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Title: Human health implications from co-exposure to aflatoxins and fumonisins in maize-based foods in Latin America: Guatemala as a case study

Author
item TORRES, OLGA - National Institute Of Public Health (INSP)
item MATUTE, JORGE - National Institute Of Public Health (INSP)
item GELINEAU-VAN WAES, JANEE - Creighton University
item MADDOX, JOYCE - Creighton University
item GREGORY, SIMON - Duke University Medical Center
item ASHLEY-KOCH, ALLISON - Duke University Medical Center
item Showker, Adele
item Voss, Kenneth
item Riley, Ronald

Submitted to: World Mycotoxin Journal
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/3/2014
Publication Date: 1/22/2015
Citation: Torres, O., Matute, J., Gelineau-Van Waes, J., Maddox, J.R., Gregory, S.G., Ashley-Koch, A.E., Showker, A.J., Voss, K.A., Riley, R.T. 2015. Human health implications from co-exposure to aflatoxins and fumonisins in maize-based foods in Latin America: Guatemala as a case study. World Mycotoxin Journal. 8(2):143-159.

Interpretive Summary: Fumonisin B1 (FB1) and aflatoxin B1 (AFB1) are toxic chemicals produced by molds. The molds that produce these two toxic chemicals are commonly found in corn and their co-occurence in corn has been demonstrated in many surveys. Combined-exposure to FB1 and AFB1 was of concern to the Joint FAO/WHO Expert Committee on Food Additives because of the known ability of AFB1 to damage genes in humans. FB1 was also of concern because of its ability to induce cells to divide after causing liver damage in animals. Humans living where corn is a dietary staple are at high risk for dietary exposure to both of these toxic chemicals. Our work has focused on Guatemala, a country in Central America where corn is consumed in large amounts every day and where intake of FB1 has been shown to be potentially quite high. In 2012 a survey was conducted which analyzed corn samples for FB1 and AFB1 from all 22 departments of Guatemala. The results show that the levels of AFB1 exposure are also potentially quite high in Guatemala, and likely throughout Central America and Mexico. The implications of co-exposure for human health are numerous, but one area of particular concern is the potential of FB1 to modulate AFB1 liver toxicity and increase the risk of liver cancer. The toxicity and carcinogenicity of FB1 in animal models is consistent with this concern. In farm and laboratory animals FB1 inhibits key enzymes in the biosynthesis of fats. The inhibition of the biosynthesis of these fats that are involved in controlling the death and survival of cells in livers of individuals exposed to AFB1 could contribute to the ability of AFB1 to cause liver cancer in humans. Studies investigating the health effects of either toxin should consider the potential for co-exposure to both toxins. Also, in countries where corn-based foods are prepared by alkaline treatment of the corn kernels, the effect of traditional processing on AFB1 levels and toxicity needs to be determined, especially for corn highly contaminated with AFB1.

Technical Abstract: Co-occurence of fumonisin B1 (FB1) and aflatoxin B1 (AFB1) in maize has been demonstrated in many surveys. Combined-exposure to FB1 and AFB1 was of concern to the Joint FAO/WHO Expert Committee on Food Additives because of the known genotoxicity of AFB1 and the ability of FB1 to induce regenerative proliferation in target tissues. Humans living where maize is a dietary staple are at high risk for exposure to both mycotoxins. Our work has focused on Guatemala, a country in Central America where maize is consumed in large amounts every day and where intake of FB1 has been shown to be potentially quite high using biomarker-based studies. In 2012 a survey was conducted which analyzed maize samples for FB1 and AFB1 from all 22 departments of Guatemala. The results show that the levels of AFB1 exposure are also potentially quite high in Guatemala, and likely throughout Central America and Mexico. The implications of co-exposure for human health are numerous, but one area of particular concern is the potential of FB1 to modulate AFB1 hepatoxicity and/or hepatocarcinogenicity. Both the mechanism of action of FB1 and its ability to promote liver carcinogenicity in rats and rainbow trout is consistent with this concern. In farm and laboratory animals FB1 inhibits ceramide synthases, key enzymes in de novo ceramide biosynthesis. The inhibition of sphingolipid signalling pathways mediating programmed cell death and activation of pathways stimulating cell proliferation in livers of individuals exposed to AFB1 could contribute to the tumorigenicity of AFB1. Studies investigating the health effects of either toxin should consider the potential for co-exposure to both toxins. Also, in countries where maize-based foods are prepared by alkaline treatment of the maize kernels, the effect of traditional processing on AFB1 levels and toxicity needs to be determined, especially for maize highly contaminated with AFB1.