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ScopeIn this study, human exposure to the mycotoxin ochratoxin A (OTA) and its thermal degradation product 2’R‐ochratoxin A (2’R‐OTA, previously named as 14R‐Ochratoxin A [22]) through coffee consumption was assessed. LC‐MS/MS and the dried blood spot (DBS) technique were used for the analysis of blood samples from coffee and noncoffee drinkers (n = 50), and food frequency questionnaires were used to document coffee consumption.Methods and resultsFor the detection of OTA and 2’R‐OTA in blood, a new sensitive and efficient sample preparation method based on DBS was established and validated. Using this technique 2’R‐OTA was for the first time detected in biological samples. Comparison between coffee drinkers and noncoffee drinkers showed for the first time that 2’R‐OTA was only present in blood from the first group while OTA could be found in both groups in a mean concentration of 0.21 μg/L. 2’R‐OTA mean concentration was 0.11 μg/L with a maximum concentration of 0.414 μg/L. Thus, in average 2’R‐OTA was approx. half the concentration of OTA but in some cases even exceeded OTA levels. No correlation between the amounts of coffee consumption and OTA or 2’R‐OTA levels was observed.ConclusionThe results of this study revealed for the first time a high exposure of coffee consumers to 2’R‐OTA, a compound formed from OTA during coffee roasting. Since little information is available regarding toxicity and possible carcinogenicity of this compound, further OTA monitoring in blood including 2’R‐OTA is advisable.

The nephrotoxic and carcinogenic mycotoxin ochratoxin A (OTA) is a worldwide contaminant in food commodities and also found frequently in human biological fluids. Dietary contaminants ingested by nursing mothers can appear in breast milk. But the rate of lactational transfer of OTA has not been investigated so far at various stages of breastfeeding. Therefore, and to investigate OTA exposure of Chilean infants, we conducted a longitudinally designed study in mother-child pairs (n = 21) with parallel collection of maternal blood, milk and of infant urine samples over a period of up to 6 months. Validated analytical methods were applied to determine OTA concentrations in all biological samples (n = 134). OTA was detected in almost all maternal blood plasma, at concentrations ranging between 72 and 639 ng/L. The OTA concentrations in breast milk were on average one quarter of those measured in plasma (M/P ratio 0.25). Interestingly, a higher fraction of circulating OTA was excreted in colostrum (M/P 0.4) than with mature milk (M/P ≤ 0.2). Infants exposure was calculated as daily intake from our new data for OTA levels in breast milk, and taking into account milk consumption and body weight as additional variables: Chilean infants have an average intake of 12.7 ± 9.1 ng/kg bw during the first 6 days after delivery while intake with mature milk results in average values close to 5.0 ng/kg bw/day. Their OTA exposure is discussed in the context of tolerable intake values suggested by different scientific bodies. Moreover, the study design enabled a comparison of OTA intake and infant urine concentrations over the breastfeeding period. The statistical analysis of n = 27 paired values showed a good correlation (r = 0.57) for this type of studies and thereby confirms that urinary OTA analysis in infants is a valid biomarker of exposure.

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