PUBLIC HEALTH ASSESSMENT
BARRINGTON, STRAFFORD COUNTY, NEW HAMPSHIRE
The tables in this section list the contaminants of concern. Weevaluate these contaminants in the subsequent sections of thepublic health assessment and determine whether exposure to them haspublic health significance. ATSDR selects and discusses thesecontaminants based upon the following factors:
- Concentrations of contaminants on and off the site.
- Field data quality, laboratory data quality, and sample design.
- Comparison of on-site and off-site concentrations with health assessment comparison values for (1) noncarcinogenic endpoints and (2) carcinogenic endpoints.
- Community health concerns.
In the data tables that follow under the On-site Contaminationsubsection and the Off-site Contamination subsection, the listedcontaminant does not mean that it will cause adverse health effectsfrom exposures. Instead, the list indicates which contaminantswill be evaluated further in the public health assessment.
The data tables include the following acronyms:
- CREG = Cancer Risk Evaluation Guide
- EMEG = ATSDR Environmental Media Evaluation Guide
- MCLG = EPA Maximum Contaminant Level Goal
- MCL = EPA Maximum Contaminant Level
- PMCLG = EPA Proposed Maximum Contaminant Level Goal
- LTHA = EPA Lifetime Health Advisory
- ppm = parts per million
- ppb = parts per billion
- RfD = Reference Dose
Comparison values for public health assessments are contaminantconcentrations in specific media that are used to selectcontaminants for further evaluation. These values includeEnvironmental Media Evaluation Guides (EMEGs), Cancer RiskEvaluation Guides (CREGs), and other relevant guidelines. CREGsare estimated contaminant concentrations based on a one excesscancer in a million persons exposed over a lifetime. CREGs arecalculated from EPA's cancer slope factors. EPA's maximumContaminant Level Goal (MCLG) is a drinking water health goal. EPAbelieves that the MCLG represents a level that no known oranticipated adverse effect on the health of persons should occurwhich allows an adequate margin of safety. Proposed MaximumContaminant Level Goals (PMCLGs) are MCLGs that are being proposed. Maximum Contaminant Levels (MCLs) represent contaminantconcentrations that EPA deems protective of public health(considering the availability and economics of water treatmenttechnology) over a lifetime (70 years) at an exposure rate of 2liters water per day. While MCLs are regulatory concentrations,PMCLGs and MCLGs are not. EPA's Reference Dose (RfD) and ReferenceConcentration (RfC) are estimates of the daily exposure to acontaminant that is unlikely to cause adverse health effects.
To identify possible facilities that could contribute to the (i.e.,air, surface water, etc.) contamination near the Tibbetts Roadsite, ATSDR searched the 1987, 1988, 1989, and 1990 Toxic ChemicalRelease Inventory (TRI). TRI is developed by the U.S.Environmental Protection Agency (EPA) from the chemical release(air, water, and soil) information provided by certain industries. TRI did not contain information on toxic chemical release in thetown of Barrington, New Hampshire, or in the site's zip code.
Between 1982 and 1991, various samples of on-site environmentalmedia were collected and analyzed. The collection and analyses ofthese samples were initiated by NH DPHS, EPA, and NHWSPCC.
For the purposes of this public health assessment on-site isconsidered the fenced portion of the residential property alongTibbetts Road.
Pre-Removal Soil Contamination
Sampling of soils before the soil removal operation indicated thepresence of VOC's, semi-volatile organic compounds (SVOC), PCB's,metals, and dioxin and furan isomers. The most highly contaminatedsoils were located within the three areas of the former drum storage:Areas A, B, and C (Figures 1 and 2). This suggests that liquid wastesfrom the drums may have been discharged onto the soils (4). Between1984 and 1985, about 48 soil samples were collected. The depth ofthese samples ranged from 0-6 inches up to about 3 feet. The sampleswere analyzed for either, VOC's, SVOC's, PCB's, selected heavy metals(i.e., lead, cadmium, and total chromium), or dioxin/furan isomers(congeners). The maximum contaminant concentrations for on-site pre-removal soils are presented in Table 1.
Maximum - ppm
a- Soil samples obtained from depths ranging from 0-6 inches to 3 feet. ATSDR considers only the top three inches of soil to be surface.
b- EMEG and Rfd comparison values reported for pica children.
c- Next highest concentration detected was 6.4 ppm.
d- Dioxin equivalent concentration calculated using EPA's 1989 ToxicEquivalency Factors (TCF) (9). The calculation is based on ahypothetical scenario where all of the highest results were foundtogether in one location. Furthermore, the scenario assumes that withineach of the isomer groups, only the most toxic isomer is present; anassumption which is very unlikely.
NA- Not available.
ND- Not detected.
Post-Removal Soil Contamination
In 1990 and 1991, 23 soil samples were collected. The depth of thesesamples ranged from 0-6 inches up to 2 feet (1). The samples wereanalyzed for VOC's, SVOC's, PCB's/pesticides, and heavy metals. Themaximum contaminant concentrations for on-site post-removal soils arepresented in Table 2. The soil data from Table 2 indicates that thesoil removal operation has appreciably reduced contaminantconcentrations--most below applicable comparison values.
Maximum - ppm
a- Soil samples obtained from a depth ranging from 0-6 inches to 2 feet. ATSDR considers only the top three inches of soil to be surface.
b- EMEG and Rfd comparison values reported for pica children.
c- PCB detected was Arochlor 1260. Arochlor 1260 was detected in onlytwo samples--the other sample contained 0.550J ppm and was a duplicate.
NA- Not available.
J- Quantitation is approximate due to limitations identified during thequality control review.
NS- Not sampled.
ND- Not detected.
Groundwater - Monitoring Wells
Between 1984 and 1991, the on-site overburden aquifer (shallowgroundwater) and bedrock aquifer (deep groundwater) were sampled on sixdifferent occasions. The current on-site monitoring network includeseight overburden and three bedrock aquifer wells. Samples from thesewells were analyzed for either VOC's, SVOC's, PCB's/pesticides, or heavymetals. The maximum contaminant concentrations detected in samples ofon-site groundwater are shown in Table 3. As shown in Table 3, elevated levels of various metals were detected in samples of on-sitegroundwater. It is difficult to determine if all of these metals are aresult of the activities and disposal practices at the site becausethere were no analyses of groundwater samples from a backgroundmonitoring well as a comparison. No background wells exist because thesite is on a drainage divide and no upgradient well are available thatEPA believes would be representative of natural groundwater conditions.
|a- Metals are reported as unfiltered/filtered.|
b- Rfd comparison values are reported for children.
c- Metal concentration for filtered and unfiltered samples are above referenced background levels (10,11).
d- Rfd for chromium +6/chromium +3.
B- Contaminant also detected in a blank sample.
J- Quantitation is approximate due to limitation identified during the quality control review.
|R- Not reported.|
ND- Not detected.
In 1984, the NHWSPCC collected three on-site samples of surface water(standing water) from the former drum disposal Area B. These sampleswere analyzed for VOC's (4). In addition, in 1990, EPA collected onesample of ponded water on-site as a screening sample. This sample wasanalyzed for VOC's, SVOC's, and PCB's/pesticides (1). The maximumcontaminant concentrations detected in these samples are presented inTable 4.
ND- Not detected.
NA- Not available.
No quantitative on-site air sampling has been performed. During fieldactivities for the RI, qualitative air screening was performed usingseveral instruments that detect the presence of certain contaminantsonly. In addition, qualitative screening of air samples was performedduring the drum and soil removal operations (4). The quality of on-siteair before the drum and soil removal and when the former owner wasengaging in activities at his residence (e.g., burning interiors ofcars) is impossible to determine without quantitative ambient airsampling results. However, based on the description of past on-siteconditions and activities, it is likely that ambient air, at least on alocalized level, was appreciably contaminated.
Between 1982 and 1991, various samples of off-site environmental mediawere collected and analyzed. The collection and analyses of thesesamples were initiated by NH DPHS, EPA, and NHWSPCC.
For the purposes of this public health assessment off-site is consideredareas outside the fenced portion of the residential property alongTibbetts Road.
In 1985, EPA obtained seven samples of off-site soil ranging in depthfrom 0-6 inches to three feet. The samples were analyzed for either,VOC's, SVOC's, or PCB's (1). None of these analyzed contaminants weredetected above applicable comparison values. In addition, in 1985, EPAobtained an additional eleven off-site soil samples and analyzed themfor dioxin and furan isomers (1). Using a similar scenario, aspresented in the notes to Table 1, the dioxin equivalent concentrationfor off-site soil samples was calculated and determined to be equal to0.0000084 ppm.
Ground Water - Monitoring and Residential Monitoring Wells
Between 1984 and 1991, off-site overburden and bedrock aquifer weresampled on six different occasions. The current off-site monitoring network includes 18 overburden and 11 bedrock aquifer monitoring wells. In addition, 11 of the residential wells that were capped in 1987 wererestored for use as monitoring wells to supplement the 11 bedrockmonitoring wells that have been installed (1). Samples from these wellswere analyzed for either VOC's, SVOC's, PCB's/pesticides, or heavymetals. In addition, one water sample, obtained in 1985, from an on-site monitoring well was analyzed for dioxin/furan isomers--no isomerswere detected (4). The maximum contaminant concentrations detected insamples of off-site groundwater are shown in Table 5. As shown in Table 5, elevated levels of various metals were detected in samples of off-site groundwater. It is difficult to determine if all of these metalsare a result of the activities and disposal practices at the sitebecause there were no analyses of groundwater samples from a backgroundmonitoring well as a comparison. No background wells exist because thesite is on a drainage divide and no upgradient well are available thatEPA believes would be representative of natural groundwater conditions.
|a- Metals are reported as unfiltered/filtered.|
b- Rfd comparison values are reported for children.c- Metal concentration for filtered and unfiltered samples are above referenced background levels (10,11).
d- Rfd for chromium +6/chromium +3
B- Contaminant also detected in a blank sample.
J- Quantitation is approximate due to limitation identified during the quality control review.
|NR- Not reported.|
ND- Not detected.
Ground Water - Residential Wells
Between 1982 and 1987, water samples from about 14 residential wellswere obtained and analyzed for VOC's. In addition, one water sampleobtained from an off-site residential well was analyzed for dioxin/furanisomers--no isomers were detected (4). The former site owner'sresidential well was sampled in 1982. The water sample was analyzed forVOC's--no VOC's were detected. During the RI (EPA) and subsequently (NHDES), water from the Len-Kay Campground bedrock well has been sampledand analyzed for VOC's. Except for the most recent samples obtainedsince May 1992, all samples did not show the presence of VOC's. Watersamples obtained in May, June, and October, 1992 showed the presence oftrichloroethene at concentrations of 17, 14, and 9.4 ppb, respectively(12). Other contaminants detected in the Len-Kay Campground well (1,2-DCE, 2.8 ppb; benzene, 0.81 ppb) were not above health comparisonvalues. In addition to the Len-Kay Campground well, water samples fromanother private (residential) well in the area of the site indicatedelevated concentrations of acetone, propylene glycol, iron, andmanganese. The maximum concentrations of acetone and propylene glycolwere 55,000 and 640,000 ppb, respectively. The most recent sample ofwater from this well did not indicate the presence of propylene glycolabove detection limits; however, acetone was detected at 52,100 ppb. Iron and manganese were detected in the May 13, 1992 water sample at aconcentration of 18.5 ppm and 23.4 ppm, respectively. The November 16,1992 sample of water from this private well was not analyzed for ironand manganese. Currently available information indicates that thepresence of propylene glycol is probably related to a plumbing accident. Propylene glycol is a common constituent of plumbing antifreezes (12). Although residential and monitoring well data indicate that the acetoneand manganese contamination, or at least a part of it, is probably notrelated to the Tibbetts Road site, this cannot be definitivelyestablished at this time.
Only benzene and trichloroethene were detected in samples of residentialwell water at concentrations above applicable comparison values. However, other VOC's, below comparison values, were detected in severalother water samples from residential wells. The highest concentrationsand number of detections of these other contaminants were from Well 1R. The predominant contaminants from the other residential wells weretrichloroethene and benzene. The maximum and range of thesecontaminants detected in residential well water samples before and afterbottled water was provided (1985), respectively, are shown in Table 6.
b- Range of detected contaminant concentrations after bottled water was provided in 1985.
c- Contaminant concentration detected during first sampling of well.
d- Contaminant concentration represents only time detected.
e- Contaminant concentration represents only time detected after bottled water provided.
J- Quantitation approximate due to limitations identified during quality control review; also reported as "less than" as detection limit of 5.0J.
ND- Not detected.
NA- Not available.
In 1984, the NHWSPCC collected two off-site samples of surface water--one from standing water near the lawn of an adjacent residence and onefrom Swain's Lake. These samples were analyzed for VOC's. No VOC'swere detected in these samples (4). Between 1990 and 1991, EPAcollected surface water samples from an intermittent unnamed brook (2samples) southwest of the site, northwest wetlands (1 sample), BellamyRiver (1 sample), and Swain's Lake (3 samples). These samples wereanalyzed for either VOC's and/or SVOC's (1). The only contaminantdetected above a drinking water comparison value was trichloroethene at9 ppb (estimated value). The only contaminants (VOC's) detected were insamples from the intermittent unnamed brook.
In 1991, EPA collected sediment samples from the Bellamy River (1sample), the northwest wetlands (1 sample), the intermittent unnamedbrook (1 sample), and the Swain's Lake (3 samples). These samples wereanalyzed for VOC's, SVOC's, PCB's/pesticides, and metals (1). Nocontaminants were detected above applicable comparison values and/orbackground soil levels.
No quantitative off-site air sampling has been performed. During fieldactivities for the RI, qualitative air screening was performed usingseveral instruments that detect the presence of certain contaminantsonly (1).
Most of the Quality Assurance/Quality Control (QA/QC) data were notavailable for review for this public health assessment. However, it isbelieved that most of the data presented here were produced by qualifiedlaboratories contracted by NHDPHS, NHWSPCC, or EPA. Furthermore, all ofthe samples collected or analyzed by the contractors of NH DES, NHWSPCC, or EPA have passed strict QA/QC requirements. All dataqualifiers, as reported in the documents reviewed for this public healthassessment, were reported in the tables presented in the Environmental Contamination and Other Hazards Section above.
Based on observations obtained during the site visit, the houseremaining on-site is considered a physical hazard to anyone who wouldtrespass on-site. Because of the fire, that partially destroyed thehouse, the structure that remains is in a dilapidated condition. However, based on information obtained from the EPA RPM, we have noreason to believe that trespassing within the fenced area is occurring. In addition, we believe that the neighbors near the site are keenlyaware of the site and would report any trespassing within or near thefenced area.
To determine whether nearby residents are exposed to on-sitecontaminants or to those migrating from the site, ATSDR evaluates theenvironmental and human exposure components that lead to human exposure. This pathways analysis consists of five elements: A source ofcontamination, transport through an environmental medium, a point ofexposure, a route of exposure, and an exposure population. The firstthree elements represent an environmental pathway--the last two elementsrepresent a human exposure pathway.
ATSDR categorizes an exposure pathway as a completed or potentialexposure pathway if the exposure pathway cannot be eliminated. Completed pathways exist when the five elements of a pathway link thecontaminant source to a receptor population. Completed pathwaysindicate that exposure to a contaminant probably have occurred in thepast, probably are occurring, or probably would occur in the future. Potential pathways, however, exist when information and data on one ormore elements in a pathway are missing. Potential pathways indicatethat exposure to a contaminant could have occurred in the past, could beoccurring now, or could occur in the future. An exposure pathway can beeliminated if at least one of the five elements is missing and willnever be present. Table 7 identifies the completed exposure pathways,and Table 8 identifies the potential exposure pathways. The discussionthat follows these two tables incorporates only those pathways that areimportant and relevant to the site.
|PATHWAY NAME||EXPOSURE PATHWAY ELEMENTS||TIME|
|On-site Soils and|
|Former On-Site Residents andother children playing on-site/|
|Private Wells||TRS||Groundwater||Off-Site Residentialand Len-Kay Well(tap)||Ingestion|
|Private Residential and Len-KayWells Near Site/30 (residentialonly)||Past|
|EXPOSURE PATHWAY ELEMENTS||TIME|
|On-site ambient air|
On-site waste materials
|Former On-Site Residents and otherchildren who played on-site/|
8-10 (same persons as completedpathway)
|Persons who reside on property inthe future/|
Past Residential Setting Pathway
Because of past recreational activities (children playing) andnormal activities at the former on-site residence, it is probablethat exposure to soils and surface water on-site occurred. Thehighest amount of exposure probably occurred to contaminants nearthe former drum disposal areas and in areas near where the interiorof automobiles were burned. Please refer to Table 7 for theelements of this completed pathway.
Contamination of on-site soils and surface waters occurredprimarily because of the disposal practices and other activitiesconducted by the owner of the residence along Tibbetts Road (thesite). Leaking drums and alleged dumping of waste materials ontothe on-site soils were probably the main mechanism for thecontamination of the on-site environmental media.
For children who played on-site, soil ingestion and skin contact(dermal) exposure were two probable routes of exposure. Soilingestion is an important route of exposure, particularly forchildren less than 6 years old (13). Soil ingestion is greater foryoung children because of their greater hand/mouth activity. However, because the ages of children who played on-site are notknown, it is difficult to determine the amount of soil they mayhave incidentally ingested. Furthermore, given the climaticconditions of New Hampshire, it is likely that cold weather andsnow precluded recreational activities and contact withcontaminated media during the cold months. ATSDR has thereforeestimated that exposure to residential soils on site probablyoccurred for six months in the year. Persons, especially children,could have been exposed to contaminants at the site from around1950 until around 1985 when the soil removal operation began. Itis believed, based on accounts from two neighbors, that only oneother family's children frequently played on-site. Therefore, webelieve that the most appreciable exposure, through the abovepathways, most likely occurred primarily to the children whoformerly lived at the site and secondarily to the children of oneother family who played on-site. Given the present conditions atthe site, it is highly improbable that appreciable incidentalexposure to children is currently occurring. Adults who formerlyresided at the site, especially the former owner, were alsoprobably exposed to site contaminants. Therefore, about 8-10persons were probably exposed through this pathway.
As shown in Table 1, on-site soils were contaminated with elevatedlevels of VOC's, SVOC's, PCB's, dioxin and furan isomers, and heavymetals. Even though some of the maximum contaminant concentrationsreported in Table 1 were found in soils at depths not usuallyaccessible for exposure, it is likely that children were exposed tothese contaminant levels, or higher, when the waste materials wereintroduced into the soil media. Therefore, we are assuming thatexposure to these contaminant levels found in subsurface soils onceoccurred. On-site ponded or standing water contained elevatedlevels of VOC's. The most appreciable contaminant concentrationshave been remediated by EPA. However, the contaminantconcentrations shown in Tables 2 and 4 possibly remain on-site.
Private Well Pathways
Past exposure pathways are probable from contamination of waterthrough the use of about eleven residential wells. Please refer toTable 7.
Based on the results of groundwater monitoring in the overburdenand bedrock aquifers, on-site and off-site groundwater iscontaminated with VOC's, SVOC's, and heavy metals (see Tables 3 and 5). The source of these contaminants is the past disposal andother activities at the Tibbetts Road site. On-site contaminatedgroundwater plumes have migrated predominantly towards the west andnortheast in the overburden aquifer. However, based on theoverburden groundwater hydrology, some limited radial migration(all directions) of contaminants away from the site has occurred. The radial migration is because the site is higher topographicallythen the surrounding areas. The overburden aquifer appears todischarge contaminants to the bedrock aquifer primarily to thenortheast. This is evidenced by a distinct contaminant plume tothe northeast (1). Contaminant migration from the overburdenaquifer to the bedrock aquifer has been retarded due to thepresence of an impermeable till layer between the aquifers. Contaminant migration in bedrock fractures is also probablyoccurring. Groundwater monitoring generated for the RI indicatethat the groundwater contaminant plumes appear to be relativelystable; that is, it is not spreading rapidly and is static orslowly decreasing in concentration (1).
Of the twelve residential wells exhibiting contamination, elevenwells, at least for one sample, contained contaminantconcentrations that were above their respective comparison valuesfor either trichloroethene or benzene (Table 6). Given the levels of contamination in Well 1R, detected in the first sampling of thewell in 1982, the proximity of the Well 1R to the site, and thefact that Well 1R appears to communicate with the overburdenaquifer, it is highly likely that the highest exposure to site-contaminants occurred through the use of this well. Given theworst case scenario, persons who used Well 1R were probably exposedfrom the 1970's, when the house was built, until 1985, when bottledwater was provided. Furthermore, it is difficult to determine thecomplete range of contaminants (i.e., SVOC's and heavy metals) inwhich persons using residential wells were exposed to becauseresidential well water samples were only analyzed for VOC's.
Before bottled water was provided in 1985, we estimate that about30 persons were exposed through ingestion, inhalation, and skincontact. Since these contaminants evaporate into the air fromwater during showers or baths, persons become exposed to thesecontaminants as they breathe the indoor air in their house. Inaddition, these contaminants will absorb across the skin duringshowers and baths thus increasing exposure (15). Therefore,persons were exposed via the non-ingestion routes (i.e., inhalationand skin contact) during the period between when bottled water wasprovided (1985) and when the municipal water line was completed(1987). Exposures through these non-ingestion routes have beenestimated to be comparable to those from direct ingestion of water(15).
Past exposures are probable to those who consumed water from theLen-Kay Campground well. As previously indicated, sampling ofwater from this well contained trichloroethene at concentrationsabove the drinking water health comparison value. In addition, oneresidential well (bedrock well), located about one-half mile fromthe site, was shown to be contaminated with acetone (may be partlysite-related), manganese (may not be site-related), and propyleneglycol (probably not site-related). Current site data andinformation, however, cannot definitively establish if the acetoneand manganese contamination is related to the site. Although thecontaminant plumes appear to be well defined in the overburdenaquifer and all residences within a quarter-mile of the site areconnected to the Swain's Lake Water Supply System, continuedsampling of water from residential (especially those with bedrockwells) and monitoring wells is needed to ensure that any possiblefuture exposures are ceased or reduced.
Past Residential Setting
Because of past recreational activities (children playing) andnormal activities at the former on-site residence, it is possiblethat children and adults breathed volatilized contaminants andcontaminated soil dusts in outdoor ambient air. Furthermore,children possibly ingested or came into contact with (skin contact)waste materials contained in drums or spilled onto the ground. Thehighest amount of exposure possibly occurred near the former drumdisposal areas and near the areas where the interior of automobileswere burned. In addition, indoor dusts could have beencontaminated because of the tracking of contaminants from theoutdoors into the house. Please refer to Table 8 for the elements of this potential pathway.
No outdoor ambient air data for volatilized contaminants and soildusts, and for indoor soil dusts are available to characterize theconcentrations that children and adults were possibly exposed to. Since this pathway relates, in part, to localized ambient aircontamination in the past, partially caused by on-site activities(e.g., burning interiors of automobiles), these data will never beavailable. Given the former conditions of the site and activitiesthat occurred there, it is possible that exposure through thispathway could have been significant. We estimate that 8-10 personswere possibly exposed through this pathway.
Future Residential Setting
If the site is used in the future for a residential setting, thenexposure to soil contaminants remaining on-site is possible. Please refer to Table 8. The primary activity that would result inthis exposure would be recreational activities (children playing). As indicated above, for children who might play on-site, soilingestion is an important route of exposure, particularly forchildren less than 6 years old. Soil ingestion is greater foryoung children because of their greater hand/mouth activity. Thecontaminants that remain in on-site soils of potential concern arelead, cadmium, and PCB's (Table 2).
This section will discuss the health effects in persons exposed tospecific contaminants (for completed pathways), discuss healthoutcome data and address specific community health concerns. Toevaluate health effects, ATSDR has developed a Minimal Risk Level(MRL) for certain contaminants commonly found at hazardous wastesites. The MRL is an estimate of daily human exposure to acontaminant below which non-cancer, adverse health effects areunlikely to occur. MRLs are developed for each route of exposure,such as ingestion and inhalation, and for the length of exposure,such as acute (less than 14 days), intermediate (15 to 364 days),and chronic (equal to or greater than 365 days). ATSDR presentsthese MRLs in Toxicological Profiles. These chemical-specificprofiles provide information on health effects, environmentaltransport, human exposure, and regulatory status. The followingdiscussion is based on the ATSDR Toxicological Profiles foracetone, benzene, bis(2-ethylhexyl) phthalate, cadmium, 1,2-dichloroethenes, dioxin equivalent, ethylbenzene, lead, manganese,methyl isobutyl ketone, polychlorinated biphenyls (PCBs),tetrachloroethene, toluene, trichloroethene, and 1,2,4-trichlorobenzene.
Since ATSDR has no methodology to determine the amount ofabsorption of chemicals through the skin, ATSDR does not have MRLsfor skin exposure. For this reason, it is difficult to determinethe health effects from skin exposure.
ATSDR has determined that past residents of the on-site buildingand children who played on the site were exposed to severalcontaminants. Those contaminants are listed in Table 10. Eachcontaminant will be listed by route of exposure. To estimate theexposure dose, it was assumed that adults, non-pica children andchildren with pica behavior would ingest 50, 100 and 5000milligrams (mg) of soil per day, respectively. Given the weatherconditions in New Hampshire, exposure was estimated for 6 monthsout of a year. For ingestion of surface water, the typicaldrinking water ingestion rate of 1 liter per day for a child wasadjusted to a more realistic level of 1 ml (0.001 L). Thisincidental ingestion rate is estimated for children who played inseasonal standing water that occurred mostly in spring.
Children who played on the site were exposed to acetone throughingestion and skin contact with surface water (Table 9). Inaddition, residents who used a private well located one-half mileaway from the site were also exposed to acetone in well water(Table 10). Although the ATSDR does not have a chronic MRL foracetone, using the highest concentration of acetone detected insurface water (1 ppm), the ingestion exposure for children does notexceed the intermediate MRL or EPA's oral RfD (Table 9). Adversehealth effects are unlikely to occur in children who ingested thislevel of acetone in surface water. Since ATSDR has no methodologyto determine the amount of absorption of chemicals through theskin, ATSDR does not have MRLs for skin exposure. In medicine,acetone is used topically as a cleansing agent prior to injectionor vaccination. Therefore, It is unlikely that the children whowere exposed to such dilute acetone on the site experienced thedryness or inflammation of the skin associated with prolongedtopical application of pure acetone.
However, the ingestion exposure in adults and children who used theresidential well located one-half mile from the site exceeds theRfD or the intermediate MRL (Table 10). The estimated dose forinfants and younger children (less than seven years old) is some 55or 28 times higher than the RfD or the intermediate MRL,respectively. The estimated ingestion doses for older children andadults are also about 18 or 9 times higher than the RfD or theIntermediate MRL, respectively. Both the RfD and the intermediateMRL were derived based on 13-week laboratory animal studies forliver and kidney problems, and for macrocytic anemia, respectively. It is possible that adults, children and infants who drank theacetone-contaminated well water from this one residential welllocated one-half from the site might experience liver and kidneyproblems as well as macrocytic anemia. However, acetone found inthe well water may be partly related to the site since the amountof acetone at the site is substantially lower than that detected inthe residential well water located one-half mile away from thesite.
Potential ingestion exposure to acetone in groundwater both on andoff site exceeds EPA's RfD for acetone. This could pose asignificant potential health threat if the chemical migrates intoany currently active drinking water well or any well that might beconstructed in the area in the future.
Exposure to benzene occurred in residents who lived on site and children who played on the site, as well as some residents wholived near the site through several completed exposure pathways(Tables 9 and 10). In addition, workers at a certain business andcampers who use the Len-Kay Campground well water were also exposedto benzene (Table 11). Before the removal of surface soil in 1986,past exposure to benzene occurred in adults and children throughsoil ingestion on site (Table 9). Although the ATSDR does not haveMRLs for benzene, the estimated doses for benzene are on theaverage 1,000,000 times lower than doses that caused white bloodcell problems in animals (17). While this toxicological evaluationis based on data from a mixture of surface and subsurface soils, itis possible to speculate that the benzene values are representativeof levels in surface soil while the site was active, and beforeremediation in 1986. The benzene exposure in children throughingestion of surface water while playing on the site is 100,000times lower than doses that caused white blood cell problems inlaboratory animals after chronic/long-term exposure (17). It isunlikely that adults and children would suffer any non-carcinogenicadverse health effects from their exposures (Table 9). Inaddition, subsequent analysis of on-site soil (Table 2) and on-site surface water (Table 4) after remediation in 1986 did not detect any benzene contamination.
Exposure to benzene occurred in residents off site throughingestion, skin contact and inhalation from the use of benzenecontaminated water from private wells located near the site (Table10). Although ATSDR does not have MRLs for benzene exposure, thelevels of benzene in most of the private wells (2R, 4R, 15R and47S), before bottled water was provided in 1985, or municipal watersupply was introduced in 1987, did not exceed ATSDR's CREG of0.0012 mg/L (Table 6) or EPA's MCL in drinking water of 0.005 mg/L. It is unlikely that residents who drank, showered, or bathed withbenzene contaminated well water between the 1970s and 1987 willsuffer any non carcinogenic health effects. During this period,the estimated ingestion dose for benzene from the most contaminatedwell is about 10,000 times lower than doses that caused white bloodcell problems in laboratory animals after chronic/long-termexposure (17).
The estimated ingestion exposure in workers at a certain businessand campers who use the Len-Kay Campground well water was some1,000,000 times lower than the doses that caused white blood cellproblems in laboratory animals after 103 weeks of chronic/long-termexposure (17). Adverse health effects are unlikely to occur because of the low levels and short duration of exposure.
The United States Department of Health and Human Services (DHHS),EPA, and the International Agency for Research on Cancer (IARC)consider benzene as a human carcinogen, based on human and animalstudies. Based on this information, persons who were exposed tobenzene in the most contaminated residential well near the site mayhave a slightly low increased risk of developing additional cancerover a lifetime. However, children who were exposed to benzene insurface water on the site, and persons exposed to benzene in Len-Kay Campground well may have no increased risk of developing cancerover a lifetime from their exposure.
Potential exposure to benzene from groundwater both on and off site(Tables 3 and 5) could pose a health problem if this amount ofbenzene migrated into a current or future drinking water well. However, benzene, toluene and xylene (BTX) mixtures biodegrade ingroundwater under high dissolved oxygen, as well as in certainanaerobic environments. The level of benzene present ingroundwater will therefore decrease as BTX is degraded over time.
Residents who lived on the site and children who played on the sitewere exposed to DEHP through ingestion of soil (Table 9). Althoughour evaluation is based on data for mixtures of surface-subsoilsamples, it is likely that adults and children who lived on thesite, and other children who came to play there, were exposed toDEHP between 1950 and 1986. However, estimated exposure dose foradults, and normal as well pica children did not exceed EPA's oralRfD for DEHP ingestion. In addition, the estimated dose of DEHPfor pica and normal children are about 10,000 and 1,000,000 times,respectively, lower than doses that caused systemic effects inanimals (18). It is therefore unlikely that adults and childrenwill suffer any non-carcinogenic health effects from theirexposures. Although the EPA has classified DEHP as probable humancarcinogen, it is unlikely that adults or children will developadditional cancer because of these low levels of exposure to DEHP. The level of DEHP detected in soil after remediation in 1986 isinsignificant (Table 2), and none has been detected in monitoringwells on or off site (Tables 3 and 5). Current or future exposureto DEHP is therefore unlikely.
Exposure to cadmium through ingestion of soil occurred in residentson site (Table 9). Cadmium exposure occurred in residents from1950 until the time they moved out of the house. In addition,children who played on the site between 1950 and 1986 were probablyexposed to higher levels of soil cadmium (Table 1) than childrenwho may have occasionally jumped the fence to play on the siteafter remediation in 1985 (Table 2). Although our evaluation isbased on data from surface-subsoil samples, the ingestion exposurein adults and children did not exceed ATSDR's chronic MRL or EPA'soral RfD for cadmium (Table 9). Adverse health effects areunlikely to occur from these past exposures. In addition, there isno evidence to suggest that humans or animals orally exposed tocadmium had increased incidence of cancer (19). Potential exposureto cadmium remaining in soil on site is unlikely to pose any healthproblems due to the low levels detected after remediation in 1986(Table 2).
Exposure to tetrachlorodibenzo-dioxins probably occurred in theformer residents and children who played on the site throughingestion from dioxin contaminated soil. The ingestion exposure todioxin in children exceeded ATSDR's MRLs or EPA's oral RfD(Table 9) or FDA's risk specific dose of 0.000000000057 mg/kg/day. However, the estimated doses for normal and pica children were100,000 - 1,000,000 times lower than the minimum toxic dose of0.0001 mg/kg/day that produced chloracne in nonhuman primates (20). Although the present evaluation is based on dioxin equivalent insurface-subsoil samples, it is highly unlikely that children whoplayed on the site will suffer any adverse health effects fromtheir exposures. As stated in the pathways analyses section, it isprobable that residents including children who lived on the sitewere also exposed to dioxin from ambient air. However, becausedata for ambient air are unavailable, the public healthsignificance of past exposures cannot be determined.
Although DHHS, EPA, and IARC have classified dioxin as a probablehuman carcinogen, the excess/additional cancer risk associated withthese exposures is insignificant.
Since dioxins in soil are generally bound to the organic enrichedportions of the soil, it is unlikely that any appreciable amountsof dioxins remained in surface soils after surface soil wasexcavated in 1986.
The former residents and children who played on site were probablyexposed to ethylbenzene through ingestion of contaminated soil. Although this evaluation is based on data from surface-subsoilsamples, and the ATSDR does not have MRLS for ethylbenzene, theestimated dose of ethylbenzene from soil did not exceed EPA's oralRfD (Table 9). No adverse health effects are likely to occur foradults and children from their past exposures. Subsequent samplingdid not detect ethylbenzene in soil (Table 2).
Potential exposure to the chemical present in groundwater both onand off site could pose a health threat if the chemical migratedinto well water at the campground. However, based on informationin the pathways analyses section, contaminant concentrations aredecreasing in the plume. Studies have also shown (21) that givensufficient time, ethylbenzene will be essentially biodegraded ingroundwater.
Lead was detected in soil samples analyzed before (Table 1) andafter surface soil excavation and removal (Table 2) in 1986. It istherefore probable that exposure to lead occurred in residents, andchildren who played on the site. ATSDR does not have MRLs and theEPA has no oral RfDs for lead. Inhaling or ingesting more than500-1,000 micrograms of lead per gram of soil was a rangepreviously considered by the CDC that could cause elevated bloodlead levels in children. However, the CDC has since withdrawn thisguideline due to the seriousness of lead exposure among children inthe United States of America. Lead exposure can cause a decreasein intelligence (IQ) score, slow growth, and cause hearingproblems.
Lead exposure is particularly dangerous for the unborn childrenbecause of the great harm it does to the developing fetus. Pregnant women exposed to lead can pass lead to the unbornchildren, causing premature birth, low birth weight, andmiscarriages. At high levels, lead can damage the brain andkidneys, and raise blood pressure in men, and cause infertility. Lead acetate and lead phosphate have been determined by TheNational Toxicology Program (NTP), an Organization within the DHHS,to cause cancer in humans. However, this conclusion is based onanimal studies (14, 22).
The level of lead in the exposed population is not known. Riskcharacterization of lead exposure generally involves usingmathematical models to predict blood lead levels that will resultfrom any given range of lead uptake. Two of these models, theIntegrated Uptake/Biokinetic (IU/BK) model (developed for the EPA)and a statistical model developed by the Society of EnvironmentalGeochemistry and Health (SEGH), allow blood lead levels to berelated quantitatively to uptake rates and can provide estimates ofthe frequency distribution of blood lead levels associated with anygiven uptake lead exposure scenario. In the absence of any healthguideline, it is not possible to determine whether adverse healtheffects could occur at these exposures. In addition, the levels oflead detected in soil after remediation in 1985 (Table 2) was aboutone half the levels before remediation (Table 1). In the absenceof any environmental data, health guidelines, and blood lead levels of the exposed population, it is difficult to determine whetherhealth effects could occur in persons who might be so potentiallyexposed.
Other heavy metals detected in groundwater both on and off site(Tables 3 and 5) include aluminum, arsenic, beryllium, chromium,cobalt, mercury, nickel, and vanadium. However, potential exposureto arsenic, chromium, cobalt, mercury, nickel, and vanadium isunlikely to cause any adverse health effects due to theinsignificant ingestion doses for adults and children who may bepotentially exposed. Potential exposure to the highest levels ofaluminum and beryllium may pose some health concerns if thechemicals migrated into any current or future drinking well waterin the area.
METHYL ISOBUTYL KETONE (MIBK)
MIBK was detected in on-site surface water samples analyzed beforesite remediation in 1985. However, subsequent analyses did notdetect MIBK in surface water (Table 9). Very little information isavailable on the toxic effects associated with exposure to MIBK. Because ATSDR does not have a Toxicological Profile or MRLs, andEPA has no oral RfD for MIBK, it is not possible to determinewhether adverse health effects will occur in children from theirpast exposures.
POLYCHLORINATED BIPHENYLS (PCBs)
Former on-site residents and children who played on the site wereexposed to PCBs from soil. The estimated PCB exposure in adultsand children exceeded ATSDR's chronic MRL for PCBs (Table 9). Exposure of experimental animals to small amounts of PCBs (between0.005 and 0.2 mg/kg/day) for several months caused reproductive,neurobiological and hematological effects, and the suppression ofimmunological functions (23). The estimated doses for adults andchildren also exceeded the experimental doses. It is probable thatmild forms of some of these health effects could occur in theexposed people on site, although the manifestation of any symptomswould partly depend on the presence in PCB mixtures of other toxiccontaminants such as chlorinated dibenzofurans. This conclusion isbased on data from surface-subsoil samples. However, the amountsof PCBs detected in soil after excavation and removal of surfacesoil in 1986 did not exceed ATSDR's chronic MRL, suggesting thatmost of the PCB contamination was associated with the uppermostorganic soil layer.
The EPA, DHHS, and IARC consider PCBs to be probable humancarcinogens. Data regarding occupational and accidental exposuresof humans to PCBs are inconclusive, due to confounding exposures orthe lack of documentation of exposure. A statistically significantexcess risk of liver cancer has been reported in a 16-year follow-up study in Japan (14). We estimate that former residents on sitewho were exposed between 10 and 30 years to PCBs may have aslightly high increased risk of developing cancer over a lifetimebecause of their exposures.
Exposure to tetrachloroethene occurred in the former occupants ofthe site building through ingestion of contaminated soil. Inaddition, children who played on the site were also exposed totetrachloroethene through skin contact and ingestion of surfacewater (Table 9). The ingestion exposure in adults and childrenfrom soil prior to remediation in 1986, did not exceed ATSDR'sintermediate MRL or EPA's oral RfD (Table 9). It is unlikely thatnon carcinogenic health effects would occur in residents from theirpast exposures. In addition, potential exposure to trace amountsof the chemical remaining in soil (Table 2) after remediation in1986 would not pose any health problems for future occupants of thesite.
Children's ingestion of PCE in surface water before remediation didnot exceed EPA's oral RfD. Non-cancer health effects are unlikelyto occur for children from their exposures. In addition,subsequent analysis of surface water samples did not detecttetrachloroethene (Table 4).
The chemical is present in groundwater both on and off site in theresidential neighborhoods (Tables 3 and 5). However, the potentialingestion exposure to levels of tetrachloroethene in groundwater isnot likely to cause adverse health effects in the potentiallyexposed persons. In addition, research indicates thattetrachloroethene does not readily transform in water, and that theamount of tetrachloroethene recovered at the end of migrationthrough the aquifer was essentially the same as that added. However, breakdown of tetrachloroethene is fairly more rapid inwater at room temperature than at normal environmental conditions(24).
IARC and DHHS consider PCE to be a possible carcinogen based onanimal studies. According to the EPA, there is limited evidencethat PCE has caused cancer in at least one rodent species. Epidemiological studies suggest a possible association betweenchronic PCE exposure and increased cancer risk. Based on thisinformation children who were exposed to PCE in both surface waterand soil on site have a slightly low increased risk of developingadditional cancer over a lifetime because of exposure to low levelsPCE.
Exposure to toluene occurred in former residents through ingestionof toluene-contaminated soil on site. In addition, children whoplayed on the site were exposed to toluene through ingestion of andcontact with surface water. Although ATSDR does not have MRLs fortoluene, the estimated doses for adults and children do not exceedEPA's oral RfD for toluene (Table 9). It is unlikely that adversehealth effects would occur in adults and children from their pastexposures to toluene. In addition, trace amounts of toluene weredetected in soil (Table 2) and surface water (Table 4) afterremediation was carried out in 1986. However, health effects areunlikely to occur from potential exposure to these low levels oftoluene. There is no conclusive evidence that toluene iscarcinogenic in animals or humans (25).
The potential ingestion exposure to toluene in groundwater both onand off site is likely to cause adverse health effects. Inaddition, biodegradation process will substantially reduce tolueneas the BTX mixture is degraded, although the rapidity of thisprocess would depend on the subsurface environment.
Exposure to 1,2,4-tichlorobenzene occurred in the former residentsand in children who played on the site for periods between 1970sand 1986 (Table 1). The chemical was successfully removed duringremediation of the site in 1986. ATSDR does not have MRLs or aToxicological Profile for 1,2,4-trichlorobenzene. However, theingestion exposure from soil in adults and children did not exceedEPA's oral RfD for 1,2,4-trichlorobenzene (Table 9). Adults and children are unlikely to experience any adverse health effectsbecause of exposure to low levels of 1,2,4-trichlorobenzene.
Exposure to TCE occurred to former residents and children whoplayed on the site, and to nearby residents through severalcompleted exposure pathways (Tables 9 and 11). Although ATSDR doesnot have chronic MRLs for TCE, the ingestion exposure in adults andchildren from soil on site did not exceed ATSDR's intermediate MRLfor TCE (Table 9). The highest estimated ingestion dose from soilis some 10,000 times lower than the doses that caused renalproblems in animals. Non carcinogenic health effects are unlikelyto occur for adults and children because of exposure to low levelsof TCE in soil. Moreover, the estimated dose of TCE in surfacewater for children who played on the site did not exceed ATSDR'sintermediate MRL for TCE (Table 9). In addition, the highestestimated ingestion dose for TCE from surface water is about1,000,000 times lower than doses that caused renal problems inanimals. It is therefore unlikely that noncarcinogenic healtheffects would occur in children because of exposure to low levelsof TCE in surface water.
TCE exposure occurred in residents off site through ingestion, skincontact and inhalation from the use of TCE contaminated water fromprivate wells located near the site. However, the ingestionexposure in adults and children did not exceed ATSDR's intermediateMRL for TCE. In addition, the levels of TCE in all the eleven TCEcontaminated wells before bottled water was provided in 1985 (Table6) did not exceed WHO's drinking water guidance level of 30 ppbbased on a carcinogenic end point. The highest estimated dose ofTCE from well water before municipal water was provided in 1987 isabout 10,000 times lower than the TCE dose that caused renalproblems in laboratory animals (26). It is unlikely that adultsand children who drank, showered, or bathed with TCE contaminatedwell water between the 1970s and 1987 would suffer any noncarcinogenic health effects because of their exposure to low levelsof TCE in water.
TCE exposure occurred in workers at a business and campers who usethe Len-Kay Campground well water. The estimated dose of thehighest level of TCE in the well water (0.017 ppm) does not exceedATSDR's intermediate MRL for TCE. In addition, our estimated dosesfor adults and children were approximately 100,000 times lower thanthe lowest dose that caused renal problems in laboratory animalsafter 52 weeks of chronic/long-term exposure (26). Workers at thecampground who used the well water, and campers (summer residents)who also used the well water are unlikely to suffer noncarcinogenicadverse health effects because of low levels and short duration ofexposure.
IARC does not consider TCE to be a human carcinogen. According tothe EPA, there is limited evidence that TCE has caused cancer in atleast one rodent species. Based on this evidence residents whowere exposed to TCE in the most contaminated well water or in soilhave no risk of developing excess/additional cancer over alifetime. Moreover, workers at a certain business, and campers whoused the Len-Kay Campground well water and who were exposed to TCEare not likely to develop any additional cancer because of theirexposure to low levels of TCE. However, long-term use of the Len-Kay Campground Well water should be reconsidered because continuousexposure to even low levels of a suspect carcinogen should beavoided.
TCE found in surface water (Table 4) on site after remediation isexpected to volatilize into the atmosphere. The level of TCE(0.011 ppm) remaining in soil (Table 2) after excavation ofcontaminated surface soil in 1986 remediation would migrate andleach from the surface and subsurface soils. Therefore, potentialexposure to TCE from any reoccurring surface water and soils wouldbe insignificant. However, the potential exposure to TCE fromgroundwater both on and off site could pose a health problem if thechemical were to migrate further into any current or futuredrinking water wells. Although the levels of TCE in groundwaterwill biodegrade over time, the products of any such microbialdegradation may include dichloroethene and vinyl chloride. However, the potential public health significance of these productswould depend upon their concentrations in groundwater and exposurescenarios that might occur in the future.
OTHER ORGANIC CHEMICALS
The potential risk from exposure to other organic chemicalsremaining in groundwater on and off site including 2-butanone, 4-methyl-2-pentanone, napthalene and 2-methylnapthalene is difficultto determine because health guidelines are unavailable.
Workers at a certain business and campers who use the Len-KayCampground were exposed to 1,2,DCE in well water. However,although there are no chronic MRLs or RfDs, the estimated ingestionexposure does not exceed the intermediate MRL (Table 11). Inaddition, the estimated dose in the Len-Kay Campground well usersis some 100,000 times lower than the experimental dose that causedno observed adverse effects in laboratory animals after 90 days ofsubchronic/intermediate exposure (27). Adverse health effects areunlikely to occur because of the low levels and short duration ofexposure. However, potential exposure to 1,2-DCE in groundwater issignificant, especially for infants and young children, because ofthe high levels of 1,2-DCE in groundwater on and off site (Tables3 and 5).
Residents who used the residential well located one-half mile fromthe site were exposed to iron in well water. Although there are noMRLs or RfDs for iron, the estimated doses (Table 10) exceed therecommended dietary allowances (RDAs) established by the NationalResearch Council (NRC) for all healthy individuals (28). However,the estimated dose for infants and young children was notsubstantially different from the RDA for young children. Theestimated doses of iron ingested from the residential well water(containing 18.5 ppm) is additional to a daily intake of 10-11 mgof iron from typical United States diets (28). However,deleterious effects of daily intakes between 25 and 75 mg areunlikely in healthy persons. In people without genetic defectsthat increase iron absorption, there are no reports of irontoxicity from foods other than long-term ingestion of home brewsmade in iron vessels (28). In addition, the percentage of ironabsorbed from a meal decreases as the amount of iron presentincreases. Therefore, adverse health effects are unlikely to occurbecause of the low levels of exposure.
Manganese exposure occurred to residents who used a residentialwell water one-half mile from the site. The ingestion exposure inadults and children is some 9-23 times higher than RfD (Table 10). Moreover, the estimated doses for adults and children are about 9-38 times greater than the amount of manganese in well water thatcaused less serious forms of mild neurological signs in humansafter 50 years of exposure (29). In addition, the estimated dosefor infants and young children also exceeds by more than twomagnitudes the experimental dose that caused less seriousneurological degeneration, and altered brain enzymes in neonatalrats after 60 days of intermediate/subchronic exposure (29). It istherefore possible that mild forms of neurological signs mightoccur in the exposed persons after 50 years of exposure. There isalso a possibility that infants and young children who drankmanganese-contaminated water from the residential well located one-half mile from the site might experience less serious forms ofdiminished brain function after less than one year of continuousexposure. However, this conclusion is based on the results ofanimal experiments only. The amount of manganese found in thisresidential well may be site-related.
Potential exposure to manganese is highly significant and couldcause adverse health effects in adults and children who may be potentially exposed because of the very high levels of manganesefound in groundwater on and off site (Tables 3 and 5).
Propylene glycol is a colorless, odorless, water-soluble liquidconsidered safe for use in commercial formulations of foods, drugs,and cosmetics and antifreezes. Propylene glycol is commonly usedin the pharmaceutical industry as a solvent for drugs, as astabilizer for vitamins, and in ointment for medicinalapplications. This widespread use of propylene glycol stems fromits low level of toxicity (30).
Exposure to propylene glycol occurred in residents who used the residential well located one-half mile from the site. There are noMRLs or RfDs for propylene glycol. The estimated dose for adultsand older children (seven years and older) were lower than the dosethat caused less serious acute exanthem (mild skin rashes) inhumans after 24 hours of short duration of exposure (30). Adultsand older children are unlikely to suffer any adverse healtheffects from their acute or short duration of exposure. However,the estimated dose for infants and young children (less than sevenyears old) is two times higher than the dose that caused lessserious acute exanthem (mild skin rashes) in humans after 24 hoursof short duration of exposure in humans (30). It is possible thatinfants and young children (less than seven years old) who wereexposed to the highest level of propylene glycol in well watermight suffer less serious form of mild skin rashes after shortduration of exposure. However, the estimated doses for infants,children and adults are 10-100 times lower than the lowestexperimental doses that caused no adverse effects in laboratoryanimals after two years of chronic/long-term exposure (30). It ishighly unlikely that adverse health effects will occur as a resultof chronic/long-term exposure because of the low levels ofexposure. Potential exposure to propylene glycol is insignificantbecause information in the contamination section of this documentindicates that analysis of recent samples have not detectedpropylene glycol in the well water.
|Health Guideline for Ingestion - mg/kg/day|
|Methyl Isobutyl Ketone||Surface Water||None||None||None|
|Health Guideline for Ingestion -|
|Health Guideline for Ingestion -|
|TCE||Len-Kay Well||0.1||Int. MRL||No|
Health outcome data were not evaluated for this site because thepopulation of concern (about 50-75) is a very small population. This would make it very unlikely that any health effects due to thesite could be detected. In addition, no previous health studies onthe population near the Tibbetts Road site were identified duringthe gathering of data and information for this public healthassessment.
We have addressed each of the community concerns as follows:
- Can EPA help residents who live near the site obtain taxabatement on their properties? In addition, can EPA help toget the on-site building demolished ?
Under Superfund legislation, EPA is in charge of remediatingand inspecting the site; however, ATSDR is not aware of anyauthority EPA has to obtain tax abatements. Nevertheless,this concern will be forwarded to EPA.
According to the EPA's Record of Decision, EPA is planning toremove the existing on-site building and debris.
- Is the on-site building a possible source of contaminants thatcould be spread to nearby residents by fire or by rodents whoreportedly reside at the house ?
Since sampling of the interior of the on-site building has notoccurred, a definitive answer to this concern cannot be given. According to the EPA RPM, no evidence exists of waste disposalactivities inside the house. However, it is probable that theformer residents of the house tracked contaminants fromoutside into the house. Any possible contaminants remainingin the house would be in dusts. Children who once resided inthe house may have been exposed to contaminated dusts. It is,however, unlikely that any remaining contaminated dusts wouldresult in a significant exposure pathway because of a fire orrodents tracking contaminants.
- Can EPA connect additional residents to the Swains Lake WaterDistrict for free ?
Since this concern/issue is related to EPA, we will forward itto them.
- Could children who played on site experience learningdisabilities, liver cancer, and neonatal death that werereported in some family members who once lived on the site?
Learning disabilities refer to one of several types ofproblems. Those problems include difficulties listening,speaking, reading, writing or with arithmetic.
There are many causes of learning disabilities such asexposure to drugs, alcohol, and lack of oxygen in the womb. Exposure to lead has been associated with learningdisabilities. It is difficult to determine the cause of mostcases of learning disabilities.
The likelihood of developing a learning disability fromexposure to lead increases with the blood lead level. At thelower levels of exposure (less than 15 ug/dL of lead inblood), effects that might occur would not be likely to causelearning disabilities or other effects that could be detected.There are many sources of lead to which children may beexposed. Those include lead containing paint, industrialemissions, automobile exhausts, food, dust and water.
Based on data and information reviewed, contaminants on sitecan be traced to the work practices on the site. Ourevaluation shows that former residents on site were probablyexposed to high levels of these contaminants. In addition tolead, some of the contaminants on site are human carcinogens. We determined that persons who were exposed to PCBs on sitefor periods between 10 and 30 years before site remediation in1986 may have a high increased risk of developing cancer overa lifetime. It is unlikely that the children who paidoccasional visits to the site would develop cancer and noncarcinogenic health effects from their exposures to PCBs.
- Are health problems such as stomach pains, vomiting,meningitis, respiratory disorders, kidney disease, high bloodpressure, and skin cancer suffered by a few residents causedby chemicals in private well water ?
Benzene and TCE were the only chemicals analyzed for inresidential drinking wells within the vicinity of the site. Benzene is a known human carcinogen. Several epidemiologicalstudies have shown a causal relationship between benzeneexposure and leukemia in humans. Benzene induces aplasticanemia in humans--these effects are shown 10 years afterexposure. Based on the data evaluated, it is unlikely thatthe health problems reported by some of the residents werecaused by exposure to benzene in their drinking water. Inaddition, it is unlikely that low amounts of benzene indrinking water caused noncarcinogenic health effects inhumans. However, the additive effects of probable exposure tobenzene in ambient air cannot be determined, because ambientair data are unavailable. Our evaluation shows that exposureto levels of benzene in residential drinking well water beforebottled water was provided may have a slightly low increasedrisk of developing cancer over a lifetime.
The International Agency for Research on Cancer (IARC) doesnot consider TCE to be a human carcinogen. According to theEPA, however, there is limited evidence that TCE has causedcancer in one species of rodents. Based on this evidence wehave determined that residents who were exposed to TCE intheir drinking well water may have no apparent risk ofdeveloping cancer over a lifetime. Although TCE exposurethrough inhalation in both the workplace and recreationalsetting has been shown to result in liver and kidney problems,our evaluation has shown that exposure to levels of TCE inresidential well water is unlikely to have caused those healtheffects. However, the additive effects of exposure to TCE inambient air, and to any other chemicals in the drinking waterbefore bottled water was provided cannot be determined becausedata for TCE in air and other chemicals in water areunavailable.