RE: Complete Testing of Potentially Contaminated Corn Should Be Done Before It Is Moved

October 7, 2002

To Whom It May Concern:

Based upon the opinions of scientists and veterinarians in Iowa and the collective body of scientific knowledge on toxins produced by mold in corn, the following investigations should be conducted before any of the suspect corn on the Rosman farm is moved or considered for sale into the open market:

1) The corn should be tested for the toxins moniliformin, fusaproliferin and beauvericin

The corn in question has tested positive for high quantities of Fusarium subglutinans mold. This mold is known to produce moniliformin, fusaproliferin and beauvericin. Moniliformin causes lung and liver lesions in animals, and is the suspected cause of a fatal heart ailment in humans (Keshan disease). Fusaproliferin and beauvericin are toxic to human cells. The corn HAS NOT BEEN TESTED for the presence of these toxins.

2) The corn should be re-tested for zearalenone

Low levels of the mycotoxin zearalenone (ZEN), a compound known to cause pseudopregnancy in sows, have been found in the corn. ZEN also has estrogenic effects in humans, and may promote breast cancer. Additional samples should be tested to see if higher levels exist in “hot spots” within the corn storage bins.

3) Cattle fed the suspect corn should be tested for the presence of ZEN in their urine

Cows fed the suspect corn have lower conception rates, another known effect of ZEN. The animals’ urine should be tested for ZEN and its breakdown products, a proven method for determining whether cattle have eaten ZEN-contaminated feed.

4) The corn should be re-tested for the potent toxin, fumonisin

The corn is also infested with Fusarium moniliforme mold. This mold is known to produce high levels of fumonisins, powerful toxins that causes brain disease in horses, lung and liver disease in swine, and cancer in rats at extremely low doses. They are also a suspected cause of cancer in humans. Thus, the FDA recommends no more than 2-4 parts per million fumonisin in food.

5) Allow time for results of tests to find endocrine disruptor that are already in progress

USDA scientists are presently testing Mr. Rosman’s corn for an endocrine disruptor recently found in corncobs that causes reproductive failure in rats when present even at extremely low levels.

See below for a more full explanation of the need to save the suspect corn for testing and references to scientific studies to support the recommendations made above.

Does an Unidentified Substance in Mold-Infested, Genetically Engineered Corn Cause Pig Disease?

Mystery of Suspect Corn Must be Solved to Protect Food, Farmers & the Environment

Immediate USDA action is needed to prevent potentially contaminated corn on the farm of Jerry Rosman of Harlan, Iowa, from being sold on the open market. USDA and Iowa State University researchers, among other scientists, are concerned that this mold-infested corn fed to pigs could possibly be the source of extraordinary reproductive problems on Mr. Rosman’s swine farm: pseudopregancies in which the sows show all the outward signs of pregnancy, but do not give birth. According to USDA Research Leader Mark Rasmussen:

“They are not the only farm in Iowa to have reported this problem … I would like to ask that the corn suspected of causing reproductive problems in swine be held for purposes of scientific research… Animal reproduction studies, especially with swine, will require considerable quantities of the suspect corn.”

The corn fed to swine experiencing pseudopregnancies is known to be infested with high levels of Fusarium molds. Fusarium molds produce mycotoxins implicated in many forms of animal disease, including pseudopregnancies in swine. While some work has been done to test for common mycotoxins in the suspect corn, experts acknowledge that negative results do not by any means rule out a mycotoxin threat to human and animal health. According to mycotoxin expert Dr. Gary Munkvold:

“Rosman is convinced his problem is related to the Fusarium, and he is probably right. Unfortunately, it is widely acknowledged that there are unknown mycotoxins that we do not know how to detect.”

There are many other reasons that the ad hoc testing conducted up to this point could have missed a potentially severe threat to animal or human health. Many unexplored avenues of research make it urgent that this corn be saved for thorough, deliberate scientific testing:

1) Sampling could miss hot spots: The mold that produces mycotoxins often grows in “hot spots” in bins of corn. Mycotoxin tests that come up negative, or show the presence of trace quantities, could very well mean that the particular samples tested missed these hot spots of mold/mycotoxin.

2) Substance known to cause pseudopregnancy found in two samples: The mycotoxin zearalenone has long been known to cause pseudopregnancy in sows. Two samples of Mr. Rosman’s feed corn were found to contain 0.04 ppm and 0.05 ppm zearalenone equivalent (see Appendix 1). Though below the level normally associated with pseudopregnancy, these trace amounts indicate the presence of zearalenone-producing mold, which could be producing much larger quantities of zearalenone elsewhere in the stored corn, making repeat tests necessary. Mr. Rosman’s cows are being fed the suspect corn, and have shown slightly lower conception rates; this is another known effect of ZEN. The animals’ urine should therefore be tested for ZEN and its breakdown products, a proven method for determining whether ZEN-contaminated feed has been consumed. Though not well-studied, zearalenone has human health impacts that include estrogenic effects and possibly, at low doses, stimulation of breast cancer cells. Studies on toxicity to genes and chromosomes have yielded mixed results.

3) Testing for other possible toxins is not complete: Mr. Rosman’s feed corn and that of 4 other producers whose sows suffered the same pseudopregnancy problem were all reportedly found to contain two species of mold: Fusarium moniliforme and Fusarium subglutinans . It is unclear whether the suspect corn has been adequately tested for all of the toxins known to be produced by these two species.

4) Fusarium moniliforme and fumonisins: F. moniliforme is known to produce highly toxic fumonisins . Fumonosins are known to cause a brain disease in horses, lung and liver disease in swine and cancer in rats at extremely low levels. Fumonisins may also cause esophageal and liver cancer in humans. Although disputed, some think that a fumonisin is the culprit in a 1991 outbreak of anencephaly: babies born with stunted or missing brains. The FDA is concerned enough that it recently set recommended maximum levels for fumonisin in human foods of just 2-4 parts per million. While fumonisin tests on Rosman’s feed came up either negative or in one case at 1.16 ppm, repeat testing may be advisable because of the “hot spot” problem or other difficulties.

5) Fusarium subglutinans and unusual mycotoxins: “Some strains of F. subglutinans are known to be highly toxic to experimental animals.” One strain of F. subglutinans found to be toxic to ducklings and rats was isolated from South African corn in an area with a “high incidence of human esophageal cancer.” F. subglutinans is known to produce three unusual mycotoxins – monilformin, fusaproliferin and beauvericin . It is unclear whether any tests have been conducted for the latter three compounds on samples of suspect feed corn.

a) Moniliformin toxic to animals and possibly humans: Two recent studies have associated ingestion of moniliformin and moniliformin and/or fumonisin B1 with adverse effects – including decreased weight gain; heart, lung and liver lesions; and death – in pigs fed diets containing moniliformin at levels of 100-200 parts per million. Moniliformin is also a suspected cause of a fatal heart disease (Keshan disease):

“Moniliformin (MON) is a widely occurring mycotoxin, produced mainly by Fusarium proliferatum and Fusarium subglutinans in corn, that has been shown to be acutely toxic for various animal species and is a suspected cause of Keshan disease in China.”

b) Fusaproliferin and beauvericin toxic to human cell lines: Several studies have shown that these two compounds produced by F. subglutinans are toxic to several human cell lines. Beauvericin has been shown to induce programmed cell death and cause DNA fragmentation.

6) An unknown toxin could be the cause: Besides these known mycotoxins which may not have been tested for, a yet unidentified toxin could be involved: “Symptoms occurring in animals that consume Fusarium-contaminated feeds cannot always be attributed to known toxins.”

7) Recently discovered endocrine-disruptor in corn also suspected: Scientists are also pursuing another lead suggested by a recent rat study conducted at Baylor University. A substance isolated from corncob bedding material commonly used in animal experimentation has been found to severely impair the reproductive behavior of male and female rats. It also stimulates cancerous proliferation in human breast and prostatic cell cultures. This same endocrine-disrupting substance was also discovered in fresh corn on the cob and in corn tortillas, making human exposure likely. This substance is potent at extremely low levels and is not broken down by heat.

8) Genetically engineered corn may be more susceptible to mold: Rosman grew and fed his hogs Roundup Ready corn and StarLink, which are resistant to the herbicides Roundup (glyphosate) and Liberty (glufosinate), respectively. Some of the varieties also produce an insecticidal toxin known as Bt. Other producers with pseudopregnant hogs also fed varieties of engineered corn. Use of glyphosate on herbicide-resistant soybeans has been associated with higher levels of Fusarium mold in the soil. Glufosinate also appears to promote Fusarium growth, in that it kills a fungus that competes with Fusarium. More research is needed to determine whether the higher levels of herbicide applied to engineered corn also promote growth of the suspect molds, and whether these molds produce the substance causing pseudopregnancy.

Studies on mycotoxin levels in Bt versus non-Bt corn have yielded inconsistent results. Odvody found higher levels of one very potent mycotoxin (aflatoxin) on Bt corn versus non-Bt. Munkvold demonstrated higher levels of another mycotoxin (fumonisin) in non-Bt corn, but only when artificially infested with mold; in corn that was naturally infested, some Bt varieties showed higher fumonisin levels. For other mycotoxins (e.g. zearalenone, trichothecenes), there appears to be little or no difference in levels.

Whatever the cause of the pseudopregnancy outbreak, it must be solved in the interests of farmers and the public. USDA scientists have conducted initial investigations and requested that Mr. Rosman’s corn be saved for further scientific research. Planned or ongoing studies include further testing of the corn for estrogenic activity, as well as rat and swine reproduction studies. According to USDA scientists, swine feeding studies would require large quantities of corn. The USDA should secure this suspect corn to guard public health, protect farmers from suffering a fate similar to Jerry Rosman’s, and to help scientists solve the riddle of a potential new toxin in the environment.

Endnotes:

Open letter from Mark Rasmussen, Ph’D, Research Leader, Food Safety and Enteric Diseases, National Animal Disease Center, Agricultural Research Service, USDA.

Quoted in Block, Tom (2002). “Pseudopregnancies puzzle swine producer,” Iowa Farm Bureau Spokesman, May 4, 2002.

Whitlow & Hagler (2002). “Mycotoxins in feeds; feed quality,” Feedstuffs, No. 28, Vol. 74, July 10, 2002.

Chang et al (1979). “Effects of the mycotoxin zearalenone on swine reproduction,” Am. J. Vet. Res. 40(9), pp. 1260-67.

Whitlow & Hagler (2002), op. cit.

Peraica & Domijan (2001). “Contamination of food with mycotoxins and human health,” Arh Hig Rada Toksikol 52(1), pp. 23-35.

Kuiper-Goodman et al (1987). “Risk assessment of the mycotoxin zearalenone,” Regul. Toxicol. Pharmacol. 7(3), pp. 253-306.

Dees et al (1997). “Dietary estrogens stimulate human breast cells to enter the cell cycle,” Environmental Health Perspectives, 105 (Supplement 3), pp. 633-6.

El-Makawy et al (2001). “Genotoxic evaluation for the estrogenic mycotoxin zearalenone,” Reprod. Nutr. Dev. 41, pp. 79-89.

Block, Tom (2002), op. cit.

“Fumonisin Levels in Human Foods and Animal Feeds: Final Guidance,” Food and Drug Administration, Center for Food Safety and Applied Nutrition, November 9, 2001.

Whitlow & Hagler (2002), op. cit.

Beil, Laura (2001). “Corn toxin examined in border birth defects; diet may have put Hispanics at risk,” The Dallas Morning News, March 4, 2001.

FDA Guidance on fumonisin. See endnote xi.

Logrieco et al (1996). “Fusaproliferin production by Fusarium subglutinans and its toxicity to Artemia salina, SF-9 insect cells, and IARC/LCL 171 Human B Lymphocytes,” Applied and Environmental Microbiology 62(9), pp. 3378-84.

Ibid

To cite three of many studies: Shepherd et al (1999). “Production of the mycotoxins fusaproliferin and beauvericin by South African isolates in the Fusarium section Liseola,” J. Agric. Food Chem. 47(12), pp. 5111-5. Torres et al (2001). “Fusarium species (section Liseola) and its mycotoxins in maize harvested in northern Argentina,” Food Addit. Contam. 18(9), pp. 836-43. Castella et al (1999). “Effects of termperature, incubation period and substrate on production of fusaproliferin by Fusarium subglutinans ITEM 2404,” Nat. Toxins 7(4), pp. 129-32.

Harvey et al (2001). “Toxicity of moniliformin from Fusarium fujikuroi culture material to growing barrows [i.e. castrated pigs],” J. Food Prot. 64(11), pp. 1780-84.

Harvey et al (2002). “Toxicity of fumonisin from Fusarium verticillioides culture material and moniliformin from Fusarium fujikuroi culture material when fed singly and in combination to growing barrows,” J. Food Prot. 65(2), pp. 373-7.

Pineda-Valdes & Bullerman (2000). “Thermal stability of moniliformin at varying temperature, pH, and time in an aqueous environment,” J. Food Prot. 63(11), pp. 1598-601.

Logrieco et al (1998). “Beauvericin production by Fusarium species,” Applied and Environmental Microbiology 64(8), pp. 3084-88.

Munkvold et al (1998). “Occurrence of fusaproliferin and beauvericin in Fusarium-contaminated livestock feed in Iowa,” Applied and Environmental Microbiology 64(10), pp. 3923-26.

Markaverich et al (2002). “A novel endocrine-disrupting agent in corn with mitogenic activity in human breast and prostatic cancer cells,” Environmental Health Perspectives 110(2), pp. 169-77.

Block, Tom (2002), op. cit.; personal communication

Kremer et al (2000). “Herbicide impact on Fusarium spp. and soybean cyst nematode in glyphosate-tolerant soybean,” American Society of Agronomy publication. For abstract, see http://www.biotech-info.net/fungi_buildup_abstract.html.

Ahmad, I. (1995). “Effect of phosphinothricin on nitrogen metabolism of Trichoderma species and its implications for their control of phytopathogenic fungi,” Pesticide Biochemistry and Physiology 53(1), pp. 49-59.

Benbrook, Charles (2001). “Factors shaping trends in corn herbicide use,” AgBioTech InfoNet Technical Paper No. 5, July 23, 2001.

Odvody et al (2000). “Aflatoxin and insect response of near-isogenic Bt and non-Bt commercial corn hybrids in South Texas,” Presentation at Aflatoxin/Fumonisin Workshop 2000, October 25-27, 2000, Yosemite, CA.

Munkvold et al (1998). “Comparison of fumonisin concentrations in kernels of transgenic Bt maize hybrids and nontransgenic hybrids,” Plant Disease, Vol. 83, No. 2, pp. 130-38.

Bakan et al (2002). “Fungal growth and Fusarium mycotoxin content in isogenic traditional maize and genetically modified maize grown in France and Spain,” J. Agric Food Chem 2002, 50(4), pp. 728-31.