Environmental tobacco smoke promotes heart disease

Y. Liu, J. Zhang, Ronald R Watson

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Environmental tobacco smoke, a mixture of cigarette sidestream smoke (85%) and mainstream smoke (15%), originates from the smoldering end of a cigarette between puffs as well as exhaled tobacco smoke. It is responsible for involuntary or "passive" smoking by nonsmokers. Over the last 15 years, epidemiology and experimental studies have consistently shown that environmental tobacco smoke increases the risk of developing acute cardiovascular disease, acute myocardial infarction, sudden death, and stroke. Environmental tobacco smoke also produces chronic effects with atherosclerosis at epicardial coronary arteries, the aorta, the carotid cerebral arteries, and large arteries, in the peripheral circulation. These adverse effects are due to the effects of cigarette smoke on lipids, greater platelet aggregation, endothelial cell damage, and oxidant injury. This review will discuss the recent evidence linking mainstream and environmental tobacco smoke with cardiovascular disease, possible mechanisms by which environmental tobacco smoke causes cardiovascular disease, and the prospect for treatment using antioxidants.

Original languageEnglish (US)
Pages (from-to)589-594
Number of pages6
JournalCardiovascular Reviews and Reports
Volume21
Issue number11
StatePublished - 2000

Fingerprint

Smoke
Tobacco
Heart Diseases
Tobacco Products
Cardiovascular Diseases
Tobacco Smoke Pollution
Cerebral Arteries
Acute Disease
Sudden Death
Platelet Aggregation
Carotid Arteries
Oxidants
Aorta
Atherosclerosis
Coronary Vessels
Epidemiology
Endothelial Cells
Arteries
Antioxidants
Stroke

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Environmental tobacco smoke promotes heart disease. / Liu, Y.; Zhang, J.; Watson, Ronald R.

In: Cardiovascular Reviews and Reports, Vol. 21, No. 11, 2000, p. 589-594.

Research output: Contribution to journalArticle

@article{612b83ecf5b14ac0893a1866983f77b4,
title = "Environmental tobacco smoke promotes heart disease",
abstract = "Environmental tobacco smoke, a mixture of cigarette sidestream smoke (85{\%}) and mainstream smoke (15{\%}), originates from the smoldering end of a cigarette between puffs as well as exhaled tobacco smoke. It is responsible for involuntary or {"}passive{"} smoking by nonsmokers. Over the last 15 years, epidemiology and experimental studies have consistently shown that environmental tobacco smoke increases the risk of developing acute cardiovascular disease, acute myocardial infarction, sudden death, and stroke. Environmental tobacco smoke also produces chronic effects with atherosclerosis at epicardial coronary arteries, the aorta, the carotid cerebral arteries, and large arteries, in the peripheral circulation. These adverse effects are due to the effects of cigarette smoke on lipids, greater platelet aggregation, endothelial cell damage, and oxidant injury. This review will discuss the recent evidence linking mainstream and environmental tobacco smoke with cardiovascular disease, possible mechanisms by which environmental tobacco smoke causes cardiovascular disease, and the prospect for treatment using antioxidants.",
author = "Y. Liu and J. Zhang and Watson, {Ronald R}",
year = "2000",
language = "English (US)",
volume = "21",
pages = "589--594",
journal = "Cardiovascular Reviews and Reports",
issn = "0197-3118",
publisher = "Le Jacq Communications, Inc.",
number = "11",

}

TY - JOUR

T1 - Environmental tobacco smoke promotes heart disease

AU - Liu, Y.

AU - Zhang, J.

AU - Watson, Ronald R

PY - 2000

Y1 - 2000

N2 - Environmental tobacco smoke, a mixture of cigarette sidestream smoke (85%) and mainstream smoke (15%), originates from the smoldering end of a cigarette between puffs as well as exhaled tobacco smoke. It is responsible for involuntary or "passive" smoking by nonsmokers. Over the last 15 years, epidemiology and experimental studies have consistently shown that environmental tobacco smoke increases the risk of developing acute cardiovascular disease, acute myocardial infarction, sudden death, and stroke. Environmental tobacco smoke also produces chronic effects with atherosclerosis at epicardial coronary arteries, the aorta, the carotid cerebral arteries, and large arteries, in the peripheral circulation. These adverse effects are due to the effects of cigarette smoke on lipids, greater platelet aggregation, endothelial cell damage, and oxidant injury. This review will discuss the recent evidence linking mainstream and environmental tobacco smoke with cardiovascular disease, possible mechanisms by which environmental tobacco smoke causes cardiovascular disease, and the prospect for treatment using antioxidants.

AB - Environmental tobacco smoke, a mixture of cigarette sidestream smoke (85%) and mainstream smoke (15%), originates from the smoldering end of a cigarette between puffs as well as exhaled tobacco smoke. It is responsible for involuntary or "passive" smoking by nonsmokers. Over the last 15 years, epidemiology and experimental studies have consistently shown that environmental tobacco smoke increases the risk of developing acute cardiovascular disease, acute myocardial infarction, sudden death, and stroke. Environmental tobacco smoke also produces chronic effects with atherosclerosis at epicardial coronary arteries, the aorta, the carotid cerebral arteries, and large arteries, in the peripheral circulation. These adverse effects are due to the effects of cigarette smoke on lipids, greater platelet aggregation, endothelial cell damage, and oxidant injury. This review will discuss the recent evidence linking mainstream and environmental tobacco smoke with cardiovascular disease, possible mechanisms by which environmental tobacco smoke causes cardiovascular disease, and the prospect for treatment using antioxidants.

UR - http://www.scopus.com/inward/record.url?scp=0034426748&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034426748&partnerID=8YFLogxK

M3 - Article

VL - 21

SP - 589

EP - 594

JO - Cardiovascular Reviews and Reports

JF - Cardiovascular Reviews and Reports

SN - 0197-3118

IS - 11

ER -