Health Effects Support Document for Naphthalene Printed on Recycled Paper Health Effects Support Document for Naphthalene U. S. Environmental Protection Agency Office of Water ( 4304T) Health and Ecological Criteria Division Washington, DC 20460 www. epa. gov/ safewater/ ccl/ pdf/ naphthalene. pdf EPA 822 R 03 005 February 2003 iii Naphthalene   February 2003 FOREWORD The Safe Drinking Water Act ( SDWA), as amended in 1996, requires the Administrator of the Environmental Protection Agency ( EPA) to establish a list of contaminants to aid the Agency in regulatory priority setting for the drinking water program. In addition, the SDWA requires EPA to make regulatory determinations for no fewer than five contaminants by August 2001. The criteria used to determine whether or not to regulate a chemical on the Contaminant Candidate List ( CCL) are the following:

The contaminant may have an adverse effect on the health of persons.

The contaminant is known to occur or there is a substantial likelihood that the contaminant will occur in public water systems with a frequency and at levels of public health concern.

In the sole judgment of the Administrator, regulation of such contaminant presents a meaningful opportunity for health risk reduction for persons served by public water systems.

The Agency's findings for all three criteria are used in making a determination to regulate a contaminant. The Agency may determine that there is no need for regulation when a contaminant fails to meet one of the criteria. The decision not to regulate is considered a final Agency action and is subject to judicial review.

This document provides the health effects basis for the regulatory determination for naphthalene. In arriving at the regulatory determination, data on toxicokinetics, human exposure, acute and chronic toxicity to animals and humans, epidemiology, and mechanisms of toxicity were evaluated. In order to avoid wasteful duplication of effort, information from the following risk assessments by the EPA and other government agencies were used in development of this document.

U. S. EPA 1987. U. S. Environmental Protection Agency. Summary Review of Health Effects Associated with Naphthalene. Washington, D. C.: Office of Health and Environmental Assessment, EPA/ 600/ 8 87/ 005F U. S. EPA. 1990. U. S. Environmental Protection Agency. Naphthalene Drinking Water Health Advisory. Office of Water. March.

ATSDR. 1995. Agency for Toxic Substances and Disease Registry. Toxicological Profile for Naphthalene ( update). Department of Health and Human Services. CRC Press, Boca Raton, FL 1997.

U. S. EPA 1998a. U. S. Environmental Protection Agency. Toxicological Review of Naphthalene ( CAS 91 20 3) in support of summary information on the Integrated Risk Information System ( IRIS). August 1998. iv Naphthalene   February 2003 U. S. EPA 1998b. U. S. Environmental Protection Agency. Integrated Risk Information System ( IRIS): Naphthalene. Cincinnati, OH. September 17, 1998.

Information from the published risk assessments was supplemented with information from recent studies of naphthalene identified by literature searches conducted in 1999 and 2000 and the primary references for key studies.

Generally a Reference Dose ( RfD) is provided as the assessment of long term toxic effects other than carcinogenicity. RfD determination assumes that thresholds exist for certain toxic effects, such as cellular necrosis. It is expressed in terms of milligrams per kilogram per day ( mg/ kg day). In general, the RfD is an estimate ( with uncertainty spanning perhaps an order of magnitude) of a daily exposure to the human population ( including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime.

The carcinogenicity assessment for naphthalene includes a formal hazard identification. Hazard identification is a weight of evidence judgment of the likelihood that the agent is a human carcinogen via the oral route and of the conditions under which the carcinogenic effects may be expressed.

Guidelines that were used in the development of this assessment may include the following: the Guidelines for Carcinogen Risk Assessment ( U. S. EPA, 1986a), Guidelines for the Health Risk Assessment of Chemical Mixtures ( U. S. EPA, 1986b), Guidelines for Mutagenicity Risk Assessment ( U. S. EPA, 1986c), Guidelines for Developmental Toxicity Risk Assessment ( U. S. EPA, 1991a), Proposed Guidelines for Carcinogen Risk Assessment ( 1996a), Guidelines for Reproductive Toxicity Risk Assessment ( U. S. EPA, 1996b), Guidelines for Neurotoxicity Risk Assessment ( U. S. EPA, 1998c); Recommendations for and Documentation of Biological Values for Use in Risk Assessment ( U. S. EPA, 1988); Use of the Benchmark Dose Approach in Health Risk Assessment ( U. S. EPA, 1995); and Memorandum from EPA Administrator, Carol Browner, dated March 21, 1995.

The chapter on occurrence and exposure to naphthalene through potable water was developed by the Office of Ground Water and Drinking Water. It is based primarily on unregulated contaminant monitoring ( UCM) data collected under SDWA. The UCM data are supplemented with ambient water data, as well as information on production, use, and discharge. v Naphthalene   February 2003 ACKNOWLEDGMENT This document was prepared under the U. S. EPA contract No. 68 C 01 002, Work Assignment No. B 02 with Sciences International, Alexandria, VA. The Lead U. S. EPA Scientist is Joyce Morrissey Donohue, Ph. D., Health and Ecological Criteria Division, Office of Science and Technology, Office of Water. vi Naphthalene   February 2003 TABLE OF CONTENTS FOREWORD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . iii ACKNOWLEDGMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . v LIST OF TABLES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix LIST OF FIGURES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . x 1.0 EXECUTIVE SUMMARY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 1 2.0 IDENTITY: CHEMICAL AND PHYSICAL PROPERTIES . . . . . . . . . . . . . . . . . . . . 2 1 3.0 USES AND ENVIRONMENTAL FATE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 1 3.1 Production and Use . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 1 3.2 Environmental Release . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 1 3.3 Environmental Fate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 3 3.4 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 4 4.0 EXPOSURE FROM DRINKING WATER . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 1 4.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 1 4.2 Ambient Occurrence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 1 4.2.1 Data Sources and Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 1 4.2.2 Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 2 4.3 Drinking Water Occurrence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 3 4.3.1 Data Sources, Data Quality, and Analytical Methods . . . . . . . . . . . . . . . 4 4 4.3.2 Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 13 4.4 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 16 5.0 EXPOSURE FROM MEDIA OTHER THAN WATER . . . . . . . . . . . . . . . . . . . . . . . . 5 1 5.1 Exposure from Food . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 1 5.1.1 Concentration in Non Fish Food Items . . . . . . . . . . . . . . . . . . . . . . . . . 5 1 5.1.2 Concentrations in Fish and Shellfish . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 1 5.1.3 Intake of Naphthalene from Food . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 3 5.2 Exposure from Air . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 4 5.2.1 Concentration of Naphthalene in Air . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 4 5.2.2 Intake of Naphthalene from Air . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 5 5.3 Exposure from Soil . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 5 5.3.1 Concentration of Naphthalene in Soil . . . . . . . . . . . . . . . . . . . . . . . . . . 5 5 5.3.2 Intake of Naphthalene from Soil . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 6 5.4 Other Residential Exposures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 7 5.5 Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 7 vii Naphthalene   February 2003 6.0 TOXICOKINETICS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 1 6.1 Absorption . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 1 6.2 Distribution . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 2 6.3 Metabolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 3 6.4 Excretion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 6 7.0 HAZARD IDENTIFICATION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 1 7.1 Human Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 1 7.1.1 Short Term Studies and Case Reports . . . . . . . . . . . . . . . . . . . . . . . . . . 7 1 7.1.2 Long Term and Epidemiological Studies . . . . . . . . . . . . . . . . . . . . . . . 7 3 7.2 Animal Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 4 7.2.1 Acute Toxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 4 7.2.2 Short Term Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 6 7.2.3 Subchronic Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 7 7.2.4 Neurotoxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 10 7.2.5 Developmental/ Reproductive Toxicity . . . . . . . . . . . . . . . . . . . . . . . . 7 10 7.2.6 Chronic Toxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 14 7.2.7 Carcinogenicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 18 7.3 Other Key Data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 23 7.3.1 Mutagenicity and Genotoxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 23 7.3.2 Ocular Toxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 24 7.3.3 Hematological Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 29 7.3.4 Immunotoxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 29 7.3.5 Hormonal Disruption . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 30 7.3.6 Physiological or Mechanistic Studies . . . . . . . . . . . . . . . . . . . . . . . . . 7 30 7.3.7 Structure Activity Relationship . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 34 7.4 Hazard Characterization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 35 7.4.1 Synthesis and Evaluation of Major Noncancer Effects . . . . . . . . . . . . 7 35 7.4.2 Synthesis and Evaluation of Carcinogenic Effects . . . . . . . . . . . . . . . 7 37 7.4.3 Mode of Action and Implications in Cancer Assessment . . . . . . . . . . 7 53 7.4.4 Weight of Evidence Evaluation for Carcinogenicity . . . . . . . . . . . . . . 7 53 7.4.5 Potentially Sensitive Populations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 56 8.0 DOSE RESPONSE ASSESSMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 1 8.1 Dose Response for Noncancer Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 1 8.1.1 RfD Determination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 1 8.1.2 RfC Determination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 2 8.2 Dose Response for Cancer Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 2 9.0 REGULATORY DETERMINATION AND CHARACTERIZATION OF RISK FROM DRINKING WATER . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 1 9.1 Regulatory Determination for Chemicals on the CCL . . . . . . . . . . . . . . . . . . . . 9 1 9.1.1 Criteria for Regulatory Determination . . . . . . . . . . . . . . . . . . . . . . . . . . 9 1 9.1.2 National Drinking Water Advisory Council Recommendations . . . . . . 9 2 9.2 Health Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 2 viii Naphthalene   February 2003 9.2.1 Health Criterion Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 3 9.2.2 Hazard Characterization and Mode of Action Implications . . . . . . . . . 9 3 9.2.3 Dose Response Characterization and Implications in Risk Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 4 9.3 Occurrence in Public Water Systems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 7 9.3.1 Occurrence Criterion Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 7 9.3.2 Monitoring Data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 8 9.3.3 Use and Fate Data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 9 9.4 Risk Reduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 10 9.4.1 Risk Criterion Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 10 9.4.2 Exposed Population Estimates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 11 9.4.3 Relative Source Contribution . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 11 9.4.4 Sensitive Populations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 13 9.5 Regulatory Determination Decision . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 14 10.0 REFERENCES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 1 APPENDIX A: Abbreviations and Acronyms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . A 1 APPENDIX B: Naphthalene Occurrence Data for Public Water Systems ( Round 1 and Round 2) . . . . . . . . . . . . . . . . . . . . . . . . . . . . B 1 ix Naphthalene   February 2003 LIST OF TABLES Table 2 1. Chemical and Physical Properties of Naphthalene . . . . . . . . . . . . . . . . . . . . . . 2 1 Table 3 1. Environmental Releases ( in pounds) for Naphthalene in the United States ( 1988   1998) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 2 Table 4 1. Naphthalene Detections and Concentrations in Ground Water . . . . . . . . . . . . . 4 3 Table 4 2. Cross section States for Round 1 ( 24 States) and Round 2 ( 20 States) . . . . . . . 4 7 Table 4 3. Summary Occurrence Statistics for Naphthalene . . . . . . . . . . . . . . . . . . . . . . 4 10 Table 5 1. Naphthalene And Methylnaphthalene Concentrations in Meat Samples. . . . . . 5 2 Table 5 2. Concentrations of Naphthalene in Vegetables . . . . . . . . . . . . . . . . . . . . . . . . . . 5 3 Table 5 3. Median Concentrations of Naphthalene and Methylnaphthalene in Harp Seals . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 3 Table 5 4. Concentrations of Naphthalene in Residential Dust ( mg/ g) . . . . . . . . . . . . . . . 5 5 Table 5 5. Exposure to Naphthalene in Media Other than Water . . . . . . . . . . . . . . . . . . . . 5 8 Table 7 1. Terminal Body Weights in Controls and in Fischer 344 Rats Exposed to Naphthalene by Gavage for 13 Weeks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 8 Table 7 2. Summary of Developmental and Reproductive Data on Naphthalene . . . . . . 7 11 Table 7 3. Survival and Incidence of Non neoplastic Lesions in B6C3F 1 Mice Exposed to Naphthalene by Inhalation for Their Lifetime . . . . . . . . . . . . . . . 7 15 Table 7 4. Incidence and Severity of Nonneoplastic Lesions in the Noses of Rats in a Two year Naphthalene Inhalation Study . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 17 Table 7 5. Incidence of Neoplasms in Male and Female F344/ N Rats in a Two year Naphthalene Inhalation Exposure Study . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 21 Table 7 6. Summary of Studies of Naphthalene Ocular Toxicity in Animals . . . . . . . . . 7 25 Table 7 7. Summary of Key Studies of Noncancer Toxic Effects of Naphthalene . . . . . . 7 39 Table 9 1. Dose Response Information from Five Key Studies of Naphthalene Toxicity . 9 6 Table 9 2. National Population Estimates for Naphthalene Exposure via Drinking Water . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 11 Table 9 3. Comparison of Average Daily Intakes from Drinking Water and Other Media . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 12 Table 9 4. Ratios of Exposures from Various Media to Exposures from Drinking Water . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 13 x Naphthalene   February 2003 LIST OF FIGURES Figure 2 1. Chemical Structure of Naphthalene . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 1 Figure 4 1. Geographic Distribution of Cross section States. Round 1 ( left) and Round 2 ( right) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 7 Figure 4 2. States with PWSs with Detections of Naphthalene for all States with Data in URCIS ( Round 1) and SDWIS/ FED ( Round 2). . . . . . . . . . . . . . . . . . . . . . . . 4 14 Figure 4 3. States with PWSs with Detections of Naphthalene ( any PWSs with Results Greater than the Minimum Reporting Level [ MRL]) for Round 1( above)

and Round 2 ( below) Cross section States. . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 17 Figure 4 4. Cross section States ( Round 1 and Round 2 Combined) with PWSs with Detections of Naphthalene ( above) and Concentrations Greater than the Health Reference Level ( HRL; below) . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 18 Figure 6 1. Proposed Pathways For Naphthalene Metabolism . . . . . . . . . . . . . . . . . . . . . . . 6 4 1 1 Naphthalene   February 2003 1.0 EXECUTIVE SUMMARY The U. S. Environmental Protection Agency ( EPA) has prepared this Drinking Water Support Document to assist in determining whether to establish a National Primary Drinking Water Regulation ( NPDWR) for naphthalene. Case study reports from humans and laboratory studies with animals demonstrate that naphthalene can have adverse effects on the oxidation state of hemoglobin ( methemoglobinemia), the structural integrity of the red blood cell membrane ( hemolysis), the activity of selected hepatic enzymes, and body weight gain following oral exposure. It also contributes to the formation of cataracts in certain species and strains of laboratory animals. These effects tend to occur at moderate to high doses that are unlikely to be found in public water systems. Accordingly, regulation of naphthalene in public water does not present a meaningful basis for health risk reduction. Prolonged inhalation exposure to naphthalene, such as can occur in the workplace, may present risks to humans, but risk from other exposure routes is minimal.

Naphthalene ( Chemical Abstracts Services Registry Number 91 20 3) is a bicyclic aromatic hydrocarbon with the chemical formula C 10 H 8. In purified form, naphthalene is a white crystalline solid that is sparingly soluble in water ( 0.031 g/ L). Naphthalene is a natural constituent of coal tar and crude oil. It is obtained in purified form from these raw materials by fractional distillation. The available historical data suggest that both production and consumption of naphthalene are declining in the United States. Crystalline naphthalene is used by consumers as a moth repellant and as a deodorizer in toilets and diaper pails. Approximately 60% of the naphthalene consumed in the United States is used commercially in the manufacture of phthalate plasticizers, resins, phthaleins, dyes, pharmaceuticals, insect repellants, and other products.

Direct releases to air account for more than 90% of the naphthalene entering environmental media. In comparison, about 5% of the naphthalene entering the environment is released to water and about 2.7% is discharged to land. Releases to water occur primarily from coal tar production and distillation processes. Other contributing sources include effluents from wood preserving facilities and oil spills. Over half of the releases to water occur to surface water.

Naphthalene is lost from surface water primarily by volatilization. Estimates for half life range from 4.2 to 7.3 hours. A small fraction ( less than 10%) is associated with organic material and settles into sediments. Naphthalene remaining in the water column is degraded by photolysis ( half life = 71 hours) and/ or biodegradation processes ( highly variable half life depending on naphthalene concentration, nutrient supply, and water temperature).

Naphthalene has been detected in untreated ambient ground water samples reviewed and/ or analyzed by the U. S. Geological Survey National Ambient Water Quality Assessment ( NAWQA) program. Detection frequencies and concentrations for all wells are relatively low; however, occurrence is considerably higher for urban wells when compared to rural wells. Naphthalene has been detected at slightly higher frequencies in urban and highway runoff. Concentrations in runoff are low. Naphthalene has also been found at Agency for Toxic 1 2 Naphthalene   February 2003 Substances and Disease Registry ( ATSDR) HazDat and Comprehensive Environmental Response, Compensation and Liability Act ( CERCLA) National Priority List ( NPL) sites across the country, and releases have been reported through the Toxic Release Inventory.

Naphthalene has been detected in public water system ( PWS) samples collected under the provisions of the Safe Drinking Water Act ( SDWA), although only 0.43% and 0.24% of total samples from two rounds of sampling showed detections. Significantly, the values for the 99th percentile and median concentrations of all samples are less than the Minimum Reporting Level ( MRL). For Round 1 samples with detections, the median concentration is 1.0 µ g/ L and the 99th percentile concentration is 900 µ g/ L. Median and 99th percentile concentrations for Round 2 detections are 0.74 µ g/ L and 73 µ g/ L, respectively. Public water systems with detections constitute only 1.2% of Round 1 systems and 0.8% of Round 2 systems, representing an estimated 769 systems ( Round 1) and 491 systems ( Round 2) when extrapolated to the national level. National estimates for the population served by PWSs with detections are also low, especially for detections greater than the Health Reference Level ( HRL).

Nationally aggregated data for naphthalene in media other than water are generally not available. The available data from localized studies suggest that naphthalene levels in fish and non fish food items are generally low unless they have been smoked or grilled. Estimates for daily intake of naphthalene via the diet ranged from 40.7 to 237 ng/ kg day for a 70 kg adult and 204 to 940 ng/ kg day for a 10 kg child. Comparison of the available data indicates that, based on rough estimates of average intakes for naphthalene, most exposure occurs through inhalation. Estimated intakes from air are approximately 5 to 45 fold greater than those from food and water.

Naphthalene is absorbed when administered orally, although no studies were identified that quantified the rate or extent of uptake. Dermal absorption of naphthalene has been inferred from toxicity observed in human neonates who were reportedly exposed by dermal contact with clothing that had been stored with naphthalene mothballs or naphthalene flakes. No empirical data that describe the rate or extent of naphthalene absorption following inhalation exposure were identified in the materials reviewed for this report. Physiologically based pharmacokinetic modeling results suggest that inhaled naphthalene is absorbed rapidly into the blood.

After distribution, naphthalene is extensively metabolized. As many as 21 metabolites ( including oxidized derivatives and conjugates) have been identified in the urine of humans and animals exposed to naphthalene. The factors that influence the relative proportions of individual metabolites include species, tissue type, and tissue concentration of naphthalene. The available evidence suggests that the naphthalene metabolites 1,2 naphthoquinone and 1,4 naphthoquinone are the primary toxic species.

Information on the human health effects of naphthalene have been obtained from medical case reports of accidental or intentional ingestion. These reports identify hemolytic anemia as the significant outcome of oral exposure to large doses of naphthalene in humans. There is one report of cataracts in humans, but it was published in the early twentieth century and, thus, has limited applicability because of uncertainties regarding compound purity and exposure 1 3 Naphthalene   February 2003 conditions. There are no reliable human toxicity data for subchronic or chronic exposure to naphthalene.

Studies of occupational exposure to naphthalene are limited to a single report of possible naphthalene related cataracts in chemical workers and two limited epidemiological studies that provide ambiguous evidence of associations between occupational naphthalene exposure and cancer. Owing to their numerous limitations, none of these studies is useful in characterizing the potential risks associated with human exposures to naphthalene.

Individuals deficient in the enzyme glucose 6 phosphate dehydrogenase ( G6PD) have been identified as a potentially sensitive population for naphthalene exposure. Individuals with this deficiency have low erythrocyte levels of reduced glutathione, a compound that normally protects red blood cells against oxidative damage. G6PD deficient neonates, infants, and the fetus are particularly sensitive to naphthalene toxicity because the metabolic pathways responsible for conjugation of toxic metabolites ( a prerequisite for excretion) are not yet well developed. In addition, they have low levels of methemoglobin reductase. This enzyme catalyzes the reduction of methemoglobin, an oxidized form of hemoglobin that occurs in association with hemolytic anemia.

Short term administration of an average daily dose of 262 mg/ kg day to a single dog resulted in signs of hemolytic anemia, including decreased hemoglobin concentration, decreased hematocrit, presence of Heinz bodies, extreme leukocytosis, and reticulocytosis. Other signs noted included pronounced lethargy and ataxia. In mice, short term oral exposure to naphthalene at doses up to 53 mg/ kg day had no apparent adverse effects. Adverse effects observed in mice exposed to 267 mg/ kg day included increased mortality and decreased terminal body weights ( 4   10%) in males and females, decreased absolute thymus weights ( 30%) in males, increased bilirubin in females, and increased spleen and lung weights ( relative and absolute) in females. Neither red cell hemolysis nor cataract formation was observed in the naphthalene exposed mice. Liver changes ( increased liver weight, increased lipid peroxidation, moderate increases in serum enzyme activity) have been reported in rats exposed to relatively high doses of naphthalene ( approximately 1,000 mg/ kg day or more) when administered for durations of 10 days to 9 weeks. However, no effects on liver weight were noted in a 14 day gavage study at doses up to 267 mg/ kg day. Naphthalene related cataract formation has been reported in rabbits, mice and rats following acute and short term oral exposures.

The subchronic oral toxicity of naphthalene has been investigated in rats and mice. Male and female rats administered 400 mg/ kg day by corn oil gavage for 13 weeks exhibited diarrhea, lethargy, hunched posture, and rough coats during the study, and one high dose male rat died during the last week of exposure. Body weights were significantly decreased in males at 200 mg/ kg day and in males and females at 400 mg/ kg day. In a similar study conducted in mice, transient signs of toxicity ( lethargy, rough coats, decreased food consumption) were observed at 200 mg/ kg day and above. Female mice exposed to naphthalene exhibited dose related decreases in body weight reaching a maximum of 24.5% in females receiving 200 mg/ kg day. A second oral exposure study in mice observed changes in organ weight and enzyme alterations indicative of impacts on liver function at 133 mg/ kg day. 1 4 Naphthalene   February 2003 Relatively little information is available regarding the neurological effects of naphthalene exposure in experimental animals. Two studies ( one each in rabbits and pregnant rats) have noted treatment related signs of neurotoxicity ( lethargy, slow respiration including periods of apnea, body drop and labored breathing, and/ or inability to move after dosing) at doses of 50 to 450 mg/ kg day. These effects were transient in pregnant rats at doses of 50 to 150 mg/ kg day. However, the subchronic studies discussed above found no clinical signs of neurotoxicity at similar doses.

The reproductive and developmental toxicity of naphthalene has been evaluated in rats, mice and rabbits. The results of these studies suggest that naphthalene is a very weak reproductive and developmental toxicant, with detectable effects occurring only at doses associated with substantial maternal toxicity.

The 2 year inhalation National Toxicology Program ( NTP) bioassays of naphthalene reported increased incidences of non neoplastic nasal lesions in male rats exposed for 6 hours/ day to 10 ppm. In mice, there was chronic inflammation of the lungs and nasal epithelium accompanied by hyperplasia There are no oral exposure studies that are considered adequate to fully assess the carcinogenic potential of naphthalene. No tumors were identified in a study of rats orally administered 42 mg/ kg day for over 2 years. However, the published report contains limited experimental detail. NTP concluded that there was some evidence of carcinogenic potential in female mice exposed by inhalation to 30 ppm naphthalene for 2 years. Clear evidence for carcinogenic potential was observed in male and female rats exposed to 60 ppm naphthalene ( approximately 20 mg/ kg day) by inhalation for 2 years. However, statistical significance was achieved only for tumors of the respiratory track ( lungs in mice; nasal cavity in rats). Several studies have been conducted in which naphthalene was administered by routes of exposure other than inhalation or diet. No carcinogenic responses were observed in these studies and each has at least one limitation that makes it inadequate for assessing the potential for lifetime risk.

The mutagenic and genotoxic potential of naphthalene has been evaluated in numerous in vitro and in vivo assays. The results of most studies were negative, suggesting that the mutagenic and genotoxic potential of naphthalene and its metabolites are weak.

When naphthalene was evaluated for EPA's Integrated Risk Information System ( IRIS), prior to completion of the NTP bioassay in rats, it was classified in Group C: possible human carcinogen. This classification was based on inadequate human data for exposure to naphthalene via the oral and inhalation routes and on limited evidence of carcinogenicity in animals exposed via the inhalation route. Using the 1996 Proposed Guidelines for Carcinogen Risk Assessment, the human carcinogenic potential of naphthalene via oral or inhalation routes " cannot be determined." Following completion of the IRIS review, the NTP bioassay in rats showed clear evidence for carcinogenic activity within the nasal cavity, but not in other tissues. The new data strengthen the association of carcinogenicicty with the inhalation route of exposure and weaken the tenuous association with the oral route. For this reason, the carcinogenic potential of naphthalene via the inhalation route may need to be re evaluated. 1 5 Naphthalene   February 2003 A quantitative cancer dose response assessment for naphthalene was not conducted for IRIS. This decision was made because adequate chronic oral animal data are lacking and because the available human data are inadequate to evaluate a plausible association with cancer. Although statistically significant increases in the incidence of respiratory system tumors were reported in female mice ( lung) and rats ( nasal cavity) exposed to naphthalene via inhalation for 2 years, this evidence is considered insufficient to assess the carcinogenic potential of naphthalene in humans exposed via the oral route. The existing data on the tumorigenic effects of naphthalene by the oral route of exposure are inadequate to support a judgment and, therefore, would be categorized as Group D, " not classifiable". 2 1 Naphthalene   February 2003 Naphthalene 2.0 IDENTITY: CHEMICAL AND PHYSICAL PROPERTIES Naphthalene is a bicyclic aromatic hydrocarbon with the chemical formula C 10 H 8 ( Figure 2 1). Pure naphthalene is a white, water insoluble solid in crystalline or marble like form and has a distinct mothball odor. The chemical and physical properties of naphthalene are summarized in Table 2 1.

Figure 2 1. Chemical Structure of Naphthalene Table 2 1. Chemical and Physical Properties of Naphthalene Property Information Chemical Abstracts Registry ( CAS) No. 91 20 3 Registry of Toxic Effects of Chemical Substances No. QJ0525000 RCRA Waste No. U165 EPA Pesticide Chemical Code 055801 Synonyms Tar Camphor; Albocarbon; Naphthene; Naphthalin; Naphthaline; Mothballs; Mothflakes; White Tar; Dezodorator; Mighty 150; Mighty RD1 Registered Trade Name Caswell No. 587 ® Chemical Formula C 10 H 8 Molecular Weight 128.19 Boiling Point 218oC Melting Point 80.5oC Vapor Pressure 0.087 mm Hg Partition Coefficients Log K ow 3.29 Log K oc 2.97 Solubility in Water 0.0031 g/ 100 mL Organic Solvents Benzene, Alcohol, Ether, Acetone Source: ATSDR ( 1995); ChemIDplus ( 2000) 3 1 Naphthalene   February 2003 3.0 USES AND ENVIRONMENTAL FATE 3.1 Production and Use Naphthalene is naturally present in fossil fuels such as petroleum and coal, and is generated when wood or tobacco are burned. Naphthalene is produced in commercial quantities from either coal tar or petroleum. Most of the naphthalene produced in the United States comes from petroleum by the dealkylation of methylnaphthalenes in the presence of hydrogen at high temperature and pressure. Another common production method is the distillation and fractionation of coal tar.

Naphthalene is a natural constituent of coal tar and crude oil ( 11% and 1.3%, respectively) ( Merck Index, 1996). Purified naphthalene is obtained from coal tar or petroleum products by fractional distillation. Fractional distillation is the process of heating a liquid until its more volatile constituents pass into the vapor phase. This vapor is then cooled to recover constituents by condensation ( Encarta, 2000). Different constituents will vaporize at different boiling points, thus permitting separation of constituents. Most naphthalene is recovered in the middle fraction ( ATSDR, 1995). This fraction is subsequently purified by treatment with sulfuric acid, sodium hydroxide, and water, followed by sublimation or a second fractional distillation. U. S. manufacturers produced 1.09 × 105 metric tons of naphthalene in 1996 ( CEH, 2000).

Naphthalene production in the United States dropped from 900 million pounds per year ( lbs/ yr) in 1968 to 354 million lbs/ yr in 1982. Approximately 7 million lbs of naphthalene were imported and 9 million lbs were exported in 1978. By 1989, imports had dropped to 4 million lbs, and exports increased dramatically to 21 million lbs ( ATSDR, 1995).

U. S. consumption of naphthalene was 1.08 x 105 metric tons in 1996 ( CEH, 2000). Naphthalene is used in the production of phthalic anhydride, which is an intermediate in the manufacture of phthalate plasticizers, resins, phthaleins, dyes, pharmaceuticals, insect repellants, and other products ( U. S. EPA, 1998a). These uses account for approximately 60% of naphthalene consumption in the United States ( CEH, 1997). Crystalline naphthalene is used as a moth repellant and as a deodorizer for diaper pails and in toilets ( U. S. EPA, 1998a). In the past, naphthalene was used medicinally as an antiseptic, expectorant, and anthelminthic, and for treatment of gastrointestinal and skin disorders ( ATSDR, 1995). Most naphthalene consumption ( 60%) is through use as an intermediary in the production of phthalate plasticizers, resins, phthaleins, dyes, pharmaceuticals, and insect repellents. Crystalline naphthalene is used as a moth repellent and a solid block deodorizer for diaper pails and toilets. Naphthalene is also used to make the insecticide carbaryl, synthetic leather tanning agents, and surface active agents ( ATSDR, 1995).

3.2 Environmental Release Naphthalene is listed as a toxic release inventory ( TRI) chemical. In 1986, the Emergency Planning and Community Right to Know Act ( EPCRA) established the Toxic 3 2 Naphthalene   February 2003 Release Inventory ( TRI) of hazardous chemicals. Created under the Superfund Amendments and Reauthorization Act ( SARA) of 1986, EPCRA is also sometimes known as SARA Title III. The EPCRA mandates that larger facilities publicly report when TRI chemicals are released into the environment. This public reporting is required for facilities with more than 10 full time employees that annually manufacture or produce more than 25,000 pounds, or use more than 10,000 pounds, of TRI chemical ( U. S. EPA, 1996d, 2000a).

Under these conditions, facilities are required to report the pounds per year of naphthalene released into the environment both on and off site. The on site quantity is subdivided into air emissions, surface water discharges, underground injections, and releases to land ( see Table 3 1). For naphthalene, air emissions constitute most of the on site releases. Also, surface water discharges exhibit no obvious trend over the period for which data is available ( 1988   1998), but discharges hit a low in 1996 and 1997, and increased again in 1998. These TRI data for naphthalene were reported from 47 States ( excluding ID, NH, and VT), indicating the widespread production or use of this chemical ( U. S. EPA, 2000b).

Table 3 1. Environmental Releases ( in pounds) for Naphthalene in the United States ( 1988   1998).

Year On Site Releases Off Site Releases Total On & Off site Releases Air Emissions Surface Water Discharges Underground Injection Releases to Land 1998 3,374,439 34,148 191,677 1,251,040 827,708 5,679,012 1997 2,449,488 13,333 187,927 82,204 491,124 3,224,076 1996 2,863,431 11,836 296,776 301,513 582,717 4,056,273 1995 2,690,669 43,311 44,318 32,085 474,106 3,284,489 1994 2,889,514 28,557 97,186 47,017 496,501 3,558,775 1993 2,744,887 31,179 79,814 49,886 334,985 3,240,751 1992 2,626,986 28,925 78,227 1,667,150 667,556 5,068,844 1991 2,927,511 31,508 39,112 55,278 983,371 4,036,780 1990 3,912,253 36,821 28,130 143,196 919,225 5,039,625 1989 3,523,562 146,983 39,552 118,409 1,054,602 4,883,108 1988 5,165,426 22,518 50,946 123,697 1,359,184 6,721,771 source: U. S. EPA ( 2000b)

Although the TRI information can be useful in giving a general idea of release trends, it is far from exhaustive and has significant limitations. For example, only industries that meet TRI criteria ( at least 10 full time employees and manufacture and processing of quantities exceeding 25,000 lbs/ yr, or use of more than 10,000 lbs/ yr) are required to report releases. These reporting criteria do not account for releases from smaller industries. Threshold manufacture and processing quantities also changed from 1988   1990 ( dropping from 75,000 lbs/ yr in 1988 to 50,000 lbs/ yr in 1989 to 25,000 lbs/ yr in 1990), creating possibly misleading data trends. Finally, the TRI data are meant to reflect releases and should not be used to estimate general exposure to a chemical ( U. S. EPA, 2000c, d).

Naphthalene is also included in the Agency for Toxic Substances and Disease Registry's ( ATSDR) Hazardous Substance Release and Health Effects Database ( HazDat). This database 3 3 Naphthalene   February 2003 records detections of listed chemicals in site samples. Naphthalene was detected in 44 States; States without detections are AK, AZ, HI, NV, ND, and UT ( ATSDR, 2000). The National Priorities List ( NPL) of hazardous waste sites, created in 1980 by the Comprehensive Environmental Response, Compensation and Liability Act ( CERCLA), is a listing of some of the most health threatening waste sites in the United States. Naphthalene was again detected at sites in all but six States ( HI, NE, NV, NM, ND, and WV) ( U. S. EPA, 1999a).

3.3 Environmental Fate Direct releases to the air account for more than 90% of the naphthalene entering environmental media ( ATSDR, 1995). The primary discharge source is residential combustion of wood and fossil fuels. Other residential sources of naphthalene include tobacco smoke and the vaporization of moth repellants. Naphthalene may also be released to air during coal tar production and distillation, aeration processes in water treatment plants, and from use of naphthalene during chemical manufacturing ( ATSDR, 1995).

About 5% of environmental naphthalene is released into water, primarily from coal tar production and distillation processes ( ATSDR, 1995). Other contributors to water releases include effluents from wood preserving facilities and oil spills. More than half of these releases are to surface water ( ATSDR, 1995). According to ATSDR ( 1995), only about 2.7% of naphthalene releases are discharged to land, but that number increased to 37% in the most recent year for which data are available ( Table 3 1). Sources for release to land include coal tar production, naphthalene production, publicly operated treatment works ( POTWs) sludge disposal, and the use of naphthalene containing organic chemicals.

The primary removal process for naphthalene in air is through reactions with hydroxyl radicals. Naphthalene will also react with atmospheric N 2 O 5, nitrate radicals, and ozone. The major products of these reactions are 1 and 2 naphthol and 1 and 2 nitronaphthalene. The halflife of atmospheric naphthalene is less than 1 day ( ATSDR, 1995).

Naphthalene is lost from surface water via several mechanisms. Volatilization into the air is the most important route of loss from surface water ( ATSDR, 1995). Mackay and Leinonen ( 1975) estimated a half life of 7.2 hours for the volatilization of naphthalene ( quantity not stated) from an aqueous solution 1 meter deep. Southworth ( 1979) estimated that a 10 fold increase in current velocity would accelerate volatilization 2 to 3 times. Rodgers et al. ( 1983) estimated a volatilization rate constant of 0.16 hour 1, which resulted in a half life of 4.3 hours ( U. S. EPA, 1986d).

A small fraction ( less than 10%) of naphthalene in water will be associated with particulate matter and will settle into sediments ( ATSDR, 1995). Naphthalene that remains in surface water will be degraded through photolysis and biodegradation processes. Naphthalene undergoing photolysis has a half life of about 71 hours ( ATSDR, 1995). Biodegradation of this chemical also occurs quite rapidly, although degradation time will vary with naphthalene concentration, water temperature, and the availability of nutrients ( U. S. EPA, 1986d). In general, the rate of biodegradation increases as the concentration of naphthalene increases. The half life 3 4 Naphthalene   February 2003 of naphthalene in oil polluted water versus unpolluted water is approximately 7 and 1,700 days, respectively ( ATSDR, 1995).

Volatilization from soil surfaces and biodegradation are important processes for the removal of naphthalene from soil ( U. S. EPA, 1986d). The estimated volatilization half lives for naphthalene from soil containing 1.25% were 1.1 day from soil 1 cm deep and 14 days from soil 10 cm deep. Maximum biodegradation is reported to occur at a pH of 8 and in the presence of a positive redox potential ( U. S. EPA, 1986d). Naphthalene is degraded to carbon dioxide and salicylate by aerobic microorganisms ( ATSDR, 1995). Therefore, soil aerobic conditions strongly influence the half life of the chemical. In addition, soil organic matter is an important factor in degradation time because the adsorption of naphthalene to organic matter significantly decreases its bioavailability to microorganisms.

3.4 Summary In summary, most of naphthalene's consumption is through its use as an intermediary in the production of phthalate plasticizers, resins, phthaleins, dyes, pharmaceuticals, and insect repellents. Its production in the United States declined from 1968 to 1982; however its import decreased and export increased from 1978 to 1989. The widespread use and production of naphthalene in the United States is evidenced by its presence in hazardous waste sites in at least 44 States ( at NPL sites), its presence in site samples in at least 44 States ( listed in ATSDR's HazDat), and its direct release into the environment in at least 47 States ( based on TRI data). 4 1 Naphthalene   February 2003 4.0 EXPOSURE FROM DRINKING WATER 4.1 Introduction This section of the report examines the occurrence of naphthalene in drinking water. While no complete national database exists of unregulated or regulated contaminants in drinking water from public water systems ( PWSs) collected under the Safe Drinking Water Act ( SDWA), this report aggregates and analyzes existing state data that have been screened for quality, completeness, and representativeness. Populations served by PWSs exposed to naphthalene are estimated, and the occurrence data are examined for regional or other special trends. To augment the incomplete national drinking water data and to aid in the evaluation of occurrence, information on the ambient occurrence of naphthalene is also reviewed.

4.2 Ambient Occurrence To understand the presence of a chemical in the environment, an examination of ambient occurrence is useful. In a drinking water context, ambient water is source water existing in surface waters and aquifers before treatment. The most comprehensive and nationally representative data describing ambient water quality in the United States are being produced through the United States Geological Survey's ( USGS) National Ambient Water Quality Assessment ( NAWQA) program. However, as NAWQA is a relatively young program, complete national data are not yet available from their entire array of sites across the nation.

4.2.1 Data Sources and Methods The USGS instituted the NAWQA program in 1991 for the purpose of examining water quality status and trends in the United States. NAWQA is designed and implemented in such a manner to allow consistency and comparison between representative study basins located around the country, facilitating interpretation of natural and anthropogenic factors affecting water quality ( Leahy and Thompson, 1994).

The NAWQA program consists of 59 significant watersheds and aquifers referred to as " study units." The study units represent approximately two thirds of the overall water usage in the United States and a similar proportion of the population served by public water systems. Approximately one half of the nation's land area is represented ( Leahy and Thompson, 1994).

To facilitate management and make the program cost effective, approximately one third of the study units at a time engage in intensive assessment for a period of 3 to 5 years. This is followed by a period of less intensive research and monitoring that lasts between 5 and 7 years. This way all 59 study units rotate through intensive assessment over a ten year period ( Leahy and Thompson, 1994). The first round of intensive monitoring ( 1991   1996) targeted 20 watersheds. This first group was more heavily slanted toward agricultural basins. A national synthesis of results from these study units and other research initiatives focusing on pesticides and nutrients is being compiled and analyzed ( Kolpin et al., 1998; Larson et al., 1999). 4 2 Naphthalene   February 2003 For volatile organic chemicals ( VOCs), the national synthesis will compile data from the first and second rounds of intensive assessments. Study units assessed in the second round represent conditions in more urbanized basins, but initial results are not yet available. However, VOCs were analyzed in the first round of intensive monitoring and data are available for these study units ( Squillace et al., 1999). The minimum reporting level ( MRL) for most VOCs, including naphthalene, was 0.2 µ g/ L ( Squillace et al., 1999). Additional information on analytical methods used in the NAWQA study units, including method detection limits, are described by Gilliom and others ( in press).

Furthermore, the NAWQA program has compiled, by study unit, data collected from local, State, and other Federal agencies to augment its own data. The data set provides an assessment of VOCs in untreated ambient groundwater of the coterminous United States for the period 1985   1995 ( Squillace et al., 1999). Data were included in the compilation if they met certain criteria for collection, analysis, well network design, and well construction ( Lapham et al., 1997). They represent both rural and urban areas, but should be viewed as a progress report as NAWQA data continue to be collected that may influence conclusions regarding occurrence and distribution of VOCs ( Squillace et al., 1999).

The National Highway Runoff Data and Methodology Synthesis has reviewed 44 highway and urban runoff studies implemented since 1970 ( Lopes and Dionne, 1998). Two national studies were included in this review: the National Urban Runoff Program ( NURP) and studies associated with the U. S. EPA National Pollution Discharge Elimination System ( NPDES) municipal stormwater permits. NURP, conducted in the 1970s and early 1980s, had the most extensive geographic distribution. The NPDES studies took place in the early to mid 1990s ( Lopes and Dionne, 1998). Naphthalene was an analyte in both studies.

4.2.2 Results Naphthalene was detected in both rural and urban wells of the local, State, and Federal data set compiled by NAWQA ( Table 4 1). The data represent untreated ambient ground water of the coterminous United States for the years 1985   1995 ( Squillace et al., 1999). Detection frequencies and median concentrations are low, especially for rural areas. Occurrence of naphthalene in rural areas is an order of magnitude lower than in urban areas, a trend generally observed for VOCs throughout the United States ( Miller, 2000). The exception to this trend for naphthalene is the maximum concentration, a parameter more likely to be influenced by extreme values ( outliers) that do not well represent the overall data.

The NURP and NPDES studies analyzing urban and highway runoff also found naphthalene ( Lopes and Dionne, 1998). Naphthalene was detected in 11% of NURP samples, making it among the 3 most detected VOCs in the study. Its detection frequency was 7% in the NPDES studies. The maximum concentration was 2.3 µ g/ L in NURP samples and 5.1 µ g/ L in NPDES samples. 4 3 Naphthalene   February 2003 Table 4 1. Naphthalene Detections and Concentrations in Ground Water.

Location Detection frequency (% of sampled wells > MRL*) Concentration percentiles ( of detections; µ g/ L) Percent exceeding HAL** ( 20 µ g/ L)

median maximum all wells drinking water wells Urban 3.0 % 3.9 43 0.4 0 Rural 0.2 % 0.4 70 0.1 0 after Squillace et al.( 1999). * MRL for naphthalene in water: 0.001 µ g/ L ** U. S. EPA ( 1996e); ATSDR ( 1996)

The maximum values for urban and highway runoff are well below the Health Advisory Level ( HAL) of 20 µ g/ L cited by Lopes and Dionne ( 1998), the HAL in effect at the time ( U. S. EPA, 1996e). The ground water studies also reported few exceedances of the 20 µ g/ L HAL ( Squillace et al., 1999). The maximum values for runoff and groundwater are considerably less than the current HAL of 100 µ g/ L ( U. S. EPA, 2000e) and even more so for the Health Reference Level ( HRL) of 140 µ g/ L used as a preliminary health effects level for the drinking water data analysis presented below.

4.3 Drinking Water Occurrence The Safe Drinking Water Act, as amended in 1996, required PWSs to monitor for specified " unregulated" contaminants, on a five year cycle, and to report the monitoring results to the States. Unregulated contaminants do not have an established or proposed National Primary Drinking Water Regulation ( NPDWR), but they are contaminants that were formally listed and required for monitoring under federal regulations. The intent was to gather scientific information on the occurrence of these contaminants to enable a decision as to whether or not regulations were needed. All non purchased community water systems ( CWSs) and non purchased nontransient non community water systems ( NTNCWSs), with greater than 150 service connections, were required to conduct this unregulated contaminant monitoring. Smaller systems were not required to conduct this monitoring under federal regulations, but were required to be available to monitor if the State decided such monitoring was necessary. Many States collected data from smaller systems. Additional contaminants were added to the Unregulated Contaminant Monitoring ( UCM) program in 1991 [ 56 FR 3526] ( U. S. EPA, 1991b) for required monitoring that began in 1993 [ 57 FR 31776] ( U. S. EPA, 1992).

Naphthalene has been monitored under the SDWA UCM program since 1987 ( 52 FR 25720) ( U. S. EPA, 1987a). Monitoring for naphthalene under UCM continued throughout the 1990s, but ceased for small public water systems ( PWSs) under a direct final rule published January 8, 1999 ( 64 FR 1494) ( U. S. EPA, 1999b). Monitoring ended for large PWSs with promulgation of the new Unregulated Contaminant Monitoring Regulation ( UCMR) issued September 17, 1999 ( 64 FR 50556) ( U. S. EPA, 1999c) and effective January 1, 2001. At the time the UCMR lists were developed, the Agency concluded there were adequate monitoring 4 4 Naphthalene   February 2003 data for a regulatory determination. This obviated the need for continued monitoring under the new UCMR list.

4.3.1 Data Sources, Data Quality, and Analytical Methods Currently, there is no complete national record of unregulated or regulated contaminants in drinking water from public water systems collected under SDWA. Many States have submitted their unregulated contaminant PWS monitoring data to EPA databases, but there are issues of data quality, completeness, and representativeness. Nonetheless, a significant amount of State data is available for UCM contaminants that can provide estimates of national occurrence.

The National Contaminant Occurrence Database ( NCOD) is an interface to the actual occurrence data stored in the Safe Drinking Water Information System ( Federal version; SDWIS/ FED) and can be queried to provide a summary of the data in SDWIS/ FED for a particular contaminant. The data used in this report were derived from the data in SDWIS/ FED and another database called the Unregulated Contaminant Information System ( URCIS).

The data in this report have been reviewed, edited, and filtered to meet various data quality objectives for the purposes of this analysis. Hence, only data meeting the quality objectives described below were used, rather than all available data from a particular source. The sources of these data, their quality and national aggregation, and the analytical methods used to estimate a given contaminant's national occurrence ( from these data) are discussed in this section ( for further details see Cadmus, 2000a, b).

UCM Rounds 1 and 2 The 1987 UCM contaminants include 34 volatile organic compounds ( VOCs), divided into two groups: one with 20 VOCs for mandatory monitoring, and the other with 14 VOCs for discretionary monitoring [ 52 FR 25720]. Naphthalene was among the 14 VOCs included for discretionary monitoring. The UCM ( 1987) contaminants were first monitored coincident with the Phase I regulated contaminants, during the 1988   1992 period. This period is often referred to as " Round 1" monitoring. The monitoring data collected by the PWSs were reported to the States ( as primacy agents), but there was no protocol in place to report these data to EPA. These data from Round 1 were collected by EPA from many States over time.

The Round 1 data were put into a database called the Unregulated Contaminant Information System, or URCIS. Most of the Phase 1 regulated contaminants were also VOCs. Both the unregulated and regulated VOCs are analyzed using the same sample and the same laboratory methods. Hence, the URCIS database includes data on all of these 62 contaminants: the 34 UCM ( 1987) VOCs, the 21 regulated Phase 1 VOCs, 2 regulated synthetic organic contaminants ( SOCs), and 5 miscellaneous contaminants that were voluntarily reported by some States ( e. g., isomers of other organic contaminants).

The 1993 UCM contaminants include 13 SOCs and 1 inorganic compound ( IOC) [ 56 FR 3526]. Monitoring for the UCM ( 1993) contaminants began coincident with the Phase II/ V 4 5 Naphthalene   February 2003 regulated contaminants in 1993 through 1998. This is often referred to as " Round 2" monitoring. The UCM ( 1987) contaminants were also included in the Round 2 monitoring. As with other monitoring data, PWSs reported these results to the States. During the past several years, EPA has requested that the States submit these historic data to EPA.

The details of the actual individual monitoring periods are complex. The timing of required monitoring was staggered relative to different size classes of PWSs, and the program was implemented somewhat differently by different States. While Round 1 includes the period from 1988   1992, it also includes results from samples analyzed prior to 1988 that were " grandfathered" into the database ( for further details see Cadmus, 2000a, b).

Developing a Nationally Representative Perspective The Round 1 and Round 2 databases contain contaminant occurrence data from a total of 40 and 35 primacy entities ( largely States), respectively. However, data from some States are incomplete and biased. Furthermore, the national representativeness of the data is problematic because the data were not collected in a systematic or random statistical framework. These State data could be heavily skewed to low occurrence or high occurrence settings. Hence, the State data were evaluated based on pollution potential indicators and the spatial/ hydrologic diversity of the nation. This evaluation enabled the construction of a cross section from the available State data sets that provides a reasonable representation of national occurrence.

A national cross section from these State Round 2 contaminant databases was established using the approach developed for the EPA report A Review of Contaminant Occurrence in Public Water Systems ( U. S. EPA, 1999d). This approach was developed to support occurrence analyses for EPA's Chemical Monitoring Reform ( CMR) evaluation. It was supported by peer reviewers and stakeholders. The approach cannot provide a " statistically representative" sample because the original monitoring data were not collected or reported in an appropriate fashion. However, the resultant " national cross section" of States should provide a clear indication of the central tendency of the national data. The remainder of this section provides a summary description of how the national cross sections for the URCIS ( Round 1) and SDWIS/ FED ( Round 2) databases were developed. The details of the approach are presented in other documents ( Cadmus, 2000a, b), to which readers are referred for more specific information.

Cross Section Development As a first step in developing the cross section, the State data contained in the URCIS database ( that contains the Round 1 monitoring results) and SDWIS/ FED database ( that contains the Round 2 monitoring results) were evaluated for completeness and quality. For both the URCIS ( Round 1) and SDWIS/ FED ( Round 2) databases, some State data were unusable for a variety of reasons. Some States reported only detections, or their data had incorrect units. Datasets only including detections are obviously biased. Other problems included substantially incomplete data sets without all PWSs reporting. Also, data from Washington, D. C. and the Virgin Islands were excluded from this analysis because it was difficult to evaluate them for the current purposes in relation to complete State data ( Cadmus, 2000b, Sections II and III). 4 6 Naphthalene   February 2003 The balance of the States remaining after the data quality screening were then examined to establish a national cross section. This step was based on evaluating the States' pollution potential and geographic coverage in relation to all States. Pollution potential is considered to ensure a selection of States that represent the range of likely contaminant occurrence and a balance with regard to likely high and low occurrence. Geographic consideration is included so that the wide range of climatic and hydrogeologic conditions across the United States are represented, again balancing the varied conditions that affect transport and fate of contaminants, as well as conditions that affect naturally occurring contaminants ( Cadmus, 2000a, Sections III. A. and III. B.).

The cross section States were selected to represent a variety of pollution potential conditions. Two primary pollution potential indicators were used. The first factor selected indicates pollution potential from manufacturing/ population density and serves as an indicator of the potential for VOC contamination within a State. Agriculture was selected as the second pollution potential indicator because the majority of SOCs of concern are pesticides ( Cadmus, 2000a, Section III. A.). The 50 individual States were ranked from highest to lowest based on the pollution potential indicator data. For example, the State with the highest ranking for pollution potential from manufacturing received a ranking of 1 for this factor and the State with the lowest value was ranked as number 50. States were ranked for their agricultural chemical use status in a similar fashion.

The States' pollution potential rankings for each factor were subdivided into four quartiles ( from highest to lowest pollution potential). The cross section States were chosen from all quartiles for both pollution potential factors to ensure representation, for example, from: States with high agrochemical pollution potential rankings and high manufacturing pollution potential rankings; States with high agrochemical pollution potential rankings and low manufacturing pollution potential rankings; States with low agrochemical pollution potential rankings and high manufacturing pollution potential rankings; and States with low agrochemical pollution potential rankings and low manufacturing pollution potential rankings ( Cadmus, 2000a, Section III. B.). In addition, some secondary pollution potential indicators were considered to further ensure that the cross section States included the spectrum of pollution potential conditions ( high to low). The cross sections were then reviewed for geographic coverage throughout all sectors of the United States.

The data quality screening, pollution potential rankings, and geographic coverage analysis established national cross sections of 24 Round 1 ( URCIS) States and 20 Round 2 ( SDWIS/ FED) States. In each cross section, the States provide good representation of the nation's varied climatic and hydrogeologic regimes and the breadth of pollution potential for the contaminant groups ( Table 4 2 and Figure 4 1). 4 7 Naphthalene   February 2003 Table 4 2. Cross section States for Round 1 ( 24 States) and Round 2 ( 20 States).

Round 1 ( URCIS) Round 2 ( SDWIS/ FED)

Alabama Alaska* Arizona California Florida Georgia Hawaii Illinois Indiana Iowa Kentucky* Maryland* Minnesota* Montana New Jersey New Mexico* North Carolina* Ohio* South Dakota Tennessee Utah Washington* West Virginia Wyoming Alaska* Arkansas Colorado Kentucky* Maine Maryland* Massachusetts Michigan Minnesota* Missouri New Hampshire New Mexico* North Carolina* North Dakota Ohio* Oklahoma Oregon Rhode Island Texas Washington*

* cross section State in both Round 1 and Round 2 Figure 4 1. Geographic Distribution of Cross section States. Round 1 ( left) and Round 2 ( right). 4 8 Naphthalene   February 2003 Cross Section Evaluation To evaluate and validate the method for creating the national cross sections, the method was used to create smaller State subsets from the 24 State, Round 1 cross section and aggregations. Again, States were chosen to achieve a balance from the quartiles describing pollution potential, as well as a balanced geographic distribution, to incrementally build subset cross sections of various sizes. For example, the Round 1 cross section was tested with subsets of 4, 8 ( the first 4 State subset plus 4 more States), and 13 ( 8 State subset plus 5) States. Two additional cross sections were included in the analysis for comparison: a cross section composed of 16 biased States eliminated from the 24 State cross section for data quality reasons and a cross section composed of all 40 Round 1 States ( Cadmus, 2000a, Section III. B. 1).

These Round 1 incremental cross sections were then used to evaluate occurrence for an array of both high and low occurrence contaminants. The comparative results illustrate several points. The results are quite stable and consistent for the 8, 13 and 24 State cross sections. They are much less so for the 4 State, 16 State ( biased), and 40 State ( all Round 1 States) crosssections The 4 State cross section is apparently too small to provide balance both geographically and with pollution potential, a finding that concurs with past work ( U. S. EPA, 1999d). The CMR analysis suggested that a minimum of 6   7 States was needed to provide balance both geographically and with pollution potential, and the CMR report used 8 States out of the available data for its nationally representative cross section. The 16 State and 40 State cross sections, both including biased States, provided occurrence results that were unstable and inconsistent for a variety of reasons associated with their data quality problems ( Cadmus, 2000a, Section III. B. 1).

The 8, 13, and 24 State cross sections provide very comparable results, are consistent, and are usable as national cross sections to provide estimates of contaminant occurrence. Including data from more States improves the national representation and the confidence in the results, as long as the States are balanced relative to pollution potential and spatial coverage. The 24 and 20 State cross sections provide the best nationally representative cross sections for the Round 1 and Round 2 data.

Data Management and Analysis The cross section analyses focused on occurrence at the water system level; i. e., the summary data presented discuss the percentage of public water systems with detections, not the percentage of samples with detections. By normalizing the analytical data to the system level, skewness inherent in the sample data, particularly over the multi year period covered in the URCIS data, is avoided. System level analysis was used since a PWS with a known contaminant problem usually has to sample more frequently than a PWS that has never detected the contaminant. Obviously, the results of a simple computation of the percentage of samples with detections ( or other statistics) can be skewed by the more frequent sampling results reported by the contaminated site. This level of analysis is conservative. For example, a system need only have a single sample with an analytical result greater than the MRL, i. e., a detection, to be counted as a system with a result " greater than the MRL." 4 9 Naphthalene   February 2003 Also, the data used in the analyses were limited to only those data with confirmed water source and sampling type information. Only standard SDWA compliance samples were used; " special" samples, or " investigation" samples ( investigating a contaminant problem that would bias results), or samples of unknown type were not used in the analyses. Various quality control and review checks were made of the results, including follow up questions to the States providing the data. Many of the most intractable data quality problems encountered occurred with older data. These problematic data were, in some cases, simply eliminated from the analysis. For example, when the number of data with problems was insignificant relative to the total number of observations, they were dropped from the analysis ( for further details see Cadmus, 2000c).

As indicated above, New Hampshire generally is included in the 20 State, Round 2 national cross section. Naphthalene occurrence data from the State of New Hampshire, however, are biased. New Hampshire reported only 5 samples from 3 systems for naphthalene with each system showing a detection. Though these results are simple detections not violating a health effect standard, and inclusion of the data does not significantly affect overall summary statistics, to maintain a consistent method for managing biased data, New Hampshire's naphthalene data were omitted from Round 2 cross section occurrence analyses and summaries presented in this report.

Occurrence Analysis To evaluate national contaminant occurrence, a two stage analytical approach has been developed. The first stage of analysis provides a straight forward, conservative, broad evaluation of occurrence of the CCL regulatory determination priority contaminants as described above. These descriptive statistics are summarized here. Based on the findings of the Stage 1 analysis, EPA will determine whether more intensive statistical evaluations, the Stage 2 analysis, may be warranted to generate national probability estimates of contaminant occurrence and exposure for priority contaminants ( for details on this two stage analytical approach, see Cadmus, 2000c).

The summary descriptive statistics presented in Table 4 3 for naphthalene are a result of the Stage 1 analysis and include data from both Round 1 ( URCIS, 1987   1992) and Round 2 ( SDWIS/ FED, 1993   1997) cross section States ( minus New Hampshire). Included are the total number of samples, the percent samples with detections, the 99th percentile concentration of all samples, the 99th percentile concentration of samples with detections, and the median concentration of samples with detections. The percentages of PWSs and population served indicate the proportion of PWSs whose analytical results showed a detection( s) of the contaminant ( simple detection, > MRL) at any time during the monitoring period; or a detection( s) greater than half the Health Reference Level ( HRL); or a detection( s) greater than the Health Reference Level. The Health Reference Level, 140 µ g/ L, is a preliminary estimated health effect level used for this analysis.

The HRL was derived as a preliminary estimated health effect level using the Reference Dose ( RfD) for naphthalene of 2 × 10 2 mg/ kg day. The RfD is an estimate ( within an order of magnitude) of the daily oral dose to the human population that is likely to be without appreciable 4 10 Naphthalene   February 2003 Table 4 3. Summary Occurrence Statistics for Naphthalene.

Frequency Factors 24 State Cross Section1 ( Round 1) 20 State Cross Section2 ( Round 2) National System & Population Numbers3 Total Number of Samples 45,567 94,915

Percent of Samples with Detections 0.43% 0.24%

99th Percentile Concentration ( all samples) < ( Non detect) < ( Non detect)

Health Reference Level 140 : g/ L 140 : g/ L

Minimum Reporting Level ( MRL) Variable4 Variable4

99th Percentile Concentration of Detections 900: g/ L 73 : g/ L

Median Concentration of Detections 1.0 : g/ L 0.74 : g/ L

Total Number of PWSs 13,452 22,926 65,030 Number of GW PWSs 12,034 20,525 59,440 Number of SW PWSs 1,502 2,401 5,590 Total Population 77,209,916 67,498,059 213,008,182 Population of GW PWSs 42,218,746 25,185,032 85,681,696 Population of SW PWSs 41,987,010 42,313,027 127,326,486 National Extrapolation5 Occurrence by System Round 1 Round 2 PWSs with detections (> MRL) 1.18% 0.75% 769 491 Range of Cross Section States 0   28.24% 0   4.48% N/ A N/ A GW PWSs with detections 1.08% 0.62% 642 368 SW PWSs with detections 1.93% 1.92% 108 107 PWSs > 1/ 2 Health Reference Level ( HRL) 0.01% 0.01% 10 6 Range of Cross Section States 0   1.53% 0   0.06% N/ A N/ A GW PWSs > 1/ 2 Health Reference Level 0.02% 0.01% 10 6 SW PWSs > 1/ 2 Health Reference Level 0.00% 0.00% 0 0 PWSs > Health Reference Level 0.01% 0.00% 10 0 Range of Cross Section States 0   1.53% 0.00% N/ A N/ A GW PWSs > Health Reference Level 0.02% 0.00% 10 0 SW PWSs > Health Reference Level 0.00% 0.00% 0 0 Table 4 3 ( continued)

Frequency Factors 24 State Cross Section1 ( Round 1) 20 State Cross Section2 ( Round 2) National System & Population Numbers3 4 11 Naphthalene   February 2003 Occurrence by Population Served National Extrapolation5 Round 1 Round 2 PWS Population Served with detections 2.910% 4.790% 6,198,000 10,204,000 Range of Cross Section States 0   37.22% 0   31.41% N/ A N/ A GW PWS Population with detections 4.005% 1.162% 3,431,000 995,000 SW PWS Population with detections 1.323% 6.950% 1,685,000 8,849,000 PWS Population Served > 1/ 2 Health Ref Level 0.007% 0.002% 16,000 5,000 Range of Cross Section States 0   0.23% 0   0.01% N/ A N/ A GW PWS Population > 1/ 2 Health Ref Level 0.013% 0.007% 11,000 6,000 SW PWS Population > 1/ 2 Health Ref Level 0.000% 0.000% 0 0 PWS Population Served > Health Ref Level 0.007% 0.000% 16,000 0 Range of Cross Section States 0   0.23% 0.000% N/ A N/ A GW PWS Population > Health Ref Level 0.013% 0.000% 11,000 0 SW PWS Population > Health Ref Level 0.000% 0.000% 0 0 1. Summary Results based on data from 24 State Cross Section, from URCIS, UCM ( 1987) Round 1. 2. Summary Results based on data from 20 State Cross Section ( minus New Hampshire), from SDWIS/ FED, UCM ( 1993) Round 2. 3. Total PWS and population numbers are from EPA March 2000 Water Industry Baseline Handbook. 4. See text for discussion 5. National extrapolations are from the 24 State data and 20 State data using the Baseline Handbook system and population numbers.  PWS = Public Water Systems; GW = Ground Water; SW = Surface Water; MRL = Minimum Reporting Level ( for laboratory analyses);  Health Reference Level = Health Reference Level, an estimated health effect level used for preliminary assessment for this review; N/ A = Not Applicable  The Health Reference Level used for naphthalene is 140 : g/ L. This is a draft value for working review only.  Total Number of Samples = the total number of analytical records for naphthalene.  99th Percentile Concentration = the concentration value of the 99th percentile of either all analytical results or just the samples with detections ( in : g/ L).  Median Concentration of Detections = the median analytical value of all the detections ( analytical results greater than the MRL) ( in : g/ L).  Total Number of PWSs = the total number of public water systems with records for naphthalene.  Total Population Served = the total population served by public water systems with records for naphthalene.  PWS with detections, % PWS > ½ Health Reference Level, % PWS > Health Reference Level = percent of the total number of public water systems with at least one analytical result that exceeded the MRL, ½ Health Reference Level, Health Reference Level, respectively.  PWS Population Served with detections, % PWS Population Served > ½ Health Reference Level, % PWS Population Served > Health Reference Level = percent of the total population served by PWSs with at least one analytical result exceeding the MRL, ½ Health Reference Level, or the Health Reference Level, respectively. 4 12 Naphthalene   February 2003 risk of adverse effects over a lifetime of exposure. This dose was converted to a drinking water equivalent concentration of 700 : g/ L by multiplying the RfD by the default body weight for an adult ( 70 kg) and dividing the result by the default daily intake of drinking water for an adult ( 2 L). For derivation of the HRL, it was assumed that about 20% of an individual's total exposure to naphthalene was attributable to drinking water. Multiplication of the drinking water equivalent concentration by 0.2 yields the HRL of 140 : g/ L. The HRL was derived as follows:

HRL = RfD × BW × RSC DI Where:

RfD = Reference dose for HCBD in drinking water, 2 × 10 4 mg/ kg day BW = Body weight of an adult, 70 kg DI = Daily intake of water for an adult, 2 L RSC = Relative Source Contribution, default value of 20%

Therefore:

HRL = ( 2 × 10 2 mg/ kg day) × ( 70 kg) × 0.20 2 L = 140 : g/ L The 99th percentile concentration is used here as a summary statistic to indicate the upper bound of occurrence values because maximum values can be extreme values ( outliers) that sometimes result from sampling or reporting error. The 99th percentile concentration is presented for both the samples with detections and for all of the samples, because the value for the 99th percentile concentration of all samples is below the MRL ( denoted by "<" in Table 4 3). The 95th percentile concentration of all samples and the median ( or mean) concentration of all samples are omitted because these also are below the MRL. Only 0.43% and 0.24% of all samples recorded detections of naphthalene in Round 1 and Round 2, respectively.

As a simplifying assumption, a value of half the MRL is often used as an estimate of the concentration of a contaminant in samples/ systems whose results are less than the MRL. With a contaminant with relatively low occurrence, such as naphthalene in drinking water occurrence databases, the median or mean value of occurrence using this assumption would be half the MRL ( 0.5 × MRL). However, for these occurrence data, this is not straightforward. For Round 1 and Round 2, States have reported a wide range of values for the MRLs. This is in part related to State data management differences as well as real differences in analytical methods, laboratories, and other factors.

The situation can cause confusion when examining descriptive statistics for occurrence. For example, for Round 2, most States reported non detections as zeros, resulting in a modal 4 13 Naphthalene   February 2003 MRL value of zero. By definition the MRL cannot be zero. This is an artifact of State data management systems. Because a simple meaningful summary statistic is not available to describe the various reported MRLs, and to avoid confusion, MRLs are not reported in the summary table ( Table 4 3).

In Table 4 3, national occurrence is estimated by extrapolating the summary statistics for the 24 and 20 State cross sections ( minus New Hampshire) to national numbers for systems and population served by systems, using the Water Industry Baseline Handbook, Second Edition ( U. S. EPA, 2000f). From the handbook, the total number of CWSs plus NTNCWSs is 65,030, and the total population served by CWSs plus NTNCWSs is 213,008,182 persons ( see Table 4 3). To arrive at the national occurrence estimate for a particular cross section, the national estimate for PWSs ( or population served by PWSs) is simply multiplied by the percentage for the given summary statistic [ i. e., for Round 1, the national estimate for the total number of PWSs with detections ( 769) is the product of the percentage of Round 1 PWSs with detections ( 1.18%) and the national estimate for the total number of PWSs ( 65,030)].

Round 1 ( 1987   1992) and Round 2 ( 1993   1997) data were not merged because they represent different time periods and different States ( only eight States are represented in both rounds). Also, each round has different data management and data quality problems. The two rounds are only merged for the simple spatial analysis overview presented in Section 4.3.2 and Figures 4 2 and 4 4.

4.3.2 Results Occurrence Estimates While States with detections of naphthalene are widespread ( Figure 4 2), the percentages of PWSs by State with detections are modest ( Table 4 3). In aggregate, the cross sections show that approximately 0.8   1.2 % of PWSs in both rounds experienced detections (> MRL), affecting 3.0   4.8 % of the population served ( approximately 6   10 million people). Percentages of PWSs with detections greater than half the Health Reference Level (> ½ HRL) are much lower for both rounds: 0.01%. The percentage of PWSs exceeding the Health Reference Level (> HRL) is also very small ( Table 4 3). Detections > HRL were only reported in Round 1: 0.01% percent of PWSs, affecting a population of approximately 16,000. There were no samples in Round 2 with concentrations above the HRL.

Note that for the Round 1 cross section, the total number of PWSs ( and the total population served by the PWSs) is not the sum of the number of ground water and surface water systems ( or the populations served by those systems). Because some public water systems are seasonally classified as either surface or ground water, some systems may be counted in both categories. The population numbers for the Round 1 cross section are also incomplete. Not all of the PWSs for which occurrence data were submitted reported the populations they served. ( However, the population numbers 4 14 Naphthalene   February 2003 Naphthalene Detections in Round 1 and Round 2 All States States not in Round 1 or Round 2 No data for Naphthalene States with No Detections ( No PWSs > MRL) States with Detections ( Any PWS > MRL) Figure 4 2. States with PWSs with Detections of Naphthalene for all States with Data in URCIS ( Round 1) and SDWIS/ FED ( Round 2). 4 15 Naphthalene   February 2003 presented in Table 4 3 for the Round 1 cross section are reported from approximately 95% of the systems.)

The national estimates extrapolated from Round 1 and Round 2 PWS numbers and populations are not additive either. In addition to the Round 1 classification and reporting issues outlined above, the proportions of surface water and ground water PWSs, and populations served by them, are different between the Round 1 and 2 cross sections and the national estimates. For example, approximately 63% of the population served by PWSs in the Round 2 cross section States are served by surface water PWSs ( Table 4 3). Nationally, however, that proportion changes to 60%.

Both Round 1 and Round 2 national cross sections show a proportionate balance in PWS source waters compared to the national inventory. Nationally, 91% of PWSs use ground water ( and 9% surface waters): Round 1 shows 89% and Round 2 shows 90% of systems using ground water. The relative populations served are not as closely comparable. Nationally, about 40% of the population is served by PWSs using groundwater ( and 60% by surface water). Round 2 data is most representative with 37% of the cross section population served by ground water; Round 1 shows about 55%.

There are differences in the occurrence results between Round 1 and Round 2, as should be expected. The differences are not great, however, particularly when comparing the proportions of systems affected. The results range from 0.8 to 1.2% of PWSs with detections of naphthalene and range from 0.00 to 0.01% of PWSs with detections greater than the HRL of 140 µ g/ L. These are not substantively different, given the data sources. The differences in the population extrapolations appear greater, but still constitute relatively small proportions of the population. Less than 5.0% of the population served by PWSs in either round were served by systems with detections and only 0.01% of the population served by Round 1 PWSs were served by systems with detections greater than the HRL.

The Round 2 cross section provides a better proportional balance relative to the national population of PWSs and may have fewer reporting problems than Round 1. The non zero estimate of the national population served by PWSs with detections greater than the HRL using Round 1 data can also provide an upper bound estimate in considering the data.

Regional Patterns Occurrence results are displayed graphically by State in Figures 4 2, 4 3, and 4 4 to assess whether any distinct regional patterns of occurrence are present. Combining Round 1 and Round 2 data ( Figure 4 2), there are 47 States reporting. Four of those States have no data for naphthalene, while another 11 have no detections of the chemical. The remaining 32 States have detected naphthalene in drinking water and are well distributed throughout the United States. In contrast to the summary statistical data presented in the previous section, this simple spatial analysis includes the biased New Hampshire data. 4 16 Naphthalene   February 2003 The simple spatial analysis presented in Figures 4 2, 4 3, and 4 4 suggests that special regional analyses are not warranted because naphthalene occurrence at concentrations below the HRL is widespread. While no clear geographical patterns of occurrence are apparent, comparisons with environmental use and release information are useful ( see also Chapter 3).

The 47 TRI States reporting releases of naphthalene to the environment include all of the States that detected it in drinking water except New Hampshire. Also, four of the six States that have not detected naphthalene in site samples reported to ATSDR's HazDat database, and three of the six States where it was not detected at CERCLA NPL sites, have detected it in drinking water.

4.4 Conclusion Naphthalene is naturally present in fossil fuels, such as petroleum and coal, and is generated when wood or tobacco are burned. Naphthalene is produced in commercial quantities from either coal tar or petroleum. Most naphthalene consumption ( 60%) is through use as an intermediary in the production of phthalate plasticizers, resins, phthaleins, dyes, pharmaceuticals, and insect repellents. Crystalline naphthalene is used as a moth repellent and a solid block deodorizer for diaper pails and toilets. Naphthalene is also used to make the insecticide carbaryl, synthetic leather tanning agents, and surface active agents.

Naphthalene has been detected in untreated ambient ground water samples reviewed and/ or analyzed by the USGS NAWQA program. Detection frequencies and concentrations for all wells are relatively low; however, occurrence is considerably higher for urban wells when compared to rural wells. Naphthalene has been detected at slightly higher frequencies in urban and highway runoff. Concentrations in runoff are low, with maximum concentrations well below the HRL of 140 µ g/ L. Naphthalene has also been found at ATSDR HazDat and CERCLA NPL sites across the country and releases have been reported through the Toxic Release Inventory.

Naphthalene has also been detected in PWS samples collected under SDWA. Occurrence estimates are low for Round 1 and Round 2 monitoring with only 0.43% and 0.24% of all samples showing detections, respectively. Significantly, the values for the 99th percentile and median concentrations of all samples are less than the MRL. For Round 1 samples with detections, the median concentration is 1.0 µ g/ L and the 99th percentile concentration is 900 µ g/ L. Median and 99th percentile concentrations for Round 2 detections are 0.74 µ g/ L and 73 µ g/ L, respectively. Systems with detections constitute only 1.2% of Round 1 systems and 0.8% of Round 2 systems ( an estimate of 769 ( Round 1) and 491 ( Round 2) systems nationally). National estimates for the population served by PWSs with detections are also low, especially for detections greater than the HRL. It is estimated that less than 0.01% of the national PWS population is served by systems with detections greater than the HRL ( approximately 16,000 people). 4 17 Naphthalene   February 2003 Naphthalene Occurrence in Round 1 States not in Cross Section No data for Naphthalene 0.00% PW Ss > MRL 0.01  1.00% PWSs > MRL 1.00  4.00% PWSs > MRL* * Outliers: S tate of Alabama a t 28.3%; State of Florida at 7.0%

States not in Cross Section No data for Naphthalene 0.00% PWSs > MRL 0.01  1.00% PWSs > MRL 1.00  4.00% PWSs > MRL* * State o f New Hampshire is an outlier at 100% Naphthalene Occurrence in Round 2 Figure 4 3. States with PWSs with Detections of Naphthalene ( any PWSs with Results Greater than the Minimum Reporting Level [ MRL]) for Round 1( above) and Round 2 ( below) Cross section States. 4 18 Naphthalene   February 2003 Naphthalene Occurrence in Round 1 and Round 2 States not in Cross Section No data for Naphth alene 0.00% PW Ss > MRL 0.01  1.00% PWSs > M RL 1.00  4.00% PWSs > M RL* * Outliers: S tate of Alabama a t 28.3%; State of Florida at 7.0%; State of New Hampshire at 100%

Naphthalene Occurrence in Round 1 and Round 2 States not in Cross Section No data for Naphthalene 0.01  1.00% PWSs > HRL 1.00  4.00% PWSs > HRL 0.00% PWSs > HRL Figure 4 4. Cross section States ( Round 1 and Round 2 Combined) with PWSs with Detections of Naphthalene ( above) and Concentrations Greater than the Health Reference Level ( HRL; below). 5 1 Naphthalene   February 2003 5.0 EXPOSURE FROM MEDIA OTHER THAN WATER 5.1 Exposure from Food 5.1.1 Concentration in Non Fish Food Items Naphthalene contamination levels in non fish food items are generally low, unless they have been exposed to smoke. Naphthalene was detected in two of 13,980 samples of foods analyzed in six U. S. states ( Minyard and Roberts, 1991). Naphthalene and methylnaphthalene levels in meat samples that were not exposed to fire or smoke are listed in Table 5 1 below. Naphthalene and methylnaphthalene levels were observed to be higher in foods contaminated by smoke during fire exposure ( Johnston et al., 1994; Snyder et al., 1996). Naphthalene levels in homogenized milk samples stored in low density polyethylene ( LDPE) bottles were low ( 0.02 : g/ mL) at the time of purchase, increased to 0.1 : g/ mL 30 days later, and averaged 0.25 : g/ mL at the expiration date ( Lau et al., 1994). Lau et al. ( 1994) hypothesized that residual naphthalene present in the LDPE packaging ( 1.5 to 2.0 : g/ g) was the source of the naphthalene contamination in the milk samples. A later study by the same authors ( Lau et al., 1995) observed that the level of naphthalene in LDPE milk bottle material had been reduced to 0.1 to 0.4 : g/ g due to a new packaging method.

Dietary naphthalene concentrations were evaluated using duplicate diet food samples from adults and children residing in low income housing in North Carolina ( Chuang et al., 1999). In the adult diets, naphthalene concentrations were found to average 3.75 ± 5.35 : g/ kg ( range = 0.01 to 18.7), whereas in the child diets, naphthalene concentrations were 4.08 ± 10.9 : g/ kg ( range = 0.01 to 54.9).

Naphthalene concentrations from vegetables grown in an industrial area of Thessaloniki, Greece are summarized in Table 5 2 ( Kipopoulou et al., 1999). As shown in the tabulated data, naphthalene was detected in all tissue samples and ranged from 0.37 to 63 : g/ kg dry weight depending on the vegetable type.

Naphthalene and methylnaphthalene ( isomer not specified) were detected in five male and five female harp seals ( Phoca groenlandica) caught in southern Labrador on the eastern coast of Canada in 1994 ( Zitko et al., 1998). Reported median concentrations of naphthalene and methylnaphthalene in harp seal tissues are presented in Table 5 3.

5.1.2 Concentrations in Fish and Shellfish In the United States, naphthalene was not detected in 83 biota samples ( median detection limit 2.5 mg/ kg) reported from 1980 to 1982 in the STORET database ( Staples et al., 1985). Reported naphthalene concentrations ranged from 5 to 176 nanograms per gram ( ng/ g) in oysters, from 4 to 10 ng/ g in mussels, and from less than 1 to 10 ng/ g in clams obtained from United States waters ( Bender and Huggett, 1989). In shore crabs collected from the San Francisco Bay area, average naphthalene concentrations were 7.4 ng/ g ( Miles and Roster, 1999). Naphthalene was detected in all samples of seven fish and two shellfish species taken from Kuwaiti waters 5 2 Naphthalene   February 2003 Table 5 1. Naphthalene And Methylnaphthalene Concentrations in Meat Samples.

SAMPLE NAPHTHALENE CONCENTRATION ( ng/ g) METHYLNAPHTHALENEa CONCENTRATION ( ng/ g) REFERENCE Fried chicken 26 27 Johnston et al., 1994 Beef 26 26 Johnston et al., 1994 Hot dog 25 5 Johnston et al., 1994 Young turkey breast 17 6 Johnston et al., 1994 Smoked chicken 11.7 Not evaluated Snyder et al., 1996 Smoked chicken 5 13 Johnston et al., 1994 Boneless beef 5 2 Johnston et al., 1994 Boneless turkey breast 4 0 Johnston et al., 1994 Cooked beef 3 2 Johnston et al., 1994 Corned beef 3 2 Johnston et al., 1994 Ham 2.5 Not evaluated Snyder et al., 1996 Corned beef 1.7 Not evaluated Snyder et al., 1996 Boneless beef LOQb Not evaluated Snyder et al., 1996 Turkey breast LOQb Not evaluated Snyder et al., 1996 Beef roast 0 Not evaluated Snyder et al., 1996 Boneless turkey 0 Not evaluated Snyder et al., 1996 a The isomer of methylnaphthalene was not specified. b LOQ = limit of quantitation ( 1 ng/ g ( 1 part per billion)) for the method used, which involved supercritical fluid extraction followed by gas chromatograph mass spectrometer analysis; the concentration was determined using naphthalene d8 as an internal standard. 5 3 Naphthalene   February 2003 that were polluted with crude oils; reported concentrations of naphthalene ranged from 2.06 to 156.09 ng/ g dry weight ( Saeed et al., 1995).

2 Methylnaphthalene was reported at concentrations ranging from 0.4 to 320 : g/ g in fish from Ohio waters, but neither isomer of methylnaphthalene was detected in muscle tissue of fish from polluted areas of Puget Sound ( GDCH, 1992). Methylnaphthalenes were detected in oysters collected in Australia at less than 0.3 to 2 : g/ g.

5.1.3 Intake of Naphthalene from Food Factors that may contribute to high dietary naphthalene intake include consumption of grilled foods. Assuming food ingestion of 0.76 to 4.43 kg per day for adults, ( Chuang et al., 1999) a daily average intake of 2.85 to 16.6 : g of naphthalene can be calculated from the dietary concentration data of Chuang et al. ( 1999). Assuming food ingestion of approximately 0.5 to 2.3 kg per day for children ( Chuang et al., 1999), an average daily intake of 2.04 to 9.4 : g of naphthalene can be calculated from the dietary concentration data of Chuang et al. ( 1999).

Table 5 2. Concentrations of Naphthalene in Vegetables VEGETABLE TYPE CONCENTRATION (: g/ kg dry weight)

Range Median Cabbage ( n= 8) 0.37   15 5.0 Carrot ( n= 6) 8.9   30 21 Leek ( n= 5) 6.3   35 18 Lettuce ( n= 8) 4.9   53 42 Endive ( n= 3) 27   63 29 Source: Kipopoulou et al. ( 1999)

Table 5 3. Median Concentrations of Naphthalene and Methylnaphthalene in Harp Seals Compound Tissue Concentration ( ng/ g wet weight)

Muscle Kidney Liver Blubber Female Male Female Male Female Male Female Male Naphthalene 3.10 2.90 4.30 4.15 4.70 4.15 21.00 23.50 Methylnaphthalene 1.50 1.55 1.70 1.40 1.70 1.40 8.30 8.85 Source: Zitko et al. ( 1998) 5 4 Naphthalene   February 2003 Using the average ranges of naphthalene intake determined above, an estimated daily intake of 40.7 to 237 ng/ kg day can be calculated for a 70 kg adult, and an average daily intake of 204 to 940 ng/ kg day can be calculated for a 10 kg child. Values for individuals will vary depending upon dietary composition.

5.2 Exposure from Air 5.2.1 Concentration of Naphthalene in Air The average reported concentration for 67 ambient air samples in the United States was 0.991 parts per billion ( ppb) ( 5.19 : g/ m3), and the majority ( 60) of these samples and the highest concentrations were collected at source dominated locations ( Shah and Heyerdahl, 1988). Howard ( 1989) reported a median naphthalene level in urban air in 11 U. S. cities of 0.18 ppb ( 0.94 : g/ m3). Chuang et al. ( 1991) reported an average naphthalene concentration of 170 : g/ m3 in outdoor air in a residential area of Columbus, Ohio. Naphthalene was detected in ambient air in Torrance, California, at a concentration of 3.3 : g/ m3 ( Propper, 1988). Patton et al. ( 1997) reported a naphthalene concentration of 1.50 × 10 4 : g/ m3 in an air sample collected from the Department of Energy's Hanford site in Washington State. Average naphthalene concentrations detected in ambient air at five hazardous waste sites and one landfill in New Jersey ranged from 0.08 to 0.88 ppb ( 0.42 to 4.6 : g/ m3) ( La Regina et al., 1986). Atmospheric concentrations of naphthalene in total suspended particles were reported to range from 0.003 to 0.095 : g/ m3 ( median = 0.017) in the city of Ionia, Greece and from 0.002 to 0.179 : g/ m3 ( median = 0.030) in the city of Sindos, Greece ( Kipopoulou et al., 1999).

1 Methylnaphthalene and 2 methylnaphthalene have also been detected in ambient air. Shah and Heyerdahl ( 1988) reported average concentrations of 0.086 and 0.011 ppb ( 0.51 and 0.065 : g/ m3) for 1 methylnaphthalene and 2 methylnaphthalene, respectively. ATSDR ( 1995) indicated that these data were obtained from source dominated areas where the highest concentrations were detected. Methylnaphthalene ( isomer not specified) was detected in ambient air at a hazardous waste site in New Jersey; however the concentration was not reported ( La Regina et al., 1986). A mean concentration of 0.252 ppb ( 1.5 : g/ m3) 2 methylnaphthalene was reported for indoor air ( Shah and Heyerdahl, 1988).

Naphthalene has been detected in indoor air samples, and residential indoor concentrations are sometimes higher than outdoor air levels. Published average indoor concentrations of naphthalene in various locations within homes range from 0.860 to 1,600 : g/ m3 ( Chuang et al., 1991; Hung et al., 1992; Wilson et al., 1989; Lau et al., 1995). However, ATSDR ( 1995) suggested that the upper range value reported in Chuang et al. ( 1991) might be erroneous and indicated that a more representative upper limit concentration for indoor air might be 32 : g/ m3, recorded in buildings in heavily trafficked urban areas of Taiwan ( Hung et al., 1992). Lau et al. ( 1995) reported mean naphthalene vapor concentrations of 5 to 41 : g/ m3 and less than 3 to 100 : g/ m3 in office and laboratory air, respectively. Concentrations of naphthalene vapor were found to be high ( 350 : g/ m3) in a flat that had been freshly painted with lacquer paint ( Lau et al., 1995). Measurements of naphthalene concentrations in both indoor and outdoor air were obtained from 24 low income homes in North Carolina in 1995 ( Chuang et al., 1999). 5 5 Naphthalene   February 2003 Indoor air concentrations ranged from 0.33 to 9.7 : g/ m3 ( mean ± Std Dev = 2.2 ± 1.9), whereas outdoor air concentrations were lower and ranged from 0.057 to 1.82 : g/ m3 ( mean ± Std Dev = 0. 43 ± 0.51).

In homes with residents who smoke, indoor and outdoor air concentrations of naphthalene were reported to be 2.2 : g/ m3 and 0.3 : g/ m3, respectively ( Gold et al., 1991; IARC, 1993). A similar analysis of air in homes without smokers detected indoor and outdoor air concentrations of 1.0 : g/ m3 and 0.1 : g/ m3, respectively. Lofgren et al. ( 1991) reported an average concentration of naphthalene inside automobiles in commuter traffic of about 4.5 : g / m3.

5.2.2 Intake of Naphthalene from Air Assuming an average ambient concentration level of 5.19 : g naphthalene/ m3 and an average inhalation rate of 15.2 m3/ day ( U. S. EPA, 1996c), an average daily dose of 1,127 ng/ kgday can be calculated for a 70 kg adult. An estimated average daily dose of 4,515 ng/ kg day can be calculated for a 10 kg child assuming an inhalation rate of 8.7 m3/ day ( U. S. EPA, 1996c). Individual intake will vary depending on factors including activity, geographic location, and inhalation rate.

5.3 Exposure from Soil 5.3.1 Concentration of Naphthalene in Soil Chuang et al. ( 1995) analyzed house dust samples obtained from carpet in homes in Columbus, Ohio. They reported mean naphthalene levels of 530 : g/ kg ( measured following Soxhlet extraction) and 350 : g/ kg ( measured using sonication extraction). Measurements of naphthalene concentrations in household dust were obtained from 24 low income homes in North Carolina in 1995 ( Chuang et al., 1999). Concentrations ranged from < 10 to 4,300 : g/ kg, depending on the location of sampling ( Table 5 4).

Table 5 4. Concentrations of Naphthalene in Residential Dust ( mg/ g)

LOCATION CONCENTRATION (: g/ kg)

Range Mean ± Std Dev House Dust 20  4,300 330 ± 850 Entryway Dust 10  1,310 110 ± 260 Pathway Soil < 10  40 10 ± 10 Source: Chuang et al. ( 1999) 5 6 Naphthalene   February 2003 Low levels of naphthalene and methylnaphthalenes have been found in uncontaminated soils and sediments, while higher levels have been reported for samples taken near sources of contamination. Wild et al. ( 1990) reported that naphthalene levels in untreated agricultural soils ranged from 0 to 3 : g/ kg. Published naphthalene concentrations in contaminated soils included up to 66 : g/ kg in sludge treated soils ( Wild et al., 1990), 6,100 : g/ kg in coal tar contaminated soil ( Yu et al., 1990) and 16,700 : g/ kg in soil from a former tar oil refinery ( Weissenfels et al., 1992). Kipopoulou et al. ( 1999) reported naphthalene concentrations in agricultural soil from Thessaloniki, Greece ranging from 3.1 to 78 : g/ kg dry weight ( median = 17). For methylnaphthalene ( isomer not specified), Yu et al. ( 1990) reported a concentration of 2,900 : g/ kg in coal tar contaminated soil.

For sediments, naphthalene was detected in 7 percent of 267 sediment samples entered into the STORET database ( 1980 to 1982); the median concentration for all samples was reported to be less than 500 : g/ kg ( Staples et al., 1985). Coons et al. ( 1982) performed a separate analysis of the STORET data and reported that concentrations in positive sediment samples ranged from 0.02 to 496 : g/ kg.

Naphthalene and methylnaphthalene have been detected in marine and estuarine sediments near petroleum production and transport facilities. Brooks et al. ( 1990) reported average concentrations of 54.7 and 61.9 : g/ kg naphthalene and 50.4 and 55.3 : g/ kg methylnaphthalenes at 10 and 25 miles, respectively, from an offshore multi well drilling platform. The study also reported that naphthalene and methylnaphthalene concentrations in nearby noncontaminated estuarine sediments were 2.1 and 1.9 : g/ kg, respectively. Sharma et al. ( 1997) analyzed sediments from 52 sites in the upper part of the Laguna Madre system, a large coastal basin located south of Corpus Christi, Texas, that supports the Gulf Coast Intracoastal Waterway and petroleum production wells and pipelines. They detected methylnaphthalene at four sites, and the mean concentrations identified at these four sites ranged from 9,400 to 81,000 : g/ kg dry weight. The Laguna Madre site with the highest concentration of methylnaphthalene receives dredged material from the waterway and other canals.

5.3.2 Intake of Naphthalene from Soil Humans may be exposed to soil naphthalene by inhalation of airborne soil particles, by ingestion of food borne soil residues, by ingestion of household dust, or by direct ingestion of soil. Exposure by inhalation of airborne soil particles is accounted for in Section 5.4. Infants and toddlers ingest soil and household dust by hand to mouth transfer during everyday activities, and may therefore be exposed to higher levels of soil naphthalene than the general population.

Assuming average ingestion of 50 milligram ( mg) of soil per day by adults ( U. S. EPA, 1996c), and house dust concentrations from 0.02 to 4.3 milligram per kilogram ( mg/ kg) ( average = 0.33), the estimated average daily intake for a 70 kg adult is calculated to be 0.00001 to 0.003 mg/ kg day ( average = 0.00002). An estimated intake range of 0.0002 to 0.043 mg/ kg day ( average = 0.0033) was calculated for a 10 kg child, assuming ingestion of 100 mg of soil per day ( U. S. EPA, 1996c). For comparison with intake from other media, these ranges have been 5 7 Naphthalene   February 2003 converted to units of 10 to 3,000 ng/ kg day ( average = 20) for adults, and 200 to 43,000 ng/ kgday ( average = 3,300) for a 10 kg child ( Table 5 5).

5.4 Other Residential Exposures Naphthalene, 1 methylnaphthalene, and 2 methylnaphthalene have been identified in cigarette smoke ( HSDB, 1999). Schmeltz et al. ( 1978) reported levels of 3 : g napthalene, 1 : g 1 methylnaphthalene, and 1 : g 2 methylnaphthalene in the smoke from one commercial U. S. unfiltered cigarette. Sidestream smoke levels of 46 : g, 30 : g, and 32 : g per cigarette were reported for these three compounds, respectively ( Schmeltz et al., 1976).

Use of naphthalene containing moth repellents also contributes to naphthalene in indoor air. Lau et al. ( 1995) measured 350 : g/ m3 naphthalene in the air inside a cupboard containing approximately 36 grams of mothballs. Unvented kerosene space heaters, gas cooking and heating appliances, as well as wood burning fireplaces, might also contribute to indoor air concentrations of naphthalene ( HSDB, 1999; Chuang et al., 1995).

In Taiwan, mosquito coils are frequently burned despite being categorized as a source of indoor air pollution. Lin and Lee ( 1997) identified naphthalene in smoke resulting from the burning of two prevalent brands of mosquito coils. Burning one gram of the mosquito coils yielded 20.98 or 30.45 : g of naphthalene vapor and 7.35 or 9.23 : g of particulate bound naphthalene, depending on the brand. The study authors estimated that the concentration of naphthalene in the air would be up to 3.35 : g/ m3 after burning a mosquito coil for 6 hours in a 40 cubic meter ( m3) room.

5.5 Summary Estimated concentration and intake values for naphthalene in media other than water are summarized in Table 5 5. Inspection of the data reveals that, based on average intakes, most exposure occurs through inhalation, with average intakes being approximately 5 to 27 fold greater than those from food and up to about 5 fold greater than those from soil. However, soil may be a significant route of exposure for children living in areas with soils containing high levels of naphthalene. 5 8 Naphthalene   February 2003 Table 5 5. Exposure to Naphthalene in Media Other than Water PARAMETER MEDIUM Food Air Soil*

Adult Child Adult Child Adult Child Concentration in medium [ average] [ 3.75] : g/ kg [ 4.08] : g/ kg [ 5.19] : g/ m3 0.02   4.3 [ 0.33] mg/ kg Estimated daily intake ( ng/ kg day) [ average] [ 40.7   237] ** [ 204   940] ** [ 1,127] [ 4,515] 10   3,000 [ 235] 200   43,000 [ 3,300]

* based on household dust concentrations ** range based on different total food intakes ( 0.076 to 4.43 kg/ day adults; 0.5 to 2.3 kg/ day child) ( Chuang et al., 1999) 6 1 Naphthalene   February 2003 6.0 TOXICOKINETICS 6.1 Absorption Oral Exposure Naphthalene is readily absorbed when administered orally as inferred from the occurrence of adverse effects after exposure. Toxic effects have been reported in humans, dogs, mice, rats, and rabbits following oral exposures to naphthalene, although the extent of absorption was not quantified ( ATSDR, 1995).

Bock et al. ( 1979) instilled 14C naphthalene into isolated rat intestinal loops. When assayed 30 minutes after instillation, 84% of the administered dose was recovered unmetabolized in the portal blood, while only 1% remained in the luminal contents. Absorption is believed to occur by passive diffusion across the intestinal membranes, with the rate of absorption determined by the partition coefficient between the contents of the intestinal lumen and the lipids of the intestinal membranes ( ATSDR, 1995).

No studies were identified that quantified the rate and extent of naphthalene absorption in humans following ingestion. However, the results of case reports confirm that significant amounts of naphthalene ingested by humans may be absorbed and that adverse effects may result ( Zuelzer and Apt, 1949; Mackell et al., 1951; Bregman, 1954; MacGregor, 1954; Chusid and Fried, 1955; Gidron and Leurer, 1956; Haggerty, 1956; Santhanakrishnan et al., 1973; Gupta et al., 1979; Shannon and Buchanan, 1982; Ojwang et al., 1985; Kurz, 1987).

Dermal Exposure Evidence of naphthalene toxicity has been described in human neonates who reportedly were exposed by dermal contact with diapers that had been stored with naphthalene mothballs or naphthalene flakes ( Schafer, 1951; Dawson et al., 1958). However, inhalation of naphthalene vapors could not be excluded as a contributing route of exposure ( ATSDR, 1995; U. S. EPA, 1998a).

Turkall et al. ( 1994) applied 3.3 : g/ cm2 of naphthalene to the shaved skin of male rats and sealed the area of application under a glass cap for 48 hours. Dermal absorption occurred rapidly, with approximately 50% of the dose being absorbed in 2.1 hours.

Inhalation Exposure No empirical data that describe the rate or extent of naphthalene absorption following inhalation exposure were identified in the materials reviewed for this report. NTP ( 2000) developed a physiologically based pharmacokinetic model to describe the uptake of naphthalene in rats and mice following inhalation exposure. The model was calibrated using blood time course data for naphthalene ( parent compound). Results from this model suggest that inhaled naphthalene is absorbed rapidly into the blood ( Blood: air partition coefficient of 571). On the 6 2 Naphthalene   February 2003 basis of estimates of naphthalene metabolism generated by the model, approximately 22% to 31% of inhaled naphthalene is absorbed by rats and 65% to 73% of inhaled naphthalene is absorbed by mice.

6.2 Distribution Oral Exposure Absorbed naphthalene is expected to be distributed throughout the body ( U. S. EPA, 1998a). Eisele ( 1985) evaluated the distribution of naphthalene following oral administration to pigs, to chickens, or to a single cow. A single 0.123 mg dose of radiolabeled naphthalene/ kg ( 4.8 Ci/ kg) was administered to young pigs, and distribution was monitored at 24 and 72 hours. Adipose tissue had the highest percentage of the label ( 3.48 ± 2.16% dose/ mg tissue) at 24 hours post administration. Lower percentages were reported in the kidney ( 0.96% dose/ mg tissue), liver ( 0.26 ± 0.06% dose/ mg tissue), lungs ( 0.16% dose/ mg tissue), heart ( 0.09 ± 0.04% dose/ mg tissue) and spleen ( 0.07 ± 0.01% dose/ mg tissue). At 72 hours, the percentage of the label in adipose tissue had decreased to 2.18 ± 1.16% dose/ mg tissue, while the activity in the liver was 0.34 ± 0.24% dose/ mg tissue. Activities of 0.96% dose/ mg tissue were determined in the kidneys and lung.

Eisele ( 1985) also administered oral doses of 0.006 mg radiolabeled naphthalene/ kg day ( 0.22 Ci/ kg day) to pigs daily for 31 days. Repeated administration resulted in a pattern of distribution that differed from the pattern observed following a single oral dose. Following repeated doses, the highest tissue concentration of naphthalene occurred in the lung ( 0.15% dose/ mg tissue). The heart and liver each contained 0.11% dose/ mg tissue, and 0.03% dose/ mg tissue was reported in adipose tissue. The spleen and the kidney had 0.09 ± 0.05% and 0.09% dose/ mg tissue, respectively.

Following single or repeated administration to one dairy cow, naphthalene was reported to distribute to milk, with the highest concentration in the lipid fraction ( Eisele, 1985). After 31 days, the highest tissue concentration was reported in the liver, and the lowest concentration was reported in adipose tissue.

Data for distribution of naphthalene or its metabolites in humans are unavailable. However, there is evidence that naphthalene can cross the placenta in humans. Erythrocyte hemolysis of sufficient magnitude to cause anemia was reported in infants born to mothers that had consumed naphthalene while pregnant ( Zinkham and Childs, 1957, 1958; Anziulewicz et al., 1959). The glucose 6 phosphate dehydrogenase status ( see Section 7.4.5) of the infants was not indicated in the materials reviewed for this document.

Dermal Exposure No data describing the distribution of naphthalene following dermal exposures in humans were identified in the materials reviewed for this document. 6 3 Naphthalene   February 2003 Turkall et al. ( 1994) applied 14C radiolabeled naphthalene ( 3.3 : g/ cm2) to the skin of rats. At 48 hours post application, the highest concentration ( 0.56% of the initial dose) was observed at the application site. Approximately 0.01% 0.02% of the initial dose was recovered in the ileum, duodenum, and kidney. Presence of the radiolabel in the ileum and duodenum was considered by the authors as evidence for biliary excretion of naphthalene metabolites.

Inhalation Exposure A recent case report of hemolytic anemia in a neonate whose mother inhaled naphthalene during the 28th week of gestation suggests that inhaled naphthalene can cross the placenta ( Athanasiou et al., 1997). No other data describing the distribution of naphthalene in humans or animals following inhalation exposure were identified in the materials reviewed for this document.

6.3 Metabolism Overview of Metabolic Pathways The in vivo and in vitro metabolism of naphthalene in mammalian systems has been extensively studied ( U. S. EPA 1998a). As many as 21 metabolites, including oxidized derivatives and conjugates, have been identified in the urine of animals exposed to naphthalene ( Horning et al., 1980; Wells et al., 1989; Kanekal et al., 1990). Factors that potentially influence the relative proportions of individual metabolites include species, tissue type, and tissue concentration of naphthalene ( U. S. EPA, 1998a). The initial step in naphthalene metabolism is catalyzed by cytochrome P 450 monooxygenases, and results in the formation of the arene epoxide intermediate 1,2 naphthalene oxide ( Figure 6 1). 1,2 Naphthalene oxide can undergo spontaneous rearrangement to form naphthols ( predominately 1 naphthol). The resulting intermediates may be further metabolized by oxidation reactions, resulting in the formation of di, tri, and tetrahydroxylated intermediates ( Horning et al., 1980). Some metabolites may undergo conjugation with glutathione, glucuronic acid, or sulfate ( ATSDR, 1995; U. S. EPA, 1998a). Glutathione conjugates undergo additional reactions to form cysteine derivatives ( thioethers). These cysteine derivatives may be further metabolized to mercapturic acids and may be excreted in the bile ( U. S. EPA, 1998a).

An alternative pathway of naphthol metabolism involves enzymatic hydration by epoxide hydrolase. This reaction results in the formation of trans 1,2 dihydro dihydroxynaphthalene, also referred to as naphthalene 1,2 dihydrodiol ( U. S. EPA, 1998a). Trans 1,2 dihydrodihydroxynaphthalene can be converted to 1,2 naphthalenediol by catechol reductase, and with subsequent oxidation to 1,2 naphthoquinone and hydrogen peroxide. In addition, 1,2 naphthoquinone may rearrange to form 1,4 naphthoquinone and vice versa ( U. S. EPA, 1998a). The 1,2 naphthoquinone and 1,4 naphthoquinone metabolites may be the primary toxic metabolites, rather than the 1,2 naphthalene epoxide intermediate. This conclusion is based on observations that 1,2 naphthoquinone and 1,4 naphthoquinone were cytotoxic and genotoxic to human lymphocytes, and that 6 4 Naphthalene   February 2003 OH OH OH OH O O O OH OH OH OH O O OH GSH GSH GSH OH Naphthalene 2 Naphthol 1 Naphthol 1,4 Naphthalenediol 1,4 Naphthoquinone Naphthalene 1,2 oxide 1,2 Dihydro 1,2 naphthalenediol 1,2 Naphthalenediol 1,2 Naphthoquinone Glutathione Conjugates Cysteine Conjugates Derivatives ( Thioethers) Glutathione S transferase Epoxide hydrolase Catechol reductase Figure 6 1. Proposed Pathways For Naphthalene Metabolism Source: U. S. EPA ( 1998a) 6 5 Naphthalene   February 2003 they depleted glutathione. In contrast, the epoxide was not cytotoxic or genotoxic, and did not deplete glutathione ( Wilson et al., 1996).

Studies of Naphthalene Metabolism in Humans Data describing the metabolism of naphthalene in humans are limited. Human lung microsome preparations from three individuals aged 60 to 77 years metabolized naphthalene to dihydro 1,2 naphthalenediol and three glutathione adducts ( Buckpitt and Richieri, 1984; Buckpitt and Bahnson, 1986). There was considerable variation in the amount of each metabolite formed by each of the three individuals. Buonarati et al. ( 1990) subsequently identified these adducts as trans 1( S) hydroxy 2( S) glutathionyl 1,2 dihydronaphthalene; trans 1( R) glutathionyl 2( R) hydroxy 1,2 dihydronaphthalene; and trans 1( S) hydroxy 2 S glutathionyl 1,2 dihydronaphthalene.

Tingle et al. ( 1993) investigated naphthalene metabolism using microsomes prepared from six histologically normal human livers. The primary stable metabolite was 1,2 dihydro 1,2 naphthalenediol, generated by the action of epoxide hydrolase on 1,2 naphthalene oxide, whereas, 1 naphthol was a minor metabolite. Inhibition of epoxide hydrolase increased the amount of 1 naphthol formed.

Analysis of urine indicates that naphthols ( specifically 1 and 2 naphthol), 1,2 naphthoquinone, and 1,4 naphthoquinone are formed in humans exposed to naphthalene ( Zuelzer and Apt, 1949; Mackell et al., 1951).

Animal Studies of Naphthalene Metabolism There is some evidence that metabolism of naphthalene may vary among species. Urinary mercapturic acid excretion increased in a dose dependent manner following the administration of naphthalene to rats via gavage ( Summer et al., 1979). In comparison, glucuronic acid and sulfate conjugates were the primary conjugates excreted in the urine of chimpanzees, based on limited data collected from two animals ( Summer et al., 1979).

Urinary metabolites identified in rats and rabbits following the oral administration of naphthalene included 1 and 2 naphthol, 1,2 dihydro 1,2 naphthalenediol, 1 naphthyl sulfate, and 1 naphthylglucuronic acid ( Corner and Young, 1954). With the exception of 1 naphthylglucuronic acid in the urine of guinea pigs, the same metabolites were also identified in the urine of mice, rats and guinea pigs following intraperitoneal injection. A glucuronic acid conjugate of 1,2 naphthalenediol was also likely present in all species; however, the presence of this metabolite was not confirmed. In addition, the urine of rats and rabbits contained 1,2 dihydro 2 hydroxy 1 naphthyl glucuronic acid, while in guinea pigs, unconjugated 1,2 naphthalenediol was excreted.

Horning et al. ( 1980) administered a 100 mg/ kg intraperitoneal dose of naphthalene to male Sprague Dawley rats. The majority of the administered dose ( 80 95%) was excreted in the urine as conjugated glucuronide, sulfate, and thioether metabolites; the major metabolites 6 6 Naphthalene   February 2003 identified were: 1 naphthol, 2 naphthol, 1,2 naphthalenediol, cis and trans 1,2 dihydro 1,2 naphthalenediol, cis and trans 1,4 dihydro 1,4 naphthalenediol, and 1,1, 2,7 and 2,6 naphthalenediol.

Stillwell et al. ( 1982) identified 1 naphthol, trans 1 hydroxy 2 methylthio 1,2 dihydroxynaphthalene, trans 1,2 dihydro 1,2 naphthalenediol, methylthionaphthalene, and 2 naphthol as the major metabolites in the urine of male mice that received naphthalene by intraperitoneal injection. Seven sulfur containing metabolites were identified, with the N acetyl S( 1 hydroxy 1,2 dihydro 2 naphthenyl) cysteine being the primary sulfur metabolite identified.

Bakke et al. ( 1990) identified the glucuronic acid conjugate and the dihydro 1 hydroxy 2 cysteine derivative of dihydronaphthalenediol in the urine of calves. The cysteine derivative was excreted in slightly larger amounts. The two metabolites accounted for approximately 81% of the administered dose.

6.4 Excretion Oral Exposure Limited information exists on the excretion of orally ingested naphthalene by humans. The results of a case study indicated that naphthol was present in human urine four days postingestion ( Zuelzer and Apt, 1949). Smaller amounts were found at five days post ingestion. Naphthol was not present in subsequent specimens. Mackell et al. ( 1951) reported that 1 and 2 naphthol, 1, 2 naphthoquinone, and 1,4 naphthoquinone were present in the urine of an 18 month old infant 9 days after ingestion. At 13 days post ingestion, all metabolites except 1,4 naphthoquinone were still detectable. These results suggest that urinary excretion may be extended following the ingestion of naphthalene. In some exposure scenarios, delayed dissolution and absorption from the gastrointestinal tract may also contribute to an extended pattern of excretion. Zuelzer and Apt ( 1949) noted that naphthalene was visible in fecal matter after the ingestion of naphthalene flakes or mothballs in several individuals.

Boyland and Sims ( 1958) reported that only trace amounts of mercapturic acids were detected in the urine of a man who ingested a 500 mg dose of naphthalene, an observation that is consistent with the findings in non human primates described below.

Animal studies indicate that the majority of ingested naphthalene is eliminated as metabolites in the urine, with a small fraction eliminated in the feces ( U. S. EPA, 1998a). Bakke et al. ( 1985) administered oral doses of radiolabeled naphthalene to rats. At 24 hours postadministration the majority of the label ( 77 93%) was recovered in the urine, while 6 7% was recovered in the feces.

Urinary excretion of premercapturic acids and mercapturic acids represents a major excretory pathway ( accounting for approximately 80% of urinary metabolites) in rodents ( Stillwell et al., 1978; Chen and Dorough, 1979). However, thioethers were not detected in the 6 7 Naphthalene   February 2003 urine of chimpanzees ( Summer et al., 1979) or rhesus monkeys ( Rozman et al., 1982) administered oral doses of up to 200 mg naphthalene/ kg. This result suggests that minimal glutathione conjugation occurs in these species ( ATSDR, 1995). Urinary metabolite data collected from two chimpanzees suggests that naphthalene is excreted primarily as glucuronide and sulfate conjugates in this species ( Summer et al., 1979).

Animal evidence exists for enterohepatic recirculation of naphthalene metabolites. Experiments with normal bile duct cannulated and germ free rats ( Bakke et al., 1985) suggest that premercapturic acid metabolites of naphthalene are excreted in the bile and subsequently converted by the intestinal microflora to 1 naphthol. The newly formed 1 naphthol is then subject to absorption and re circulation.

Dose dependent increases in urinary thioether levels were reported in rats that received gavage doses of 30, 75, or 200 mg naphthalene/ kg ( Summer et al., 1979). The levels of thioethers excreted accounted for approximately 39%, 32%, and 26%, respectively, of the dose levels tested.

Dermal Exposure No studies were located that documented the excretion of naphthalene in humans following dermal exposures.

Turkall et al. ( 1994) evaluated the excretion of dermally applied 14C labeled naphthalene by rats over a 48 hour period. A dose of 3.3 : g/ cm2 of neat naphthalene or naphthalene adsorbed to clay or sandy soils was applied to the shaved skin of rats under a sealed plastic cap. In all cases, excretion was primarily through the urine ( 70 87%). Exhaled air accounted for 6 14% of the administered dose, and 2 4% was recovered in feces. Less than 0.02% of the label was exhaled as carbon dioxide.