Short-tailed shrews: Toxicity and residue relationships of DDT,dieldrin, and endrin

Experiments involving dietary toxicity and residue relationships of DDT, dieldrin, and endrin were conducted with short-tailed shrews. Dietary concentrations of DDT dissolved in vegetable oils were usually more toxic than diets containing comparable amounts of powdered DDT. Younger shrews, particularly females, were more tolerant of powdered DDT than older animals; yet, there were no conspicuous age differences in toxicity of DDT dissolved in oils. In comparison to other mammals, short-tailed shrews are not unusually sensitive to DDT, dieldrin, or endrin on the basis of two-week feeding tests. The influence of age and sex on toxicity of DDT, endrin, and dieldrin was sometimes more important than body weight. Of those shrews of the same age and sex that were fed the same dietary dosage, heavier shrews were more tolerant than lighter individuals; and, heavier shrews tended to lose a greater percentage of body weight before death. There was a range of 15 to 105 DDT equivalents in brains of shrews dying on dietary dosages of DDT. Six shrews fed a high level of DDT seemed to have unusual metabolite capabilities and died with apparent lethal levels of DDD in their brains. Levels of dieldrin in brains of shrews that died on a dietary dosage of dieldrin ranged from 3.7 to 12.6 ppm. In the rates of gain and loss experiments where shrews were given diets containing 400 ppm DDT or 50 ppm dieldrin up to 17 days, high residues were noted in tissues of shrews after two weeks on a contaminated diet and a few died at that time. After shrews were placed on clean food, it was determined that >50% of the dieldrin residues in carcass and brain were lost in <2 weeks. Males and females fed DDT for 17 days lost >50% of residues of DDT and metabolites in brains after 2 weeks on clean food; males lost nearly 50% of residues in carcasses after two weeks on clean food compared with a loss of only 11% in females.     

Pre- and Postnatal Exposure to 3,3′,4,4′-Tetrachlorobiphenyl: II. Effects on the Reproductive Capacity and Fertilizing Ability of Eggs in Female Mice

This study investigated the effects of 3,3′,4,4′-tetrachlorobiphenyl (TCB) on the reproductive capacity of female mice. Female C57BL/6J mice (F-0) were fed diets containing 0, 3, or 30 ppm TCB for 2 weeks before pairing with nontreated C57BL/6J males for a 10-day breeding period. Females were continued on their treatment diet throughout mating, gestation, and lactation. Female offspring (F-1) were fed the same diet as their dams throughout the study. The reproductive capacity of F-1 females was examined by mating with non-treated B₆D₂-F₁ males. In addition, the fertilizing ability of eggs from F-1 females was examined in vitro by insemination with sperm from nontreated B₆D₂-F₁ males. Fecundity in F-0 females after mating was 80%, 71%, and 47% in the 0, 3, and 30 ppm treatment groups, respectively. Four-day and 21-day survival indices were lower for offspring of 30 ppm TCB-treated F-0 females than for offspring of the control females. Fecundity in F-1 females was the same among all treatment groups, however, all offspring born to 3- and 30-ppm TCB-treated F-1 females died before 4 days of age. Although the litter size at birth was not affected, the in vitro fertilizing ability of eggs in the 3- and 30-ppm treatment groups was lower than in the control group. This decrease in fertilizing ability was associated with an increase in degenerated eggs. F-0 females treated with 30 ppm TCB had enlarged livers during pregnancy and lactation. At 5 and 6 weeks, liver enlargement and thymus atrophy were apparent in F-1 females exposed to 30 ppm TCB. This study demonstrated impaired reproductive capacity and decreased egg fertilizing ability in TCB-treated female mice. Received: 15 May 1997/Accepted: 22 July 1997     

Effects of dietary exposure to fumonisins from Fusarium moniliforme culture material (M-1325) on the reproductive performance of female mink

Adult female mink (Mustela vison) were fed diets that contained Fusarium moniliforme culture material that provided low- or high-dose dietary concentrations of 86 or 200 ppm fumonisin B₁, 22 or 42 ppm fumonisin B₂, and 7 or 12 ppm fumonisin B₃, respectively, from approximately two weeks prior to breeding through gestation and lactation. Breeding performance of the females was not affected by consumption of the fumonisin diets. However, 58% of the mated females fed the high-dose diet (254 ppm total fumonisins) whelped compared to 100% of those fed the control and low-dose diets (115 ppm fumonisins). There was a statistically significant, dose-dependent decrease in kit (young mink) body weights at birth and a notable, but non-significant, decrease in litter size. The percentage of stillborn kits was directly proportional to the concentration of fumonisins in the dams' diets. Fumonisin concentrations in milk collected from those fed the high-dose diets were approximately 0.7% of the dietary fumonisin concentrations. Lactational exposure to fumonisins did not significantly decrease kit survival from birth through three weeks of age. Hepatic cell vacuolation was present in 25% of the control and 80% of the high-dose adults. No treatment-related gross or histologic lesions were observed in the kit mink. Numerous differences in hematologic and serum chemical parameters were noted between the control and fumonisin-exposed mink.     

Trophic and maternal transfer of selenium in brown house snakes (Lamprophis fuliginosus)

Excessive concentrations of dietary Se are toxic to oviparous vertebrates (i.e., fish and birds) but little is known about its accumulation and effects in reptiles. We exposed female brown house snakes, Lamprophis fuliginosus, to 10 and 20 microg/g Se by injecting seleno-D,L-methionine into their prey items and compared the snakes to individuals receiving background levels of approximately 1 microg/g dietary Se. Snakes were fed meals equaling 25% of their body mass 2-3 times a month for 10 months. Snakes exposed to excessive Se accumulated significant concentrations of Se in kidney, liver, and ovarian tissue, but accumulation had no effect on female survival, food consumption, growth, or body condition. Fewer females exposed to excessive Se reproduced than females exposed to 1 microg/g Se (67% vs. 91%, respectively), but the reduction in reproductive activity was not statistically significant. Total reproductive output of females did not differ among the three dietary treatments. However, snakes exposed to 10 and 20 microg/g Se transferred significant concentrations of Se to their eggs. In the 20 microg/g treatment, maternal transfer resulted in Se concentrations in eggs that surpassed all suggested reproductive toxicity thresholds for birds and fish. Further studies are needed to more rigorously determine whether maternal transfer of Se in this snake species affects the viability of developing embryos or the health of offspring.     

Shell thinning and reproductive impairment in black ducks after cessation of DDE dosage

Captive black ducks (anas rubripes) were fed dietary DDE [1,1-dichloro-2,2-bis (p-chlorophenyl)ethylene] at 10 ppm (dry weight; about 2 ppm on a natural diet basis) for 2 breeding seasons, then untreated feed for 2 succeeding years. Residues of DDE in the carcasses of adults declined 90% during the 2-year clean-up period. Following 2 years of dietary DDE, mean residues in eggs reached 64.9 ppm. Even after 2 years on clean feed, DDE residues in the eggs averaged 6.2 ppm or 9.5% of the mean DDE level reached after 2 years on treated feed. Shells of eggs from treated hens were about 20% thinner than shells of eggs from controls. Stoppage of DDE dosage resulted in progressively thicker shells, yet even after 2 years on untreated feed hens laid eggs with shells about 10% thinner than control hens. After DDE was removed from the diet, DDE residues in the eggs decreased, shell thickness increased, and reproductive success improved. Hens previously exposed to DDE, but then fed clean feed for 2 years, still produced significantly fewer surviving ducklings than did control hens.     

Eggshell thickness and reproduction in American kestrels exposed to chronic dietary lead

American kestrels (Falco sparverius) were randomly paired and fed 0, 10, or 50 ppm metallic lead in their diet from November 1979–May 1980. Lead levels were elevated in bones and livers of birds receiving the treated diets, particularly the 50 ppm treatment group. Differential deposition of lead was noted between males and females, with the highest levels in the females. No adverse effects were evident with respect to survival, egg laying, or initiation of incubation in any treatment group nor was fertility or eggshell thickness affected. Little or no lead was transferred to the egg contents and although lead was present in the shell, the levels were too variable for this to be considered a useful measure of exposure.     

The effect of mirex on reproduction of Japanese quail and on characteristics of eggs from Japanese quail and chickens

Laying White Leghorn chickens were fed mirex at 0, 5, 10, 20, 40, 80, and 160 ppm for 12 weeks, and laying Japanese quail were fed mirex at 0, 5, 40, and 80 ppm for 12 weeks. The data suggest that dietary mirex at these levels did not affect egg production, egg weight, shell thickness, shell calcium, the proportion of broken eggs, or the proportion of soft-shelled eggs of either chickens or quail. Statistical significance (P < 0.05) associated with dietary mirex was detected in the analysis of eggshell weight for chickens; however, because a dose-response relationship of shell weightvs. level of mirex fed was not evident, this observation was attributed to chance. The data suggest that dietary mirex did not affect eggshell weight, fertility, or hatchability of quail. Mirex accumulation in eggs and carcasses of both species was proportional to dose and was slightly higher in quail than in chickens.     

Reproduction and residue accumulation in black ducks fed toxaphene

Three sets of 15 pairs of black ducks (Anas rubripes) were given 0, 10, or 50 ppm toxaphene in a dry mash diet for a period of 19 months, which included two breeding seasons. Survival of adults was not affected, but the weights of treated males were depressed during the summer months. Egg production, fertility, hatchability, eggshell thickness, growth, and survival of young did not vary with toxaphene ingestion in either breeding season. However, the mean number of days required to complete a clutch was lower in birds fed toxaphene than in birds on the control diet. Clutches of hens fed 50 ppm toxaphene showed improved hatching success in the second year of the study.Carcass wet-weight (70% moisture) residues in adults and the young birds averaged from 50 to 100% of the dietary concentration (7% moisture); egg residues showed a similar trend. Carcass residues did not reflect those found in the livers or brains of the adults, which seldom exceeded 0.5 ppm. Toxaphene residues were found in the brain of only one 10 ppm bird, but were present in nearly all of the 50 ppm birds. Toxaphene residues were present in the liver all all birds ingesting toxaphene.     

Reproductive,immunologie, and cytogenetic effects of dietary 3,3′,4,4′-tetrachloroazoxybenzene exposure to mice

The effects of chronic dietary exposure to 3,3,4,4-tetrachloroazoxybenzene (TCAOB) on the reproductive efficiency of female Swiss-Webster mice were measured. The immunocompetence of their offspring was assayed at weaning. No indications of toxicosis were seen in the adult females with the exception of a reduction in the thymus weight of the animals consuming 10 ppm TCAOB. Pup mortality to weaning and the percentage of females whelping were not affected by 0.1 ppm, 1 ppm, or 10 ppm of TCAOB in the diet. There was, however, a significant reduction in the number of pups (at birth and at weaning) per female whelping at 10 ppm TCAOB in the diet. The thymus weight and plaque-forming-cell response of the pups were also significantly reduced below control levels. The lymphocyte blastogenic response to Concanavalin-A and lipopolysaccharide, and total peripheral blood leukocyte count, were not affected by the concentrations of TCAOB tested. Dietary treatment of female mice with relatively high concentrations of this chemical resulted in reduced reproductivity capacity, but only moderate immuno-suppression of their offspring exposed duringin utero and early postnatal development.Spleen cells of mice exposedin vivo to TCAOB for 28 days via the diet were examined for chromosome damage and sister chromatid exchange. TCAOB was investigated because of its similarity to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD); TCAOB caused significantly increased chromatid breakage, suggesting that it may be affecting protein synthesis or may be a mutagen. However, TCAOB did not result in a significant increase in sister chromatid exchanges or isochromatid breaks even at a dietary concentration of 40 ppm.     

Toxicity to fathead minnows of endrin in food and water

Fathead minnows (Pimephales promelas) were exposed during a partial chronic toxicity study to endrin concentrations in the water or food, or both, for 300 days encompassing reproduction. Tissue residues were analyzed at preset intervals for first-generation fish, and were also determined for embryos, larvae at hatch, and 30-day progeny. Gas-chromatographic and liquid-scintillation techniques were used to monitor the contribution of endrin from each source. The food was clams that had accumulated 14C-endrin when exposed to an endrin water concentration similar to that to which the fish were exposed. Higher endrin tissue residues were accumulated from the water than from food. Maximum concentration factors were 0.8 from the food and 13,000 from the water. Residues contributed by endrin in the food were additive to those from the water at all life stages. Endrin in the food (0.63 ppm) significantly reduced survival of the fathead minnows, and fish exposed to both endrin sources had lower survival than those exposed to either source alone. Endrin residues in embryos and larvae were highest and larval survival lowest for progeny of adults exposed to endrin in both food and water. Survival of 30-day progeny was significantly reduced at all test exposures (0.63 ppm in the food, water exposures of 0.14 and 0.25 ppb, and all combinations of food and water exposure).     

Reproductive Performance of Two Generations of Female Semidomesticated Mink Fed Diets Containing Organic Mercury Contaminated Freshwater Fish

Semidomesticated female mink (Mustela vison) were fed daily diets containing 0.1 ppm, 0.5 ppm, and 1.0 ppm of total mercury. Piscivorous and nonpiscivorous fish naturally contaminated with organic mercury were used to prepare the diets. Twenty-month-old females (G1 generation) that were exposed to the experimental diets for approximately 400 days in 1994 and 1995 and their 10-month-old female offspring (G2 generation) that were exposed to mercury for approximately 300 days in 1995, were all mated to 10-month-old males. Males were fed the diet containing 0.1 ppm mercury 60 days prior to the mating season. Diets containing 0.1 ppm and 0.5 ppm were not lethal to G1 and G2 females for an exposure period of up to 704 days. At the age of 11 months, mortalities occurred in 1994 for G1 females (30/50) and in 1995 for G2 females (6/7) fed the 1.0 ppm mercury diet after 90 days and 330 days of exposure, respectively. The length of the gestation periods and the number of kits born per female were not different among dietary groups for the two generations of females. The proportion of females giving birth was low for all groups, except for the G1 females fed the 0.1 ppm diet. There was an inverse relationship between whelping proportion and exposure group, but was not statistically significant. There was evidence that kits were exposed to mercury both in utero and/or during lactation as indicated by the presence of mercury in their livers. Mercury exposure did not influence the survival and growth of neonatal kits. Received: 11 November 1997/Accepted: 24 August 1998     

Pre- and Postnatal Exposure to 3,3′,4,4′-Tetrachlorobiphenyl: I. Effects on Breeding Ability and Sperm Fertilizing Ability in Male Mice

This study investigated the effects of 3,3′,4,4′-tetrachlorobiphenyl (TCB) on the reproductive performance and in vitro sperm fertilizing ability of male mice. C57BL/6J female mice (F-0) were fed diets containing 0, 3, or 30 ppm TCB for 2 weeks before pairing with nontreated males for a 10-day breeding period. Females were continued on their treatment diet throughout mating, gestation, and lactation. Male offspring (F-1) were given the same diet as their dams throughout this study. F-1 males at 7 and 17 weeks of age were mated to nontreated B₆D₂-F₁ female mice. Body weight, litter size, and survival indices of offspring sired by F-1 males were recorded. Sperm fertilizing ability of F-1 males at 9 and 19 weeks of age was examined in vitro using eggs collected from nontreated B₆D₂-F₁ females. Sperm motion analysis was performed at the same time. When 7- and 17-week-old F-1 males were mated to nontreated females, no differences in fecundity, litter size, sex ratio, or survival indices among any of the treatments were observed. However, sperm fertilizing ability of 30 ppm–treated F-1 males at 19 weeks of age was less than that of the control mice. Testes weights were greater in 3-week-old, 30 ppm–treated mice. Received: 16 August 1996/Accepted: 18 February 1997     

Effects of methyltestosterone on reproduction in the Japanese quail (Coturnix coturnix japonica)

Although the hormone-mediated effects of the synthetic androgenic hormone methyltestosterone (MT) are well characterized in mammals, little is known about endocrine and other toxic effects on reproduction in birds. In a one-generation study, MT was administered to adult Japanese quail (12 pairs per group) at dietary dose levels of 0, 10, 50, and 110 ppm for a period of 3 weeks. Reproductive performance was severely affected in the groups receiving 50 and 110 ppm MT. In females, the egg-laying rate was reduced not only related to the dose administered but also to the duration of treatment. The administration of 110 ppm, and to a lesser extent, of 50 ppm MT resulted in an immediate and dramatic decrease in the total number of eggs laid, which complicated reliable assessment of other reproduction-related parameters. In males, the findings suggested inhibition of spermatogenesis at dose levels of 50 ppm and above, resulting in a subsequent reduction in male fertility.     

2,4-Dichlorophenyl-p-Nitrophenyl Ether (TOK)

In a two-generation reproduction study, rats were fed dietary levels of 0, 20, 100, and 500 ppm of 2,4 dichlorophenyl-p-nitrophenyl ether (TOK) (1.8 to 1.1 mg/kg/ day, 9.2 to 5.2 mg/kg/day, and 46 to 26 mg/kg/day, respectively). The survival of the offspring was not affected at the 0 and 20 ppm dietary levels. At the 100 ppm dietary level the survival of the offspring to weaning was reduced and at the 500 ppm dietary level no offspring survived the neonatal period in the two breedings of the first generation.

In further studies rats were dosed during pregnancy either by stomach tube or by adding TOK to the diet. The reduction in the number of surviving litters was caused by poorly developed lungs in the exposed groups. Technical TOK had the same effect as 99% pure TOK. Furthermore, 2,7-dichlorodibenzodioxin, which may be a contaminant of TOK, does not affect the maturation process of the lungs when given at a dose of 0.04 mg/kg/day on days 7 to 15 of gestation.     

DDT thins shells of eggs from mallard ducks maintained onad 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.Published with the approval of the Director of the North Dakota Agricultural Experiment Station as Journal Article No. 462.     

Toxicologic studies with japanese quail fed winter wheat grown on municipal sludge-amended soil

Winter wheat was grown on soil amended with 100 dry tons per acre (224 metric tons/ha) of municipal sewage sludge from Syracuse, New York. The grain contained 1.43 and 0.98 ppm (mg/kg) dry weight, respectively, of cadmium and nickel. This wheat was incorporated as 60% of a semi-synthetic diet and fed to male and female Japanese quail for two generations. Male quail from the F₁ generation fed sludge-grown wheat showed induction of hepatic microsomal enzymes,i.e., aminopyrene-N-demethylase and aniline hydroxylase, that indicated foreign compounds present in the wheat. Cadmium was significantly higher (p < 0.05) than controls in kidney, liver, and testes and nickel in the liver of the male quail (F₀) fed the sludge-grown grain. Cadmium in kidney and liver (but not in eggs) and nickel in liver was significantly higher (p < 0.05) than controls in the females fed the sludge-grown wheat. Birds from the F₁ generation showed no significantly different (p > 0.05) concentrations of cadmium in kidney, liver, or eggs between the two dietary treatments. There were no observable changes in the tissue ultrastructure of liver and kidney as examined by electron microscopy in any of the treatment groups.     

The chronic toxicity of 3-chloro-4-methyl benzamine HCl to birds

3-Chloro-4-methyl benzamine HCl (DRC-1339), an avian toxicant, was fed to five species of birds for periods up to 120 days. The 30-day LC₅₀ of uniformly treated feed for starlings was 4.7 ppm and the 90-day LC₅₀ was 1.0 ppm. The 28-day LC₅₀ for coturnix was 18 ppm. The 30-day LC₅₀ for pigeons was less than 100 ppm. Pheasants fed diets containing 2% DRC-1339 baits diluted to a rate of 286 ppm of DRC-1339 died within 22 days. Bobwhite quail fed similar diets suffered some mortality at levels as low as 2.9 ppm, but most survived 10 times this dosage level for the 120-day test period. Application of the Kenaga Index of Chronicity, resulted in the conclusion that DRC-1339 was cumulatively toxic to birds.Reproduction in coturnix was adversely affected by treatments at 10 ppm of DRC-1339 and above. Reproduction in pigeons was adversely affected by a treatment of 25 ppm. In coturnix, DRC-1339 caused an increased incidence of egg breakage and decreased both egg and live chick production. In pigeons, DRC-1339 caused an increase in the proportion of infertile eggs. Reproductive ability of first generation offspring was not affected when parent coturnix and pigeons were fed DRC-1339.These data emphasize the need for care in the use of DRC-1339. The bait should be used only as registered and care exercised in storage and disposal of unused baits to avoid poisoning of nontarget species.     

Effects of Chronic Dietary Cadmium on Hepatic Glutathione Levels and Glutathione Peroxidase Activity in Starlings (Sturnus vulgaris)

The effects of chronic exposure to dietary cadmium on the levels of hepatic glutathione (GSH) and on the activity of the glutathione peroxidase enzymes (GSH-Px) were studied for the first time in starlings (Sturnus vulgaris). Thirty-three individuals (17 females and 16 males) were divided into three groups: One represented the untreated control and two were respectively fed with diets containing 10 and 50 ppm cadmium chloride (CdCl₂). The total duration of treatment was 22 weeks. The three groups respectively accumulated mean hepatic Cd residues of 2.29, 75.71, and 208.49 ppm. Hepatic GSH increased in the treated groups respectively 24% and 52% in comparison to controls. Total GSH-Px activity in the liver was inhibited in the group fed with 50 ppm, due to inhibition of the selenium-dependent fraction of the enzyme, while the selenium-independent fraction did not change significantly. During the treatment, after 14 weeks of exposure to cadmium, the 50 ppm–treated group showed a 47% decrease of the activity of the selenium-dependent GSH-Px and a 50% increase of the somatic liver index in comparison with controls. Received: 17 February 1999/Accepted: 12 October 1999     

The reproductive effects of dietary heptachlor in mink (Mustela vison)

Adult female mink were fed diets containing 0 (control), 6.25, 12.5, and 25 ppm (g/g) technical grade heptachlor prior to and throughout the reproductive period (181 days) to evaluate the effects of heptachlor consumption on reproduction and offspring viability and to assess the extent of placental and mammary transfer of heptachlor epoxide to mink offspring. Feeding 12.5 and 25 ppm resulted in significant reductions in feed consumption and body weights of female mink. Mortality was 0, 8, 67, and 100% for the control, 6.25, 12.5, and 25 ppm groups, respectively. All females in the 25 ppm group died within 88 days. Mink fed the two higher heptachlor diets displayed clinical signs indicative of central nervous system involvement just prior to death. Females were mated with males on the same dietary treatments. Whelping success rates were 67, 83, 27, and 0% for the control, 6.25, 12.5, and 25 ppm groups, respectively. High mortality in the 12.5 and 25 ppm groups accounted for the lack of reproductive success. Gestation length, litter size and birth weight of kits were not significantly affected by adult female consumption of 6.25 ppm heptachlor while kits whelped by females on the 12.5 ppm diet weighed significantly less than control kits at birth. Survival of kits in the 12.5 ppm group from birth to three weeks of age was also adversely affected. At three and six weeks of age, kit body weights in both the 6.25 and 12.5 ppm groups were significantly less than body weights in control kits. Examination of heptachlor epoxide concentrations in newborn and developing kits indicated both placental and mammary transfer of the chemical from the dams to the kits. The LC50 for the 181-day exposure period for female mink was 10.5 ppm heptachlor and the LOAEL, based on reduced kit growth, was 6.25 ppm.     

Eggshell thinning in ring doves exposed top,p′-dicofol

Ring doves (Streptopelia risoria) were brought into breeding condition and, after laying two clutches of two eggs each, were fed one of three experimental diets containing either 33.4 ppm dicofol (1, 1-bis(p-chlorophenyl)-2,2,2-trichioroethanol), 37 ppmp,pi DDE (2,2-bis (p-chlorophenyl)-1,1 dichloroethylene), or no toxicant (control). Mean shell thicknesses of eggs produced on experimental diets were: control, 156 x; DDE, 145 ; and dicofol 142 . Birds fed DDE produced eggs with shells a mean 5.6% thinner than pre-treatment eggs, while birds fed dicofol produced eggs with shell means 7.2% thinner. No change in shell thickness was found in eggs from control doves. Analysis of covariance revealed a statistically significant effect of decreasing eggshell thickness over time in doves fed DDE and dicofol diets but not in control birds. Egg production was significantly lower in both dicofol-fed and DDE-fed birds when compared with controls. Control birds produced a mean of 1.97 eggs per clutch. Dicofol- and DDE-treated birds produced 1.88 and 1.79 eggs per clutch, respectively. The proportion of eggs found cracked or broken in the nest was greatest in birds fed dicofol, with 16.9% of all eggs broken or cracked, compared to 7.9% of eggs from the DDE group and 5.7% of eggs from control group. Selected eggs were analyzed for residues of dicofol, dichlorobenzophenone (DCBP), and DDE in the yolk. For the birds fed the dicofol diet, DDE residues in treatment eggs ranged from 0.036 to 0.119 ppm wet weight. DDE residues in pre-treatment eggs ranged from 0.013 to 0.080 ppm. Dicofol residues ranged from 2.62 ppm to 22.58 ppm. DCBP residues ranged from 2.55 to 17.68 ppm. Only residues of dicofol showed a significant correlation with percent shell thinning.