Tobacco Smoke Pollution

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Original Article

Association between Passive Smoking and Hypertension: A Panel Study with 621.506 Adults from Brazil

Vicente Gabriel Winck Mattos et al. Gustavo Ianzer Moraes Laís Werneck de Azevedo Júlia Oleiro Mandeco … Elizabet Saes-Silva Carine Nascimento da Silva Samuel Carvalho Dumith

Abstract

Background

Passive smoking, which affects a large number of people, may create a predisposition to cardiovascular disease in a manner similar to active smoking. However, this relationship is poorly explored in the scientific literature.

Objectives

This study aimed to investigate the association between passive smoking and hypertension in an adult population in Brazil.

Methods

This panel study utilized data on the Brazilian population collected through a VIGITEL survey conducted between 2009 and 2021. The data were analyzed using Poisson regression with a 95% confidence interval (95%CI).

Results

The prevalence of hypertension in our population was 24.9% (95%CI 24.6-25.1), and passive smoking was observed in 16.3% (95%CI 16.0-16.5). The adjusted analysis revealed that passive smoking leads to a high risk of hypertension (PR=1.10; 95%CI 1.07 to 1.14), which was surprisingly close to the risk among heavy smokers (>1 pack or 20 cigarettes a day) (PR 1.09; 95%CI 1.06 to 1.13). Another noteworthy finding was the higher prevalence of hypertension among former smokers, highlighting associations that are poorly explained in the literature.

Conclusion

A significant association was found between passive smoking and hypertension, demonstrating that passive smokers are as prone to developing hypertension as heavy smokers. Therefore, we recommend a meta-analysis to consolidate the evidence on this subject and strengthen our findings.

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Original Article

Passive Cigarette Smoking Impact on Blood Pressure Response to Epinephrine and Felypressin in 1K1C Hypertensive Rats Treated or not with Atenolol

Camila A. Fleury et al. Elizandra P. M. Almeida Thiago J. Dionisio Adriana M. Calvo … Gabriela M. Oliveira Sandra L. Amaral Carlos F. Santos Flávio A. C. Faria

Abstract

Background:

Cigarette smoking is usually associated with hypertension and may modify vasoconstrictor response.

Objective:

The present study aimed to analyze and compare the interaction of passive cigarette smoking and hypertension on epinephrine and felypressin blood pressure effects after intravascular injection.

Method:

45-day male Wistar rats had the main left renal artery partially constricted and the right kidney removed (1K1C model). Rats were placed in the chamber for exposition to passive cigarette smoking (10 cigarettes) during 10 min (6 days a week). Hypertensive rats received atenolol (90 mg/kg/day) by gavage for two weeks. Hypotensive and hypertensive response, response duration and heart rate were recorded from direct blood pressure values. The significance level was 5%.

Results:

Passive cigarette smoking increased maximal hypertensive response to epinephrine in normotensive and 1K1C-atenolol treated rats and to felypressin only in 1K1C-atenolol treated rats; it also reduced epinephrine hypotensive response. Epinephrine increased heart rate in normotensive and hypertensive passive smokers or non-smoker rats. Comparing the two vasoconstrictors, epinephrine showed greater hypertensive response in normotensive smokers, 1K1C-atenolol treated smokers and non-smokers. However, in normotensive-nonsmoker rats, felypressin showed a greater and longer hypertensive effect.

Conclusions:

Our results suggest that passive cigarette smoking may reduce epinephrine vasodilation and increase hypertensive response when compared to felypressin. Therefore, felypressin may be safe for hypertensive patients to avoid tachycardia and atenolol interaction, but for normotensive and non-smoker patients, epinephrine may be safer than felypressin.

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Statement

2019: Recommendations for Reducing Tobacco Consumption in Portuguese-Speaking Countries – Positioning of the Federation of Portuguese Language Cardiology Societies

Gláucia Maria Moraes de Oliveira et al. Miguel Mendes Oscar Pereira Dutra Aloysio Achutt … Mario Fernandes Vanda Azevedo Maria Beatriz Sena e Costa Santos Ferreira Armando Serra Coelho Miryan Bandeira dos Prazeres Cassandra Soares Mário Alberto Brito Lima Évora Mário Gomes Mariotto João Araujo Morais

Introduction

Depending on the epidemiological perspective of the observer and the extent of his concept of causality, tobacco consumption can be considered the second cause in the world of death attributed to classic cardiovascular risk factors, preceded only by hypertension, and the first cause of premature death and disabilities. When understood as an immediate cause without contextualization in the complex that determines and maintains population behavior, smoking was responsible in the world for about 8.10 (7.79-8.41) million deaths and 213.39 (201.16-226.66) million healthy life years lost (disability-adjusted life-years, DALYs). Although the number of daily smokers (individuals aged 15 years and older who smoke daily) has decreased, the total number of smokers continues to increase, imposing a major global challenge for healthcare systems.

Physicians, who generally deal directly and individually with the patient, tend to consider health/illness limited to the patient’s organic commitment and personal history and are less appreciative of the “causes of the causes” and the psychosocial determinants of the phenomena and behaviors, inseparable from the ecological context and interests. Environmental pollution (which has also a contribution from smoking and is progressively increasing) is currently considered to be the most important cause of morbidity and mortality in the world’s population, extending the spectrum beyond the traditionally valued risk factors. This perspective is very important for an understanding of the resistance to smoking control and planning of strategies that are more effective to approach this issue.

[…]

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Original Article

Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure

Marcos Minicucci et al. Fernando Oliveira Priscila Santos Bertha Polegato … Meliza Roscani Ana Angelica Fernandes Beatriz Lustosa Sergio Paiva Leonardo Zornoff Paula Azevedo

Abstract

Background:

Tobacco smoke exposure is an important risk factor for cardiac remodeling. Under this condition, inflammation, oxidative stress, energy metabolism abnormalities, apoptosis, and hypertrophy are present. Pentoxifylline has anti‑inflammatory, anti-apoptotic, anti-thrombotic and anti-proliferative properties.

Objective:

The present study tested the hypothesis that pentoxifylline would attenuate cardiac remodeling induced by smoking.

Methods:

Wistar rats were distributed in four groups: Control (C), Pentoxifylline (PX), Tobacco Smoke (TS), and PX-TS. After two months, echocardiography, invasive blood pressure measurement, biochemical, and histological studies were performed. The groups were compared by two-way ANOVA with a significance level of 5%.

Results:

TS increased left atrium diameter and area, which was attenuated by PX. In the isolated heart study, TS lowered the positive derivate (+dp/dt), and this was attenuated by PX. The antioxidants enzyme superoxide dismutase and glutathione peroxidase were decreased in the TS group; PX recovered these activities. TS increased lactate dehydrogenase (LDH) and decreased 3-hydroxyacyl Coenzyme A dehydrogenases (OH-DHA) and citrate synthase (CS). PX attenuated LDH, 3-OH-DHA and CS alterations in TS-PX group. TS increased IL-10, ICAM-1, and caspase-3. PX did not influence these variables.

Conclusion:

TS induced cardiac remodeling, associated with increased inflammation, oxidative stress, apoptosis, and changed energy metabolism. PX attenuated cardiac remodeling by reducing oxidative stress and improving cardiac bioenergetics, but did not act upon cardiac cytokines and apoptosis.

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Association between Passive Smoking and Hypertension: A Panel Study with 621.506 Adults from Brazil

Abstract

Background

Objectives

Methods

Results

Conclusion

Passive Cigarette Smoking Impact on Blood Pressure Response to Epinephrine and Felypressin in 1K1C Hypertensive Rats Treated or not with Atenolol

Abstract

Background:

Objective:

Method:

Results:

Conclusions:

2019: Recommendations for Reducing Tobacco Consumption in Portuguese-Speaking Countries – Positioning of the Federation of Portuguese Language Cardiology Societies

Introduction

Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure

Abstract

Background:

Objective:

Methods:

Results:

Conclusion:

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