blood pressure and heart rate, reflecting a systemic hemodynamic response to
smoking both types of cigarettes (Figure 6).
Previous studies have shown that TC smoking causes a marked elevation in blood
pressure by sympathetic excitation, impairment of arterial baroreflex function and acute
reduction in arterial compliance [15–19,28]. The effect of TC on sympathetic drive is com‐
plex [16]. TC causes a marked increase in skin sympathetic discharge and a decrease in
MSNA. Paradoxical MSNA decrease might at first glance suggest a sympathoinhibitory
effect of TC. However, MSNA, in contrast to SSNA, is inhibited by blood pressure changes
[15–17]. Therefore, MSNA inhibition during TC smoking reflects the protective effect of
arterial baroreflexes, responding to increases in blood pressure. When the blood pressure
increase in response to TC smoking is blunted by the simultaneous infusion of sodium
nitroprusside, there is a striking increase in MSNA [16].
The recently published study by Gonzalez J et al. [23] in healthy non‐smokers, de‐
scribe similar results concerning the effect of ECs on MSNA and arterial pressure. How‐
ever, there is no estimation of SSNA [23] that is not influenced by hemodynamic load
changes due to smoking. Thus, our study provides for the first time, evidence that EC
Figure 5. Changes in MSNA and SSNA by TC, EC and sham smoking. EC, electronic cigarette;
MSNA, muscle sympathetic nerve activity; SSNA, skin sympathetic nerve activity; TC, tobacco
cigarette, SS, sham smoking.
There was no association of the change in MAP with the alterations in MSNA and
SSNA during sessions of TC, EC and sham smoking (data not shown). Moreover, nore-
pinephrine levels were not related to MSNA and SSNA changes (data not shown).
4. Discussion
To the best of our knowledge, this is the first study to have assessed the effect of both
TC and EC smoking on MSNA and SSNA in healthy smokers. Our findings indicate that
ECs have a powerful sympathetic excitatory effect, similar to that elicited by TCs. EC
smoking may act at a central level to cause a uniform increase in sympathetic nerve traffic
to blood vessels, skin and the heart. Alterations in sympathetic drive are paralleled by an
increase in blood pressure and heart rate, reflecting a systemic hemodynamic response to
smoking both types of cigarettes (Figure 6).
Previous studies have shown that TC smoking causes a marked elevation in blood pres-
sure by sympathetic excitation, impairment of arterial baroreflex function and acute reduc-
tion in arterial compliance [15–19,28]. The effect of TC on sympathetic drive is complex [16].
TC causes a marked increase in skin sympathetic discharge and a decrease in MSNA.
Paradoxical MSNA decrease might at first glance suggest a sympathoinhibitory effect of
TC. However, MSNA, in contrast to SSNA, is inhibited by blood pressure changes [15–17].
Therefore, MSNA inhibition during TC smoking reflects the protective effect of arterial
baroreflexes, responding to increases in blood pressure. When the blood pressure increase
in response to TC smoking is blunted by the simultaneous infusion of sodium nitroprusside,
there is a striking increase in MSNA [16].
The recently published study by Gonzalez J et al. [23] in healthy non-smokers, describe
similar results concerning the effect of ECs on MSNA and arterial pressure. However, there
is no estimation of SSNA [23] that is not influenced by hemodynamic load changes due to
smoking. Thus, our study provides for the first time, evidence that EC increases SSNA in
humans. The rise in SSNA was evident from the first TC and the start of EC smoking and
remained high till the end of the sessions. Although we did not seek to maintain pressure
at baseline levels by sodium nitroprusside, as performed in a previous study [16], our
current findings indicate that the effects of TC and EC smoking on MSNA are comparable.
The sympathoexcitatory effect of ECs, in addition to SSNA increase, is further supported
by a significant rise in plasma norepinephrine and tachycardia, which were of a similar
magnitude to those during the TC session. Importantly, blood pressure increase was similar
8. Int. J. Environ. Res. Public Health 2022, 19, 3237 8 of 11
during TC and EC sessions, facilitating interpretation of the sympathetic traffic results.
This is in line with a previous work [23], highlighting the unfavorable impact of vaping on
arterial pressure. The use of the control arm strengthens our findings since sham smoking
was associated with a lack of significant MSNA change and a significantly lower increase
in SSNA compared to TC and EC smoking.
increases SSNA in humans. The rise in SSNA was evident from the first TC and the start
of EC smoking and remained high till the end of the sessions. Although we did not seek
to maintain pressure at baseline levels by sodium nitroprusside, as performed in a previ‐
ous study [16], our current findings indicate that the effects of TC and EC smoking on
MSNA are comparable. The sympathoexcitatory effect of ECs, in addition to SSNA in‐
crease, is further supported by a significant rise in plasma norepinephrine and tachycar‐
dia, which were of a similar magnitude to those during the TC session. Importantly, blood
pressure increase was similar during TC and EC sessions, facilitating interpretation of the
sympathetic traffic results. This is in line with a previous work [23], highlighting the un‐
favorable impact of vaping on arterial pressure. The use of the control arm strengthens
our findings since sham smoking was associated with a lack of significant MSNA change
and a significantly lower increase in SSNA compared to TC and EC smoking.
Figure 6: EC smoking, similar to TC smoking, may act at a central level to cause a uniform increase
in sympathetic nerve traffic to blood vessels, skin and the heart. Alterations in sympathetic drive
are paralleled by an increase in blood pressure and heart rate, reflecting a systemic hemodynamic
response to smoking of both types of cigarettes. These unfavorable effects of ECs mimicking those
by TCs may chronically lead to increased risk of cardiovascular events. BP, blood pressure; CV,
cardiovascular; EC, electronic cigarette; HR, heart rate; TC, tobacco cigarette.
The acute tachycardic effect of TC smoking had a similar pattern to that observed
during the EC session. Although it is established that nicotine, as a sympathomimetic sub‐
stance, in TCs induce the increase in cardiac sympathetic nerve activity reflected by in‐
creased heart rate, the contribution of other non‐nicotine combusted organic constituents
is largely unexplored [4,15–22,27]. Especially in the EC setting, the data are scarce, sup‐
porting mostly the main contribution of nicotine to EC‐related unfavorable change in car‐
diac sympathetic nerve activity as observed in heart rate variability parameters as well as
blood pressure increase [1,20,22,23,26]. Adding more fuel to this controversy, air pollution
with similarities to TC smoke without nicotine can increase cardiac sympathetic drive via
Figure 6. EC smoking, similar to TC smoking, may act at a central level to cause a uniform increase
in sympathetic nerve traffic to blood vessels, skin and the heart. Alterations in sympathetic drive
are paralleled by an increase in blood pressure and heart rate, reflecting a systemic hemodynamic
response to smoking of both types of cigarettes. These unfavorable effects of ECs mimicking those
by TCs may chronically lead to increased risk of cardiovascular events. BP, blood pressure; CV,
cardiovascular; EC, electronic cigarette; HR, heart rate; TC, tobacco cigarette.
The acute tachycardic effect of TC smoking had a similar pattern to that observed
during the EC session. Although it is established that nicotine, as a sympathomimetic
substance, in TCs induce the increase in cardiac sympathetic nerve activity reflected by
increased heart rate, the contribution of other non-nicotine combusted organic constituents
is largely unexplored [4,15–22,27]. Especially in the EC setting, the data are scarce, sup-
porting mostly the main contribution of nicotine to EC-related unfavorable change in
cardiac sympathetic nerve activity as observed in heart rate variability parameters as well
as blood pressure increase [1,20,22,23,26]. Adding more fuel to this controversy, air pol-
lution with similarities to TC smoke without nicotine can increase cardiac sympathetic
drive via reactive oxygen species and pathways of lung vagal afferent C-fibers [22,28–30].
Nowadays, there are data that show that, although particulate size and number in ECs
have considerable overlap with air pollution and TC smoke, the levels of toxic substances
are lower. In addition, it is supported that flavorings, solvents and/or contaminants in ECs
are not linked to acute sympathetic system changes [22,30], as evident in vaping without
nicotine [23].
9. Int. J. Environ. Res. Public Health 2022, 19, 3237 9 of 11
Norepinephrine levels that are not specific to MSNA and SSNA and reflect acute
changes in nervous tone, were found to be increased at the end of TC but not EC sessions
compared to baseline, and, also, they were not related to the parameters of microneurogra-
phy. This could be due to both MSNA and SSNA being influenced by nicotine and diverse
axes and feedback mechanisms, while norepinephrine level alterations are the severe result
of the nicotine-induced local release of catecholamines from adrenergic nerve terminals [4].
Moreover, given that the studied EC contained nicotine, one could not exclude different
reactions of non-nicotine ECs, as explored recently [23]. From a pathophysiological point of
view, nicotine and other toxic agents such as the gases and fine particulate matter (PM2.5;
defined as 2.5 mm in hydrodynamic diameter) in cigarette smoke are implicated in the
pressor result and autonomic system shifting to sympathetic predominance [1,4]. Ad-
junct mechanisms for the observed smoking effects include a 1-adrenoceptor–mediated
vasoconstriction, vasopressin release and endothelial dysfunction [1,4,31,32].
The subjects in the current study were males and healthy with preserved baroreflex
axis. This is not the case for patients with hypertension, diabetes mellitus and heart failure
who are characterized by baroreflex failure and might be more sensitive to TC and EC
smoking by not diminishing acutely MSNA while maintaining high hemodynamic load and
heart rate [4]. Thus, clinical research in these higher risk cardiovascular states for the impact
of TC and EC smoking on sympathetic tone will provide additional pathophysiological
explanations for their augmented overall risk. Especially in the elderly, it was shown
that heart rate is less increased after smoking compared to younger subjects and, also,
the MSNA-related sympathetic activity is not suppressed, rendering smoking even more
hazardous [17]. Our study population consisted of males with a mean age of 34 years
and, thus, older than the participants in another previous study in which the sympathetic
response to TC and EC smoking was more pronounced [16]. This age gap could partially
explain the differences in MSNA and SSNA reaction to acute smoking exposure between
our study and the previous one [16]. Finally, our population consisted of smokers in
contrast to the recently published work by Gonzalez J et al. [23] in which only non-smokers
participated. It is possible that TC and EC smoking might have a diverse effect on autonomic
regulation and hemodynamic modulation according to the smoking status of the studied
subjects [16,17,23]
Cardiac mortality associated with smoking is non-linear with the risk being binary,
meaning that the consumption of 1–3 cigarettes per day correlates to the risk induced by 20
cigarettes per day [28]. On these lines, with the acute exposure to TC and EC smoking, the
unfavorable changes in mean arterial pressure and heart rate along with MSNA and SSNA
are observed with the first cigarette and maintained after the second one, and, in the case of
EC, at 5 min the impact is comparable to that of 30 min. Given that experienced EC smokers
can increase their nicotine absorption significantly by puff duration compared to naïve
subjects [33] such as those in our study, it is possible that the unfavorable effects of vaping
are underestimated. These results suggest that exposure to low levels of nicotine is adequate
to elicit important systemic changes in humans that are then enhanced and maintained by
the continuation of TC or EC smoking. Specific for our study, the alterations of sympathetic
drive by TC and EC smoking were evident in the already increased sympathetic activation
that is present in habitual TC smokers [18].
The study results are limited by the inclusion of only males; however, there are gender
differences to blood pressure effects of smoking, and this baroreflex diverse reaction to
acute TC and EC exposure could influence the sympathetic response [4]. The lack of
active nicotine and cotinine estimation along with no spontaneous cardiovagal baroreflex
sensitivity calculation limits our findings, along with the fact that smoking with a drinking
straw is still different than the physique of the cigarette and subjects were not blinded.
Moreover, no repeated measurements for hemodynamic and sympathetic parameters on
each participant were made. There was also no sham EC testing as well as no EC without
nicotine as in a previous work [23]. Finally, the effect of TC and EC smoking on sympathetic
drive, blood pressure and heart rate after the acute phase were not assessed.
10. Int. J. Environ. Res. Public Health 2022, 19, 3237 10 of 11
5. Conclusions
This is the first study showing that inhaling ECs acutely increases mean arterial
pressure and heart rate, decreases MSNA and augments SSNA in healthy smokers. These
findings provide novel insights into the unfavorable impact of vaping on the cardiovascular
system and support further research for the overall effects of EC.
Author Contributions: Conceptualization, K.N. and C.T.; data curation, I.L., D.K. and I.A.; formal
analysis, K.D., I.L. and C.M.; investigation, I.L., I.A., C.T. and K.T.; methodology, K.D., K.N., D.K.,
C.M., I.A. and C.T.; supervision, K.N. and K.T.; writing—original draft, K.D.; writing—review
and editing, K.N., D.T. and K.T. All authors have read and agreed to the published version of the
manuscript.
Funding: This research received no external funding.
Institutional Review Board Statement: The present study complies with the Declaration of Helsinki
and the locally appointed ethics committee has approved the research protocol.
Informed Consent Statement: Informed consent was obtained from all subjects involved in the
study.
Acknowledgments: I would like to thank INAKEN for the support.
Conflicts of Interest: The authors declare no conflict of interest.
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