Evaluating the relationship between prenatal exposures and non-nutritive suck as an early indicator of neurodevelopment

• In Event: Effects of Environmental Exposures on Birth and Early developmental Outcomes

Abstract

Sensitive tests of early neurofunction are essential in infancy. However, there are few that can be administered in the first year of life, restricting researchers to standardized tests that frequently underestimate delays. Infant non-nutritive suck (NNS) - a suck pattern that occurs in the absence of nutrients, such as sucking on a pacifier - is the first oral motor skill infants develop and is considered an early measure of central nervous system function. Sucking behavior begins in utero at approximately 15 weeks’ gestation and is stable and well-patterned by 34 weeks’ gestation. Poor sucking has been linked to reduced scores on the Bayley Scales of Infant and Toddler Development at 2 years, and poor motor skills, language comprehension, and IQ scores at 5 years of age. Initial studies have shown that prenatal exposure to phthalates (a class of chemicals that are added to consumer products as plasticizers and solvents) is related to altered NNS patterning in infants, suggesting NNS could also be used as an indicator for fetal neurotoxicity. We are further investigating this connection using data from two U.S. birth cohorts. One cohort is predominantly composed of white, non-Hispanic individuals from high socioeconomic backgrounds (n=72). The second cohort is predominantly Hispanic individuals from low socioeconomic backgrounds (n=143). Thus far, we have examined the relationship between prenatal maternal stress and NNS across both cohorts in 209 mother-infant dyads. Prenatal stress was assessed in the third trimester in both cohorts using the 10-item Perceived Stress Scale. When infants were 1-12 weeks old, NNS was measured using our custom research pacifier which yields NNS duration (sec), amplitude (CmH20), frequency (Hz), suck burst, suck cycles, and cycles per burst. Multiple linear mixed models revealed higher prenatal maternal stress was associated with fewer but longer NNS bursts. To expand on this project, we recently examined prenatal phenol exposure (measured throughout pregnancy via maternal urine samples) and NNS data available in a combined sample of 212 and found that increased prenatal concentrations of 2,4-dichlorophenol and 2,5-dichlorophenol were independently associated with more NNS bursts with lower amplitude. Higher prenatal benzophenone-3 exposure was also associated with more bursts while higher propylparaben exposure was only associated with lower amplitude, similar to findings for higher prenatal exposure to di-2-ethylhexyl terephthalate. Greater bisphenol-F exposure was related to lower frequency, similar to what was observed with higher prenatal exposure to mono-2-ethylhexyl phthalate, the main metabolite of the antiandrogenic phthalate di-2-ethylhexyl phthalate. Higher triclosan exposure was related to higher frequency, and greater methylparaben exposure was associated with more cycles per burst. The mechanisms of these relationships are currently unknown, but prenatal phthalate, phenol, and stress exposures have all been linked to changes in anogenital distance measurements in infants, suggesting the changes we have observed could be related to in utero androgen levels. The investigation of this potential mechanism is currently underway. Together, these data indicate NNS is a useful tool for early detection of possible deficits in neurodevelopment due to prenatal exposures.

Authors

• Megan L Woodbury, Northeastern University
  Presenting Author

• Emily Zimmerman

• Andréa Aguiar

• Max T. Aung

• Sarah D. Geiger

• Deborah Watkins

• Shukhan Ng

• Gerdia Huerta-Montañez

• Jose Cordero

• John Meeker

• Susan Schantz

• Akram Alshawabkeh