Background: Aflatoxin, a potent fungal toxin, contaminates 25% of crops worldwide. Since 2004, 477 aflatoxin poisonings associated with eating contaminated maize have been documented in Eastern Kenya, with a case-fatality rate of 40%.Objective: We characterized maize aflatoxin contamination during the high-risk season (April–June) after the major harvests in 2005, 2006 (aflatoxicosis outbreak years), and 2007 (a non-outbreak year).Methods: Households were randomly selected each year from the region in Kenya where outbreaks have consistently occurred. At each household, we obtained at least one maize sample (n = 716) for aflatoxin analysis using immunoaffinity methods and administered a questionnaire to determine the source (i.e., homegrown, purchased, or relief) and amount of maize in the household.Results: During the years of outbreaks in 2005 and 2006, 41% and 51% of maize samples, respectively, had aflatoxin levels above the Kenyan regulatory limit of 20 ppb in grains that were for human consumption. In 2007 (non-outbreak year), 16% of samples were above the 20-ppb limit. In addition, geometric mean (GM) aflatoxin levels were significantly higher in 2005 (GM = 12.92, maximum = 48,000 ppb) and 2006 (GM = 26.03, maximum = 24,400 ppb) compared with 2007 (GM = 1.95, maximum = 2,500 ppb) (p-value < 0.001). In all 3 years combined, maize aflatoxin levels were significantly higher in homegrown maize (GM = 17.96) when compared with purchased maize (GM = 3.64) or relief maize (GM = 0.73) (p-value < 0.0001).Conclusions: Aflatoxin contamination is extreme within this region, and homegrown maize is the primary source of contamination. Prevention measures should focus on reducing homegrown maize contamination at the household level to avert future outbreaks.
Aflatoxins contaminate approximately 25% of agricultural products worldwide. They can cause liver failure and liver cancer. Kenya has experienced multiple aflatoxicosis outbreaks in recent years, often resulting in fatalities. However, the full extent of aflatoxin exposure in Kenya has been unknown. Our objective was to quantify aflatoxin exposure across Kenya. We analysed aflatoxin levels in serum specimens from the 2007 Kenya AIDS Indicator Survey – a nationally representative, cross-sectional serosurvey. KAIS collected 15,853 blood specimens. Of the 3180 human immunodeficiency virus-negative specimens with ≥1 mL sera, we randomly selected 600 specimens stratified by province and sex. We analysed serum specimens for aflatoxin albumin adducts by using isotope dilution MS/MS to quantify aflatoxin B1-lysine, and normalised with serum albumin. Aflatoxin concentrations were then compared by demographic, socioeconomic and geographic characteristics. We detected serum aflatoxin B1-lysine in 78% of serum specimens (range =
Acute aflatoxin exposure can cause death and disease (aflatoxicosis) in humans. Aflatoxicosis fatality rates have been documented to be as high as 40% in Kenya. The inclusion in the diet of calcium silicate 100 (ACCS100), a calcium montmorillonite clay, may reduce aflatoxin bioavailability, thus potentially decreasing the risk of aflatoxicosis. We investigated the efficacy, acceptability and palatability of ACCS100 in a population in Kenya with recurring aflatoxicosis outbreaks. Healthy adult participants were enrolled in this double-blinded, crossover clinical trial in 2014. Following informed consent, participants (n = 50) were randomised to receive either ACCS100 (3 g day−1) or placebo (3 g day−1) for 7 days. Treatments were switched following a 5-day washout period. Urine samples were collected daily and assessed for urinary aflatoxin M1 (AFM1). Blood samples were collected at the beginning and end of the trial and assessed for aflatoxin B1-lysine adducts from serum albumin (AFB1-lys). AFM1 concentrations in urine were significantly reduced while taking ACCS100 compared with calcium carbonate placebo (β = 0.49, 95% confidence limit = 0.32–0.75). The 20-day interval included both the placebo and ACCS100 treatments as well as a washout period. There were no statistically significant differences in reported taste, aftertaste, appearance, colour or texture by treatment. There were no statistically significant differences in self-reported adverse events by treatment. Most participants would be willing to take ACCS100 (98%) and give it to their children (98%). ACCS100 was effective, acceptable and palatable. More work is needed to test ACCS100 among vulnerable populations and to determine if it remains effective at the levels of aflatoxin exposure that induce aflatoxicosis.
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