Misplaced Pages

This is an old revision of this page, as edited by T Cells (talk | contribs) at 21:57, 27 July 2015 (ce). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

This article or section is in a state of significant expansion or restructuring. You are welcome to assist in its construction by editing it as well. If this article or section has not been edited in several days, please remove this template. If you are the editor who added this template and you are actively editing, please be sure to replace this template with {{in use}} during the active editing session. Click on the link for template parameters to use. This article was last edited by T Cells (talk | contribs) 9 years ago. (Update timer)

Chlorine gas poisoning, also known as bertholite poisoning, occurs after the inhalation of chlorine gas beyond the threshold limit value. Chlorine gas is a toxic gas and pulmonary irritant with intermediate water solubility that causes acute damage to the receptors in the epithelium of the respiratory tract. The dose inhaled determines the toxicity on the respiratory tract. Occupational exposures constitute the highest risk of toxicity and common domestic exposure results from the mixing of chlorine bleach with acidic washing agents such as acetic, nitric and Phosphoric acid. Prolonged exposure to low concentration of chlorine gas may have lethal effects, as can short-term exposure to high concentrations.

Chlorine gas damages the respiratory tract using a chloride shift mechanism involving the exchange of bicarbonate (HCO₃) and chloride (Cl) across the membrane of red blood cells (RBCs).

The cell membranes of red blood cells are impermeable to hydrogen ions but exchange bicarbonate ions for chloride ions using the anion exchanger protein Band 3 and a rise in intracellular bicarbonate causes chloride intake and bicarbonate export. As a result, blood chloride concentration is lower in systemic venous blood than in pulmonary circulation because the levels of CO₂ and therefore bicarbonate are higher in systemic venous blood, providing less of a driving force for exchange. Excess chlorine gas in the lung and bloodstream deregulate the affinity of hemoglobin for oxygen through the chloride ion acting as an allosteric inhibitor.

Symptoms of mild acute poisoning include sneezing, tearing, nose irritation and throat irritation, while larger exposures can lead to significant toxicity of the respiratory tract and heart and sometimes death. Following acute poisoning, long-term sequelae often occur and chronic exposure to low levels of chlorine gas can lead to memory loss.

Signs and symptoms

Chlorine gas poisoning only causes severe damage to the respiratory tract and is therefore not harmful to all forms of life like carbon monoxide poisoning. It is easily absorbed through the lungs and its inhalation result in CNS damage and death. Different people and races may have different chlorine gas tolerance levels. Chlorine gas exposure may lead to a significantly shorter life span due to heart damage. Individual tolerance level for chlorine gas may be altered by several factors, such as metabolic rate, hematological disorders and barometric pressure.

Acute poisoning

The primary manifestations of chlorine gas poisoning develop in the organ systems most dependent on oxygen use: the central nervous system and the heart. The initial symptoms of acute chlorine gas poisoning include dyspnea, nausea and vomiting, violent cough, chest pains, lightheadedness, headache and muscle weakness. These symptoms are synonymous to those of influenza or other illnesses such as gastroenteritis or foodborne illness. Headache is the most common symptom of acute chlorine gas poisoning; it is often described as dull, frontal, and continuous. Increasing exposure produces cardiac abnormalities including fast heart rate, cardiac arrhythmia, hypotension and respiratory arrest. Less common symptoms of acute chlorine gas poisoning include hypertension, myocardial ischemia, muscle necrosis, skin lesions and pneumonia.

Chronic poisoning

Chronic exposure to relatively low levels of chlorine gas may cause persistent headaches, lightheadedness, nausea and vomiting. Like carbon monoxide poisoning, upon removal from exposure to carbon monoxide, symptoms usually resolve themselves, unless there has been an episode of severe acute poisoning. Sea water is a large source of chlorine and a typical source of poisoning is exposure to the organic solvent dichloromethane, found in some paint strippers.

Background

Chlorine gas is a toxic gas, a pulmonary irritant with intermediate water solubility that causes acute damage to the receptors in the epithelium of the respiratory tract.

Chlorine gas was first used as a chemical weapon in World War I on April 22, 1915 by Germany in the Second Battle of Ypres. Based on the soldiers' description of chlorine gas, it had the distinctive smell of a mixture of pepper and pineapple. It also tasted metallic and stung the back of the throat and chest. Chlorine gas often reacts with water in the mucosa of the lungs to form hydrochloric acid, an irritant that can be lethal.

The damage caused by chlorine gas can be minimized or prevented by the use of activated charcoal commonly found in gas masks, or other filtration methods, which makes the overall chance of death by chlorine gas much lower than those of other chemical weapons. The use of chlorine gas poisoning as a chemical weapon was pioneered by a German scientist later to be a Nobel laureate, Fritz Haber of the Kaiser Wilhelm Institute, Berlin in collaboration with the German chemical conglomerate IG Farben, who developed methods for discharging the gas against an entrenched enemy. It was reported that Haber's role in the use of chlorine gas as a deadly weapon drove his wife, Clara Immerwahr, to suicide.

Following its usage in the World War I, Theodore Gray wrote in his book The Elements: A Visual Exploration of Every Atom in the Universe, "Chlorine was used as a poison gas during the grueling trench-warfare phase. Soldiers would position a line of gas cylinders at the front lines, wait for the wind to shift towards the enemy, then open the valves and run like hell. This practice---sometimes overseen personally by Fritz Haber, a man whose positive contributions to humanity are listed under nitrogen (7)--- was slowly phased out as experience showed that roughly equal numbers of soldiers on both sides died regardless of who set off the gas."

Pathophysiology

Chlorine gas is non-combustible gas at room temperature and atmospheric pressure. It is heavier than air in its pure state causing it to remain close to the ground level, thereby increasing the exposure time. The odour threshold level for chlorine gas is approximately 0.3 - 0.5 ppm accounting for why the differentiation of toxic air levels from permissible air levels may seemed difficult until irritative symptoms develop. The degree of exposure determines the lethality and severity of symptoms and rapidity of onset increase. Chlorine gas is moderately soluble in water to form chlorine water (HOCl) or hypochloric acid and hydrochloric (HCl) acids. A mixture of Chlorine and ammonia gas, reacts to form chloramine gas. In the presence of water, chloramines decompose to form ammonia and hypochlorous acid or hydrochloric acid. Due to the affinity of chloramine for water, chloramine exposures result in rapid symptom development. The exact mechanisms by which the effects of chlorine gas poisoning are induced upon bodily systems are complex and poorly understood. The mechanisms of the biological activity of chlorine gas poisoning are not fully understood. The anatomic site of injury varies, depending on the produced chemical species. Hydrochloric acid is more souble in water than chlorine gas. Hydrochloric acid primarily target the upper respiratory mucous membranes and the epithelia of the ocular conjunctivae. Hypochlorous acid have a similar injury pattern with hydrochloric acid and more soluble in water than hydrochloric acid. The concentration of the inhaled gas, duration of exposure, water contents of the tissues exposed and individual susceptibility play a crucial role on the fatality of exposure. Acute inflammation of the conjunctivae, pharynx, nose, trachea and bronchi are immediate effects of chlorine gas poisoning. Chlorine gas poisoning poses severe pathological threats. The pathological effects of the poisoning includes Pneumonia, Pulmonary edema, Pneumonitis, Multiple pulmonary thrombosis and Ulcerative tracheobronchitis but the hallmark of the pathological effects is "pulmonary edema", clinically manifested as "dyspnea", hypoxia and adventitious lung sounds.Cite error: A <ref> tag is missing the closing </ref> (see the help page).

Etiology

Occupational exposures constitute the highest risk of toxicity and common domestic exposures result from the mixing of chlorine bleach with acidic washing agents such as acetic, nitric and phosphoric acid. They also occur as a result of the chlorination of table water. Other exposure risks occur during industrial or transportation accidents. Wartime exposure is rare.

Epidemology

In 2011, the annual report of the American Association of Poison Control Centers' National Poison Data System confirmed that the United States has the highest exposure to chlorine gas. It reported that "3,988 exposures to chlorine gas, 1,524 single exposures to chlorine gas when household acid is mixed with hypochlorite, and 701 single exposures to chloramine gas". On July 26, 2015, it was reported that 14 people died and several others were injured from a chlorine gas explosion in Nigeria. Globally, it constitutes a major cause of toxic release incidents.

references

1. http://www.ncbi.nlm.nih.gov/pubmed/439544
2. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2908650/
3. Crandall ED, Mathew SJ, Fleischer RS, Winter HI, Bidani A (1981). "Effects of inhibition of RBC HCO₃/Cl exchange on CO2 excretion and downstream pH disequilibrium in isolated rat lungs". J. Clin. Invest. 68 (4): 853–62. doi:10.1172/JCI110340. PMC 370872. PMID 6793631.{{cite journal}}: CS1 maint: multiple names: authors list (link)
4. Nigen AM, Manning JM, Alben JO (25 June 1980). "Oxygen-linked binding sites for inorganic anions to hemoglobin". J. Biol. Chem. 255 (12): 5525–9. PMID 7380825.{{cite journal}}: CS1 maint: multiple names: authors list (link)
5. http://www.ncbi.nlm.nih.gov/books/NBK236056/
6. http://www.atsdr.cdc.gov/MMG/MMG.asp?id=198&tid=36
7. http://misc.medscape.com/pi/iphone/medscapeapp/html/A820779-business.html
8. http://www.ncbi.nlm.nih.gov/pubmed/3303382
9. http://m.tih.sagepub.com/content/9/3/439.refs
10. http://www.ncbi.nlm.nih.gov/pubmed/3789518
11. Smil, Vaclav (2004-04-01). Enriching the Earth: Fritz Haber, Carl Bosch, and the Transformation of World Food Production. p. 226. ISBN 978-0-262-69313-4.
12. "Battle of Ypres" The Canadian Encyclopedia
13. "Weapons of War: Poison Gas". First World War.com. Retrieved 2007-08-12.
14. "The element, a visual exploration". Google books. Retrieved July 27, 2015.
15. https://books.google.co.uk/books?id=w06jNbLXFZgC&pg=PA134&lpg=PA134&dq=Jones+RN,+Hughes+JM,+Glindmeyer+H,+Weill+H.+Lung+function+after+acute+chlorine+exposure&source=bl&ots=byMAI8K7e3&sig=8gcHdH1ggs4y84k8bvYcoO9JsJU&hl=en&sa=X&ved=0CBYQ6AEwBWoVChMI_KrOh5T6xgIVxbwUCh0a5w5c
16. https://books.google.co.uk/books?id=Yc0RBwAAQBAJ&pg=PA127&lpg=PA127&dq=Jones+RN,+Hughes+JM,+Glindmeyer+H,+Weill+H.+Lung+function+after+acute+chlorine+exposure&source=bl&ots=k8-HE1DGL1&sig=DnuYEkskB9I_hvr9QmaJX26jzM8&hl=en&sa=X&ved=0CBsQ6AEwB2oVChMI_KrOh5T6xgIVxbwUCh0a5w5c
17. http://www.ncbi.nlm.nih.gov/books/NBK208283/
18. http://www.cdc.gov/healthywater/swimming/data/mmwr-pool-chemicals.html
19. http://www.ncbi.nlm.nih.gov/pubmed/17851445
20. http://www.ncbi.nlm.nih.gov/pubmed/23272763
21. http://www.thisdaylive.com/articles/14-dead-scores-injured-as-chlorine-gas-explodes-in-jos/215656/

• Toxic effects of substances chiefly nonmedicinal as to source
• Gases
• Medical emergencies
• Suicide methods
• Industrial hygiene