Mercury levels in pregnant women, children, and seafood from Mexico City.

BACKGROUND: Mercury is a global contaminant of concern though little is known about exposures in México. OBJECTIVES: To characterize mercury levels in pregnant women, children, and commonly consumed seafood samples. METHODS: Use resources of the Early Life Exposures in Mexico to Environmental Toxicants (ELEMENT) birth cohorts to measure total mercury levels in archived samples from 348 pregnant women (blood from three trimesters and cord blood), 825 offspring (blood, hair, and urine) and their mothers (hair), and 91 seafood and canned tuna samples from Mexico City. RESULTS: Maternal blood mercury levels correlated across three trimesters and averaged 3.4 µg/L. Cord blood mercury averaged 4.7 µg/L and correlated with maternal blood from trimester 3 (but not trimesters 1 and 2). In children, blood, hair and urine mercury levels correlated and averaged 1.8 µg/L, 0.6 µg/g, and 0.9 µg/L, respectively. Hair mercury was 0.5 µg/g in mothers and correlated with child's hair. Mean consumption of canned tuna, fresh fish, canned sardine, and shellfish was 3.1, 2.2, 0.5, and 1.0 times per month respectively in pregnant women. Mean mercury content in 7 of 23 seafood species and 5 of 9 canned tuna brands purchased exceeded the U.S. EPA guidance value of 0.3 µg/g. CONCLUSIONS: Mercury exposures in pregnant women and children from Mexico City, via biomarker studies, are generally 3-5 times greater than values reported in population surveys from the U.S., Canada, and elsewhere. In particular, mercury levels in 29-39% of the maternal participants exceeded the biomonitoring guideline associated with the U.S. EPA reference dose for mercury.

RETRACTED: Paraoxonase I polymorphisms and attention/hyperactivity in school-age children from Mexico City, Mexico.

Globally, organophosphate (OP) pesticide usage and exposure is widespread. Studies have found that fetuses and infants are more sensitive than adults to environmental toxicants and that prenatal exposure to low levels of OPs has been associated with Attention Deficit Hyperactivity Disorder-Like Phenotypes (ADHD-LP). Paraoxonase 1 (PON1) is an enzyme involved in detoxifying some OPs and its polymorphisms influence enzyme activity and quantity. The objective of this study was to examine whether maternal and/or child PON1 genotypes (PON1R192Q and PON1L55M) were associated with ADHD-LP in a Mexico City, Mexico birth cohort. PON1R192Q and PON1L55M genotypes in mothers (PON1R192Q: N=531; PON1L55M: N=458) and children (PON1R192Q: N=532; PON1L55M: N=478) from blood DNA were determined. We assessed ADHD-LP for children between the ages of 6 and 13 using Conners' Parent Rating Scales-Revised (CRS-R), Conners' Continuous Performance Test (CPT), and the parent scores for Behavior Assessment System for Children-2 (BASC2). Multivariable linear regression models were used to test relationships between ADHD-LP and PON1 polymorphisms. In these models, significant associations were observed with maternal genotypes but not with the child genotypes. A higher DSM IV Hyperactivity/Impulsivity score (ß=3.27 points; 95% CI (0.89, 5.65)) and a 2.17 higher score in child DSM IV Total (95% CI (0.05, 4.29)) were observed for maternal PON155MM in comparison to PON155LM+LL. The childattention problems score was 2.27 points higher (95% CI (0.002, 4.53) for maternal PON1192QQ in comparison to PON1192QR+RR. Because maternal PON1 polymorphisms were associated with child ADHD-LP, this may be a viable biomarker of susceptibility for ADHD-LP.

Prenatal and Early Childhood Exposure to Lead and Repeated Measures of Metabolic Syndrome Risk Indicators From Childhood to Preadolescence.

Background: Exposure to lead (Pb) during the early life stages has been associated with the development of metabolic syndrome (MetS). Longitudinal studies of Pb exposure in critical developmental windows in children are limited. Methods: Our study included 601 mother-child dyads from the PROGRESS (Programming Research in Obesity, Growth, Environment and Social Stressors) birth cohort. Blood lead levels (BLLs) were assessed during the second and third gestational trimesters, in cord blood at delivery, and at ages 1, 2, and 4 years. Bone lead levels in the patella and tibia were assessed at 1 month postpartum and evaluated in separate models. To account for cumulative exposure (prenatal, postnatal, and cumulative), we dichotomized the BLLs at each stage visit and determined the following: "higher" if a BLL was at least once above the median (HPb) and "lower" if all BLLs were below the median (LPb). We analyzed fasting glucose, HbA1c, triglycerides (TGs), total cholesterol (TC), high-density lipoprotein cholesterol (cHDL), low-density lipoprotein cholesterol (cLDL), body mass index, waist circumference (WC), body fat percentage, and systolic (SBP) and diastolic blood pressure (DBP) at two study visits between 6 and 12 years of age and created cutoff points based on the clinical guidelines for each indicator. Mixed effects models were used to analyze each outcome longitudinally for each BLL score, adjusting for child's sex, size for gestational age, child's age, maternal parity, mother's age, and socioeconomic status. Results: We observed associations for HPb exposure and TC in all stages (OR = 0.53, 95%CI = 0.32-0.86) and postnatally (OR = 0.59, 95%CI = 0.36-0.94) and for prenatal HPb and TGs (OR = 0.65, 95%CI = 0.44-0.95). HPb at all stages was associated with WC (OR = 0.27, 95%CI = 0.08-0.86), BMI (OR = 0.33, 95%CI = 0.11-0.99), SBP (OR = 0.53, 95%CI = 0.32-0.85), and DBP (OR = 0.57, 95%CI = 0.34-0.95). Pb levels in the patella were associated with cHDL (OR = 1.03, 95%CI = 1.00-1.07) and those in the tibia with TGs (OR = 0.95, 95%CI = 0.91-0.99). Conclusion: Early life exposure to Pb may alter early indicators of MetS. A follow-up of these children will allow for more definition on the impact of longer-term exposures.