Case Control Study

The objective of the case control study was to identify the risk factors for developing acute aflatoxicosis, and to quantify aflatoxin exposure in the affected population by measuring the aflatoxin level in maize and the level of aflatoxin adducts in serum. Little is known about risk factors associated with outbreaks of aflatoxicosis in this region of Africa or what protective factors may prevent exposure and/or mitigate disease. In addition, few studies have measured aflatoxin levels in biological samples from clinical cases, because unbound aflatoxin remains in circulation for only 13-90 minutes following exposure (Krishnamacha-ri et al, 1975). Between 1% and 4% of the ingested aflatoxin, however, binds irreversibly with proteins, primarily albumin, to form adducts.


• In February 2004, the onset of rains in the affected areas was earlier than expected, which forced the farmers to harvest and store maize grain with a high moisture content. Due to the severe shortage of maize, the grain was not stored in a granary (to prevent theft), but instead was stored on the floor of the huts where the families live. The roofs of the huts are thatched with grass. During the rains, some roofs leak which increases the moisture content of the grain on the floor even further. If the moisture content of the grain is > 12%, then the conditions are conducive for growth of the mold that produces aflatoxin.

• The early rains in 2004 were followed by hot humid conditions in March and subsequent months. These conditions formed an ideal environment for the growth of the aflatoxin-producing fungi and the subsequent contamination of the grain with aflatoxins.

• The consumption of contaminated maize was the primary risk for developing aflatox-icosis. Maize taken from households where affected individuals lived had higher afla-toxin contamination levels than did maize obtained from other households where no one was affected by aflatoxicosis.

• Food collected from households in the affected areas contained high levels of aflatoxins, suggesting that the aflatoxicosis outbreak was caused by aflatoxin poisoning.

• Affected individuals had higher serum levels of the aflatoxin Bj-lysine adducts than did unaffected control individuals (1.2 ng/ml vs. 0.15 ng/ml). Individuals who died of aflatox-icosis had higher aflatoxin B1-lysine adduct levels than did individuals who survived (3.2 ng/mg vs. 0.5 ng/mg) although this difference was not statistically significant (Azziz-Baumgartner et al, 2005). These levels of aflatoxin adducts are the highest ever reported.

• Levels of aflatoxin B1-albumin adducts in apparently unaffected individuals were consistent with levels previously documented in studies that measured the level of aflatox-in B1-albumin adducts in African populations with a high incidence of liver cancer (Peers and Linsell, 1973).

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