Aflatoxin exposure and child nutrition: measuring anthropometric and long-bone growth over time in Nepal

Abstract

Background Naturally occurring aflatoxins may contribute to poor growth and nutritional statuses in children. Objectives We analyzed the relationship between contemporary and lagged aflatoxin exposure and 1) length-for-age z-score (LAZ); and 2) length, knee-heel length, stunting, weight-for-age z-score (WAZ), and weight-for-length z-score (WLZ). Methods We conducted a longitudinal birth cohort study involving 1675 mother-infant dyads in rural Nepal. Participants were repeatedly visited from pregnancy to 2 years of age (2015–2019). One blood sample was collected during pregnancy and 4 samples were collected from the children at 3, 6, 12, and 18–22 months of age to measure concentrations of aflatoxin B1 (AFB1)-lysine adduct. Multivariate linear fixed-effects and logistic models with generalized estimating equations were used to identify associations between child growth and aflatoxin exposure. Results AFB1-lysine adducts were detected in the majority of children (at 3 months, 80.5%; at 6 months, 75.3%; at 12 months, 81.1%; and at 18–22 months, 85.1%) and in 94.3% of pregnant women. Changes in contemporary ln child AFB1-lysine adduct concentrations were significantly associated with changes in LAZ (β, −0.05; 95% CI, −0.09 to −0.02; P = 0.003), length (β, −0.19; 95% CI, −0.29 to −0.10; P < 0.001), knee-heel length (β, −0.09; 95% CI, −0.13 to −0.05; P < 0.001), and WAZ (β, −0.04; 95% CI, −0.07 to −0.005; P = 0.022). Serum aflatoxin concentrations were associated with stunting (OR, 1.18; 95% CI, 1.05–1.32; P = 0.005). Similar results were found in the models using changes in contemporary ln AFB1 adjusted for changes in child weight, with significant associations with changes in WLZ (β, −0.07; 95% CI, −0.10 to −0.03; P < 0.001). Changes in time-lagged ln AFB1 (unadjusted and adjusted for changes in child weight) were associated with changes in length and knee-heel length. Conclusions Our results add to the growing body of evidence confirming chronic aflatoxin exposure and suggest that exposure is significantly correlated with various negative growth outcomes, which may vary by child weight status. This trial was registered at clinicaltrials.gov as NCT03312049.

Exposure to multiple mycotoxins, environmental enteric dysfunction and child growth: Results from the AflaCohort Study in Banke, Nepal

“…These findings add to the body of evidence hypothesising that aflatoxin can be a significant contributor to poor child growth. Our results support other studies that demonstrate a link between aflatoxin exposure and poor child growth in low-income countries (Andrews-Trevino et al, 2021;Y. Gong et al, 2002;Gong et al, 2004;Turner et al, 2007).…”

“…AflaCohort Study data (Andrews-Trevino et al, 2021). In this current study, we did not find any significant interaction effects with other mycotoxins or with EED, as noted by the lack of statistical significance of the interaction terms across all models.…”

Longitudinal Assessment of Prenatal, Perinatal, and Early-Life Aflatoxin B1 Exposure in 828 Mother–Child Dyads from Bangladesh and Malawi

“…We will discuss our data in the context of prior work by presenting estimated albumin-normalized values alongside our volume-normalized results, as well as with appropriate conversions to account for known quantitative biases of other AFB 1 -lysine analytical methods ( 49 ). Using these conversions, the level of exposure we observed in Bangladesh is very similar to those reported recently from Nepal by Andrews-Trevino et al ( 18 ), with medians of 1.20 pg/mg in maternal samples during pregnancy (equivalent to ∼0.053 pg/μL), 0.72 pg/mg in 3-mo-old children (0.032 pg/μL), and 1.11 pg/mg at 18–22 mo (0.049 pg/μL). Similarly, we report levels of exposure in Malawi mothers, which, after conversion, are similar to maternal concentrations in other African populations, such as Ghana (mean, 10.9 pg/mg; equivalent to 0.481 pg/μL) ( 50 ) and Uganda (median, 5.83 pg/mg; equivalent to 0.256 pg/μL) ( 51 ), while being higher than concentrations recently reported in pregnant Rwandan women (median, 1.7 pg/mg; equivalent to 0.071 pg/μL) ( 52 ).…”

“…In fact, most of the studies that have failed to find an association between aflatoxin exposure and child growth outcomes have had small sample sizes, have not adjusted for key variables such as seasonality or breastfeeding practices, or both ( 66 , 72–75 ). Moreover, while some have suggested that null results may have been the result of low aflatoxin exposures, perhaps below a critical threshold for biological effect ( 75 ), the recently published study in Nepalese subjects from Andrews-Trevino and colleagues ( 18 ) revealed highly significant reductions in postnatal LAZ, WAZ, WLZ, length, and knee-heel length in association with aflatoxin exposures that were lower than those in many of the prior studies that have reported no association. Notably, the AFB 1 -lysine concentrations that Andrews-Trevino et al reported in Nepal are similar to those we measured in Bangladeshi mothers and children.…”

“…Aflatoxin exposure and its effects on child growth have been reported extensively in west African populations, with most investigations in this region demonstrating that either maternal or child exposures are associated with reduced birth weight ( 50 ), WAZ ( 63 , 71 ), LAZ/HAZ ( 63 , 65 , 71 ), and/or WLZ ( 71 ). In contrast, studies exploring these questions in eastern Africa and southeast Asia have produced conflicting results both supporting ( 18 , 19 , 51 ) and not supporting ( 66 , 72–75 ) a role for aflatoxin in fetal growth restriction and childhood stunting. However, those studies that do not control for key determinants of aflatoxin exposure—such as seasonality and breastfeeding, as we show in the present report—may bias results towards the null ( 61 , 75 ), while other studies with similar sample sizes, populations, and exposures may reveal an effect of aflatoxin on growth parameters due to more complete statistical accounting of variance components ( 71 ).…”