Technical DDT Research Articles

Studies on the chemical control of the mirid bug, Helopeltis antonii Sign, in the cashew

Laboratory and field studies were made to investigate the toxicity, mode of action, and persistence of technical DDT and y BHC when applied to the cashew in Sri Lanka to control the mirid bug, Helopeltis antonii Sign. The insecticides were tested at concentrations previously used in field trials. Mirid nymphs were placed on the nuts and the rate of knockdown and mortality after exposure for a test period was recorded. These tests showed that BHC had a higher toxicity and acted more quickly than DDT. BHC had a powerful and transient fumigant action over DDT, which had no fumigant effect at all. Persistence was studied by treating cashew leaves and nuts growing under natural conditions and then testing the residual deposit at intervals. It was concluded that BHC would be more effective than DDT when treating mature cashews because, in addition to its higher toxicity and quicker action, its fumigant action would compensate for incomplete coverage by low-volume spraying.

Effects of DDT and its metabolites on the adrenal gland of Japanese quail

The effects of the ingestion of technical grade DDT, p, p′-DDT and p, p′-DDE on the weights and histological and histochemical structure of the adrenals of male and female Japanese quail were studied. The adrenal weights in all treatment groups showed a tendency to increase, as also did the percentage of the adrenals' cortical tissue. No changes were detected in the nuclear size of the cortical and medullary cells. The lipid content of the interrenal cords remained constant during the experiment. A stimulation of the adrenal cortex by DDT and its metabolites via a hyperplasia is discussed.

DDT and Metabolite Accumulation in Adrenal, Liver, and Brain of Broiler Chickens

Four-week old broiler chickens were fed rations with varying levels of technical grade DDT for a 4-week period. DDT and metabolite concentrations were measured in adrenal, liver, and brain. Accumulations per gram of tissue were greatest in the adrenals, followed by those in the liver, then in the brain.All birds fed 2700 p.p.m. of DDT died within 12 days after beginning feeding, and moderate signs of toxicity, such as ataxia and trembling, appeared in those fed 900 p.p.m. Although both DDT metabolites, p,p′-DDE and p,p′-DDD, were found in the tissues, the higher levels of the former indicated that the aerobic conversion of DDE occurs more readily than the anaerobic conversion. Significant quantities of o,p′-DDT appear only in tissues of birds fed high levels of the technical grade DDT.

Carcinogenicity of DDT (dichlorodiphenyl trichloroethane) in pure inbred Swiss mice.

Inbred Swiss mice were treated with technical DDT (1) orally with the diet or by intubation; (2) subcutaneously and (3) by skin painting. The total duration of the experiment was 80 weeks. There was no difference in body growth and mortality between the experimental and control groups. Toxic manifestations of DDT were observed in treated mice in the form of tremor, convulsions and corneal opacity usually after 40 weeks. Oral and subcutaneous DDT treatment resulted in a significant increase in the incidence of tumours mainly of lymphoid tissues, lung and liver. The highest tumour incidence was recorded in the group of mice receiving DDT by subcutaneous injections. Males and females were equally susceptible. No evidence of carcinogenicity was observed in the painted group.

Sensitivity of the alga [formula omitted][formula omitted] to some pesticides

Indoor cultures of the green alga Scenedesmus acutus were tested for sensitivity to varying concentrations of seven insecticides and three fungicides. The growth rates of the organisms were considerably reduced by BHC and DDT analogues even at low concentrations of 500 ppb and 1 ppm. Lindane above 5 ppm and Technical BHC and DDT at 100 ppm were lethal to this alga. Of the three fungicides, TMTD (Tetra Methyl Thiurum Disulfide) was most toxic resulting in death of the culture at 10 and 100 ppm. Blitox (Copper-oxy chloride) and Zineb (Zinc Ethylene-Bis dithiocarbamate) considerably retarded growth at all concentrations. This alga was more sensitive to Lindane, BHC (Technical), DDT and TMTD. The growth rate appeared to be influenced by the concentration of pesticide present in the algal culture. As Scenedesmus acutus is being considered as a source of Single Cell Protein (SCP) for human consumption, knowledge on the sensitivity of this alga to pesticide contamination will be useful.

Long-term administration of DDT or phenobarbital-Na in Wistar rats.

In lifespan studies, outbred male and female Wistar rats were given either technical DDT mixed into the diet at a dose of 500 parts per million (ppm) or phenobarbital-sodium dissolved in drinking water at a dose of 500 ppm. Liver-cell tumors developed in treated animals but not in controls. The incidence of liver tumors was 45% in the DDT-treated group and 44% in the phenobarbital-sodium-group. When evaluated by sex, DDT-treated females and males had incidences of 56% and 35%, respectively, while in the phenobarbital-sodium group, the respective incidences were 32% and 59% in females and males. These data show a varying susceptibility between the sexes, with regard to induction of liver-cell tumors by the two compounds. In both treated groups, the number of nodular tumors per rat and the average size increased with age and were greater in females. None of these tumors and metastasized. Histologically, the liver tumors were nodular growths, which compressed surrounding parenchyma did not infiltrate it. The total incidence of extrahepatic tumors was higher in controls than in treated animals. In this connection, we must mention the apparent, but not significant, reduction of adrenal tumors in treated rats compared to the controls.

Dosage relationships associated with DDT in milk

Separate reports imply that DDT is more toxic to infant rats if they receive it via their mothers' milk rather than via stomach tube. Therefore, the effect of DDT in milk was reinvestigated, and the study was expanded to include dosage-response measurements. The results were consistent with earlier findings that young rats are no more susceptible than adults to poisoning by DDT and may be more resistant, depending on circumstances. A comparison of isomers and potential metabolites in technical DDT and in tissues indicated either lack of absorption or rapid excretion of o,p′-isomers, resistance of the blood-brain barrier to o,p′-DDT, and the increase of DDD and DDE through metabolism. The concentration of DDT in the brains and whole bodies of pups from dams dosed at 200 mg/kg/day was higher than would be predicted by extrapolation from lower dosages, suggesting relative inability of the dams to metabolize and eliminate the compound at a dosage fatal to some of them. However, the highest brain level for a pup that died following dosing of its mother was 44 ppm, compared to 83 ppm (the highest level for a surviving pup of the same kind) and compared to 132–177 ppm (the range for pups killed by DDT administered to them by stomach tube). A slight deficiency of weight gain and significantly less stomach contents of pups of mothers treated at 200 mg/kg/day indicated their relative failure to feed although their mothers produced adequate milk. Based on the concentration of DDT in rat milk and on the amount of DDT measured in litters fed exactly 24 hr, it was calculated that rats secreted milk at the rate of 26.6 and 34.5 ml/dam/day when DDT was administered ip and op, respectively. Based on the analyses of litters, the dams secreted into their milk 12.6 to 30.2% of the DDT administered to them, the mean being 24.6% in those receiving the compound from their diet at an average rate of 32.4 mg/kg/day. The concentration of DDT in the milk of rats receiving DDT at a dietary level of 200 ppm was far higher than any level reported for human milk. Infants are in no danger from DDT in their mothers' milk unless the dosage of the mother is one that approaches, or perhaps reaches, a level toxic to her.

Prolonged ingestion of commercial DDT and PCB; effects on progesterone levels and reproduction in the mature female rat

A report linking human polycystic ovary with increased exposure to environmental DDT (Heinrichs et al. 1971) prompted the present study comparing effects of PCB and DDT or their combination on reproduction in female rats under more realistic conditions with respect to level (75 and 150 ppm), route of administration (dietary contaminant), and period of exposure (8 and 36 weeks). Evaluation of estrous cycle length, mating frequency, number and size of litters; as well as plasma levels of DDT, PCB, progesterone (P), and 17 alpha=hydroxyprogesterone (17 alpha=OH-P), permitted comparison of short and long term reproductive changes from ingestion of two levels of DDT and/or PCB. PCB reduced plasma progesterone (p less than .01) while plasma 17alpha OH-P was unchanged by PCB or DDT. High DDT and PCB abolished reproduction. Histologically, distinct ovarian stromal changes accompanied 150 ppm of PCB, while increased numbers of more prominent follicular cysts were evident with 150 ppm of DDT. Although DDT and PCB generally reduced or abolished litter production, no treatment tested significantly altered litter size. Long term chronic ingestion of more realistic levels of technical DDT (85% p,p', 15% o,p'-DDT) in these studies did not lead to polycystic ovaries in adult rats comparable to those reported following i.v. administration of pure o,p'-DDT to immature rats. Plasma DDT levels above 800 ppb are clearly detrimental to reproduction, while levels below 500 ppb had lettle effect. Finally, we present the first evidence reported to our knowledge demonstrating that prolonged ingestion of PCB (150 ppm) markedly reduces reproduction (p less than .05) accompanied by significantly reduced progesterone in plasma (p less than .01) as well as by histologically characteristic ovarian stromal changes not seen with DDT alone.

Influence of high levels of DDT in the diet on liver microsomal estrogen metabolism in the laying hen.

Two experiments were conducted with laying hens to evaluate the effect of technical grade DDT on estrogen metabolism by liver microsomes using an assay which measured the metabolism of estradiol-17beta-4-14C. In Experiment I feeding 500 ppm DDT in the diet had no significant effect on estrogen metabolism after 10 days. However, the metabolism was increased after 18 days and more than doubled after 51 days. In Experiment II hens were fed diets containing 0, 300, 600 or 1200 ppm DDT and estrogen metabolism by liver microsomes was examined at 0, 7, 14, 21 and 35 days. A significant increase in estrogen metabolism was seen at 14 days with the feeding of 600 or 1200 ppm DDT and at 21 days with 300 ppm DDT. The ability to metabolize estrogen reached a maximum increase of approximately two-fold in all hens fed DDT. This required 14 days when the birds were fed 1200 ppm DDT, 21 days when fed 600 ppm DDT and 35 days when fed 300 ppm DDT. The increase in estrogen metabolism caused by DDT was found to be dose and time dependent.

Toxicity of high dietary levels of DDT in laying hens.

White Leghorn hens were fed diets containing 0, 300, 600, or 1200 ppm technical grade DDT for three 28-day periods. The 1200 ppm diet caused tremors and 33% mortality in the final period, but no gross toxicity symptoms were seen in birds fed the other diets. Egg production was decreased during the third period by 600 or 1200 ppm. Egg weight was decreased during the third period by 600 or 1200 ppm. Egg weight was decreased during the last two periods by 1200 ppm. Shell thickness was decreased in all three periods by feeding 600 or 1200 ppm DDT. Dietary DDT caused no change that could be detected by shell beta backscatter. Shell weight as a percent of total egg weight was decreased by 600 or 1200 ppm DDT.

DDT and DDE Effects on Migratory Condition in White-Throated Sparrows

The onset of spring migratory condition, as measured by Zugunruhe and weight increase, was delayed at least 1 week in caged white-throated sparrows (Zonotrichia albicollis) fed diets containing 5 or 25 ppm technical DDT. Migratory fat stores, determined by extraction from birds sacrificed early in the migratory period, showed a dose-dependent depression which was statistically significant only at the high dose level. Late in the period there were indications of increased Zugunruhe in treated birds. In the high treatment group, this increased activity was significantly (P < 0.05) correlated with the log of body concentration of DDE, a metabolite of ingested DDT. A similar experiment with birds fed DDE produced no effect early in the spring migratory period. Late in the period, Zugunruhe showed significant and dose-dependent increases. Daytime activity was not significantly altered. J. WILDL. MANAGE. 39(3):520-527 Several sublethal effects of organochlorine pesticides on avian reproduction, physiology, and behavior have been documented (see Pimentel 1971 or Stickel 1968 for recent reviews). Although physiological components important in the initiation or maintenance of migratory condition are known to be altered, there is no published information on the possible effects of pesticides on migratory behavior or physiology. These pesticide-sensitive components include gonadal hormones (Peakall 1967, 1969, 1970), adrenal hormones (Meier and Martin 1971, Newcomer 1959, Srebocan et al. 1971), storage fat (Keith 1970, Tinsley and Lowry 1972), and the thyroid (Jefferies 1969, Jefferies et al. 1971, Jefferies and French 1972). According to Wilson and Farner (1960) the thyroid does not function in normal control of the migratory cycle. However, thyroid dysfunction could affect the positive energy balance needed for storage of migratory fat. Ulfstrand et al. (1971) indicated that chemically similar pol chlorinated biphenyls (PCBs) increased migratory activity of caged European robins (Erithacus rubecula) in a twonight test. This study was undertaken to determine if spring migratory condition was affected in caged white-throated sparrows fed diets treated with either technical DDT (78.9 perc nt p,p'-DDT, 21.1 percent o,p-DDT) or p,p'-DDE at 5 and 25 ppm, dry weight. The research was not designed to determine causes of a possible effect. The DDT study was conducted in spring, 1970, and the DDE study was made during the following spring. I thank E.P. Odum and C.W. Helms for their encouragement and advice and T. Richardson for assistance with statistical

Dieldrin and DDT effects on reproduction and some hepatic mixed-function oxidases in the mallard duck.

Mallard ducks were fed 2, 20, or 200 ppm of technical DDT or chemically purep,p′-DDT, or 1, 5, or 10 ppm of dieldrin for 343 days, which included parts of two laying seasons. All 18 ducks fed 200 ppm ofp,p′-DDT and 17 of 18 ducks fed 200 ppm of technical DDT died during the experiment. The insecticides did not affect fertility or hatchability significantly. Tremors were exhibited by hatchlings from eggs laid during the second laying season by ducks fed ten ppm of dieldrin and from the one remaining duck fed 200 ppm of technical DDT. Liver weights or hepatic microsomal aniline hydroxylase and aminopyrineN-demethylase activities were not significantly affected in either ducklings or adults by the insecticides. Cytochrome P450 concentration in hepatic microsomes of ducklings was increased significantly by feeding 200 ppm of DDT or ten ppm of dieldrin. Pesticide residues in eggs were variable but were higher the second season than the first and were dose dependent.

The accumulation and distribution of pp′DDT and related compounds in an apple orchard .I. residues in the soil

AbstractSoils from an orchard sprayed annually (1953‐1969) with technical DDT (77% pp′DDT and 22 % pp′DDT) were analysed for residues from 1964 until 1969. The amount of DDT found after 17 years was 21 %pp′DDTout of 27.1 kg/ha applied, and 7 % of pp′DDT out of 7.6 kg/ha. The vertical distribution of residues (pp′DDT, pp′DDE, pp′TDE and pp′DDT) showed a linear relationship between log amount and depth, with approximately 80% in the top 10 cm of soil. At depths from 50 to 210 cm, residue values were too small to be determined (i.e. &lt; 1 ng/g dry wt). The surface distribution in the orchard showed a systematic pattern of circular areas of residues, with maximum values centred at each trunk (7.5 μg/g) and decreasing rapidly to each alley (1.9 ug/g). The levels of pp′DDT had reached a steady state (3‐4 kg/ha) and the half‐life time was calculated as 3.0 j′ears. pp′DDE (1.8 kg/ha) was the main metabolite of pp′DDT. Small amounts of pp′TDE were also found, pp′DDT was less persistent than pp′DDT, with a half‐life time of 1.5 years.

Effect of Flooding and Organic Matter Applications on DDT Residues in Soil

AbstractA field in Coachella Valley, California which had received repeated applications of technical DDT to sweet corn (Zea mays L.) for ear worm [Heliothis yea (Boddie)] control was flooded 48 days, with and without organic matter amendments, to determine whether DDT soil concentrations could be effectively reduced. Applications of 180 and 45 metric tons/ha of feedlot manure and 18 and 5.6 metric tons/ha of alfalfa (Medicago sativa L.) meal were disked to a depth of 15 cm. Redox potentials in all flooded plots rapidly dropped below −150 mV at both the 7.5‐ and 15‐cm soil depths. All flooded plots including control plots showed a rapid decrease in soil levels of DDT isomers accompanied by a rapid accumulation of the respective DDD isomers in the top 15 cm. Flooding had little effect on the DDE isomers. By the end of the flood period p,p′‐DDT had decreased from 8.1 µg/g to 0.5 to 1.6 µg in flooded plots receiving organic amendments while the p,p′‐DDD level increased from zero to 4.2 to 5.6 µg/g. The rates of disappearance of DDT and the formation of DDD were significantly lower in the flooded plots receiving no organic amendments. After 18 days flooding the rates of p,p′‐DDT losses and DDD gains were in the order of 180 metric tons/ha manure ≃ 18 metric tons/ha alfalfa &gt; 5.8 metric tons/ha alfalfa ≃ 45 metric tons/ha manure &gt; control. The transformation of DDT isomers to DDD isomers occurred to a lessor extent at 15–30, 30–45, and 45–50 cm soil depths. The data indicate that flooding organic matter‐amended soil effectively reduced DDT concentrations to very low levels. The fate of DDD in flooded soils is unknown. However, through the formation of DDD, the conversion of DDT to the potentially hazardous DDE is prevented.

DDT thins shells of eggs from mallard ducks maintained on ad libitum or controlled-feeding regimens.

Mallard ducks were fed diets containing various levels of technical DDT or chemically purep,p'-DDT, or dieldrin. Either technical DDT orp,p'-DDT at 20 ppm or greater, or dieldrin at 10 ppm caused a statistically significant reduction in eggshell thickness, weight, and calcium. Shells of eggs from ducks fed 40 ppm ofp,p'-DDT were about 20% thinner than those from control ducks, and shells of eggs from ducks fed 10 ppm of dieldrin were about 6% thinner than those from controls. The reduction in eggshell thickness was linear with increasing dose of DDT to 40 ppm, and with increasing dose of dieldrin through all levels studies. Eggshell thinning occurred regardless of whether the diets containing DDT were fed underad libitum or controlled conditions. DDT fed at 200 ppm was lethal to the ducks. Neither DDT nor dieldrin affected weight of the eggs or rate of egg production.

Immune Response in Broilers Fed Technical Grade DDT

Four experiments were conducted using White Rock males. Beginning at four weeks of age, mash containing levels of technical grade DDT up through 625 p.p.m. was fed ad libitum. At six weeks the chicks were inoculated intravenously with either killed Salmonella pullorum (SP) or a purified Bovine Serum Albumin (BSA) antigen. SP antibody titers were determined on sera collected every 48 hours for two weeks and BSA antibody titers were measured using sera collected every 72 hours for a three-week period.Under the conditions of these experiments, ingestion of technical grade DDT did not consistently influence the antibody titers to SP or BSA of these chickens. At only the sixth day post-inoculation of one experiment was there a difference among treatments. At that time SP titers were significantly higher in birds receiving 50 p.p.m. than in those receiving 0 or 500 p.p.m. DDT.In a fifth experiment 0 to 2700 p.p.m. technical grade DDT was fed to four-week-old chicks. All birds fed 2700 p.p.m. died within 12 days after starting on the treated feed. Despite outward signs of toxicity in birds fed 900 p.p.m., a significant difference in antibody response to SP antigen was not observed.

Fertility, Hatchability and Progeny Performance of Laying Hens Fed High Levels of DDT in the Diet

Three groups of White Leghorn hens were fed a commercial laying ration supplemented with 0, 300 or 600 p.p.m. technical DDT for 93 days prior to and during a 40 day measurement period. Fertility, hatchability, chick mortality, chick body weight and chick liver and adipose tissue DDT residues were studied. Egg production was reduced by both 300 and 600 p.p.m. in the hens diet. Fertility was significantly reduced in the 300 but not in the 600 p.p.m. group when compared to the 0 p.p.m. group. There were no significant differences in the hatchability of fertile eggs. Chick mortality was significantly increased in the 300 (7.6% mortality) and 600 p.p.m. (76.5% mortality) groups and chick body weight was significantly decreased in both DDT groups. The majority of the chick mortality in the 600 p.p.m. group occurred in the first three days after hatching. Concentration of DDT residues in chick liver and fat increased as the DDT ingestion by the hens increased.

Some Effects of DDT, Toxaphene and Polychlorinated Biphenyl on Thyroid Function in Bobwhite Quail

Bobwhite quail were given technical grade DDT, Toxaphene (Tox), or Polychlorinated Biphenyl (PCB) at 5, 50 or 500 p.p.m. in their feed for 4 months. At monthly intervals groups of quail (usually 10) from each experimental group were tested and compared with control birds. Thyroid, adrenal, liver, and body weights were measured as were the 2-hour thyroidal I131 uptakes. Generally, only the higher dosages were effective in producing changes. DDT: DDT early increased the uptake of I131 by the thyroid and by 4 months the 2-hour uptake had returned toward control levels. The thyroid gland was found to be significantly enlarged after 3 months on treatment and remained enlarged thereafter. DDT produced no consistent effect on body or adrenal weights, but the livers were enlarged after 2 months on high dosage treatment. Toxaphene: Toxaphene stimulated thyroid growth and I131 uptake. In the former case, the effects were statistically significant only at the 4-month period while the total thyroid uptake of I131 was significantly increased at 3 and 4 months on treatment. When expressed as percentage of dose of I131 taken up per mg. of thyroid, the uptake was significantly greater after 2 and 3 months on treatment. Toxaphene in high dose rate significantly decreased body weights at all time periods studied. At all dose levels used, Tox seemed to produce adrenal hypertrophy by 3 months. The effects of this chemical on liver weights was slight or none at all. PCB: PCB seemed to depress thyroid size at low dose levels or early in the experiment and to stimulate growth at higher dose levels or later in the experiment. The enlarged glands of the high PCB group took up more iodide than the controls, but each unit weight of these thyroids took up the same amount of iodide as the controls. On the other hand, the thyroids from birds receiving the lower two doses of PCB took up the same amount of iodide as the controls, but each mg. of thyroid took up less. PCB had no consistent effect on body weight or adrenal weight, but produced a very dramatic increase in liver weight. These results are discussed.

Liver tumours in CF-1 mice exposed for limited periods to technical DDT.

Groups of CF-1 mice were given 250 ppm of DDT mixed into the diet for 15 weeks or 30 weeks and killed at different time intervals. Following 30 weeks of treatment a similar proportion of male mice bearing hepatomas was observed at 65, 95, and 120 weeks from the beginning of the experiment. In females the incidence of hepatomas increased from the 65th to the 95th week. More mice had hepatomas larger than 10 mm at 95 and 120 weeks than at 65 weeks. A similar pattern was observed in mice exposed for 15 weeks but the incidence of hepatomas was much lower than after 30 weeks' exposure.

Tumors in CF-1 mice exposed for six consecutive generations to DDT.

CF-1 minimal inbred mice of 6 consecutive generations (parents, F1-F5) were fed 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (technical DDT) mixed into the diet at dose levels of 2, 10, 50, and 250 ppm for their lifespans. The experiment involved 3987 mice, including DDT-exposed and negative and positive controls. Exposure to all A levels of DDT significantly increased liver tumors (hepatomas) in males (50–55.9% in the 2, 10, and 250 ppm groups and 86% in the 250 ppm DDT groups, compared to 29.5% in controls). In females, hepatoma incidence increased considerably after exposure to 250 ppm DDT (65.5% compared to 4.7% in controls), whereas 10 and 50 ppm DDT only slightly increased the incidence (9 and 13%, respectively). No effect was noted at the level of 2 ppm DDT in females. The average lifespan of males with hepatomas decreased in DDT-treated groups (84 wk at the 250 ppm DDT level, 101–104 wk at the levels of 2, 10, and 50 ppm, as compared to 114 wk in controls). In females, only the highest dose level shortened the average lifespan of hepatoma-bearing mice (94 wk compared to 104 wk in controls). DDT did not alter tumor incidence at sites other than the liver, though an apparent, but not significant, increase in lung tumor incidence was noted at the levels of 2 and 10 ppm DDT. No progressive increase of hepatoma incidence from generation to generation was noted in DDT-treated mice. However, considerable variations in the incidence of tumors of the liver, lungs, and hematopoietic tissue were observed between the generations within each treatment group, including controls. One metastasizing hepatoma was found in controls and 13 in 4 DDT-treated groups. Malignant liver tumors, tentatively termed “hepato-blastomas,” also occurred, with a slightly increased incidence in the 10 and 50 ppm groups (3.9 and 3.1%, respectively, as compared to 0.9% in controls) and a significant increase in the 250 ppm group (7.1%). Ten of 56 tumors of this type found in DDT-treated mice metastasized to the lungs.