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Neurodevelopmental disorders are increasing globally, and metal exposure may play a significant role as an environmental factor. This cross-sectional study aimed to identify metal mixture patterns and assess their impact on children’s neurodevelopment. Data from 962 children (aged 4–5 years) participating in the Spanish INMA cohort study were analysed. Urinary metal concentrations (cobalt (Co), copper (Cu), molybdenum (Mo), selenium (Se), lead (Pb), zinc (Zn), and arsenic speciation) were used as exposure biomarkers. Principal component analysis (PCA) revealed four latent exposure variables representing uncorrelated metal mixture patterns. Linear regression analyses examined the associations between these variables and children’s neuropsychological functions assessed through the McCarthy Scales of Children’s Abilities. The first latent exposure variable (Cu, Se, Pb, Zn) and the second (inorganic arsenic, monomethylarsonic acid) showed negative associations with verbal executive function (ß=  − 1.88, 95% confidence interval (CI) =  − 3.17 to − 0.59) and gross motor function (ß=  − 1.41, 95% CI =  − 2.36 to − 0.46), respectively. Conversely, the third variable (Mo, Co) and the fourth (arsenobetaine) exhibited positive associations with visual and verbal span functions (ß= 1.14, 95% CI = 0.16 to 2.12) and fine motor function (ß= 1.01, 95% CI = 0.11 to 1.92), respectively. This study suggests that even relatively low levels of metal latent exposures, notably inorganic arsenic and a mixture of metals including Pb, adversely affect children’s neuropsychological development function scores, while exposure to arsenobetaine and a mixture of Co and Mo has a positive impact.

The gastrointestinal tract (GIT) microbiota has been identified as an important reservoir of antibiotic resistance genes (ARGs) that can be horizontally transferred to pathogenic species. Maternal GIT microbes can be transmitted to the offspring, and recent work indicates that such transfer starts before birth. We have used culture-independent genetic screenings to explore whether ARGs are already present in the meconium accumulated in the GIT during fetal life and in feces of 1-week-old infants. We have analyzed resistance to ß-lactam antibiotics (BLr) and tetracycline (Tcr), screening for a variety of genes conferring each. To evaluate whether ARGs could have been inherited by maternal transmission, we have screened perinatal fecal samples of the 1-week-old babies’ mothers, as well as a mother–infant series including meconium, fecal samples collected through the infant’s 1st year, maternal fecal samples and colostrum. Our results reveal a high prevalence of BLrand Tcrin both meconium and early fecal samples, implying that the GIT resistance reservoir starts to accumulate even before birth. We show that ARGs present in the mother may reach the meconium and colostrum and establish in the infant GIT, but also that some ARGs were likely acquired from other sources. Alarmingly, we identified in both meconium and 1-week-olds’ samples a particularly elevated prevalence of mecA(>45%), six-fold higher than that detected in the mothers. The mecA gene confers BLrto methicillin-resistant Staphylococcus aureus, and although its detection does not imply the presence of this pathogen, it does implicate the young infant’s GIT as a noteworthy reservoir of this gene.