Determining Fetal Manganese Exposure from Mantle Dentine of Deciduous Teeth

Studies addressing health effects of manganese (Mn) excess or deficiency during prenatal development are hampered by a lack of biomarkers that can reconstruct fetal exposure. We propose a method using the neonatal line, a histological feature in deciduous teeth, to identify regions of mantle dentine formed at different prenatal periods. Micromeasurements of Mn in these regions may be used to reconstruct exposure at specific times in fetal development. To test our hypothesis, we recruited pregnant women before 20 weeks gestation from a cohort of farmworkers exposed to Mn-containing pesticides. We collected house floor dust samples and mother’s blood during the second trimester; umbilical cord blood at birth; and shed deciduous incisors when the child was ∼7 years of age. Mn levels in mantle dentine formed during the second trimester (as ⁵⁵Mn:⁴³Ca area under curve) were significantly associated with floor dust Mn loading (<i>r</i>_spearman = 0.40; <i>p</i> = 0.0005; <i>n</i> = 72). Furthermore, ⁵⁵Mn:⁴³Ca in sampling points immediately adjacent the neonatal line were significantly associated to Mn concentrations in cord blood (<i>r</i>_spearman = 0.70; <i>p</i> = 0.003; <i>n</i> = 16). Our results support that Mn levels in mantle dentine are useful in discerning perinatal Mn exposure, offering a potentially important biomarker for the study of health effects due to environmental Mn exposure

Associations within adipokines in children over the birth - 9-year period (N = 80).

<p>Associations within adipokines in children over the birth - 9-year period (N = 80).</p

Demographic characteristics of mothers and children from the CHAMACOS Study, Salinas Valley, CA (N = 80).

<p>Demographic characteristics of mothers and children from the CHAMACOS Study, Salinas Valley, CA (N = 80).</p

Child adipokine levels and size by cluster.

<p>Child adipokine levels and size by cluster.</p

(A) Individual child adiponectin trajectories.

<p>Black rectangles indicate age at which adiponectin was measured. Orange, blue, and green trajectories comprise groups 1A, 2A, and 3A, respectively, as identified by vertically-shifted mixture modeling (VSMM). (B) VSMM-defined adiponectin trajectory groups. (C) Individual child leptin trajectories. Purple, orange, and dark blue trajectories comprise groups 1L, 2L, and 3L. (D) VSMM-defined leptin trajectory groups.</p

Relationship between adiponectin, leptin, and size (birth weight and BMI) in children from birth to 9 years of age (N = 80).

<p>Relationship between adiponectin, leptin, and size (birth weight and BMI) in children from birth to 9 years of age (N = 80).</p

Adiponectin and Leptin Trajectories in Mexican-American Children from Birth to 9 Years of Age

<div><p>Objectives</p><p>To address molecular mechanisms underlying obesity development, we examined patterns of critical metabolism-related hormones, adiponectin and leptin (adipokines), over childhood.</p><p>Subjects and Design</p><p>Plasma adiponectin and leptin were measured in 80 Mexican-American children at birth and again at 2, 5, and 9 years from the ongoing prospective cohort followed by the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS). We used a mixture modeling approach to identify patterns in adipokine trajectories from birth to 9 years.</p><p>Results</p><p>Leptin was positively related to child body size within all ages, however adiponectin had inverse and weaker associations with BMI at 2, 5, and 9 years. Correlations between adipokine levels over the 0–2, 2–5, and 5–9-year periods increased for both leptin (r = 0.06, 0.31 and 0.62) and adiponectin (r = 0.25, 0.41 and 0.46). Our mixture modeling approach identified three trajectory clusters for both leptin (1L [slowly-rising], 2L [rapidly-rising], and 3L [stable]) and adiponectin (1A [steep-dropping and rebounding], 2A [moderately-dropping], and 3A [stable]). While leptin groups were most separated over the 2–9-year period, adiponectin trajectories displayed greatest heterogeneity from birth to 2 years. Children in the rapidly-rising 2L group had highest BMI and waist circumference at 9 years. Further, children with greater birth weight had increased odds of belonging to this high risk group (OR = 1.21 95% CI 1.03, 1.43, compared to stable group 3L). Children whose mothers consumed more sugar-sweetened beverages during pregnancy were at risk of being in the steep-dropping 1A group (OR = 1.08, 95% CI 1.01, 1.17, compared to stable group 3A).</p><p>Conclusion</p><p>Our results highlight developmental differences in leptin and adiponectin over the childhood period. Leptin closely reflects child body size however factors affecting adiponectin and long-term consequences of its changes over infancy need to be further explored.</p></div