Glycols human exposure

Stewart, R.D., J.E.Peterson, P.E.Newton, CL.Hake, MJ.Hosko, AJ.Lebrun, and G.M.Lawton. 1974. Experimental human exposure to propylene glycol dinitrate. 

Stewart RD, Peterson JE, Newton PE, et ah Experimental human exposure to propylene glycol dinitrate. Toxicol ApplPharmacol 30 377-395, 1974... 

In studies involving human exposure (Rengstorff and Mershon, 1969a, b), CS (0.1% or 0.25% in water 1.0% in triocyl phosphate) sprayed or administered as ophthalmic drops onto the eyes, caused apraxia of eyelid opening with blepharospasm upon eyelid closure for 10 to 135 s. It also caused a transient conjunctivitis but no comeal damage upon further inspection with a slit lamp. Rabbit eyes contaminated with CS as a solution (0.5-10% in polyethylene glycol), as a solid, or thermally dispersed as a smoke (15 min at 6,000 mg/m ) showed a greater toxicity with solution. CS in solution caused profuse lacrimation, conjunctivitis, iritis, chemosis, keratitis, and corneal vascularization at concentrations at or above 1%. 

Pederen LM. Biological studies in human exposure to and poisoning with organic solvents. Pharmacol Toxicol 1987 3 1-38. Porter GA. The treatment of ethylene glycol poisoning simplified. N Eng J Med 1988 319(2) 109-110. 

There are sufficient data to characterize the acute and chronic toxicity of propylene glycol in laboratory animals, including nonhuman primates. In humans, information on toxicity is limited to medical case studies. However, because of the similarities in the toxicokinetic profile of propylene glycol across species, the toxicity data from the animal studies can be extrapolated to human exposures. 

The Toxics Release Inventory (TRI), which contains information for 1994, became available in May of 1996. This database will be updated yearly and should provide a list of industrial production facilities and emissions. Currently, no information is available in the TRI database for 2-butoxyethanol because the database contains such information only for the general toxic chemical category of glycol ethers and not for specific glycol ethers (EPA 1995). No information is available in the TRI database for 2-butoxy-ethanol acetate because this chemical is not included under SARA, Title III, and therefore is not among the chemicals that facilities are required to report (EPA 1995). There is a need for such information in order to assess the potential for human exposure to these chemicals from their release from industrial production facilities. Limited or no information was found in the available literature on current disposal methods (including efficiencies, the need for improvement, and the amount disposed of) for 2-butoxyethanol no information in these areas was found for 2-butoxyethanol acetate. Additional information on disposal methods and the amounts of 2-butoxyethanol and 2-butoxyethanol acetate disposed of by each method is needed. 

In recent years, health concerns have caused substitution of propylene glycol-based products for the ethylene glycol-based products to avoid human exposure. 

In the case of human exposure to ethylene glycol, oxalic acid was found to be the end-product of metabolism. It precipitated to crystals of calcium oxalate monohydrate in the tubular lumen, causing acute kidney injmy with extensive intracellular intraluminal crystal depositions, and subsequently acute oxalate nephropathy. ... 

Toxicology. Dipropylene glycol methyl ether (DPGME) at very high concentrations causes narcosis in animals, and it is expected that severe exposure will produce the same effect in humans. Because the propylene glycol ethers are metabolized differently from the ethylene glycol ethers, they are not associated with potent teratogenic, spermatotoxic, or hematopoietic effects. ... 

National Institute for Occupational Safety and Health Criteria for a Recommended Standard Occupational Exposure to Ethylene Glycol Monomethyl Ether, Ethylene Glycol Monoethyl Ether, and Their Acetates. Pub No 91-119, Cincinnati, OH, US Department of Health and Human Services, Public Health Service, 1991... 

The primary function of the kidneys is to rid the body of waste materials that are either ingested or produced by metabolism, and to control the volume and composition of the body fluids. The toxins absorbed by the different routes are biotransformed and enter the blood. They are then eliminated through the urine, feces, and air. Since the kidneys receive approximately a quarter of the cardiac output, it is an important organ for the exposure of toxicants and their metabolites. Recent incidents of pet food toxicity and diethylene glycol toxicity indicate that contamination of animal and human food and drugs, respectively, can lead to severe mortahty and morbidity as a result of renal toxicity. 

Hess R, Bartels MJ, Pottenger LH. Ethylene glycol and estimate of tolerable levels of exposure based on a review of animal and human data. Arch Toxicol 2004 78 671 -680. 

Exposure to Otto Euel II is likely to cause eye and respiratory irritation in humans exposed to significant levels. In addition, headaches of presumed vascular origin are possible based on experience by torpedo maintenance workers. In experimental exposure to volunteers to propylene glycol dinitrate vapor, headaches were reported by some subjects at concentrations of 0.2 ppm for up to 8 h. 

No epidemiological studies or case reports of ill effects in healthy humans attributable to chronic exposure to polyethylene glycols were found in the available literature. 

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