Page 672 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Toxic Gases and Vapors Chapter | 48 637

VetBooks.ir have been reported in humans with chronic irritant expo- Prevention
sures. Cardiac arrhythmias, nausea, vomiting, diarrhea,
Losses of detection ability (odor fatigue and/or olfactory
and abdominal pain are also common.
nerve paralysis), ill-advised entries into closed spaces, and
misguided attempts to rescue casualties have all been asso-
Diagnostic Testing ciated with many deaths. The use of electronic exposure
Measurements of H 2 S metabolites, such as sulfide and monitors (both personal and in spaces) and the immediate
thiosulfate in whole blood and/or urine as well as breath- availability of personal protective equipment have saved
ing zone air sampling/monitoring, are useful (Caravati, many lives. Great care should be taken not to stir or agitate
2004). manure tanks, septic tanks, sludge pits, cesspools, or set-
tling ponds. The use of hydrochloric acid and/or sulfuric
acid-based drain cleaners should be avoided.
Postmortem Findings
Greenish discoloration of gray matter, viscera, and bron-
chial secretions is a classical indicator in fresh tissues, but
the coloration is lost with formalin fixation (Park et al., Oxides of Nitrogen (Silo Filler’s Disease)
2009). Fresh tissues may also have a distinctive sulfide Overview, Uses, and Sources of Exposure
smell and may undergo accelerated decomposition.
The main gas involved is nitrogen dioxide (NO 2 ), although
other reactive oxides of nitrogen may also be present
Treatment
(Lowry and Schuman, 1956; Jonas, 1984; Pladson, 1984;
The immediate treatment priority is the prompt removal Douglas et al., 1989; Epler, 1989; Gurney et al., 1991;
of the patient from the source of exposure (Reiffenstein Zwemer et al., 1992; Leavey et al., 2004). NO 2 has a
et al., 1992; Smith, 1997; Milby and Baselt, 1999; Albin, bleach-like odor, a reddish-brown to yellow color, and
2000; Caravati, 2004; Woodall et al., 2005; Chou et al., leaves a yellow stain on silage, wood, or other contact
2006; Khoshniat, 2008; Oesterhelweg and Puschel, 2008; materials. It is heavier than air. The most commonly
Ballerino-Regan and Longmire, 2010). Rescuers need to encountered source in veterinary medicine is from silos
take great care not to become casualties in such circum- that have been recently filled with fresh organic material
stances. The next treatment priority is resuscitation and (notably corn or other grains) or from silage pits. NO 2 is
provision of 100% oxygen (Caravati, 2004). Induction of formed when NO in fresh silage or silo contents comes in
methemoglobinemia by administration of nitrites, based contact with oxygen in the air. Silage gas also typically
on the predilection of sulfide to bind to ferric ions form- contains carbon dioxide. Silo gas has been a cause of mor-
ing sulfmethemoglobin and thus potentially removing the tality in dairy cattle (Haynes, 1963; Verhoeff et al., 2007).
sulfide from cytochrome oxidase and reactivating aerobic Toxic (and potentially lethal) levels of NO 2 can
metabolism, has been suggested as an antidotal therapy. develop within hours on top of the material in the silo or
In clinical reality, induction of methemoglobinemia is silage pit (Groves and Ellwood, 1989). Within silos, the
only of benefit if performed within seconds to minutes of gas tends to seep down through the silo chute. The risk is
exposure. Hydroxycobalamin has been proposed as an highest when feedstuffs that are high in nitrates are
antidote for H 2 S poisoning on the basis that the patho- ensiled or used for silage. Gas production typically peaks
physiology resembles that of acute cyanide poisoning at approximately 24 h, but it may last for several days.
(Truong et al., 2007; Fujita et al., 2011). This antidote Other veterinary-relevant sources of NO 2 include kero-
seems to have some effect under laboratory conditions. sene heaters, unvented gas stoves, gas heaters, and
However, its effectiveness under field conditions has not tobacco smoke.
been adequately investigated. Hyperbaric oxygen has also
been proposed as being beneficial; however, it is rarely
available in veterinary practice (Smilkstein et al., 1985; Toxic Dose
Whitcraft et al., 1985; Lindenmann et al., 2010).
The US EPA National Ambient Air Quality Standards
lists 0.053 ppm as the 24-h time-weighted average upper
Prognosis limit for NO 2 in air. Levels of 25.9 ppb (SD, 18.1 ppb)
The prognosis is variable depending on the duration of are known to increase the risk of pediatric asthma in
apnea and the degree of CNS hypoxia (Caravati, 2004). A humans (Belanger et al., 2006). Brief exposures to
few individuals appear to recover without any subsequent 200 ppm can be fatal, and exposure to 50 ppm can result
problems; however, a significant proportion of survivors in significant pulmonary edema. A 1-h exposure to 1 ppm
will develop subsequent neurological problems associated is associated with deleterious effects in the lung. The
with brain hypoxia. human odor threshold is approximately 0.1 0.2 ppm.