Introduction

Lead poisoning has been known since antiquity. Occupational exposure occurs in mines, smelters and foundries, storage battery production, and with heating or grinding of lead-painted metal, as well as in a variety of other settings. Children may be directly involved in such work, or indirectly exposed through any of their parents’ occupation. Emissions increased ten-fold in the 20th century, and substantial environmental exposure is common in hot-spots close to occupational sources. In addition there is wide-spread environmental exposure from leaded petrol and lead paint. Oral intake is the predominant exposure route in children.    After inhalation or ingestion, lead is quickly distributed to soft tissue and red blood cells. It is also incorporated in bone, and after some time, the skeleton harbours most of the body burden of lead. Blood lead (B-Pb) is the traditional biomonitoring medium, reflecting the adverse effects of lead. The half time for lead in blood and soft tissue is about one month. However, lead in bone, which has a half life of about a decade, also contributes to B-Pb.  The effects of lead on the central nervous system are the most important ones. But lead can also cause peripheral neuropathy, anemia, kidney disease, and increase the risk of hypertension. Several recent risk assessments concluded that effects of lead exposure can be demonstrated also at low-level exposure, which was previously considered "safe" and for some effects no threshold has been documented. Thus, the European Food Safety Authority recently lowered the recommended tolerable intake by more than a factor of five.   Although important preventive measures have been taken to decrease exposure to lead, the problem remains, and recent research has demonstrated dimensions previously not considered.