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Plasma lipoprotein(a), Lp(a), is the most important known genetically controlled independent risk factor for the prediction of early atherosclerosis (AS) and coronary artery disease (CAD) in a significant subpopulation of Caucasians. A sensitive, specific 'capture' enzyme linked immunosorbent assay (ELISA) is reported for the assay of human plasma Lp(a). There is no interference from low density lipoprotein (LDL), plasminogen, or from endogenous lipids, hemoglobin, or bilirubin. An immobilized polyclonal rabbit antibody 'captures' the Lp(a) ligand, and then a monoclonal murine antibody 'recognizes' it. Alkaline phosphatase conjugated rabbit antimouse IgG and para-nitrophenyl phosphate substrate 'detect' and 'indicate' colorimetrically the amount of Lp(a) bound. Quantitation is relative to a commercially available secondary clinical standard. The frequency distribution for a predominantly Caucasian reference population is highly skewed toward the higher concentrations. The median plasma Lp(a) concentration for healthy Caucasians is 80 mg per 1. Relative risk for early myocardial infarction (MI) increases as plasma Lp(a) levels increase above 300 mg per 1. Approximately 20 percent of Caucasians have plasma Lp(a) values above 300 mg per 1. The frequency distributions of plasma Lp(a) in Blacks and Caucasian type II diabetics are different from the healthy Caucasian reference population. The percentiles of Lp(a) values greater than 300 mg per 1 in these latter groups is three times higher. Thorough epidemiologic and clinical studies where groups are segregated by race and ethnic origin are needed for accurate clinical interpretation of plasma Lp(a) results. Only neomycin and niacin are shown to lower plasma Lp(a) levels therapeutically, although anabolic steroid medication causes lower plasma Lp(a) concentrations. Endocrine malfunction also may influence plasma Lp(a) levels.