Lead concentration in feces and urine of exposed rats by x-ray fluorescence and electrothermal atomic absorption spectrometry D. Guimarães, a * M. L. Carvalho, b M. Becker, c A. von Bohlen, c V. Geraldes, d I. Rocha d and J. P. Santos a Measurements made in feces and urine of Wistar rats exposed to lead acetate (n = 20) in drinking water since the fetal period were compared with those obtained from a control group (n = 20) in order to assess the age influence on Pb excretion. The measurements were made in different collections of rats aging between 1 and 11 months. To determine the Pb content of the samples, total reflection X-ray fluorescence (TXRF) and electrothermal atomic absorption spectrometry (ETAAS) were used for the urine samples and energy dispersive X-ray fluorescence (EDXRF) was used for the feces. The results show high concentrations of Pb being eliminated from the organism by urine and feces in contaminated rats. Values vary from (600  140) mgl 1 to (5 460  115) mgl 1 in urine and from (4 500  300) mgg 1 to (11 400  3 300) mgg 1 in dry feces. The control rats show, in general, low lead concentrations or below detection limits. The fecal/urinary ratio was studied. It was shown to be about three to four orders of magnitude and positively correlated with time. It was verified in feces and urine that excretion decreases with the animal age and that this decrease is made by different levels of excretion. The excretions of Pb in urine and in feces are positively correlated. A good agreement was found between the results obtained with TXRF and ETAAS for urine samples. This work also stresses the suitability of these techniques in the study of Pb intoxication. Copyright © 2011 John Wiley & Sons, Ltd. Introduction Lead poisoning is a particularly insidious public health threat. Because Pb is ubiquitous in the environment, this heavy element turns out to be an inevitable and undesired constituent of body tissues with no known physiological requirements in the organ- ism. [1] Mainly in the last three decades, the Pb poisoning has received significant attention. The Pb content of gasoline was reduced, use of lead solder in food-containing seals was removed, and household paints with high Pb concentrations were forbidden. Several efforts are still being made to eradicate the remaining sources of environmental Pb contamination. [2] One of the main lead intake routes is the ingestion, which is responsible for most of the children intoxications. Once ingested, the fraction of Pb that is retained by the body and available to interact with body metabolic processes varies considerably. Several factors may affect absorption, such as the chemical form of the compounds ingested, the pH of the stomach, the size of the contaminated particles, the age (children absorbs ~30–40% and adults ~8–10%; absorption rate is also higher in younger animals [3] ), and the simultaneous ingestion of nutrients that affect the solubilization and binding of Pb. [4,5] Absorbed Pb that is not stored in the tissues, namely in bone, is filtered and excreted through the main excretory routes: kidney to urine, and liver to bile and then to feces. Small amounts are also excreted through other minor routes of excretion, such as sweat, saliva, hair, nails, and breast milk. [6–8] The mechanisms for fecal excretion of absorbed Pb are still not clear. However, it is believed that pathways of excretion may include secretion into the bile and passing directly by blood to intestine walls. [9] Feces have normally the highest Pb concentra- tions, corresponding to the majority of the Pb that is not absorbed into the blood. The upper limit of Pb concentration considered acceptable in humans is about 50 mgg 1 in dry feces. [10] At low Pb level exposures, the excretion in feces is about half that in urine or less. [11] The Pb excretion in urine is mainly through glomerular filtra- tion. [12] Because of the easy sample collection, the absence of health risk and for being non-invasive, urine is one of the most con- venient samples for human biomonitoring and to assess Pb expo- sure. [13–16] However, these measurements do not reflect the body lead burden, in part because of the wide variation in renal excretion * Correspondence to: D. Guimarães, Centro de Física Atómica, CFA, Departa- mento de Física, Faculdade de Ciências e Tecnologia, FCT, Universidade Nova de Lisboa, 2829-516 Monte da Caparica, Portugal. E-mail: dianafcg@gmail.com a Centro de Física Atómica, CFA, Departamento de Física, Faculdade de Ciências e Tecnologia, FCT, Universidade Nova de Lisboa, 2829-516 Monte da Caparica, Portugal b Centro de Física Atómica, CFA, Departamento de Física, Faculdade de Ciências, Universidade de Lisboa, Av. Prof. Gama Pinto 21649-003, Lisboa, Portugal c Leibniz- Institut für Analytische Wissenschaften – ISAS – e.V., Bunsen-Kirchhoff- Str. 11, 44139, Dortmund, Germany d Instituto de Fisiologia, Faculdade de Medicina de Lisboa and Instituto de Medicina Molecular, Lisboa, Av. Prof. Egas Moniz, 1649-028 Lisboa, Portugal X-Ray Spectrom. 2012, 41, 80–86 Copyright © 2011 John Wiley & Sons, Ltd. Research article Received: 20 June 2011 Revised: 8 November 2011 Accepted: 23 November 2011 Published online in Wiley Online Library: 21 December 2011 (wileyonlinelibrary.com) DOI 10.1002/xrs.2361 80