1 

# PETITION TO THE

ENVIRONMENTAL PROTECTION AGENCY TO BAN LEAD SHOT, BULLETS, AND

FISHING SINKERS UNDER THE

TOXIC SUBSTANCES CONTROL ACT

P Lead-poisoned bald eagle, photo credit U.S. Fish and Wildlife Service, Dr. Rhoda M. Ralston



### PETITIONERS

CENTER FOR BIOLOGICAL DIVERSITY

AMERICAN BIRD CONSERVANCY

ASSOCIATION OF AVIAN VETERINARIANS

PROJECT GUTPILE

PUBLIC EMPLOYEES FOR ENVI RONMENTAL RESPONSIBILITY

PETITION FOR RULEMAKING

UNDER THE TOXIC SUBS TANCES CONTROL ACT

August 3, 20102 EXECUTIVE SUMMARY

Pursuant to the Toxic Substances Co ntrol Act (“TSCA”, 15 U.S.C. § 2601 et seq. ), Petitioners Center for Biologi cal Diversity, American Bird Conservancy, Association of Avian Veterinarians, Project Gutpile a nd Public Employees for Environmental Responsibility hereby petition the Environmen tal Protection Agency (“EPA”) to revise rules governing toxic substances to ban the manufacture, pr ocessing and distribution in commerce of lead shot, bullets, and fishing sinkers. Petitioners request that the EPA consider this rulemaking pursuan t to section 6(a) of TSCA.

Based on information extending back to Ro man times more than 2,000 years ago, lead has long been identified as a highly toxic substance with lethal properties and numerous pathological effects on living organisms. Health effects fr om lead exposure can run the gamut from acute, paralytic poisoning and seizures to subtle, long-term mental impairment, miscarriage and impotence. Lead is a cumulative metabolic poison affecting a large number of biological functions in cluding reproduction, growth, development,

behavior and survival. Even low levels of exposure to lead can cause neurological damage, and there may be no safe level of lead in the body tissues of fetuses and young. Despite this knowledge, lead continues to be used in manufactured products, many of which are sources of toxic lead exposu re to wildlife and to human beings.

In recent decades the federal government ha s begun to implement regulations to reduce the exposure of human beings to lead in dr inking water, paint, gasoline, toys, toxic dumps, lead wheel balancing weights and both indoor and out door shooting ranges. Strict recycling regulations have been imposed on disposal of lead-aci d batteries. However, spent lead ammunition and lost lead fishi ng tackle are uncontrolled and lead remains widely encountered and distribut ed in the environment from these sources. The continued availability of traditional lead bullets a nd shot exposes any animal that preys or scavenges on targeted wildlife to lead’s toxi c effects. Particularly susceptible are avian scavengers that encounter lead in carcasses left in the wil d, in gut piles (viscera) from animals cleaned in the wild, and in wounded prey species that survive hunting and carry lead ammunition in their bodies. Sensitive spec ies such as bald and golden eagles and endangered California condors are frequently killed by lead poisoning or suffer chronic sublethal effects of lead poi soning from scavenging meat cont aining lead fragments from ammunition. Lead shotgun pellets and lead fish ing tackle accumulate in both aquatic and terrestrial habitats, where animals encounter a nd ingest these lead it ems, often mistaking them for food, grit or bone fragments. Mo re than 130 species of animals (including mammals, upland birds, raptors, waterfowl, am phibians and reptiles) have been reported

in scientific literature as be ing exposed or killed by ingest ing lead shot, bullets, bullet fragments, fishing tackle or prey contaminated with lead ammunition.

Ducks, geese and swans have received prot ection from hunting sour ces of lead poisoning since 1991 by a federal requirement to use onl y nontoxic shot for hunting waterfowl, but

similar restrictions in terrestrial habitats are scattered and localized. Data now show that over 75 terrestrial species of birds are known to be poisoned by spent lead from ammunition. Mourning doves are particularly susc eptible to ingesting lead shot pellets,3 and lead poisoning may kill as many as 20 million doves per year in the United States. Lead fishing sinkers and jigs continue to cau se the needless deaths of waterfowl species such as trumpeter swans, ducks, geese and loons.

Ammunition and tackle manufacturers now ma rket a wide variety of non-lead, nontoxic bullets, shotgun pellets and fishi ng tackle that can replace le ad projectiles and weights. There is no technological or commercial reason why nontoxic ammunition and fishing tackle with comparable effectiveness should not be substituted for th eir lead counterparts.

Several states have mandated nontoxic shotgun ammunition for upland game bird hunting, and states in the Northeast have be gun to require non-lead fishing weights and lures in an effort to protect loons and other wildlife. Those states with only a partial ban, such as California’s requirement for big ga me hunting with nontoxic ammunition within the eight-county range of Ca lifornia condors, continue to have high rates of lead poisoning in wildlife.

The EPA has long held that whenever a to xic substance customarily used in the manufacture of commercial pr oducts can be replaced by a nontoxic substitute, articles

made of the toxic substance should be rem oved from the market. All hunting and fishing gear containing lead could econom ically be replaced with e ffective, nontoxic alternatives, thus making a strong argument for EPA regulatory action.

TSCA grants the EPA the broad authority to re gulate chemical substances that “present an unreasonable risk of injury to health or the environment” (15 U.S.C. § 2061). The EPA may regulate the manufactur e, processing, distribution, us e or disposal of such chemical substances. Specific control mechanisms include: prohibitions on an entire or certain use of a chemical substance; lim itations on allowable concentration levels; labeling or recordkeeping require ments; and obligations to issu e notice of risks of injury (15 U.S.C. § 2605(a)). The EPA has already decl ared that lead is a toxic substance, and has removed nearly all products containing lead from the market. The requirement for nontoxic shotgun shot, bullets, and fishing gear may be achieved with the EPA prohibiting the manufacture, processing, or distribution in commerce of a chemical substance for a particular use (15 U.S.C. § 2605(a)(2)(A)(i)). The EPA is specifically prohibited from regulating ammunition or fire arms under TSCA, but toxic components of ammunition can be regulated if nontoxic alte rnatives are commercially available. The petitioners have waited until nontoxic alternativ es have become available to submit this petition in an effort to clearly indicate that this petition is not an attempt to regulate

ammunition or firearms.

States that have mandated nontoxic shotgun ammunition for upland game bird hunting and nontoxic fishing gear continue to have active hunting and fishing communities that have successfully transitioned away from lead products. Market forces in these states have caused a full line of nontoxic replacement products to be made available to the public, demonstrating that comm ercially available alternatives exist and the economic consequences of removing lead from the environment will be minimal. The EPA is compelled under TSCA to grant this petition and develop regulations to require nontoxic alternatives to lead sporting products.4 TABLE OF CONTENTS

EXECUTIVE SUMMARY ...............................................................................................2

I. PETITIONERS AND STANDING TO FILE .....................................................5

II. NATURE OF THE REQUESTED REGULATION...........................................7

III. REASON FOR THE REQUEST..........................................................................8

A. Introduction................................................................................................8 B. Sources and Quantities of Lead in the Environment From Hunting, Shooting Sports, and Fishing ..................................................................10 C. Pathways of Lead Exposure....................................................................12

D. Toxic Effects of Lead Ammunition on Wildlife ....................................16 E. Lead Ammunition Poisonings by Species ..............................................20

1. California Condor........................................................................20 2. Bald and Golden Eagle ................................................................28 3. Turkey Vulture.............................................................................31 4. Other Raptors...............................................................................31

5. Waterfowl .....................................................................................32

6. Game Birds...................................................................................35

7. Cranes and Rails ..........................................................................36

8. Corvids..........................................................................................36 9. Song Birds.....................................................................................37

10. Mammals ......................................................................................38 11. Amphibians and Reptiles ............................................................38

F. Toxic Effects of Lead Sinker s and Fishing Tackle on Wildlife............39

G. Toxic Effects of Lead Ammuniti on and Fishing Tackle on Humans ..42

H. Alternatives to Lead Ammunition and Sinkers.....................................47 1. Availability, Performance, a nd Toxicity of Non-Lead Bullets

and Shot ........................................................................................47 2. Availability, Performance, a nd Toxicity of Non-Lead Fishing

Tackle............................................................................................51

IV. EXISTING REGULATIONS .............................................................................53 A. Existing Federal and State Lead Ammunition Regulations.................53 B. Existing State Lead Sinkers and Fishing Tackle Regulations .............55

V. AUTHORITY TO ACT.......................................................................................57 A. Authority to Regulate Lead Shot and Bullets........................................58 B. Authority to Regulate Le ad Sinkers and Fishing Tackle.....................58

VI. DESCRIPTION OF FEDERAL REGULATIONS REQUESTED.................59

VII. CONCLUSION ....................................................................................................60

VIII. REFERENCES.....................................................................................................625 1. PETITIONERS AND STANDING TO FILE

Section 21 of the Toxic Substances Control Ac t (“TSCA” or the “Act”, 15 U.S.C. § 2601

et seq. ) provides that “any person” may petiti on the Environmental Protection Agency Administrator (“EPA”) to initiate a proceeding for the “issuance, amendment, or repeal of a rule” (15 U.S.C. § 2620(b)(3 )). Petitioners therefore have standing to petition the EPA to initiate proceedings to ban lead shot, bul lets, and fishing sinkers under section 2605 of

TSCA.

Petitioner Center for Biological Diversity (“ Center”) is a non-profit organization that works to protect endangered species and wild places through science, policy, education, citizen activism, and environmental law. Th e Center and its 255,000 online activists and members have an ongoing interest in protec ting wildlife from l ead poisoning. Since 2004, the Center has taken action through a “Get the Lead Out” campaign to change policies to regulating lead to prev ent toxic lead from entering the food chain. The Center has been a leading proponent of regulations on lead ammunition to protect endangered California condors, bald and golden eagles, and other wild life species at risk from lead poisoning.

Center for Biological Diversity 351 California Street, Suite 600 San Francisco, CA 94104

Contact: Jeff Miller E-mail: jmiller@biologicaldiversity.org

Petitioner American Bird Conservancy conser ves native wild birds and their habitats throughout the Americas, and acts to safeguard the rarest bird speci es, restore habitats, and reduce threats to bird species. The Amer ican Bird Conservancy has been a leading organization working to reduce all mortality threats to birds from habitat destruction, collisions with buildings and wind turbines, a nd from toxins such as hazardous pesticides

and lead.

American Bird Conservancy 1731 Connecticut Ave., NW Washington, DC 20009 Contact: Michael Fry

, Director of Conservation Advocacy E-mail: mfry@abcbirds.org

Petitioner Association of Avian Veterinarians is an international professional organization of practitioners advancing and promoting avian medici ne, stewardship, and conservation through education of its members, the veterinary comm unity and those they

serve.

Association of Avian Veterinarians

P.O. Box 811720 Boca Raton, FL 338416 Contact: Adina Rae Freedman, Executive Director E-mail: aavcentraloffice@gmail.com

Petitioner Project Gutpile is an educati onal organization compri sed of hunters that provides educational resources for lead-free hunt ers and anglers. Project Gutpile has been promoting non-lead ammunition and raising lead awareness in the hunting community

since 2002.

Project Gutpile Contact: Anthony Prieto

E-mail: projectgutpile@gmail.com

Petitioner Public Employees for Environm ental Responsibility (“PEER”) is a 10,000 member national alliance of local, state and federal resource professionals working to protect the environment. P EER members include government scientists, land managers, environmental law enforcement agents, field sp ecialists, and other re source professionals committed to responsible management of America’s public resources.

Public Employees for Environmental Responsibility

P.O. Box 4057 Georgetown, CA 95634 Contact: Karen Schambach, California Field Director E-mail: capeer@peer.org

TSCA requires that within 90 days after filing of a petition, the EPA shall either grant or deny the petition (15 U.S.C. § 2620(b)(3)). If the Administrator grants the petition, the Administrator shall promptly commence an ap propriate proceeding. If the Administrator denies the petition, the Admi nistrator shall publish in the Federal Register the

Administrator’s reasons for such denial (15 U.S.C. § 2620(b)(3)).7 II. NATURE OF THE REQUESTED ACTION

Petitioners Center for Biologi cal Diversity, American Bird Conservancy, Association of Avian Veterinarians, Project Gutpile a nd Public Employees for Environmental Responsibility request that the EPA adopt regulations prohibiting the manufacture, processing, and distribution in commerce of lead shot, lead bullets, lead fishing sinkers, and other lead-containing fishing gear, pursu ant to TSCA (15 U.S. C. § 2605(a)(2)(A)(i)). Such regulations are needed to protect vulne rable wildlife species from the ongoing threat of lead poisoning, as well as to safeguard human health.

TSCA mandates that the EPA must regulat e chemical substances where there is a

“reasonable basis to conclude” that such s ubstances “present an unreasonable risk of injury to health and or the environment” (15 U.S.C. § 2605(a)). TSCA authorizes the EPA to prohibit “the manufacturing, proces sing, or distribution in commerce” of a chemical substance for a particular use or uses (15 U.S.C. § 2605(a)(2)(A)(i)).

Lead used in shot, bullets, and fishing sinkers is a “chemical substance” falling within the scope of TSCA. As defined by the Act, “Ex cept as provided in subparagraph (B), the term “chemical substance” means any organic or inorganic substan ce of a particular molecular identity, including (i) any combina tion of such substan ces occurring in whole or in part as a result of a chemical reaction or occurring in nature and (ii) any element or uncombined radical” (15 U.S.C. § 2602(2)(A)).

Most other uses of lead, such as lead-bas ed paints, plumbing pipe and fixtures, and leaded gasoline, are already subject to st rict regulation (15 U. S.C. §§ 2681-2692). In January 2008, lead and lead compounds were added to the Priority Testing List (40 C.F.R. 716.120; see also 15 U.S.C. § 2603(e)), requiring cer tain lead manufacturers to submit unpublished health and safety reports to the EPA (73 Fed. Reg. 5109-5115; Jan. 29, 2008). Automobile wheel balancing wei ghts will be phased out with an EPA proposed rule scheduled for 2011. Manufacturer s of consumer products intended for use by children who also manufacture lead or lead compounds are required to report certain health and safety data to the EPA. However, there is currently no specific regulation of lead shot, bullets or fi shing sinkers under TSCA.8 III. REASON FOR THE REQUEST

A. INTRODUCTION

Lead has been used by humankind for millennia. Lead had numerous uses in ancient Egypt and it is believed that toxicity arising from the use of lead in water pipes, pottery, cosmetics, food and wine may have contri buted to the fall of the Roman Empire (Hernberg 2000). The properties of lead as a biocide have been well known for hundreds of years. It is now unquestioned scientific know ledge that lead is a toxic substance with potentially lethal as well as numerous pat hological effects on liv ing organisms of all sorts. Despite this knowledge, lead has cont inued to be used in a wide variety of manufactured products, many of which are cont inued sources of toxic lead exposure to human beings and to wildlife.

The use of lead for hunting dates back hundred s of years, and lead has been used in fishing activities for thousands of years. The effects of lead in modern shot, bullets, and fishing sinkers on fish and wildlife have b een well documented and reviewed (e.g. Pain 1992; Fisher et al. 2006; Rattner et al . 2007). Recognizing these threats, some jurisdictions began plac ing restrictions on the use of lead ammunition and tackle in the 1970s and 1980s. Despite restrictions, signifi cant amounts of lead continue to be deposited in aquatic and upland habitats and enter the food chain from hunting and fishing activities. Legal and illegal hunti ng using lead ammunition may directly or secondarily expose wildlife to lead and deposit bioavailable lead into the environment. Skeet/trap shooting and target practice activi ties also deposit signifi cant amounts of lead in geographically localized areas. Signif icant amounts of lead end up in aquatic environments from lost or discarded fishing tackle, including lures, sinkers, lead core fishing line, downrigger cannonballs, weights, and a variety of fishing traps and nets that employ the use of lead.

Lead can remain in the environment relativel y intact and stable for decades, and, under

some environmental conditions it can be read ily released and taken up by plants or animals (ATSDR 2007). Absorbed or ingested lead can cause a range of biochemical, physiological, and behavioral effects in sp ecies of invertebrates, fish, amphibians, reptiles, birds, and mammals. Wildlife can be exposed to lead through feeding in aquatic environments and ingesting contaminated vegetation and sediments, feeding on invertebrates or vertebrates containing lea d, or ingesting lead pellets or fragments directly, mistaking them for food, grit, or bone. Although lead is a naturally occurring metal in the environment, for biological systems it is a nonessential metal with no

functional or beneficial role at the molecular or cellular level. Ingested lead substitutes in dysfunctional ways for calcium in biochemi cal interactions, with harmful effects on neurological functions, bone structure, renal function, repr oductive functions, pancreatic functions, and muscular functions, among others.

Lead is toxic to organisms at very low levels , and has lethal and severe sublethal effects at higher levels (IPCS 1989; Nordic Council of Ministers 2003). Lead can act as a neurotoxin, and numerous studies indicate that blood lead concentrations even below 109 micrograms per deciliter can have advers e developmental effects on intellectual functioning and social-behaviora l conduct in humans (Needleman et al. 1990; Canfield et al. 2003; Ris et al. 2004). Huma n fetuses and young children are particularly sensitive to even low levels of lead exposure and can easily suffer permanent neurological damage.

Clinicians now assert that there is no safe level of lead in the body tissues for fetuses and young children (e.g. Canfield et al. 2003; Lanphear et al. 2005, 2006; Ca rlisle et al. 2009).

In recent decades the federal government ha s taken various regulat ory actions to reduce the exposure of humans to lead in drinking water, paint, gasoline, toys, toxic dumps, automobile wheel balancing weights, and indoor and outdoor shooti ng ranges. However, other lead sources causing significant contamination are still uncontrolled, and lead exposure to wildlife has recently been wide ly documented and is not adequately regulated.

Toxic lead shotgun pellets a nd bullet fragments from hunting accumulate in both aquatic and terrestrial habitats, where animals often eat them because they are mistaken for grit or food (seeds). Birds frequently ingest spent lead shotgun pellets as grit normally consumed to aid grinding of foods in the gizzard during digestion. Ducks, geese, and swans have received much protection from this source of lead poisoning since 1991 through the federal requirement to use only nontoxic shot for hunting waterfowl, but

similar restrictions in terrestrial habitats are few, scattered, and localized. Research has shown that over 75 terrestrial species of bi rds are known to be poisoned by spent lead ammunition (Eisler 1988; Fisher et al. 2006).

Evidence has accumulated over the past century and it is now incontrovertible fact that lead fragments in the bodies of animals shot with lead bullets or l ead shotgun pellets are a serious source of lead exposure to scavengi ng animals that eat meat containing lead fragments and residue (Calve rt 1876; Holland 1882; Grinne ll 1894; Bowles 1908). Lead fragments in meat also pose potential health risks to humans who eat lead-tainted game, especially subsistence hunters dependent upon hunted game for food. Critically endangered California condors, bald and golde n eagles, ravens, and other scavenging birds are frequently killed or harmed by this source of lead poisoning. Spent lead shotgun pellets on the ground in fields where upland game birds are hunted are also ingested by birds as grit making herbivorous birds as well as carnivorous bi rds victims of lead poisoning. Mourning doves are particularly sensitiv e to this, as they are hunted in fields where they congregate to feed, and spent lead pellets are th e appropriate sized grit for

doves.

More than 130 species of animals (including upland birds, raptors, waterfowl, mammals and reptiles) have been documented being exposed or killed by ingesting lead shot, bullets, bullet fragments, or prey contaminated with lead ammunition (Environment Canada 1995; Tranel and Kimmel 2009). As lo ng as ammunition manufactured with lead projectiles and lead fishing tackle remain s available for purchase and use, numerous species of wildlife will continue to be poisoned by lead and human health will be threatened, posing an unreasonable risk of in jury to human health and the environment.10 B. Sources and Quantities of Lead in the Environment from Hunting, Shooting Sports, and Fishing Activities

Hunting

The density of spent lead shot in wetlands or fields is related to hunting intensity. In waterfowl hunting areas, prior to the national requirement for nontoxic shot, densities of spent shot have been reported from about 50,000 pellets to over 2 million pellets per acre (Bellrose 1959; Pain 1992; Rocke et al. 1997). Areas with regular hunting from fixed position blinds or pits resulte d in significant accumulation of spent lead. Prior to the banning of lead shot for waterfowl hunting, an estimated 2,721 metric tons of spent lead shot were deposited in U.S. wetlands each year (Pain 1992), and spent shot accumulated near the surface of sediments in aquatic se ttings, increasing the amount of lead shot available to waterfowl over time (Pain 1992). The depth of lead fragments in soil and their availability can be influenced by land management practices such as cultivation, and lead shot and bullets can persist for decades to hundreds of years (Fredrickson et al. 1977; Jorgensen and Willems 1987; Kendall et al. 1996).

Significant lead shot deposition continues t oday in upland fields used for hunting and densities of spent lead shot can reach over 400,000 pellets pe r acre (Schulz et al. 2002). Castrale (1989) estimated densities of 11,000 pellets/acre in a field managed for dove hunting in Indiana. Lewis and Legler (1968) estimated 43,600 pellets/acre in a field managed for dove hunting in Tennessee. Essl inger and Klimstra (1983) estimated 44,000 pellets/acre in a field managed for goose hunti ng in Illinois. Fredrickson et al. (1977) estimated 122,800 pellets/acre in uncultivated fiel ds near duck blinds in Missouri. Best et al. (1992a) estimated 344,000 pellets/acre in an area frequented by dove and quail hunters in New Mexico. The Washington Fish and Wildlife Nontoxic Shot Working Group in 2001 estimated densities of 188,000 and 344,000 pelle ts/acre at two pheas ant release sites in Washington.

Despite the ban on lead shot for waterf owl hunting, large amounts of spent lead ammunition continue to be deposited in the environment through hunting of big game, upland species, furbearers, and from predat or control activities (Scheuhammer and Norris 1995; Schulz et al. 2002). Lead from shot, bullets and bullet fragments in tissue or

entrails of wounded or dead animals has been increasingly recognized as a threat to many avian species (Jannsen et al. 1986; H unt et al. 2006; Knopper et al. 2006).

To give an idea of the quantity of potenti ally lead-tainted carcasses available to scavengers, Fry and Maurer ( 2003) quantified hunter-shot car casses available to condors in their California range before the Californi a lead ammunition ban went into effect, and concluded that gut piles and w hole carcasses left in the fi eld by hunters were a highly significant source of lead within the condor range. From hunti ng survey data for the eight counties encompassing the condor range in Ca lifornia, Fry and Maurer (2003) estimated an annual average of 36,000 big game an imals (17,000 wild pigs, 11,000 coyotes and 8,000 deer) were taken each year by sport hunt ers in this area. Fry and Maurer (2003)11 assumed that only a very few gut piles ar e actually buried, hidden successfully, or removed from the field. Deer and pigs are ge nerally field dressed and gut piles discarded in the field; coyotes are gene rally left in the field inta ct. The Fry and Maurer (2003) figures do not account for poaching, which lik ely significantly increases the number of

deer carcasses available. The data also do not account for the ta ke of thousands of permitted depredated pigs and deer shot by ranchers, and do not account for small game such as ground squirrels shot by varmint hunt ers. The carcasses of these large animals left in the field would be the primary s ource of hunter-shot food for condors. Fry and Maurer (2003) estimated th at almost 28,000 tree squirrel, rabbit, and ground squirrel

carcasses are left in the field within the c ondor range annually. Even animals as small as ground squirrels shot with .22 caliber bullets can contain lead frag ments at biologically relevant levels that may constitute a l ead-hazard for other sc avenging birds of prey (Harmata and Restani 1995: Knopper et al. 2006).

Shooting Sports

Target, trap and skeet shooting can result in substantial accumulation of spent lead in localized areas, and lead from spent shot at shooting ranges can become bioavailable to terrestrial and aquatic plants, invertebrates, and vertebrates (Scheuhammer and Norris 1995). Individual shooting ranges can deposit as much as from 1.4 to 15 tons of lead shot and bullets each year; estimate s of the annual amount of lead shot and bullets deposited at the roughly 9,000 outdoor shooting ranges in the U.S. range from 72,600 to 80,000 metric tons (Tanskanen et al. 1991; USEPA 2001; Craig et al. 2002; USGS 2008). Kendall et al. (1996) estimated mean densities of spent lead shot at trap, skeet, and sporting clay ranges in the United States at 3.7 billion pellets/acre. Large concentrations of lead at shooting ranges (up to 17,000 gram s per square meter) cluster in small areas because of stationary targets, trajectories of launched targets, and concentration of shooters (Darling and Thomas 2003). Significan t amounts of fine particulate lead can concentrate near shooting stations.

Studies of the dissolution of lead from shot at terrestrial shooting ranges suggest that onehalf of a lead shot pellet would release into the soil within 40 to 70 years and that the

entire lead shot would transf orm in 100 to 300 years, with mechanical disturbance of soil enhancing transformation rates (Jorgensen and Willems 1987; Scheuhammer and Norris 1995; Hardison et al. 2004). Lead concentratio ns in soil at shooting ranges have been shown to be up to 55,000 mg/kg, over 10,000 tim es background levels (Scheuhammer and Norris 1995). Lead leaching into soil or sediment exceeding cr iteria for hazardous waste and dissolved lead entering surf ace water and ground water exceeding water quality criteria has been docum ented at many U.S. shooting ranges (Murray et al. 1997; Bruell et al. 1999; Craig et al. 1999; Rooney et al. 1999; Ch en et al. 2002; Cao et al. 2003a, 2003b; Soeder and Miller 2003; Sorvai et al. 2006). A study of shooting ranges over water showed high shot density in the soil/sediment fall zone and lead concentrations in water samples two orde rs of magnitude above EPA water quality criteria (Stansley et al. 1992).12 Fishing

Accurate quantitative information on how mu ch lead is entering the environment from lead fishing weights and tackle sinkers is not available, but approximations can be made from the quantities of lead fishing tackle so ld in the U.S., assuming most or many sinkers are purchased to replace those lost while fi shing (Scheuhammer et al 2003), and from studies of sinker and tackle loss by anglers. Roughly 4,000 metric tons of lead fishing sinkers are sold annually in the U.S. (Sche uhammer et al 2003; US GS 2008). Studies of

sinker and tackle loss rates am ong recreational anglers vary - a variety of factors can influence whether lead will be lost, including the type of fishing activity, the location of the activity, the time of year, and the skill of the angler. Fishers lost 2-3 sinkers per angling day in the United Ki ngdom (Bell et al. 1985). Angler s in the U.S. reported losing 0.18 sinkers/hour, and 0.23 hooks and lures/hour, with 2% of angler s reporting losing a fish with tackle still attached (Duerr 1999) . Radomski et al. (2006) reported average loss

rates on Minnesota lakes of 0.0127 lures per hour, 0.0081 large sinkers per hour, 0.0057 split shot sinkers per hour, 0.0247 jigs per hour, and 0.0257 hooks per hour; for a

estimated total of one metric ton of lead lost for 6,000 anglers in 2004. Assessments of lead fishing tackle along U.S shorelines have found 0.01 sinkers/square meter of shoreline in areas of low ang ling pressure up to 0.47 sinkers/m 2 in areas of high angling pressure (Duerr and DeStefano 1999), with much higher densities (up to 190 sinkers/m 2 ) in studies in Europe (Cryer et al. 1987; Sears 1988). Am ounts of lead fishing weights produced and approximations of lo st tackle indicate that fishing can introduce significant amounts of lead into aquatic environments . The USEPA (1994) estimated in 1994 that 450 million toxic fishing sinkers containing l ead or zinc are produced each year and potentially entering the environment.

The fate of elemental lead in aquatic envi ronments is influenced by water chemistry, wave action, water flow, and pH (see Sche uhammer and Norris 1995). In lakes, lead particles may be adsorbed onto sediment and so il particles. The bioavailability of lead is related to the presence of organic matter a nd sediments and acidity. In coastal ocean waters, lead sinkers may easily be abraded by wave action against rocks, releasing small fragments into the water column.

C. Pathways of Lead Exposure

Lead has been widely dispersed throughout the environment from activities such as mining, smelting, manufacturing, and engine combustion. Many historical documented instances of lead exposure among terrestrial wi ldlife species have been associated with small contaminated areas, such as around metal smelters, shooting ranges, lead paint contaminated buildings, or locations with intense hunting pressu re (Blus et al. 1991, Henny et al. 1991; Blus et al. 1995; Sileo et al. 2001; Lewi s et al. 2001). Manufacture of leaded gasoline, lead-based paints and pestic ides, and use of lead solder in cans has now been nearly eliminated in the U.S. The EP A recently granted a petition to ban lead automobile wheel balancing weights, and will produce regulations requiring non-lead wheel weight alternatives in 2011 (USEPA 2009). A petition to phase out the largest13 remaining permitted use of leaded gasoline, that for piston-driven aircraft, was filed with the EPA in 2010, and EPA recently solicited co mments on that petition (USEPA 2010).

Environmental distribution of lead from hunti ng and fishing is widespread, although it is difficult to estimate the magnitude of lead e xposure compared to other sources, such as legacy residues of leaded gasoline exhaust deposition, emissions from smelters, improper disposal of paint chips and dust, and lead ground to dust from lead wheel weights falling

off vehicles. Lead from shot , bullets and fragments in he avily hunted fields, wetlands, and shooting areas can be directly ingested or solubilized and biol ogically incorporated into food items (Ma 1989; Stansley and Roscoe 1996; Hui 2002). Studies at shooting ranges have shown increased lead levels in terrestrial and aquatic plants (Manninen and Tanskaanen 1993; Peterson et al. 2993; Mell or and McCartney 1994; Rooney et al. 1999; Hui 2002), and lead concentrations in invertebrates have been shown to be elevated due to uptake of lead near shooting ranges (Hui 2002; Labare et al. 2004). There has been increasing evidence documenting significant depos ition of spent lead shot and bullets and lost fishing sinkers and tackle, and subseque nt ingestion by numerous bird and mammals species, as discussed below.

Aquatic Environments

There is extensive documentation of direct ingestion of lead shot, bullet fragments, sinkers, and jigs by dabbling and diving ducks, swans, loons and other water birds.

There is very little information on lead releas ed from spent shot or fishing weights in aquatic habitats which could be solubili zed and taken up by invertebrates or fish (Stansley et al. 1992; Hui 2002). For rept iles and amphibians near heavily hunted wetlands and shooting ranges, consumption of waterborne lead and ingestion of leadcontaminated sediments and food items are likely exposure pathways (Stansley and Roscoe 1996; Borkowski 1997; Camus et al. 1998; Hammerton et al. 2003; Pattee and Pain 2003; Lance et al. 2006). Although direct ingestion of lead shot or ammunition fragments by aquatic inverteb rates, reptiles, and amphibians seems unlikely, numerous studies describe injuries to fish incurred by tackle (oft en containing lead) and small fragments passing through fish digestive track could release lead. Although there is no documentation of such lead uptake or poisoning in fish, there are reported cases of lead poisoning of turtles that ha ve ingested lead fishing tackle (Borkowski 1997; Scheuhammer et al. 2003b). Hooked fish can ingest or retain a ttached lead fishing tackle such as hooks and jigs, and become a potenti al pathway of lead exposure for predatory birds consuming fish containi ng such lead fishing gear. Marsh birds feeding in wetland

areas that are hunted with lead ammunition i ngest lead, which has been documented in flamingoes, rails, shorebirds, terns, and he rons (Artman and Martin 1975; Kaiser et al. 1980; Maedgen et al. 1982; Custer and Mulher n 1983; Hall and Fisher 1985; Locke et al. 1991; Beck 1997; Mateo et al. 1997; Acora 2005).14 Terrestrial Environments

The most significant lead exposur es and effects are due to dir ect ingestion of spent lead shot and bullet fragments by waterfowl (Sa nderson and Bellrose 1986) and certain upland game species (Kendall et al. 1996, Schulz et al. 2006). Secondary poisoning of birds consuming wounded or dead prey contaminated with lead ammunition and scavenging of gut piles with spent lead ammunition or fr agments is a significant source of toxic exposure to predatory and scavenging birds, with particularly deadly effects on bald eagles and California con dors (Pattee and Hennes 1983; Kramer and Redig 1997; Meretsky et al. 2000; Church et al. 2006; Hunt et al. 2006; Pauli and Buskirk 2007). The recent use of stable lead isotope ratios has provided evidence that ammunition sources are responsible for lead exposure in wild birds (Scheuhammer and Templeton 1998; Scheuhammer et al. 2003a; Church et al. 2006, Finkelstein et al. 2010).

Granivorous (seed-eating) bird species may ingest lead shot as grit, or perhaps mistaking it for berries, which may be similar in appearance after drying and falling (Calvert 1876; Campbell 1950; Hunter and Rosen 1965; Fimr eite 1984; Best 1992; Scheuhammer et al. 1999; Lewis et al. 2001; Potts 2004; Butler 2005a, 2005b; Rodrigue et al. 2005). Lead exposure has been documented in doves foragi ng at intensive hunti ng or target-shooting areas (Fisher et al. 2006 Schulz et al. 2002). Species that fora ge primarily on seeds on the ground may have higher risk, but even bird species with very different foraging strategies, such as woodpeckers, can acqui re lead - presumably by ingesting lead fragments embedded in trees or on the ground (Mörner and Peterson 1999). Of birds and mammals examined in a firearm shooting field, 33% were found to have elevated lead tissue levels and 17% to have pot ential subclinical or clinical lead exposure (Lewis et al. 2001). Deer are thought to i ngest lead fragments on th e ground at shooting ranges

because of the taste of lead salts on oxid ized fragment surfaces (Lewis et al. 2001).

Animals that scavenge hunte r-killed carcasses are at the highest risk of encountering severely toxic concentrations of lead . A recent study by Hunt et al. (2006, 2009) evaluated radiographic evidence of lead frag ments in 38 deer killed by licensed hunters using center fire rifles with lead-based coppe r jacketed, soft point bullets in Arizona from 2002 to 2004. Metal fragments were found to be broadly distributed along wound channels, 94% of samples of deer killed with lead-based bullets c ontained fragments and 18 out of 20 (90%) offal piles contained lead fragments. The authors concluded that the data demonstrated a high potential for scavenger exposure to lead. Meanwhile, the carcasses and gut piles from deer killed by non-lead copper expanding bullets (or “Xbullets”) showed little evidence of fragmentation (Hunt et al. 2006, 2009).

Reports from experimental and field observations conclude that all bird species would be susceptible to lead poisoning af ter ingesting and retaining shot in the gastrointestinal system (Fisher et al. 2006). Raptor and scave nger species that feed on animals killed with

lead ammunition would be at high risk for exposure to lead in this way. Animals that consume lead particles that have fragme nted in hunter-killed carcasses may be at particular risk because the small size and ir regular shape of fragments make them more absorbable in the digestive process.15 Fisher et al. (2006) listed fi fty-nine terrestrial bird speci es worldwide that have been exposed to lead from ammunition sources, in cluding raptors, galliforms, gruiforms, columbiforms, and gulls. Vyas et al. (2000, 2001) identified lead in s ong birds resident on a shotgun trap and skeet range. Fisher et al. (2006) reviewed publishe d literature on lead poisoning of 32 species of wild birds in the United States from spent lead ammunition. Documented cases of ingestion and poisoni ng by lead from ammunition in terrestrial birds globally include 33 rapt or species and 30 species from Gruiformes

, Galliformes and various other avian taxa, incl uding ten globally threatened or near threatened species (Pain et al. 2009). Lead poisoning is of partic ular conservation concer n in long-lived slow breeding species, especially t hose with initially small populations. A recent review by the Minnesota Department of Natural Res ources found over 130 species of animals (including upland birds, raptors, waterfowl, and reptiles) have been reported in scientific literature as being exposed or killed by ingesting lead shot, bullets, bullet fragments, or prey contaminated with lead ammuniti on (Tranel and Kimmel 2009). In the United States, Kendall et al. (1996) found that upla nd game birds ingest substantial amounts of lead shotgun pellets and deduced that raptor s must incur secondary ingestion of pellets because their prey ingested it. Rifle-shot prairie dogs and ground squirrels may contain fragmented lead particles that could be inge sted by scavengers or raptors (Knopper et al. 2006; Pauli and Buskirk 2007). Kramer and Re dig (1997) compiled data on more than 2,000 bald eagles, demonstrating that lead shot pellets, likely from crippled waterfowl and lead fragments in offal and unrecovered d eer carcasses, were responsible for elevated

lead levels in more than 98% of birds admitte d to a veterinary hospital and raptor center. Recently, Church et al. (2006) and Chesley et al. (2009) linked isot opically labeled lead

in California condors with rifle bullets sold in the same region, substantiating that condors were ingesting lead and were dying and suffering sublethal effects from bullet fragments.

Terrestrial birds are exposed to lead mainly through ingestion. Galliforms and doves probably ingest spent shot as grit which is re tained in their gizzar ds, although there is considerable uncertainty as to why doves ingest lead and steel shot pellets (Schulz et al. 2002). Approximately 2.5% of hunter-shot doves contained lead shot in their digestive system, giving a rough estimate of the proporti on of doves that ingest shot. A similar percentage of doves collected on fields where hunt ers used steel shot ingested steel shot. Estimates of the 2005 U.S. dove population are 350-600 million birds (Dunks et al. 1982; Schulz et al. 2006), and experiment al studies indicate that nearly all doves that ingest shot will die as a result of this ingestion. Schul z et al. (2006) estimated that from 8.8 to 15 million doves may be killed each year from inge sting lead shot pellets. If scavengers consume these poisoned doves and secondarily co nsume the lead pellets, it is estimated that up to one million scavenging birds and mammals could die annually from ingesting poisoned doves alone.

Raptors and other scavenging bi rds are usually poisoned throu gh ingesting lead shot or bullet fragments in dead or in jured prey or gut piles (Fri end 1987; Kendall et al. 1996).

Common ravens have been shown to have elevated blood lead levels during hunting season due to ingestion of lead in rifle-shot big game offa l piles (Hatch 2006; Craighead16 and Bedrosian 2007, 2008). In Canada, upland game birds and mammals, the primary food source of many raptors, are now more likely to contain lead shot than waterfowl, as lead shot is prohibited for waterfowl hunting (Clark and Scheuhammer 2003).

D. Toxic Effects of Lead Ammunition on Wildlife

Lead has long been recognized as a pois on to living organisms (Grinnell 1894; Engsted 1932; Horton 1933), with negative effects on general health, reproduction, and behavior (Ris et al. 2004). Lead was highlighted as an important cause of mortality in wildlife populations in the late 1950s, when ingesti on of spent hunting lead pellets or fishing sinkers was recognized to cause death in a wi de range of wild wate rfowl (Bellrose 1959). Reports of poisoned wildlife have continued fr equently since that time (e.g. Bates et al. 1968; Irwin and Karstad 1972; Sanderson and Bellrose 1986; Kramer and Redig 1997; Schulz et al. 2006).

It is well recognized that lead fragments can be absorbed fr om the gastrointestinal tract of birds and mammals, cause damage in various organs, and result in behavioral changes, significant illness, and even death depending on the amount ingested (Reiser and Temple 1981; Kramer and Redig 1997; Fisher et al. 2006).

Lead fragments or pellets inge sted by birds may be rapidly re gurgitated (in the pellets of raptors, for example), retained for varying periods, or completely dissolved with the resulting lead salts absorbed into the bloodstream. The likelihood of a bird becoming poisoned is related to the rete ntion time of lead items, frequency and history of exposure to lead, and factors such as nutritional status and environm ental stress (Pattee and Pain 2003). A proportion of exposed birds will die, and mortality can occur following the ingestion of just one pellet of lead shot (Pain and Rattner 1988) . Ingestion of lead particles usually results in some absorpti on, and in cases where sufficient lead is absorbed, poisoning ensues. Lead concentra tions are generally highest in the blood directly after absorpti on, and in liver and kidneys for days to months after absorption. Lead deposited in bone can remain for year s, and reflects lifetim e exposure (Pain 1996).

Lead is a non-essential elemen t and the activity of blood enzymes appears to be affected by extremely low concentrations. Other than in cases of point source contamination, high

concentrations of lead in the tissues of birds result primarily from the ingestion of lead ammunition or fishing weights.

Various authors have attempted to define tis sue concentrations in birds indicative of excessive lead exposure, sub-lethal poisoni ng and acute poisoning (F ranson et al. 1996; Pain 1996), but there is no definitive consensu s on “background” lead levels for wild

birds. Environmental sources of lead are al most exclusively anthropogenic, with a small

contribution from natural sources such as volcan oes. Lead is rarely found in nature in its elemental metal form, and the most common s ource is galena or PbS, which has a very low solubility in water. Wildlife can ge t low level exposure to lead from unknown sources, including natural accumulation in pl ants and ingestion by herbivores, and deposition by leaded gasoline exhaust, now a ttenuated with regulation. “Baseline” lead

concentrations in wildlife can vary between taxa, and the diagnosis of poisoning is17 usually based on signs of poisoning in combina tion with blood lead le vels in live birds, and on tissue concentrations, sometimes in combination with evidence of exposure to lead in dead birds. For example, the Diagnos tic Center for Populati on and Animal Health (Michigan State University, Lansing MI) de fined background blood l ead levels as <35 μg/dL for eagles (W. Rumbeiha, pers. comm. ), while Pattee et al. (1990) defined background levels as <20 μg/dL, and Feierabe nd and Myers (1984) defined them as <10 μg/dL. The generally accepted blood lead leve ls for wild birds have been <20 μg/dL as background; 20 to <50 μg/dL indicating subclinical poisoning; 50 to 100 μg/dL indicating clinical poisoning; and >100 μg/d L representing severe clinical poisoning (Friend 1985, 1999; Franson 1996; Pain 1996; Pattee and Pain 2003). For condors, blood lead levels above 10 μg/dl, rather than 20 μg/dl, could have detrimental effects on condors and ought to be considered the begi nning of toxic exposure (Fry et al. 2009). The background levels of 20ug/dl are now unders tood to indicate significant exposure, because animals held in captivity usually have background levels of 4 μg/dl or less (Walters et al. 2010).

A threshold toxic level for wildlife is di fficult to measure because the effects on the nervous system at low doses can be subtle and difficult to det ect without specific quantifiable behaviors. In a ddition, predisposition and suscep tibility to lead can vary between individuals within a species (Pattee et al. 1981, Carpenter et al. 2003). There is probably no toxic lead threshold for any animal , as lead is a neurotoxin with no biological function. Lead salts are rarely encountered in the environment, and animals do not have

well established metabolic or detoxification mechanisms to biochemically protect themselves from adverse effects of exposure. Even a minor decrease in fitness to a bird surviving in a hostile and competitive envi ronment caused by small amounts of lead ingestion may result in a proximate death fr om many causes. In long-lived bird species, such as condors, eagles, and ravens, this has the potential to skew the normal age structure toward younger and non-breeding bi rds and negatively influence long-term population viability. As the duration of peri odic and chronic exposur e increases in the condor population so does the likelihood of death by lead-poisoning. It is unknown whether wildlife species sustain sublethal e ffects on coordination and cognitive behaviors similar to those demonstrated in humans, but it is likely that repetitive sub-lethal exposures to lead will cause permanent neur ological and behavioral decrements in all species of wildlife (Canfield et al. 20 03; Lanphear et al. 2003; Ris et al. 2004).

Lead is a non-specific poison affecting all body systems. Birds can suffer from both acute and chronic lead poisoning (Bellrose 1959; Redig 1985; Sanderson and Bellrose 1986; Eisler 1988; Scheuhammer and Norris 1996). Birds with acu te lead poisoning can appear normal, but experience massive tissue destructi on to internal organs and death within a few days (Sanderson and Bellrose 1986). Bird s with chronic lead poisoning may develop appetite loss, anemia, anor exia, reproductive or neurol ogical impairment, immune suppression, weakness, and susceptibility to predation and starvation (Grandy et al. 1968; Kimball and Munir 1971; Finley a nd Deiter 1978; Hohman et al. 1995).

The effects of toxicosis in birds commonly incl ude distension of the proventriculus, green watery feces, weight loss, anemia and drooping posture (Hanzlik 1923; Quortrup and18 Shillinger 1941; Redig et al. 1980; Reiser a nd Temple 1981; Franson et al. 1983; Custer et al. 1984; Sanderson and Be llrose 1986; Mateo 1998). Sub-le thal toxic effects are exerted on the nervous system, kidneys and circ ulatory system, resulting in physiological, biochemical and behavioral changes (Sch euhammer 1987). Vitamin metabolism can be affected (Baski and Kenny 1978) and birds can go blind (Pattee et al. 1981). Lead toxicosis depresses the activity of certain bl ood enzymes, such as delta aminolevulinic acid dehydratase, essential for cellular energy and hemoglobin production, and may impair immune function (Redig et al. 1991; Grasman and Scanlon 1995). Over longer periods, haematocrit and hemoglobin levels ar e often reduced. Finkels tein et al. (2010)

found that sub-lethal concentr ations of lead in blood (20 μg/dL), resulted in a 60%

decrease in the levels of aminole vulinic acid dehydratase in condors.

As a result of physiological and behavioral changes, birds may become increasingly susceptible to predation, starva tion and infection by disease, increasing the pr obability of death from other causes (Scheuhammer and Norris 1996). Lead can also affect reproductive success (Cheatum and Benson 1945; Elden 1954; Buerger 1984; Buerger et al. 1986). Grandjean (1976) showed a corr elation between thin eggshells and high concentrations of lead in European kestrels ( Falco tinnunculus ). Lead poisoning significantly decreased egg production in captive Japanese quail, Coturnix japonica (Edens and Garlich 1983). In ringed turtle doves ( Streptopelia risoria ), significant testicular degeneration has been reported in adults following shot ingestion and seminiferous tubules may be devoid of sp erm (Kendall and Scanlon 1981; Veit et al. 1982). Experimental studies on Cooper’s hawks ( Accipiter cooperii ) showed detectable amounts of lead in eggs when adults had high levels in their blood (Snyder et al. 1973). In nestlings of altricial species, such as the American kestrel ( Falco sparverius ), body length, brain, liver and kidney weights can be depressed (Hoffman et al. 1985a), along with reduced survival and disrupted brain, liver and kidney function (Hoffman et al. 1985b).

Under some circumstances, there may be sex di fferences in the probability of exposure to or poisoning by lead, at leas t in western marsh-harriers ( Circus aeruginosus ), as significantly more females than males trappe d had elevated lead concentrations, for unexplained reasons (Pain et al. 1993). Lead exposure may also reduce the likelihood of birds returning to an area to breed (M ateo et al. 1999). Locke and Friend (1992) concluded from their wide-ranging study that all bird species would be susceptible to lead poisoning after ingesting and retaining shot. A ll raptor species that feed on game could potentially be exposed at some time to l ead ingestion, the likelihood varying according to the proportion of game in the diet, the si ze of game taken, the season, and the local hunting intensity (Pain et al. 1993).

Burger and Gochfeld (2000) found that chro nic lead exposure resulted in delayed behavioral response time in both la boratory and wild herring gulls ( Larus argentatus ). Kelly and Kelly (2005) documented moderately elevated blood lead levels increased the

risk of collision with overhead power lines for mute swans ( Cygnus olor ). Mallards ( Anas platyrhynchos ) experimentally fed lead exhibited he molytic anemia during the first week of exposure and neurological impairment duri ng the second week (Mateo et al. 2003). In19 experimentally fed turkey vultures ( Cathares aura ) and bald eagles ( Haliaeetus luecocephalus ), lead ingestion decreased weight and muscle mass and caused blindness (Pattee et al. 1981, 2003). Blood pressure increa ses and renal damage have also been observed in rodents after experimental lead exposure (Victery 1988; Staessen et al. 1994). Bagchi and Preuss (2005) found that acute l ead exposure had lasti ng effects including lowered bone density and increased blood pressu re one year after e xposure in laboratory

rats.

In spite of the abundance of evid ence that lead is toxic to wi ldlife, poisoning rates are not

well understood. While massive die-offs are r eadily visible, daily losses of individual

animals are more difficult to detect. This is because sick animals will often isolate themselves, and then are quickly predated upon after death. In one study, observers were given 30 minutes to discover 100 placed carca sses and only found 6 (Stutzenbaker et al. 1983). In another study in which researchers pl anted carcasses, over 60% of the carcasses were gone within 3 days and over 90% were gone within 8 days (Humburg et al. 1983; Stutzenbaker et al. 1983).

Sub-lethal lead poisoning may weaken rapt ors and leave them unable to hunt, or make them more susceptible to mortality from vehi cles, power lines, and steel traps (Redig et al. 1980; Fry and Maurer 2003). It has also been suggested that rapt ors intoxicated with lead may suffer impaired hunting ability and ma y scavenge to a greate r extent or be less

selective in their choice of prey (Pain et al. 1993). Sampling methods to determine the exposure to lead intoxication in wildlife have inherent biases as with any wildlife health

assessment in the field.

Long-lived species are particularly susceptible to bioaccumulation of lead in bone tissues, and repeated lead ingestion and accumula tion in long-lived species can reduce bone mineralization, which could mean an increase in bone fragility (Gangoso et al. 2009). . Gangoso et al. (2009) found unusua lly high level of frequency of fractures and even leg amputations in an Egyptian vulture ( Neophron percnopterus ) population with high exposure to ingestion of lead ammunition.

The non-lethal effects of lead toxicosis may be difficult to recognize at a distance in freeranging wild animals. Subtle neurological si gns are easy to miss even in domesticated animals that can be physically examined. Wild animals that have died from or have been debilitated by lead poisoning may elude cap ture due to behavior al or physiological changes, or be removed from the population if lead exposure is associated with high levels of mortality (Miller et al. 1998).

Lead poisoning due to ingestion of spent shot or bullet fragments has had populationlevel effects for some bird species with low recruitment rates, depressed populations, or in recovery, such as the California condor, bald eagle, trumpeter swan, sandhill crane, and spectacled eider (He nnes 1983; Grand et al. 1998; Church et al. 2006).20 E. Lead Ammunition Poisonings by Species

Information on lead poisoning of wildlife sp ecies in the United States from lead

ammunition is detailed below. Information on lead poisoning of wildlife species in

Canada and other countries is included in some instances where there is additional research on the effects and prevalence of lead toxicosis for certain species.

1. California Condor ( Gymnogyps californianus )

The potential effects of lead ammunition in non-waterfowl hunting practices has now received national attention in part because of recent documentation of harmful levels of lead exposure in the endangered California condor population. Elevated blood lead levels in free-flying California condor s have been well described (L ocke et al.1969; Wiemeyer et al. 1986; Janssen et al. 1986; Pattee et al. 1990; Meretsky et al. 2000; Fry and Maurer 2003; Redig et al. 2003; Woods et al. 2006; Hunt et al. 2006; Sullivan et al. 2006; Parish et al. 2006; Church et al. 2006). Wild condor s in California are cap tured once or twice per year, and blood samples are taken as part of an extensive lead monitoring program for the reintroduced population. C ondors with concentrations below 20 μg/dl in blood are considered to have only background exposur e, concentrations between 20–59 μg/dl indicate elevated exposure to lead, concentrations betw een 60–99 μg/dl suggest birds may be clinically affected, a nd levels above 100 μg/dl indicate acute toxicity (Redig et al. 1983). Fry and Maurer (2003) a nd Fry et al. (2009) report that since blood monitoring was implemented in California in 1997, 83% of all free-flying condors tested have had detectable exposure to lead. A recent review of medical records from captive condors at the San Diego Wild Animal Park was conduc ted to identify blood l ead reference ranges for condors not exposed to lead sour ces in the wild (Dujowich et al. 2005). Among 95 captive born condors tested, all had blood lead le vels below detection limits of 6 μg/dl with one exception testing at 11.0 μg/dl (Dujowich et al. 2005).

For the condors released in southern California (Ventura, Santa Barbara and San Luis Obispo counties) since 1992, blood lead concen trations were evaluated in 214 samples from 44 individuals (Hall et al. 2007). Forty- four percent (95/214) of these blood samples obtained during captures from 1997 to 2004 had lead concentrations consistent with elevated levels of exposure (>20 μg/dl), w ith 8% (18/214) at clinically significant concentrations and 3% (7/214) at acutely t oxic concentrations (Hall et al. 2007). Seventy seven percent of the individual condors tested (34/44) showed elevated exposure; 32% of condors (14/44) had concentrations considered to be clinically significant, and 14% (6/44) had concentrations consis tent with acute toxicity in at least one of their samples.

Half of the individuals had elevated levels in multiple samples suggesting repeated exposure events (Hall et al. 2007). Subadults (age 4-5 years) in this cohort had higher exposure than adults classified as 6 year s and older (Hall et al. 2007). Condors were

found to have increased blood l ead concentrations the second year after release reaching a peak 4 years post-release and then generally declining (Hall et al. 2007). Highest lead concentrations coincide with the age class most likely to forage widely, but detailed comparisons of condor movements and lead co ncentrations have not been done on a large scale for the California population.21 The frequency of elevated blood lead concentr ations reported for the condors released in southern California is higher than that observed in the condors released by the Ventana Wildlife Society in Big Sur, California. Si nce 1997, 33 condors releas ed in Big Sur were repeatedly sampled to produce a total of 126 independent measurements of blood lead concentration. This group reports 21% ( 27/126) of samples to be above background levels, with only 3% (4/126) of samples at clinically significant levels and only 2% (2/126) indicative of acute toxicity (S orenson and Burnett 2007). Condor lead concentrations were significantly higher in year 6 and year 8 post-release (Sorenson and Burnett 2007). Most of the birds released at Big Sur (21/33) visited southern California at some point, and for those that did so, they did this on average 2 years post release (Sorenson and Burnett 2007). The authors at tributed the lower prevalence of lead exposure in the Big Sur population to their fi nding that out of 26 observed feeding events on wild prey, 20 were California sea lions in contrast to only 3 observations of condors feeding on deer, which were far more likely to be hunter-shot (Sorenson and Burnett 2007).

Petterson et al. (2009) collect ed 63 blood samples from 20 condors at Pinnacles National Monument from 2003 to 2007 and compared blood l ead values before and after release. Of 63 post-release samples, 24 (38%) were above background (20–59 μ g/dL), two (3.2%) were clinically affected (60–99 μ g/dL), and two more (3.2%) were indicative of acute toxicity ( ≥ 100 μ g/dL). Fifteen (75%) of individuals sampled were exposed at least once and eight (40%) were exposed on two or more occasions. Petterson et al. (2009) found a significant difference comparing samples collec ted before release and within one year after release from the same individuals, re vealing that even young, inexperienced condors in this area are vulnerable to lead exposure.

A complete recount on lead in toxication events of wild and captive-reared condors in California and Arizona (1992 to 2002) was compiled by Fry in 2003 with information from the Condor Recovery Program. Currently, condors with greater th an 40 μg/dl lead in blood measured with a portable lead analyzer in the field are br ought into captivity for

chelation treatment to reduce blood lead c oncentrations. Among condors released in southern California, at least 8 had been brought back into captivity and received emergency chelation therapy as of 2007 (Hall et al. 2007). Four of these birds had lead levels exceeding 180 μg/dl and were likely to have died or been severely debilitated without emergency interv ention (Hall et al. 2007).

Free-flying condors are also captu red once or twice per year in Arizona to measure lead exposure. Out of a total of 437 samples, 31% (137/437) had elevated lead concentrations (15-59 μg/dl), and 9% (39/437) exceeded 60μg/ dl (Parish et al. 2006). Chelation therapy

was administered 66 times to a total of 28 individuals from 1996 to 2005 in Arizona (Parish et al. 2006).

In addition to capture and treatment of c ondors found with high lead levels, management practices in both California and Arizona include supplemen tal feeding to reduce lead exposure. Several reports sugge st that the condor mortality due to lead would be much22 higher if the free-flying popul ation were not intensively managed by supplemental feeding and chelation treatment to minimize th e impact of lead exposure events (Fry and Maurer 2003; Woods et al. 2006; Pattee et al. 2006; Hall et al. 2007; Mee and Snyder 2007).

Causes of condor mortality were reviewed in detail for 41 free flying condors that died in

California and Arizona between 1992 and 2002 (Fry and Maurer 2003). Of the 41 condor carcasses found and examined, lead toxicity was documented as the cause of death in 12% (5/41) (Meretsky et al. 2000; Fry a nd Maurer 2003). Preda tion (22%; 9/41) and power line electrocutions and col lisions (20%; 8/41) were iden tified as the leading causes

of reintroduced condor mortalit y in California and Arizona during this time frame (Fry and Maurer 2003). While power line collisions and electrocutions were particularly problematic for the early condor releases in California, mortality due to this cause has been reduced substantially in recent y ears since power line aversion training was instituted as part of th e reintroduction program (Mee and Snyder 2007). The coarse terrain and wide-ranging movements of the condor make it difficult to find deceased

animals within a timeframe that allows for the accurate determination of causes of death. Unless carcasses are recovered in fresh post-mortem condition, it can be exceedingly difficult to identify causes of death th at are only recognizab le by microscopic examination of tissues or laboratory analyses of samples. It can also be difficult to distinguish whether or not dise ase or intoxications have alte red an individual’s behavior and initiated a chain of events leading to trauma or some other cause of death. The exceedingly high blood lead levels reported in some free-flying condors suggest that these birds may have compromised abilities to avoid hazards. Therefore, cause of death could not be accurately determined for 20% (8/41) of recovered condor carcasses. An additional 11 condors were lost to follow up during this time period. While likely dead,

these condors were never recovered.

A more recent review of th e 66 condors released in sout hern California found that among

the 34 condors that died in this area from 1992-2005, exact cause of death could be determined for 18 birds (Hall et al. 2007). L ead toxicity is believe d to be the primary cause of death in 3 of these birds (17%). Ag es at death for the three condors with lead poisoning were 1.7, 2.5 and 4.8 years. Condor deaths due to lead toxicity have not been reported for the 33 condors rel eased in Big Sur, California (Sorenson and Burnett 2007).

Out of a total of 26 condor deaths observed in Arizona between 1996 and 2005, at least 6 and perhaps as many as 8 (23-31%) died from lead poisoning (Woods et al. 2006; Parish et al. 2006). Mainly because of a marked r ecent increase in the number of lead-related

mortalities in condors released in Arizona , lead poisoning is now the leading known cause of death in free-flying condors. Data presented in these repor ts do not include the

additional 5 released condors in California a nd 3 condors in Arizona that have died due to lead poisoning from lead ammunition si nce 2007 (Peregrine Fund 2010; VWS 2010). At

least 30 condors in California and Arizona ha ve now died from lead exposure proven or thought to be from ingestion of lead ammun ition fragments or lead shot, with many more deaths suspected to involve lead poisoning.23 Chronic and frequent sub-leth al lead exposure for condors has been well-documented. A disturbing number of the released condors mu st undergo frequent chelation therapy to save their lives from lead poisoning due to continual exposure to lead. In 2006 alone, 95% of all Arizona condors had lead exposur e and 70% of the Arizona population had to receive life-saving chelation treatment. In 2007 there were 50 cases of lead exposure in Arizona condors, and although data have not been released for 2008 and 2009, the Peregrine Fund reported having to treat “a la rge portion” of the wild Arizona condor population with chelation thera py for increased lead levels during the winter of 2008 and a “significant amount” of lead exposure to c ondors in the winter of 2009 (Peregrine Fund 2010). In June of 2008, 7 condors fell ill from lead poisoning in one feeding event near or on Tejon Ranch, the highest lead exposure even t in Southern California in 10 years. In 2008 the blood lead levels of 72 free-flying c ondors in California were tested; from January to June, 59 percent of the condors sampled had blood lead levels that were considered above background (>10 micrograms/ deciliter) levels; 45 percent of condors exhibited blood lead levels above backgr ound levels during July-December 2008 (CFGC 2009).

Lead poisoning has begun to interfere with th e first breeding of re leased condors in the wild; one of the lead poisoning deaths in California in 2008 was a parent with a chick in the nest; in 2009 a breeding condor died of lead poisoning; and in December 2008 the first condor female to successfully hatch, a nd fledge, a wild-produced condor in Arizona in close to a century died of lead poisoning, as did her wild-produced offspring. In early 2010, the first California condor chick to hatch inside a national park in more than a century was severely lead poisoned, likely from eating carrion contaminated with fragments of lead bullets. The condor chick and its male parent had to be taken from the

nest at Pinnacles National Monument for tr eatment and the chick could suffer lasting neurological damage as a result.

If lead exposure is not high enough to cause acute intoxication and death or to impair survival skills, lead should be eliminat ed from the body gradually through natural processes. Fry and Maurer (2003) calculated an average depuration ra te (or half-time for lead elimination from blood) of 13.34±2.87 days. This finding, along with the high proportion of samples with elevated blood le vels (see Fry et al. 2009), suggest that condors are frequently and repeatedly expos ed to lead in the wild. The clinical consequences of recurrent lead poisoning are uncertain, but will likely result in long-term neurological injury (Fry et al. 2009). Fry et al. (2009) analyzed 469 blood samples taken

from 95 different condors in California si nce 2000, and found that 79 of these condors (83%) have had at least one significant lead exposure in cident, and some condors have been intoxicated multiple times (up to 13 times for one condor). There were 276 separate

documented incidents of blood l ead levels in excess of 10 μ g/dL; and 27 poisonings in

excess of 50 μ g/dL that required emergency clinical care to prevent permanent injury or death. Similar observations of high lead levels in blood and tissues of sympatric species, such as vultures, eagles, hawks and ravens in the condor range support the conclusion that environmental lead is widely availabl e to scavenging birds (W iemeyer et al. 1988; Pattee et al. 1990).24 Many studies have attributed lead exposure in condors to le ad bullet fragment ingestion when eating hunted animal carcasses (Locke et al. 1969; Janssen et al. 1986; Meretsky et al. 2000; Fry and Maurer 2003; Hunt et al. 2006 ; Woods et al. 2006; Church et al. 2006). Lead from environmental sources, such as air and water pollution, may accumulate in animals, but environmental exposure is not li kely to result in leve ls high enough to cause mortality (Pattee et al. 1990). The very high leve l of lead detected in most individuals of the free-flying condor population is consistent with a highl y concentrated source of exposure not typically found in air, water or so il unless in an area contaminated from lead mining and smelting activities.

Condors are exclusively carrion feeders, and the condor diet includes deer, sea lions, whales, squirrels, rabbits, skunks, coyotes, pi gs and cattle. The relative proportion of these various components in condor diet is very hard to assess given the difficulties involved in directly observing condor feeding behavior in the wild. Observed condor feeding behavior in southern California, although sporadic, has most commonly involved deer and cow or calf carcasses (Hopper M ountain NWR unpublished data). Intensive monitoring of the condors rel eased in Arizona has resulte d in the documentation of condors feeding on 78 deer, 42 elk, 10 c oyotes, 51 domestic livestock and 16 miscellaneous animals (Hunt et al. 2007). Condors released in Big Sur are the only population with a diet that includes marine mammals. Out of 26 feeding observations made on condors released in Big Sur, 77% involved sea lion carcasses and only 15% involved deer and elk carcasses (Sorenson and Burnett 2007). In 1984, Wiemeyer et al.

evaluated environmental contaminants includi ng biologically incorporat ed lead in condor prey species, testing muscle, fat and placenta from cattle, sheep and mule deer ( Odocoileus hemionus ). Lead levels in thes e potential food items were low in all but one muscle sample from the head of a hunter k illed deer (17.5 parts per million, ppm) and one cattle placenta sample (1.82 ppm; Wiemeyer et al. 1984).

Deer killed by hunters, predat ion, vehicular collisions, fire and disease ar e potential food

sources for condors. Condors have been dire ctly observed feeding on deer killed by hunters, and there are several observations of multiple condors feeding on deer offal piles in California (Hopper Mountain NWR unpublished data) and Arizona (Hunt et al. 2007).

In the Kaibab Plateau in Arizona 15 of the 55 deer carcasses invol ved in condor foraging events were hunter-killed (Hunt et al. 2007). Animal carcasses that have been shot with lead ammunition are likely to co ntain fragments of lead even if the bullet passed through the carcass or if the primary shot fragment has been removed (Hunt et al. 2006). Offal piles left in the field are also very likely to contain lead fragments, since these piles usually contain thoracic organs and hunters of ten aim for the thorax when targeting large mammals (Hunt et al 2006).

Inter-annual variation and seas onal trends in lead exposure have been observed in all condor populations. The 44 condors released in southern California showed substantial

inter-annual variation in blood lead concentrations with samples from 2001-2004 having a significantly lower mean than sample s from 1997-2000 (Hall et al. 2007). This temporal trend has been explained by a move in release, food pr ovisioning and trapping (sampling) location from the Sierra Ma dre Mountains to Hopper Mountain NWR in25 2001. Condors trapped at the Sier ra Madre site had a signif icantly higher mean lead

concentration than condors trapped at Hopper Mountain. Th e Sierra Madre site is characterized by greater public access and hunting activity than the Hopper Mountain site (Hall et al. 2007). Increases in blood lead le vels in condors tested during the deer hunting season have also been reported by Hall et al (2007), but samp ling effort was not distributed evenly in all seasons. In fact , sampling between January and May was very limited (with only 20/214 samples in these mont hs). This study noted that while mean lead concentration was significantly highe r in condors sampled during deer hunting season, elevated lead exposure wa s detected at other times of the year with 38% (20/53) of blood samples collected in June having le ad concentrations exceeding 20 μg/dl. Blood samples in the 33 condors at Big Sur also show ed inter-annual and seasonal variation in lead concentration with samples obtained in 2005 and samples obtained in September and October showing the highest mean concentr ation of lead (Sorenson and Burnett 2007). This peak in lead concentr ations in the Big Sur condor population does correspond with the time period in which hunter-s hot deer are most prevalent in the coast range (Fry and Maurer 2003).

The studies conducted on the introduced condor population in Arizona by Hunt et al. (2006) show correlations between increased lead exposure and foraging in deer hunting areas during and just following the hunting seas on. Spikes in blood lead levels of condors during November and December correspond with the deer hunting seasons and condor movement to deer hunting areas (Parish et al. 2009). Since condors began foraging in the Kaibab Plateau in 2002, detected lead expos ures have been temporally and spatially clustered and highly predictable (Hunt et al . 2007). Blood lead levels in condors visiting the Kaibab Plateau were significantly highe r than condors not visi ting this intensively hunted area, and evidence of lead intoxicat ion in live and dead condors have peaked annually in November and December from 2002 to 2004, coincident with the deer hunting season (Hunt et al. 2007) . Increased proficiency of condors at finding carrion in the wild corresponds with a grea ter incidence of lead exposur e, and information collected on food types supports the hypothesis that l ead ammunition residues in rifle- and shotgun-killed animals are the principle sour ce of lead contamination among condors in

northern Arizona and southern Utah (Parish et al. 2009). Ches ley et al. (2009) evaluated lead isotopic ratios from blood samples of 47 condors in Arizona over 3 years and collected 12 metal fragments from 6 birds w ith elevated blood l ead levels, directly linking ingested lead ammuniti on fragments to lead in the blood of Arizona condors. Lead poisoning has been the leading cause of death among reintroduced condors in Arizona from 1996 to 2007 (Parish et al. 2009).

Condor lead intoxications re ported in both California a nd Arizona during non-deer hunting seasons suggest that de er hunting practices are not the only pot ential source of

lead for condors. Firearms are used in th e California condor range year-round for taking non-game animals, such as ground squirrels a nd coyotes, which are typically left in the field and available for scavenging species (P attee et al.1990). Rabbits , squirrels, coyotes, and pigs shot with lead ammunition likely pose a similar risk fo r exposure as do hunterkilled deer carcasses, and these animals are more likely to be left in the field if they are not a food source or trophy for hunters. Condor s have been observed feeding on hunted26 pigs at private dumps and piles of dead ground squirrels shot for pest control (Johnson et al. 2007). Two rifle-killed coyotes were observed as a food source for condors in Arizona, and hunted coyotes have been suggest ed as a potential source for summer lead exposure in condors (Parish et al

. 2006, Hunt et al. 2007).

Direct evidence of consumption of amm unition by condors is extremely difficult to obtain given the lag time between likely inge stion/exposure and debi litation or death. In addition, ingested lead fragments can pass thr ough the digestive tract or be completely digested and absorbed if very small. Radi ographs are unlikely to detect radio-opaque particles less than 1 mm in diameter, and sim ilarly sized particles may be easily missed at surgery or necropsy. Nonetheless, physical evidence of ammunition inside the stomachs

of individual condors that have died or have been diagnosed with high blood lead levels, have occurred in 14 cases in Arizona (Parri sh et al. 2006). Of these 14 condors, 7 (3 alive, 4 dead) had shotgun pellets and 7 (6 al ive, 1 dead) had spent rifle bullets in their digestive tracts either on radiographs or during necropsy (Parish et al. 2006). In California, from 1984 to 2002, 7 condors had meta l detected in their gastro-intestinal tracts, but identification of fr agments and analysis of samples for lead content were not performed (Fry and Maurer 2003).

Ammunition was implicated as the main source of lead exposure in released condors in recent studies by Church et al. (2006) and Ches ley et al. (2009). The Church et al. (2006) study compared lead isotopic (207 Pb /206 Pb ) ratios in blood samples from released freeflying condors in Central California and prerel ease condors in Southern California; tissue samples from possible condor diet items (cal ves, road-killed deer and a sea lion); and samples from ammunition sold for bird and mammal hunting at stores within the condor range. The lead isotope ratios in free-flying condors differed significantly from those in captive pre-release condors providing further evidence that the sources of exposure for free-flying condors were diffe rent from the sources causing background levels of exposure in captive condors. Furthermore, the low background concentrations of lead

detected in non-hunter killed condor diet samples had isotop ic ratios similar to those described for environmental lead in rivers, lakes, atmospheric dust and urban aerosols. These findings provided evidence that “envi ronmental” sources of lead, such as background levels in water, so il and non-hunter killed carcasse s, were not responsible for the elevated lead exposures observed in fr ee-flying condors in California. The lead isotopic ratios in the elevated free-flying condor samples we re similar to those found in the ammunition samples tested (Church et al. 2007).

The lead isotope ratio technique has been also recently applied as a forensics tool to trace

lead sources involved in condor deaths. A feather from one condor (#165) released in Arizona and found dead nearly 3 years later (June 2000) from acute lead poisoning with 16-17 shotgun pellets in its stomach was analyz ed for lead concentration and lead isotope composition (Church et al. 2006). The lead isotopic ratio in the feather from this condor (in the area of the rachis and vane with most recent growth) closely matched that detected in ammunition samples from stores in Californi a (Church et al. 2006). Further analysis of

concentrations of tota l lead in the bones of three other dead condors (#132, 175 and 181) strongly suggest that lead poi soning or debilitation induced by lead contributed to their27 deaths, but the isotopic ratio in tissues from condors #175 and # 181 were unlike those of the ammunition samples tested to date. Howeve r, the isotope ratio in tissues from condor #132 closely matched that of the ammunition sa mples tested in the study by Church et al (2006).

Finkelstein et al. (2010) comp ared blood and feather lead isotopic composition in leadpoisoned condors to spent ammunition from a recovered pig carcass fed upon by the birds to provide irrefutable evidence for exposure to lead-based ammunition. Finkelstein et al. (2010) also analyzed lead isotope ratios in 65 releas ed California condors and demonstrated that lead in the condors (isot ope ratio values of between 0.81 and 0.83) is within the range of that found in bullet samples, most of which were turned in by hunters

in California. Pre-release birds had lower con centrations of lead in their blood, and their isotopic ratios were higher (0.83 to 0.85). Pa rmentier et al. (2009) s howed that the lead concentration and isotopic composition of c ondor feathers examined changed following a documented ammunition-exposure event, arrivi ng at values that matched exactly the isotopic composition of recovered ammunition.

Further lead isotopic analyses of ammuniti on and other potential point sources in the condor’s habitat, along with bone s, feathers and blood of ot her condors have developed a

more conclusive association between ammunition-derived lead intoxications and condor mortalities. Feathers are a pa rticularly instructive forensic tool to reconstruct lead poisoning in California condors. Finkelstein et al. (2010) used sequential feather sampling and analysis to show that feather lead concentra tions can help estimate annual lead exposure risk and give better long-ter m monitoring of lead exposure. Sampling two or more growing primary feathers over a year will provide a time series of lead exposure and capture 60% of a bird’s annual lead exposure history, co mpared to only 10% of an annual exposure history reflected in one or two blood samples collected over the same time period.

Parmentier et al. (2009) demonstrated from evaluating lead concen tration and stable isotopic measurements in growing condor feathers that lead -exposed condors are suffering sub-clinical toxicity, based on δ -aminolevulinic acid dehydratase (ALAD) inhibition by lead. Preliminary results of nine condors with blood lead concentrations ranging between 1.9-64.0 μ g/dL show a significant inve rse relationship between blood lead concentration and ALAD activity, indi cating significant inhibition of ALAD at

blood lead levels below those wh ere clinical chelation treatm ent is indicated. Church et al. (2009) showed increases in phosphorus and enzymes in condors with high blood lead levels that may be indicative of lead-induced nerve tissue damage or renal disease and kidney dysfunction.

The population-level impact of condor exposure to lead may be difficult to quantify but is clearly significant. For small populations in pa rticular, increased adul t bird mortality at any measurable rate is likely to affect population dynamics (Westemeier et al. 1998; Fisher et al. 2006). Re-intr oduced condor populations are cu rrently being intensively managed to reduce lead exposure, and the pr oportionate mortality due to lead exposure would almost certainly be higher if individual animal interventions ceased. While28 intensive management has been an important component of condor recovery efforts to date, its practicality in the long term is questionable as the condor population grows in size. More importantly, such close m onitoring and frequent recapturing are counterproductive to the establishment of a behaviorally normal self-sustaining wild condor population (Condor Recovery T eam, Lead Exposure Reduction Steering Committee, 2003). In order to ensure the r ecovery of the California condor, lead ammunition must cease being one of the species’ greatest threats.

2. Bald Eagle ( Haliaeetus leucocephala ), Golden Eagle ( Aquila chrysaetos ), and Other Eagles

Bald eagles share some demographic and eco logical factors with free-ranging condors that make this species vulnerable to lead in toxication; they scavenge on carcasses, they are long-lived, they have low recruitment rate s, and their numbers have been reduced in recent decades (Pattee et al. 1990). Bald eagles that ingest lead shot embedded in the

tissues or the intestinal tract of waterfowl demonstrate acute and chronic symptoms of lead poisoning (Hoffman et al. 1981; Miller et al. 2001). The experimental intoxication of bald eagles with lead shot conducted by Pattee et al. (1981) found that it took between 10 and 133 days (median 20 days) for mortality to occur. The range of time for lead shot

retention in the stomach varied between 0.5 and 48 days. Mean lead levels in dead animals were 16.6 ppm (wet weight) in liver and 6.0 ppm (wet weight ) in kidney (Pattee et al. 1981). In a complementary study, Hoffm ann et al. (1981) report mean blood lead levels in eagles dosed with 10 #4 lead shot (0.21g each) to be 80 μg/dl after 24 hours and 280 μg/dl after 72 hours. Mean blood lead levels as high as 270 μg/dl have been detected in apparently healthy free-ranging bald eagle s but subclinical effects may be difficult to document (Reiser and Temple 1981). Foreign bo dies, including lead fragments, may be regurgitated by eagles so that fragments may not be detected in the gastrointestinal tract at the time of capture or blood tests, even if the fragments contributed substantially to elevated lead exposure levels prior to bei ng ejected. Mateo et al . (2003) recognized the importance of accounting for this unique phys iology in raptors and recommend collecting regurgitated pellets at raptor roosting sites to study the pr esence, frequency, seasonality and prey associated with th e ingestion of lead shot.

The secondary poisoning of bald eagles by lead shot in crippled waterfowl was part of the impetus for the final decision to ban the use of lead for hunting wate rfowl (Kendall et al. 1996; Kramer et al. 1997). Coon et al. (1969) reported that 7% of 45 bald eagle carcasses had high enough lead levels to be lethal. Ka iser et al. (1990) re ported 9% of 158 bald eagle carcasses had elevated lead levels in th e liver. In one study, 97% of bald eagles and 86% of golden eagles had elevated blood leve ls of lead (Harmata and Restani 1995).

Pattee and Hennes (1983) found that elevated lead levels in bald eagles corresponded well (89%) with late fall and winter wa terfowl hunting seasons. However, a study attempting to trace lead poisoni ng in bald eagles to diet pref erence did not find significant differences in blood lead levels among eag les feeding on fish and eagles feeding on

waterfowl in an area where waterfowl hun ting was intensive (Miller et al. 1998). According to the Wisconsin Department of Na tural Resources, about 15 to 20 percent of29 all bald eagle deaths in that state are due to lead pois oning (Eisele 2008; Strom et al. 2009), usually from eating animals that were wounded with lead ammunition or from scavenging gut piles during and after the deer hunting season. Lead poisoning cases in bald eagles begin to increase in October, peak in December and tail off in late winter, which coincides exactly with Wisconsin's deer hunting season s, suggesting huntercrippled game and lead contaminated offal are the cause.

A 16 year review of lead levels in bald and golden eagles in Minnesota and Wisconsin by Kramer and Redig (1997) found that observed blood lead concentrations in both species declined following the ban on lead shot in waterfowl hunting, but there was no change in the prevalence of lead poisoning, at tributable in part to conti nued availability of gut piles from hunter-killed deer. In that study, 21% (138/654) of eagles admitted to the centers had evidence of lead poisoning, and only one had radiographic evidence of lead fragments in the gastro-intestinal tract (K ramer and Redig 1997). Other potential sources of lead, such as fish contaminated with lead fishing sinkers, a nd hunting activities not included in the lead shot ban were suggested as causes for the substantial number of cases reported during this time period. Cl ark and Scheuhammer (2003b) found, not surprisingly, that upland game birds and mammals, the primary foods for many raptors, were more likely to contain lead shot than waterfowl 12 years after the ban on lead shot for waterfowl hunting. Lead shot from upla nd game hunting and lead bullet fragments from big game hunting and “varmint” shooting are a significant cause of continued lead toxicity for bald and golden eagles (Harmata and Restani 1995; Fisher et al. 2006; Hunt et al. 2006; Pauli and Buskirk 2007).

Golden eagles share some feeding ecology and behaviors with California condors and bald eagles and therefore may be exposed to some of the same fact ors that predispose condors to lead intoxication. In the study by Pattee et al. (1990) on the lead hazards

within the California condor range, golden eagles were suggested as a model species to assess lead exposure in California condors b ecause they are abundant in the condor range and they have been observed feeding on the same carcasses as condors. Between 1985 and 1986, 36% of the 162 golden eagles evaluate d within the Califor nia condor range had elevated blood lead levels, and 2.5% had le vels greater than 1 00ug/dl, indicative of clinical lead poisoning. This st udy also reported seasonal trends in lead levels in tissues of golden eagles within th e California condor range which coincided with the deer hunting season (Pattee et al. 1990).

Wildlife rehabilitators in Iowa began gatheri ng lead poisoning information on bald eagles in 2004, analyzing blood, liver, or bone sa mples for 62 eagles (Neumann 2009). Thirtynine eagles showed lead levels in their blood above 0.2 ppm or lead levels in their liver above 6 ppm, which could be lethal poisoning without chelation treatment. Seven eagles showed exposure levels of lead (betw een 0.1 ppm and 0.2 ppm in blood samples, between 1 ppm and 6 ppm in liver samples, and between 10 ppm and 20 ppm in bone). Several of the eagles admitted with traumatic injuries showed underlying lead exposure or poisoning. Over fifty percent of the eagles being admitted to Iowa wildlife rehabilitators have ingested lead. Behavioral observations, tim e-of-year data analysis, and x-ray information point to lead shrapnel left in slug-shot white-tailed deer ( Odocoileus30 virginianus ) carcasses to be a source of this i ngested lead (Neumann 2009). Thousands of bald eagles winter in Iowa, up to one fifth of the lower 48 states population.

The Washington Department of Fish and W ildlife conducted a four-year study of golden eagles in Washington that showed increased lead levels in golden eagles.

Spring migrating eagles sampled in we st-central Montana between 1983 and 1985

showed elevated blood-lead le vels in 85% of 86 golden eagle s and 97% of 37 bald eagles, with the source thought to be shot from wate rfowl hunting and fragme nted lead-core rifle bullets in ground squirrels (Harmata and Restani 1995). Domenech and Langner (2009) sampled blood from 42 golden eagles in Montan a captured on migrati on during the fall of

2006 and 2007 and found that 58% had elevated bl ood-lead levels, attributed to ingestion of lead-tainted carcasses or offal piles. Of the eagles evaluated by Domenech and Langner (2009), 18 contained background lead levels of 0–10 μ g/dL, 19 eagles were

considered sub-cl inically exposed at 10–60 μ g/dL, two birds were clinically exposed (60–100 μ g/dL), and three exhi bited acute exposure of >100 μ g/dL. Eagles with lower, but detectable blood lead levels may have ha d earlier exposure with the majority of the lead already deposited in other organs and bone.

Bedrosian and Craighead (2009) measured bloo d lead levels of 47 bald eagles and 16 golden eagles in the southern Yellowstone Ecosystem around Grand Teton National Park, Wyoming during and after large-game hunts for two years. They found a median blood

lead level of 41.0 μ g/dL (range = 3.2–523 μ g/dL), 74.9% of all birds tested exhibited elevated lead levels (>20 μ g/dL), and 14.3% exhibited levels associated with clinical poisoning (>100 μ g/dL). The median blood lead leve ls for eagles during the hunting season was significantly higher than the non-hunting season (56.0 vs. 27.7 μ g/dL, respectively; P = 0.01). The magnitude of lead in the blood of Wyoming eagles is extremely high and likely results in the d eath of some individuals (Bedrosian and Craighead 2009).

Lead poisoning is a significant cause of death in some upland-foraging raptors in Canada (such as golden eagles) that may feed on dead or wounded upland prey with embedded lead shot or bullet fragments (Scheuhammer 2009).

Kurosawa (2000) first reported lead poisoning in sea eagles in Japan, and Saito (2009) reported on 129 mortalities of Steller’s sea-eagles ( Haliaeetus pelagicus ) and white-tailed eagles ( Haliaeetus albicilla ) on the island of Hokkaido, Japan from 1996 to 2007 diagnosed as lead poisoning fatalities. Necropsies and radiogra phs revealed lead fragments from rifle bullets and from shot gun slugs in the digestive tracts of poisoned eagles, providing evidence that a source oflead was spent ammunition from leadcontaminated Sika deer carcasses, which ar e a major food source for wintering eagles.

Post mortem examinations of more than 390 white-tailed sea eagles ( Haliaeetus albicilla ) in Germany, an umbrella species for othe r scavenging birds, have shown that lead poisoning is the most significant cause (23% of mortality) of death (K rone et al. 2009). Krone (2004) also reported lead poisoning of seal eagles in Greenland. Potential sources of lead were waterfowl such as geese and carca sses of game animals or their remains (gut31 piles) shot with lead-containing bullets. Capt ured geese and shot game animals examined by radiograph revealed embedded shot pellet s and large numbers of lead particles.

3. Turkey Vulture ( Cathartes aura ) and other Vultures

While mortality due to lead exposure in tu rkey vultures is not well documented, dead turkey vultures sampled with in the condor range have been documented as having elevated lead exposure (Weimeyer et al. 1988). Experimental lead in toxication studies in turkey vultures suggest that vultures can succumb to lead poisoning, although studies have demonstrated that turkey vultures are ab le to tolerate very highly elevated lead concentrations in blood. One experimental intoxication study, conducted by Carpenter et

al

. (2003), administered turkey vultures daily oral doses of one, three or ten BB-sized lead shot (0.35 to 0.45 grams) over a six m onth observation period. While most measured parameters were similar to those reported fo r other avian species, survival time (143 to 211 days), even at the higher level of exposur e, was much longer than reported for other species, suggesting turkey vulture s may be less sensitive to the deleterious effects of lead ingestion (Carpenter et al. 2003) . In a separate experimental trial by Reiser and Temple (1981), one turkey vulture was more susceptibl e to lead intoxication than two red-tailed hawks (it is difficult to generalize to the spec ies level and rule out individual responses with this sample size).

Additional reports on individual cases of lead toxicosis in turkey vultures have been published. Clark and Scheuhammer (2002) evalua ted 184 raptors (16 different species) in Canada and the highest bone l ead concentration was found in a turkey vulture, suggesting this bird was likely exposed to a series of s ublethal doses of lead in carrion. Platt et al. (1999) observed histopathological peripheral ne uropathy in a turkey vulture with toxic

blood lead concentrations. Another case report describes a griffon vulture ( Gyps fulvus ) evaluated at a wildlife rescue hospital in Spai n that was clinically ill and died after eight days of supportive care with one 0.4 gram lead shot fragment found in its gizzard (Mateo et al. 1997).

Gangoso et al. (2009) examined the sub-lethal effects of lead contamination on Egyptian vultures ( Neophron percnopterus ), comparing two populations in Spain with differing exposures to the ingestion of lead ammun ition. Blood lead levels were higher in the Canary Island population than the Iberian Peninsula population, showing clear seasonal trends peaking during the Canary Island hunting season. Bone lead concentration increased with age, reflecting a bioacc umulation effect. The bone composition was significantly altered by this contaminant: the mineralizati on degree decreased as lead concentration levels increased (Gangoso et al. 2009).

4. Other Raptors

Lethal effects from ingestion of lead shot by predatory and scavenging raptors feeding on

hunter-killed carcasses have been do cumented in red-tailed hawks ( Buteo jamaicensis ), northern goshawks ( Accipiter gentilis ), and great horned owls ( Bubo virginianus ). Pain32 and Amiard-Triquer (1993) and Pain et al. (1993) documented exposure of marsh harriers

in France.

5. Waterfowl

In North America, ducks and geese for y ears suffered significant losses from lead poisoning by ingesting spent lead shot on th e bottom of ponds and marshes. Grinnell (1894) first reviewed lead poisoning in waterfowl and ot hers documented poisonings shortly thereafter (Bowles 1908; McAtee 1908; Wetmore 1919; Munr o 1925). It was

estimated that about 1.6 to 3.9 million waterfow l died each year in North America from lead poisoning before the national ban on lead shot for waterfowl hunting in 1991 (Bellrose 1959; Feierabend 1983). Lead poisoni ng from spent lead shot caused an estimated 2 to 3 percent of the annual losse s of North American waterfowl between 1938 and 1954 (Bellrose 1959). In Washington, prio r to the ban on waterfowl hunting with lead shot, biologists reported that 4.1-4.5% of harvested waterfowl contained ingested lead shot in their digestiv e tracts (Jeffrey 1977; Driver and Kendall 1984), however the extent of lead poisoning in the entire Washington waterfowl population was unknown. Within six years of the ban, there was an esti mated 64% decline in ingestion of lead shot by waterfowl on the Mississippi flyway (Ande rson et al. 2000). Of examined ducks whose gizzards contained ingested pellets, 68% of mallards, 45% of ring-necked ducks, 44% of scaup, and 71% of canvasbacks cont ained only nontoxic s hot (Anderson et al. 2000). Samuel and Bowers (2000) demonstrat ed a 44% reduction in lead exposure (defined as >0.2 ppm in blood) and of bl ack ducks in Tennessee comparing exposure from 1986-1988 with the post-lead shot ban from 1997-1999. Similar decreases in mean bone lead concentrations in hatch-year ducklings were shown in Canada after implementation of lead shot bans (Stevenson et al. 2005). After nontox ic shot regulations for most migratory game birds were estab lished and implemented nationwide from 1990 to 1999 in Canada, the incidence of elevated lead exposure in hatch year ducks declined dramatically, testifying to the effectivene ss of the regulations and a generally high compliance by hunters (Scheuhammer 2009).

The effects of ingested lead shot on wate rfowl have been well documented (Bellrose 1959; Dieter and Finley 1978; Roscoe et al. 1979; Sanderson and Bellrose 1986; Pain and Rattner 1988; Rattner et al. 1989; Pain 1996; Franson et al. 1996; Friend 1999; Pattee and Pain 2003). As few as one or two ingested lead shot pellets can cause waterfowl to waste away and die over a period of several weeks. Ducks debilit ated by lead may be more vulnerable to hunting and may have impaired migratory behavior (Bellrose 1951). Lead shot ingestion rates for waterfow l are related to density of sp ent shot (Rocke et al. 1997).

Swans

Swan lead fatalities from ingestion of spent lead shot have been o ccurring since at least 1925 (Munro 1925). Some of the most dramatic examples of mass mortality of waterfowl due to ingestion of lead shot involve the deaths of thousands of wintering trumpeter

swans and tundra swans in northwestern Washi ngton state and southern British Columbia (Lagerquist et al. 1994; Degern es et al. 2006). Swan mortaliti es continue to regularly33 occur although use of lead shot was prohibi ted in wetland areas ove r 10 years previously.

The use of lead shot for waterfowl hunti ng was banned in Whatcom County, Washington in 1989 and Sumas Prairie, British Columbia in 1992 but lead shot continues to be permitted for upland hunting and target s hooting and for hunting doves, pigeons, and American woodcock. Lagerquist et al. (1994) found that 35 percent of the 110 trumpeter

and tundra swan carcasses collected and di agnosed from 1986 to 1992 had lead liver concentrations diagnostic of lead poisoning. Degernes et al. (2006) found that 81 percent of 400 trumpeter and tundra swan carcasses co llected from 2000 to 2002 died from lead poisoning. Swan mortality could be high because swans can forage deeper into bottom sediments than other waterfowl, and be expos ed to shot deposited years earlier. Large die-offs or consistent mortality prompt concern that lead poisoning could negatively impact populations. From 2000 to 2001, over 30 0 trumpeter swans died in Whatcom County from ingestion of lead shot (WDFW 2000). Th e 2001 population of trumpeter swans in this area was 916, and it is likely th at lead poisoning is affecting the population

in this area.

From 1999 to 2008, more than 2,500 trumpeter ( Cygnus buccinator ) and tundra swans ( Cygnus columbianus ) have died from lead poisoning from ingesting lead shot in northwestern Washington and s outhwestern British Columbia around just a single lake in (Shore 2009; Wilson et al. 2009). Swans at Judson Lake, which straddles the U.S./Canadian border in the Fraser Valley, begi n to die from lead poisoning about three

weeks after their arrival in November from summer nesting grounds in the Yukon. Swans arrive on the wintering grounds with low blood lead levels, bu t some birds subsequently become exposed to lead afte r ingesting lead shot (Smith et al. 2009). Some of the poisoned swans were found to have ingested mo re than 100 lead shot. Ingestion of only two to three pellets may cause mortality in approximatel y three weeks. It is unknown whether the swans are ingesting lead shot fr om feeding on the bottom of the lake, left over from the days before the lead shot ban, or from nearby fields wh ere they also forage,

and where lead shot is sti ll legal to use in the hunting of doves and other upland game birds. Relatively high densities of spent lead shot occur in fields and water bodies where hunting and target shooting occur on the U.S. side of Judson Lake (Smith et al. 2009).

Wilson et al. (2009) confirmed lead shot in 80% of intact remains of dead swans from Judson Lake given toxicological testi ng. A multi-agency working group identified suspected sources of the lead shot, determini ng the type and size of shot in lead poisoned swans and measuring lead isotope ratios in lead poisoned and non-lead poisoned swans.

Patterns of lead ratios in shot from suspected source areas, in shot from gizzards of leadpoisoned swans, and in liver of lead poisone d swans were compared. Swan gizzards had a mix of lead shot sizes typically used fo r upland game bird hunting (#6) and target shooting (#7.5–8) and predominately nontoxic sh ot sizes typically used for upland game bird hunting (#4–6). 56% of the lead ratios measured in the shot collected from

sediment/soil fell within the range found for shot collected from the swan gizzards, indicating that swans are not consuming the whole range of shot sizes recovered from agricultural fields and water-bodies. Prelimin ary results are inconclusive, but Wilson et al. (2009) suspect lead shot for trap or skeet practice in areas frequented by waterfowl may be partially responsible. Two recent test s of hazing or preventing swans from using a34 major roost site at Judson Lake (2006- 2007 and 2007-2008) resulted in a 50% reduction in lead-related swan fatalities, compared to th e average of the five previous years (Smith et al. 2009). Judson Lake is a source of lead shot poisoning sw ans but it clearly is not the only source.

Efforts to restore trumpeter swans in Wiscons in are also being hampered by persistent die-offs due to lead poisoning. According to the Wisconsin Department of Natural Resources, about 30 percent of a ll trumpeter swan deaths in Wi sconsin are related to lead poisoning from ingesting lead shot or lead fishing sinkers on the bottom of water bodies (Eisele 2008). Strom et al. (2009) reported that approximately 25% of trumpeter swan

fatalities in Wisconsin have been attributed to lead toxicity, and about 15% of livesampled trumpeter swans in Wisconsin had blood lead levels above background concentrations (20 μ g/dL).

Loons

According to the Wisconsin Department of Natural Resources, about 35 percent of all

loon deaths in Wisconsin are related to l ead poisoning, from picking up lead shot or

sinkers on the bottom of water bodies (Eisele 2008). Pokras et al. (2009) demonstrated that common loons in New England ingest spent lead shot through examining lead objects found in 118 of 522 loon carcasses recove red from the six New England states from 1987 to 2000. A total of 222 lead objects were recorded from the loons’ gizzards, with 11% of the items recovered being l ead ammunition, primarily shotgun pellets, but

also one .22 caliber bullet and one .44 –.45 caliber bullet. Ev ers (2004) reported that in New England, a 14-year study diagnosing cau ses of mortality in 522 common loons documented 44% of the breeding adults died from lead toxicosis, from either lead shot or

sinkers. Substantial rates of lead-related mort ality are also known for loons in Michigan and Minnesota. In New Hampshire, the inges tion of lead sinkers and jigs accounted for

40 to 71% of identified annual adult mortality during the breeding season.

Eiders

Lead shot is still used in many parts of rural Alaska for subsistence waterfowl hunting and legal use of lead shot for upland ga me hunting can occur in waterfowl breeding habitats. Availability of spent shot may be prolonged by permafrost, which frequently

underlies wetlands used for br eeding and retards the sinking of shot beyond the reach of feeding waterfowl. Lead pois oning of spectacled eiders ( Somateria fischeri ), a federally threatened species, in the Yukon-Kuskokwim De lta of Alaska, has been shown to be due to ingestion of lead shot (Franson et al. 1995; Brown et al. 2006). Radiograph studies showed that nearly 12 percent of eider a dults and 2.5 percent of eider ducklings had ingested lead shot (Flint et al. 1997; Franson et al. 1998). Adult female eiders died of lead poisoning and predation, and eggs from female s exposed to lead survived at much lower rates (Flint and Grand 1997; Grand et al. 1998). Mortality from lead exposure was suggested as a significant impact impeding th e recovery of the lo cal spectacled eider populations in the 1990s, which were already depressed (Grand et al. 1998). Matz and Flint (2009) analyzed blo od of spectacled eiders ( Somateria fischeri ), king eiders ( S.35 spectabilis ), common eiders ( S. mollissima ) and long-tailed ducks ( Clangula hyemalis )

on the Yukon-Kuskokwim Delta and the North Sl ope of Alaska for total lead and lead isotope ratios. Lead shot can have distinct, ore-specific signatures. Isotopic signatures from birds with relatively high blood lead concentrations were most similar to the isotopic signatures of lead shot, while si gnatures from birds with low blood lead concentrations closely matched those of local sediments. Lead concentrations in sediment samples were very low making sedime nts an unlikely source for high blood

concentrations.

6. Game Birds

Lead exposure and poisoning from ingesting spent lead shot has been documented in many species of upland game birds such as chukar ( Alectoris chukar ), grey partridge ( Perdix perdix ), ring-necked pheasant ( Phasianus colchicus ), wild turkey ( Meleagris gallopavo ), scaled quail ( Callipepla squamata ), northern bobwhite ( Colinus virginianus ), American woodcock ( Scolopax minor ), ruffed grouse ( Bonasa umbellus ), and mourning dove ( Zenaida macroura ) (Campbell 1950; Damron and Wilson 1975; Best et al. 1992; Yamamoto et al. 1993; Kendall et al. 1996; A koshegyi 1997; Keel et al. 2002; Battaglia et al. 2005; Butler 2005; Fisher et al. 2006, Schulz et al. 2006).

Mourning doves are particularly at risk for l ead poisoning because they frequent and feed at high-risk habitats in terms of high concentrat ions of spent lead shot (Lewis and Legler 1968; Hass 1977; Kendal and Scanlon 1979a, 1979b; Kendall 1980; Burger et al. 1983; Carrington and Mirarchi 1989; Castrale 1989; Best et al. 1992; Kendall et al. 1996; Burger et al. 1997; Schulz et al. 2002). Por tions of the dove populations feeding on these sites ingest lead pellets, and shot ingestion by doves in creases during the hunting season ((Kendall et al. 1996; Otis et al. 2008; Franson et al. 2009). Virt ually all doves that ingest pellets succumb to the direct or indirect effects of lead poisoning (Schulz et al. 2006; Schulz et al. 2007). Kendell et al . (2006) identified in creased susceptibility to cold as a mortality mechanism caused by lead toxicosi s in doves. Spent shot concentrations on managed dove fields have been documente d as high as 348,000 pellets per acre (Best et al. 1992).

Sampling and evaluation of lead exposure of hunter-harvested doves is the usual source for estimating lead ingestion (S chulz et al. 2002, 2006) with 2.5-45.3% of doves having lead shotgun pellets in their digestive tracts. Schulz et al . (2009) suggested that doves feeding in fields hunted with l ead shot that ingest multiple le ad pellets may die quickly of

acute lead toxicosis and become unavailable to harvest, resulting in an underestimates of lead shot ingestion rates, such as for prev ious studies finding rela tively few doves with ingested lead shot despite feeding in areas wi th high lead shot avai lability. Schulz et al. (2007, 2009) administered lead shot to captive doves and confirmed rapid and acute lead

toxicosis.

Franson et al. (2009) evaluated lead expos ure in 4,884 hunter-harvested mourning doves from Arizona, Georgia, Missouri, Oklahom a, Pennsylvania, South Carolina, and Tennessee. The frequency of ingested lead pellets in gizzards of doves on hunting areas36 where the use of lead shot was permitted was 2.5%. On areas where nontoxic shot was required, 2.4% of mourning doves had ingested steel shot. Doves without ingested lead pellets had lower bone lead concentrations in areas requiring the use of nontoxic shot than in areas allowing the use of lead s hot. Schulz et al. (2006) calculated from comparing hunting statistics a nd population estimates that approximately as many doves are poisoned lethally by lead shotgun pellets (8.8 million t o15 million per year) as are shot by sport hunters on an annual basis. The number of mourning dove s harvested in the U.S. is approximately 20 million birds annually.

Bingham et al. (2009) documented ingestion of lead pellets by hunter-harvested chukars in four counties in western Utah, finding inge sted lead-pellets in 8.74% of gizzards from 286 birds. Toxicology results show elevated concentrations of lead (>0.5 ppm, ranging from 0.7 to 42.6 ppm) in 50 bird livers (14%). The arid, rocky, and alkaline nature of chukar habitat which reduces pellet sett lement and dissolution, and the similar appearance of lead pellets to chukar food sources leads to ingestion of lead pellets by

chukars.

American woodcock are exposed to lead on their breeding grounds in Wisconsin, resulting in high accumulations of lead in bone tissue (Strom et al. 2009). Bone lead

concentrations considered to be toxic in wa terfowl were observed in all age classes of woodcock. Although stable isotope analysis of bone samples was not able to conclusively identify the source of the lead, the data sugge st a local and dietary source (Strom et al. 2009).

The frequency of elevated lead accumulation in some hatch year upland game birds (such as Hungarian partridge) in Canada can be co mparable to that experienced by hatch year ducks prior to nontoxic shot regulations.

7. Cranes and Rails

A number of gruiformes have been shown to ingest lead shot, including greater sandhill cranes ( Grus canadensis tabida ), American coots ( Fulica americana ), clapper rails ( Rallus longirostris ), king rails ( Rallus elegans ), Virginia rails ( Rallus limicola ), and sora ( Porzana carolina ) (Jones 1939; Kennedy et al. 1979; Windingstad et al. 1984; Franson and Hereford 1994; Wingstad 1998; Fisher et al. 2006). The consequences of poisoning incidents for the critically e ndangered Mississippi sandhill crane ( Grus canadensis pulla ) could be considerable, given a population th at has only recently grown to about 100 individuals (Johnsgard 1983; LaRoe et al . 1995). Whether endangered whooping cranes ( Grus americana ) ingest lead pellets dur ing their migration across Canada and the U.S. is

unknown.

8. Corvids

Scientists tested blood lead levels in 302 ravens that s cavenged on hunter-killed large ungulates and their offal in and around Gr and Teton National Park, Wyoming in 2004 and 2005 (Craighead and Bedrosian 2007, 2008). Bl ood-lead levels of ravens increased37 dramatically during hunting season, roughly five times higher than the rest of the year, likely due to ravens consuming lead bullet fr agments left behind in gut piles of hunted elk, deer, and moose. Blood samples were ta ken during a 15-month period spanning two hunting seasons, from mid-September 2004 to mid-December 2005. Forty-seven percent of the ravens tested during the hunting seas on exhibited elevated blood lead levels ( ≥ 10 μg/dL) while only 2% tested during the non-hunting season exhibited elevated lead levels. Offal is the primary food source of ravens during the time of exposure and Craighead and Bedrosian (2007) also identifi ed un-retrieved offal piles of hunter-killed game as a point source for lead contamination in the area. These substantial increases in blood-lead levels correspond al most exactly with the open and close of hunting season. Just after the start of hunting season, blood-lead levels begin to rise. Shortly after the end of hunting season, they return to normal. Blood-l ead levels show a spike again in the late spring, when melting snow uncovers gut piles left from the previous hunting season. 100 percent of the ravens at th e study site feed on gut piles at some point throughout the hunting season and get exposed to lead.

Craighead and Bedrosian (2009) collected an additional 237 blood samples from ravens in the same study area spanning an additional two hunting seasons. The samples had a

median blood lead level of 10.0 μ g/dL with a range of 2.7–51.7 μ g/dL. The median blood lead level of 84 additional samples collect ed during the non-hunting season was only 2.2

μ g/dL with a range of 0.0–19.3 μ g/dL. Fifty percent of the hunting season samples had

blood lead levels >10 μ g/dL, while only 3% were greater than 10 μ g/dL during the nonhunting season.

Craighead and Bedrosian also documented that the blood lead levels of ravens around Grand Teton dropped corresponding with in creased use of non-lead ammunition by hunters on the National Elk Refuge and in Grand Teton National Park. In fall of 2009 researchers distributed 194 boxes of copper bul lets to hunters with permits for the park and the refuge, captured 46 ravens (which t ypically scavenge the discarded gut piles) during hunting season and tested their blood fo r lead. An estimated 24 percent of hunters in the area used copper bullets in 2009, and there was a corresponding 28 percent drop in blood lead levels in ravens compared with wh at would have been expected (Hatch 2010).

Research has yet to be done on lead expos ure to magpies, which occasionally feed on carrion and could also ingest lead by eating hunter-ki lled carcasses.

9. Song Birds

Lead poisoning from ingested spent lead ammunition has been documented in several songbird species in the United States , including white-throated sparrow ( Zonotrichia

albicollis ), dark-eyed junco ( Junco hyemalis ), brown-headed cowbird ( Molothrus atar ), yellow-rumped warbler ( Dendroica coronata ), brown thrasher ( Toxostoma rufum ), and blue-headed vireo ( Vireo solitarius ) (Vyas et al. 2000, 2001; Lewis et al. 2001).38 10. Mammals

Elevated levels of lead have been found in several species of small mammals near shooting ranges, such as shrews, mice, vol es, and squirrels, hares, opossums, and raccoons (Tataruch and Onderscheka 1981; Erickson and Lindsey 1983; Ma 1989; Stansley and Roscoe 1996; Lewi s et al. 2001). It was not de termined whether elevated

blood lead levels were due to di rect ingestion of l ead particles, or whether plants growing

on lead-contaminated soil bioaccumulated l ead, which was ingested by the herbivorous mammals. Woolf et al. (1982) identified lead in liver of wild white-tailed deer ( Odocoileus virginianus ).

Ingestion of lead by carrion scavenging mammals, such as coyotes, grizzly bears, black bears, wolves, wolverines, and mountain lions feeding on varmint carcasses, and gut piles and carcasses of big game during the hunti ng season has rarely been studied. Large carnivores such as black bears ( Ursus americanus ), grizzly bears ( U. arctos) , wolves ( Canis lupis), and coyotes ( C. latrans) scavenge to varying degrees on ungulate offal piles abandoned by hunters. Cougars ( Puma concolor ) may periodically be exposed to lead at biologically significant levels becau se of the tendency to occasionally scavenge. Rogers et al. (2009) have begun collecting sa mples of liver, hair, blood, and feces from black and grizzly bears, wolves, coyotes, and cougars in Grand Teton, Wyoming, and tested samples for the presence of lead. Roge rs et al. (2009) docum ented elevated lead blood levels in grizzly bears during hunting season, when th ey scavenge the remains of big game. Preliminary data by Rogers et al. (2009) showed that of 13 Grand Teton grizzly bears sampled during hunting season, 46 percent showed elevated blood lead levels above 10 μg/dl, while 11 bears sample d outside of hunting season had undetectable lead in their blood. The potential consequen ces for large mammalian scavengers are as yet unstudied.

11. Amphibians and Reptiles

A few studies have found elevated concentratio ns of lead in tissues of amphibians and reptiles near shooting ranges and heavily hunted areas (Stansley and Roscoe 1997; Stansley et al. 1997; Hamme rton et al. 2003; Pattee and Pain 2003), with exposure presumed to be due to ingestion of lead in food items or dissolved in water, although ingestion of small lead fragments may be possible. Lead poisoning has been shown to cause mortality and to impact egg and tadpole development and growth rates in amphibians (Dilling and Healey 1926; Kaplan et al. 1967; Khangaro t et al. 1985; PerezColl et al. 1988; IPCS 1989; Stansley et al . 1997; Rice et al. 1999; Sparling et al. 2006).

American alligators have been documented i ngesting lead bullets after feeding on nutria that had been shot (Camus et al. 1998).39 F. Toxic Effects of Lead Sinker s and Fishing Tackle on Wildlife

Waterbirds are lead poisoned from ingesting le ad fishing sinkers or jigs lost by anglers on the bottom of water bodies. Sport anglers attach lead weights to fishing lines to sink the hook, bait, or lure into the water. Some a nglers use lead-weighte d hooks, called jigs. A sinker or jig can accidentally detach from a line and fall into the water or the hook or line may become tangled and the line may break or be cut. Aquatic birds may ingest lead objects while collecting gizzard stones or by preying on live bait or escaped fish with attached fishing gear. Many ducks and other wa ter birds forage for food in the mud at the

bottom of lakes. Most of these birds also swallow small stones a nd grit that aid in grinding up their food. Some of the grit ma y contain lead from fishing tackle.

Since birds do not generally ingest lead fishing weights greater than 2 ounces, the greatest hazard to water birds from lead fish ing tackle seem to be the smaller weights used by sport anglers (Scheuhammer and No rris 1995). However, Franson et al. (2003) found a pyramid sinker weighing 2.75 ounces in a common loon and found 5 sinkers in other water birds greater than 25 mm in diamet er. Observed sizes of lead objects in the gizzards of waterfowl may be somewhat smalle r at necropsy than at the time they were first ingested, due to the grinding action of the gizzard and the presence of small stones against which lead objects are abraded. Birds such as loons may ingest fishing weights while ingesting bait attached to tackle (F ranson and Cliplef 1992; Stone and Okoniewski 2001; Evers 2004). Once ingested, lead objects re tained within the ventriculus of birds will be abraded and will be partially dissolved by acid in the digestive tract, and absorbed into the blood with potentia lly toxic effects (IPCS 1989; Scheuhammer and Norris 1995, 1996; NCM 2003; Scheuhammer et al . 2003b; Pokras et al. 2009).

Lead fishing sinkers and jigs are documente d to cause lead poisoning mortality in numerous species of water birds and wading bi rds, and the problem is particularly acute for mute swans ( Cygnus olor ), whooper swans ( Cygnus cygnus ), trumpeter swans ( Cygnus buccinator ), sandhill cranes ( Grus canadensis, ), Canada geese ( Branta

canadensis ), mallards ( Anas platyrhynchos ), brown pelicans ( Pelecanus occidentalis ), and common loons ( Gavia immer ) (Locke et al. 1982; Windingsta d et al. 1984; Blus et al. 1989; Pain 1992; Pokras and Chafel 1992; USEPA 1994; Scheuhammer and Norris 1995, 1996; Daoust et al. 1998; Friend 1999; Stone a nd Okoniewski 2001; Franson et al. 2003; Sidor et al. 2003).

Loons

Common loons and pelicans are known to ingest lead objects more frequently compared to 26 other species of water birds sampled acr oss the United States (Franson et al. 2003). Franson et al. (2003) found that 11 of 313 co mmon loons brought sick to rehabilitation centers or live-trapped had inge sted lead fishing weights, in cluding split shot, jig heads, and a pyramid sinker. Franson and Cliplef (1992) reviewed records of 222 dead loons

examined between 1976 and 1991 and found that 14 died of lead poisoning, with lead fishing weights found in the stomachs of 11 of these loons. Waterbirds trapped when40 apparently healthy rarely s how evidence of lead sinker i ngestion (Franson and Cliplef 1992).

Lead poisoning from ingesting lead fishing sinkers or jigs is a frequent cause of death for

adult common loons in the northeastern Unite d States, accounting for about 50 percent of mortality of examined dead loons, and is the single most important mo rtality source in for loons new England (Pokras et al. 1992). Locke et al. (1982) reported a common loon poisoned that died from inges ting lead fishing sinkers in Ne w Hampshire; Pokras et al (1992) examined 60 dead loons collected fr om 1989 to 1992 and 27 (45%) had ingested lead sinkers; Pokras and Chafel (1992) f ound that 16 of 31 (52%) dead adult loons collected from 1989 to 1990 ingested lead sinkers; Stone and Okoniewski (2001) found that lead poisoning caused 21% of the deat hs of 105 common loons examined from new York between 1972 and 1999; and Sidor et al. (2003) examined 254 dead or moribund and found that 44% died of lead poisoning. Ev ers (2004) reported th at in New England, a 14-year study diagnosing causes of mortal ity in 522 common loons documented 44% of the breeding adults died from lead toxicosi s. Substantial rates of lead-related mortality are also known for loons in Michigan and Mi nnesota. In New Hampshire, the ingestion of lead sinkers and jigs accounted for 40 to 71% of identified annual adult mortality during the breeding season.

Pokras et al. (2009) quantified the size, mass, and types of lead fishing gear regularly ingested by common loons, coll ecting loon carcasses from the six New England states between 1987 and 2000 and submitting them for necropsy. Of the 522 loon carcasses examined, 118 (22.6%) had ingested lead object s, and 73 of these 118 loons, 73 had more than one object in their gizza rd, for a total of 222 lead obj ects recorded. Lead sinkers (48%) were the most frequently ingested object, followed by jighead s (19%), split shot (12%), ammunition (primarily shotgun pellets), lead wires or tapes, and unknown items. Fifty percent of loons with ingested shot gun pellets had either two or three such projectiles present. About 36% of loons with ingested l ead had other fishing-related objects (mostly hooks, swivels and monofilament line) present in th e gastro-intestinal tracts. All loons ingesting lead objects also had elevated liver lead levels consistent with lead poisoning. Of the 222 lead objects inge sted, 94% weighed less than 10 g and the largest object weighed 25 g. Ninety-four percen t of the lead objects were less than 25.4 mm in length; 44% had a length of less than 10 mm.

Lead poisoning from fishing we ight ingestion was the leadin g cause of deaths diagnosed

for common loons in easter n Canada from 1983 to 1995, in areas where loon breeding habitats overlap with spor t fishing (Scheuhammer et al. 2003b). (Scheuhammer 2009)

concluded from a review of available data th at ingestion of small lead sinkers or jigs

accounts for about 20–30% of recorded mort ality of breeding adult common loons in

Canada in habitats that e xperience high recreatio nal angling activity. Daoust et al. (1998)

found that 5 of 31 common loons collected w ith ingested fishing weights from the

Maritime Provinces in Canada between 1992 and 1995 had died of lead poisoning.

Ensor et al. (2002) found 17% of loons examin ed in Minnesota died of lead poisoning; Franson and Cliplef (1992) reported lead poisoning in 7 of 77 common loons from41 Minnesota and 2 of 17 loons from Wisconsin; and lead fishing tackle accounted for 52 percent of mortalit ies among adult and immature loons in New Hampshire from 1976 through 2000, by far the largest single cause of adult loon mortality in the state (Loon Preservation Committee). (Strom et al. 2009) re ported that approximately 30% of dead loons in Wisconsin submitted for necropsy since 2006 were found to be lead-poisoned, and lead fishing gear was recovered from the ga strointestinal tracts of loons in all cases where lead toxicity was a major c ontributor to the cause of death.

Swans

Lead poisoning from ingesting lead fishing si nkers was documented as the cause of death for 4 of 18 trumpeter swans examined in Montana, Idaho and Wyoming from 1976 to 1987 (Blus et al. 1989).Locke and Young (1973) reported the lead poisoning related mortality of a tundra swan that ingested a l ead sinker. A study in Britain found that lead poisoning from ingestion of fish ing weights was the leading cause of death (up to 90%) for declining mute swans (S impson et al. 1979; Birkhead 1982; Birkhead and Perrins 1985; Kirby et al. 1994), a trend which reversed when a ban on small lead fishing weights was implemented in Britain in 1987 (Delaney et al. 1992; Owen 1992; Kirby et al. 1994; Perrins et al. 2003; Kelly and Kelly 2004). Con tinued mute swan mortality in the region is thought to be from ingestion of lead weight s lost prior to the ba n or during illegal use after the ban (Perrins et al. 2003).

Cranes

Two sandhill cranes diagnosed with lead poi soning died after ingesting lead fishing weights (Windingstad et al. 1984) and an endangered Mississi ppi sandhill crane died of lead poisoning with an unidentified lead object in its gizzard (Franson and Hereford 1994).

Other Birds

Other species reported to ingest lead sinkers in clude redheaded ducks ( Aythya

americana ), pochard ( Aythya ferina ), greater scaup ( Aythya marila ), wood ducks ( Aix

sponsa ), black ducks ( Anus rubripes ), red-breasted mergansers ( Mergus serrator), whitewinged scoters ( Melanitta fusca ), double-crested cormorants ( Phalacrocorax auritus ), white pelicans ( Pelecanus erythrorhynchos ), great blue herons ( Ardea herodias ), snowy egrets ( Egretta thula ), great egrets (Ardea alba ), black-crowned night-herons ( Nycticorax nycticorax ), white ibis ( Eudocimus albus ), laughing gulls ( Larus atricilla ), herring gulls ( Larus argentatus ), royal terns ( Sterna maxima ), and bald eagles (Mudge 1983; USEPA 1994; Scheuhammer and Norris 1995; Friend 1999; Franson et al. 2003; Scheuhammer et al. 2003b).42 Reptiles

Borkowski (1997) documented a snapping turtle that ingested a lead fishing sinker, resulting in elevated blood lead, and there are reports of turtles suffering from lead toxicosis after ingesting lead fishi ng weights (Scheuhammer et al. 2003b).

G. Toxic Effects of Lead Ammuniti on and Fishing Tackle on Humans

The toxic effects of lead on humans have been known since Roma n times (Nriagu 1983; Needleman 1999; Hernberg 2000; Tong et al. 2000; Nriagu 2009). Lead is an extraordinarily toxic element, and when i ngested it attacks organs and many different body systems, including the bl ood-forming, nervous, urinary, and reproductive systems (USDHHS 1999). The effects of lead poisoni ng can include: damage to the brain and central nervous system; kidney disease; high blood pressure; anemia; and damage to the reproductive system, including decreased se x drive, abnormal menstrual periods, impotence, premature ejaculation, sterility, re duction in number of sperm cells, damage to sperm cells resulting in birth defects, mis carriage, and stillbirth, painful gastrointestinal irritation, diarrhea, loss of appetite, weakness and dehydration, nerve disorders, memory and concentration problems, muscle and joint pain (USDHHS 1999). In large enough doses, lead can cause brain damage leadi ng to seizures, coma, and death (USDHHS 1999). Chronic overexposure to low levels of lead can cause health impairments to develop over time, and irreversible dama ge can occur without obvious symptoms (USDHHS 1999). Lead exposure can adversely affect the nervous sy stem (resulting in impaired cognition, reduced motor coordi nation, and palsy), renal system, and cardiovascular system (IPCS 1977; Needle man et al. 1990; Goyer 1996; Needleman 2004; Khan 2005). Lead is especially dange rous to fetuses and young children and poisoning is even more pronounced because th e lead is absorbed faster and disrupts development, causing slow growth, developmen t defects, and damage to the brain and nervous system. Some studies link elevated bone or blood lead levels with aggression and delinquent behavior and atten tion deficit hyperactivity disord er (Nevin 2000; Needleman et al. 2002; Needleman 2004; Braun et al. 2006).

In humans, blood lead concentration of 10 micr ograms of lead per deciliter is currently considered an elevated level, although some researchers and health professionals have advocated for a threshold of 5 micrograms or even 2 micrograms. A blood lead level of 60 micrograms per deciliter in a human would require immediate medi cal attention. Lead accumulates in humans mainly in bones, with lead in blood and other tissues reflecting

more recent exposure.

Human exposure to lead in the United Stat es has decreased as lead plumbing, paint, solder, toys, and gasoline have been phased out and replaced. Public health agencies have regulated lead in industrial ac tivities and consumer products, and have to varying degrees begun to address and remediate lead exposur e from shooting ranges, but have focused little attention on hunting or fish ing activities that may be an important source of lead exposure in certain communities, occupations, or activities.43 Hunters who use lead bullets are at risk of lead poisoning in seve ral ways. One exposure

mechanism is inhalation of airborne lead cr eated by friction from l ead slugs against the gun barrel (KDHE 2004), whereby inhaled lead enters the bloodstream and is distributed throughout the body. Hunters who handl e lead bullets are also at risk of ingesting lead residue (KDHE 2004)

. The most serious exposure is from accidental ingestion of lead shot pellets or lead bullet fragments in the meat (Carey 1977; Tsuji et al. 1997, 1999; Scheuhammer et al. 1998; Johansen et al. 2001, 2004, 2005; Bjerregaard et al. 2004; Mateo et al. 2007). Health effect s in human beings following i ngestion of whole lead shot pellets have been reported in many cases, a nd ingestion of meat tissues containing minute flakes or fragments of metallic lead from the passage of lead shot or lead bullet fragments through the tissues is also possible (S cheuhammer and Norris 1995; Khan 2005).

Published literature on lead concentrations a nd lead isotope patterns from subsistence hunters in the circumpolar North indicates that elevated human lead exposure is

correlated with use of lead ammunition (Verbrugge et al . 2009). The mechanisms of exposure include ingestion of lead dust, am munition fragments, and shot pellets in harvested meat, and inhalation of le ad dust during ammunition reloading. Epidemiological studies and risk assessment modeling indicate that regular consumption of game meat harvested with lead ammunition and contamin ated with lead residues may cause relatively substantial increases in blood lead compared to background levels, particularly in children (K osnett 2009). A Canadian study of blood lead levels in hunters (Nieboer 2001) showed that lead pellets from wild game harvested with lead shot is a major source of exposure to lead in Native American communities in Canada. Blood lead levels were demonstrated to be higher in Native hunting communities than in a nearby reference group. Blood lead levels were also hi gher in men than women, consistent with greater participation of males in hunting and greater consumption of bagged wild fowl.

Blood lead levels were shown to increase in male hunters during the hunting season, and one of the measured lead isotope ratios al so changed in a manner consistent with exposure to lead derived from leaded ammunition. Of 132 subsistence hunters radiographed, 15% showed ingested lead pelle ts, with 8% located in the lumen of the digestive tract and 7% in the appendix (Tsuji and Nieboer 1997). Fifteen recent studies in Canada, Greenland, and Russia ha ve linked lead shot found in game animals to higher levels of lead in people who eat those game animals (Carey 1977; Tsuji et al. 1997, 1999; Scheuhammer et al. 1998; Johansen et al. 2001, 2004, 2005; Bjerregaard et al. 2004; Mateo et al. 2007; Tranel a nd Kimmel 2009). Studies showing significantly higher lead exposure in people from hunting communities have major implications for the public health hazards of lead in ammunition (Dew ailley et al. 2001; Levesque et al. 2003).

In Alaska, ammunition-related lead exposures include ingestion in shot game, use of certain indoor firing ranges and melting and casting lead to make bullets. Titus et al. (2009) quantified the popul ation of Alaska at potential ri sk of lead exposure from eating game shot with lead ammunition. Alaska ha s 84,000 licensed resident hunters, many of whom rely on wild game for a significant part of their diet. About 29,000 hunters kill about 7,300 moose annually in Alaska. In ru ral Alaska, where reliance on ungulate meat is high, about 100 kg of moose and caribou m eat is consumed per person annually, and small game, marine mammals, and waterfowl ha rvested with firearms also contribute to44 the local diet. Sixty percent of households in rural Alaska harvest game animals and 86% consume wild game.

A study of lead concentrations in tissue s of waterfowl killed by shotgun (Frank 1986) showed high amounts of lead (>100 mg/kg) and confirmed the presence of lead fragments by X-ray. Particles of lead ranged from irregular fragments 1–2 mm in length to very fine dust, resulting from the disr uption of lead shot pellets upon collision with bone (Frank 1986). Researchers have also det ected lead fragments visible by radiograph in carcasses of squirrels shot with bullets (Harmata a nd Restani 1995; Knopper et al. 2006). The flesh of any species of game animal killed with lead shot or lead bullets can become contaminated with high concentra tions of lead through this mechanism. Studies

have demonstrated that lead bullets can sh atter into hundreds of fragments when fired from a high-powered rifle (Hunt et al. 2009b; Cornicelli and Grund 2009). Bedrosian and Craighead (2009) showed extensiv e fragmentation of lead bulle ts in an elk carcass shot with a .30-06 rifle. In an X-ray of the resu lts, lead fragments a ppear as white shards spread throughout a la rge area in the elk’s body. Hunt et al. (2009b) found that lead fragments in shot game spread far beyond the in ternal organs and can move into the meat that humans eat. X-rays of meat from a butch ered game animals showed bullet fragments in steaks packaged for human consump tion. While most big-game hunters discard “blood-shot” meat that’s been pierced by bulle t fragments, the California research shows that fragments can be packaged even by experienced butchers.

A recent study by the Minnesota Department of Natural Resources found that when lead bullets explode inside an animal, imperceptib le dust sized particles of lead can infect meat up to a foot and a half away fr om the bullet wound (C ornicelli and Grund 2009). Cornicelli and Grund (2009) conducted a ra diograph study of bullet fragmentation patterns in carcasses to determine the potential risk of lead contamination of deer meat in the Minnesota venison donation program. Th e study assessed lead levels in deer and domestic sheep shot using di fferent types of bullets and firearms commonly used for hunting in Minnesota, including: a centerfire rifle with lead bullets designed to rapidly expand upon impact used for hunting mid-sized ga me such as deer, lead bullets designed to retain a high percentage of their weight, and non-lead co pper bullets; a shotgun using a 1-ounce Foster lead slug, commonly used throughout the Minnesota shotgun-only zone;

and an inline muzzleloader with two comm on bullets types used during Minnesota’s hunting seasons.

Cornicelli and Grund (2009) showed that using bullets with no exposed lead (a copper case completely surrounds the lead core) or bullets made of coppe r significantly reduce (or eliminate) lead exposure . Non-exposed lead core bul lets averaged nine copper fragments in the animal with an average maximum distance from the wound channel of seven inches. By design, copper bullets leave no lead and th e few copper fragments that were seen on x-ray were less than an inch from the exit wound. Both of these bullet designs fragmented very little and left no lead. Ballistic tip lead bullets (rapid expansion) had the highest fragmentation rate, with an average of 141 lead fragments per carcass and an average maximum distance of 11 inches from the wound channel. In one carcass, a lead fragment was found 14 inches from the exit wound. Soft point lead bullets (rapid45 expansion) left an average of 86 lead frag ments at an average maximum distance of 11

inches from the wound channel. Bonded lead -core bullets (controlled expansion, exposed lead core) left an average of 82 lead frag ments with an average maximum distance of nine inches from the wound. Lead shotgun slugs left an average of 28 lead fragments at an average maximum distance of five inch es from the wound channel. Muzzleloader bullets (245-grain and 300-gr ain respectively) left an av erage of three and 34 lead fragments, respectively, at an average ma ximum distances of one and six inches, respectively. Lead fragments were found so far from exit wounds that routine trimming likely would not remove all of the fragments. Only about 30 percent of fragments were

within two inches of the ex it wound, and the vast majority were dispersed further from the carcass. In some cases, low levels of lead were detected as far away as 18 inches from the bullet exit hole. Rinsing of a carcass produc ed mixed results, tending to reduce lead around the wound channel but also transp orting lead away from the wound. Lead ammunition shot into the hindquarters of a deer, where heavy bones are found, resulted in extensive fragmentation so pronounced that a hunt er would likely not wa nt to utilize this meat as there would be no way to remove a ll the fragments. Having venison processed at a meat processor will likely result in an in creased risk of lead exposure because venison from different hunters is typically mixed during the grinding pr ocess and the vast majority of hunting bullets are made from lead. Cornicelli and Grund (2009) found that 27% of the ground venison and 2% of the whole muscle cuts tested had detectable lead fragments.

In a highly publicized recent case, packets of venison shot with lead ammunition and donated by hunters to feed the hungry tested posi tive for lead contamination. Cornatzer et al. (2009) studied 100 randomly selected ground venison packages donated to the Community Action Food Centers of North Dakot a by hunters. The packages were studied by high resolution computerized tomography im aging and x-ray fluoroscopy for detection of metal fragments. Analysis of randomly selected ground venison samples showed 59 packages out of 100 had one or more visibl e lead fragments. One sample had 120 ppm lead. Cornatzer et al. (2009) concluded ther e is a health risk from lead exposure to humans consuming ground veni son. Food banks and shelters in North Dakota pulled the meat from their shelves after the report. Th e Centers for Disease Control and Prevention and the North Dakota Department of Health ra n a test to find out th e health effects of lead-shot game. The agency compared blood-lead levels of people who regularly eat meat

shot with lead bullets with the levels of those who don't eat much wild game. The results

were inconclusive. Those who ate the lead-shot meat had slightly higher blood-lead levels than those who did not, but none of the 738 people in the study had levels above the government's threshold for danger. The h ealth department recommended that children younger than 6 and pregnant women stop eating venison shot with lead bullets because those groups are at particular risk for l ead poisoning, even at low levels. Avery and Watson (2009a) conducted a survey of all w ild game meat donation programs throughout

the United States to determine the amount of venison and other game donated annually. Venison donation programs operate in all 50 st ates and in at least four Canadian provinces. For the 2007/2008 hunting season 75 programs reported providing an average of 34,943 pounds of hunted game meat annually, a total of 2.6 million pounds of meat or approximately 10 million meals.46 Hunt et al. (2009) radiographed 30 evisce rated carcasses of white-tailed deer ( Odocoileus virginianus ) shot by hunters with standard le ad core, copper-jacketed bullets under normal hunting conditions. All d eer carcasses brought to proce ssors contained fragments (15–409 fragments counted in radiographs), a nd despite a high ra te of removal of fragments by processors to avoid contamination, 80% were unable to do so entirely. Hunt et al. (2009) demonstrated that people risk exposure to bi oavailable lead when they eat

venison from deer killed with standard lead-based rifle bulle ts and processed under normal commercial procedures. Ten million hunters, their families, and low-income

beneficiaries of venison donati ons in the U.S. are at ris k. The evidence includes a high proportion (80%) of examined deer showing at least one bullet fragment in one or more ground meat packages, a substantial frequency of contamination (32% of all ground meat packages), a majority (93%) of assaye d fragments identified as lead, isotopic homogeneity of bullet lead with that f ound in the meat, and increased blood lead concentrations in swine fed fragment-c ontaining venison, meaning the lead is

bioavailable to humans as well. Hunt et al. (2009) concluded that in a majority of cases, one or more consumers of a hunter-killed, commercially-processed deer will consume

bullet lead.

Pain et al. (2010) found that eating the meat of animals hunted using lead ammunition can be more dangerous for health than was previously thought, especially for children and people who consume large qua ntities. Pain et al. (2010) analyzed the meat of six species of game birds (red partridge, pheasant, wood pigeon, grouse, woodcock and mallard) shot by hunters in the United Kingdo m, and found that lead levels in cooked game meat exceeded the maximum allowances set by the European Union, due to the presence of remains of ammunition, even af ter lead pellets were removed. Depending on the species and type of recipe used, betw een 20% and 87.5% of the samples analyzed exceeded 100 parts per billion of the fresh weight of meat.

Watson and Avery (2009) assessed the numbers and proportions of state populations that hunt and may be at risk of lead exposure from lead-bas ed ammunition, from lead handling ammunition (e.g., hunters who load th eir own ammunition), inhalation of vapor upon firing, or ingestion of game meat contaminated with bu llet fragments and shot.. In 2006, 12.5 million people (6% of the population) aged 16 years and older in the United States hunted on 220 million days, including an estimated 1.6 million children aged 6 to 15 years.

Elevated blood lead levels resulting in bi ochemical effects, disease and neurotoxicity have been documented for people who freque nt or work at indoor and outdoor firing ranges (Fischbein et al. 1979; Novotny et al . 1987; Chisholm 1988; Valway et al. 1989; Peddicord and LaKind 2000; Gulson et al. 2002 ). Exposure may be due to handling lead materials during reloading as well as inhalati on of lead dust. Sportsmen who reload rifle and pistol ammunition and cast their own lead bu llets are at particular risk of exposure to

lead.47 Watson and Avery (2009) assessed the numbers and proportions of state populations that may be at risk of lead exposure from fishing gear, from handling and making lead sinkers, and through accidental ingesti on. In 2006, 30 million people (13% of the population) aged 16 years and older in the United States fished on 517 million days. As of 1994 approximately 800,000 to 1.6 million peopl e in the United States manufactured lead fishing weights in their homes, often in enclosed garages or basements, representing approximately one-third of the lead sinke rs produced in the country (USEPA 1994). Melting lead to produce fishing tackle such as lead sinkers and jigs can result in lead poisoning through inhalation of l ead dust and fumes (USEPA 2004).

H. Alternatives to Lead Ammunition and Sinkers

In promulgating a rule in response to a Sec tion 6 petition, the EPA must consider ‘the benefits of such substance or mixture for various uses and the availability of substitutes for such uses” as well as “the reasonably ascertainable economic consequences of the rule, after consider ation of the effect on the national economy, small business, technological innovation, the environmen t, and public health” (15 U.S.C. § 2605(c)(1)(C)-(D)). This petition identifies below commercially available alternatives to lead rifle bullets, rimfire bulle ts, shotgun pellets, fishing sinker s, and jigs containing lead. Not all products available in lead are currently available as nontoxic alternatives, but the demonstrated technology indicates that all products could be produced in nontoxic alternatives within a short period of time , if manufacturers ar e provided a transition period for expanding upon current designs and stocks of ammunition and fishing gear.

1. Availability, Performance, a nd Toxicity of Non-Lead Bullets

and Shot

Stroud and Hunt (2009) reviewed basic bullet materials availa ble to bullet manufacturers, which include lead alloys, lead with external copper wash, lead core with copper jacket, pure copper, and bismuth. Lead and bismuth are highly frangible, whereas pure copper bullets tend to remain intact after impact. Bullet fragmentation increases the degree of lead contamination in tissue ingested by scavengers feeding on hunter-killed animal remains. Modern bullet design, velocity, composition, and bone impact are significant

factors in the character and di stribution of lead particles in carcasses, gut piles, and

wound tissue left in the field by hunters. Prior to the 1900s, bu llets were made entirely of lead. Their velocities were relatively slow (< 2,000 feet per second), and their tendency to fragment was accordingly lower than that of modern ammunition. Development of smokeless powder in the 1890s increased bul let speeds above 2000 feet (610 m) per second, causing lead bullets to melt in the barrels and produce fouling which reduced accuracy. Copper jacketed lead-core bullets were therefore developed, which permitted velocities that may exceed 3,000 or even 4,000 ft/sec in modern firearms. Standard hunting bullets now typically travel at 2,600 to 3,100 ft/sec, speeds highly conducive to fragmentation. Plastic-tipped “hollow-point bu llets” used for varmint hunting are actually designed to completely fragment, leaving the en tire mass of the lead bullet to contaminate

the carcass.48 Although the terms “lead-free,” “non-lead” and “nontoxic” are used interchangeably, as a result of the manufacturing pro cess, trace levels of lead can exist in any metal projectile used for bullets, including copper, resulting in ammunition that is not 100% lead-free, but that is functionally nontoxic to wildlife and humans. The Fish and Wildlife Service

definition of “nontoxic” shot to be used in waterfowl hunting specifies in 50 C.F.R. 20.21(j) several alloys containing not more than 1% lead. Steel shot can be coated with metals such as zinc (which always contains lead as an impurity) as long as the coating does not exceed 1% of the weight of the s hot. The California Department of Fish and

Game has established a maximum amount of lead content in projectile s considered to be nontoxic at 1% by weight, given scientific consensus that this threshold for lead content will preclude risk to condors, which are typica lly more sensitive to lead than other taxa, from lead fragmentation. Toxicological mode ling of this amount of lead impurity in bullet fragments indicates that even if c ondors consume major fragments of bullets, the dissolution of lead is unlikely to raise the blood lead levels above 1 μ g/dL, a low level equivalent to the blood lead levels of condor s being raised in Los Angeles or San Diego

Zoos on a lead-free diet (Fry et al. 2009).

For all but the smallest caliber bullets (those used for varmint hunting), nontoxic ammunition is widely available. Currentl y available alternatives are either made completely of non-lead materials, such as coppe r, or designed such that a lead interior is protected from exposure upon impact. Other designs have been proposed and it is expected that the increase in demand w ill result in greater options of nontoxic ammunition. Non-lead bullets generally have equivalent, if not superior, performance when compared to their lead counterparts. C opper bullets were originally designed for the “premium” market not because of concerns over lead poisoning but rather for their enhanced ballistic capabilities.

Oltrogge (2009) reviewed the success of am munition manufacturers in developing leadfree, expanding-nose centerfire bullets. The Barnes Bullet Company succeeded in 1985 in designing lead-free copper bul lets that demonstrate good ex pansion without shedding copper particles. They have proper rotational moment of inertia, are made in traditional bullet weights, and despite the lower densit y, the over-all loaded cartridge lengths are within specification. These and other factors make them as capable as traditional leadcored bullets. They are on the market as the X- Bullet series, in several varieties, chief of which are the Triple Shock and the MRX. Th e latter is shorthand for Maximum Range XBullet, which has an all-metal tungsten-composite core that is more dense than lead. It shoots further, with flatter trajectory, than any other lead-free bullet and surpasses many lead-containing bullets. Oltrogge (2009) reviewed some of th e science of achieving these lead-free, centerfire bullets. Nosler a nd other companies are now making all-copper centerfire bullets, and availability is increasing.

Currently there are a number of lead-free copper hunting bulle ts produced, at least one of which—the Barnes X Bullet—is widely availabl e. The Barnes X is made out of copper, a material that is lighter and more rigid than lead. Barnes produces a number of X-type bullets, including the X, XLC, and Triple Shoc k X, in a wide variety of calibers suitable for hunting game such as deer, elk, pig, a nd coyote. In order to promote proper49 expansion, Barnes bullets are de signed with a hollow point that is fluted so that the tip peels back to form a mushroom upon impact. Barnes bullets have a ballistic coefficient between .220 and .555, depending upon the calibe r and cartridge used. Barnes also reports that its bullets retain close to 100% of their weightafter hitting most targets. Thus, Barnes bullets are lead-free alternat ive ammunition that offers equivalent or superior performance to that of high-quality lead bullets.

Another alternative bullet, composed of tungsten, tin, a nd bismuth (“TTB”) is being developed by various ammuniti on manufacturers and the military has been experimenting with a so-called “gr een” bullet that relies on the same metals to replace lead (Mikko 1999).

The California Department of Fish and Game certifies nontoxic ammunition for use while hunting big-game and non-game species in the range of the California condor in California, including deer, bear, wild pig, elk, pronghor n antelope, coyote, ground squirrels, and other nongame wildlife. Such ammunition must use a projectile or bullet

which has been certified to contain ≤ 1% lead by weight. As a result of the manufacturing process, trace levels of lead likely exist in any projectile. DFG established a maximum amount of lead content in projectiles to be 1% by weight, given scie ntific consensus that

this threshold for lead conten t will preclude risk to the c ondor from lead fragmentation. Typically, the certified n ontoxic identified projectiles have far less than 1% lead content. As of April 2010, the Department had certified nontoxic ammunition from 24 manufacturers. A list of DFG approve d nontoxic ammunitions can be found at http://www.dfg.ca.gov/wildlife/ hunting/condor/certifiedammo.html. The Arizona Game and Fish Department also publishes a list of non-lead rifle ammunition available for big game hunters, including 120 bullets in va rious calibers produced by 13 ammunition manufacturers, as well as 7 manufacturers who provide custom-loaded non-lead rifle

ammunition. The information can be found at http://www.azgfd.gov/pdfs/w_c/condors/Non-LeadAmmo.pdf

Both rifle bullets and .22 caliber rimfire bul lets are currently marketed with non-lead

alternatives. Ammunition in .22 rimfire was made available only after California required the use of nontoxic .22 ammunition in the range of California condors. Prior to that time, expert testimony was presented to the California Fish and Game Commission saying nonlead .22 caliber rimfire was impossible to produce. However, commercially available .22

caliber ammunition was available four months after the Commission decision to ban lead

.22 ammunition.

In one survey, 90% of hunters and ranchers surveyed approved of the use of copper bullets (Ritter 2006). According to post-hunt su rvey results in Arizona, 88% of successful

hunters who used non-lead ammunition said it performed as well as or better than lead bullets. In addition, 72% of a ll hunters said they would re commend the all-copper bullets to other hunters (Seng 2006). In general, expe rts appear to endorse the use of non-lead bullets (AGFD; Rees).50 Nontoxic shotgun ammunition is widely availabl e on the market, largely as the result of federal regulations requiring its use while hunting for waterfowl (50 C.F.R. § 20.134).

Certification of nontoxic shot is conducted by the US Fish and Wildlife Service, and acceptable alloys must be not more than 1% lead. Shotguns, the dominant firearm used for waterfowl hunting, are also used for upland hunting of small game, such as squirrels, rabbits, and birds, and in many states are used for hunting larger game such as deer and pigs using solid slugs.

Commercially available nontoxic shotgun ammun ition consists of shot composed either of steel, tungsten (including tungsten-ir on, tungsten-bronze, t ungsten-nickel-iron, tungsten-matrix, tungsten-nick el-iron, tungsten-ti n-iron-nickel, tungsten-tin-bismuth, tungsten-tin-iron, and tungsten polymers), bismuth, or tin (WFGA 2001). It should be noted, however, that nontoxic shot is not cu rrently available for all gauges and pellet sizes, particularly smaller shot sizes ( #71⁄2 and #8) which are popular for hunting upland game birds (WFGA 2001).

The use of nontoxic shot for hunting upland game is mandated on a variety of federal and state lands, and nontoxic shot is used by upl and hunters across at least 1.33 million acres nationwide (WFGA 2001). For example, a number of individual National Wildlife Refuges require the use of nontoxi c shot, as do a number of st ates such as South Dakota, Wisconsin, and Maine.

The performance of nontoxic shot is also roughly equivalent to that of lead shot. Nonlead shot, particularly steel, is lighter than lead and thus has reduced velocity at greater distances, whereas bismuth shot has a density a lmost equivalent to th at of lead. Tungsten alloy shot of several compositions is superior to lead and steel shot, and can be used in double barreled shotguns and older steel barre led shotguns which would be damaged by the higher muzzle pressures created by steel shot. Tungsten all oy shot shells are currently much more expensive ($2.20- 3.50 per cartridge) than e ither lead ($0.25-0.75 per cartridge) or steel shot ($0.40-$0.60 per cartridge).

After the federal ban on lead shot for hunti ng waterfowl, there were hunter complaints

about the effects of non-lead shot on shot gun barrels. Older shotguns not designed for

steel shot have a risk of dama ge to the barrels due to increas ed pressure of the hard steel shot which may cause “ring-bulge” deformation of the barrel at the choke of older fixed choke shotguns. Double barrel shotguns are also susceptible to barrel damage with steel shot. “Hevi-shot”®, composed of tungsten, ni ckel, and iron will not damage barrels of older shotguns, although it is considerably more expensive than steel shot. All modern single barreled shotguns ma nufactured after 1990 use interchangeable choke tubes designed for steel and other nontoxic shot, and will not be damaged by any nontoxic shot.

The U.S. Fish and Wildlife Service certifie s and approves non-lead, nontoxic shot for use in waterfowl hunting (USFWS 2010). The Service has currently approved 12 nontoxic shot types. A full list can be found at http://www.fws.gov/migratorybirds /CurrentBirdIssues/nontoxic.htm51 Mandating the use of non-lead ammunition fo r hunting would impose some additional costs on some in the hunting community. Howeve r, the incremental cost of alternative ammunition is typically a tiny fraction of the total that hun ters spend on their sport. According to the federal government, the averag e big game hunter in California spends just over $800 per hunting trip. Of that $800, approximately $173 dollars are spent on all “hunting equipment”, with bullets represen ting a fraction of that cost (USDOI/DOC 2003). Likewise the cost of shot is a sma ll portion of annual waterfowl or game bird hunting expenses (Scheuhammer and Norris 1995). The Minnesota Department of Natural Resources reports that effective nontoxic alternatives to lead shot are available, and at costs comparable to lead (Trane l and Kimmel 2009). The price of non-lead ammunition has continued to drop over time as demand has risen. As demand continues to increase and subsequent production costs fall, nontoxic bullets and shot will likely become less expensive. On a larger scale, the costs to purcha se non-lead ammunition would likely be more than offset the societ al costs involved in cleaning up and managing

lead wastes from lead ammunition.

2. Availability, Performance, a nd Toxicity of Non-Lead Fishing

Tackle

Fishing sinkers and jigs do not have to be made of lea d. Inexpensive and ecologically sound alternatives to lead fishing weights made from non-poisonous materials such as tin, bismuth, steel, and recycled glass are available. Sinkers made of materials other than lead have gained varying levels of acceptance among anglers, with tradeoffs regarding cost

and effectiveness. At least 10 substitutes for lead fishing tackle are on the market: tungsten (plastic composites and putty), stai nless steel, carbon st eel, tin, tin/bismuth, brass, ceramics, glass, pewter, and zinc (Scheuhammer and Norris 1995; Scheuhammer et al. 2003b; MOEA 2006). Most fishi ng tackle stores in the U.S. already carry alternatives to lead fishing tackle and sinkers (Sch euhammer and Norris 1995, 1996; Simpson 2001; Scheuhammer et al. 2003b; Mi chael 2006). Some states a nd non-profit organizations offer small-scale programs that exchange angler-owned lead tackle for non-lead substitutes. Fishing jigs and weights containing lead are requ ired to carry a warning label in California (Proposition 65 warning) because lead has been identified by California as causing cancer. As a result, retailers and purchaser s of fishing gear in nearly all states can currently identify gear cont aining lead, and can routinel y avoid using lead-containing products, if they so choose. No t all states require a lead warning, but because California is a large market, most manufacturers routin ely label fishing gear packages that are

retailed in most states.

Metals such as bismuth and tungsten are more expensive than lead, and others such as

zinc are known to be toxic to birds and ot her biota (Grandy et al. 1968; Zdziarski et al. 1994; USEPA 1994; Levengood et al. 1999).

Tungsten, one of the more widely used alterna tives to lead fishing tackle, is sold as a tungsten-plastic composite and as tungsten putty, a specialty it em marketed to flyfishers. Tungsten putty can be molded into varying sh apes and sizes and affi xed to fishing line, allowing anglers to vary the si nk rate of their fly presentati on. Tungsten is comparable to52 lead in density and can be manufactured to be more dense than lead, allowing for smaller tackle. Tungsten tackle can also have noise-m aking attributes that may attract fish in some situations. Tungsten is more expensiv e than lead, and tungs ten tackle requires plastic sleeves to cover sharp e dges, and additional expense.

Stainless steel tackle is adve rtised as having fish-attracti ng qualities due to the noise it makes bumping along the bottom. Stainless steel tackle is larger than lead tackle of equivalent weights. Carbon steel tackle is available on the inte rnet. Some carbon steel

tackle is made from recovered waste steel mixed with resins, within a cotton sleeve. Anglers can add or subtract steel balls on a th ree-way swivel to adjust the sink rate to hold bait on the bottom. This gear is gaini ng popularity in river fi sheries and steel is replacing lead in a variety of commercial traps. Iron is one of the less expensive alternatives to lead, but ha s the disadvantage of corrodi ng after exposure to water.

Tin is a malleable metal that allows angler s to reuse split shot many times. The lower density of tin also allows for a slower sink ra te, potentially keeping the bait in the “strike zone” longer. Tin tackle tends to be larger and more expensive than lead, but is widely

available. Bismuth is a brittle metal that can be used in non-split fishing weights such as egg, worm, swivel, bullet slips, and jig heads (Scheuhammer and Norris 1995). Bismuth/tin compounds are popular among angl ers who manufacture their own jigs, partly due to better pa int quality on jig heads using this material. A disadvantage is that bismuth is a relatively expensive metal.

Brass fishing tackle is advertised as produc ing sound with fish-attracting qualities. Brass is an alloy of copper and zinc, and metallic zi nc is known to be highl y toxic to birds when ingested. Also, brass fishing t ackle often includes lead mixe d in with brass, and is not lead-free, even though the lead is bound in a state not thought to be toxi c (MOEA 2006).

Fishing tackle made of glass tends to be la rger and more expensiv e than lead. Certain types of glass can be made to “glow” af ter exposure to light, a quality purported to improve fish biting frequency. Glass sinkers are available primarily through the internet. Ceramic fishing tackle is also cons iderably larger than lead tackle.

Zinc was used as a replacement for lead sinkers until it was demonstrated that the industrial grade zinc used in th e tackle was more toxic in aq uatic environments than lead. Lead-free pewter tackle is anot her potential alternative, but pe wter is not in wide use and not currently available to consumers. It is e xpected that pewter tackle will need to be larger than lead equivale nts and more expensive.

In 1994 the EPA determined that the economic impact of switching to nontoxic fishing sinkers will be nominal (EPA 1994). Simila rly, when the National Wildlife Refuge System implemented “Lead-Free Fishing Areas,” they acknowledged that nontoxics sometimes cost more than lead weights but st ated that as sinkers only comprise 3% of yearly equipment costs, the increase did not create a burden for anglers (Federal Regulation 50 CFR 32 and 36, proposed rule).53 IV. EXISTING REGULATIONS

A. Existing Federal and State Lead Ammunition Regulations

In 1991 the USFWS banned the use or possess ion of lead shot wh ile hunting waterfowl (50 C.F.R. § 20.21(j)). This regulation was passed as a result of a lawsuit brought by a coalition of environmental groups, filed under the Endangered Species Act, in response to lead poisoning of waterfowl and secondary poisoning of eagles caused by lead shot. Regulations were phased in nationally over a five year period, w ith additional zones designated as requiring nontoxic shot each year. By September 1, 1991, every state was designated as a nontoxic shot zone for hunting waterfowl, coots and certain other species (50 C.F.R. 20.108). While bans on the use of lead shot for hunting waterfowl will inevitably reduce the likelihood of poisoning of raptors that prey on or scavenge waterfowl, they do nothing to pr event the poisoning of raptors that feed on hunted species away from wetlands or those that feed on a range of avian and mammalian prey. Lead ammunition is still permitted for upland hun ting on non-federal lands by most states. Continued lead poisoning of condors, eagles, and upland game birds, has prompted some

additional restrictions on us e of lead ammunition in National Parks, National Wildlife Refuges, and on public lands in some states. Ot her than the regulations pertaining to lead shot for waterfowl, the federal government does not regulate the method of take by hunting, deferring to state regulations on federal lands.

A 2006 survey of existing nontoxic shot regula tions for hunting waterfowl contacted 50 U.S. states, 10 Canadian provi nces and 2 Canadian territor ies (D.J. Case & Associates 2006). In 2006, 23 states had nontoxi c shot regulations for dove, crane, rail, snipe, quail, and/or pheasant hunting on some state-mana ged lands that go beyond those required by federal law for waterfowl hunting (Alaska, Ca lifornia, Illinois, Iowa, Kansas, Kentucky, Louisiana, Maryland, Michigan, Minnesota , Missouri, Nebraska, New Jersey, New Mexico, New York, North Carolina, North Dakota, Ohio, Oregon, South Dakota, Utah, Washington, and Wyoming). Some of these re strictions apply to public, but not private land, and in 7 states the restrictions only apply to mourning dove and/or marsh species such as snipe and rails. In ge neral, the regulations are more widespread for species that overlap in habitat with waterfowl (such as cr ane rail, and snipe), and to a lesser degree, doves, and are less restrictive for upland game birds such as grouse, quail and pheasant.

Of the 40 states that allow dove hunti ng, 16 have some level of nontoxic shot requirements specific to dove hunting.

There have are only been a few state efforts to restrict use of lead ammunition within the range of special-status species, such as the California condor, spect acled eider and other

water birds:

Alaska

Lead exposure to the threatened spectacled eider and other wa ter birds led to regulations in Alaska in 2007 that prohibit use of lead shot “T” size and smaller for hunting small game, furbearers, and unclassified game in the Yukon-Kuskokwim Delta.54 California

The Ridley-Tree Condor Preservation Act wa s signed into law in California in 2007, effective July 1, 2008, requiring hunters to use non-lead ammunition for hunting big game (such as deer, elk, pigs, and bighorn sh eep) and shooting coyotes within the condor range, which encompasses all or portions of 13 central and southern California counties and seven deer-hunting zone s. The California Fish a nd Game Commission approved additional regulations in 2007 expanding th e non-lead requirements to hunting of nongame mammals and birds and prohibiting the us e of lead .22-caliber and smaller-rimfire cartridges for non-game hunting in the condor range. In February 2010, California state Assembly member Pedro Nava proposed legisl ation to ban the use of lead shot in California’s 627,000 acre network of State Wildli fe Areas – this legislation passed the state Assembly but was reje cted by the Senate in 2010.

Wisconsin

In fall of 2008 Wisconsin started requiring dove hunters on public la nds to use nontoxic shot (Eisele 2008).

National Parks

In March 2009 the National Park Service announced that it would begin to develop regulations to eliminate the use of lead a mmunition in all National Parks by the end of 2010, but has yet to initiate any rulemaking. Grand Teton National Park and National Elk Refuge in Wyoming asked hunters to voluntar ily switch to non-lead bullets beginning in

fall of 2009.

International

As part of the International Update Repor t on Lead Poisoning in Waterbirds in 2000, 74 of 137 responding countries had implemented regul ations on the use of lead shot, and 37 more countries indicated lead shot legi slation was being prepared (Beintema 2001). Restrictions range from voluntar y measures to partial bans a pplied to certain species and areas, to outright statutory bans for all wate r bird hunting. Use of lead shot to hunt any water bird species is banned outright in Canada, Denmark, Finland, Norway and Switzerland (Beintema 2001). Due to extensive lead poisoning of eagles, in 2001 the Ministry of the Environment in Japan manda ted use of nontoxic rifl e bullets or shotgun slugs for hunting on the isla nd of Hokkaido, Japan (Saito 2009). Canadian national regulation in 1999 prohibited th e use of lead shot for hunting all migratory birds anywhere in Canada (exempting upland speci es such as American woodcock, mourning doves, and rock doves. (Scheuhammer 2009).

Avery and Watson (2009b) summarized interna tional lead ammunition legislation, noting that 29 countries have implement ed voluntary or legislative rest rictions on the use of lead ammunition. The types of bans varied wide ly and ranged from partial, voluntary55 restrictions of the use of lead shot to a total ban on the use and import of lead

ammunition. Two counties have banned all form s of lead ammunition. Six countries have a partial ban on the use of lead bullets in addi tion to full bans on lead shot. Four countries

have banned the use of lead shot for a ll hunting. Fourteen countries and Australian

territories have banned the us e of lead shot in wetlands or for waterfowl hunting. Two countries have voluntary or r ecommended restrictions in place. Eleven countries and Australian territories have a partial ban on lead shot. Seven countries have implemented increasingly strict regulations on lead ammunition over time.

B. Existing Federal and State Lead Sinkers and Fishing Tackle Regulations

Federal

In 1994 the EPA proposed a nationwide ban on the manufacture, importation, processing, and distribution of fishing si nkers less than 25 mm containi ng lead or zinc (USEPA 1994), but these regulations were not ratified and have been abandoned.

Lead tackle is banned on some National Wildlife Refuge s that have loon and swan populations and one National Park. As of 2008, only 7 national Wildlife refuges in the U.S. had regulations prohibiting use of lead we ights, sinkers, or fishing tackle: Bear Lake NWR in Idaho, Union Slough NWR in Iowa, Rachel Carson NWR in Maine, Assabet River NWR in Massachusetts, Seney NWR in Michigan, Red Rock lakes NWR in Montana, and Rappahannock River Valley NW R in Virginia (Franson et al. 2003; Michael 2006). Yellowstone National Park has banned leaded fishing tackle and weights small enough to be ingested by wildlife. In March 2009 the National Park Service announced that it would begin to develop regula tions to eliminate the use of lead fishing

tackle in all National Parks by the end of 2010, but has yet to initiate any rulemaking.

In 1999 the USFWS announced it would establis h additional lead-free fishing areas on more National Wildlife Refuges and wilderne ss areas used by loons, and waterfowl production areas on federal lands in Alaska, Florida, Main e, Minnesota, and Wisconsin (USEPA 1999; USFWS 1999). However, the USFWS has not followed through on regulations, a final rule on the use of lead fi shing tackle on federal refuges has yet to be made, and this effort appears to have been shelved.

A few states subsequently moved forward w ith banning lead associated with fishing activities. Only Maine, New Hampshire, New York and Vermont have established

statewide bans on the sale and/or use of lead sinkers and jigs in the sizes that are most likely to be ingested by wildlife. Massachuse tts has a partial ban, a nd the other 45 states have no lead fishing regulations at all.

Maine

Maine passed legislation in 2001 (effective Ja nuary 1, 2002) that prohibits the sale of

lead sinkers one-half ounce or less.56 Massachusetts

Massachusetts prohibits the use of lead sinkers for fishing in certai n reservoirs visited by loons - the Quabbin and Wachusett Reservoirs.

New Hampshire

New Hampshire became the first state to ban th e use of lead sinkers. Legislation passed in 1998 (effective in 2000) prohibits the use of lead sinkers up to one ounce and lead jigs up to one inch in length, in lakes and ponds in the state. This legislation was later expanded in 2006 to include a ll waters of the state.

New York

New York in 2004 prohibited the sale of lead fishing sinkers (inc luding "split shot") weighing one-half ounce or less.

Vermont

Vermont passed legislation prohibiting the use (effective January 1, 2007) and sale (effective January 1, 2006) of lead fishi ng sinkers weighing one- half ounce or less.

International

Restrictions on the sale and use of lead fish ing sinkers and jigs are in place in Canada, Denmark, and Great Britain. In 1997, Canada amended its Wildlife Area Regulations to prohibit possession of any lead sinker or jig weighing less than 50 grams while fishing in any National Wildlife Area where sport fish ing is allowed, and also amended the National Parks Fishing Regulations to prohibit the possession and use of lead sinkers or jigs while fishing in national parks. Great Br itain banned the use of lead sinkers weighing less than one ounce in 1987, due to the harm lead was causing swans, diving birds, and wading birds, and after determining that vo luntary efforts were ineffective. Reported cases of lead poisoning in swans from the Ri ver Thames in England dropped from a peak of 107 in 1984 to 25 in 1988, one year after the ban on sale of lead fishing weights (Sears and Hunt 1991).57 V. AUTHORITY TO ACT

In adopting the Toxic Substances Contro1 Ac t, Congress declared its policy that (1) “adequate data should be developed with respec t to the effect of ch emical substances and

mixtures on health and the environment” a nd (2) “adequate authority should exist to regulate chemical substances and mixtures wh ich present an unreasona ble risk of injury

to health or the environment.”

To promulgate a rule under TSCA secti on 2605(a), the EPA must find there is a

“reasonable basis to conclude” that activities involving a chemical substance “presents or will present an unreasonable risk to health or the environment.” Factual certainty of the magnitude of risk to health and environm ent is not required; the EPA may base its decision not only on known facts, but also on scientific theories, projections and extrapolations from available data, and m odeling using reasonable assumptions (59 Fed. Reg. 11122, 11138, citing H.R. Rep. No. 1341, 94 th Cong., 2d Sess. 32 (1976)).

In its determination that a risk is “unreas onable,” the EPA must weigh the risks to be reduced by the Act regulation and the conseque nces of such regulation. Section 6(c) of

TSCA outlines four basic considerations to be weighed: A) the effects of the chemical on health and the magnitude of human exposure, B) the effects of the chemical on the environment and the magnitude of environm ental exposure, C) the benefits of the chemical for various uses and the ability of substitutes for such uses, and D) the reasonably ascertainable economic consequences of the rule, after consideration of the effect on the national economy, small business, technological innovation, the environment, and public hea lth (15 U.S.C. § 2605(c)(1)).

The EPA must consider whether the risk to be addressed by regulat ion may be prevented

or reduced to a sufficient extent under othe r federal laws (15 U.S.C. § 2608(a)(1)(A)). The purpose of this provision is to avoid overlap and duplication between the Act and

other federal laws. The EPA has determined that other federal laws do not sufficiently prevent or reduce the risk posed by lead and that “some activit ies, the regulation of which could protect [health and environment] (e.g., regulation of the manu facture, processing,

and distribution in commerce of chemical subs tances) are clearly within the purview of [the] EPA” (15 U.S.C. § 2608(a)(1)(A), at 11137-38).

In the 1994 proposal to ban lead sinkers, th e EPA preliminarily determined that other laws were, in fact, insufficient to reduce th e unreasonable risk of harm to health and environment (59 Fed. Reg. 11122). The EPA r ecognized that, in th e area of wildlife protection, there was some overlap between th e statutory authoritie s administered by the Department of the Interior and the EPA, but that “some activities, the regulation of which could protect wildlife (e.g., re gulation of the manufacture, processing, and distribution in commerce of chemical substances), are clearly within the purview of the EPA” (59 Fed. Reg. 11122).

Currently, there are some limited and inconsis tent regulations rega rding lead ammunition and fishing tackle in some states and on some National Wildlife Refuges and National58 Parks. While these measures are a good start to eliminating the risk of lead exposure to wildlife and humans, and demonstrate that regul ation of lead is po ssible and substitute

ammunition and tackle are available for fi shing and hunting activ ities, they are no substitute for comprehensive, sweeping regulation of lead shot , bullets, and sinkers by the

EPA.

A. Authority to Regulate Lead Shot and Bullets

Lead used in shot, bullets and sinkers is a “chemical substance” falling within the scope of the Act (15 U.S.C. § 2602(2)(A)). 1 Although certain substances are excluded from the definition of “chemical substances,” these excl usions do not apply to lead shot or bullets (15 U.S.C. § 2602(B)). Section 2602(B)(v) excl udes from Act regulation “any article the sale of which is subject to the tax imposed by section 4181 of the Internal Revenue Code of 1986.” Section 4181 of the Internal Revenue Code taxes firearms, shells, and cartridges (26 U.S.C. § 4181). However, shot and bullets are not subj ect to this tax. In fact, a 1968 Revenue Ruling states, “The manu facturers excise tax imposed upon sales of shells and cartridges by section 4181 of the Internal Revenue Code of 1954 does not apply to sales of separate parts of ammunition such as cartridge cases, primers, bullets, and powder” (Rev. Rul. 68-463, 1968-2 C.B. 507 (emphasis added)). This ruling has been confirmed by subsequent administrati ve decisions (See, for example, Fed. Tax Coordinator ¶ W-2911(2d.)). Because shot and bullets, as separate parts of ammunition,

are not taxed under section 4181 of the Inte rnal Revenue Code, the section 2602(B)(v) exception of TSCA does not apply. Thus, lead sh ot and bullets are prop erly classified as “chemical substances” subj ect to TSCA regulation.

B. Authority to Regulate Lead Sinkers and Fishing Tackle

The EPA expressed its authorit y to regulate lead sinkers under the Toxic Substances Control Act in 1994 by proposing a ban on lead sinkers (USEPA 1994). The EPA proposed a rule under section 6(a) of TSCA to prohibit the manufacturing, processing,

and distribution in commerce in the United Stat es, of certain smaller size fishing sinkers containing lead and zinc, and mixed with othe r substances, including those made of brass, due to unreasonable risk of inju ry to human health or the en vironment. This proposal was issued in response to a citizens’ petition to require that the sa le of lead fishing sinkers be accompanied by a label or notice that such products are toxic to wildlife. The EPA recognized the risk that lead sinkers presented to wildlife, and recognized that a labeling requirement would not go far enough to reduce this risk.

To date, the rule has not been finalized. In 2005 EPA issued a proposal to withdraw the proposed rule, but to date has not done so (see 70 Fed. Reg. 27625). It is possible that the “Common Sense in Fishing Regulations Act,” introduced to the Senate in 1995, prompted the EPA to hold-off on a final rulemaking as it directed the EPA not to issue the ban on

1 “Except as provided in subparagraph (B), the term “chemical substance” means any organic or inorganic substance of a particular molecular identity, including (i) any combination of such substances occurring in whole or in part as a result of a chemical reacti on or occurring in nature and (ii) any element or

uncombined radical.”59 lead sinkers (Sen. 505, 104 th Cong. (March 6, 1995)). When introducing the bill, Senator Harkin declared that the proposed ban was not hing more than “government regulation run amok” and that the risks presented by lead sinkers were not unreasonable (Sen. 505, 104 th
Cong. (March 6, 1995), Senator Harkin, Stat ements on Introduced Bills and Joint Resolutions). However, the bill was never pass ed and EPA has still not acted to ban lead

sinkers.

VI. DESCRIPTION OF FEDERAL REGULATIONS REQUESTED

Petitioners request that the EPA issue a proposed rule under section 6(a) of TSCA to prohibit the manufacturing, processing, and dist ribution in commerce in the United States of lead ammunition (including bullets and shotgun pellets) and l ead fishing tackle (including sinkers, jig heads, weight s, and all other fishing tackle).60 VII. CONCLUSION

This petition has set forth the facts establishi ng the indisputable toxicity of lead hunting bullets and shotgun pellets and lead fishing gear to wildlife and to humans. The scientific literature on the sources, quanti ties, and pathways of exposure of lead in the environment from hunting, shooting sports, and fishing is comprehensive and conclusive, as is

information on the toxic effects and health ri sk of lead ammunition and fishing tackle on wildlife and humans. The banning of lead ammu nition for hunting in wetlands has greatly

reduced the massive former mortalities of waterfowl and correspondingly reduced lead consumption by predators and scavengers of wa terfowl, such as bald eagles, as well as humans. However, other uses of lead a mmunition have continued unabated, causing unnecessary widespread incidental morta lity of many bird and mammal species.

Lead-based bullets fragment on impact, di stributing toxic lead particles widely throughout carcasses, and making it impossible for scavenging animals or humans to avoid ingesting lead along with meat. Norm al butchering processes do not remove this lead. This health risk potent ially affects large numbers of people, particularly hunters and their families and in areas where wild game is a significant part of the diet. Lead has been

shown to affect adults and children at far lower concentr ations in body tissues than formerly thought, and at lower concentrati ons than current regulations acknowledge.

Many species of wildlife ingest spent lead shot pellets or lead fishing weights, while others ingest lead fragments from the carca sses and gut piles of shot animals on which they feed. More than 130 speci es of wildlife are affected by lead from these sources in this way, and in some species thousands or tens of thousands of individuals die from lead ingestion every year in North America. For most species there has been no assessment of the effect of lead-caused mortality on population levels. However, population level effects have been shown in well-studied species such as the California condor, bald eagle, trumpeter swan, sandhill cran e, and spectacled eider.

The widespread poisoning of many species of wildlife requires a response from the EPA to regulate and enforce a ban on lead ammun ition and lead fishing tackle. This petition presents strong evidence that lead shot, bullets and sinkers pose an unreasonable risk to

health and the environment and that this ri sk cannot be prevente d through action under other federal laws. In evaluating unreasonable risk the EPA must consider: A) the effects of the chemical on health and the magnitude of human exposure; B) the effects of the chemical on the environment and the magnit ude of environmental exposure; C) the benefits of the chemical for various uses and the ability of substitutes for such uses; and D) the reasonably ascertainable economic conseq uences of the rule, af ter consideration of the effect on the national economy, small business, technologi cal innovation, the environment, and public health (15 U.S.C. § 2605(c)(1)). Regulation under section 2605 of the Toxic Substances Control Act requires only “a reasonable basis to conclude” that a risk is unreasonable. Scientific theories, pr ojections of trends fr om currently available data, modeling using reasonable assumptions, and extrapolations from limited data may help to establish risk (H.R. Rep. No. 1341, 94 th Cong., 2d Sess. 32 (1976)). The data presented in the petition supports the conclusion that the risk is such that lead shot,61 bullets and sinkers should be banned under the Act. The recent granting of a Section 21 petition to ban lead wheel-balancing weights is further evidence that the EPA is aware of

the environmental hazards of lead. This petition demonstrates that commercially available alternatives to hunting projectiles and fishing gear are, or can be made, available to replace lead-containing spor ting equipment currently on the market.62 VIII. REFERENCES

Adler, F.E.W. 1944. Chemical analyses of or gans from lead-poisoned Canada geese. Journal of Wildlife Management 8(1):83-85.

African-Eurasian Water Bird Agreement (AEMA). 2002. Special Edition: Lead poisoning in waterbirds through the ingesti on of spent lead shot. AEMA Newsletter, Special Issue #1. 28 pp.

Agency for Toxic Substances and Disease Registry (ATSDR). 2007. Toxicological Profile for Pb. http://www.atsdr.cdc. gov/substances/toxsubstance.asp?toxid=22

Akoshegyi, I. 1997. Lead poisoning of pheasants caused by lead shots. Magyar Allatorvasok Lapja 119(6):328-336.

Ancora, S., N. Bianchi, C. Leonzio, and A. Renzoni. 2008. Heavy metals in flamingos ( Phoenicopterus ruber ) from Italian wetlands: The problem of ingestion of lead shot. Environmental Research. In press.

Anderson, W.L. 1975. Lead poisoning in waterfow l at Rice Lake, Illinois. Journal of Wildlife Management 39:264-270.

Anderson, W.L., and S. P. Havera. 1985. Blood lead, protoporphyrin, and ingested shot for detecting lead poisoning in waterfow l. Wildlife Society Bulletin 13(1):26- 31.

Anderson, W.L. and S.P. Havera. 1989. L ead poisoning in Illinois waterfowl (1977- 1988) and implementation of nontoxic shot regul ations. Illinois Natural History Survey Biological Notes 133.

Anderson, W.L., S.P. Havera, and B.W. Zerc her. 2000. Ingestion of Lead and Non-Toxic Shotgun Pellets by Ducks in the Mississippi Flyway. Journal of Wildlife Management

64:848-857.

ANZECC (Australian and New Zealand Envi ronment and Conservation Council). 1994. Report to the Australian a nd New Zealand Environment and Conservation Council on alternative shot to lead in hunting. Pr epared by NSW Nationa l Parks and Wildlife Service, April. 32 pp.

Arizona Game and Fish Department (AGF D). Non-Lead Brochure. Available at www.azgfd.gov/pdfs/w_c/condor s/nonlead_brochure.pdf.

Arizona Game and Fish Depa rtment (AGFD). What the E xperts Say About Non-Lead Bullets. Available at http://condor info.org/What_the_Experts_Say.pdf.

Artmann, J.W. and E.M. Martin. 1975. Incidenc e of ingested lead shot in sora rails.

Journal of Wildlife Mana gement 39(3):514-519.63 Avery, D., and R.T. Watson. 2009a. Distri bution of Venison to Humanitarian Organizations in the USA and Canada. In R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spen t Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Avery, D., and R.T. Watson. 2009b. Regulati on of lead-based ammunition around the

world. In R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Bagchi, D. and H.G. Preuss. 2005. Effects of Acute and Chronic Oval Exposure of Lead on Blood Pressure and Bone Mineral Density in Rats. Journal of Inorganic Biochemistry

99:1155-1164

.

Bagley, G.E. and L.N. Locke. 1967. The occurrence of lead in tissues of wild birds.

Bulletin of Environmental Cont amination and Toxicology 2:297-305.

Baksi, S.N. and A.D. Kenny. 1978. Effect of Lead Ingestion on Vitamin D3 Metabolism in Japanese Quail, Res. Commun. Chem. Path. Pharmacol. 21, 375-378

.

Bates, F.Y., D.M. Barnes, and J.M. Higb ee. 1968. Lead Toxicosis in Mallard Ducks.

Bull. Wildl. Dis. Assoc. 4:116-125

.

Battaglia, A., S. Ghidini, G. Campanin i, and R. Spaggiari. 2005. Heavy metal contamination in little owl ( Athene noctua ) and common buzzard ( Buteo buteo ) from northern Italy. Ecotoxicology and En vironmental Safety 60(1):61-66.

Baxter, G.S., C. Melzer, D. Byrne, D. Fi elder, and R. Loutit. 1998. The prevalence of spent lead shot in wetland sediments and i ngested by wild ducks in coastal Queensland. The Sunbird 28(2):21-25.

Beaven, L. 2004. Army reconsiders green bullets in light of new studies. Army Times

, August 2, 2004.

Beck, N. 1997. Lead shot ingestion by the common snipe ( Gallinago gallinago ) and the jacky snipe ( Lymnocryptes minimus ) in northwestern France . Gibier Faune Sauvage (France):65-70.

Bedrosian, B., and D. Craighead. 2009. Blood le ad levels of Bald and Golden Eagles sampled during and after hunting seasons in the Greater Yellowstone Ecosystem.

Extended abstract in R. T. Watson, M. Fuller, M. P okras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.64 Beintema, N.H. 2001. Lead Poisoning in Wate rbirds. International Update Report 2000.

Wetlands International Wa geningen. www.unep-aewa.org

Beintema, N. (compiler). 2004. Non-toxic shot : A path towards sustainable use of the

waterbird resource. African- Eurasian Wate rbird Agreement, Technical series No. 3.Accessed Feb. 8, 2007. Available online: http://www.unepaewa.org/publications/te chnical_series/ts3_non-t oxic_shot_english.pdf

Bell, D.V., N. Odin, and E. Torres. 1985. A ccumulation of Angling Litter at Game and

Coarse Fisheries in South Wales. U.K. Biological Conservation 34:369-379.

Bellrose, F.C. 1959. Lead Poisoning as a Mo rtality Factor in Wa terfowl Populations. Ill.

Nat. Hist. Surv. Bull. 27:2335-288

.

Bengtson, F.L. 1984. Studies of lead toxicity in Bald eagles at the Lac Qui Parle Wildlife Refuge. Master’s thesis. Un iversity of Minnesota. 106 pp.

Best, T.L., T.E. Garrison, and C.G. Schmid t. 1992. Ingestion of lead pellets by scaled quail ( Callieppla squamata ) and northern bobwhite ( Colinus virginianus ) in southeastern

New Mexico. Texas Journal of Science 44:99-107.

Best, T.L., T.E. Garrison, and C.G. Schmitt. 1992. Availability and Ingestion of Lead Shot by Mourning Doves ( Zenaida macroura ) in Southeastern New Mexico. The

Southwestern na turalist 37:287-292.

Beyer, W.N., J.W. Spann, L. Sileo, and J.C. Franson. 1988. Lead Poisoning in Six Captive Avian Species. Arch. Environ. Contam. Toxicol. 17:121-130

.

Beyer, W.N., J.C. Franson, L.N. Locke, R.K. Stroud, and L. Sileo. 1998. Retrospective study of the diagnostic criteria in a lead-poisoning survey of waterfowl. Archives of Environmental Contamination and Toxicology 35(3):506-512.

Bihrle, C. 1999. Testing new ground - Steel s hot study finds facts for pheasant hunters. North Dakota Outdoors Magazine , September-October 1999:1-7.

Bingham, R.J., R.T. Larsen, J.A. Bissone tte, and J.T. Flinders. 2009. Causes and consequences of ingested lead pe llets in Chukars. Extended abstract in R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Birkhead, M. 1982. Causes of Mortality in the Mute Swan Cygnos olor on the River Thames. Journal of Zoology 198:15-25.

Birkhead, M. and C. Perrins. 1985. The Breeding Biology of Mute Swan Cygnus olor on the River Thames With Special Reference to Lead Poisoning. Biological Conservation

32:1-11.65 Bjerregaard, P., P. Johansen, G. Mulvad, H.S. Pedersen, and J.C. Hansen. 2004. Lead

sources in human diet in Greenland. Environmental Health Perspectives 112(15):1496-

1498.

Bjorn, H., N. Gyrd-Hansen, and I. Kraul. 1982. Birdshooting lead pellets and grazing

cattle. Bulletin of Environmental Contamination and Toxicology 29:174-176.

Blus, L.J., R.K. Stroud, B. Reiswig, and T. McEneaney. 1989. Lead Poisoning and Other Mortality Factors in Trumpeter Swans. E nvironmental Toxicology and Chemistry 8:263-

271.

Blus, L.J., C.J. Henry, D.J. Hoffman, and R.A. Grove. 1991. Lead Toxicosis in Tundra Swans Near a Mining and Smelti ng Complex in Northern Idaho. Arch. Environ. Contam.

Toxicol. 21:549-555

.

Blus, L.J. 1994. A review of lead poisoning in swans. Comparative Biochemistry and Physiology, Part C 108(3):259-267.

Blus, L.J.,C.J. Henry, D.J. Hoffman, and R.A. Grove. 1995. Persistence of High Lead

Concentrations and Associated Effects in Tundra Swans Captured Near a Mining and Smelting Complex in Northern Idaho. Ecotoxicology (8)2: 125-132

.

Borkowski, R. 1997. Lead Poisoning and Inte rnal Perforations in a Snapping Turtle ( Chelydra serpentina ) Due to Fishing Gear Ingesti on. Journal of Zoo and Wildlife

Medicine 28:109-113.

Bowles, J.H. 1908. Lead poisoni ng in ducks. A uk 25(3):312-313.

Braun, J.M., R.S. Kahn, T. Froelich, P. Aui nger, and B. Lamphear. 2006. Exposures to

Environmental Toxicants and Attention Defic it Hyperactivity Disorder in U.S. Children. Environmental Health Perspectives 114;1904-1909.

Brown, C.S., J.Luebbert, D. Mulcahy, J. Schamber, and D.H. Rosenberg. 2006. Blood lead levels of wild Steller’s eiders ( Polysticta stelleri ) and black scoters ( Melanitta nigra ) in Alaska using a portable bl ood lead analyzer. Journal of Zoo and Wildlife Medicine 37(3):361-365.

Brownlee, W.C., K. Brown, and L.A. Johns on. 1985. Steel vs. lead shot: a ten-year evaluation on Murphree Wildlife Management Area. Unpublished mimeo. Texas Parks

and Wildlife Federal Aid Project W-106-R. 12 pp.

Bruell, R., N.P. Nikolaidis, and R.P. Long. 1999. Evaluation of Remedial Alternatives of Lead From Shooting Range Soil. Envir onmental Engineering Science 16:403-414.66 Buerger, T.T., R.E. Mirarchi and M.E. Lisa no.1983. Lead shot ingestion in a sample of Alabama mourning doves. Journal of Al aska Academy of Science 54:119.

Buerger, T. 1984. Effect of lead shot inge stion on captive mourni ng dove survivability and reproduction. M.S. thesis. Auburn University, Auburn, Alabama. 39 pp.

Buerger, T., R.E. Mirarchi, and M.E. Lisa no. 1986. Effects of lead shot ingestion on captive mourning dove survivability and repr oduction. Journal of Wildlife Management 50(1):1-8.

Burger, J., R.A. Kennamer, I.L. Brisbi n, and M. Gochfeld. 1997. Metal levels in Mourning doves from South Carolina: Pote ntial hazards to doves and hunters.

Environmental Rese arch 75(2):173-186.

Burger, J., R.A. Kennamer, I.L. Brisbin, and M. Gochfeld. 1998. A risk assessment for consumers of mourning doves. Risk Analysis 18(5):563-573.

Burger, J. and M. Gochfeld. 2000. Metals in Albatross Feathers From Midway Atoll: Influence of Species, Age, and Nest Location. Environ. Res. 82(3): 207-21

.

Butler, D. A. 1990. The incidence of lead sh ot ingestion by waterfowl in Ireland. Irish

Naturalists' Journal Belfast 309-131.

Butler, D.A. 2005. Incidence of lead shot inges tion in red-legg ed partridges ( Alectoris rufa ) in Great Britain. Veterinary Record: Journal of the British Veterinary Association 157(21):661.

Butler, D.A., R.B. Sage, R.A.H. Draycott, J.P. Carroll, and D. Pottis. 2005. Lead exposure in ring-necked pheasants on shooti ng estates in Great Britain. Wildlife Society Bulletin 33(2):583-589.

Cade, T.J. 2007. Exposure of California condors to lead from spent ammunition. Journal of Wildlife Management 71(1):2125-2133.

Calle, P.P., D.F. Kowalczyk, F.J. Delin, a nd F.E. Hartman. 1982. Effect of hunters’

switch from lead to steel s hot on potential for oral lead poisoning in ducks. Journal of American Veterinary Medica l Association 181(11):1299-1301.

Calvert, H.S. 1876. Pheasants poisoned by swallowing shot. The Field 47:189.

Campbell, H. 1950. Quail picking up lead sh ot. Journal of Wildlife Management 14:243-

244.

Camus, A.C., M.M. Mitchell, J.F. Williams, and P.L.H. Jowett. 1998. Elevated Lead Levels in Farmed American Alligators Alligator mississippiensis Consuming Myocastor67 coypus Meat Contaminated by Lead Bullets. J ournal of World Aquaculture Society

29:370-376.

Canfield, R. L., C.R. Henderson, Jr., D.A. Cory-Slechta, C. Cox, T.A. Jusko, B.P. Lanphear. 2003. Intellectual Impairment in Children with Blood Lead Concentrations Below 10 micrograms Per Deciliter. New England Journal of Medicine 348:1517-26.

Cantarow, H.O. and M. Trumper. 1944. Lead poisoning. Williams and Wilkins Co.

Baltimore.

Cao, X., L.Q. Ma, M. Chen, D.W. Hardison, and W.G. Harris. 2003. Lead

Transformation and Distribution in the Soils of Shooting Ranges in Florida, USA.

Science of the Total Environment 307:179-189.

Cao, X., L.Q. Ma, M. Chen, D.W. Hardison, and W.G. Harris. 2003. Weathering of Lead

Bullets and Their Environmental Effects at Outdoor Shooting Ranges. Journal of Environmental Quality 32:526-534.

Carey, L.S. 1977. Lead shot appendicitis in no rthern native people. Journal of Canadian Association of Radiology 28:171-174.

Carlisle, J.C., K.C. Dowling, D.M. Sieg el, and G.V. Alexeeff. 2009. A blood lead benchmark for assessing risks from childhood le ad exposure. J Environ Sci Health A Tox Hazard Subst Environ Eng. 2009 Oct;44(12):1200-8.

Carpenter, J.W., O.H. Pattee, S.H. Fritts, B.A. Rattner, S.N. Wiemeyerr, J.A. Royle, and M.R. Smith. 2003. Experimental Lead Poisoning in Turkey Vultures ( Cathartes aura ). J. Wildl. Dis. 39(1):96-104

.

Carrington, M.E. and R.E. Mirarchi. 1989. Effect s of lead shot ingestion on free-ranging mourning doves. Bulletin of Environmenta l Contamination and Toxicology 14:89-95.

Case, D.J. and Associates. 2006. Non-toxic shot regulation inventory of the United States and Canada. D.J. Case and Associates, Mishawaka, IN. 29 pp.

Castrale, J.S. 1989. Availability of spent lead shot in fields managed for mourning dove hunting. Wildlife Society Bulletin 17:184-189.

Cheatum, E.L., and D. Benson. 1945. Effects of lead poisoning on reproduction of

mallard drakes. Journal of W ildlife Management 9(1):26-29.

Chen, M., S. Daroub, L.Q. Ma, W.G. Harris, and X. Cao. 2002. Characterization of Lead

in Soils of a Rifle/Pistol Range in Central Florida, USA. Soil and Sediment

Contamination 111:1-17.68 Chesley, J., P. Reinthal, C. Parish, K. Sullivan, and R. Sieg. 2009. Evidence for the

source of lead contamination with in the California Condor. Abstract in R.T. Watson, M. Fuller, M. Pokras, and W.G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Chiba, A., N. Shibuya, and R. Honma. 1999. Description of a Lead-poisoned Middendorff's Bean Goose, Anser fabalis middendorffii , Found at Fukushima-gata, Niigata Prefecture, Japan. Japanese Journal of Ornithology 47:87-96.

Chisolm, J.J., Jr. 1971. Lead poisoning. Sc ientific American 224(2):15-23.

Chisholm, J.J. 1988. Blood Lead Levels and I ndoor Target Practice. Journal of the

American Medical Association 259:1385.

Church, M.E., Gwiazda, R., Risebrough, R.W ., Sorenson, K., Chamberlain, C.P., Farry, S., Heinrich, W., Rideout, B.A., and Smit h, D.R. 2006. Ammunition is the principal source of lead accumulated by California condors re-introduced to the wild.

Environmental Science a nd Technology 40(19):6143-6150.

Church, M.E., Gwiazda, R., Risebrough, R.W ., Sorenson, K., Chamberlain, C.P., Farry, S., Heinrich, W., Rideout, B.A., and Smit h, D.R. 2008. Response on “Ammunition is the principal source of lead accumulated by Calif ornia condors re-introduced to the wild”.

Environmental Science and T echnology, Web release date: 1/31/2008. Available online: http://pubs.acs.org/cgi-bin/abstract .cgi/esthag/asap/abs/es702174r.html

Church, M., K. Rosenthal, D. R. Smith, K. Parmentier, K. Aron, and D. Hoag. 2009. Blood chemistry values of California Condors exposed to lead. Abstract in R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.) . Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Clark, A.J. and A.M. Scheuhammer. 2003. Lead Poisoning in Upland-Foraging Birds of Prey in Canada. Ecotoxicology 12(1-4):23-30

.

Clausen, B., K. Haarbo, and C. Wolstrup. 1981. L ead pellets in Danish cattle. Nordisk Veterinary Medicine 33:65-70.

Clausen, B., and C. Wolstrup. 1979. Lead poisoning in game from Denmark. Denmark Review of Game Biology 11:1-22.

CNN. 2009. Should Hunters Sw itch to ‘Green’ Bullets?

Coburn, D.R., D.W. Metzler, and R. Treich ler. 1951. A study of absorption and retention

of lead in wild waterfowl in relation to c linical evidence of lead poisoning. Journal of Wildlife Management 15(2):186-192.69 Cornatzer, W.E., E.F. Foga rty, and E.W. Cornatzer. 2009. Qu alitative and quantitative detection of lead bullet fragments in random venison packages donated to the Community Action Food Centers of North Dakota, 2007. In R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Cornicelli, L. and M. Grund. 2009. Examini ng Variability Associated With Bullet Fragmentation and Deposition in White-Taile d Deer and Domestic Sheep: Preliminary Results. Minnesota Department of Natural Resources.

Craig, J.R., D. Edwards, J.D. Rimstidt, P.F. Scanlon, Y.K. Collins, O. Schabenberger,

and J.B. Birch. 2002. Lead Distribution on a Public Shotgun Range. Environmental Geology 41:873-882.

Craig, J.R., J.D. Rimstidt, C.A. Bonnaff on, T.K. Collins, and P.F. Scalon. 1999. Surface Water Transport of Lead at a Shooting Range. Bulletin of Environmental Contamination and Toxicology 63:312-319.

Craig, T.H., J.W. Connelly, E.H. Craig, and T. L. Parker. 1990. Lead concentrations in Golden and Bald eagles. Wilson Bulletin 102(1):130-133.

Craighead, D. and B. Bedrosian. 2008. Blood le ad levels of Common ravens with access to big-game offal. Journal of Wildlife Management 72(1):240-245.

Craighead, D. and B. Bedrosian. 2009. A rela tionship between blood lead levels of Common Ravens and the hunting season in the southern Yellowstone Ecosystem. In R. T. Watson, M. Fuller, M. Pokras, and W. G. H unt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho,

USA.

Cryer, M.J., J. Corbett, and M.D. Wi nterbotham. 1987. The Deposition of Hazardous Litter by Anglers at Coastal and Inland Fi sheries in South Wales. Journal of Environmental Management 25:125-135.

Custer, T.W., and B.L. Mulhern. 1983. Heavy metal residues in pre-fledgling blackcrowned night-herons from three Atlantic Coast colonies. Bulletin of Environmental Contamination and Toxicology 30:178-185.

Custer, T.W., J.C. Franson, and O.H. Pa ttee. 1984. Tissue Lead Distribution and Hematologic Effects in American Kestrels ( Falco sparverius ) Fed Biologically Incorporated Lead. J. Wildlife Dis. 20, 39-43

.

Daoust, P.-Y., G. Conboy, S. McBurney, and N. Burgess. 1998. Interactive Mortality

Factors in Common Loons From Maritime Ca nada. Journal of Wild life Diseases 34:524-

531.70 Damron, B.L., and H.R. Wilson. 1975. Lead toxicity of bobwhite quail. Bulletin Environmental Contamination Toxicology 14:489-496.

Darling, C.T.R. and V.G. Thomas. 2003. The Di stribution of Outdoor Shooting Ranges in

Ontario and the Potential for Lead Pollution of Soil and Water. Science of the Total

Environment 313:235-243.

Darling, C.T.R. and V.G. Thomas. 2005. Lead bioaccumulation in earthworms,

Lumbricus terrestris , from exposure to lead compounds of differing solubility. Science of the Total Environment 346(1-3):70-80.

Daury, R.W., F.E. Schwab, and M.C. Bateman. 1994. Prevalence of ingested lead shot in American black duck ( Anas rubripes ) and ring-necked duck ( Aythya collaris ) gizzards

from Nova Scotia and Prince Edward Isla nd. Canadian Field-Natu ralist 108(1):26-30.

Decker, R.A., A.M. McDermid, and J.W. Prideaux. 1979. Lead poisoning in two captive king vultures. Journal of American Veterinary Medial Association 175:1009.

Degernes, L., S. Heilman, M. Trogdon, M. Jordan, M. Davison, D. Kraege, M. Correa, and P. Cowen. 2006. Epidemiologic Investigation of lead Poisoning in Trumpeter and Tundra Swans in Western Washington St ate, USA, 2000-2002. Journal of Wildlife

Diseases 42:345-358.

Delaney, S.J., J.D. Greenwood, and J. Kirby. 1992. The National Mute Swan Survey 1990. JNCC Report Number 74, Joint Nature Conservancy Council, Peterborough, UK.

DeLong, J. P. 2004. Effects of management prac tices on grassland birds: Golden Eagle.

Northern Prairie Wildlife Research Center, Jamestown, ND. 22 pages.

Demayo, A., M.C. Taylor, K.W. Taylor, a nd P.V. Hodson. 1982. Toxic effects of lead and lead compounds on human health, aquatic life, wildlife, plants, and livestock. CRC

Critical Reviews in Envir onmental Control 12(4):257-305.

DeMent, S.H., J.J. Chisolm, Jr., J.C. Barber , and J.D. Strandberg. 1986. Lead exposure in an “urban” Peregrine falcon and its avian pr ey. Journal of Wildlif e Diseases 22(2):238-

244.

DeMent, S.H., J.J. Chisolm, Jr., M.A. Ec khaus and J.D. Strandberg. 1987. Toxic lead exposure in the urban rock dove. Jo urnal Wildlife Diseases 23:273-278.

Dewaily, E., B. Levesque, J-F. Duchesnes, P. Dumas, A. Scheuhammer, C. Gariepy, M. Rhainds, J-F. Proulx. 2000. Lead shot as a so urce of lead poisoning in the Canadian Arctic. Epidemiology 11(4):146.

Dewailly E., P.Ayotte, and S. Bruneau. 2001. Exposure of the Inuit population of Nunavik (Arctic Quebec) to lead and mercury. Arch. Environ. Health 56:350-357.71 Dieter, M.P. and M.T. Finley. 1978. Erythrocyte δ -Aminolevulinic Acid Dehydrates Activity in Mallard Ducks: Duration of Inhi bition After Lead Shot Dosage. Journal of Wildlife Management 42:621-625.

Dilling, W.J. and C.W. Healey 1926. Influence of lead and the Metallic Ions of Copper, Zinc, Thorium, Beryllium and Thallium on the Germination of Frog’s Spawn and on the Growth of Tadpoles. Annals of Applied Biology 13:177-188.

D.J. Case & Associates. 2006. Non-Toxic Shot Regulation Inventory of the Untied States and Canada. Report to the Ad Hoc Mourning Dove and Lead Toxicosis Working Group. Final Report, August 2006.

Domenech, R. and H. Langner. 2009. Blood-lead levels of fall migrant Golden Eagles in

west-central Montana. Extended abstract in R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Sp ent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Donázar, J.A., C.J. Palacios, L. Gangoso, O. Ceballos, M.J. Gonzalez, and F. Hiraldo. 2002. Conservation status and limiting factors in the endangered population of Egyptian vulture ( Neophron percnopterus ) in the Canary Islands. Biological Conservation 107(1):89-97.

Dorgelo, F. 1994. Alternatives for lead shot a nd fishing sinkers in the Netherlands. Issue Paper presented at the OECD Workshop on Lead Products and Uses, 12-15 September, Toronto, Ontario. 5 pp.

Driver, C. J, and R. J. Kendall. 1984. Lead shot ingestion in Waterfowl in Washington State, 1978-1979. Northwest Sci. 58:103-107.

Duerr, A.E. 1999. Abundance of Lost and Discar ded Fishing Tackle and Implications for Waterbird Populations in the United States. Masters thesis. School of Renewable Natural Resources, University of Arizona, Tucson, Arizona.

Duerr, A.E. and S. DeStefano. 1999. Using a Me tal Detector to Determine Lead Sinker Abundance in Waterbird Habitat. Wildlife Society Bulletin 27:952-958.

Edens, F.W. and J.D. Garlich. 1983. Lead-I nduced Egg Production Decrease in Leghorn and Japene Quail Hens, Poultry Sci. 62, 1757-1763

.

Eisele, T. 2008. Outdoors: Time to Get the Lead Out of A ll Hunting, Fishing. Special to The Capital Times 3/12/2008.

Eisler, R. 1988. Lead Hazards to Fish, Wildlif e and Invertebrates: A Synoptic Review. USFWS Biol. Rep. 8, 1-4

.72 Elder, W.H. 1954. The effect of lead poisoning on the fertility and fecundity of domestic

mallard ducks. Journal of Wild life Management 18(3):315-323.

Elliott, J.E., K.M. Langelier, A.M. Scheuhammer, P. H. Sinclair, and P. E. Whitehead. 1992. Incidence of lead poisoning in bald eag les and lead shot in waterfowl gizzards from British Columbia, 1988-91. Canadian Wildlife Service Program Note No. 200. 7

pp.

Engstad, J.E. 1932. Foreign bodies in th e appendix. Minnesota Med. 15:603-6xx. Ensor, K.L., D.D. Helwig, and L.C. Wemm er. 1992. Mercury and Lead in Minnesota Common Loons ( Gavia immer ). Water Quality Division, Mi nnesota Pollution Control Agency, St. Paul, Minnesota. 32 pp.

Environment Canada. 1995. A review of the environmental impacts of lead shotshell ammunition and lead fishing weights in Canada . Canadian Wildlife Service. Occasional Paper No. 88. Hull, Quebec.

Erickson, D.W., and J.S. Lindsey. 1983. Lead and cadmium in mu skrat and cattail tissues. Journal of Wildlife Management 47(2):550-555.

Erne, K., and K. Borg. 1969. Lead poisoning in Swedish wildlife. In: metals and ecology. Swedish Natural Science Council, Ecology Research Commissioners Bulletin 5:31-33.

Estabrooks, S.R. 1987. Ingested lead shot in Northern red-billed whistling ducks ( Dendrocygna autumnalis ) and northern pintails ( Anas acuta ) in Sinaloa, Mexico. Journal of Wildlife Diseases 23(1):169.

Ethier, A.L.M., B.M. Braune, A.M. Sche uhammer, D.E. Bond. 2007. Comparison of lead residues among avian bones. Envi ronmental Pollution 145(3):915-919.

Evers, D.C. 2004. Status assessment and conservation plan for the Common Loon (Gavia immer) in North America. U.S. Fish and Wildlife Service, Hadley, MA.

Fawcett, D. and J. van Vessem. 1995. Lead poisoning in waterfowl: international update report 1995. JNCC Report, No. 252. Joint Nature Conservation Committee, Peterborough, UK.

Feierabend, J.S. 1983. Steel Shot and Lead Po isoning in Waterfowl. National Wildlife Federation Science and technical Series Number 8. 62 pp.

Fimreite, N. 1984. Effects of lead shot ingestion in willow grouse. Bulletin of Environmental Contamination and Toxicology 33(1):121-126.

Finkelstein, M.E., D. George, S. Scherbinsk i, R. Gwiazda, M. Johnson, J. Burnett, J. Brandt, S. Lawrey, A.P. Pessi er, M. Clark, J. Wynne, J. Grantham, and D.R. Smith. 2010.

Feather Lead Concentrations and 207 Pb/ 206 Pb Ratios Reveal Lead Exposure History of73 California Condors ( Gymnogyps californianus ). Environ. Sci. Technol. 2010, 44, 2639–

2647.

Finley, M.T., and M.P. Dieter. 1978. Influen ce of laying on lead accumulation in bone of mallard ducks. Journal of Toxicology and Environmental Health 4:123-129.

Fischbein, A., C. Rice, L. Sakozi, S.H. Kon, M. Petrocci, and I.J. Selikoff. 1979. Exposure to Lead at Firing Ranges. Journa l of the American Medical Association

241:1141-1144.

Fisher, I.J., D.J. Pain, and V.G. Thomas . 2006. A Review of Lead Poisoning From

Ammunition Sources in Terrestrial Birds. Biological Conservation 131:421-432

.

Flint, P.L. and J.B. Grand. 1997. Survival of Spectacled Eider Adult Females and Ducklings During Brood Rearing. Journa l of Wildlife Management 61:217-221.

Flint, P.L., M.R. Petersen, and J.B. Gr and. 1997. Exposure of Spectacled Eiders and Other Diving Ducks to Lead in Western Alaska. Canadian Jour nal of Zoology 75:439-

443.

Florida State University College of Medici ne (FSUCM). 2004. Firearms tutorial. Internet Pathology Laboratory for Medical Education (available at http://medlib.med.utah.edu/WebPath/ TUTORIAL/GUNS/GUNBLST.html).

Frank, A. 1986. Lead fragments in tissues from wild birds: a cause of misleading results.

Sci. Total Environ. 54 :275–281.

Franson, J.C. and D.J. Cliplef. 1992. Causes of Mortality in Common Loons. Pages 2-59

in W.N. Beyer, G.H. Heinz, and A.W. Re dmon-Norwood, editors. Proceedings from the 1992 Conference on the Loon and its Ecosystem: Status, Management, and Environmental Concerns, August 22-24, 1992, Co llege of the Atlantic, Bar Harbor,

Maine.

Franson, J.C. and S.G. Hereford. 1994. Lead Poisoning in a Mississippi Sandhill Crane.

Wilson Bulletin 106:766-768.

Franson, J.C., L. Sileo, O.H. Pattee, and J. F. Moore. 1983. Effects of Chronic Dietary Lead in American Kestrels ( Falco spaverius ). J. Wildlife Dis. 19,110-113

.

Franson, J.C., M.R. Petersen, C.U. Meteyer, and M.R. Smith. 1995. Lead Poisoning of Spectacled Eiders ( Somateria fischeri ) and of a Common Eider ( Somateria mollissima ) in

Alaska. Journal of Wildlife Diseases 31:268-271.

Franson, J.C., N.J. Thomas, M.R. Smith, A.H. Robbins, S. Newman, and P.C. McCartin. 1996. A Retrospective Study of Post-Mortem Findings in Red-Tailed Hawks, J. Raptor Res. 30, 7-14

.74 Franson, J.C., M.R. Petersen, L.H. Creekmore, P.L. Flint, and M.R. Smith. 1998. Blood Lead Concentrations of Spectacled Eide rs Near the Kashunuk River, Yukon Delta National Wildlife Refuge, Alaska. Ecotoxicology 7:175-181.

Franson, J.C., S.P. Hansen, T.E. Creekmore, C. J. Brand, D.C. Evers, A.E. Duerr, and S. DeStefano. 2003. Lead Fishing Weights and Other Fishing tackle in Selected Waterbirds.

Waterbirds 26:345-352.

Franson, J.C., S.P. Hansen, and J.H. Schul z. 2009. Ingested shot and tissue lead concentrations in Mourning Doves. In R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spen t Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Fredrickson, L.H., T.S. Bask ett, G.K. Brakhage, and V.C. Cravens. 1977. Evaluating Cultivation Near Duck Blinds to Reduce Lead Poisoning Hazard. Journal of Wildlife Management 41:624-631.

Friend, M. 1987. Field Guide to Wildlife Diseases. USFWS

.

Friend, M. 1999. Lead. Pages 317-334 in M. Friend and J.C. Franson, editors. Field

Manual of Wildlife Diseases: General Field Pr ocedures and Diseases of Birds. U.S. Geological Survey, Biological resources Division. Information and technology Report 1999-2001. Washington, D.C.

Fry, D.M. 2003. Assessment of Lead Cont amination Sources Exposing California

Condors. Species conservation and recovery report 2003, California Department of Fish and Game: San Diego, Calif

.

Fry, M., K. Sorenson, J. Grantham, J. Burn ett, J. Brandt, and M. Koenig. 2009. Lead

intoxication kinetics in condor s from California. Abstract in R.T. Watson, M. Fuller, M. Pokras, and W.G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Gangoso, L., P. Alvarez-Lloret, A.A.B. Rodr iguez-Navarro, R. Mateo, F. Hiraldo, and J.A. Donazar. 2009. Long-Term Effects of L ead Poisoning on Bone Mineralization in Vultures Exposed to Ammunition Sources. Environmental Pollution 157 569-574

.

Garcia-Fernandez, A.J., E. Martinez-Lopez, D. Romero, P. Maria-Mojica, A. Godino, and P. Jimenez. 2005. High levels of blood lead in griffon vultures (Gyps fulvus) from Cazorla Natural Park (southern Spain) . Environmental Toxicology 20(4):459-463.

Garcia Fernandez, A. J., M. Motas Guzman, I. Navas, P. Maria Mojica, A. Luna, and J. A. Sanchez Garcia. 1997. Environmental exposure and distribution of lead in four species75 of raptors in southeastern Spain. Archiv es of Environmental Contamination and Toxicology 33:76-82.

Godin, A. J. 1967. Test of grit types in alleviat ing lead poisoning in mallards. U.S. Fish Wildlife Service, Spec. Scientific Re port- Wildlife 107. Washington, D.C. 9 pp.

Goyer, R.A. 1996. Toxic Eff ects of Metals. Pages 691-736 in C.D. Klaassen, M.O. Amdur, and J. Doull, editors. Cassarett and Doull’s Toxicology: The Basic Science of

Poisons. 5 th ed. McGraw-Hill, New York.

Grand, J.B., P.L. Flint, M.R. Petersen, and C.L. Moran. 1998. Effect of Lead Poisoning on Spectacled Eider Survival Rates. J ournal of Wildlife Management 62:1103-1109.

Grandjean, P. 1976. Possible eff ect of lead on egg-shell th ickness in kestrels 1874-1974.

Bulletin of Environmental Contamin ation and Toxicology 16(1):101-106.

Grandy, J.W. IV, L.N. Locke, and G.E. Bagley. 1968. Relative Toxicity of Lead and Five Proposed Substitute Shot Types to Pen-R eared Mallards. Jour nal of Wildlife Management 32:483-488.

Grasman, K.A., and P.F. Scanlon. 1995. Effect s of acute lead ingestion and diet on antibody and T-cell-mediated immunity in Japanese quail. Arch. Environ. Contam. Toxicol. 28, 161–167.

Grinnell, G.B. 1894. Lead-poisoning. Forest and Stream 42(6):117-118.

Guitart, R., J. Serratosa, V.G. Thomas. 2002. Lead poisoned wildfowl in Spain: A significant threat for human c onsumers. International Journa l of Environmental Health Research 12(4):301-309.

Guitart, R., J. To-Figueras, R. Mateo, A. Bertolero, S. Cerradelo, and A. MartinezVilalta. 1994. Lead poisoning in waterfowl from Ebro delta, Spain: calculation of lead exposure thresholds for mallards. Archiv es of Environmental Contamination and Toxicology 27:289-293.

Gulson, B.L., J.M. Palmer, and A. Bryce. 2002. Changes in the Blood Lead of a

Recreational Shooter. The Science of the Total Environment 293:143-150.

Haldimann, M., A. Baumgartner, and B. Zimm erli. 2002. Intake of lead from game meat – a risk to consumers’ health. European Food Research and T echnology 215(5):375-379.

Hall, M., J. Grantham, R. Posey, and A. Mee. 2007. Lead Exposure Among Reintroduced

California Condors in Southern California. California Condors in the 21 st Century, American Ornithologists Uni on and Nuttall Ornithological Club

. A. Mee, L.S. Hall and J. Grantham (eds.).76 Hall, S. L., and F. M. Fisher. 1984. Lead c oncentrations in tiss ues of marsh birds: relationship of feeding habits and grit preference to spent sh ot ingestion. Department of Biology, Rice Univ., Hous ton, Texas. Mimeo, 8 pp.

Hall, S. L., and F. M. Fisher. 1985. Lead c oncentrations in tiss ues of marsh birds: relationship of feeding habits and grit preference to spen t shot ingestion. Bulletin of Environmental Contamination and Toxicology 35:1-8.

Hammerton, K.M., N. Jayasinghe, R.A. Jeffree, and R.P. Lim. 2003. Experimental Study of Blood Lead Kinetics in Estuarine Crocodiles ( Crocodylus porosus ) Exposed to Ingested Lead Shot. Archives of Envir onmental Contamination and Toxicology 45:390-

398.

Hanning, R.M., R. Sandhu, A. MacMillan, L. Moss, L.J.S. Tsuji, and E. Nieboer Jr. 2003. Impact on blood Pb levels of maternal and ea rly infant feeding practices of First Nation Cree in the Mushkegowuk Territory of northern Ontario, Canada. Journal of Environmental Monitoring 5:241 – 245.

Hanzlik, P. J. 1923. Experimental plumbism in pigeons from the administration of metallic lead. Archiv für experimente lle Pathologie und Pharmakologie 97:183-201.

Hardison, D.W. Jr., L.Q. Ma, T. Luongo, and W. G. Harris. 2004. Lead Contamination in Shooting Range Soils From Abrasion of l ead Bullets and Subsequent Weathering.

Science of the Total Environment 328:175-183.

Harmata, A.R. and M. Restani. 1995. Environm ental contaminants and cholinesterase in blood of vernal migrant bald and golden eagles in Montana. Intermountain Journal of

Sciences 1(1):1-15.

Harper, M.J. and M. Hindmarsh. 1990. Lead poisoning in magpie geese Anseranas semipalmata from ingested lead pellets at Bool Lagoon Game Reserve (South Australia).

Australia Wildlife Research 17:141-145.

Hass, G. H. 1977. Unretrieved shooting loss of mourning doves in north central South Carolina. Wildlife Society Bulletin 5:123-125.

Hatch, C. 2006. Lead Bullets Poison Ravens, Maybe People. Jackson Hole News &

Guide , September 16, 2006.

Hatch, C. 2010. Lead in Ravens Drops With Copper Bullets. Jackson Hole News &
Guide, February 24, 2010.

Hawkins, A. S. 1965. The lead poisoning problem in the four flyways. Pages 21-60 in N. A. Cox, (Chair), Wasted Wa terfowl. Report by Mississipp i Flyway Central Planning

Committee.77 Hennes, S.K. 1985. Lead shot ingestion and l ead residues in migran t bald eagles at the Lac Qui Parle Wildlife Management Area, Minn esota. Master’s thesis. University of

Minnesota.

Henny, C.J., L.J. Blus, D.J. Hoffman, R. A. Grove, and J.S. Hatfield. 1991. Lead Accumulation and Osprey Production Near a Mi ning Site in the Coeur d’ Alene River,

Idaho. Arch. Environ. Contam. Toxicol. 21, 415-424

.

Herbert, C. E., V. L. Wright, P. J. Zwa nk, J. D. Newson, and R. L. Kasul. 1984. Hunter performance using steel and lead loads for hunting ducks in coastal Louisiana. Journal Wildlife Management 48(2):388-398.

Hernberg, S. 2000. Lead Poisoning in Historical Perspective. American Journal of

Industrial Medicine 38:244-254

.

Hoffman, D.J., O.H. Pattee, S.N. Wiemeyer, and B. Mulhern. 1981. Effects of Lead Shot Ingestion on Delta-Aminolevulinic Acid Dehyratase Activity, Hemoglobin Concentration, and Serum Chemistry in Bald Eagles. J. Wildl. Dis. 17:423-431

.

Hoffman, D.J., J.C. Franson, O.H. Pattee, C.M. Bunck, A. Anderson. 1985. Survival, Growth and Accumulation of Ingested L ead in Nestling American Kestrels ( Falco sparverius ). Arch. Environ. Contam. Toxicol. 14, 89-94

.

Hoffman, D.J., J.C. Franson, O.H. Pattee, C.M. Bunck, and H.C. Murray. 1985. Biochemical and Hematological Effects of Lead Ingestion in Nestling American Kestrels ( Falco sparverius ). Comp. Biochem. Physiol. 80C, 431-439

.

Hohman, W. L., J. L. Moore, and J. C. Franson. 1995. “Winter survival of immature

Canvasbacks in inland Louisiana.” Journa l of Wildlife Management 59(2):384-392.

Holland, G. 1882. Pheasant poisoning by swallowing shot. The Field 59:232.

Holmes, R. S. 1975. Lead poisoning in waterfowl: dosage and dietary study. Summary of Illinois Natural History Survey Study- 1948-1953. Joint Report of Illinois Natural History Survey and Olin Cor poration, Winchester Group. 70 pp.

Holt, G., A. Froslie, and G. Norheim. 1978. Lead poisoning in Norwegian waterfowl (author’s translation). 1978. Nordisk Veterinaer Medici n. 30(9):380-386.

Honda, K., D. P. Lee, and R. Tasukawa. 1990. Lead poisoning in swans in Japan. Environmental Pollution 65(3):209-218.

Horton, B.T. 1933. Bird shot in verminform a ppendix: a cause of ch ronic appendicitis. Surgical Clinics of North America 13:1005-1006.78 Hui, C.A. 2002. Lead Distribution Throughout Soil, Flora and an Invertebrate at a Wetland Skeet Range. Journal of Toxicol ogy and Environmenta l Health 65:1093-1107.

Humburg, D. D., S. L. Sheriff, P. H. Geissl er, and T. Roster. 1982. Shot shell and shooter

effectiveness: lead vs. steel shot for duc k hunting. Wildlife Societ y Bulletin 10(2):121-

126.

Humburg, D.D., D. Graber, S. Sheriff, a nd T. Miller. 1983. Estimating autumn-spring waterfowl nonhunting mortality in north Missour i. North American Wildlife and Natural

Resources Conference Transactions 48:241-256.

Hunt, W.G., W. Burnham, C.N. Parish, and K. Burnham. 2006. Bullet Fragments in Deer Remains: Implications for Lead Exposure in Scavengers, Wildlife Society Bulletin

34:168-171

.

Hunt, W.C., C.N. Parish, S.C. Farry, T. G. Lord, and R. Sieg. 2007. Movements of

Introduced Condors in Arizona in Relation to Lead Exposure. California Condors in the

21 st Century, American Ornithologists Union and Nuttall Ornithological Club

. A. Mee, L.S. Hall and J. Grantham (eds.).

Hunt, W.G., R.T. Watson, J.L. Oaks, C.N. Pa rish, K.K. Burnham, R.L. Tucker, J.R. Belthoff, and G. Hart. 2009. Lead Bullet Fragme nts in Venison from Rifle-Killed Deer: Potential for Human Dietary Exposure. PLoS ONE

Hunt, G., W. Burnham, C. Parish, K. Bur nham, B. Mutch, and J. L. Oaks. 2009a. Bullet fragments in deer remains: Implicatio ns for lead exposure in scavengers. In R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.) . Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Hunt, W.G., R.T. Watson, J.L. Oaks, C.N. Pa rish, K.K. Burnham, R.L. Tucker, J.R. Belthoff, and G. Hart. 2009b. Lead bullet fragme nts in venison from rifle-killed deer: potential for human dietary exposure. Reproduced in R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Hunter, B. F., and M. N. Rosen. 1965. Occurrence of lead poisoning in a wild pheasant (Phasianus colchicus). Calif ornia Fish and Game 51:207.

International Programme on Chemical Sa fety (IPCS). 1989. Lead Environmental Aspects. Environmental health Criteria 85. World Health Organi zation, International Programme on Chemical Safety, Geneva, Switzerland.

Iowa Department of Natural Resources, “Trends in Iowa Wildlife Populations

and Harvest 2007.”79 Irwin, J.C. and L.H. Karstad. 1972. The toxicity for Ducks of Disintegrated Lead Shot in

a Stimulated Marsh Environment. J. Wildl. Dis. 8:149-154

.

Janssen, D. L., J. E. Oosterhuis, J. L. Allen, M. P. Anderson, D. G. Kelts, and S. N. Wiemeyer. 1986. Lead poisoning in free ranging California condors. J. Amer. Vet. Med.

Assoc. 189:1115-1117.

Jeffrey, R. G. 1977. Incidence of ingested sh ot in waterfowl taken during the 1973-74 and 1976-77 season in Washington. Washington De t. Game, Game Manage. Div. Rep. 8 pp.

Johansen, P., G. Asmund, and F. Riget. 2001. Lead contamination of seabirds harvested with lead shot — implicati ons to human diet in Green land. Environmental Pollution 112(3):501-504.

Johansen, P., G. Asmund, and F. Riget. 2004. High Human Exposure to Lead Through Consumption of Birds Hunted With Lead Shot. Environmenta l Pollution 127:125-129.

Johansen, P., H.S. Pedersen, G. Asmund, and F. Riget. 2005. Lead shot from hunting as a

source of lead in human blood. E nvironmental Pollution 142(1):93-7.

Johns, F. M. 1934. A study of punctate stippli ng as found in the lead poisoning of wild ducks. Journal of Laboratory a nd Clinical Medicine 19:514-517.

Johnsgard, P.A. 1983. Cranes of the World.

Johnson, C.K., T. Vodovoz, W.M. Boyce, and J.A.K. Mazet. 2007. Lead Exposure in California Condors and Sentinel Species in Calif ornia. Report prepared for the California Department of Fish and Game. Universi ty of California, Davis, February 2007.

Jorgensen, S.S. and M. Willems. 1987. The Fate of Lead in Soils: The Transformation of Lead Pellets in Shooting Range Soils. Ambio 16:11-15.

Jones, J. C. 1939. On the occurrence of lead shot in stomachs of North American gruiformes. Journal of Wildlife Management 3:353-357.

Jordan, J. S. 1951. Lead poisoning in wild wa terfowl. Illinois National History Survey Biology Notes 26:18.

Jordan, J. S., and F. C. Bellrose. 1950. Shot alloys and lead poisoning in waterfowl.

Transactions of North Ameri can Wildlife Conference 15:155-170.

Kaiser, G. W., K. Fry, and J. G. Ireland. 1980. Ingestion of lead shot by dunlin. The Murrelet 61(1):37.80 KDHE (Kansas Department of Health and Environment). 2004. Adult blood lead epidemiology and surveillance program. http://www.kdhe.state.ks.us /ables/hobby.html#hunting/.

Kaplan, H.M., T.J. Arnholt, and J.E. Payne. 1967. Toxicity of Lead Nitrate Solutions for Frogs ( Rana pipiens ). Lab Animal Care 17:240-246.

Keel, M.K., W.R. Davidson, G.L. Doster, a nd L.A. Lewis. 2002. Northern bobwhite and lead shot deposition in an upland habitat. Ar chives of Environmen tal Contamination and Toxicology 43:318-322.

Kelly, A. and S. Kelly. 2000. Are Mute Swans With Elevated Blood Levels More Likely

to Collide With Overhead Powerlines? Waterbirds 28:331-334

.

Kelly, A. and S. Kelly. 2004. Fishing Tackle Injury and Blood Lead Levels in Mute

Swans. Waterbirds 27:60-68.

Kendall, R. J. 1980. The toxicology of lead s hot and environmental lead ingestion in avian species with emphasis on the biologi cal significance in m ourning dove populations. Ph.D. thesis. Virginia Polytech Institut e and State University, Blacksburg. 289 pp.

Kendall, R. J., G. R. Norman, and P. F. Scanlon. 1980. Lead concentrations in ruffed grouse (Bonasa umbellus) collected from southwestern Virginia, USA. Virginia Journal of Science 31(4):100.

Kendall, R.J. and P.F. Scanlon. 1981. Effects of Chronic Lead Ingestion on Reproductive Characteristics of Ringed Turtle Doves ( Streptopelia risoria ) and on Tissue Lead Concentrations of Adults and Their Progeny. Environ. Pollut. Series A 26, 203-214

.

Kendall, R.J., G.W. Norman, and P.F Scanl on. 1984. Lead concentration in ruffed grouse collected from Southwestern Virg inia. Northwest Science 58:14-14.

Kendall, R.J. and P.F. Scanlon. 1979a. Lead concentrations in mourning doves collected from middle Atlantic game management areas . Proceedings of the Annual Conference of

Southeast Association Fish Wildlife Agencies 33:165-172.

Kendall, R. J., and P. F. Scanlon. 1979b. Lead levels in mourning doves collected from Mid-Atlantic States in 1977. Virg inia Journal of Science 30:69.

Kendall, R.J., T.E. Lacher, C. Bunck, B. Daniel , C.E. Driver, C.E. Grue, F. Leighton, W. Stansley, P.G. Watanabe, and M. Whitwort h. 1996. An Ecological Risk Assessment of Lead Shot Exposure in Non-Waterfowl Avia n Species: Upland Game Birds and Raptors. Environmental Toxicology and Chemistry 15:4-20

.81 Kennedy, J. A., and S. Nadeau. 1993. Lead s hot contamination of waterfowl and their

habitats in Canada. Canadian Wildlife Serv ice Technical Report Se r. No. 164, Canadian Wildlife Service, Ottawa. 109 pp.

Kennedy, S., J. P. Crisler, E. Smith, and M. Bush. 1979. Lead poisoning in sandhill

cranes. Journal of American Veteri nary Medical Association 171:955-958.

Kenntner, N., Y. Crettenand, H-J. Fünfst ück, M. J. Janovsky, and F. Tataruch. 2007. Lead poisoning and heavy metal exposure of golden eagles ( Aquila chrysaetos ) from the European Alps. Journal of Ornithology 148(2):173-177.

Kenntner, N., F. Tataruch, and O. Krone. 2001. Heavy metals in soft tissue of whitetailed eagles found dead or moribund in Germany and Austria from 1993 to 2000. Environmental Toxicology and Chemistry 20(8):1831-1837.

Khan, A.N. 2005. Lead Poisoning. Emedicine in stant access to the minds of medicine. www.emedicine.com/radio/topic386.htm.

Khangarot, B.S., A. Sehgal, and M.K. Bhas in. 1985. Man and Biosphere – Studies on the Sikkim Himalayas. Part 5: acute toxicity of selected heavy metals on the tadpoles of Rana hexadactyla . Acta Hydrochimica et Hydrobiologica 13:259-263.

Kimball, W. H. and Z. A. Munir. 1971. Th e corrosion of lead shot in a simulated waterfowl gizzard. Journal of Wildlife Management 35(2):360-365.

King, M. 1993. Bismuth shot now established as a legal alternativ e to steel in the Northern Territory. Australian S hooters Journal, January 1993:56-57.

Kingsford, R. T., J. Flanjak, and S. Black. 1989. Lead shot and ducks on Lake Cowal.

Australian Wildlife Research 16:167-172.

Kingsford, R.T., J. L. Kacprzak, and J. Zi aziaris. 1994. Lead in livers and gizzards of waterfowl shot in New South Wales, Austra lia. Environmental Pollution 85(3):329-335.

Kirby, J., S. Delany, and J. Quinn. 1994. Mute Swans in Great Britain – A Review, Current Status and Long-Term Tr ends. Hydrobiologia 279/280:467-482.

Knopper, L.D., P. Mineau, A.M. Sche uhammer, D.E. Bond, and D.T. McKinnon. 2006. Carcasses of Shot Richardson’s Ground Squirre ls May Pose Lead Hazards to Scavenging

Hawks. The Journal of Wild life Management 70(1)

.

Koh, T.S., and Harper, M.J. 1988. Lead-poisoning in Black Swans, Cygnus atratus

, exposed to lead shot at Bool lagoon Game Reserve, South Australia. Australian Wildlife

Research 15:395-403.82 Kosnett, M.J. 2009. Health effects of low dos e lead exposure in a dults and children, and preventable risk posed by the consumpti on of game meat harvested with lead

ammunition. In R. T. Watson, M. Fuller, M. Pokras, a nd W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Kramer, J.L. and P.T. Redig. 1997. Sixteen Years of Lead Poisoning in Eagles, 1980- 1995: An Epizootiologic View. J.E. Cooper and A.G. Greenwood (eds.). Journal of Raptor Research 31:327-332

.

Kringer, F., W. L. Anderson, and J. A. Ellis. 1980. Effectiveness of steel shot in 2 3⁄4 in 12 gauge shells for hunting mourning doves. Illinois Department of Conservation Management Notes No. 3. Springfield, Illinois. 10 pp.

Krone, O., Willie, F., Kenntner, N., Boertma nn, D., Tataruch, F. 2004. Mortality factors, environmental contaminants, and parasites of white-tailed sea eagles from Greenland.

Avian Diseases 48:417-424.

Krone, O., N. Kenntner, A. Trinogga, M. Nadjaf zadeh, F. Scholz, J. Sulawa, K. Totschek, P. Schuck-Wersig, and R. Zieschank. 2009. L ead poisoning in White-tailed Sea Eagles: Causes and approaches to solutions in Germany. In R.T. Watson, M. Fuller, M. Pokras, and W.G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Kurosawa, N. 2000. Lead poisoning in Stelle r’s sea eagles and White-tailed sea eagles. Pages 107-109 in Ueta, M. and McGrady, M.J. (eds). First Sympos ium on Steller’s and White-tailed sea eagles in East Asia.

Labare, M.P., M.A. Butkus, D. Riegner, N. Schommer, and J. Atkinson. 2004. Evaluation

of Lead Movement from the Abiotic to Biotic at a Small-Arms Firing Range. Environmental Geology 46:750-754.

Lagerquist, J.E., M. Davison, and W.J. Fo reyt. 1994. Lead Poisoning and Other Causes of Mortality in Trumpeter ( Cygnus buccinator ) and Tundra ( C. columbianus ) Swans in Western Washington. Journal of Wildlife Diseases 30:60-64.

Lakhani, H. 1982. Benefit-cost analysis: Subs tituting iron for lead shot in waterfowl hunting in Maryland. Journal of E nvironmental Management 14:201-208.

Lance, V.A., T.R. Horn, R.M. Elsey and A. de Peyster. 2006. Chronic incidental lead ingestion in a group of cap tive-reared alligators ( Alligator mississippiensis ): possible contribution to reproductive failure . Toxicology and Pharmacology 142:30–35.

Langelier, K. 1994. Lead shot poisoning in Canadian wildlife. Prepared for the Animal Welfare Foundation of Canada, Vancouver, B.C. 46 pp.83 Langelier, K. M., J. E. Elliott, and A. M. Scheuhammer. 1991. Bioaccumulation and toxicity of lead in bald ea gles (Haliaeetus leucocephalus) of British Columbia. Western Canada Wildlife Health Workshop, 15-16 February, Victoria, B.C.

Lanphear, B.P., K.N. Dietrich, and O. Berger . 2003. Prevention of lead toxicity in US

children. Ambul. Pediatr. 3(1):27-36.

Lanphear, B.P., R. Hornung, J. Khoury, K. Yo lton, P. Baghurst, D.C. Bellinger, R.L. Canfield, K.N. Dietrich, R. Bornschein, T. Gr eene, S.J. Rothenberg, H.L. Needleham, L. Schnaas, G. Wasserman, J. Graziano, and R. Roberts. 2005. Low-level environmental lead exposure and children's intellectual f unction: an international pooled analysis. Environ Health Perspect. 2005 Jul;113(7):894-9.

Lanphear, B.P., R. Hornung, J. Khoury, K. Yolt on, and K.N. Dietrich. 2006. Lead and IQ in Children: Lanphear et al . Respond. Environ Health Perspect. 2006 February; 114(2):

A86–A87.

LaRoe, E.T., G.S. Farris, C.E. Puckett, P.D. Doran, and M.J. Mac. 1995. Our Living

Resources. A Report to the Nation on the Distri bution, Abundance, and Health of U.S. Plants, Animals, and Ecosystems. U.S. Dept . Interior, National Biological Service

.

Levengood, J.M., G.C. Sanderson, W.L. Anderson, G.L. Foley, L.M. Skowron, P.W. Brown, and J.W. Seets. 1999. Acute Toxicity of Ingested Zinc Shot to Game-Farm

Mallards. Illinois Natural Hi story Survey Bulletin 36:1-36.

Levesque, B., J. F. Duchesne, C. Gariepy, M. Rhainds, P. Dumas, A. M. Scheuhammer, J. F. Proulx, S. Dery, G. Muckle, F. Da llaire, and E. Dewailly. 2003. Monitoring of

umbilical cord blood lead levels and sources assessment among the Inuit. Occupational

and Environmental Medicine 60:693-695.

Lewis, J. C., and E. Legler, Jr. 1968. L ead shot ingestion by mourning doves and

incidence in soil. Journal of Wildlife Management 32(3):476-482.

Lewis, L.A., R.J. Poppenga, W.R. Davidson, J.R. Fischer, and K.A. Morgan. 2001. Lead

Toxicosis and Trace Elements in Wild Bi rds and Mammals at a Firearms Training Facility. Arch. Environ. Contam. Toxicol. 41:208-214

.

Locke, L. N., and G. E. Bagley. 1967a. Case report: coccidiosis and lead poisoning in Canada geese. Chesapeake Science 8(1):68-69.

Locke, L.N., M.R. Smith, R.M. Windingsta d, and S.J. Martin. 1991. Lead poisoning of a marbled godwit. Prairie Naturalist 23(1):21-24.

Locke L.N. and M. Friend. 1992. Lead Poisoning of Avian Species Other Than

Waterfowl. Lead Poisoning in Waterfowl , D.J. Pain (ed.), pp. 19-22.84 Locke, L.N., S.M. Kerr, and D. Zoromski. 1982. Lead Poisoning in Common Loons ( Gavia immer). Avian Diseases 26:392-396.

Ma, W. 1989. Effect of Soil Pollution With Metallic Lead Pellets on Bioaccumulation and Organ/Body Weight Alterations in Sm all Mammals. Archives of Environmental Contamination and Toxicology 18:617-622.

Maedgen, J. L., C. S. Hacker, G. D. Schr oder, and F. W. Weir . 1982. Bioaccumulation of lead and cadmium in the royal tern and sandwich tern. Archives of Environmental Contamination and Toxicology 11:99-102.

Manninen, S., and N. Tanskanen. 1993. Transfer of lead from shotgun pellets to humus and three plant species in Finnish shooting range. Archives of Environmental Contamination and Toxicology 24:410-414.

Mateo, R. R. Molina, J. Grifols, and R. Guitart. 1997. Lead Poisoning in a Free Ranking Griffin Culture ( Gyps fulvus ). Vet. Rec. 140:47-48

.

Mateo, R. 1998. La Intoxicacion Por Ingest ion de Objtos de Polmo en Aves: Una Revision de Los Aspectos Epidemiologicos y Clinicos. La Intoxicacion por Ingestion de Perdigones de Plomo en Aves Silvestres: Aspe ctos Epidemiologicos y Propuestas para su Prevencion en Espana, Doctoral Thesis, Univ ertat Autonoma de Barcelona, Barcelona

, pp. 5-44.

Mateo, R. J. Estrada, J.Y. Paquet, X. Riera, L. Domingues, R. Guitart, and A. MartinezVilata. 1999. Lead Shot Inge stión by Marsh Harriers ( Circus aeruginosus ) From the Ebro Delta, Spain. Environ. Pollut. 104, 435-440

.

Mateo, R., J.C. Doltz, J.M. Aguilar Serrano, J. Belliure, and R. Guitart. 1997. An epizootic of lead poisoning in greater flamingos ( Phoenicopterus ruber roseus ) in Spain. Journal of Wildlife Diseases 33(1):131-134.

Mateo, R., R., A.J. Green, C.W. Jeske, V. Urios, and C. Gerique. 2001. Lead poisoning in the globally threatened marbled teal and white-headed duck in Spain. Environmental Toxicology Chemistry 20(12):2860-2868.

Mateo, R., M. Taggard, and A.A. Meharg. 2003. Lead and Arsenic in Bones of Birds of Prey From Spain, Env. Poll. 126:107-114

.

Mateo, R., R., A.J. Green, H. Lefranc, R. Baos, and J. Figuerola. 2007. Lead poisoning in wild birds from southern Spain: a comp arative study of wetland areas and species affected, and trends over time. Ecotoxicolo gical Environmental Science 66(1):119-126.

Mateo, R., M. Rodríguez-de la Cruz, M. Re glero, and P. Camarero. 2007. Transfer of lead from shot pellets to game meat during cooking. Scie nce of the Total Environment 372(2-3):480-485.85 Matz, A. and P. Flint. 2009

. Lead isotopes indicate lead shot exposure in Alaska-breeding

waterfowl. Abstract in R.T. Watson, M. Fuller, M. P okras, and W.G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

McAtee, W. L. 1908. Lead poisoning in ducks. Auk. 25(4):472.

Mellor, A. and C. McCartney. 1994. The Eff ects of Lead Shot Deposition on Soil and Crops at a Clay Pigeon Shooting Site in Northern England. Soil Use and Management

10:124-129.

Meretsky, V. J., N. F. R. Snyder, S. R. Bei ssinger, D. A. Clendenen, and J. W. Wiley. 2000. Demography of the California condor: Implications for re establishment. Conservation Biology 14:4:957-967.

Michael, P. 2006. Fish and Wild life Issues Related to the Use of Lead Fishing Gear. Washington State: Washingt on Department of Fish and Wildlife, Fish Program. http://www.wa.gov/fish/papers/ lead_fishing_gear/fpt_06-13.pdf.

Mikko, D. 1999. U.S. Military “Green Bullet.” Association of Firearm and Tool Mark Examiners Journal, Volume 31 Number 4, Fall 1999. U. S. Army Criminal Investigation Laboratory, Forest Park Georgia.

Miller, M.J.R., M. Restani, A.R. Harmata, G.R. Bortolotti, and M.E. Wayland. 1998. A Comparison of Blood Lead Levels in Bald Ea gles From Two Regions on the Plains of

North America. Journal of Wildlife Diseases 34:704-714

.

Miller, M.J.R., M.E. Waylands, and G. R. Bortolotti. 2001. Hemograms for and Nutritional Condition of Migrant Bald Eagles Tested for Exposure to Lead. J. Wildl. Dis. 37(3):481-488

.

Minnesota Office of Environmental Assistan ce (MOEA). 2006. Let’s Get the Lead Out! Non-Lead Alternatives for Fishing Tackle . www.pca.state.mn.us/oea/reduce/sinkers.cfm.

Mohler, L. 1945. Lead poisoning of geese near Lincoln. Nebraska Bird Review 13(2):49-

50.

Mörner, T., and L. Petersson. 1999. Lead poi soning in woodpeckers in Sweden. Journal

of Wildlife Diseas es 35(4):763-765.

Mudge, G.P. 1983. The Incidence and Significan ce of Ingested Lead Pellet Poisoning in British Waterfowl. Biological Conservation 27:333-372.

Munro, J. A. 1925. Lead poisoning in trumpe ter swans. Canadian Field-Naturalist 39(7):160-162.86 Murray, K., A. Bazzi, C. Carter, A. Ehlert, A. Harris, M. Kopec, J. Richardson, and H. Sokol. 1997. Distribution and Mobility of Lead in Soils at an Outdoor Shooting Range.

Journal of Soil Contamination 6:79-93.

Nakade, T., Y. Tomura, K. Jin, H. Taniyama , M. Yamamoto, A. Kikkawa, K. Miyagi, E. Uchida, M. Asakawa, T. Mukai, M. Sh irasawa, and M. Yamaguchi. 2005. Lead poisoning in Whooper and Tundra swans. Jour nal of Wildlife Dis eases 41(1):253-256.

National Wildlife Health Laboratory. 1985. Bald eagle mortality from lead poisoning and other causes 1963-84. Unpublished report. U.S. Fish and Wildlife Service, Washington, D.C. 48 pp.

Needleman, H.L., A. Schell, D.M. Bellinger, A. Leviton, and E.N. Allred. 1990. The long-term effects of exposure to low doses of lead in childhood. An 11-Year follow up report. New England Journal of Medicine 322(2):83-88.

Needleman, H.L. and D.M. Bellinger. 1991. The health effects of low level exposure to

lead. Annual Review of Public Health12:111-140.

Needleman, H.L. 1999. History of Lead Poisoni ng in the World. Intern ational Conference on lead Poisoning Prevention and Treatment , Bangalore, February 8-10, 1999. Bangalore, India: The George Foundation. www.l eadpoisoning.net/gener al/history.htm.

Needleman, H.L. 2004. Lead Poisoning. A nnual Review of Medicine 55:209-222.

Needleman, H.L., C. McFarland, R.B. Ness, S.E. Fienberg, and M.J. Tobin. 2002. Bone Lead Levels in Adjudicated Delinquents: A Case Control Study. Neurotoxicology and Teratology 24:711-717.

Neumann, K. 2009. Bald Eagle lead poisoning in winter. In R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Nevin, R. 2000. How Lead Exposure Relates to Temporal Changes in IQ, Violent Crime, and Unwed Pregnancy. Environmenta l research Section A 83:1-22.

Nieboer, E. 2001. The definitive identification of lead shotshell as a major source of lead exposure in native communities. Health Canada and Environment Canada, Toxic

Substances Research Initiative # 287.

Nordic Council of Ministers (NCM). 2003. L ead Review. Nordic Council of Ministers Report 1, Issue 4. www.norden.org/pub/miljo/miljo/sk/US20031308.pdf.

Novotny, T., M. Cook, J. Hughes, and S.A. Lee. 1987. Lead Exposure on a Firing Range.

American Journal of P ublic health 77:1225-1226.87 Nriagu, J.O. 1983. Lead and Lead Poisoning in Antiquity. John Wiley and Sons. New

York.

Nraigu, J.O. 2009. History in lead and lead poisoning in history. Abstract in R. T. Watson, M. Fuller, M. Pokras, and W. G. H unt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho,

USA.

Ochiai, K., T. Kimura, K. Uematsu, Umematsu, and C. Itakura. 1999. Lead poisoning in wild waterfowl in Japan. Journal of Wildlife Diseases 35(4):766-769.

Ochiai, K., K. Hoshiko, K. Jin, T. Tsuuzuki, and C. Itakura. 1993. A survey of lead poisoning in wild waterfowl in Japan. J ournal of Wildlife Diseases 29(2):349-352.

Ochiai, K., K. Jin, C. Itakura, M. Goryo, K. Yamashita, N. Mizuno, T. Fujinaga, and T. Tsuzuki. 1992. Pathological study of lead poisoning in whooper swans ( Cygnus cygnus ) in Japan. Avian Dis eases 36(2):313-323.

Odland et al. 1999. Elevated blood lead concentrations in ch ildren living in isolated communities of the Kola Peninsula, Russia. Ecosystem Health 5(2):75-81.

O’Halloran, J., A. A. Myers, and P. F. Duggan. 1988. Lead poisoning in swans and

sources of contamination in Ireland. Journal of Z oology (London) 216:211-223.

Old Deer Hunter Associati on (ODHA). 2004. The Importance of Ballistic Coefficient When Selecting Ammo and Bullets (available at http://www.clcweb.net/Shooting/ Ballistics/ ballistics.htm l ).

Oltrogge, V. 2009. Success in developing lead-f ree, expanding nose centerfire bullets. In R.T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho,

USA.

Osmer, T.L.G. 1940. Lead shot: its danger to water-fowl. The Scientific Monthly 50(5):455-459.

Oswkttera, GD, Bucka, WB, and WE Lloyda. 1973. Epidemiology of Lead Poisoning in Cattle- A Five-Year Study in Iowa. Clin ical Toxicology, Volume 6(3): 367 – 376.

Owen, M. 1992. Progress on Lead Shot in the UK: 1991. Wildfowl 43:223.

Pain, D.J. 1991. Lead shot densities and settle ment rates in Camargue marshes, France. Biological Conservation 57:273-286.88 Pain, D. J. (ed). 1992a. Lead poisoning of waterfowl: a review. IWRB Special Publication No. 16, Slimbridge, United Kingdom.

Pain, D.J. 1992b. Lead poisoning in birds: a so uthern European perspective. Pages 109- 114 in C M. Finlayson, G. E. Hollis and T. J. Davis (eds), Managing Mediterranean Wetlands and Their Birds, Proceedings of an IWRB International Symposium, Grado, Italy, 1991. IWRB Special publicatio n, Slimbridge, United Kingdom.

Pain, D.J. 1992. Lead Poisoning of Waterfowl: A Review. Pages 7-13 in D.J. Pain, editor. Lead Poisoning in Waterfowl. Proceedings of the International Waterfowl and Wetlands Research Bureau Workshop, Brussels, Be lgium 1991. IWRB Special Publication 16, Slimbridge, U.K.

Pain, D. J., and C. Amiard-Triquet. 1993. Lead poisoning of raptors in France and elsewhere. Ecotoxicology and Environmental Safety 25:183-192.

Pain, D. J., C. Bavoux, G. Burneleau, L. Eon, and P. Nicolau-Guillaum. 1993. Lead poisoning in wild populations of marsh harriers (Circus ae ruginosus) in the Camargue and Charente-Maritime, France. Ibis 135:379-386.

Pain, D. J., J. Sears, and I. Newton. 1994. Lead concentrations in bird s of prey in Britain.

Environmental Pollution 87:173-180.

Pain, D.J. 1996. Lead in Waterfowl. Environmental Contaminants in Wildlife: Interpreting Tissue Concentrations . W.M. Beyer, G.H. Heinz, and A.W. RedmanNorwood (eds.), pp. 251-262.

Pain, D. J., C. Bavoux, and G. Burneleau. 1997. Seasonal blood lead concentrations in

marsh harriers Circus aeruginosus from Charente-Maritime, France: Relationship with the hunting season.

Pain, D.J. and B.A. Rattner. 1988. Mortality and Hematology Associated With the Ingestion of One Number Four Lead Shot in Black Ducks, Anas rubripes

. Bull. Environ.
Contam. Toxicol. 40, 159-164

.

Pain, D.J., C. Amiard-Triquet, C. Bavoux, G. Burneleau, . Eon, and P. NicolauGuillaumet. 1993. Lead Poisoning in Wild Populations of Marsh Harrier ( Circus aeruginosus ) in the Camargue and Charente-Maritime, France. Ibis 135, 379-386

.

Pain, D.J., I.J. Fisher, and V.G. Thomas . 2009. A global update of lead poisoning in

terrestrial birds from ammunition sources. In R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Sp ent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Pain, D.J., R.L. Cromie, J. Newth, M.J. Brow n, E. Crutcher, P. Hardman, L. Hurst, R. Mateo, A.A. Meharg, A.C. Moran, A. Raab, M.A. Taggart, and R.E. Green. 2010.89 Potential Hazard to Human Health from Exposur e to Fragments of Lead Bullets and Shot

in the Tissues of Game Animals. Plos One , 5 (4): e10315 DOI: 10.1371/journal.pone.0010315.

Parish, C.N., W.G. Hunt, E. Feltes, R. Si eg, and K. Orr. 2009. Lead exposure among a reintroduced population of California Condors in norther n Arizona and southern Utah. In R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlif e and Humans. The Peregrine Fund, Boise, Idaho, USA.

Parmentier, K., R. Gwiazda, J. Burnett, K. Sorenson, S. Scherbinski, C. Vantassell, A. Welch, M. Koenig, J. Brandt, J. Petters on, J. Grantham, R. Risebrough, and D. Smith. 2009. Feather Pb isotopes reflect exposur e history and ALAD i nhibition shows subclinical toxicity in Ca lifornia Condors. Abstract in R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Pattee, O.H., S.N. Wiemeyer, B. Mulher n, L. Sileo, and J.W. Carpenter. 1981. Experimental Leadshot Po isoning in Bald Eagles. J. Wildl. Manage. 45:806-810

.

Pattee, O.H., P.H. Bloom, J.M. Scott, and M.R. Smith. 1990. Lead Hazards Within the Range of the California Condor. The Condor 92:931-937

.

Pattee, O.H. and D.J. Pain. 2003. Lead in the Environment. Handbook of Ecotoxicology

, D.J. .Hoffman, B.A. Rattner, G.A. Burton, and J. Cairns (eds.), pp. 373-408.

Pauli, J.N. and S.W. Buskirk. 2007. Recreationa l Shooting of Prairie Dogs: A Portal for Lead Entering Wildlife Food Chains. Journal of Wildlife Management 71:103-108

.

Peddicord, R.K. and J.S. LaKind. 2000. Ecol ogical and Human Health Risks at an Outdoor Firing Range. Environmental Toxicology and Chemistry 19:2602-2613.

The Peregrine Fund. 2010. California Condor Rel eases in Arizona--Notes from the Field.

Available at http://www.peregrinefund.org/archived_not es.asp?category=California%20Condor%20R

eleases%20in%20Arizona&cnoteid=272

Perez-Coll, C.S., J. Herkovitz, and A. Salibian. 1988. Embryotoxicity of Lead to Bufo

arenarum . Bulletin of Environmental Cont amination and Toxicology 41:247-252.

Perrins, C.M., G. Cousquer, and J. Waine. 2003. A Survey of Blood Lead Levels in Mute

Swans Cygnus olor . Avian Pathology 32:205-212.

Perry, M. C., and J. W. Artmann. 1979. Incidenc e of embedded shot and ingested shot in oiled ruddy ducks. Journal of W ildlife Management 43(1):266-269.90 Peterson, S., R. Kim, and C. McCoy. 1993. Ecol ogical Risks of Lead Contamination at a Gun Club: Waterfowl Exposure Via Multiple Dietary Pathways. 14 th Annual Meeting of the Society of Environmental To xicology and Chemistry. Abstract.

Petterson, J.R., K.J. Sorenson, C. Vantassell, J. Burnett, S. Scherbinski, A. Welch, and S. Flannagan. 2009. Blood-lead concentrations in California Condors released at Pinnacles National Monument, California. Abstract in R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Sp ent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Platt, S.R., K.E. Helmick, J. Graham, R.A. Be nnett, L. Phillips, C.L. Chrisman, and P.E. Ginn. 1999. Peripheral neuropathy in a turkey vult ure with lead toxicosis. Journal of the American Veterinary Medi cal Association 8:1218-1220.

Pokras, M.A. and R. Chafel. 1992. Lead Toxi cosis From Ingested Fishing Sinkers in Adult Common Loons ( Gavia immer) in New England. Journal of Zoo and Wildlife

Medicine 23:92-97.

Pokras, M.A., M.R. Kneeland, A. Major, R. Miconi, and R.H. Poppenga. 2009. Lead objects ingested by Common Loons in New England. Extended abstract in R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.) . Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Potts, G.R. 2004. Incidence of ingested l ead gunshot in wild grey partridges ( Perdix perdix ) from the UK. European Journal of Wildlife Research 51(1):31-34.

Quortrup, E.R. and J.E. Shillinger. 1941. 3,000 w ild bird autopsies on western lake areas. American Veterinary Medi cal Association Journal.

Radomski, P., T. Heinrich, T.S. Jones, P. Rivers, and P. Talmage. 2006. Estimates of Tackle Loss for Five Minnesota Walleye Fisheries. North American Journal of Fisheries Management 26:206-212

.

Rattner, B.A., W.J. Fleming, and C.E. Bunc k. 1989. Comparative Toxicity of Lead Shot in Black Ducks ( Anas rubripes ) and Mallards ( Anas platyrhynchos ). Journal of Wildlife

Diseases 25:175-183.

Rattner, B.A...[et al.]. 2007. Contaminant Expos ure and Effects--Terrestrial Vertebrates (CEE-TV) Database. Version 7.0. [Updated May 2007; Accessed Feb. 4, 2008]. U.S. Geological Survey, Patuxent Wildlife Resear ch Center , Laurel, Maryland. Available online: http://www.pwrc.us gs.gov/contaminants-online

Redig, P. T. 1979. Lead poisoning in raptors. Hawk Chalk 18(2):29-30.91 Redig, P.T. 1984. An investigation into the e ffects of lead poisoning on bald eagles and other raptors: Final report. Endangered Sp ecies Program. Study 100A-100B. University of Minnesota, St. Paul, Minneso ta. Unpublished report. 41 pp.

Redig, P. T. 1985. A report on lead toxicosis stud ies in bald eagles. Final Report, U. S. Dept. of Interior, Fish and Wild life Service Project No. BPO #30181-0906.

Redig P.T, D.R. Smith, and L. Cruz-Martin ez. 2009. Potential sources of lead exposure for Bald Eagles: A retrospective study. Extende d abstract in R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Redig, P.T., C.M. Stowe, D.M. Barnes, and T.D. Arent. 1980. Lead Toxicosis in Raptors.

J. Am. Vet. Assoc. 177:941-943

.

Redig, P.T., E.M. Lawler, S. Schwartz, J. L. Dunnette, B. Stephenson, and G.E. Duke. 1991. Effects of Chronic Exposure to Sublethal Concentrations of Lead Acetate on Heme Synthesis and Immune Functi on in Red-Tailed Hawks. Arch. Environ. Contam. Toxicol.

21:72-77

.

Rees, C. Triple-Shock X-Bullet. Petersen’s Rifle Shooter . Available at http://www.rifleshootermag.com/ammunition/triple_0723/index.html

Reid, V.H. 1948. Lead shot in Minnesota wa terfowl. Journal of Wildlife Management 12(2):123-127.

Reiser, M.H. and S.A. Temple. 1981. Effects of Chronic Lead Int oxication on Birds of Prey. Recent advances in the study of raptor diseases, 21-25 . J.E. Cooper and A.G. Greenwood (eds.), pp. 21-25.

Rice, D.A., M.F. McLoughlin, W.J. Blanch flower, T.R. Thompson. 1987. Chronic lead poisoning in steers eatin g silage contaminated with lead shot – dia gnostic criteria.

Bulletin of Environmental C ontaminant Toxicology 39(4):622–629.

Rice, T.M., B.J. Blackstone, W.L. Nixdorf, and D.H. Taylor. 1999. Exposure to Lead Induces Hypoxia-Like Responses in Bullfrog Larvae ( Rana catesbeiana ). Environmental Toxicology and Chemistry 18:2283-2288.

Ris, M. D., K.N. Dietrich, P.A. Succop, O.G. Berger and R.L. Bornschein. 2004. Early exposure to lead and neuropsychol ogical outcome in Adolescen ce. Journal International Neuropsychological Society 10: 261-270.

Ritter, J. 2006. Lead Poisoning Eyed as Threat to California Condor,. USA Today (10/23/2006). Available at http:// www.usatoday.com/news/nation/2006-10-23- condor_x.htm92 Rocke, T.E., C.J. Brand, and J.G. Mensik. 1997. Site-Specific Lead Exposure From Lead Pellet Ingestion in Sentin el Mallards. Journal of Wildlife Management 61:228-234.

Rodrigue, J., R. McNicoll, D. Leclair, and J. F. Duchesne. 2005. Lead concentrations in ruffed grouse, rock ptarmigan, and willow ptarmigan in Quebec. Archives of Environmental Contamination and Toxicology 49(1):334-340.

Rogers, T., B. Bedrosian, D. Craighead, H. Quigley, and K. Foresman. 2009. Lead ingestion by scavenging mammalian carnivore s in the Yellowstone ecosystem. Extended

abstract in R.T. Watson, M. Fuller, M. Pokras, and W.G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Rooney, C.P., RG. McLaren, and R.J. Creswell. 1999. Distribution a nd Phytoavailability

of Lead in a Soil Contaminated With Lead Shot. Water, Air, and Soil Pollution 116:535-

548.

Roscoe, D.E., S.W. Nielsen, A.A. Lamola, and D.. Zuckerman. 1979. A Simple, Quantitative Test for Erythrocytic Protoporphyrin in Lead-Poisoned Ducks. Journal of

Wildlife Diseases 15:127-136.

Saito, K. 2009. Lead poisoning of Steller’s Sea-Eagle ( Haliaeetus pelagicus ) and Whitetailed Eagle ( Haliaeetus albicilla ) caused by the ingestion of lead bullets and slugs, in Hokkaido Japan. In R.T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implicati ons for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Sanderson, G.C. and F.C. Bellrose. 1986. A Revi ew of the Problem of Lead Poisoning in

Waterfowl. Ill. Nat. Hist. Surv. Spec. Publ. 4

.

Scheuhammer, A. M. 1987. The chronic toxici ty of aluminum, cadmium, mercury, and

lead in birds: a review. Environmental Pollution 46:263-295.

Scheuhammer, A.M. 2009. Historical perspectiv e on the hazards of environmental lead

from ammunition and fish ing weights in Canada. In R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Scheuhammer, A.M. and S. L. Norris. 1995. A review of the environmental impacts of

lead shotshell ammunition and lead fishi ng weights in Canada. Canadian Wildlife Service, Environment Canada, Ottawa.

Scheuhammer, A.M. and S.L. Norris. 1996. Th e Ecotoxicology of Lead Shot and Lead Fishing Weights. Ecotoxicology 5:279-295.93 Scheuhammer, A. M., J. A. Perrault, E. Rout hier, B. M. Braune, and G. D. Campbell.

1998. Elevated lead concentrations in edible portions of game birds harvested with lead

shot. Environmental Pollution 102:251-257.

Scheuhammer, A. M., C. A. Rogers, and D. Bond. 1999. Elevated lead exposure in American woodcock ( Scolopax minor ) in eastern Canada. Archives of Environmental Contamination and Toxicology 36:334-340.

Scheuhammer, A.M., S.L. Money, D.A. Ki rk, and G. Donaldson. 2003b. Lead Fishing Sinkers and Jigs in Canada: Review of Thei r Use Patterns and Toxic Impacts on Wildlife. Occasional Paper 108. Canadian Wildlife Se rvice, Environmental Canada, Ottawa, Ontario, Canada.

Schulz, J.H., J.J. Millspaugh, B.E. Washbur n, G.R. Wester, J.T. Lanigan III, and J.C Franson. 2002. Spent-Shot Availability and Ingestion on Areas Managed for Mourning Doves. Wildlife Society Bulletin 30:112-120.

Schulz, J.H., J.J. Millspaugh, A.J. Bermudez, X. Gao, T.W. Bonnot, L.G. Britt, and M.

Paine. 2006. Acute Lead Toxicosis in Mourni ng Doves. Journal of Wildlife Management

70:413-421.

Schulz, J. H., J. J. Millspaugh, X. Gao, a nd A. J. Bermudez. 2007. Experimental lead pellet ingestion in mourning doves ( Zenaida macroura ). American Midland Naturalist

158:177-190.

Schulz, J. H., P. I. Padding, and J. J. Millspaugh. 2006. Will mourning dove crippling rates increase with nontoxic-shot regulations ? Wildlife Society Bulletin 34(3), 861-864.

Schulz, J.R., R.A. Reitz, S.L. Sheriff, a nd J.J. Millspaugh. 2007. Attitudes of Missouri

Small Game Hunters Toward Nontoxic-Shot Regulations. J. Wildlife Management 71(2):628–633; 2007)

Schulz, J. R., G. E. Potts, J. E. Cornely, J.J. Millspaugh, and M.A. Johnson. 2009. The Question of Lead: Considerations for M ourning Dove Nontoxic-sh ot Regulation. The

wildlife Professional 2009: 46-49. The Wildlife Society.

Schulz J.H. R.A. Reitz, S.L. Sheriff, J.J. Millspaugh, and P.I. Padding. 2009. Small game hunter attitudes toward nontoxic shot, and cr ippling rates with nontoxic shot. In: M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Schulz J.H, J.J. Millspaugh, and L.D. Va ngilder. 2009. Policy considerations for a Mourning Dove non-toxic shot regulation. In: R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.94 Schulz, J.H., X. Gao, J.J. Millspaugh, and A. J. Bermudez. 2009. Acute lead toxicosis and experimental lead pellet ingestion in Mourning Doves. Extended abstract in R.T. Watson, M. Fuller, M. Pokras, and W.G. Hunt (Eds.) . Ingestion of Lead fr om Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Sears, J. 1988. Regional and Seasonal Varia tions in Lead Poisoning in Mute Swan Cygnus olor in Relation to the Distribution of L ead and Lead Weights in the Thames Area, England. Biological Conservation 46:115-134.

Sears, J. and A. Hunt. 1991. Lead Poisoning in Mute Swans, Cygnus olor , in England. Pages 383-388 in J. Sears and P.J. Bacon, editors. Wildfowl. Supplement 1, Third IWRB International Swan Symposium. The Wildfowl & Wetlands Trust and the International Waterfowl and Wetlands Research Bureau, Slimbridge, U.K.

Seng, P.T. 2006. Non-Lead Ammunition Program Hunter Survey. Final Report to the Arizona Game and Fish Department . Available at www.azgfd.gov/w_c/documents/Ammo SurveyFINALReport2-23-06_001.pdf.

Shillinger, J. E., and C. C. Cottam. 1937. The importance of lead poisoning in waterfowl.

Transactions of the North Amer ican Wildlife Conference 2:398-403.

Shore, R. 2009. Mystery of the Toxic Swans: Explores the Fraser Valley’s Avian EcoDisaster. Canadian Te levision documentary.

Sidor, I.F., M.A. Pokras, A.R. Major, R.H. Poppenga, K.M. Taylor, and R.M. Miconi. 2003. Mortality of Common Loons in New England, 1987 to 2000. Journal of Wildlife

Diseases 39:306-315.

Sileo, L., L. H. Creekmore, D. J. Audet, M. R. Snyder, C. U. Meteyer, J. C. Franson, L. N. Locke, M. R. Smith, and D. L. Finley. 2001. Lead poisoning of waterfowl by

contaminated sediment in the Coeur d’Al ene River. Archives of Environmental Contamination and Toxicology 41:364–368.

Simpson, J. 2001. Weighting Environmentally Fr iendly Metal Weight Alternatives for Change. Walleye In-Sider Magazine 12:56-57.

Simpson, V.R., A.E. Hunt, and M.C. French. 1979. Chronic Lead Poisoning in a Herd of

Mute Swans. Environmental Pollution 18:187-202.

Smith, M.C., M.A. Davison, C.M. Schexnider, L. Wilson, J. Bohannon, J.M. Grassley, D. K. Kraege, W.S. Boyd, B.D. Smith, M. Jord an, and C. Grue. 2009. Lead shot poisoning in swans: Sources of pellets within Whatco m County, WA, USA, and Sumas Prairie, BC,

Canada. Extended abstract in R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA. DOI 10.4080/ilsa.2009.020195 Snyder, N.F., H.A. Snyder, J.L. Lincer , and R.T. Reynolds. 1973. Organochlorines, Heavy Metals, and the Biology of North American Accipiters. Bioscience 23, 300-305

.

Soeder, D.J. and C.V. Miller. 2003. Ground-Wa ter Contamination From Lead Shot at Prime Hook National Wildlife Refuge, Su ssex County, Delaware. Water resources Investigation Report 02-4282. U.S. Geologica l Survey, Baltimore, Maryland. 26 pp.

Sorvai, J., R. Anitikainen, and O. Pyy. 2006. Environmental Contamination at Finnish Shooting Ranges – the Scope of the Problem and Management Options. Science of the

Total Environment 333:21-31.

Sparling, D.W., S. Krest, and M. Ortiz-Sant aliestra. 2006. Effects of Lead-Contaminated

Sediment on Rana sphenocephala Tadpoles. Archives of E nvironmental Contamination and Toxicology 51:458-466.

Staessen, J.A., R.R. Lauwerys, C.J. Bulpitt, R. Fagard, P. Linjen, H. Roels, L. Thijs, and A. Amery. 1994. Is a Positive Association Between Lead Exposure and Blood Pressure Supported by Animal Experiments? Current Opinion in Nephrology and Hypertension

3:257-263

.

Stansley, W. and D.E. Roscoe. 1996. The Uptake and Effects of Lead in Small Mammals and Frogs at a Trap and Skeet Range. Arch ives of Environmental Contamination and Toxicology 30:220-226.

Stansley, W., L. Widjeskog, and D.E. Roscoe . 1992. Lead Contamination and Mobility in Surface Water at Trap and Skeet Ranges. Bulletin of Environmental Contamination and Toxicology 49:640-647.

Stansley, W., M.A. Kosenak, J.E. Huffman, and D.E. Roscoe. 1997.Effects of LeadContaminated Surface Water From a Trap and Skeet Range on Frog Hatching and Development. Environmental Pollution 96:69-74.

Stevenson, A.L., A.M. Scheuhammer, and H. M. Chan. 2005. Effects of Nontoxic Shot regulations on lead Accumu lation in Ducks and American Woodcock in Canada.

Archives of Environmental Cont amination and Toxicology 48:405-413.

Stein, S. 1979. Lead shot poisoni ng in red-tailed hawks. 77 pp.

Stone, W.B. and J.C. Okoniewski. 20 01. Necropsy Findings and Environmental

Contaminants in Common Loons from New Yo rk. Journal of Wildlife Diseases 37:178-

184.

Strom, S.M., J.A. Langenberg, N.K. Busi nga, and J.K. Batten. 2009. Lead exposure in

Wisconsin birds. In R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.96 Stroud, R.K., and W.G. Hunt. 2009. Gunshot wounds: A source of lead in the

environment. In R. T. Watson, M. Fuller, M. Pokras, a nd W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Stutzenbaker, C.D., K. Brown, and D. Lobprie s. 1983. An assessment of the accuracy of documenting waterfowl die-offs in a Texas coastal marsh. Special Report. Federal Aid Project W-106-R, Texas Parks and W ildlife Department, Austin, Tex. 21 p.

Tanskanen, H., I. Kukkonen, and J. Kaija . 1991. Heavy Metal Pollution in the Environment of a Shooting Range. Geological Survey of Finland, Special Paper 12:187-

193.

Tataruch, F., and K. Onderscheka. 1981. Leve ls of environmental pollutants in wild animals in Austria (II)- amounts of lead and cadmium in the organs of European brown hare. Zeitschrift for Jagdwissenschaft 27:153-160.

Tavecchia, G., R. Pradel, J. Lebreton, A. R. Johnson, and J. Mondain-Monval. 2001. The effect of lead exposure on survival of adu lt mallards in the Camargue, southern France. Journal of Applied Ecology 38(6):1197-1207.

Thomas, V.G. 1997. The environmental and ethical implications of lead shot

contamination of rural lands in North America. Journal of Agricultural and Environmental Ethics 10(1):41-54.

Thomas, V.G. 2003. Harmonizing approval of nontoxic shot and sinkers in North America. Wildlife Society Bulletin 31(1):292-295.

Thomas, V.G., and Guitart, R. 2003a. Evaluati ng non-toxic substitutes for lead shot and fishing weights. Environmenta l Policy and Law 33(3-4):150-154.

Thomas, V.G., and Guitart, R. 2003b. Lead pollution from shooting and angling, and a common regulative approach. Environm ental Policy and Law 33(3-4):143-149.

Thomas, V.G., and Guitart, R. 2005. Role of international conven tions in promoting avian conservation through re duced lead toxicosis: progr ession towards a non-toxic agenda. Bird Conservation Internatio nal 15:147-160.

Thomas, V.G., and M. Owen. 1996. Preventing l ead toxicosis of European waterfowl by regulatory and non-regulatory means. Environmental Conservation 23(4):358-364.

Titus, K., T.L. Haynes, and T.F. Paragi. 2009. The importance of Moose, Caribou, deer and small game in the diet of Alaskans. In R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spen t Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.97 Tong, S., Y.E. von Schirnding, and T. Prapamontol. 2000. Environmental Lead Exposure: A Public Health Problem of Globa l Dimensions. Bulletin of the World Health Organization 78:1068-1077.

Trainer, D.O., and R. A. Hunt. 1965. Lead poi soning of waterfowl in Wisconsin. Journal of Wildlife Management . 29(1):95-103.

Trainer, D.O., and R. A. Hunt. 1965. Lead poisoning of whistling swans in Wisconsin. Avian Diseases 9(2):252-264.

Tranel, M.A., and R.O. Kimmel. 2009. Impact s of lead ammunition on wildlife, the environment, and human health—A literature review and implications for Minnesota. In R.T. Watson, M. Fuller, M. Pokras, and W.G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho,

USA.

Trautman, M.B., W.E. Bills, and E.L. Wickli ff. 1939. Winter losses fr om starvation and exposure of waterfowl and upland game birds in Ohio and other Northern states. The Wilson Bulletin 51(2):86-104.

Tsuji, L.J.S. and E. Nieboer. 1997. Lead Pell et Ingestion in the Fi rst Cree Nation of the Western James Bay Region of Northern Onta rio, Canada; Implications for a Nontoxic Shot Alternative. Ecosystem Health 3:54-61.

Tsuji, L.J.S., E. Nieboer, J.D. Karagatzid es, and D.R. Kozlovic. 1997. Elevated dentine

lead levels in adult teeth of First Nation people from an isolated region of northern Ontario, Canada. Bulletin of Environmenta l Contamination and Toxicology 59:854-860.

Tsuji, L.J.S., E. Nieboer, J.D. Karagatz ides, R.M. Hanning, and B. Katapatuk. 1999. Lead

Shot Contamination in Edible Portions of Game Birds and its Dietary Implications. Ecosystem Health 5:183-192.

U. S. Department of Health and Human Services (USDHHS). 1999. Toxicological profile for lead. Agency for Toxic Subs tances and Disease Registry, July 1999. Available at http://www.atsd r.cdc.gov/toxprofiles/tp13.pdf/.

United States Environmental Protection Agen cy (USEPA). 1994. Lead Fishing Sinkers: Response to Citizens’ Petition and Proposed Ba n; Proposed Rule. Fede ral Register Part III, Volume 40, part 745:11121-11143.

United States Environmental Protecti on Agency (USEPA). 1999. 1999-2000 RefugeSpecific Hunting and Sport Fishing Regula tions: Proposed Rule. Federal Register Volume 64, Number 154:43834-43854.98 United States Environmental Protection Ag ency (USEPA). 2001. Best Management Practices for Lead at Outdoor Shooting Ranges, EPA-902-B-01-001. U.S. Environmental Protection Agency, Division of Enfor cement and Compliance Assistance, RCRA Compliance Branch, New York. www.epa .gov/region02/waste/lead shot/epa_bmp.pdf.

United States Environmental Protection Ag ency (USEPA). 2004. Humans and Lead Fishing Sinkers. www.epa.gov/owowwtr1/fish/humans.html.

United States Environmental Protection Agen cy (USEPA). 2009. Lead Wheel Weights; Regulatory Investigation. Available at http://yosemite.epa.gov/opei/rulega te.nsf/byRIN/2070-AJ64?opendocument

United States Environmental Protection Agency. 2010. Request for comments on petition to phase out leaded aviation ga soline. http://www.ep a.gov/otaq/aviation.htm

United States Fish and Wildlife Serv ice (USFWS). 1999. Establishing “Lead Free Fishing Area” and the Prohibition of the Use of Certain Fishing Si nkers and Jigs Made With Lead on Specific Units of the National Wildlife Refuge System. Federal Register

64:17992.

United States Fish and Wildlife Service (USFWS). 2010. Nontoxic shot regulations for hunting waterfowl and coots in the U.S. Di vision of Migratory a nd Bird Management. http://www.fws.gov/migratorybirds /CurrentBirdIssues/nontoxic.htm

U.S. Geological Survey (USGS). 2008 Lead S hot and Sinkers: Weight y Implications for

Fish and Wildlife Health. USGS Press Release 7/11/2008

.

Valway, S.E., J.W. Martyny, J.R. Miller, M. Cook, and E.J. Mangione. 1989. Lead Absorption in Indoor Firing Range Users. Am erican Journal of Public Health 79:1029-

1032.

Veit, H.P., R.J. Kendall, and P.F. Scanlon. 1982. The Effect of Lead Shot Ingestion on the Testes of Adult Ringed Turtle Doves ( Streptophelia risoria ). Avian Dis. 27, 442-452

.

Ventana Wildlife Society (VWS). 2010. C ondor Reintroduction Notes from the Field. Available at http://www.ventanaw s.org/species_condors_fieldnotes/

Verbrugge, L.A., S.G. Wenzel, J.E. Bern er, and A.C. Matz. 2009. Human exposure to lead from ammunition in the circumpolar north. In R.T. Watson, M. Fuller, M. Pokras, and W.G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Victery, W. 1988. Evidence for Effects of Chr onic Lead Exposure on Blood Pressure in Experimental Animals: An Overview, Environmental Health Perspectives 78:71-76

.99 Vyas, N.B., J.W. Spann, and G.H. Heinz. 2001. Lead shot toxicity to passerines. Environmental Pollution 111 (1):135-138.

Vyas, N.B., J.W. Spann, G.H. Heinz, W.N. Be yer, J.A. Jaquette, and J.M. Mengelkoch. 2000. Lead poisoning of passerines at a trap and skeet range. Envi ronmental Pollution 107 (1):159-166

.

Vermeer, K., and D.B. Peakall. 1979. Trace metals in seaducks of the Fraser River Delta intertidal area, British Columbia. Marine Pollution Bulletin 10(7):189-193.

Wallace, B.M., R.J. Warren, and G.D. Gaines. 1983. Lead shot incidence in sandhill cranes collected from Alaska, Canada, a nd Texas. Prairie Naturalist 15(4):155-156.

Walters J.R., S. R. Derickson, D. M. Fry, S. M. Haig, J.M. Marzluff, and J.M. Wunderle,

Jr. 2010. Status of the California Condor and Efforts to Achieve its Recovery. Auk. In

Press

Washington Department of Fish and Wildlife (WDFW) 2000. Unpublished data. Available at http://wdfw.wa.gov/fish /papers/lead_fishing_gear/index.htm

Washington Fish and Game Association (W FGA). 2001. Report to the Washington Fish

and Wildlife Commission: the use of nontoxic shot for hunting in Washington. Washington Department of Fish and Wildlife Nontoxic Shot Working Group.

Watson, R.T. and D. Avery. 2009. Hunters and angl ers at risk of lead exposure in the

United States. In R. T. Watson, M. Fuller, M. Pokras, a nd W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Wayland, M. and T. Bollinger. 1999. Lead e xposure and poisoning in bald eagles and golden eagles in the Canadian prairie pr ovinces. Environmenta l Pollution 104:341-350.

Wayland, M., E. Neugebauer, and T. Bollinger. 1999.Concentrations of lead in liver, kidney, and bone of Bald and Golden eagles. Archives of Environmental Contamination and Toxicology 37(2):267-272.

Weimeyer, S.N., A.J. Krynitsky, and S.R. W ilbur. 1983. Environmental contaminants in tissues, foods, and feces of California condors. Pages 428-439 in S. R. Wilbur and J. A. Jackson (eds), Vulture Biology and Manage ment. University of California Press, Berkeley, California.

Weimeyer, S.N., J.M. Scott, M.P. Anderson, P.H. Bloom, and C.J. Stafford. 1988.

Environmental Contaminants in California Condors, Journal of Wildlife Management

52:238-247.100 Wetmore, A. 1919. Lead poisoning in waterfow l. U.S. Department Agr. Bulletin 793. 12

pp.

Whitehead, P.J. and K. Tschirner. 1991. L ead shot ingestion and lead poisoning of magpie geese Anseranas semipalmata foraging in a northern Aust ralian hunting reserve. Biological Conservation 58:99-118.

Wilson, I.D. 1937. An early report of lead poi soning in waterfowl. Science, New Series 86(2236):423.

Wilson, L.K., G. Grigg, R. Forsyth, M. Tolksdorf, V. Bowes, M. Smith, and A. Scheuhammer. 2009. Lead poisoning of Trumpete r Swans in the Pacific Northwest – Can recovered shot pellets help to eluc idate the source? Extended abstract in R. T. Watson, M. Fuller, M. Pokras, and W. G. Hunt (Eds.). Ingestion of Lead from Spent Ammunition: Implications for Wildlife and Humans. The Peregrine Fund, Boise, Idaho, USA.

Windingstad, R.M., S.M. Kerr, L.N. Locke, and J.J. Hunt. 1984. Lead Poisoning of Sandhill Cranes ( Grus Canadensis ). Prairie Nat. 16, 21-24

.

Wingstad, R.M. 1988. Nonhunting mortality in sandhill cranes. Journal of Wildlife Management 52(2):260-263.

Woolf, A., J.R. Smith, and L. Small. 1982. Me tals in livers of white-tailed deer in

Illinois. Bulletin Environmental Contamination Toxicology 28:189-194.

Yamamoto, K., M. Hayashi, M. Yoshimura, H. Hayashi, A. Hiratsuka, and Y. Isii. 1993. The prevalence and retention of lead pellets in Japa nese quail. Archives of Environmental Contamination and Toxicology 24:478-482.

Zdziarski, J.M., M. Mattix, R.M. Bush, and R. J. Montali. 1994. Zinc Toxicosis in Diving

Ducks. Journal of Zoo and Wildlife Medicine 25:438-445.

Zwank, P.J., V.L. Wright, P.M. Shealy, and J.D. Newsom. 1985. Lead toxicosis in waterfowl in two major wintering areas in L ouisiana. Wildlife So ciety Bulletin 13(1):17-

26.