Environmental risk factors for heart disease.
In this review, we discuss current evidence linking environmental pollutants to cardiovascular disease (CVD). Extensive evidence indicates that environmental factors contribute to CVD risk, incidence, and severity. Migrant studies show that changes in the environment could substantially alter CVD risk in a genetically stable population. Additionally, CVD risk is affected by changes in nutritional and lifestyle choices. Recent studies in the field of environmental cardiology suggest that environmental toxins also influence CVD. Exposure to tobacco smoke is paradigmatic of such environmental risk and is strongly and positively associated with increased cardiovascular morbidity and mortality. In animal models of exposure, tobacco smoke induces endothelial dysfunction and prothrombotic responses and exacerbates atherogenesis and myocardial ischemic injury. Similar mechanism may be engaged by other pollutants or food constituents. Several large population-based studies indicate that exposure to fine or ultrafine particulate air pollution increases CVD morbidity and mortality, and the plausibility of this association is supported by data from animal studies. Exposure to other chemicals such as polyaromatic hydrocarbons, aldehydes, and metals has also been reported to elevate CVD risk by affecting atherogenesis, thrombosis, or blood pressure regulation. Maternal exposure to drugs, toxins, and infection has been linked with cardiac birth defects and premature CVD in later life. Collectively, the data support the notion that chronic environmental stress is an important determinant of CVD risk. Further work is required to assess the magnitude of this risk fully and to delineate specific mechanisms by which environmental toxins affect CVD.
O'Toole
Timothy E
TE
Institute of Molecular Cardiology, Division of Cardiovascular Medicine, Department of Medicine, University of Louisville, Louisville, KY 40202, United States of America.
Conklin
Daniel J
DJ
Bhatnagar
Aruni
A
D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000503:physiopathology; D050197:Atherosclerosis / Q000209:etiology / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000503:physiopathology*; D003329:Coronary Vasospasm / Q000209:etiology / Q000503:physiopathology; D004032:Diet; D004730:Endothelium, Vascular / Q000503:physiopathology; D004781:Environmental Exposure / Q000009:adverse effects*; D004785:Environmental Pollutants / Q000009:adverse effects*; D015438:Health Behavior; D006330:Heart Defects, Congenital / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology; D009930:Organic Chemicals / Q000009:adverse effects; D052638:Particulate Matter / Q000009:adverse effects; D012307:Risk Factors; D013927:Thrombosis / Q000209:etiology / Q000503:physiopathology; D014028:Tobacco Smoke Pollution / Q000009:adverse effects
D004785:Environmental Pollutants; D009930:Organic Chemicals; D052638:Particulate Matter; D014028:Tobacco Smoke Pollution