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Emissions of hydrogen sulfide (H2S) gas are commonly encountered in sour gas processing operations. In this study, systemic biochemical changes were assessed in Fischer 344 rats after a repeated exposure regime (8 h/ day, 5 days/ wk for 5 wk) to atmospheres containing 0, 1, 10, and 100 ppm (0, 1.4, 14, and 140 mg/ m 3) H2S. Biochemical activities were analyzed in lung, brain, and liver mitochondria for cytochrome oxidase, and in erythrocytes for superoxide dismutase and glutathione peroxidase. Exposure at the lowest concentration (1 ppm) did not cause any significant changes in these biochemical activities; however, rats exposed to increased concentrations of H S 2 (10 and 100 ppm) showed significantly lower activity (p < .05) of cytochrome oxidase in lung mitochondria than the control rats (0 ppm). The cytochrome oxidase activity in brain mitochondria also appeared to be lower in rats exposed to 10 ppm and 100 ppm H2S than in the control rats, but the differences were not statistically significant. In liver mitochondria, the activity of cytochrome oxidase was not affected by these exposures. A small decrease (~8% ) in superoxide dismutase activity of erythrocytes was observed in rats exposed to 100 ppm H2S. It is suggested that repeated exposures to even low concentrations of H 2S can reduce the activity of a critical mitochondrial enzyme, cytochrome oxidase, in lungs and possibly other tissues. This reduction in mitochondrial cytochrome oxidase could be an early-stage biochemical event of H2S toxicity in pulmonary tissues. [ABSTRACT FROM AUTHOR]

The Acute Toxicopathy of Intravenous Diacetoxyscirpenol (Anguidine) in Swine. COPPOCK, R. W., GELBERG, H. B., HOFFMANN, W. E., AND BUCK, W. B. (1985). 5, 1034–1049. Diacetoxyscirpenol (DAS, anguidine) was given intravenously to swine at 0.0,0.5, and 1.0 mg/kg body wt. In mitotically and metabolically active tissues such as gastrointestinal epithelium and lymphoid aggregates the effects of DAS mimicked radiation poisoning. A quadratic dose-response relationship between the cytotoxicity of DAS and damage to enterocytes was found. Enterocytes in different anatomical regions of the bowel had differing susceptibilities to the toxic effects of DAS. In lymphoid tissues, DAS was preferentially cytotoxic to B-lymphocyte-rich tissues as compared to T-lymphocyte-rich tissues. In all pigs dosed with DAS the bone marrow was void of hemopoietic elements. DAS was cytotoxic to cells with specialized ion pumps, namely, renal tubular, gastric parietal, and salivary ducts. Cell damage in the exocrine and endocrine pancreas and adrenal gland accounted for changes in blood glucose. Endothelial necrosis and hemorrhage were observed in the brain. These findings were compared with those reported for other 12,13-epoxytrichothecenes and ionizing radiation and we concluded that a similar mechanism of cytotoxicity could exist. [ABSTRACT FROM PUBLISHER]

This paper describes a large-scale investigation into the effects of licensed air emissions from sour-gas processing plants on the health and productivity of beef cow-calf herds in the province of Alberta, Canada. In conjunction with a geographical information system, two atmospheric-dispersion models were used to assess historical exposures at 5726 beef cow-calf farm-sites from 1987 to 1990. We did secondary analyses of health, productivity, and management data, from a government-extension survey previously administered to beef cow-calf producers across the province. Statistical models (adjusted for potential confounding and clustering within herd and over time) were used to determine associations with estimates of sour-gas emission exposure. All analyses were conducted at the herd-level. There were no significant (P>0.05) detrimental associations of exposure and the annual herd risk for culling, calf-crop delivered, calf-crop season profile, stillbirth and twinning, calfhood mortality, or calf-crop weaned.

The dispersion of air pollutants from all 231 licensed sour-gas processing plants in Alberta, Canada, was modeled on a monthly basis over a 10-year period (1985-1994). Exposure estimates for sulfur dioxide (SO(2)-used as a surrogate for exposure to combusted emissions) then were assigned to 1382 provincial dairy farms using a geographical-information system. Individual average and peak exposure for periods prior to each of 15 months of age and conception (four exposure-averaging periods for each of two dispersion models) were estimated for 163,988 primiparous female dairy-cattle between 1986 and 1994. Monthly or annual average farm-site exposure estimates likewise were assigned to associated herd-level data sets for the biologically relevant period of interest for each of three additional reproductive outcomes: monthly herd-average calving interval, stillbirth risk, and twinning risk. In one of the main-effects models, the maximum (i.e., peak) monthly sour-gas exposure experienced by individual-animals from birth to conception was associated with an increased time to first-calving in the very-highest exposure category (hazard ratio=0.86, 95% CI=0.80, 0.92). This equates to a decreased hazard (lambda) of calving (in each month subsequent to 22 months of age) for the highest-exposure animals (lambda=0.170) versus the zero-exposure animals (lambda=0.198) in a model with referent values for agro-ecological region and season of birth. The dose-response was not consistent across the full range of exposure categories. There was significant (P=0.003) interaction of emissions with agro-ecological region. After accounting for the interaction, a more-consistent dose-response was evident for some (but not all) agro-ecological regions. This suggests that any effect of emissions on dairy-heifer reproduction is subject to modification by features of soil type, vegetative cover, and/or climate. The increase in monthly herd-average calving interval on farms exposed to the very-highest levels of emissions appeared quite small and of limited practical importance within the range of expected exposures. There was no association between exposure and the risk for twinning. Herds exposed to higher emissions exhibited a slight decrease in risk for stillbirth.

Crude and refined petroleum contain a complex mixture of aliphatic, aromatic, polyaromatic and heterocyclic hydrocarbon compounds. The objective of our research was to investigate early-stage biochemical changes in rats exposed to low dosages of petroleum hydrocarbons. The animals were repeatedly exposed, per oral by gavage, to low dosages (0.5-2.5 ml/kg) of an Alberta crude oil (ACO) and their general health and systemic biochemical parameters were assessed. Rats exposed to these doses of ACO did not show any apparent symptoms of intoxication. Similarly, no significant changes were observed in clinical parameters of systemic impairment. Systemic biochemical assessment has shown that ACO exposure caused marked changes in the activities of several cytochrome P-450 (CYP)-linked polysubstrate monooxygenase enzymes in liver, kidney and lung tissues. Exposure to ACO caused dose-dependent increases in the hepatic activities of ethoxyresorufin-O-deethylase, a CYP 1A1/A2-linked enzyme; pentoxyresorufin-O-dealkylase, a CYP 2B-linked enzyme, and ethoxycoumarin-O-deethylase, a CYP 2B/1A-linked enzyme. Temporal assessment showed that these systemic biochemical changes were reversible in nature. Analysis of biomarker chemicals provided evidence that in exposed animals petroleum hydrocarbons were mainly distributed in the adipose tissues.

On a temporal basis, air has immense capacity for moving a large mass of pollutants. Mammals and birds are exposed to pollutants in air by the inhalation (nose and mouth), cutaneous or ocular routes. Most laboratory studies on air pollutants have been limited to single air pollutants and very little research has been done on the complex mixture of compounds that exist in ambient air. Complex mixtures are further complicated by dynamic chemical reactions that occur after the emissions leave point sources. Exposure parameters are also important in the toxicity of air pollutants. Intermittent exposure of monkeys to ozone increased the adverse pulmonary effects. Superimposing spikes of 0.8 ppm nitrogen dioxide on a baseline of 0.2 ppm, as occurs on a calm winter day, increased the susceptibility of mice to bacteria-induced pneumonia. Sulfur dioxide at concentrations of 5 ppm increased pulmonary resistance by 39%. Sulfuric acid is the predominate acid particle in the atmosphere. Exposure for 1 h to > 200 micrograms sulfuric acid/m3 depressed bronchomucociliary clearance. Concentrations of 100 micrograms/m3 of photochemical products caused headaches and 510 micrograms/m3 produced cough and chest pain. For chemical interactions in dose response, nitrogen dioxide is synergistic with ozone and ammonium sulfate. When all 3 chemicals are used in mixture, the response was 340%. Atmospheric conditions, such as fog, can alter the toxicity of air pollutants. The dose response to a single chemical can be altered by chemical mixtures and pre-existing disease conditions. Understanding these relationships is important for establishing no observable adverse effect levels. Mechanisms for multiple chemical interactions are multifaceted. One chemical may interfere with the metabolism or detoxification of another. Others may interact at cell receptors. To understand the effects of multiple chemical interactions of air pollutants, there is a need for a blend of epidemiological, laboratory and field studies. Studies are expensive. In the rural agricultural settings, the economic and environmental health risks are high. Should field observations and chemical problems be used as "red flags" for action?

In 26 hr laboratory trials a dose of 1000 micrograms/kg microcystin-LR (MC-LR) caused 100% mortality in rainbow trout, while no mortality was observed at doses of 400 micrograms/kg or less. The liver to body mass ratio increased in fish exposed to the toxin which was likely due to water retention in the liver. In contrast to mammalian studies, hemorrhage of the liver was rare in fish. Exposure to MC-LR caused widespread hepatocellular swelling and lysis of hepatocyte plasma membranes, resulting in liquifactive necrosis (organelles floating in a milieux of cellular debris). Kidney lesions in the fish consisted of coagulative tubular necrosis with a dilation of Bowman's space. Lesions observed in the liver and kidney of fish exposed to MC-LR were considerably different than those previously reported for mammals.

The toxicologic pathology of petroleum and oilfield-related chemicals is reviewed, and a field guide for toxicopathologic evaluation of cattle is given. Cattle will voluntarily ingest petroleum and chemicals used in the exploration, production and transportation of crude petroleum. Variability in chemical composition of petroleum from different fields will alter the type and severity of lesions observed. When airborne pollutants are present, cattle are continually exposed and make excellent sentinel animals. The lung, kidney, liver, gastrointestinal tract, heart and brain are target organs for petroleum hydrocarbons. Exposure to elemental sulfur can produce pulmonary pathology. Sulfur-containing gases are irritating to the mucosa of the eye and respiratory tract. Arsenic and lead cause lesions in the gastrointestinal tract, brain, liver and kidney. Glycols are hepato-, nephro- and neurotoxic, and oral exposure to diethylene glycol produces corneal lesions. Invert drilling fluids are fetotoxic. Nonpesticide organophosphate esters target the peripheral and central nervous systems. Toxicopathy is a strategic tool in the diagnosis of intoxications occurring in cattle after exposure to oilfield chemicals. Cattle are sensitive to oilfield pollutants and are a useful biomonitoring species.

Cattle are poisoned by petroleum and substances used in drilling and operating oil and gas wells. The most common reported route of exposure for non-gaseous material is oral. Exposures occur when the petroleum or chemicals used in oil and gas field activities are available to cattle and when water and feed-stuffs are contaminated. Cattle, as a leisure activity, explore and ingest crude oil. Based on morbidity patterns in cattle herds, the amount of toxic substance ingested is variable. When water and feedstuffs are contaminated, a larger number in a herd generally are affected. Cattle have been poisoned by a wide variety of chemical mixtures. For substances high in volatile hydrocarbons, the lung is a target organ. Hydrocarbons also target the kidney, liver and brain. Exposure-linked abortions have been reported in cattle. Diethylene glycol targets the brain, liver and kidney. The reported threshold dose of unweathered oil for cattle ranges from 2.5 to 5.0 ml/kg bw, and the reported threshold dose for weathered oil is 8.0 ml/kg.

Nonpesticide phosphate esters induce delayed neurotoxicity in cattle. The most common exposures are to complex mixtures of triaryl phosphate used in lubricating oils. Oral ingestion is most common, but dermal exposures have also occurred. Clinical signs of cholinesterase (ChE) inhibition may or may not be seen. Depending on the biochemical targets, the percent reduction in blood ChE is variable and can be < 30% of normal activity. Organophosphate ester-induced delayed neurotoxicity cannot be predicted by inhibition of blood ChEs. Signs of delayed neurotoxicity occur 2 to 25 d after exposure; these signs are neurologic deficiencies of the antigravity muscles and the muscles of the urinary bladder and larynx. Affected cattle may dribble urine and some may be mute. Signs of ChE inhibition generally are not observed in animals with neurological deficiencies. Pathologic findigs are axonopathy and myelin degeneration of nerves with long axons located in both the peripheral and central nervous systems. In the spinal cord, location of the affected nerve tracts is variable. Degenerative changes occur in motor neurons. Calves are less susceptible to organophosphate ester-induced delayed neurotoxicity than cows. A dose of 500 mg triaryl phosphate/kg body weight will produce complete paralysis in a mature cow in 26 d.

The death of common loons (Gavia immer) was associated with a small spill of bunker-C oil off the Chicago shoreline of Lake Michigan. Petroleum oil was not found on the feathers or in the lungs of the birds. Botulinus toxins C and E were found in heart blood. Because the carcasses were autolysed, botulism toxins could have been produced postmortem. An average of 97 micrograms PCBs (Aroclor 1254 standard) and 2.2 micrograms dieldrin/g of body fat also were found. Concentrations of heavy metals in one bird were 0.25 microgram of total mercury and 0.5 microgram of lead/g of liver, respectively. The loons had abundant body fat suggesting they were not debilitated at the time of death.

High-moisture corn was treated with a propionic acid preservative and stored in a 40,000 bushel steel bin. This corn heated and spoiled in storage and subsequently was retreated with the preservative. The out-of-condition corn was used as an ingredient in the ration for a dairy herd of cows and replacement heifers. The finished feed was cultured for fungi and assayed for mycotoxins. Results were 750,000 Fusarium spp colonies/g of feed, and 1.5 mg zearaleonone and 1.0 mg deoxynivalenol/kg of feed. Frequent episodes of behavioral estrus of 2 to 5 d duration, that were not synchronized with the ovarian cycle, were observed. Cows in the second and third trimester of pregnancy also has episodes of behavioral estrus. Idiopathic vaginitis was diagnosed. Mammary development occurred in the prepubertal heifers. Cows bred in true estrus were found in true estrus 35 to 55 d later. All of the heifers with precocious mammary development were subsequently culled from the herd because of sterility.

Fischer-344 rats were exposed for 4 hr to various concentrations of hydrogen sulfide (H2S) gas and killed either immediately or at 1, 24, or 48 hr after exposure. Mitochondrial fractions from lung tissues were assayed for the activities of respiratory chain enzymes. Exposure of rats to a low concentration (10 ppm) of H2S caused no significant changes in the activities of lung mitochondrial enzymes. However, exposure to sublethal concentrations of H2S (50-400 ppm) produced marked and highly significant depressions in the activities of cytochrome c oxidase and succinate oxidase complexes of the respiratory chain. The inhibition of cytochrome c oxidase activity in lungs was most severe (greater than 90%) in rats that died from acute exposure to greater than 500 ppm H2S. In rats exposed to 200 and 400 ppm H2S, a marked recovery in cytochrome c oxidase activity of lungs was observed at 24 and 48 hr postexposure. Studies in vitro with rat lung mitochondria showed that low concentrations of sulfide also caused a similar and selective inhibition of cytochrome c oxidase activity. This effect was reversed upon removal of sulfide either by washing or by oxidation with methemoglobin. The nature of sulfide inhibition of cytochrome c oxidase was noncompetitive with respect to ferrocytochrome c. Because the activities of NADH-cytochrome c reductase and succinate-cytochrome c reductase were not significantly altered by H2S exposure and in vitro treatments with low concentrations of sulfide, it is concluded that under physiological conditions H2S would block the respiratory chain primarily by inhibiting cytochrome c oxidase. Such a biochemical impairment would lead to functional (histotoxic) hypoxia in the lung tissues.

Diacetoxyscirpenol (DAS) was given IV to pigs (0, 0.5, and 1.0 mg/kg of body weight), cattle (0 and 0.5 mg/kg), and dogs (0 and 0.5 mg/kg). Blood was collected and hemograms were done at 0.5-hour intervals for 8 hours. The animals were euthanatized at 8 hours after treatment, and bone marrow samples were taken and examined by light microscopy. Moderate to severe necrosis of bone marrow hematopoietic elements was found in animals given DAS. The sequential increase in the type and number of abnormal cells in the blood suggested a successive destruction of the hematopoietic elements. A marked left shift in the neutrophil population was found in animals given DAS. Metarubricytes and large platelets were found in the blood of animals given DAS. Lymphocytes were replaced with immature cells. Pathologic changes were most severe in the pigs given a dosage of 1.0 mg of DAS/kg. The order of species sensitivity to DAS was pigs greater than dogs much greater than cattle.

During 1977, 4,976 oil and gas wells were drilled in Oklahoma to an average depth of 4,892 feet. There were 2,253 successful oil wells and 1092 successful gas wells (26). The Oklahoma Animal Disease Diagnostic Laboratory investigated several cases where livestock in close proximity to drilling sites became ill or die. The case histories emphasize the need for a careful and complete diagnostic work-up. The identification and quantification of petroleum hydrocarbons, toxic chemicals and heavy metals in intestinal contents and tissues are diagnostically significant. The most difficult cases involve chronically ill and poor-doing animals following exposure to oil field wastes. The potential for litigation exists whenever cattle in close proximity to drilling and production sites become ill or die. Many of these cases could be prevented if livestock were prevented access to such sites by fencing or other means. The circumstantial evidence in many cases suggests the need for additional research on the toxicity of petroleum hydrocarbons, drilling muds and other oil dield wastes. Improves diagnostic methods should benefit both the livestock and oil industries.

In swine and cattle given 0, 0.1, or 0.5 and 0, 0.5 mg of diacetoxyscirpenol (DAS)/kg of body weight, IV, respectively; DAS had a large volume of distribution and total body clearance. The shortness of the interval between halothane and DAS exposures significantly (P greater than 0.05) decreased DAS biotransformation. Urinary excretion of DAS as a parent compound was not an important route of elimination. In swine and cattle, DAS was transformed by sequential deacetylation to monoacetoxyscirpenol and scirpentriol.

Studies were conducted to ascertain in vitro effects and effects of percutaneous application (in vivo) of dichlorvos (2,2-dichlorovinyl dimethyl phosphate; DDVP) on cholinesterase activities in bovine erythrocytes and plasma. Treatment in vitro of erythrocytes and plasma with DDVP resulted in concentration- and time-dependent inhibition of erythrocyte acetylcholinesterase (AChE) and plasma cholinesterase (ChE) activities. Mean (+/- SD) DDVP concentrations required to cause 50% enzyme inhibition were 15.7 +/- 3.3 microM and 43.1 +/- 5.7 microM for AChE and ChE, respectively; however, these values required to achieve this inhibition were markedly decreased with increasing incubation time. The inhibited AChE activity failed to be reactivated after incubation of erythrocytes with 2-pyridine aldoxime methiodide (2-PAM); however, limited reactivation of inhibited AChE and ChE activities was observed with excess concentration of 2-PAM. Percutaneous application of a DDVP-containing livestock spray on cattle also caused a marked decrease in the in vivo activities of AChE and ChE; however, the inhibited enzyme activities were reactivated rapidly after incubation with 2-PAM.

Pigs (n = 19) were given 0, 0.1, 0.5, or 1 mg of diacetoxyscirpenol (DAS)/kg of body weight, and heifers (n = 7) were given 0 or 0.5 mg of DAS/kg. Animals were anesthetized and exsanguinated 8 hours after administration of DAS, and liver, kidney, skeletal muscle, mesenteric lymph node, and spleen were analyzed for DAS. Diacetoxyscirpenol was not detected in tissues from animals not given DAS. All tissues from pigs and calves given DAS contained at least traces (less than or equal to 10 ng/g of tissue) of DAS.

Aflatoxicosis was diagnosed in 600 feeder pigs, of which 400 died, 150 were destroyed, and 50 were marketed. The pigs were exposed to 2,500 to 3,500 micrograms of aflatoxins/kg of feed. Drought-stressed damaged corn infected with Aspergillus flavus was stored under ambient conditions in a glass-lined silo, and this storage environment provided conditions that favored rapid fungal growth and mycotoxin production.

Alfalfa, estimated to contain 25.89 mg lead (Pb)/kg of air dried sample, was ensiled in a glass-lined bottom-unloading silo. Three weeks later air dried haylage from the bottom of the silo contained 118.6 mg of Pb/kg. The concentration of Pb in the haylage was sufficient to induce saturnism in a dairy herd. During the disposal process, the concentration of Pb was determined in each 11.3 m3 load of silage. These data provide evidence that Pb migrated and concentrated in the bottom of the silo.

Study was made of the pharmacokinetics and toxicopathy of deoxynivalenol (DON, vomitoxin) given IV to swine. In the 24 hours after swine were given DON, clinical signs of vomiting, diarrhea, muscular weakness, tremors, and twilight coma were similar to those observed with other 12,13-epoxytrichothecenes. Hypoglycemia and pancreatic islet cell lesions were observed which indicated that DON-induced changes in intermediary metabolism may be an insidious aspect of DON intoxication. Histopathologic examination of all organ systems revealed pancreatic acinar and islet cell necrosis and mild lympholysis of the mesenteric lymph nodes. The renal excretion of DON was altered by IV infusion of saline solution. Pharmacokinetic findings may indicate that DON was both secreted and reabsorbed by the renal tubules. The half-life of DON ranged from 2.08 to 3.65 hours. Residues of DON were not found in skeletal muscle of swine at 24 hours after dosing.

Small animals are exposed to a variety of household products. The most common route of exposure is oral by direct ingestion or from grooming soiled fur and feet. The majority of household products are complex chemical mixtures. The clinician must determine the body burden of toxic or potentially toxic substances and the potential for a combination of chemicals to produce intoxication in a particular species and then plan a course of action. Toxicoses of selected household and commercial products are discussed in detail. Animals are exposed to a variety of antiseptics by numerous routes. Potential for iatrogenic intoxication from antiseptics is also discussed. An abridged version of this article will be published in the 10th edition of CURRENT VETERINARY THERAPY: SMALL ANIMAL PRACTICE, RW Kirk, editor, WB Saunders Co, Philadelphia, PA.

Weather conditions in northern Illinois favored infection of pasture grasses with Claviceps purpurea. A herd of 52 Holstein heifers selectively grazed the seedheads of an orchard grassbromegrass pasture infected with C purpurea and were poisoned. Peptide alkaloids were found in the sclerotia. Clinical signs of intoxication included lameness, edema of the hind limbs, epilation, areas of skin necrosis, and diarrhea. Pathologic findings included myopachynsis of arterioles in the deep dermal areas, lungs, kidney, spleen, submucosa of small intestines and cerebral cortex, focal cracks on the hoofs, and multifocal areas of detachment of the hoof wall. Of the 52 heifers, 3 died on the farm, 1 was euthanatized, and 3 were sold. The remaining heifers conceived without difficulty, and subsequent calvings were uncomplicated.