Lead Toxicity in Mute Swans

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for obvious reasons, the visits of the adult birds are nee ·1 b · f · Id · essart y ne This wou !11ean, tn consequence, that exposure of sub-adult birds· to t~e tdm1ttedly a~ _Yethundefined lead source at The Lough i~ re 1 at1ve y gre .at~r an . 1s t us reflected in the blood picture. Although 1t 1s unlikely that the source of increased lead th · L · · was e River ee - s.ince 1t would be washed away by the swift river flow - g.rab samplmg and dredging has failed to confirm that the birds obtained lead at The ~ough. The few lead weights found there and .zero trace lead levels m .the wate: are _ . pe~plexing and may reflect the madequac~ of t~e sampling techniques. Further research is obviously necessary tn this area .. Ne:ertheless, preliminary results from grab sampl.es at ~he Lough indicate that the sub-littoral is silty and has very little gnt. Thus any spent lead or lead shot having fallen into the "":ater or bee.n caught ~n the vegetation would soon be picked up by blfds searching for gnt. · The cygnets at The Lough, as expected, had low levels in their blood (8 .28-29.80µg/100mls) compared to adult or sub-adult birds. However, cygnets contaminated at The Lough had demonstratively higher levels than those of adults at 'country sites'. The only cygnet value lower (8.28µg/100mls) was from a very young bird - introduced into The Lough from Kanturk - where its parents had been killed . Note that the other cygnet in the sample had hatched at The Lough. However, blood lead levels are known to fluctuate and it has been suggested that this may be due to temporal variations in exposure. (Birkhead 1983). Indeed the degree· of exposure as indicated by the blood picture is not now regarded as a totally reliable correlation as the elevated blood lead levels following an acute exposure are not necessarily maintained for more than seven to ten days. A good example of this problem was noted in The Lough sample. The very first bird examined on 4th October 1983 had a blood lead level of 354µg/ 1 OOmls. Some three weeks later this elevated level had more than halved (31st October 1983 the blood lead level was 104µg/1 OOmls). Comparable variation in blood lead levels has also been noted by Birkhead (1983). Because of the interpretation difficulties which these fluctuations cause, it has been recommended that further assessment of the damage caused by high lead levels be obtained by measuring zinc protoporphygrin in the eryth~ocyte (Bush et al 1982). This is because one of the susceptible enzymes is ferrochelatase which catalyses the conversion of protoporphrin into haem (Lee 1981). This inhibition of protoporphyrin synthesis causes anaemia, a characteristic of lead poisoning. Although only two corpses :vere av~ilable for post:morte'!: examination, they proved sufficient to illustrate the differer. .. ~ between a lead poisoned bird and one with very low, presumably non- - 145 -
toxic lea? l~vels. The post-mortem examinations in this study revealed the first mc1dence of a Mute Swan ~atality ~aused by lead poisoning in Ireland. The syn:ptoms were consistent with the findings of previous workers. Both Simpson et al (1979) and Birkhead (1981) refer to the ab~orr:ial car:iag~ ?f the neck .as a pronounced symptom of lead poisomng. This cltmcal feature 1s caused by partial paralysis of the alimentary track that inhibits peristalsis with a resultant clogging of the gizzard, proventriculus and eventually the oesophagus. Jordan and Bellrose (1951) found impacted gizzards in 44% of lead poisoned ducks and a distinct starvation syndrome, which resulted in an enlarged gallbladder, a symptom also found in this study. · Quantitative chemical analysis of soft tissues employed in this investigation provided sufficient evidence to incriminate lead as the cause of fatality. The level of lead in the liver of the poisoned bird ( 44. 3 µg/ g wet matter) exceeds the level (SO~tg/ g dry matter 0111.z.i'µg/ g wet matter) widely recognised as lethal in plumbism. Similarly the kidney lead level (111. 78µg/ g w .m.) exceed the limit (125µg/g d.m. or 31.25µg/g w .m.) required to confirm death due to lead poisoning. (Clarke and Clarke 1975, Birkhead 1982). The blood lead was also greatly elevated. Little data on the diagnostic value of the remaining tissues is published. Nevertheless, the levels found in kidney, liver and other tissues were greater than that of the cygnet by many orders of magnitude and were presumably toxic (Table 6). The toxic effect of lead on the kidneys of many organisms including swans is under intensive investigation (Birkhead 1982 and Chisholm 1971). Much of the excess lead is concentrated in the form of dense inclusion bodies in the nucleii of the proximal and distal tubule cells (Locke, Bagley and Irby 1966). The significance of the inclusion bodies found in this study were that they were located in the nucleus, mitochondria and cytoplasm. Although the size and number of inclusion bodies is known to vary Table 6 Details of two swans taken for post mortem LEAD Sex Age Nr. of Lead shot in Gizzard µg/lOOmls µg/gm (wet matter) Blood Breast \ Heart Kidney Liver Muscle Pancreas Male Sub-Adult 4 652 4.24 57.34 11!.78 44.43 43.78 Male Cygnet 0 18.6 1.86 2.4 5.11 - 146 -.
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0004067t:.7 1~11111 /I llll II llll
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This thesis is dedicated to my moth
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ABSTRACT Lead toxicity in Mute swan
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- what are the best methods for the
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Benson, W.W., Brock, O.W., Gabrica,
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CHAPTER 1 DETERMINATION OF HAEMOGLO
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MATERIALS AND METHODS Blood was obt
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standards are now available, it is
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I ' ABSTRACT The use of blood lead
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developed and (c) information on bl
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MATERIALS AND METHODS Study sites.
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Swans were sexed by cloacal examina
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Red blood cell protoporphyrin .. Th
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RESULTS Blood Lead Levels Diel vari
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16.00 24.CO 2.00 7.00 - ~ ~--1_ J l
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for corrected lead values (ug /g Rb
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Table 2. Blood lead levels of indiv
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30 20 (A) n = 357 10 0-.99 1- 2- 3-
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Blood lead is very labile (Chamberl
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median value of lead in April is si
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elevated lead levels. (2) Haemoglob
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Chisolm, J.J. & Browne, D.R. (1975)
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Ohi, G., Seki, H., Akiyama, K. & Ya
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CHAPTER 3: SECTION 1 LEAD POISONING
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mammals' (Finley et al. 1976). This
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commute from areas up to 20km away
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TABLE 1: Causes of death in Irish s
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I 4. Coiled shot: malleable stainle
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CHAPTER 3: SECTION 2 LEAD POISONING
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I INTRODUCTION The importance of le
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42,000 anglers visit the State each
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MATERIALS AND METHODS Study sites B
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30KM f Fig.l Map of Ireland indicat
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lead. X-ray. They were subsequently
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RESULTS Blood levels Blood lead lev
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I Table.II Proportion of lead poiso
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I of the gizzard and oesophagus and
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Table IV. 11 (of 41) X-rayed swans
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Table V. Median water lead levels (
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of pellets had occured. What is sig
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irds by Bellrose (1959) in the U.S.
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I the pellets as they moved in shor
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i Chamberlain, A.G. (1985). Predict
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Ong, C.N. & Lee, W.R. (1980). Inter
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SUMMARY Reference levels of some bi
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I adults, immatures, females and ma
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I centrifugation in microhaematocri
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RESULTS All blood samples included
Page 99 and 100: Table 1. Mean (± s.e.) maximum and
Page 101 and 102: Table 3. Haematological and biochem
Page 103 and 104: Table 5. Haemoglobin, haematocrit a
Page 105 and 106: Table 6. Age, sex, blood lead level
Page 107 and 108: DISCUSSION The normal range of haem
Page 109 and 110: considered when using protoporphyri
Page 111 and 112: I the blood constituents, reflectin
Page 113 and 114: REFERENCES Bates, F.Y., Barnes, D.M
Page 115 and 116: i Lucas, A.M. and Jamroz, C. (1961)
Page 117 and 118: CHAPTER 5 TISSUE LEAD LEVELS AND HA
Page 119 and 120: INTRODUCTION Lead poisoning through
Page 121 and 122: I r MATERIALS AND METHODS Collectio
Page 123 and 124: I RESULTS Tissue lead levels Tissue
Page 125 and 126: Table 1. Tissue lead levels (ug/ g)
Page 127 and 128: Table 3 Age, sex, blood lead level
Page 129 and 130: DISCUSSION Tissue lead levels have
Page 131 and 132: which had collided had raised blood
Page 133 and 134: REFERENCES Anders, E., Dietz, D.D.,
Page 135 and 136: O'Halloran, J., Myers, A.A. and Dug
Page 137 and 138: many others for helping to catch sw
Page 139 and 140: APPENDIX 1 LEAD LEVELS IN MUTE SWAN
Page 141 and 142: intense fishing in summer and large
Page 143 and 144: area of 4m 2 , were taken. The samp
Page 145 and 146: levels of the birds on the Lee also
Page 147 and 148: i oesophagus, proventriculus and gi
Page 149: in blood. In general, healthy birds
Page 153 and 154: London area. Part 2 Biological Effe
Page 155 and 156: Prelin1inary results of ringing Mut
Page 157 and 158: Ringed Mute S1rans ?f the. 61 I r~~
Page 159: Acknowledgments Ringed Mute S1ra11s
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Lead Toxicity in Mute Swans

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