WATERWAY-305
Flammability | 1 | |
Toxicity | 3 | |
Body Contact | 3 | |
Reactivity | 2 | |
Chronic | 3 | |
SCALE: Min/Nil=0 Low=1 Moderate=2 High=3 Extreme=4 |
Water treatment chemical.
Contact with combustible material may cause fire.
Harmful by inhalation.
Toxic if swallowed.
Causes burns.
Risk of serious damage to eyes.
Very toxic to aquatic organisms.
Toxic effects may result from the accidental ingestion of the material; animal experiments indicate that ingestion of less than 40 gram may be fatal or may produce serious damage to the health of the individual. The material can produce chemical burns within the oral cavity and gastrointestinal tract following ingestion. Ingestion of acidic corrosives may produce burns around and in the mouth. the throat and esophagus. Immediate pain and difficulties in swallowing and speaking may also be evident. Swelling of the epiglottis may make it difficult to breathe which may result in suffocation. More severe exposure may result in vomiting blood and thick mucus, shock, abnormally low blood pressure, fluctuating pulse, shallow respiration and clammy skin, inflammation of stomach wall, and rupture of esophageal tissue. Untreated shock may eventually result in kidney failure. Severe cases may result in perforation of the stomach and abdominal cavity with consequent infection, rigidity and fever. There may be severe narrowing of the esophageal or pyloric sphincters; this may occur immediately or after a delay of weeks to years. There may be coma and convulsions, followed by death due to infection of the abdominal cavity, kidneys or lungs. Hydantoin derivatives may damage the stem cell which acts as the precursor to components of the blood and, as a result, produce blood dyscrasias. Most blood cells originate from a single pluripotent stem cell which are present in the circulating blood, but differentiates only in intact bone marrow. When the number stem cells decreases to below 10% of their normal value, pancytopenia (a reduction in the number of red and white blood cells and platelets) develops in the peripheral blood, with a latency period corresponding to the lifetime of the individual blood cells. Granulocytopenia (a reduction in granular leukocytes) develops within days and thrombocytopenia (a disorder involving platelets), within 1-2 weeks, whilst loss of erythrocytes (red blood cells) need months to become clinically manifest. The erythrocyte count reveals 0.8% loss per day, on average, following the complete stop of red blood cell formation. Aplastic anaemia develops due to complete destruction of the stem cells. Hydantoin is cardiotoxic, producing dysrhythmias or other conductance disturbances. Some hydantoin derivatives (such as phenytoin) are able to cross the placenta and are embryotoxic and/or teratogenic. Repeated or prolonged exposure to acids may result in the erosion of teeth, swelling and or ulceration of mouth lining. Irritation of airways to lung, with cough, and inflammation of lung tissue often occurs. Chronic exposure may inflame the skin or conjunctiva.
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 acid corrosives may produce pain, tears, sensitivity to light and burns. Mild burns of the epithelia generally recover rapidly and completely. Severe burns produce long-lasting and possibly irreversible damage. The appearance of the burn may not be apparent for several weeks after the initial contact. The cornea may ultimately become deeply opaque resulting in blindness.
The material can produce chemical burns following direct contactwith the skin. Skin contact is not thought to produce harmful health effects (as classified using animal models). Systemic harm, however, has been identified following exposure of animals by at least one other route and the material may still produce health damage following entry through wounds, lesions or abrasions. Good hygiene practice requires that exposure be kept to a minimum and that suitable gloves be used in an occupational setting. Open cuts, abraded or irritated skin should not be exposed to this material. Skin contact with acidic corrosives may result in pain and burns; these may be deep with distinct edges and may heal slowly with the formation of scar tissue. 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. The material may cause moderate inflammation of the skin either following direct contact or after a delay of some time. Repeated exposure can cause contact dermatitis which is characterized by redness, swelling and blistering.
If inhaled, this material can irritate the throat andlungs of some persons. Inhalation of dusts, generated by the material, during the course of normalhandling, may be harmful. Corrosive acids can cause irritation of the respiratory tract, with coughing, choking and mucous membrane damage. There may be dizziness, headache, nausea and weakness. Swelling of the lungs can occur, either immediately or after a delay; symptoms of this include chest tightness, shortness of breath, frothy phlegm and cyanosis. Lack of oxygen can cause death hours after onset.
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. 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 acids may result in the erosion of teeth, swelling and or ulceration of mouth lining. Irritation of airways to lung, with cough, and inflammation of lung tissue often occurs. Chronic exposure may inflame the skin or conjunctiva. 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.