Water Quality for Wyoming Livestock & Wildlife - Coming Soon!

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supplementing with 17 ppm Cu for six months resultedin no signs of adverse effects. 308 Cattle grazing a reclaimedmine tailing site containing 21-44 ppm Mo and13-19 ppm Cu for three consecutive summers exhibitedno signs of Mo toxicity. 217,309,310 No adverse effects werenoticed in a cannulated steer consuming sun-cured haycontaining 49.68 ppm Mo and 19.09 ppm Cu. 311 Ineach of these studies, low S in both the diet and waterwas offered as being a possible explanation for the lack ofclinical signs observed.SummaryHorses, like most monogastric animals, are very resistantto the effects of Mo as compared to ruminants. Cattle arecommonly cited as slightly more susceptible to molybdenosisthan sheep, and limited quantitative data suggestmule deer are relatively resistant compared to cattle.Therefore, drinking water Mo concentrations that are safefor cattle are probably also safe for horses, other classesof livestock, and wild cervids. Although there is quite abit of variability in the reports summarized above, andsome (large) amount of dietary Mo may cause poisoningregardless of Cu status, the bottom line seems to be thattotal dietary Cu:Mo ratios of less than 2-4 can result inchronic toxicity and decreased production in cattle, especiallyif dietary S is higher than absolutely necessary.As with many substances, the effects of forage and waterMo concentrations are additive, and, in some areas of thewestern United States, forage Mo concentrations are alreadytoxic or very nearly toxic. Under these conditions,any additional Mo intake contributed by drinking wateris potentially dangerous. In these areas, however, producersare likely already aware of the problem and feedingsupplemental Cu. A more normal situation wouldbe cattle grazing “typical” Wyoming forage containing 7ppm Cu (or supplemented to that level) and negligibleMo (~1 ppm). Under these conditions the critical safe4:1 ratio would be exceeded whenever drinking watercontains 375 μg Mo/L.We recommend that, in the absence of other data,drinking water for livestock and wildlife containless than 0.3 mg/L. If dietary Mo is higher, which isnot unusual in this region, water Mo concentrationsshould be adjusted downward accordingly.24
6 Nitrate and NitriteThe nitrate (NO 3-) and nitrite (NO 2-) ions are intermediatesin the biological nitrification cycle and the primarysource of nitrogen (N) for plants in the soil. Plants accumulateNO 3-from soil to synthesize protein via a multistepprocess; excessive NO 3-accumulation as a result ofthis process may cause poisoning of grazing animals. 312Nitrate or NO 2-may contaminate water as a result ofcontact with natural minerals (e.g. niter), agriculturalrunoff (fertilizer, manure) or industrial processes. 312-314Nitrate is the more stable of the two N species and thereforemore common in surface waters. 315 Nitrite (NO 2-)usually results from biological reduction of NO 3-, but itmay also be an industrial contaminant or exist in groundwaters where pH and redox potential prevent oxidationto NO 3-. 315 Both ions are extremely water-soluble andtherefore water-mobile.EssentialityAlthough N is an essential macro element for mammals,NO 2and NO 3are not essential per se.MetabolismWhile the NO 3-ion is readily absorbed in the upper gastrointestinal(GI) tract and possesses intrinsic toxicologicproperties such as vasodilation, the condition referred toas “nitrate poisoning” actually depends upon reduction ofNO 3-to NO 2-in the upper GI tract. 312,316-318 This processoccurs in human infants 319,320 , and it is the basis of currenthuman drinking water standards, but nitrate toxicityis primarily a problem in ruminant species, as the rumenmicroflora are well-suited to catalyze NO 3-reduction.Radiotracer studies indicate that NO 2-, formed fromNO 3-in the rumen, may either be further reduced andincorporated via NH 3into amino acids or reduced vianitric oxide to N and expelled. 321 Unfortunately, neitherof the latter pathways (i.e. amino acids or N) is as fast asthe initial reduction to NO 2-, and dangerous NO 2-concentrationsaccumulate in the GI tract when assimilatorypathways are overloaded. 321-323 Under the proper dietaryconditions (mainly adequate carbohydrates) the assimilatorypathways can adapt to high NO 3-concentrations,and very little NO 3-or NO 2-escape the rumen. 314,322,324-327Sustained exposure to moderately high NO 3diets resultsin induction of the assimilatory pathways, and this abilitymay be acquired by transfer of GI flora from one ruminantto another. 322,323 Once absorbed into the bloodstream,the NO 3-ion is rapidly distributed throughoutthe body water and excreted via urine and saliva, whereasthe NO 2-ion is oxidized to NO 3-via a coupled reactionwith hemoglobin and eliminated as NO 3-. 316,318,328,329Other differences between ruminants and monogastricsin the metabolism of the NO 2-and NO 3-ions, whilenot directly tied to the ruminal metabolism of NO 3-,probably reflect evolutionary pressure of the constantbackground of NO 2-ruminants receive from ruminalmetabolism. The blood t 1/2of NO 2-is similar in monogastricsand ruminants, but the elimination of NO 3-fromblood is much slower in monogastrics 316 and the normalbackground metHb concentration is higher in monogastrics.330 In ruminants only a small portion of an oral doseof NO 3is eliminated in the urine, whereas in monogastricsmost ingested NO 3is eliminated via urine. 314Some sources suggest the NO 3-ion is more bioavailablein water than feedstuffs. 312-314 The experiments thisconclusion was drawn from, however, were based uponaqueous NO 3-administered directly into the stomach vs.contaminated feedstuffs offered ad libitum. 314 The mostimportant determinant of NO 3toxicity seems to be howrapidly a given dose of NO 3-is administered, rather thanwhether it is in feed or water. 314,331,332 For example, thesingle oral median lethal dose (SOLD 50) of NaNO 3incows was reported to be 328 mg/kg BW when given atonce, but when the same dose was spread over 24 hours,the LD 50increased to 707-991 mg/kg. 331ToxicityAlthough the most common source of NO 3poisoning inlivestock is contaminated feedstuffs, NO 3--contaminateddrinking water has poisoned people and animals. 320,333-336The mechanism of poisoning involves GI microbialreduction of the NO 3-ion to NO 2-, which is absorbedinto the bloodstream where it oxidizes the ferrous ironatoms (Fe +2 ) in hemoglobin (Hb) to the ferric (Fe +3 )state, resulting in methemoglobin (metHb), which can-25
Page 1 and 2: Water Qualityfor Wyoming Livestock
Page 3: AbbreviationsADG - average daily ga
Page 6 and 7: 7 pH 31Function. . . . . . . . . .
Page 8 and 9: animal drinks. Water intake is tech
Page 10 and 11: ter or “mg X/L”. If the substan
Page 12 and 13: tion between the erythrocytic and p
Page 14 and 15: in diseases such as cancer. 10,20,2
Page 17 and 18: 3 BariumBarium (Ba), an alkaline ea
Page 19 and 20: exposed to 100 mg Ba 2+ /L had depr
Page 21 and 22: 4 FluorideFluorine (F) is the most
Page 23 and 24: lost weight and many died at the hi
Page 25: Our search of the literature pertai
Page 28 and 29: elatively stable; however, once unb
Page 32 and 33: not transport oxygen from the lungs
Page 34 and 35: Winter and Hokanson 381 fed varying
Page 37 and 38: 7 pHpH is defined as “the negativ
Page 39: for basic drinking water. From a pu
Page 42 and 43: efficiency. 436,437 Absorption of S
Page 44 and 45: significantly impaired in the same
Page 47 and 48: 9 Sodium ChlorideSodium chloride (N
Page 49 and 50: containing 15,000 mg NaCl/L for 21
Page 51 and 52: 10 SulfurSulfur (S) occurs in natur
Page 53 and 54: in feed or water consumption. The a
Page 55 and 56: 11 Total Dissolved Solids (TDS)Tota
Page 57: 12 SummaryElementShort (days - week
Page 61 and 62: 14 Bibliography1. National Research
Page 63 and 64: 35. Klug H.L., Lampson G.P. and Mox
Page 65 and 66: 69. Harding J.D., Lewis G. and Done
Page 67 and 68: 104. Choudhury H. and Cary R. (2001
Page 69 and 70: 136. Boyd E.M. and Abel M. (1966).
Page 71 and 72: 171. Mullenix P.J., Denbesten P.K.,
Page 73 and 74: 203. Schultheiss W.A. and Van Nieke
Page 75 and 76: 237. Tolgyesi G. and Elmoty I.A. (1
Page 77 and 78: 269. ANZECC (2000). Australian and
Page 79 and 80: 301. Huber J.T., Price N.O. and Eng
Page 81 and 82:
332. Crowley J.W., Jorgensen N.A.,
Page 83 and 84:
366. Walker R. (1990). Nitrates, ni
Page 85 and 86:
399. Wu L., Kohler J.E., Zaborina O
Page 87 and 88:
432. Naftz D.L. and Rice J.A. (1989
Page 89 and 90:
464. Glenn M.W., Jensen R. and Grin
Page 91 and 92:
498. Knott S.G. and McCray C.W.R. (
Page 93 and 94:
532. Harvey R.W., Croom J. WJ, Pond
Page 95 and 96:
567. Koletsky S. (1959). Role of sa
Page 97 and 98:
602. Gooneratne S.R., Olkowski A.A.
Page 99 and 100:
633. McAllister M.M., Gould D.H., R
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