Human inhalation exposure to ethylene glycol

Abstract

Two male volunteers (A and B) inhaled 1.43 and 1.34 mmol, respectively, of vaporous (13)C-labeled ethylene glycol ((13)C(2)-EG) over 4 h. In plasma, (13)C(2)-EG and its metabolite (13)C(2)-glycolic acid ((13)C(2)-GA) were determined together with the natural burden from background GA using a gas chromatograph equipped with a mass selective detector. Maximum plasma concentrations of (13)C(2)-EG were 11.0 and 15.8 micromol/l, and of (13)C(2)-GA were 0.9 and 1.8 micromol/l, for volunteers A and B, respectively. Corresponding plasma half-lives were 2.1 and 2.6 h for (13)C(2)-EG, and 2.9 and 2.6 h for (13)C(2)-GA. Background GA concentrations were 25.8 and 28.3 micro mol/l plasma. Unlabeled background EG, GA and oxalic acid (OA) were detected in urine in which the corresponding (13)C-labeled compounds were also quantified. Within 28 h after the start of the exposures, 6.4% and 9.3% (13)C(2)-EG, 0.70% and 0.92% (13)C(2)-GA, as well as 0.08% and 0.28% (13)C(2)-OA of the inhaled amounts of (13)C(2)-EG, were excreted in urine by volunteers A and B, respectively. The amounts of (13)C(2)-GA represented 3.7% and 14.2% of background urinary GA excreted over 24 h (274 and 88 micromol). The amounts of (13)C(2)-OA were 0.5% and 2.1% of background urinary OA excreted over 24 h (215 and 177 micromol). From the findings obtained in plasma and urine and from a toxicokinetic analysis of these data, it is highly unlikely that workplace EG exposure according to the German exposure limit (MAK-value 10 ppm EG, 8 h) could lead to adverse effects from the metabolically formed GA and OA.

Acute pulmonary toxicity and inflammation induced by combined exposure to didecyldimethylammonium chloride and ethylene glycol in rats

“…Ingestion of EG is known to promote renal injury (Porter, 2012). In contrast, inhalation of EG has been thought to be relatively safe, as healthy volunteers exposed to aerosolized EG did not show any abnormal symptoms in clinical studies (Wills et al, 1974;Carstens et al, 2003;Upadhyay et al, 2008).…”

Glyoxal [MAK Value Documentation, 2004]

“…This C 2 body is either introduced into the intermediary metabolism (for example by transamination to glycine or after reaction with pyruvic acid or 2-ketoglutaric acid) or transformed into oxalic acid in a further oxidation step (Carstens et al 2003) (Figure 2.). …”

Comparative efficacy trials with alcohol added d‐phenothrin formulations against Aedes aegypti under open‐field condition

“…aegypti by forming hydrogen bonds with atmospheric water, thus increasing droplet size and inhibiting evaporation of the insecticidal droplets. Despite its beneficial effects, airborne ethylene glycol poses risks to operators and the public because it is highly toxic and causes numerous illnesses, including confusion, nausea, vomiting, central nervous system dysfunction, cardiovascular impairment, elevated anion gap metabolic acidosis, acute kidney injury and upper respiratory tract irritation 14,15 . This warrants the need for safer adjuvant alternatives.…”