Exposure to environmental pollutants has been associated with cellular aging in children and adolescents. Individuals may vary, however, in their sensitivity or vulnerability to the effects of environmental pollutants. Larger hippocampal volume has emerged as a potential index of increased sensitivity to social contexts. In exploratory analyses (N = 214), we extend work in this area by providing evidence that larger hippocampal volume in early adolescence reflects increased sensitivity to the effect of neighborhood pollution burden on telomere length (standardized β = -0.40, 95% CI[-0.65, -0.15]). In contrast, smaller hippocampal volume appears to buffer this association (standardized β = 0.02). In youth with larger hippocampal volume, pollution burden was indirectly associated with shorter telomere length approximately 2 years later through shorter telomere length at baseline (indirect standardized β = -0.25, 95% CI[-0.40, 0.10]). For these youth, living in high or low pollution-burdened neighborhoods may predispose them to develop shorter or longer telomeres, respectively, later in adolescence.
Inuit communities in Northern Quebec (Canada) are exposed to environmental contaminants, particularly to mercury, lead and polychlorinated biphenyls (PCBs). Previous studies reported adverse associations between these neurotoxicants and memory performance. Here we aimed to determine the associations of pre- and postnatal exposures to mercury, lead and PCB-153 on spatial navigation memory in 212 Inuit adolescents (mean age = 18.5 years) using a computer task which requires learning the location of a hidden platform based on allocentric spatial representation. Contaminant concentrations were measured in cord blood at birth and blood samples at 11 years of age and at time of testing. Multivariate regression models showed that adolescent mercury and prenatal PCB-153 exposures were associated with poorer spatial learning, whereas current exposure to PCB-153 was associated with altered spatial memory retrieval at the probe test trial. These findings suggest that contaminants might be linked to different aspects of spatial navigation processing at different stages.
Iron is needed for normal development in adolescence. Exposure to individual environmental metals (e.g., lead) has been associated with altered iron status in adolescence, but little is known about the cumulative associations of multiple metals with Fe status. We used data from the 2017-2018 National Health and Nutrition Examination Survey (NHANES) to examine associations between a metal mixture (lead, manganese, cadmium, selenium) and iron status in 588 U.S. adolescents (12-17 years). We estimated cumulative and interactive associations of the metal mixture with five iron status metrics using Bayesian Kernel Machine Regression (BKMR). Higher concentrations of manganese and cadmium were associated with lower log-transformed ferritin concentrations. Interactions were observed between manganese, cadmium, and lead for ferritin and the transferrin receptor, where iron status tended to be worse at higher concentrations of all metals. These results may reflect competition between environmental metals and iron for cellular uptake. Mixed metal exposures may alter normal iron function, which has implications for adolescent development.
Introduction: Heavy metals such as Lead (Pb) and Mercury (Hg) can affect adipose tissue mass and function. Considering the high prevalence of exposure to heavy metals and obesity in Mexico, we aim to examine if exposure to Pb and Hg in adolescence can modify how fat is accumulated in early adulthood.
Methods: This study included 100 participants from the ELEMENT cohort in Mexico. Adolescent Pb and Hg blood levels were determined at 14-16 years. Age- and sex-specific adolescent BMI Z-scores were calculated. At early adulthood (21-22 years), fat accumulation measurements were performed (abdominal, subcutaneous, visceral, hepatic, and pancreatic fat). Linear regression models with an interaction between adolescent BMI Z-score and Pb or Hg levels were run for each adulthood fat accumulation outcome with normal BMI as reference.
Results: In adolescents with obesity compared to normal BMI, as Pb exposure increased, subcutaneous (p-interaction = 0.088) and visceral (p-interaction < 0.0001) fat accumulation increases. Meanwhile, Hg was associated with subcutaneous (p-interaction = 0.027) and abdominal (p-interaction = 0.022) fat deposition among adolescents with obesity.
Conclusions: Heavy metal exposure in adolescence may alter how fat is accumulated in later periods of life.
Children are exposed to many trace elements throughout their development. Given their ubiquity and potential to have effects on children's neurodevelopment, these exposures are a public health concern. This study sought to identify trace element mixture-associated deficits in learning behavior using operant testing in a prospective cohort. We included 322 participants aged 6-7 years recruited in Mexico City with complete data on prenatal trace elements measurements (third trimester blood lead and manganese levels, and & urine cadmium and arsenic levels), demographic covariates, and the Incremental Repeated Acquisition (IRA), an associative learning task. Weighted quantile sum (WQS) regression models were used to estimate the joint association of the mixture of all four trace elements and IRA performance. Performance was adversely impacted by the mixture, with different elements relating to different aspects of task performance suggesting that prenatal exposure to trace element mixtures yields a broad dysregulation of learning behavior.
The experience of poverty embodies complex, multidimensional stressors that may adversely affect physiological and psychological domains of functioning. Compounded by racial/ethnic discrimination, the financial aspect of family poverty typically coincides with additional social and physical environmental risks such as pollution exposure, housing burden, elevated neighborhood unemployment, and lower neighborhood education levels. In this study, we investigated the associations of multidimensional social disadvantage throughout adolescence with autonomic nervous system (ANS) functioning at 17 years. Two hundred and twenty nine low-income Mexican-American adolescents (48.6% female) and their parents were assessed annually between the ages of 10 and 16. Participants' census tracts were matched with corresponding annual administrative data of neighborhood housing burden, education, unemployment, drinking water quality, and fine particulate matter. We combined measures of adolescents' electrodermal response and respiratory sinuses arrhythmia at rest and during a social exclusion challenge (Cyberball) to use as ANS indices of sympathetic and parasympathetic activity, respectively. Controlling for family income-to-needs, youth exposed to greater cumulative water and air pollution from ages 10-16 displayed altered patterns of autonomic functioning at rest and during the social challenge. Conversely, youth living in areas with higher housing burden displayed healthy patterns of autonomic functioning. Altogether, results suggest that toxin exposure in youths' physical environments disrupts the ANS, representing a plausible mechanism by which pollutants and social disadvantage influence later physical and mental health.

