Chlorine respiratory toxicity

The interplay between the chemical and biological properties of the threat agent, on the one hand, and the specific attack scenario, on the other, can influence the lethality of the attack. Table 2-2 shows the relative respiratory toxicities (expressed as the lethal concentration of toxin at which 50 percent of test animals are killed, or LCT50, in milligrams per minute per cubic meter) of a variety of toxic gases compared with chlorine gas, which was used as a chemical weapon in World War I. According to Table 2-2, the nerve agent sarin (GB) has a respiratory toxicity approximately 100 times that of chlorine, while sulfur mustard (HD) is about 7 times more toxic. However, the lethality of an attack... 

Upper respiratory toxicants include hydrogen halides (hydrogen chloride, hydrogen bromide), oxides (nitrogen oxides, sulfur oxides, sodium oxide), and hydroxides (ammonium hydroxide, sodium dusts, and potassium hydroxides). Lower respiratory toxicants include monomers (such as acrylonitrile), halides (fluorine, chlorine, bromine), and other miscellaneous... 

Shroff, C.P., M.V.Khade, and M.Srinivasan. 1988. Respiratory cytopathology in chlorine gas toxicity A study in 28 subjects. Diagn. Cytopathol. 4(1) 28—32. 

The toxic action of bromine is similar to that of chlorine and can cause physiological damage to humans through inhalation and oral routes. It is an irritant to the mucous membranes of the eyes and upper respiratory tract. Severe exposures may result in pulmonary edema. Chronic exposure is similar to therapeutic ingestion of excessive bromides. 

PHMB is very toxic to fish and aquatic life. It is moreover irritating to skin and may cause sensitization by skin contact. It can cause irritation to the eyes, nose and respiratory tract. The PHMB is not compatible with most common swimming pool chemicals. Not compatible with chlorine and chlorinated chemicals and bromine donors. Not compatible with ionic sterilizers, copper based QAC-algicides, anionic detergents, water softening chemicals, persulfate oxidants etc. The defence of the inventors of PHMB is that one should not combine it with other biocides because it should be a bactericide/algicide. But the algicidal properties of PHMB are very weak in brochures and manuals the dose is 200 ppm. 

Animal studies also indicate that the respiratory system is a major target of toxicity following inhalation exposure to chlorine dioxide. Dalhamn (1957) reported the results of several inhalation studies in laboratory animals. In one study, a single 2-hour inhalation exposure of four rats to a chlorine dioxide concentration of 260 ppm (728 mg/m ) resulted in pulmonary edema and nasal bleeding. Respiratory distress was reported in three other rats subjected to 3 weekly 3-minute exposures to decreasing concentrations of airborne chlorine dioxide from 3,400 to 800 ppm (from 9,520 to 2,240 mg/m ) bronchopneumonia was observed in two of these rats. In a third rat study, repeated exposure to approximately 10 ppm (28 mg/m ) of chlorine dioxide (4 hours/day for 9 days in a 13-day period) resulted in rhinonhea, altered respiration, and respiratory infection. No indications of adverse effects were seen in rats exposed to approximately 0.1 ppm (0.28 mg/m ) of chlorine dioxide 5 hours /day for 10 weeks. 

EPA (IRIS 2002) has derived an RPC of 2x10 " mg/m for chlorine dioxide based on a LOAEL of 2.76 mg/m (1 ppm) for respiratory effects (peribronchiolar edema and vascular congestion in the lungs) in rats exposed to chlorine dioxide vapors 5 hours/day, 5 days/week for 2 months (Paulet and Desbrousses 1972). The LOAEL was converted to a LOAEL hec of 0.64 mg/m and divided by an uncertainty factor of 3,000 (10 for extrapolation of a chronic RPC from a subchronic study, 3 for interspecies extrapolation using dosimetric adjustments, 10 for intrahuman variability, and 10 to account for extrapolation from a LOAEL for mild effects and for the lack of inhalation developmental and reproductive toxicity studies). 

Toxic or potentially toxic agents may be inhaled into the respiratory tract where they may cause localized effects such as irritation (e.g., ammonia, chlorine gas), inflammation, necrosis, and cancer. Chemicals may also be absorbed by the lungs into the circulatory system, thereby leading to systemic toxicity (e.g., CO, lead). 

Among the many toxicants that cause convulsions are chlorinated hydrocarbons, amphetamines, lead, organophosphates, and strychnine. There are several levels of coma, the term used to describe a lowered level of consciousness. At level 0, the subject may be awakened and will respond to questions. At level 1, withdrawal from painful stimuli is observed and all reflexes function. A subject at level 2 does not withdraw from painful stimuli, although most reflexes still function. Levels 3 and 4 are characterized by the absence of reflexes at level 4, respiratory action is depressed and the cardiovascular system fails. Among the many toxicants that cause coma are narcotic analgesics, alcohols, organophosphates, carbamates, lead, hydrocarbons, hydrogen sulfide, benzodiazepines, tricyclic antidepressants, isoniazid, phenothiazines, and opiates. 

Bromine is toxic when inhaled or ingested. Like chlorine and fluorine, it is an irritant to the respiratory tract and eyes because it attacks their mucous membranes. Pulmonary edema may result from severe bromine poisoning. The severely irritating nature of bromine causes a withdrawal response in its presence, thereby limiting exposure. 

Inhaled chlorine is predominantly retained in the upper respiratory tract (Nodelman and Ultman 1999a, b), and is a known irritant. At low doses (<2.5 ppm for up to 2 h), approximately 95% of chlorine is effectively scrubbed in the upper respiratory tract. At higher concentrations, it reaches the lungs and can exert toxic effects (EPA 1994). 

There are no animal toxicity studies specifically on dermal exposure to chlorine gas, but most of the inhalation studies involved whole-body exposures. Those studies reported irritation of the mucous membranes of the respiratory tract and the eyes. 

Additional studies on the toxicity of chlorine in experimental animals are needed to better define the health effects of exposure at concentrations of 0.5—4 ppm, 24 h/d for up to 10 d. These studies should include evaluation of short-term effects, on pulmonary function and on long-term effects such as inflammation of the respiratory tract and pulmonary fibrosis. Studies are also needed on the interactive effects of chlorine with other gases found in disabled submarines. 

SAFETY PROFILE A human poison by ingestion and moderately toxic by inhalation. A poison by ingestion and inhalation experimentally. Corrosive. The action of bromine is essentially the same as that of chlorine, irritating the mucous membranes of the eyes and upper respiratory tract. Severe exposure may result in pulmonary edema. Usually, however, the irritant qualities of the chemical force the worker to leave the exposure area before serious poisoning can result. Chronic exposure is similar to the therapeutic ingestion of excessive bromides. See also BROMIDES. Regular physical examinations should be made of people who work with bromine or bromides. Flammable in the form of liquid or vapor by spontaneous chemical reaction with reducing materials. A... 

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