MORTALITY OF COMMON LOONS IN NEW ENGLAND, 1987 TO 2000

JOURNAL OF WILDLIFE DISEASESThursday May 15 2003 08:49 AMAllen Press • DTPro System

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Journal of Wildlife Diseases, 39(2), 2003, pp. 306–315q Wildlife Disease Association 2003

MORTALITY OF COMMON LOONS IN NEW ENGLAND, 1987 TO 2000

Inga F. Sidor,1,5,6 Mark A. Pokras,1 Andrew R. Major,2 Robert H. Poppenga,3 Kate M. Taylor,4and Rose M. Miconi11 Tufts University School of Veterinary Medicine, Wildlife Clinic, 200 Westboro Road, North Grafton,Massachusetts 01536, USA2 US Fish and Wildlife Service, 70 Commercial Street, Suite 300, Concord, New Hampshire 03301, USA3 Laboratory of Pathology and Toxicology, New Bolton Center, University of Pennsylvania, Kennett Square,Pennsylvania 19348, USA4 Loon Preservation Committee, P.O. Box 604, Moultonborough, New Hampshire 03254, USA5 Current address: Department of Pathobiology, University of Connecticut, 61 North Eagleville Road, U-89, Storrs,Connecticut 06269-3089, USA6 Corresponding author (email: [email protected])

ABSTRACT: Diagnostic findings are presented on 522 common loons (Gavia immer) found deador moribund in New England (Connecticut, Maine, Massachusetts, New Hampshire, Rhode Is-land, and Vermont, USA) between 1987 and 2000. Common loon numbers and range in NewEngland have decreased from historic levels over the last century due to a number of proposedfactors. Goals of this study were to identify and categorize causes of mortality and quantify naturalversus anthropogenic causes. The majority of identifiable mortality in chicks was from intraspecificaggression (25%) and other causes of trauma (32%). Death in immature loons was primarily fromfungal respiratory disease (20%) and trauma (18%). Causes of adult loon mortality differed sig-nificantly in breeding and wintering habitats. Wintering adults primarily died of trauma (17%)and infection (11%) and had significantly poorer body condition than breeding loons. In breedingadults, confirmed and suspected lead toxicosis from ingested fishing weights accounted for almosthalf of all mortality. Direct anthropogenic factors accounted for 52% of loon mortality in thisstudy. Because of high carcass recovery rates, we believe these data are a good representation ofloon mortality in New England. Results highlight the importance of human influences on con-servation and management of the common loon in New England.

Key words: Anthropogenic factors, Aspergillus, common loon, Gavia immer, lead toxicosis,New England, trauma.

INTRODUCTION

Common loons (Gavia immer) havebeen proposed as indicators of aquatichealth in the northern lake ecosystemsthey inhabit (Scheuhammer et al., 1998)and are the subjects of intense study.Loons are listed as a threatened or endan-gered species in several northeasternstates. Because of a variety of environmen-tal and human factors, their numbers andrange in New England have decreasedfrom historic levels over the last century(McIntyre and Barr, 1997). Despite recov-ery over the last few decades due to man-agement of these populations, mortalityhas increased in some areas (New Hamp-shire Loon Preservation Committee, un-publ. data). Previous studies of loon mor-tality have documented lead toxicosis, oilspill contamination, respiratory aspergillo-sis, botulism, trauma, net or monofilamentfishing line entanglement, and an emacia-

tion syndrome of unknown etiology asleading causes of death (Brand et al., 1988;Pokras et al., 1991; Forrester et al., 1997;Augspurger et al., 1998; Daoust et al.,1998). Environmental contaminants, suchas mercury and organochlorines, are ele-vated in some populations as well, thoughit is debated whether this is linked to in-creased mortality (Frank et al., 1983; For-rester et al., 1997; Barr, 1986; Augspurgeret al., 1998).

This mortality study of New England’scommon loons was begun in 1987 after acase of lead toxicosis due to fishing sinkeringestion was found in New Hampshire.The goals were to identify and quantifynatural and anthropogenic causes of mor-tality in this population. This report sum-marizes results of 12 yr of collection andanalysis of loons from across New Englandand compares these results with those ofprevious studies.

SIDOR ET AL.—LOON MORTALITY IN NEW ENGLAND 307



FIGURE 1. Location of common loon carcassesexamined from New England, 1987–2000. The num-ber of loons collected per site is indicated by the sizeof the corresponding circle. No site had between 13and 19 loons collected.

MATERIALS AND METHODS

From 1987 to 2000, 522 dead or moribundloons were submitted to the Wildlife Clinic atTufts University School of Veterinary Medicine(TUSVM) in North Grafton, Massachusetts.Loons were collected from both interior andcoastal regions in Connecticut (n56), Maine(n5173), Massachusetts (n5118), New Hamp-shire (n5184), Rhode Island (n511), and Ver-mont (n530) (between 478259N, 668559W and41809N, 738459W) by state and federal wildlifeagencies, wildlife rehabilitators, veterinarians,and non-profit organizations. Geographic dis-tribution of loons collected for this study isshown in Figure 1. Sick or injured loonsdeemed non-releasable were euthanized by in-travenous injection of sodium pentobarbital(Beuthanasia-D Special Euthanasia Solution,Schering-Plough Animal Health Corp., Union,New Jersey, USA), according to currently ac-cepted veterinary protocol (American Veteri-nary Medical Association, 2000). Carcasses col-lected from remote areas were frozen as soonas possible after collection, and kept frozen un-til the time of examination, usually 3–6 mopostmortem. Each bird was weighed and radio-graphed and complete gross necropsy was per-formed. Age class categories were chick (pre-fledging, on natal lake), immature (fledged, justbefore migration away from the natal lake oron saltwater after migration), or adult, as dif-ferentiated by plumage. Breeding and winter-ing adult populations were distinguished by theseason and site of collection and plumage.Body condition was subjectively scored as good,thin, or emaciated, as assessed by the abun-dance of subcutaneous, mesenteric, and peri-cardial fat stores and amount of pectoral mus-cle mass. Birds scored as good had abundantfat stores and pectoral muscle mass obscuring

a barely palpable keel. Thin loons had adequateto scant amounts of fat and a palpable keel.Emaciated loons had no fat depots, severely at-rophied pectoral muscle mass, and a prominentkeel. Sex was determined by direct visualizationof the gonad if carcass condition allowed posi-tive identification (n5451). The entire liver wascollected for lead and other contaminant anal-ysis, and stored in glass jars (I-Chem, Divisionof Nalge, New Castle, Delaware, USA) at270 C.

Liver lead was determined by inductivelycoupled plasma-atomic emission spectroscopyat one of three laboratories specified by the USFish and Wildlife Service (Hazleton Environ-mental Services, Inc., Madison, Wisconsin,USA, n549; Research Triangle Institute, Re-search Triangle Park, North Carolina, n521);and University of Pennsylvania, New BoltonCenter, Laboratory of Pathology and Toxicolo-gy, Kennett Square, Pennsylvania, USA,n5189). Detection limits varied by laboratorybetween 0.05 and 1.0 part per million (ppm).Values below the detection limit were includedin the calculations at the detection limit. Spe-cific toxicologic analysis techniques are detailedin Pokras et al. (1991) and Dahlquist and Knoll(1978). If the carcass was in suitable condition,a standard set of tissues was taken for histo-pathology, including esophagus, proventriculus,ventriculus, intestine, cecum, pancreas, liver,gall bladder, spleen, heart, trachea, lung, kid-ney, gonad, adrenal, thyroid, pectoral muscle,sciatic nerve, and brain, including any signifi-cant gross lesions. These tissues were fixed in10% neutral buffered formalin, dehydrated,and embedded in paraffin; 5 mm sections werestained with hematoxylin and eosin and exam-ined by light microscopy at the Tufts UniversitySchool of Veterinary Medicine Department ofPathology.

Determination of ultimate cause of deathwas based on history, clinical signs, and radio-graphic, gross, and microscopic findings. As de-scribed in Beyer et al. (1998) and Friend(1999), a diagnosis of lead toxicosis was madewhen a liver lead concentration .6 ppm wetweight was found in conjunction with either alead object in the ventriculus or clinical, gross,or histologic signs typical for lead toxicosis, orboth. A diagnosis of suspected lead toxicosiswas made when a lead object was present inthe ventriculus, with or without clinical or grosssigns, but liver lead levels were not determinedor were ,6 ppm. This category also included aloon euthanized because of the radiographicpresence of lead in its ventriculus, but whichhad liver lead ,6 ppm. Presence of lead objectsin the ventriculus was determined by radio-graphic and direct visualization of items of me-

308 JOURNAL OF WILDLIFE DISEASES, VOL. 39, NO. 2, APRIL 2003



tallic density. Metallic objects found in the ven-triculus were tested by a commercial qualitativecolorimetric swab method (Lead CheckSwabsq, HybriVet Systems, Inc., Framingham,Massachusetts); an intense pink color on theswab confirmed the presence of lead in the ob-ject.

The category of trauma included birds ob-served struck by boats and those with injuriesindicative of blunt trauma that was not consis-tent with loon aggression. A few trauma caseswere loons attempting to land on wet asphaltsurfaces that resemble open water. A diagnosisof intraspecific trauma was based on observa-tions in the field or by lesions consistent withpecking or penetrating beak wounds. Thesewounds included punctures of pectoral musclesand sternum or abdomen, with hemorrhageand laceration of internal organs, or, in chicks,wounds and feather loss at the back of the headand neck. The category of fishing gear mortalityincluded deaths caused by ingestion of fishinggear, with penetrating gastrointestinal woundsand peritonitis caused by hooks or gastric ob-struction by other gear, but not including in-gestion of lead sinkers. Entanglement with netsor monofilament line was also included in thiscategory.

Fungal respiratory infections were consid-ered a cause of death only when loons pre-sented with massive involvement of multiple airsacs, lung parenchyma, and other tissues.These lesions were identified grossly by thepresence of typical yellow, caseous, fungalplaques and nodules but were not cultured.When possible, the presence of Aspergillus sp.was confirmed histologically in these lesions bythe presence of typical branching, thin-walled,and septate hyphae. Cases not confirmed werecategorized as suspected fungal respiratory dis-ease.

Bacterial infection was diagnosed by histo-logic examination of involved tissues or by di-agnostic culture. Bacterial cultures were takenby culture swab from gross lesions suggestiveof bacterial infection. Cultures were submittedto the Tufts Veterinary Diagnostic Laboratory(North Grafton, Massachusetts) for isolationand identification by standard microbiologictechniques.

Loons with gunshot wounds generally exhib-ited both an entrance and an exit wound or hadbullet or pellet fragments lodged in tissues.Mortality associated with oil was diagnosed bythe presence of significant amounts of oil onthe feathers, with obvious disruption of water-proofing, with or without evidence of ingestionor internal lesions. Parasitic infections were de-termined to be the ultimate cause of death onlywhen significant gross or microscopic lesions,

or multi-systemic involvement was present.Parasites were identified by class as nematodes,cestodes, or trematodes but were not speciatedfor the purposes of this study; a subset of thesehelminths has been described previously (Chaf-el and Pokras, 1992). Predation was deter-mined by the presence of puncture wounds orlacerations not consistent with intraspecific at-tacks. Loon chicks deemed victims of predationwere typically recently hatched and found onor near the nest. Miscellaneous causes of mor-tality were identified based on their uniqueclinical, gross, and microscopic presentations.The category of unknown mortality includedloons with no significant gross or histologic le-sions and those found emaciated with minorfungal respiratory infections but no other ob-vious lesions, as well as carcasses too decom-posed for thorough examination.

Body weight data for live loons were collect-ed from 1995–97 as part of an on going captureand banding project in Maine and New Hamp-shire. Adult breeding loons were captured onfreshwater lakes by a spotlighting technique, aspreviously described (Evers, 1992). Bodyweight was measured to the nearest 50 g usinga 5 or 10 kg spring scale (Pesola Prazisionwaa-gen AG, Baar, Switzerland) and a mesh bag tocontain the loon.

Annual common loon censuses were con-ducted by Loon Preservation Committee fieldbiologists in New Hampshire to catalog individ-ual loons and the breeding success of pairs.Lakes were prioritized for visitation accordingto a three-tiered system. Tier I lakes had a cur-rent history of loon pairs defending territories(minimum of 3 yr continuous occupancy ornewly occupied) and required at least three sitevisits. Any lakes other than Tier I lakes that hada history of loon pairs were designated Tier IIlakes. Tier II lakes support loon pairs on anirregular basis and at least one visit was re-quired. Tier III lakes had few loon sightings onrecord. These lakes were visited as time al-lowed and prioritized by making observationson lakes not surveyed in the previous year. Allobservations were made from boat or by shore-line observations using 103 binoculars and/or15–453 spotting scopes.

Annual mortality was estimated by use of thebiologic effects submodel of the Natural Re-source Damage Assessment Model for Coastaland Marine Environments (NRDAM/CME,National Technical Information Service,Springfield, Virginia, USA).

General statistical and data analyses wereperformed using commercially available soft-ware (SPSS version 6.1, SPSS Inc., Chicago,Illinois, USA). Differences in mean weight andliver lead values between groups were com-




TABLE 1. Population of common loons in NewHampshire with mortality estimates and carcass re-coveries, 1996–99.

Year

Totaladult loons

in NewHampshirea

Estimatedannual

mortalityb

Looncarcassesrecovered

Percentrecovered

1996199719981999Average

450474493481474.5

4547494847

1513141213.5

33%28%29%25%28%

a Data collected by New Hampshire Loon Preservation Com-mittee.

b Assumes 10% annual mortality, as estimated by NRDAMmodel.

TABLE 2. Causes of common loon mortality in New England, 1987–2000, by age class and season.

Primary cause of death

Chick

n %

Immature

n %

Breedingadult

n %

Winteringadult

n %

All loons

n %

UnknownLead toxicosisa

TraumaIntraspecific traumaFishing gearFungal respiratory diseasea

28—b

3326

2—

27—32252

—

193

1234

13

295

1856

20

4511130112418

184412

497

394

17—

96

394

17—

96

13111892403937

252318877

InfectionGunshotOilMiscellaneousParasitesPredationTotal loons examined

10——

112

103

10——112

5—

312

—65

8—

523

—

48111

—254

23

,1,1,1—

11545

——

100

11545

——

30138842

522

62221

,1

a Combined confirmed and suspected cases.b None found.

pared using independent-samples t-tests. Cat-egorical variables were compared using a chi-square test. A Kolmogorov-Smirnov test wasused to assess normal distribution of variables.The Fisher’s exact test was used to comparedistributions of causes of mortality betweengroups using the shareware program Exact2xK(Abramson and Gahlinger, 2001). All state-ments of statistical significance are based onP,0.05.

RESULTS

Population, estimated mortality, and re-covery data of adult breeding loons fromNew Hampshire for 4 yr of the study arein Table 1. Mortality data for all loons in-

cluded in the study are summarized in Ta-ble 2.

Cause of death varied significantly byage group (P50.001) and habitat(P50.0008). The majority of identifiablemortality in chicks (n5103) was from in-traspecific aggression and other causes oftrauma. Death in immature loons (n565)was primarily from fungal respiratory dis-ease and trauma. Causes of adult loonmortality differed significantly in breedingand wintering habitats. Wintering adults(n5100) primarily died of trauma and in-fection. In breeding adults (n5254) con-firmed and suspected lead toxicosis fromingested fishing weights accounted for al-most half of all mortalities. There was nosignificant difference (P50.34) in causes ofmortality between sexes.

Body weight and subjective body con-dition scores of adult loons varied signifi-cantly by gender, habitat, and cause ofdeath. Weight was normally distributedwithin the population (P50.0001). Maleadult loons were significantly heavier thanfemale adult loons (P50.001), withweights of 4.261.2 kg (mean 6 SD,n5171) and 3.361.0 kg, (n5146), respec-tively. Wintering adult loons had signifi-cantly (P50.001) lower mean body weights




TABLE 3. Average adult loon body weight for eachcategory of mortality.

Primary cause of death

Averageweight

(kg)

Stan-dard

devia-tion(kg) n

Intraspecific traumaLead toxicosisTraumaFishing gearShotUnknownInfectionFungal respiratory diseaseMiscellaneousOilParasitesAll adult loonsa

4.54.33.73.63.53.43.43.43.32.61.63.8

1.31.01.31.41.31.21.10.91.10.3—1.2

11106

453012781522

651

331

a In cases where body weight was recorded.

FIGURE 2. Liver lead histogram for commonloons with confirmed and suspected lead toxicosis.n571.

TABLE 4. Association of clinical signs and presenceof gastrointestinal lead objects in confirmed and sus-pected lead toxicosis.

Confirmedlead toxicosis

Suspectedlead toxicosis

Liver lead (ppm,wet weight)

Lead object aloneClinical signs aloneLead object and

clinical signsTotal loons

.6 ppm

243

41

68

Not tested or2–6 ppm

220

28

50 FIGURE 3. Liver lead histogram for commonloons with non-lead associated mortality. n5194.

of 2.960.9 kg (n594) and significantly(P50.001) poorer subjective body condi-tion scores (91% versus 62% thin or ema-ciated body condition score) than breedingloons which had average weights of4.161.2 kg (n5237). Table 3 lists meanbody weights for adults in each category ofmortality. Weights of live breeding adultsfrom comparable populations, with aver-age weights of 5.460.8 kg (n583), weresignificantly higher than those of loonsfound dead (P50.001). Comparisons ofweights of chicks or immature loons werenot performed because variability in agewould confound results. Suspected andconfirmed categories for both lead toxico-sis and fungal respiratory infection were

combined for these comparisons of bodyweight.

Table 4 delineates the assignment ofloons to the categories of confirmed orsuspected lead toxicosis. These categoriesdo not include five loons that had liverlead levels .6 ppm but had no clinicalsigns or lead objects present in the gastro-intestinal tract. Four of the 28 birds withclinical signs and lead objects, included inthe suspected toxicosis column, werefound to have slightly elevated liver leadlevels between 2 and 6 ppm. Histogramsof liver lead values for loons in the com-bined categories of confirmed and sus-pected lead toxicosis, or other causes ofdeath are presented in Figures 2 and 3,respectively. Average liver lead value inloons dying from confirmed lead toxicosiswas 17.668.8 ppm wet weight (n568),compared to 1.062.5 ppm (n5194) in oth-er loons, including suspected lead intoxi-cation.

Typical clinical signs found with loonswho had ingested lead included weaknessand beaching, drooped wing posture, headtremors, and open-mouth breathing ordyspnea. Typical necropsy findings includ-ed green staining of feathers at the vent,impaction and dilatation of esophagus and




proventriculus with food items, dark greenor black staining of ventriculus lining, adistended gall bladder, and dilation of in-testine or cecum. Hepatic Kupffer cell he-mosiderosis was often found on histologicexamination of loons with elevated liverlead levels, which is suggestive of hemo-lytic anemia (Cullen and MacLachlan,2001). Acid-fast renal inclusions were onlyrarely found.

Severe, systemic Aspergillus infectionswere confirmed in 14 loons and suspectedin 23 others. Less severe lesions associatedwith fungal respiratory disease were foundin 59 loons assigned to other categories ofmortality. Causes of mortality for these 59loons differed significantly (P,0.008) fromthose loons without fungal lesions(n5329). Loons in the categories of infec-tion, trauma, and gunshot were most likelyto be affected, with lesions found in seven(23%), 18 (20%), and three (23%) birds inthese categories, respectively. Fungalgrowths in air sacs were found significantlymore often in adult or immature birdsfrom wintering populations (P,0.003).Adult loons with fungal lesions had signif-icantly (P,0.002) reduced body weights(3.461.0 kg, n556) compared to thosewithout (3.861.2 kg, n5275). Frequencyof fungal lesions differed significantly byage group (P,0.00001), with immatureloons being most likely to be affected(46%, n530), compared to adults (17%,n560) and chicks (6%, n56). No signifi-cant difference in prevalence of fungal le-sions was found between male and femaleloons (P,0.8).

The miscellaneous category containedseveral diverse cases. Neoplastic lesionswere the cause of death in two adult birds.These were a hepatic biliary ductular ad-enocarcinoma and a metastatic tumor ofpossible hepatic origin. Another loon diedfrom complications of egg binding andperitonitis. One small adult loon asphyxi-ated after attempting to swallow a largefish. Another had gross changes in the kid-ney consistent with severe renal disease;histopathology was inconclusive because of

autolytic changes in tissues. Two loons de-veloped aspiration pneumonia after treat-ment and gavage at rehabilitation centers.Finally, after being observed separatedfrom its parents during inclement weather,a loon chick became exhausted anddrowned.

Direct anthropogenic causes of mortal-ity, including confirmed and suspectedlead toxicosis, fishing gear ingestion or en-tanglement, oil, gunshot, and most cases oftrauma (assumed to result from boat col-lision) accounted for 270 of 522 (52%) cas-es of loon mortality among all age cate-gories.

DISCUSSION

The loon population in New England isunusual in the degree of scrutiny it re-ceives. The breeding loons in Massachu-setts, Maine, and, especially, New Hamp-shire are monitored closely from the timethey arrive in spring until the young fledgeand migrate in the fall. This is possible inpart because loon populations in this re-gion, at the most southern extreme of theirbreeding range, are small as compared tomore northern and less developed areas.Although every loon carcass was notfound, our recovery was high, averaging anestimated 28% in recent 4 yr of the studyin New Hampshire, as compared to the6% recovery rate of wild waterfowl mor-talities reported by Stutzenbaker et al.(1986). Given this recovery of carcasses,we believe this study to be a good indi-cator of overall mortality in this regionwith a few caveats described below.

This study emphasizes the importanceof anthropogenic influences on this popu-lation of loons. Figure 1 shows that collec-tion of loon carcasses was focused in aband along the New England coast andcentral/southern areas of New Hampshire,correlating with areas of high human pop-ulation density and, therefore, more close-ly examined lakes. Our study highlightsmortality occurring on the breedinggrounds. Loons dying on the ocean aremuch less likely to wash ashore than those




dying on lakes and the amount of time acarcass lasts on the beach may be signifi-cantly limited by wind and weather con-ditions and scavenging (Forsell, 1999).

This study does not include an estimat-ed 400 loons killed in a large oil spill offthe Rhode Island coast in spring 1996 be-cause full necropsy data were not avail-able. Oil spills are a recognized danger formany seabirds and have a large impact onflightless, wintering loon populations. Sev-eral previous studies of loon mortality havealso been associated with epizootics ofvarying etiologies (Brand et al., 1988; For-rester et al., 1997; Augspurger et al.,1998). The comparative effect of the mor-talities reported here on regional loonpopulations is unknown.

Because this was a study of wild birdsand the carcasses were often collecteddays after death, decomposition affectedaccurate determination of the cause ofdeath. In cases where tissues were consid-erably decomposed, subtle metabolic orinfectious diseases would be harder to de-tect, and obvious traumatic injuries may begiven more weight. Additionally, becausecultures were not routinely performed inthis study, bacterial disease was probablyunder-diagnosed. Deaths due to predationof chicks were likely underrepresented inour sample because of the lack of physicalevidence.

Habitat differences in body weights andmortality likely reflect the harsher environ-ment and seasonal stresses of the coastalwintertime feeding grounds. Energy re-quirements for the winter molt would alsoadd additional metabolic stress, resultingin higher rates of infectious and opportu-nistic disease. This is supported by ourfindings on fungal respiratory disease. As-pergillosis was more likely to be seen inboth adult and immature birds found onsaltwater in this study, and Aspergillus sp.has been reported as a common infectiousagent in other populations of winteringloons (White et al., 1976; Alexander,1991).

High human recreational pressure in

the breeding territories on freshwater hy-pothetically leads to increased interactionsbetween boats and loons, with resulting in-creases in traumatic injuries, line entangle-ment, and opportunity for exposure to leadfishing weights. Differences in mortalitybetween age classes can similarly be ex-plained by the differences in habitat andenvironmental pressures. Immature loonmortality appears to follow the patterns ofboth wintering adult and chick mortality,with trauma and Aspergillus infection asleading causes of death, reflective of theseloons’ presence in both the breeding andwintering habitats.

Differences in body weights and bodycondition were seen associated with sev-eral different factors. Female loons areabout 25% smaller than males, despitetheir lack of dimorphism in plumage. Ex-amination of the variations in body weightcompared to cause of death gives an in-dication of the probable chronicity of theindividual syndromes. For instance, loonswith relatively chronic parasitic or fungaldisease have low body weights; whereasloons dying of traumatic injuries have rel-atively higher body weights. Loons killedby other loons had the highest bodyweights, consistent with the acute, trau-matic manifestations of territorial aggres-sion observed in the field. Birds foundwith gunshot wounds typically did not dieacutely but had chronic infections orwounds that would impair foraging ability,with intermediate body weights at death.

Lead intoxication in this population isassociated with relatively high bodyweights compared to other causes of mor-tality. Apart from signs of lead toxicosis,few lesions were seen in these birds. Webelieve this indicates a relatively acutedeath, which is consistent with our clinicaland field experience in this study. Otherstudies have found that loons with leadtoxicosis are generally in poor body con-dition (Daoust, et al., 1998), and lesionssimilar to starvation are observed in otherlead poisoned waterfowl (Beyer et al.,1998). However, Sanderson and Bellrose




(1986) indicate that weight loss is not al-ways seen, especially in cases of acute tox-icosis. Why this population of loons re-sponds differently than that in the Cana-dian study is unclear, but may reflect themultifactorial nature of wildlife mortalityand environmental stressors.

Liver lead levels of .6 ppm were con-sidered indicative of toxicosis in this study,and levels between 2 and 6 ppm were con-sidered suggestive. This is consistent withthe literature in waterfowl and other birds(Franson, 1996; Pain, 1996). Although el-evated liver lead levels have been reportedin loons, no studies have attempted to de-termine threshold levels (Franson, 1996).Examining our data for lead levels foundin unexposed and clinically affected birdsin Figures 2 and 3, it can be seen that themajority of unexposed loons have lead lev-els at or below the threshold of detection(0.05–1.0 ppm), while the majority ofloons found with ingested lead objectshave levels much greater than 6 ppm.There were eleven loons in the populationof loons with non-lead associated mortalitythat had elevated levels; we suspect thesecases represented undetected exposure tolead objects in the environment. We sug-gest that in loons, conservative criteria forlead toxicosis are similar to those reportedin other waterfowl, although any liver lead.2 ppm is suggestive of exposure. As hasbeen previously proposed, in the face ofgross and microscopic evidence of toxico-sis, the presence, but not necessarily thedegree, of elevations should be considereddiagnostic (Franson, 1996).

The results of this study are similar topreliminary reviews of these data, whichreported breeding loon mortality due tolead ingestion at 52% (Pokras et al., 1991;Pokras and Chafel, 1992). Lead toxicosis isstill the largest cause of mortality in thispopulation. Adult loon mortality due tolead toxicosis in New England was almosttwice as common as in adjacent Canadianmaritime populations (26%) (Daoust et al.,1998). This contrast may be due to thesmaller sample size of loons in that study

(n531) or differences in monitoring ofpopulations and collection of carcasses. Itmay also reflect differences in regionallandscape, human population, or land andwetland usage. If a few lakes in southernNew Hampshire, which are heavily usedfor recreation and have high adult lead-associated mortality approaching 100%,are removed from the analysis, the region-al rates become comparable (data notshown).

Our results support the hypothesis thatanthropogenic causes are the most signif-icant determinants of loon mortality inNew England, accounting for approxi-mately half of all deaths in our study.These reasons for loon mortality are es-pecially significant when considering sus-tainability of their populations in this re-gion. Taken in conjunction with other in-direct factors such as habitat encroach-ment and environmental contamination,these effects may be compounded (Mc-Intyre, 1975; Yonge, 1981; Barr, 1986). Al-though wildlife mortality is dependent ona complex set of factors and stressors, it isclear from our data that future conserva-tion and management of loon populationsmust consider human influences.

ACKNOWLEDGMENTS

The authors would like to thank the manyindividuals and groups without whom this studywould not have been possible. The biologists ofNew Hampshire’s Loon Preservation Commit-tee, Maine Audubon Society, BioDiversity Re-search Institute, and Vermont Institute of Nat-ural Science were instrumental in collection ofloons for this study. Support was also providedby members of the New England Loon StudyWorkgroup, including US Fish and WildlifeService, New Hampshire Fish and Game De-partment, Massachusetts Division of Fish andWildlife, Maine Department of Inland Fisher-ies and Wildlife, Vermont Department of Fishand Wildlife, and Canadian Wildlife Service.Legions of Tufts University School of Veteri-nary Medicine students assisted in field andlaboratory with collection and necropsy of car-casses. Thanks to G. Patronek for statistical ad-vice. This work was funded in part by donationsand grants from the US Fish and Wildlife Ser-vice, US Environmental Protection Agency,New Hampshire Charitable Trust, Massachu-




setts Environmental Trust, Davis ConservationFoundation, National Fish and Wildlife Foun-dation, and Wood Family Foundation.

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Received for publication 12 December 2000.

MORTALITY OF COMMON LOONS IN NEW ENGLAND, 1987 TO 2000

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