Particulate and vapor phase constituents of cigarette mainstream smoke and risk of myocardial infarction

被引:154
作者
Smith, CJ [1 ]
Fischer, TH
机构
[1] RJ Reynolds Tobacco Co, Bowman Gray Tech Ctr, Res & Dev, Winston Salem, NC 27102 USA
[2] Univ N Carolina, Sch Med, Dept Pathol & Lab Med, Francis Owen Blood Res Lab, Chapel Hill, NC 27516 USA
关键词
mainstream smoke; atherogenic potential; arrhythmia;
D O I
10.1016/S0021-9150(01)00570-6
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
On pharmacological and compositional grounds, cigarette mainstream smoke (MS) aerosol can be broadly categorized as consisting of the following constituents: carbon monoxide, other vapor phase components, particulate matter ('tar') and nicotine. The relative risk of coronary artery disease for smoking 20 cigarettes per day has been estimated by meta-analysis of five large prospective epidemiology studies to be 1.78. These four major smoke components are simultaneously delivered to the active smoker as a complex aerosol composed of several billion semi-liquid particles per cm(3) within the mixture of combustion gases. Fractional attribution of the 78% increase in reported risk to a given constituent is problematic because of the complex mixture. However, a significant literature exists which suggests that some general statements regarding smoke constituent-associated risks for development or exacerbation of myocardial infarction are supportable. First, the atherogenic potential of MS is associated with the particulate and vapor phases and not with CO. Nicotine might exert an indirect effect on atherosclerotic plaque development by increasing shear forces in main conduction arteries. Similarly, the thrombogenic potential is associated primarily with the particulate and vapor phases and also possibly with nicotine via platelet aggregation. Vasoconstriction probably results from the actions of nicotine and hypoxia from carbon monoxide. Finally, the arrhythmia-inducing potential may result from catecholamine release following nicotine exposure, with a questionable contribution from carbon monoxide. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:257 / 267
页数:11
相关论文
共 117 条
  • [1] *AM HEART ASS, 1998, HIGH BLOOD PRESS STA
  • [2] ANDERSSON K, 1993, INT J OBESITY, V17, P678
  • [3] [Anonymous], 1986, RECENT ADV TOBACCO S, DOI DOI 10.3109/08958378.2012.744781
  • [4] Bainton D.F., 1988, INFLAMMATION BASIC P, P265
  • [5] SIGNIFICANCE OF SMOKING IN PATIENTS RECEIVING THROMBOLYTIC THERAPY FOR ACUTE MYOCARDIAL-INFARCTION - EXPERIENCE GLEANED FROM THE INTERNATIONAL TISSUE PLASMINOGEN-ACTIVATOR STREPTOKINASE MORTALITY TRIAL
    BARBASH, GI
    WHITE, HD
    MODAN, M
    DIAZ, R
    HAMPTON, JR
    HEIKKILA, J
    KRISTINSSON, A
    MOULOPOULOS, S
    ERNESTO
    PAOLASSO
    VANDERWERF, T
    PEHRSSON, K
    SANDOE, E
    SIMES, J
    WILCOX, RG
    VERSTRAETE, M
    VONDERLIPPE, G
    VANDEWERF, F
    [J]. CIRCULATION, 1993, 87 (01) : 53 - 58
  • [6] HEMODYNAMIC STRESS AND EXPERIMENTAL AORTOILIAC ATHEROSCLEROSIS
    BASSIOUNY, HS
    ZARINS, CK
    KADOWAKI, MH
    GLAGOV, S
    [J]. JOURNAL OF VASCULAR SURGERY, 1994, 19 (03) : 426 - 434
  • [7] Evaluation of the genotoxic and cytotoxic potential of mainstream whole smoke and smoke condensate from a cigarette containing a novel carbon filter
    Bombick, DW
    Bombick, BR
    Ayres, PH
    Putnam, K
    Avalos, J
    Borgerding, MF
    Doolittle, DJ
    [J]. FUNDAMENTAL AND APPLIED TOXICOLOGY, 1997, 39 (01): : 11 - 17
  • [8] EFFECT OF NICOTINE ON CULTURED BOVINE AORTIC ENDOTHELIAL-CELLS
    BOOYSE, FM
    OSIKOWICZ, G
    RADEK, J
    [J]. THROMBOSIS RESEARCH, 1981, 23 (1-2) : 169 - 185
  • [9] Chemical and biological studies of a new cigarette that primarily heats tobacco. Part 1. Chemical composition of mainstream smoke
    Borgerding, MF
    Bodnar, JA
    Chung, HL
    Mangan, PP
    Morrison, CC
    Risner, CH
    Rogers, JC
    Simmons, DF
    Uhrig, MS
    Wendelboe, FN
    Wingate, DE
    Winkler, LS
    [J]. FOOD AND CHEMICAL TOXICOLOGY, 1998, 36 (03) : 169 - +
  • [10] Bottcher M, 1999, J CARDIOVASC RISK, V6, P299