ABSTRACT
The objective of this study was to evaluate the association between in utero exposure to fluoride (F) and Mental and Psychomotor Development (MDI and PDI) evaluated through the Bayley Scale of Infant Development II (BSDI-II) in infants. The sample included 65 mother-infant pairs. Environmental exposure to F was quantified in tap and bottled water samples and F in maternal urine was the biological exposure indicator; samples were collected during the 1st, 2nd and 3rd trimester of pregnancy. The mean values of F in tap water for the 1st, 2nd and 3rd trimester were 2.6±1.1mg/l, 3.1±1.1mg/l and 3.7±1.0mg/l respectively; above to 80% of the samples exceeded the reference value of 1.5mg/l (NOM-127-SSA1-1994). Regarding F in maternal urine, mean values were 1.9±1.0mg/l, 2.0±1.1mg/l and 2.7±1.1mg/l for the 1st, 2nd and 3rd trimester respectively. The infants with MDI and PDI scores less than 85 points were 38.5% and 20.9% respectively. After adjusting for potential confounding factors (gestational age, age of child, marginalization index and type of water for consumption), the MDI showed an inverse association with F levels in maternal urine for the first (ß=-19.05, p=0.04) and second trimester (ß=-19.34, p=0.01). Our data suggests that cognitive alterations in children born from exposed mothers to F could start in early prenatal stages of life.
Subject(s)
Cariostatic Agents/adverse effects , Cognition Disorders/etiology , Developmental Disabilities/chemically induced , Fluorides/adverse effects , Maternal Exposure/adverse effects , Prenatal Exposure Delayed Effects/chemically induced , Adolescent , Adult , Female , Humans , Infant , Male , Mexico , Pregnancy , Prenatal Exposure Delayed Effects/physiopathology , Young AdultABSTRACT
We studied the effect of silymarin and dimercaptosuccinic acid (DMSA), a chelating agent that was administered individually or in combination against lead (Pb) toxicity in rats. Wistar rats (200 ± 20) were randomly divided into five groups. Group A served as a control. Groups B-E were exposed to 2000 ppm of lead acetate in drinking water for 8 weeks. Group B served as a positive control. Group C received silymarin (100 mg kg(-1) orally) for 8 weeks. Group D received DMSA (75 mg kg(-1) orally) once daily for the last 5 days of treatment. Group E received DMSA and silymarin as groups C and D, respectively. The effect of Pb was evaluated and accordingly the treatments on blood lead levels (BLLs), renal system, and genotoxic effects were calculated using comet assay. The BLLs were significantly increased following the exposition of lead acetate. The administration of silymarin and DMSA provided reduction in BLLs. Silymarin and DMSA provided significant protection on the genotoxic effect of Pb. The toxic effect of Pb on kidneys was also studied. Our data suggest that silymarin and DMSA improve the renal histopathological lesions.
