Page 105 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition
P. 105
72 SECTION | I General
VetBooks.ir bertholite (Budavari, 2000). It is a greenish-yellow Toxicity
diatomic gas with an irritating, pungent, or suffocating
Inhalation is the main route of chlorine gas exposure.
odor (Lewis, 2000; Budavari, 2000). Chlorine gas is
heavier than air and will settle in low areas. Chlorine gas is very irritating on contact and can be caus-
tic to the eyes, skin, nose, throat, and mucous membranes.
Ocular exposure can result in severe or permanent eye
Pharmacokinetics/Toxicokinetics injury. Dermal exposure may cause erythema, pain, and
irritation. Both liquid chlorine and high concentrations of
The initial effects of chlorine gas exposure can appear
gaseous chlorine can cause dermal burns (Raffle et al.,
very rapidly, depending upon the concentration. Due to
1994). Signs of exposure to chlorine gas include: rhinor-
chlorine’s water solubility and chemical reactivity, it can
rhea, ataxia, syncope, muscle weakness, dermatitis, dys-
have a greater effect on the lower respiratory tract as a
pnea, tachypnea, pneumonia, bronchospasm and acute
large percentage bypasses the upper airways. Respiratory,
lung injury. High concentrations may cause laryngos-
dermal, and ocular irritation starts immediately and acute
pasm, cardiovascular collapse, tachycardia, and respira-
lung injury peaks in 12 24 h.
tory arrest (Noe, 1963). Respiratory symptoms may be
immediate or delayed up to several hours depending on
Mechanism of Action the concentration (Bingham et al., 2001). Hypoxia is com-
Chlorine gas is a strong irritant, and in concentrated mon and death may be rapid. See Table 5.1 for severity
of signs expected after inhalation at certain ppm concen-
amounts may be corrosive to mucous membranes when
trations of chlorine gas.
inhaled or ingested. When chlorine combines with tissue
Symptoms generally disappear within 6 h after mild
water it produces hydrochloric acid and reactive oxygen
exposures but may continue for more than 24 h with
species. These free radicals are potent oxidizers, causing
severe exposures. Moderate to severe exposures can result
further tissue damage. Nitric oxide (NO) formation is dis-
in chronic respiratory dysfunction (Decker, 1988).
rupted causing increased inflammation (Honavar et al.,
2014). The damage to the respiratory epithelium leads to
alveolar capillary congestion followed by high fibrinogen Treatment
edematous fluid (Noe, 1963). Hypoxemia results from
development of atelectasis, emphysema, and membrane Move animals into fresh air and monitor for respiratory
formation. Acute lung injury and development of acute distress. If coughing or dyspnea develops, evaluate for
respiratory distress syndrome (ARDS) can occur. Death hypoxia, acidosis, respiratory tract irritation, bronchitis or
usually occurs within 48 h from cardiac arrest secondary pneumonitis. Oxygen supplementation along with intuba-
to hypoxia (Decker, 1988). tion and ventilation may be needed. Beta adrenergic
TABLE 5.1 Different Effects of Exposure Levels of Chlorine Gas
Values in ppm Effect
0.2 3.5 Odor detection (some tolerance develops)
1 3 Mild mucous membrane irritation that can be tolerated for up to 1 h
3 Extremely irritating to the eyes and respiratory tract
5 Severe irritation of eyes, nose, and respiratory tract; intolerable after a few minutes
14 21 Immediate irritation of the throat; dangerous if exposed for 30 60 min
15 Irritation of the throat
30 Moderate irritation of the upper respiratory tract; immediate chest pain, vomiting, dyspnea, cough
35 50 Lethal in 60 90 min
40 60 Toxic pneumonitis and acute lung injury; dangerous for even short periods
430 Lethal over 30 min
1000 Fatal within a few minutes
Source: Data from Lewis, R.J., 2000. Sax’s dangerous properties of industrial materials, 10th edn. Van Nostrand Reinhold Company, New York, NY, HSDB,
2005. Hazardous Substances Data Bank. (Edition expires in 2005.) National Library of Medicine, Bethesda, MD (Internet Version). Thomson MICROMEDEX,
Greenwood Village, CO; Bingham, E., Chorssen, B., Powell, C.H., 5th edn., 2001. Patty’s Toxicology, vol. 3. John Wiley & Sons, New York, NY.