Page 105 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition
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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.
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