Advanced Water and Waste Water Engineering

Abstract.

This report makes use of the site investigation findings as described in the various section to evaluate further the potential pollutant linkages identified. A combination of qualitative and quantitative techniques is used as described below. The comparison of contaminant concentrations measured in water at a site with generic assessment criteria. Generic assessment criteria are typically conservative to ensure that they are applicable to the majority of sites and normally apply to only a limited number of pollutant linkages.

Introduction:

Acenaphthene, also known as 1,2-dihydroacenaphthylene or 1,8-ethylenenaphthalene, is a tricyclic aromatic hydrocarbon that occurs in coal tar. It is used as a dye intermediate, in the manufacture of some plastics, and as an insecticide and fungicide (EPA, 1980). Acenaphthene has been detected in cigarette smoke, automobile exhausts, and urban air; in effluents from petrochemical, pesticide, and wood preservative industries (EPA, 1980); and in soils, groundwater, and surface waters at hazardous waste sites.

Exposure Assessments:

No absorption data are available for acenaphthene; however, by analogy to structurally-related polycyclic aromatic hydrocarbons (PAHs), it would be expected to be absorbed from the gastrointestinal tract and lungs (EPA, 1988). The anhydride of naphthalic acid was identified as a urinary metabolite in rats treated orally with acenaphthene (Chang and Young, 1943).

Although a large body of literature exists on the toxicity and carcinogenicity of PAHs, primarily benzo[a]pyrene, toxicity data for acenaphthene are limited. Acenaphthene is irritating to the skin and mucous membranes of humans and animals (Sandmeyer, 1981; Knobloch et al., 1969). Acute toxicity data for animals include oral LD₅₀s of 10 g/kg for rats and 2.1 g/kg for mice (Knobloch et al., 1969) and an intraperitoneal LD₅₀ of 600 mg/kg for rats (Reshetyuk et al., 1970). Oral exposure of rats to daily 2-g doses of acenaphthene for 32 days produced peripheral blood changes, mild liver and kidney damage, and pulmonary effects (Knobloch et al., 1969). Subchronic oral exposure to acenaphthene at doses of > 350 mg/kg for 90 days produced increased liver weights, hepatocellular hypertrophy, and increased cholesterol levels in mice. Reproductive effects included decreased ovary weights at doses of > 350 mg/kg and decreased ovarian and uterine activity as well as smaller and fewer corpora lutea at 700 mg/kg/day (EPA, 1989). Adverse effects on the blood, lungs, and glandular tissues were reported in rats exposed daily to 12 mg/m³ of acenaphthene for 5 months (Reshetyuk et al., 1970).

A reference dose (RfD) of 6E-1 mg/kg/day for subchronic oral exposure (EPA, 1993a) and 6.E-2 mg/kg/day for chronic oral exposure to acenaphthene (EPA, 1993b) was calculated from a no-observed- adverse-effect level (NOAEL) of 175 mg/kg/day from a 90-day gavage study with mice. The critical effect was hepatotoxicity. Data were insufficient to derive an inhalation reference concentration (RfC) for acenaphthene (EPA, 1993a,b).

Effect Assessment:

Neukomm (1974) reported negative results in a predictive carcinogenicity test based on neoplastic induction in the newt, Triturus Cristatus. Acenaphthene was injected subcutaneously at unspecified dose levels. Mutagenicity studies of ancenaphthene in Salmonella typhimurium gave negative results in strain with and without S-9 metabolic activation and in strains with s-9 metabolic activation.

Acenaphthene also had no effect on the recombination rate of two auxotrophic strains of Escherichia coli, as indicated by the low level of prototroph induction also tested acenaphthene for mutagenicity in Micrococcus. Acenaphthene has been shown to produce nuclear and cytological changes in microbial and plant species. The changes observed, including increased cell size and DNA content are associated with disruption of the spindle mechanism during mitosis. Because there is no known correlation between these effects and the biological impact of acenaphthene on mammalian cells studies examining these changes will not be summarized here. Studies concerning these mitotic effects are reviewed in US EPA.

Risk Characterization:

Sub Chronic:

The 2 g/kg of acenaphthene in olive oil to seven young rates daily for 32 days. The effects observed were loss of body weight, changes in peripheral blood, increased aminotransferase levels in blood serum, mild morphological damage to the liver and kidneys, and mild bronchitis and localized inflammation of the peribronchial tissue. No information was provided regarding the use of controls.

In a subchronic gavage study, male and female CD-1 mice were administered 0, 175, 350, or 700 mg/kg/day of acenaphthene for 90 days (EPA, 1989). There were no treatment-related effects on survival, body weight, or total food intake. No clinical signs of toxicity or ophthalmologic alterations were observed. Statistically significant (p0.05) increases in liver weights accompanied by microscopic alteration (cellular hypertrophy) occurred in mid- and high-dosed rats (both sexes). Additionally, high-dosed males and mid- and high-dosed females had significantly (p0.05) increased cholesterol levels. In females, acenaphthene elicited adverse effects on the reproductive system characterized by decreased ovary weights (mid- and high-dosed mice, p0.05) and decreased activity of the ovaries and uterus, as well as fewer and smaller corpora lutea (high-dosed mice). Although increased liver weights without accompanying microscopic alterations or increased cholesterol levels were also observed at the low dose, this change was considered to be adaptive rather than adverse, providing a lowest-observed-adverse-effect level (LOAEL) of 350 mg/kg/day and a no-observed-adverse-effect level (NOAEL) of 175 mg/kg/day.

Comments:

These screening criteria have been taken from the World Health Organization Guidelines for Drinking Water Quality (1984). The health value is a guideline value representing the concentration of a contaminant that does not result in any significant risk to the receptor over a lifetime of exposure.

EQS have been released by the EA for dangerous substances, as identified by the European Commission (EC) Dangerous Substances Directive. EQS can vary for each substance, for the hardness of the water and can be different for fresh, estuarine or coastal waters.

Conclusion:

Because of the lack of data for the carcinogenicity and threshold toxicity of acenaphthene, risk assessment values cannot be derived. The ambient water quality criterion of 0.2 mg/l is based on organoleptic data which has no known relationship to potential human health effects.

The best documented effect of acenaphthene is its ability to cause nuclear and cytologic changes in plants. No correlation between these effects on mammalian cells is known. Acenaphthene has tested negative in mutagenicity studies in microorganisms and in a carcinogenicity study in the newt, Triturus cristatus. Despite the negative results the fact that acenaphthene is a PAH a class of chemicals that contain carcinogens,  indicates that the primary issue requiring resolution is the carcinogenicity of acenaphthene by oral or inhalation exposure. Acenaphthene has been found in both air and water, so that both routes of exposure may be important. If adequate testing determines that acenaphthene is not carcinogenic efforts should be made to define thresholds for non carcinogenic toxicity. Data are needed to determine the target organs or systems most likely to be injured by exposure to acenaphthene. Because acenaphthene has a relatively low vapor pressure substantial levels in air are unlikely and initial testing by oral exposure to determine sub chronic developmental and reproductive toxicity may be more immediately necessary.

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