ObjectiveLow-level postnatal lead exposure is associated with poor intellectual development in children, although effects of prenatal exposure are less well studied. We hypothesized that prenatal lead exposure would have a more powerful and lasting impact on child development than postnatal exposure.DesignWe used generalized linear mixed models with random intercept and slope to analyze the pattern of lead effect of the cohort from pregnancy through 10 years of age on child IQ from 6 to 10 years. We statistically evaluated dose–response nonlinearity.ParticipantsA cohort of 175 children, 150 of whom had complete data for all included covariates, attended the National Institute of Perinatology in Mexico City from 1987 through 2002.Evaluations/MeasurementsWe used the Wechsler Intelligence Scale for Children–Revised, Spanish version, to measure IQ. Blood lead (BPb) was measured by a reference laboratory of the Centers for Disease Control and Prevention (CDC) quality assurance program for BPb.ResultsGeometric mean BPb during pregnancy was 8.0 μg/dL (range, 1–33 μg/dL), from 1 through 5 years was 9.8 μg/dL (2.8–36.4 μg/dL), and from 6 through 10 years was 6.2 μg/dL (2.2–18.6 μg/dL). IQ at 6–10 years decreased significantly only with increasing natural-log third-trimester BPb (β = −3.90; 95% confidence interval, −6.45 to −1.36), controlling for other BPb and covariates. The dose–response BPb–IQ function was log-linear, not linear–linear.ConclusionsLead exposure around 28 weeks gestation is a critical period for later child intellectual development, with lasting and possibly permanent effects. There was no evidence of a threshold; the strongest lead effects on IQ occurred within the first few micrograms of BPb.Relevance to Clinical PracticeCurrent CDC action limits for children applied to pregnant women permit most lead-associated child IQ decreases measured over the studied BPb range.

Objective: To evaluate the validity of a food-frequency questionnaire (FFQ) for assessment of the dietary intakes of polyunsaturated fatty acids (PUFAs) against a biochemical marker of fat intake, erythrocyte cell membrane phospholipid levels, during pregnancy. Design: Cross-sectional analysis. Setting: Developmental Neurobiology Department, National Institute of Perinatology, Mexico City. Subjects: One hundred forty-six healthy pregnant women during the last trimester of pregnancy. Among women enrolled, the first 35 pregnant women (24%) had their erythrocytes analysed for fatty acid status. Methods: We administered an FFQ and compared intakes of PUFAs against their erythrocyte cell membrane concentrations, processed by gas chromatography. Erythrocyte cell membrane ALN concentration (%/total) was only marginally related to ALN dietary intake (mg day 21 ) (b ¼ 0:52; 95% CI: -0.020 -1.10, P ¼ 0.061). However, after adjustment for long-chain n-3 PUFA/AA, this association reached significance (b ¼ 0:44; 95% CI: 0.026-0.825, P ¼ 0.038). Main dietary sources for n-3 PUFAs were canned tuna fish and fresh catfish; for n -6 these were eggs and cow's milk. The use of this FFQ in these pregnant Mexican women provided estimates of average long-term intakes of PUFAs and correlated reasonably well with their erythrocyte cell membrane phospholipid status. However, we need to consider that, during pregnancy, there is a faster turnover of PUFAs from fat storage that may modify the profile of erythrocyte PUFAs and lower the correlation between dietary intake and erythrocyte PUFAs.

We determined the secular trend in blood lead levels in a cohort of 321 children born in Mexico City between 1987 and 1992. Blood lead level was measured every 6 months during a 10-year period. We modeled the effect of yearly air lead concentration nested within the calendar year in which the child was born, family use of lead-glazed pottery, socioeconomic status, year in which the child was born, age of the child at the time of blood lead measurement, place of residence, and an indicator variable for subjects with complete or incomplete blood lead values. The yearly mean of air lead of the Valley of Mexico decreased from its highest level of 2.80 μg/m3 in 1987 to 0.07 μg/m3 in 2002. The contribution of air lead to blood lead according to year of birth was strongest for subjects born in 1987 and fell to nearly zero for children born in 1992. The geometric mean of the entire cohort rose from 8.4 μg/dL in the first year of life to 10.1 μg/dL in the second and decreased thereafter until it reached 6.4 μg/dL at 10 years of age. Children of families who used lead-glazed ceramics had blood lead levels 18.5% higher than did children of nonusing families. Children who belonged to the lowest socioeconomic levels had blood lead levels 32.2% higher than did those of highest socioeconomic levels. Children who lived in the northeast part of the city had blood lead levels 10.9% higher compared with those who lived in the southwest.

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Lead (Pb) is a developmental neurotoxicant found in industrial activities, many of them already prohibited worldwide. This study aimed to evaluate current blood Pb (PbB) levels in children in Cordoba, Argentina, and to compare these with similar studies performed before Pb was banned in gasoline in 1996. We also sought to identify mechanistically relevant biomarkers by measuring δ-aminolevulinic acid dehydratase (δ-ALAD), superoxide dismutase (SOD), and catalase (CAT) activities. We finally aimed to determine whether sociodemographic characteristics are associated with Pb toxicity. Blood samples collected from 161 healthy children between September 2009 and February 2010 revealed mean PbB levels of 2.58 ± 0.30 µg/dl. Enzymatic δ-ALAD, CAT, and SOD activities showed no significant variations when plotted against PbB levels. Finally, children living in the suburbs have higher PbB levels than their city counterparts, while low socioeconomic status increased δ-ALAD inhibition compared with that of middle-income children. Overall, these results evidenced a substantial reduction in exposure to Pb in this pediatric population over a decade after Pb was restricted in gasoline and reveal the importance of pursuing novel biomarkers of toxicity along with the sociodemographic profile to complement Pb diagnosis.