Page 252 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Respiratory Toxicity Chapter | 13 219

VetBooks.ir Carbon Monoxide damage. Data from rats trained to run a reversed contin-
gency maze suggested that H 2 S may impair learning by
CO is a product of incomplete combustion of hydrocarbon
increasing the animals’ susceptibility to interference from
fuels. It has background levels of about 0.02 ppm in rural
areas, 13 ppm in urban areas and 40 ppm in areas of high irrelevant stimuli (Partlo et al., 2001).
urban traffic. Improperly vented or adjusted heaters, and Hydrogen sulfide is readily detectable as a rotten egg
fires, especially those burning more coolly, are frequent smell. Humans and presumably animals can detect hydro-
sources of increased CO. gen sulfide at 0.025 ppm (Carson, 2004). Above 200 ppm,
however, hydrogen sulfide paralyzes the olfactory appara-
CO binds about 250 times as tightly to hemoglobin
tus so it may not be detectable by smell. Higher concen-
as oxygen, forming carboxyhemoglobin (COHb).
trations seem to paralyze smell more rapidly. Thus,
Oxygen is displaced by CO, limiting the ability to take
animals or humans may have only a very brief instant to
up oxygen and give off carbon dioxide in the lungs.
smell hydrogen sulfide at high concentrations; it is dan-
Because of their high respiratory exchange efficiency,
gerous to ignore the smell because its duration can be so
birds are unusually sensitive to CO (Brown et al., 1997).
brief.
They often require relatively more oxygen per unit body
Hydrogen sulfide is heavier than air and insoluble in
weight because they have smaller body sizes and more
the water of manure pits (Carson, 2004). Thus it can exist
active metabolisms.
as bubbles in swine manure pits inside hog houses, ready
Measurement of COHb is diagnostic of CO intoxica-
to be released and expose animals and workers on agita-
tion (Carson, 2004). In humans, ,3% COHb is
tion. Taking appropriate steps to protect rescuers, exposed
considered normal; 6% 8% causes drifting of atten-
people or animals not breathing should be dragged out-
tion; 10% 20% headaches; 20% 30% dizziness;
side. If breathing is not reestablished spontaneously, arti-
30% 60% tachypnea, tachycardia and confusion; and
ficial respiration should be applied until spontaneous
60% fatality. Birds respond more acutely than mam-
respiration returns.
mals, and canaries have been used as sentinels for
miners (Brown et al., 1997; Carson, 2004). Treatment
requires, at a minimum, fresh circulating air; 100% Nitrogen Dioxide and Ozone
oxygen may be lifesaving. Prognosis depends on the
amount of COHb and the hypoxic brain damage. NO 2 is considered with ozone (O 3 ), because NO 2 is a
Pulmonary function should be monitored for at least 2 prooxidant and O 3 an oxidant. In agriculture, NO 2 can
weeks, and in some cases 6 weeks. come from silage or relatively airtight silos, where it is
usually found towards the top (Carson, 2004). Indoor air
Methane NO 2 and O 3 can come from second-hand cigarette smoke.
NO 2 exposure from newly opened silage bags may mod-
Methane (CH 4 ) becomes an asphyxiant at .85%; it is an
estly affect hungry cattle if exposure levels are unusually
explosion hazard at 10% 15%. It is substantially lighter
high (i.e., in large confined animal feeding operations
than air and will flow above water in a swamp (Carson,
dairies), but usually they are more likely to affect care-
2004).
takers in upright silos. NO 2 has low water solubility, and
can pass through the upper airway and permanently dam-
Hydrogen Sulfide age pulmonary parenchyma where residence times are
Since hydrogen sulfide (H 2 S) is insoluble in water, it may longer. At ambient NO 2 (2 3 ppm) there is little damage
expose the deepest recesses of the lung. At 50 150 ppm or clinical signs. At higher levels, e.g., 20 ppm, it induces
level H 2 S causes pulmonary edema (Carson, 2004). In lung edema. Animals develop coughing, some fluid in the
vitro, H 2 S induces apoptosis of aorta smooth muscle cells, lungs, death of type I epithelial cells, coalescing alveoli,
regulated by mitogen-activated protein kinase (ERK and an increased collagen production but no morphologic
MAPK) that activates caspase-3 (Yang et al., 2004). H 2 S evidence of fibrosis (Gregory et al., 1983; Pickrell et al.,
is less toxic to birds than to other animals; 1987a; Mauderly et al., 1987; Carson, 2004). Animals
2000 3000 ppm will change respiratory rate and depth, that die at varying times after exposure have evidence of
while 4000 ppm will kill them in about 15 min. The pulmonary edema and emphysema.
mechanism may relate to the greater gas exchange effi- Birds are unusually sensitive to NO 2 and O 3 , depend-
ciency of parabronchi (Brown et al., 1997). ing on exposure level. Caged pet birds may be sensitive
Hydrogen sulfide’s ability to paralyze the respiratory to second-hand cigarette smoke, especially in the presence
tract is its greatest danger to animals and humans of heating/combustion sources. Newly hatched chicks die
(Carson, 2004). Above 500 2000 ppm, mammals are after 5 days’ exposure to 1 4ppm O 3 ; exposure to
said to take the second, but not the third, breath. Above 0.3 0.7 ppm O 3 causes pulmonary hemorrhage in these
500 ppm, H 2 S begins to cause permanent neurologic chicks (Brown et al., 1997). Pulmonary hemorrhage in