Acenaphthene exposure

Diboration of a,/ -unsaturated ketones is promoted by platinum(O) complexes. Reaction of 4-phenyl-3-buten-2-one with bis(pinacolato)diboron in the presence of a platinum catalyst affords a boryl-substituted (Z)-boron enolate, that is, a 1,4-diboration product, in high yield with high stereoselectivity (Scheme 8). The isolated boron enolate is easily hydrolyzed by exposure to water, giving / -boryl ketones in high yields.66 Similar diboration of a,/ -unsaturated ketones has also been achieved with Pt(bian)(dmfu) (bian = bis(phenylimino)acenaphthene, dmfu = dimethyl fumarate).67 Although the... 

FIGURE 3.4 Biofouling reduces the exchange kinetics of PRCs (deuterated acenaphthene and fluorene) between the nonpolar Chemcatcher sampler (fitted with either fouled or unfouled LDPE membranes) and water. The experiment was performed in a laboratory flow-through calibration system at a water temperature of 11°C with simulated water turbulence of 40 rpm. MD(t)/MD(0) is the fraction of the PRC remaining in the sampler during exposure. 

Skin contact is the most common accidental exposure pathway. Acenaphthene may irritate or burn skin. Exposure can also be through ingestion or inhalation. Its vapor can be poisonous if inhaled. 

Acenaphthene can cause hepatotoxicity in rats and mice. Little information is available regarding acute exposure to acenaphthene. It is biotransformed in the liver. On the basis of a mouse oral subchronic study in which hepatotoxicity was seen as the major effect, the no-observed-adverse-effect level and the... 

Chronic human exposure data are not available. Currently, acenaphthene is under review by US Environmental Protection Agency for evidence of human carcinogenic potential. This does not imply that this agent is necessarily a carcinogen. The nitro-derivative of acenaphthene (5-nitroacenaphthene) is a possible carcinogen to humans. 

Oral Exposure. The only MRLs available for this fraction are acute and subchronic MRLs for naphthalene, an intermediate MRL for acenaphthene, and a chronic MRL for 1-methyl naphthalene these MRLs are listed in Table 6-6. Although more health effects data are available for oral exposure than for inhalation exposure to the constituents of this fraction, selection of surrogate values to use for oral exposure to this fraction is problematic. The acute and intermediate MRLs for naphthalene, 0.05 and 0.02 mg/kg/day, are equivalent to or lower than any other MRLs for this fraction, including the chronic MRL for 1-methyl naphthalene. The compounds in this fraction tend to cause hepatic and renal effects. Naphthalene and 1-methyl naphthalene have respiratory effects following oral exposure it is expected that... 

Intermediate-Duration Exposure. One intermediate-duration study was located that evaluated the carcinogenic potential of acenaphthene. Male and female mice exposed to 0, 175, 350, or 700 mg/kg/day acenaphthene by gavage for 13 weeks showed no evidence of tumorigenesis at necropsy (EPA 1989c). 

No acute, or chronic oral MRLs were derived for PAHs because there are no adequate human or animal dose-response data available that identify threshold levels for appropriate noncancer health effects. Serious reproductive and developmental effects in animals associated with acute oral exposure to PAHs have been reported. These are not appropriate end points for the derivation of an MRL. Noncancer effects noted in longer term oral toxicity studies in animals include increased liver weight (generally not considered to be adverse) and aplastic anemia (a serious effect), neither of which is an appropriate end point for the derivation of an MRL. Intermediate-duration oral MRLs were derived for acenaphthene. anthracene, fluoranthene, and fluorene. 

An MRL of 0.6 mg/kg/day has been derived for intermediate-duration oral exposure (15-364 days) to acenaphthene. 

Exposure of individuals installing treated fence posts, lumber, and timbers via inhalation of creosote volatiles (e g., acenaphthene and naphthalene) can also occur when freshly treated materials are handled under calm, hot, sunny conditions (USDA 1980). Exposure may be even greater during warmer months when ambient temperatures are higher. Acenaphthene, fluorene, phenanthrene, anthracene, and fluoranthene were observed to undergo more volatilization from creosote-treated wood at 30 °C than at 4 °C (Gevao and Jones 1998). 

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