Risks for animal health related to the presence of ergot alkaloids in feed

Abstract

The European Commission requested EFSA to provide an update of the 2012 Scientific Opinion of the Panel on Contaminants in the Food Chain (CONTAM) on the risks for animal health related to the presence of ergot alkaloids (EAs) in feed. EAs are produced by several fungi of the Claviceps and Epichloë genera. This Opinion focussed on the 14 EAs produced by C. purpurea (ergocristine, ergotamine, ergocornine, α- and β-ergocryptine, ergometrine, ergosine and their corresponding 'inine' epimers). Effects observed with EAs from C. africana (mainly dihydroergosine) and Epichloë (ergovaline/-inine) were also evaluated. There is limited information on toxicokinetics in food and non-food producing animals. However, transfer from feed to food of animal origin is negligible. The major effects of EAs are related to vasoconstriction and are exaggerated during extreme temperatures. In addition, EAs cause a decrease in prolactin, resulting in a reduced milk production. Based on the sum of the EAs, the Panel considered the following as Reference Points (RPs) in complete feed for adverse animal health effects: for pigs and piglets 0.6 mg/kg, for chickens for fattening and hens 2.1 and 3.7 mg/kg, respectively, for ducks 0.2 mg/kg, bovines 0.1 mg/kg and sheep 0.3 mg/kg. A total of 19,023 analytical results on EAs (only from C. purpurea) in feed materials and compound feeds were available for the exposure assessment (1580 samples). Dietary exposure was assessed using two feeding scenarios (model diets and compound feeds). Risk characterisation was done for the animals for which an RP could be identified. The CONTAM Panel considers that, based on exposure from model diets, the presence of EAs in feed raises a health concern in piglets, pigs for fattening, sows and bovines, while for chickens for fattening, laying hens, ducks, ovines and caprines, the health concern related to EAs in feed is low.

Keywords: animal health risk assessment; ergot alkaloid; exposure; feed; toxicity.

FIGURE 1

Structures exemplifying the three main groups of ergot alkaloids.

FIGURE 2

Epimerisation of Δ^9,10‐ergolenes via enolisation at C‐8 (D‐lysergic acid (8‐(R))‐derivative (suffix ‘ine’), into the corresponding isolysergic acid (8‐(S))‐derivative (suffix ‘inine’).

FIGURE 3

Number of samples by sampling country.

FIGURE 4

Number of samples by sampling year.

FIGURE 5

Overview of quantified and left‐censored samples (all reported EAs below LOD/LOQ) at Feed level 1.

FIGURE 6

Overview of quantified and left‐censored analytical results (below LOD/LOQ) across different types of EAs. Quantified samples (at least one EA quantified, n = 789) were assessed to identify the average contribution of the different EAs to the total concentration. Overall, the ‘ine’ epimers represent on average 77% of the total EA concentration vs. the 23% of the ‘inine’ epimers. Although only a small number of feed samples referred to processed commodities (e.g. ‘Compound feed’, ‘Malting barley and malt fines’), in these samples the proportion of ‘inine’ epimers was slightly higher (⩍ 30%) as compared to unprocessed feed (results not shown). This shift from ‘ine’ epimers to ‘inine’ epimers seems to be related to processing and it was already described in the 2017 EFSA scientific report on EAs (EFSA, 2017). The three most abundant EAs were ergotamine, ergosine and ergocristine; the three together represent on average 59% of the total EA concentration (see Table 7).

FIGURE I.1

Relative potencies for the effect of EAs in the bovine lateral saphenous vein bioassay (Craig et al., 2015). EV, ergovaline; ET, ergotamine; ECo, ergocornine; ECs, ergocristine; ECp, ergocryptine; EM, ergometrine; LA, lysergic acid.

FIGURE I.2

Relative potencies for the effect of EAs in the bovine ruminal artery and vein bioassays (Foote et al., 2011). EV, ergovaline; ET, ergotamine (not tested); ECo, ergocornine (not active in vein assay); ECs, ergocristine; ECp, ergocryptine; EM, ergometrine (not active in vein assay); LA, lysergic acid (not active in both assays).

FIGURE I.3

Relative potencies for the effect of EAs in the bovine mesenteric artery and vein bioassays (Egert et al., 2014). EV, ergovaline (not tested in the artery assay); ET, ergotamine; ECo, ergocornine; ECs, ergocristine; ECp, ergocryptine; EM, ergometrine; LA, lysergic acid (not included in this study).

FIGURE I.4

Relative potencies for the effect of EAs in the equine medial palmar artery and vein bioassays (Klotz & McDowell, 2017). EV, ergovaline; ET, ergotamine; ECo, ergocornine; ECs, ergocristine; ECp, ergocryptine; EM, ergometrine; LA, lysergic acid. LA was not included in this study and ET was only tested on arteries.