Lead is a common element in the earth's crust, serving useful purposes in industry, but serving no purpose in the human body. Increase in blood pressure is an important public health problem with numerous factors contributing to many facets of the disease. The relationship of lead exposure and increased blood pressure has long been considered, but only recently critically investigated. Reports of subtle changes in calcium metabolism and renal function, as well as in vitro studies examining end-arteriolar smooth muscle contractility, link lead exposure and increased blood pressure. This paper critically examines the evidence associating chronic low-level lead exposure and increased blood pressure. The review focuses on epidemiological, clinical, and toxicological data. The epidemiological evidence is consistent with low-level exposure to lead causing an elevation in blood pressure. The strength of that association, and the dose-response characteristics, are less certain. Individual resistance and susceptibility could affect the degree of blood pressure elevation. The results of animal and in vitro studies are consistent with the epidemiological evidence, and suggest biologically plausible mechanisms for the association. The most probable mechanisms are intracellular perturbations in calcium metabolism mediated by direct lead effects at the end-arteriole, and indirect effects via renal dysfunction. Better indices of lead exposure and lead activity are needed to quantify these effects in humans. New and safer methods of chelating lead suggest interesting approaches for studying the relationship between lead and hypertension. This link could have significant implications in determining what constitutes a 'safe' level of environmental lead exposure, and whether a proportion of essential hypertension could be 'cured' by chelation therapy.