ZINC DITHIONITE
Flammability | 0 | |
Toxicity | 2 | |
Body Contact | 2 | |
Reactivity | 1 | |
Chronic | 2 | |
SCALE: Min/Nil=0 Low=1 Moderate=2 High=3 Extreme=4 |
Reducing agent. Brightening groundwood, kraft and other paper pulps; treatment of beet and
cane sugar juices; depressant in mining flotations, bleaching textiles, vegetable oils,
straw, hemp, vegetable tannins, animal glues. As reducing agent, particularly in dyeing
with indigo and vat dyes. Used as a bleach, for soap, straw; removing dyes from dyed
fabric. Part of a redox catalyst system for synthetic rubber production. Oxygen scavenger
in water treatment, reduction of metals in waste treatment.
O4-S2-Zn, ZnS2O4, "zinc hydrosulphite", "zinc hydrosulfite"
Contact with acids liberates toxic gas.
Irritating to eyes, respiratory system and skin.
Accidental ingestion of the material may be damaging to the health of the individual.
This material can cause eye irritation and damage in some persons.
This material can cause inflammation of the skin oncontact in some persons. The material may accentuate any pre-existing dermatitis condition. Skin contact is not thought to have harmful health effects, however the material may still produce health damage following entry through wounds, lesions or abrasions. Open cuts, abraded or irritated skin should not be exposed to this material. 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.
Inhalation may produce health damage*. The material can cause respiratory irritation in some persons. The body's response to such irritation can cause further lung damage. Inhalation of dusts, generated by the material during the course of normal handling, may be damaging to the health of the individual. Persons with impaired respiratory function, airway diseases and conditions such as emphysema or chronic bronchitis, may incur further disability if excessive concentrations of particulate are inhaled. Sulfur dioxide irritation probably results from the action of sulfurous acid as the highly soluble gas dissolves in mucous fluid. Short-term exposure causes bronchoconstriction measurable as an increase in flow-resistance. The magnitude is concentration-dependent.. Chief effects are upper respiratory tract irritation and severe acute exposure may cause oedema of the lungs and possible respiratory paralysis. These exposures have produced severe obstructive and restrictive defects up to 3 months post-exposure; these have failed to respond to bronchodilators. Such exposures have also, on rare occasions, been associated with moderately severe obstructive illness and persistent, productive cough. Systemic effects of acute poisoning are not known but regular exposure may deaden the sense of smell. Symptoms include throat irritation, coughing, tightness of chest, difficulty with breathing, tear formation (lachrymation), eye smarting and suffocating feeling. Substantial exposures produce direct respiratory tract irritation, cough, burning, lachrymation, conjunctival injection, difficulty in swallowing, and otopharyngeal erythema. Other symptoms may include vomiting, diarrhoea, abdominal pain, fever, headache, vertigo, agitation, tremor, convulsions, and peripheral neuritis. High dose acute exposure may produce immediate bronchospasm and pulmonary oedema with respiratory failure/ paralysis, inflammation of the conjunctivae and inflammation of the tongue.
Long-term exposure to respiratory irritants may result in disease of the airways involving difficult breathing and related systemic problems. Limited evidence suggests that repeated or long-term occupational exposure may produce cumulative health effects involving organs or biochemical systems. 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. Repeated exposure of animals to airborne sulfur dioxide (SO2) can produce a thickening of the mucous layer in the trachea and an increase in goblet cells and mucous glands similar to pathological changes found in chronic human bronchitis. Chronic exposure to sulfur dioxide (SO2) particulate complexes, present in polluted air, have been associated with the aggravation of chronic cardiovascular diseases such as asthma, chronic pulmonary disease, and coronary artery disease (this may occur at levels of 6-10 ug/m3 for 24 hours), An association exists between persistent cough and sputum production, particularly in women and non-smokers. A 10-year follow study on workers exposed to a mean sulfur dioxide concentration of up to 33 ppm did not reveal an increased prevalence of chronic respiratory disease or decreased pulmonary function. By contrast, studies of smelter workers, exposed to concentrations below 2 ppm, suggest that chronic respiratory disease may develop and that workers exposed at concentrations exceeding 1 ppm show accelerated loss of pulmonary function. Although SO2 is not a carcinogen, the apparent increases in mortalities amongst arsenic- exposed smelter workers was greater when exposures included both high arsenic concentrations and moderate to high SO2 exposures, suggesting that SO2 might act as a promoter. Intermittent exposure of rats to benz[a]pyrene along with inhalation of SO2 at 4-10 ppm, 1-6 hours per day, 5 days per week, produced substantial increases in respiratory tract squamous cell carcinomas compared to that associated with exposure to B[a]P or SO2 alone. Sulfites and bisulfites can cause narrowing of the airways, stomach upset, flushing, low blood pressure. tingling sensation, itchy wheal, swelling and shock, and asthmatics are especially prone. They induce allergic-like reactions which can occur on first contact with the material.