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Wiesen, Liesl M.
Blood lead concentrations in the cat population of Tampa, FL
h [electronic resource] /
by Liesl M. Wiesen.
[Tampa, Fla] :
b University of South Florida,
ABSTRACT: Where lead pollutes urban soils, both human and animals risk exposure. This exposure gives rise to similar health risks across species. A group of 50 outdoor living cats from inner city Tampa, Florida were tested for blood lead concentration (BLC). Most cats had no measurable lead loads, 14 percent had levels less than or equal to 6 micrograms per decaliter. Soil samples were taken from the home location of each cat. None of these samples, which ranged from 2.6 microgram per gram to 170 micrograms per gram, had hazardous levels of lead. Overall, BLCs were lower than expected. In addition, the BLCs were lower than those found in older industrial cities. The reduction of the use of lead as well as Tampa's location in the newly developed Sunbelt, may be responsible for the overall low levels found in the region's outdoor living cat population.
Thesis (M.A.)--University of South Florida, 2006.
Includes bibliographical references.
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Adviser: Robert Brinkmann, Ph.D.
x Environmental Science and Policy
t USF Electronic Theses and Dissertations.
Blood Lead Concentrations In The Cat Population Of Tampa, Florida by Liesl M. Wiesen A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science Department of Environmental Science & Policy College of Arts and Sciences University of South Florida Major Professor: Robert Brinkmann, Ph.D. Sylvia Gografe, D.V.M., Ph.D. Graham Tobin, Ph.D. Date of Approval: February 13, 2006 Keywords: soil, street sweeping, urban pollu tion, lead toxicosis, animal sentinels Copyright 2006 Liesl Wiesen
Table of Contents List of Tables ii List of Figures iii Abstract iv Chapter One Introduction 2 Lead in Environment 2 Lead in Soil 5 Lead Pollution in Tampa 7 Human Health Effects 9 Animal Health Effects 13 Chapter Two Methodology 23 Study Area 23 Blood Lead Sampling 25 Street Sediment Sampling 28 Lab Analysis 30 Statistical Analysis 30 Chapter Three Results 32 Raw Data 32 Descriptive Statistics 38 Correlations 40 A Closer Look 41 Chapter Four Discussion and Conclusions 50 References Cited 58 i
List of Tables Table 1 Bureau of Land Management Limits on Lead in Soil for Land Management 5 Table 2 Clinical Symptoms of Lead Poisoning in Humans 11 Table 3 Exposure Routes for Animals 15 Table 4 Clinical Symptoms of Lead Poisoning in Animals 19 Table 5 Street Sediment Sites 33 Table 6 Blood Lead Concentrations a nd Street Sediment Lead Levels 35 Table 7 BLCs listed by Date Collected 37 Table 8 ANOVA and Regression of Transformed Data 41 ii
List of Figures Figure 1. Study Area 24 Figure 2. Cat Project Data Sheet 27 Figure 3. Study Area with Study Sites Marked 29 Figure 4. Highlighted Site s Mentioned in Text 38 Figure 5. Blood Lead Concentrations of Sampled Cats 39 Figure 6. Site #15-LW-05 43 Figure 7. Site #16-LW-05 44 Figure 8. Site #23-LW-05 45 Figure 9. Site #29-LW-05 46 Figure 10. Site #30-LW-05 47 Figure 11. Site #32-LW-05 48 iii
Blood Lead Concentrations in the Cat Population in Tampa, Florida Liesl M. Wiesen ABSTRACT Where lead pollutes urban soils, both hu man and animals risk exposure. This exposure gives rise to similar health risk s across species. A group of 50 outdoor living cats from inner city Tampa, Florida were te sted for blood lead concentration (BLC). Most cats had no measurable lead loads, 14% had levels 6 g/dl. Soil samples were taken from the home location of each cat. None of these samples, which ranged from 2.6 g/g to 170 g/g, had hazardous levels of lead. Overall, BLCs were lower than expected. In addition, the BLCs were lower than those found in older industrial cities. The reduction of the use of lead as well as Tampas location in the newly developed Sunbelt, may be responsible for the overal l low levels found in the regions outdoor living cat population. iv
1 Chapter 1 Introduction Lead pollution is geographically distribut ed along busy roadways and in older urban neighborhoods throughout the United States. The uses of leaded gasoline and lead paint are the most common sources of urban l ead pollution and are most often implicated as sources for both human and animal lead toxicosis. Exposure to urban soil lead pollution can cause a variety of physiological and neurological symptoms. While we know a great deal about lead poisoning and its distribution in the human population, the distribution of lead exposure in urban animal populations has not been widely studied. Cats, both feral and domestic, are a co mmon and wide-ranging urban animal. Where lead exists in the soil, cats should show exposure leve ls due to their behavior and feeding patterns. If human and animal expos ure risks are assumed equal, then a resident population of animals could serve as indicato rs of the health risks to humans in that neighborhood. In addition, we know very little about the risk to urban animals from lead pollution in cities. In order to assess the di stribution of blood lead levels in cats, blood lead concentrations were m easured in samples taken from 50 outdoor living cats that were collected from older neighborhoods in Tampa. Samples were obtained with the assistance of Hillsborough County Animal Services (HCAS) personnel. Soil samples from the streets at the home addresses of th ese cats were collected and tested for lead content.
2 Prior to reviewing the results of the res earch, I will examine some of the current literature on urban lead pollution a nd its health effects, with a closer regional look at lead in Tampa, Florida. Lead in the environment Lead is a naturally occurring metal (Irw in, et.al., 1997). Ev idence of the use of lead can be dated as far back as 7000 BC to the beginning of the development of metallurgy. Surface level lead contaminati on and lead intoxication, resulting from mining and fabrication, followed soon after and persists into modern times (Lessler, 1988). In the U.S., lead is the fifth most commonly used metal. It is used in many products including: construction material, piping, safety equipment, petroleum products, bearings, paint, ceramics, plastics, electronic devices, batteries, ammunition, solder, and other metal products and alloys (Irwin, et.a l., 1997). Additional commercial and recreational activities can release lead into the environment: sewage sludge containing lead is applied to soils, smelting adds lead to the air and water, the burning of fossil fuels releases lead into the air, lead based pestic ides were used in fruit orchards, wastes from mining and metal recycling operations leach into the soil, and lead is released at firing ranges and hunting preserves in the form of spent ammunition (Billus, 1999, Kilbourne, 1998, Irwin, et.al., 1997, Yokel and Delistraty, 2003, Aranguren, 1996, EPA, 2000). Perhaps the most damaging sources of lead pollu tion are leaded gasoline and lead paint. These two sources are the most often implicat ed sources of lead toxicosis in both humans and animals. While they are not widely used in the United States today, their impact is evident in polluted soils and sediments in most urban settings.
3 Leaded gas is created when tetramethy llead and tetraethyllead is added to gasoline to increase the octane rating, ther eby reducing engine knoc k. The lead is not burned within the engine but released as lead chloride via the exhaust. This airborne lead is then precipitated onto the surrounding wa ter and soil. The i mmediate effect of exhausted lead is air pollution; the legacy is soil pollution. It is estimated that by 1960, 200 million t ons of lead were used in gasoline (Irwin, et.al., 1997). As a result, higher levels of lead were deposited adjacent to roadways where vehicle use was dense. Urban areas, places where cars commonly accelerate, gas stations, and areas plagued by traffic jams, a ll can have potentially hazardous levels of lead contamination in the soil due to the use of leaded gas in the past (Aranguren, 1996). As the health effects of lead exposure became more apparent within the public health community, the U.S. petroleum industr y and the American public converted from leaded to unleaded gasoline (Irwin, et.al ., 1997). The introduc tion of the catalytic converter in 1975 reduced the use of leaded ga s. In 1986, lead content limits were put into effect. Unleaded gas may contain 0.013 grams of lead per liter; leaded gas may contain no more than 0.025 g /L. The 1990 Clean Air Act amendments prohibited the sale of leaded gas in the US for most uses (Irwin, et.al., 1997). By 1995, its use in the U.S. was reduced by 99.5% (Happel, 1995). Leaded gasoline can easily be absorbed via the skin, lungs an d gastrointestinal tract (Berny, et.al., 1992, Goodman and Gilman, 1975). The symptoms of leaded gas intoxication include weakness, fatigue, headach e, nausea, vomiting, and diarrhea (Irwin, et.al., 1997). The ease of absorption explains the correlation between leaded gas use and high blood lead levels (Kilbourne, 1998). Intere stingly, the decrease in the use of leaded
4 gas corresponded with a compar able decrease in human bl ood lead levels between 1976 and 1980 (CDC, 1991). Unfortunately the legacy of leaded gaso line will be long lasting. Lead is very stable in soils and tons of it was depos ited along roadsides where humans and animals continue to be exposed (CDC, 1991). Contam inated soil and leaded gasoline are still reported as sources in poisoning cases in the Un ited States as late as 1992 (Berny, et.al., 1992). Before lead was introduced into the ur ban environment via automobiles it was applied to structures in the form of lead paint. In 1977 the Consumer Product and Safety Commission limited the lead in paint to 0.06% down from a high level of 50% (Happel, 1995, Ramsey, et.al., 1996). Seventy four percent of homes in the U.S. built before 1980 have lead paint somewhere in the structure. This explains the prev alence of paint related lead poisoning cases (CDC, 1991). The Federa l Lead-Based Paint Poisoning Prevention Act requires the detection and control of lead paint in public and private buildings (Schierow, 1998). Various agencies within the U.S. a nd state governments developed regulations governing the use and presence of lead. A br ief look at these regulations reveals lead pollution as an issue of both national and lo cal concern. The Environmental Protection Agency lists lead as on e of the 25 most hazardous substanc es at Superfund sites. Lead is defined as a class B2 carcinogen and an an imal carcinogen (Irwin, et.al., 1997). The 1986 Safe Drinking Water Act prohibits the use of lead in pipes, solder, and flux in water systems for human consumption. Lead free pi ping is defined as 0.2% lead content in flux and 8% lead content in pipes. Another agency, the federal Bureau of Land
5 Management defined limits for lead levels in soil based on the likelihood of human or wildlife exposure. Concentrations below the li mits stated in Table 1 are not expected to cause adverse health problems. At the state level, Florida has set a water quality standard for lead in wetlands at 30 g/L (Irwin, et.al., 1997). All the regulations and pub lic health efforts aimed at reducing lead in the environment are largely successful. The CDC estimates a 37% reduction in lead pollution and reported an overall drop in cases of lead poisoning from 1976 to 1980 (Lessler, 1988). But leads behavior once it enters the environment and settles into soil and sediment is perhaps its most in sidious feature and the least studied. Table 1: Bureau of Land Management Limits on Lead in Soil for Land Management (From Irwin et. al. 1997). Species Lead Level Rabbit 44 mg/kg Mule deer 438 mg/kg Mallard 152 mg/kg Child camper 1000 mg/kg Lead in the soil Lead is very stable in soil and sedime nts (Billus, 1999). This means that once lead is deposited onto the soil surface it does not degrade; it has low solubility and only migrates by certain physical means. It ge nerally remains where it was deposited and
6 remains a health threat at that location (CDC, 1991, Turj oman and Fuller, 1987, Chow, 1970, Kilbourne, 1998, Brinkmann, 1994). Urban soils can acquire lead from leaded gas use and from paint on older structures. Even when an older home is removed from a site, the lead will remain in the soil (Aranguren, 1996). Along roadwa ys a general rule of lead deposition seems to apply: the higher the traffic volume, the greater the lead content of the soil. Factors such as wind direction, air turbulence, and road slope modify lead deposition to some extent (Chow, 1970). This soil based lead can find its way back onto the road by erosion processes. This street sediment can contain lead attached to fine sediment grains from throughout the local wate r shed. Road runoff then transports this contaminated sediment into local wa ter bodies (Brinkmann and Tobin, 2001). Lead can most often be found in the first 2 to 5 cm of soil. Retention can depend on organic content and soil pH (Irwin, et.a l., 1997, Turjoman and Fuller, 1987). A study of very early lead mining waste piles in Br itain found movement ra tes of 0 to 70 years per meter and pH seemed to be a principle dete rmining factor in the translocation of lead (Maskall, et.al., 1995). Tropical soils have not been studied as extensively but lead seems to behave similarly to temperate soils (Mogollon, et.al., 1997) In addition, an organic content greater than 5% retains lead. Thus, heavily vegetated areas retain more of the deposited lead than soils that are like ly to erode (Friedland and Johnson, 1985). Aquatic sediments also retain large amounts of the lead deposited in the water. In this way retention ponds can be used to cleanup road runoff before the water is released into another wetland. All in all, a significant amount of lead was deposited in U.S. soils. An estimation of the mean soil concentration of lead in the U.S. is 32 g/g (Irwin, et.al., 1997).
7 Despite the fact that lead is stable in soils and sediments, only a small portion of that lead is available to plants and organi sms (Maskall, et.al., 1995). Bioavailability can be affected by multiple factors. Particle size, chemical form and age of exposure are intrinsic characteristics that affect absorption. The older the lead deposit, the smaller the bioavailable portion (Yokel and Delistraty, 2003). The behavior of an organism and its access to soil can also affect the amount of lead absorption or ingestion that can occur (CDC, 1991). With some bioavailable lead in the roadsi de soil it can be expe cted to be in and on the roadside plants as well. Many types of plants can absorb lead (Mogollon, et.al., 1995). Grasses growing on roadsides have a hi gher lead content than grasses growing elsewhere (Chow, 1970). In addition, plant lead levels are influe nced by traffic volume and distance from roadways, similar to soil lead levels (M otto, et.al., 1970). Lead pollution in Tampa For the study area of Hillsborough County, Florida, the Toxic Release Inventory data show that74,894 pounds of lead a nd lead compounds were released in 2002 (USEPA, 2002). The Hillsborough County Health Department reports 103 cases of lead poisoning for the same year (Hillsborough C ounty, 2003). Several studies examine lead pollution in Tampa in more detail. In 1994, Brinkmann undertook a soil survey of certain residentia l areas of Tampa, Florida. Lead concentrations ranging from 0 to 9160 g/g were found. The higher concentrations were located in the older ne ighborhoods of Tampa. Brinkmann asserted
8 that this evidence of hazardous levels of lead in older areas of the city highlighted the need to look more closely at pollu tion issues in southern urban areas. In 1995, Happel continued this work by l ooking at lead concentr ations in Tampas neighborhoods from a socio economic perspectiv e. It is often noted that the higher incidence of lead poisoning of lower inco me children is not solely a matter of environment, but that income, housekeeping habits, and personal hygiene also play impact whether or not an individual is expos ed to lead. Happel studied three distinct neighborhoods defined by income and race : poor black, wealthy white, and median income and mixed ethnicity. She found hazardous levels of soil lead, defined as greater than 500g/g, in all three neighborhoods. He r study demonstrates that the process of gentrification often includes extensive renovation and rest oration of structures. Depending on age, these structures may contain lead based paint that is then released onto the surrounding soil. In addition, she found that high lead levels in soil are common in older areas of Tampa regardless of income levels. In 1996, Hafen and Brinkmann investigated soil lead levels along the interstate system that bisects Tampa. They confirme d that the distance from highly trafficked roads was correlated with soil lead levels. Th e highest levels occurred closer to the roadway. Hazardous lead levels, greater than 500 g/g, were found in half of the samples collected in the inters tate right of way. In Tampa, residential neighborhoods closely border the urban interstate system. This puts residents at risk from the lead that originates at the roadside. In 1998, Lewis returned to Tampas neighborhoods. She completed a detailed look at lead levels in soils within a portion of Port Tampa City. Lewis assessed homes of
9 different ages with varying lawn features su ch as sheds and fences. Predictably, high lead levels were found near older homes. In addition, lead was high near painted lawn features (i.e. sheds) and near new homes that replaced older structures. Finally in 1999, Billus studied the lead le vels in street sweepings collected from a variety of Tampa neighborhoods and industria l areas. Most samples contained lead levels ranging from 200 g/g to 1100 g /g This suggests that even though lead gasoline is no longer used, lead remain s a problem associated with roadways. Additional studies of the composition of street sediment conducted in 2001 found that lead occurs in street sediment regardless of the type of la nd use. Lead content in street sediment averaged 65 g/g across Tampa. Hazardous levels were not found in this series of studies (Brinkmann and Tobin, 2001). It is evident that lead pollution exists in soils and sediments in Tampa, Florida. Where lead exists, exposure risks exist. When leads stability in soils is taken into account, the exposure risk will exist for decad es. Residential areas by definition have humans in residence. Many of these i ndividuals end up with lead poisoning through normal screening processes. The Hills borough County Health Department reported 103 cases of lead poisoning for 2003 (Hillsboroug h County, 2003). Where humans live, their domestic animals live. The following secti on examines some of the health impacts of lead poisoning in humans and in animals. Human Health Effects Once lead enters the body, all of its actions are toxic. At a mo lecular level, lead interferes with chemical r eactions by binding with oxygen, nitrogen, sulfur, carboxyl and
10 phosphoryl groups (Li, et.al., 2003, Goodman and Gilman, 1975). Lead is a neurotoxin. It can disrupt glucose metabolism and energy production within the nervous system and it interferes with the action of neurotransmitte rs (Ballantyne, 1988). This accounts for the occurrence of neural symptoms in bot h lead exposure and lead toxicity. Lead, when orally ingested, is primarily absorbed through the lower intestine and the colon (Goodman and Gilman, 1975). It tr avels via the bloodstream to every system of the body and initially concen trates in the soft tissues (CDC, 1991). While in the blood stream, lead associates with the erythroc ytes and high blood lead concentrations can cause anemia (Goodman and Gilman, 1975). The body reacts to lead in the same way it reacts to calcium. Long term exposure to lead will result in bones with a high lead content (Irwin, et.al., 1997, Goodman and Gilman, 1975). Within the bone, high lead levels can inhibit the development of red bl ood cells in the bone marrow. Lead poisoning can be the cause of the symptom of anemia. Lead stored in the bones, under conditions of illness or pregnancy, can be released back into the blood stream. In these circumstances lead poisoning can reoccur (Le ssler, 1988). The biological half life for lead in bones is approximately ten years. Lead is naturally excreted from the body by urine and feces (Goodman and Gilman, 1975). A summary of the clinical symptoms of lead poisoning in humans is provided in Table 2.
11 Table 2: Clinical symptoms of lead poisoni ng in humans. Adapted from Irwin, et.al., 1997, CDC, 1991, Goodman and Gilman, 1975. Syndrome Symptoms Acute poisoning by ingestion Metallic ta ste, dry throat, thirst, abdominal pain, nausea, vomiting, diarrhea, constipation, peripheral circulatory collapse, neuromuscular symptoms, central nervous system symptoms (includes headache, insomnia, depression, coma, and death), kidney damage, hemolytic symptoms (includes anemia and hemoglobinuria) Lead encephalopathy due to chronic exposure Headache, insomnia, vomiting, visual disturbances, irritability, short term memory loss, restlessness, delirium, hallucinations, convulsions, coma, death from exhaustion and respiratory failure Lead poisoning w/o encephalopathy Decr eased activity, lethargy, anorexia, vomiting, abdominal pain, constipation Lead is a cumulative poison. Multiple small doses can be as detrimental as a single large dose (CDC, 1991). The cumulative dose that a person or animal receives over time depends on many factors: amount i ngested, duration of exposure, background exposure, type of lead, nutritional status, ag e, and season of the year (CDC, 1991). Lead poisoning cases seem to appear on a seasonal basis. Nutritional deficiencies in iron, calcium, protein and zinc can increase a pe rson or animals lead exposure symptoms (CDC, 1991). Acute lead poisoning is typi fied by a blood lead concentration (BLC) 100 g/dl. Even with treatment, permanent kidney and nerve damage may occur at these
12 levels. Lead poisoning without encepha lopathy generally occurs with a BLC 70 g/dl (CDC, 1991). Lead exposures below these levels can have biological effects as well. Currently these sublethal effects are more common th an outright poisoning and are of greater concern to health care officials and envir onmental professionals. Chronic low level exposure to lead can cause neurological problems, anemia, and kidney dysfunction (Irwin, et.al., 1997). In these situations, the immune system is suppressed, thus increasing susceptibility to infections (Goodman and Gilman, 1991). Chromosomal changes can occur with in male gonads (CDC, 1991). Pre gnant women, fetuses and very young children are especially vulnerabl e to low level lead exposure. The biological stress of pregnancy can cau se bone lead to be released into the mothers blood stream. Depending on the amount released, the woman may start to exhibit symptoms of lead poisoning. But even very small amounts of lead will effect natal development (Gulson, et.al., 2003). The developing brain will have fewer phospholipids, galactolipids, plasmalogen and ch olesterol. This means there is an overall decrease in brain weight and the number of brain cells (Ballantyne, 1988). After birth the infant continues to be exposed to maternal lead via milk (Goodman and Gilman, 1975). The resulting interference with neural and overall development can lead to the child having decreased intelligence, decreased grow th, poor hearing and posture, and a greater chance of being born premature and ha ving a low birth weight (CDC, 1991). The neural development alteration leads to behavioral and cognitive effects in children. Aggression and antisoc ial behavior is connected wi th lead exposure in early childhood (Li, et.al., 2003). Lead exposed chil dren can have lower IQs and lower school
13 success rates. A long term study in Australi a of children exposed to lead via a lead smelter found that the cognitive effects were only partially reversed by reducing blood lead levels (Tong, et.al., 1998) A BLC as low as 10 g/dl was associated with these detrimental effects (CDC, 2001). Ten g/dl is the current CDC threshold level, a BLC above this level should trigger remedial action. The Center of Disease Control and Prev ention (CDC) is at the forefront of the public health initiatives to prevent chil dhood lead exposure in this contry and the organization has a goal to eliminate it by 2010. The CDCs 1991 Preventing Lead Poisoning in Young Children lays out the agencys recommendations for monitoring and elimination of lead exposure. This re port marked the official lowering of the threshold level from 25 g/dl to 10 g/dl based on new scientific knowledge of lead effects at low exposure levels. The ultimate goal is to reduce all childrens BLC below the threshold mark. The health effects of low level lead exposure may seem minor, but cognitive deficiencies can affect a child thr oughout life. Population level effects are also a concern for the CDC. These possible populat ion level effects rais e concerns over lowlevel exposure in animals as well. Currently, blood lead concentr ation (BLC) measurements are the diagnostic test of choice for identifying low-level exposure cases (Fikes and Dorman, 1994). This is a standard test available at medical and vete rinary labs. There is a positive correlation between total body load and environmental e xposure to lead (Irwin, et.al, 1997). Blood lead concentrations increase by 3 to 7 g/dl for every 1,000 g/g lead in the contaminated soil source (CDC, 1991). Lead remains in the blood for about one month after exposure (Irwin, et.al., 1997). In addi tion, BLC will reach a maximum level with
14 constant lead exposure and therefore BLC can represent a chronic level of exposure as well as a short-term acute e xposure (Berny, et.al, 1994). Animal Health Effects Animals and humans share the exposure pathways and health effects of lead exposure. The domestic animals that share our homes and yards have the same or greater chance of developing toxic levels of lead e xposure as humans. Some health authorities recommend that if an animal is diagnosed w ith lead toxicity, child ren in that household should be screened for lead exposure. Conversely if it is known that owners have been exposed to lead, household animals should be screened (Dowsett, 1994). Population level concerns become important when wildlife is considered. Cognitive and reproductive problems can have devastati ng effects on local animal communities. A list of reported exposure pathways for animals is presented in Table 3.
15 Table 3: Exposure routes for animals. Adap ted from Berny, et.al, 1992, Irwin, et.al, 1997, EPA, 2000, Morgan, et.al., 1991. Exposure Possibility Lead Exposure Pathway Lead based paint Contaminated soils Processed food Lead tainted meat Time spent outside Wine bottles Caulking Oils and greases Solder Pottery Linoleum Roofing Nursing Lead ammunition Owners occupation Glazers putty Leaded gas Asphalt Polluted water sources Discarded batteries Lead water pipes Drapery weights Newsprint Rug padding Fishing sinkers Golf balls The toxic effects of lead can be found in all species. Lead pollution in aquatic environments negatively affects the resident fish. Even small amounts of lead increases mucous formation and fin erosion, interrupts metabolism, delays development and slows growth, alters behavior, and suppresses repr oduction (Irwin, et.al ., 1997). Amphibians absorb aquatic lead through their permeable skin. Highly contaminated water, from mining and highways for example, corresponds to high total body lead levels in the resident amphibians (EPA, 2000). Reproduction and development is impaired in these populations. Fewer larvae survive due to the competition between lead and oxygen uptake and due to an increased susceptibility to predation. A study of tadpoles from a wetland polluted by lead ammunition, for ex ample, revealed stunted tail growth, incurvation of the spine, edema and reduced body size (EPA, 2000).
16 Waterfowl are also affected by water polluted with lead ammunition. The exposure pathway is commonly the ingestion of lead ammunition as grit. Ingestion often leads to direct toxicity and death. It is es timated that 3 to 4 lead shots will kill a duck and that 10 will kill a goose (Irwin, et .al., 1997). Sublethal levels of lead exposure can cause neurological dysfunction, immune suppressi on, a decrease in reproductive function, thinner eggshells, and slower growth of chicks (Irwin, et .al., 1997, EPA, 2000). Direct lead poisoning deaths were recorded in many species of birds including: greater flamingos, trumpeter swans, canvasbacks, less er scaups, and spectacled eiders. Annual deaths of waterfowl in the U.S. caused by l ead shot ingestion was estimated in 1990 at 1.6 to 2.4 million animals (EPA, 2000). The us e of lead shot is now banned in many areas around the world. Wild mammals are primarily impacted by contamination of air and soil. Plants growing on roadsides absorb lead. When th ese plants are ingested by herbivores the animal absorbs a portion of the lead. The l ead can then work its way up the food chain (EPA, 2000). Researchers studying the lead st ored in the livers of small mammals found high body loads when animals were collected near high traffic roadways. A comparison was also done between urban and rural living insectivores. The urban animals had 11 to 367 g/g lead in the liver compared to 4.7 to 16 g/g in the livers of rural living animals (Irwin, et.al., 1997). Lead poisoning cases in urban zoo dwelling animals are linked to lead originating from highly trafficked roadways. Lead exposure risks are the same for do mestic animals as for wild animals and humans. Lead is an equal opportunity toxin. Livestock can be exposed in pasture or in the barn. In cattle, lead poisoning results fr om the ingestion of 6 to 7 mg/kg of lead
17 (Irwin, et.al., 1997). In horses, 3 to 4 mg/kg can cause acute lead poisoning. These doses are lower than acute toxic doses for humans (Lessler, 1988). A review of lead poisoning reports to the French national animal pois on hotline (Centre National DInformations Toxicologiques Veterinaires) revealed that 57% of calls involved cattle. In this set of cases, the exact source of the lead was mostly untraceable, but when the source was known, lead ammunition, paint and contamin ated soil were identified (Berny, et.al., 1992). Lead exposure in sheep can cause mis carriage and sterility ( Irwin, et.al., 1997). Studies of sheep pastured near the mines of mid-Wales found that ingesting contaminated soil was the main exposure pathway. Interest ingly, seasonal variati ons are noted. Higher levels of lead were found in both grass and sh eep in March and May. The reasons for the seasonality of lead pois oning are not known (Abrahams and Steigmajer, 2003). Among domestic animals, dogs and cattl e are most often treated for lead poisoning (Merck, 2002). In the veterinary fi eld little treatment or screening occurs for exposures that do not cause clinical signs As with humans, young animals are more susceptible to lead exposure (Merck, 2002, Ber ny, et.al., 1992). Adult dogs can absorb 5 to 10% of the lead ingested, whereas puppies can absorb 40 to 50% of the lead ingested (Fikes and Dorman, 1994). The level of lead that constitutes lead poisoning varies. Thirty-five to forty g/dl is the current level in veterinary medicine at which symptoms most commonly begin to manife st (Morgan, 1994, Berny, et.al., 1994). As in human medicine, new research is discovering advers e effects at blood lead concentration lower than previously expected. On average, dogs brought in for treatment in one Boston hospital had a BLC around 93 g/dl, cats 133 g /dl, birds 380 g/dl, and rabbits 280 g/dl. It should be remembered that these numbers resulted from the review of only one
18 hospitals records. Among the cases presente d to this hospital, 7 animals exhibited symptoms with BLC < 40 g/dl (Morgan, 1994, Morgan, et.al., 1991). Background levels in suburban dogs are approximately 5 to 10 g/dl. Berny, et. al. (1994) used 10 g/dl to define cases of lead poisoning in their series of studies of human and animal exposures. This is below symptom levels as they are currently unde rstood, but it enabled a direct comparison between the humans a nd animals within the study. As with livestock, in most cases the source of the le ad that caused poisoning is unknown. When it is known, paint is the most common source of lead toxicity (Morgan, et.al., 1991). Incidences of lead poisoning seem to have a seasonal aspect. The annual peak occurs in February and March with minor peak s in late summer and early fall. The true reason for this trend is not known. In the previously discussed Welsh sheep study, plant lead content increased during th is period. This would incr ease the amount of lead being ingested by grazing animals. Sunlight incr eases the production of vitamin D, which in turn could increase lead absorption. Highe r temperatures and more time spent outside will also increase lead exposure a nd absorption (Berny, et.al, 1992). As with humans, most of the total body bur den of lead in other animals is stored in bone, with a small portion in the kidneys and the liver (Fikes and Dorman, 1994). Nutritional status influences lead absorp tion and symptom manifestation (Merck, 2002). A low calcium and high fat diet increases th e bodys absorption of lead (Nafe, 1988). The gastrointestinal symptoms and the neur ological symptoms may appear in any combination (Turner and Fairburn, 1979). Cats tend to have more neurological effects, while dogs have gastrointestinal symptoms. Even with treatment and clinical recovery,
19 vascular damage in the brain and damage to the kidneys may be permanent (Nafe, 1988). The clinical symptoms of lead poisoning in animals are summarized in Table 4. Table 4: Clinical symptoms of lead poisoni ng in animals. Adapted from Turner and Fairburn, 1979, Fikes and Dorman, 1994, Irwin, et.al., 1997. Syndrome Symptoms Neurological Hyperexcitability, epileptic form convulsions, tremors, partial paralysis hyperesthesia, depression, cha nges in gait or posture, ataxia, blindness Gastrointestinal Anorexia, wasting, vomiti ng, constipation, diarrhea, thirst, kidney damage, contracted intestines, di scoloration of tongue and throat, immune system suppression Behavioral changes develop in animals as a result of lead exposure. This is an important symptom link with human lead to xicity. Lead exposure produces similar symptoms and effects in humans and animals; therefore it can be presumed that the emotional and cognitive changes are similar as well. Lead exposed animals can appear agitated and aggressive (Li, et.al., 2003). In rodents, lead exposure is linked to aggressive behavior. In 1983 a case study repo rted on sheep dogs that were poisoned by the paint in their kennels. The dogs became too agitated to work. Moving the dogs to a new kennel slowly restored the dogs workab ility (Nicholls and Handson, 1983). It is reported that lead poisoned dogs bark and cr y continuously, run without purpose in many directions, and indiscriminate ly bite at anything. Diffe rential diagnoses for lead poisoning include rabies and distemper (Fikes and Dorman, 1994). Cats experimentally dosed to a BLC of 20 to 80 g/dl exhibited an increase in predatory aggression. When
20 the cats were withdrawn from the lead contam inated diet the effect was reversed (Li, et.al., 2003). Animals can be exposed to lead duri ng gestation and lactation by the same mechanisms that work in humans (Luthman, et.al., 1992). Lead crosses the placenta and the blood brain barrier and is excreted in m ilk (Fikes and Dorman, 1994, Merck, 2003). Neonatal laboratory rats were exposed to lead in order to assess l eads effects on brain development and motor skills development. Exploratory behavior and coordination were negatively affected by lead exposure. Upon wit hdrawal of the lead, th e rats only partially recovered normal behavior patterns and abilities (Luthman, et.al, 1992) Cats may be less affected by the physical symptoms of lead poisoning. This is perhaps due to two factors. Feline sympto ms are nonspecific so misdiagnosis could be occurring, or cases may simply be under repo rted in the literature (Irwin., et.al., 1997, Hoffheimer, 1988). Cats seem to show symp toms at blood lead concentrations below that of symptomatic dogs. In a study of 8 lead poisoned cats; the BLCs were 10 to 30 g/dl (Hoffheimer, 1988, Fikes and Dorman, 1994). It is generally assumed that cats do not come in contact with lead as often as dogs due to the selectivity of their eating habits. Dogs are more likely to swallow foreign objects or chew on the woodwork, for example (Hoffheimer, 1988). Cats, however, have groom ing habits that may lead to unintentional ingestion of contaminated soil. Cleaning of coats, feet, and nails can include the ingestion of soil and paint (Hawke, et.al., 1992, Berny, et.al., 1995). Indoor cats are not entirely safe from exposure either. C ontaminated house dust is a common exposure source for both children and animals. Wi ndowsills are often identified as having the
21 highest lead levels of any indoor location (B erny, et.al., 1995). Outdoor cats, strays, and feral cats also can be exposed via the total body lead conten t of their prey. Two studies demonstrate that humans and animals have similar exposure opportunities; one in Boston, Massachusetts and one in Granite City, Illinois. In Boston, animal lead toxicity case data from 1 987 to 1992 were examined for clinical and demographic trends (Morgan, 1994). Th e veterinary hospital used a BLC of 40 g/dl to define a lead toxicity case. Mammals, bird s, and reptiles treated for lead toxicity had BLCs ranging from 40 to 620 g/dl with a mean of 120 g/dl. Fifty-nine percent of the cases had unknown sources of lead Thirty-four percen t of the cases traced the source of poisoning to lead paint. Demographically, ow ners that lived in low-income regions of the city presented the most animals with lead toxicity. A lead smelter in Granite City, Il l heavily contaminated the surrounding residential community (Berny, et.al., 1992, 1994, 1994a, 1995). After the smelter shut down in 1982, a long-term study of residents and their pets commenced. The researchers were interested if a correlation existed between human exposure levels and exposure levels of their pets and if there was a re lationship between soil contamination and the animals BLC. Could the animals act as sentinels for the human population? The CDC threshold level of 10 g/dl defined a case. This allowed comparison of animal cases to human cases. None of the 110 animals studied had BLCs > 35 g/dl, but 30% had a BLC > 10 g/dl. A significant co rrelation was found between hi gh BLC in pets and high BLC in their owners. An owner or family member was 6 times more likely to have a high BLC if a pet also had a high BLC. There was no significant difference between the number of cases of dogs and cats. The importa nt factor in the animals BLC was the time
22 spent outside. A significant correlation was found between BLC in both pets and owners and the homes environmental lead levels. The presence of lead paint, in addition to the high soil contamination, would further increase blood lead levels. In fact, the correlation for animal BLC with environmental levels was higher than that for their owners. The authors overall conclusions were that animal s did indeed share lead exposure risk with their owners; pets could be used as sentin els for lead exposure for their owners. It is clear from the above discussion that lead pollution is a se rious problem in the United States. It is also evident that lead is present in soils and sediments in Tampa and that individuals in the Tampa Bay area are tr eated for lead poisoning each year. What is unknown is whether or not animals in th e region are poisoned by exposure to lead pollution. The hypothesis of the thesis is that outdoor living cats in the city of Tampa do not have blood lead levels that indicate lead poisoning. In order to test this hypothesis, I examine the following research questions: Ar e outdoor living cats exposed to lead via the soil? Are their blood lead concentrations related to soil lead levels? If so, are there location attributes that influences these conditions? In order to address these questions, blood samples were obtained from 50 out door living cats from Tampa for blood lead concentration testing. In addition, street sediment samples were taken from each cats home address and tested for lead conten t. The following chapter reviews the methodology used to complete the study.
23 Chapter 2 Methodology This chapter reviews the methods used in the study and discusses the study area and why it was chosen. Study Area The study area is contained within the city limits of Tampa, Fl orida, a large city on the coast of west central Florida. The city covers 112.07 square miles and has a human population of 303,447. Previous studies id entified high levels of lead in soils and street sediment in the city. The work of Happel (1995), Brinkmann (1994), Hafen and Brinkmann (1996), and Billus (1999) indicate that older portions of the city have higher levels of lead in the soil than newer areas. Thus, the study area is focused within portions of the city that deve loped prior to 1940. The study area ( Figure 1) consists of U.S. Zip Codes 33602, 33603, 33604, 33605, 33606, 33607, 33609, 33610, 33611, 33614, 33615, 33619, 33629, 33634, and 33635. This area covers the Port of Tampa, Ybor City, the downtown business district, Seminole Heights, and Sulphur Springs. Land use is industrial, commercial, and residential and covers the original foundati ons of the city of Tampa (Jahoda, 1973). Twelve to thirty percent of the homes in the study area were built before 1940 according to 2000 census data ( http://factfinder.census.gov ).
25 Blood Lead Sampling Blood was collected from 50 randomly chosen cats by Hillsborough County Animal Services (HCAS). The animals were selected regarding the following exclusion criteria: 1) adult, 2) no b ites, 3) not owner surrendered, 4) no blood loss trauma, and 5) origin with the study area based on the zip c ode where the animal was collected. The cats were domestic shorthairs that were estimated to be adults in relatively good health. HCAS regulations excluded cats brought into the shelter for bite qua rantine. When cats are surrendered to the shelter, their owners have the option to exclude the animals from any research activities. To comply, this group of animals was not sampled. Since age and sex has not been found to be associated with increased BLC in cats (Berny, 1994), those parameters were not considered selection criterion. An analysis of lead toxicosis cases in dogs did not find any significant di fference between breeds. Breed differences are less obvious in cats. Nevertheless, only domestic shorthair cats were used in the study to prevent the possibility of breed diffe rences. This breed is the most commonly found outdoor living cat and thus their exclusive use in this study did not reduce the pool of cats available. Direct measures of the demographic char acteristics of the outdoor cat population in Tampa do not exist. However, HC AS does keep track of annual impoundment numbers. In 2003, Animal Services impounded 17, 240 cats, 54.5% of the total animals the organization handled. 15,881 of these cats were euthanized (Hillsborough County Animal Services, 2004). The cats utilized in this study were randomly selected out of a group of impounded cats destined for routine euthanasia Prior to death, experienced Animal
26 Services staff of the HCAS obt ained the blood samples. Cats were sedated with ketamine (10-20mg/kg), as per standard procedure prio r to euthanasia. A jugular puncture was done after cleaning the area w ith an alcohol swab. Blood wa s drawn into a glass whole blood tube with sodium heparin (72 USP freeze dried for lead determination 13x75mm, 5.0 ml draw Hemogard Brown Stopper; BD V acutainer Systems Preanalytical Solutions; Fisher Scientific International) and refrigerated (Li, et.al., 2003, Berny, et.al, 1994a). Each animal was identified by their Anim al Services impound number. HCAS staff provided weight, sex, age, loca tion of pickup, date of collect ion, and name of collector. All data were recorded on a standardized fo rm designed specifically for this study (Figure 2). Blood samples were drawn from January to May to avoid seas onal effects. All procedures were approved by the University of South Floridas Institutional Animal Care and Use Committee.
27 Zip codes: 33602, 33603, 33604, 33605, 33606, 33607, 33609, 33610, 33611, 33614, 33615, 33619, 33629, 33634, 33635 Give location address as completely as possi ble. Use more than one line if necessary. Clearly label tubes. Mix Well, any clots could affect results Refrigerate samples; call Liesl Wiesen @ 972-2000 ext 6386 or 234-3180 to pick up the samples and the data sheets. Figure 2: Data sheet provided to Hillsborough County Animal Services. Date Impound # Weight SexAge Location initials
28 Street Sediment Lead Sampling Street sediment samples were collected at each address from which a cat was sampled. Sites that supplied multiple cats were only sampled once, resulting in 40 sample sites (Figure 3). Sediment samples were taken on two successive Saturdays. The collection days had similar weather conditions and no large rain even ts occurred between dates. Sampling occurred at or near each addr ess. The actual loca tion of soil collection was determined by the physical conditions at each address. Every effort was made to collect at the curb directly in front of addre ss. In some cases, this was not possible, and soil was collected from nearby pavement marg ins, storm drains, and storm ditches. Approximately 100g of sediment was taken fr om each site and placed in a pre numbered plastic bag with an individual plastic spoon. Nitrile gloves were worn and changed between sites. Notes were made of the type of pavement configura tion, a description of the neighborhood and if any mammal (wild or do mestic) could be seen in the immediate vicinity. A handheld Magellan 315 GPS unit was used to obtain the site coordinates used later in map construction.
30 Lab Analysis Blood samples were submitted to Florida Department of Agriculture & Consumer Services Division of Animal Industry/Kissimm ee Diagnostic Lab in Kissimmee, Florida for analysis. The atomic absorption test is sensitive to 0.01g/g (1g/dl). EDTA, succimer, and pencillamine, all drugs used to treat lead toxicosis, can interfere with testing. Due to the origin of the cats used in the study, it was not anticipated that the animals had exposure to these drugs. As with any study, there is a range of possible human errors and other difficulties that could affect study outcome. Errors th at could occur during sample collection and delivery include misidentifications of cat orig in, mislabeling of tubes, storage problems, and delivery delays. The criteria for cats to be included in the study cannot account for undetected pregnancy in females and for cats that were abandoned by owners at a distance from their original home. Possible an alysis errors at the lab were safe guarded against by providing enough blood from each cat for two BLC tests. Street sediment samples were submitted to Millennium Laboratories, Inc. of Tampa Fl, which is certified by the National Environmental Laboratory Accreditation Conference (NELAC). EPA lead testing pr otocol #7421 was used using an atomic absorption furnace. Statistical analysis In this study, a blood result =>10 g/dl is considered a high BLC rating. Berny, et. al. (1994) uses 10 g/dl to define cases of lead poisoning in their series of studies of human and animal exposures. This is belo w symptom levels, as they are currently understood.
31 For each type of sample, standard descriptive statistics were calculated (mean, median, range, and standard deviation). Th e data were transformed to create normal distributions. A correlation coefficient was cal culated via simple linear regressions in order to gain an understanding of the relationship between BL C and street sediment lead. In addition, each site at which high BLC s or street sediment lead was examined in detail to assess whether or not there are loca l contributing factors to the elevated levels. Specifically, age of home, distance to major transportation route, and land use were examined.
32 Chapter 3 Results The results are in many ways unexpected. They demonstrate that lead pollution, as analyzed in this study, is quite low and th at there is no evidence of lead poisoning of cats in the population I studied. In this ch apter, the raw data for both BLC and street sediment lead is presented by location along w ith the general descri ptive statistics for each data set and the correlation statistics between BLC and street sediment lead. The problems and possibilities of the data are then discussed. The chap ter concludes with an examination of specific sites where cats were collected that are of particular interest. Specifically, the sites where BLC level between 1 and 6 g/dl and the highest and lowest values of the street sediment lead range ar e evaluated for any unique characteristics that may influence the results. The Raw Data The raw data are presented in Tables 5 and 6 organized by zip code and site number. Two facts about these data sets are immediately evident. First, only 8 out of 50 cats were found to have any measurable BLC. Four cats had BLC equal to 1 g/dl, 2 cats had 2 g/dl, and 1 cat each had 5 and 6 g/dl. The 42 remaining cat s, 84% of all cats sampled, had BLCs equal to 0. No cats had levels greater to or equal to 10 g/dl, which represents a case as previously defined. The cats of Tampa, at least those selected in my study, do not seem to be suffering from lead e xposure. Second, all of the sediment lead
33 levels are lower than the accepted hazardous level of 500 g/g. Lead levels in the collected street sediment ranged from 2.6 g/g dw to 170 g/g dw. Table 5: Street Sediment sites. Site number Zip Code Description Animals 01-LW-05 33635 Older trailer park, curb ed paved street 1 possum, 2 cats 02-LW-05 33615 Cul de sac housing development, paved street with cement ditches on both sides 03-LW-05 33615 Older development, drainage down road center 04-LW-05 33615 Older development, same as 03-LW-05, drainage down road center 2 cats 05-LW-05 33615 Apartment complex, uncurbed parking lot 1 cat 06-LW-05 33634 Duplex housing complex, paved with cement ditches on both sides 07-LW-05 33614 Older urban neighborhood, paved road with grass shoulder 08-LW-05 33614 Older urban neighborhood, close commercial development, paved with cement ditches on both sides 09-LW-05 33614 Older urban nei ghborhood, paved with grass shoulder 10-LW-05 33607 Older urban neighborhood, paved with cement ditches on both sides 11-LW-05 33605 Commercial, automotive, paved with curb, alley paved with dirt shoulder 12-LW-05 33603 Older urban nei ghborhood, paved with grass shoulder 13-LW-05 33604 Commercial empty lot, paved with curbs 14-LW-05 33604 Older urban nei ghborhood, brick with stone curb 15-LW-05 33604 Old neighborhood, I-275, paved with curbs only at corners 5 cats 16-LW-05 33604 Older urban nei ghborhood, paved with some curbing, near commercial 17-LW-05 33604 Older urban ne ighborhood, paved with grass/sand shoulder 1 cat, 1 dog,
34 Table 5: (Continued). Site Number Zip Code Description Animals 18-LW-05 33604 Older urban neighborhood, paved with cement drainage on one side 1 cat, 1 dog 19-LW-05 33604 50s neighborhood, house under renovation, paved with grass shoulder 20-LW-05 33607 50s neighborhood, paved with grass shoulder 21-LW-05 33602 Older urban nei ghborhood, brick with stone curb, corner lot 1 cat 22-LW-05 33607 Old neighborhood, paved with stone curb, near commercial 23-LW-05 33607 Older urban neighborhood, near commercial, abandoned property, paved with grass/sand shoulder 24-LW-05 33609 50s/60s neighborhood, near commercial, paved with grass shoulder 25-LW-05 33606 Infill condos in older urban neighborhood, paved with granite curb 2 cats 26-LW-05 33629 Renovated older neighborhood, paved with cement drainage both side 27-LW-05 33611 Older urban nei ghborhood, paved with sand shoulders 1 cat 28-LW-05 33605 Old neighborhood, redone cigar worker housing behind Cuesta Ray factory, paved with curbs 2 cats, 1 dog 29-LW-05 33605 Old neighborhood, paved with curb 30-LW-05 33610 Older urban nei ghborhood, paved with grass shoulder 31-LW-05 33610 New apartment complex, paved with curbed parking areas 32-LW-05 33605 Older neighborhood, paved with curbs 33-LW-05 33604 Older neighborhood, paved with sand shoulder 34-LW-05 33604 Older riverfront condos, paved street with sand shoulder 35-LW-05 33610 Commercial aluminum yard, paved parking lot, paved road with sand shoulder 36-LW-05 33610 Rural, paved with drainage ditches 37-LW-05 33619 Commercial, near residential, paved with drainage ditch (recently dug out) 38-LW-05 33619 Rural, paved with cement drainage both sides 39-LW-05 33619 New rural apartment complex, paved with curbed parking
35 Table 5: (Continued). Site Number Zip Code Description Animals 40-LW-05 33619 Rural, paved with grass median and cement drainage Table 6: Blood Lead Concentrations and Street Sediment Lead Levels. Zipcode Site Number BLC (g/dl) Lead (g/g dw) 33602 21-LW-05 0 5.7 33603 12-LW-05 0 74 33604 13-LW-05 0 65 14-LW-05 0 94 15-LW-05 2 29 16-LW-05 1 (cat1) 0 (cat 2) 18 17-LW-05 0 26 18-LW-05 0 8.8 19-LW-05 0 18 33-LW-05 0 (cat 1) 0 (cat 2) 13 34-LW-05 0 7 33605 11-LW-05 0 (cat 1) 0 (cat 2) 0 (cat 3) 56 28-LW-05 0 120 29-LW-05 1 (cat 1) 6 (cat 2) 2 (cat 3) 1 (cat 4) 55 32-LW-05 1 22 33606 25-LW-05 0 23 33607 10-LW-05 0 74 20-LW-05 0 (cat 1) 0 (cat 2) 14 22-LW-05 0 160 23-LW-05 0 (cat 1) 5 (cat 2) 2.6 33609 24-LW-05 0 30 33610 30-LW-05 0 170 31-LW-05 0 21 35-LW-05 0 41
36 Table 6: (Continued). Zipcode Site Number BLC (g/dl) Lead (g/g dw) 36-LW-05 0 67 33611 27-LW-05 0 8.2 33614 07-LW-05 0 12 08-LW-05 0 16 09-LW-05 0 8.9 33615 02-LW-05 0 5.1 03-LW-05 0 3.3 04-LW-05 0 (cat 1) 0 (cat 2) 4.7 05-LW-05 0 7.6 33619 37-LW-05 0 47 38-LW-05 0 17 39-LW-05 0 3.5 40-LW-05 0 31 33629 26-LW-05 0 11 33634 06-LW-05 0 3.2 33635 01-LW-05 0 9 Table 7 presents the BLC data organi zed by sampling date. Previous studies demonstrated that there is a seasonal fluctuat ion in blood lead concentrations, with peaks in the spring and fall. The data collected from the Tampa cats seem to illustrate the spring peak. Blood samples were taken from January 2005 to May 2005. All the cats that produced BLC of 1 to 6 g/dl were sampled in February and March.
37 Table 7: BLCs listed by date collected. Date BLC (g/dl) Date BLC (g/dl) 1/20/05 0 3/25/05 0 1/26/05 0 3/28/05 0 1/26/05 0 3/28/05 0 2/16/05 2 3/29/05 0 2/23/05 1 3/29/05 0 2/26/05 0 3/30/05 0 2/28/05 0 3/31/05 0 3/2/05 5 3/31/05 0 3/3/05 1 3/31/05 0 3/3/05 0 4/4/05 0 3/7/05 0 4/4/05 0 3/9/05 0 4/5/05 0 3/9/05 0 4/19/05 0 3/9/05 0 4/19/05 0 3/9/05 0 4/19/05 0 3/9/05 1 4/19/05 0 3/9/05 6 4/22/05 0 3/9/05 2 4/22/05 0 3/15/05 1 4/28/05 0 3/21/05 0 4/28/05 0 3/21/05 0 5/5/05 0 3/25/05 0 5/5/05 0 3/25/05 0 5/5/05 0 3/25/05 0 5/5/05 0 3/25/05 0 5/5/05 0 The highlighted site numbers in Figure 4, which represent the locations that produced a positive BLC level and/or the lowest and highest street sediment lead levels, will be discussed individually later in this chapter.
39 Descriptive Statistics The blood lead concentrations found in this group of 50 outdoor living cats were predominantly zero. Figure 5 presents a fr equency graph of the BLC data. With 42 cats having a BLC = 0, the median of the data set is 0. The mean BLC is 0.4 g/dl with a range of 6 g/dl. The standard deviation is 1.2. The data were not normally distributed and required a logarithmic transformation in order to complete appropriate statistical analysis (Glantz and Slinker, 2001). After log transformation of the nonzero BLC values, the mean is 0.26 with a standard deviation of 0.32. All BLCs were below the previously defined case level of 10 g/dl. No cases of significant lead expos ure, as previously defined, were identified in this study. 0 5 10 15 20 25 30 35 40 45 01234567 BLC (microgram/dl)frequency Figure 5: Blood Lead Concentrations of Sampled Cats. The street sediment lead levels found at the 40 locations has a mean of 34.9 g/g dw. The median of the raw data set is 19. 5 and has a range of 167.4 g/g lead. The
40 standard deviation is 41.1. After log tran sformation of the 40 lead values, the mean equals 1.26 and the standard deviation is 0.5. All lead levels are below the accepted hazardous level of 500 g/g. Method detection limits, as reported by the lab, ranged from 0.021 to 2.7. Correlations Using SAS 9.1, simple linear regres sions and ANOVAS were run using the raw data and the log transformed data. Street sediment lead was used as the independent variable and BLC as the dependent variab le. No significant association was found between street sediment lead and BLC in eith er regression. Because both raw data sets (BLC and street sediment lead) do not sati sfy the basic data assumptions needed for regression (linearity, normality, and constant variance) the regression using the untransformed data is statistically meani ngless. The data sets generated by log transformation of the raw data meet these assumptions. The transformed data improved the regression as illustrated by the P va lue of the overall F test (raw P = 0.9375, transformed P = 0.3926). The P value represen ts the probability of observing a value as extreme or more extreme than the observed value. A low P value is preferred. The transformed data produced a correlation coefficient of 0.35 (R2 = 0.1238). R2 represents the coefficient of determination, the square ro ot of which is the correlation coefficient. The coefficient of determination measures th e fraction of the variance in the dependent variable that the regression model explains. An R2 equal to 1 would mean that the model fully explains the variance of the dependent variable. An R2 of 0.1238 leaves 87% of the variance in the blood lead concentrations unexplained. The full SAS output of the ANOVA and the regression of the transformed data are presented in Table 8.
41 Table 8: ANOVA and Regression of Transformed data. Source DF Sum of SquaresMean Square F ValuePr >F Model 1 0.48254 0.48254 0.85 0.3926 Error 6 3.41405 0.56901 Corrected Total7 3.89659 Root MSE 0.75433 R-Square 0.1238 Dependent Mean 0.59844 Adj R-Sq -0.0222 Coeff Var 126.04957 Variable DF Parameter Estimate Standard Error T value Pr > |t| Intercept 1 1.42175 0.93297 1.52 0.1764 X 1 -0.25012 0.27161 -0.92 A Closer Look Six sites containing either the highest BL C or the highest lead concentration in street sediment are discussed below. By taki ng a closer look at the si x sites, local factors may emerge that affect the lack of correla tion between street sediment lead and cats BLCs. Three of these sites produced a cat or cats with a BLC greater than zero. One site produced one cat with a BLC of 5g/dl and had the lowest street sediment lead (2.6 g/g) in the group. One site represents the highest street sediment lead (170 g/g) in the group but the corresponding cat had a BLC equal to zer o. All of the chosen sites have a land use classification of residential. Even though the study clearly demonstrates that low levels of lead are found in blood samples colle cted from outdoor living cats and from site
42 sediment, it is unclear why certain cats had relatively high blood lead levels and whether or not particular characteri stics of the vicinity where the cats were living have any influence on the blood lead levels. Each of the six sites is described using basic geographic characteristics including age of st ructure, type of construction, and local subdivision. All information presented below pertaining to the year the structure was built, and the construction type was obtai ned from the Hillsborough County Property Appraisers Office ( www.hcpafl.org ). The six chosen sites, discussed in detail below, are all from areas where structures date from before 1957. The sites are older than the collective mean and median building age of the sample population. Thus higher soil lead levels and lead exposure risk based on building age, a factor which is used by many agencies as a predictor of risk, was expected.
43 Figure 6: Site #15-LW-05. Site # 15-LW-05 is located in West Central Tampa, a neighborhood with paved streets and curbed corners (Figure 6). Th e address is located approximately 140 feet from I-275. The property contains a wood frame, 10 unit apartment house built in 1923. The one cat sampled from this site had a BLC of 2 g/dl. The street sediment collected from the site contained 29 g/g dw lead. Five cats were observed at or near the address.
44 Figure 7: Site #16-LW-05. Site #16-LW-05 is located in the Irvington Heights neighborhood of Tampa. The streets are paved but are without curbs (Figur e 7). This site contains wood frame home built in 1957. The home and its neighbors are poorly kept and are located a block from commercial development. Two cats were samp led from the site. One had a BLC of 1 g/dl and the other had 0 blood lead. The st reet sediment collected from the site contained 18 g/g dw lead. No cats were observed at the site.
45 Figure 8: Site #23-LW-05. Site #23-LW-05 is located in West Tampa, a neighborhood with paved streets without curbs (Figure 8). The home on this property was built in 1949 and is covered with vinyl siding. A commercial building a nd an abandoned property flank the site. The two cats sampled from the site had BLCs of 0 and 5 g/dl. The street sediment collected from the site contained 2.6 g/g dw lead. Intriguingly, this site provided the lowest lead level collected and the s econd highest BLC recorded.
46 Figure 9: Site #29-LW-05. Site #29-LW-05 is located in the Ybor Heights neighborhood of Ybor City with paved streets with curbs (Figure 9). Th e wooden house on this property was built in 1930. The four cats sampled from the site had BLCS of 1, 6, 2, and 1 g/dl. The site produced the highest BLC out of all 50 cats samp led. The street sediment collect from the site contained 55 g/g dw lead.
47 Figure 10: Site #30-LW-05. Site #30-LW-05 is located in the Semi nole Heights neighborhood of Tampa. The streets are paved streets without curbs (Figure 10). The prope rty contains a house built in 1955 of concrete block. The cat sampled from this site had a BLC of 0. However, this site produced the highest soil lead level of 170 g/g dw.
48 Figure 11: Site #32-LW-05. Site #32-LW-05 is located in the Su lphur Springs neighborhood and has paved streets with curbs (Figure 11). The wood fram e house on this property was built in 1952. The cat sampled from this site had a BLC of 1 g/dl. The street sediment collected from the site contained 22 g/g dw lead. This property is located approximately a block from railroad tracks. There are some commonalities and differe nces among the six homes selected for detailed analysis. All of the six homes we re built between 1923 and 1955. Lead paint was in widespread use in homes during this period. Four of the six properties are adjacent to major transportations routes (int erstate highway and railroad) or commercial development. These routes could be additional sources of lead.
49 The age of the buildings located at site can be used as an indicator of the likelihood of lead being found in and around th e structure. According to the CDC, 74% of the homes in the U.S. built before 1980 ha ve lead paint somewhere in the structure (CDC, 1991). The average age of the buildi ngs on the all 40 study sites is 28.28 years. The median year built is 1969. The six chosen sites are all older than 1957. These sites are older than the collective mean and median building age, thus higher soil lead levels and lead exposure risk is associated with building age.
50 Chapter 4 Discussion and Conclusions Based on the data, the h ypothesis that outdoor living cats in Tampa do not have lead poisoning is true. However, it must be st ated that the sample (n=50) is small. Yet other information can be extracted from the research. Are outdoor living cats exposed to lead via the soil? Based on the data collect ed in this study of the outdoor living cat population in Tampa, soil based lead is not a significant hazard to resident felines. Only 8 out of 50 cats were found to have any measurable BLC. 84% of all Tampa cats sampled had BLCs equal to 0 and none of the cats had levels greater to or equal to 10 g/dl. Are blood lead concentrations related to soil lead levels? While such a relationship has been found in other studies no significant correla tion was found between lead levels in street sediment and the BL Cs found in the cats. The transformed data produced an R2 = 0.1238. This leaves 87% of the variance in the blood lead concentrations unexplained. What are the possible factors affecting the data? First, mathematically, there are too few non zero BLC data points for meaningf ul comparisons to be made to street sediment lead. The total sampling time ran from Ja nuary to May, but all positive BLCs occurred in February and March only. S econd, more accurate sourcing of the cats may improve the accuracy of the relationship between lead exposure and BLC. In this study,
51 the information provided by HCAS and the ow ner surrendering the cats was trusted. There is no way of knowing the accuracy of this information or the duration of the cats residency at that address. Third, lower leve ls of lead than expected were found in the street sediment. It is interesting to note th at several studies carried out in the areas of Tampa in the 1990s found some of the same ar eas with hazardous levels of lead in the soil and street sediments. The reduced leve ls found in this study ten years later, could indicate a reduction in lead exposure risk. There are imperfections in blood lead te sting as well. Methodology may not be sensitive enough to be reliable at low lead leve ls. Individual labs can vary in accuracy and methodology (CDC, 1991). BLC will not be representative of the length of exposure or the total lead burden in the body (Fikes and Dorman, 1994). Nevertheless, blood lead testing is the standard method used to measure human exposure to lead. These results may seem unexpected, but tr ends toward lower BLCs and lower soil lead pollution have been found worldwide. The cause or causes of these trends is commonly thought to be changing environmenta l policy, i.e. the banning of leaded gas, and aggressive public health monitoring. The CDC has tracked a reduction in human blood lead concentrations since 1975. In addition, the National Health and Nutrition Examination Survey (NHANES) found a decrease in BLCs in all age groups and in all racial/ethnicity groups. From 1976 to 1994, th e number of children 1 to 5 years of age with BLCs 10 g/dl decreased from 77.8% of the population to 4.4% (CDC, 2005). More recent data show a con tinuation of this downward trend. In 1997, 130,512 children were reported to have elevated BLCs. By 2001, this number was 74,887 children (CDC, 2003). For the entire U.S. population duri ng the period 1999 to 2002, the percentage of
52 elevated BLCs was 0.7%. The geometric mean of the blood lead levels for the human population in 1991 to 1994 was 2.3 g/dl and in 1999 to 2002 it was 1.6 g/dl (CDC, 2005). At the state level, researchers st udying New York State children born between 1994 and 1997 found that BLCs decreased by 44%. In 1994, 6.9% of children had elevated blood lead levels compared to 3.9% in 1997 (Haley and Talbot, 2004). To compare these percentages and means to those obtained in the current study, 16% of the Tampa cats had some measurable blood lead leve l. None of the cats had elevated lead levels that indicate dangerous exposures. Perh aps the lack of lead poisoning is directly related to the overall decrease in lead in the environment. Decreases in soil lead levels and in lead deposition rates correspond to these recorded decreases in blood lead levels. Pr evious studies of soil samples in Tampa, Florida found hazardous levels of lead. The Hafen study in 1996 of soil lead levels along the local interstate highway system examined 224 samples, one third of which contained lead levels greater than 500 g/g. The mean of the lead level found was 317 g/g. The Billus study of Tampa street sweepings undert aken in 1999 found hazardous lead levels in 2% of samples. The mean of the lead level found was 65 g/g. By contrast, this current study found no samples with lead levels greater than 500 g/g. The mean of the lead levels is 1.26 g/g Over the period of a decade, the average lead level in soil samples decreased by 79%. Other studies illustrate that Tampas is not a unique case. Similar decreases in lead levels and/or de position rates have been found in road dust, sediment cores, peat bogs, mosses, and clam shells. An examination of Pb/Ca ratios in North Carolina clam shells dating from 1949 to 2002 showed a lead peak in the late 1970s a nd a slow but steady decline in lead since
53 1982 (Gillikin, et.al., 2005). The authors of the study account the removal of leaded gas from use in the U.S for the decline. In the U. K., a study of lead levels in street sediment during 1999 and 2000 showed a reduction in lead levels. Leaded gas was removed from use in the U.K. in January 2000 (Massadeh and Snook, 2002). Patroon Creek, NY has been heavily impacted by industrial polluti on. An examination of sediment cores revealed a decline in lead deposition rates resulting from the 1984 shutdown of a National Lead Industries plant (Arnason and Fletcher 2003). Mosses in Fi nland show decreasing lead concentrations following the banning of lead ed gas in that region (Poikolainen, et.al., 2004). Finally, a study of lead levels in pe at bogs in the Czech Republic found a peak in lead deposition around 1980 that corresponds to a regional peak in coal mining. Deposition rates have declined with the introduction of unleaded gas starting in 1990 (Novak, et.al., 2003). This brief overview of international inqui ries into modern lead pollution research has already alluded to the proposed causes of this ever improving state of the environment with respect to lead pollution. The story of lead pollution is illustrative of the effectiveness of environmental regulation when coupled with a strong public health initiative. Time and again, studies find marked downward trends in BLCs and soil lead that corresponds to the regional banning of leaded gas. Sec ondarily, the removal of lead paint from homes is considered a contribu tor (Haley and Talbot 2004). According to CDC figures, the number of homes built before 1950 which are likely to contain lead paint, has decreased from 27.5 million in 1990 to 25.8 million in 2000 (CDC, 2003). These policies, coupled with aggressive health monitoring progr ams, affect cities such as Tampa. The success of removing l ead from gas and paint, and reducing other
54 sources of lead pollution has positive implications for Tampas cats and other domestic animals. Outdoor living cats have a low ri sk of accumulating high doses of lead from ingesting soil during grooming activities. They do not run the risk of suffering long term health effects due to lead toxicosis. The neurological, mental, and behavioral development of kittens is not impeded by the effects of lead. Juveniles and adult cats should not have the cognitive and reproductive problems associated with lead exposure. The reduction of the use of lead may be res ponsible for the overall low levels of lead found in the regions outdoor livi ng cat population. Overall, lead seems to pose less of a risk to wildlife and domestic an imals than previously thought. As with most scientific inquiries, this study raises as many new possibilities as answers to the original questions. This study was designed using the assumption that some cases greater than or equal to 10 g /dl would be found in a random sample of 50 cats. This assumption proved to be wrong. While this is positive news about the environmental quality of the city of Tampa, this assumption resulted in a lack of statistically significant correlations. A larger study with better sourced cats, with owner and vet cooperation, is needed to better establish the re lationship between exposure to street sediment lead and feline BLC. In this study blood samples were taken from the cats over the shortest possible time. This was done in order to minimize any seasonal effects on the BLCs. However some hint of seasonality may have appeared in the data. The total sampling time ran from January to May, but all positive BLCs occurred in February and March. The sampling of more cats during this two month period may produce more BLCs greater than zero. Conversely, a long itudinal study of feline BLCs over a period of years may be
55 useful in illuminating possible seasonal trends any trends in overall BLCs over the span of years, and help pinpoint the relationship between soil lead exposure and the cats blood lead levels. There is another aspect to this study be sides an investigatio n into the possible effects of lead pollution on an urban cat population. This study looked at cats housed by the local animal control agency. This is a first look at a previously unstudied population of shelter cats and th is lack of knowledge is both a hi ndrance and an opportunity. While making inquiries concerning the cats and bl ood sampling for this study, it was discovered that while various solutions to feline populati ons control are advocat ed and studied, very little is known about the general population as a whole. For example, an accurate estimate of the feline population of Hillsbor ough County was not available. How this population was related in size to populations in the other coun ties of Florida is also not known beyond the level of the educated guess. Domestic cat home ranges can vary widely, but for females in urban settings home ranges can average around 0.27 ha and 0.29 ha (0.0010 and 0.0011 square miles). Urban males have larger ranges, approximately 4 ha (0.0154 square miles). Home range size depends on food availability and location and in the case of males, on breeding status (Turner and Bateson, 2000). Using these appr oximations, the study cats represent the soil lead pollution of the neighborhood and mi crowatershed surrounding their home addresses. It should be noted though that the demographics and movement patterns of the urban cat population in Tampa is not known. Further research in to this particular population will provide a more accurate popula tion estimate and an improved picture of urban cats in a southern city.
56 This cat population information would be critical in evaluatin g the usefulness of cats as an animal sentinel for environmental h ealth issues. The use of animal species to investigate exposure risk for human populat ion has some advantages over direct monitoring of human health. Animal monito ring may have lower associated costs and provide researchers easier acce ss to subjects. In choosing an appropriate species for monitoring the population should be widely distributed over the area in question, producing more uniform monitoring of exposur e risk over the area than human sampling may provide. Such investigations, in additi on to providing useful information for human health and safety, will lead to greater knowledge of common species. The research would require interdisciplinar y cooperation among the fields of veterinary medicine, human medicine, zoology, and environmental scie nce. But investigations into the use of animal sentinels are rare and have produced mixed results. The Berny studies in Granite City, Ill made use of dogs and cats and found that animal exposure risk was a good indicator of the exposure risk of their ow ners (Berny, et.al., 1992, 1994, 1994a, 1995). Pigeon populations have been used as sentin els in urban and industrial environments. However, the lead levels in the tissues a nd feathers of the urba n pigeon population of Seoul and Ansan, Korea did not significantly correspond to atmospheric lead levels (Nam, et.al., 2004, 2004a). In conclusion, this study looked at the concentration of lead in blood samples obtained from 50 outdoor living cats from older neighborhoods in Tampa. Only 8 of these cats had any measurable BLCs. Afte r log transformation the mean BLC is 0.26 g/dl. Seeking to investigate the correlati on between the lead in the environment with the lead accumulated by the cats, 40 street sediment samples were taken from the
57 locations from which the cats were collected None of the samples had hazardous levels of lead. The mean lead is 1.26 g/g after log transformation. Using the log transformed data an R2 of 0.12 was obtained by regression analysis There is no statistical correlation between street sediment lead levels and the BLC of cats. By taking a closer look at the location at which cats had any measurable BLC, the age of housing emerged as a possible indicator of exposure risk. The very low inci dence of measurable l ead in the blood of the sampled cats leads to the conclusion that lead is not a significant threat to feline health in Tampa.
58 References Cited Abrahams, P. and Steigmajer, J. 2003. Soil ingestion by sheep grazing the metal enriched floodplain soils of Mid-Wales. Environmental Geochemistry and Health 25:17-24. Aranguren, F. 1996. The spatial distribution of lead contamination in roadside soils of Trujillo City, Venezuela. Masters Thesis. Arnason, J.G., and Fletcher, B.A. 2003. A 40+ year record of Cd, Hg, Pb, and U deposition in sediments of Patroon Re servoir, Albany County, NY, USA. Environmental Pollution. 123(3):383-91. Ballantyne, B. 1988. Perspectives in Basic and Applied Toxicology. Butterworth & Co. Ltd., London. Berny, P., Cote, L., and Buck, W. 1992. Case reports of lead poisoning in dogs from the National Animal Poison Control Center a nd the Centre National DInformations Toxicologiques Veterinaires: Anecdote or Reality? Veterinary and Human Toxicology 34(1):26-31. Berny, P., Cote, L. and Buck, W. 1994. Lo w blood lead concentration associated with various biomarkers in household pets. American Journal of Veterinary Research 55(1): 55-62. Berny, P., Cote, L. and Buck, W. 1994a. Re lationship between soil lead, dust lead, and blood lead concentrations in pets and their owners: evaluation of soil lead threshold values. Environmental Research. 67: 84-97. Berny, P., Cote, L. and Buck, W. 1995. Can household pets be used as reliable monitors of lead exposure to humans? The Science of the Total Environment. 172: 163173. Billus, M. 1999. Investigation into the appl ication of street sweeping waste as a soil amendment. Masters Thesis. Brinkmann, R. 1994. Lead pollution in soil s adjacent to homes in Tampa, Florida. Environmental Geochemistry and Health. 16 (2): 59-66. Brinkmann, R. and Tobin, G. 2001. Urban sediment removal: the science, policy, and
59 management of street sweeping. Kluwer Academic Publishers, Boston. Census 2000. http://www.census.gov/geo/www/tractez.html on 10/18/03 Centers for Disease Control. 1991. Prev enting lead poisoning in young children. Downloaded from www.cdc.gov/nceh/lead/publicatio ns/plpyc/contents.htm on 6/9/03 Centers for Disease Control. 2001. Blood lead levels in young children United States and selected states. 1996 1999. Journal of the American Medical Association. 285: 286 287. Centers for Disease Control. 2003. Surveill ance for elevated blood lead levels among children United States, 1997-2001. MMWR Surveillance Summaries. 52(SS10):1-21. Centers for Disease Control. 2005. Blood lead levels United States, 1999-2002. MMWR weekly. 54(20):513-516. Chow, T. 1970. Lead accumulation in roadside soil and grass. Nature 225: 295-296. Dowsett, R. and Shannon, M. 1994. Childhood plumbism identified after lead poisoning in household pets. The New England Journal of Medicine. 331 (24): 1661-1662. EPA Office of Emergency and Re medial Response. May 2000. Lead at Outdoor Firing Ranges. Fikes, J. and Dorman, D. 1994. Diagnosis and therapy of neurotoxi cological syndromes in dogs and cats: neurotoxic metals, part 3. Progress in Veterinary Neurology 5(1): 5 12. Friedland, A., and Johnson, A. 1985. Lead distribution and fluxes in a high-elevation forest in northern Vermont. Journal of Environmental Quality 14(3):332 336. Gillikin, D.P., Dehairs, F., Baeyens, W., Nav ez, J., Lorrain, A., and Andre, L. 2005. Interand intra-annual variations of Pb/Ca ratios in clam shells ( Mercenaria mercenaria ): a records of anthropogenic lead pollution? Marine Pollution Bulletin. Aug. 4. Glantz, S., and Slinker, B. 2001. App lied Regression and Analysis of Variance. 2nd edition. McGraw-Hill, Inc., New York. Goodman, L. and Gilman, A. 1975. Th e pharmacological basis of therapeutics 5th edition. Macmillan Publishing Co. New York.
60 Gulson, B. Mizon, K., Korsch, M., Palmer, J ., and Donnelly, J. 2003. Mobilization of lead from human bone tissue during pre gnancy and lactation a summary of long-term research. The Science of the Total Environment 303: 79-104. Hafen, M. and Brinkmann, R. 1996. Analysis of lead in soils adjacent to an interstate highway in Tampa, Florida. Environmental Geochemistry and Health. 18: 171179. Haley, V., and Talbot, T. 2004. Geographic an alysis of blood lead levels in New York State children born 1994 1997. Environmental Health Perspectives. 112(15):1577-1582. Happel, S.B. 1995. The spatial distribution of lead in soil in three differing socioeconomic neighborhoods in Tampa, Florida. Masters Thesis. Hawke, C., Maddison, J., Poulos, V., and Wa tson, A. 1992. Erthrocyte protoporphyrin concentrations in clinically normal cats and cats with lead toxicity. Research in Veterinary Science. 53: 260 263. Hillsborough County Animal Services. 2004. Fis cal year statistical status resulting from operations. Hillsborough County Health Department. May 9, 2003. EPI-Notes. Hillsborough County Property Appraisers Office. http://www.hcpafl.org on 7/29/05. Hoffheimer, M. 1988. Lead poisoning in a cat. The Compendium on Continuing Education for the Practicing Veterinarian. 10(6): 724, 728. Irwin, R.J., VanMouwerik, M., Stevens, L., Seese, M.D. and Basham, W. 1997. Environmental Contaminants Encyclopedia. National Park Service, Water Resources Division, Fort Collins, Colorado. Gasoline, Leaded entry. Lead entry. Jahoda, G. 1973. River of the Golden Ibis. University Press of Florida, Gainesville, Fl. Kilbourne, C.A. 1998. Lead contamination of schoolyard soils in Trujillo, Venezuela. Masters Thesis. Lessler, M. 1988. Lead and lead pois oning from antiquity to modern times. Ohio Journal of Science. 88(3): 78 84. Lewis P. R. 1998. The distribution of lead in soils in a portion of Port Tampa City, Florida. USF Masters Thesis. Li, W., Han, S., Gregg, T., Ke mp, F., Davidow, A., Louria, D., Siegel, A. and Bogden, J.
61 2003. Lead exposure potentiates predat ory attack behavior in the cat. Environmental Research. 92(3). Luthman, J., Oskarsson, A., Olson, L., and Hoffer, B. 1992. Postnatal lead exposure affects motor skills and expl oratory behavior in rats. Environmental Research 58: 236-252. Maskall, J., Whitehead, K. and Thornton, I. 1995. Heavy metal migr ation in soils and rocks at historical smelting sites. Environmental Geochemistry and Health 17(3): 127-138. Massadeh, A.M., Snook, R.D. 2002. Determina tion of Pb and Cd in road dusts over the period in which Pb was remove d from petrol in the UK. Journal of Environmental Monitoring. 4:567-72. Merck Vet Manual on line. 2002. Lead poisoning. Downloaded from www.merckvetmanual.com on 5/23/03. Mogollon, J., Bifano, C., and Davies, B. 1995. Distribution of metals in mechanical fractions of soils from a lake catchment in Venezuela. Environmental Geochemistry and Health. 17: 103111. Morgan, R., Pearce, L., Moore, F., and Rossi, T. 1991. Demographic data and treatment of small companion animals with lead poisoning: 347 cases (1977-1986). Journal of American Veterina ry Medical Association. 199(1): 98 102. Morgan, R. 1994. Lead poisoning in small companion animals: an update (1987-1992). Veterinary and Human Toxicology. 36 (1): 18-22. Motto, H., Daines, R., Chilko, D. and Motto, C. 1970. Lead in soils and plants: its relationship to traffic volume and proximity to highways. Environmental Science and Technology. 4(3): 231 237. Nafe, L. 1988. Selected Neurotoxins. Veterinary Clinics of North America: Small Animal Practice 18(3): 593-604. Nam, D., Lee, D., and Koo, T. 2004. Factor s causing variations of lead and cadmium accumulation of feral pigeons. Environmental Monitoring and Assessment. 95:23-35. Nam, D., Lee, D., and Koo, T. 2004a. Mon itoring for lead pollution using feathers of feral pigeons from Korea. Environmental Monitoring and Assessment. 95:13-22. Novak, M., Emmanuel, S., Vile, M., Erel, Y., Veron, A., Paces, T., Wieder, R., Vanecek,
62 M., Stepanova, M., Brizova, E., and Hovorka J. 2003. Origin of lead in eight Central European peat bogs determined from isotope ratios, strengths, and operation times of regional pollution sources. Environmental Science & Technology 37(3):437-445. Nicholls, T.J. and Handson, P.D. 1983. Behavi oural change associated with chronic lead poisoning in working dogs. The Veterinary Record. 112: 607. Poikolainen, J., Kubin, E., Piispanen, J., a nd Karhu, J. 2004. Estimation of the longrange transport of mercury, cadmium, and lead of Northern Finland on the basis of moss surveys. Artic, Antarctic, and Alpine Research. 36(3):292-297. Ramsey, D., Casteel, S., Faggell, A., Chastain, C., Nunn, J., and Schaeffer, D. 1996. Use of orally administered succimer for treatment of lead poisoning in dogs. Journal of the American Veterinary Medical Association 208(3): 371-375. Schierow, L. 1998. Lead-based paint pois oning prevention: federal mandates for local government. CRS Report for Congress. Tong, S., Baghurst, P., Sawer, M., Burns, J., and McMichael, A. 1998. Declining blood lead levels and changes in c ognitive function during childhood. Journal of the American Medical Association 280(22):1915 1919. Turjoman, A., And Fuller, W. 1987. Behavior of lead as a migrating pollutant in Saudi Arabian soils. Arid Soil Research and Rehabilitation. 1(1): 31-45. Turner, D., and Bateson, P. eds. 2000. The Domestic Cat: the biology of its behavior. 2nd edition. Cambridge University Press, Cambridge, UK. Turner, A. and Fairburn, A. 1979. Lead poisoning in the cat. Australian Veterinary Practitioner. 9(4): 205 207. USEPA. TRI data. 2002. www.epa.gov/tri/ Yokel, J. and Delistraty, D. 2003. Arseni c, lead and other trace elements in soils contaminated with pesticide resi dues at the Hanford site (USA). Environmental Toxicology. 18:104-114.