Fumonisin exposure and the sphinganine/sphingosine ratio in urine, serum and buccal cells in adults from Burkina Faso, West Africa

Abstract

Fumonisins are mycotoxins that frequently contaminate maize, a dietary staple in Burkina Faso. Fumonisins have been linked with both the incidence of oesophageal cancer, and to neural tube defects. However, epidemiological studies of these associations are hampered by lack of validated exposure biomarkers. One candidate biomarker is the sphinganine/sphingosine (Sa/So) ratio in biological samples. Twenty husband-wife pairs aged 20-40 were recruited from Dingasso-1, western Burkina Faso. Plate ready food was sampled over three consecutive days (day one to three) for fumonisin B 1 and B 2 , to provide a measure of total fumonisin intake. The Sa/So ratio was determined in (1) first morning urines taken on days two to four, (2) buccal cells and (3) serum on days one and four only. Fumonisin intake was moderate (mean 0.81 µg/kg bw/day (range 0.01-2.40 µg/kg bw/day) compared to exposures reported in China and South Africa. For each person the mean fumonisin intake over three days was compared to the mean Sa, So and Sa/So ratio in urine, buccal cells and serum. A modest positive trend between mean fumonisin intake and mean serum Sa/So was observed ( P =0.067). When individuals were dichotomised based on the median fumonisin intake (<0.75 µg/kg bw/day), the serum Sa/So ratio was moderately higher ( P =0.044) in the high intake group (geometric mean 0.64; 95% CI: 0.54, 0.75) compared to the low intake group (0.49; 95% CI: 0.41, 0.59). Neither urinary nor buccal cell Sa/So ratio was associated with mean fumonisin intake. Neither mean individual Sa nor So level for urine, buccal cells or urine was associated with mean individual fumonisin intake. The study population was exposed to moderate levels of fumonisin with limited evidence of altered Sa/So ratio. Further work on serum Sa/So ratio is merited in comparison with other biomarker approaches such as urinary fumonisin B 1 or sphingolipid 1-phosphate metabolites.