Effects of early and recent mercury and lead exposure on the neurodevelopment of children with elevated mercury and/or developmental delays during lactation: A follow-up study.

This follow-up study of 82 children investigated the potential impact of early and recent exposure to mercury and lead on their neurodevelopmental performance at 5-8 years of age (2017-2018). Early exposure of these children to mercury, methylmercury, and lead was assessed during lactation at 3-12 months old, as well as their mother's exposure using measurements from a cross-sectional study (2011-2013). Only infants who failed to pass the neurodevelopment screening tools and/or had elevated mercury were included in this study. Urine and hair were sampled during the follow-up study to assess the children's recent exposure to mercury, methylmercury, and lead. Their cognitive performance and visual-motor integration were also measured using the Test of Non-Verbal Intelligence (TONI) and the Beery-Visual-Motor Integration (Beery VMI), respectively. The association between alterations in urinary porphyrins excretion and exposure to metals was analyzed and their influence on the children's neurodevelopment was explored. Linear regression models revealed a significant negative association between the infants' mercury exposure during lactation and the TONI Quotient (ß = -0.298, 95%CI = -4.677, -0.414) and Beery VMI Age Equivalent scores at age 5-8 (ß = -0.437, 95%CI = -6.383, -1.844). The mothers' blood methylmercury was inversely and significantly associated with their children's TONI Quotient (ß = -0.231, 95%CI = -8.184, -0.331). In contrast, the children's Beery VMI Age Equivalent scores were positively and significantly associated with the hair methylmercury of the mothers (ß = 0.214, 95%CI = 0.088, 3.899) and their infants (ß = 0.256, 95%CI = 0.396, 4.488). These relationships suggest the presence of negative confounding that we did not take into account. Unlike mercury, there was some evidence that lead in breast milk had an inverse relationship with the children's visual-motor coordination skills. Our study did not show a clear association between children's recent exposure to metals and neurodevelopment. However, a significant inverse association was observed between the TONI Quotient and the interaction of hair methylmercury × ∑porphyrins (ß = -0.224, 95%CI = -0.86, -0.049), implying that porphyrins are a sensitive measure of low body-mercury burden. Although lead induced higher ∑porphyrins excretion in urine (ß = 0.347, 95%CI = 0.107, 0.525), their interaction did not influence children's neurodevelopmental scores. The interactions between metals and porphyrins might provide insights into their potential contributory role in the pathogenesis associated with neurological disorders or other diseases. Despite the small sample size of the present study, its findings about the association between toxic metal exposure and the high risk of poor neurodevelopmental performance are worrying, particularly at an early age, and additional research is needed using larger sample sizes.

Prenatal and postnatal lead exposure and early cognitive development: longitudinal study in Saudi Arabia.

The goal of this study was to assess the effect of prenatal and postnatal lead exposure on early cognitive development of infants using the Bayley Scale of Infant Development (BSID-I) at the age of 6, 12, 18, and 24 months in a longitudinal study. Based on the results of 653 cord blood lead levels, infants were classified into three groups for neuropsychological assessments: low lead risk (<10th percentile) and high lead risk (>10th percentile) of the distribution of cord blood lead level were designated as low (< or = 1.045 microg/dL) and high (> or = 3.466 microg/dL) lead risk groups. Blood lead levels in between the <10th and >90th percentile were designated as mid lead risk group. A total of 66 infants were supposed to be selected from each group for a follow-up study. Of these, only 106 participated 6 months after the study. During the follow-up study, the dropout was very high with attrition rates of 74.5%, 52.8%, and 39.6% during the 12, 18, and 24 months. Mean blood lead levels increased from 3.36 to 4.45 microg/dL between the ages of 6 and 24 months, but the standardized Mental Development Index (MDI) and Psychomotor Development Index (PDI) decreased from 99.26 and 98.13 (6 months old) to 93.29 and 82.52, respectively (24 months old). Due to the high rate of attrition, most of the infants in the low group were lost. Therefore, we used the 75th percentile of blood lead levels as a cutoff in the statistical analyses. After adjustment for a large number of confounding variables, prenatal lead exposure was found to be significantly associated with the standardized MDI and PDI scores at the age of 6 months old with a P value of 0.02 for both. A borderline significant effect of prenatal lead exposure was also seen on standardized PDI scores at the age of 24 months (P = 0.09). On the other hand, no relationship was seen between postnatal blood lead levels and concurrent cognitive development scores. Such an observation is not conclusive because of low statistical power due to small sample size. Our results provide additional evidence for low prenatal lead exposure effects on cognitive development in Saudi infants living in a rural area.

Longitudinal study of prenatal and postnatal lead exposure and early cognitive development in Al-Kharj, Saudi Arabia: a preliminary results of cord blood lead levels.

Extensive data shows a direct link between low-level lead exposure during early development and deficits in neurobehavioral-cognitive performance evident late in childhood through adolescence. Our previous studies confirmed the transfer of lead from the mother to the fetus as well as the effect of low lead exposure on neuropsychological behavior in school children. Such results led us to design a longitudinal survey to evaluate the effect of prenatal and/or postnatal lead exposure on early cognitive development among selected group of children from birth to 2 years of age. During the first stage of this study (between March and July 2004), we measured lead levels in 653 umbilical cord blood samples taken from healthy Saudi mothers delivering at King Khalid Hospital, Al-Kharj. This gave a good opportunity to look at the prevalence of increased blood lead levels in umbilical cord blood and to identify risk factors for prenatal lead exposure. The mean cord lead levels were 2.21 +/- 1.691 microg/dl in the range of 0.284-17.276 microg/dl. Only 1.23% of the newborns had blood lead levels >10 microg/dl, the Center for Disease Control level of concern. To investigate risk factors affecting cord blood lead levels, only subjects with lead levels above the 75th percentile (2.475 microg/dl) were selected in the multiple regression models. We observed that cord blood lead levels were significantly influenced by maternal age, the location of residence and intake of prenatal supplements. Controlling for newborn's head circumferences confounders, it was found that cord blood lead levels were significantly and negatively associated with newborn's head circumference (beta = -0.158, p = 0.036). The negative association was seen between intake of prenatal supplements and cord blood lead levels emphasizing the role of prenatal supplementations during pregnancy. The significant reductions in newborns, head circumferences due to lead exposure may have serious implications for their future performance and achievement. This study reveals that even at low prenatal lead exposure, all possible measures to inspect lead sources in our environment and reduce lead exposure should be taken.