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PETITIONED PUBLIC HEALTH ASSESSMENT

ESCAMBIA BRUNSWICK WOOD
(a/k/a BRUNSWICK WOOD PRESERVING)
BRUNSWICK, GLYNN COUNTY, GEORGIA


APPENDIX B: SOIL PATHWAY CONSULTATION


PUBLIC HEALTH CONSULTATION

SOIL AND SEDIMENT PATHWAY EVALUATION

BRUNSWICK WOOD PRESERVING
BRUNSWICK, GLYNN COUNTY, GEORGIA
EPA FACILITY ID: GAD981024466

December 31, 1998


TABLE OF CONTENTS

SUMMARY

BACKGROUND

DISCUSSION

COMMUNITY HEALTH CONCERNS

CONCLUSIONS

RECOMMENDATIONS

REFERENCES

TABLES

FIGURES

APPENDICES


SUMMARY

Brunswick Wood Preserving (BWP) is a former wood-preserving facility located on approximately 84 acres on Perry Lane Road, Brunswick, Glynn County, Georgia. BWP began treating utility poles and marine piles at the site in 1958. The facility initially handled only oil-based preservatives (e.g., creosote and pentachlorophenol [PCP]), but, by 1970, BWP had constructed a separate facility for chromated copper arsenate (CCA) wood treatment. BWP declared bankruptcy in 1991 and completely ceased operations.

Following facility closure, the U.S. Environmental Protection Agency (EPA) conducted a preliminary environmental investigation in which they determined that wood-preserving compounds used in BWP industrial processes had contaminated on-site soil and sediment. EPA also discovered that some compounds may have entered nearby Burnett Creek.

In response to the potential immediate health hazards, EPA initiated a two-phase removal action of the contaminated materials, beginning in 1991. EPA disassembled the facility's process area and excavated and stockpiled contaminated soil , but insufficient funding delayed completion of the removal action. Prior to the delay, however, stockpiled soil had been stored on site in fully contained cells. The cells were covered, lined, and equipped with leachate collection systems to prevent migration of contaminants. While the site was inactive, access was controlled by security guards. In November 1996, the Georgia Department of Natural Resources (GADNR) secured funding to begin removal of the cells of stockpiled soil. Most of the contaminated soil has now been removed from the site.

The Agency for Toxic Substances and Disease Registry (ATSDR) prepared a health consultation for BWP in 1992 to identify potential health concerns associated with site conditions. ATSDR concluded that contaminants, including PCP, dioxin, and creosote, existed in the on-site soil at levels above acceptable health guidelines. Since the 1992 health consultation, ATSDR has received a request from a Brunswick community member to investigate potential health hazards, including the possibility that contact with contaminated on-site soil could have harmed the health of on-site workers or trespassers.

In response to the community member's concern, ATSDR evaluated potential exposures to contaminated on-site soil at the BWP site. Although elevated levels of creosote and CCA compounds, including polycyclic aromatic hydrocarbons, PCP, dioxins/furans, arsenic, and chromium, had been found in on-site soil, workers and trespasser most likely did not come in contact with contaminated soil at levels associated with public health hazards. ATSDR concluded that adverse health effects could result if workers or trespassers contacted the most contaminated soil frequently and for extended periods--a highly unlikely scenario--but that the infrequent and short-term contact that most likely occurred would not harm their health.

ATSDR also evaluated potential exposure to contaminants in sediment from the on-site lagoons and drainage ditches, soil from the perimeter of the site, and sediment from Burnett Creek. ATSDR concluded that soil and sediment in these areas were either inaccessible or contained contaminants at levels that do not pose health hazards.

ATSDR concludes that the soil or sediment pathway posed no apparent public health hazard in the past, nor is it expected to pose a health hazard currently or in the future, because the contaminated media is being removed and a guarded patrol continues to control unauthorized access to the site.


BACKGROUND

Statement of Issues

The Agency for Toxic Substances and Disease Registry (ATSDR) received a request from a Brunswick, Glynn County, Georgia community member to investigate potential health concerns associated with the Brunswick Wood Preserving (BWP) facility. The individual expressed concern that contact with contaminated on-site soil could have harmed the health of on-site workers or trespassers (ATSDR, 1993a). In response to the request, ATSDR reviewed available environmental site data, including information and analytical data provided by the U.S. Environmental Protection Agency (EPA), Georgia Department of Natural Resources (GADNR), Glynn County Health Department, and Community Based Environmental Project (CBEP), to determine whether the contaminated on-site soil poses or did pose a public health concern. As part of a thorough evaluation of potential health hazards, ATSDR additionally evaluated related media, including soil collected from the perimeter (off site) of the site and sediment from on-site lagoons and drainage ditches and Burnett Creek, which abuts the site.

Site Description

BWP is a former wood-preserving facility, located on approximately 84 acres on Perry Lane Road, Brunswick, Georgia (see Figure 1). The site is situated in northwest Brunswick, approximately 5 miles from the downtown area, and is bounded to the south and east by railroad tracks, residential property, and wooded areas, to the north by Perry Lane, and to the west by Burnett Creek (ATSDR, 1992). The 50-acre production area consisted of two wood-treating process areas, former (buried) impoundment area, lagoons, a lumbering area, a drip stockpile area, and several drainage ditches (see Figure 2). The boundary along Perry Lane is secured with a fence and guarded gates. The other boundaries are not fenced or are inadequately fenced, but a security patrol controls access to the site (EPA, 1997a, 1997b).

History

The BWP facility was one of four facilities that made up Brunswick Wood Treating Company (EPA, 1991b). BWP treated utility poles and marine piles from 1958 to 1991, when the site was abandoned. The Brunswick facility initially handled only oil-based preservatives (e.g., creosote and working solutions of technical grade pentachlorophenol [PCP] in diesel fuel), but, by 1970, BWP had also constructed a separate facility for chromated copper arsenate (CCA) wood treatment (EPA, 1991a).

Pressure treatment with PCP and creosote was performed in the southwest portion of the site; the CCA process was performed in the northwest corner of the site, near the lagoons. Following treatment by either method, BWP's wood products were dried in drip tracks and stored in treated wood storage areas prior to shipment. The creosote and PCP pressure treatment process generated a large amount of wastewater , which was treated on site before its release to surface water bodies (the closest being Burnett Creek). Neither the process areas, the drip tracks, nor the storage areas were underlain with concrete slabs or other material that might have prevented wood-preserving compounds from washing into the surrounding soil (EPA, 1991a). As a result of normal operations, storage practices, and several documented large-scale spills, wood preservatives and spent wastewater were released to surrounding soil. Visibly stained soil existed throughout much of the site at the time of EPA's 1991 investigations (EPA, 1994).

BWP used several on-site lagoons (also referred to as surface impoundments) for storing diesel fuels or for disposing of wastewater from treatment operations. It is believed that material stored in lagoons significantly contaminated the underlying soil. During the mid-1970s or mid-1980s, two lagoons located in the south west end of the site were closed, drained, excavated, and paved. These paved areas were later used as a parking lot. Some of the excavated material was transported to and stored in one of the two other lagoons located on the east end of the site.

In early 1991, BWP declared bankruptcy and completely ceased operations following a fire at the facility. Because the facility was unable to take corrective actions or continue operating a waste-water treatment system, EPA entered into a Consent Decree with the various owners/operators and initiated a two-phase emergency removal action program. The first phase began on May 29, 1991, and included 1) abating an emergency situation posed by contaminants released from the site's waste-water treatment system, 2) draining several small holding tanks, and 3) disassembling the CCA process area (EPA, 1991a).

During the first phase, EPA also conducted a preliminary assessment of environmental media, determining that elevated levels of wood-preserving compounds were present in the process area's soil at depths up to 9 feet below ground surface. Contaminants identified in soil included PCP, polycyclic aromatic hydrocarbons (PAHs), arsenic, and chromium. EPA also identified dioxins and furans, which are impurities of PCP. Appendix A provides a brief description of these contaminants. In addition, EPA conducted limited on-site groundwater monitoring and found that wood-preserving compounds released to the on-site soil had migrated vertically to the underlying surficial aquifer beneath the site (EPA, 1991a).

The second phase of the removal action started in January 1992 and included demolition of the CCA process area, the construction of cells for staging of excavated soil, and the excavation of the soil underlying a creosote/PCP lagoon to the west of the creosote/PCP process area. EPA stored more than 127,000 tons of excavated contaminated soil in four on-site lined and covered cells. A lack of funding resources delayed removal activities, and stockpiled contaminated soil remained on site for several years. From these actions, all but a few of the site structures were demolished and removed and large areas of contaminated soil were excavated and stockpiled (EPA, 1997b). Only two lagoons and visibly contaminated soil (at the location of a former lagoon/surface impoundment) remain on site (EPA, 1997b).

GADNR secured funding in November 1996 to begin removing the cells containing stockpiled soil (Permar, 1996). In February 1997, EPA placed the site on the National Priorities List (NPL) and began final cleanup measures at the site (EPA, 1997a). Three of the four soil cells have been removed and removal of the final cell is expected by early 1998.

This health consultation is a continuation of ATSDR's assessment process. In 1992, EPA requested ATSDR to evaluate whether BWP site conditions pose health concerns for nearby residents or individuals accessing the site (ATSDR, 1992). ATSDR determined that on-site workers, those engaged in remedial activities, and individuals who gained unauthorized access to the site may have directly contacted contaminated soil.

Since the 1992 health consultation, ATSDR has received a petition from a Brunswick community member concerned about worker and trespasser exposure to on-site contaminants (ATSDR, 1993a). As followup to the ATSDR recommendation in the 1992 health consultation, and in response to the community member's concern, ATSDR is preparing this health consultation to evaluate whether on-site soil posed a health hazard to workers or site trespassers. In addition, ATSDR addresses whether sediment in on-site lagoons and drainage ditches posed a health hazard and whether these contaminants have migrated to off-site areas (i.e., off-site [perimeter] soil, Burnett Creek) at levels of health concern.

Land and Natural Resources Use

The land in the vicinity of the BWP site is used for a combination of light industrial, commercial, and residential purposes. The Brunswick area has experienced a great deal of pollution; the EPA has identified 17 other hazardous waste sites in the Brunswick area and is conducting Superfund cleanups at three other sites.

Much of the area encompasses large tidal marshes. The marshes are habitat and feeding area for a number of species of animals and birds, including migratory birds and several endangered species (EPA, 1991b). Burnett Creek, a tidally-influenced creek, flows within 100 feet of the western end of the site. Burnett Creek flows from the site toward Cowpen Creek, then the Turtle River, the Brunswick River, and eventually into the Atlantic Ocean (EPA, 1997b). Another marsh area, Dixon Swamp, lies east of the site and is subject to seasonal flooding.

A concrete flume connects Burnett Creek to the site. Because of the poor integrity of the flume, groundwater is probably leaching into it and traveling to Burnett Creek. Although the flume was plugged during removal measures, the plug has not effectively prevented contaminated groundwater from traveling to Burnett Creek (EPA, 1997a). Several drainage ditches convey surface water runoff along western boundary and along the active railroad tracks along the southwestern end of the site. One significant ditch flows along Perry Lane, then across the main entrance of the site, and ultimately empties into Burnett Creek (EPA, 1997b).

A strong commercial seafood fishing industry prospers in Brunswick. Commercial harvesting of shrimp and blue crabs occurs below the U.S. 341 bridge, one-half mile south of the site (EPA, 1991a). Contamination was detected in the surface water and fish in the area (and attributed to a variety of sources), and in response, GADNR issued a fish consumption advisory for Purvis Creek, Gibson Creek, and parts of the Turtle River, all of which are located approximately 2 to 3 miles south-southeast of the BWP site (EPA, 1995). Recreational harvesting of finfish and shellfish for local consumption also occurs along all reaches of Burnett Creek, including areas adjacent to the site (EPA 1991a, 1997a).


DISCUSSION

Assessment Methodology

For each environmental medium at a site, ATSDR examines the type and concentrations of relevant contaminants. In preparing this document, ATSDR used comparison values to screen contaminant concentrations and select chemical of concerns--a chemical that exceeds one or more comparison values--that warrant further evaluation. Comparison values are concentrations of chemicals that can reasonably (and conservatively) be regarded as harmless, assuming default conditions of exposure. The comparison values generally include ample safety factors to ensure protection of sensitive populations. Because comparison values do not represent thresholds of toxicity, exposure to contaminant concentrations above comparison values will not necessarily produce health effects. Comparison values used in this document are discussed in Appendix B. ATSDR then considers how people might come into contact with the contaminants. This information is essential to determining public health hazards because, for any given chemical, exposure concerns vary according to the method of exposure and the concentrations of contaminants. A list of acronyms and a glossary are provided in Appendix C and Appendix D, respectively.

Potential exposure pathways for BWP include soil, air, and groundwater pathways. In response to the petitioner's concern about worker and trespasser exposure to contaminated on-site soil, this document evaluates the on-site soil exposure pathway in more detail, considering any information gathered during removal or remedial activities conducted since ATSDR's 1992 health consultation. ATSDR also addresses potential health hazards from exposure to sediment in on-site lagoons and drainage ditches and areas potentially affected by off-site migration of contaminants to determine whether these pathways pose a health concern for workers, trespassers, or perhaps to other persons. ATSDR has evaluated the air and groundwater exposure pathways in separate documents.

Evaluation of the Soil and Sediment Pathway

Soil and Sediment Monitoring Results

EPA sampled soil and sediment during 1991 and 1993 preliminary site investigations and most recently during 1997 remedial investigation activities to assess the distribution of CCA, PCP, creosote, and dioxin/furan contamination (EPA, 1991c, 1994, 1997a). EPA collected on-site composite soil samples from the CCA, lumbering, and drip/stockpile areas and from the locations of former lagoons. During the 1997 environmental investigations, off-site soil sampling occurred along the perimeter of the site. EPA also sampled sediment from the on-site lagoons, on-site drainage ditches, and Burnett Creek. All samples were analyzed for creosote compounds (i.e., PAHs), PCP, and metals, and selected samples were analyzed for dioxins/furans and volatile organic compounds.

The contaminants and the maximum concentrations detected in the soil and sediment samples collected during the site investigations are summarized in Tables 1 through 4, along with comparison values for each contaminant. Contaminants exceeding comparison values, and therefore identified as contaminants of concern in soil and sediment at BWP, consist of PCP, dioxins/furans, PAHs, benzene, arsenic, and chromium.

On-Site Soil and Sediment

Soil sampling revealed that concentrations of PAHs, dioxins/furans, arsenic, chromium, and PCP in on-site soil and sediment exceeded comparison values. The following describes the level of contamination present in soil and sediment:

  • A maximum PCP concentration of 5,000 milligrams per kilogram (mg/kg) (well above the ATSDR comparison value of 6 mg/kg) was detected in soil collected from an on-site waste pile. Concentrations of PCP up to 1,000 mg/kg were sporadically detected in the drip and stockpile area. Lower concentrations were present in sediment collected from the drainage ditch (up to 431 mg/kg) and the lagoon (up to 66 mg/kg).

  • Dioxin and furan contamination was typically present where there were high concentrations of PCP. The highest concentrations of dioxins/furans were measured at 0.14 mg/kg 2,3,7,8-TCDD-equivalents (TEQs) and 0.31 mg/kg TEQs in lagoon sediment;(1) concentrations are above the ATSDR comparison value for 2,3,7,8-TCDD (0.001 mg/kg). Lower concentrations (0.00005 to 0.02741 mg/kg TEQs) were generally found in on-site soil. Drainage ditch samples were not analyzed for dioxins/furans.

  • PAHs measured as benzo(a)pyrene equivalents were detected in on-site soil at levels up to 17.67 mg/kg--above the ATSDR comparison value for benzo(a)pyrene of 0.1 mg/kg. PAHs were frequently found in soil of the drip and stockpile area, but some of the highest concentrations were detected beneath the former lagoons, where contamination extended to 8 feet below ground surface. Lower levels of PAHs were measured in the lagoon sediment (up to 9.05 mg/kg TEQs). Drainage ditch samples were not analyzed for PAHs.

  • Elevated levels of arsenic (up to 8,800 mg/kg) and chromium (up to 4,700 mg/kg) were sporadically detected above the ATSDR comparison values (0.5 mg/kg and 6 mg/kg, respectively) in the CCA area soil. Similar levels were reported in samples collected from the on-site lagoons. Much lower levels (generally below 10 mg/kg) were found in the majority of samples collected from remaining portions of the BWP site, however.

As of 1997, contaminated soil and waste piles were excavated to depths up to 8 feet below ground surface and most of the excavated material has been removed from the site. EPA and GADNR expect to remove the final cell of excavated soil and waste by early 1998. Clean soil and gravel have replaced contaminated soil in the excavated areas.

Past Exposures to On-Site Soil and Sediment

BWP workers and trespassers could have been exposed to contaminants in soil or sediment through skin contact or incidental ingestion. To evaluate the likelihood, if any, of the chemicals of concern at the BWP site causing adverse health effects, ATSDR estimated the dose of these chemicals to which people might have been exposed, based on site-specific considerations. ATSDR reviewed the scientific literature and evaluated potential noncancer (noncarcinogenic) and cancer (carcinogenic) health effects associated with the levels of contaminants of concern detected at BWP. Appendix F describes this process in more detail and presents the assumptions used in estimating doses.

Although high levels of contaminants were detected in sediment in the lagoons and the drainage ditches, water covering these areas limited access to the underlying sediment. Therefore, it is unlikely that workers or trespassers contacted sediment in these areas during past site operations. Because sediment soil contamination was fairly wide spread, workers or trespassers probably came in contact with contaminated soil; however, the extent to which workers and trespassers came in contact with contaminants in soil, including the frequency and duration of exposures, are not known with certainty. In the absence of this site specific information, ATSDR developed a scenario using very conservative assumptions when estimating worker and trespasser exposures to contaminants in soil. ATSDR assumed that a 70-kilogram worker performed outdoor activities in the contaminated area 5 days a week over 20 years, and that a 50-kg trespasser (assuming a child/teenager between the ages of 7 and 14 years) accessed contaminated areas, 2 days a week over a 7-year period. ATSDR also assumed that, during these activities, individuals were incidentally exposed to the most contaminated soil; therefore, ATSDR used maximum measured concentrations of contaminants in on-site soil (see Table 1) in estimating exposure doses. For exposure through skin, ATSDR assumed that approximately 10% of a worker's or trespasser's skin surface was exposed to soil.

On the basis of these very conservative assumptions, ATSDR derived exposure doses and excess cancer risk for workers and trespassers. Estimates for exposure to arsenic and dioxins/furans via dermal contact or incidental ingestion exceeded health guidelines (i.e., minimal risk levels [MRLs] and Reference Doses [RfDs]). In addition, cancer risk estimates for workers and trespassers contacting or ingesting arsenic and dioxins/furan in soil, or contacting PCP in soil exceed acceptable cancer guidelines. Therefore, workers or trespassers who were most likely to come in contact with or inadvertently ingest these contaminants in soil may have an increased likelihood of developing adverse health effects or cancer if exposed to the highest levels of these contaminants over an extended period. The exposure doses, however, most likely overestimate the actual exposures incurred by workers and trespassers. The likelihood that workers in their routine responsibilities or trespassers during their intermittent access came in contact with the most contaminated soil for an extended period is remote. If workers or trespassers did contact soil with the highest concentrations, exposure most likely was intermittent and brief. Moreover, workers entering these areas most likely wore protective clothing, which would reduce exposure and any associated health effects. Therefore, likely actual exposures incurred by workers or trespassers would not be expected to result in adverse health effects.

ATSDR concludes that past exposures to on-site soil and sediment, which were likely sporadic and of short duration, are not a public health concern. ATSDR determined that a health hazard may have existed for workers or trespassers if they came in contact with the most contaminated soil on a regular basis for an extended period of time. The likelihood that such exposures occurred is very low, however.

Present and Future Exposures to On-Site Soil and Sediment

Present or future exposure to contaminated soil and sediment is unlikely to occur. A fence along Perry Lane and security patrols currently limit unauthorized access, and there is no current evidence that trespassing is occurring. Workers involved in the cleanup or removal measures should wear protective clothing to limit exposures; if exposure were to occur, it would be infrequent and of a short duration. As mentioned previously, EPA and GADNR have excavated areas of soil contamination and removal of the excavated material is expected to be completed by early 1998. This action is intended to reduce contaminant levels in the soil and sediment to levels with which workers can safely come in contact in the future. Once the soil is removed, the site should not pose a health hazard in the future to the general public, as long as site use is limited to industrial- and commercial-related purposes.

Off-Site (Perimeter) Soil

EPA collected soil samples from along the perimeter of the site to determine whether soil contaminants may have migrated beyond the site boundaries. These samples were analyzed for VOCs, semivolatile organic compounds (SVOCs) (including PAHs), PCP, dioxins/furans, and metals. The benzo(a)pyrene equivalents (up to 3.5 mg/kg) exceeded the corresponding comparison value for benzo(a)pyrene (0.1 mg/kg); however, the levels are within background concentrations reported for benzo(a)pyrene in urban/industrial environments (0.06 to 14 mg/kg) (ATSDR, 1995). Other off-site sources associated with PAHs, including railroad operations, may be contributing to the slightly elevated levels in soil. The maximum level for arsenic (2.8 mg/kg) also slightly exceeded ATSDR's CREG, but was below both the RMEG (20 mg/kg) and the mean background soil concentration of 5 mg/kg (ATSDR, 1993c).

It is unlikely that the exposure to PAHs or arsenic in the perimeter soil would pose a health hazard for trespassers, workers, or nearby residents. The perimeter soil contained contaminants at levels that were even much lower than levels detected on-site that were found to pose no public health hazard.

Burnett Creek Sediment

Burnett Creek sediment contained slightly elevated levels of dioxins/furans and PAHs in downstream sections of the creek, and slightly higher concentrations of arsenic in upstream portions. This finding indicates that dioxin, arsenic, and creosote compounds from BWP may have migrated from the site, but that other upstream sources also could be responsible for arsenic in Burnett Creek.

Although arsenic, PCP, and dioxins/furans were present in the Burnett Creek sediment at levels just slightly above ATSDR's comparison values, the levels do not pose a health hazard to the users of Burnett Creek, assuming people are not contacting sediment on a frequent basis. Although one report suggests that nearby residents may have used Burnett Creek for swimming, there are no current indications that people use the creek for recreation in ways (e.g., wading) that would result in significant dermal contact with sediment (EPA, 1991a).

Indirect exposure to contaminants may occur through fish consumption because fish may accumulate even very low levels of contaminants that may be in sediment. Following a spill of PCP from BWP into the Burnett Creek, GADNR closed the creek to fishing for approximately one year. GADNR analyzed fish samples from the creek for PCP in 1989 and 1990 and concluded that PCP levels in the fish tissue did not present a public health hazard to persons consuming Burnett Creek fish (EPA, 1991a). EPA also requested ATSDR to evaluate potential health hazards for persons consuming fish that potentially accumulated site-related contaminants. At the time, ATSDR concluded that PAHs and metals in sediment were unlikely to accumulate to harmful levels in Burnett Creek fish, but information was insufficient to comment on other contaminants, most notably, dioxins/furans (EPA, 1991a).

ATSDR does not know with certainty the extent to which people fish in the creek or whether fish are accumulating low levels of site-related contaminants, such as dioxins/furans. ATSDR reviewed scientific literature to understand the relationship between dioxin/furan concentrations in sediment and uptake by fish. Findings from limited available studies provide some evidence that elevated fish tissue concentrations correlate to high dioxin/furan sediment concentrations, but differences in fish species and lipid content may influence uptake (Sherman, 1992). One study indicates that fish accumulated dioxins/furans to levels greater than 0.0000025 mg/kg TEQs from sediment containing dioxin/furan concentrations ranging from 0.0000141 mg/kg TEQs to 0.000142 mg/kg TEQs (Ling, 1995). The 0.0000025 mg/kg TEQ limit has been used by the Food and Drug Administration as a basis for issuing fish consumption advisories for dioxins/furans, but it is currently under review (FDA, 1981; ATSDR, 1989). Because sediment concentrations measured in Burnett Creek are similar to the literature-based values, dioxins/furans may be accumulating in Burnett Creek fish, if they reside exclusively in the stream area near the site. It is possible that dioxin/furan sediment contamination in Burnett Creek might be additive to existing levels in fish downstream from the site, increasing the potential for exposure to multiple contaminants.

ATSDR calculated cancer risk for an average adult (60kg) from eating fish using the FDA TEQ and assumed consumption rates from previous studies (the 1988 West study, a 1988 survey in New York, a 1985 survey in Wisconsin, and a 1980 survey by Rupp, National Marine Fisheries for the North-Central region of the U.S.). From these studies ATSDR used 15g/d for sport-fishers and 7.3g/d for self-caught fish as reasonable but yet conservative daily consumption estimates. ATSDR calculations indicate that elevated cancer risk is not significant for an average adult who consumes 2 fish meals or less per month over a 70 year period from Burnett Creek. For persons who consume 4 fish meals or more per month over a 70 year period from Burnett Creek theoretical cancer risk is slightly elevated. If people consume fish from the creek, then fish monitoring data are needed to more fully evaluate this exposure pathway.


COMMUNITY HEALTH CONCERNS

ATSDR received a request from a Brunswick community member to investigate potential exposures to site-related contaminants. ATSDR is addressing the concern about contamination at the site through this health consultation. To date, Glynn County Health Department has not received inquires or concerns from the community or documented any site-related health effects (GCHD, 1997). ATSDR will continue to monitor community concerns (e.g., communicate with the Glynn County Health Department) as a continuation of the health consultation process.


CONCLUSIONS

Based on a review of available data and discussions with local, state, and federal environmental and health officials, ATSDR developed the following conclusions and assigned public health hazard categories for the soil and sediment exposure pathway at the site. A description of ATSDR conclusion categories is provided in Appendix G.

  • Elevated levels of PAHs, PCP, dioxins/furans, arsenic, and chromium (all associated with wood preserving compounds) have been detected in BWP on-site soil and sediment.

  • On-site soil or sediment posed no apparent public health hazard to workers and trespassers in the past, except for persons who may have routinely contacted the most contaminated soil over an extended period of time. Most workers and trespassers, however, did not frequently work in or access areas with the highest levels of contamination. Rather they would have only contacted contaminants infrequently and briefly.

  • On-site soil and sediment pose no apparent public health hazard, now or in the future, assuming future industrial or commercial use. EPA has removed the majority of the contaminated soil and sediment from the site and replaced it with clean soil and gravel. Furthermore, a security patrol controls unauthorized access to the site.

  • Soil samples taken along the perimeter of the site contained only low levels of site-related compounds. Contaminants levels in off-site soil are not likely to pose a public health hazard.

  • Burnett Creek sediment contained slightly elevated levels of dioxin, PAHs, and arsenic. People do not appear to use the creek for the type of activities that permit extended contact with sediment. Therefore, infrequent contact with the slightly elevated levels of arsenic, dioxin, or PAHs present in the creek sediment does not pose a public health hazard.

  • Indirect exposure to site-contaminants through consumption of Burnett Creek fish pose an indeterminate public health hazard. Burnett Creek fish may be accumulating even low levels of site-related contaminants (e.g., dioxins/furans) in sediment to levels associated with public health hazards to people who eat fish from Burnett Creek. Supporting fish sampling data, however, are not available to enable a full evaluation.

RECOMMENDATIONS

The following recommendations identify actions that ATSDR has determined necessary to characterize further potential public health hazards associated with BWP.

  • If persons fish along Burnett Creek near the site, ATSDR recommends actions be taken (e.g., fish monitoring) to determine the extent, if any, to which Burnett Creek fish are accumulating site-related contaminants (e.g., dioxins) to levels that could pose health hazards to persons consuming Burnett Creek fish.

If requested, ATSDR will review additional data available from the forthcoming RI and will revise the findings of this public health consultation, if necessary.


REFERENCES

ATSDR. 1989. Agency for Toxic Substances and Disease Registry. U.S. Public Health Service. Toxicological Profile for 2,3,7,8-Tetrachloro-dibenzo-p-dioxin. June 1989.

ATSDR. 1990. Agency for Toxic Substances and Disease Registry. U.S. Public Health Service. Toxicological Profile for Creosote. TP-90-09. December 1989.

ATSDR. 1992. The Brunswick Wood Preserving Site Health Consultation. Brunswick Glynn County, Brunswick, Georgia. Agency for Toxic Substances and Disease Registry. May 15 1992.

ATSDR. 1993a. The Brunswick Wood Preserving Site Petition Decision Summary. Brunswick, Glynn County, Brunswick, Georgia. Agency for Toxic Substances and Disease Registry. December 15, 1993.

ATSDR. 1993b. Agency for Toxic Substances and Disease Registry, U.S. Department of Health and Human Services. Pentachlorophenol Toxicity. Case Studies in Environmental Medicine. 23. September 1993.

ATSDR. 1993c. Agency for Toxic Substances and Disease Registry. U.S. Public Health Service. Toxicological Profile for Arsenic. TP-92/02. April 1993.

ATSDR. 1993d. Agency for Toxic Substances and Disease Registry. U.S. Public Health Service. Toxicological Profile for Chromium. TP-92/08. April 1993.

ATSDR. 1994. Agency for Toxic Substances and Disease Registry, U.S. Department of Health and Human Services. Toxicological Profile for Pentachlorophenol (Update). TP-93/12. May 1994.

ATSDR. 1995. Agency for Toxic Substances and Disease Registry, U.S. Department of Health and Human Services. Draft Toxicological Profile for Polycyclic Aromatic Hydrocarbons (Update). August 1995.

EPA. 1989a. Interim procedure for estimating risk associated with exposure to mixtures of chlorinated dibenzo-p-dioxin and dibenzo furans (CDDs and CDFs) and the 1989 update. March 1989.

EPA. 1989b. Environmental Protection Agency (EPA). Exposure Factors Handbook. EPA/600/8-89/043. 1989.

EPA. 1991a. Memorandum from Greer C. Tidwell, Regional Administrator, U.S. Environmental Protection Agency to Don Clay, Assistant Administrator, Office of Solid Waste and Emergency Response, U.S. Environmental Protection Agency. Re: Request for a $2 Million Exemption for the Escambia Wood Preserving-Brunswick Site in Brunswick, Glynn County, Georgia.

EPA. 1991b. Removal Action Fact Sheet. Escambia Wood Preserving-Brunswick Site in Brunswick, Glynn County, Georgia.

EPA. 1991c. Final report preliminary assessment Brunswick Wood Preserving Site, Brunswick. GA. November, 1991. U.S. Environmental Protection Agency/ERT.

EPA. 1992. Environmental Protection Agency (EPA), Dermal Exposure Assessment: Principles and Applications. Interim Report. Office of Research and Development. EPA/600/8-91/001B. January 1992.

EPA. 1993. Environmental Protection Agency (EPA), Office of Research and Development, Washington, DC. Provisional Guidance for Quantitative Risk Assessment of Polycyclic Aromatic Hydrocarbons. EPA/600/R-93/089.

EPA. 1994. Draft expanded site inspection. Escambia Brunswick Wood, Brunswick Glynn County, GA. Waste Management Division. U.S. Environmental Protection Agency. Region IV. February 28, 1994.

EPA. 1995. Brunswick/Glynn County Community Based Environmental Project Brunswick, Glynn County Work plan. U.S. Environmental Protection Agency. November 1995.

EPA. 1996. Brunswick Wood Preserving. HRS Documentation. U.S. Environmental Protection Agency. June 26, 1996.

EPA. 1997a. Personal correspondence between Eastern Research Group, Inc. and Brian Farrier, U.S. Environmental Protection Agency.

EPA. 1997b. Remedial investigation work plan for Brunswick Wood Preserving Superfund site. Brunswick, Glynn County, Georgia. February 1997.

FDA. 1981. Talk paper: Dioxin in fish. Food and Drug Administration. U.S. Department of Health and Human Services. August 28, 1981.

GCHD. 1997. Personal correspondence between Eastern Research Group, Inc. and Jane Britt, Glynn County Health Department. January 1997.

IRIS. 1997. Integrated Risk Information System. U.S. Environmental Protection Agency. August 1997.

Kissel, J. Richter, K., Duff, R. et al. 1995. Dermal soil exposure: Investigation of soil contact and skin coverage. Office of Health and Environmental Assessment. (Review Draft) U.S. Environmental Protection Agency. June 1995.

Ling, Y. D. Soong, and M. Lee. 1995. PCDD/DFs and coplanar PCBs in sediment and fish samples from Er-Jen River in Taiwan. Chemosphere, 331:2863-72.

MADEP. 1995. Massachusetts Department of Environmental Protection (MADEP), Bureau of Waste Site Cleanup and Office of Research and Standards. Guidance for Disposal Site Risk Characterization. July 1995.

Nisbet, I.C. and P.K. LaGoy. 1992. Toxic equivalency factors (TEFs) for polycyclic aromatic hydrocarbons (PAHs). Regul. Toxicol. Pharm. 16:290-300.

Permar, J. 1996. Toxic Wastes. The Islander. November 4.

Ryan, E., E. Hawkins et al. 1987. Assessing Risk from Dermal Exposure at Hazardous Waste Sites. In Bennet, G. And J. Bennet, eds. Superfund '87: Proceedings of the Eighth National Conference; November 16-18; Washington, D.C. The Hazardous Material Control Research Institute.

Sherman, R., R.Keenan, and D. Gunster. 1992. Reevaluation of dioxin bioconcentration and biaccumulation factors for regulatory purposes. J. Toxicol. Environ. Health. 37:211-229

Wester, R., H. Maibach et al. 1993a. In vivo and in vitro percutaneous absorption and skin decontamination of arsenic from water and soil. Fundamental and Applied Toxicology. 20:336-340.

Wester, R., H. Maibach et al. 1993b. Percutaneous absorption of pentachlorophenol from soil. Fundamental and Applied Toxicology. 20:68-71.


TABLES

TABLE 1. Maximum Contaminant Concentrations in On-Site Soil

Contaminant Maximum Concentration
(mg/kg)
Comparison Value
Concentration
(mg/kg)
Reference
2,3,7,8-TCDD equivalents 0.02741 0.001 ATSDR's Interim Policy Level
PAHs
Benzo(a)pyrene equivalents
3,249
17.67
no value
0.1
CREG
Arsenic 8,800 20
0.5
RMEG
CREG
Chromium 4,700 300 RMEG
Pentachlorophenol 5,000 6 CREG

mg/kg: milligrams per kilogram

RMEG: Reference Dose Media Evaluation Guide
CREG: Cancer Risk Evaluation Guide (1 x 10-6 excess cancer risk)

Sources: EPA, 1991c, 1994, 1997a


TABLE 2. Maximum Contaminant Concentrations in On-Site Sediment

Contaminant Drainage Ditches (mg/kg) Lagoon Sediment
(mg/kg)
Comparison Value
Concentration
(mg/kg)
Reference
2,3,7,8-TCDD equivalents NA 0.140 0.001 ATSDR Interim Policy Level
PAHs
Benzo(a)pyrene equivalents
NA
NA
1,267
9.05
no value
0.1
CREG
Arsenic < 10 13,000 20
0.5
RMEG
CREG
Chromium 30 4,700 300 RMEG
Pentachlorophenol 431 1,200 6 CREG

mg/kg: milligrams per kilogram

RMEG: Reference Dose Media Evaluation Guide
CREG: Cancer Risk Evaluation Guide (1 x 10-6 excess cancer risk)
NA: not analyzed for

Sources: EPA, 1991c, 1994, 1997a


TABLE 3. Maximum Contaminant Concentrations in Off-Site (Perimeter) Soil

Contaminant Maximum Concentration
(mg/kg)
Comparison Value
Concentration
(mg/kg)
Reference
2,3,7,8-TCDD equivalents 0.000047 0.001 ATSDR's Interim Policy Level
PAHs
Benzo(a)pyrene equivalents
66.8*
3.5
no value
0.1
CREG
Arsenic 2.8 20
0.5
RMEG
CREG
Chromium 18 300 RMEG
Pentachlorophenol 0.10* 6 CREG

mg/kg: milligrams per kilogram
*Laboratory data sheets indicate that the values are estimated concentrations.

RMEG: Reference Dose Media Evaluation Guide
CREG: Cancer Risk Evaluation Guide (1 x 10-6 excess cancer risk)

Sources: EPA, 1997a


TABLE 4. Maximum Contaminant Concentrations in Burnett Creek Sediment

Contaminant Burnett Creek Comparison Value
Upstream
(mg/kg)
Downstream
(mg/kg)
Concentration
(mg/kg)
Reference
2,3,7,8-TCDD equivalents 0.0004 0.00049 0.001 ATSDR's Interim
Policy Level
PAHs
Benzo(a)pyrene equivalents
ND 16.17
0.297
no value
0.1
CREG
Arsenic 2.8 0.27 20
0.5
RMEG
CREG
Chromium 20 0.81 300 RMEG
Pentachlorophenol ND 0.570 6 CREG

mg/kg: milligrams per kilogram

RMEG: Reference Dose Media Evaluation Guide
CREG: Cancer Risk Evaluation Guide (1 x 10-6 excess cancer risk)
ND: not detected

Sources: EPA, 1991c, 1994, 1997a


FIGURES

Area Map
Figure 1. Area Map

Site Map
Figure 2. Site Map


APPENDICES

APPENDIX A: WOOD PRESERVING CONSTITUENTS

The wood preserving constituents used during plant operations included creosote and pentachlorophenol. The following is a summary of these wood preserving compounds.

Creosote and PAHs

The type of creosote used for wood preserving is a complex mixture of many chemicals created by high-temperature treatment of coal; it is also known as coal tar creosote. The primary way that creosote contaminates soil is through wastewater effluent leaching from unlined settling ponds at wood treatment facilities. Although approximately 300 chemicals have been identified in creosote, the major constituents of potential health concern are polycyclic aromatic hydrocarbons (PAHs) and phenols. PAHs typically represent 85 % of a creosote mixture while phenols represent 2 % to 17 % (ATSDR, 1990).

Because creosote consists primarily of PAHs, the fate of the mixture often parallels that of PAHs. PAHs are formed during the incomplete burning of coal, oil, wood, or other organic substances. More than 100 PAHs exist and most are ubiquitous in air and soil. PAHs do not dissolve readily in water and may strongly adsorb to soil. Their mobility correlates roughly to their molecular weight. Lower molecular weight PAHs or light PAHs (e.g., acenaphthene, acenaphthylene, anthracene, and naphthalene) tend to volatilize from water and exhibit moderate ability to adsorb to soil (which may hinder their solubility and movement in water). Heavy PAHs (e.g., chrysene, benzo(a)pyrene, and benzo(b)fluoranthene) do not readily volatilize from water and have a stronger tendency to adsorb to carbon in soil, thus impeding movement within groundwater (ATSDR, 1995).

Pentachlorophenol

Pentachlorophenol is another man-made substance used for wood preserving that does not occur naturally in the environment. Impure pentachlorophenol, the form typically found at hazardous waste sites, exists as dark gray to brown dust, beads, or flakes. Like creosote, the pentachlorophenol found in soil is most likely the result of waste leaking from unlined storage lagoons at former wood preserving facilities. Although pentachlorophenol can leach through soil to contaminate groundwater, certain conditions (e.g., acidic soil) may encourage adsorption of pentachlorophenol to soil and reduce the potential for leaching to groundwater (ATSDR, 1993a, 1994).

Metals

Metals such as arsenic and chromium are chemicals associated with the CCA wood preserving activity. These metals often attach strongly to soil and sediment, but they can dissolve in water or release from industrial discharges and move deeper in the soil to the underlying groundwater (ATSDR, 1993c, 1993d).

Dioxins and Furans

Polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDF) are common impurities in technical grade pentachlorophenol. PCDDs and PCDFs are classes of compounds that are loosely referred to as dioxins and furans, respectively. The more than two hundred possible dioxin and furan isomers belong to one of eight different homologue categories or series. (A homologue is a group of structurally related chemicals that have the same degree of chlorination. There are eight homologues of dioxins, monochlorinated through octachlorinated. An isomer is a substance that belongs to the same homologue class.) The potency of these isomers varies with structure, with the maximum potency belonging to isomers containing chlorine in the 2,3,7,8-lateral ring positions. Current evidence indicates that the most toxic dioxin is 2,3,7,8-tetrachlorodibenzodioxin (2,3,7,8-TCDD) (ATSDR, 1989).

Although 2,3,7,8-TCDD may leach through soil that contain very low organic carbon content, the compound tends to be relatively immobile in most other types of soil. The estimated environmental half-life of 2,3,7,8-TCDD in soil may be 1 to 3 years, but is as much as 10 to 12 years in the deeper soil layers (ATSDR, 1989).


APPENDIX B: COMPARISON VALUES

Comparison values for ATSDR public health assessments are contaminant concentrations that are found in specific media and that are used to select contaminants for further evaluation. The values provide guidelines that are used to estimate a dose at which health effects might be observed. Comparison values used in the Environmental Contamination and Other Hazards and the Public Health Implications sections of this public health assessment are listed and described below.

Cancer Risk Evaluation Guides (CREGs) are estimated contaminant concentrations that would be expected to cause no more than one excess cancer in a million (1 x 10-6) persons exposed over a lifetime. CREGs are calculated from EPA's cancer slope factors, which indicate the relative potency of a carcinogenic chemical.

Environmental Media Evaluation Guides (EMEGs) are based on ATSDR minimal risk levels (MRLs) and factor in body weight and ingestion rates. Reference Dose Media Evaluation Guides (RMEGs) are the same as EMEGs only they are based on EPA reference doses (RfDs).

A Minimal Risk Level (MRL) is an estimate of daily human exposure to a chemical (in mg/kg/day) that is likely to be without an appreciable risk of deleterious effects (noncarcinogenic) over a specified duration of exposure. MRLs are based on human and animal studies and are reported for acute (< 14 days), intermediate (15-364 days), and chronic (> 365 days) exposures. MRLs are published in ATSDR Toxicological Profiles for specific chemicals.

EPA's Reference Dose (RfD) is an estimate of the daily exposure to a contaminant that is unlikely to cause adverse health effects. However, RfDs do not consider carcinogenic effects.


APPENDIX C: LIST OF ACRONYMS

ABS absorption factor
AF adherence factor
AT averaging time
ATSDR Agency for Toxic Substances and Disease Registry
BW body weight
BWP Brunswick Wood Preserving
CBEP Community Based Environmental Project
CCA chromated copper arsenate
CF conversion factor
CPF Cancer Potency Factor
CREG Cancer Risk Evaluation Guide (1 x 10-6 excess cancer risk)
ED exposure duration
EF exposure frequency
EMEG environmental media evaluation guide
EPA U.S. Environmental Protection Agency
EPD Georgia Environmental Protection Division
EDS EPA's Environmental Services Division
GADNR Georgia's Department of Natural Resources
kg kilogram
mg/kg milligrams per kilogram
µg/kg micrograms per kilogram
MRL ATSDR's minimal risk level
NA not analyzed
ND not detected
NPL National Priorities List
PAH polycyclic aromatic hydrocarbon
PCDD polychlorinated dibenzo-p-dioxins
PCDF polychlorinated dibenzofurans
ppb parts per billion
ppm parts per million
PCP pentachlorophenol
RfD EPA's Reference Dose
RI remedial investigation
RMEG ATSDR's reference dose media evaluation guide
SA skin surface area
TCDD 2,3,7,8-tetrachlorodibenzodioxin
TEFs 2,3,7,8-tetrachlorodibenzodioxin toxic equivalency factors
TEQs 2,3,7,8-tetrachlorodibenzodioxin equivalents
VOCs volatile organic compounds


APPENDIX D: GLOSSARY

Carcinogen:
Any substance that may produce cancer.


Comparison Values:
Estimated contaminant concentrations in specific media that are not likely to cause adverse health effects, given a standard daily ingestion rate and standard body weight. The comparison values are calculated from the scientific literature available on exposure and health effects.


Concentration:
The amount of one substance dissolved or contained in a given amount of another. For example, sea water contains a higher concentration of salt than fresh water.


Contaminant:
Any substance or material that enters a system (the environment, human body, food, etc.) where it is not normally found.


Dose:
The amount of a substance to which a person is exposed. Dose often takes body weight into account.


Environmental Contamination:
The presence of hazardous substances in the environment. From the public health perspective, environmental contamination is addressed when it potentially affects the health and quality of life of people living and working near the contamination.


Exposure:
Contact with a chemical by swallowing, by breathing, or by direct contact (such as through the skin or eyes). Exposure may be short term (acute) or long term (chronic).


Groundwater:
Water beneath the surface of the ground in a saturated zone.


Health Consultation:
A response to a specific question or request for information pertaining to a hazardous substance or facility (which includes waste sites). It often contains a time-critical element that necessitates a rapid response; therefore, it is a more limited response than an assessment.


Ingestion:
Swallowing (such as eating or drinking) chemicals that have gotten in or on food, drinks, utensils, cigarettes, or hands. After ingestion, chemicals can be absorbed into the blood and distributed throughout the body.


Media:
Soil, water, air, plants, animals, or any other parts of the environment that can contain contaminants.


Petitioned Health Consultation:
A public health consultation conducted at the request of a member of the public. When a petition is received, a team of environmental and health scientists is assigned to gather information to ascertain, using standard public health criteria, whether there is a reasonable basis for conducting a public health consultation. Once ATSDR confirms that a public health consultation is needed, the petitioned health consultation process is essentially the same as the public health consultation process.


Potentially Exposed:
The condition where valid information, usually analytical environmental data, indicates the presence of contaminant(s) of a public health concern in one or more environmental media contacting humans (i.e., air, drinking water, soil, food chain, surface water), and there is evidence that some of those persons have an identified route(s) of exposure (i.e., drinking contaminated water, breathing contaminated air, having contact with contaminated soil, or eating contaminated food).


Risk:
In risk assessment, the probability that something will cause injury, combined with the potential severity of that injury.


Route of Exposure:
The way in which a person may contact a chemical substance. For example, drinking (ingestion) and bathing (skin contact) are two different routes of exposure to contaminants that may be found in water.


Volatile organic compounds (VOCs):
Substances containing carbon and different proportions of other elements such as hydrogen, oxygen, fluorine, chlorine, bromine, sulfur, or nitrogen; these substances easily become vapors or gases. A significant number of the VOCs are commonly used as solvents (paint thinners, lacquer thinner, degreasers, and dry cleaning fluids).

APPENDIX E: TEF APPROACH

TCDD Toxic Equivalents (TEQs)

The more than two hundred possible dioxin and furan isomers belong to one of eight different homologue categories or series. The potency (or relative toxicity) of these isomers varies with structure, with the maximum potency belonging to isomers containing chlorine in the 2,3,7,8-lateral ring positions. Current evidence indicates that the most toxic dioxin is 2,3,7,8-tetrachlorodibenzodioxin (2,3,7,8-TCDD).

Dioxins and furans include compounds with various levels of chlorination from 0 to 8. Compounds with the same number of chlorine molecules are referred to as isomers. The arrangement of the chlorines on the basic molecule determines the specific congener. Isomers with four chlorine molecules include the most toxic forms, and congeners with chlorines in the 2,3,7, and 8 positions are the most toxic forms within each isomer group. The most toxic form is 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD), while the related furan is only slightly less toxic. Other dioxins and furans can range from slightly less toxic to 1,000 times less toxic. In dealing with mixtures of dioxins and furans, a system has been developed to weigh concentrations of congeners and isomers by factors that relate their toxicity to that of 2,3,7,8-TCDD, generating "TCDD equivalency factors" (EPA, 1989a). These factors are then used to assess the health risks of a dioxin/furan mixture.

Throughout this health consultation, concentrations of dioxin and related compounds have been presented as TCDD equivalents (or TEQs). The TEQ is a weighted concentration of total polychlorinated dibenzo-p-dioxins (PCDDs) in a mixture that compensates for the differences in toxicity among the 2,3,7,8-TCDD analogs. The equivalent factors used in this evaluation are as follows:

Compound

EPA/89 TEF

Tetrachlorodibenzodioxin (TCDD)
          2,3,7,8-TCDD
          other TCDDs


1
0

Pentachlorodibenzodioxin (PeCDD)
          1,2,3,7,8-PeCDD
          other PeCDDs


0.5
0

Hexachlorodibenzodioxin (HxCDD)
          2,3,7,8-HxCDD
          other HxCDD


0.1
0

Heptachlorodibenzodioxin (HpCDD)
          1,2,3,7,8-HpCDD


0.001

Octachlorodibenzodioxin (OCDD)

0.001
Compound EPA/89 TEF
Tetrachlorodibenzofuran (TCDF)
           2,3,7,8-TCDD
           other TCDFs

0.1
0

Pentachlorodibenzofuran (PeCDF)
           1,2,3,7,8-PeCDF
           2,3,4,7,8-PeCDF
           other PeCDF


0.05
0.5
0

Hexachlorodibenzofuran (HxCDF)
           2,3,7,8-HxCDF


0.1

Heptachlorodibenzofuran (HpCDF)
           2,3,7,8-HpCDF
           other HpCDF


0.01
0

Octachlorodibenzofuran

0.0001

Using this convention, the concentration of each isomer in a mixture (Ccongener) is multiplied by the appropriate factor (TEFcongener) (listed above) and the sum of all the weighted PCDDs in the mixture is represented by the TCDD Toxic Equivalent. The following equation is used to calculate the TEQs:

mathematical equation


Benzo(a)pyrene Toxic Equivalents

The benzo(a)pyrene toxic equivalent is a weighted concentration of carcinogenicity of polycyclic aromatic hydrocarbon (PAHs) in a mixture that compensates for the differences in toxicity among the different PAHs. A TEF has been assigned to 17 individual PAH compounds based on laboratory evidence of carcinogenicity and on their prevalence at hazardous waste sites. Although the TEF approach assumes that the carcinogenic activity of PAH mixtures depends primarily on the carcinogenic PAHs, noncarcinogenic PAHs are included because they may increase the potency of the carcinogenic PAHs (Nisbet and LaGoy, 1992).

The relative weight is 1 for benzo(a)pyrene is 1; 0.1 for benzo(a)anthracene, benzo(b)fluoranthene, benzo(k)fluoranthene, ideno(1,2,3-c,d)pyrene; 0.001 for anthracene, benzo(g,h,i)perylene, and chrysene; 0.0001 for acenaphthene, acenaphthylene, fluoranthene, fluorene, 2-methylnapthalene, phenanthrene, and pyrene. The benzo(a)pyrene toxic equivalent is calculated in the same manner as described above for the TCDD toxic equivalent. ATSDR used the benzo(a)pyrene equivalent to evaluate the likelihood for cancer effects to occur from contact with or incidental ingestion of soil and sediment.

Because the TEF approach, and therefore the benzo(a)pyrene equivalent, is relevant for cancer effects of PAHS only, ATSDR used the maximum PAHs values for samples collected on site to estimate exposure doses for noncancer effects. The PAH value is the sum of the concentrations of the 17 individual PAHs used to estimate the benzo(a)pyrene equivalent.


APPENDIX F: ESTIMATED EXPOSURE AND HEALTH EFFECTS

Estimates of Human Exposure Doses and Determination of Health Effects

Deriving Exposures Doses

ATSDR estimated the human exposure doses dermal contact with or incidental ingestion of on-site soil by workers and trespasser. Deriving exposure doses requires evaluating the concentrations of the contaminants to which people may have been exposed and how often and how long exposure to those contaminants occurred. Health effects are also related to individual characteristics such as age, gender, and nutritional status that influence how a chemical might be absorbed, metabolized, and eliminated by the body. Together, these factors help influence the individual's physiological response to chemical contaminant exposure and potential noncancer (noncarcinogenic) or cancer (carcinogenic) outcomes. In the absence of exposure specific information, ATSDR applied several conservative exposure assumption to define site-specific exposures as accurately as possible for residents near the BWP site.

Evaluating Potential Health Hazards

The estimated exposure doses are used to evaluate potential noncancer and cancer effects associated with chemicals of concern. When evaluating noncancer effects, ATSDR uses standard health guidelines, including ATSDR's Minimal Risk Levels (MRLs) and EPA's Reference Doses (RfDs), to determine whether adverse effects will occur. The chronic MRLs and RfDs are estimates of daily human exposure to a substance that are unlikely to result in adverse noncancer effects over a specified duration. ATSDR compares estimated exposure doses associated with BWP exposure scenarios to conservative health guidelines such as MRLs or RfDs for each contaminant. If the exposure dose is greater than the MRL or RfD, then a possibility for noncancer effects to occur exists.

To evaluate cancer effects, ATSDR uses Cancer Potency Factors (CPFs) that define the relationship between oral exposure doses and the increased likelihood of developing cancer over a lifetime. The CPFs are developed using data from animal or human studies and often require extrapolation from high exposure doses administered in animal studies to the lower exposure levels typical of human exposure to environmental contaminants. The CPF represents the upper-bound estimate of the probability of developing cancer at a defined level of exposure; therefore, they tend to be very conservative (i.e., overestimate the actual risk) in order to account for a number of uncertainties in the data used in the extrapolation.

ATSDR estimated the potential for cancer to occur using the following equation. The estimated exposure doses and CPF values for the contaminants of concern are incorporated into the equation:

Lifetime Cancer Risk = Estimated exposure dose (mg/kg/day) x CPF (mg/kg/day)-1

Although no risk of cancer is considered acceptable, it is impossible to achieve a zero cancer risk. Consequently, ATSDR often uses a range of 10-4 to 10-6 estimated lifetime cancer risk (or 1 new case in 10,000 to 1,000,000 exposed persons), based on conservative assumptions about exposure, to determine whether a concern regarding cancer effects is valid. This range is consistent with values adopted by EPA for evaluating the need for cleanup at hazardous waste sites. All the chemicals of concern detected at the BWP site are considered to be human carcinogens or probable human carcinogens. ATSDR was not able to evaluate cancer risk for exposure to chromium, however, because a CPF has not been established for this chemical.

When estimating exposure doses for carcinogenic effects of dioxins/furans and PAHs, ATSDR uses a Toxic Equivalency Factor Approach (TEF) (EPA, 1993) to account for the fact that toxicity values are not available for all the dioxins/furans or PAHs detected in soil or sediment at the site. TEF approach is described in Appendix E.

In addition to estimating the likelihood of noncancer and cancer effects, ATSDR reviewed the literature to evaluate possible health effects associated with exposure at the doses/concentrations estimated for the three pathways described above.

Evaluation of On-Site Soil and Sediment Past Exposure Pathways

Dermal Contact With Soil/Sediment

ATSDR used the following equation to estimate human exposure doses for dermal (skin) contact with soil and sediment at the BWP site:

Estimated Exposure Dose = Conc. x CF x SA x ABS x AF x EF x ED
                                   BW x AT

where:

Conc. = Maximum contaminant concentration in on-site soil (mg/kg)
CF = Conversion factor: 10-6 kg/mg
SA = Skin surface area available for contact (cm2/event):
  • Worker: 2,300 cm2 (hands, forearms) (EPA, 1989b)
  • Trespasser: 6,170 cm2 (hands, arms, legs, and feet) (EPA, 1989b)
ABS = Absorption Factor (unitless) for dermal exposure
AF = Skin to soil adherence factor = 0.6 mg/cm2-event (EPA, 1992)
EF = Exposure frequency, or number of exposure events per year of exposure:
worker = 5 days/week x 50 weeks/year; trespasser =2 days/week x 50 weeks
ED = Exposure duration, or the duration over which exposure occurs: work = 20 years; trespasser = 7 years
BW = Body weight (kg): worker = 70 kg; trespasser (age 7-14) = 50 kg
AT = Averaging time, or the time period over which cumulative exposures are averaged (ED x 365 days/year for noncancer effects; 70 years x 365 days/year for cancer effects)

Assumptions for Estimating Human Exposure Dose:

  • Assessing exposure to contaminants from dermal contact involves determining the amount of contaminant actually absorbed into the body rather than the amount that comes into contact with the outer skin. Therefore, exposures that occur through dermal contact were calculated as absorbed doses. A dermal absorption factor (ABS-dermal) was used to approximate how much of the contaminant contacting the body is actually absorbed. The ABS-dermal values for the chemicals of concern represent the percentage of the contaminant concentration contacted (see Table F-1).

  • The skin surface area (SA) available for contact per exposure event was assumed to be 10% of the 95th percentile values for the whole body of adults and a trespasser (hands, arms, legs, and feet) (EPA, 1992). Although estimates of exposed skin are fairly realistic, it is likely that less than the estimated area of exposed skin actually becomes covered with soil.

  • The amount of soil adherence to skin (the adherence factor [AF]) per exposure event was assumed to be 0.6 mg/cm2, the midpoint of the range recommended by EPA for dermal exposure to soil (EPA, 1992). Measurements of soil adherence for workers, however, reportedly approach only 0.2 mg/cm2 for hands and approximately 0.02 mg/cm2 for other exposed parts of the body (Kissel et al., 1995).

  • The exposure frequency (EF), or number of exposure events per year, was assumed to be 250 days per year for a worker, based on a 5 day a week exposure over 50 week per year, and 100 days per year for trespassers, based on a 2 day a week exposure over 50 weeks a year.

  • The duration of exposure (ED) was assumed to have occurred over 20 years for a worker and 7 years for a trespasser. These values most likely overestimate the actual duration of exposure.

  • The averaging time (AT) for noncancer effects was assumed to be 20 years or 7 years for 365 days/year, and 70 years for 365 days/years (or 25,550 days) for cancer effects.

  • No health guidelines for carcinogenic and noncarcinogenic effects are available for the dermal route of exposure. Therefore, the values available for the oral route of exposure were adjusted to account for exposure occurring through the skin rather than from ingestion.

Likelihood of Health Effects From Contact With On-Site Soil and Sediment

Worker Exposure

Noncancer Effects: If a worker were exposed to the maximum detected concentration of arsenic or dioxins/furans in on-site soil 5 days a week for 50 weeks over 20 years, exposure doses would exceed chronic MRLs/RfDs (see Table F-2). These estimates suggest that a worker contacting soil containing the maximum levels of arsenic or dioxins/furans over an extended period may experience adverse health effects. Estimated exposure doses for PAHs, chromium, and PCP are below health guidelines and, therefore, are not likely to pose noncancer health effects.

Cancer Effects:ATSDR estimated the increased likelihood of developing cancer to range between 3 and 9 new cases in 10,000 persons exposed to soil containing the highest concentrations of arsenic, PCP, or dioxins/furans (see Table F-3). The estimates suggest that if workers were exposed to the highest measured levels of arsenic, PCP, dioxins/furans for extended periods of time they would have a slight to moderate increased likelihood of developing cancer. Cancer risk estimates for exposure to PAHs in soil are within acceptable range used by ATSDR.

Trespasser Exposure

Noncancer Effects: If a trespasser (7 to 14 years) were exposed to the maximum detected concentration of arsenic or dioxins/furans a 2 days per week for 50 weeks over 7 years, exposure doses would exceed chronic health guidelines (see Table F-2). These estimates suggest that contact with the most contaminated on-site soil may result in adverse noncancer health effects. Estimated exposure doses for PAHs, chromium, and PCP were below health guidelines and, therefore, are not likely to result in noncancer health effects.

Cancer Effects: Arsenic, PCP, and dioxin/furan doses exceed levels of potential concern regarding cancer when exposures to maximum levels are assumed to be twice a week for 50 weeks during the year for 7 years (see Table F-3). The estimates suggest that trespassers exposed to the highest levels of these compounds have a slight to moderate increased likelihood of developing cancer. Cancer risk estimates for PAHs are within acceptable ranges used by ATSDR.

Many uncertainties exist regarding the extent that chemicals are absorbed by the human skin, especially when evaluating soil or sediment exposures (EPA, 1992). In this evaluation, ATSDR estimated absorbed doses based on very conservative assumptions about skin contact and absorption. Additionally, ATSDR used very conservative assumptions about frequency and duration of workers' or trespassers' contact with the most contaminated soil. In fact, most persons probably did not routinely contact the most contaminated soil over an extended period of time. Together, the assumptions used likely overestimate the exposure and potential health hazards for workers and trespassers. Therefore, actual worker or trespasser exposures most likely would no result in an increased likelihood of developing noncancer or cancer effects.

Incidental Ingestion of Contaminated On-Site Soil and Sediment

 

Estimated Exposure Dose = Conc. x IR x CF x EF x ED
                                                         BW x AT

where:

Conc. = Maximum contaminant concentration in site soil (mg/kg)
IR = Ingestion Rate (mg/day): 50 mg/day for adults; 100 mg/day for trespassers.
CF = Conversion factor (10-6 kg/mg)
EF = Exposure frequency, or number of exposure events per year of exposure:
worker = 5 days/week x 50 weeks/year; trespasser = 2 days/week x 50 weeks.
ED = Exposure duration, or the duration over which exposure occurs: work = 20 years; trespasser = 7 years
BW = Body weight (kg): worker = 70 kg; trespasser (age 7-14) = 50 kg
AT = Averaging time, or the time period over which cumulative exposures are averaged (ED x 365 days/year for noncancer effects; 70 years x 365 days/year for cancer effects)

Assumptions for Estimating Human Exposure Dose:

  • A soil ingestion rate of 50 mg/day was based on an assumption that soil on the hands is incidentally ingested while eating or smoking, and that soil adheres to the palms of the hands. A more typical value for ingestion over an entire day is probably less than 50 mg/day, assuming a worker spends only part of their day at BWP. The soil ingestion rate also assumes that the contaminant in soil is bioavailable as the pure chemical, whereas the actual bioavailablity may be substantially less.

  • The exposure frequency (EF), or number of exposure events per year, was assumed to be 250 days per year for a worker, based on a 5 day a week exposure over 50 week per year, and 100 days per year for trespassers, based on a 2 day a week exposure over 50 weeks a year.

  • The duration of exposure (ED) was assumed to have occurred over 20 years for a worker and 7 years for a trespasser. These estimate most likely overestimate the actual duration of exposure.

  • The averaging time (AT) for noncancer effects was assumed to be 20 or 7 years for 365 days/year and 70 years for 365 days/years (or 25,550 days) for cancer effects.

Likelihood of Health Effects From Incidental Ingestion of Soil and Sediment

Worker Exposure

Noncancer Effects: The estimated exposure dose for a worker who inadvertently ingests soil containing the maximum concentration of arsenic or dioxins/furans 5 days a week for 50 weeks over 20 years, exceeds the health guidelines. Therefore, workers incidentally ingesting the highest levels of arsenic and dioxins/furans over an extended period may develop adverse noncancer effects. Estimated doses associated with even the highest concentrations of PAHs, PCP, and chromium, however, are below ithin health guidelines, and therefore are not a health concern.

Cancer Effects: Arsenic and dioxin/furan doses exceed levels of potential concern regarding cancer (that the likelihood of developing cancer ranges from 6 to 20 new cases in 10,000 exposed individuals), when exposures to maximum levels are assumed to be 5 days a week for 50 weeks during the year for extended periods (e.g., 20 years). The estimates suggest that workers exposed to the highest levels have a slight to moderate increased likelihood of developing cancer. Cancer estimates for PAHs and PCP are within acceptable ranges used by ATSDR.

Trespasser Exposure

Noncancer Effects: If a trespasser (7 to 14 years) were exposed to the maximum concentration of arsenic or dioxins/furans 2 days per week for 50 weeks over 7 years, the exposure dose would exceed chronic MRLs. These estimates suggest that incidental ingestion of the highest levels of arsenic or dioxins/furans over an extended period may result in adverse noncancer health effects. Estimated doses associated with even the highest concentrations of PAHs, PCP, and chromium, however, are below health guidelines, and therefore are not a health concern.

Cancer Effects: Arsenic and dioxin/furan doses exceed levels of potential concern regarding cancer when exposures to maximum levels are assumed to be twice a week for 50 weeks during the year for an extended period. These estimates suggest the increased likelihood of developing cancer to range between 2 and 7 new cases per 10,000 exposed individuals. Therefore, trespassers inadvertently ingesting soil containing the highest concentrations of arsenic and dioxins/furans may have a slight increased chance of developing cancer. Cancer risk estimates for PAHs and PCP are within acceptable ranges used by ATSDR.

Very conservative assumptions were used to derive exposure doses and increased likelihood of developing cancer. Most workers and trespassers did not routinely ingest soil containing the highest concentrations. Rather, their infrequent contact, if any, would not be expected to result in exposures associated with adverse health effects.

Review of Toxicological Literature

ATSDR also reviewed the toxicological literature to further evaluate whether arsenic, PCP, or dioxins/furans at levels detected in on-site soil and sediment in the past may have been harmful to the on-site workers or trespassers.

Arsenic

Doses estimated for dermal contact and incidental ingestion of the maximum concentrations of arsenic exceed the chronic MRL/RfD, suggesting that long-term exposure could result in adverse health effects. In reviewing the toxicological data, ATSDR did not identify any human studies of adverse effects from dermal contact or incidental ingestion of contaminated soil at levels similar to those present in BWP. Results from available animal studies or human studies show that at very high concentrations, arsenic can irritate the skin, eye, throat, and gastrointestinal tract; decrease the number of red and white blood cells; damage blood vessels; and cause abnormal heart functions.

The most sensitive endpoints for chronic oral exposure to humans appear to be skin problems (e.g., hyperkeratosis, hyperpigmentation), neurological effects, and gastrointestinal irritations (e.g., vomiting, abdominal pain). The health guideline is based on a study in which the lowest observed levels at which adverse effects have been reported range from 0.014 mg/kg/day to 0.05 mg/kg/day for skin and gastrointestinal effects in human exposed to arsenic in drinking water for up to 45 years (ATSDR, 1993a). Although the study demonstrates an association between arsenic in drinking water and adverse health effects, it has a number of weaknesses and uncertainties, including exposure to other nonwater sources of arsenic, genetic susceptibility to arsenic, and poor nutritional status of the exposed population. Arsenic exposure may have been underestimated in the study, which may have led to an overestimation of the actual risk. The weakness and uncertainties identified in the study, along with the fact that it examines drinking water, not soil exposures, may limit the study's usefulness in assessing adverse noncancer effects for workers and trespassers exposed to contaminated soil.

Furthermore, dermal contact may not lead to significant exposures. In fact, studies indicate that the primary route of nonoccupational exposure is by ingestion of food and water and that dermal contact is not likely to contribute significantly to the overall uptake of arsenic.

Arsenic has been classified as a human carcinogen by EPA. (In contrast to most human carcinogens, arsenic does not cause cancer in laboratory animals when administered orally.) The cancer potency factor used to derive the excess cancer estimates is the same study used to derive the health guidelines for arsenic. In the study, the lowest levels associated with the onset of cancer (skin) were observed in people drinking water containing 170 to 800 parts per billion (ppb) arsenic for a 45-year exposure period (ATSDR, 1993a). The study demonstrates an association between arsenic in drinking water and skin cancer, however, the weaknesses and uncertainties identified in the study, may limit the study's usefulness in assessing cancer for workers and trespassers exposed to contaminated soil.

Dioxins and Furans

ATSDR estimated that exposures doses for contact with or incidental ingestion of on-site soil with the highest levels of dioxins/furans exceed health-based guidelines, suggesting that long-term exposure could result in adverse health outcomes. The most widely studied and most toxic dioxin, 2,3,7,8-TCDD, can be ingested via contaminated water or food products, or inhaled in contaminated air. Some evidence from experimental animal studies links 2,3,7,8-TCDD exposure with liver damage and digestive disorders (loss of appetite, weight loss). Human exposure can result in skin disorders, including chloracne. Only limited human and animal data are available for studying the effects of chloracne and, therefore, dose relationship information in humans is not available (ATSDR, 1989).

ATSDR did not identify any human studies of adverse effects from dermal contact or incidental ingestion of dioxin/furan-contaminated soil at levels similar to those present in BWP. Some studies suggest that 2,3,7,8-TCDD in soil is not as readily adsorbed as is 2,3,7,8-TCDD administered to animals in experimental studies.

The extent of dioxin's carcinogenicity is still being evaluated by the scientific community. Although sufficient human data are still not available, animal data suggest that dioxin (primarily 2,3,7,8-TCDD) may be a relatively strong cancer-causing agent. Most studies of their carcinogenic potential show that the liver appears to be the primary target. Other dioxin forms (isomers and congeners) can cause many of the same effects, but usually require much greater doses than associated with concentrations detected in BWP soil (ATSDR, 1989). The cancer potency factor of 156,000 mg/kg/day-1 was based on data from a study in which rats received oral doses of 2,3,7,8-TCDD in their diet. Although the study has relevance to human exposure from food, this study may not be relevant to worker and trespasser exposures occurring through contact with or ingestion of soil.

Pentachlorophenol (PCP)

Exposure doses associated with contacting soil containing the maximum soil concentrations exceeded the health based guidelines for workers and trespassers. The toxicological literature indicates that human exposure to PCP can cause irritation, systemic effects (e.g., effects on the liver, kidneys, blood, lungs, nervous system, and immune system), and, in some people, allergic responses. Some of the health effects shown to be associated with PCP (e.g., certain skin conditions) may be due to the impurities, such as dioxins/furans, present in commercial PCP (ATSDR, 1993b; ATSDR, 1994; IRIS, 1997).

Effect levels noted in these studies were typically much higher than the exposure doses estimated for BWP workers or trespassers. The lowest observed effect level of 10 mg/kg/day for liver and kidney effects was reported in experimental animals administered PCP in the diet (IRIS, 1997). This study was used as the basis for developing the chronic RfD. By contrast, the highest dose estimated for contact or incidental ingestion with BWP soil is 500 to approximately 5,000 times lower than the lowest literature-based value.

An increase likelihood of cancer was demonstrated in laboratory animals following oral administration of PCP. PCP was not shown to be a tumor promotor in experimental animal studies following dermal exposure, however. It also should be noted that several human studies have not established an association between much higher PCP exposure and cancer. Although PCP has been classified a probable human carcinogen, that conclusion is based on evidence from studies in which laboratory animals were administered high oral doses of PCP. Therefore, these findings may have limited relevance to workers and trespassers contacting PCP in soil at the BWP.

Based on this review, contaminants present in soil and sediment have been shown to produce toxic effects in experimental animal and some human studies, but at much higher doses (and via different exposure routes) than estimated by ATSDR for dermal contact or incidental ingestion of soil or sediment at the BWP site.

TABLE F-1. Absorption Factors for Dermal Exposure to Soil

Contaminant

ABS-dermal
(percent)
References ABS-oral
(percent)
References
Arsenic 3.2 a 95 b
Chromium 1 c not available
assumed 100
d
PAHs/
benzo(a)pyrene
equivalents
10 e 91 f
PCP 24.4 g 90 h
2,3,7,8-TCDD
equivalents
3 c 80 I

Key:

ABS-dermal= Absorption Factor for dermal exposure (percent contact)
ABS-oral= Absorption Factor for oral exposure (percent intake)

Sources:
a Wester et al., 1993a
b ATSDR, 1993c
c EPA, 1992
d MADEP, 1995
e Ryan et al., 1987
f ATSDR, 1995
g Wester et al., 1993b
h ATSDR, 1994
I ATSDR, 1989


TABLE F-2. Estimated Exposure Doses--Noncancer Effects
Dermal Contact with On-Site Soil

Contaminant

Maximum Contaminant
Concentration (mg/kg)

Estimated Exposure Dose (mg/kg/day) Adjusted
Health Guideline
Chronic Orala
(mg/kg/day)
Basis for Health
Guideline
Worker Trespasser
2,3,7,8-TCDD
equivalents
0.02741 1.0 x 10-8 2.0 x 10-8 8.0 x 10-10 MRL
PAH a 3,429 0.005 0.007 0.03 RfD for pyrene
Arsenic 8,800 0.004 0.006 0.00023 MRL/RFD
Chromium 4,700 0.0006 0.001 0.005 RfD
PCP 5,000 0.02 0.02 0.03 RfD

a Adjusted Health Guideline = Health Guideline x Oral Absorption Factor.

b Sum of the concentrations of the 17 individual PAHs in soil.

Key: mg/kg = milligrams per kilogram; mg/kg/day = milligrams contaminant per kilogram body weight per day; MRL = Minimal Risk Level; RfD = Reference Dose.


TABLE F-3. Estimated Exposure Doses--Cancer Effects
Dermal Contact With On-Site Soil

Contaminant

Maximum Contaminant
Concentration (mg/kg)

Estimated Exposure Dose-Cancer (mg/kg/day) Adjusted
Cancer Potency
Factora
(mg/kg/day)
Lifetime Excess Cancer Estimateb
Worker Trespasser Worker Trespasser
2,3,7,8-TCDD equivalents 0.02741 3 x 10-9 2.0 x 10-8 195,000 6 x 10-4 3 x 10-4
Benzo(a)pyrene equivalents 17.67 7 x 10-6 4 x 10-5 8 5 x 10-5 3 x 10-5
Arsenic 8,800 0.001 0.0006 1.6 6 x 10-4 9 x 10-4
Chromium 4,700 0.0002 0.0001 NA NA NA
PCP 5,000 0.005 0.002 0.13 6 x 10-4 3 x 10-4

a Adjusted CPF = CPF / Oral Absorption Factor

b Lifetime Cancer Risk = Estimated Exposure Dose(Cancer) x Cancer Potency Factor.

Key: mg/kg = milligrams per kilogram; mg/kg/day = milligrams contaminant per kilogram body weight per day.


TABLE F-4. Estimated Exposure Doses--Noncancer Effects
Incidental Ingestion of On-Site Soil

Contaminant

Maximum Contaminant
Concentration (mg/kg)

Estimated Exposure Dose (mg/kg/day) Health Guideline
Chronic Oral
(mg/kg/day)
Basis for Health
Guideline
Worker Trespasser
2,3,7,8-TCDD equivalents 0.02741 1.3 x 10-8 2.0 x 10-8 1.0 x 10-9 MRL
PAH a 3,429 0.002 0.002 0.03 RfD for pyrene
Arsenic 8,800 0.004 0.005 0.0003 MRL/RfD
Chromium 4,700 0.002 0.003 0.005 RfD
PCP 5,000 0.002 0.003 0.03 RfD

a Sum of the concentration of the 17 individual PAHs in soil.

Key: mg/kg = milligrams per kilogram; mg/kg/day = milligrams contaminant per kilogram body weight per day; MRL = Minimal Risk Level; RfD = Reference Dose.


TABLE F-5. Estimated Exposure Doses--Cancer Effects
Incidental Ingestion of On-Site Soil

Contaminant

Maximum Contaminant Concentration (mg/kg)

Estimated Exposure Dose-Cancer (mg/kg/day) Cancer Potency Factor (mg/kg/day) Lifetime Excess Cancer Estimatea
Worker Trespasser Worker Trespasser
2,3,7,8-TCDD equivalents 0.02741 4.0 x 10-9 2.0 x 10-9 156,000 6 x 10-4 2 x 10-4
Benzo(a)pyrene equivalents 17.67 3.0 x 10-6 1.0 x 10-6 7.3 2 x 10-5 7 x 10-6
Arsenic 8,800 0.001 0.0005 1.5 2 x 10-3 7 x 10-4
Chromium 4,700 0.0007 0.0003 NA NA NA
PCP 5,000 0.0007 0.0003 0.13 8 x 10-5 3 x 10-5

a Lifetime Cancer Risk = Estimated Exposure Dose (Cancer) x Cancer Potency Factor.

Key: mg/kg = milligrams per kilogram; mg/kg/day = milligrams contaminant per kilogram body weight per day.


APPENDIX G: ATSDR PUBLIC HEALTH HAZARD CONCLUSION CATEGORIES

No Public Health Hazard

Sites for which data indicate no current or past exposure or no potential for exposure and therefore no health hazard.

No Apparent Public Health Hazard

Sites where human exposure to contaminated media is occurring or has occurred in the past, but the exposure is below a level of health hazard.

Potential/Indeterminate Public Health Hazard

Sites for which no conclusions about public health hazard can be made because data are lacking.

Public Health Hazard

Sites that pose a public health hazard as the result of long-term exposures to hazardous substances.

Urgent Public Health Hazard

Sites that pose a serious risk to the public health as the result of short-term exposures to hazardous substances.


1. See Appendix E for an explanation of TEQs and benzo(a)pyrene equivalents.



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