Contribución de la dieta a la exposición al plomo de niños de 1 a 7 años en La Plata, Buenos Aires / Contribution of diet to lead exposure among children aged 1 to 7 years in La Plata, Buenos Aires

Introducción. El plomo es un metal tóxico, que, aun en bajas concentraciones sanguíneas, es capaz de alterar el normal desarrollo neurológico de los niños, por lo que no existe un nivel aceptable de plombemia. La absorción de plomo de los alimentos es la mayor contribución a los niveles de plombemia de la población no expuesta laboralmente o a ambientes contaminados. El objetivo fue determinar la contribución dietaria a la exposición al plomo en niños de 1 a 7 años de edad que concurrían por controles de salud al Hospital de Niños de La Plata. Población y métodos. El estudio se realizó entre junio de 2015 y mayo de 2016. Se realizó un cuestionario de frecuencia de consumo de alimentos sobre 91 niños cuya edad promedio ± desvío estándar fue de 3,0 ± 1,7 años, sobre la cual se seleccionaron los alimentos por analizar. Se compraron los alimentos seleccionados en diversos comercios de la región. Se armaron muestras compuestas de diversos grupos de alimentos. Se determinó la concentración de plomo en los grupos de alimentos y, finalmente, se estimó la ingesta diaria de plomo de la población estudiada. Resultados. La ingesta diaria de plomo fue de 138 µg/día.Los grupos de alimentos que tuvieron mayor contribución fueron los productos cárnicos procesados (15,4%), los panificados (14,8%), la leche (12,5%) y la carne (11,7%). Conclusiones. Los niños de 1 a 7 años que concurren a un hospital público de La Plata tienen una carga de plomo en la dieta de 138 µg/día.

Introduction. Lead is a toxic metal which, even at low blood levels, can alter normal neurodevelopment in children, so no blood lead level is acceptable. Lead absorption from diet accounts for the highest contribution to blood lead levels in the population who is not exposed to contaminated environments or because of their occupation. The objective of this study was to determine the contribution of diet to lead exposure among children aged 1 to 7 years who attended Hospital de Niños de La Plata for health check-ups. Population and methods. The study was conducted between June 2015 and May 2016. A questionnaire on the frequency of food intake was administered to 91 children whose average age ± standard deviation was 3.0 ± 1.7 years, and foods included in the analysis were selected based on this questionnaire. Selected foods were purchased from different regional stores. Composite samples were made up of different food groups. Lead levels corresponding to each food group were determined and, finally, the daily intake of lead was estimated for the studied population. Results. The daily intake of lead was 138 µg/day. The food groups with the higher intake rates were processed meat products (15.4%), bakery products (14.8%), milk (12.5%), and meat (11.7%). Conclusions. Children aged 1 to 7 years attending a public hospital in La Plata have a lead burden from dietary intake of 138 µg/day.

Contribution of diet to lead exposure among children aged 1 to 7 years in La Plata, Buenos Aires. / Contribución de la dieta a la exposición al plomo de niños de 1 a 7 años en La Plata, Buenos Aires.

INTRODUCTION: Lead is a toxic metal which, even at low blood levels, can alter normal neurodevelopment in children, so no blood lead level is acceptable. Lead absorption from diet accounts for the highest contribution to blood lead levels in the population who is not exposed to contaminated environments or because of their occupation. The objective of this study was to determine the contribution of diet to lead exposure among children aged 1 to 7 years who attended Hospital de Niños de La Plata for health check-ups. POPULATION AND METHODS: The study was conducted between June 2015 and May 2016. A questionnaire on the frequency of food intake was administered to 91 children whose average age ± standard deviation was 3.0 ± 1.7 years, and foods included in the analysis were selected based on this questionnaire. Selected foods were purchased from different regional stores. Composite samples were made up of different food groups. Lead levels corresponding to each food group were determined and, finally, the daily intake of lead was estimated for the studied population. RESULTS: The daily intake of lead was 138 µg/day. The food groups with the higher intake rates were processed meat products (15.4%), bakery products (14.8%), milk (12.5%), and meat (11.7%). CONCLUSIONS: Children aged 1 to 7 years attending a public hospital in La Plata have a lead burden from dietary intake of 138 µg/day.

INTRODUCCIÓN: El plomo es un metal tóxico, que, aun en bajas concentraciones sanguíneas, es capaz de alterar el normal desarrollo neurológico de los niños, por lo que no existe un nivel aceptable de plombemia. La absorción de plomo de los alimentos es la mayor contribución a los niveles de plombemia de la población no expuesta laboralmente o a ambientes contaminados. El objetivo fue determinar la contribución dietaria a la exposición al plomo en niños de 1 a 7 años de edad que concurrían por controles de salud al Hospital de Niños de La Plata. POBLACIÓN Y MÉTODOS: El estudio se realizó entre junio de 2015 y mayo de 2016. Se realizó un cuestionario de frecuencia de consumo de alimentos sobre 91 niños cuya edad promedio ± desvío estándar fue de 3,0 ± 1,7 años, sobre la cual se seleccionaron los alimentos por analizar. Se compraron los alimentos seleccionados en diversos comercios de la región. Se armaron muestras compuestas de diversos grupos de alimentos. Se determinó la concentración de plomo en los grupos de alimentos y, finalmente, se estimó la ingesta diaria de plomo de la población estudiada. RESULTADOS: La ingesta diaria de plomo fue de 138 µg/día. Los grupos de alimentos que tuvieron mayor contribución fueron los productos cárnicos procesados (15,4%), los panificados (14,8%), la leche (12,5%) y la carne (11,7%). CONCLUSIONES: Los niños de 1 a 7 años que concurren a un hospital público de La Plata tienen una carga de plomo en la dieta de 138 µg/día.

Alteration and recovery of the antioxidant system induced by sub-chronic exposure to microcystin-LR in mice: its relation to liver lipid composition.

The effects of MC-LR on antioxidant system in liver and kidney and its effects on hepatic lipid composition after prolonged exposure to sublethal doses of microcystins (MCs) were studied in mice. Mice were treated i.p. with 25 microg of MC-LR/kg body weight or saline solution every 2 days for a month (inflictive stage), then progression or recovery was studied for 1 and 2 months of wash-out. During the inflictive stage, MC-LR-induced oxidative damage and significant changes in liver lipids of treated mice were compared with control mice. A clear dependence of the enzyme defense system was demonstrated with reduced glutathione and alpha-tocopherol availabilities and a concomitant elevation in NOx production. Sub-chronic MC-LR toxicosis produced alterations in lipid components that included a decreased EFA/non-EFA, SFA/PUFA, and n-3/n-6 ratios all of which exhibited a pattern of slow recovery during the recovery periods.

Hepatic recovery after damage produced by sub-chronic intoxication with the cyanotoxin microcystin LR.

The effect of sub-chronic exposure of intraperitoneal (i.p.) injections of microcystin-LR (MC-LR) on microscopic tissue architecture, hepatic function and lipid peroxidation has been studied in liver and kidney of mice. Mice were treated i.p. with 25 microg of pure MC-LR/kg body weight or saline solution for 1 month (every 2 days) with the aim of producing an inflictive stage with evident damage. Histopathological analysis of dissected livers of mice showed a disrupted lobar architecture and the development of cytoplasmatic vacuoles. According to this, a significant increase in hepatic lipid content and in lipid peroxidation levels in liver and kidney was found in MC-LR-treated animals when compared with controls. Moreover, serum alkaline phosphatase and aspartate aminotransferase activities showed a significant alteration in MC-LR-treated animals. After damage, progression or recovery was studied for 1 and 2 months of wash-out. The recovery from liver damage was evident at the cytological and physiological level, only the recovery of lobar architecture was incomplete along the period investigated. In conclusion, the present study demonstrates the ability of hepatic tissue to recover from damage produced by sub-chronic MC-LR administration. The dynamic interplay between damage and tissue-repairing response in determining the ultimate outcome of toxicity should be considered in risk-assessment studies.