Inhalation of chlorine

In the nine deaths listed above, it should be noted and understood that all nine persons died from inhaling chlorine gas. They may have had other injuries, but the cause of death was inhalation of chlorine gas. 

Ploysongsang Y et al Pulmonary function changes after acute inhalation of chlorine gas. Southern Med J 7 5-.2 i-26, 1982... 

Information regarding respiratory effects in orally-exposed animals is limited to a report of a significantly increased incidence of nasal lesions (goblet cell hyperplasia and inflammation of nasal turbinates) following 90 days of exposure to chlorine dioxide in the drinking water at concentrations that resulted in estimated doses as low as 2 mg/kg/day in males and 8 mg/kg/day in females (Daniel et al. 1990). These nasal effects were likely caused by inhalation of chlorine dioxide vapors released from the water rather than a systemic respiratory effect following oral exposirre. 

During the latter half of World War I and the early postwar years, there was serious concern that men poisoned by inhalation of chlorine, phosgene, and mustard (the three most common and deadly agents) would develop tuberculosis and cancer. Limited studies were begun, but it proved difficult to produce evidence to support the idea. Achard, Wilson and Mackintosh,Sergent and Haas,6 ... 

Demnati, R., R.Fraser, H.Ghezzo, J.G.Martin, G.Plaa, and J.L.Malo. 1998. Time-course of functional and pathological changes after a single high acute inhalation of chlorine in rats. Eur. Respir. J. 11(4) 922—928. 

Schwartz, D.A., D.D.Smith, and S.Lakshminarayan. 1990. The pulmonary sequelae associated with accidental inhalation of chlorine gas. Chest 97(4) 820-825. 

Corticosteroid use is controversial. Animal models have shown positive results in hastening recovery from severe chlorine gas poisoning however, administration to humans has not been shown to provide any significant change (Traub et al, 2002). Wang et al (2004) demonstrated that pigs exposed to chlorine gas responded better to a combination of aerosolized bronchodilators and corticosteroids (terbu-taline, budesonide) than to either therapy alone. Sheep nebulized with 4% sodium bicarbonate had decreased mortality and improved oxygenation after inhalation of chlorine gas (Chisholm et al, 1989). 

Exposures to single toxic chemicals in and around the house produce many well-known identifiable effects in people. An example of such an effect is respiratory irritation following inhalation of chlorine bleach fumes. Often, individuals develop clinical symptoms that are associated with mixtures of chemicals, for example, headache and dizziness following inhalation of paint fumes containing toluene and glycol ethers. 

Inhalation of chlorine and hexane vapors can occur if special care is not exercised. 

In December 1993, the Chemical Industry Institute of Toxicology issued its report on a study on the chronic inhalation of chlorine in rats and mice. Rats and mice were exposed to chlorine gas at 0.4, 1.0 or 2.5 ppm for up to 6 hours a day and 3-5 days/week for up to 2 years. There was no evidence of cancer. Exposure to chlorine at all levels produced nasal lesions. Since rodents are obligatory nasal breathers, how these results should be interpreted for humans is not clear [5]. 

Wegman DH, Peters JM, Boundy MG et al (1982) Evaluation of respiratory effects in miners and millers exposed to talc free of asbestos and silica. Br J Ind Med 39 233-238 Wells IP, Bhatt RCV, Flanagan M (1985) Kaolinosis a radiological review. Clin Radiol 36 579-582 Williams JG (1997) Inhalation of chlorine gas. Postgrad Med J 73 697-700... 

Toxicity of Chlorine Sanitizers. Chlorine-based swimming-pool and spa and hot-tub sanitizers irritate eyes, skin, and mucous membranes and must be handled with extreme care. The toxicities are as follows for chlorine gas, TLV = 1 ppm acute inhalation LC q = 137 ppm for 1 h (mouse) (75). The acute oral LD q (rats) for the Hquid and soHd chlorine sanitizers are NaOCl (100% basis) 8.9 g/kg (76), 65% Ca(OCl)2 850 mg/kg, sodium dichloroisocyanurate dihydrate 735 mg/kg, and trichloroisocyanuric acid 490 mg/kg. Cyanuric acid is essentially nontoxic based on an oral LD q > 20 g/kg in rabbits. Although, it is mildly irritating to the eye, it is not a skin irritant. A review of the toxicological studies on cyanuric acid and its chlorinated derivatives is given in ref. 77. 

The threshold limit value—time integrated average, TLV—TWA, of chlorine dioxide is 0.1 ppm, and the threshold limit value—short-term exposure limit, STEL, is 0.3 ppm or 0.9 mg /m of air concentration (87,88). Chlorine dioxide is a severe respiratory and eye irritant. Symptoms of exposure by inhalation include eye and throat irritation, headache, nausea, nasal discharge, coughing, wheezing, bronchitis, and delayed onset of pulmonary edema. Delayed deaths occurred in animals after exposure to 150—200 ppm for less than one hour. Rats repeatedly exposed to 10 ppm died after 10 to 13 days of exposure. Exposure of a worker to 19 ppm for an unspecified time was fatal. The ingested systemic effects of low concentration chlorine dioxide solutions are similar to that of chlorite. 

AH volatile organic solvents are toxic to some degree. Excessive vapor inhalation of the volatile chloriaated solveats, and the central nervous system depression that results, is the greatest hazard for iadustrial use of these solvents. Proper protective equipment and operating procedures permit safe use of solvents such as methylene chloride, 1,1,1-trichloroethane, trichloroethylene, and tetrachloroethylene ia both cold and hot metal-cleaning operations. The toxicity of a solvent cannot be predicted from its chlorine content or chemical stmcture. For example, 1,1,1-trichloroethane is one of the least toxic metal-cleaning solvents and has a recommended threshold limit value (TLV) of 350 ppm. However, the 1,1,2-trichloroethane isomer is one of the more toxic chloriaated hydrocarboas, with a TLV of only 10 ppm. 

Human incidents have been reported in workers involved in the production or uses of PCNs. In the United States as well as in Germany and Austraha, the severity of the PCN-induced toxicosis was higher after exposure to the higher chlorinated PCN mixtures. In humans the inhalation of hot vapors was the most important route of exposure and resulted in symptoms including rashes or chloracne, jaundice, weight loss, yellow atrophy of the hver, and in extreme cases, death (75,77—79). 

Some authorities question whether dmnkeimess can result from the inhalation of ethyl alcohol vapors. Experience has demonstrated that in any event such intoxication is indeed rare (281). There is no concrete evidence that the inhalation of ethyl alcohol vapor will cause cirrhosis. Liver function is definitely impaired during alcohol intoxication (282), making the subject more susceptible to the toxic effects of chlorinated hydrocarbons. 

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. 

List all obvious hazards. Most processes include a number of hazards that are already fully recognized, such as the flammability of propane or the inhalation toxicity of chlorine. 

Partial what-if analyses for the two example processes described in Section 4.0 are shown in Tables 4.9 and 4.10. Although for actual, more complex analyses, the what-if tables for each line or vessel would be separate, for these examples, a single table was developed. A preliminary hazard analysis (PHA) would identify that the intrinsic hazards associated with HF are its reactivity (including reactivity with water, by solution), corrosivity (including carbon steel, if wet), toxicity via inhalation and skin contact, and environmental toxicity. The N2 supply system pressure is not considered in this example. The specific effects of loss of containment could be explicitly stated in the "loss of HF containment" scenarios identified. Similarly, the effects of loss of chlorine containment, including the reactivity and toxicity of chlorine, could be specified for the second example. 

Ocular Effects. A case-control study of office workers was conducted by Baj et al. (1994) to evaluate the risks of chronic exposures to inhaled formaldehyde, phenol and isomers of organic chlorohydrocarbons from Ksylamit which is a widely used liquid wood preservative reported to consist of a mixture of chlorinated benzenes, pentachlorophenol, alpha-chloronaphthalene, chloroparafifin, and kerosene . Twenty-two workers (18 women and 4 men) exposed for at least 6 months were the cases, and 29 non-exposed, non-smoking volunteers matched for age, sex, and place of residence were the controls. The authors indicate that all of the exposed workers developed chronic complaints, among them burning eyes, but that no remarkable increase in morbidity was found during the 6 months of exposure to Ksylamit , nor during the 3-year follow-up study (details of which were not provided). The authors attribute these symptoms to the irritant effect of the inhaled Ksylamit probably (based on the references provided) due to the formaldehyde vapor they assert emanates from the woodpreserving liquid. 

Horn HJ, Weir RJ Inhalation toxicology of chlorine trifluoride. I. Acute and subacute toxicity. AMA Arch Ind Health 12 515-521, 1955... 

A chronic-duration inhalation MRL was not derived for chlorine dioxide because chronic inhalation exposure studies in humans or animals are not available. An approach using an uncertainty factor for extrapolating from intermediate- to chronic-duration exposure was not used because it is not known whether respiratory irritation, observed during intermediate-duration inhalation exposure to chlorine dioxide, might result in more persistent effects in cases of chronic-duration exposure. Furthermore, it is not likely that humans would be chronically exposed to significant concentrations of chlorine dioxide vapors in environmental or occupational settings. 

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. 

Cardiovascular Effects. Infoimation regarding cardiovascular eiJects in humans following inhalation exposure to chlorine dioxide is limited to a single account of tachycardia that developed in a woman several hours after having been exposed to an unknown concentration of chlorine dioxide that had triggered respiratory effects severe enough to force her to leave the area where she had been bleaching dried flowers (Elkins 1959). The tachycardia was likely secondary to the primary respiratory effects. 

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