Chlorine gas poisoning
| Chlorine poisoning | |
|---|---|
| Classification and external resources | |
| Specialty | Emergency medicine |
| ICD-10 | T59.4 |
Chlorine gas poisoning is illness resulting from the effects of exposure to chlorine beyond the threshold limit value.
The signs of acute chlorine gas poisoning are primarily respiratory, and include difficulty breathing and cough; listening to the lungs will generally reveal crackles. There will generally be sneezing, nose irritation, and throat irritation. 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, or a headache.
Chronic exposure to relatively low levels of chlorine gas may cause pulmonary problems like acute wheezing attacks, chronic cough with phlegm, and asthma.
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.
Humans can smell chlorine gas at ranges from 0.1–0.3 ppm. According to a review from 2010: "At 1–3 ppm, there is mild mucus membrane irritation that can usually be tolerated for about an hour. At 5–15 ppm, there is moderate mucus membrane irritation. At 30 ppm and beyond, there is immediate chest pain, shortness of breath, and cough. At approximately 40–60 ppm, a toxic pneumonitis and/or acute pulmonary edema can develop.... Concentrations of about 400 ppm and beyond are generally fatal over 30 minutes, and at 1,000 ppm and above, fatality ensues within only a few minutes."
The concentration of the inhaled gas and duration of exposure and water contents of the tissues exposed are the key determinants of toxicity; moist tissues like the eyes, throat, and lungs are the most susceptible to damage.
Once inhaled, chlorine gas diffuses into the epithelial lining fluid (ELF) of the respiratory epithelium and may directly interact with small molecules, proteins and lipids there and damage them, or may hydrolyze to hypochlorous acid and hydrochloric acid which in turn generate chloride ions and reactive oxygen species; the dominant theory is that most damage is via the acids.
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