SDS

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 early
neurotoxic effects are also the only symptoms attributed to unmetabolised ethylene glycol. Together with metabolic changes, they occur during the period of
30 minutes to 12 hours after exposure and are considered to be part of the first stage in ethylene glycol intoxication. In cases of acute intoxication, in which a
large amount of ethylene glycol is ingested over a very short time period, there is a progression of neurological manifestations which, if not treated, may
lead to generalized seizures and coma. Ataxia, slurred speech, confusion, and somnolence are common during the initial phase of ethylene glycol
intoxication as are irritation, restlessness, and disorientation. Cerebral edema and crystalline deposits of calcium oxalate in the walls of small blood vessels
in the brain were found at autopsy in people who died after acute ethylene glycol ingestion.
Effects on cranial nerves appear late (generally 5-20 days post-ingestion), are relatively rare, and according to some investigators constitute a fourth, late
cerebral phase in ethylene glycol intoxication. Clinical manifestations of the cranial neuropathy commonly involve lower motor neurons of the facial and
bulbar nerves and are reversible over many months.
Reproductive Effects: Reproductive function after intermediate-duration oral exposure to ethylene glycol has been tested in three multi-generation
studies (one in rats and two in mice) and several shorter studies (15-20 days in rats and mice). In these studies, effects on fertility, foetal viability, and male
reproductive organs were observed in mice, while the only effect in rats was an increase in gestational duration.
Developmental Effects: The developmental toxicity of ethylene glycol has been assessed in several acute-duration studies using mice, rats, and rabbits.
Available studies indicate that malformations, especially skeletal malformations occur in both mice and rats exposed during gestation; mice are apparently
more sensitive to the developmental effects of ethylene glycol. Other evidence of embyrotoxicity in laboratory animals exposed to ethylene glycol exposure
includes reduction in foetal body weight.
Cancer: No studies were located regarding cancer effects in humans or animals after dermal exposure to ethylene glycol.
Genotoxic Effects: Studies in humans have not addressed the genotoxic effects of ethylene glycol. However, available in vivo and in vitro laboratory
studies provide consistently negative genotoxicity results for ethylene glycol.
PROPYLENE CARBONATE
for propylene carbonate:
Numerous adequate and reliable acute toxicity tests are available on propylene carbonate. Oral and dermal tests meet OECD and EPA test guidelines.
Propylene carbonate is practically nontoxic following acute exposures; the oral LD50 is >.5000 mg/kg and the dermal LD50 is >3000 mg/kg. No further
testing is recommended.
Subchronic studies (13- 14 weeks) of propylene carbonate by inhalation (aerosol) and oral (gavage) routes were conducted in rats according to current
guidelines. The oral study indicated low systemic toxicity from propylene carbonate (NOAEL = 5000 mg/kg/day). In the inhalation study, no systemic toxicity
was seen at concentrations up to 1000 mg/m”; however, there was periocular irritation and swelling in a few males at 500 and 1000 mg/m3. A dermal
carcinogenicity study in mice did not indicate tumorigenic potential or systemic toxicity from 2 years of exposure to propylene carbonate. No further testing
is recommended.
There is a negative Ames in vitro mutagenicity assay of propylene carbonate. A single intraperitoneal injection of 1666 mg/kg propylene carbonate did not
induce an increase in micronuclei when examined after 30,48 and 72 hours. The mutagenicity battery is satisfactorily filled; no further mutagenicity testing
is recommended.
Gavage administration of propylene carbonate to pregnant rats days 6-15 of gestation resulted in systemic toxicity at doses of 3000 and 5000 mg/kg/day,
including mortality (not seen in 13 week study of non-pregnant rats). The NOAEL for maternal toxicity was 1000 mg/kg/day. This indicates that pregnant rats
are more susceptible to propylene carbonate than are non-pregnant rats. There were no significant differences in live litter size, average fetal weight,
percentage of males, or malformed fetuses.
No studies of the effect of propylene carbonate on reproduction are available. However, no adverse effects on testis, ovaries, or accessory sex organs were
noted in rats following oral or inhalation of propylene carbonate for 13 weeks. Therefore, reproductive effects from propylene carbonate are unlikely
DIETHYL CARBONATE
Exposure to the material for prolonged periods may cause physical defects in the developing embryo (teratogenesis).
Equivocal tumorigen by RTECS criteria
COPPER
for copper and its compounds (typically copper chloride):
Acute toxicity: There are no reliable acute oral toxicity results available. In an acute dermal toxicity study (OECD TG 402), one group of 5 male rats and 5
groups of 5 female rats received doses of 1000, 1500 and 2000 mg/kg bw via dermal application for 24 hours. The LD50 values of copper monochloride
were 2,000 mg/kg bw or greater for male (no deaths observed) and 1,224 mg/kg bw for female. Four females died at both 1500 and 2000 mg/kg bw, and one
at 1,000 mg/kg bw. Symptom of the hardness of skin, an exudation of hardness site, the formation of scar and reddish changes were observed on application
sites in all treated animals. Skin inflammation and injury were also noted. In addition, a reddish or black urine was observed in females at 2,000, 1,500 and
1,000 mg/kg bw. Female rats appeared to be more sensitive than male based on mortality and clinical signs.
No reliable skin/eye irritation studies were available. The acute dermal study with copper monochloride suggests that it has a potential to cause skin
irritation.
Repeat dose toxicity: In repeated dose toxicity study performed according to OECD TG 422, copper monochloride was given orally (gavage) to Sprague-
Dawley rats for 30 days to males and for 39 - 51 days to females at concentrations of 0, 1.3, 5.0, 20, and 80 mg/kg bw/day. The NOAEL value was 5 and 1.3
mg/kg bw/day for male and female rats, respectively. No deaths were observed in male rats. One treatment-related death was observed in female rats in the
high dose group. Erythropoietic toxicity (anaemia) was seen in both sexes at the 80 mg/kg bw/day. The frequency of squamous cell hyperplasia of the
forestomach was increased in a dose-dependent manner in male and female rats at all treatment groups, and was statistically significant in males at doses
of =20 mg/kg bw/day and in females at doses of =5 mg/kg bw/day doses. The observed effects are considered to be local, non-systemic effect on the
forestomach which result from oral (gavage) administration of copper monochloride.
Genotoxicity: An in vitro genotoxicity study with copper monochloride showed negative results in a bacterial reverse mutation test with Salmonella
typhimurium strains (TA 98, TA 100, TA 1535, and TA 1537) with and without S9 mix at concentrations of up to 1,000 ug/plate. An in vitro test for
Chemwatch: 5351-42
Version No: 2.1.1.1
Page 8 of 15
Toro Flex Force Lithium Ion Battery (UN3480)
Issue Date: 07/05/2019
Print Date: 08/05/2019
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