The Effects of Prenatal and Postnatal Substance Exposure on C-Reactive Protein, Magnified by Behavioral Problems

• In Event: Developmental psychophysiology and developmental psychopathology: Temporal and contextual considerations

Abstract

Background. Exposure to tobacco and cannabis during developmental periods of enhanced vulnerability (e.g., in utero and early childhood) can have long-lasting effects on health. One potential mechanism underlying these associations is via alteration of inflammatory pathways. Using data from a longitudinal study of mother/infant dyads, we examined relations between prenatal and postnatal cannabis and tobacco exposure and inflammation in early childhood. Given previous research demonstrating associations between inflammation and attention-deficit/hyperactivity disorder (ADHD), the substance exposure-inflammation linkage was then investigated as a function of child ADHD symptoms.
Method. One hundred four mother/infant dyads (57% female children; 22% Caucasian) were recruited from a local hospital during their first prenatal appointment. Repeated assessments were conducted at 10 time points: at each trimester, at birth, and when children were 2, 9, 16, 24, 36, and 60 months old. Biomarker analysis of infant meconium (first neonatal feces) provided information about prenatal exposure to tobacco (n= 30), tobacco and cannabis (n = 19), or neither substance (n = 55). Postnatal exposure was assessed by maternal self-report via a Timeline Follow-Back Interview at each postnatal study visit. Prenatal and postnatal substance exposure indices were used to predict early childhood inflammation, as indexed by salivary c-reactive protein (CRP) levels measured at 60 months. Teacher reports of child ADHD symptoms, measured via Swanson, Nolan, and Pelham-IV (SNAP-IV) at the 60-month assessment, were examined as moderators of the relations between tobacco and cannabis exposure and child inflammation.
Results. Prenatal concurrent tobacco and cannabis exposure was associated with lower levels of CRP in early childhood, whereas postnatal cannabis exposure was associated with higher levels of CRP. Importantly, prenatal tobacco exposure alone did not predict CRP levels in early childhood, nor did postnatal tobacco exposure. Behavioral problems related to ADHD symptoms moderated the effect of postnatal cannabis exposure on CRP levels. Such that, children with higher ADHD symptoms showed stronger positive relations between postnatal cannabis exposure and CRP levels, adjusting for postnatal tobacco exposure and prenatal substance exposure. Of note, although postnatal tobacco and cannabis exposure were assessed as separate continuous predictors, most mothers who reported cannabis use also reported some level of tobacco use. All models included child BMI, sex, race, and maternal educational attainment as covariates.
Conclusion. This study expands upon the known relations between prenatal and postnatal substance exposure and immunological outcomes in early childhood, underscoring the importance of assessing cannabis use during gestation in combination with tobacco use. These findings suggest that the effect of postnatal cannabis exposure on elevated inflammation in early childhood is stronger among children with higher levels of behavioral problems related to ADHD symptoms.

Authors

• Shauna G Simon, University of California - Irvine
  Presenting Author

• Rina D. Eiden, The Pennsylvania State University
  Non-Presenting Author

• Danielle S Molnar, Brock University
  Non-Presenting Author

• Jenna L. Riis, Institute for Interdisciplinary Salivary Bioscience Research, University of California, Irvine
  Non-Presenting Author