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The 90 Day Plan

Saturday, July 3, 2010

What is a dispersant?

One example of a dispersant for oil

  • Canada: addition of 2-butoxyethanol to list of toxic substances., Coat., Reg. Environ., 2005, , 2005-09-01, Pages -

2-Butoxyethanol has been added to the list of toxic substances under schedule 1 of the Canadian Environmental Protection Act 1999. The risk assessment for 2-butoxyethanol determined that concentrations of 2.3 ppm posed a risk to health. Consumer exposure modelling suggested that the use of products containing 2-butoxyethanol in an indoor setting could exceed this concentration. The Canadian authorities determined that of four hundred and forty four cleaning, painting and coating products containing 2-butoxyethanol available for indoor use around two hundred and sixty contained 2-butoxyethanol at concentrations which exceeded the limit values. The regulations exclude outdoor use, use in manufacturing, use in scientific research as a solvent or analytical standard.

Chronic exposure to 2-butoxyethanol increased liver hemangiosarcomas in male mice. The mechanism for the selective induction of hemangiosarcomas by 2-butoxyethanol in unknown but has been suggested to occur through non-DNA-reactive mechanisms. The occurrence of liver hemangiosarcomas in male mice has been linked to oxidative damage subsequent to RBC hemolysis and iron deposition and activation of macrophages (Kupffer cells) in the liver, events that exhibit a threshold in both animals and humans. 2-Butoxyethanol is metabolized to 2-butoxyacetaldehyde and 2-butoxyacetic acid, and although the aldehyde metabolite is short lived, the potential exists for this metabolite to cause DNA damage. The present study examined whether 2-butoxyacetic acid and its metabolites, 2-butoxyacetaldehyde and 2-butoxyacetic acid, damaged mouse endothelial cell DNA using comet assay. No increase in DNA damage was observed following 2-butoxyethanol (1 - 10 mM), 2-butoxyacetaldehyde (0.1 - 1.0 mM), or 2-butoxyacetic acid (1 - 10 mM) in endothelial cells after 2, 4, or 24 h exposure. Additional studies examined the involvement of hemolysis and macrophage activation in 2-butoxyethanol carcinogenesis. DNA damage was produced by hemolyzed RBCs (10 × 1064 h), ferrous sulfate (0.1 - 1.0 µM; 2 - 24 h), and hydrogen peroxide (50 - 100 µM; 1 - 4 h) in endothelial cells. Hemolyzed RBCs also activated macrophages, as evidenced by increased tumor necrosis factor (TNF)α, while neither 2-butoxyethanol nor butoxyacetic acid increased TNF-α from macrophages. The effect of activated macrophages on endothelial cell DNA damage and DNA synthesis was also studied. Coculture of endothelial cells with activated macrophages increased endothelial cell DNA damage after 4 h or 24 h and increased endothelial cell DNA synthesis after 24 h. These data demonstrate that 2-butoxyethanol and related metabolites do not directly cause DNA damage. Supportive evidence also demonstrated that damaged RBCs, iron, and/or products from macrophage activation (possibly reactive oxygen species) produce DNA damage in endothelial cells and that activated macrophages stimulated endothelial cell proliferation. These events coupled together provide the events necessary for the induction of hemangiosarcomas by 2-butoxyethanol.

Male B6C3F1 mice and F344 rats were treated by gavage with 1 or 5mM 2-butoxyethanol (BE) for 7 days. In addition, hepatocytes were treated with BE, its metabolite 2-butoxyacetic acid (BAA) or iron sulfate. BE induced oxidative stress in the liver of mice. Neither BE nor BAA induced changes in the oxidative stress parameters examined in either rat or mouse hepatocytes, whereas iron affected the biomarkers. Mouse hepatocytes were more sensitive to oxidative damage from iron sulfate than rat hepatocytes. Induction of hepatic oxidative stress by 2-butoxyethanol in vivo occurs secondary to induction of haemolysis and iron deposition in the liver.

SHE cells were treated with 2-butoxyethanol (BE), its 2-butoxyacetic acid (BAA) metabolite or ferrous sulfate for 7 days. BE and BAA did not induce cellular transformation, but ferrous sulfate increased morphological transformation via oxidative stress. The level of oxidative DNA damage increased following ferrous sulfate treatment. The results support the proposal that iron produced through haemolysis, and not BE or BAA, is responsible for the observed hepatocarcinogenicity of BE in rodents.

Male B6C3F1 mice and F344 rats were treated by oral gavage with 0-900 or 0-450 mg/kg/day 2-butoxyethanol, respectively, for 7-90 days. Haemolysis and iron deposition in Kupffer cells increased in a dose-dependent manner, haematocrit decreased and spleen weight increased. Mouse liver showed increased oxidative damage and DNA synthesis in hepatocytes and endothelial cells. The results are discussed in terms of the induction of liver tumours in mice.

  • EPA proposes delisting of 2-butoxyethanol from hazardous air pollutant (HAP) classification., Coat., Reg. Environ., 2004, , 2004-03-01, Pages -

The Environmental Protection Agency (USEPA) proposes to remove ethylene glycol monobutyl ether (2-butoxyethanol, EGBE) from its list of hazardous air pollutants (HAPs). EGBE has been found to damage red blood cells but it does not cause cancer in humans at exposure levels likely to be encountered in air. EPA will consider any new medical evidence presented which indicates other health risks before making a final decision. EGBE is used as a coalescent in waterborne coatings. The ruling is significant because many EPA restrictions on volatile organic compound (VOC) emissions relate only to HAPs rather than any broader classification.

2-Butoxyethanol, a forestomach carcinogen in mice exposed by inhalation, has been shown to enter the forestomach as a result of grooming and ingestion of material condensed on the skin and fur during exposure. On entering the stomach, it is metabolised by dehydrogenase enzymes to 2-butoxyacetic acid which was found to cause a marked hyperkeratosis in the forestomach following oral dosing. There was a marked species difference in the metabolism of 2-butoxyethanol in forestomach fractions with the maximum rates up to one order of magnitude greater in mouse than rat. The dehydrogenases responsible for this metabolism were heavily concentrated in the stratified squamous epithelium of the forestomach of both rats and mice, whereas in the glandular stomach the distribution was more diffuse. In human stomach both enzymes were evenly distributed throughout the epithelial cells of the mucosa. It is concluded that 2-butoxyethanol is ingested following inhalation exposure and concentrates in the forestomach where it is metabolised to 2-butoxyacetic acid which causes cellular damage, increased cell replication, hyperkeratosis and ultimately tumours. Differences in structure and enzyme distribution between the rodent and human stomach suggest that the responses seen in the mouse are unlikely to occur in humans.

  • V. J. Cogliano, Y. Grosse, R. A. Baan, M. B. Secretan, F. El Ghissassi. Meeting report: summary of IARC monographs on formaldehyde, 2-butoxyethanol, and 1-tert-butoxy-2-propanol., Environ. Health Perspect., 2005, 113, 1205, Volume 113, Issue 9, 2005-11-01, Pages 1205-1208

An international, interdisciplinary working group of expert scientists met in June 2004 to develop IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans (IARC Monographs) on formaldehyde, 2-butoxyethanol, and l-tert-butoxy-2-propanol. Each IARC Monograph includes a critical review of the pertinent scientific literature and an evaluation of an agent's potential to cause cancer in humans. After a thorough discussion of the epidemiologic, experimental, and other relevant data, the working group concluded that formaldehyde is carcinogenic to humans, based on sufficient evidence in humans and in experimental animals. In the epidemiologic studies, there was sufficient evidence that formaldehyde causes nasopharyngeal cancer, "strong but not sufficient" evidence of leukaemia, and limited evidence of sinonasal cancer. The working group also concluded that 2-butoxyethanol and l-tert-butoxy-2-propanol are not classifiable as to their carcinogenicity to humans, each having limited evidence in experimental animals and inadequate evidence in humans. These three evaluations and the supporting data will be published as Volume 88 of the IARC Monographs.

US EPA's integrated risk information system (IRIS) assessment of 2-butoxyethanol (EGBE) indicates that the human carcinogenic potential of EGBE cannot be determined at this time, but that "suggestive evidence" for cancer exists from laboratory animal studies (hemangiosarcoma of the liver in male mice and forestomach squamous cell papilloma or carcinoma in female mice [National Toxicology Program (NTP), 2000a. Toxicology and carcinogenesis studies of 2-butoxyethanol (CAS no. 111-76-2) in F344/N rats and B6C3F1 mice (inhalation studies). National Toxicology Program Technical Report Series No. 484. US Department of Health and Human Services, National Institutes of Health, Washington, DC]). Since the last EGBE IRIS assessment, a number of studies have provided evidence that the carcinogenic effects observed in mice are nonlinear in their mode of action and may be dependent on threshold events such as EGBE-induced hemolytic effects. EPA is in the process of considering several questions relating to this issue. First, can a plausible mode of action be determined for the two types of tumors observed in mice? Second, are the mechanisms involved applicable to humans? If so, should the mode of action be considered to result in a linear or nonlinear dose-response? These questions will be addressed within the context of the agency's new cancer guidelines and with regard to how the answers might affect a revised IRIS assessment for EGBE.

The pharmacokinetics of 2-butoxyethanol (BE; ethylene glycol butyl ether) and its metabolite butoxyacetic acid (BAA) were studied in female B6C3F1 mice to examine the observation of forestomach tumours after inhalation exposure. Oral dosing with BE caused irritation in the forestomach, but only small amounts were present on the fur after inhalation studies. Parenteral administration also resulted in forestomach lesions, indicating that sources other than grooming were responsible. BE and BAA were eliminated more slowly from forestomach tissue than blood or other tissue, and were present for a prolonged period after oral gavage or intraperitoneal injection. Thus, several factors govern the levels of BE and BAA in the forestomach, resulting in contact irritation, compensatory hyperplasia and tumorigenicity.


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