염화질소

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

0.043 [ppm]

0.52 [ppm]

3.1 [ppm]

In this study an in vitro exposure test to investigate toxicological effects of the volatile disinfection by-product trichloramine and of real indoor pool air was established. For this purpose a set-up to generate a well-defined, clean gas stream of trichloramine was combined with biotests. Human alveolar epithelial lung cells of the cell line A-549 were exposed in a CULTEX() device with trichloramine concentrations between 0.1 and 40 mg/cu m for 1 hr. As toxicological endpoints the cell viability and the inflammatory response by the cytokines IL-6 and IL-8 were investigated. A decreasing cell viability could be observed with increasing trichloramine concentration. An increase of IL-8 release could be determined at trichloramine concentrations higher than 10 mg/cu m and an increase of IL-6 release at concentrations of 20 mg/cu m. Investigations of indoor swimming pool air showed similar inflammatory effects to the lung cells although the air concentrations of trichloramine of 0.17 and 0.19 mg/cu m were much lower compared with the laboratory experiments with trichloramine as the only contaminant. Therefore it is assumed that a mixture of trichloramine and other disinfection by-products in the air of indoor pool settings contribute to that effect.

IDENTIFICATION AND USE: Nitrogen chloride is a yellow, oily liquid, which explodes easily. It was used as a flour bleach (no longer permitted in US). It is a volatile chlorination by-product and a potent respiratory irritant present in swimming pools. HUMAN STUDIES: The most commonly reported symptoms consisted of cough, dyspnea, tearing eyes and blocked or runny nose. Airway hyperreactivity to histamine was also detected in exposed subjects. Cases of workers who developed occupational asthma following exposure to airborne nitrogen chloride in indoor chlorinated swimming pools are reported. Epidemiology studies show that lifeguards and trainers experience ocular and respiratory irritative symptoms from nitrogen chloride more frequently than employees not exposed. Cleaning and disinfecting workers in the food industry are at risk of developing eye, nasal, and throat irritation symptoms. Although nitrogen chloride exposure does not seem to carry a risk of developing permanent bronchial hyperresponsiveness (BHR), the possibility of transient BHR cannot be ruled out. Altered levels of innate immunity proteins in the upper airways of exposed individuals may pose as potential biomarkers. ANIMAL STUDIES: The expiratory bradypnea indicative of upper airway irritation in mice was evaluated during a 60-min oronasal exposure to increasing concentrations of nitrogen trichloride. The maximal response of nitrogen trichloride was reached in 10 min. In rats pulmonary edema appears to contribute significantly to mortality produced by inhalation of nitrogen chloride. The subchronic toxicity of 0.2-90 ppm nitrogen chloride in the drinking water of rats was investigated using biochemical, hematological, and histopathological parameters. Nitrogen chloride at level of >2 ppm induced adaptive histopathological changes in thyroids and kidneys of animals of both sexes.

/EPIDEMIOLOGY STUDIES/ BACKGROUND: Several members of a swimming club complained of respiratory symptoms associated with attending a municipal indoor swimming pool. Trichloramine, a volatile chlorination by-product and a potent respiratory irritant, was the most probable culprit, but the exact cause for its presence in excessive concentrations remained elusive. METHODS: Twenty-two competitive swimmers and six coaches were evaluated during the outbreak and nine swimmers and four coaches were re-evaluated one year later. Symptoms were recorded by non-standardized history taking; pulmonary function testing included spirometry, measurement of fraction of exhaled nitric oxide (FENO) and histamine provocation. Concentrations of trichloramine in air were measured repeatedly by the method of Hery. RESULTS: The most commonly reported symptoms consisted of cough (n=16), dyspnea (n=13), tearing eyes (n=10) and blocked or runny nose (n=6). Mean FEV1% predicted was 109.1%. Mean FENO level was 19.7 ppb (higher than 25 ppb in 3 subjects). Airway hyperreactivity to histamine (PC20 = 8 mg/mL) was detected in 22/26 subjects. Measured trichloramine concentrations in air exceeded the maximal concentration (WHO) of 0.5 mg/cu m four times between May and October 2011 and four times between January and March 2012. Polyamine compounds, present in glue used for repairing pipework, were identified as a probable external source of nitrogen resulting in increasing trichloramine concentrations. After the removal of the presumed cause of the excessive trichloramine concentrations, most subjects improved clinically, but several subjects remained symptomatic and had bronchial hyperreactivity. DISCUSSION: A high prevalence of airway hyperreactivity, accompanied by symptoms of upper and lower airways, was detected in swimmers who had been repeatedly exposed to high trichloramine concentrations. A glue containing polyamines, used to repair a pipework, was suspected to be the source of this excessive production of trichloramine.

/EPIDEMIOLOGY STUDIES/ Ten indoor swimming pools in Taipei, Taiwan were included in the study to assess the exposure of people to airborne trichloramine (NCl3) and also to discover the factors that might affect the associated concentrations. An active air sampling method was performed to determine the levels of NCl3, while questionnaires were administered to swimming pool workers, including lifeguards, swimming instructors, and management employees. The results show that the concentrations of trichloramine ranged from 0.017 to 0.15 mg/cu m, which were generally lower than what have been reported from other studies. Symptoms of sore throat and phlegm were more frequent among lifeguards and swimming instructors (exposure group) than management employees (reference group) (odds ratios were 11.28 and 4.22 for sore throat and phlegm, respectively). It seems that the current exposure limit for airborne NCl3, which was recommended by WHO, was not lower enough to protect the health of pool attendants. Regulated level of free available chlorine in Taipei (i.e., 0.3-0.7 ppm) is lower than what is required in other countries (e.g., 1-3 ppm in the UK). This might be the main reason why the concentrations of NCl3 reported elsewhere were higher than what were found in this research. Further international comparisons will help to elucidate if low free chlorine concentration should be adopted as an operating standard. For the indoor swimming pools in Taipei, the air quality is suggested to be improved, since even with the low concentrations of NCl3, higher respiratory ailments among pool workers were observed.

/LABORATORY ANIMALS: Acute Exposure/ The expiratory bradypnoea indicative of upper airway irritation in mice was evaluated during a 60-min oronasal exposure to increasing concentrations of chlorine and nitrogen trichloride. The airborne concentration resulting in a 50% decrease in the respiratory rate of mice (RD50) was calculated for each chemical. Chlorine and nitrogen trichloride showed dissimilar concentration-response curves. While the maximal response of nitrogen trichloride was reached in 10 min, the maximal response of chlorine was reached between 45 and 60 min of exposure. The results showed both chemicals to have an irritant potency of the same order of magnitude. The RD50 values of chlorine and nitrogen trichloride were 3.5 and 2.5 ppm, respectively. On the basis of a TLV-STEL (threshold limit value for short-term exposure limit) equal to 0.1 RD50 and a TLV-TWA (time-weighted average) equal to 0.03 RD50, the current TLVs for chlorine seem too high (1 and 0.5 ppm, respectively) and should be reduced to 0.5 and 0.1 ppm, respectively. For nitrogen trichloride, 0.3 ppm and 0.1 ppm are proposed as TLV-STEL and TLV-TWA, respectively.

/LABORATORY ANIMALS: Acute Exposure/ The LC50 of nitrogen trichloride (NCl3) was determined in rats following a one hour inhalation exposure. Five groups of 10 animals per group were exposed to a concentration range of NCl3 from 58 ppm to 157 ppm. The one hour LC50 is 112 ppm with the 95% confidence interval between 107 ppm and 117 ppm. All mortality occurred during or within one day following the exposure. Gross necropsy of the animals which died as a result of exposure to NCl3 showed noticeable fluid in the trachea and lungs. This was not the case for those animals which survived the exposure (gross necropsies performed 14 days post-exposure). Pulmonary edema appears to contribute significantly to mortality produced by NCl3.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ The subchronic toxicity of 0.2-200 ppm dichloramine and 0.2-90 ppm trichloramine in the drinking water of rats was investigated using biochemical, hematological, and histopathological parameters. Animals in the highest dose groups consumed 5-15% less fluid than controls with no significant decrease in body weight gain. No clinical signs of toxicity were observed in either case. Both males and females dosed with 90 ppm trichloramine had significantly increased relative kidney/body weights and the females had increased hepatic glutathione S-transferase and UPD-glucuronosyltransferase activities. No significant changes were detected in other xenobiotic metabolizing enzymes or in serum biochemistry, urine biochemistry, or hematology. Both dichloramine and trichloramine induced minimal to mild adaptive histopathological changes in thyroids and kidneys of animals of both sexes. Dichloramine, but not trichloramine, was associated with histological changes in the gastric cardia characterized by epithelial hyperplasia at concentrations of 2 ppm and above in the males and 200 ppm in the females. This study indicates that dichloramine produced mild histological effects at drinking water concentrations of >0.2 ppm in males (0.019 mg/kg/day) and >2 ppm in females (0.26 mg/kg/day) while trichloramine produced biochemical and mild histological effects at levels of >2 ppm both in males (0.23 mg/kg/day) and in females (0.29 mg/kg/day).

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. obtain medical attention. /Explosives/

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . /Explosives/

/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam (Valium) or lorazepam (Ativan) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Explosives/

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Chlorine and related compounds/

For more Antidote and Emergency Treatment (Complete) data for Nitrogen chloride (6 total), please visit the HSDB record page.

4.0E+03(G)

Volatile

Mutagen

1

0.1

4.0E+03 (G)

Volatile

Mutagen

1

0.1