Document NEZVpy6rxQ8GbRazebx9YmdKp

' l^c^ -:Hopct!lb.-Vxr^ Abstract. Tcn-day-old mallard ducklings fed a polychlorinated biphenyl at concentrations of 25, 50, and 100 parts per million for 10 days suffered no apparent clinical intoxication. Five days later these birds were challenged with duck hepatitis virus, and they suffered significantly higher mortality than birds which were not exposed to the polychlorinated biphenyl. Polychlorinated biphenyls (PCB) along with DDE [l,l-dichloro-2,2-bis(p-chlorophenyl) ethane] are reported - to be the most abundant of the chlo rinated hydrocarbon pollutants in the global ecosystem (1). Despite the fact that PCB's have been in wide use since 1930 (2), they remained eco logically inconspicuous until 1966 when 10-day feeding trial, no birds died or became clinically ill, although duck lings in the group given 100 ppm PCB were noticeably hypcrcxcitablc after day 3 as were those in the 50-ppm group 4 days after treatment. Body weights of birds receiving PCB in their diet were significantly heavier at the end of the 10-day feeding trial isolation units where they were main tained on PCB-frcc feed and water for 3 days before being- challenged with DHV. No birds died or became clinically ill during the interim period between PCB feeding and virus chal lenge although two birds were lost from the 100-ppm group due to accidents. On day 15 of the experiment all but, a Swedish chemist reported their pres than those fed the diet without PCB the untreated controls (birds not re- ence in the tissues of pike and other (Table 1). The heaviest body weights ceiving either PCB or DHV) were in- * wildlife (3). Since then, their presence occurred in birds fed the highest con oculated intraperitoneally with 1.5 1 has been reported in additional wild-, life of Europe and North America (/, 4). These compounds are interesting because they are an important source of interference in the chemical detec tion of DDT and its metabolites (5) and because they are a potential hazard in centrations of PCB, and the > trend ap peared to be linear. Differences in body weights among treatment means were highly significant (F = 20.30, d.f. = 4, 119) when tested by analysis of covariance. No statistical comparisons between individual treatment means LD-J (50 percent effective lethal dose for dtlcks) of DHV per bird. The first birds died about 47 hours after inoculation. Mortality was recorded hourly for the remainder of the 80hour experimental period with one cxcoption; there were no observations be the environment; on a weight basis PCB preparations have been shown to have an estradiol-degrading potential about were made. A similar analysis of liver weights (determined as a percentage of final body weight) disclosed highly sig tween hours 63 through 69. The onset of mortality in all groups given PCB .plus DHV began at least 8 to 16 hours- five limes that of p,p'~DDE or techni nificant differences among treatment before that in the control group treated cal grade DDT [ 1,1,1 -trichloro-2,2-bis- means (F = 5.82, d.f. = 4, 18). These with the virus only (Fig. 1). In addi (p-chlorophcnyl)cthane] (7). differences appeared to be within tion, mortality levels occurring among As part of an investigation of possi ble interactions between organochlorinc groups treated with PCB rather than : PCB-plus-virus treatment groups at the between treated and untreated groups ; end of the experiment were significantly pollutants and infectious diseases, this (Table 1). The small sample sizes (N = higher at the .01 level of probability. ' study was initiated to determine 5) necessitates caution in interpretation than for ducklings receiving the virus whether any interaction, antagonistic or of liver weight data. No interpretation only (chi square = 7.49, d.f. =. 1). synergistic, occurs with PCB and duck of differences among body ana liver There was no significant difference in ' -hepatitis virus (DHV) in mallards weights are offered at this time. mortality among ducklings receiving the (Anas platyrhynchos). . different concentrations of PCB plus ' Four separate diets, three with PCB : Tabic 1. Final mean body and liver weights and one without, of a standard duck starter ration were fed to groups of of mallard ducklines aflcr being fed PCB ' (Aroclor 1254, Monsanto, St. Louis) for 10 days. Numbers in parentheses arc the number virus (chi square = 3.79, d.f. = 2). No birds in the untreated group died (Table 2). 10-day-old mallard ducklings. The three of birds used. The liver and body weights PCB diets contained Aroclor 1254 (in . were adjusted by covariance for o common starting mean; the liver weight was determined a com oil premix) concentrations cal ' as percentage of body weight. The final con AH birds that died during the experi ment had gross pathognomonic liver lesions, indicating typical duck hepa culated to be 25, 50, and 100 parts per trol did not receive cither PCB or D1IV. titis infection (6). No other gross million (ppm). These diets were fed to five groups of 22. ducklings each, three jyincipal and two control groups , (Table f). -- . All birds were leg-banded with color ' coded, numbered bands, weighed, and fed their respective diets for 10 days. Treatment (pPpCmll) PCB + DHV PCB + DHV PCB + DHV DHV control Control 100 50 25 0 0 Body weight (B) 381.6(25) 368.8 (25) 352.8 (25) 315.2(25) 309.6(25) JJvcr weight (e) 0.046 (5) .037 (5) .029 (5) .036 (4) .034 (5) lesions, with the exception of varying amounts of edema within the peri cardium and_ thoracic cavity of some birds, were observed. There did not ap- , pear to be any relation between treat- : ment and the presence or absence of edema. Histological and residue analy On day 11 each bird was weighed sis have not been completed at this again, and every fifth bird from each treatment group was killed. Tissues vr ' . , . time. Twelve days after the experiment be ' The suggestions that PCB may render were collected for residue analysis, his ' tology, and liver weights. During the gan, birds were placed in crates and a host more susceptible to certain types transported approximately 5 miles to of infectious agents is the significant lover] 18 December 1970 OSW 282008 SCIENCE, Vol. 170 STLCOPCB4063336 finding in this study. None of the conccntrations of PCB fed resulted in de tectable chemical intoxication even with the physical stresses of weighing, handling, confinement, and crowding during transportation, transportation it self, or relocation in a different environ ment. However, when the stress of an infectious agent was added, these sublethal concentrations appeared to in fluence the resulting mortality rates, causing two- to fourfold increases (14 percent among virus controls versus 35 to 65 percent among groups receiving PCB plus DHV) and reduced incuba tion time (Fig. 1 and Table 2). Similar increases in mortality were obtained with other organochlorine compounds in our laboratory (7). In those studies 30-day-old mallard duck lings which had been fed sublelhal con centrations of p.p'-DDT or dieldrin exhibited three- to ninefold increases in mortality over that of DHV controls (6 percent among virus controls versus 19 to 59 percent among groups receiv ing dieldrin plus DHV, and 19 to 40 percent among groups receiving p,p'DDT plus DHV). It is unlikely that in all these instances mortality in the DHV control groups would be less than Tabic 2. Mortality among mallard ducklings caused by DHV during an RO-hour experimental period. No observations were made between 31 to 47 and 62 to 70 houn. The final control did not receive cither PCB or'DHV. Treatment PCB (ppm) No. of deaths/ total sample Mortality Percentage Onset (hours) Cessation (hours) PCB + DHV PCB + DHV PCB + DHV DHV control . Control 100 50 25 8/18 13/20 7/20 3/21 0/20 44.4 65.0 35.0 14.3 Oh 31-47 55. 31-47 62-70 75 76 ' 75 . 73 60 >, 40 20 - __y -e - 50 60 70 80 Time (hours) Fig. 1. Mortality among mallard ducklings exposed to both PCB and DHV, DHV only, or neither agent, (a) 100 ppm PCB + DHV; (b) 50 ppm PCB + DHV; (c) 25 DSW 282009 STLCOPCB4063337