Effects of dietary nickel on survival and growth of mallard ducklings

Mallard (Anas platyrhynchos) ducklings were fed nickel sulphate in their diet from day one to 90 days of age. Ducklings fed 1,200 ppm nickel began to tremor and show signs of paresis after 14 days of dosage (age) and 71% of this group died within 60 days of age. Birds fed 1,200 ppm nickel weighed significantly less (P<0.05) at 28 days of age than birds fed the other diets. Weights of ducklings fed untreated food or dietary dosages of 200 and 800 ppm nickel diets were not significantly different (P>0.05). The weight/length ratio of the humerus (an expression of bone density) from the 800 ppm diet females was significantly lower (P<0.05) than the control fed females at 30 and 60 days and for all ducklings fed 1,200 ppm at 30 days of age. The organ-weight/body-weight ratios for heart, liver, and gizzard did not differ from controls or between any dosage group. Liver nickel residues from ducklings that died during this study ranged between 1.0 to 22.7 ppm and kidney residues ranged between 2.7 to 74.4 ppm. Liver and kidney tissues from all ducklings that survived to 90 days of age contained less than 1.0 ppm nickel.     

Chlorfenapyr and mallard ducks: overview, study design, macroscopic effects, and analytical chemistry

The first commercial pesticide derived from a class of compounds known as halogenated pyrroles was registered for use in the United States in 2001. Chlorfenapyr degrades slowly in soil, sediment, and water and is highly toxic to birds. Information on biochemical or histological endpoints in birds is lacking; therefore, a two-year study was conducted to provide information needed to develop diagnostic criteria for chlorfenapyr toxicosis. In the first year, male mallard ducks were fed concentrations of 0, 2, 5, or 10 ppm technical chlorfenapyr or 5 ppm of a formulated product in their diet during a 10-week chronic exposure study. Survival, body weight, feed consumption (removal), behavior, and molt progression were monitored. Feed and liver were analyzed for chlorfenapyr and two metabolites. Five of 10 ducks in the 10-ppm group died, and neurotoxic effects were observed in the 5- and 10-ppm groups. Feed removal increased for ducks receiving chlorfenapyr and body weights of 5- and 10-ppm ducks were reduced. Loss of body fat, muscle atrophy, and bile retention were suggestive of metabolic disruption or a decreased ability to digest and absorb nutrients. Liver and kidney weights and liver and kidney weight/body weight ratios exhibited a positive response to concentrations of chlorfenapyr in the diet. Emaciation and elevated organ weight/body weight ratios are candidates for a suite of indicators of chronic chlorfenapyr exposure. Liver is the preferred tissue for chemical confirmation of 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     

Copper Pellets Simulating Oral Exposure to Copper Ammunition: Absence of Toxicity in American Kestrels (<Emphasis Type="Italic">Falco sparverius</Emphasis>)

To evaluate the potential toxicity of copper (Cu) in raptors that may consume Cu bullets, shotgun pellets containing Cu, or Cu fragments as they feed on wildlife carcasses, we studied the effects of metallic Cu exposure in a surrogate, the American kestrel (Falco sparverius). Sixteen kestrels were orally administered 5 mg Cu/g body mass in the form of Cu pellets (1.18–2.00 mm in diameter) nine times during 38 days and 10 controls were sham gavaged on the same schedule. With one exception, all birds retained the pellets for at least 1 h, but most (69%) regurgitated pellets during a 12-h monitoring period. Hepatic Cu concentrations were greater in kestrels administered Cu than in controls, but there was no difference in Cu concentrations in the blood between treated and control birds. Concentration of the metal-binding protein metallothionein was greater in male birds that received Cu than in controls, whereas concentrations in female birds that received Cu were similar to control female birds. Hepatic Cu and metallothionein concentrations in kestrels were significantly correlated. Histopathologic alterations were noted in the pancreas of four treated kestrels and two controls, but these changes were not associated with hepatic or renal Cu concentrations, and no lesions were seen in other tissues. No clinical signs were observed, and there was no treatment effect on body mass; concentrations of Cu, hemoglobin, or methemoglobin in the blood; or Cu concentrations in kidney, plasma biochemistries, or hematocrit. Based on the parameters we measured, ingested Cu pellets pose little threat to American kestrels (and presumably phylogenetically related species), although the retention time of pellets in the stomach was of relatively short duration. Birds expected to regurgitate Cu fragments with a frequency similar to kestrels are not likely to be adversely affected by Cu ingestion, but the results of our study do not completely rule out the potential for toxicity in species that might retain Cu fragments for a longer time.     

Mercury residues in tissues of dead and surviving birds fed methylmercury.

Concentrations of mercury in passerine birds fed diets containing 40 ppm methylmercury were similar in tissues of birds that died from mercury poisoning and in those that were sacrificed after half the group had died. Residues were higher in tissues of birds that died, but the differences were not statistically significant. Residue levels were highest in livers, followed by kidneys and brains. Levels of mercury were similar in breast muscle, carcass, and whole body. Mercury levels were highest in redwinged blackbirds, lowest in grackles, and intermediate in starlings and cowbirds. Mercury concentrations exceeded 20 ppm in all tissues of all species and were similar to levels reported in wild birds known to have died of mercury poisoning.     

Mercury residues in tissues of dead and surviving birds fed methylmercury

Summary Concentrations of mercury in passerine birds fed diets containing 40 ppm methylmercury were similar in tissues of birds that died from mercury poisoning and in those that were sacrificed after half the group had died. Residues were higher in tissues of birds that died, but the differences were not statistically significant. Residue levels were highest in livers, followed by kidneys and brains. Levels of mercury were similar in breast muscle, carcass, and whole body. Mercury levels were highest in redwinged blackbirds, lowest in grackles, and intermediate in starlings and cowbirds. Mercury concentrations exceeded 20 ppm in all tissues of all species and were similar to levels reported in wild birds known to have died of mercury poisoning.     

Toxicity of Lead-Contaminated Sediment to Mute Swans

Most ecotoxicological risk assessments of wildlife emphasize contaminant exposure through ingestion of food and water. However, the role of incidental ingestion of sediment-bound contaminants has not been adequately appreciated in these assessments. This study evaluates the toxicological consequences of contamination of sediments with metals from hard-rock mining and smelting activities. Lead-contaminated sediments collected from the Coeur d'Alene River Basin in Idaho were combined with either a commercial avian maintenance diet or ground rice and fed to captive mute swans (Cygnus olor) for 6 weeks. Experimental treatments consisted of maintenance or rice diets containing 0, 12 (no rice group), or 24% highly contaminated (3,950 μg/g lead) sediment or 24% reference (9.7 μg/g lead) sediment. Although none of the swans died, the group fed a rice diet containing 24% lead-contaminated sediment were the most severely affected, experiencing a 24% decrease in mean body weight, including three birds that became emaciated. All birds in this treatment group had nephrosis; abnormally dark, viscous bile; and significant (p ≤ 0.05) reductions in hematocrit and hemoglobin concentrations compared to their pretreatment levels. This group also had the greatest mean concentrations of lead in blood (3.2 μg/g), brain (2.2 μg/g), and liver (8.5 μg/g). These birds had significant (α = 0.05) increases in mean plasma alanine aminotransferase activity, cholesterol, and uric acid concentrations and decreased plasma triglyceride concentrations compared to all other treatment groups. After 14 days of exposure, mean protoporphyrin concentrations increased substantially, and mean δ-aminolevulinic acid dehydratase activity decreased by more than 95% in all groups fed diets containing highly contaminated sediments. All swans fed diets that contained 24% lead-contaminated sediment had renal acid-fast intranuclear inclusion bodies, which are diagnostic of lead poisoning in waterfowl. Body weight and hematocrit and hemoglobin concentrations in swans on control (no sediment) and reference (uncontaminated) sediment diets remained unchanged. These data provide evidence that mute swans consuming environmentally relevant concentrations of Coeur d'Alene River Basin sediment developed severe sublethal lead poisoning. Furthermore, toxic effects were more pronounced when the birds were fed lead-contaminated sediment combined with rice, which closely resembles the diet of swans in the wild. Received: 12 July 2001/Accepted: 11 October 2002     

Dietary vitamin E and pulmonary biochemical and morphological alterations of rats exposed to 0.1 ppm ozone

Three groups of 28 1-month-old male Sprague-Dawley rats each were fed a basal vitamin E-deficient diet and supplemented with either 0, 11, or 110 ppm vitamin E for 38 days, and were then exposed to 0 or 0.1 ppm ozone continuously for 7 days. Following ozone exposure, the level of reduced glutathione (GSH) and activities of GSH peroxidase, GSH reductase, glucose-6-phosphate dehydrogenase (G-6-PD), and lactate dehydrogenase (LDH), but not of malic dehydrogenase, were significantly elevated in the lungs of rats fed the vitamin E deficient diet. The level of GSH and activities of GSH peroxidase and G-6-PD were also significantly increased in the lungs of the animal group fed the 11 ppm vitamin E diet, while none of the biochemical measurements made was significantly altered by ozone in the 110-ppm vitamin E diet fed rats. Scanning electron microscope examination revealed that five out of six rats on the vitamin E-deficient diet and four out of six from the 11-ppm vitamin E diet had detectable lesions following ozone exposure, as compared with only one of the six exposed animals from the 110-ppm vitamin E diet. The lesion was restricted to bronchiolar epithelium and alveoli immediately adjacent to the bronchiole-alveolar duct junction. None of the control animals had detectable lesions. The results suggest that exposure to ozone at 0.1-ppm level can produce detectable pulmonary damage, and that dietary vitamin E alters pulmonary susceptibility to ozone exposure.     

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.     

Immune dysfunction in rats fed a diet deficient in copper

Rat pups maintained on copper (Cu)-adequate (6ppm), Cu-deficient (2 ppm) or Cu-depleted (0 ppm) diets from parturition were killed at 8-wk. Liver Cu and serum-ceruloplasmin levels confirmed that on the 0- and 2-ppm diets, a Cu-deficient state was induced. Although body weight was unaffected by the deficiency, the liver, heart, and thymus weights (% body weight) were altered. Hepatomegaly occurred in females fed 0-ppm Cu and males fed 2-ppm Cu. Heart weights increased in both sexes fed 0-ppm Cu. Thymus weights decreased in male rats fed 0-ppm Cu. Antibody titers and natural killer-cell cytotoxicity were markedly suppressed in the animals fed 0-ppm Cu. Male rats given 2-ppm Cu showed reduced antibody titer. Delayed-type hypersensitivity and prostaglandin E2 levels were not significantly affected. These studies suggest that certain components of the immune system are Cu dependent.     

Effects of methylmercury on reproduction in American kestrels

Sixty breeding pairs of captive American kestrels (Falco sparverius) were exposed to a range of sublethal dietary concentrations of mercury (Hg), in the form of methylmercuric chloride, and their subsequent reproduction was measured. Egg production, incubation performance, and the number and percent of eggs hatched decreased markedly between 3.3 and 4.6 mg/kg dry weight of Hg (1.2 and 1.7 mg/kg wet wt), in the diet. The number of fledglings and the percent of nestlings fledged were reduced markedly at 0.7 mg/kg dry weight (0.3 mg/kg wet wt) and declined further between 2 and 3.3 mg/kg dry weight (0.7 and 1.2 mg/kg wet wt). Dietary concentrations of >or=4.6 mg/kg dry weight (1.7 mg/kg wet wt) were associated with total fledging failure. The estimated decline in fledged young per pair (24%, Bayesian regression) for kestrels consuming 0.7 mg/kg dry weight (0.3 mg/ kg wet wt) raises concerns about population maintenance in areas subject to high inputs of anthropogenic Hg. Mercury concentrations in 20 second-laid eggs collected from all groups were related to dietary concentrations of Hg, and the Hg concentrations in 19 of these eggs were related to eggs laid and young fledged. Concentrations of Hg in eggs from the highest diet group (5.9 mg/kg dry wt; 2.2 mg/kg wet wt) were higher than egg concentrations reported for either wild birds or for captive birds (nonraptors) fed dry commercial food containing 5 mg/kg methylmercury. Accumulation ratios of Hg from diets to eggs were higher than those reported for feeding studies with other species.     

Mercury accumulation and loss in mallard eggs

Female mallards (Anas platyrhynchos) were fed diets containing 5, 10, or 20 ppm mercury as methylmercury chloride. One egg was collected from each bird before the start of the mercury diets and 15 eggs were collected from each bird while it was being fed mercury. The mercury diets were then replaced by uncontaminated diets, and each female was allowed to lay 29 more eggs. Mercury levels in eggs rose to about 7, 18, and 35 ppm wet-weight in females fed 5, 10, or 20 ppm mercury, respectively. Mercury levels fell to about 0.16, 0.80, and 1.7 ppm in the last egg laid by birds that had earlier been fed 5, 10, or 20 ppm mercury, respectively. Higher concentrations of mercury were found in egg albumen than in yolk, and between 95 and 100% of the mercury in the eggs was in the form of methylmercury.     

Studies on combined effects of organophosphates and heavy metals in birds. I. Plasma and brain cholinesterase in coturnix quail fed methyl mercury and orally dosed with parathion

Summary We found that mercury potentiated the toxicity and biochemical effects of parathion. Male Coturnix quail (Coturnix coturnix japonica) were fed a sublethal concentration of morsodren (4 ppm as methyl mercury) for 18 weeks. This resulted in an accumulation of 21.0 ppm of mercury in the liver and 8.4 ppm in the carcass. Birds fed clean feed and those fed morsodren-treated feed were orally dosed with 2, 4, 6, 8, and 10 mg/kg parathion, and their 48-h survival times compared. The computed LD₅₀ was 5.86 mg/kg in birds not fed morsodren and 4.24 in those fed the heavy metal. When challenged with a sublethal, oral dose of parathion (1.0 mg/kg), morsodren-fed birds exhibited significantly greater inhibition of plasma and brain cholinesterase activity than controls dosed with parathion. Brain cholinesterase activity was inhibited 41% in morsodren-fed birds and 26% in clean-fed birds dosed with parathion, which suggested that the increase in parathion toxicity in the presence of morsodren was directly related to the inhibition of brain cholinesterase.     

Mallard reproductive testing in a pond environment: A preliminary study

A 2-year preliminary study was conducted on mallard ducks (Anas platyrhynchos), to determine the feasibility of using outdoor pond enclosures for reproductive studies and to evaluate the effects of the insecticide chlorpyrifos on mallard reproduction. No significant reproductive effects were observed for mallards receiving 8 ppm (mg/kg of feed) chlorpyrifos in their diet. Birds receiving 80 ppm chlorpyrifos hatched significantly (p < 0.05) fewer ducklings per successful nest (5.8) than controls (10.2). None of the ducklings on treatment ponds survived to 7 days. Control birds produced 8.4 ducklings per successful nest surviving to 7 days or longer. Birds in the 80 ppm treatment group consumed less feed than did controls (p < 0.01). Weight loss from reduced feed consumption did not occur to the extent expected, indicating that birds supplemented their diets with natural foods found in and around the ponds. In spite of relatively low treated feed consumption, brain acetylcholinesterase was significantly (p < 0.05) depressed (57% of controls) for 80 ppm treated birds. Studies on indoor penned mallards fed 80 ppm chlorpyrifos in their diet also resulted in acetylcholinesterase depression to the same extent, but at much higher feed consumption levels. The study demonstrated the potential of using outdoor pond enclosures to evaluate chemical effects on food consumption, brain acetylcholinesterase, and reproduction in mallards. Improvements to the study design and to the pond enclosures are discussed.     

Fiber-degrading enzyme increases body weight and total serum cholesterol in broiler chickens fed a rye-based diet

Broiler chickens were fed diets based on either outer or inner endosperm from rye. These diets were fed with or without a fiber degrading enzyme to study the effects of the dietary fiber fraction on production results, body composition, serum lipid concentrations and apparent ileal digestibility of nutrients. Elimination of the dietary fiber effect by the enzyme generally improved the production results and caused an increase in total serum cholesterol concentrations. On average, at d 21 of the experiment chickens fed the enzyme supplemented outer endosperm diet had body weights and serum total cholesterol concentrations -23% and 37% higher, respectively, than those of birds fed the corresponding unsupplemented diet. The body fat content tended to be higher and the protein content was generally lower in chickens fed enzyme-supplemented diets. Chickens fed the unsupplemented outer endosperm diet had a low apparent ileal crude fat digestibility of only 23%, and birds fed the enzyme-supplemented diet had crude fat digestibility that was 113% higher but still lower than that of birds fed the inner endosperm diet. Birds fed enzyme-supplemented diets generally had higher apparent ileal digestibilities of organic matter, crude protein, starch, crude fat and dietary fiber components.     

Effects of methylmercury on approach and avoidance behavior of mallard ducklings

Summary Mallard ducks were fed a control diet or a diet containing 0.5 or 3 ppm mercury (as methylmercury dicyandiamide) based on the dry feed. These mercury diets are approximately equivalent to 0.1 and 0.6 ppm mercury in a natural succulent diet. I measured for the ducklings the approach behavior in response to a tape-recorded maternal call and the avoidance of a frightening stimulus.There were no significant differences among controls and ducklings from mercury-treated parents in the percentage of ducklings that approached the tape-recorded call. Control ducklings, however, moved back and forth toward the call more than ducklings from mercury-treated parents and also spent more time in the end of the runway near the loudspeaker than ducklings whose parents were fed a diet containing 0.5 ppm mercury.Compared to control ducklings, ducklings from parents fed a diet containing 0.5 or 3 ppm mercury were hyper-responsive in the test of avoidance of a frightening stimulus.Mallard eggs collected in the wild have been found to contain levels of mercury exceeding the 1 ppm (wet-weight) found in the eggs of hens fed a diet containing 0.5 ppm, but there are no reports of mallard eggs collected in the wild that were found to contain as much mercury (6 to 9 ppm) as eggs from hens fed a diet containing 3 ppm mercury. On a dry-weight basis, the concentration of mercury in the eggs was about 6 times as great as that in the feed for ducks fed the 0.5 ppm mercury diet and about 6 to 9 times as great for ducks fed the 3 ppm mercury diet.     

Toxicity of Lead-Contaminated Sediment to Mallards

Because consumption of lead-contaminated sediment has been suspected as the cause of waterfowl mortality in the Coeur d'Alene River basin in Idaho, we studied the bioavailability and toxicity of this sediment to mallards (Anas platyrhynchos). In experiment 1, one of 10 adult male mallards died when fed a pelleted commercial duck diet that contained 24% lead-contaminated sediment (with 3,400 μg/g lead in the sediment). Protoporphyrin levels in the blood increased as the percentage of lead-contaminated sediment in the diet increased. Birds fed 24% lead-contaminated sediment exhibited atrophy of the breast muscles, green staining of the feathers around the vent, viscous bile, green staining of the gizzard lining, and renal tubular intranuclear inclusion bodies. Mallards fed 24% lead-contaminated sediment had means of 6.1 μg/g of lead in the blood and 28 μg/g in the liver (wet-weight basis) and 1,660 μg/g in the feces (dry-weight basis). In experiment 2, we raised the dietary concentration of the lead-contaminated sediment to 48%, but only about 20% sediment was actually ingested due to food washing by the birds. Protoporphyrin levels were elevated in the lead-exposed birds, and all of the mallards fed 48% lead-contaminated sediment had renal tubular intranuclear inclusion bodies. The concentrations of lead in the liver were 9.1 μg/g for mallards fed 24% lead-contaminated sediment and 16 μg/g for mallards fed 48% lead-contaminated sediment. In experiment 3, four of five mallards died when fed a ground corn diet containing 24% lead-contaminated sediment (with 4,000 μg/g lead in this sample of sediment), but none died when the 24% lead-contaminated sediment was mixed into a nutritionally balanced commercial duck diet; estimated actual ingestion rates for sediment were 14% and 17% for the corn and commercial diets. Lead exposure caused elevations in protoporphyrin, and four of the five mallards fed 24% lead-contaminated sediment in a commercial diet and all five fed the contaminated sediment in a corn diet had renal intranuclear inclusion bodies. Lead was higher in the livers of mallards fed 24% lead-contaminated sediment in the corn diet (38μg/g) than in the commercial diet (13 μg/g). Received: 9 April 1998/Accepted: 21 October 1998     

Barbiturate potentiation in mercury poisoning

Summary Barbiturate potentiation was observed in Japanese quail fed dietary levels of 4, 21, and 24 ppm Hg as methyl mercuric chloride. Gross symptoms of mercury poisoning were not observed until after BP was observed. After the initial increase in BP time was observed in the birds receiving 4 and 12 ppm mercury, there followed a plateau in response until those birds receiving 24 ppm Hg began to show gross symptoms of toxicity and the, BP time markedly rose again. Pronounced BP persisted 7 weeks after removal of mercury from the diet reflecting the long biological half-life of mercury as the methyl derivative. Selenium effectively prevented BP after 7 days exposure to toxic levels of methyl mercury chloride. Therefore, results suggest that early toxic effects of mercury can be observed readily by BP and that this environmental contaminant may influence drug activity or increase the sensitivity of the nervous system to sodium pentobarbital.Scientific Article No.A1993, Contribution No.4935 of the Maryland Agricultural Experiment Station.     

Concentrations versus amounts of biomarkers in urine: a comparison of approaches to assess pyrethroid exposure

Background

In 2005, 84% of Wayana Amerindians living in the upper marshes of the Maroni River in French Guiana presented a hair mercury concentration exceeding the limit set up by the World Health Organization (10 μg/g). To determine whether this mercurial contamination was harmful, mice have been fed diets prepared by incorporation of mercury-polluted fish from French Guiana.

Methods

Four diets containing 0, 0.1, 1, and 7.5% fish flesh, representing 0, 5, 62, and 520 ng methylmercury per g, respectively, were given to four groups of mice for a month. The lowest fish regimen led to a mercurial contamination pressure of 1 ng mercury per day per g of body weight, which is precisely that affecting the Wayana Amerindians.

Results

The expression of several genes was modified with mercury intoxication in liver, kidneys, and hippocampus, even at the lowest tested fish regimen. A net genetic response could be observed for mercury concentrations accumulated within tissues as weak as 0.15 ppm in the liver, 1.4 ppm in the kidneys, and 0.4 ppm in the hippocampus. This last value is in the range of the mercury concentrations found in the brains of chronically exposed patients in the Minamata region or in brains from heavy fish consumers. Mitochondrial respiratory rates showed a 35–40% decrease in respiration for the three contaminated mice groups. In the muscles of mice fed the lightest fish-containing diet, cytochrome c oxidase activity was decreased to 45% of that of the control muscles. When mice behavior was assessed in a cross maze, those fed the lowest and mid-level fish-containing diets developed higher anxiety state behaviors compared to mice fed with control diet.

Conclusion

We conclude that a vegetarian diet containing as little as 0.1% of mercury-contaminated fish is able to trigger in mice, after only one month of exposure, disorders presenting all the hallmarks of mercurial contamination.     

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.