“…There are few available studies and no routine surveys for the presence of CPA in grains or other commodities, in part because of the lack of regulatory requirements for testing, the relative difficulty of the analytical methods used in its detection ( Moldes-Anaya et al, 2009 ; Diaz et al, 2010 ), and probably also in part because many researchers have concluded, despite the dearth of data, that CPA is a relatively “benign” toxin, that it is not likely to be present in sufficient concentrations in food or feed to pose a significant problem or that efforts to reduce aflatoxin contamination will indirectly result in reductions in CPA contamination ( Byrem et al, 1999 ; Burdock and Flamm, 2000 ; Chang et al, 2009a ). Other researchers have expressed concern that the potential for harm to humans or animals from exposure to CPA has not been adequately evaluated or addressed ( Stoltz et al, 1988 ; Dorner et al, 1994 ; Kubena et al., 1994 ; Balachandran and Parthasarathy, 1996b ; Prasongsidh et al, 1997 ; Kumar and Balachandran, 2009 ) and several studies have demonstrated the presence of CPA in food and feed items sampled from various locations around the world, sometimes at levels in the range of 2.8 to 12 μg/g (Stolz et al, 1988; Widiastuti et al, 1988 ; Urano et al, 1992 ; Balachandran and Parthasarathy, 1996b ). This risk becomes more serious when CPA-producing “atoxigenic” strains are intentionally applied to a major food and feed crop such as maize, under conditions that favor colonization of the plant by the introduced strain.…”