In a recent study published in Environmental Research, researchers examined the effects of prenatal exposure to chemicals on early child language ability.
Language development is complex and influenced by genetics, prenatal factors, and socialization. The prenatal period is critical for brain development since chemicals can cross the placenta and affect fetal development. Although much research has been centered on the effect of chemicals on child neurodevelopment, there is little work specifically focused on their early language ability.
About the study
In the present study, researchers evaluated how prenatal exposure to chemicals impacts children's language ability. Participants were recruited in the Norwegian Mother, Father, and Child cohort study (MoBa). They were recruited during their first ultrasonography appointment at 17 weeks' gestation throughout the country from 1999 to 2008.
The study population for the present analysis was drawn from nested MoBa sub-studies, which focused on attention-deficit/hyperactivity disorder (ADHD). The authors leveraged 1) a preschool ADHD sample in which parents indicated ADHD-like symptoms of their children, which was later assessed onsite, 2) ADHD cases from the National Patient Registry (NPR), and 3) a random sample from MoBa regardless of ADHD-like symptoms.
Urine samples were obtained from mothers at around 17 weeks of gestation. Maternal urine levels of metabolites of 12 phthalates, six organophosphorus pesticides (OPs), and four organophosphate esters (OPEs) metabolites were measured. Parents specified the communication abilities of their children using the shortened version of the Ages and Stages questionnaire communication subscale on the 18-month MoBa questionnaire.
During the onsite ADHD assessment, parents/teachers reported on expressive language ability using the child development inventory (CDI) and the expressive language subscale. Principal component analyses (PCA) were performed for each chemical family (phthalates, OPEs, and OPs).
Structured equation modeling was applied to examine the effects of phthalates, OPEs, and OPs on child communication at 18 months and expressive language at preschool age. In addition, sensitivity analyses were performed to study associations between prenatal chemical exposure and child communication at 18 months.
Mothers in the preschool ADHD sample were aged 30 years on average, and most subjects completed college or higher education. The children were approximately three years old and born during 2004-07. Mothers in the preschool ADHD sample were more likely to be nulliparous. PCA revealed two underlying factors for phthalates and one each for OPs and OPEs.
The first phthalate factor had high loadings of mono-iso-butyl-phthalate (MiBP), mono-n-butyl phthalate (MnBP), and monobenzyl phthalate (MBzP), referred to as low molecular-weight phthalates (LMWPs). The second phthalate factor had high loadings of di-iso-nonyl phthalate (DiNP) and di(2-ethylhexyl) phthalate (DEHP), referred to as high molecular-weight phthalates (HMWPs).
The OP factor showed high loadings of diethyl phosphate (DEP) and dimethyl phosphate (DMP), while the OPE factor showed high loadings of di-n-butyl phosphate (DNBP) and diphenyl phosphate (DPHP). Metabolites within chemical families had greater correlations than between families. Prenatal exposure to OPs was associated with lower communication at 18 months.
18-month communication was positively associated with expressive language at preschool age. The authors observed a negative effect of OPs on parent-reported communication at 18 months. Prenatal exposure to higher LMWP levels was associated with lower expressive language at preschool age. Findings from sensitivity analyses were similar to those in the primary analysis.
In summary, the researchers assessed associations between prenatal exposure to three chemical families (phthalates, OPEs, and OPs) and early childhood language development. They found a negative association between prenatal OP exposure and preschool-age expressive language through communication deficits at 18 months.
Moreover, negative associations between LMWPs and preschool-age expressive language were also evident, independent of the effects on communication at 18 months. Prenatal OPE exposure was not associated with language ability at any age. Although participants were from the well-characterized MoBa cohort, the sample was disproportionately represented by older married females with fewer high-risk behaviors.
Notably, children with ADHD-like symptoms were oversampled, limiting the generalizability. Taken together, the findings revealed that prenatal OP or phthalate exposures were associated with language development deficits at 18 months and preschool age. Future research should differentiate between language production and comprehension and focus on broad language development constructs.