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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?

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.

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.

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.

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.