L. Rello,a E. García-Ruiz,b M.A. Belarrab and M. Resanob*
aDepartment of Clinical Biochemistry, “Miguel Servet” Universitary Hospital, Paseo Isabel La Católica 1–3, 50009 Zaragoza, Spain
bDepartment of Analytical Chemistry, University of Zaragoza, Pedro Cerbuna 12, 50009 Zaragoza, Spain. E-mail: [email protected]
Introduction
Eliminating childhood lead poisoning: a worldwide concern
Lead exposure is an international issue. Pb may enter biological systems (as Pb2+) via food (e.g. food contaminated from cans containing Pb solders in the joints), water (e.g. use of lead pipes), air and soil (the combustions of leaded fuels have contributed to the accumulation of atmospheric and soil Pb). In the USA, the major source of ingestion in young children seems to be the dust and chips originating from old lead paint (used from 1884 to 1978).1 Foetuses and very young children (up to 36 months of age) are more sensitive than adults to relatively high blood lead levels because their brains and nervous systems are still developing and their blood-brain barrier is still incomplete. Childhood lead exposure has been correlated with school absenteeism, low class ranks, poorer vocabulary, longer reaction times and diminished hand-eye coordination, among other neurobehavioural disorders.
The level of public awareness on lead exposure in children may be summarised with the following recommendation for the US government included in the 2005 Policy Statement of the American Academy of Pediatrics (AAP): “Identify all children with excess lead exposure and prevent further exposure to them”. The threshold limit of lead poisoning in children has been established by the Centers for Disease Control and Prevention (CDCP) as 100 µg Pb L–1. In this context, the development of a fast, reliable and cost-efficient procedure for Pb control in those areas of risk can be considered of the upmost importance.
