SDS

asthma and atopic eczema (neurodermatitis) which is associated with increased IgE synthesis.
Exogenous allergic alveolitis is induced essentially by allergen specific immune-complexes of the IgG type; cell-mediated reactions (T
lymphocytes) may be involved. Such allergy is of the delayed type with onset up to four hours following exposure.
Goitrogenic:.
Goitrogens are substances that suppress the function of the thyroid gland by interfering with iodine uptake, which can, as a result, cause an
enlargement of the thyroid, i.e., a goitre
Goitrogens include:
Vitexin, a flavanoid, which inhibits thyroid peroxidase thus contributing to goiter.
Ions such as thiocyanate and perchlorate which decrease iodide uptake by competitive inhibition; as a consequence of reduced thyroxine
and triiodothyronine secretion by the gland, at low doses, this causes an increased release of thyrotropin (by reduced negative feedback),
which then stimulates the gland.
Lithium which inhibits thyroid hormone release.
Certain foods, such as soy and millet (containing vitexins) and vegetables in the genus Brassica (e.g. broccoli, brussels sprouts, cabbage,
horseradish).
Caffeine (in coffee, tea, cola, chocolate) which acts on thyroid function as a suppressant.
ETHYLENE CARBONATE
The material may produce severe irritation to the eye causing pronounced inflammation. Repeated or prolonged exposure to irritants may
produce conjunctivitis.
The material may cause skin irritation after prolonged or repeated exposure and may produce a contact dermatitis (nonallergic). This form of
dermatitis is often characterised by skin redness (erythema) and swelling epidermis. Histologically there may be intercellular oedema of the
spongy layer (spongiosis) and intracellular oedema of the epidermis.
for ethylene carbonate
Mammalian toxicity:
Reliable acute toxicity tests are available on ethylene carbonate. Ethylene carbonate is practically nontoxic following acute
oral exposure in a test that meets OECD and EPA test guidelines; the LD50 is >5000 mg/kg. The dermal LD50 is >2000 mg/kg, in a test that
meets OECD and EPA test guidelines.
Ethylene carbonate is rapidly metabolized to ethylene glycol. Following gavage administration to rats, ethylene carbonate is rapidly converted
into ethylene glycol; the half-life for disappearance of ethylene carbonate from blood was 0.25 hours. As a result, the mammalian toxicity of
ethylene carbonate is nearly identical to that of ethylene glycol for endpoints where both have been tested
Ethylene carbonate was mixed in the diet of 26 male and 26 female Crl: CD(SD) rats for 18 months at concentrations of 25,000 ppm for males
and females and 50,000 ppm for females; males were also fed 50,000 ppm for 42 weeks, and 40,000 ppm for 16 weeks. Survivors were
observed to 24 months. Compound intake (mg/kg/day) was not reported, but is estimated to be approximately 250 and 500 mg/kg/day. No toxic
effects were found in females, but increased mortality was seen in males at both dose levels. No high-dose males survived week 60 and only 10
low-dose males survived to week 78. Males had severe nephrotoxicity, characteristic of ethylene glycol toxicity.
The following
in vitro
genotoxicity tests were conducted on ethylene carbonate, without indications of genotoxicity: an Ames mutagenicity assay,
an unscheduled DNA synthesis assay using rat hepatocytes, and a cell transformation assay using BALB/3T3 cells. No
in vivo
genotoxicity
studies on ethylene carbonate were found; however, ethylene glycol has been tested and was negative in a rat dominant lethal assay.
Gavage administration of ethylene carbonate to pregnant rats days 6-15 of gestation resulted in systemic toxicity at doses of 3000 mg/kg/day,
including post-dose salivation. The NOAEL for maternal toxicity was 1500 mg/kg/day. Similar to ethylene glycol, there were increased soft tissue
(hydrocephalus, umbilical herniation, gastroschisis, cleft palate, misshapen and compressed stomach) and skeletal malformations at 3000
mg/kg/day, but not at 1500 mg/kg/day.
For ethylene glycol:
Ethylene glycol is quickly and extensively absorbed through the gastrointestinal tract. Limited information suggests that it is also absorbed
through the respiratory tract; dermal absorption is apparently slow. Following absorption, ethylene glycol is distributed throughout the body
according to total body water. In most mammalian species, including humans, ethylene glycol is initially metabolised by alcohol.
dehydrogenase to form glycolaldehyde, which is rapidly converted to glycolic acid and glyoxal by aldehyde oxidase and aldehyde
dehydrogenase. These metabolites are oxidised to glyoxylate; glyoxylate may be further metabolised to formic acid, oxalic acid, and glycine.
Breakdown of both glycine and formic acid can generate CO2, which is one of the major elimination products of ethylene glycol. In addition to
exhaled CO2, ethylene glycol is eliminated in the urine as both the parent compound and glycolic acid. Elimination of ethylene glycol from the
plasma in both humans and laboratory animals is rapid after oral exposure; elimination half-lives are in the range of 1-4 hours in most species
tested.
Respiratory Effects.
Respiratory system involvement occurs 12-24 hours after ingestion of sufficient amounts of ethylene glycol and is
considered to be part of a second stage in ethylene glycol poisoning The symptoms include hyperventilation, shallow rapid breathing, and
generalized pulmonary edema with calcium oxalate crystals occasionally present in the lung parenchyma. Respiratory system involvement
appears to be dose-dependent and occurs concomitantly with cardiovascular changes. Pulmonary infiltrates and other changes compatible with
adult respiratory distress syndrome (ARDS) may characterise the second stage of ethylene glycol poisoning Pulmonary oedema can be
secondary to cardiac failure, ARDS, or aspiration of gastric contents. Symptoms related to acidosis such as hyperpnea and tachypnea are
frequently observed; however, major respiratory morbidities such as pulmonary edema and bronchopneumonia are relatively rare and usually
only observed with extreme poisoning (e.g., in only 5 of 36 severely poisoned cases).
Cardiovascular Effects.
Cardiovascular system involvement in humans occurs at the same time as respiratory system involvement, during the
second phase of oral ethylene glycol poisoning, which is 12- 24 hours after acute exposure. The symptoms of cardiac involvement include
tachycardia, ventricular gallop and cardiac enlargement. Ingestion of ethylene glycol may also cause hypertension or hypotension, which may
progress to cardiogenic shock. Myocarditis has been observed at autopsy in cases of people who died following acute ingestion of ethylene
glycol. As in the case of respiratory effects, cardiovascular involvement occurs with ingestion of relatively high doses of ethylene glycol.
Nevertheless, circulatory disturbances are a rare occurrence, having been reported in only 8 of 36 severely poisoned cases.Therefore, it appears
that acute exposure to high levels of ethylene glycol can cause serious cardiovascular effects in humans. The effects of a long-term, low-dose
exposure are unknown.
Gastrointestinal Effects.
Nausea, vomiting with or without blood, pyrosis, and abdominal cramping and pain are common early effects of acute
ethylene glycol ingestion. Acute effects of ethylene glycol ingestion in one patient included intermittent diarrhea and abdominal pain, which were
attributed to mild colonic ischaemia; severe abdominal pain secondary to colonic stricture and perforation developed 3 months after ingestion,
and histology of the resected colon showed birefringent crystals highly suggestive of oxalate deposition.
Musculoskeletal Effects.
Reported musculoskeletal effects in cases of acute ethylene glycol poisoning have included diffuse muscle tenderness
and myalgias associated with elevated serum creatinine phosphokinase levels, and myoclonic jerks and tetanic contractions associated with
hypocalcaemia.
Hepatic Effects
.
Central hydropic or fatty degeneration, parenchymal necrosis, and calcium oxalate crystals in the liver have been observed at
autopsy in cases of people who died following acute ingestion of ethylene glycol.
Renal Effects.
Adverse renal effects after ethylene glycol ingestion in humans can be observed during the third stage of ethylene glycol toxicity
24-72 hours after acute exposure. The hallmark of renal toxicity is the presence of birefringent calcium oxalate monohydrate crystals deposited in
renal tubules and their presence in urine after ingestion of relatively high amounts of ethylene glycol. Other signs of nephrotoxicity can include
tubular cell degeneration and necrosis and tubular interstitial inflammation. If untreated, the degree of renal damage caused by high doses of
ethylene glycol progresses and leads to haematuria, proteinuria, decreased renal function, oliguria, anuria , and ultimately renal failure. These
changes in the kidney are linked to acute tubular necrosis but normal or near normal renal function can return with adequate supportive therapy.
Metabolic Effects.
One of the major adverse effects following acute oral exposure of humans to ethylene glycol involves metabolic changes.
These changes occur as early as 12 hours after ethylene glycol exposure. Ethylene glycol intoxication is accompanied by metabolic acidosis
which is manifested by decreased pH and bicarbonate content of serum and other bodily fluids caused by accumulation of excess glycolic acid.
Other characteristic metabolic effects of ethylene glycol poisoning are increased serum anion gap, increased osmolal gap, and hypocalcaemia.
Serum anion gap is calculated from concentrations of sodium, chloride, and bicarbonate, is normally 12-16 mM, and is typically elevated after
ethylene glycol ingestion due to increases in unmeasured metabolite anions (mainly glycolate).
Neurological Effects:
Adverse neurological reactions are among the first symptoms to appear in humans after ethylene glycol ingestion. These
Chemwatch:
5351-42
Version No:
6.1.1.1
Page
8
of
15
Toro Lithium Ion Battery [60V, 40V, 24V, 20V]
Issue Date:
13/10/2020
Print Date:
13/10/2020
Continued...