s 363.739 U24atac 1987 Black and Veatch Assessment of the toxicity of arsenic, cadmium, lead and zinc in soil, plants, and livestock in the Helena Valley of Montana Activities trolled Sites -Zone II 2EZ Environmental Protection Agency Hazardous Site Control Division Contract No. ott-Ol-7251 ADMINISTRATIVE DUPLICATE Stat? tocu. mTs % 77 S9630 C0L^0N |0fcO8<3O Di rr-oz QCT' Ls - \%«t U» lHILL Black & Veatch ICF PRC Ecology and Environment SF FILE NUMBER KCM IV Remedial Planning Activities at Selected Uncontrolled Hazardous Waste Sites -Zone II ±ajj*~~ *± Environmental Protection Agency X*tf2. Hazardous Site Control Division Contract No. 68-01-7251 ADMINISTRATIVE OUPLICATE $TA7£ •AfOA/ C0^CTlt T**A ^ 59S30 % n« * )Ois>OZOO ■ 14 . 'v i . jUJ '■•>, '"{*[ I in r H/U. Black & Veatch ICF PRC Ecology and Environment IX-Z OCT 2 m 1998 APR -2 :999 1 FEB 1 o 2001 rEB 6 2004 AP ?nr)7 17 S3e3r3fflNA STATE L.BRARY 3 0864 0009531 7 7 II 0141594 ASSESSMENT OF THE TOXICITY OF ARSENIC, CADMIUM, LEAD AND ZINC IN SOIL, PLANTS, AND LIVESTOCK IN THE HELENA VALLEY OF MONTANA for EAST HELENA SITE (ASARCO) EAST HELENA, MONTANA EPA Work Assignment No. 68-8L30.0 MAY 1987 0141595 TABLE OF CONTENTS Page Table of Contents List of Tables Glossary of units, 1.0 Introduction symbols, acronyms and terms i v vi 1 . 1 Purpose 1 . 2 Scope 1.3 Methods 1.4 Site Description 1 1 1 3 Literature Review and Hazard Levels for Livestock 2.1 Ar sen ic 2.2 2.3 2.4 Arsenic literature review Livestock arsenic hazard levels 1 Toxic arsenic hazard levels for cattle 2 Toxic arsenic hazard levels for horses 3 Toxic arsenic hazard levels for sheep 4 Toxic arsenic hazard levels for goats Cadmium literature review Cadmi urn 2.2.1 2.2.2 Livestock cadmium hazard levels 2.2.2.1 Toxic cadmium hazard levels for cattle 2.2.2.2. Toxic cadmium hazard levels for horses 2.2.2.3 Toxic cadmium hazard levels for sheep Lead 2.3.1 2.3 2 2 2 2 3 3 3 Zinc 2,4.1 2.4 2 2 2 Lead literature review Livestock lead hazard levels 1 Toxic lead hazard levels 2. Toxic lead hazard levels 3 Toxic lead hazard levels Zinc literature review Livestock zinc hazard levels for cattle for horses for sheep Tox ic Toxic Toxic goats zinc hazard levels for cattle zinc hazard levels for horses zinc hazard levels for sheep and Literature Review and Hazard Levels for Soils and Plants 5 5 16 17 19 21 21 21 21 33 33 36 36 39 39 50 50 53 55 56 56 66 66 69 69 74 3.1 Arsenic in soils and plants 3.1.1 Arsenic literature review 3.1.2 Arsenic in soils 3.1.2.1 Total arsenic in soils 3.1.2.2 Extractable soil arsenic 3.1.3 Arsenic in plants 75 75 84 84 i i 014159b 3.2 Cadmium in soils and plants 88 3.2.1 Cadmium literature review 88 3.2.2 Cadmium in soils 90 3.2.2.1 Total cadmium in soils 90 3.2.2.2 Extractable soil cadmium 109 3.3.3 Cadmium in plants 109 3.3 Lead in soils and plants 110 3.3.1 Lead literature review 110 3.3.2 Lead in soils 111 3.3.2.1 Total lead in soils 111 3.3.2.2 Extractable soil lead 116 3.3.3 Lead in plants 117 3.4 Zinc in soils and plants 118 3.4.1 Zinc literature review 118 3.4.2 Zinc in soils 228 3.4.2.1 Total zinc in soils 118 3.4.2.2 Extractable soil zinc 131 3.4.3 Zinc in plants 132 4.0 Hazard Levels for Water 134 4.1 Water Quality Levels for Livestock 134 4.2 Water Quality Levels for Irrigation 136 5.0 Regulatory Criteria From Other Technologies 138 5.1 Criteria from Land Application of Sewage Sludge 138 5.2 Criteria from Coal Overburden Suitability for Root Zone Material 143 5.3 Criteria for Defining Hazardous Wastes 143 5.4 Criteria for Metal Contaminants Based on Land Use 143 .5.5 Summary 143 6.0 Appendix 151 6.1 Toxicology Mechanisms of Metals for Livestock 151 6.1.1 Arsenic toxicology 151 6.1.2 Cadmium toxicology 153 6.1.3 Lead toxicology 156 6.1.4 Zinc toxicology 159 6.2 Toxicology Mechanisms of Metals for Plants 161 6.2.1 Arsenic toxicology 161 6.2.2 Cadmium toxicology 163 6.2.3 Lead toxicology 165 6.2.4 Zinc toxicology 166 6.3 Computerized Data Base Utilized 168 7.0 References Cited 174 i i i .-* n - > •• 0141597 LIST OF TABLES Number Page 1 Background arsenic levels in livestock fluids and hair 7 2 Background arsenic levels in livestock tissues 8 3 Elevated arsenic levels in livestock fluids and hair 9 4 Elevated arsenic levels in livestock tissues 11 5 Diagnostic levels of arsenic in cattle 18 6 Diagnostic levels of arsenic in horses 20 7 Diagnostic levels of arsenic in sheep and goats 22 8 Background cadmium levels in livestock fluids and hair 24 9 Background cadmium levels in livestock tissues 25 10 Elevated cadmium levels in livestock fluids and hair 27 11 Elevated cadmium levels in livestock tissues 29 12 Diagnostic levels of cadmium in cattle 34 13 Diagnostic levels of cadmium in horses 37 14 Diagnostic levels of cadmiun in sheep and goats 38 15 Background lead levels in livestock fluids and hair 40 16 Background lead levels in livestock tissues 4 1 17 Elevated lead levels in livestock fluids and hair 43 18 Elevated lead levels in livestock tissues 45 19 Diagnostic levels of lead in cattle 51 20 Diagnostic levels of lead in horses 54 21 Diagnostic levels of lead in sheep and goats 57 22 Background zinc levels in livestock fluids and hair 59 23 Background zinc levels in livestock tissues 60 24 Elevated zinc levels in livestock fluids and hair 61 25 Elevated zinc levels in livestock tissues 63 26 Diagnostic levels of zinc in cattle 67 27 Diagnostic levels of zinc in horses 70 28 Diagnostic levels of zinc in sheep 71 29 Diagnostic levels of zinc in goats 73 30 Phytotoxicity of total arsenic in soils 76 31 Phytotoxicity of extractable arsenic in soils 78 32 Phytotoxicity of arsenic in vegetation 80 33 Comparison between concentra ted HC1 and NaHCC>3 for determination of extractable soil arsenic (ppm) 83 34 Interpretive guide for concentrated HC1 soil extractable arsenic 8 5 35 Relative tolerance of crops to arsenic 86 36 Phytotoxicity of total cadmium in soils 91 37 Phytotoxicity of extractable cadmium in soils 96 38 Phytotoxicity of cadmium in vegetation 99 39 Phytotoxicity of total lead in soils 112 40 Phytotoxicity of extractable lead in soils 114 41 Phytotoxicity of lead in vegetation ■ 115 42 Phytotoxicity of total zinc in soils 119 43 Phytotoxicity of extractable zinc in soils 122 44 Phytotoxicity of zinc in vegetation 124 45 Water quality criteria for arsenic, cadmium, lead, and z i nc 13 5 46 Irrigation water criteria for arsenic, cadmium, lead, and zinc 137 4" Maximum permissible cumulative metal loadings from sewage sludge to agricultural lands 139 i v 0141598 48 Suitability criteria for soil overburden used as root zone mater ials . 14 4 49 EP toxicity testing for hazardous materials 145 50 Identification of hazardous wastes (California) 146 51 Acceptable concentration of contaminants in soils (United Kingdom) 147 52 Suggested hazarad criteria for soil based on regulatory agency data 150 ^--ifri 0141599 Glossary of Units, Symbols, Acronyms and Terms Units kg kilogram; kg = 103 g g gram = 10-3 kg mg milligram; mg = 10-3 g ug microgram; ug = 10-3 mg ng nanogram; ng = 10-3 ug L liter; L = 1 dm3 ml milliliter; ml = 10-3 l Symbols ppm ppb ug/g mg/kg mg/L ug/L ug/ml ng/ml A c r o n ym s parts per million = ug/g = mg/kg parts per billion = 10-3 ppm, ng/g = ug/kg microg ram/gram milligram/kilogram mill igram/1 i ter microgram/1 iter microg ram/mi 11 ili ter na nog ram/mi lliliter AA Arsanilic acid ALA-D Delta aminolevulinic dehydratase AAS Atomic absorption spectrophotometry AOAC Association of Official Agricultural Chemists AWT Ash weight basis CCM Copper carbonate method CEC Cation exchange capacity d Day DTPA Diethylenetr i ami nepentaacetic acid DW Dry weight basis EDTA Ethylenediaminetetraacet ic acid EPA Environmental Protection Agency EPA CV Environmental Protection Agency cold vapor method ES Emission spectrographic FEP Blood-free erthrotyte porphyrins FLAAS Flameless atomic absorption spectrophotometry GLC Gas liquid chromatography INAA Instrumental neutron activation analysis IPAA Instrumental photon activation analysis LD20 A dose which is lethal for 20 percent of the test subjects MMC Methyl mercuric chloride MMH Methyl mercuric hydroxide Mo Month MSMA Monosodium acid methanear sona te MW Mining waste MYC Mycorrhiza ND Not determined v 1 0141600 NOAA National Oceanic and Atmospheric Administration NR Not reported NRC National Research Council NS Not significant OM Organic Matter Content pH Negative logarithm, base 10, of H+ concentration PMA Phenyl mercuric acetate RNAA Radiochemical neutron activation analysis SCS U.S. Soil Conservation Service SSMS Spark source mass spectrometry USDA United States Department of Agriculture USGS United States Geological Survey WW Wet weight basis Wks Weeks XRFL X-ray fluorescence YR Yield reduction Terms acute - Sharp; poignant. Having a short and relatively severe course. chronic - Persisting over a long period of time. phytotoxic - Pertaining to a phytotoxin. Inhibiting the growth of plants. toxicosis - Any disease condition due to poisoning. criterion - A standard by which something may be judged. V I I 1.0 INTRODUCTION Vyl41DUl This document consists of a literature review and presents candidate hazard levels for assessment of selected environmental hazards associated with the East Helena smelter complex. A substantial amount of material was reviewed but additional material will no doubt be added to these data as the study progresses. This document has been prepared specifically for the Helena Valley, Montana area and use of this document for evalua- tion of other sites should be done only after appropriate consid- eration of site specific conditions. 1 . 1 Purpose This document is a literature review from which hazard levels were developed to assess potential risk to plants and livestock from chemical element levels found in soil, plants, livestock and water present in the vicinity of the East Helena smelter. These hazard levels will enable determination of the potential danger to these agricultural resources. It is the intent of this review to assess only the potential risk to agricultural production. This document does not address any subsequent risk to the human population from consumption of these agricultural products. 1.2 Scooe - The scope of this document (Volume 1) is confined to the metals arsenic, cadmium, lead and zinc present in soil, water, plants and livestock and their toxic affects to plants and livestock. In addition, a brief discussion on the toxicology mechanisms of these four metals to livestock and vegetation is included. Volume 2 presents similar data for plants and soils for the metals copper, mercury, selenium, silver and thallium. 1.3 Methods Portions of the literature presented in this document were procured through the use of a computer search utilizing numerous data bases. Data bases utilized included AGRICOLA, BIOSIS, CAB 0141602 Abstracts, CRIS-USDA, ENVIROLINE, MEDLINE, NTIS, Pollution Abstracts, SCISEARCH and Water Resources Abstracts. A brief description of these data bases is included in section 6.3. Conventional library methods were also employed for researching abstracts, periodicals and other materials. No attempt was made to determine the relative importance of field studies versus greenhouse studies, but study settings are given in appropriate tables to enable the reader to evaluate this variable. No attempt was made to evaluate synergistic or antagonistic effects of these metals although some of these mechanisms are documented in the text. Levels of impact or an evaluation of an acceptable impact have not been determined but this data is included in appropriate tables when reported in the referenced literature. The authors conducted a meeting to establish normal, tolera- ble, uncertain and toxic levels of metals in soils, plants, and livestock. At this meeting all literature was discussed followed by establishment of hazard levels based on the reviewed litera- ture . Background values for all parameters were generally derived directly from data in the reviewed literature and are the minimum and maximum or only value reported for normal or control parame- ters. The background range will no doubt expand as more data become available. The tolerable level represent the maximum concentrations at which no toxicity has been noted. These levels were not available for many parameters. The uncertain range represents the chemical level at which both nontoxic and toxic results have been reported by various studies. This result stems from variations in individual animal tolerances, variations in experimental designs, and by synergistic or antagonistic effects of other constituents. Toxic concentrations have been derived from two major sources: 1) the results of individual studies and 2) criteria reported as toxic in toxicology manuals, texts, and special Dubli cat ions. '-?}?. U .; 0141603 Data derived under conditions similar to those found in the Helena Valley merited greater consideration than other data. For example, a toxic soil level for wheat on calcareous loamy soils was more applicable than a toxic soil level for cabbage on sandy acid soils. The hazard levels presented in this document are thus site specific for crops and conditions present in the Helena Valley as much as allowed by the reviewed literature. In some cases, a site specific evaluation was not possible. Site specific conditions for the Helena Valley are presented in the following section (1.4) . Once hazard levels were developed they were compared to means and ranges of soil/plant chemical levels measured in the Helena Valley and control sites. 1.4 Site Description The Helena Valley is located in west central Montana and trends in a west northwest direction. It is 35.4 km (22.1 mi) long and 17.1 km (10.7 mi) wide. The valley is bounded on the northeast by the Big Belt Mountains, on the south by the Elkhorn Mountains and the Boulder Batholith, and on the west by mountains forming the continental divide. Lower portions of the valley are occupied by Lake Helena and Hauser Lake formed by dams on Prickly Pear Creek and the Missouri River. Elevations range from 1,113 m (3650 ft) mean sea level at Hauser Lake to 2,560 m (8,400 ft) in the surrounding mountains. Geological materials on the valley floor consist of quaternary and tertiary sediments that are consolidated or poorly consolidated. Soils are moderately calcareous and composed of silt and clay (Miesch and Huffman 1969). Typical soil series mapped in portions of the Helena Valley are the Hilger, Martinsdale, Musselshell, and Sappington series all of which contain horizons that are "strongly to violently" effervescent (Soil Conservation Service 1977b) . Except for an area in the immediate vicinity of East Helena surficial soil pH values range from about 7.1 to 8.6 (EPA, 1986) Soil profiles are poorly to moderately developed on both quaternary and tertiary parent materials. The Helena Valley is semi-arid and receives less than 25.4 cm (10 in) of annual precipitation. The 0141bU4 adjacent mountains receive up to 76.2 cm (30 in) of annual precipitation (Soil Conservation Service 1977). The climate is modified continental with an average annual temperature of 6.3°C (43.3°F) (National Oceanic and Atmospheric Administration (NOAA) 1983). Average January and July temperatures at Helena are -8°C (18.1°F) and 20°C (67.9°F) respectively (NOAA 1983). Agricultural crops in the Valley are alfalfa, small grains (usually wheat, barley and some oats) and range land. The Helena Valley is the site for two incorporated cities: Helena and East Helena with approximate populations of 23,900 and 2,400 respectively (1980 census). The two cities are located 6.4 (4 mi) and 1 km (0.6 mi) from the smelter complex, respectively. The valley has been the site of a lead smelter since the Helena and Livingston facility was built in East Helena in 1888. The smelter was purchased by its present owner (American Smelting and Refining Company) in 1899. The Anaconda Company built a zinc plant adjacent to the smelter in 1927 to recover zinc from waste products. In 1955 the American Chemet Company constructed a paint pigment plant utilizing zinc oxide from the zinc facility. *:j^: 0141605 2.0 LITERATURE REVIEW AND HAZARD LEVELS FOR LIVESTOCK There are three general -approaches to determining the body burden of heavy metals in livestock. These are: 1) analyzing internal organ tissues; 2) analyzing accessible body fluids and materials; and 3) the _i_n vivo determination of heavy metals utilizing radiometric analyses. A considerable amount of data has been published on background and elevated heavy metal levels in livestock organs. In most situations these organs are not available for large scale studies. Liver and bone samples may be procured through biopsy procedures. Data on blood, milk, hair, feces and urine are more limited, but sufficient in some parame- ters to allow their use in a livestock survey for some heavy metals. The third method offers much promise in future studies but facilities for radiometric determinations are few at this time. The following sections outline documented levels of selected heavy metals in various animal substances and their sig- nificance in determining toxicosis. All values are reported on a wet weight basis unless noted. 2 . 1 Arsenic 2.1.1 Arsenic literature review Arsenic poisoning is the second most common metaloid toxin. The element is ubiquitous and has been found in all plant and ar.:nal tissues under normal background conditions (Schroeder and Baiassa 1966). Several forms: arsanilic acid; sodium arsanilate; 3-n i tro-4-hydroxyphenylarsonic acid, have been used as feed addi- tives to increase weight gain and feed efficiency and to control disease in swine, poultry and other livestock. Most documented cases of arsenic poisoning in livestock have been acute or subacute, usually from ingesting treated forage (Edwards and Clay 1979, Weaver 1962, McCulloch and St. John 1940, Selby et al. 1974, Selby et al. 1977), contaminated feed (Beregland et al . 1976, Selby et al . 1977), dipping powder and herbicides (Moxham and Coup 1968) and various refuse (McParland 0141606 and Thompson 1971, Selby et al. 1977). Very few cases of natural arsenic poisoning have been reported. Fitch et al. (1939) studied the poisoning of livestock in the Waiotapu Valley in New Zealand and attributed it to arsenic from geothermal sources. Many cases of chronic arsenic poisoning may be partially masked by the effects of other heavy metal poisoning (especially lead, copper, cadmium and zinc) usually associated with arsenic in metallurgical mining, smelting and refining industries. It has been suggested that some tolerance to arsenic is acquired by livestock with chronic exposure (McCulloch and St. John 1940) . A considerable difference exists between the effective toxicity of various forms of arsenic. Levels of total arsenic found in marine invertebrates and fish have been found to be toxic to aquatic organisms and fish when the arsenic was present as arsenic trioxide (Schroeder and Balassa 1966). Bucy et al. (1955) found differences in the toxicity of organic arsenic compounds to sheep, with 3-ni tro-4-hydr oxyphenylarsonic acid the least toxic. The study found arsanilic acid to be less toxic than potassium arsenite and that the latter was not very palatable to lambs. All arsenic concentrations in livestock substances have been reported as total arsenic. The arsenic hazard levels presented in this document are thus based on total arsenic. Tables 1-4 list background and elevated arsenic levels in livestock fluids, h^ir and tissues. The highest concentration of arsenic in tissues has been found in the spleen, liver and kidneys (Peoples 1964, Edwards and Clay 1979, Rosiles 1977, Knapp et al. 1977). Cattle that have not been exposed to arsenic have kidney levels from 0.0 (Peoples 1964) to 0.25 ppm (wet weight) (Dickinson 1972). Doyle and Spaulding (1978) reported a value of 0.06 ppm for 100 cattle tested by the National Bureau of Standards. One hundred and ninety Australian cattle tested by Flanjak and Lee (1979) had a mean value of 0.018 ppm for kidney tissue. 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L' S <%i fM F a> c C j( >: Ji i' j: rn ■o • • ' □ cr o 0 \ w w jj 'j C B - .. 10 in vi u1 u1 L" iT' u' C C/< in u — - E E E E E o k- <: < <: c O -.-.--.- u < < < LP [u a, 0141611 w *o rtiiniriiriu^ifi^ifiiriifiiriiri ir> — • — J-^XC£-Cff,^ff'CT»O^O^CTi^ff'0»ffi ffi T ^J A U U U--'— • — — — — — • — — ^- _ 4 „^ bJ iJ bf QJ OJ 4)*D T3 T3 -■-----■■-■----,-. ■i " '/ i ■ *- *. a i a i c ', ". i . c i o u u c c c c c c c c c uuuooooo flT*T)0)0>0)r3333-J3333r3 >, >. >- — — w u- x: x: sz x x w xjjjjjoOOOUUUOOOU >C T « C C x X -----«-_. dojojoocoooooooooooojc rxxzz^-f-Ht-Hf-HF-f-f-i-e-ibH p> c cr a1 01 ? ai a1 a; jj jj jj > > > 10 T3 fC c C r u u U 0) a 0) -- in tr m i~> ±J jj ij u k, *C TO B3 < rt < n o f^ rif«. ^ ^m^^-.^w-i^^^^^jj c »- C fl t — E >,iJ C « o & c - > c *0 w. c ■0 >.o I ^ • 0 " - « - c - o 2 m 13 -._.,--- EEE : ^ p tr P1 ,\ J£ J( i E C* CT1 ^ • f E E £ . . r^ v ec 2 < < ' -< m w to n «c x E I1 0141612 ranged from 0.09 to 0.26 ppm (mean 0.15) in six lambs analyzed by Bucy et al. (1955). Puis (1981, 1985) has given a range of 0.01 to 0.3 ppm for normal arsenic levels in sheep kidney tissue. Arsenic levels in normal liver tissue from cattle have been reported as 0.013 ppm (n = 190) and 0.06 ppm (n = 100) by Flanjak and Lee (1979) and Doyle and Spaulding (1978), respectively. Normal ranges for cattle liver have been given as 0.03-0.40 ppm (Puis 1981) and less than 0.5 ppm (NRC 1977). Buck et al. (1976) has stated normal levels are usually less than 0.5 ppm. Background arsenic levels in sheep liver have been reported as 0.03 ppm for 440 animals tested by Spaulding (1975), and 0.05 to 0.21 ppm (mean 0.15 ppm) for six lambs studied by Bucy et al. (1955). Normal sheep liver levels given by Puis (1981) are 0.03 to 0.20 ppm. Horse liver and kidney background levels of less than 0.4 ppm have been reported by Puis (1981). Insufficient data exist to determine background levels of arsenic in spleen tissue, but limited data suggest that in some cases elevated arsenic concentrations in the spleen may be higher than in liver or kidney tissue (Table 4). Elevated arsenic levels in kidney, liver and spleen have been demonstrated in a number of experimental and accidental situa- tions. Peoples (1964) found concentrations greatest in the spleen (2.0 ppm) and liver (1.2 ppm) of cattle fed 1.25 mg/kg arsenic acid for eight weeks. Bucy et al . (1955) found arsenic concentra- tions nearly equal in the kidneys and liver of lambs fed up to 0.4 percent of their diet as organic arsenic compounds. Levels were sharply elevated from background concentrations with diets of 500 ppm organic arsenic content. Cattle kidney levels as high as 53 ppm have been reported by Underwood (1977). The level at which chronic poisoning -occurs has not been well documented. Reduced weight gains, which are only rarely noticed, are generally the first signs of chronic arsenic poisoning. Increasing levels to 1000 ppm arsanilic acid in the diet of swine produced posterior paresis or quadriplegia in 15 days (Ledet et al. 1973). Levels of 7.5 to 7.8 and 6.8 to 12.3 ppm (wet weight) for kidneys and liver, respectively, were noted in sheep fed 0.05 12 J. 3 1 M 0141613 percent organic arsenic compounds compared to 0.15 ppm found in the same organs of controls (Bucy et al. 1955). Buck et al. (1976) cited a level of 10 ppm in kidney and liver tissues as diagnostic of arsenic poisoning. Peoples (1964) found 0.35 ppm arsenic in the kidneys of cows receiving up to 1.25 ppm arsanilic acid diet and noted no toxic effects. A study by Bennett and Schwartz (1971) found sheep liver arsenic levels equal to or greater than 10.6 ppm in all experimental sheep that died from lead arsenate poisoning. The same study also revealed that all surviving sheep had liver concentrations of less than 3.8 ppm arsenic. Kidney and liver tissue arsenic levels associated with chronic arsenic poisoning in cattle were reported as 5.0 to 53 ppm and 7.0 to 70 ppm, respectively (Puis 1981). It should be noted however that under acute conditions, clinical toxicity has been reported in cattle exhibiting liver arsenic concentrations as low as 1.6 ppm (Dickinson 1972) and numerous clinical toxicity cases have been documented in the 1.6 to 5 ppm range (Edwards and Clay 1979, Rosiles 1977, Knapp et al. 1977, Hatch and Funnell 1969, Bergeland et al . 1976, Riviere et al . 1981). Puis (1981) reported toxic levels in horse kidney at 10.0 ppm and 7.0 to 15 ppm in liver. Bucy et al . (1955) noted arsenic levels in sheep kidney tissue decreased rapidly following removal of arsenic from the diet. Dickinson (1972) has suggested that cattle could deplete an elevated kidney arsenic content to a value less than that of diagnostic significance but still succumb to irreversible tubular damage . The affinity of arsenic for sulfhydryl groups results in high arsenic concentrations in sulfhydryl rich keratinized tissues such as skin and hair (Riviere et al . 1981). The arsenic content of hair has been used to determine exposure of humans to this element (Bencko and Symon 1977). Normal levels found in cattle hair have been published by Riviere et al. (1981), Dickinson (1972) and Orheim et al . (1974) at values of 0.09 to 0.10 ppm 0.81 to 2.7 ppm and 0.13 to 0.84 ppm, respectively. The publication of Dickinson (1972) is not clear with respect to the sampling time for "before treatment" results which would appear to be anomalously high at 13 0141614 1.1 to 2.7 ppm arsenic, compared to the control animal at 0.81 ppm arsenic, therefore the 2.7 ppm value has not been included in the background range. Edwards and Clay (1979) found a range of 0.11 to 0.55 ppm (mean .36 ppm) in 10 control cows they sampled. Lewis (1972) found no arsenic in the hair of nonexposed horses he studied. Puis (1981) has reported a normal range of arsenic concentration in cattle hair of 0.5 to 3.0 ppm. Cattle and horses exposed to industrial pollution have been found to have elevated arsenic levels in the hair. Orheim et al . (1974) reported values of 3.7 to 19.0 ppm arsenic in cattle exposed to smelter emissions. Cattle poisoned from arsenic in feed and water (mining waste) exhibited hair arsenic values of 6.3 to 21.0 ppm with a mean of 13.6 ppm (Bergeland et al . 1976). Cattle consuming 5.5 ppm arsenic in feed suffered acute toxicosis and were found to have 0.80 to 3.40 ppm arsenic in their hair (Riviere et al. 1981). Bergeland et al. (1976) reported subclinical poisoning ("unthrifty") in cattle exhibiting hair arsenic concentrations as low as 2.4 ppm. Insufficient data exist on normal arsenic levels in wool or horse hair to properly interpret concentrations produced by chronic low level arsenic exposure. It has been shown that the amount of arsenic in human hair increases with age and that sex may have some influence on concentrations observed (Ohmori et al . 1975) . To what degree these parameters affect arsenic in live- stock hair is not well documented. The literature suggests that arsenic levels in hair above 3.5 ppm may indicate exposure to some arsenic source and that levels above 2 ppm are suspect. An investigation by Edwards and Clay (1979) indicated that arsenic levels in cattle hair can be expected to return to normal levels one year after exposure has ceased. Individual variations among animals may make large group analyses necessary if one assumes that the variations in arsenic levels in livestock hair are similar to those observed in humans (Bencko and Symon 1977). Urine, blood and milk arsenic data for livestock are not commonly found in the literature. Peoples (1964) found arsenic acid was eliminated in the urine of dairy cattle in proportion to lit 0141815 *> ' J i - ! intake. Lakso and Peoples (1975) noted both trivalent and pentavalent forms of arsenic were methylated in the body and largely excreted via the urine. Urinary excretion in cattle is rapid with 54 to 98 percent of the daily intake eliminated in the urine (Peoples 1964). Normal urine arsenic levels for cattle and horses are reported as 0.5 and 0.4 ppm, respectively (Puis 1981) . Lakso and Peoples (1975) found a range of 0.17 to 0.31 ppm arsenic in urine of control cattle that they tested. Selby and Dorn (1974) found 1400 ug/100 ml of arsenic in the urine of acutely poisoned steers. Puis (1981) noted urine levels of 2 to 14 ppm and 100 to 150 ppm as indicative of acute toxicosis in cattle and sheep, respectively. Background arsenic concentrations in cattle blood have been reported as 0.03 to 0.07 ppm (Edwards and Clay 1979). Blood arsenic levels may be more insensitive to intake at low levels than are arsenic levels in urine. Peoples (1964) found no change in arsenic blood levels among cattle fed 0.0 to 1.25 mg/kg body weight arsenic acid. Shar iatpanahi and Anderson (1984a, 1984b) found blood arsenic levels increased rapidly following ingestion of monosodium methanear sonate in sheep and goats. A near steady state approximately 3 orders of magnitude above background levels was observed within 10 days under daily ingestion of 10 mg/kg body weight of arsenic. These authors also reported a rapid decline in blood arsenic levels following removal of arsenic from the diet. Edwards and Clay (1979) found low concentrations of arsenic (0.03 to 0.12 ppm) in the blood of cattle exposed to toxic concentra- tions of arsenic in contaminated forage one year prior to sam- pling. The concentration range was not significantly different from non-exposed cattle. Puis (1981) has given normal blood arsenic levels as 0.05 and 0.01 ppm for cattle and swine,, respec- tively. High blood levels for sheep were reported as 0.04 to 0.08 ppm and toxic levels were given as 0.17 to 1.0 and 5.0 ppm for cattle and sheep, respectively (Puis 1981). Levels of arsenic in normal milk have been reported to range from 0.0005 to 0.17 ppm (NRC 1977, Iyengar 1982). Peoples (1964) found nc significant correlation between arsenic in milk and 15 0141616 rsenic in the diet of cattle. Weaver (1962) found no significant rsenic in the milk from a cow showing symptoms of arsenic oisoning. Calvert and Smith (1972) found arsenic in cattle milk ncreased from 0.015 to 0.026 ppm only at the highest diet level ed (3.2 mg As/kg body weight). Lesser amounts produced no ncrease in milk arsenic levels. Underwood (1977) has reported ilk arsenic levels of 0.07 to 1.5 ppm in chronically poisoned attle. The literature suggests that while small quantities of rsenic may appear in milk of exposed individuals, it is doubtful hat any significance with respect to arsenic exposure can be ttached to it. In conclusion, arsenic concentration of the kidney, liver and ossibly the spleen have been shown to correlate with arsenic ntake. Elevated levels of arsenic in hair, urine and blood have Iso been shown to occur in exposed individuals. Due to individ- al variations, large groups of subjects should be used to etermine the significance of hair and blood arsenic levels. Both lood and urine arsenic levels have been shown to fluctuate uickly in response to arsenic intake. Urine levels are generally bout one order of magnitude greater than those found in blood and re therefore subject to less sampling and analytical error than he lower levels found in blood. It is the opinion of the authors hat exposure to arsenic can be adequately determined through the se of hair and blood samples providing appropriate analytical lethods can be developed for the latter. The additional accuracy rovided by urine analysis would be unlikely to justify the dditional expense of sample collection and urine analysis for an nitial livestock survey but could be very useful for more etailed studies. The utility of milk, may be of questionable alue . 2.1.2 Livestock arsenic hazard levels Background and elevated levels of arsenic have been docu- lented in many studies (Tables 1, 2, 3 and 4). This data base has ieen used to select arsenic hazard levels documented in the rollowing sections. 16 0141617 2.1.2.1 Toxic arsenic hazard levels for cattle The toxic concentration of arsenic in cattle blood was reported as 0.17 - 1.0 ppm by Puis (1981) (Table 5). No other data were found in the reviewed literature on elevated arsenic levels in cattle blood. Puis (1981) reported arsenic concentra- tions of 2-14 ppm in cattle urine was indicative of arsenic toxicosis. Peoples (1964) found up to 7.95 ppm in the urine of cows which consumed a diet of 1.25 mg/kg "arsenic acid" without apparent toxicity. Lakso and Peoples (1975) reported total arsenic in cattle urine of 4.86 and 6.35 ppm for cows fed 2.75 mg/kg sodium arsenate and 1.75 mg/kg potassium arsenite respec- tively without any toxicity symptoms. The lack of cases of documented toxicity in the 2 to 8 ppm urine arsenic range suggests that a toxic hazard level of 8 to 14 ppm arsenic in cattle urine may be more appropriate but, due to the limited data base, Puis' (1981) range of 2 to 14 ppm has been recommended for this parame- ter . Toxic arsenic levels 1.5 and 5 ppm in cattle kidney and liver tissue respectively have been recommended (Table 5) . All kidney arsenic levels above 1.5 ppm found in the reviewed literature were associated with toxicity. In most of these cases, poisoning was acute and therefore observed concentrations were relatively low. Kidney concentration criteria for chronic arsenic poisoning in cattle was reported as 5.0 to 53 ppm (Puis 1981). Few data were found in the review to determine the accuracy of this range. Acute arsenic toxicity was reported for cattle with liver arsenic levels as low as 1.6 ppm (Dickinson 1972), and toxicity was common in the 2 to 5 ppm range (Table 4). The highest nontoxic value for cattle liver arsenic content found in the literature was 1.2 ppm (Peoples 1964). The range from 1.6 to 5 ppm represents the range in which acute poisoning has been documented (Dickinson 1972, Rosiles 1977) but is below typical values reported for chronic poisoning (Puis 1981). Puis (1981) reported toxic cattle liver concentration ranges of 2.0 to 15 and 7.0 - 70 ppm for acute and chronic poisoning, respectively. The higher animal tissue concentrations 17 0141618 • O^ — * C< •D -H OD C DC «! C — i C ■— o -. _ ED I C E IT} — — Oi 0) x: p^ w u C Si m z r tt (J — -4 ft) O cr E f-> c — > t» ft! c B - -** •c — o o f* C r* , • i ~~ - CO ES — I ^» a> *~ c- i — < 1 •o r-* CD Q fc- a* C* O^ m o *c *H © — cs - r — ' * w B ^ c S S> u a> c w >- a> — B •- 01 B u o u u TJ 3 T 3 u 0 wi O *! m C l/l N ^ N -V. m tn 3 ppm in cattle hair, if statistically significant, should be an indication of excessive exposure to this element. Milk arsenic levels remained low (<1 ppm) even under moderate exposure to arsenic (Peoples 1964). The toxic hazard level for cattle milk (1.5 ppm) was based on this level observed in a chronic toxicity case reported by Underwood (1977). 2.1.2.2 'oxic arsenic hazard levels for horses Few arsenic toxicity data for horses were found in the literature. The toxic hazard levels for horse kidney and liver tissues, 10 ppm and 7-15 ppm respectively, were concentrations reported by Puis (1981) (Table 6). The toxic level for arsenic in horse hair, 4 ppm, was based on a study by Lewis (1972) of horses in the Helena Valley. Arsenic content of mane hair in affected horses ranged from 0 to 4.5 ppm. The mane hair of one horse that died of the "smoked syndrome" contained 4.4 ppm arsenic. Two out of the three affected animals had mane hair arsenic levels greater than 4 ppm. No subclinical evaluation was attempted in this study and the affected animals also exhibited high concentrations of ]? 0141620 u c — ZO 4J C7- X -t = CD — cs — in m i 3 Z *3 in - .- X — a' Oj > z -. - — = a 2C ._':'; 0141621 lead and cadmium. Thus, the suggested horse hair arsenic hazard level represents a level of excessive exposure based on a very limited amount of data. It should be used with caution. 2.1.2.3 Toxic arsenic hazard levels for sheep The toxic blood and urine arsenic concentrations for sheep were reported as >5 ppm and >100 ppm , respectively (Puis 1981) (Table 7) . Values for blood and urine (14.5 ppm and 341 ppm) in two related studies by Shar iatpanahi and Anderson (1984a, 1984b) generally supported the toxic concentrations reported by Puis (1981). No additional support was found in the literature. Sheep kidney and liver toxic arsenic concentrations of >7 ppm and >8 ppm, respectively were based on data from Bucy et al . (1955). They found similar toxic effects produced by arsanilic acid, 3N-3-Ni tr o-4-Hydr oxyphenylarsonic acid and potassium arsenite at these levels. These hazard levels were in general agreement with the toxic level of >10 ppm for both organs reported by Puis (1981) . The toxic hazard level of 0.18 ppm arsenic in sheep milk was based on one study (Shar iatpanahi and Anderson 1984a). Animals in this study exhibited mild clinical symptoms of arsenic poisoning (Anderson 1985). The hazard level should be used with caution until additional data are available. 2.1.2.4 Toxic arsenic hazard levels for goats All toxic hazard levels for goats were based on the study of Shar iatpanahi and Anderson (1984b) (Table 7). These values should be used with caution until additional data are available. 2.2 Cadmium 2.2.1 Cadmium Literature Review Most experimental data regarding cadmium toxicity have utilized dietary cadmium levels far exceeding those commonly found in nature (Hinesly et al. 1985). Hinesly et al. (1985) concluded 1 ppm (dry weight) of biologically incorporated dietary cadmium 21 0141622 Q.CD Q.CO *J C* jj e* H) -J TO — ' m u r* l^ • TO C ■v TO c ■* .c o f\ X o — LO l/> 10 tn kJ TJ u •v * & c * * C ~T « — *D to -< c ~-t c CO < B CO < lO C* C9 ff> »M X) •^ -< -o r a a' — c ■ t ■D £ C "*" to CO T3U 13 -C C ^ «> C -w to co ^ to cc re a> — T> TO & — n n c to < 1 '— m 3 CB T3 T 3 T 3 u 0 u 0 *0 1/1 (0 tfi N \ N -V (D IP (C Ifl — _i X -I ai 01 T3 > 0> » O 0) C 0 ■a r u c TO V) N \ - w X — a> U > kJ tO LJ Ifl TO \ fl ■.. N W n tn TO — ' r — X a> s o > > u ov .* a - fcj _- j i> 01 0' 0 U u u u w ■C 3 ■O 3 r V O ~ o TJ O rc to «3 LO u tn N V. N \ 10 \ 01 > > o & C 01 * - o J .- J m J 22 0141623 "will have little if any effect on the health and performance of poultry." Exposure of livestock to excessive cadmium may result more from ingesting contaminated soils than from contaminated forage. The liver and kidneys are the main reservoirs of cadmium in vertebrates (Tables 8-11). Concentrations in muscle tissue are always quite low (Doyle et al . 1974, Osuna et al . 1981, Mills and Dalgarno 1972), but elevated forage cadmium levels will cause slight increases in muscle concentrations as well as significant increases in liver and kidney cadmium levels (Johnson et al . 1981). All studies of elevated cadmium in diet or water refer- enced in Table 11 produced increased cadmium levels in liver and kidneys. Other pathogenic states or abnormalities were produced by varying additions of dietary cadmium. In studies of lambs and the Long Evans strain of laboratory rats, 5 mg/kg in the diet or drinking water caused reduced growth or hypertension (Doyle et al. 1974, Schroeder and Vinton 1962). The experimental periods were long in both examples, 163 days for lambs and 1 year for rats. Production of metal lothionein by internal organs protects the animal from damage by the elevated concentration of the toxic metal until this protective mechanism is thwarted by prolonged overexposure. This mechanism is discussed more fully in Appendix section 6.1.2. The determination of the exposure of livestock to cadmium is difficult because of the scarcity of data on cadmium in readily available samples such as hair, blood or urine. The few documents available indicate that animal hair is a controversial tool for this assessment. Limited data suggest the background range for cattle hair cadmium concentrations will be 0.6 ppm or less (Powell et al. 1964, Wright et al . 1977). Available data suggest that cadmium in animal hair will likely be significantly correlated to dietary intake at diet levels above 50 ppm. Interpretation of hair data from lower diet levels may be difficult. Hammer et al . 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Elevated levels of cadmium in hair have been detected in animals exposed to dust from lead ore trucks and smelter emissions. Wright et al. (1977) found a good correlation between cadmium in cattle hair and cadmium (as cadminate) in feed for the range of 0 to 500 ppm. These authors found subclinical toxicosis associated with 15 to 21 ppm cadmium in hair resulted in reproduction problems (abnormal or dead calves). Lewis (1972) found an association between cadmium levels in horse mane hair with distance from a primary lead smelter. Diets containing 5 to 60 ppm cadmium did not produce any signifi- cant differences in cadmium levels found in sheep wool (Doyle et al. 1974). Combs et al . (1983) found cadmium in rat and goat hair was not significantly correlated to dietary cadmium at levels up to 15.9 and 18.5 mg/kg. Typical background concentrations of cadmium in the urine of livestock are less than 0.15 ppm for cattle (Wright et al. 1977) 0.0003 to 0.0213 ppm for horses (Elinder et al . 1981) and 0.01 to 0.03 ppm for sheep (Wright et al. 1977). Urinary excretion of cadmium does not appear to increase significantly in animals until proteinuria occurs, at which time cadmium excretion increases dramatically (Friberg 1952). Thus, increased urinary cadmium is an indication of kidney damage probably caused by the metal and does not indicate the extent of subclinical cadmium exposure. However, Roels et al. (1981) found a significant relationship between the total body burden of cadmium and urine cadmium levels in humans that lacked any renal dysfunction. Background cadmium concentrations in livestock blood are 0.005 to <0.05, <0.006 to 0.012 and 0.003 to 0-.17 for cattle, horses, and .sheep respectively (Penumarthy et al . 1980, Powell et al . 1964, Doyle et al . 1974, Mills and Dalgarno 1972). Roels et al. (1981) found a relation- ship between blood cadmium levels and total body burden but the correlation coefficient was 0.45. Doyle et al. (1972) reported increased blood cadmium when lambs were fed a diet containing 60 ppm; no significant blood effects were observed at lower dietary levels. Osuna et al . (1981) found no significant increase in the 31 0141632 blood cadmium level in swine fed 83 ppm cadmium in the diet. There were no significant differences in blood cadmium levels of lambs fed diets containing 0.7, 3.5 and 7.1 ppm cadmium (Mills and Dalgarno 1972). Similar results were obtained for goats that were fed 5.3 ppm cadmium (Dowdy et al . 1983). Cousins et al . (1973) reported that reduced hematocrit, due to induced iron deficiency, was the most sensitive indicator of cadmium toxicity in swine. Few data were found in the literature for hematocrit values and cadmium exposure relationships for other livestock species. Wright et al. (1977) reported little difference between blood cadmium concentrations in controls and cattle feed diets up to 500 ppm cadmium (clinical toxicosis). These authors found blood cadmium concentrations averaged 0.04 for all 12 of their test animals on diets of 0 to 500 ppm cadmium. Puis (1981) also reported that blood cadmium levels are not diagnostical ly elevated even in toxic environments. The cadmium content of cattle milk has been found to vary seasonally, generally being highest during the spring and summer (Murthy and Rhea 1968). Market milk tested by the same authors ranged from 0.017 to 0.030 ppm (mean of 0.026 ppm) and they found a range of 0.020 to 0.037 ppm in 32 individual animals tested in the Cincinnati area. Typical background values found in the literature ranged from 0.0001 ppm (Cornell and Pallansch 1973) to the 0.037 found by Murthy and Rhea (1968). Sharma et al . (1979) found no significant increase in milk cadmium levels from cattle fed up to 11.3 ppm cadmium in the diet. Levels of cadmium milk from three Holstein cows that were kept on a diet of 250-300 ppm cadmium for 2 weeks remained below the 0.1 ppm detection limit (Miller et al. 1967). Similarly, a study by Dowdy et al. (1983) found no increase in the cadmium levels in milk from goats that were fed up to 5.3 ppm cadmium. The most reliable indicator of cadmium exposure in livestock is the determination of metal levels in the liver and/or kidney. Mean cadmium concentrations in these organs from two-year-old slaughter cattle from non-polluted areas of the Northern Great Plains were reported to be 0.06 and 0.22 ppm (wet weight), respec- tively (Munshower 1977). These values were lower than the levels 32 0141G33 reported by Kreuzer et al . (1975) or the U.S. Department of Agriculture (USDA 1975), but these later surveys included older animals of uncertain age and background. The maximum ranges found in the literature for cattle kidney and liver tissue were 0.075 to 4 ppm (Penumarthy et al . 1980, Baxter et al . 1983) and 0.034 to 0.84 ppm (Penumarthy et al. 1980, Doyle and Spaulding 1978) re- spectively. It should be noted that both maximums were converted from the reported dry weight figures using the conversions found by Munshower and Neuman (1979). The highest apparently nontoxic concentration of cadmium in cattle kidney tissue found in the reviewed literature is the 57 ppm (dry weight basis) found by Baxter et al. (1982). The effect of 19 ppm cadmium in cattle kidney tissue (Sharma et al. 1982) was not clearly stated. Penumarthy et al. (1980) found cattle background kidney and liver cadmium levels of 0.075 to 2.500 ppm and 0.034 to 0.430 ppm, re- spectively. Similar values for horses were given as 0.840 to 5.000 ppm and 0.830 to 4.100 ppm. Because of the difficulty and expense involved in the acquisition of liver or kidney samples from animals in the field, a survey of animal hair may be a more realistic approach to determining cadmium exposure in a large group of animals. Urine may have some future potential, but little background data are available for interpretation. Cadmium in feces may provide an estimate of dietary intake (Chaney 1980). 2.2.2 Livestock cadmium hazard levels Documented cadmium levels in livestock fluids, tissues and hair are presented in Table 8, 9, 10 and 11. Cadmium hazard levels were derived from this data base. 2.2.2.1 Toxic cadmium hazard levels for cattle Cadmium levels in cattle blood are not a good diagnostic indicator of cadmium toxicity (Puis 1981) (Table 12). Powell et al. (1964) found the blood cadmium level in bull calves on a diet of 2560 ppm cadmium (toxic) to be <0.10 ppm. This value was within the same order of magnitude as most background blood 33 ■D O o c o w o fc 0141634 3 - O " O. 2 O u> a. - E a z.. - =u C C a. tr fl' C — 0 — L E - 1 " i - z T = ; c 'fl 9 > t -J 1 ■£ C - : e.' — : it — r -v C. - 3^ 0141G35 cadmium concentrations (0.005 to <0.05 ppm) (Table 8). The diagnostic use of cadmium in blood is not recommended. Cadmium concentrations in cattle urine are also of limited diagnositc use. The narrow range between background values (<0.15 ppm) and the only toxic concentration reported in the reviewed literature (0.7 ppm, Wright et al. 1977) (Table 10) suggests urine may not be a reliable indicator of cadmium toxicity. Toxic hazard levels selected for cadmium levels in cattle kidneys and liver are 44 ppm and 25 ppm respectively. The kidney hazard level is based on studies by Powell et al. (1964) and Wright et al. (1977) in which all concentrations equal or greater than 44 ppm cadmium in cattle kidneys were associated with toxico- sis. Similar results were obtained by these authors for cadmium concentrations in cattle liver, meaning all values in excess of 24.4 ppm were associated with toxicity. Puis (1981) reported values of 100 to 250 ppm and 50 to 160 ppm cadmium in cattle kidneys and liver, respectively, as toxic under chronic condi- tions . The recommended toxic hazard level for cadmium concentrations in cattle hair is >9 ppm cadmium. This hazard level was derived from the work of Powell et al . (1964) who found cadmium concentra- tions from 9 to 13 ppm in cattle hair to be associated with toxicosis. Wright et al . (1977) found levels of 15 to 21 ppm to be associated with subclinical toxicosis and levels of 57 to 88 ppm to be associated with clinical toxicosis. These authors found cadmium concentrations in cattle hair usually reached 100 ppm before death. Puis (1981) reported 40 to 100 ppm cadmium in cattle hair as toxic. The >9 ppm toxic cadmium hazard level should be an indication of possible subclinical toxicosis and should only be applied to large herds of cattle where statistical- ly valid and representative data can be obtained. Large varia- tions in hair cadmium concentrations between individual animals make an absolute application of this hazard level meaningless. 35 0141636 2.2.2.2 Toxic cadmium hazard levels for horses Data for toxic cadmium concentrations in the tissues of horses were very limited (Table 13). The recommended toxic cadmium hazard level for horse kidneys (75 ppm) is based on the results of Elinder et al . (1981). These authors found a signifi- cant (<0.05) relationship between cadmium concentration and histopathological changes in horse kidney cortex, and noted an increase in the frequency of the histopathological changes at cortex concentrations exceeding 75 ppm. The 80 ppm toxic hazard level for horse liver cadmium concen- tration is based on one sample from a horse that died from apparently being "smoked" from smelter emissions (Lewis 1972). To what extent ether metals may have affected this animals is unknown. This hazard level should be used with extreme caution until additional data are obtained. The hazard level for toxic concentrations of cadmium in horse hair is also based on the very limited data of Lewis (1972). This author reported a poor correlation between mane hair cadmium concentrations and cadmium concentrations in liver and kidney tissues. The use of this parameter is not recommended until additional support data are obtained. 2.2.2.3 Toxic cadmium hazard levels for sheeD - The toxic hazard level reported for cadmium in sheep blood is 0.1 to 0.2 ppm (Puis 1981) (Table 14). This range overlaped the background range for this parameter and is not considered diagnos- tic . The diagnostic level for toxic concentrations of cadmium in sheep kidney tissue (53 ppm) is based on the study of Wright et al. (1977) who found this level was associated with reproductive failure in sheep. With one exception, all sheep kidney tissue levels in excess of 53 ppm were associated with a degree of toxicity, where as all levels less than 53 ppm, with one excep- tion, were not associated with toxicity. The 53 ppm hazard level agrees well with the 50 to 400 ppm criteria reported by Puis (1981) for toxic concentration of cadmium in sheep kidney tissue. -jA c E '. D — D 0141637 w cr o C* fN — i /s *"" „, 1 DC 1 — - ~~t cr* 1 X JJ \ u Q> w I O w I U U 3 *■* ' 0) Q. in c r- C» i *— ea 5 rsi crv ™ V) — <— c . — _ — c^ c V f f%, — c >■ cs cc >. X >* 3 C» JZ C w JZ _r cs l • JJ c= a- o JJ B jj -J c; u * *o )_i u v c c c r; re _ IB C -3 > O CI o _: c > — — 0) t. a = o o z r rsj go C5> — ' o ^ — I cs Qj —< i in — co in T3 CD 1 o> C CT\ i *u • ^-* T TO ~-t 1 c — < — C 0) — 1 TO TO in Qm 1 (rt in 1 (^ u -< rn -o -< i/i o> d — c 3 a- c - 10 o c i E -J 1 - - I — = — d T — —> ±J "T • ^ rv CS C CD 3= C* r~ . C9 J-> IB c^ — 0) o — o o Q a S- ai it ~ 1 o — ' i l i m "-" i 1 < i V) 1 | —• i i i ■V 3 i i a. i i cr\ — c — 1 (0 in jj u- a 5 i 0141633 r-* (%J ~~ — SB- 'S I ±J cc a> c o oi 0i t 3 ■- V es c — 01 in cr> =s — :-. es -3 ex ~ es — ™ u fed 3 O O s r ■ — w v — D ; 1 re E- H _ •O c D O 6 o — o > e c. 01 > — u c. c c >. 0. a1 > c u 0' c, > -: c z 36 0141639 A sheep liver concentration of 13 ppm cadmium was selected based on the study of Doyle and Pfander (1975). These authors have reported reduced growth in lambs was associated with 13.2 ppm cadmium in liver tissue. Reduced feed efficiency and reduced growth were reported for sheep with liver cadmium concentrations in the 40 to 60 ppm range (Table 12), and Puis (1981) reported a toxic concentration of cadmium in sheep liver to be 50 to 600 ppm. The 13 ppm hazard level for this parameter should be used with caution until additional data are obtained. The toxic hazard level (>20 ppm) of cadmium in sheep wool (hair) is based on the >20 ppm cadmium Wright et al . (1977) found in the wool of sheep fed toxic levels of cadmium (as cadminate) over a 49 week period. Doyle and Pfander (1975) noted cadmium levels of 0.7 to 1.22 ppm in the wool of sheep fed 5 to 60 ppm cadmium (as CdCl2) over a 163 day period, but these levels also overlap typical background values (Table 9) . 2.3 Lead 2.3.1 Lead literature review The literature search revealed a considerable amount of data on lead levels in various animal tissues and other substances (Tables 15-18). These data suggest that lead levels in kidney and liver, which accumulate lead, and blood are good indicators of lead toxicosis. Concentrations of lead in these three tissues are elevated in all documented cases of lead toxicity. Furthermore, a considerable volume of data on background or control levels is also available (Ruhr 1984, Doyle and Younger 1984, Zmudski et al. 1983, Burrows and Borchard 1982, Schmitt et al . 1971, Dollahite et al. 1978, Buck et al. 1976). Fewer data are available on lead levels in spleen, heart, brain, pancreas, bone and hair (Tables 15-18) . Blood lead levels appear to be a good indicator of chronic toxicosis but are not as dependable for diagnosis in acute or subacute cases. 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C w a s > — ™ 3 3 3 S 3 3 sc ^ i b S-CBtT-l 1 i : ^ O B t 3 U C 'J U fN O — .X X IN ^ Of ■ I CD IT " - : (% (N v IN ' ^5 I CD — - U U — — w - — « o o ma • *j — c V V) Oi Zs c z o „ z. n. 3 |~ r. r- r- JZ o^ o-1 o^ o* ±J 4J w oi (i b » EC. O t C' <. rz '-J jj L £ C jQ c — — c- I 3 - - — *~> O U U IB V 01 O 01 £ ^ ^ ^ ^ [/; u jj *j jJ < u u u u < < < < zi n n xj n 0141646 j e 3 - ol&c -^ s -* -j* — - Csj V W"i ---.--*. e E E :- E Q, 1 c o o O — C * t^N E \ £ --- £ Q. V -T E "N CTN. ■s. ^ i CT E = C* a * .» ^ -. a. CD ■" „ O c U6 0141647 a moderate decline within a few hours. Allcroft (1951) found blood lead levels in calves up to 4 ppm within 12 hours of ingestion, a value which fell to 1 to 1.5 ppm in the following 48 to 72 hours, but remained elevated above background levels for one to two months. Zmudski et al . (1983) found that maximum blood lead levels in calves occurred six hours after intake of the metal. After 12 hours only about one half of the peak concentra- tion remained, but this level was still in excess of 10 times background. Sheep blood lead levels were shown to peak 4 hours following ingestion of lead acetate (Blaxter, 1950b). Buck et al . (1976) suggested that bovine blood levels from 0.10 to 0.35 ppm were significant as a primary etiological agent or as a predis- posing or contributory factor in lead toxicity. Background blood lead levels up to 0.21 ppm in cattle have been reported by Ruhr (1984). Similar background levels for horses range from 0.04 to 0.26 ppm. These values compare favorably with those reported for cattle (0.02 to 0.20 ppm), horses (0.04 to 0.25 ppm) and sheep (0.02 to 0.25 ppm) by Puis (1981). Burrows et al . (1981) found blood lead concentrations of 0.35 ppm or greater in nine percent of 118 horses and ponies he sampled in the North Idaho silver/lead belt. Two of these horses had blood lead levels of 0.7 ppm, but none of the horses exhibited signs of clinical toxicosis. It has been shown that high to toxic levels of zinc intake will prevent clinical signs of lead toxico- sis in horses. This may help explain observed cases of high blood lead levels where no signs of clinical toxicosis were observed (Willoughby et al . 1972b). Several horses investigated by Schmitt et al. (1971) displayed symptoms of advanced lead toxicosis at blood lead levels ranging from 0.20 to 0.34 ppm. It is evident from the literature that a great deal of variation exists in indi- vidual animal absorption, excretion or metabolism of lead (Dollahite et al. 1978, Zmudski et al. 1983). Attempts to use more specific blood parameters such as delta-aminolevul inic dehydratase (ALA-D) and blood-free erythrocyte porphyrins (FEP) to determine the level of blood lead have met with limited success. Osweiler and Ruhr (1978) found a good correlation (r = 0.9) of FEP ^7 0141648 with blood lead levels in calves, but poor correlation of ALA-D with blood lead or with FEP . A study by George and Duncan (1981) found levels of FEP in blood of experimental calves to be more uniform than blood lead levels and that FEP levels continued to rise 3 months following deletion of lead from the diet. These authors suggested the FEP test could be more sensitive than blood lead levels for subclinical lead exposure. Ruhr (1984) found no significant correlation of FEP or ALA-D with blood lead levels in normal cattle. This may have been due to the low blood lead levels in the nonexposed cattle he sampled. Blumenthal et al. 1972 found a correlation coefficient (r) of 0.11 between the ALA-D test and blood lead levels in children. These authors calculated that the ALA-D test would miss 33 percent of the positive cases. Furthermore, there are too few data to establish lead dose and ALA-D response in cattle (Bratton and Zmudski 1984). Lead levels in kidney and liver tissues, both background and elevated levels, are well defined for most livestock. Background levels for cattle kidneys range from 0.11 ppm (calves) to 1.77 ppm (Zmudski et al . 1983, Prior 1976). Similar levels for cattle liver range from 0.11 ppm (Penumarthy et al. 1980) to 1.44 ppm (Prior 1976). Background levels reported for horses range from 0.03 ppm to 1.3 ppm and 0.08 ppm to 1.4 ppm (Penumarthy et al. 1980) for kidney and liver tissues, respectively (Table 16). Puis (1981) has reported normal lead levels for horse kidney and liver at 0.5 ppm (wet weight). The tissue lead levels which are diag- nostically significant for lead poisoning have been reported by numerous authors. Fenstermacher et al . (1946) concluded that 10 ppm (dry weight) in liver tissue was a likely indication of lead toxicosis. Buck et al . (1976) stated that kidney or liver levels equal to or greater than 10 ppm (wet weight) were diagnostically significant for ruminants. Lead levels of 3.0 to 5.0 ppm and 5.0 to 140 ppm (wet weight) in kidney tissue have been considered an indication of lead exposure or chronic lead toxicity, respec- tively, in horses (Puis 1981). Acute lead poisoning has been characterized in cattle by kidney cortex levels above 25 ppm (dry weight) (Todd 1962, Garner and Papworth 1967), whole kidney levels i48 0141649 of 10 to 700 ppm (wet weight) (Puis 1981) and liver levels of 5 to 300 ppm (wet weight) (Puis 1981). Chronic lead exposure may produce kidney and liver lead levels 50 ppm (wet weight) (Table 18). Kidney tissues with 12 ppm lead have been reported in cattle killed from lead toxicosis (Every 1981) and levels as low as 4.5 ppm in foal kidney have been associated with chronic lead poison- ing (Schmitt et al . 1971). Levels of lead have been reported for spleen, heart, brain, bone, pancreas, hair and milk for several species (Tables 15-18). These values are generally an order of magnitude less than corresponding levels in kidney and liver tissues and are thus, subject to greater analytical error in de- termining the degree of lead toxicosis. Elevated lead levels in hair have been associated with chronic lead toxicosis in horses (Lewis 1972). A study of elements in cattle hair has determined that there are large variations in elemental concentrations among individuals within the same group and that lead levels in cattle hair show only a slight correlation to other metals (Ronneau et al. 1983). Significant correlations (p = 0.01) between hair and liver concentrations of cattle were found by Russell and Schoberl (1970). Dorn et al. (1974) found one to two orders of magnitude increase in lead concentrations in hair of cows exposed to industrial pollution when compared to controls. Levels of lead in milk are generally low, but have been used to estimate the degree of chronic lead poisoning. Milk lead levels are usually about two orders of magnitude less than kidney and liver samples and thus milk samples are less sensitive and more prone to contamination. Murthy et al . (1967) reported background levels of lead in milk from cattle ranged from 0.023 to 0.079 ppm with a mean of 0.047 ppm. Hammond and Arcnson 11964) reported a mean and range of .0.009 and 0.006. to 0.013, respec- tively, in 8 animals. Lead levels in cattle milk indicative of toxicosis have been given as 0.10 to 0.25 ppm (Puis 1981). This author also indicated that a dietary intake of 100 ppm lead was associated with lead toxicosis. In summary, it appears that kidney and liver tissues offer the best indication of lead toxicosis. Because of the expense and A9 0141650 limited opportunity to obtain these samples, the analysis of blood may provide a good alternative. Blood lead levels are moderately well defined in the literature and sampling and analysis are relatively simple. The specific blood parameters of ALA-D and FEP may provide a means of determining lead intoxication in the future, but at the present, insufficient data exist to fully utilize these parameters for livestock toxicolog ical evaluation. Hair samples may be used to indicate long term chronic lead exposure if a sufficiently large sample base is obtained. A hair lead content of 10 ppm has been reported as indicative of exces- sive lead exposure (Puis 1981). More detailed studies could make use of biopsy tissues of liver and bone, and feces can be analyzed to' determine dietary exposure (Decker et al . 1980). 2.3.2 Livestock lead hazard level The data contained in Table 15, 16, 17, and 18 and other publications were used to develop lead hazard levels in the following sections. 2.3.2.1 Toxic lead hazard levels for cattle The 0.35 ppm toxic blood level selected for cattle is based on several publications (Table 19). Buck et al . (1976) suggested the level was indicative of probable clinical toxicosis. Buck (1975) stated ".Concentrations >0.35 ppm in cattle should be considered as evidence of unusual exposure," That statement was based on the observation of 142 animals, of which 52 exhibited symptoms of clinical lead toxicosis and had blood lead levels ranging from 0.19 to 3.80 ppm, with a mean of 0.81 ppm lead. Hammond and Aronson (1964) observed that, in acute lead poisoning in cattle, blood lead levels were never less than 0.35 mg/1 . The 0.35 ppm blood lead concentration was reported by Puis (1981) as indicative of toxicosis in cattle0 The value is supported by other data from the reviewed literature (Tables 15 and 17). The highest concentration of lead in cattle blood at which toxicosis has not been noted is the 0.29 ppm reported by Sharma et al. (1982) . en c ^-> •D C o M g O L 3 10 in DQ z: — rn -T « *. \D cs «—. *— . 0* LO ,— ^ r- cc — - ON er» *-4 ^ C — O V) J£ i/, c u ^-i o 3 D u 03 a. < E TO A M u M3 rg ID H AJ r~ cc jC »c OJ O^ 0> to — . — i AJ — ■H w «— - 1 t. 01 •—I JC 1 — ■ CD VI • E t O T J* 0* rsi *^ — £ 1 — * CO u .—1 ^ D re re ~ 1 c^ r — ' E kj — 1 1 •—* CL 1 N ^O o 1 W 0) cr* 1 VD «. — • in » 73 -< 1 — D . — i ^r C — — i fM C^ — i U «J <*- cc cc D >. o* *D CT\ CO ^ hJ J.' ~- C — i Q. : Of ' TO ' ' « o > u • «■-. n f-i »o Ql — i \D — i CO w -o C T r- ■D one cy c* a, -< X * ^ re u — re 0J T3 c jc u re CC - —J ~ rsi CL s I l _ PNl rg CD •t; C* nj 0' • 0) nj t_3 I TJ C in re C5 • JC cs> re V c re ' en in ~ es ° 0.' T3 C e 3 rs r o — ' — I IS <3 3 a. IN CT\ - c re £ a1 it E a 10 0! O £ O re ^3 re - u 3 re C N en re \ ~ tn i — — OJ o > o 1 . — - CD OJ OJ '-' T) O — kj u u ^ r re 3 re c N O r. in re en re \ x \ r w. en ~- >.-■ c 0J 4) ai c > c > — 0J ■a iv u hj — j ~ & 0' o — kj u 3 r^ 0 N UI re v. x I" — u a c > > 0J — - a> -. o '. tu u - r T3 3 u c u o re en re in N \. N \ re in re in I — i X — c 0' 0' u > JC > — a -i Cj re ■J — ■ lJ ~ r - 01 B C o 0J r re > 51 0141652 Background concentrations for lead in cattle kidney tissue range from <0.05 ppm to 2.29 ppm (Flanjak and Lee 1979). The highest nontoxic value reported for this parameter was 4.04 ppm found in the kidneys of dairy cattle fed lead acetate (Sharma et al. 1982). The toxic lead hazard level of 6 ppm for cattle kidney tissue is based on the study of Logner et al. (1984). These authors fed elevated lead (as lead sulfate) to calves for 7 weeks and noted acute toxicity symptoms and one fatality in the 4 calves receiving a diet with 1501 ppm lead. The surviving calves exhibited a mean kidney lead concentration of 6.38 ppm. This level agrees with other data in the reviewed literature in that all levels >6 ppm were associated with toxicity and all levels <6 ppm were nontoxic. A 10 ppm lead concentration in cattle kidney tissue was reported as toxic by Puis (1981) and Buck (1976). Background lead concentrations in cattle liver tissue range from <0.05 to 1.44 ppm (Flanjak and Lee 1979, Prior 1976). The toxic lead hazard level for liver tissue of 5-12 ppm is based on the 5 to 300 ppm criteria reported by Puis (1981). All cattle liver lead levels in excess of 5 ppm reported in the reviewed literature were associated with toxicosis. All values less than the 5 ppm, with the exception of a 3.5 ppm value reported by Logner et al. (1984), were nontoxic. Buck et al . (1976) stated that liver levels >10 ppm lead we.re diagnostical ly significant for ruminants . The typical background range for lead in cattle hair has been reported as 0.5 to 5.0 ppm (Puis 1981) and apparently may average close to 5 ppm near highly developed areas such as Los Angeles (USDA 1975). The toxic hazard level of 10 ppm lead in cattle hair is the value given by Puis (1981). No other data were found in the reviewed literature to substantiate this hazard level. Background values for lead in cattle milk range from 0.02 to 0.420 ppm (Keheo et al. 1940, Murthy 1974). The toxic hazard level for cattle milk (0.15 ppm) is based on the work of White et al. (1943) who noted mild lead poisoning symptoms associated with this level. The 0.15 ppm level is in agreement with the toxic 52 0141653 level of 0.10 to 0.25 ppm lead reported by Puis (1981) for cattle milk. 2.3.2.2 Toxic lead hazard level for horses The basis of the toxic hazard level for lead in horse blood (>0.34 ppm) is, in part, the report of Schmitt et al . (1971) (Table 20). These authors found toxicosis in horses with blood lead levels that ranged from 0.20 to 0.75 ppm. Some of the observed toxicity symptoms in this study were likely due to zinc contamination. Burrows and Borchard (1982) noted that after feeding contaminated hay containing lead acetate (423 ppm) for 5 to 6 weeks, ponies exhibited blood levels consistently _> 0 . 3 ppm. These authors found that blood lead concentrations "did not increase consistently at onset of clinical toxicologic signs or just before death". Blood lead levels in four ponies fed lead acetate did not decrease below 0.39 ppm after clinical toxicosis was noted and most concentrations were _> 0 . 5 ppm (Burrows and Borchard, 1982). The 0.34 ppm level is the lowest toxic value found in the reviewed literature that is still above maximum background values. Puis (1981) reported a toxic range of 0.33 to 0.50 ppm for this parameter. The toxic hazard level for lead in horse urine (0.50-5.0 ppm) is the range noted by Puis (1981). Few data were found from the literature to substantiate this range but it was generally supported by the report of Schmitt et al. (1971). The selected lead hazard value of 10 ppm for horse kidney tissue is based on the findings of Buck et al. (1976) and Schmitt et al . (1971). Schmitt et al . (1971) observed toxicity in foals with kidney levels ranging from 4.5 to 20 ppm. The apparent toxicity in this study was likely due in part to high levels of zinc. Eamens et al. (1984) reported one case of clinical toxicity with a kidney tissue level of 8 ppm lead. Puis (1981) noted toxicity ranges for horse kidney tissue of 5.0 to 140 ppm and 20 to 200 ppm for chronic and acute poisoning, respectively. Buck et al. (1976) suggested 10 ppm in kidney tissue as diagnostic criteria for lead poisoning. 53 0 H E a' Li — al lrmm Jtf ~-l U — J* , — •0 r» 3 — ( U — 1 c C* m en 3 CO CD T3 — - — CD _ .— « ~-i n D _* ^ _« — n -— •— ' 3 V i — i CO ,_■ r- in T o iTl *-4 , in cr\ c* in cd w cm u CD (T _i 1 ,™i — i l c* — 1 —4 L4 o» en i — w 3 f4 3 3 — — i AJ cs> a. (9 — a. 1 aj fM 1 w Q a> V) CD in „< in — , — * m s ■■ o\ CD in jj 3 « \0 -J VD — 1 — ^ H rsi ~^ jj cs G, *. p^ ■k IC r*» ra — ■ 3 — es jj c* B e*\ p-* B> a. E ~* a — " — JJ Of ^2 Cft u U JJ *"" •0 0141854 — — H c — ' in u E « a' to — ■ u E 3 TO U JJ ID JJ a> O W 0J LJ 0) _ CO r>j — ** r B ID jj 1 jj a a> B QJ r\j j-j jj u — ' cn o Q rsj aj E U c D - 0 """ 'j it "J m - — ° in U > ai u ^ c a' jj c 01 s n — * c — 3-i ts — o j"» ^ >-c^ X — ' £ — ' XJ ~— JJ — kd — TO • It • e _* E — 5 re = re c c oi jj a> jj C tt) c a in rsj S — ' • r- ■ CO CM C^ B> C^ — — " 1 — - 1 — * r- in \j? in C6 — C5 — • 3 © 3 - a> . a. j B" Sv c u c - = T *■ 0 -" if, C 6 C ^ — - -c J - z T y] N ^v TO it: ~ pH 1 kj :< a( & > J w re N tn re 0) > kj o a> u w o *Q t*; Sfc. I*. * o — > j^ — i QJ CI. 0141655 The 10 ppm toxic hazard level for horse liver tissue is based on Schmitt et al. (1971), Eamens et al. (1984) and Buck et al. (1976). Schmitt et al. (1971) found a range of 9.0 to 48 ppm lead in horse liver tissue of animals exposed to industrial pollution near Trail, British Columbia. Eamens et al . (1984) found 10.0 ppm lead in liver tissue of a horse exhibiting clinical toxicity symptoms. Similar levels (11.8-17.2 ppm) were found associated with clinical toxicity by Knight and Burau (1973). With the exception of one horse with a liver tissue lead concentration of 11.4 ppm (Dollahite et al. 1978), all horse liver tissue samples with >10 ppm lead were associated with toxicity. Puis (1981) gave ranges of 4 to 50 ppm and 10 to 500 ppm in horse liver tissue as indicative of chronic and acute toxicosis, respectively Buck et al. (1976) indicated that the 10 ppm lead concentration in liver tissues was diagnostic of lead poisoning . The reports of Lewis (1972) and Burrows and Borchard (1982) are the basis of the toxic hazard level for horse hair. Lewis (1972) found elevated lead concentrations (9.6 to 25.8 ppm) in 3 of 4 affected horses studied in the Helena Valley. The effects of the interaction of elevated levels of other metals on the apparent toxicity noted in this study were not documented. Burrows and Borchard (1982) studied ponies on diets of contami- nated hay (from the Coeur d'Alene River Basin, Idaho) and on diets with added lead acetate and found hair lead concentrations of 12.2 and 13.4 ppm for the two groups respectively. These authors suggested that the interaction of cadmium in the contami- nated hay "markedly increased ... the severity and rapidity of development of the clinical toxicologic signs and hematologic changes" . No elevated horse milk data were found in the reviewed literature (Table 17). The toxic hazard level is the Level published by Puis (1981). 2.3.2.3 Toxic lead hazard levels for sheep Fick et al. (1976) found concentrations of lead in sheep olood from 0.18 to 0.28 were nontoxic. Blaxter (1950a) noted sheep blood lead levels of _> 0.45 ppm were associated with toxicosis, which was the basis of the toxic hazard level for this 55 0141656 parameter (Table 21). Puis (1981) reported sheep blood lead levels in the range of 1.0 to 5.0 ppm were toxic. Toxic lead concentrations in sheep urine were noted by Blaxter (1950a) and ranged from 0.28 to 0.81 ppm. The 0.28 to 0.32 ppm toxic hazard level for lead in sheep urine should be used with caution until more data are available. Toxic lead levels in sheep kidney and liver tissues were reported as 5 to 200 ppm and 10 to 100 ppm respectively (Puis 1981). With minor exceptions, data in the reviewed literature tended to support these ranges. The toxic hazard level for lead concentrations in sheep wool (25 ppm) was reported by Puis (1981). No data were found in this review to substantiate this value. 2.4 Zinc 2.4.1 Zinc literature review Zinc is an essential element and most animals can tolerate relatively high dietary levels. Few cases of natural zinc poisoning of livestock have been reported in the literature. Most episodes of poisoning involve contamination of livestock feed (Allen 1968, Grimmett et al . 1937, Sampson et al . 1942, Davies et al. 1977). Experimental zinc toxicosis in livestock has been studied and described in several reports and much of these data are reviewed here. The uptake of toxic amounts of zinc affects many organs directly or interferes with the metabolism of several other elements, notably iron, copper, calcium and cadmium. Cadmium acts synergisticly with high levels of zinc, enhancing the toxic effects of zinc (Thawley et al . 1977). Cadmium also tends to reduce the absorption and retention of zinc (Miller 1969) . Zinc absorption is higher in young animals than in older animals, making them more susceptible to zinc poisoning (Davies et al. 1977). The degree to which the diet composition affects this re- lationship remains unresolved. Diets containing 200-400 ppm zinc have been shown to produce clinical copper deficiency in diets 56 0 H 1 V C 2 J* -*' U u « _< u. ^ Uj » r-> — fN| m P4 T •a «"-» e* C ~ c — i *D <0 — C «0 — CB •— ■ z \c r «x- •0 — r- _ r* I t-i ^ cr* r. — « CT\ & C3 a — tS ec -- cr jj CS cr\ w <—» C* — 0141657 —4 C» — « - El — a. z 13 B h 1 c. o = g = re rv if r^ = — s — — c JJ — a — ■£ CC re •*■ IT — -H • >c 3. «_ rsi r-- — 3 — s re =■ re X CT\ £ r cs _ 5 * - — - v a • jj n CC JJ a U U5 re jj jj a z a> a C5 re > o w IB J- re * a Qj a 0) L L 0 ~ i. •~ *C -- - s - >. a =■ o a c i cc ot Cw — "J T-J >*- 3 > ^ a. .* a — ^ — _: r V 1 i O — 57 0141658 with low copper content (Hill and Matrone 1970). Campbell and (Mills (1979) produced a severe copper deficiency in pregnant ewes on diets of 750 ppm zinc. The form of zinc is another important factor in zinc toxic- ity. Smith (1977) found that zinc sulfate was more rapidly excreted in the urine of sheep than was zinc oxide. Zinc sulfate has also been shown to accumulate less in tissues when given at the same concentration as zinc oxide (Miller et al . 1970). The sex of beef cattle has been shown to affect the amount of zinc ac- cumulated in tissues, but the threshold level of zinc (900 ppm Zn diet) necessary to produce toxicosis was found to be similar for both heifers and steers (Ott et al . 1966b). It is apparent from this discussion that a given amount of zinc, within limits, may or may not produce toxicosis. Many studies have attempted to determine threshold toxic levels of zinc in various animals. These studies are summarized in Tables 22-25. Excessive absorption of zinc is controlled up to a certain dietary level by the body's homeostatic mechanisms. In lambs, 'this system is effective up to a dietary concentract ion of ap- proximately 1000 ppm (Ott et al . 1966c). For calves, the level is somewhat lower, as large increases in tissue zinc content have been observed at dietary levels of 638 ppm (Miller et al. 1971). Higher levels of zinc overwhelm -the homeostatic mechanisms and significant increases of zinc have been observed in liver, kidney, pancreas and blood serum (Tables 24 and 25). Miller et al. (1971) found that zinc levels in whole blood did not correlate with dietary zinc levels up to 638 ppm. Similarly, normal skeletal muscle has been shown to be highly insensitive to dietary zinc. These two livestock tissues would be of little use in" monitoring zinc exposure. Zinc levels in blood serum, liver, kidney and pancreas have been shown to correlate with dietary levels of the element. These three organs tend to accumulate similar metal levels and are about two orders of magnitude greater than levels found in serum. Allen et al . (1983) found that the pancreas is the only organ consistently affected by zinc toxicosis and 'suggested that pathological changes observed in the pancreas could 58 0141G59 to -c — 5 z" z: *7Z~ in M> f* WW * * 3, yj-.TTH'^^^ """ ^ 2 — — — — vC^CCr-r- ^ 3 \. — — — • ^ ^ C C ff* C" . . . — — . <-i *i — — (D TO (0 > C C--N 1 ..-■■-- TO TO TO TO O^ Qj 1 Qj TO TO *"* "2 - - - 1- - -' V 1 Q T >. »- q (Jj Q; Cl ftj jc jc C C (D • — ^^fOTOOOTOOi o a 0 IT, W 1/1 " a. w > > ^ >*- d> ru to to to Cj CT> C1 J* ff1 0s — sC VC — __ — TO VC \D —■ — o> 0- *^ TO — TO C r jj > — • — a, *> ■J c «o rc 0 O w w It j-» «m 0i c z *- a a c 0 c u yp : QJ C7* 0> — (0 T u QJ — wo: 0> ON ■D — C — a- DC w 0* 4J 0J — es k. 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CD • r— ON .— < «-t 0 Li C 3 3 a. ^— ^— ^^ *U ^H ® vo r- r- \D Oi CT\ w — 0 v£> —i r— ( DC ' r- a in 3 ^ a 01 13 O (V 10 u ai > e a o t-i a u ID CO c (0 M Ch 0) -— i JJ T ffl "*■ a> qj r- ^H CD (-1 JJ m 4-» — . m hJ 1 o 1 CD i *X o> T) p* 1 (~M Cft • c S (— « IN TO ts — * • — i I-* .—1 .— < J£ CD • TO CT> iH I—! -H TO c 3 a. rH (0 TO 1 (0 *J *J *£> 4J a> a n QJ i — i kd u 4J a* oj JJ .—I ^H G «— 1 i— < CO -M CTi c 01 I ^ T ■D • C r»i ie 3-. >0 c re. O CS -*: cc *- i p- TO cm • & *T i — «T pH X) in 1 1 1 VC — c^ CC m Cr- ^ • r* r- CNJ __ 10 TO • cr 4J (0 — ' 01 4J t/1 M 0j W QJ QJ ^ C C _ w C £ 0 OJ is. O = re - ro C U •a k-t u 3 ra 0 N ir. 10 \ ~ U! rH E o> 3 > u c 01 _ U3 OJ 0) o ■c U "0 « fc-t u u - ra 3 (C z N O N to (0 t/3 ro \ z •-N. VI 1/1 rH >. — T a c a O > ~ > o 01 -r 01 ^_ J -" ^ c u: T u u r ra c n l" ra \ I I" — u 0) 01 > > 0) >«^ - _ c 01 u u u kj ~ 3 TJ 3 — 0 M C It w ra 1/3 N \ N \ ra V. ra 1/1 r IH x F-< c 0) w 5> x 7* — i a < — i 0. ra j — J r: £ 67 0141658 values for zinc in whole blood are apparently slightly higher than respective values for serum. The background range for zinc in whole blood is 1.02 to 3.74 ppm (Miller et al . 1968, Bertrand et al. 1981). The background range for zinc in .cattle kidney tissue reported by Flanjak and Lee (1979) (12.9 to 31.6 ppm) encompasses all other background values found in the literature. The highest reported nontoxic value for this parameter was 76 ppm (Ott et al. 1966d). The toxic hazard level suggested for zinc concentrations in cattle kidney tissue is 130 to 140 ppm. This range is based on the 130 ppm level reported to be toxic by Puis (1981) and the 140 ppm found to be toxic by Allen et al. (1983). Flanjak and Lee (1979) reported the maximum background range (13.4 to 99.2 ppm) of zinc in cattle liver tissue and Ott et al . (1966d) noted that 86 and 159 ppm in calf liver tissue were nontoxic but also noted that 136 ppm was toxic. The 86 ppm tolerable level for this parameter is thus based on the highest nontoxic value below the lowest reported toxic value. The toxic hazard level of 300 ppm for cattle liver tissue is based on the work of Ott et al . (1966d). These authors reported toxicity at liver zinc concentrations of 136 to 326 ppm. Several authors reported nontoxic liver zinc levels in the interval of 136 to 186 ppm. All values derived from the literature which exceeded 300 ppm were associated with zinc toxicity. Puis (1981) reported a value of >500 ppm as the toxic concentration of zinc in cattle liver tissue. Background values of zinc in cattle hair have been reported to range from 79.2 ppm (Miller et al. 1965b) to 142 ppm (Ott et al. 1966d). Zinc concentrations in cattle hair associated with toxicity ranged from 154 to 173 ppm (Table 24). With one excep- tion (158 ppm) , all values which exceeded the suggested 154 ppm hazard level were toxic. Puis (1981) reported a range of 100 to 150 ppm zinc in cattle hair as high ("levels elevated well above normal but not necessarily toxic"). No other data were found in the reviewed literature for this oarameter. 68 ' ' 0141669 The range of background concentrations of zinc in cattle milk is 2.8 to 4.780 ppm (Dorn et al. 1975, Parkash and Jenness 1967). The toxic hazard level of 8.4 ppm zinc in cattle milk is the level reported by Puis (1981) as indicative of toxicosis. This value was derived from Miller et al„ (1965a) who noted a slight reduc- tion in milk production at that level but no other apparent toxicity to the 24 dairy cows used in the study. 2.4.2.2 Toxic zinc hazard levels for horses The hazard level for toxic zinc concentrations in horse blood is based on only one study provided by Eamens et al . (1984) (Table 27). This hazard level should be used with care. The suggested hazard level for toxic concentrations of zinc in whole blood of horses (5-15 ppm) is the range reported by Puis (1981). No additional support data were found in the reviewed literature. Diagnostic levels for zinc in horse kidney and liver tissues were reported between 295 to 580 ppm and 1300 to 1900 ppm, respectively (Puis 1981). The limited data of Eamens et al . (1984) suggested ranges of 180 to 580 ppm and 1200 to 1900 ppm zinc in horse kidney and liver tissue respectively may be more ap- propriate. The hazard level for the toxic concentration of zinc in horse hair (280 ppm) is based on the very limited data of Lewis (1972). The 280 ppm level was the concentration found in a single horse that subsequently died. The hair of other horses in the study ranged from 140 to 430 ppm zinc. Toxicity was not noted in a number of horses with hair zinc levels above 280 ppm. This level should best be considered as an indication of possible excessive exposure to zinc and as with most hair data, sufficient numbers of animals should be sampled to provide a meaningful statistical confidence. 2.4.2.3 Toxic zinc hazard levels for sheep and goats The toxic hazard level reported for zinc in sheep serum is 7.1 to 44 ppm (Table 28). This range was derived from data reported by Ott et al. (1966c). These authors reported reduced 69 , CO CB c E er QJ in 'J c 3 E 1) O J o () o in i — i 0) > c c X) c r e r- 9 CTn CO «— 4 | 1 ?N *■" 1 1 1 1 tn l •p* 1 1 1 as 3 1 1 1 '~* Of 1 1 I rsi -J 1 E — a> 0) as cm in — in CD V) m r*- in c CC c cm cr* <-■> • T 01 QJ ^H ~^ 1 E 1 F. 1 — i . at CM — — ^J QJ 3 a. a' SI 0) 01 0 0 0 u u •a ^ u T 3 •D = _ ^ TJ = " 0 Li O c ^ Li C IZ to Ni? ~ L". A n\ S^s N\ id in fC w = cr ,«; CJ E > ■o > 11 ? u > 3 CJ o oi c 0/ 01 o Li kj o — T) — > fcj 01 (B — 1 (0 ~- = 0) 01 > > u 01 J* 0) _ *J •J 0141 *. «.> 70 70 0141671 I U VP Oi\D — r-i cr< —* ,-t CD *o *-• cr* c -« *n • — ' ij 3 1 0) n. .- J u T1 iJ £ r* o IQ ■*» « n* © — u m cd CD Ol *— \o 00 CT* cr* cd £ VD f* cr £ C^ — ' i-< (J*-. rr in ~^ •■H — ' . r- m X — « *£> . _j — < U • z. ' •—* f* 10 0i ~* — _. cc 1 J-» «0 «J C^ ' tfi in — ' in 01 m to JJ I 0> •0 tfl 0) o •O *D ^. AJ *- C »- J-» 7 * C O Cb .-4 — < iw < 0' C — it t 3 - C C u .= in < (T1 (Ti — * -- ID a ID *■> z & ID " c E > It w c C 0. c — ~ at w > ai Oj > — t\ k in ic — = a1 > w a' ._ _ t c C — 71 0141672 feed efficiency in sheep with serum zinc concentrations as low as 5.24 ppra. All serum values in excess of 7.1 ppm, found in the reviewed literature, were associated with severe toxicity. Puis (1981) reported a 30 to 50 ppm toxic range for this parameter. The' toxic hazard level for zinc concentrations in sheep kidney, 185 to 325 ppm, is based in part on the publication of Ott et al . (1966c). Data for sheep liver zinc concentrations indi- cated most values above 185 ppm were associated with toxicity (Table 25). The only exception was a value of 2153 ppm (dry weight) reported by Telford et al. (1982). Puis (1981) reported a toxic concentration for zinc in sheep kidney tissue as 1000 ppm. This concentration would appear too high based on the reviewed 1 i ter a ture . The 400 ppm toxic hazard level for zinc in sheep liver tissue has been derived largely from the work of Ott et al. (1966c) who found that concentrations near or above this level were associated with toxicosis. Data from the reviewed literature suggest toxicity is not uncommon in the 200 to 400 ppm range for this parameter. All sheep liver zinc levels in excess of 400 ppm, were toxic. No zinc toxicity data for goats were found in the litera- ture reviewed (Table 29). 72 c 0141673 c r 0' 3 E Q' D -> cu JO IT c ■- 0 0 w hJ ^ c ~ Jf u u TO B a* IT i n • TO • ID in jj Ps) 0) 01 — - 0) 1 c — • rg r c o c it ■c e ie it ■o e IT a 0 C o> 0 0 y u o o ~ _ u u u "^ - k. — c 5 — 3 u C 3 3 ^ c <- C c w *" LC ^- LC 2\ N \ IT V. * 10 C i- It IT. — W fT ^ . d , > > > IS *- — O 0.' O — o; > C 0' ■o — o 5 w 0. ._ - n .* a 73 0141674 3.0 LITERATURE REVIEW AND HAZARD LEVELS FOR SOILS AND PLANTS Heavy metal levels in soils and plants are of concern for two primary reasons: 1) decreased crop and livestock production; and 2) the introduction of certain toxic metals into the food chain and their consumption by humans. The "soil-plant barrier" (Chaney 1983) reduces the risk from exposure to certain elements which are either not translocated to plant foliage (lead) or produce phytotox ici ty in the plant at concentrations safe for animals (zinc, arsenic). Of the selected four metals evaluated in this manuscript (arsenic, cadmium, lead and zinc) only cadmium readily passes the soil-plant barrier. It should be noted, that ingestion of soil and dust by livestock or humans bypasses the soil plant barrier and increases the risk of exposure to toxic concentrations of all pollutants. It has been shown that extractable soil levels of lead, cadmium and zinc generally show better correlations with plant uptake than do total soil levels (Neuman and Gavlak, 1984). Chelating agents such as EDTA and DTPA have been extensively used to evaluate agronomic characteristics of soils and overburden materials in western states. The correlation of total or extrac- table arsenic levels with vegetation uptake has been more diffi- cult to define and a special discussion has been included for a review of this problem. Numerous technical problems present themselves when universal phytotoxic hazard levels for soils and plants are to be defined. Some of the more important of these are: the toxic element, soil pH, soil organic matter content, soil cation exchange capacity (CEC) , soil texture and the plant species involved. In general, there is an inverse relationship between microelement availability to plants and the soil pH (Logan and Chaney 1.983). Molybdenum and selenium are the only notable exceptions, both of which become more available at higher pH. The Soil Survey of Broadwater County Area, Montana includes a portion of the Helena Valley study area and all background sites. All mapped soil units, except small areas which are poorly drained, exhibit calcareous to strongly Ik 0141G75 calcareous conditions (U.S. Soil Conservation Service, 1977). Mean pH values of surface soils (0-4 inch) for the background sites and the project area are 8.0 and 7.2 respectively. The pH values in the project area ranged from 4.7 to 8.2 and, except for an area in and near the City of East Helena, were generally >6.5 (EPA, 1986). A pH level of >6 . 5 is considered to be effective in reducing the availability of metals (Chaney 1973, CAST 1976). The selected phytotoxic soil criteria are generally based on soil pH levels greater than 6.5 when these data were available. Other parameters are discussed in the following sections on specific element levels . All elemental levels for plants and soils are reported in parts per million (ppm) dry weight basis unless otherwise noted. 3.1 Arsenic in soils and plants 3.1.1 Arsenic literature review Arsenic is present in all soils, with typical values ranging from 0.1 to 40 ppm total arsenic. In plants, background concen- trations vary from 0.01 to 5 ppm ( Kabata-Pend ias and Pendias 1984). Natural elevated soil values of up to 8000 ppm have been noted in a few rare cases (Kabata-Pendi as and Pendias 1984). However, such excessive levels are usually due to soil application of arsenic-containing pesticides, or less frequently, from smelting operations. Inorganic arsenate of low solubility makes up the largest fraction of soil arsenic. The availability of this arsenic to plants and the potential for plant toxicity is depend- ent upon many factors, some of the major ones being: soil pH, texture, and fertility level; and plant species (Wauchope 1983). The interactions possible from these factors complicate the interpretation of phytotoxic soil and plant arsenic levels. In general, soils with higher levels of easily soluble arsenic will increase the risk of reducing plant growth (Walsh et al . 1977). The results of a number of studies regarding toxic levels of arsenic in soils and plants are summarized in Tables 30, 31 and 32. 75 0141G76 04 ^ ^ ^» ^ * --*»< - ■ — — .- ■ o o o o o o o o 3 * * * o o o o o o o o o • %, (. C £ .C C > > • * * £ t 1 t b kr r c c c c c c t. * C o c o > > *e « r * 4> * — — «, i O C O C *- *• o c c t - -> w- s t : j ^ ir» ^> *o z » Oi a a o» «■ a » *^ ^ **"* ^ C. C B. 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W 3 Oi O1 TO 3 re jj C c re CV JJ Ad JJ ■— «m g ^ ^ e E — re jj 0i jQ TO jO TO TO JJ "T ~ - - - — w c E jj 01 JO E >■ E 0' c TO TO 01 TO TO a. 01 Z 0 - re — O C X L K cc EQ cc oa CO E E- u u u — CO H 3 80 0141631 It has been noted by investigators that chemical analysis of the total soil arsenic is not a reliable indicator of potentially phytotoxic levels in vegetation (Albert and Arndt 1931, Vandecaveye et al. 1936, Woolson et al. 1971b). This has led to attempts to develop soil tests for plant-available soil arsenic that can be correlated with symptoms of plant toxicity. A greenhouse study by Benson and Reisenauer (1951) found no satis- factory correlation between soil extractable arsenic and plant growth by four different extracting solutions (NaCl , NaOAc + CH3COOH, H2S04, NH4F+HCL) Vandecaveye et al . (1936) believed that the condition of field crops in the state of Washington was closely related to the amount of readily soluble arsenic. However, others have noted that such easily soluble arsenic is best used as an indicator only for those soils that have had recent arsenic applications (Carrow et al. 1975, Jacobs et al. 1970). Johnston and Barnard (1979) evaluated 14 different arsenic extracting solutions on four New York soils. The arsenic extrac- tion ability for the 14 solutions was (in increasing order): water = IN NH4CI = 0.5M CH3COONH4 = 0.5M NH4NO3 < 0.5M (NH4)2S04 < 0.5N NH4F = 0.5M NaHC03 < 0.5M (NH4)2C03 < 0.5N HC1 + .025N H2S04 < 0.5N HC1 = 0.5M Na2CC>3 = 0 . 5M KH2PC>4 < 0.5N H2SC>4 = 0.1N NaOH. They made no specific recommendations for the use of any particu- lar solution, but noted that basic solutions were more effective in arsenic extraction than were neutral solutions, and that phos- phorus and arsenic reacted ' simi larly to solutions containing bicarbonate or hydrogen ions. The soil chemistry of arsenic is similar to that of phospho- rus; its principle chemical form is that of arsenate (As04~3) which has been occluded or adsorbed on hydrous aluminum and iron oxides (Ganje and Rains 1982). Like phosphorus, it is also often present as precipitates of slightly soluble compounds of Al , Fe, Ca and Mg . Lesser amounts of arsenic are associated with soil clays and organic matter. This similarity between arsenic and phosphorus has led to the use of phosphorus extracting solutions for the determination of plant-available arsenic. Perhaps the two most commonly used extractants for phosphorus that have been sub- Si 0141GS2 sequently applied to arsenic extraction are: NaHCC>3 (developed for use primarily on alkaline soils); and a mixture of 0.05N HC1 and 0.025N H2SO4 (used for neutral and acidic soils). In a study by Woolson et al . (1971a) these two methods (NaHCC>3, HCI + H2SO4) and four others were evaluated for determining arsenic availability to corn on 28 different soils from different areas of the United States. Most of the soils were from the east and only five had an alkaline pH, the highest being 7.50. The NaHCC>3 and mixed dilute acid solutions were both recommended for use, because of their relative simplicity and for their good correlations of available arsenic with reduced plant growth. A later study by these same researchers (Woolson et al. 1973) revealed the complexity of determining plant-available arsenic in the soil. They found that plants growing on different soils that contained the same extractable arsenic levels experienced varying degrees of arsenic toxicity. This was attributed to the variabil- ity in the chemical and physical properties of the soils (texture, organic matter and pH) . Jacobs and Keeney (1970) also noted the influence of soil texture on arsenic phytotoxici ty , with arsenic being more toxic on sandy soils than on finer-textured soils. Such findings suggest that the general application of extractable soil arsenic levels to estimating phytotoxicity in field situa- tions is limited. Ganje and Rains (1982), in their review of methods of analysis for soil-arsenic, state that when selecting an extracting solution to determine plant-available arsenic, no single extractant can be used as a universal indicator of arsenic availability and that each soil type or soil area must be treated independently. The literature indicates that the selection of a soil-arsenic extracting solution is a complicated decision. Present methods have been shown to have limited applicability to field situations where an interpretation of phytotoxic levels is desired. For the Helena Valley study area a decision was made to employ a method for determination of soil extractable arsenic that has been developed and applied successfully to problems of arsenic-contami- nated soils of this region. 82 0141683 Heilman and Ekuan (1977) investigated soil extractable arsenic levels around the ASARCO smelter near Tacoma, Washington. They extracted soil arsenic with concentrated HC1 in a 1:5 soil to acid ratio; the same method was used for the Helena Valley investigation. These investigators determined a significant correlation (r = .625) between extractable soil arsenic and the arsenic levels present in above ground garden biomass. The correlation was also significant (r = .475) between extractable soil arsenic and below ground garden biomass (roots). These results suggest determination of extractable soil arsenic with concentrated HC1 is indicative of the soil arsenic level that the plant can absorb. Therefore this method has merit for the deter- mination of plant available arsenic in soils. As a check between soil test levels obtained from this method and the NaHCC>3 method (which may be considered a more standard method), duplicate samples from two soils (one with high and one with low arsenic levels) were extracted with both solutions, and analyzed for arsenic (Table 33). All work was performed by the Soil, Plant, and Irrigation Water Testing Laboratory at Montana State University, Bozeman, MT. Table 33. Comparison between concentrated HC1 and NaHC03 for determination of extractable soil arsenic (ppm) . Concentrated Sample HC1 NaHCC>3 "2518 40.46 36.34 2518-2 37.31 No Data STD-C 3.01 2.67 STD-C-2 1.98 1.50 The samples designated STD-C are in-house laboratory stan- dards used for quality control. The close agreement in soil- arsenic levels provided by the two extracting solutions suggests that the concentrated HC1 method provides results similar to the NaHC03 method for these soils. 33 Tha analytical method and accompanying interpretive guide was developed by N.R. Benson (Benson and Reisenauer 1951, Benson 1968) primarily through many years of field experience in diagnosing arsenic toxicity problems in orchard vegetation in central and eastern Washington (A.R. Halvorson, personal communication 1985). Soil arsenic is extracted with concentrated HC1 (12. 3M) in a 1:5 soil to acid ratio for a period of one hour, and standard instru- mentation methods are used to determine actual concentrations. Interpretation of the results of the analysis in terms of poten- tial phytotoxicity can be made by refering to Table 34. Benson and Reisenauer (1951) rated the relative tolerance of crops to arsenic (Table 35). Crops such as those found in the Helena Valley (e.g. barley, wheat, alfalfa) were considered not tolerant to soil arsenic. The tolerance of wheat to soil arsenic was compared to peach and apricot fruit trees. The interpretation is that grain and forage crops will do poorly when the concen- trated HC1 extractable soil arsenic exceeds 50 ppm (Tables 34 and 35) . This result compliments other investigations of the effect of soil extractable arsenic on crops (Table 32) . These investigators found significant yield reduction of vegetable crop when extract- able arsenic was in the range of 6 to 48 ppm. 3.1.2 Arsenic in soils 3.1.2.1 Total arsenic in soils The phytotoxic and tolerable levels of total arsenic in soils of the Helena Valley are 100 and 25 ppm, respectively (Table 30). The 100 ppm concentration has been selected primarily based on data of Woolson et al . (1973) and Steevens et al. (1972) who noted large yield reductions in oats, corn, peas and potatoes at 100 ppm total soil arsenic. All total soil arsenic values equal or greater than 100 ppm in the reviewed literature were associated with phytotoxicity. Soil characteristics, especially texture and organic matter content, strongly influence the relative toxicity of arsenic. Weaver et al . (1984) reported phytotoxicity of 8k 0141685 Table 3*. Interpretive guide for concentrated HC1 soil ex- tractable arsenic Soil Depth feet As Level ppm Interpretation 0-3 0-1 1-3 0-1 1-3 0-3 0-1 1-3 Below 25 ppm 25-50 ppm Below 2 5 ppm 25-50 ppm 50-100 ppm Below 25 ppm 50-100 ppm Above 100 ppm Above 50 ppm As is probably not a problem, May reduce growth of sensitive trees, such as apricot and peach. Should not seriously affect growth of apple, pear, and cherry. Symptoms of As toxicity may appear on apricot and peach during hot summer. Newly planted apple, pear, and cherry may be reduced in growth, but should still grow well. Survival of apricot and peach doubtful unless planted with As-free soil. Symptoms of As toxicity should be severe on established apricot and peach. May limit growth of newly planted apple, pear, and cherry. Significant reduction in growth of any newly planted trees should be anticipated. Avoid planting stone fruits. Hazardous to plant any new trees under these conditions. A (Washington State Cooperative Extension Service, 1975). 85 Table 35. 01416S6 Relative tolerance of crops to arsenic' Tolerant Moderately Tolerant Not Tolerant Apples Pears Grapes Raspberries Dewberr ies Rye Mint Asparagus Cabbage Carrots Parsnips Potatoes Swiss chard Tomatoes Bluegrass Italian rye grass Kentucky bluegrass Meadow fescue Orchard grass Red Top Tree Fruit and Berry Crops Cherries Peaches Strawberries Apricots Field and Truck Crops Beets Corn Squash Turnips Forage Crops Crested wheat grass Timothy Barley Oats Wheat Beans Cucumbers Onions Peas Alfalfa Alsike clover Ladino clover Strawberry clover Sweet clover White clover Vetch Smooth brome Sudan grass "Benson and Reisenauer, 1951. 86 0141S87 bermuda grass at concentrations which ranged from 45 to 90 ppm in sand and clay soils respectively. Phytotoxic criteria reported in the literature for total arsenic in soils ranged from 15 to 50 ppm (Kitagishi and Yamane 1981, Kloke 1979, Linzon 1978 and El-Bassam and Tietjen 1977). Numerous cases of phytotoxici ty were reported in the 45 to 100 ppm range (Table 30). For many situations, a phytotoxic level of 50 ppm would appear appropriate. A tolerable level of 25 ppm total soil arsenic is based on the low or no yield reductions that have been reported at or below this level (Table 30). The only important exception is the 22 percent yield reduction for oats at a 10 ppm total soil arsenic concentration that was noted by Woolson et al. (1973). 3.1.2.2 Extractable soil arsenic It is highly probable that extractable arsenic soil concen- trations greater than the 50 ppm hazard level suggested for the Helena Valley will be phytotoxic (Table 31). Jacobs et al. (1970) reported 100 percent yield reductions (no growth) for snap beans and peas at the 100 ppm extractable (Bray P-l) arsenic level. Considerable phytotoxici ty was noted at levels less than 50 ppm extractable (various methods) soil arsenic (Table 31) and a phytotoxic concentration as low as 10 ppm may be an appropriate hazard level in some circumstances.- It is apparent from the reviewed data that soil factors have much less influence on phytotoxic extractable arsenic levels as compared to phytotoxic total arsenic levels in soils (Tables 30, 31). The tolerable extractable soil arsenic concentration of 2 ppm is based on the limited work of Vandecaveye et al. (1936) , who noted no toxicity in barley and alfalfa at or below that level, and the observations of Walsh et al . (1977), who reported phyto- toxicity to soybeans at an extractable arsenic level of 3 ppm (Table 31) . 3.1.3 Arsenic in plants Phytotoxic arsenic levels in plant tissues have been reported from 5 to 20 ppm (Table 32). The suggested 20 ppm hazard concen- 87 0141688 tration is based on two publications, Davis et al . (1978) and Weaver et al . (1984). Davis et al . (1978) reported arsenic concentrations in the shoots of barley were toxic in a range of 11 to 26 ppm and determined a level of 20 ppm was the "upper critical level" at which a 10 percent yield reduction could be expected. Bermuda grass leaves containing 20 ppm arsenic were associated with plants exhibiting reduced growth (Weaver et al . 1984). These authors found bermuda grass leaves, stems and roots often exceeded 15, 25, and 200 ppm respectively in plants grown in soils contain- ing 45 ppm arsenic. All plant tissue arsenic concentrations >20 ppm found in the reviewed literature were associated with phyto- toxicity. Kabata-Pendias and Pendias (1984) reported a phytotoxic range of 5 to 20 ppm for arsenic in unspecified plant tissue. Numerous references reported "intermediate range" arsenic levels (those values between traces and toxicity). Typical values for plant tops of alfalfa, red clover, and oats were reported as 0.05, 0.37, and 0.62 ppm respectively (Liebig, 1966). This source reported high range (elevated but not showing toxicity symptoms) values for alfalfa, red clover and barley as 3.15 to 14 ppm, 6.26 ppm and 12.3 ppm, respectively. Data from the reviewed literature indicated that no cereal and forage crops or edible vegetable portions contained a concentration of arsenic greater than the 3 ppm tolerable level suggested for the Helena Valley. Woolson (1973) calculated, through the use of regression equations, the phytotoxic tissue levels producing a yield reduction of 50 percent in 6 vegetables. This study indicated only lima beans, an arsenic sensitive crop, had a tolerance level less than 3 ppm for the calculated yield reductions. 3.2 Cadmium in soils and plants 3.2.1 Cadmium literature review Cadmium levels in plants and soils rarely exceed 1 ppm (Kabata-Pendias and Pendias 1984). Areas with naturally occurring high levels of cadmium in soils have been documented to have up to 22 ppm total cadmium, with soil parent material up to 33 ppm total 35 0141689 cadmium (Lund et al . 1981). In areas where soils have been contaminated, soil concentrations may approach 1000 ppm, and plants may accumulate cadmium to levels in excess to 200 ppm, (dry weight), depending on the species (Kabata-Pendi as and Pendias 1984). In contaminated soils the highest cadmium concentrations are found in surface layers and decrease rapidly with depth, due to the low mobility of this element. Total soil cadmium levels are not good indices of the availability of the element to the plant, as much of the total cadmium in soil may be bound in compounds of low solubility (Pickering 1980). Cadmium, like many metals, is more mobile and thus more available to plants in soils of low pH (4.5 to 5.5). Alkaline soils exhibit low cadmium mobility, and decrease the risk of plant toxicity even in heavily contaminated soils ( Kabata-Pendias and Pensias 1984). It has been shown, however, that whereas the availability of cadmium for plant uptake is decreased by liming, cadmium added to the soil does result in increased uptake by plants (Baker et al . 1979). Chang et al . (1982) found that the uptake of cadmium and zinc in barley cultivars was more influenced by the soil type (and pH) than by the specific barley cultivar. Similar findings by White and Chaney (1980) indicated that soil types strongly influence zinc, cadmium and manganese uptake in soybeans and that organic matter was more effective than hydrous oxides of iron and manga- nese in moderating the uptake of excessive soil heavy metals. A study by Haghiri (1974) suggested that the soil cation exchange capacity (CEC) largely determined the uptake of cadmium in oat shoots and that organic matter had little effect on the uptake of this element other than increasing the CEC. The study found that the concentration of cadmium in soybean shoots increased with in- creasing soil temperature. Chaney et al . (1976) revealed that increased levels of soil zinc increased cadmium uptake by soy- beans. Boggess et al . (1978) reported that significant differ- ences existed in the susceptibility of soybeans to cadmium among several varieties tested. These authors found that the observed susceptibility was due more to plant uptake characteristics than 8Q UI ^± I SJ J U to the tolerance of plants to cadmium. Considerable variation in cadmium accumulation has been demonstrated for many vegetable and grain crops grown on the same soil (Davis 1984). In recent years interest in cadmium in soils and plants has intensified because of its presence in sewage sludge. This aspect has been the subject of much research and several reviews (Hansen and Chaney 1984, Logan and Chaney 1983, Sommers 1980, Singh 1981, Standish 1981, Webber et al . 1983, Williams 1982, Rundle et al. 1984, Page 1974, Page et al . 1983, and Lutrick et al . 1982). Land application of sludge may potentially cause phytotoxici ty pro- blems, but of greater concern is the high potential for introduc- tion of cadmium into the food chain, where it may create health hazards (Nriagu 1980). A summary of many scientific studies of plant uptake of soil cadmium is presented in Tables 36, 37 and 38. 3.2.2 Cadmium in soils 3.2.2.1 Total cadmium in soil A total soil cadmium hazard level of 100 ppm was selected for the Helena Valley based on two major factors: 1) all total soil cadmium concentrations greater than 100 ppm found in the reviewed literature were associated with yield reductions regardless of plant type, and 2) the lack of and variability of data, especially with respect to higher pH levels (6-7), in the total soil cadmium range of 40 to 100 ppm (Table 36). Other phytotoxic total soil cadmium criteria reported in the literature ranged from 3 to 8 ppm (Melsted 1973, Linzon 1978). However, nonsignificant or no yield reductions were reported for several plant species at 40 ppm total soil cadmium (John 1973). Data of Khan and Frankland (1984) suggested highly significant yield reductions occur in the biomass of wheat, oat and radish roots at 50 ppm total soil cadmium. 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T k- 4 4 - 4 a — "T r ^- 4JT4ltal44k-^6. 3 3 3 4 k- 4 c e 3 k-. c" l- e. c t- I--- i t i. - OOOmifci i ox.— N^ifliv.X.KUV. -J - -J X >,k- ^XJ >.X >,X. ^^.^SvfcO >, I I ■ t. 4 '^ 4 t C ' 4 J- 4 4 4 ~ ^ 4 c c c nwviMrt - — c— c — — — . « ,■ — 0OO£«CC*9O*O«£*9 C*0£c* 107 0141703 - - C 01 r > £ i - IS c e ~ cccccccccccc 3 3 333333333333 ooocoooooooooooo O* P* ^ ^ Q* P* ^ ^ ^ ^ O O - L1 U L U U L L CD 0 *^ ffi 0 0 EC ffl £ 23 CC tT1 CT O* (J1 *: T - t CC3CCCCCCCCCCCC OO-hOOOOOOOOOOOO XXMXXXXX 2ZZ2ZZ2 « M Vt ■ ■ ■ M ^ i. fcj i- i, ». _. O O 0 o o o o — L_ — 1_ — _ _ o o o c o o o WW Wlfi W w w N. \ W \ \ \ ■----»-- -- f .- v W! * j- 3 3 3 3 3 3 3 O O O O O O O O O a. CO 1) V & » a t C c — — — — — - a t : c ' t> t i a &■ a. > cy ft. s. «.' e. ' w » C CS O O i , s ■ B O 4. «, V t_? -J "*•* •J u * "S. \ * \ W *3 «r ■c M >. * ■1 C* tJ c 17 M tr (T> «• C"T T1 t V •D 4-T Cv CT - (V b 4r ti i. c n a: EC V) 4> ^ r >, X >. >, >. >l\ >*\ >i %> ft> " II -■ - 1 4> ^ u _ .. u t, „ a. u M „ p C c r ■ * c c .T K .- 1 o. ■ ■ a. ft cc J CC 2 ■ V} 3 J 108 0141703 of cadmium that may enter the food chain at either 100 or 50 ppm total soil cadmium concentration. The total soil cadmium tolerable concentration of 4 ppm was selected for the Helena Valley based on the generally small or nonsignificant yield reductions reported below this level, compared to the higher yield reductions (up to 46.8% for corn shoots) noted at the 5 ppm total soil cadmium level. 3.2.2.2 Extractable soil cadmium The DTPA extractable soil cadmium phytotoxic and tolerable concentrations selected for the Helena Valley were 30 and 2 ppm, respectively (Table 37). All extractable cadmium concentrations, found in the reviewed literature, that were in excess of 30 ppm were phytotoxic. The hazard level was based on the 25 percent yield reductions that were noted for wheat grain and white clover at concentrations of 30 and 29 ppm, respectively (Bingham et al. 1975). Numerous occurrences of phytotoxici ty were noted for a number of species in the 4.8 to 30 ppm extractable cadmium range (Table 37) . Of particular interest were the 22 and 25 percent yield reductions for alfalfa and wheat grain at extractable soil cadmium levels of 22 and 23 ppm respectively (Bingham et al . 1976, Mitchell et al. 1978). Extractable soil cadmium concentrations between 2 and 4.8 ppm were associated with both yield increases and yield decreases. Concentrations less than the suggested 2 ppm tolerable level were not generally significantly phytotoxic except under specific experimental conditions (Table 37). 3.2.3 Cadmium in plants The phytotoxic concentration of cadmium in plant tissues (50 ppm) selected for the Helena Valley was based on the literature in which most concentrations greater than 50 ppm were associated with phytotoxicity . The only exceptions were slight yield increases noted for lettuce and alfalfa at levels of 51.1 and 57.6 ppm, respectively (Table 38). Large yield reductions in ryegrass and wheat grain (50 and 42 percent, respectively) were reported at tissue cadmium levels at or near 40 ppm, (Dijkshoorn et al. 1979, 109 Mitchell et al. 1978) and very large yield reductions for field beans, peas, carrots and wheat grain were noted in the 27 to 40 ppm range (Table 38). Davis et al . (1978) found barley shoot cadmium concentrations of 14 to 16 ppm to be phytotoxic. These authors noted that 15 ppm cadmium in barley shoots was associated with 10 percent yield reduction. It is clear that the 50 ppm phytotoxic hazard level for cadmium concentrations in plant tissue will be associated with phytotoxi ci ty in nearly all cases and that phy totoxici ty may occur in many species at notably lower concen- trations. All of the above cadmium concentrations far exceed recommended levels for forage and will likely increase the probability of high levels of cadmium entering the food chain. A tolerable plant tissue cadmium level of 10 ppm was sug- gested based on the generally low yield reductions that were noted in the literature below this concentration (Table 38). The alfalfa study of Taylor and Allinson (1981) was of particular importance in that these authors reported several cases of increased production up to the 10 ppm cadmium concentration in alfalfa tops. Again, the 10 ppm tolerable level selected for the Helena Valley will allow much higher cadmium concentrations in forages than the maximum recommended level (0.5 ppm) (NRC 1980). 3.3 Lead in soils and plants 3.3.1 Lead literature review Mean values for total lead concentration in soil range from 10 to 67 ppm, while common levels in plants range from 0.5 to 4 ppm (Kabata-Pendias and Pendias 1984). Meyer et al. (1982) found that background soil lead levels ranged from 3 to 23 ppm (mean of 12 ppm) for 290 locations in the United States. In urban areas soil lead values may be considerably higher due to contamination from automobile exhaust and industrial activity. Lead is not an essential plant element, and is apparently taken up passively from the soil. While plant toxicity to lead has been noted, it is extremely rare even when excessive amounts of lead are added to the soil (Cannon 1976). This is because lead is one of the least 110 0141711 mobile of the heavy metals, resulting in generally low lead levels in the soil solution and minimal plant uptake. Chumbley and Unwin (1982) determined that there was no significant correlation between total soil lead and plant lead levels. The low mobility of lead is governed primarily by soil pH, texture, cation exchange capacity and organic matter content (Zimdahl and Arvik 1973, Pepper et al . 1983) . Little specific research has been directed toward the deter- mination of plant and soil lead toxicity levels. Rather, concern has centered around the introduction of lead into the human food chain from plants (either from lead taken up from the soil or from aerially deposited lead on plant surfaces), or from ingestion of lead that is in soil or dust. Tables 39, 40 and 41 summarize the limited number of studies where the phytotoxic concentration of lead in soil and plant tissue has been documented. 3.3.2 Lead in soils 3.3.2.1 Total lead in soils The suggested total soil lead hazard concentration for the Helena Valley is 1000 ppm. Phytotoxic levels of total soil lead were reported by many authors (Table 39). Values ranged from 100 ppm to 1000 ppm. It must be noted that considerable crop damage may occur to sensitive crops or other crops grown in soils with higher available lead content (i.e. lower pH) at levels considera- bly lower than the selected hazard level (Table 39). The above problem was exemplified in the following reviewed literature. McLean et al . (1969) noted significant reductions in alfalfa yields at total soil lead levels of 100 to 1000 ppm in soils with a pH range of 4.9 to 5.7. These authors reported nonsignificant yield reductions at 1000 ppm total soil lead at a pH of 6.3 and no yield reductions at a pH of 7.5. Similar results were reported by these authors for oats: the only significant yield reduction occurred at 1000 ppm total lead at a pH of 5.2. John and VanLaer- hoven (1972) found a 30 percent yield reduction in lettuce but no effect to oat yield at a total soil lead level of 1000 ppm and a 111 0141712 - V <^ &• &■ <*• "■ — c c c c c c o a a * •.' *' >>>>>> &* & &* &* ^* ^ ^* ^ ^ 3 * w « « * | #t Bl 01 V< *0 • ' : c c > « ■ c c c c c c c c c "C T t TJ T tl t) . t~* r- T> CCCCCC***»'C I Mil fct*O^^^^^TJ"0^> cccccccc ECCCCCC* t,*cccccccce 3 z. c r £■ £■ U iJ *J I.-' * * * - ». r «" "' a a c > > — 3 3 — i a, &, o. a. *: ' ■ — c c • o — — ■c « rf - c « TIT) C C ' c * « — >. >.- — ■ n - < f- h a y* tn w» *> V* »^ *W ^.w^w..— wnwiui — — — — w , «. * l in w V) 2 Z Z i ■"■ M Q. 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[J u ft" u x: fti o u w ft. -J u o V) — X. O «l J ar. aJ IO J X IT) X, a \ « 01 \ fa. "S. M 3 X. >, Vi an \\ * w X M o >.^ tr >. 0 *- %> V) — ftl ft n =a»"U ft in >, 17> ►- O — C AOf-CsV a-iCC«J> C XI vi in vi (y c > > fti 0 - > «J "C Om CPV. *» i^ ■- u c— mx— cr c — — — m c - a Pa, O. O. C cro c « iZ J f - C - «■ i- .. c — B - 0« O — — k* C « •» ■- 3 « « M * RJ W o o o — — ft* cv - a, -. s ft r c. *' -• 1 M • «^0»Cir-u-«>-''". >i >->..', C X >, iv, --x a. >s >, >- L- >-. L. 3 U 3 X. XX. o u X >*>.>, u « C2 >.*m V. *. *j ft. V(iO>'i'lVli\a>l|iil 3 • 4-' £. Of.** ftl W 3 3 • ' ft 4 ft 3 ft C ft — c — a, — MM W « C — • — -> C « (*■ — ■ — — a' — > O1 »' \r> • .- r If U • •- — — *j ax v -< • JS w-., iD-i-tlCai.^-.' H >' H i M tf ** *' ft) at w u V 0-X W a* •• 0 * « * <£0«"'«i£i«*<» « ■- O fti O £ ft) ft ft. ftl r. C«<0ftift«aVtf*< U CD in cO (OtBUiHaiMtoffiiaaicffiaj CD to WaJMU ffi (Q J J c isaajftuxjiat c 130 0141731 Chaney 1980). Typical phytotoxic criteria for total soil zinc were reported by various authors as 250 to 500 ppm (Kitagishi and Yamane 1981, Chapman 1960, El-Bassam and Tietjen 1977, Linzon 1978, Kabata-Pendias 1979, Kloke 1979, Melsted 1973, Chaney et al . 1978) . The suggested 500 ppm hazard level for the Helena Valley is also the level suggested by Chaney et al . (1978) and has been selected because it best fit data from the reviewed literature (Table 42) . The tolerable total soil zinc concentration (200 ppm) is based on the observation that reductions in yields of most species, with the exception of soybeans, were generally low at concentrations less than 200 ppm while levels greater than 200 ppm were shown to result in yield reductions for many crops. Vegeta- tive yields for two of the specific crops of interest for the Helena Valley, barley and wheat, were reported to be decreased by 16 percent and 18 percent at total soil zinc concentrations of 200 ppm and 300 ppm respectively (Boawn and Rasmussen 1971). Mitchell et al . (1978) noted reductions in wheat grain yields of 3 to 14 percent in the 100 to 180 ppm total soil zinc range and 12 to 29 percent at 340 ppm total soil zinc. No data were found in the reviewed literature relating alfalfa yields and total soil zinc levels below 200 ppm. 3.4.2.2 Extractable soil zinc The 60 ppm phytotoxic extractable soil zinc hazard level has been selected utilizing data reported by Boawn (1971), Boawn and Rasmussen (1971) and Walsh et al . (1972) (Table 43). Boawn (1971) reported normal yields for 12 leafy vegetables at a DTPA extract- able soil zinc concentration of 55 ppm. Boawn and Rasmussen (1971) noted a 16 percent reduction in the vegetative yield of barley at 88 ppm DTPA extractable soil zinc and Walsh et al . (1972) reported a 66 percent yield reduction of snap bean pods at 47 ppm DTPA extractable soil zinc. The 5 ppm DTPA extractable soil zinc tolerable level is based on the observations of Boawn and Rasmussen (1971) who noted no yield reductions for a number of 131 0141732 crops, including wheat, barley and alfalfa, at or below this level . An argument can be made to revise both the phytotoxic and tolerable extractable zinc levels upward to 125 ppm and 40 ppm respectively. The 60 ppm phytotoxic hazard level was selected based on two phytotoxic occurrences noted above (Table 43). Significant yield reductions for most crops were rare at DTPA extractable zinc concentrations less than 146 ppm. The first significant yield reductions for wheat and alfalfa were reported at DTPA extractable soil zinc concentrations of 146 ppm and 195 ppm, respectively (Boawn and Rasmussen 1971). Some yield reduc- tions may occur in barley at DTPA extractable soil zinc concentra- tions less than 125 ppm but the level appears more appropriate for wheat, alfalfa and clover which are grown extensively in the Helena Valley. No significant yield reductions were noted in the reviewed literature for any crops at DTPA extractable soil zinc concentra- tions less than 40 ppm. The maximum background extractable (IN HC1) zinc concentration found in the reviewed literature was 26 ppm (Dudas and Pawluk 1977) and Walsh et al . (1972) noted a yield increase for corn grain at a 29 ppm 0.1 NHC1 extractable soil zinc concentration. The maximum yield of rye was noted at 40 ppm 0.1N MgSC>4 extractable zinc (Chapman 1966) . 3.4.3 Zinc in plants There is a wide range of zinc phytotoxic levels reported among some plant species, different plant types and for different parts of plants (Table 44). Reported phytotoxic zinc levels range from 60 ppm for wheat plants (Takkar and Mann 1978) to values greater than 800 ppm for swiss chard (Boawn 1971) (Table 44). Most values for crops of concern (cereal grains and forages) fall within the range of 189 ppm to 560 ppm (35 and 20 percent yield reductions, respectively) found by Mitchell et al. (1978) and Boawn and Rasmussen (1971). Boawn and Rasmussen (1971) reported 20 percent yield reductions for barley, wheat and alfalfa at above ground plant tissue levels of 540 ppm, 560 ppm and 295 ppm, 132 0141733 respectively. Zinc phytotoxici ty to barley seedlings was reported | in the range of 160 to 320 ppm (Davis et al . 1978). It is apparent that the suggested plant tissue phytotoxic level of 500 ppm zinc will produce phytotoxici ty in most plants. Only two values in excess of the suggested 500 ppm plant tissue phytotoxic level were found not to be phytotoxic (508 ppm for corn forage and 527 ppm for lettuce shoots) (Mortvedt and Giordano 1975, Mitchell et al. 1978). Phytotoxic criteria levels reported in the litera- ture ranged from 100 to 400 ppm zinc (Kabata-Pendias and Pendias 1984) . The suggested 50 ppm tolerable zinc level in vegetation is based on the lowest phytotoxic tissue level found for crops of interest (barley, oats, wheat, alfalfa and other forage crops). The value 51 ppm was reported for a 20 percent yield reduction in wheat (Boawn and Rasmussen 1971). These authors also reported a 20 percent yield reduction for sweet corn and sorghum at zinc tissue levels of 41 and 34 ppm respectively. These values were the only occurrences of phytotoxici ty found in the reviewed I literature at levels less than the 50 ppm suggested tolerable concentration. 133 « i 0141734 4.0 HAZARD LEVELS FOR WATER A large number of factors influence the suitability of water for livestock consumption and for irrigation purposes. Some of these are discussed in the following sections. A computer litera- ture review was not conducted for this subject. 4.1 Water Quality Levels for Livestock A number of factors, including animal tolerance, water con- sumption and forage ingestion, are involved in the determination of the suitability of a water source for livestock. Water con- sumption by livestock is influenced by the species, the age, the condition of the animals and climatic factors. Temperature changes have been shown to vary water consumption in cattle by a factor of three (Rittenhouse and Sneva 1973). The moisture content of forage affects water consumption and some species such as sheep have been shown to subsist entirely on dew or snow (3utcher 1973). Water consumption by domestic livestock varies between 1 and 4 gallons per day for sheep or goats and 10 to 16 gallons per day for dairy cattle (Federal Water Pollution Control Administration 1968) . It is clear that any given amount of heavy metal in water will likely affect individual animals in a slightly different manner. The heavy metal content of forage and soil is another factor which influences the allowable amount of heavy metals in livestock drinking water. Contaminated water will only exacerbate toxicosis produced from ingesting contaminated forage. Mayland et al . (1975) estimated cattle ingested soil in the amount of 100 to 1500 g/animal/day . In areas with high levels of heavy metals in soils, this source may represent a considerable fraction of the total heavy metal intake in some animals. Several organizations have established suitability criteria levels for most consti tutents found in water. Criteria for arsenic, cadmium, lead and zinc are reviewed in Table 45. 13^ 0141735 Table 45. Water quality criteria for arsenic, cadmium, lead and zinc. Use As Cd Pb Zn Reference mg/L DRINKING WATER 0.05 0.01 0.05 5 EPA 1983, USPHS 1962 LIVESTOCK WATER 0.2 0.05 0.1 25 NRC 1974 LIVESTOCK WATER 0.5 0.05 0.1 50 Dyer and Johnson 1975 LIVESTOCK WATER 0.05 0.01 0.05 — Federal Water Pollu- tion Control Adminis- tration 1968 (FWPCA) Standards for arsenic have been based on total arsenic and are usually reported on the toxicity of arsenic trioxide (Peoples 1983). Methylated forms have been shown to be one hundred times less toxic than inorganic forms. With the exception of rats, arsenic is rapidly eliminated from the bodies of most animals (Peoples 1964). Chronic toxicity in livestock has been demon- strated at levels of 50 mg/kg forage (NRC 1980). Problems may occur on the most contaminated soils (greater than 100 ppm arsenic) if livestock ingest considerable quantities of the soil. A survey of water quality in the Helena Valley in 1972 found no arsenic values greater than 0.03 mg/L (Soukup 1972). Dyer and Johnson (1975) suggested 0.5 mg/L may be a more appropriate maximum level for arsenic in livestock water but, given the possibility of intake from other sources, the 0.2 mg/L level may provide a better margin of safety. Arsenic toxicosis may still occur in very extreme cases in which ingestion of soil by live- stock is the major contributing factor. Both lead and cadmium tend to accumulate in animal tissues and therefore are more prone to cause toxicosis in chronic poisoning cases. Allcroft (1951) found that both soluble and insoluble (lead acetate and lead carbonate respectively) forms of lead were absorbed at about the same rate. Puis (1981) has given 135 0141736 I V ** dietary intake levels of >100 ppm lead as toxic to cattle. Soukup (1972) found a maximum lead value of 0.044 mg/L in Helena Valley water, well below the permissible criteria of 0.1 mg/L. The possibility of high levels of lead in forage and soil, suggests that the drinking water criteria of 0.05 ppm lead may be most ap- propriate for the Helena Valley. The most appropriated hazard level for cadmium concentrations in livestock water of the Helena Valley will depend on cadmium levels found in forage and soils under background conditions. The 0.5 ppm criteria reported by the NRC (1974) may be the most applicable. Chaney (1984) and NRC (1980) have given a value of 0.5 mg/kg cadmium in forage as the chronic toxicosis tolerance level. However data discussed by Hansen and Chaney (1984) showed that the 0.5 mg/kg cadmium value was based upon conservative estimates for cadmium accumulation in animal livers. They felt that when the Cd:Zn ratio is <1.0%, cadmium in feed may reach 5 ppm with little accumulation in liver and kidney tissues of animals. However, the drinking water standard and the FWPCA livestock criteria of 0.01 mg/L may be insufficient to prevent cadmium toxicosis under conditions of heavy contamination. Zinc tolerence is high in animals and dietary intake exceed- ing 2000 ppm may be required to produce zinc toxicosis (Puis 1981). The 1972 study of the Helena Valley indicated a maximum forage content of 232.0 ppm (dry wt . ) zinc (Hindawi and Neely 1972). Soils sampled in the same study contained a maximum of 5200 ppm zinc and the mean for sites 0.67 to 10 miles from the smelter was found to be 79 ppm (Miesch and Huffman 1972) . It is apparent that the recommend zinc limit of 25 mg/L for livestock water will provide a sufficient margin of safety except in areas with very high soil contamination. No data were found that would document the heavy metal content of snowmelt runoff and its consumption by livestock. 4.2 Water Quality Levels for Irrigation Water quality criteria for irrigation must take into consid- eration the nature of the specific water constituent, soil charac- 136 0141737 teristics, plant species and climatic variables. Irrigation methods can also influence the relative toxicity of some elements. Sprinkler irrigation can result in foliar absorption or adsorption of minerals at levels detrimental to plant growth if the water contains excessive levels of some constituents (Federal Water Pollution Control Administration 1968). Ground application of the same water may not produce any adverse effects due to soil chemical and physical properties that may reduce some elements to insoluble forms and adsorption of elements by soil constituents with high cation exchange capacity. Helena Valley waters analyzed by Soukup (1972) contained no levels above the more restrictive irrigation criteria for all soils for arsenic, cadmium, lead and zinc (Table 46) . Table 46. Irrigation water criteria for arsenic, cadmium, lead, and zinc. Use As Cd Pb Zn Reference mg/L Irrigation All Soils 0.1 0.01 5 2 NRC 1972 Irrigation Fine Textured Soils 2.0 0.05 10 10 NRC 1972 The use of contaminated surface runoff, waters receiving in- dustrial effluent or polluted ground water could result in waters exceeding existing irrigation guidelines. 137 0141733 5.0 REGULATORY CRITERIA FROM OTHER TECHNOLOGIES Several state, provincial and national regulatory agencies have attempted to set limits for metal contaminants in soils and/or to define metal hazard levels in waste materials. These hazard levels have been developed from different technologies and view soils from different perspectives. Much of the criteria come from four sources: (1) sewage sludge amendment of agricultural soils; (2) coal overburden materials used as rooting zone material in revegetation attempts; (3) defining hazardous materials using various extraction techniques; and (4) setting limits for metal contaminants in soil based on the intended future use of the soil. The criteria presented in this section are provided for a compari- son to hazard levels suggested in this document for the Helena Valley. These criteria were not used to determine the Helena Valley hazard levels. Tables 47 to 51 summarize this regulatory information . 5.1 Criteria from Land Application of Sewage Sludge Metals commonly present in sludge have been classified (CAST, 1978) as those that are likely to pose little hazard (manganese, iron, aluminum, chromium, arsenic, selenium, antimony, mercury and lead) for land application and those which pose significant hazard (cadmium, copper, molybdenium, nickel and zinc). Many national regulatory agencies have set maximum cumulative loading levels of these elements for agricultural lands (Table 47) . These loading levels have been set to prevent toxicity to humans or animals from crops grown on treated agricultural lands. It is of interest to note that Norway and Sweden prescribe very low cumulative loading levels while the Uni'ted Kindom and United States allow signifi- cantly higher levels. Cumulative loading levels are given in kg of metal/ha. Conversion to mg of metal/kg of soil is based on a one acre furrow slice (6 to 7" depth) weighing two million pounds. 138 L. (0 CT. 3 — IS 2 ~ in S C L. in cr c o CJ £ O ID c o U (J o a i u ui O - _ N in 10 U u -£ in in E - 1) a E 3 E x IB r 13 01 0141739 o *r — E QD X 3 ON o»> — I — i — I o 1 1 tn u Q. C jz Ul z Ul o — » \ u rsi u. -*•! 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X) 01 2 co CO on on to • U 10 01 XI X) a 3 CD CO ON ON a. — X) a 0) 3 CD CO ON'On to • a. _ u ID o> X) X) Oi 3 CO CD ON ON U) • a. — u io a E S r-l 0 u XI z o c 10 u •o c 10 >. — c u 10 01 E £ u jj OI 01 'J z 10 ro 10 ro 10 ro 10 10 10 ro 10 ^J jj JJ jj JJ jj « JJ JJ jj jj o c c o o o 3 o o o 0 E- r- E- s- e- H ~ f- f- f- *— ' E T E B* E 10 c 0" 01 s CO • \ m CTN IN E IN 3 55 U> OS Ji I o> E es ro n x: cs on D» E E 0" E ■s 9 £ IT S B IT J* E ro JC 10 c c c = c c c E c c z = o R 0 o o 3 o 0 0 - 0 o » .■J ._ tpj •*4 •*N — — — — — XI Jj jj JJ JJ JJ jj JJ JJ 4J u ro 10 (0 10 10 n 10 ro rt 10 10 10 jj in jj in JJ in JJ m x^ 1/ JJ V) jj in jj V) JJ in JJ m jj (/) o a (1) 01 a 01 r., 01 a 1 a 0) a 0) a 01 Q, 0) r„ 01 a oi a r> o rr> 0 ON o a R C" 0 C^ 0 ^ 0 0» 0 c- 0 ON R ty 0 On 0 m u 01 ij 01 w ■ 01 kJ 01 u 01 tj 0) u 01 u 01 u 01 >j 01 u > u > U > u > U > (J > U > u > u > O > U > u > u c o u E 3 Cl o to a en — Si D. 141 0141742 e u u w O 0) C O U CJ - c — XJ 01 r 01 o cj CI 01 0> a' 01 xi XI XI JO XI -C X) □ 0) a; a> 01 3 S 3 3 ^ fc . » *r rn T "-( *T <"-! •f r-i 00 cc CO =T CD CO CO CO en o> cn -r ON ffv o*\ cr> to « !/) . 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Ul Ul 3 3 M •o 0 C 0 re OJ t-i E u a> — JJ 0 0 re > a in 10 MJ h 0 «* ~~* OJ ^1 u tm tr 9 o> v> X o> — i w — 0.' Ul u re jr •c H* -V > Qj u re c FH Vj ■« 4J re re w UT re E C ._ - .4- 3 * i- 3 C U) -- i/. OJ O OJ ^H ^ -j * u TJ 0' X C z • M U OJ > cr re re X. 3 3 a, — — ~ (J >" 1/3 -J X - a 142 0141743 5.2 Criteria from Coal Overburden Suitability for Root Zone Mater lal Because strip mining for coal in the western United States increased significantly in the 1970s several state regulatory agencies established guidelines for the analysis of soils and overburden materials to determine their suitability as root zone materials in revegetation attempts. Suitability guidelines and suspect levels were set by some states and are shown in Table 48. The levels for cadmium, lead and zinc established by Montana as being suspect, have been rescinded, but not yet replaced. New proposed guidelines are under consideration. 5.3 Criteria for Defining Hazardous Wastes The Resource Conservation and Recovery Act (RCRA) set criteria for determining if a waste is hazardous. Part of this act defines the EP Toxicity Test (40 CFR) 261.24, 19 May 1980). The levels of arsenic, cadmium and lead that are defined as the concentration of contaminants which will produce characteristic EP Toxicity are shown in Table 49. The state of California has also taken a similiar approach to defining hazardous materials by using two criteria; soluble threshold limit concentration (STLC) , and total threshold limit concentraction (TTLC) . These criteria are given in Table 50. 5.4 Criteria for Metal Contaminants Based on Land Use The British Department of Environment has set draft guide- lines for the concentration of contaminants in soils based on land use. These criteria are given in Table 51. 5.5 Summary Table 52 summarizes the hazard criteria for arsenic, cadmium, lead and zinc concentrations. These data are a synthesis of information from state, provincial and national regulatory agencies. Heavy emphasis is given to maximum cumulative loadings of sludge to agricultural soils. TO 0141744 U w n E c 0 N * rf ^ O* 2 ^ ^ ^ - i' 0 c U1 n QJ in D Z V "O l_ -O i_ 0) > o Q, O D. O o. o a. o 3 t/, Z> lO z> w 3 v> 0 1/1 1- u JO It - cc jQ I. c. I.. I ]kk 01417 45 fr C r-, » CO v- C ._.— CD _ e -o 0141746 t_ o u L (J U u < < < < «i < < u o u L U u o c 01 E (V o o o> c o u u ■o — Ol zz >*- 3 —I ID C7* ID D cc — n ID 01 CD > E 0 ID X CO "D 3 c •M o T — * >*4 o 01 CS AJ in JJ • o ID in (D •-« r w kri ID rN AJ X *J JJ — Q. X o B u — CD t- in ID 01 OJ > E O ID X) 10 ID E 3 C — o •O —••* z : i - in *j • v ID CO ID « u I w .— ax 5 u — cy ID 01 0) > E O id a to ID 0 s- a 01 > 0) F a E ID x ID V- a 10 E s c — 0 - — — c 01 CS jj (A u o ID in n i — sr U u ID rg 4D ■= *j AJ -*4 a X 0 B u — CD I- n 01 > D 0 01 > a F a E ID x ID to IS <-- E 3 c — o - •— .— O 0) e» MJ CO *J o ID in ID — T u. 1-1 ID rM — T J-» *J — £* X O s L — 01 fc- c c u c 01 u >. 3 ID w 3 o r. a -u X ID u a r o IS u 1/1 0) l/l <-. 3 u- O — L. n N n c 0 It u CD '-• c o a in CD EC ID ID 0 0) = B O JJ — X X 3 CD — (J -. i- E C O £ — o tO X> — < (J - ct oi -ic 3 {?>•" E CD in 3 ID in > 0 0 a S in c. — DS •z x c H 0) D U ID 01 — O _i u E c O -C — o £ IT IT X — N 01 a> 3 r cs jj B 01 in 3 id w > o o a E « CD — CD O ^ — X c XI in aj CD 3 m- u — u e = o x — o W JJ -^ u j^ — ■ \ 01 CT> 3 E CS) AJ • CD -H 3 — . ID ID W > O 0 a E w CD — ■ CC T3 ^h in jj cd ID CD — U AJ l-i E C o x: — o t- jj — o V. 01 c 3 E CS CD — 3 — i 10 ID W > o c a e w id — CD O JJ — x: c DO W XJ o> 3 »•« U - i- E C O X — O HI JJ -< o \ 01 ~ 3 F tn u 01 3 N — ■H ID ID to > o 0 a E VI 0 •r* DS - o X ^ in xj id CD — — - =; O X — E- *J — a> j: j< tT s. — CT> 0) E 3 B B -^ s C — 3 N« ■H M ID K 11! > 0 D d. E in 0 •** 21 ~ Cd C aj X) In jj cd hue: o c — o LG -J — U ^ m xv oi ID Cd — O -; u E c O X — o (- a> -i u \ o; ~ 3 E s aj to CD 0 C a g v> Cd • ^ K ~ err JC CT S ■*• tT 0) = 3 B — XJ :=■ 01 L" 3 N _ V* (5 n H > O 0 a E V) 01 — O- o z c LP -3 CD - 3 C m (0 3 S o to - 3 o en c LI 111 - 3 3 O to 3 O CO m - 3 o to XI II in < V) < - u 146 X X C 0141V47 a £ O o o> C O ■a o c jj SI E 1/3 in c 01 > c ID 01 JJ *U "~ C — SC 0) 3 = — i E 0' o E 0J > o X) E E t/) W) 0) 0' > :> 0 o XI X a n c u E o X IT U-l <: 0 a ~- O E IB JJ E — JJ o »•* 0 c in 0 H — v it o X 10 o XI E e cs> > U1 Of 0) o U -" > > „o a — 0 c IQ ^ o 0 £ £ |Q 4-» W R3 n JJ m O C *w Ifl If. <. t- -- o < < E C — CD'; C ■a o i/i C ID C "k r. W c C o c 0 3 TZ- a. 01 u cu 01 u =» 3 ID in 3 O S. a. w X id u: a c o a c E 3 IT! Ifl C JJ ._ 1 (J tfl O W ID 10 ^ 0i m Q. E J-1 W Cj. o " C J3 - u- - QJ O X — O U TJ U — ■ c — S. O >- T3 Ifl C — " o, cm £ O" « (- u 10 XT CT — J.' o EJi E >. ts u jj ■ — •» ft U ra lfl O 01 <0 ID ^ 0i o> &. E JJ o kJ c X c **J u oi o c m O U *D U •" ai > X 10 1/1 < U-riH O "> to o *0 10 ** tl ID E u ID cr w c x: C u-i 01 o c 11 > c X 10 0 ID in c c o o - » ••-« Cu - - > jj •— ... _• o ra 0 to 0 01 Qj £ JJ 10 10 o> o m c x: C >" u oi o c in hi o u *o o —< C c 0 0 * - — •M | 1 jj jj JJ «« — < U 10 B 0 ■ ID rH 0 m e jj 10 CT> ^ C J= C u- U o c HM O T3 o — Ifl < 01 V > > 0 0 X X 10 10 in 10 < < CI 0/ > > 0 c s> X ID ID c • u -- Ifl c c 0 u 01 H 01 U) -1 T3 3 m u E id OJ UJ CT> ja fO 4-1 a E 0) D u ■•- — u TD • — < 01 0 Z w __ LT\ jj c . ts " -I T3 -H |fl c 01 01 CP"0 u u 10 ID o*.-« ^l .M •*! J^ o J< 0 ty o \ in \ in > in u* it \ E >■ E >. & >< S !- C9 u E " t n •«r "D in Tj 0 — in c ■-J ui .-. 01 w 01 c in t-t e o -J "0 0) *D jj « IS 10 sj E u j a a E H Oh o in u> a1 .^ □>•- i tr o .* o Ji 01 s, in \ cr n- >. E >- E u rsi u m Tg -h -O rN ifl >v-i c JJ Oi 01 — Ifl CT>"0 c in u u 01 ID ID ID E " j a> < 0> o in < c t/i in < c o ■0 u 1^7 0141748 E (J O III c o D ^ a 0 u 01 01 u >. 3 ib m 3 o sz D.U x ib 01 W •c c ra a. N W IB II TJ V 3 C •— 4ml E c 3 0 (J 13 OJ r _ LP, u 4) c ^ - ■8 E OJ E in IB OJ xj Tp ~ c — ■ :*. OJ 3 Z> (- IT — O X) 01 01 > _> 0 c X- X IB 10 Ul (A < < ■0 Xl y~i 01 OJ TJ u — a. o > > O a a o c sz — O E o - 0 E x X *J IB *J £ U) IB 4J E tmi IB n Oi J-J CB . -\ .^ E C C LTl 14-1 0 C in c 01 (.' E- — tt o t- — V to < < W O IB 0j in E L) IB IB — < JJ IB c x: c **-i o o c - CD u- c •D IB -I V O SZ O w -D it C- u 0; c ib l-i U O"1 N' X O ■— IB E- U-. tn sz in o 0) in D. £ CP O w C w-i fc-i 01 O IB 10 IB IB — c E D D C SZ o c — O O T3 0 — ' 0 "* 0>-< CT>— < j<: — .* O X 0 X m c in CP E E > s >, •v — in V c ■•* 0) — i 01 1 — 1 C 0 _-t •v X 0J IB IB i~t 3 a a E IB a, O. in to cr — r E 01 :■ o IB < 01 > 0 a u n < E to D XI IB u < OJ < — f- Xl a. O IB c U-l U . *-l & 0 r ib c E in kj •- ' E — E to o XI 0 XI IB C» 0< M *r in If. in ~ c IB it E E - - c X C 0 O •» ■. — 11 — — JJ 4^ > 4J •- * iH u IB 0 m o IB IB ~-l XI Oi VI E ml IB IB Cn k-i c xr c y-j 0J o c in — O TJ o ■~ < '-- c IB 5 3 = - O - ■"'" --I O It in o in io ib — 0i in a E *-> id tT o u c sz toe is E c C u-i *" O O TJ U • 01 Q: > > o o XI - IB 10 in 10 < < Cj a! > > o o XI XI 10 IB in in < < \ IT O cn E m E IS B s >, in in kj on -H -z) in in X-i c jj o> a> — in iyo c in u w oi io 10 10 E i- mZ CT» < tr tn J^ -4 CT— ' \.-« Ji ■- o o \ o E in cr> m B E , es >, Ci u CO b rsi *D IM *D •D U 0 io XI a c io ... oi — CO xi oi io = a a a o w c 10 c — 01 — -D 10 L4 E io to cr c to 0' > c XI 10 to < x — \ o a> in E es >, CO u fM »D rg in c 01 01 C7>T3 u _ IB 10 XI D. li*8 c 0141749 r. u E CTi E - a E 01 U C Ci — T3 C O U U — z ai Q Oi 01 > E ■* • ** — — » IB aj JJ — — c ■-* K 01 3 D fr- < rH 6" £ u. D Q 0 uJ U jj z flj E E in M — ■ E c 4J S M E m s CD N ^ 0) > o 01 0 < — O re u: c n x c u N a OJ u 01 u >^ 3 « w 3 o c a, jj X ™ u c - in 4J .., _ U IB m o m re -h 0 W £ -J re a* u c jr c **j 0) o c — O T3 O — in = re E r oi > o .0 re gg < o 01 tfl re E — O a u 3 Wh 2 re = o a re in — a C — u c re o — re o a :* — VD ~. O in i -i in 5 C >, m E w ^N >0 (S — in ,x w £ w ■a \ 0 E , r"> w 01 CT> C m ■-" re >i oi re u — re Q. > - re "D — c a re ■a r .- m c ui oi re E - < c* — 01 JJ c — C'U 01 0 - oi re [j..- - c a. Oi 4J — o m > E — m o p- o C V C 1/5 E O l/l E N re w *D £ 3 4-i in — < 01 (J Ui • "O c mi — (J- c — re i* oi £) E re E 3 C-; -i < n. 1 IlQ UJ-4 KJU Table 52. Suggested hazard criteria for soil based on regulatory agency data. Arsenic Cadmium Lead Zinc mg/kg Soil, Total level 6-10 Soil, ExtractableA level 2-5 1.5-2.0 1.0 1000 20 150-300 40-130 VDPTA extractant for Pb , Cd and Zn; HC1 extractant for As 150 0141752 6.0 APPENDIX 6.1 Toxicology Mechanisms of Metals for Livestock 6.1.1 Arsenic toxicology Arsenic is second only to lead for heavy metal poisoning of domestic livestock (Sahli 1982, Buck et al. 1976). Arsenic intoxication can occur through inhalation or ingestion of arsenic bearing compounds. The trivalent forms of arsenic are generally more toxic than are pentavalent forms (Franke and Moxon 1936) and inorganic compounds are generally more toxic than organic forms (Savchuck et al . 1960). The most common means of arsenic poison- ing is through ingestion of contaminated food and the most affected livestock are cattle, sheep, and horses (Sahli 1982, Selby et al. 1977). Arsenic poisoning in livestock by inhalation of arsenic compounds is not well documented. Absorption of arsenic is dependent upon the means of exposure (inhalation or ingestion), the form of arsenic, the species of animal, and the condition of the animal. Soluble forms such as sodium arsenite are readily absorbed by all body surfaces but less soluble forms such as arsenic trioxide are not as well absorbed and are partially eliminated by excretion in the feces (Buck et al. 1976). Less than 10 percent of the usually soluble forms appear in the feces (NRC 1980). Absorbed arsenic is transported via the blood to most body tissues. In peracute, acute, or subacute poisoning, arsenic tends to accumulate in the liver and kidneys, with levels of 2 to 100 ppm (wet weight) found in these organs in dying animals. High levels have also been observed in skin tissues, hair, and spleen. Absorbed arsenic compounds are generally excreted via urine, with lesser amounts in milk and feces (Peoples 1964, Lakso and Peoples 1975, Shar iatpanahi and Anderson 1984a). Bennett and Schwartz (1971) found that a considerable portion of arsenic from lead arsenate fed to sheep was excreted in feces within 3 to 7 days. Phenylarsonic compounds are generally excreted rapidly by the urinary system in domestic animals, with 50 to 75 percent excreted within one day and the 151 0141753 remaining 25 percent excreted in 8 to 10 days (NRC 1977). Shar iatpanahi and Anderson (1984a) found that the half life of arsenic in blood of sheep and goats was 3.2 and 2.1 days, respec- tively after monosodium methanearsonate was removed from the diet. Dehydrated animals and those in poor condition are more suscepti- ble to poisoning, probably due to reduced excretion via the kidneys. Some ingested inorganic arsenate and arsenite have been shown to be methylated i_n vivo by both ruminants and nonruminants (Laksc and Peoples 1975, Tsukamoto et al. 1983). The action is apparently endogenous and the result of intestinal microflora (Penrose 1975). This action may reduce the toxicity of these compounds . The toxicosis of arsenic is generally attributed to the trivalent form (Buck et al . 1976). Arsenic reacts with sulfhydryl groups in cells inhibiting sulfhydryl enzyme systems such as pyruvate oxidase, which is essential for proper fat and carbohy- drate metabolism in the cell. Arsenic also uncouples oxidative phosphorylation by substituting for phosphorus; labile arsenylated oxidation products are substituted for stable phosphorylated intermediates (Riviere et al . 1981). Tissues most affected are the alimentary tract, kidney, liver, lung and epidermis (Buck et al. 1976). Capillary damage, especially in the splanchnic area, results in transudation of plasma into the intestinal tract and sharply reduced blood volume. Blood pressure falls to shock levels, the heart muscle becomes depressed, and general circula- tory failure occurs. The capillary transudation of plasma in vesicles results in edema of the gastrointestinal mucosa, eventu- ally leading to epithelial sloughing and the discharge of plasma into the gastrointestinal tract .(Radeleff 1970). Chronic arsenic poisoning through faulty diets containing phenylarsonic feed additives are well documented (NRC 1977). Toxicosis by phenylarsonic compounds apparently involves periph- eral nerve degeneration and symptoms include incoordination, inability to control body and limb movements, and ataxia. The condition may progress to quadriplegia (Ledet et al . 1973) 152 0141754 The rapid excretion of arsenic from the system in sublethal doses prevents any large bioaccumulat ion of arsenic in livestock. Selby (1974) recommended a 14 day market withholding time for a single dose of arsenic and a 6 week period for multiple arsenic exposure. These authors suggested that arsenic intoxicated cattle "...usually will represent a minimal hazard to man as a food source . " Although epidemiological studies have implicated arsenic as a carcinogen in humans, no literature was found indicating similar implications in domestic livestock. The average elapsed time from the beginning of skin treatments with arsenic compounds (Fowler's solution) to the development of ephi thel iomatous growth in humans has averaged 18 years (NRC 1977). It is thus likely that similar occurrences in livestock would not have sufficient time to develop, and possible metabolic differences such as exhibited by rats, may produce a different syndrome. 6.1.2 Cadmium toxicology Uptake of cadmium by domestic livestock is generally re- stricted to ingestion via contaminated food supplies or soil. Natural inhalation of cadmium at levels necessary to produce toxicosis in livestock is poorly documented. Cadmium poisoning through inhalation has been limited to human subjects, usually associated with industrial exposure. Cadmium contamination of livestock food sources may occur from airborne fallout, which accumulates on or in forage, or from excessive levels in forage grown on contaminated soils. Two of the major sources of cadmium contamination are from the land disposal of sewage sludge high in heavy metals and from mining and smelting operations. It is likely that most instances of cadmium poisoning in domestic livestock (ruminants and horses) are the result of the ingestion of contaminated feed. Absorption of cadmium is apparently not controlled by a homeostatic mechanism and therefore accumulation of cadmium in the body will occur regardless of the existing body burden or level of intake (NRC 1980). Absorption through the gastrointestinal tract 153 0141755 has been shown to range from 0.3 percent to 5 percent in various animals (Doyle et al. 1974, Moore et al. 1973, Miller et al. 1967) and is similar to the 2.7 percent absorption found for humans (Newton et al. 1984). Data suggest diets deficient in protein and calcium may increase cadmium absorption or retention (Larsson and Piscator 1971, Suzuki et al. 1969). Elevated concentrations of zinc, copper, iron, selenium or ascorbic acid tend to reduce the deleterious effects of this element (Pond and Walker 1972, Hill et al. 1963, Gunn et al . 1968). Cadmium retained by the gastrointes- tinal tract appears to represent the fraction most rapidly cleared from the body, usually within 4 to 12 days for cows and goats (NRC 1980). Lesser amounts of absorbed cadmium are excreted via bile, intestinal tract wall and urine. Very small amounts (.002 ppm) of cadmium have been detected in milk from Holstein cows which suggests milk is not an important factor in the excretion of cadmium from the body (Miller et al. 1967). Excretion of cadmium via the urine increases markedly following renal damage but prior to tissue damage, urine is an erratic indicator of cadmium exposure . The most common signs of cadmium poisoning in livestock are reduced growth rates in young animals, anemia, infertility, abortions and deformed young. Sheep fed cadmium have lost the crimp in their wool, a characteristic of copper deficiency (NRC 1980). The physiological action of cadmium within the body is intimately associated with zinc metabolism. Cadmium apparently leaves the blood rapidly following absorption and accumulates to some extent in most organs in the body. Both zinc and cadmium are known to induce the synthesis of the protein thionein to which the metals become bound (Cousins 1979). Cadmium metallothionein eventually accumulates in the liver and kidneys; kidneys have the highest concentration. The degradation of metallothionein has been shown to follow the order thionein < zinc metallothionein < cadmium metallothionein. When cadmium metallothionein is de- graded, the released cadmium ions are quickly incorporated into nascent chains of thionein and retained within the bodv (Cousins 15* 0141756 ..... : i 1979). The cadmium metallothionein is thus maintained in the kidneys. Cadmium then interferes with zinc in enzymes necessary for reabsorption and catabolism of proteins, producing tubular proteinuria. Development of proteinuria in humans takes a number of years of chronic exposure (more than 10). High concentrations of cadmium in kidneys of livestock fed cadmium in their diet suggests that this condition will occur in domestic animals if the exposure time is of sufficient duration. However, with the possible exception of horses, it is unlikely that animals would be maintained for such long periods, especially in large commercial operations. Cadmium has been shown to decrease uptake of calcium by bone in rats and chronic exposure via water and food in the presence of a calcium deficient diet has been implicated in the development of the Itai-Itai disease in humans. Osteoporosis has been observed in horses and foals near a zinc smelter and has been attributed to direct cadmium poisoning or "the result of a conditioned copper deficiency associated with high intakes of zinc and cadmium" (Gunson et al . 1982) . Studies of the effect of cadmium on the reproduction of livestock strongly indicate a high incidence of abortions and deformed offspring. A diet of 50 ppm cadmium succinate produced dead and abnormal calves and lambs (Wright et al. 1977). Goats on a diet of 75 ppm experienced 50 percent abortions, with no normal young (Anke et al. 1970). The tendency of cadmium to accumulate in the kidney and liver of livestock and the low rate of elimination from the body make bioaccumulation of cadmium very important as a means of introduc- ing this element into the human food chain. There is less danger, however, from consumption of livestock muscle tissues which accumulate very little cadmium (Table 12) . Available data strongly suggests carcinogenic effects of cadmium on humans. Many studies involving subcutaneous injections of cadmium chloride or other cadmium salts in rats have produced sarcoma. Similar studies with oral ingestion of cadmium in rats and mice did not suggest cadmium was carcinogenic in the doses 155 0141757 given (Friberg et al . 1974). Only a small amount of literature exists concerning the long-term carcinogenic effects of low level chronic cadmium poisoning in domestic livestock. Zinc is antagonistic to cadmium and the effects of cadmium poisoning have been somewhat attenuated by increasing zinc in the diet. The antagonistic nature of zinc has reduced the risk of exposure to cadmium in some areas polluted by smelters. Simi- larly, supplemental calcium, iron, copper, selenium and ascorbic acid in the diet has decreased the effects of cadmium toxicity. Lead appears to be synergistic and increases cadmium toxicity. 6.1.3 Lead toxicology Lead poisoning is the most common form of heavy metal poisoning in livestock and has been the subject of many reports and literature reviews (Amnerman et al . 1977, Aronson 1972, Buck 1970). Ingestion and subsequent absorption of lead in the gastrointestinal tract is the primary mode of absorption in domestic animals although Dogra et al. (1984) found bovine lungs with lead concentrations up to 4268 ppm in industrial areas. Sources of lead include contaminated feed, forage, and soils, along with lead-bearing debris (storage batteries, used crankcase oil, paint, leaded gasoline, etc.). Lead compounds are generally insoluble and some soluble forms (lead acetate) develop insoluble compounds (lead sulfate) in the gastrointestinal tract. Ruminants and nonruminants absorb less than three percent and about 10 percent of ingested lead, respectively (National Research Council (NRC) 1972). Research has shown that excessive dietary calcium and phosphorus decrease lead absorption in rats and lambs (NRC 1980). High zinc intake has a beneficial effect on lead toxicity in horses (Schmitt et al . 1971, Willoughby et al . 1972) and swine (Hsu et al. 1975). Horses may be more prone to lead poisoning than ruminants, but the higher number of incidents reported for horses may be partially the result of ingestion of higher levels of contaminated soils (Buck et al. 1976). Swine, sheep, goats, and chickens are apparently somewhat resistant to lead intoxica- tion (Damron et al . 1969, Staples 1975, NRC 1980). 156 0141758 Excretion of lead occurs through urine, feces, milk, and hair. Studies with rats (Castellino et al . 1966) and sheep (Blaxter and Cowie 1946, Pearl et al. 1983, Bennett and Schwartz 1971) suggest that fecal excretion, via bile and by secretion of lead and epithelial exfoliation in the gastrointestinal tract, may be greater than or equal to urinary excretion. Fecal excretion of ingested lead has been reported to range from 82 to 99 percent for sheep (Bennett and Schwartz 1971, Pearl et al. 1983, Blaxter 1950, Fick et al 1976) and high lead levels were found in feces of experimental horses (Willoughby et al. 1972). Chronic exposure to low levels of lead have been shown to produce a near steady state in adult humans, sheep (Pearl et al. 1983), and cattle (Allcroft 1951) where metabolic excretion of lead approximately equals lead absorpt i on . The estimated minimal cumulative fatal dosage of lead in cattle is 6 to 7 mg/kg body weight per day (Buck et al. 1976). Allcroft (1951) fed lead as lead acetate to an experimental steer at a dose of 5 to 6 mg/kg body weight per day for 33 months before any signs of clinical toxicosis occurred. Hammond and Aronson (1964) observed no effects in cattle consuming 3.0 to 3.5 mg lead/kg body weight per day for several months. Cattle fed 6.25 mg lead/kg body weight lead per day died within 24 days (Doyle and Younger 1984), and calves on milk diets containing lead levels of 2.7 mg/kg body weight per day died within 20 days (Zmudski et al. 1983). Horses have been reported to be poisoned at lead levels of 1.7 mg/kg body weight per day. Evidence clearly indicates that livestock can be poisoned by moderately low chronic lead levels. Clinical signs of lead poisoning include anorexia, excessive salivation, diarrhea, blindness, muscle twitching, hyperirrita- bility, depression, convulsions, grinding teeth, ataxia, circling, bellowing ("roaring in horses") and incoordination. Lack of muscular control of lips and the rectal sphincter has been observed in ponies (Burrows and Borchard 1982). Absorbed lead is initially distributed to soft tissues via the blood. Some of the lead is later redeposited in bone where it accumulates and forms the bulk of the body's lead burden. Lead 157 0141739 affects all major body organs and has been found concentrated in kidneys, liver, spleen, heart and brain. Circulating lead combines with erythrocytes and results in increased fragility of red blood cells and their subsequent premature destruction. Lead also depresses bone marrow and as a result fewer red blood cells are produced. The above effects of blood result in the develop- ment of microcytic hypochronic anemia in some animals species. Lead causes rupture of lysosomes and release of acid phosphatase that is required for energy production and protein synthesis. Lead disrupts heme synthesis by interfering with several enzymes and blocks metabolism of aminolevulinic acid which causes abnor- mally large amounts of deltaminolevulinic acid to appear in plasma and urine. Chronic lead poisoning causes degeneration of kidney and liver tissues with necrosis of the renal tubule cells. Acute poisoning produces necrosis of the gastrointestinal mucosa. The central nervous system is affected by decreased blood supply due to capillary damage which produces edema or collapse of small arteries. Extensive brain lesions have been noted in both chronic and acute lead poisoning in cattle (Christian and Tryphonas 1971). These lesions involve the cerebral cortex, thalamus, hypothalamus, medulla oblongata and proximal cervical spinal cord. Pharyngeal or buccal paralysis in cattle and laryngeal and pharyngeal paralysis in horses may be produced by damage to either cranial nerves or the brain stem nuclei. Incoordination and degeneration of muscle control occurs through segmental demyel ination of peripheral nerves. Lead has been shown to adversely affect reproduction in several animal species, including humans. Sheep grazing in lead mining areas have exhibited high rates of abortions and failures to conceive. Pregnant goats on lead-supplemented diets (lead acetate, 50 to 6,400 mg Pb/kg/day) aborted 6 to 8 days after starting the lead diets (Dollahite et al. 1975). There is evidence that lead can cross the placenta and affect fetal development (Barltrop 1969). 158 The large accumulation of lead in livestock organs and bone represents a potentially significant source of lead in the human diet . No documentation has been found relating chronic exposure of livestock to lead and the subsequent development of cancer. Studies of rats and mice subjected to rather high doses of lead compounds via oral or parenteral administrations exhibited malignant and benign renal neoplasms (Environmental Protection Agency 1977) . The synergistic effects of lead and cadmium have been documented for ponies and calves (Burrows and Borchard 1982, Lynch et al . 1976b). Zinc appears to be antagonistic to lead and inhibits symptoms of lead toxicity in young horses (Willoughby et al. 1972b). These authors found that, in the presence of toxic amounts of lead and zinc, the symptoms and tissue lead accumula- tion normally associated with lead toxicity were suppressed and that the clinical symptoms were those associated with zinc toxicity. Willoughby et al . (1972b) found that dietary doses of lead and zinc necessary to experimentally produce clinical toxicity in foals were considerably higher than lead and zinc levels in diets associated with natural toxicosis, thus suggesting interaction with unknown additional elements occurred in the natural poisoning cases. Lead has been shown to also, disrupt tissue levels of iron, copper and manganese in cattle (Doyle and Younger 1984). There is conflicting data concerning the effect of calcium on the absorption and excretion of lead (Pearl et al . 1983, Willoughby et al. 1972). 6.1.4 Zinc toxicology Animals have high tolerances for zinc, and only under large, excessive exposures have toxic effects been documented. Diets with 3,000 ppm have been required to induce zinc toxicosis experi- mentally, and 1,000 ppm zinc has not produced adverse effects if there has been an adequate amount of copper and iron in the diet. Ott et al. (1966a) has shown that 1000 to 2000 ppm zinc is necessary to adversely affect the performance of lambs. Zinc is 159 0141761 an essential element, and all body tissues contain some zinc. Metabolic problems with zinc generally involve a zinc deficiency. Although inhalation of industrial dust has resulted in deposition of up to 13,311 ppm zinc in bovine lungs (Dogra et al , 1984) the normal route of zinc absorption is through the gastroin- testinal tract. The approximate minimum requirement of zinc in the diet is 40 to 100 ppm for young domestic animals (NRC 1980) . Absorption of zinc is controlled by homeostatic mechanisms when zinc ingestion is within normal ranges. These mechanisms have been shown to become markedly less effective at higher (600 ppm) levels of zinc intake in calves (Miller et al . 1970, 1971). Zinc absorption in humans has been reported to range from 16 to 77 percent of the total amount ingested (EPA 1977). Sheep absorbed 13 percent of a 39 mg per day zinc diet (Doyle et al. 1974). Zinc deficiency and underweight conditions increase absorption while excessive dietary calcium with phytate decreases zinc absorption. Zinc is primarily excreted in the feces, with lesser amounts in urine. Small amounts are also found in milk, saliva, sweat and hair, the latter is commonly used as an indicator of body zinc levels (Miller et al. 1965b). Manifestations of excess dietary zinc include reduced weight gains, anemia, reduced bone ash, decreased iron, copper and manganese in tissues, and diminished utilization of calcium and phosphorus (Ott et al. 1966 c,d). Lameness has been observed in horses receiving up to 186 mg/kg body weight zinc, and severe bone and cartilage abnormalities have been observed in swine receiving 268 ppm dietary zinc. Diets with 2,000 to 4,000 ppm zinc have produced an arthritis-like syndrome, internal hemorrhaging and 33 to 50 percent mortality in swine (Brink 1959). Absorbed zinc binds to sulfyhdryl, amino, imidazole and phosphate groups. Zinc is necessary for several zinc metal- loenzyme and metalloprotein systems, including carbonic anhydrase, carboxypeptidases A and B, alcohol dehydrogenase, glutamic dehydrogenase, D-glyceraldehyde-3-phosphate dehydrogenase, lactic dehydrogenase, malic dehydrogenase, alkaline phosphatase, aldo- lase, superoxide dismutase, r ibonnuclease and DNA polymerase 160 (Riordan and Vallee 1976, Chesters 1978). The toxic effects of excessive zinc include disrupting bone mineralization (by depress- ing calcium and phosphorus levels and by decreasing the cal- cium: phosphorus ratio), interference with copper metabolism (lessened activity of cytochrome oxidase and catalase), and reduced iron concentrations in some tissues (iron deficiency anemia and reduced hepatic iron stores) (NRC 1979) . Zinc chloride has been shown to induce testicular tumors when injected into the active gonads of some fowl, but there is no evidence that zinc is carcinogenic when ingested. Some studies suggest zinc supplements may inhibit tumor growth. Zinc is antagonistic to cadmium and can reduce many of the adverse effects produced by cadmium when the diet is supplemented with zinc. Animals receiving both zinc and lead exhibit lower lead in bones but higher levels of lead in kidneys and liver. The neurologic dysfunction associated with high lead intake has been absent in the presence of supplemented zinc in the diet. Zinc is antagonistic to copper and may produce copper deficiencies at elevated levels (Eamens et al . 1984). Zinc also disrupts levels of calcium, phosphorus and iron, as indicated above. 6.2 Toxicology Mechanisms of Metals for Plants The toxicology of metals in plants may involve different biochemical mechanisms in different species and varieties (Foy et al. 1978). Numerous other factors also influence the toxicity of heavy metals. These factors and plant toxicology mechanisms are presented in the following sections. 6.2.1 Arsenic toxicology Wh-ile elemental arsenic is not toxic, many of its compounds are toxic. Chief among these are arsenate (AsC>4~3) and arsenite (As02"2). Other common forms are methanearsenate and dimethyl- arsenate, which are commercially prepared as post-emergence herbicides, but may also be synthesized in trace amounts in the soil by microorganisms. Plants take up relatively small amounts 161 0141/03 of arsenic from soils and the arsenic levels in natural soils are rarely high enough to cause phy totox ici ty . Aerial deposition of arsenic from smelters, or long-term application of arsenical pesticides may elevate soil values to phytotoxic levels. Plant toxicity to arsenic occurs when: 1) abnormally high arsenic levels are produced in soil, either deliberately or accidentally by man's activities; 2) a change in soil chemistry increases arsenic availability; and 3) plant foliage is sprayed with arsenical compounds (Wauchope 1983). Symptoms of arsenic toxicity include wilting of new-cycle leaves, followed by retardation of root and top growth (Liebig 1966) . Arsenite is 4 to 100 times more toxic and its compounds are more available to plants than arsenate (Wauchope 1983). However, in most cases arsenite is rapidly oxidized to arsenate in the soil. Arsenic phytotoxicity is a four-stage process: 1) absorp- tion onto plant surfaces; 2) movement to the plant interior; 3) translocation to the site of action; and 4) a biochemical reaction that is toxic (Wauchope 1983). Both arsenate and arsenite are rapidly and intensely adsorbed to plant roots, resulting in very high concentrations in the root vicinity (Machlis 1974). Because of its extremely high toxicity to cell membranes, very limited translocation of arsenite occurs once the chemical has penetrated the cuticle and entered the apoplast phase of the plant system. Membrane degradation is the result of arsenite oxidation by sulfhydryl groups, causing cessation of root functions and foliar necrosis upon contact (Speer 1973). Internal injury of this type is manifested as wilting due to loss of turgor. Arsenate is less toxic and therefore is more readily trans- located. If sub-lethal concentrations are present in the soil, substantial accumulation may occur in foliage (Liebig 1966). Translocation occurs both intra- and extracellularly , including xylem and phloem transport. Arsenate does not react with sulfhy- dryl groups, nor does it degrade cell membranes like arsenite. Its main toxic effects are apparently due to its disturbance of phosphorus metabolism in plants. Studies have shown that the chemistry of arsenate and phosphate is very similar and they tend 162 to replace one another chemically, but not functionally. Such substitution of arsenate for phosphate may cause decoupling of oxidative phosphorylation in mitochondria and inhibit leaf uptake of chemicals. Further, as arsenate is translocated throughout the plant it may interfere with cell organelles such as chloroplasts in which phosphorus plays an important role (NRC 1977). Porter and Sheridan (1981) noted reduction in the nitrogen fixing activity at low levels (1 mg/L of added arsenic) and inhibition of photosynthesis and respiration at very high levels (100 mg/L). 6.2.2 Cadmium toxicology Cadmium is an element serving no apparent essential biologi- cal function, yet it is often readily taken up, translocated and accumulated by plants. It is found in very low concentrations in natural soils and generally only reaches phytotoxic levels due to anthropogenic activities. Plant uptake occurs both through roots and leaves. Uptake of soil-cadmium is influenced by several factors including pH, CEC, plant species and varieties and age (Jastrow and Koeppe 1980, Boggess et al. 1978). Recently, added chloride was shown to increase the level of soluble soil-cadmium (Bingham et al. 1984). A study of cadmium uptake and transloca- tion from solution has shown most of the cadmium to be retained in plant roots (Jarvis et al. 1976). Symptoms of cadmium toxicity include stunting and chlorosis. While much is known about the tox icological effects of cadmium, little has been discovered con- cerning the biochemical basis for plant toxicity. Cadmium is chemically allied with zinc and often substitutes for zinc in plant metabolic activities; this substitution may.be a reason for its phytotoxici ty . Vallee and Ulmer (1972) proposed that cadmium toxicity is in part due to the replacement of zinc by cadmium at certain enzyme sites. Root et al. (1975) stated that excess cadmium may cause chlorosis in corn leaves due to decreased zinc uptake and subsequent changes in the Fe:Zn ratios. Cadmium interference with zinc uptake and translocation in beans was documented by Hawf and Schmid (1967). In contrast, added cadmium levels significantly increased the zinc concentration of tomato 163 0I417SS leaf tissue (Smith and Brennan 1983). Other researchers have reported both interference and enhancement of zinc uptake by cadmium in different plants and at varying levels of cadmium concentration (Hinesly et al. 1982, Pepper et al. 1983, Chaney et al. 1976). Gerritse et al . (1983) found that increasing zinc in the soil solution apparently increased cadmium uptake at high solution concentrations of cadmium and decreased uptake at low solution concentractions . Air pollution (as ozone) may interact synergistically with cadmium to reduce crop yields, causing ozone toxicity symptoms to develop at cadmium levels that normally would be harmless (Czuba and Ormrod 1974). Hovmand et al . (1983) reported that atmospheric cadmium accounted for 20 to 60 percent of the total amount of cadmium in some agricultural crops in Denmark . More than 70 percent of the total amount of cadmium in tree leaves near a zinc smelter was found to be associated with the cell wall. The remaining cadmium was distributed among the cytosol , vacuole sap and cell organelles (Ernst, 1980) . Such a compar tmentali zation of cadmium in cell walls may protect the more susceptible metabolic sites of the cell. Cadmium content in cell organelles is related to their function and potential for ion uptake. For example, chloroplasts will accumulate much more cadmium than mitochondria. Lee et al . (1976) found that cadmium may either stimulate or inhibit a large number of plant enzyme systems, which may cause subsequent biochemical chain reactions. Enzyme inhibition has been shown to be the result of cadmium affinity for sulfhydryl groups. Such disruption of enzyme systems has been shown to affect nitrate uptake in corn seedlings and amino group catalysis and nitrogen fixation by legumes (Mathys 1975, Volk and Jackson 1973, Huang et al. 1974). Cadmium may also negatively affect photosynthesis. It has often been associated with reduced chlorophyll content, possibly due to interference with the biosynthesis of photosynthetic pigments and biomembranes . Enzymes needed for catalytic activity may also be inactivated by cadmium because cadmium will bind with \M 0141786 sulfhydryl groups. Reduced carbon dioxide fixation may result from cadmium substitution for zinc in zinc metal loenzymes and sub- stitution for manganese may cause inhibition of electron flow in plant photosystems (Ernst 1980). Plant respiration may be enhanced or inhibited depending upon species-specific carbohydrate metabolism. Cadmium has been shown to cause pronounced swelling of mitochondria, with a resultant decrease in respiration rate (Bittell and Miller 1974). Like numerous other metals, cadmium may have a strong effect on the properties of DNA. It has been demonstrated that cadmium may decrease cell viability, increase single-strand breakage of DNA and inhibit cell division (Mitra and Bernstein 1978) . 6.2.3 Lead toxicology Lead is considered a nonessential element for plant growth. Lead uptake from soils is dependent on many factors, including soil pH, cation exchange capacity (CEC), organic matter, calcium content, plant species and the soluble metal concentration. Climatic conditions such as precipitation, temperature and the length of daylight also influence lead uptake. Lead uptake is enhanced by low pH conditions and by soils with little organic matter. Organic matter is known to have a high CEC and tends to adsorb or bind most metal cations. Thus, high CEC or organic matter content renders soil lead less availa- ble to plants. Low pH conditions enhance the solubility of most metals, including lead, making them more available for plant uptake. The addition of phosphate and liming have been shown to reduce lead uptake by plants by forming low solubility compounds such as lead hydroxide, carbonate and phosphate (Demayo et al . 1982) . Plant species also differ in their lead uptake. Lead tends to collect in the top layer of soil and, therefore, shallow rooted plants such as annual grasses take up more lead than deep rooted perennials such as alfalfa. Absorption of lead by plants is both by root uptake and absorption through foliage of airborne lead fallout. Most of the literature indicates that uptake by roots is the primary means of 165 0141767 lead absorption (Zimdahl and Arvik, 1973). Translocation of lead from the root system to other parts of the plant is poor, with roots generally accumulating the highest lead concentration. The translocation is predominantly apoplastic in nature (Holl and Hampp 1975). Indirect evidence suggests transport is via sieve tubes which are part of the phloem (food) transport system in plants. Some lead may be precipitated in root dictyosomes, possibly due to phosphatase enzymes (Haque and Subramanian 1982) . The dictyosome vesicles contain cell wall precursors and as the dictyosomes move to the cell walls and fuse to it, the lead may be bound at that site. Translocation of lead is apparently enhanced when the soil solution is deficient in other nutrients. Many researchers have found increased lead levels in all plant tissues growing in a nutrient solution containing lead. The fruiting and flowering parts of plants have been found to accumulate the least amount of lead (NRC 1972). The toxicosis of lead in plants is expressed by reduced growth and vital processes such as photosynthesis, mitosis and water absorption. Lead accumulates in tissues with high mitotic activity and appears to be bound to polyuronic acids of the cell walls (Holl and Hampp, 1975). High concentrations of lead are found in organelles such as mitochondria, chloroplasts and also in nuclei. The lead is apparently bound to certain phosphate groups in cells . Roots that are in contact with lead degenerate because of a decrease in cell division in root meristems. The photosynthetic process is hindered by diminished CO2 fixation by chloroplasts and by the disturbance that lead causes in the transport of electron between the site of primary electron donor and water oxidation (Holl and Hampp 1975). The activity of many enzymes is inhibited due to blocking by lead of sulfhydryl groups in proteins due to changes in the phosphate levels of living cells. 6.2.4 Zinc toxicology Zinc is an essential element in plant metabolism. Zinc deficiency in crops is the most common micronutr ient deficiency in 166 0141763 the United States (NRC 1979) . Zinc phytotox ici ty exists naturally in only isolated instances with most toxicity problems related to anthropogenic sources such as in metal mining, smelting and refining . Zinc uptake by plants is influenced by the soil pH, soil composition, CEC, organic matter, phosphorus levels, and soluble zinc concentrations. Uptake is also influenced by the form of zinc. Zinc oxides, carbonates, phosphates and sulfides are generally less soluble and therefore less toxic than similar concentrations of soluble zinc salts. Zinc availability to plants is enhanced in low pH in soils where the solubility of many metals is increased. The potential for zinc toxicosis is reduced in soils high in calcium and magnesium and the increase of soil pH from the liming of agricultural soils reduced zinc toxicosis (Lee and Page 1967) . The fixation of zinc through microbial activity also reduces zinc available for plant uptake. Studies suggest plants remove 1 to 3 percent of the zinc added to a soil (Taylor et al. 1982) . Absorption of zinc is influenced by copper, phosphorus, and iron levels. Copper and zinc are antagonistic and the absorption of one usually depresses absorption of the other. Phosphorus in excessive amounts can reduce zinc uptake and, conversely, exces- sive zinc apparently depresses phosphorus metabolism. Excess iron tends to intensify a zinc deficiency. Translocation of zinc ccurs through the xylem (water transports system) and a small amount may be redistributed via the phloem (food transport system) . Normal zinc concentrations in plants range from 15 to 150 ppm (dry matter) with zinc toxicosis commonly occurring at levels of 400 ppm (dry matter) (Gough et al. 1979). The suscepti- bility of plants to zinc toxicity varies among species. Boawn and Rasmussen (1971) have shown that monocotyledonous species (corn, sorghum, barley and wheat) were more sensitive to excess zinc than were dicotuledmons species (beans, peas, some leafy vegetables and clover). Symptoms of zinc toxicity include stunted growth, reduced yields, reduced size of leaves, necrosis of leaf tips and o 167 0141759 shoot apices, a reddish tint near the basal part of leaves and curling and distortion of foliage. Zinc is an enzyme cofactor and binds pyridine nucleotides to the protein portion of enzymes. Zinc atoms also stabilize the structure of yeast alcohol dehydrogenase and are an essential component in a variety of dehydrogenases, proteinases, peptidases and zinc metal loenzyme carbonic anhydrase (NRC 1979) . Lack of zinc, therefore, produces a general failure in the metabolic system; RNA doesn't form, resulting in lowered protein formation, less total nitrogen and DNA lesions. 6.3 Computerized Data Base Utilized The following data bases have been computer searched for this document. Descriptions are quoted directly from Dialog database catalog for 1985. AGRICOLA File 10, 110 1970-present, 2,826,000 records, monthly updates (National Agricultural Library, Beltsville, MD ) . AGRICOLA (formerly CAIN) is the cataloging and indexing database of the National Agricultural Library (NAL) . This massive file provides comprehensive coverage of worldwide journal and monographic literature on agriculture and related subjects. Since AGRICCLA represents the actual holdings of the National Agricul- tural Library, there is substantial coverage of all subject matter normally contained in a very large library. File 110 contains the citations for the years 1980-1978. File 10 contains citations from 1979 to the present. Both files have similar format and identical coverage and pricing. BIOSIS PREVIEWS Files 5, 55, 255 1969-present , 4,566,000 records, biweekly updates (BioSciences Information Service, Philadelphia, PA). BIOSIS PREVIEWS contains citations from both 3iological Abstracts and 5:clrg:cal Abstracts/RRM (formerly entitled Bio- research Index1 , the major publications of BioSciences Information 168 014.1770 Service of Biological Abstracts. Together, these publications constitute the major English language service providing comprehen- sive worldwide coverage of research in the life sciences. Over 9,000 primary journals and monographs as well as symposia, reviews, preliminary reports, semi-popular journals, selected institutional and government reports, research communications, and other secondary sources provide citations on all aspects of the biosciences and medical research. Searchable abstracts are available for Biological Abstracts records from July 1976 to the present. File 5 contains all the citations from 1981 through the present. The citations for the years from 1977 through 1980 are available in File 55, and citations for the years 1969-1976 are available in File 255. CAB ABSTRACTS File 50 1972-present , 1,760,000 records, monthly updates (Commonwealth Agricultural Bureaux, Farnham Royal, Slough, England) . CAB ABSTRACTS is a comprehensive file of agricultural and biological information containing all records in the 26 main abstract journals published by Commonwealth Agricultural Bureaux. Over 8,500 journals in 37 languages are scanned, as well as books, reports, and other publications. In some instances less accessi- ble literature is abstracted by scientists working in other countries. About 130,000 items are selected for publication yearly; significant papers are abstracted, while less important works are reported with bibliographic details only. The following journals are included in CAB ABSTRACTS: Agricultural Engineering Abstracts; Animals Breeding Abstracts; Apicultural Abstracts; Arid Lands Abstracts; Dairy Science Abstracts; Field Crop Abstracts; Forest Products Abstracts; Forestry Abstracts; Helminthological Abstracts (A & B) ; Herbage Abstracts; Horticultural Abstracts; Index Veter inarius; Nutrition Abstracts and Reviews (A & B) ; Plant Breeding Abstracts; Proto- zoological Abstracts; Review of Applied Entomology (A & B) ; Review of Medical and Veterinary Mycology; Review of Plant Pathology; 169 0141771 Rural Development Abstracts; Rural Extension, Education and Training Abstracts; Leisure, Recreation and Tourism Abstracts; Rural Sociology Abstracts; Soils and Fertilizers; Veterinary Bulletin; Weed Abstracts; and World Agricultural Economics. CRIS/USDA File 60 Last two years, 35,700 records, monthly updates (U.S. Department of Agriculture, Beltsville, MD) . CRIS (Current Research Information System) is a valuable current-awareness database for agriculturally related research projects. The projects described in CRIS cover current research in agriculture and related sciences, sponsored or conducted by USDA research agencies, state agricultural experiment stations, state forestry schools, and other cooperating state institutions. Currently active and recently completed projects within the last two years are included. The subject coverage of CRIS encompasses the following disciplines: biological, physical, social and behavioral sciences related to agriculture in its broadest applications, including natural resource conservation and management; marketing and economics; food and nutrition; consumer health and safety; family life, housing, and rural development; environmental protection; forestry; outdoor recreation; and community, area, and regional development . ENVIROLINE File 40 1971-present, 115,500 records, monthly updates ( ElC/Intell i- gence, New York, NY). ENVIRONLINE, produced by the Environment Information Center, covers the world's environmental information. Its comprehensive, interdisciplinary approach provides indexing and abstracting coverage of more than 5,000 international primary and secondary source publications reporting on all aspects of the environment. Included are such fields as: management, technology, planning, law, political science, economics, geology, biology, and chemistry as they relate to environmental issues. Literature covered 170 0141772 includes periodicals, government documents, industry reports, proceedings of meetings, newspaper articles, films and monographs. Also included are rulings from the Federal Register and patents from the Official Gazette. MEDLINE Files 152, 153, 154 1966-present , 4,687,000 records, monthly updates (U.S. National Library of Medicine, Bethesda , MD) . MEDLINE (MEDLARS onLINE), produced by the U.S. National Library of Medicine, is one of the major sources for biomedical literature. MEDLINE corresponds to three printed indexes: Index Medicus, Index to Dental Literature, and International Nursing Index. MEDLINE covers virtually every subject in the broad field of biomedicine. MEDLINE indexes articles from over 3000 interna- tional journals published in the United States and 70 countries. Citations to chapters or articles from selected monographs are also included. MEDLINE is indexed using NLM ' s controlled vocabulary MeSH (Medical Subject Headings) . Over 40% of records added since 1975 contain author abstracts taken directly from the published articles. Over 250,000 records are added per year, of which over 70% are English language. NTIS File 6 1964-present, 1,122,000 records, biweekly updates (National Technical Information Service, [NTIS], U.S. Department of Com- merce, Springfield, VA) . The NTIS database consists of government-sponsored research, development, and engineering plus analyses prepared by federal agencies, their . contractor s or grantees. It is the means through which unclassified, publicly available unlimited distribution reports are made available for sale from such agencies as NASA, DDC, DOE, HHS (Formerly HEW), HUD, DOT, Department of Commerce, and some 240 other units. State and local government agencies are now beginning to contribute their reports to the file. 171 0141773 The NTIS database includes material from both the hard and soft sciences, including substantial materials on technological applications, business procedures, and regulatory matters. Many topics of immediate broad interest are included, such as environ- mental pollution and control, energy conversion, technology transfer, behavioral/societal problems, urban and regional planning . POLLUTION ABSTRACTS File 41 1970-present, 110,000 records, bimonthly updates (Cambridge Scientific Abstracts, Bethesda, MD) . POLLUTION ABSTRACTS is a leading resource for references to environmentally related literature on pollution, its sources, and its control. The following subjects are covered by the POLLUTION ABSTRACTS database: Air Pollution, Environmental Quality, Noise Pollution; Pesticides, Radiation, Solid Wastes, and Water Pollution . SCISEARCH Files 34, 87, 94, 186 1974-present , 6,189,000 records, biweekly updates (Institute for Scientific Information, Philadelphia, PA) SCISEARCH is a multidiscipl inary index to the literature of science and technology prepared by the Institute for Scientific Information (ISI). It contains all the records published in Science Citation Index (SCI) and additional records from the Current Contents series of publications that are not included in the printed version of SCI. SCISEARCH is distinguished by two important and unique characteristics. First, journals indexed are carefully selected on the basis of several criteria, including citation analysis, resulting in the inclusion of 90 percent of the world's significant scientific and technical literature. Second, citation indexing is provided, which allows retrieval of newly published articles through the subject relationships established by an author's reference to prior articles. SCISEARCH covers every area of the pure and applied sciences. 172 W-i- 111 (<1 The ISI staff indexes all significant items (articles, reports of meetings, letter, editorials, correction notices, etc.) from about 2600 major scientific and technical journals. In addition, the SCISEARCH file for 1974-75 includes approximately 38,000 items from Current Contents — Clinical Practice. Beginning January 1, 1976, all items from Current Contents — Engineering, Technology, and Applied Science and Current Contents — Agriculture, Biology, and Environmental Sciences that are not presently covered in the printed SCI are included each month. This expanded coverage adds approximately 58,000 items per year to the SCISEARCH file. WATER RESOURCES ABSTRACTS File 117 1968-present , 176,000 records, monthly updates (U.S. Dept. of the Interior, Washington, D.C.). Water Resources Abstracts is prepared from materials col- lected by over 50 water research centers and institutes in the United States. The file covers a wide range of water resource topics including water resource economics, ground and surface water hydrology, metropolitan water resources planning and management, and water-related aspects of nuclear radiation and safety. The collection is particularly strong in the literature on water planning (demand, economics, cost allocations), water cycle (precipitation, snow, groundwater, lakes, erosion, etc), and water quality (pollution, waste treatment). WRA covers predomi- nantly English-language material and includes monographs, journal articles, reports, patents and conference proceedings. 173 0141775 7.0 REFERENCES CITED Akinsoyinu, 0., 0.0. Tewe and A.U. Mba. 1979. Concen- tration of trace elements in milk of West African dwarf goats affected by state of lactation. Journal of Dairy Science. V.62, pp 921- Albert, W.B. and C.H. Arndt. 1931. The concentration of arsenic as an index of arsenic toxicity to plants. S.C. Agric. Exp. Sta. 44th Ann. Rpt . Alberta Environment. 1982. Guidelines for the applica- tion of municipal wastewater sludges to agricultural lands in Alberta. Standards and Approvals Division. Earth Sciences Division. Edmonton, Alberta, Canada. Allcroft, R. 1951. 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V. 2(1), pp 31-36. Boggess, S.F., S. Willavize, and D.E. Koeppe. 1978. Differ- ential response of soybean varieties to soil cadmium. Agronomy Journal. V 70, pp. 756-760. Bratton, G.R. and J. Zmudski. 1984. Laboratory diagnosis of Pb poisoning in cattle: A re-assessment and review. Vet- erinary and Human Toxicology. V. 26(5), pp. 387-392. Bremner, I. 1979. The toxicity of cadmium, zinc, and moly- bdenum and their effects on copper metabolism. Proc. Nutr. Soc. V. 38, pp. 235-242 Bremner, I., B.W. Young and C.F. Mills. 1976. Protective effect of zinc supplementation against copper toxicosis in sheeD. British Journal of Nutrition. V. 36, pp. 551-561'. Brink M.F., D.E. Becker, S.W. Terrill and A.H. Jensen. 1959. Zinc toxicity in the weanling pig. Journal of Animal Science. V. 18, pp.- 836-842^ 177 0141779 British Columbia, 1982. Guidelines for use with the regulation under the Waste Management Act for control of the discharge of sludge to land. 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