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Chlorine poisoning is illness resulting from the effects of exposure to chlorine beyond the threshold limit value.

Signs and symptoms

The signs of acute chlorine gas poisoning are primarily respiratory, and include difficulty breathing and cough. There may also be skin irritation or chemical burns and eye irritation or conjunctivitis. A person with chlorine gas poisoning may also have nausea, vomiting, a runny nose, or a headache.

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.

Holding 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, symptoms usually resolve themselves upon removal of exposure to the gas, 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.

Prolonged exposure to low concentration of chlorine gas may have lethal effects, as can short-term exposure to high concentrations.

Causes

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.

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.

Other exposure risks occur during industrial or transportation accidents. Wartime exposure is rare.

Mechanism

causes acute damage to the receptors in the epithelium of the respiratory tract.

Chlorine gas is non-combustible at room temperature and pressure. It is heavier than air in its pure state, causing it to remain near 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 seem difficult until irritative symptoms develop. The degree of exposure determines the lethality and severity of symptoms and rapidity of onset.

Chlorine gas dissolves in water to form chlorine water (HOCl) or hypochloric acid and HCl. Chlorine reacts with ammonia gas to produce Chloramine, commonly used as a disinfectant. Chloramine decomposes in the presence of water to produce hydrochloric acid or hypochlorous 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. HCL is more soluble in water than chlorine gas. Hydrochloric acid primarily target the upper respiratory mucous membranes and the epithelia of the ocular conjunctivae. Hypochlorous acid has a similar injury pattern to hydrochloric acid and is 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, pneumonitis, tracheobronchitis, pulmonary edema, multiple pulmonary thrombosis and ulcerative but the hallmark of the pathological effects is "pulmonary edema", clinically manifested as "dyspnea", hypoxia and adventitious lung sounds.

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.

Diagnosis

Treatment

Outcomes

Epidemiology

History

Society and culture

On July 26, 2015, it was reported that 14 people died and several others were injured from a chlorine gas explosion in Nigeria.

References

Template:Research help

1. Jones R, Wills B, Kang C. Chlorine gas: an evolving hazardous material threat and unconventional weapon. West J Emerg Med. 2010 May;11(2):151-6. PMID 20823965 PMC 2908650
2. White CW, Martin JG. Chlorine gas inhalation: human clinical evidence of toxicity and experience in animal models. Proc Am Thorac Soc. 2010 Jul;7(4):257-63. Review. PMID: 20601629 PMC 3136961
3. Agency for Toxic Substances and Disease Registry via the CDC. Medical Management Guidelines: Chlorine Page last reviewed: October 21, 2014. Page last updated: October 21, 2014
4. Gerald F O'Malley, GF et al. Chlorine Toxicity Medscape Drugs & Diseases, Ed. Dembek, ZF. Updated: Dec 11, 2015
5. Squadrito GL, Postlethwait EM, Matalon S. Elucidating mechanisms of chlorine toxicity: reaction kinetics, thermodynamics, and physiological implications. Am J Physiol Lung Cell Mol Physiol. 2010 Sep;299(3):L289-300. Review. PMID 20525917 PMC 2951076

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