ARS | Publication request: Development of biomarkers to assess fumonisin exposure and birth defects

Submitted to: Meeting Abstract
Publication Type: Book / Chapter
Publication Acceptance Date: July 24, 2012
Publication Date: October 10, 2012
Citation: Riley, R.T., Voss, K.A., Showker, A.J., Torres, O., Matute, J., Maddox, J.R., Rainey, M., Gardner, N.M., Sachs, A., Gregory, S.G., Ashley-Koch, A.E., Krupp, D., Gelineau-Van Waes, J. 2012. Development of biomarkers to assess fumonisin exposure and birth defects. In: Binder, E.M., editor. Proceedings of the World Nutrition Forum, October 10-13, 2012, Marina Bay, Singapore. p. 249-256.

Technical Abstract: Fumonisin is suspected to be a risk factor for increased incidence of neural tube defects (NTD) in humans where maize is consumed in large amounts and diets are likely to be deficient in folate. In susceptible mice, fumonisin induction of NTD appears to be closely linked to disruption of sphingolipid metabolism. Human data on fumonisin exposure and the threshold of exposure necessary for disruption of sphingolipid metabolism are currently lacking. If fumonisin is a risk factor for NTD, or any other disease, in humans then it is likely to be linked to disruption of sphingolipid metabolism. Human studies are currently in progress in Guatemala to determine if elevated urinary fumonisn levels can be correlated with evidence of increased levels of sphingoid base 1-phosphates using the sphinganine 1-phosphate to sphingosine 1-phosphate ratio as a mechanism-based biomarker. As of May 2012, we have collected data on FB contamination of the maize (n=117) in three Departments in Guatemala and have collected and analyzed urine for FB and blood spots for sphingosine 1-phosphate and sphinganine 1-phosphate (n=1,240 female; n=101 males). The results show that many maize consumers in Guatemala are exposed to fumonisins and that the use of blood spots as a tool for assessing fumonisin disruption of sphingolipid metabolism is promising.