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Residual effects of Dichloro-Diphenyl-Trichloro Ethane (DDT) in Poultry Diets

S.Venkata Rama Rao & N.K. Praharaj
Project Directorate on Poultry, Hyderabad .

About 85-90% of Poultry feed consists of food grains or the by products from plant source only. The increased food grain production has become more dependants on the use of synthetic chemicals to control insects or pests. At the same time the use of these chemicals in modem land and water management has posed a potential health hazards not only to livestock and poultry but to human beings also. Amongst the several chemicals used to control pests and insects contamination of stored food grains, DDT is being used widely. If proper care is taken during application of this chemical to control the diseases of plants, no residue could be detected in grains, the residual episodes usually follow due to errors in dosage rates, dosing with undesirable combinations of Chemotherapeutic agents. Narsinga Rao (1990) analyzed the residual DDT content in several feed ingredients used in poultry and livestock nutrition and observed that the residual amounts were much higher in maize, grains, brains, feed mixtures, eggs and livestock feed (0.049, 1.0, 0.24, 8.01, and 3.38 ppm respectively) than the maximum permissible levels fixed by FAO/WHO (0.10,0.10,0.10, 0.50 and 0.10 ppm respectively). The main purpose of this article is to discuss the residual effects of DDT in poultry production, starting from the mechanism of its action, symptoms of DDT toxicity, and also the residual effects of DDT on egg and meat production, shell thickness, fertility, hatchability, mortality and mechanism of its excretion.

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Mode of Action and Toxicity:-

DDT (Dichloro-Diphenyl Trichloro Ethane) was synthesized by Zeilder in 1874. Since then it has been widely used to control insect populations on farms around houses, and also to treat ectoparasites on poultry. It is soluble in fat solvents, and readily absorbed through the skin. Absorption from vegetable oil suspensions is 10 times greater than from mineral oil suspensions (Clarke and Clarke 1967), but absorption from the digestive tract is poor (Saint Omer 1970).

The mode of toxicity of the DDT is not known clearly, but it influences the efflux of potassium ions from the axon of nerves, Subsequently it was established that DDT inhibits Na+, K+, Mg++ and ATP-ase activity in the nerve ending. This enzyme is involved in ion transport in the nervous system. A good correla­tion between the degree of its inhibition by analogs of DDT and their toxicity has been observed in mosquito larvae. The DDT toxicity in chicken are nervous disorders such as hyper excitability and tremors (Rosenberg and Adler 1950). There are no typical necropsy findings. Affected birds may have signs of trauma. In lingering cases effected birds may be emaciated due to anorexia (Robinson et al. 1967). Ultra structural studies have shown that there are sig­nificant changes in nerve cells (De Los Reyes and Moral 979).

Symptoms of Toxicity:-

Manifestations of DDT toxicity in layers are loss of weight, moulting, cessation of lay, marked tremors, ataxia, downward bending of the neck, and a marked tendency to rest on the hocks or lie on their sides. Chick’s manifest nervous signs, hyper excitability and fine tremors.

Ingestion of 400 ppm DDT in the feed for 30 days resulted in 50% mortality in the adult quails (Smith etal. 1969).

Effect onEgg Production:-

Feed containing 310 ppm DDT led to a significant drop in egg production (20%) in laying hens within a month, and 2500 ppm caused a 70% drop in 30 days and almost 100% within 60 days. (Rubin et al. 1968). Armbrecht and Dewitt (1963) indicated that the Japanese quail may be intermediate in pesticide sensitivity compared to Bob White quail, ring neck pheasants and other wild birds. Cross et al. (1962) found that up to 300 ppm DDT had no effect on egg weight or egg production, but 700 ppm resulted in Zero per cent egg production.

Effect on Egg Shell Thicknespread use of chlorinated hydro­carbon pesticides, particularly DDT, has been correlated with a decrease in the egg shell thick­ness of aquatic birds (Onlendorf et al. 1978). In 1970, Smith et al. reported egg shell thickness in White leghorn hens fed 10 ppm DDT in the diet. There were changes in the physical characteris­tics of the egg shells, including reduced porosity which may be associated with reduced hatchability.

Residual Storage in Body Fat and Egg Yolk:-

As the DDT is a fat soluble chlorinated hydro carbon, it tends to accumulate in the fatty tissues of hens and in the egg yolk. Stadelman et al. (1965) found that exposure to the equivalent of 10 to 15 ppm DDT resulted in 4-6 ppm residue in the egg yolk. The residue remained for 26 weeks after removal of the pesticide from the diet. Smith etal. (1970) found that l0 ppm DDT ingestion for two months resulted in 117 ppm of both DDT and its metabolite. DDE, DDT in the fat and 5.0 ppm in the yolk. The amount of residue deposited per unit weight of a bird may differ in layers and broilers. Liska et al. (1965) reported that low levels of DDT (less than 1 ppm) in the ration resulted in higher residue levels in broilers than in mature laying hens. This might' be due to higher rate of tissue formation in broilers than by laying hens. and it would also possible mat the laying hen has a mechanism for excreting fat soluble contaminants through the egg yolk, whereas the broiler cannot effectively excrete these contaminants. The amount of DDT deposited was twice (358 ppm) to its metabolite DDE (184 ppm) in egg yolk of quail, fed400 ppm DDT for 60 days (Smith et al. 1969).

Effect on Fertility and Hatchability:-

Jones and summers (1968) concluded from studies with Japanese quails that eggs could carry sufficient quantities of DDT or its metabolites to cause high chick mortality after hatching. Sauter and Steele (1972) reported that even 0.1 ppm DDT significantly reduced hatchability due to increased embryonic mortality throughout the incubation period. Rubin et al. (1968) observed that hatchability of chicken eggs was impaired by 0.062% DDT (620 ppm) in the diet. Health et al. (1969) reported that concentrations of 10 and 40 ppm of DDE in feed severely impaired reproduction in Mallard ducks. Zero hatchability was resulted when 500 ppm DDT was fed to Japanese quails (Smith et al. 1969).

Methods to Overcome the Residual Toxicity:-

Contamination of animal feeds with extremely low levels of chlorinated hydrocarbon insecticides results in significant residues of these materials in the tissues. Many factors which affect pesticide metabolism have been studied in order to develop methods to hasten pesticide depletion from body tissues of poultry. Wesley et al. (1969a) showed that hens exhibited detectable DDT residues 22weeksafterdosing. Wesley et al. (1966b) presented data which suggested that starvation increased the depletion rate of DDT from the tissues.

The effects of forced molting and dietary protein levels on pesticide depletion were studied by Wesley et al. (1966a). They found that forced molting followed by feed restricting to 20% of normal intake of a high protein diet resulted in higher pesticide depletion rates than the same procedure with a low protein diet or a control diet with no forced molting. Donaldson et al. (1968) found that fat depletion by starvation resulted in increase in concentration of the DDT in the remaining body fat due to a lack of dilution by the deposition of new fat tissue. The interaction between dietary calcium and DDT was studied by Bitman et al. (1969) and they found that, DDT and DDE caused a greater reduction in egg shell thickness when fed to Japanese quail in a diet deficient in calcium, Cecil et al. (1971) observed the reduction was much less when birds fed adequate calcium diet. Lesser amount of residue was deposited in the fat of pullets fed high calcium diet (3.5%) that the pullets fed low calcium diet (1.5%).


Commonly DDT is being used either to control pest infestation or as a preservative in food grain storage. Improper dosage may lead to accumulation of some quantum of this pesticide in food grains, which is turn leads to decrease in egg production, reduction in egg shell thickness, fertility, hatchability of eggs. However accumu­lation of DDT or its metabolite DDE, in both body fat and egg yolk is another concern to human health. The residual toxicity can be re­duced or minimized by dilution of contaminated feed ingredient with pesticide free feed ingredient, high protein diet, starvation, forced molting or by giving optimum level of calcium in diet.