Page 701 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

666 SECTION | IX Gases, Solvents and Other Industrial Toxicants

VetBooks.ir mucosal congestion, and mucosal and serosal hemorrhage (1989, 1990a,b) showed that PBCO was embryotoxic and
that the toxicity was different from hypoxia induced by
and inflammation in all areas of the gastrointestinal tract.
sealing the eggs with wax. Mineral oil (USP) was not
Isolated necrosis of enterocytes, superficial erosions, mild
acute cryptitis and neutrophilic and lymphocytic exudates toxic to chicken embryos. On day 9 of incubation, PBCO
were also observed. was applied below the airspace to the surface of the egg
shell. Dosages ranged from 2 to 30 μL PBCO/egg.
Renal Pathology of Petroleum Hepatic lesions were observed 2 days after treatment, and
renal and splenic lesions observed on the third day. The
Renal lesions have been observed in cattle dosed with a livers were observed to have superficial yellowish zones
light crude oil (Bystrom, 1989). These lesions were that were multifocal to diffuse. These yellowish zones
shrunken or collapsed glomeruli (2 5ina4 3 field), and mineralization corresponded to areas of hepatocellular
mild focal necrosis of epithelial cells in the collecting necrosis. Hepatic histopathology was hepatocellular
ducts, and inflammatory cells that were observed in the vacuolization, hepatocellular necrosis with mineralization,
renal cortex. Parker and Williamson (1951) reported and perivascular and multifocal accumulations of hetero-
degeneration of the kidney in cattle after they consumed phils. Hepatocellular necrosis was dose-dependent. The
tractor vaporizing oil. Tubulointerstitial nephrosis with number of mitotic figures in the liver increased with the
renal vascular thrombi observed in 1 out of 51 cattle fol- dose of PBCO.
lowing environmental exposure to aviation turbine engine Renal lesions were primarily limited to the mesoneph-
fuel (Barber et al., 1987). Renal lesions were not observed ros. The capillaries of the glomeruli were distended and
in surviving animals slaughtered 124 days later. Renal cellular casts and mineralization were observed in the
histopathology was observed in sheep poisoned by inges- renal tubules. Splenic lesions were limited to increased
tion of natural gas condensate (Adler et al., 1992). The granulopoietic cells arranged in distinct cords. Other path-
lesions were tubular epithelial necrosis, granular eosino- ological findings were ascites and subcutaneous edema.
philic casts (negative for hemoglobin), protein droplet Edema fluid was more pronounced after the third day of
filled Bowman’s space, and in many renal tubules, incubation. In another study, the toxicity of PBCO was
inflammatory cells were observed around tubular casts. evaluated in chicken embryos (Lusimbo and Leighton,
1996). The chicken embryos were exposed to oil on day 9
of incubation. The oil was placed on the eggshell over a
Nervous System Pathology of Petroleum
prominent blood vessel of the chorioallantoic membrane.
Histopathology of the CNS was observed in sheep poi- Dosages ranged from 0 to 16 μL PBCO/egg, and embryo-
soned by ingestion of natural gas condensate (Adler et al., nal mortality was dose-dependent. Lesions were observed
1992). Mild perivascular hemorrhage was seen in the pia in the liver, subcutaneous tissues, bursa of Fabricius and
matter and white matter of the cerebellum and cerebrum. pipping muscle (musculus complexus). Hepatic lesions
Increased separation between the pia and arachnoid mem- were multifocal to locally extensive areas of hepatic
branes was prominent, and edema was observed in the necrosis and mineralization. Large fluid-filled vesicles
stroma of the choroid plexus. were observed on the dorsocaudal aspect of 5% and 16%
of embryos dosed with 1 and 2 μL of PBCO, respectively.
The bursa of Fabricius had depleted lymphoid tissue and
Cardiac Pathology of Petroleum
the interstitium was infiltrated with heterophils. Lesions
Adler et al. (1992). observed cardiac pathology in sheep in the pipping muscle were edema and hemorrhage,
that ingested natural gas condensate. Gross pathological sparse multifocal fragmentation, and occasional vacuola-
changes included epicardial hemorrhages, serosangui- tion of the myofibers. Exposure to PBCO at 4 μL
neous pericardial fluid, pale-appearing myocardium, and decreased weight gains during a 3-week posthatching
reddened endocardium. Histopathology was segmental observation period.
myocardial necrosis and calcification. The myofibrils had
loss of cross striations and a beaded appearance. There TOXICOLOGY OF SOUR PETROLEUM
were multifocal areas infiltrated with lymphocytes,
macrophages, and occasional neutrophils. The cardiac Sour petroleum can be defined as petroleum that contains
blood vessels were congested. more than 0.5% sulfur (mass/mass). Sweet crude oil gener-
ally has a sulfur content of ,0.5%. A common constituent
in sour petroleum is H 2 S, which has the odor of rotten
Pathological Effects of Petroleum in Embryos
eggs. Sour gas at the wellhead can have greater than 20%
Studies on the embryotoxicity of Prudhoe Bay Crude Oil hydrogen sulfide. Sour petroleum can be burned for a vari-
(PBCO) have been reported. Couillard and Leighton ety of reasons including production testing of wells,