Petroleum Product Poisoning in Animals

Petroleum product toxicosis may involve the respiratory, GI, or integumentary systems or the CNS. In some cases of ingestion, no clinical signs are evident; however, small animals are reported to show oral irritation, salivation, and champing of jaws, followed by coughing, choking, and vomiting. Pneumonia due to aspiration of hydrocarbons into the lungs is usually the most serious consequence of ingestion of these materials. Aspiration can occur during vomiting by monogastrics or eructation of rumen contents. Pulmonary damage can occur from a combination of volatility, viscosity, and surface tension. Higher volatility promotes access of vapors to the lung and airways and displaces alveolar oxygen. Risk of pulmonary toxicosis is increased by products of lower viscosity and surface tension, with increased penetration into smaller airways and spread of the product to a larger lung surface area.

Acute bloat from petroleum products in ruminants has been reported after consumption of highly volatile hydrocarbons such as gasoline or naphtha. CNS signs may be a result of the anesthetic-like action of low-molecular-weight aliphatic hydrocarbons and/or cerebral anoxia that can result from lung damage or displacement of oxygen by the more volatile hydrocarbons. Some compounds, when absorbed in high doses, may sensitize the myocardium to endogenous catecholamines. Anorexia, decreased rumen motility, and mild depression may begin in ~24 hours and last 3–14 days, depending on dose and content. Hypoglycemia may occur several days after ingestion. These clinical signs and weight loss may be the only responses observed in animals that do not bloat or aspirate oil. Some animals do not reestablish normal rumen function after ingestion and can develop a chronic wasting condition.

After ingestion of oil, the feces may not be affected until several days later, when they become dry and formed, in the case of kerosene or lighter hydrocarbon fractions; in contrast, heavier hydrocarbon mixtures (eg, motor oil) tend to be cathartic. Oil may be found in feces and rumen contents up to 2 weeks after ingestion. Regurgitated or vomited oil may be evident as residue on the muzzle and lips.

CNS signs attributable to pulmonary, dermal, or GI absorption of hydrocarbons or cerebral anoxia include excitability (associated with aromatic fractions, such as benzene, toluene, etc), depression (aliphatic or saturated low-molecular-weight hydrocarbons), shivering, head tremors, visual dysfunction (sometimes associated with lead contamination), and incoordination. Acute pneumonia and possibly pleuritis (coughing, tachypnea, shallow respiration, reluctance to move, head held low, weakness, oily nasal discharge, and dehydrated appearance) occur in some animals that aspirate highly volatile mixtures; deaths usually occur within days. Respiratory signs may be limited to dyspnea shortly before death in animals that aspirate heavier hydrocarbons. Increased PCV, Hgb, and BUN, indicating mild to moderate hemoconcentration, are associated with development of pneumonia. Neutropenia, lymphopenia, and eosinopenia occur initially and are followed by a relative increase in neutrophils.

There are a few anecdotal reports of abortion after exposure. Laboratory data in rodents support the occurrence of increased fetal loss and decreased fetal growth. However, the doses necessary to affect the fetus were also sufficient to profoundly affect maternal health and weight. Anecdotal cases of near-term pregnant cows exposed to petroleum hydrocarbons resulted in relaxation of pelvic ligaments and lack of udder development before calving, poor mothering of calves, and marked immunosuppression in newborn calves. The associated table summarizes some of the clinical signs of petroleum hydrocarbon toxicosis in ruminants.

• Presence of petroleum hydrocarbons and matching of the hydrocarbon fingerprint of the hydrocarbon fingerprint of the toxic source with biological samples

• Necropsy and histopathologic examination to rule out alternative causes of death, particularly in chronic cases

A hydrocarbon odor may be detected in the lungs, ruminal contents, and feces of animals suffering from petroleum product toxicosis. Even if ingested in large doses, hydrocarbons may not be detected in ruminal contents after ~4 days. Adding warm water to a sample of GI contents may cause any oily contents to collect at the surface; however, finding oil in the GI tract does not in itself indicate a diagnosis of poisoning; most oils have low toxicity if not aspirated. Samples of GI contents, lung, liver, kidney, fat (especially perirenal), and the suspected source hydrocarbon material should be collected for chemical analysis to demonstrate presence of hydrocarbons in tissue (particularly lung) and GI contents and to match those found in tissues and ingesta with the suspected source, or to match the hydrocarbon "fingerprint." Limited anecdotal data in cattle suggest that hydrocarbons, particularly the alkylated naphthalenes, can be detected in perirenal fat for almost 45 days after exposure.

Samples must be carefully protected from cross-contamination during necropsy and transportation to the laboratory. Instructions from the receiving diagnostic laboratory should be checked to ensure collection equipment and transport containers (certified trace clean containers) are appropriate to prevent contamination and evaporative loss of important components. If a legal issue is involved, all sampling must be well documented and photos taken, if appropriate. Positive chemical findings together with appropriate clinical and histopathologic findings are confirmatory. Diagnosis in oil-field situations has historically been complicated by involvement of other toxicants, eg, explosives, lead from grease and “pipe dope,” arsenicals, organophosphate esters, caustics (acids or alkalis), and saltwater or brine water.

• Supportive therapy for to assist breathing

• Removal of hydrocarbons from skin with mild soap or detergents and cool water

Treatment for petroleum product toxicosis that can cause aspiration pneumonia or hydrocarbon contamination of tissues (lung or peritoneal) must be avoided. Bloat pressure should be released by passing a stomach tube if absolutely necessary to save the life of the animal; using a trocar risks forcing oil into the peritoneal cavity, which results in peritonitis. Passing a stomach tube dramatically increases the risk of aspiration, and extreme caution is necessary. In the absence of bloat, the main objectives are to prevent aspiration and to mitigate GI dysfunction. Rumenotomy to remove ruminal contents and replace them with healthy ruminal material is safer. More chronic cases involving primarily hypofunction of the rumen may also respond to this procedure. Cathartics, if used, should be of the saline or sorbitol type; however, there is no evidence that they improve prognosis. Use of oil-based cathartics for petroleum ingestion is no longer supported.

Activated charcoal has occasionally been suggested for use in small animals. Although it does not effectively adsorb petroleum distillates, it may be given if necessary to adsorb additives and other contaminants. Gastric lavage is generally contraindicated for petroleum and volatile hydrocarbon ingestions. Care should be taken to avoid inducing vomiting and aspiration. Small animals with acute respiratory distress may require supplemental oxygen and positive-pressure ventilation, used cautiously because of existing physical pulmonary damage. Frequent purging of ventilators is necessary to eliminate volatile hydrocarbons.

Animals with evidence of bacterial respiratory infection may require broad-spectrum antimicrobial treatment. Pathogens can be introduced into the lungs from aspirated rumen or stomach contents mixed with the hydrocarbons. However, the use of steroids in hydrocarbon aspiration may further reduce the chance of recovery and is generally contraindicated. Treatment of aspiration pneumonia is rarely effective, and the prognosis is poor. Because clinical signs of aspiration may not appear for several days, however, prognosis based on initial clinical findings may be misleading.

Most high-molecular-weight compounds pass through the GI tract unchanged. Most of the petroleum hydrocarbons are highly lipophilic and will be stored for varying times in tissues with high lipid content, including fat, nervous tissue, and the liver. Some of the absorbed compounds are metabolized into more toxic by-products (eg, benzene, toluene, and n-hexane). Although most of these compounds do not remain in the body for prolonged periods, little is known about exactly how long tissue levels persist in highly exposed animals or the effects on fetuses. The potential for tissue residues must be considered before the slaughter of animals intended for human consumption. FARAD should be contacted for an estimate of a withdrawal time, if available, with consultation with the state veterinarian and FDA regional office for petroleum hydrocarbon exposures in food animals.

In poisoning including that involving cutaneous exposure, the offending material should be removed from the skin with the aid of soap or mild detergents and copious amounts of cool water. The skin should not be brushed or abraded. Further treatment depends on the clinical signs and is largely restricted to supportive therapy.

Petroleum product poisoning can be avoided only by preventing access to these materials via proper storage of home and farm chemicals and well-maintained fencing around high-risk petroleum facilities. In very active petroleum fields, production animal owners must be vigilant to protect water and pasture/feed sources and watch for accidental releases at work sites and along pipelines.

Anecdotal reports of petroleum product toxicosis in the literature have documented producer concerns about the effect of oil fields on cattle health and production. Some observational studies have suggested that exposure to emissions from sour gas processing plants and sour gas flares (natural gas containing hydrogen sulfide) may be associated with an increased risk of certain reproductive losses in cattle. Researchers are examining these findings and exploring the impact of oil and gas field emissions on the immune system.

• FARAD web site: DeDonder KD, Gehring R, Baynes RE, Tell LA, Vickroy TW, Riviere JE. FARAD Perspective. Oil and petroleum product exposure to livestock.

• Coppock RW, Christian RG. Petroleum. In: RC Gupta, ed. Veterinary Toxicology Basic and Clinical Principals. Elsevier: New York. 2012: 745-778.

• Also see pet health content regarding petroleum product poisoning.