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al., 2005b

nd: non-detected. aGeometric mean.

bData from an eight month longitudinal study with 200 children aged 1-3 years at recruitment, tested for AF-alb in ''February, June and 3October of 2001.

nd: non-detected. aGeometric mean.

bData from an eight month longitudinal study with 200 children aged 1-3 years at recruitment, tested for AF-alb in ''February, June and 3October of 2001.

2000, 2003, 2005a,b). These levels result from early weaning and introduction to family foods. The common family foods, e.g., maize, are contaminated with aflatoxins. Aflatoxin-albumin adducts can be detected in sera of Beninese children aged less than one year of age (Gong et al., 2003). Various studies of children from West Africa have found a uniformly high occurrence of exposure across countries and over time (Table 1). Comparisons across countries, however, should be interpreted cautiously because the data are drawn from different studies whose designs are not directly comparable. Nevertheless, the overall observations leave no doubt that children are chronically exposed to high levels of aflatoxins in this part of the world.

The pattern of aflatoxin exposure in early infancy is dynamic because the infant will initially consume exclusively breast milk and then be slowly introduced to weaning foods followed by family foods. The weaning food, typically a thin cereal gruel made from maize, sorghum or millet, is introduced early, sometimes by two months of age. The nature of the weaning food, the relative quantities compared to breast milk and the duration of weaning before the introduction of family foods will affect the amount of aflatoxin exposure during this potentially critical developmental period. Factors affecting the weaning process also vary and may depend on seasonal variation in availability of different foods, sibling number, local cultural practices, and maternal or infant health. Despite the variation in individual circumstances, the general pattern is that as weaning foods slowly replace breast milk the level of aflatoxin exposure increases markedly (Gong et al., 2002, 2003, 2004).

The period of breast-feeding is generally associated with lower levels of aflatoxin-albumin in a child's blood (Turner et al., 2007) because the mother's metabolism limits transfer of dietary aflatoxins into the milk. Little is known about how the components of breast milk might interfere with the absorption of aflatoxins from milk, a point worthy of additional research. However, there may be some toxic impact of aflatoxin metabolites even during this period of life, because the hydroxylated metabolite, aflatoxin M1, can be transferred to breast milk (IARC, 2002). This metabolite is less carcinogenic than the parent aflatoxin B1 found in food but may still possess cytotoxic activity.

Whilst aflatoxins have long been investigated in the etiology of HCC, there has been remarkably little attention paid to the other potential adverse effects on health despite the widespread exposure. Given the growing belief that early life exposures influence health and disease later in life (Barker, 2002), aflatoxin exposure in children should receive more attention. This point was highlighted by a recent World Health Organization/Center for Disease Control, USA report on aflatoxins (Strosnider et al., 2006).

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