1) Chlorine is used extensively in pulpmills, where wood chips are processed into pulp as part of the paper manufacturing process (Kennedy et al, 1991).

a) PREHOSPITAL: Remove contaminated clothing and wash exposed skin with water.
b) HOSPITAL: Remove contaminated clothing and wash exposed skin with water.

a) SHAMPOOS: Green hair caused by shampooing has occurred. The cause was copper leaching from household plumbing following water acidification due to non-pH-controlled fluoridation (Barrett, 1977; Cooper & Goodman, 1975).

a) INCIDENCE: In a series of 86 patients whose chlorine exposure cases were reported to a poison control center, 3 (4%) developed eye irritation or burning (Bosse, 1994). In a retrospective review of 598 poison center chlorine cases, 248 cases (41.5%) involved exposure to tablets; 320 (53.5%), exposure to liquid chlorine; and the remainder, to both. Eye irritation was reported in 8.5% of patients (LoVecchio et al, 2005).

a) INCIDENCE: In a series of 86 patients whose chlorine exposure cases were reported to a poison control center, 5 (6%) developed nasal irritation or burning (Bosse, 1994). In a retrospective review of 598 poison center chlorine cases, 248 cases (41.5%) involved exposure to tablets; 320 (53.5%), exposure to liquid chlorine; and the remainder, to both. Nasal complaints were reported in 9.7% of patients (LoVecchio et al, 2005).

a) INCIDENCE: In a series of 86 patients whose chlorine exposure cases were reported to a poison control center, 12 (14%) developed throat irritation, burning, or soreness (Bosse, 1994).

a) Weak pulse, hypertension followed by hypotension, and cardiovascular collapse may occur (Done, 1976; Noe, 1963).

a) Severe exposure may cause tachycardia (Mohan et al, 2010; Kose et al, 2009; Vohra & Clark, 2006; Done, 1976; Noe, 1963).
b) CASE SERIES: Following a train derailment that released 42 to 60 tons of chlorine gas within a small town, tachycardia (greater than 100 bpm) was reported as an immediate and persistent finding in 27 of 63 patients (43%) and as a delayed finding in 8 of 63 patients (13%) (Van Sickle et al, 2009).

a) Two cases have been reported in which exposure to chlorine gas produced ventricular ectopic beats. Neither required the use of antiarrhythmics (Edwards et al, 1983).

a) CASE SERIES: Following a train derailment that released 42 to 60 tons of chlorine gas within a small town, hypertension (systolic pressure greater than 140 mmHg or diastolic pressure greater than 90 mmHg) was reported as an immediate and persistent finding in 18 of 63 patients (29%) and as a delayed finding in 10 of 63 patients (16%) (Van Sickle et al, 2009).

a) CASE SERIES: Derailment of a train carrying three 90-ton tanker cars of chlorine released 42 to 60 tons of chlorine gas within a small town, resulting in the hospitalization of 71 people and the deaths of 9 people (8 at the scene of the accident and 1 on the first day of hospitalization). Although asphyxia was determined to be the primary cause of death, autopsies detected cardiomegaly in 8 of the 9 deceased individuals. Cardiomegaly was also a radiologic finding in 3 of the hospitalized patients (Van Sickle et al, 2009).

a) CASE REPORT: A 74-year-old woman, with diabetes, presented to the emergency department profoundly hypoxic and (oxygen saturation 50%) and comatose after inhaling fumes from the combination of sodium hypochloride and hypochloric acid. Examination of the patient revealed tachycardia, miosis, rales and rhonchi of the lungs, and a Glasgow Coma Scale score of 5. Laboratory data revealed respiratory acidosis and an elevated blood glucose level (946 mg/dL). An ECG demonstrated anterior superior hemiblock and loss of R-wave progression, and an elevation in her cardiac enzymes was noted, indicating a non-Q myocardial infarction. A brain CT scan initially detected no abnormalities except for slight edema; however, a repeat CT, performed 1 day later, revealed an infarct of the right middle cerebral artery and effacement of right sulci. Despite aggressive supportive care, the patient's condition continued to deteriorate and she died on hospital day 5 (Kose et al, 2009).

a) INCIDENCE: In a series of 86 patients whose chlorine exposure cases were reported to a poison control center, 45 (52%) developed cough (Bosse, 1994). In a retrospective review of 598 poison center chlorine cases, 248 cases (41.5%) involved exposure to tablets; 320 (53.5%), exposure to liquid chlorine; and the remainder, to both. Cough was reported in 70.1% of patients (LoVecchio et al, 2005).
b) INCIDENCE: In a series of 281 workers who had been repeatedly exposed to chlorine, 67% complained of cough (Courteau et al, 1994).

a) INCIDENCE: In a series of 86 patients whose chlorine exposure cases were reported to a poison control center, 44 (51%) developed shortness of breath (Bosse, 1994). In a retrospective review of 598 poison center chlorine cases, 248 cases (41.5%) involved exposure to tablets; 320 (53.5%), exposure to liquid chlorine; and the remainder, to both. Shortness of breath was reported in 38.1% of patients (LoVecchio et al, 2005).
b) INCIDENCE: In a series of 281 workers who had been repeatedly exposed to chlorine, 54% complained of shortness of breath (Courteau et al, 1994).
c) CASE REPORT: A 7-year-old developed dyspnea and coughing after inhaling chlorine fumes from a can of chlorine tablets used for an indoor swimming pool. The patient was treated with 100% oxygen (O2) via face mask to maintain an O2 saturation above 94% and was also given 1 treatment of albuterol by nebulizer without improvement. The patient was then given nebulized sodium bicarbonate over 20 minutes, with a dramatic improvement in symptoms and a decrease in nasal flaring and retraction. The patient was discharged the following day with no further symptoms (Douidar, 1997).
d) CASE REPORT: Coughing and dyspnea occurred in a 9-year-old girl who was swimming and inhaled chlorine released from aerosolized swimming pool purification tablets. Her O2 saturation the day following exposure was 90% on room air. Lung examination revealed moderate intercostal and supraventricular retractions, tachypnea, and bilateral wheezing. A chest radiograph showed bilateral interstitial infiltrates. The patient recovered with supplemental O2 and bronchodilator therapy. After 4 months, pulmonary function tests indicated a mild reversible obstructive pattern, but medication was not required to perform normal activities of daily living (Vohra & Clark, 2006).
e) CASE SERIES: In a series of 13 children who had been exposed to chlorine gas at a swimming pool, 5 patients were admitted to the hospital secondary to hypoxia, with pulse oximetry reading ranging from 85% to 93% on room air. Of these 5 patients, 4 were found to have mild carbon dioxide (CO2) retention with PCO2 readings of 45, 47, 47, and 50 mmHg. The authors suggested that CO2 retention may occur relatively frequently following chlorine gas exposure (Sexton & Pronchik, 1998).
f) CASE REPORT: A 42-year-old man developed respiratory distress following inhalation of chlorine powder used to treat his pool. Dyspnea, cough, chest tightness, and eye pain, tearing, and blurred vision occurred shortly after inhalation. Physical examination revealed mild expiratory wheezes and bilaterally injected sclerae, Although his initial chest X-ray was unremarkable and he received treatment with bronchodilators, his condition rapidly worsened and he developed increasing dyspnea, cough, and bilateral crackles. He was intubated approximately 60 hours after exposure for worsening symptoms and a post intubation chest x-ray revealed pulmonary edema, acute respiratory distress syndrome, and small pleural effusions. A bronchoscopy demonstrated hyperemic mucosa and mucosal pallor. With supportive care, including ventilator support and inhaled beta-agonists, the patient was eventually extubated and discharged without sequelae 14 days later. A follow-up one year later revealed no long term lung related complications (Endrizzi et al, 2015).

a) Typical findings following mild to moderate acute exposure include wheezing, throat irritation, coughing, dyspnea, burning chest pain, and feelings of suffocation (Centers for Disease Control and Prevention (CDC), 2011; Mohan et al, 2010; Courteau et al, 1994; Anon, 1984). Bronchospasm may occur with acute exposure (Sexton & Pronchik, 1998).
b) INCIDENCE: In a series of 86 patients whose chlorine exposure cases were reported to a poison control center, 29 (34%) developed chest pain, burning, irritation, or heaviness (Bosse, 1994).

a) Laryngeal edema, hoarseness, and stridor may develop (Hathaway et al, 1996; Martinez & Long, 1995; Anon, 1984).

a) More severe exposures may lead to laryngeal spasms, cyanosis, and respiratory arrest (Lawson, 1981; Hedges & Morrissey, 1979; Done, 1976; Noe, 1963).

a) More severe exposures may lead to acute lung injury (Van Sickle et al, 2009; Sexton & Pronchik, 1998; Heidemann & Goetting, 1991), and death may follow within 24 hours (Martinez & Long, 1995; Anon, 1984).
b) CASE REPORT: A 14-year-old healthy male with a history of asthma developed respiratory failure and acute lung injury following exposure to chlorine gas (result of mixing vinegar and household bleach in an unventilated room). The patient was managed using mechanical ventilation with positive end-expiratory pressure (up to 12 mmHg), along with intravenous methylprednisolone and nebulized albuterol. The patient was successfully extubated on day 19, with no evidence of permanent pulmonary injury (Traub et al, 2002).
c) CASE REPORT: A 42-year-old man developed respiratory distress following inhalation of chlorine powder used to treat his pool. Dyspnea, cough, chest tightness, and eye pain, tearing, and blurred vision occurred shortly after inhalation. Physical examination at hospital arrival revealed mild expiratory wheezes and bilaterally injected sclerae. Although his initial chest X-ray was unremarkable and he received treatment with bronchodilators, his condition rapidly worsened and he developed increasing dyspnea, cough, and bilateral crackles. He was intubated and a second chest x-ray revealed pulmonary edema, acute respiratory distress syndrome, and small pleural effusions. A bronchoscopy demonstrated hyperemic mucosa and mucosal pallor. With supportive care, including ventilator support and inhaled beta-agonists, the patient was eventually extubated and discharged without sequelae 14 days later (Endrizzi et al, 2015).

a) CASE REPORT: Dyspnea, hypoxemia, and pneumonitis occurred in a 9-year-old girl who, while swimming, was exposed to chlorine released from aerosolized swimming pool purification tablets. Her oxygen saturation approximately 12 hours after exposure was 90% on room air. Lung examination revealed moderate intercostal and supraventricular retractions, tachypnea, and bilateral wheezing. A chest radiograph showed bilateral interstitial infiltrates. The patient recovered with supplemental oxygen and bronchodilator therapy. After 4 months, pulmonary function tests revealed a mild, reversible obstructive pattern, but medication was not required to perform normal activities of daily living (Vohra & Clark, 2006).

a) CASE REPORT: A 23-year-old healthy man developed acute bronchiolitis after exposure to chlorine gas (concentration unknown) for approximately 5 minutes while exercising. Respiratory symptoms became progressively worse (tachypnea, bilateral wheezing), and a chest x-ray obtained 36 hours after exposure showed diffuse small nodular opacities. Scant blood-tinged sputum was also observed. A CT scan of the chest was consistent with diffuse bronchiolitis (ie, ill-defined centrilobular nodules along the peribronchovascular structure and mild air trapping). Following treatment (albuterol and prednisone), the patient was discharged; pulmonary functions studies repeated at 12 weeks were markedly improved (Kanne et al, 2006; Parimon et al, 2004).

a) Flexible fiberoptic bronchoscopy 3 to 7 days after exposure to chlorine gas revealed evidence of tracheobronchitis (congestion, edema, scattered hemorrhage, and sloughing) in 14 patients. Of the 9 patients with previously normal lungs, 6 had evidence of mild obstructive lung disease, and 2 had mild restrictive disease on initial pulmonary function testing. Pulmonary function tests returned to normal over the next 6 months. In the 5 patients with preexisting COPD, there was no improvement in pulmonary function tests 6 months after exposure (Abhyankar et al, 1989).

a) Persistent reactive airways dysfunction syndrome (RADS) has occasionally been reported after exposure to chlorine gas (Mohan et al, 2010).
b) CASE REPORT: A 30-year-old man with a history of childhood asthma not requiring medication for 20 years developed severe shortness of breath and wheezing after a chlorine gas cylinder exploded in his face. Nocturnal and exertional dyspnea and wheezing and reversible airflow obstruction requiring inhaled bronchodilators and steroids persisted for 6 years (Donnelly & FitzGerald, 1990).
c) CASE REPORT: A 25-year-old man with a history of mild childhood asthma not requiring treatment for 20 years developed dyspnea and wheezing after working in a chlorine-filled enclosed environment. He was treated with aminophylline, inhaled beta-agonists, and inhaled and oral steroids over the next 4 years. Pulmonary function testing 4 years after exposure revealed severe partially reversible obstructive disease (Moore & Sherman, 1991).
d) CASE REPORT: A 39-year-old woman with atopy and a family history of asthma developed mild reversible obstructive disease, as shown by pulmonary function testing, after mixing sodium hypochlorite and hydrochloric acid in a confined space. Symptoms persisted for 2 years after exposure (Deschamps et al, 1994).
e) CASE REPORT: Two patients developed reactive airways disease after chlorine exposure. Both patients improved over time (Demeter & Cordasco, 1992).
f) CASE SERIES: In a series of 71 workers considered at moderate to high risk of developing RADS because of repeated exposure to chlorine, 51 underwent spirometry 18 to 24 months after exposure ended. Of those workers, 16 had obstructive pulmonary disease and 29 showed hyperresponsiveness on methacholine challenge (Bherer et al, 1994).

a) CASE REPORT: A 26-year-old woman presented with severe dyspnea and wheezing approximately 2 days after inhaling the chlorine gas produced by mixing 5% sodium hypochlorite and 18% hydrochloric acid. Physical examination revealed hyperemia and edema of her vocal cords and laryngeal structures, and diffuse rhonchus was heard following auscultation of her lungs. A CT scan of the patient's neck and thorax indicated emphysema of the neck and pneumomediastinum. Following treatment with 50% humidified oxygen and administration of bronchodilators and IV corticosteroid infusion, the patient recovered. A repeat CT scan performed 6 days later showed complete resolution of the pneumomediastinum (Akdur et al, 2006).
b) CASE REPORTS: Two patients, a 13-year-old girl and a 15-year-old boy, presented to the emergency department 10 minutes after inhaling chlorine gas. Chest radiographs of both patients revealed pulmonary edema and a chest CT scan indicated pneumomediastinum. Both patients recovered following supportive care, including oxygen therapy (Li et al, 2011).

a) PULMONARY SEQUELAE: Increased airway reactivity to inhaled methacholine and decreased residual volume have been described for up to 12 years following an acute exposure (Schwartz et al, 1990; Decker, 1988).
b) Patients at increased risk for development of prolonged sequelae were older and had marked airflow obstruction and air trapping immediately following exposure (Schwartz et al, 1990).
c) CASE REPORT: A 3.5-month-old infant exposed to chlorine gas had wheezing and persistent airway obstruction as shown by pulmonary function testing for 1 year after exposure (Givan et al, 1989).
d) CASE SERIES: Pulp mill workers who reported transient exposures to high levels of chlorine gas showed increased airflow obstruction on pulmonary function tests compared to controls (Kennedy et al, 1991).
e) CASE SERIES: Bronchoscopy was performed on 28 patients 5 to 25 days after unintentional exposure to approximately 66 parts per million (ppm) of chlorine gas. Cytopathologic features of bronchial brushings included varying degrees of bronchial mucosal damage and acute inflammatory response. On day 15, bronchoscopy of 7 patients who had persistent cough and respiratory distress showed evidence of secondary bacterial invasion. Bronchoscopy of these same 7 patients on day 25 revealed evidence of repair by fibrosis (Shroff et al, 1988).
f) CASE SERIES: Episodes of high chlorine gas exposure in pulp mill workers have been associated with evidence of obstructive disease on pulmonary function testing, decreasing FEV1/FVC over time, and self-reported respiratory symptoms (chest tightness, sputum production, wheezing, and cough) (Henneberger et al, 1996; Salisbury et al, 1991). Most of these workers were also exposed to other irritant gases (Salisbury et al, 1991).
g) CASE SERIES: In a population of 113 people who were exposed to chlorine gas following a train derailment, the probability of having been admitted to the hospital after the initial exposure was related to the person's distance from the spill. Three weeks after exposure there was no detectable difference in lung function that could be related to distance from the spill or initial severity of injury (Jones et al, 1986).
h) CASE SERIES: Following a train derailment that released 42 to 60 tons of chlorine gas within a small town, 63 patients were hospitalized on the day of the accident. All of the patients presented with at least 1 pulmonary complaint, with wheezing being the most common immediate/persistent physical pulmonary finding (46%). Other respiratory findings included rales/crackles, cough, decreased breath sounds, rhonchi, labored breathing, retractions, and tachypnea. Of those findings, the most prevalent delayed sign was rales/crackles, occurring in 18 of the 71 patients (29%) (Van Sickle et al, 2009).

a) The long-term effects of acute chlorine exposure on pulmonary function have been debated in the literature. A historical study suggested a lack of permanent effect (Weill et al, 1969), while current findings include persistent pulmonary abnormalities (eg, a decrease in total lung capacity, functional residual capacity, and vital capacity and a significant increase in residual volume and airway resistance over several years and persistent reactive airways dysfunction syndrome) (Williams, 1997; Deschamps et al, 1994; Demeter & Cordasco, 1992; Moore & Sherman, 1991).
b) LONGITUDINAL STUDY
c) REACTIVE AIRWAY DYSFUNCTION SYNDROME
d) INFLUENZA-LIKE SYMPTOMS

a) Headache is the most frequently reported neurological complaint (Centers for Disease Control and Prevention (CDC), 2011; Courteau et al, 1994; CDC, 1991; Hedges & Morrissey, 1979).
b) INCIDENCE: In a series of 281 workers who had been repeatedly exposed to chlorine, 63% complained of headache (Courteau et al, 1994). In another series of 82 workers, headache was reported in 24% to 29% of patients (Sexton & Pronchik, 1998).

a) Agitation and anxiety may develop in patients with significant respiratory compromise (Noe, 1963).

a) CNS depression ranging from lethargy to coma may develop in patients with severe pulmonary injury (Heidemann & Goetting, 1991).

a) The significant neurobehavioral findings reported in 97 patients after exposure to spilled chlorine and potassium cresylate compared with a referent population included differences in simple reaction time, balance with eyes closed, vocabulary score, and information. Forty-eight of 90 patients had abnormal visual quadrants in visual fields. At 3 years postexposure, additional findings included differences in choice reaction time, balance with eyes open, color errors, immediate and delayed verbal recall, Culture Fair Test results, fingertip number writing errors, and blink reflex latency (Kilburn, 2003).

a) CASE REPORT: A 74-year-old woman, with diabetes, presented to the emergency department profoundly hypoxic (oxygen saturation 50%) and comatose after inhaling fumes from the combination of sodium hypochloride and hypochloric acid. Examination of the patient revealed tachycardia, miosis, rales and rhonchi of the lungs, and a Glasgow Coma Scale score of 5. Laboratory data revealed respiratory acidosis and an elevated blood glucose level (946 mg/dL). An ECG demonstrated anterior superior hemiblock and loss of R-wave progression, and an elevation in her cardiac enzymes was noted, indicating a non-Q myocardial infarction. A brain CT scan initially detected no abnormalities except for slight edema; however, a repeat CT, performed 1 day later, revealed an infarct of the right middle cerebral artery and effacement of right sulci. Despite aggressive supportive care, the patient's condition continued to deteriorate and she died on hospital day 5 (Kose et al, 2009).

a) Salivation, nausea, retching, and vomiting are typical findings following exposure (Mohan et al, 2010; Harbison, 1998; CDC, 1991; Hryhorczuk, 1986).
b) INCIDENCE: In a series of 82 individuals who were exposed to chlorine gas, 24% to 29% developed vomiting (Sexton & Pronchik, 1998).

a) INCIDENCE: In a series of 82 individuals who were exposed to chlorine gas, 24% to 29% developed abdominal pain (Sexton & Pronchik, 1998).

a) Metabolic acidosis has been reported following severe (fatal) exposure to chlorine gas or trichloro-s-triazinetrione powder (Martinez & Long, 1995; Adelson & Kaufman, 1971) . The acidosis is probably due to poor peripheral tissue oxygenation secondary to severe hypoxemia. Metabolic acidosis with hyperchloremia has been reported (Szerlip & Singer, 1984).
b) CASE SERIES: Following a train derailment that released 42 to 60 tons of chlorine gas within a small town, metabolic acidosis and respiratory acidosis were reported in 9 and 25 patients, respectively, of 55 patients who had an arterial blood gas measurement (Van Sickle et al, 2009).

a) Liquid chlorine may cause cutaneous burns. Gaseous chlorine will irritate the skin and may cause burns in high concentrations (Raffle et al, 1994; Anon, 1984).
b) Severe dermal, ocular, and pulmonary burns developed in a man who was exposed to chlorine gas after he added water to a pail containing trichloro-s-triazinetrione; the mixture exploded (Hathaway et al, 1996; Martinez & Long, 1995).

a) In a retrospective review of 598 poison center chlorine cases, 248 cases (41.5%) involved exposure to tablets; 320 (53.5%), exposure to liquid chlorine; and the remainder, to both. Skin complaints were reported in 2.5% of patients (LoVecchio et al, 2005).

a) CASE REPORT: Hyperglycemia (blood glucose level 946 mg/dL) was reported in a 74-year-old diabetic woman after inhaling fumes from the combination of sodium hypochloride and hypochloric acid (Kose et al, 2009).

a) Chlorine (as hypochlorite) was teratogenic at 100 parts per million (ppm) when given to pregnant rats in their water (Meier, 1985). Biochemical and metabolic effects were observed in newborn rats (RTECS , 2000).

a) As a whole, these various studies relating exposure to chlorinated by-products in drinking water with adverse human reproductive outcomes are very difficult to compare. They have examined different end points, have used different methods of dosimetry, and in any case dosimetry is very complex. Although the results are suggestive, they should be interpreted with caution (Reif et al, 1996).

a) Recurrent respiratory symptoms should be evaluated by pulmonary function testing, although it is not indicated in the immediate exposure period (Traub et al, 2002).
b) Persistent abnormalities have been noted on pulmonary function tests for up to 12 years after acute exposures (Schwartz et al, 1990).
c) Eighteen children, ages 6 to 12 years, were exposed to chlorine gas after an excessive amount of chlorine was accidentally added to a swimming pool. Acutely, all children had respiratory symptoms and reduced lung function as determined by FVC and FEV1, low fractions of nitric oxide in exhaled air (FE(NO)), and high exhaled breath condensate leukotriene B4 levels. Lung function returned to normal within 15 days for all the children. The fractions of nitric oxide in exhaled air reached normal values within 2 months, and the exhaled breath condensate leukotriene B4 levels progressively declined over 8 months (Bonetto et al, 2006).
d) Eighty-four school children who lived near a chemical plant that had a chlorine gas leak underwent pulmonary function testing 2 weeks after exposure. Compared with a control group, the exposed children had statistically significant decreases in mean values for VC, FVC, FEV1, PEFR, and V75. Overall evaluation of their pulmonary function tests revealed that 20 of the 84 children (24%) had a normal pattern, 56 (66%) had an obstructive pattern, and 8 (10%) had a restrictive pattern (Pherwani et al, 1989).
e) Respiratory symptoms after exposure to chlorine gas were more common and more likely to be present at 15 to 30 days after the exposure in patients with chronic respiratory diseases and smokers or ex-smokers. Effects of exposure on lung function tended to be higher in smokers and ex-smokers (Agabiti et al, 2001).

a) A double-blind, placebo-controlled study was conducted to determine the efficacy of nebulized sodium bicarbonate for treatment of reactive airways dysfunction syndrome (RADS) following chlorine gas inhalation. Forty-four patients with persistent RADS for at least 3 months with initial onset within 24 hours of chlorine gas inhalation were given either nebulized sodium bicarbonate (n=22) or nebulized placebo (n=22). All patients also received corticosteroids and nebulized short-acting beta-agonists. FEV1 values were significantly higher at 120 and 240 minutes in the nebulized sodium bicarbonate group as compared with the nebulized placebo group (p less than 0.05). The quality of life scores in both groups, determined from questionnaires, also improved significantly following treatment (p less than 0.001), but there was no significant difference between the groups (Aslan et al, 2006).
b) CASE REPORTS: Dramatic improvement of early respiratory symptoms was noted following humidification with a 5% sodium bicarbonate solution in an anecdotal report (Done, 1976) and with a 3.75% sodium bicarbonate solution in 3 male patients with mild symptoms in another anecdotal report (Vinsel, 1990).
c) CASE SERIES: In a retrospective review of 86 cases of chlorine gas exposure that were treated with nebulized sodium bicarbonate (3 mL of 8.4% sodium bicarbonate mixed with 2 mL normal saline administered as a nebulizer treatment with oxygen or air), 69 patients were treated and released from the emergency department. Of these, 7 also received inhaled bronchodilators, 1 patient received steroids, 2 were discharged with bronchodilators, and 1 patient was discharged with a course of steroids. Condition was improved on discharge in 53 patients, 23 of whom were asymptomatic. Condition was not specified in 16 patients who were treated and released. Seventeen patients required hospital admission. No patient appeared to suffer an adverse effect that could be attributed to sodium bicarbonate (Bosse, 1994a).
d) Steroid and bicarbonate treatments were inadequate supportive therapies for patients with acute chlorine intoxication in a case series of 106 patients (Guloglu et al, 2002).
e) Clinically, humidification with 5% sodium bicarbonate does not seem to produce a notable thermal reaction within the lung parenchyma. This most likely occurs due to the dilute concentration used.

a) A study in sheep that were exposed to chlorine gas for 4 minutes and then randomized to receive 8 mL of nebulized normal saline or 4% sodium bicarbonate demonstrated a higher PCO2 and lower PO2 in the control group. Sodium bicarbonate did not worsen outcome, as measured by mortality and postmortem pathologic evaluation, and appeared to improve arterial blood gas values (Chisholm et al, 1989).

a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)

1) Chlorine
b) Under Study

1) Listed as: Chlorine
2) REL:
3) IDLH:

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Chlorine
2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Chlorine
3) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Chlorine
4) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Chlorine
6) MAK (DFG, 2002): Not Listed
7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

1) Listed as: Chlorine
2) Table Z-1 for Chlorine:

a) 66 ppm for 1H - cough and dyspnea; headache
b) 500 ppb for 2D-intermittent -- tolerance behavior affected

a) 400 ppb for 6H/2Y-intermittent -- changes to nose, eyes, ears, and taste
b) 9100 ppb/for 6H/5D- intermittent -- decreased weight gain and weight loss; changes to sense organs; structural and functional changes to trachea or bronchi

a) 400 ppb for 6H/2Y-intermittent-- changes to the sense organs
b) 9 ppm for 6H/6W-intermittent-- changes to white blood count, phosphatases, kidney, bladder, and ureter
c) 9100 ppb for 6H/5D-intermittent -- decreased weight gain or weight loss; changes to the sense organs; structural or functional changes to bronchi or trachea