“…Examples of candidate markers for consumption of potentially harmful foods include: metabolites of ethyl alcohol [ethyl glucuronide (EtG), ethyl sulfate (EtS), phosphatidyl ethanol (PEth)] and 5-hydroxytryptophol (HTOL) ( Maenhout et al, 2013 ; Reid et al, 2011 ) (note that since PEth is synthesized via phospholipase D, it serves as a definitive metabolite, but one for which sewage has apparently not yet been monitored); DON-15-GlcA, which is the most important glucuronic acid (GlcA) conjugate of deoxynivalenol (DON; also known as vomitoxin)—one of the most prevalent Fusarium mycotoxins (common contaminant of grains worldwide, especially wheat, barley, maize, and oats) ( Gruber-Dorninger et al, 2017 ; Huybrechts et al, 2015 ); and 1-methyl-histidine (a marker for meat consumption), but not 3-methyl-histidine, which can be formed via muscle catabolism ( Fraser et al, 2016 ; Lindsay and Costello, 2017 ). Note, however, that although conjugates provide an assurance that they originate from metabolism and therefore reflect exposure, their inherent chemical instability introduces added challenges in performing back-calculations to quantify exposure (e.g., Banks et al, 2017 ).…”