Document DGX297qdGedREykaonO2ZL535

p, Wheeler Effects of 15 Common Environmental Pollutants on Eggshell Thickness in Mallards and Coturnix by Max A. Hafcki.k and Michaud K. Ti cker , ,, Introduction Bureau of S/mrt Fisheries and ftiIdlife Denier W ildtifr Research Center Bldg, 1A, Pvnrrr Federal Centrr Deni er, Colo. 80225 Eggshell thinning has been documented In several species of fish-eating and raptorial birds in recent years (ANDERSON et al. 1969, FYFE et al. 1969, HICKEY and ANDERSON 1968, KEITH et al. 1970). High residue levels of DDE, the principal metabolite of DDT, were found in the affected birds and their eggs. Most re searchers believe that DDE is the causative agent In the shell thinning phenomenon (ANDERSON ec al. 1969, CADE et al. 1971, FYFE et al. 1969, HICKEY and ANDERSON 1968, KEITH et al. 1970, PEAKALL 1970 b). However, laboratory studies with birds given DDE have not shown shell thinning of the magnitude (as much as 30%) seen in some species of wild birds (R1SEBR0UCH et al. 1971). For ex ample, studies with penned ducks (HEATH et al. 1969, L0NGC0KE et al. 1971) have shown that DDE can cause eggshell thinning of 13 to 23X. The lower degree of thinning in ducks may be duo to species differences, or to the possibility chat the responses of this and other species under laboratory conditions may not be re presentative of those of fish-eating and raptorial birds in the wild. However, it is also possible that additional chemicals are partly responsible for the greater shell thinning and reproduc tive failure seen in some wild birds. Long and extensive use of DDT hes led to the ubiquitous occurrence of the stable metabolite DDE In the environment (HICKEY 1969), but other chemicals, such as mercury, lead, and polychlorinated biphenyls, have also been shown to be widespread environmental pollutants (KNAPP 1970, LA2RUS et al. 1970, PEAKALL and LINGER 1970). This study was conducted to investigate the capacity of some of these compounds to cause egg shell thinning. Fifteen common pesticides and environmental pollutants, including DDE, were tested by a rapid, short-term screening procedure in two conson species of laboratory birds. Procedure Eighty-four unmated female coturnix quail (Coturnix coturnix japonica) were randomly distributed Into 16 groups of 6 each and placed in individual Indoor cages on a regimen of 14 hours of UghL and 10 hours of dark. Eighty female mallards (Anas platyrhynchos) in their first reproductive season were randomly distributed into 16 groups of 5 birds each and placed in outdoor cages. Eggs were collected from ail birds for 6 days to obtain en average pre-treatment eggshell thickness. Each group was orally administered a single dose of one of the chemicals, by gelatin capsule through glass tubing to the level of the proventrlculua. So that maximum shell-chlnnlng potential for each chemical would be expressed, dosages were chosen to be high but 96 Tlull'lm l Fn. ii-.nm.nut Oniumiiidinn 41 Tnirc'Jn|-. V.il II. IV.. I (i> 19*4 U, S|'<etr. fsr.. V>t - 08 iU' U: of fin Uali : at 13 of re-' he re of lita h ae Shown I *t I to t|g- trnlx end r iy loor tin en- >ut not lethal. Eggs laid after treatment were collected and measured for 6 days, except tor eggs from the DDE-treated mallards, which were collected for 18 days, and chose from che Aroclor-treated mallards, which were collected for 10 days. Eggs (Including membranes) were measured at the equator to the nearest 5 microns with a micrometer. Results and Discussion Table 1 lists the chemicals and dosagea given, and shows the 12 treatments that had no apparent effect on eggshell thickness. Figures 1, 2, and 3 show the results with the 14 treatments chat caused eggshell thinning in coturnlx or mallards. The graphs show that single oral doses of several chemicals and pesticides caused temporary eggshell thinning in coturnlx and mallards. But the only ' prolonged eggshell thinning observed was that caused by p.p'-DDE In mallards. Much of the eggshell thinning observed in coturnlx was probably caused by low food consumption in the treated birds. Food consumption was greatly reduced during the first few day9 after treatment In coturnlx that showed eggshell thinning (Figure 1), but not in the coturnlx which did not exhibit eggshell thin ning (Table 1). Figure 1 shows that untreated birds, when fasted for 36 hours, laid thln-shelled eggs for a few days during and j after the fast. This pattern was quite similar to that shown by I the chemically treated birds. Mallard food consumption was not measured because of inclement weather and outdoor pens, but lower food consumption after treat ment probably had some transitory shell effect, as in the coturnlx. Mallards that have been fasted for a few days in some of our other studies have laid egga with thinner shells during and shortly after the faat. The timing of the eggshell thinning In mallards given DDE differed from that seen with the other compounds tested (Figure 3). These birds were still laying thin-shelled eggs at 6 days post treatment, so eggs were collected for an additional 12 days. Even by this time, there was no appreciable recovery to normal shell thickness. Not only did thinning last longer, but maximum thinning also occurred more quickly (within about 20 hours after treatment). PEAKALL (1970 a) also found thinning in the first eggs laid after ring doves (Streptopelia rlsoria) were Injected with DDE. The fact that birds treated with a single dose of DDE lay thin-shelled eggs in less than 24 hours suggests that eggshell thinning is not associated with enzyme induction. In this amount of time, liver microsomal enzymes probably could not be Induced at levels sufficient to cause the thinning observed. ' Except for the pattern shown by DDE, the shell thinning pro duced by the compounds tested appears to be associated with re duced food consumption caused by sublethal intoxication and could be termed toxic thinning. In contrast, the shell-thinning re sponse to DDE appears to occur in the absence of any other clinical sign of Intoxication. Thus It appears that DDE, the major degradation product of DDT In the environment, can be a very quick-acting eggshell-thinning agent with long-term effects. This suggests that birds exposed to DDE on the winter grounds or during migration north could lay thin-shelled eggs, even though the food supply where they nested was not significantly contami nated. 99 MQNS 08572Q TABLE 1 Chemicals tested for eggshell-thinning effects Compound Single Oral Dose (mg/kg) Coturnix Mallards Aroclor 125W (PCB) Ceresan M^/ 2,4-D acid p,p'-DDE 500 500 250 . 12SS-' o,p'-DDT pp'-DDT DDT Dieldrln Chlordecone Heptachlor Parathion Carbary1 Sodium arsenite Tetraethyllead Toxaphene 12&/ 12j^ 125^ 10/ 2.5 1000 6 io/ 1000 500 1500 . 500 1000 2000 60E7 25=/ 1000 }* looo^ 100 5/Trade name of Monsanto for polychlorinated biphenyl containing 542 chlorine. Reference to trade names does not Imply endorsement of commercial products by the Federal Govern ment . k/Trade name of DuPont for N-(ethylmercuri)- p-tolusne sulfonanllide. . 5/Caused no appreciable eggshell thinning (Re duction between pre- and post-treatment thickness, <5 microns). 100 HONS 085721 IO O S H IU T M IC K N III fM IC ftO N S l t 8.8*/fc Mi Hi 1M /!> ! 800 Mf/h Aracler 1384 z 0 M V I CeeVre I 8,0 nif/k| ttoyll** AVI OIT-TIIATMINf Figure 1. Treatments causing short-term eggshell thinning In coturnix (six birds per treatment). Dotted lines represent average 6-day pre-treatment eggshell thickness. Figure 2. Treatments causing short-term eggshell thinning in mallards (five birds per treatment). Dotted lines represent average 6-day pre-treatment eggshell thickness. Eggs collected for days 7 through 10 averaged greater than normal thickness. HUNS 085722 I r Central Figure 3 Effects of p,p`-DDE on mallard eggshell thickness (five birds per treatment). Dotted lines represent average 6-day pre-treatment eggshell thickness. 9 2000 mi/ltg p.p'DDI ` `............ a 4 * I 10 11 M M II OATS POST-TRKATMIMT References ANDERSON, D. W., J. J. HICKEY, R. W. RISEBROUGH, E. F. HUGHES, and R. E. CHRISTENSEN: Can. Field Natur. 83, 91 (1969). CADE, T. J., J. L. LINCER, C. M. WHITE, D. G. ROSENEAU, and L. C. SWARTZ: Science 172. 935 (1971). FYFE, R. W., J. CAMPBELL, B. HAYSON, end K. HODSON: Can. Field Natur. S3, 191 (1969). HEATH, R. C., J. W. SPANN, and J. F. KKEXTZER: Nature 224, 47 (1969). HICKEY, J. J.: Atlantic Natur. 24, B6 (1969). HICKEY, J. J., and D. W. ANDERSON: Science 162, 271 (1966). KEITH, J. 0., L. A. WOODS, JR., and E. G. HUNT: Trane. 35th North Aver. Wildl. Natur. Resources Conf., p 56 (1970). KNAPP, C.. E.: Environ. Sci. Techol. 4, 890 (1970). LAZRUS, A. L., E. LORANCE, end J. P. LODGE, JR.: Environ. Scl. Techol. 4, 55 (1970). LONGCORE, J. R., F. B. SAMSON, and T. U. WHITTENDALE, JR.: Bull- Env. Cont. and Toxicol. 6, 485 (1971). PEAKALL, D. B.: Science 168, 592 (1970 a). PEAKALL, D. B.: Sci. Aair. 222, 73 (1970 b). PEAKALL. D. B., and J. L. LINCER: BioSclence 20. 958 (1970). RISEBROUGH, R. W., F. C. SIBLEY, and M. N. KIRVEN: Aver. Lrdi 25, 8 (1971). 1Q2 HONS 085723