There is an emerging hypothesis that exposure to cadmium (Cd), mercury (Hg), lead (Pb), and selenium (Se) in utero and early childhood could have long-term health consequences. However, there are sparse data on early life exposures to these elements in US populations, particularly in urban minority samples. This study measured levels of Cd, Hg, Pb, and Se in 50 paired maternal, umbilical cord, and postnatal blood samples from the Boston Birth Cohort (BBC). Maternal exposure to Cd, Hg, Pb, and Se was 100% detectable in red blood cells (RBCs), and there was a high degree of maternal–fetal transfer of Hg, Pb, and Se. In particular, we found that Hg levels in cord RBCs were 1.5 times higher than those found in the mothers. This study also investigated changes in concentrations of Cd, Hg, Pb, and Se during the first few years of life. We found decreased levels of Hg and Se but elevated Pb levels in early childhood. Finally, this study investigated the association between metal burden and preterm birth and low birthweight. We found significantly higher levels of Hg in maternal and cord plasma and RBCs in preterm or low birthweight births, compared with term or normal birthweight births. In conclusion, this study showed that maternal exposure to these elements was widespread in the BBC, and maternal–fetal transfer was a major source of early life exposure to Hg, Pb, and Se. Our results also suggest that RBCs are better than plasma at reflecting the trans-placental transfer of Hg, Pb, and Se from the mother to the fetus. Our study findings remain to be confirmed in larger studies, and the implications for early screening and interventions of preconception and pregnant mothers and newborns warrant further investigation.

Acetaminophen is the most commonly used medication for analgesic and antipyretic purposes among mothers during pregnancy and infants in early life.^1-8 More than 65% of women in the United States and 50% in Europe ever used acetaminophen during pregnancy.^7,9 Despite its widespread use, previous studies in animals and humans have found an association between prenatal acetaminophen exposure and increased risks of adverse childhood outcomes, including asthma,^10,11 cryptorchidism,¹² and neurodevelopmental disorders, including attention-deficit/hyperactivity disorder (ADHD)^12-20 and autism spectrum disorder (ASD).^17,21,22

In the last 25 years, the United States has experienced a dramatic increase in the already epidemic use of opioids, resulting in unprecedented levels of overdose, opioid use disorder, and other harms related to opioids.^1,2 Nationwide, the rate of opioid use disorder among women delivering newborns more than quadrupled between 1999 and 2014.³ Opioid drug use during pregnancy, whether heroin or prescription painkillers, harms the health of mother and child.^4-7 A major consequence is opioid-associated neonatal abstinence syndrome (NAS), defined by signs of withdrawal that infants develop after in utero exposure to opioids.⁸ Newborns with severe NAS require inpatient pharmacologic intervention, with a mean length of hospitalization of 16 days in the United States.^9-11

In the United States, preterm birth affects 1 in 9 live births and 1 in 5 live births among African Americans.¹ In contrast to the well-established association between term low birthweight and adult diseases, much less is known about the role of preterm birth in the later development of chronic diseases. Such information is needed in light of the persistently high rates of incidence of preterm birth and survival among those born preterm in the United States.² Available studies have linked preterm birth to insulin resistance^3-7 and type 2 diabetes in childhood,³ young adulthood,^4,5 and middle-adulthood.^6,8

In the United States, more than 50% of women of reproductive age are overweight or obese (OWO), with the prevalence at about 80% in non-Hispanic black women.¹ Maternal obesity has been linked to offspring obesity.^2,3 This transgenerational transmission may originate in utero⁴ and amplify the obesity epidemic in current and future generations.^5,6 However, questions remain regarding what early-life factors can enhance or mitigate the adverse effects of maternal obesity on child obesity and what underlying molecular mechanisms are involved.