Page 703 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

668 SECTION | IX Gases, Solvents and Other Industrial Toxicants

VetBooks.ir Experimental Studies on Hydrogen Sulfide 439 ppm H 2 S for 4 h. Rats exposed to 439 ppm H 2 S
showed perivascular and pulmonary edema 1 h postexpo-
Hydrogen sulfide is a toxic gas. It also has been shown to
sure. The edema cleared postexposure at hour 18. The
be produced endogenously at micromolar levels in all
olfactory epithelium is considered a sensitive target for
organ systems and performs regulatory functions in cell
H 2 S(Lopez et al., 1988b; Dorman et al., 2004). Ciliated
cycles, apoptosis, is important in reducing oxidative stress
cells in the nasal passages, trachea, and bronchi are also
and functions as a gasotransmitter (Olas, 2015). Toxicity
sensitive targets for airborne irritants including H 2 S and
studies on H 2 S have shown that it has a steep dose
SO 2 . Ciliated cells transport mucus or foreign particulate
response curve, is an irritating gas and uncouples mito-
matter from the lower respiratory tract toward the pharynx
chondrial electron transport at the cytochrome c oxidase
where it is swallowed, and from the nasal passages to exit
target (Khan et al., 1990; Haouzi et al., 2016). There is evi-
at the nares.
dence to suggest that H 2 S interactions with cysteine can be
an important factor in acute H 2 S poisoning. Exposure to
high level of H 2 S causes abolishment of cardiac contrac- Exposure to Environmental Sulfur
tions while rhythmic contractions persist. Hydrogen sulfide
Sulfur removed from sour petroleum can be stored in
poisoning inhibits L-type calcium channels and the effects
large stockpiles. The impact of elemental sulfur on cattle,
on the heart mimic poisoning by calcium channel blockers.
especially to producers near sulfur stockpiles, is a concern
Goats were essentially continuously exposed to H 2 S
to cattle producers. A study was done on the impact in
during a 96-h interval in an exposure-hood delivery system
cattle of fugitive sulfur and other pollution from sulfur
(Hayes, 1972). The exposure hood sealed around the head
mines in Poland (Janowski and Chmielowiec, 1981). The
and neck and the animals could eat and drink. Exposure
principal pollutants were sulfur dust, sulfur gases, SO 2 ,
concentrations of H 2 S were 0.0 ppm, four goats; 10 ppm,
and sulfur hydride. Fifty-five cattle within 1 km of the
four goats; 50 ppm, four goats; and 100 ppm, five goats.
mine were evaluated during the summer months on pas-
Goats exposed to 50 or 100 ppm H 2 S trembled during
ture, and during the winter months when the cattle were
physical activity. At 50 ppm of exposure, epiphora
predominantly stabled. The control group of 27 cattle was
occurred 24 h after exposure, and persisted for the remain-
kept in an area that was free of sulfur pollution, 20 km
der of the exposure interval. Epiphora also occurred with
from the mine. Clinical findings in the polluted area
exposure to 100 ppm H 2 S, and ocular injury was visible
were: decreased occurrences of infestation with external
following 24 48 h of exposure. Corneal opacities, consid-
parasites and mycotic skin infections (ringworm),
ered to be reversible, caused partial loss of vision. There
increased body temperature, heart and respiratory rates,
was an inverse relationship between exposure levels and
and decreased excitement response to pain. Other findings
the decrease intake of feed and water. Plasma concentra-
were abnormal eyes (90.4%), respiratory disease (94.2%),
tions of cortisol were increased 48% and 55% in the 50
and digestive disorders (21.1%). Clinical findings in the
and 100 ppm groups, respectively. Respiratory and heart
eye were epiphora, erythema of the conjunctiva, and
rates, and blood pressure were recorded each day at 08:00,
edema of the eyelids. Abnormal findings of the respira-
10:00, 13:00 and 16:00 h. These data suggest that initial
tory system included dyspnea, coughing, mucopurulent
exposure to H 2 S at the 10 and 20 ppm levels caused a
nasal discharge, and abnormal pulmonary sounds.
decrease in respiratory rate on day 1 of exposure. The 0.0
Digestive disorders included abnormal ruminal motility
and 10 ppm treatment groups were not different for respi-
and diarrhea. Cattle were healthier when kept indoors.
ratory rate; exposure to 50 ppm significantly decreased
Cattle in areas polluted with sulfur, as compared to con-
respiration from 19.8 respirations/min on exposure day
trols, had a decreased burden of parasites in the digestive
2 16.5 respirations/min on day 3; goats exposed to
tract. Pathological findings in the sulfur-exposed cattle
100 ppm had a significant decrease in respiratory rate on
were: the respiratory tract contained gray-yellow tinged
the last 2 days of exposure. Exposure to H 2 S did not sig-
mucus, inflammation of the trachea, thinning of cellular
nificantly alter heart rate, blood pressure, or rectal temper-
layers in the bronchi, almost to the point of squamous
ature; however, there was a trend for rectal temperature to
metaplasia, and interstitial inflammation. The authors
increase during the exposure period.
concluded that sulfur pollution produces intoxication in
the form of a chronic disease.
Pathology of Hydrogen Sulfide
Toxicology of Sulfur Dioxide in Cattle
Detailed reports on the pathology of H 2 S and sour gas in
livestock do not appear to exist in the scientific literature. Inhalation studies (head-only exposure) on SO 2 in cattle
There are reports on the toxicopathology of H 2 S in other showed that SO 2 adversely affects the immune system
species. Lopez et al. (1988a) exposed rats to 0, 83, and and metabolism, and cold ambient temperature modulates