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HEXAMETHONIUM BROMIDE
| Flammability | 1 | |
| Toxicity | 2 | |
| Body Contact | 2 | |
| Reactivity | 0 | |
| Chronic | 3 | |
| SCALE: Min/Nil=0 Low=1 Moderate=2 High=3 Extreme=4 | ||
Reagent. Quaternary ammonium ganglion- blocking agent used as anti- hypertensive agent.
C12-H30-Br2-N2, (CH3)3N(CH2)6N(CH3)3.2Br.H2O, "alpha, omega-bis(trimethylammonium)hexane
dibromide", C-6, "hexamethionium bromide", "hexamethonium dibromide",
hexamethylenebis(trimethylammonium)bromide, "1, 6-hexadiaminium, N, N, N, N'N'-
hexamethyl-, dibromide", "1, 6-hexadiaminium, N, N, N, N'N'-hexamethyl-, dibromide",
"hexonium dibromide", Esametina, Gangliostat, HB, Hexameton, Simpatoblock, Vegolysen,
Vegolysin, "quaternary ammonium compound/ antihypertensive"
Toxic to aquatic organisms.
Although ingestion is not thought to produce harmful effects, the material may still be damaging to the health of the individual following ingestion, especially where pre- existing organ (e.g. liver, kidney) damage is evident. Present definitions of harmful or toxic substances are generally based on doses producing mortality (death) rather than those producing morbidity (disease, ill-health). Gastrointestinal tract discomfort may produce nausea and vomiting. In an occupational setting however, ingestion of insignificant quantities is not thought to be cause for concern. Considered an unlikely route of entry in commercial/industrial environments. Concentrated solutions of many cationics may cause corrosive damage to mucous membranes and the esophagus. Nausea and vomiting (sometimes bloody) may follow ingestion. Serious exposures may produce an immediate burning sensation of the mouth, throat and abdomen with profuse salivation, ulceration of mucous membranes, signs of circulatory shock (hypotension, labored breathing, and cyanosis) and a feeling of apprehension, restlessness, confusion and weakness. Weak convulsive movements may precede central nervous system depression. Erosion, ulceration, and petechial hemorrhage may occur through the small intestine with glottic, brain and pulmonary edema. Death may result from asphyxiation due to paralysis of the muscles of respiration or cardiovascular collapse. Fatal poisoning may arise even when the only pathological signs are visceral congestion, swallowing, mild pulmonary edema or varying signs of gastrointestinal irritation. Individuals who survive a period of severe hypertension may develop kidney failure. Cloudy swelling, patchy necrosis and fatty infiltration in such visceral organs as the heart, liver and kidneys shows at death. Bromide poisoning causes intense vomiting so the dose is often removed. Effects include drowsiness, irritability, inco-ordination, vertigo, confusion, mania, hallucinations and coma. Other effects include skin rash, nervous system symptoms, sensory disturbances and increased spinal fluid pressure. They have been used as sedatives and depress the central nervous system. Toxicity is increased if dietary chloride is reduced. Repeated ingestion can cause a syndrome with acne, confusion, irritability, tremor, memory loss, weight loss, headache, slurred speech, delusions, stupor, psychosis and coma.
Although the material is not thought to be an irritant, direct contact with the eye may produce transient discomfort characterized by tearing or conjunctival redness (as with windburn).
The material is not thought to produce adverse health effects or skin irritation following contact (as classified using animal models). Nevertheless, good hygiene practice requires that exposure be kept to a minimum and that suitable gloves be used in an occupational setting.
The material is not thought to produce adverse health effects or irritation of the respiratory tract (as classified using animal models). Nevertheless, good hygiene practice requires that exposure be kept to a minimum and that suitable control measures be used in an occupational setting. 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. Respiratory sensitization may result in allergic/asthma like responses; from coughing and minor breathing difficulties to bronchitis with wheezing, gasping.
There is some evidence that inhaling this product is more likely to cause a sensitization reaction in some persons compared to the general population.
Principal routes of exposure are usually by skin contact/absorption and inhalation of generated dust. 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.
