Lead (Pb) induces arterial hypertension in consequence of low exposures, which is not manifested by Pb toxic eff ects on the marrow, kidneys or other organs. Pb hypertensive effect, in the range of blood concentration from 10 to 40 μg/dl, has been evidenced by numerous experimental and population studies. However, the presence of signifi cant correlation between blood lead level and systolic and/or diastolic blood pressure is not confi rmed by some epidemiological studies. These discrepancies can be explained by the observation, that Pb-induced hypertension results rather from past than from current exposure, hence the arterial pressure values should be rather related to bone than to blood lead level. The occurrence of polymorphism of genes involved in Pb toxic effect may be another explanation. The interaction between Pb toxicity and ALAD gene polymorphisms on hematopoesis is observed in workers occupationally exposed to lead. These polymorphisms, occurring in a single form or in connection with other polymorphisms, seem to be implicated in Pb-induced hypertension, e.g., vitamin D receptor gene. The results of experimental studies show that the correlation between Pb exposure, arterial blood pressure and the presence of polymorphisms of angiotensin converting enzyme and beta(2)adrenergic receptor genes should be analysed in populations. It is likely that studies of other genes polymorphisms, genegene interactions and the interaction between genes and - environmental factors lead to the identifi cation of causes of so called spontaneous hypertension. Med Pr 2008;59(4):325-332