(7aR, cis)3,4,7a,9,10,10a-Hexahy-dro-5-methoxy-1H,12H-furo-(3'2',:4,5)furo(2,3-h)pyrano-(3,4-c)(1)chromen-1,12-dion

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

SMALL SPILLS AND LEAKAGE: If a spill of this chemical occurs, FIRST REMOVE ALL SOURCES OF IGNITION, then you should dampen the solid spill material with acetone and transfer the dampened material to a suitable container. Use absorbent paper dampened with acetone to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with acetone followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: Criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

Chemical treatment: Any chemical detoxification must reduce the mycotoxin level to within limits set by proper regulatory agencies, must have no toxic residues, and should not decrease the nutritive value of the treated commodity. These restrictions as well as simple economic considerations have narrowed the types of chemical agents likely to achieve significance in a commercially scaled detoxification process. Chemicals having good promise in this regard can be classified simply as oxidizing agents, acid, and bases. Of oxidizing systems that destroy all the aflatoxin only hydrogen peroxide has shown promise to detoxify foods and feeds. ... Aqueous suspensions of peanut meals containing 90 ppm aflatoxin /were treated/ with 6% soln of hydrogen peroxide at pH 9.5 for 30 min at 80 °C. The treatment destroyed 97% of the toxin ... . The use of acids as detoxifying agents has a definite potential in the recovery process of free fatty acids from commercial soapstock prepn. The use of inorganic and organic bases affords an efficient and relatively inexpensive means to achieve aflatoxin destruction or removal from large quantities of contaminated agricultural commodities. The refinement of edible oils is a classic example of the use of bases under conditions that would destroy or remove aflatoxins.

Administration of phonobarbital enhances hepatic transformation activities and also protects against AFB-induced toxicity, carcinogenicity and DNA binding in vivo. In cases of ingestion, feeding large quantities of an adsorbent such as activated charcoal may be used. Antioxidants such as ellagic acid and inducers of some cytochromes P450, such as indole-3-carbinol, may give a protective effect. (A704, L1879)

The main target organ in mammals is the liver so aflatoxicosis is primarily a hepatic disease. Protracted exposure to aflatoxins may cause liver damage and necrosis, cholestasis, and hepatomas. Moreover, protracted exposure to aflatoxins has been associated with hepatocellular carcinoma, acute hepatitis, Reye's syndrome, bile duct cell proliferation, periportal fibrosis, hemorrhages, mucous membrane jaundice, fatty liver changes, cirrhosis in malnourished children, and kwashiorkor. However, aflatoxins accumulate in the presence of liver disease, and the association with hepatic cancer is confounded by the occurrence of hepatitis-B. Thus, it is not clear in these various instances whether aflatoxin is a primary cause of the disease, is an innocent bystander which accumulates secondary to the disease process, or is a contributing cause in conjunction with other factors. It is also mutagenic and teratogenic. Inhaled aflatoxins may produce pulmonary adenomatosis. Aflatoxins modify the immune system by affecting antibody formation, complement, cell-mediated immunity, and phagocytosis. (A704, L1956)

LD50 Duckling (day old) oral 172.5 ug/50 g body wt

LD50 Duck oral 2450 ug/kg

TERRESTRIAL FATE: Based on a classification scheme(1), a Koc range of 682 to 2.3X10+4 for analogous aflatoxin B1(2), indicates that aflatoxin G2 is expected to have low to no mobility in soil(SRC). Volatilization of aflatoxin G2 from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.1X10-14 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Aflatoxin G2 is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 7.7X10-11 mm Hg at 25 °C(SRC), determined from a fragment constant method(4).

AQUATIC FATE: Based on a classification scheme(1), a Koc range of 682 to 2.3X10+4 for analogous aflatoxin B1(2), indicates that aflatoxin G2 is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 1.1X10-14 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 3(SRC), from an estimated log Kow of 0.71(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), aflatoxin G2, which has an estimated vapor pressure of 7.7X10-11 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase aflatoxin G2 may be removed from the air by wet and dry deposition(SRC). Aflatoxin G2 absorbs UV light at wavelengths of 256 and 363 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

Commercially available market basket samples were collected in Tokyo, Japan during 1986 to 1990; aflatoxin concentrations were determined in 3054 samples (803 samples of cereals, 540 samples of nuts, 540 samples of beans, 564 samples of spices, and 607 samples of other foods)(1).

Aflatoxin G2 concentrations of 6 to 96 ug/kg were reported in peanut cake samples. The limit of detection was 2 ug/kg. Food samples were obtained from markets in the Republic of Benin, West Africa(1). A market-basket survey of 296 food samples was conducted in Campinas, Brazil between May 1985 and June 1986. Aflatoxin G2 was detected in popcorn, polished rice, dried carioquinha bean, and dried mulatinho bean at contamination levels of 32, 38, 39, and 52 ug/kg, respectively(2).

Aflatoxins produce singlet oxygen upon their exposure to UV (365-nm) light. Singlet oxygen in turn activates them to mutagens and DNA binding species. Aflatoxin metabolites can intercalate into DNA and alkylate the bases through their epoxide moiety, binding particularity to N7-guanine bases. In addition to randomly mutating DNA, this is thought to cause mutations in the p53 gene, an important gene in preventing cell cycle progression when there are DNA mutations, or signaling apoptosis. (L1877, A2859, A2972)

Aspergillus strains were isolated from municipal solid waste compost from a municipal solid waste composting plant in Grenoble, France. The waste was cultured on sucrose yeast extract medium. Aflatoxon G2 produced by A. parasiticus was recovered from the first stage of composting; mycotoxin quantification 40 ug/L(1).

PRECAUTIONS FOR "CARCINOGENS": Whenever medical surveillance is indicated, in particular when exposure to a carcinogen has occurred, ad hoc decisions should be taken concerning ... /cytogenetic and/or other/ tests that might become useful or mandatory. /Chemical Carcinogens/

Koc values of 23170, 1570 and 682 were calculated(SRC) from Freundlich's adsorption coefficients of 238.49, 76.19 and 17.40 mg/kg soil, respectively, for analogous aflatoxin B1 in a silty clay loam (pH 7.3, 0.597% organic matter, CEC of 18.0 cmol/kg), a silt loam (pH 5.8, 2.818% organic matter, CEC of 11.7 cmol/kg) and a sandy loam (pH 6.0, 1.478% organic matter, CEC of 5.4 cmol/kg), respectively(1). According to a classification scheme(2), these Koc values suggest that the aflatoxins may range in mobility from low to immobile depending on the soil. Cation exchange capacity was positively correlated with the adsorption coefficient value(1). In addition, the type of clay (2:1 expanding clays were found in the silty clay loam) appears to influence the amount of adsorption to soil(1).