Page 699 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

664 SECTION | IX Gases, Solvents and Other Industrial Toxicants

VetBooks.ir or emulsifiers, and additives in refined petroleum. can occur after petroleum is inhaled. Aspiration of oil
during emesis is the most common mechanism of inhala-
A 200 mL single oral dose of odorless kerosene adminis-
tion exposure to liquid petroleum (Coppock et al., 1996;
tered to a mature dairy cow caused a 90.3% reduction in
dry matter intake, and the same dose of Stanvac odorless Coppock and Christian, 2012). Necropsy findings of oil-
solvent caused a 42.5% reduction in dry matter intake for induced chemical pneumonia have been described
a 3-day period (Reid, 1957). Emulsification of kerosene (Dungworth, 1993). Generally, the cranioventral lobes of
with a nonionic surfactant decreased the interval between the lungs are affected first. During necropsy, oil may be
exposure and the onset of effects. Similar findings were identified in the lungs by oil discoloration and a petro-
observed when kerosene was placed directly into the oma- leum odor, visible oil in the lung, oil floating to the sur-
sum. Fistulation of the rumen did not alter the response to face when a piece of lung is immersed in water or
kerosene or solvent. Studies in cattle on a heavy liquid formalin, or oil layering on the surface of the supernatant
paraffin (mineral oil) to control bloat showed that the oil when a piece of lung is homogenized. The pulmonary his-
can reduce blood and milk butter fat levels of fat soluble topathology for unweathered petroleum is similar for the
vitamins (McGillivray et al., 1959). various forms of petroleum. Histopathological changes
are proliferative, and macrophages, with a foamy-
appearing cytoplasm, are found in and tend to fill the
TOXICOPATHOLOGY OF PETROLEUM
alveoli (Dungworth, 1993). In the pathogenesis, oil-
AND OILFIELD CHEMICALS containing macrophages are found in the lymphatics,
Clinical Pathology especially those adjacent to blood vessels around bronchi.
Fibrosis and proliferation of type II macrophages are
Barber (1987) reported on the toxicology of aviation tur- prominent features. Foamy macrophages may be incorpo-
bine fuel in heifers. Ten animals were considered to have rated into the alveolar septa by fibroblastic proliferation.
elevated serum activity of aspartate aminotransferase, As determined by histochemistry and special stains, lipids
interpreted as a reflection of acute hepatic dysfunction, are found in both intracellular and extracellular sites, and
activates of γ-glutamyl transpeptidase (GGT) were within oil can be identified in the alveolar spaces. In the early
the normal range. Elevated concentrations of nonesterified stages, the lesion may be an acute necrotizing fibrinous
fatty acids were observed in 11 of the animals, two had bronchopneumonia. Generally, neutrophils, lymphocytes,
elevated concentrations of blood urea nitrogen and five and plasma cells surround the necrotic areas. Fibrinous
had a leukocytosis. Six weeks after the initial farm visit, exudate, inflammatory cells, and amorphous eosinophilic
41 of 41 animals had elevated serum activity of GGT. and oily material can fill the alveolar spaces. Empty
Bystrom (1989) found that acute sweet crude oil intoxica- spaces in the tissues suggest that liquid foreign material
tion did not alter hematological parameters. There was a may have been absorbed and subsequently washed out by
correlation between the severity of clinical signs and tissue processing. Plant material from aspirated ingesta
increased concentrations of plasma fibrinogen. The activ- may also be seen in alveoli. Fibrin hemorrhages and a
ity of hepatocellular enzymes in serum and serum glucose mixed population of mononuclear cells may be observed
were not consistently increased after acute exposure to on the pleural surface. Extensive coagulative necrosis and
sweet crude oil, but serum calcium and potassium values suppuration may be observed in the consolidated areas.
consistently decreased and bilirubin values consistently Bacteria may be present in the necrotic areas and alveoli.
increased. Rowe et al. (1973) found that hematological Hematogenous exposure of the lungs to petroleum hydro-
parameters, especially leukocyte numbers, were increased carbons also occurs. Volatile components of petroleum
as clinical signs of chemical pneumonia increased. A sin- are absorbed by the gastrointestinal tract and are volatil-
gle dose of sour crude oil caused a constant decline in ized from the blood in the lungs. An oil embolism can
plasma glucose. A transient decline in plasma glucose occur in the lungs through absorption of oil from the gas-
was also observed in calves given sweet crude oil or kero- trointestinal tract. These oil embolisms can block the
sene. Exposure to nitrates from drilling fluids can cause small blood vessels in the lungs and brain. Oil embolisms
methemoglobinemia. The concentration of nitrates can be in blood vessels of the lungs and brain have not been
determined in rumen fluid, aqueous humor (anterior reported in cattle intoxicated with crude petroleum. The
chamber of the eye), urine, and plasma. Uterine and fetal pathogenesis and observed lesions may be altered by con-
fluids can also be used. current bacterial infection and cytotoxicity of the oil.
There are reports of field and experimental-induced
petroleum intoxication. Ulceration of the ventral aspect of
Pulmonary Pathology of Petroleum
the trachea can occur in kerosene poisoning and the ulcers
The lung is a target especially for unweathered petroleum. may be covered with a pseudomembrane (Rowe et al.,
Hydrocarbon-induced chemical (inhalation) pneumonia 1973). Areas of the lung can be consolidated and have a