Prenatal Alcohol And/or Tobacco Exposure, White-Matter Microstructure, and Cognition: Analyzing a South African Birth Cohort with Neurite Orientation and Dendrite Dispersion Imaging.

BACKGROUND:Prenatal exposure to alcohol (PAE) and/or tobacco (PTE) may impact neurobiological and cognitive development years after such exposures have occurred. While such effects on cortical gray matter and cognition are widely researched, there is less research on the effects of PAE and PTE on white-matter development and cognition, particularly in non-clinical, community samples. METHODS:We analyzed white-matter microstructure and its cognitive correlates in four hundred and sixty five 8-12-year-olds in the urban Cape Town region of South Africa: 192 were prenatally exposed to alcohol and tobacco (PAE + PTE), 73 to tobacco only (PTE), 102 to alcohol only (PAE), and 98 to neither tobacco nor alcohol (CON). White-matter microstructure was quantified via neurite orientation and dendrite dispersion imaging (NODDI). The outcome variables were fractional anisotropy (FA), the neurite density index (NDI), and neurite orientation dispersion index (ODI) for 52 white-matter tracts. Cognition was measured using the Wechsler Intelligence Scale for Children-Fifth Edition (WISC-V). RESULTS:PAE (but not PTE) was associated with NDI in 35 of 52 white-matter tracts analyzed. There were no false-discovery-rate (FDR) corrected main effects of PAE or PTE on FA or ODI. For 17 of the 35 tracts affected by PAE, the corresponding NDIs were positively associated with scores on the WISC-V Processing Speed Index. CONCLUSIONS:Our previous research of neuroanatomical structure in this cohort suggested that there are stronger effects of PTE on cortical gray matter. In contrast, the present data suggest that PAE may have stronger associations with white-matter microstructure, with such effects potentially manifesting as downstream deficits in processing speed.