Mycotoxins and milk safety
Mycotoxins and milk safety: the potential to block transfer to milk
Published: September 27, 2006
By: L.W. WHITLOW, D.E. DIAZ, B.A. HOPKINS AND W.M. HAGLER, JR. - Alltech Inc.
Mycotoxins occur worldwide. They occur frequently in a variety of feedstuffs (Gareis et al., 1989; Sharma and Salunkhe, 1991; Wood, 1992) and are therefore routinely consumed by dairy cattle. These typically low levels of mycotoxins are associated with subclinical losses in milk production, increases in disease and reduced reproductive performance. In some cases, mycotoxin concentrations in feedstuffs are high enough to be associated with severe problems including death. Diagnosis of a mycotoxicosis is difficult because of nonspecific symptoms, difficulties in feed sampling and analysis, and interactions with other stress factors. However, mycotoxins should be considered as a causative factor when unidentified problems exist.
Moy (1998) reviewed the international efforts to evaluate and reduce the human risks of mycotoxins. He stated that “human health problems caused by the consumption of most mycotoxins are complex and poorly understood”, but that they may be responsible for a range of diseases.
The majority of human health risk from mycotoxins is from consumption of contaminated grains and nuts. Several mycotoxins have been shown to occur in the milk of dairy cattle. Concentrations are extremely low because only a small fraction of the amount consumed by a cow is transferred to milk in the parent form or as a derivative. The US Food and Drug Administration (FDA) has indicated that aflatoxin is the only mycotoxin that currently warrants regulation in milk (Wood and Trucksess, 1998).
Aflatoxin
Interest in mycotoxin research was renewed in the early 1960s with the discovery that aflatoxin was responsible for the outbreak of Turkey X Disease in England (Sargeant et al., 1961). It was soon discovered that aflatoxin consumed by dairy cattle resulted in a toxic metabolite in milk (Allcroft and Carnaghan, 1962; 1963).
Aflatoxin is produced primarily by Aspergillus flavus. It is of major concern because it is carcinogenic and is found worldwide, especially in warm and humid climates including a routine occurrence in the southern US. Aflatoxin occurs in several forms of which the most common are aflatoxins B1, B2, G1 and G2. Reference is most frequently made to aflatoxin B1, which is the most prevalent and the most toxic form.
Aflatoxin is expected to occur in about 20% of the corn grain grown in the southern US even in non-crisis years (Shotwell, 1991). In the midwestern region of the US, aflatoxin is not expected except in years with extreme weather conditions. In 1988-89 the midwest experienced a drought; and 8% of corn samples from seven midwestern states contained aflatoxin (Russel et al., 1991). Aflatoxin occurrence is of concern in corn, peanuts, cottonseed and sometimes soybeans but may also occur in other feed products (Wood, 1992).
Aflatoxin can reduce performance and impair health of dairy cattle, but significant toxicity is thought to occur at dietary concentrations much greater than those which can result in illegal milk residues. Although no level of aflatoxin should be considered safe, the degree of toxicity is related to dietary level of the toxin, duration of exposure, and the amount of other stresses affecting the animal. Levels of 300 to 700 ppb are considered toxic for beef cattle depending on criteria for toxicity, and other factors affecting toxicity (CAST, 1989). Garrett et al. (1968) showed gain and intake in beef cattle were affected at 700 ppb, but not at 300 ppb aflatoxin.
However, levels of ‘no effect’ cannot be determined from data with such few animals. Trends in the data, especially for increased liver weights, would indicate potential toxicity at levels as low as 100 ppb. Guthrie (1979) showed a decline in reproductive efficiency in a field case where lactating dairy cattle were consuming 120 ppb aflatoxin. When cows were changed to an aflatoxinfree diet, milk production increased over 25%.
Patterson and Anderson (1982) and Marsi et al. (1969) also suggest that 100 ppb may reduce milk production. Applebaum et al. (1982) showed that impure aflatoxin produced by culture reduced production, while equal amounts of pure aflatoxin did not. Several studies suggest that naturally contaminated feeds are more toxic than would be expected from the concentrations of assayed mycotoxins. This suggests the presence of both known and unidentified mycotoxins in naturally contaminated feeds. Milk aflatoxin residues are the result of transformation of the parent compound in the liver and its subsequent secretion into milk. Aflatoxin B1 results in milk residues of aflatoxin M1, while aflatoxin B2 results in milk residues of aflatoxin M2. Small amounts of other derivatives such as aflatoxin M4, Q1, and aflatoxicol can also be found in milk, however aflatoxin M1 is the primary residue (Wood, 1991). Van Egmond (1989) concluded that aflatoxin carry-over from feed to milk is approximately 1-2 %. Frobish et al. (1986) found greater aflatoxin transfer to milk when the toxin was supplied by contaminated cottonseed meal than when it was supplied by contaminated corn. Aflatoxin transfer to milk was not affected by concentration in the feed or by milk production level of the cow. They concluded that concentration of aflatoxin M1 in milk was approximately equal to 1.51% of the concentration of aflatoxin B1 in the diet. Therefore a concentration of 33 ppb in the total diet would result in a 0.5 ppb concentration in milk (3.9 ppb in the milk dry matter, assuming 12.8% milk solids). Figure 1 shows the decline and increase in milk aflatoxin concentrations associated with the consumption of approximately 0 or 100 ppb aflatoxin and with or without binders in the diet (Diaz et al., 1997).
The FDA sets limits on aflatoxin in corn grain according to intended use of the grain. These values are: 200 ppb or less for breeding cattle, 300 ppb or less for finishing beef cattle, and 20 ppb or less for lactating dairy cattle. The FDA has set an action level for aflatoxin M1 at no more than 0.5 ppb in milk. The limit on milk aflatoxin M1 was set without going through the formal rule-making process and thus it is not binding on the courts, the public or the agency. However, the action level provides a guideline for regulatory action (Wood, 1998). Van Egmond (1989) conducted a survey during 1987 indicating that approximately 34 countries had actual or proposed regulations on aflatoxin B1 concentrations in feedstuffs and that approximately 14 countries had actual or proposed limits on aflatoxin M1 concentrations in milk.
Regulatory pressures and a widespread awareness have helped minimize aflatoxin problems. Surveys of aflatoxin B1 concentrations in feedstuffs conducted during the 1980s resulted in lower levels than for surveys conducted in the 1970s (Van Egmond, 1989). The United States General Accounting Office (GAO, 1991) concluded that industry, federal and state programs are effective in detecting and controlling aflatoxin and that it is doubtful that additional programs or limits would reduce the risk of aflatoxin in the food supply. The GAO specifically examined the state-administered program in the state of Georgia as a part of its report. In 1989, 13% of corn samples tested by the Georgia Department of Agriculture exceeded 20 ppb. On farms, 3.9% of tested milk exceeded limits while at the retail level only 0.4% of milk was in violation. Current surveillance programs in the US aimed at reducing food residues make it very unlikely that aflatoxin will be fed at high enough levels and for sufficient duration to have significant production or health effects on dairy herds in those regions that have an active program.
Dairy cattle feeds should contain less than 20 ppb aflatoxin to prevent milk residues above 0.5 ppb. Concentrations of aflatoxin should be conservatively low because of uncertainties in sampling and analysis, nonuniform distribution of aflatoxin, and potential for more than one source of aflatoxin in the diet.
T-2 toxin
T-2 toxin, a Fusarium-produced toxin, has been associated with gastroenteritis, intestinal hemorrhages (Petrie et al., 1977) and death in cattle (Hsu et al., 1972). Serum immunoglobulins and certain complement proteins were lowered in calves receiving T-2 toxin. T-2 has been shown to reduce white cell and neutrophil count in 50 kg calves (Gentry et al., 1984) as well as immunoglobulin levels in 190 kg calves (Mann et al., 1983).
Administration of pure T-2 toxin failed to produce hemorrhagic bowel syndrome in a cow although it did produce a rumen ulcer and edema of the submucosa of the reticulum, cecum and colon (Weaver et al., 1980). Patterson et al. (1979) had previously failed to produce hemorrhagic symptoms in calves with either T-2 toxin or diacetoxyscirpenol. Together, these studies suggest that other unidentified toxins are present or that interactions with conditions in the field are somehow different than those encountered in the laboratory.
Analysis of corn grain samples from the 1988-89 drought year in the midwestern US showed a 13% incidence of T-2 toxin. T-2 toxin has been detected in 7% of over 2000 non-random samples submitted by farmers to the North Carolina mycotoxin testing program over a nine year period (Whitlow et al., 1998). In a review of mycotoxin incidence in European countries, Gareis et al. (1989) indicated that T-2 had been found to occur in over 20% of oats samples and between 3% and 5% of other grains and mixed feeds.
T-2 is metabolized in the rumen to HT-2 and acetyl HT-2 (Munger et al., 1987). These derivatives are less toxic than T-2, but are still potent toxins.
Residues of T-2 and its derivatives have been found in milk, but have a low transfer rate from feed to milk. After 72 hrs, an orally administered dose of T-2 at 0.42 mg/kg of body weight (approximately 36 ppm) was almost completely excreted in the feces and urine (Yoshizawa et al., 1981; 1982). Milk residues, which reached a maximum of about 35 ppb, suggest that about 0.2% of T-2 and its metabolites are excreted into milk. In the lactating cow administered radioactive labeled T-2 toxin, three metabolites (3'-hydroxy-T-2 toxin, 3'-hydroxy-HT-2 toxin and 3'-hydroxy-7-hydroxy- HT-2 toxin) accounted for 30-40% of the radioactivity in urine, 60-70% of radioactivity in milk and 50-60% of the radioactivity in blood plasma. Other metabolites included HT-2 toxin, neosolaniol and 4-deacetylneosolaniol. Other investigators (Robinson et al., 1979) have measured T-2 up to a peak of 160 ppb in milk on the fifth day after starting oral intubation with daily doses of 182 mg of T-2 toxin for 15 consecutive days (equivalent to about 9 ppm in the diet, assuming a daily consumption of 20 kg).
There are currently no regulations on T-2 toxin in the US.
Deoxynivalenol
In 1982 the FDA issued an advisory which recommended a level of concern for deoxynivalenol (DON) at 1 ppm in finished wheat products for human consumption, 2 ppm for wheat entering the milling process and 4 ppm for wheat by-products used in animal feeds. This advisory was updated in 1993 to 1 ppm in finished wheat products for human consumption. Advisory levels for animal feeds were changed to 5 ppm in grains and grain products (not to exceed 20% of the diet) fed to swine; 10 ppm in feeds for poultry and ruminating beef and feedlot cattle older than four months (not to exceed 50% of their diets); and 5 ppm in feed for all other animals (not to exceed 40% of their diets) (Wood and Trucksess, 1998).
Deoxynivalenol has been associated with reduced feed intake (Trenholm et al., 1985) in ruminants. Symptoms of unthriftiness, low weight gain and a trend toward reduced performance have been associated with both DON and zearalenone (e.g. Noller et al., 1979). Whitlow et al. (1991) suggested an association of DON with milk production loss. Charmley et al. (1993) demonstrated a 13% (2.85 kg) numerical decrease in 4% fat corrected milk production (statistics not available) utilizing 18 mid-lactation dairy cows (average 19.5 kg milk/day) consuming diets shown to contain no common mycotoxins other than DON, which was at levels of 2.7 to 6.4 ppm in treatment diets. While the decrease in actual milk production (1.35 kg) was not statistically significant, the decrease in fat test (3.92 vs. 3.04%) was significant. DiCostanzo et al. (1995a) cite results by Ingalls (1994) where lactating dairy cows were fed 0, 3.6, 10.9 and 14.6 ppm DON for 21 days without an apparent effect on feed intake or milk production, which averaged about 30 kg daily. Foster et al. (1986) showed that DON is associated with as yet unknown factors causing productivity losses in swine. Pure DON added to swine diets did not result in effects as severe as did similar levels of DON provided by naturally contaminated grains.
Presence of DON in feed apparently indicates that the feed is moldy. In this way, DON serves as an indicator of spoilage, and the probable presence of other mycotoxins or factors more toxic than DON itself. Smith and MacDonald (1991) have suggested that fusaric acid produced by Fusarium moniliforme may be interacting with mycotoxins such as DON to produce more severe effects. It is well documented that multiple mycotoxins often occur in the same feed sample (Abbas et al., 1989; Hagler et al., 1984), and thus several interactions are possible.
Wood and Trucksess (1998) suggest that DON may be the most widely distributed of the Fusarium mycotoxins. An Ohio study of 52 preharvest corn samples from 26 farms showed 46% of samples to contain DON (Vesonder et al., 1978). An Illinois survey of feeds from swine problem herds found 80% of samples contained DON and 12% zearalenone (Côté et al., 1984). A 1982 survey of hard, red winter wheat in Kansas and Nebraska found a mean 1.71 ppm DON in 157 samples (Shotwell et al., 1985). Fifty-eight percent of the samples contained greater than 1 ppm DON and only 8% less than 0.1 ppm. In 1993, adverse weather conditions prompted a survey of wheat and barley samples from 25 states that revealed that about 40% of samples contained more than 2 ppm DON (Trucksess et al., 1995). Analysis of corn grain samples from 1993 collected from the midwestern US showed that 70% contained DON with 19% above 1 ppm and 6% greater than 2 ppm (Wood and Trucksess, 1998). Of over 2400 samples non-randomly submitted during a nine year period by North Carolina farmers, 58% contained detectable levels of DON with positive samples averaging 1.7 ppm (Whitlow et al., 1998).
Deoxynivalenol is transformed to DOM-1 in the rumen with estimates of 24 hr degradation of about 50% (King et al., 1984). Deoxynivalenol and metabolites are rapidly excreted, primarily through urine (Côté et al., 1986a; Prelusky et al., 1984; 1987). Prelusky et al. (1984) administered DON in an oral dose of 920 mg and found less than 4 ng/ml of free and conjugated DON in the milk. DON was excreted in milk primarily as DOM-1, but excretion rate is extremely low at 0.0001% of the dose. Côté et al. (1986a) found no DON, but up to 30 ppb of DOM-1 in milk of cows fed DON at about 300 mg/day (66 ppm) for five days.
Zearalenone
Zearalenone is a Fusarium produced mycotoxin that elicits an estrogenic response in monogastrics (Sundlof and Strickland, 1986), but is of less toxicity to ruminants. A controlled study with cows fed up to 22 ppm zearalenone resulted in no obvious effects except that corpora lutea were smaller in treated cows (Weaver et al., 1986b). In a similar study with heifers receiving about 13 ppm zearalenone, conception rate was depressed about 25%; otherwise, no obvious effects were noted (Weaver et al., 1986a). A few case reports have related zearalenone to an estrogenic response in ruminants (Khamis et al., 1986; Mirocha et al., 1968; Roine et al., 1971). Large doses were associated with abortions in cattle (Kellela and Ettala, 1984, Mirocha et al., 1974).
Mirocha et al. (1968) isolated zearalenone from hay associated with infertility in dairy cattle. Other cattle responses may include vaginitis, vaginal secretions, poor reproductive performance and mammary gland enlargement in virgin heifers. In a field study by Coppock and Mostrom (1990), diets containing about 750 ppb zearalenone and 500 ppb DON resulted in poor feed consumption, depressed milk production, diarrhea and total reproductive failure. New Zealand workers (Towers et al., 1995a, 1995b; Sprosen and Towers, 1995; Smith et al., 1995) have related urinary zearalenone and zearalenone metabolites (zearalenone, zearalanone, "- and ß-zearalenol and "- and ß-zearalanol), which they refer to as ‘zearalenone’, to intake of ‘zearalenone’ and to reproductive disorders in sheep and dairy cattle. In sheep, ‘zearalenone’ was related to lower conception, reduced ovulation, and increased twinning rates. With dairy cattle, herds with low fertility were found to have higher levels of blood and urinary ‘zearalenone’ and consume pastures containing higher levels of ‘zearalenone’.
In addition, within herds, individual cows were examined by palpation and those that were determined to be cycling had lower blood ‘zearalenone’ levels than did cows that were not cycling. Differences in ‘zearalenone’ levels were attributed to selective grazing behavior. The reproductive problems in dairy cattle were associated with ‘zearalenone’ concentrations of about 400 ppb in the pasture samples.
Grain sorghum samples from 10 states harvested in 1975 and 1976 were analyzed for zearalenone with a detection limit of 100-200 ppb (Shotwell et al., 1980). Twenty-eight percent were positive, with 18% above 1 ppm. In two Virginia surveys, zearalenone was found in 19 of 42 wheat samples in 1975; but none was found in samples collected from 1976-1980 (Shotwell et al., 1977; Shotwell and Hesseltine, 1983). Eppley et al. (1974) reported that 17% of corn samples collected from Corn Belt areas from the 1972 crop where Fusarium damage was reported in association with excessive moisture contained zearalenone at levels of 0.4 to 5.0 ppm. Stoloff et al. (1976) surveyed the 1973 crop corn and found the incidence of zearalenone to be 10% in corn from the midwestern US and 1% in other regions of the US, with a maximum value of 0.4 ppm. Of over 1700 samples non-randomly submitted during a nine year period by North Carolina farmers, 17.5% contained detectable levels of zearalenone with positive samples averaging 0.7 ppm (Whitlow et al., 1998).
Shreeve et al. (1979) fed dairy cows about 1 ppm zearalenone for 11 weeks without detecting a milk residue. Prelusky et al. (1990) administered up to 6 g of zearalenone per cow daily and found a total milk residue of up to 16 ppb, which represented about 0.01% of the dose. Hagler et al. (1980) administered 5 g zearalenone in ground feed to a lactating dairy cow that was milked twice daily with samples collected until 120 hr after dosing. Only trace levels of zearalenone were found in the milk obtained at 96, 108 and 120 hr after dosing and trace levels of zearalenol were also found in the milk at 108 and 120 hr after dosing. Mirocha et al. (1981) found that zearalenone and its metabolites reached levels above 1 ppm in milk representing about 0.7% of the zearalenone dosage, which was 25 ppm for eight days.
Zearalenone is rapidly converted to "- and ß-zearalenol in rumen cultures (Kiessling et al., 1984). Ruminal degradation of zearalenone was found to be about 30% complete in 48 hrs (Kellela and Vasenius, 1982). There are no regulations for zearalenone in feed, food or milk in the US. days.
Fumonisin
Fumonisin B1 was isolated by Gelderblom et al. (1988) and shown to be a cancer promoter. Fumonisin B1 has been shown to cause leukoencephalomalacia in horses (Marasas et al., 1988), pulmonary edema in swine (Harrison et al., 1990), and hepatoxicity in rats (Gelderblom et al., 1991). While fumonisin B1 is thought to be much less potent in ruminants than in monogastrics, work by Krick et al. (1981) suggested that fumonisin was toxic to sheep. Osweiler et al. (1993) demonstrated that fumonisin B1 in large amounts (148 ppm) can cause mild liver damage in cattle even when fed for a short term (31 days), but without an effect on feed intake or weight gain. Whitlow (unpublished) has demonstrated that fumonisin B1 is toxic to dairy cattle. Fed for approximately seven days prior to freshening and for 70 days thereafter, dietary fumonisin B1 at 100 ppm significantly and dramatically reduced milk production (6 kg/cow/day) and increased serum enzymes levels indicative of liver disease.
A USDA/APHIS (Anon., 1995) survey found an average of 6.9% of 1995 corn samples from Missouri, Iowa and Illinois to contain more than 5 ppm fumonisin B1. Over 60% of corn samples collected from 1988 to 1991 from the midwest contained fumonisin B1 (Murphy et al., 1993). FDA surveys from 1994 and 1995 show that while over 45% of shelled corn samples from both years contained detectable levels of fumonisin B1, the percentages of samples which contained more than 1 ppm were 2.4% of the 1994 samples and 10.2% of the 1995 samples (Wood and Trucksess, 1998).
Fumonisin B1 carryover from feed to milk is thought to be negligible (Richard et al., 1996; Scott et al., 1994). Prelusky et al. (1996) reported studies where dairy cattle were administered fumonisin B1 either orally or intravenously. The oral dosages were approximately equal to dietary concentrations of 60 to 300 ppm. The intravenous dosages were stated to be similar to dietary concentrations of 125 to 500 ppm. No fumonisin B1 or its metabolites were detected in milk (detection limit of 0.5 ng/ml for fumonisin B1).
Maragos and Richard (1994) analyzed 155 milk samples collected in Wisconsin during a period when feeds were reported to be severely affected by mold. Additionally, 10 samples were collected in Illinois. Feed samples associated with these milk samples were not collected and thus fumonisin B1 concentrations in feed were unknown. Only one of the 165 milk samples tested positive for fumonisin B1, which was determined to be 1.29 ng/ml. This suggests that fumonisin can occur in milk, but is likely to be at very low levels.
There are no current regulations for fumonisin B1 in feed, food or milk in the US.
Ochratoxin
Ochratoxin A is produced primarily by penicillium molds and tends to be more prevalent in cooler climates (Pohland et al., 1992). Although as much as 50% of the dietary ochratoxin is destroyed within 15 minutes in the rumen (Kiessling et al., 1984), there are reports of ochratoxin toxicity in dairy cattle indicating symptoms of diarrhea, kidney damage and reduced milk production (Ribelin, 1978; Vough and Glick, 1993).
Sreemannorayoma et al. (1988) showed that calves with a functioning rumen survived ochratoxin in oral doses of 2.0 mg/kg bodyweight, while preruminant calves died when administered ochratoxin at doses of as little as 0.25 mg/kg bodyweight.
Goats were administered a single dose of radiolabeled ochratoxin A at 0.5 mg/kg (Nip and Chu, 1979).
Cumulative excretion of radioactivity over seven days indicated that 53% was excreted in the feces, 38% in the urine and 6% in milk. Of the radioactivity in milk, only a small amount was in the form of ochratoxin A, representing 0.026% of the dosage administered. In a study with lactating cows, where ochratoxin A was fed at 317 to 1,125 ppb for 11 weeks, neither ochratoxin A nor its metabolite ochratoxin " were detected in milk (Shreeve et al., 1979).
There are no regulations on ochratoxin in feed, food or milk in the US.
Treatments for mycotoxin contamination
Adsorbent materials such as clays (bentonite, zeolite) added to contaminated diets fed to rats, poultry, swine and cattle have helped reduce the effects of mycotoxins (Diaz et al., 1997; Galey et al., 1987; Harvey, 1988; Lindemann and Blodgett, 1991; Scheideler, 1990; Hayes, 1990; Smith, 1980; 1984). In most cases, clay was added to the diet at about 1%. Other absorbent materials such as activated carbon at 1% of the diet (Galvano et al., 1996), and glucomannans at 0.05% of diet dry matter (Diaz et al., 1999) have been shown effective in reducing aflatoxin in milk. Figure 2 shows the percentage reduction in milk aflatoxin associated with inclusion of various aflatoxin binders in the diet (Diaz et al., 1999). In this study inclusion of an esterified glucomannan product (Mycosorb, Alltech, Inc.) was shown to reduce milk aflatoxin concentrations by 58% in dairy cows consuming aflatoxin-contaminated diets when included at 0.05% of the diet dry matter. The reduction of milk aflatoxin was similar to that seen for a sodium bentonite product included in the diet at 1.1% of the dry matter.
Limited studies on binding of mycotoxins other than aflatoxin are also available, but such studies are difficult to conduct in vivo because of the lack of a simple biological marker to estimate binding. While there are estimates for mycotoxin binding with feed additives in vitro, such values may not reflect binding in vivo (Diaz et al., 1997) and are not the same for all mycotoxins (Devegowda et al., 1998).
Summary
While many mycotoxins are common contaminants of feedstuffs, aflatoxin is the only mycotoxin that has received regulatory action in the US as a possible contaminant in milk. This is because aflatoxin is carcinogenic and highly toxic to humans, and because milk is a primary component of the diet of infants. Several other mycotoxins or their derivatives may be found in extremely small amounts in milk. It is thought that significant residues of these other mycotoxins occur in milk only when very high, nonclinical levels are administered to cows. Additionally the derivatives are generally less toxic than the parent compound. Therefore, mycotoxins other than aflatoxin are not considered as likely human health hazards in milk.
Regulatory efforts have successfully reduced the risk of aflatoxin in the food supply in the US (GAO, 1991). Efforts to prevent aflatoxin formation, to divert contaminated ingredients away from usage in dairy feeds, and to use feed additives that reduce aflatoxin absorption by the animal have contributed to fewer milk contamination problems.
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