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HACH MONOCHLOR F REAGENT MSDS报告[下载][中文版]

Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

HACH MONOCHLOR F REAGENT

NFPA

Flammability 1
Toxicity 2
Body Contact 3
Reactivity 1
Chronic 3
SCALE: Min/Nil=0 Low=1 Moderate=2 High=3 Extreme=4

PRODUCT USE

Used for the determination of monochloramine and ammonia.

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

Harmful by inhalation.
Contact with acids liberates very toxic gas.
Causes burns.
Risk of serious damage to eyes.
May cause SENSITIZATION by skin contact.
May cause long- term adverse effects in the environment.

POTENTIAL HEALTH EFFECTS

ACUTE HEALTH EFFECTS

SWALLOWED

  The material can produce chemical burns within the oral cavity and gastrointestinal tract following ingestion.  Ingestion of alkaline corrosives may produce burns around the mouth, ulcerations and swellings of the mucous membranes, profuse saliva production, with an inability to speak or swallow. Both the esophagus and stomach may experience burning pain; vomiting and diarrhea may follow. Epiglottal swelling may result in respiratory distress and asphyxia; shock can occur. Narrowing of the esophagus, stomach or stomach valve may occur immediately or after a long delay (weeks to years). Severe exposure can perforate the esophagus or stomach leading to infections of the chest or abdominal cavity, with low chest pain, abdominal stiffness and fever. All of the above can cause death.  Accidental ingestion of the material may be harmful; animal experiments indicate that ingestion of less than 150 gram may be fatal or may produce serious damage to the health of the individual.  Salts of tartaric acid (including Rochelle salt and Seidlitz powder) and the acid itself have all produced serious poisonings or fatalities in man. Gastrointestinal symptoms are marked and include violent vomiting, diarrhea, abdominal pain and thirst followed by cardiovascular collapse and/or kidney failure.  

EYE

  The material can produce chemical burns to the eye following direct contact. Vapors or mists may be extremely irritating.  If applied to the eyes, this material causes severe eye damage.  Direct eye contact with corrosive bases can cause pain and burns. There may be swelling, epithelium destruction, clouding of the cornea and inflammation of the iris. Mild cases often resolve; severe cases can be prolonged with complications such as persistent swelling, scarring, permanent cloudiness, bulging of the eye, cataracts, eyelids glued to the eyeball and blindness.  

SKIN

  The material can produce chemical burns following direct contactwith the skin.  Skin contact with alkaline corrosives may produce severe pain and burns; brownish stains may develop. The corroded area may be soft, gelatinous and necrotic; tissue destruction may be deep.  Entry into the blood-stream, through, for example, cuts, abrasions or lesions, may produce systemic injury with harmful effects. Examine the skin prior to the use of the material and ensure that any external damage is suitably protected.  

INHALED

  Inhalation of dusts, generated by the material, during the course of normalhandling, may be harmful.  The material can cause respiratory irritation in some persons. The body's response to such irritation can cause further lung damage.  Inhaling corrosive bases may irritate the respiratory tract. Symptoms include cough, choking, pain and damage to the mucous membrane. In severe cases, lung swelling may develop, sometimes after a delay of hours to days. There may be low blood pressure, a weak and rapid pulse, and crackling sounds.  

CHRONIC HEALTH EFFECTS

  Skin contact with the material is more likely to cause a sensitization reaction in some persons compared to the general population.  Limited evidence suggests that repeated or long-term occupational exposure may produce cumulative health effects involving organs or biochemical systems.  There is some evidence that human exposure to the material may result in developmental toxicity. This evidence is based on animal studies where effects have been observed in the absence of marked maternal toxicity, or at around the same dose levels as other toxic effects but which are not secondary non-specific consequences of the other toxic effects.  Chronic intoxication with ionic bromides, historically, has resulted from medical use of bromides but not from environmental or occupational exposure; depression, hallucinosis, and schizophreniform psychosis can be seen in the absence of other signs of intoxication. Bromides may also induce sedation, irritability, agitation, delirium, memory loss, confusion, disorientation, forgetfulness (aphasias), dysarthria, weakness, fatigue, vertigo, stupor, coma, decreased appetite, nausea and vomiting, diarrhoea, hallucinations,  an acne like rash on the face, legs and trunk, known as bronchoderma (seen in 25-30% of case involving bromide ion), and a profuse discharge from the nostrils (coryza). Ataxia and generalised hyperreflexia have also been observed. Correlation of neurologic symptoms with blood levels of bromide is inexact. The use of substances such as brompheniramine, as antihistamines, largely reflect current day usage of bromides; ionic bromides have been largely withdrawn from therapeutic use due to their toxicity. Several cases of foetal abnormalities have been described in mothers who took large doses of bromides during pregnancy.  Repeated or prolonged exposure to corrosives may result in the erosion of teeth, inflammatory and ulcerative changes in the mouth and necrosis (rarely) of the jaw. Bronchial irritation, with cough, and frequent attacks of bronchial pneumonia may ensue. Gastrointestinal disturbances may also occur. Chronic exposures may result in dermatitis and/or conjunctivitis.  Long term exposure to high dust concentrations may cause changes in lung function i.e. pneumoconiosis; caused by particles less than 0.5 micron penetrating and remaining in the lung. Prime symptom is breathlessness; lung shadows show on X-ray.  Chronic exposure to cyanides and certain nitriles may result in interference to iodine uptake by thyroid gland and its consequent enlargement. This occurs following metabolic conversion of the cyanide moiety to thiocyanate. Thyroid insufficiency may also occur as a result of metabolic conversion of cyanides to the corresponding thiocyanate. Exposure to small amounts of cyanide compounds over long periods are reported to cause loss of appetite, headache, weakness, nausea, dizziness, abdominal pain, changes in taste and smell, muscle cramps, weight loss, flushing of the face, persistent runny nose and irritation of the upper respiratory tract and eyes. These symptoms are not specific to cyanide exposure and therefore the existence of a chronic cyanide toxicity remains speculative. Repeated minor contact with cyanides produce a characteristic rash with itching, papules (small, superficial raised spots on the skin) and possible sensitization. Concerns have been expressed that low-level, long term exposures may result in damage to the nerves of the eye.  Repeated or prolonged exposure with local anesthetics may result in sensitization of skin,  with the development of lesions, hives and edema. There may be anaphylactic reactions that may cause death. Prolonged eye contact may result in permanent clouding of the cornea with loss of vision, severe corneal inflammation and possible perforation.  
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