Abstract
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.
Highlights
Exposure to lead (Pb) has been declared second on the list of 10 highest priority toxic substances to public health due to established multisystem toxicity and widespread exposure by the World Health Organization (WHO) and the Agency for Toxic Substances and Disease Registration (ATSDR) [1, 2].During pregnancy, Pb has potential impacts on fetal health due to its ability to cross the placental barrier [3]; endogenous Pb exposure increases due to bone resorption [4, 5]
Developmental windows, including in utero and early childhood, are key to study the effects of Pb exposure on organ growth and development, which may contribute to adverse health outcomes later in life [7]
The median blood lead level (BLL) were higher in the prenatal stages compared to those in the postnatal stages
Summary
Exposure to lead (Pb) has been declared second on the list of 10 highest priority toxic substances to public health due to established multisystem toxicity and widespread exposure by the World Health Organization (WHO) and the Agency for Toxic Substances and Disease Registration (ATSDR) [1, 2].During pregnancy, Pb has potential impacts on fetal health due to its ability to cross the placental barrier [3]; endogenous Pb exposure increases due to bone resorption [4, 5]. Developmental windows, including in utero and early childhood, are key to study the effects of Pb exposure on organ growth and development, which may contribute to adverse health outcomes later in life [7]. One of the mechanisms of Pb toxicity is the production of reactive oxygen species, resulting in various adverse health effects such as oxidative damage to DNA, proteins, and lipids and increased lipid peroxidation in the cell membrane [9, 10]. It might modify the permeability of blood vessels, leading to vascular damage, cardiac toxicity, cardiac dysfunction, and hypertension. Another mechanism of action is its role as an endocrine disruptor, functioning as endogenous hormones and mimicking endocrine effects [4, 11]. Longitudinal studies of Pb exposure in critical developmental windows in children are limited
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