Page 704 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Petroleum Chapter | 50 669

VetBooks.ir SO 2 toxicity (Komarnisky, 2003). A summary of this soiled hair or feathers. Environmental samples include sus-
pect liquid petroleum, contaminated soil, and water.
study is given. Eight steers were progressively exposed to
room air containing 1 ppm SO 2 for 10 days, 5 ppm SO 2
for 7 days, and 20 ppm for 7 days. Four steers were
DIFFERENTIAL DIAGNOSIS
exposed to SO 2 at room temperature

(approximently18 C), and four steers were exposed to The diagnosis of petroleum toxicity can be straight
SO 2 at 216 C. In the cold environment, the metabolic forward or very difficult depending on the circumstances.

rate was increased by 33%, 39%, and 44% at 1, 5, and If the exposure is current or recent and there is direct evi-
20 ppm of SO 2 , respectively. Exposure to SO 2 in the dence of toxic substances in or on the animals and obvi-
warm environment did not significantly alter metabolic ous detrimental effects, the diagnosis may still require
rate. For a 500-kg steer intermittently exposed to 1 ppm careful assessment and testing, but should be accom-
of SO 2 , the extra feed required for maintenance and plished relatively easily. However, if the exposure has not
growth would be equivalent to 1.5 kg/day of additional been recent and clinical signs are not specific or are ones
grain or 2.1 kg/day of additional hay. Sulfur dioxide was that may have several possible causes, the diagnosis can
shown to have adverse immunotoxic effects in cattle. be very difficult. Pneumonic lesions associated with crude
Exposure of steers to 5 and 20 ppm in the cold environ- oil toxicity are easier to interpret if oil is still present in
ment decreased the respiratory bursts in neutrophils. the gastrointestinal tract or identified in the lungs. The
Exposure to SO 2 in the cold environment decreased the presence of vacuolated macrophages is helpful in differ-
threshold dose for shedding of respiratory epithelial cells entiation from infectious causes of pneumonia.
into bronchoalveolar lavage (BAL) fluid. Neutrophil num- Pneumonia initiated by toxic gases is difficult to diagnose
bers in BAL were increased by exposure to SO 2 , and because the initial site of injury is at the broncho-alveolar
exposure to cold temperature further increased neutrophil junction, the same location as the initial site of infection
numbers. Exposure to SO 2 decreased the number of pul- for several viral and bacterial pathogens. The bronchial
monary macrophages in BAL fluid. At the 20-ppm level, and alveolar reactions of necrosis, edema and cellular
lactate dehydrogenase was increased in the BAL fluid. infiltration can be indistinguishable between toxic gas
responses and infectious agent responses. In addition,
toxic gases can interfere with the normal functions of
ANALYTICAL TOXICOLOGY
cells lining the trachea and bronchi leading to reduced
The matrix containing petroleum and the chemicals associ- resistance to infection (Dungworth, 1993). Multiple toxic
ated with petroleum and oil—gas field operations can be agents may also be present at the same time, making the
assayed. The most common approach used is to match determination of the initial cause impossible. Acute neu-
chromatographic finger prints. The organic substances rological signs may result from sodium ion toxicity or the
assayed generally are extracts from specimens and samples acute effects of volatile hydrocarbons. The differential
submitted to the laboratory. Chemicals in petroleum that includes thiamine responsive polioencephalomalacia,
are resistant to biodegradation can be used as biomarkers which results in brain lesions that are indistinguishable,
(e.g., phytane and pristine). Many of the biomarkers in and lead poisoning. The analysis for sodium levels in
crude petroleum are sensitive to petroleum refining and rumen content is essential and serum osmolarity may be
up-grading processes and may not be found in refined pro- helpful. Exposure to high sulfates in water is linked to thi-
ducts. Gas found in ground water contaminated by petro- amine responsive polioencephalomalacia. The occurrence
leum wells may be different from the endogenous gas or of delayed neurotoxicity signs requires an in-depth inves-
the ratio of gases found in ground water. Ions and heavy tigation of potential causes, including the tri-alkyl/aryl
metal pollutants can be assayed in produced water and phosphate esters and pesticides, to determine possible
ground and surface water suspected of being contaminated exposure. The occurrence of ocular and respiratory irrita-
with water chemicals from oilfield operations. The ratio of tion in the presence of toxic gases is a typical sign.
substances in ground water can be compared to the ratio However, similar irritation may result from dry, dusty and
found in produced water or other contaminating sub- windy conditions and from irritating particles in feed. The
stances. During necropsy, samples and specimens need to measurement of toxic gas levels near the livestock is sel-
be taken for analytical toxicology. The best procedure is to dom possible and assumptions of exposure based on data
phone the laboratory in advance and request instructions from the emission source and nearby monitoring sites
for sampling containers and methods of preservation. The may be the only data available. Differentiation from
specimens that should be collected at necropsy are rumen infectious pinkeye may be made by isolating the infec-
and stomach contents, contents from various areas of the tious agent and ruling out toxic gas exposure.
gastrointestinal tract, liver, kidney, lung (including descrip- Poor growth and weight loss may have many possible
tion of the lobe), perirenal or bone marrow fat, brain, causes including nutritional deficiency, parasitism,