Child Aflatoxin Exposure is Associated with Poor Child Growth Outcomes: A Prospective Cohort Study in Rural Malawi

Andrew Matchado; Joshua W Smith; Kerry J Schulze; John D Groopman; Emma Kortekangas; David Chaima; Charles D Arnold; Kenneth Maleta; Ulla Ashorn; Per Ashorn; Kathryn G Dewey; Christine P Stewart

doi:10.1016/j.cdnut.2023.101962

Child Aflatoxin Exposure is Associated with Poor Child Growth Outcomes: A Prospective Cohort Study in Rural Malawi

Curr Dev Nutr. 2023 Jun 10;7(7):101962. doi: 10.1016/j.cdnut.2023.101962. eCollection 2023 Jul.

Authors

Affiliations

¹ School of Global and Public Health, Kamuzu University of Health Sciences, Blantyre, Malawi.
² Department of Nutrition, Institute for Global Nutrition, University of California, Davis, CA, United States.
³ Department of Environmental Health and Engineering, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, United States.
⁴ Department of International Health, Center for Human Nutrition, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, United States.
⁵ Center for Child, Adolescent, and Maternal Health Research, Tampere University and Tampere University Hospital, Tampere, Finland.
⁶ Department of Paediatrics, Tampere University Hospital, Tampere, Finland.

Abstract

Background: Aflatoxin (AF) exposure is associated with child growth faltering in cross-sectional studies, with limited findings from longitudinal studies.

Objectives: To evaluate the relationship between maternal AF B₁-lysine adduct concentration, child AF B₁-lysine adduct concentration, and child growth in the first 30 mo of life.

Methods: AF B₁-lysine adduct was measured in mother-child dyad plasma samples using isotope dilution mass spectrometry. Using linear regression, we assessed the relationship between AF B₁-lysine adduct concentration and child weight, height, and head and mid-upper arm circumferences at 1 wk, 6, 12, 18, 24, and 30 mo of age.

Results: In adjusted models, maternal prenatal AF B₁-lysine adduct (pg/μL) was positively associated with newborn anthropometric outcomes; largest beta coefficients for associations between standardized values were for newborn weight-for-age z-score [β = 0.13; 95% confidence interval (CI): 0.02, 0.24; P < 0.05 and β = 0.11; 95% CI: 0.00, 0.22; P < 0.05 for second and third trimester AF, respectively]. Child AF B₁-lysine adduct (pg/μL) at 6 mo was negatively associated with head circumference-for-age z-score at 6, 18, 24, and 30 mo, with beta coefficients ranging from β = -0.15; 95% CI: -0.28, -0.02 to β = -0.17; 95% CI: -0.31, -0.03; P < 0.05); 18-mo AF was negatively associated with anthropometric outcomes at 18, 24, and 30 mo, most consistently with length-for-age z-score (β = -0.18; 95% CI: -0.32, -0.04, β = -0.21; 95% CI: -0.35, -0.07, β = -0.18; 95% CI: -0.32, -0.03 at 18, 24 and 30 mo, respectively).

Conclusions: Child AF exposure was associated with impaired child growth, but maternal AF exposure was not. Exposure during infancy was linked to persistent deficit in head circumference, implying reduced brain size lasting beyond the age of 2 years. Exposure at 18 mo was linked to persistent linear growth deficit. Further research should elucidate mechanisms through which AF affects child growth.

Keywords: AF B1-lysine adduct; Malawi; aflatoxin; anthropometric outcome; child growth.