PubMed · 13765425
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H I MAIBACH, A M KLIGMAN. 1960. Dihydroxyacetone: a suntansimulating agent.. https://doi.org/10.1001/archderm.1960.01580040023004
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A procedure for the determination of 13 organophosphate insecticides (OPs) in water, sediment and biota at low ppb levels is described. Samples were extracted with dichloromethane or acetone/hexane and cleaned up with micro-column silica gel chromatography. Measurements were made by dual capillary column gas chromatography using both nitrogen-phosphorus (NPD) and electron capture (ECD) detection. Recoveries from fortified water samples ranged from 76% to 102% for all sample types. Practical detection limits ranged between 0.003 and 0.029 microg/l in natural water samples, 0.0004-0.005 microg/g w.w. for sediments, and 0.001-0.005 microg/g w.w for biota using the NPD and ECD method. Losses in sediments were experienced when sulphur was removed. Precision and accuracy were not affected in sediment samples where sulphur was not removed.
OBJECTIVES: This study investigated the hypothesis that varying the acetone content of single solution dentin bonding agents may affect the adhesive layer thickness and microtensile bond strength (MTBS) of the bonded complex, and explored whether the adhesive layer thickness is a valid predictor for MTBS. METHODS: Experimental dentin bonding agents containing (27, 37, 47, 57, or 67) mass fraction% acetone were used to bond composite resin onto occlusal dentin surfaces of extracted human molars. The adhesive layer thickness was determined by digitized image analysis. MTBS was measured after 48 h. The fracture surfaces were observed using SEM. RESULTS: With increasing acetone content, MTBS varied from 38 MPa (67% acetone) to the highest MTBS of 64 MPa (37% acetone), while the adhesive layer thickness decreased linearly. Both dependent variables demonstrated moderate inverse correlation with the acetone content (p<0.0001), but were not correlated with each other (p>0.05). Ninety-four percent of the specimens showed fractures within the adhesive layer extending toward the interfaces with the hybrid layer or the composite resin. In the groups containing 57 and 67% acetone, cracks were observed at these interfaces. SIGNIFICANCE: Rather than the adhesive layer thickness, interfacial cracks in specimens with acetone-rich bonding agents may have caused lower MTBS. Within the scope of this investigation, lower acetone concentrations, as could be anticipated from solvent evaporation during clinical use of the bonding agent, did not seem to lower MTBS, but rather improved the integrity of the dentin/adhesive bond.
Recent health risk assessments to propose a Reference Dose (RfD) for acetone (Forsyth, 2001; U.S. EPA, 2001) have been based on the results of an oral subchronic study conducted in rats and mice (Dietz et al., 1991; NTP, 1991). These assessments have utilized the traditional concept of establishing the RfD by determining the lowest experimentally determined No-Observed-Adverse-Effect Level (NOAEL) and applying various Uncertainty Factors (UFs) (U.S. EPA, 1988). This article describes a risk assessment for acetone based on the systemic toxicity observed in subchronic and developmental toxicity studies to estimate an RfD and an inhalation reference concentration (RfC) for acetone. Specifically, this approach examined the subchronic study by Dietz et al. (1991), as well as an inhalation developmental toxicity study on acetone (Mast et al., 1988) and several toxicology studies of isopropanol (IPA). This was accomplished by applying a physiologically based pharmacokinetic (PBPK) model developed previously for IPA and its metabolite acetone (Clewell et al., 2001). The incorporation of the PBPK model into the derivation of an RfD and RfC for acetone allowed for a tissue-based approach rather than an external exposure-based approach, making it possible to derive an oral RfD from an inhalation study. In addition, the use of the PBPK model to analyze data from chronic and reproductive/developmental studies conducted with IPA enabled an assessment of the potential for acetone to produce any of the effects observed in the IPA studies. This analysis provided sufficient information to reduce the need for UFs in the adjustment of the NOAEL from the oral subchronic study for the determination of an RfD. Using the PBPK model in the acetone risk assessment supports a composite UF of 60 for the subchronic study, compared to composite factors of 300 to 3000 in the other recent risk assessments. This difference resulted in an RfD of 16 mg/kg/d, compared to the values of 0.3 to 3 that have previously been estimated (Forsyth, 2001; U.S. EPA, 2001). Considering the results from the inhalation developmental study (Mast et al., 1988) resulted in an RfD of 8.7 mg/kg/d. Using this study also fills a data gap for acetone that exists if only the oral database for acetone is considered for RfD derivation. An RfC of 29 ppm was also estimated for acetone using the Mast et al. (1988) study results in combination with the PBPK model. The potential impact of endogenous acetone on a risk assessment for acetone is also discussed.