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Epidemiological evidence suggests a possible association between chronic exposures to toxigenic molds …

Biology Articles » Toxicology » High Cholesterol Levels And Chronic Exposure To Toxigenic Molds In Damp Buildings: A High Risk For Cardiovascular Diseases And Stroke » Introduction

- High Cholesterol Levels And Chronic Exposure To Toxigenic Molds In Damp Buildings: A High Risk For Cardiovascular Diseases And Stroke

Human exposure to toxigenic molds in damp buildings is a primary environmental health problem associated with adverse health effects, 1and which costs millions of dollars to insurance companies, homeowners, and schools. There is increasing concern that, a significant number of individuals exposed to chronic mold in water-damaged buildings may be at high risk of cholesterol abnormalities. 2, 3, 4Cholesterol is an important biomolecular constituent of the cell membrane structure. It serves as a precursor for the synthesis of steroid hormones and bile acids. Both dietary cholesterol and that synthesized de novo are transported through the circulation in lipoprotein particles. 3, 4The same is true of cholesteryl esters, the form in which cholesterol is stored in the cells. Cholesterol balance is essential to life yet its deposition in arteries has been associated with cardiovascular disease and stroke. 4Of particular clinical importance is the abnormal deposition of cholesterol and cholesterol-rich lipoproteins in the coronary arteries. Such deposits eventually lead to arteriosclerosis, a contributory factor in diseases of the coronary arteries. Arteriosclerosis is the hardening of the arteries and it is the cause of more than half of all mortality in developed countries and the leading cause of death in the US. 1, 2, 3, 4More than 90 million American adults, or about 50 percent, have elevated blood cholesterol levels, one of the key risk factors for heart disease, according to the National Heart, Lung, and Blood Institute's National Cholesterol Education Program. 4When it affects the coronary arteries, it is the underlying cause of most heart attacks and a common cause of cognitive heart failure and arrhythmias. 1, 2, 3

The pathological process of arterioscleroses begins very early with a fatty streak composed of lipid deposited in the intimae of arteries. Modified macrophages known as foam cells accumulate in the plaque region. These foam cells accumulate lipids, especially oxidized low-density lipoproteins. When the lesion becomes infiltrated with fibrous material it protrudes into the lumen of the artery. The lesion itself rarely occludes the artery but rather it is blood clots that form on top of the plaque that close off the channel. Chronic lesions become calcified and the elasticity of the vessel is decreased. This hardening of the arteries causes an increase in resistance to blood flow and therefore an increase in blood pressure. 1, 2, 3, 4Any vessel in the body may theoretically be affected by arteriosclerosis, but the aorta, coronary, carotid, and iliac arteries are most frequently affected. Arterioscleroses is a common cause of aortic aneurysms (a local abnormal dilation of an artery due to a congenital defect or weakness of the vessel wall) while those in the periphery are usually caused by damage due to trauma or bacterial or fungal infection. 1, 2, 3, 4

In recent years, these harmful roles of cholesterol in the body have been widely publicized because of the increase in the occurrence of cardiovascular diseases and stroke. Research evidence suggests that high levels of cholesterol are the main culprit 1, 2, 3, 4. Although, the physiological status of cholesterol in animals exposed to toxigenic molds have been reported, there is insufficient concrete evidence to support similar toxigenic mold-related occurrences in humans. The purpose of this review is to synthesize that could form the basis for discussions in the light of on-going research on the topic. The effects of chronic toxigenic mold exposures on individuals in damp buildings are reviewed to set the stage for better evaluation and assessment of their associations with the observed cholesterol abnormalities. The structure, and the regulatory mechanisms of cholesterol biosynthesis are assessed to identify the important enzymatic stages and the rate limiting steps that might be amenable to a possible influence of the mycotoxins consequent upon which abnormalities are enhanced. Invariably, the likely effects of mycotoxins on the stages of cholesterol metabolism, steady state of cellular supply, utilization, bile acids synthesis, and the associated cardiovascular diseases are evaluated.

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