Childhood aflatoxin exposure patterns in West Africa

Aflatoxin exposure has been difficult to characterize in the past, partly because the heterogeneous nature of contamination makes representative sampling of foodstuffs difficult (Whitaker, 2006). This inability to accurately measure individual exposure has in turn hampered efforts to understand the health effects of aflatoxins. Overcoming the difficulties inherent to these types of assessment has been the driving force for the development of afla-toxin exposure biomarkers (Groopman and Kensler, 1999; Wild and Turner, 2002). Anatoxins require bio-activation to a reactive aflatoxin 8,9-epoxide in order to exert their toxic effects and this metabolic activation is effected in humans by enzymes of the cytochrome P450 family, specifically CYP3A4, CYP3A5, CYP3A7 and CYP1A2 (Guengerich et al., 1998; IARC, 2002). Once activated to the epoxide, aflatoxin can bind to and damage cellular targets such as DNA and proteins. One consequence is that aflatoxin binds covalently to albumin and this aflatoxin-albumin (AF-alb) adduct can be measured in the peripheral blood as a useful biomarker of exposure over the 2-3 months prior to sampling (Wild and Turner, 2002). The ability to measure exposure using AF-alb has permitted a number of investigations of aflatoxin exposure and disease in the developing world. This chapter focuses on the consequences of aflatoxins for child health.

Aflatoxin exposure begins early in life in West Africa. The lipophilic nature of aflatoxins means that they can cross the placental barrier, and aflatoxin-albumin adducts have been reported in Gambian cord blood samples (Wild et al., 1991). This exposure continues in infancy. In The Gambia and Guinea, for example, children as young as three years of age have similar high prevalence (> 90%) and levels of adduct as observed in adults from the same populations (Allen et al, 1992; Wild et al, 1993, 2000; Diallo et al, 1995; Turner et al,

Table 1. Aflatoxin-albumin adducts in children by country.
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