Cardiovascular effects associated with air pollution: Potential mechanisms and methods of testing

被引:134
作者
Utell, MJ
Frampton, MW
Zareba, W
Devlin, RB
Cascio, WE
机构
[1] Univ Rochester, Med Ctr, Dept Med, Div Pulm, Rochester, NY 14642 USA
[2] Univ Rochester, Med Ctr, Dept Environm Med, Rochester, NY 14642 USA
[3] US EPA, Res Triangle Pk, NC 27711 USA
[4] Univ N Carolina, Dept Med, Chapel Hill, NC USA
[5] Ctr Environm Med & Lung Biol, Chapel Hill, NC USA
关键词
D O I
10.1080/08958370290084881
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
A recent series of epidemiologic reports have shown associations between fine particulate matter (PM) levels and increased cardiovascular morbidity and mortality. Elevated PM levels have been linked with cardiac events, including serious ventricular arrhythmias and myocardial infarction. A workshop brought together epidemiologists, cardiologists, and toxicologists from academia, government, and industry to examine plausible mechanisms that could be responsible for such effects, and to consider the armamentarium of noninvasive tests available to examine these relationships. Possible mechanisms considered by the participants include: (a) effects on the autonomic nervous system; (b) alterations on ion channel function in myocardial cells; (c) ischemic responses in the myocardium; and (d) inflammatory responses triggering endothelial dysfunction, atherosclerosis, and thrombosis. A large number of tests were identified to assess specific mechanistic pathways underlying the cardiovascular effects of air pollution and include: (a) autonomic control of the cardiovascular system assessed primarily by heart-rate variability; (b) myocardial substrate and vulnerability assessed by the electrocardiogram and estimations of ejection fraction and wall motion abnormalities in imaging studies; and (c) endothelial function, atherosclerosis, and thrombosis assessed by clotting parameters, cytokines, lipid profiles, and forearm blood flow. A variety of approaches ranging from molecular and genetic investigations to human clinical studies were recommended to further investigate the important epidemiologic associations.
引用
收藏
页码:1231 / 1247
页数:17
相关论文
共 39 条
[1]  
[Anonymous], 1995, HEART RATE VARIABILI
[2]   Beat-to-beat repolarization lability identifies patients at risk for sudden cardiac death [J].
Atiga, WL ;
Calkins, H ;
Lawrence, JH ;
Tomaselli, GF ;
Smith, JM ;
Berger, RD .
JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, 1998, 9 (09) :899-908
[3]  
BOSCIA JA, 2000, AM J RESP CRIT CARE, V161, pA2396
[4]   Canines as sentinel species for assessing chronic exposures to air pollutants:: Part 2.: cardiac pathology [J].
Calderón-Garcidueñas, L ;
Gambling, TM ;
Acuña, H ;
García, R ;
Osnaya, N ;
Monroy, S ;
Villarreal-Calderón, A ;
Carson, J ;
Koren, HS ;
Devlin, RB .
TOXICOLOGICAL SCIENCES, 2001, 61 (02) :356-367
[5]   Low heart rate variability in a 2-minute rhythm strip predicts risk of coronary heart disease and mortality from several causes - The ARIC study [J].
Dekker, JM ;
Crow, RS ;
Folsom, AR ;
Hannan, PJ ;
Liao, D ;
Swenne, CA ;
Schouten, EG .
CIRCULATION, 2000, 102 (11) :1239-1244
[6]  
DEVLIN RB, 2000, AM J RESP CRIT CARE, V161, pA239
[7]   Systemic and cardiovascular effects of airway injury and inflammation: Ultrafine particle exposure in humans [J].
Frampton, MW .
ENVIRONMENTAL HEALTH PERSPECTIVES, 2001, 109 :529-532
[8]   Chemokines, leukocytes, and atherosclerosis [J].
Gerszten, RE ;
Mach, F ;
Sauty, A ;
Rosenzweig, A ;
Luster, AD .
JOURNAL OF LABORATORY AND CLINICAL MEDICINE, 2000, 136 (02) :87-92
[9]   Concentrated ambient air particles induce mild pulmonary inflammation in healthy human volunteers [J].
Ghio, AJ ;
Kim, C ;
Devlin, RB .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2000, 162 (03) :981-988
[10]  
GODLESKI JJ, 2000, RES REP HLTH EFF I, V91, P5