Vol. 6 No. 2 April 1986




On March 17th and 18th I was asked to visit Fayetteville, Arkansas to provide information on the biological fate of heptachlor in food animals. Less than a week before the trip, the FDA and the Health Department for the State of Arkansas had discovered violative residues of heptachlor and heptachlor epoxide in milk samples taken from local dairy farms. The contamination problem was quickly found to be widespread and Secretary of Agriculture Lyng appointed a Task Force to look into the problem. Because of my involvement with the Food Animal Residue Avoidance Databank (FARAD), I was asked to attend to help the Task Force and dairy farmers decide what to do. This newsletter is a report on the meetings held there and also provides information on how the contamination occurred.


The contamination problem occurred due to the indirect use of seed grain as animal feed. A local cooperative opened an alcohol production unit to make ethyl alcohol for use in "gasohol". Poor quality grains which would not normally be fed to livestock can be used efficiently for ethyl alcohol production. For many years, distillers have sold the "mash" left after fermentation as livestock feed. The gasohol plant found that this was necessary also in order to make a profit. The firm did so for a few years with no problems.

The gasohol producer was offered some moldy, aflatoxin contaminated grain for use in the process and checked with FDA about using it. They said it's fine to use such grain for ETOH production but it is not to be fed to livestock (aflatoxins are not significantly affected by the fermentation). This prompted FDA inspections to monitor the mash for aflatoxins on a routine basis. During the most recent inspection for aflatoxins, the inspector noted the presence of pink colored grains in the mash. This raised a red flag that seed grain had been used in the fermentation process. FDA thought the seed was treated with captan but analysis did not show captan residues. Analysis eventually revealed the presence of technical heptachlor, and FDA notified the Arkansas, Missouri and Oklahoma Health Departments.

Heptachlor had been used to treat the seed grain to prevent the seed's destruction by a worm during germination. EPA apparently cancelled heptachlor use on seed grain in 1983 with a provision to use up existing supplies. The gasohol producer had purchased large quantities of this treated grain because it was old and useless for crop production or as animal feed. It is not clear how much contaminated grain was used, nor is it clear just where the contaminated mash went as feed. The gasohol producer did not keep detailed records but it appears the mash was sold to dairy, beef, pork, chicken and turkey producers.

The mash left over after fermentation is usually a good quality feed. The levels of carbohydrates are reduced and thus the protein level is higher than in unfermented grain. There is considerable water in the feed (50-65%) and thus it usually is not economical to transport the material very far. In addition, the storage life of the mash is short (a week or less).

The Arkansas Health Department was faced with the prospect of having to monitor numerous small dairies. They started monitoring by sampling milk from route trucks that serviced up to six small dairy farms. If heptachlor epoxide (HE) was not found in the sample, all the dairies on the route were cleared. If HE was found, they all had to dump their milk until individual samples from each farm were analyzed. This resulted in some "clean" dairies being quarantined for up to 2 weeks until individual bulk tank analysis showed they were clean. (The tolerance for HE in butterfat is 0.1 ppm.) The levels of contamination found ranged from 0.1 ppm to over 50 ppm.

The dairy producers needed to know how long it would take to clean up their herds, and how to do it. FARAD contains considerable information on heptachlor and HE fate in dairy cattle and chickens. Much of the information was extracted from "older" literature and reanalyzed to determine the biological half-life. The information from different sources is remarkably consistent. The half-life of HE in milk from dairy cattle is 58 days. (Range of 45-65 for the beta phase.) In the first 2 weeks after removal of contaminated feed, the milk levels drop about 50%, and then the 58 day t 1/2 takes over. In lactating dairy cattle, milk excretion accounts for >95% of HE excretion. Urinary and fecal excretion is very low.

Using this data, we were able to draw up a table of values which would predict the time it would take to reach tolerance. The equation used to do this is as follows:

t = ln__Abo__

Abt = tolerance of 0.1 ppm
Abo = initial milk level ppm
kel = 0.693/58 days

This information will allow each dairy producer to make the economic decision about continuing to milk, or getting rid of the herd. In many instances of severe contamination, the time may be greater than 1 year.

There is some data available from studies of beef cattle contaminated with dieldrin. It is possible to clean-up beef cattle by inducing severe weight loss and subsequent reduction in body fat (starvation). Some of the producers with severely contaminated herds of prize cattle will probably try this procedure.


In 1982, the Hawaiian Islands experienced a heptachlor milk contamination problem. The University of Hawaii did a lot of work on the contaminated cows and Dr. Dick Stanley published some recommendations to share with the farmers. The first series of recommendations said the following:


1. Feed rations to contain 18% crude fiber and 68-70% total digestible nutrient on a dry matter basis. The 18% crude fiber will stimulate milk fat synthesis and the 68- 70% total digestible nutrient energy level will provide adequate energy for optimum milk production.

2. Feed long hay if available at a minimum of 5 lbs per animal per day to stimulate higher milk fat secretion.

3. Feed whole cottonseed if available at levels of 8 to 9 lbs per animal per day. Animals fed whole cottonseed will have higher milk fat tests and the fat in the whole cottonseed will assist in the elimination of fat soluble materials in the animal's body.

4. Inject animals every other week with vitamin ADE mixture. Animal to receive 2 million units of vitamin A at each injection. Watch for vitamin A toxicity which show similar symptoms to vitamin A deficiency especially watery eyes followed by the eyes becoming cloudy.

5. Other materials fed as mechanical antidotes such as mineral oil and vegetable fat, calcium salts or bentonite as well as activated carbon with or without drugs such as phenobarbital are only very weakly effective after the animal has received the chlorinated hydrocarbon. The above materials are effective for acute poisoning when the animal eats large amounts and the material is still in the stomach and intestines. However some testing and searching is ongoing and if any of these look promising I'll let you know.

Based on FARAD literature on heptachlor elimination, I agree with these recommendations, especially for cattle whose milk level is below 2-5 ppm. There is some evidence in the literature that both activated charcoal (AC) and mineral oil (MO) may increase the fecal excretion of HE. The effect of these substances on milk levels of HE is not great. Since good data is not available on the effect of AC or MO on the rate of elimination of HE in milk, I made no recommendation for their use. Some of the dairy farmers were already trying either MO or AC, and perhaps some data will become available from their use. Phenobarbital has been suggested as a treatment to enhance the metabolism of heptachlor in the cattle. Phenobarbital would hasten the conversion of heptachlor to HE (which is what is stored in fat) and thus no benefit would be seen. Even if phenobarbital did work, the logistics and expense of handling large quantities would be impractical because it is a DEA controlled substance.

The problem for the dairy farmers is money. The federal indemnity program that helped dairies in Hawaii has virtually no money left. The Task Force is likely to recommend bolstering this fund to help the farmers. I have also heard suggestions that the government buy the contaminated herds and help the dairies replace their animals.


The milk containing >0.1 ppm HE in butterfat is being dumped to prevent human consumption. HE was detected at a level of 0.08 ppm in a composite sample of human breast milk in Arkansas and the Arkansas State Health Department told nursing mothers to stop nursing and feed formula. There are thousands of people in Arkansas who perceive that they have been poisoned. FDA representatives said that they don't think the milk represents an acute human health hazard. The 0.1 ppm tolerance was set on the basis of chronic health effects (based on the "possible" carcinogenicity of heptachlor in mice, negative in rats). It is difficult to convey the uncertainty of this data to the public. The level of 0.1 ppm in butterfat translates to 0.004 ppm (based on 4% butterfat in milk). Many people do not want any HE in milk and thus would just as soon slaughter all contaminated animals. In light of the emotionality of this whole incident, reason breaks down. (As usual with open meetings of this type, there was a nursing mother present who didn't want any HE contamination, and who is worried about her child's development; and an old fellow who said that as a child he and his whole family ate potatoes that tasted of heptachlor, and it didn't hurt them at all. Such polarized views usually do little to help arrive at a reasonable position on the problem, and often overshadow reason if there is any to be found.)

Although no solutions were found to any of the problems caused by this contamination, the meetings did help to inform the Task Force about the problems the dairies face, and helped to inform the dairies of the magnitude of the problem, how long it may take to clear up, and what mechanisms may be useful to enhance elimination (none). It also provided FARAD with the opportunity to help with the mitigation of a major pesticide contamination problem.

If you would like references for the toxicokinetic data mentioned in this newsletter, please write to me: c/o FARAD, Ext. Vet. Med., University of California, Davis, CA 95616.

Arthur L. Craigmill
Toxicology Specialist