Acute exposure

Inhalation

Glycol ethers are irritant to the skin, eyes and respiratory tract. They may cause lacrimation, rhinorrhoea, cough, dyspnoea and nausea. A high concentration may cause CNS depression.

Cherry angiomas were reported in 6 out of 7 workers exposed to EGBE which had been applied to the floor of one of the rooms at work. Cherry angiomas are red/purple smooth lesions due to permanent dilatation of blood vessels and are usually found on the trunk and proximal extremities. The workers had developed immediate symptoms of irritation with dyspnoea and nausea at the time of the incident and had removed themselves from exposure. However, some of them had to enter the treated room during the course of their work. Some of the workers had been sent home because of their symptoms, but all were well enough to return to work the next day. Cherry angiomas began to develop 4-22 weeks after the incident. When examined 8 months after the incident 6 workers complained of recurrent eye and tracheobronchial irritation and retro-orbital headache. Four of them had a dry cough. Five years after the exposure cherry angiomas continued to appear (Raymond et al., 1998).

Dermal

Glycol ethers are irritant to the skin; however, the severity depends on the particular ether (see Table 11.8). In a volunteer study where the fingers were immersed in neat EGBE for 2 hours the skin became wrinkled and less elastic. There was a decrease in finger volume and skin thickness. These effects reached a maximum 2-4 hours after cessation of exposure and then resolved. This was thought to be due to delipidisation and dehydration of the skin. In some cases there was slight erythema which resolved in 1-2 days (Johanson et al., 1988).

Table 11.8 Comparative acute irritation effects of glycol ethers in animal studies (Ballantyne and Myers, 1987)

Ether

Skin irritation

Eye irritation

Ethylene

methyl

minor

moderate

ethyl

moderate

severe

propyl

moderate

severe

butyl

moderate

severe

hepyl

moderate

severe

hexyl

severe

severe

Diethylene

methyl

minor

moderate

ethyl

minor

moderate

butyl

minor

severe

heptyl

minor

severe

hexyl

minor

severe

In rabbit studies, exposure to ethylene glycol hexyl ether for 4 hours caused mild to moderate erythema and oedema. There was some necrosis and desquamation. Diethylene glycol hexyl ether was less irritant (Ballantyne and Myers, 1987). In an animal study comparing EGEEA and EGBEA, both were found to be practically non-irritant (Truhaut et al., 1979).

Glycol ethers are irritant to eyes; however, the severity depends on the particular ether (Grant and Schuman, 1993), see Table 11.8. In rats, ethylene glycol hexyl ether and diethylene glycol hexyl ether caused severe conjunctivitis with hyperaemia, iritis, chemosis and discharge. There was full recovery (Ballantyne and Myers, 1987).

Ingestion

Ingestion of a large quantity of glycol ether (usually in a suicide attempt) results in coma, respiratory depression, convulsions and severe hypotension. Restlessness, weakness, confusion and disorientation, agitation, cyanosis and hyperventilation have been reported. Transient non-cardiogenic pulmonary oedema has been reported (Bauer et al., 1992). The onset of effects is usually rapid, i.e., within 2 hours (Gijsenbergh et al., 1989; McKinney et al., 2000), but there may be a delay in presentation because initial effects may be non-specific (8 and 18 hours: Nitter-Hauge, 1970; 12 hours: Rambourg-Schepens et al., 1988; 10 hours: Bauer et al., 1992).

Laboratory analyses may reveal severe metabolic acidosis, DIC, hepatotoxicity (abnormal LFTs and INR), reduced haemocrit and haemoglobin and evidence of renal impairment. Urine analysis may reveal proteinuria and oxalate crystals may be present. Hypocalcaemia (Nitter-Hauge, 1970), hypokalaemia (Nitter-Hauge, 1970; Rambourg-Schepens et al., 1988; Bauer et al., 1992), thrombocytopenia and non-haemolytic hypochromic anaemia (Bauer et al., 1992) have occasionally been reported. Haemolytic anaemia and haematuria may occur (Rambourg-Schepens et al., 1988; Gijsenbergh et al., 1989). Cases of ingestion of glycol ether are summarised in Table 11.9.

Table 11.9 Cases of ingestion of glycol ether

Glycol ether

Quantity

Co-ingestants

Age/sex

Results of investigations

Treatment

Outcome

Reference

DGME

NK 20-30%

Mineral spirits (65-70%), xylene (2-4%)

59 F

Acidosis, osmolar gap 12 mOsm/kg H20 Ethylene glycol and methanol not detected

Ethanol

Recovery

Wermuth and Furbee, 1997

EGBE

500 ml of 9.1% (45.5 g)

Ethanol 2.5%

53 M

Acidosis

Ethanol, haemodialysis

Recovery

Bauer et al, 1992

EGBE

500 ml of 12.7% (63.5 g)

Ethanol 3.2%

23 F

Acidosis, no osmolar gap, oxalate excretion normal

Diuresis, haemodialysis

Recovery

Gijsenberg et al, 1989

EGBE

360-480 ml of 22% (79-106 g) and 12 days later 480 ml of 22%

17 M

Acidosis, ethylene glycol not detected

Ethanol, haemodialysis on both occasions

Recovery

Gualtieri et al, 1995

EGBE

NK 5.6%

87 F

Acidosis, ethylene glycol concentration 1.1 g/1

Ethanol, haemodialysis (stopped due to arrhythmias)

Death after 3 days

Litovitz etal, 1991

EGBE

225 ml

Isopropanol

51 F

Acidosis, ethanol, ethylene glycol and methanol not detected, osmolar gap 1 mOsm/kg H20

Ethanol

Recovery

McKinney et al, 2000

EGBE

(23 g)

52 F

Acidosis, ethylene glycol concentration 0.31 g/1, oxalate crystals on biopsy

Ethanol, fomepizole,

Recovery

Nisse etal, 1998

EGBE

250-500 ml of 12% (30-60 g)

-

50 F

Acidosis, oxalates in urine

Diuresis

Recovery

Rambourg- Schepens etal, 1988

EGME

100 ml pure

-

41 M

Acidosis, oxalate in urine, methanol not detected

Ethanol

Recovery

Nitter-Hauge, 1970

EGME

100 ml pure

-

23 M

Acidosis, oxalate in urine, methanol not detected

Ethanol

Recovery

Nitter-Hauge, 1970

EGME

285 ml ? pure

-

44 M

No methanol detected

-

Death

Young and Woolner, 1946

Most cases reported involve EGBE (Rambourg-Schepens et al., 1988; Gijsenbergh et al., 1989; Litovitz et al., 1991; Bauer et al., 1992; Burkhart and Donovan, 1998; McKinney et al., 2000; Nisse et al., 1998), but cases of EGME (Nitter-Hauge, 1970) and dipropylene glycol monomethyl ether have also been reported (Wermuth and Furbee, 1997). Recovery from severe poisoning may be prolonged; residual neurological damage has been reported (Burkhart and Donovan, 1998), but this may have been a result of hypoxia following aspiration.

Renal biopsy in a patient with persistent renal impairment showed acute tubular necrosis, vascular lesions and oxalate crystal deposition in the renal parenchyma (Nisse et al., 1998). Findings in postmortem examination in two fatal cases included haemorrhagic gastritis, degenerative changes in the renal tubules and fatty degeneration of the liver (Young and Woolner, 1946).

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