Case Report

Acute renal failure, neuropathy, and myopathy after ingestion of dipropylene glycol fog solution

Abstract

Dipropylene glycol is used in several industrial products including cosmetics, emulsifiers, solvents, and as a fog solution for dance club special effects. Animal studies have suggested that dipropylene glycol has minimal toxicity. We report a case of a 32-year-old man who ingested more than 500 mL of dipropylene glycol-containing Fantasia fog solution (High Energy Lighting, Houston, TX) and subsequently developed acute renal failure, polyneuropathy, and myopathy.

A 32-year-old previously healthy male presented to the emergency department with acute abdominal and flank pain 3 days after ingestion of more than 500 mL of Fantasia fog solution, 120 ml of Nyquil, and approximately 10 tablets of 220 mg of naproxen sodium.

Upon arrival, his vital signs and physical examination were normal. At the time of presentation, his serum urea nitrogen level was 53 mg/dL (reference range, 8-25 mg/dL), and his creatinine level was 6.4 mg/dL (reference range, 0.6- 1.5 mg/dL). Initial blood gases, electrolytes, and liver func- tion tests were normal. Comprehensive urine drug screen using thin layer chromatography and gas chromatography– mass spectrometry showed negative results including drugs mentioned above. Serum acetaminophen, salicylate, metha- nol, ethanol, and plasma Ethylene glycol were undetectable. The patient subsequently had oliguria and underwent hemodialysis. On day 6, his serum urea nitrogen and Creatinine levels peaked at 171 and 17.7 mg/dL, respectively. Arenal biopsy performed on day 10 showed cortical necrosis. His physical examination revealed a left facial palsy and proximal muscle weakness. A muscle biopsy at that time showed inflammatory myositis, and an electromyograph was consistent with peripheral axonopathy. A magnetic resonance image revealed abnormal

enhancement of Cranial nerves V, VII, IX, and X.

The patient required tracheotomy and polyethylene glycol-tube placement. He was discharged to a long-term care facility. At 6-month follow-up, he had persistent neurologic deficits and still required hemodialysis.

Dipropylene glycol (DPG) is part of a class of solvents used in many commercial products. The methyl ethers of these compounds, which are soluble in both water and oil,

allow them to be ideal solvents and dispersing agents for industrial use [1]. Dipropylene glycol is used frequently in cosmetics, as well as air fresheners, antifreeze fluid, and plastics. It is also an ingredient in the fog solution used in dance clubs for aesthetic special effects. The most likely routes of exposure to DPG by humans are inhalation, dermal contact, and oral ingestion [2].

The toxicity of DPG for human beings after oral intake has not been established, and currently no data have been published regarding postingestion clinical morbidity. Several studies have been performed on rat and mouse populations, with minimal toxicity reported. In a study conducted in 2004 on rats and mice, DPG exposure after oral ingestion was shown to have variable effects [2].

There was an increased incidence of changes consistent with chronic nephropathy as well as focal liver inflammation in rats receiving oral DPG for 2 years. However, these changes were thought to be exacerbations of chronic processes typically seen in aging rats. In the mouse study, there was no significant change between controls and those given DPG [2]. There were no cases of myopathy or neuropathy in theses trials. Currently, there are no published human cases of acute renal failure, neuropathy, and myopathy after immediate ingestion of DPG.

In our review, this is the first published case of acute renal failure, polyneuropathy, and myopathy associated with immediate ingestion of DPG. The 2004 animal studies have shown DPG to be minimally toxic to rodents, with any variation in toxicity between species likely because of differences in metabolism [3].

In conclusion, minimal data are available regarding the clinical effects of immediate DPG ingestion. Current data regarding the hazards of this class of compounds in humans indicate an extremely low level of acute toxicity [4]. The clinical course seen in our patient has not been previously documented, nor has it been seen in any published animal studies. There will likely be a need for further investigation and data regarding human toxicity with immediate DPG ingestion.

Frank LoVecchio, DO, MPH Banner Poison Control Center Department of Emergency Medicine Maricopa Medical Center

Phoenix, AZ, USA E-mail address: [email protected]

0735-6757/$ – see front matter (C) 2008

635.e2 Case Report

Cameron Nourani University of Arizona School of Medicine Phoenix, AZ, USA

D.J. Watts, MD

K.L. Wallance, MD

P.M. Wax, MD

Banner Poison Control Center

Phoenix, AZ, USA

doi:10.1016/j.ajem.2007.10.010

References

1. Miller RR, Hermann EA, Calhoun LL, Kastl PE, Zakett D. Metabolism and disposition of dipropylene glycol monomethyl ether (DPGME) in male rats. Fundam Appl Toxicol 1985;5(4):721-6.
2. Hooth MJ, Herbert RA, Haseman JK, Orzech DP, Johnson JD, Bucher JR. Toxicology and carcinogenesis studies of dipropylene glycol in rats and mice. Toxicology 2004;204(2-3):123-40.
3. National Toxicology Program (NTP). Toxicology and carcinogenesis studies of dipropylene glycol (CAS No. 25265-71-8) in F344/N rats and B6C3F₁ mice (drinking water studies). Natl Toxicol Program Tech Rep Ser 2004;511:6-260.
4. Spencer PJ. New toxicity data for the propylene glycol ethers–a commitment to public health and safety. Toxicol Lett 2005;156(1): 181-8.