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PUBLIC HEALTH ASSESSMENT

CARDINAL LANDFILL
FARMINGTON, STRAFFORD COUNTY, NEW HAMPSHIRE


V. DISCUSSION - ADULT AND CHILDREN'S HEALTH ISSUES

Based on the review of environmental data and conditions at the site in the previous section, there aresix completed pathways by which people could be or could have been exposed to chemicals from thesite. In the following sections, the public health implications of these exposures will be discussed. First,in Section A, the actual exposures to these chemicals will be evaluated using estimates of exposure andthe toxicological properties of these chemicals. As part of the ATSDR Child Health Initiative and inresponse to community concerns, the susceptibility of young children or developing fetuses to thechemical exposures will be a large component of the toxicological and epidemiologic review. Second,in Section B, data on cancer diagnoses for the Town of Farmington will be presented. Finally, healthquestions from the community are answered in Section C. The combination of these differentevaluations provides the weight of evidence to support DHHS' determinations regarding public healthhazards associated with exposures.

The two pathways of greatest public health significance are the drinking water pathway and the soil gasto indoor air pathway. Therefore, most of this discussion will focus on these pathways, although theothers will also be addressed.

(A) Public Health Implications of Exposure

In this subsection, we discuss the known adverse health effects that have been associated with the typesof exposures that are or were possible at this site. To understand how adverse health effects could becaused by a specific chemical, it is helpful to review factors related to how the body processes such achemical. Those factors include the exposure concentration (how much), the duration of exposure (howlong), the route of exposure (breathing, eating, drinking, and/or skin contact), and the multiplicity ofexposure (combinations of contaminants). Once exposure occurs, a person's individual characteristicssuch as age, gender, diet, general health, lifestyle, and genetics, influence how the body absorbs,distributes, metabolizes, and excretes the chemical. Together these factors determine the potential healtheffects that can be caused by the chemical.

To evaluate potential health effects, ATSDR has developed Minimal Risk Levels (MRLs) forcontaminants commonly found at hazardous waste sites. The MRL is an estimate of daily humanexposure to a contaminant below which non-cancer, adverse health effects are unlikely. MRLs aredeveloped for oral and inhalation exposure routes, and for duration of exposure (acute: 14 days orfewer; intermediate: 15-364 days; chronic: 365 days or more). Acute MRLs are typically higher thanchronic MRLs because of the shorter duration of exposure.

ATSDR publishes MRLs in its series of chemical-specific documents called Toxicological Profiles -documents that describe health effects, environmental transport, human exposure, and regulatory statusof a chemical. The preparers of this public health assessment have reviewed the profiles for thecontaminants of concern at the site.

We may also use EPA's chemical specific Reference Doses (RfDs) and Reference Concentrations(RfCs) to determine if non-cancer health effects are possible. RfDs, which are analogous to ATSDR'sMRLs, are estimates of daily human exposure to a contaminant that is unlikely to result in adverse non-cancer health effects over a lifetime. For chemicals that are considered to be known, probable, orpossible human carcinogens, DHHS uses EPA's chemical-specific cancer potency values to determinea theoretical estimate of excess lifetime cancer risk associated with exposure to the contaminant.

In the following subsections, the two major pathways of exposure (private drinking water wells and soilgas to indoor air) are evaluated in detail: (1) the potential effects of each chemical are discussedindividually; (2) the combined effects of multiple chemicals are evaluated; (3) any special child healthissues related to the exposures are discussed; and (4) there is an overall summary of the public healthimplications of the pathway. After this, the remaining four completed pathways are discussed more briefly.

(1) Private Drinking Water Wells

At present, none of the existing private wells in the area contain contamination above health comparisonvalues. The properties where groundwater contamination currently exists above health comparisonvalues have either switched to town water or are no longer occupied. Therefore, all significant exposures to contaminated drinking water were in the past.

In the past, five drinking water wells were contaminated with chemicals from the site at levels greaterthan health comparison values (Lots 7, 9, 11, 17, and 18, see Figure 2). Four of these wells wereabandoned in the mid-1980s. The fifth (Lot 7) was planned to be abandoned at the same time but wasnot. It was closed in January 2000 following a test by DES that showed contamination with VOCs.

The range of average concentrations of each contaminant in the wells and the associated exposures are presented in the following table.

Compound Range of Average Concentration (ug/L)1 Estimated Exposure (mg/kg-d)2,4 Dose Comparison Value (mg/kg-d) Source5
Methylene Chloride 13 0.003 0.2 MRL-chronic
Tetrachloroethene 7.6 - 82 0.002 - 0.02 0.01 RfD
Trichloroethene 16 - 230 0.003 - 0.05 0.2 MRL-acute
1,2-Dichloroethene 190 - 800 0.04 - 0.2 0.02 RfD
1,2-Dichloroethane 21.8 0.004 0.2 MRL-int
Vinyl chloride 24 0.005 0.00002 MRL-chronic
Notes:
1. The second column contains the range of average concentrations of each chemical in each of the five private wells. For compounds where only one value is listed, the chemical was only detected in one well.
2. Estimated exposure is based on drinking 1 L/d and a 10 kg body weight. These parameters are for a small child which is the most conservative way to estimate exposure on a per body weight basis. Additional exposures from inhaling fumes from water and dermal exposure while showering were estimated by doubling the ingestion dose per guidance from ATSDR [35].
3. Not all of the contaminated wells contained all six of these compounds.
4. Exposures have been rounded to one significant figure.
5. MRL-chronic = ATSDR's Minimal Risk Level for chronic exposures (lasting longer than 1 year)
MRL-int = ATSDR's Minimal Risk Level for intermediate exposures (lasting longer than 14 days but less than 1 year)
MRL-acute = ATSDR's Minimal Risk Level for acute exposures (lasting less than 14 days)
RfD = EPA's Reference Dose for chronic exposures

(i) Methylene Chloride
Private Drinking Water Well Pathway

The estimated exposures to methylene chloride (0.003 milligrams per kilogram per day or mg/kg-d) arewell below the MRL for this chemical (0.2 mg/kg-d), therefore, non-cancer health effects are notexpected. The MRL was derived from a laboratory study with mice and rats that observed cellularchanges in the liver following exposure to methylene chloride. The lowest dose at which no adverseeffects were observed was 6 mg/kg-d [66]. Therefore, the estimated exposure from contaminateddrinking water was 1000 times lower than the "no observed adverse effect level" (NOAEL).

The National Toxicology Program (NTP) has classified methylene chloride as being reasonablyanticipated to be a human carcinogen based on laboratory studies with animals, but inconclusiveevidence for human carcinogenicity. All the laboratory cancer studies with animals have been atexposure levels that are thousands of times higher than those expected from the drinking water near thesite. At these higher exposures, methylene chloride is detoxified by the body using a metabolic pathway(the glutathione transferase pathway) which produces reactive byproducts which are thought to becarcinogenic agents. No cancer studies have been done at the low exposure doses typically experiencedby humans [66]. Regardless, even using the cancer potency factor that EPA has derived from the highdose animal studies, we would not expect an appreciable theoretical cancer risk from the exposures to methylene chloride in the private wells.

(ii) Tetrachloroethene (PCE)
Private Drinking Water Well Pathway

The central nervous system (CNS) is a well-established target of PCE exposure in humans, andavailable toxicity data suggests that it may be the most sensitive target [64]. ATSDR has derived anMRL for acute duration exposures (lasting less than 14 days) of 0.05 mg/kg-d. This is based on a studyin which newborn mice were exposed to 5 and 320 mg/kg-d of PCE and an increase in hyperactivity wasobserved. Although this exposure only lasted for seven days, it occurred while the CNS was developingand, therefore, was particularly sensitive to the effects of PCE [64]. The estimated exposures fromcontaminated drinking water wells were in the range of 0.002-0.02 mg/kg-d, which are less than theacute MRL and at least 250 times less than the level at which effects were observed. ATSDR has notderived MRLs for longer-term exposures to PCE because longer-term oral studies in animals have notfocused on neurological effects, the principle effect of PCE in humans.

Effects on the kidneys and liver have also been reported for people exposed to high concentrations ofPCE [64]. EPA has established a chronic RfD of 0.01 mg/kg-d based on the results of laboratory studieswith rats and mice. These studies observed liver effects in mice at a dose of 71 mg/kg-d, but no effectsat 14 mg/kg-d [40]. Estimated exposures from contaminated wells near the site were approximatelyequal to or below the RfD and 1000 times below the levels that have been demonstrated to cause aneffect. Moreover, the liver effects observed in the animal studies may not be relevant to the humanbody. Hepatic toxicity is thought to be the result of a metabolite, trichloracetic acid, not the PCE itself. Mice metabolize more PCE to trichloracetic acid than humans. Therefore, the dose at which livereffects were observed in mice is probably lower than the level at which similar effects would be seen inhumans [64].

PCE has been classified to be reasonably anticipated to be a human carcinogen by NTP, however, thetheoretical cancer risks from this exposure are expected to be low. Evidence for the humancarcinogenicity of PCE comes from studies of workers who were exposed to high concentrations of PCEthat found increases in esophageal cancer, cervical cancer, and non-Hodgkin's lymphoma. In general,these studies were confounded by concomitant exposure to other solvents, smoking and other lifestylevariables, and methodological limitations [64]. In animals, PCE exposures have been linked to livercancers in mice (but not rats), mononuclear leukemia in rats (but not mice), and small increases in theincidence of kidney cancer in male rats. The significance of these results to humans is uncertain. Livercancer in mice is thought to be related to trichloracetic acid, but this metabolite of PCE is produced lessin humans. The type of leukemia observed in the rat studies was fairly unique. And, renal damage inrats was likely the result of reactive intermediates formed by the glutathione transferase pathway. This metabolic pathway, while always active, only becomes important at very high exposures [64].

(iii) Trichloroethene (TCE)
Private Drinking Water Well Pathway

Most of the information regarding the effects of TCE in humans comes from case studies andexperiments describing the effects of TCE after inhalation exposure. These studies indicate that theprimary target of TCE in humans is the CNS [63]. Speech impairment, hearing impairment, and strokehave been observed to be more prevalent among people enrolled in ATSDR's National ExposureSubregistry for TCE [70,74].

ATSDR has not derived an MRL for chronic exposures to TCE because suitable studies are notavailable. However, 0.2 mg/kg-d has been established as the MRL for acute exposures (<14 days). ThisMRL is based on a study where mouse pups were exposed to TCE and exhibited behavioral changeslater in life. The lowest exposure at which this effect was observed was 50 mg/kg-d [63]. Estimatedexposures to TCE in the drinking water wells fell in the range of 0.003-0.046 mg/kg-d, which are atleast 1000 times less than the level at which effects were observed in the animal studies.

Animal studies indicate that effects of the liver are also possible following TCE exposure. In the liver,TCE is broken down to different metabolites, including trichloracetic acid, which can damage the livertissues [76]. A recent reassessment of non-cancer toxicity of TCE suggests an exposure level that wouldbe without effects on the liver would be in the range of 0.06-0.12 mg/kg-d [78]. The estimatedexposures from the drinking water wells are below this range.

NTP recently classified TCE as being reasonably anticipated to be a human carcinogen [72]. Moreover,a recent analysis of TCE carcinogenicity suggests a stronger association between occupationalexposures to TCE and liver and kidney cancer than previous analyses [75]. The review also suggestsassociations between TCE and Hodgkins disease and non-Hodgkins lymphoma. Laboratory studieswith animals have observed similar cancer primary sites as in humans (e.g., kidney and liver). However, using the latest available quantitative estimates of the carcinogenicity of TCE there wouldbe low theoretical risk of developing cancer from this drinking water exposure.

(iv) 1,2-Dichloroethene (1,2-DCE)
Private Drinking Water Well Pathway

The most significant effects of 1,2-DCE exposure are on the blood and the liver. ATSDR has derivedMRLs for the two 1,2-DCE isomers (cis and trans) for intermediate exposures (up to 1 year) in the rangeof 0.2-0.3 mg/kg-d. These were based on a laboratory studies that observed changes in the proportionsof cell types in the blood of rats and liver effects in mice at doses as low as 97 mg/kg-d. No effects wereobserved in the animals at 17 mg/kg-d. Other organs and endpoints were an order of magnitude lesssensitive [60]. The estimated exposures to 1,2-DCE from the contaminated wells were in the range of0.038-0.16 mg/kg-d, which is less than the intermediate MRL and at least 100 times less than the levelat which no effect was observed in the animal studies.

EPA has derived an RfD for trans-1,2-DCE of 0.02 mg/kg-d [40]. This is based on the same study thatATSDR used for the intermediate MRL and differs only in that an additional 10-fold safety factor hasbeen applied to account for extrapolation from intermediate to chronic exposures. The estimatedexposures were greater than this RfD but still were 100 times less than the "no effect" level from thestudy on which it is based. Therefore, it is unlikely that these exposures will result in adverse health effects.

Tests on the ability of 1,2-DCE to damage genetic material, which could initiate cancerous growths,have been predominantly negative. Federal and international agencies have not given 1,2-DCE a cancer classification [60].

(v) 1,2-Dichloroethane (1,2-DCA)
Private Drinking Water Well Pathway

When humans have been exposed to large amounts of 1,2-DCA the primary target organs where effectshave been observed are the CNS, liver, and kidneys [69]. Studies with laboratory animals have foundsimilar effects, as well as immunological, genotoxic, and carcinogenic effects not reported in humans.

ATSDR has derived an intermediate duration MRL of 0.2 mg/kg-d, based on a study where rats wereexposed to 1,2-DCA in drinking water for 13 weeks. Increased kidney weights were observed at thelowest dose administered, 58 mg/kg-d. While increased kidney weight is not an adverse effect, this signwas interpreted as the beginning of the toxic effects that were observed at higher concentrations [69].The estimated exposure from contaminated wells near the site was 0.004 mg/kg-d. This is 1000 timesless than the MRL and 10,000 times less than the exposure at which increased liver weights wereobserved. Therefore, these adverse health effects are not likely to develop from the exposure.

Results from animal bioassays provide sufficient evidence to suggest that 1,2-DCA is a probable humancarcinogen. However, the toxic and carcinogenic effects observed for 1,2-DCA are not from the parentchemical itself, but from reactive intermediates formed when 1,2-DCA is metabolized by the body [69]. EPA's cancer slope factor for this chemical was derived from a study in which rats and mice wereexposed to at least 5 mg/kg-d of 1,2-DCA dissolved in corn oil [40]. This type of high-dose exposureis more likely to produce carcinogenic effects than a low-dose exposure. Regardless, using EPA's cancerpotency factor derived from the high-dose study, the theoretical cancer risk from exposures to 1,2-DCA in drinking water wells is still expected to be low.

(vi) Vinyl chloride
Private Drinking Water Well Pathway

Vinyl chloride was detected in December 1999 in one drinking water well near the site (Lot 7) at aconcentration of 24 ug/L. The date when this vinyl chloride contamination began is uncertain. The wellwas tested in 1985 and vinyl chloride was not detected, but the detection limit of the analytical methodwas 10 ug/L. The well is reported to be very deep (approximately 450 feet deep) and it draws waterfrom the bedrock aquifer. There are two bedrock monitoring wells between the site and Lot 7. Vinylchloride has been consistently detected at high concentrations in one of these bedrock monitoring wells(SW104R). The concentrations have been increasing in this well over time and reached their highestlevels (3,100 ug/L) during the most recent tests in April 2000 [26,33]. The other bedrock well(MW402R), which is closer to Lot 7, was installed in February 2000 and did not contain any detectablelevels (<2 ug/L) of vinyl chloride in April 2000 [33]. Both of these monitoring wells are approximately100-120 feet deep [18,33]. The presence of very high, and increasing, concentrations of vinyl chloridein a bedrock monitoring well near Lot 7 suggests that the detection of this chemical in the drinkingwater well serving Lot 7 was not an anomaly. The absence of vinyl chloride in the other nearbymonitoring well (MW402R) does not rule out migration of vinyl chloride from the site to Lot 7 becauseMW402R is much shallower than the private well (118 vs. 450 feet, respectively). Therefore, whilethere is uncertainty about the duration and magnitude of vinyl chloride contamination in the wellserving Lot 7, we have assumed a sustained exposure to the measured concentration of 24 ug/L, whichwould be approximately equivalent to 0.005 mg/kg-d.

Workers who have been exposed to vinyl chloride at high concentrations developed signs and symptomsof intoxication such as dizziness, drowsiness, and/or headache. These high level exposures may alsoproduce lung and kidney irritation and inhibition of blood clotting. Longer term exposure of humansin occupational settings has been associated with the development of a number of other toxic effects. The most sensitive effects are changes in the tissues of the liver [61].

ATSDR has derived a chronic MRL for vinyl chloride of 0.00002 mg/kg-d. This based on a study withrats that observed changes in the liver cells of rats at an exposure dose of 0.018 mg/kg-d [61]. Theestimated exposure from the contaminated well (0.005 mg/kg-d) is much higher than the MRL and isclose to the level at which effects were observed in animals. Given that effects on the liver have beendemonstrated in humans and animals, there is little evidence for large differences between the speciesin terms of toxicity [61]. Therefore, this exposure, if it lasted for several years, could cause effects onthe liver for people who lived in this house.

A large number of studies have reported a greater than expected incidence of a rare type of cancer,angiosarcoma of the liver, among workers exposed to vinyl chloride. Other types of cancer that haveshown a statistically significant increase in incidence among vinyl chloride workers, at least in somestudies, include cancer of the brain and CNS, the lung and respiratory tract, and thelymphatic/hematopoietic system. Angiosarcoma has also been observed in laboratory studies withanimals. Therefore, vinyl chloride is considered a known human carcinogen, with angiosarcoma of theliver as the primary site of concern [61]. For a person exposed to 24 ug/L of vinyl chloride for 9 years(the average duration of residence in a home in the U.S.), there would be a moderate theoretical risk ofdeveloping cancer (an increased risk of 1:1,000). However, since the most recent residents of the homelived there for approximately half this duration, their theoretical risk of developing cancer from the exposure is expected to be low.

Data suggest that the following subsets of the human population may be more susceptible to the toxiceffects of vinyl chloride: fetuses; infants; young children; people with liver disease, irregular heartrhythms, impaired peripheral circulation, or systemic sclerosis. Other factors that may exacerbate theeffects of vinyl chloride are exposure to organochlorine pesticides, consumption of alcoholic beverages,and the use of barbiturates [61]. The most recent residents of the home served by the contaminated wellwere adults; however, they have only lived there for the last 4-5 years and earlier residents may have included children.

(vii) Combined Effects of Chemicals with Similar Toxicological Properties
Private Drinking Water Well Pathway

The six chemicals for which there was exposure from contaminated wells can be grouped into threesubsets with similar toxicological properties.

PCE, TCE, and 1,2-DCE are metabolized by the body in much the same way. For low-level exposures,they break down to trichloroacetic acid and dichloroacetic acid, which are thought to induce effects onthe liver. PCE and TCE are both detoxified by the glutathione transferase pathway at higher exposures. Metabolites from this pathway (e.g., S-[1,2-dichlorovinyl]-L-cysteine or DCVC) have been associatedwith kidney tumors.

Four of the five wells contained a combination of PCE, TCE, or 1,2-DCE. The combined exposurefrom all three chemicals was in the range of 0.002-0.2 mg/kg-d. The lowest RfD or MRL for these threecompounds is the RfD for PCE of 0.01 mg/kg-d which is based on the results of laboratory studies withmice. These studies observed effects on the liver at a dose of 71 mg/kg-d, but no effects at 14 mg/kg-d[64]. Some of the combined exposures to PCE, TCE, and 1,2-DCE were greater than the RfD for PCE,but were still 350 times lower than the levels at which effects were observed in animals. Humans areless likely to experience these effects than laboratory animals due to a different metabolism. Therefore,the combined exposures to PCE, TCE, and 1,2-DCE are not likely to result in adverse health effects inhumans.

Regarding cancerous effects, PCE and TCE both appear to be carcinogenic by the same mechanisms. Yet, when the exposures to both chemicals are combined, the theoretical excess risks of developingcancer are still expected to be low. 1,2-DCE is not considered carcinogenic.

The second group of chemicals with similar toxicological properties is 1,2-DCA and methylenechloride. Both appear to be toxic and carcinogenic due to reactive metabolites produced by theglutathione transferase pathway. However, it is not necessary to evaluate combined exposures becausenone of the contaminated wells contained both methylene chloride and 1,2-DCA at concentrationsgreater than comparison values.

Vinyl chloride has unique toxicological properties but it can be influenced by the toxic effects of otherchemicals. For example, since it is the metabolites of vinyl chloride that are toxic, the effects of vinylchloride can be increased by speeding up its metabolism. The metabolic pathway responsible forbreaking down vinyl chloride is inducible by exposures to organochlorine pesticides and Arochlor 1254(PCBs) [61]. Therefore, someone who is exposed to vinyl chloride and pesticides may experiencegreater effects than someone who is exposed to vinyl chloride alone. It is possible that exposures to othersolvents that are metabolized by this pathway (e.g., PCE, TCE, 1,2-DCE) could have a similar effect. However, 1,2-DCE metabolites have been shown to inhibit metabolic activity [60]. Therefore, the combined effects of other solvents with vinyl chloride are equivocal.

(viii) Children's Susceptibility
Private Drinking Water Well Pathway

Children differ from adults in their physiology (e.g., respiratory rates relative to body weight),pharmacokinetics (i.e., distribution, absorption, metabolism, and excretion of a chemical), andpharmacodynamics (i.e., susceptibility of an organ to the exposure) [77]. Therefore, when evaluatingchemical exposures, it is important to consider whether children would be more or less susceptible tothe effects of the exposure than adults.

For PCE, TCE, and 1,2-DCE, there is evidence that children are more susceptible to exposures thanadults. The most sensitive stage of childhood appears to be in utero (i.e., during pregnancy) and duringthe first year of life. During this time, the primary enzyme that breaks TCE as well as 80 otherchemicals down to its toxic metabolites (the CYP2E1 isoform of cytochrome P-450) may be active, butother systems of detoxification and excretion are still developing [77]. This could result in higherinternal doses of the toxic intermediates at the target organs for children than adults. Studies in micesuggest that PCE can cross the placenta and that at least one of the metabolites (trichloracetic acid) canbecome concentrated in the fetus [64].

In addition to the toxicological evidence, recent epidemiological studies suggest that exposures to PCE,TCE, or 1,2-DCE during pregnancy could result in adverse health effects for the developing fetus. Onestudy in New Jersey found that maternal residence during pregnancy in areas with PCE, TCE, or DCE-contaminated drinking water was associated with an increased risk of birth defects of the CNS, theneural tube, and the oral cleft [107]. An ATSDR study of the U.S. Marine Corps Base at CampLeJeune in North Carolina reported significantly decreased mean birth weight for babies born followingmaternal exposures to VOCs during pregnancy [63,108]. A study of childhood leukemia conductedin Woburn, Massachusetts, concluded that the incidence of childhood leukemia was associated with themother's potential for exposure to water from specific wells contaminated with PCE and TCE,particularly exposure during pregnancy [109]. Another study in New Jersey found a statisticallyelevated rate of childhood leukemia in towns served by community water supplies contaminated withTCE and PCE in the years 1979 to 1987, compared to towns without a history of such contamination[110]. Finally, a study in Arizona observed an increase in the proportion of live births with congenitalheart defects following maternal exposure to TCE in drinking water [111]. Overall, the associationsdrawn from these limited epidemiological studies of humans are suggestive, yet inconclusive, thatexposure to these VOCs (PCE, TCE, DCE) through drinking water may cause birth defects or childhoodleukemia in children exposed while a fetus.

For 1,2-DCA and methylene chloride, there is little evidence for increased susceptibility of children toexposures. The one case report of a child who was exposed to high levels of 1,2-DCA showed similareffects as adults and animals. From animal studies, there is evidence on the potential susceptibility ofchildren to effects on their immune system, particularly after large dose ingestion exposures, forexample, with accidental ingestion of household products that contain 1,2-DCA. 1,2-DCA can crossthe placental barrier and has been detected in breast milk. However, neither laboratory studies withanimals nor human epidemiological studies have found clear evidence for the association of 1,2-DCAwith developmental effects. One study in New Jersey claimed a positive association between ingestionof 1,2-DCA in drinking water and cardiac birth defects [107]. The results of this study are limitedbecause there was simultaneous exposures to other chemicals in the water supply. There is no evidencefrom either human or animal studies that children are, or are likely to be, more susceptible than adultsto inhalation, oral, or dermal exposure to methylene chloride [66,69].

Vinyl chloride has the potential to affect fetuses and young children more seriously than adults for thesame reasons that PCE, TCE, and 1,2-DCE are of concern for very young children. Vinyl chloride cancross the placental barrier and enter the blood of the fetus [61]. Animal studies have shown that subjectsexposed before adolescence or during pregnancy may have a greater death rate and increased likelihoodof developing cancer than adult animals exposed for similar periods. However, this may simply reflectthat younger animals have a longer time for the effects of the exposure to be manifested, not increasedsensitivity [61].

The susceptibility of children to toxic chemicals is a new field of research so precise estimates ofincreased risk for developmental effects are not available. If young children or pregnant women residedin the homes with contaminated wells along Watson Corner Road, there is a chance that exposures toPCE, TCE, and 1,2-DCE could have affected the health of the children or developing fetuses. Thehomes with the highest contamination and, hence, the greatest risk were lots 7, 9, 11, and 18 (Tax mapR-19). The well serving lot 7 (Tax map R-19) contained vinyl chloride at concentrations capable ofaffecting the health of adults. The latest residents of this house did not have children. However, ifprevious residents had young children and the exposures were the same, the children or developingfetuses could have experienced more severe health effects than the adults.

(ix) Summary of the Private Drinking Water Well Pathway

Currently, there are no significant exposures to contaminants in drinking water. All of the residents nearthe landfill either receive water from the town supply or are served by a well where any contaminationis below a level of health concern. A groundwater management zone will be established for the site andcontaminated neighboring properties, which will restrict the use of groundwater in this area and preventfuture exposures. DHHS recommends that all drinking water wells in the future groundwatermanagement zone be permanently removed from service (i.e., physically removed or sealed) to preventinadvertent use of the contaminated water. Furthermore, all private wells around the perimeter of thiszone should be tested yearly.

In the past, there were exposures to several VOCs in five of the private wells near the site. The mostserious exposures were for the residents of Lot 7 (Tax map R-19) where exposure to vinyl chloridecould potentially cause non-cancerous effects on the liver and a low to moderate theoretical risk ofcancer, particularly angiosarcoma of the liver. For the other four wells, the known exposures wereunlikely to result in non-cancer health effects for adult residents. However, young children ordeveloping fetuses could have been affected by the exposures. Also, there would be a low theoreticalrisk of cancer from long-term (i.e., 10-year) exposures to PCE, TCE, and 1,2-DCE in the wells servinglots 9, 11, and 18 (Tax map R-19). It is not known whether any residents of these houses lived therelong enough or if the contamination began early enough for such long-term exposures to occur.

The drinking water well that served the Peaceful Pines Mobile Home Park up until 1995 was notaffected by contamination at the site. The park currently receives water from the Town of Farmingtonmunicipal supply.

Therefore, following ATSDR's health hazard categories (see Appendix G), this pathway was a publichealth hazard in the past for five private wells along Watson Corner Road. However, currently and inthe future, this pathway would be classified as no public health hazard, because there is no exposure.


(2) Soil Gas to Indoor Air Pathway

Based on the soil gas test results and the modeled comparison values, there is currently only one areanear the site where soil gas contamination could potentially affect indoor air quality: the buffer zonebetween the mobile home park and the landfill. Up until 1999, there were three homes in this bufferarea that were occupied. Currently, two of the homes have been moved and the third has beenunoccupied since February 1999. Therefore, there are no current exposures by this pathway.

Exposures to contaminants were possible in the past, however. The indoor air of these homes was tested in 1999 and 2000 to characterize recent indoor air exposures. The compounds that exceeded comparison values in any tests are summarized in the following table.

Compound Average Concentration (ug/m3) Maximum Concentration (ug/m3) Comparison Value (ug/m3)Source1
Methylene chloride2.55.51000MRL
Benzene1.62.49NCEA
Chloromethane 4.311100MRL
Formaldehyde557910MRL
Acetaldehyde4.85.59RfC
Hexanal (Hexaldehyde) 4.14.5NANA
MIBK142380HEAST
Toluene26862000MRL
Carbon Tetrachloride0.70.7300MRL-int
1,4-Dioxane 7.37.3NANA
Notes:
1. MRL-chronic = ATSDR's Minimal Risk Level for chronic exposures (lasting longer than 1 year)
MRL-int = ATSDR's Minimal Risk Level for intermediate exposures (lasting longer than 14 days but less than 1 year)
MRL-acute = ATSDR's Minimal Risk Level for acute exposures (lasting less than 14 days)
RfC = EPA's Reference Concentration for chronic exposures
HEAST = Reference Dose from EPA's HEAST Tables FY97.
NCEA = Provisional Reference Concentration from EPA-NCEA.

Conditions before 1999 may have been different but there are no data that would allow pre-1999exposures to be estimated. Groundwater contamination near these homes was considerably higher inthe previous decade (particularly 1989-1997) which could have caused more serious indoor air contamination in these and other nearby homes.

(i) Methylene Chloride
Soil Gas to Indoor Air Pathway

ATSDR has derived an MRL for chronic exposures to methylene chloride in air of 1000 microgramsper cubic meter (ug/m3). This MRL was derived from a study of workers who were exposed torelatively high concentrations of methylene chloride at 30,000 ug/m3 (adjusted average) for more than10 years. Comparisons to a similar population did not reveal any differences in symptoms or adversehealth effects in the exposed population as judged by selected liver, cardiac, and neurologic healthparameters [66]. The measured concentrations of methylene chloride in the three homes (5.5 ug/m3,maximum) were at least 150 times less than the MRL and 5000 times less than the level that did nothave an effect on humans. Therefore, non-cancer health effects are not expected from this exposure.

As discussed in the earlier, NTP has classified methylene chloride as being reasonably anticipated tobe a human carcinogen. The only information on methylene chloride carcinogenicity in humans is fromstudies of occupational exposures which have produced conflicting results. In animal studies, inhalationof very high concentrations of methylene chloride has produced liver and lung tumors [66]. However,using the quantitative estimates of cancer risk derived by EPA from these studies, exposure to theconcentrations measured in the homes would not result in appreciable theoretical cancer risks for residents.

(ii) Benzene
Soil Gas to Indoor Air Pathway

The most noted systemic effect resulting from intermediate and chronic benzene exposure is on theblood. Specifically, a causal relation exists between benzene exposure and aplastic anemia in humans. This disorder is characterized by reduction of all cellular elements in the peripheral blood and bonemarrow. Aplastic anemia that results from benzene exposure is also associated with an increased riskof developing acute non-lymphocytic leukemia [62].

EPA has derived a draft RfC of 9 ug/m3 for chronic exposures to benzene. This value was calculatedfrom an occupational study that observed effects on blood cell counts in workers at 8,600 ug/m3(adjusted) [39]. The results of this occupational study are reliable because the benzene exposure levelswere monitored and there was little concomitant exposure to other solvents. The concentrationsmeasured in the homes were less than 2.4 ug/m3 and therefore were below the RfC and well below thelevel at which effects were observed, hence, non-cancer adverse health effects are not expected from thisexposure.

Benzene is a known human carcinogen. Data from both humans and animals indicate that benzene and/or its metabolites are capable of damaging genetic material in cells. Epidemiological and case studies of occupational exposures consistently correlate benzene exposure with acute non-lymphocytic leukemia [62]. However, using the upper-bound of the EPA's inhalation cancer potency factor for benzene, exposures to benzene at the measured concentrations would not be expected to result in any appreciable theoretical cancer risk. There is also strong evidence that there is a non-linear threshold for the carcinogenic effects of benzene which is much higher than the concentrations measured in the indoor air [104].

(iii) Chloromethane
Soil Gas to Indoor Air Pathway

The CNS, liver, and kidney are the major targets of chloromethane toxicity in both humans and animals.

ATSDR's chronic MRL for chloromethane (100 ug/m3) is based on CNS effects. Laboratory studieswith mice observed swelling and degeneration in the spinal nerves at a concentration of 100,000 ug/m3[67]. The concentrations in the houses were all less than 11 ug/m3, which is 10 times less than the MRLand 10,000 times less than the lowest level at which effects were observed. Therefore, non cancer healtheffects are not likely from this exposure.

Chloromethane exposure has been associated with kidney tumor development in male mice. However,carcinogenic effects were not observed in similarly exposed female mice or male and female rats. Therefore, the evidence that chloromethane is a carcinogen is limited. It is not known whether cancercould develop in humans exposed to chloromethane by any route [67]. Using EPA's cancer slope factorfrom the animal studies, the exposures in the indoor air of the homes would not present any appreciable theoretical risk of developing cancer.

(iv) Aldehydes (Formaldehyde, Acetaldehyde, Hexanal)
Soil Gas to Indoor Air Pathway

Although formaldehyde is commonly produced by cells in the body, it is still a highly reactive moleculethat can be directly irritating to tissues with which it comes into contact. Human and animal studiesindicate that formaldehyde can be irritating to the upper respiratory tract and eyes with inhalationexposure, to the skin with dermal exposure, and to the gastrointestinal tract with oral exposure. Studiesof animals exposed for life to formaldehyde in air or drinking water also show that formaldehydeprimarily damages tissue at portals-of-entry (i.e., the upper respiratory tract and the gastrointestinaltract); evidence for toxic effects at internal organs is less consistent. The apparent restriction offormaldehyde-induced non-cancer and cancer effects to portals-of-entry is consistent with the highlyreactive nature of formaldehyde and the existence of physiological mechanisms of protection, such asthe nasal mucosal barrier and a detoxifying metabolism of formaldehyde in most, if not all, cells [68]. Based on their chemical structure, acetaldehyde, hexanal, and other aldehydes are expected to bemetabolized by the body in the same manner as formaldehyde and have similar, if less severe, toxiceffects.

ATSDR has derived a chronic MRL for formaldehyde of 10 ug/m3. This is based on observations ofcellular changes in the nasal tissue of workers exposed to formaldehyde at 300 ug/m3 [68]. EPA hasnot established an RfC for formaldehyde but does support an RfC for acetaldehyde of 9 ug/m3. Similarto the MRL for formaldehyde, the RfC for acetaldehyde is based on observed effects on epithelial cellsof the nasopharyx in animals [40]. No minimal risk levels have been established for hexanal but itseffects are expected to be less severe than those from formaldehyde or acetaldehyde because it is alarger, and less reactive, molecule.

The measured concentrations of formaldehyde in the three homes averaged 55 ug/m3 and had amaximum value of 80 ug/m3. Acetaldehyde and hexanal both had average concentrations around 5ug/m3. Combining the concentrations of all the aldehydes yields a total aldehyde concentration of 65ug/m3 on average and less than 100 ug/m3 at maximum values, most of which is formaldehyde. Theseconcentrations (~100 ug/m3) are higher than the formaldehyde MRL and close to the concentration atwhich effects were observed in humans (300 ug/m3). Therefore, some reversible irritant effects of theupper respiratory tract and eyes are possible for sensitive individuals.

NTP considers formaldehyde to be reasonably anticipated to be a human carcinogen primarily basedon studies with laboratory animals. Studies with humans, specifically medical specialists who work withformaldehyde, found very small risks of developing nasopharyngeal cancer, but the results wereequivocal and contradictory between different studies [68]. Animal studies have produced conclusiveresults that rats exposed to high concentrations of formaldehyde develop nasal tumors. However, thetumors were only observed at the high concentrations that already damage the nasal epithelial cells(12,000-18,000 ug/m3), and not at lower exposure concentrations (400-2,000 ug/m3) [68]. Exposureto high concentrations for prolonged periods overwhelms or otherwise exhausts the inherent defensemechanisms to formaldehyde [68]. Cellular and tissue damage inflicted by unmetabolized formaldehydeis then followed by regenerative cell growth that may lead to cancerous tumors [68]. The measuredconcentrations of aldehydes in the homes were 100 times lower than the levels that have producedcarcinogenic by this mechanism. Therefore, these exposures are not likely to result the cellular damagethat could lead to nasal tumors. Furthermore, even if it is assumed that carcinogenic effects are possibleat the relatively low concentrations measured in the homes, the theoretical cancer risk would be lowbased on EPA's cancer slope factor for formaldehyde [40]. Quantitative estimates of cancer potencyby EPA show that acetaldehyde is a less potent carcinogen than formaldehyde [40]. No estimates of thepotency of hexanal are available, but its chemical structure does not indicate any increased potencyabove and beyond that of formaldehyde, and it is probably less potent.

Formaldehyde is not exclusively a "site contaminant" because it is an expected constituent of indoor airin homes with pressed wood products (e.g., manufactured homes) [68]. In 1987, an EPA survey ofrandomly-selected mobile homes measured mean formaldehyde concentrations in the range of 112-761ug/m3. Several steps to reduce formaldehyde emissions from building materials have been enacted sincethat survey. However, a pilot study in 1996 still found formaldehyde at 43-554 ug/m3 in the air of anewly constructed home [68]. In 1999, the median formaldehyde concentration in indoor air of homestested for the National Human Exposure Assessment Survey Pilot Study was 21 ug/m3 [47]. Theaverage formaldehyde concentration measured in the homes near the landfill was 55 ug/m3, which represents the combined effects of formaldehyde sources both inside and outside the homes.

(v) Methyl Isobutyl Ketone (MIBK)
Soil Gas to Indoor Air Pathway

MIBK is an eye, skin, and respiratory tract irritant and a CNS depressant [83]. The availabletoxicological information on related compounds, MEK and acetone, confirms that irritant and CNSdepression are the primary effects of this class of compounds, but also suggests moderate toxicity to theliver, blood, and kidneys. There is no evidence for carcinogenicity for this class of compounds [59].

EPA formerly supported an RfC for MIBK of 80 ug/m3 based on increased liver and kidney weights inrats. This was based on a study in which no effects were observed at 200,000 ug/m3 [38]. Even thoughthis RfC is no longer supported by EPA, it is the basis for the indoor air screening values published byEPA Region III [41] and DES [43]. The maximum measured concentration (23 ug/m3) was below theold RfC and was 9000 times below the "no effects" level. For MEK, which is the most closely relatedchemical, EPA has derived a RfC of 1000 ug/m3 to be protective of developmental effects fromexposures in utero based on laboratory studies with rats. The level at which no effects were observedin this study was approximately 3,000,000 ug/m3 [40]. Therefore, the measured concentrations of MIBK appear to be below levels of health concern.

(vi) Toluene
Soil Gas to Indoor Air Pathway

Long-term damage to the CNS is the prime concern associated with chronic human exposure to highlevels of toluene. Occupational data suggest that chronic toluene exposure impairs behavioral function. ATSDR's chronic MRL for toluene (2000 ug/m3) is based on study of two groups of workers exposedto toluene at average concentrations of 43,000 and 157,000 ug/m3, respectively. Decreased cognitiveperformance was observed in both groups [65]. The concentrations measured in the homes were lessthan 86 ug/m3. Therefore, these types of effects are not expected from the exposure.

Human and animal studies generally do not support a concern for the carcinogenicity of toluene [65].

(vii) Carbon Tetrachloride
Soil Gas to Indoor Air Pathway

The principal effects of carbon tetrachloride in humans are on the liver, the kidneys, and the CNS.ATSDR has established a minimal risk level for carbon tetrachloride for intermediate exposures at 300ug/m3. This is based on laboratory studies that did not observe effects on the livers of rats at 30,000ug/m3 exposure [57].

Carbon tetrachloride was measured at 0.7 ug/m3 in the indoor air of one home in May 1999. However,it was not detected in the soil gas or crawl space air near or beneath that home. The air tests in Februaryand March 2000 did not detect this chemical in any media (e.g., soil gas, crawl space air, indoor air, oroutdoor air). Carbon tetrachloride has been detected in the groundwater on the site, but infrequentlyand only in monitoring wells away from the mobile home park (MW5, SW111). Therefore, thesampling data does not suggest sustained exposures to this chemical in the indoor air. Furthermore, theconcentrations that were measured were at least 10,000 times lower than those at which no effects wereobserved in laboratory experiments with animals. Therefore, no adverse health effects are expected.

NTP has determined that carbon tetrachloride may reasonably be anticipated to be a carcinogen. Thereis convincing evidence from studies that oral exposure to carbon tetrachloride leads to hepatic tumors.Because the same kinds of noncarcinogenic effects are observed in the liver following oral andinhalation exposure, it seems likely that inhalation exposure could lead to liver cancer under theappropriate conditions [57]. However, using upper-bound estimates of cancer potency by the oral route,and assuming that the concentration of carbon tetrachloride measured in the indoor air stayed constant,this exposure would not result in any appreciable theoretical risk of cancer.

The major current use of carbon tetrachloride is in the production of chlorofluorocarbons, such as Freon11 and Freon 12, which are primarily used as refrigerants [57]. In 1991, production of carbontetrachloride in the U.S. was 315 million pounds [57]. Production in recent years has been decliningfollowing the adoption of an international agreement (the Montreal Protocol) to reduce concentrations of chlorofluorocarbons and other chemicals due to their effects on the atmospheric ozone layer [57].

(viii) 1,4-Dioxane
Soil Gas to Indoor Air Pathway

1,4-Dioxane is an irritant and CNS depressant, and may cause effects on the kidneys and liver [82]. Upper respiratory tract and eye irritation have been noted at 1,000,000 ug/m3 in humans [82], whichis 100,000 times higher than the concentration measured in the home (7.3 ug/m3). Therefore, no adverse health effects are expected from the exposure.

EPA has classified 1,4-dioxane as a probable human carcinogen based on laboratory studies in whichanimals developed nasal cavity, liver, and gall bladder carcinomas following high-level exposure to 1,4-dioxane in drinking water [40]. However, the carcinogenicity of this chemical by the inhalation route has not been determined.

1,4-Dioxane is used primarily as a solvent in such widely used products as paints, varnishes, lacquers, cosmetics and deodorants [84].

(ix) Combined Effects of Chemicals with Similar Toxicological Properties
Soil Gas to Indoor Air Pathway

Some of the chemicals detected in the indoor air at levels of concern have similar toxicologicalproperties or endpoints. For these groups of similarly acting chemicals, their individual effects shouldbe combined to determine if there is a cumulative risk from exposure to multiple chemicals. In thissection, groupings of similar compounds are discussed and their cumulative effects evaluated.

Methylene chloride, chloromethane, and carbon tetrachloride have similar chemical structures andtoxicological properties. They are all single-carbon, chlorinated aliphatic compounds that produce toxicbyproducts when they are metabolized in the liver. The specific metabolites are different for each of thecompounds, but the organs affected by them are the same: the CNS, liver and kidney. Of the threecompounds, the lowest MRL or RfC is the MRL for chloromethane of 100 ug/m3, which is based onobservations of CNS effects in mice. Adding the concentrations of methylene chloride, chloromethane,and carbon tetrachloride together, the maximum combined concentration of the three chemicals was17.2 ug/m3. Given that this combined exposure is less than the most sensitive MRL, itself built upona 1000 fold safety factor, simultaneous exposure to these three chemicals is not expected to produceCNS, liver, or kidney effects. Furthermore, using the cancer potency factors from EPA, the combinedcancer risk from exposures to the three chemicals at once would not result in an appreciable theoreticalcancer risk.

Although toluene and MIBK have different chemical properties (toluene is aromatic, MIBK is a ketone),they have similar toxic endpoints and appear to affect the body in the same way. Both chemicals aretoxic in their original form. Metabolism by the mixed function oxidase pathway produces non-toxicbyproducts that are excreted from the body. Neither chemical has a demonstrated potential forcarcinogenicity. The primary effect of both chemicals in humans is depression of the CNS. The lowesthealth comparison value for these compounds is the retired RfC from EPA of 80 ug/m3 based on liverand kidney increased weights. The maximum combined concentrations of toluene and MIBK wouldhave been 109 ug/m3, which exceeds the old RfC. However, no effects were observed in the animalsat concentrations as high as 200,000 ug/m3. Therefore, the combined exposures of these two chemicalsare not likely to result in adverse health effects.

While the combined exposures of MIBK and toluene are not of concern, there is evidence that ketones,like MIBK, can increase the effects of chlorinated aliphatics, particularly carbon tetrachloride [59]. Although precise mechanisms for this potentiation are not well understood, it is likely that mostpotentiators act, at least in part, by increasing the metabolism of carbon tetrachloride to its toxicintermediates, thus increasing injury [57]. The concentrations of acetone (a ketone) at which thesepotentiating effects were observed in laboratory studies were very high (6,000,000 ug/m3) [59]. So, theeffects of ketones on carbon tetrachloride toxicity are not expected to be significant at this site. However,heavy drinkers and diabetics may be more susceptible to the effects of exposure to chlorinated solventsbecause these conditions increase the endogenous concentrations of ethanol and ketones in the body.

All of the aldehydes (e.g., formaldehyde, acetaldehyde, and hexanal) have similar toxicologicalproperties thus their effects should be combined, which was described in the preceding section.

Benzene has a unique metabolism and toxicological endpoint (acute non-lymphocytic leukemia)compared to the rest of the compounds. The metabolites of benzene that are thought to be the toxicagents are phenol, catechol, hydroquinone, and muconaldehyde [62]. Benzene has been observed tointeract with other chemicals that are present at the Cardinal Landfill, especially ketones. Animals thatwere exposed to acetone (a ketone) at very high doses (863 mg/kg-d) had an order of magnitudeincrease in cytochrome P-450 enzyme activity in the liver and bone marrow. This was taken asevidence that exposure to ketones (e.g., MIBK, MEK, acetone) could increase the effects of benzene byincreasing the activity of the enzyme that metabolizes benzene [59]. The exposures to acetone in thestudy were very high (equivalent to air concentrations of 3,000,000 ug/m3) in order for this effect to beobserved, and hence, are probably not relevant to exposures by this pathway at the Cardinal Landfill.The maximum concentrations of MIBK, MEK, and acetone in the indoor air were 23, 44, and 110 ug/m3, respectively.

There is not enough information on the mode of action for 1,4-dioxane to make any conclusions aboutinteractions between this chemical and the others. However, in light of the very low concentrations ofthis chemical in the indoor air, the combined effects of this chemical with others is expected to be minimal.

(x) Children's Susceptibility
Soil Gas to Indoor Air Pathway

As stated previously, when evaluating chemical exposures, it is important to consider whether childrenwould be more or less susceptible to the effects of the exposure than adults. Special considerations forvery young children or developing fetuses will be discussed for each chemical in this section.

There is no evidence from either human or animal studies that children are, or are likely to be, moresusceptible to inhalation, oral, or dermal exposure to methylene chloride than adults. [66]

Epidemiological studies implicating benzene as a developmental toxicant have many limitations, andthus it is not possible to assess the effect of benzene on the human fetus. In animal studies, benzene hasnot been shown to be teratogenic (i.e., causing birth defects), but has been shown to be toxic to the fetus(i.e., "fetotoxic") at high concentrations that are also maternally toxic [62].

There are no human studies to determine whether children are more or less susceptible to the effects ofchloromethane than adults. Animal studies have shown that mid-to-high exposures (greater than1,000,000 ug/m3) during pregnancy resulted in offspring that were smaller than normal, withunderdeveloped bones, and possibly abnormal hearts. However, the developmental toxicity ofchloromethane is controversial and it is not known whether chloromethane could produce these samedevelopmental effects in humans [67].

Formaldehyde exposure is expected to elicit in children the same type of effects that occur in adults (e.g.,damage to portal-of-entry tissues at exposure levels that exceed tissue detoxification mechanisms).Symptoms expected to occur in children include eye, nose, and throat irritation from exposure toairborne concentrations between 500 and 4000 ug/m3, and dermal irritation from dermal contact withliquids containing more than 2% formaldehyde. The developing fetus or nursing infant would beexpected to be protected from exposure to formaldehyde by the pregnant or breast-feeding mother.Studies of animals exposed during pregnancy to formaldehyde in air, in the diet, or by the oral routehave found no distinct or consistent effects on fetal development even at exposure levels that producedsevere maternal toxicity [68].

There are some studies, however, that show that children may be more sensitive to the irritant effectsof formaldehyde. One study found an increased prevalence of physician-diagnosed chronic bronchitisor asthma among children exposed at 70 ug/m3, but not among similarly exposed adults. In anotherstudy with schoolchildren, there were reports of respiratory symptoms at concentrations as low as 50ug/m3, that went away with removal from the building [68].

There is very limited information available on the toxicity of MIBK for young children or fetuses.Exposures of pregnant rats and mice up to 7,000,000 ug/m3 by inhalation did not cause an increase inbirth defects in the offspring [83]. Toxic effects on the fetus were noted at the highest doses, which werelevels that were also maternally toxic [83]. A more extensive database is available for another ketone,acetone. Acetone appears to be toxic to rat and mouse fetuses at maternally toxic inhalationconcentrations. From limited information, acetone does not appear to be teratogenic in animals in invivo experiments. Whether acetone would cause developmental toxicity in humans under any exposureconditions is not known, but concentrations and doses used in the animal studies were much higher thanare likely to be experienced by humans [59]. Diabetics may be more susceptible to the effects of acetone[59].

Toluene has been shown to affect the developing fetus following exposure of pregnant women eitheroccupationally or as a result of solvent abuse. Developmental and behavioral effects have beenobserved in children who were exposed to toluene in utero as a result of maternal solvent abuse duringpregnancy. However, the exposure levels at which these effects were observed were very high andproduced maternal toxicity. Overall, it is not possible to state whether children would be more or lesssusceptible to the neurological effects of toluene [65].

In animals, no teratogenic or fetotoxic effects were observed in rats exposed to carbon tetrachloride either by inhalation or ingestion except at doses that produced clear maternal toxicity [57].

1,4-Dioxane was toxic to fetuses in rats (but only at levels toxic to the mothers) and was teratogenic inchicks. Since rats are mammals, the rat study is more relevant to humans. The actual human reproductive hazard is unknown [82].

Therefore, for the suite of chemicals of concern in the indoor air, developmental effects are not expectedexcept at high concentrations that would likely produce maternal toxicity. Young children may be more sensitive to the irritant effects of aldehydes.

(xi) Summary of the Soil Gas to Indoor Air Pathway

Currently, there are no exposures to site contaminants in the indoor air. The section of the PeacefulPines Mobile Home Park where this exposure pathway was recently completed was purchased byTextron in 1999 to create an undeveloped buffer zone between the landfill and the park. One house stillremains in this buffer zone area but it has not been occupied since February 1999. Therefore, accordingto ATSDR's health hazard categories, this pathway is classified as no public health hazard currently.

In the recent past (1999), there were three occupied homes in the buffer zone area of the park whereindoor air exposures were possible. However, based on indoor air quality tests, exposures to chemicalsfrom the site were unlikely to result in adverse health effects or an appreciably increased risk of cancer.Exposures to formaldehyde may have caused reversible irritation of the upper airway and eyes foryoung children or other people who are sensitive to this type of chemical. Formaldehyde is notexclusively a "site contaminant" because it is an expected constituent of indoor air of homes withpressed wood products (e.g., manufactured homes) [68]. Therefore, for the recent past (1999), theindoor air pathway would be classified as no apparent public health hazard.

In the previous decade (particularly 1989-1997), groundwater contamination near the buffer zone wasmore severe, which could have resulted in higher concentrations of contaminants in the indoor air of thenearby houses. Exposures during this period cannot be estimated because no indoor air or soil gasmeasurements were taken in this area prior to 1999. Therefore, indoor air exposures before 1999 maywell have been higher than those observed in 1999-2000 but are uncertain and, thus, are classified asan indeterminate public health hazard.

DHHS recommends frequent monitoring of soil gas on the site, along Watson Corner Road, in the bufferzone, and, if necessary, in the mobile home park to guard against any future exposures due to migrationof contaminated soil gas into developed areas.


(3) Ambient Air

Five chemicals were detected at levels of potential health concern in the ambient air. All of thesechemicals were also detected in the indoor air at similar or lower concentrations. For instance,formaldehyde concentrations outdoors (1.2 ug/m3) were considerably lower than indoors (55 ug/m3 onaverage). Average long-term background concentrations of formaldehyde in the ambient air areestimated to be 0.2 ug/m3 [68]. Due to the considerable dilution within the atmosphere, it is unlikelythat ambient air concentrations would have been much higher in the past, even if contamination on thesite had been more severe. However, the concentrations of chemicals in smoke from fires that occurredon the site in the past are unknown.

Since indoor air exposures were not expected to produce health effects, exposures to chemicals in theoutdoor air are likewise not expected to affect people's health. Therefore, according to ATSDR's healthhazard categories, this pathway is considered no apparent public health hazard.


(4) On-Site Soils and Sediments

In 1982-1984, transient puddles and streams on the site contained relatively high concentrations ofsolvents that had leached out of the waste. In later years, concentrations of these chemicals in thepuddles were below comparison values for drinking water. Contamination was detected in a few soilsamples from the site at concentrations above residential soil comparison values. The public could beexposed to the soil and water contamination only if they were to trespass on the site. However,occasional and non-intensive exposures while trespassing (e.g., riding an all-terrain vehicle) are not likely to affect a person's health.

Therefore, soil and surface water contamination on the site is considered no apparent public health hazard according to ATSDR's health hazard categories.

DHHS recommends that the site remain fenced and signs be posted to prevent the public from entering as a prudent public health precaution.


(5) Cocheco River Surface Water and Sediments

Contaminated groundwater from the site discharges to the Cocheco River near the Watson Corner Roadbridge. The groundwater is diluted by water in the stream but could potentially contaminate the river. In a similar manner as on-site surface waters, the Cocheco River water contained relatively highconcentrations of VOCs in 1982-1984. Recent tests, and tests generally since 1986, have not foundcontamination at concentrations greater than drinking water comparison values. Tests of the sedimentquality in 1990 and 1998 detected toluene and PCE but below health comparison values. People whoswim or wade in the stretch of river could have been exposed to contamination in the past. However, infrequent use of the river would not have resulted in exposures of health concern.

Therefore, following the ATSDR's health hazard categories, this pathway is considered no apparent public health hazard.

DHHS recommends that the water and sediment quality of the river should continue to be monitored until discharges of chemicals from the site are eliminated.


(6) Cocheco River Fish

Fish in the Cocheco River were tested in 1986. No contamination was found at concentrations greaterthan health comparison values, but the quality of the test results is questionable. However, surfacewater and sediment tests in the river have only sporadically detected contamination at concentrationsgreater than drinking water comparison values in the past. Recent tests did not detect any surface wateror sediment contamination at concentrations greater than comparison values. Furthermore, thepredominant contaminants at the site, VOCs, are not likely to accumulate in fish tissue due to theirphysical-chemical properties [59-61,63-66]. Therefore, despite the limitations of the fish tissue data,DHHS does not believe that consuming fish from the Cocheco River would result in exposures to sitecontaminants at levels of health concern. Following ATSDR's health hazard categories, this pathwaywould be considered no apparent public health hazard.

DHHS has a state-wide advisory for the consumption of freshwater fish from New Hampshire waterbodies to protect the public from mercury, a contaminant that is found in fish throughout the state. Thegeneral population is advised to limit their consumption to four 8-ounce meals per month. Women whoare pregnant or who may become pregnant, and women who are breastfeeding their children should onlyeat one 8-ounce meal per month. Children under the age of 7 should only eat one 3-ounce meal permonth. However, it is important to remember that fish is still an important part of a healthy diet. Fishare high in protein and low in saturated fat and cholesterol.

Regular water and sediment monitoring of the river, as recommended by DHHS in the previous section,would detect any increased contamination in the river that might produce elevated concentrations ofcontaminants in fish tissues.




(B) Health Outcome Data Review

(1) Methodology

The health outcome data evaluation for the Cardinal Landfill site is based on an analysis of availablecancer data from the New Hampshire State Cancer Registry (NHSCR). The NHSCR maintainsstatistics regarding twenty-three types of cancer for all cities and towns in New Hampshire. Cancer datafor Farmington was requested for all 23 types of cancer in an eleven-year time period of the most recentyears that cancer incidence rates were available (1987 through 1997) from the Bureau of HealthStatistics and Data Management, which maintains a close working relationship with the NHSCR. Theeleven-year time period, twice the duration typically reviewed, was selected to ensure that disease trendscould be calculated for a community with a relatively small overall population (1990 census population:5,755).

Once the data were received, they were reviewed for potential data quality issues. After conferring withthe NHSCR regarding specific issues with this data set, a total of 18 cases were removed from theoriginal data set of 273. The data that were removed included one case for which multiple primarytumors were recorded but could not be confirmed by NHSCR. For six cases, the primary tumor couldnot be confirmed. Two cases were removed due to incomplete records. In comparing the cases that were removed to the rest of the data set, the following differences were observed.

  Full Data Set Removed Data
Mean Age: 62 years old 74 years old
Males 46.7% 22.2%
Females 53.3% 77.8%
Primary Diagnosis: No significant difference between full data and removed data

Three statistical tests were performed comparing the removed data to the rest of the data set: (1) anindependent samples T-Test for age at diagnosis; (2) a Fisher's Exact Test for gender; and (3) a MonteCarlo Estimate for primary diagnosis. There are differences between the full data set and the data thathas been removed, however the only statistically significant difference is for mean age at diagnosis. Thereason for this difference is unknown. However, the fact that there is a difference will not affect theoverall results of the health outcome data review because the primary variable of interest is primarydiagnosis, which showed no significant difference between the full data set and the data that wereremoved.

Following this data quality review, a descriptive epidemiological analysis was conducted using theStandardized Morbidity Ratio technique (SMR). A detailed discussion of this technique is available inAppendix E. The data were reviewed for each type of cancer reported in Farmington according to thefollowing factors: sex and age (0-14, 15-24, 25-34, 35-39, 40-44, 45-49, 50-54, 55-59, 60-64, 65-69,70-74, 75-79, 80-84, and 85+ years). The SMR analysis was divided into two separate time periods,data from 1987-1992 and data from 1993-1997. This was done in order to make comparisons toexisting state rates for these same time periods. This process enabled us to review the observed numberof specific cancer cases, per cancer type, in Farmington and compare that value to the expected numberof cancer cases based on average rates for the State of New Hampshire.

DHHS relies heavily on the quality of the NHSCR cancer data to conduct descriptive epidemiologicalanalysis for the SMR calculations. There were no independent interviews of persons living inFarmington and no medical record reviews; therefore these analyses are subject to randommisclassification. It should also be noted that the SMR analysis is descriptive in nature and should notbe confused with an in-depth epidemiological study. However, while this method has limitations, itsatisfies the objective of the health outcome data review in that it can determine whether or not potential health impacts around the site would warrant further investigation.

(2) Results

The findings from our descriptive epidemiological analyses are illustrated in Tables 16, and 17 titled,"Cancer Incidence in Farmington, New Hampshire (1987-1992, 1993-1997)". The data is presented,by gender, in tabular form with the heading of each column describing the type of cancer, the expectednumber of cases for that particular type of cancer, followed by the observed number of cases for thatspecific cancer. A Standardized Morbidity Ratio (SMR) and 95% confidence interval (statistical tests)have been calculated for each type of cancer. Any types of cancer that have been omitted from the tablehave been excluded due to a value of less than 4 observed cases over the respective time periods(1987-1992, 1993-1997). This is done to conform to the Bureau of Health Statistics and Data Management's protocol on confidentiality in the release of cancer data.

After completing the SMR calculations, it was found that the rates for all cancer types except two were within the expected range at a 95% confidence interval. The cancer types that were found to be statistically elevated in Farmington between 1987-1992 and 1993-1997 were cervical cancer in females (SMR 8.21, SMR 6.03 respectively) and lung cancer in females 1987-1992 (SMR 2.13).

(3) Discussion

(i) Cervical Cancer

Cervical cancer is the second most common type of cancer among females worldwide [86]. In 2000,it is estimated that approximately 12,800 new cases of cervical cancer will be diagnosed in the UnitedStates, with 100 of those being diagnosed in New Hampshire [85]. There were approximately, 4,800deaths from cervical cancer nationally in 1999. In New Hampshire, the rate of cervical cancer over theperiod of 1993-1997 is 8 cases per 100,000 persons. Nationally, the Surveillance Epidemiology andEnd Results (SEER) program data for cervical cancer over the period of 1973-1997 indicates that forwhite females, the age-adjusted rate is 7.1 cases per 100,000 persons [89]. In New Hampshire, overthe period of 1987-1997 there were 660 new cases of cervical cancer reported. During that same period22 cases (or 3.3% of the New Hampshire total) were reported in Farmington.

Cervical cancer is a slow growing type of cancer, which begins in the tissues of the cervix. There aretypically no physical symptoms associated with cervical cancer until late-stage disease, however thereare medical tests that can be performed to determine the presence of the cancerous cells in the cervix[88]. The most common of these tests are pelvic exams and Pap Tests, which are completed in a clinicsetting by a gynecologist. Infection with the human papillomavirus (HPV), a sexually transmitteddisease (STD) which is found using the Pap Test, has been found to be the most significant risk factorfor the development of cervical cancer. Researchers have found that over 90% of all cervical cancertumors contain the HPV [90,91,92]. Other risk factors for cervical cancer include: (1) having firstintercourse at an early age, (2) multiple sexual partners or partners who have had multiple sexualpartners, (3) cigarette smoking, and (4) low socioeconomic status. [85,88] Currently the only knownchemical risk factor for cervical cancer is occupational exposure to tetrachloroethene. However, studiesthat have linked tetrachloroethene to the development of this disease are equivocal and have been basedonly on occupational exposure to high levels of this chemical as well as to simultaneous exposure tovarious other chemicals [64].

The five-year survival rate for invasive cervical cancer is 70%; however, for those cases of cervicalcancer detected in situ (confined to original tissues) the survival rate approaches 100%. Over the pastseveral decades, the incidence of cervical carcinoma has continued to decrease while survival rates haveincreased. This has been attributed to more frequent use of Pap screening, which detects early stagesof the disease when it is most curable [85]. The Pap test is a simple procedure that can be performedby a health care provider during a routine pelvic exam. It is recommended that this screening tool bestarted as soon as a woman reaches the age of 18 or when she first becomes sexually active [88].

For the early detection of cervical cancer, we suggest at least yearly screening by a health careprofessional for individuals who are considered at increased risk based on the risk factors discussedabove. For the general public, we support the recommendations of the American Cancer Society thatall women have a routine Pap test done by a health care professional as part of a pelvic exam. This testshould be performed annually with a pelvic exam in women who are, or have been, sexually active, or who have reached age 18.

In New Hampshire, the Breast and Cervical Cancer Early Detection Program located in the Departmentof Health and Human Services can provide further resources, educational information and outreachprograms related to cervical cancer (1-800-852-3345 ext. 4931). Also, the STD/HIV PreventionBureau within DHHS can provide information on all STD/HIV clinics in the State of New Hampshire. This bureau can be reached at (603) 271-4502.

(ii) Lung Cancer

Lung cancer is currently the second most common cancer for men and women in the United Statestoday. In 2000, it is estimated that approximately 164,100 new cases of lung cancer will be diagnosedin the United States, with 700 of those being diagnosed in New Hampshire [85]. Data from the SEERprogram for 1993-1997 reports the age-adjusted incidence of lung cancer in whites at 56.4 cases per100,000 persons. This can be compared to New Hampshire's overall age-adjusted incidence during thesame time period at 58.8 cases per 100,000 persons [89]. Overall trends in lung cancer incidence showthat males have a higher rate of disease than females but that over time both the incidence and mortalityin men has begun to decline. The incidence and mortality in females has also begun to show this sametrend, however only recently due to the fact that during the late 1980s and early 1990s, the incidenceof lung cancer in women was increasing at a higher rate than that of males [87,89]. This increase in therate of females experiencing lung cancer is likely due to social tolerance and/or acceptance of smokingamong females several decades ago, which in turn caused an increase in the numbers of women startingto use tobacco.

Lung cancer is defined as cancers that develop in the epithelial tissue in the lining of the bronchi,trachea, bronchioles and alveoli. Lung cancer is divided into two main types; small cell and non-smallcell lung cancer. Non-small cell is the most common of the two types (80% of diagnoses) with atendency to have slow growing tumors and less metastases (spreading) to other organs. Symptoms oflung cancer are a persistent cough, blood-streaked sputum, chest pain, recurring pneumonia andbronchitis, and swelling of the face and neck. However, symptoms do not usually become apparent untilthe cancer has progressed to an advanced stage. In persons who stop smoking, even after pre-cancerouscells have been found, damaged lung tissue can return to normal.

The single most important risk factor in the development of lung cancer is cigarette smoke [85]. It hasalso been shown that the amount of tobacco smoked per day, is directly proportionate to thedevelopment of lung cancer. Recent research suggests that women are at higher risk for tobacco-relatedlung cancer due to more frequent use of "light and ultra-light" type cigarettes. The higher rate of canceris thought to be due to the fact that women have been shown to inhale these types of cigarettes moredeeply than their male counterparts [93]. Other risk factors for lung cancer that are independent oftobacco use include: diet, family history, persons with tuberculosis, residential exposure to radon,various occupational exposures to substances such as arsenic, asbestos, chloromethyl ethers, chromium,mustard gas, nickel, and polyaromatic hydrocarbons [85,94]. Cigarette use in combination with theseoccupational exposures dramatically increases the risk of developing lung cancer.

Lung cancer is the number one cause of cancer mortality for both men and women with approximately,158,900 deaths nationally in 1999. The five-year relative survival rate for lung cancer is only 14%. The survival rate approaches 50% for cases where the disease is detected early, however the majorityof lung cancer is advanced by the time that it is diagnosed [84]. Although late-stage lung cancer canbe detected using a chest x-ray, there are no effective methods of screening the general population forearly-stage lung cancer. Therefore prevention is the main goal in the reduction of lung cancer incidence.

Further information about lung cancer can be obtained by contacting the American Lung Associationat (603) 669-2411. However, DHHS suggests smoking cessation programs for the prevention of lungcancer since it is largely preventable through the elimination of the use of tobacco. The TobaccoPrevention Program at the Department of Health and Human Services (603) 271-6892 can provideinformation regarding the various types of programs that are currently available.

(4) Summary of Health Outcome Data Review

The rates of 21 out of 23 cancer types in Farmington, New Hampshire between 1987 and 1997 werewithin their expected ranges at the 95% confidence level.

The rates of cervical cancer among females in Farmington were significantly elevated throughout theanalysis periods (1987-1992, 1993-1997). One of the main contributing causes to the development ofcervical cancer is concomitant exposure to the human papillomavirus [91,92].

Lung cancer in females (SMR 2.1) was found to be statistically elevated for Farmington during 1987-1992. It is unknown why there is an elevation among women for this time period. However, this trendwas not seen in a subsequent SMR analysis for the years of 1993-1997. Data for tobacco use, theprimary risk factor for lung cancer, was not available at the town level in New Hampshire; thereforeassumptions based on this risk factor could not be made.

Therefore, the elevated rates are not likely to be related to exposures to site contaminants.

For further information on the types of cancer discussed in this section please see the following websites:
National Cancer Institute
http://cancernet.nci.nih.gov
American Cancer Society
http://www2.cancer.org/crcGateway/index.cfm
1-800-ACS-2345

(5) Information on Other Health Outcome Data Sources

DHHS reviewed all possible ways to analyze health outcome data relevant to the Cardinal Landfill Site. It is our opinion that the most appropriate data evaluation that could be made, given the types of datathat the State of New Hampshire currently maintains, is the analysis of cancer data from the NewHampshire State Cancer Registry.

The other types of data that are currently available in New Hampshire are mortality data, hospitalinpatient and ambulatory care data, and state birth records. In some situations, analysis of particulardata types does not provide the answers that a community desires regarding exposure to a potentialcontaminant and the development of disease. Formal statistical analysis requires that certain standardsfor data selection be met for the appropriate calculation of results. Without these standards, data thatare analyzed and reported may not be statistically sound, thus producing results that do not reallyanswer the community's questions.

Mortality data is notoriously difficult to analyze because of both under reporting and misclassificationof the underlying cause of death [96]. This issue creates an uncertainty about the ultimate validity ofthe data to be analyzed. For example, the cause of death that is listed on a death certificate can oftentimes be the primary cause of death, such as pneumonia, even when the underlying cause of death maybe lung cancer. In other words, when a person dies from a complication of a disease rather than thedisease itself, under-reporting can occur. Another problem that is particular to cancer diagnoses, is thatmost individuals with cancer die when the disease metastasizes (spreads) to the other organs of the body. Often on death certificates, organs to which the originating cancer spread are labeled as the cause ofdeath, when in fact the originating organ is the true cause of death. This is referred to as amisclassification of the underlying cause of death.

Hospital data has many limitations to consider. First, it is based on the number of events (e.g. visits),not persons, at a given health care facility. This makes it impossible to estimate true population-basedincidence rates for a disease from these data. This is due to the fact that it is possible for persons to bedouble-counted during the course of an entire year's data collection, therefore when applying a ratederived from hospital data it will over-estimate the illness in the general population. Secondly, it mustalso be recognized that persons that are admitted into a health care facility are different from thepopulation as a whole. For the most part they can be considered to have more severe symptoms thanother persons who may have the same illness but have yet to consult a health care provider about theirhealth issues. For this reason, hospital data typically reports information about people with more severedisease, while excluding those with milder symptoms, thus underestimating the true number of peoplewith a disease. The hospitalized population may also be considered a bias group because of the factthat it represents a group of people who have access to health care facilities. Thirdly, a large andcomplicated set of standard codes is used to describe diseases and conditions in hospital data. Oftentimes, there are issues with hospital data regarding inconsistencies in coding from hospital to hospitaland within hospitals from staff member to staff member. Finally, in hospital data, case ascertainmentcan be compromised because of certain confidential variables that are not available for analysis withouta signed release form and a review of the patient's actual hospital record.

Overall, the use of birth records as a screening tool for infant mortality or morbidity is questionable[86,95]. When used as a variable within a rigorous epidemiological study, birth weight may be anappropriate measure to include as part of the analysis. However, a descriptive review of a state's birthrecords, using low-birth weight as a proxy for the development of adverse outcomes in children is inappropriate, because it is a non-specific health indicator.

For more information regarding the above mentioned data sets, please refer to the State of New Hampshire Bureau of Health Statistics and Data Management's website:
http://www.dhhs.state.nh.us/CommPublicHealth/HealthStats.nsf/vMain?Openview




(C) Community Health Concerns

When performing any public health assessment, DHHS gathers health concerns from people living inthe vicinity of the site. The health concerns that people express are then used to direct the focus of thepublic health assessment so that questions from the community are answered. At the Cardinal Landfill, DHHS accomplished this task through two activities:

  • On October 26, 1999, DHHS staff went door-to-door to distribute an educational needs assessment survey to the residents of the Peaceful Pines Mobile Home Park.
  • On November 16, 1999, DHHS held a public availability session at the Farmington Town Offices. Residents of the community were able to meet with DHHS and ATSDR staff, in a confidential setting, to discuss their health concerns and questions regarding the Cardinal Landfill. The public availability session was advertised through local media and a mass mailing.

Based on responses from the written survey and the availability session, the three most requested piecesof information were: (1) the site contaminants and possible exposure routes; (2) the extent ofcontamination; and (3) the adverse health effects that have been associated with exposures to the typesof chemicals present. This type of information is always included in a public health assessment and waspresented earlier.

The following is a list of the other questions that DHHS received while preparing the public healthassessment. Please see Appendix F for more information on DHHS' outreach activities in the community near the Cardinal Landfill.

(1) Health Concerns

  • Please describe the symptoms that have been associated with contaminants on the site.
  • How will our health be affected in the future from past exposures to site contaminants?

Reply: The major contaminants at the site are VOCs. In general, this class of chemicals isassociated with depression of the central nervous system in adults. Some of the contaminants canalso damage the liver and kidneys [60,64,65], and at least two of the chemicals on the site areknown human carcinogens [61,62]. The impacts of this contamination on the community aroundthe site depend on exposure to the chemicals. Please see the evaluation of specific exposurepathways in the text of this report.

  • Is this a real health concern? Would the Health Department live in this park?

Reply: Yes, there were significant exposures to site contaminants in the past. In particular, theresidents of five homes along Watson Corner Road were exposed to site contaminants in drinkingwater wells at concentrations greater than health comparison values. However, for these residentsand for the occupants of the Peaceful Pines Mobile Home Park, there are no current exposures tocontaminants that would be expected to result in adverse health effects.

  • Have any health related issues been traced directly to Cardinal Landfill?

Reply: No.

  • Can insomnia, headaches, diarrhea, and increased blood pressure be caused by exposure to site contaminants?
  • Can exposure to site contaminants increase stress?

Reply: While these issues are important, in general they are considered symptoms of many othertypes of conditions and not specific diseases in themselves. The effects of exposure from sitecontaminants cannot be evaluated separately from the other causes of these general symptoms.

  • Can exposure to site contaminants in the soil cause skin rashes?

Reply: Skin rashes caused by chemicals are most likely from exposures by the dermal route (skincontact with the chemical). This type of pathway is not currently significant at the Cardinal Landfillsite.

  • How can the chemicals from the site affect children? Are they more at risk?
  • Are there long-term health concerns for children? If so, what are they? We have grandchildren and are concerned about when they came over to visit on the weekends. Is it possible that their health could have been affected due to contamination from site chemicals?

Reply: At this site, there are two exposures to which children could be more susceptible than adults.First, exposure to contaminated drinking water in five wells along Watson Corner Road as eithera developing fetus or as a young child might result in long-term health effects. Four of the fivecontaminated wells were abandoned in 1985. The fifth, serving Lot 7, was abandoned in January2000. None of these wells served the mobile home park (see section V(A)(1)(viii)). Second, childrenmay also be more sensitive to the reversible irritant effects of formaldehyde in indoor air (please seesection V(A)(2)(x)).

  • Do any of the chemicals found affect diabetes?

Reply: VOCs, the predominant type of contaminant at the site, have not been associated with thedevelopment or exacerbation of diabetes. The major risk factors for diabetes vary by type. In TypeI, the risk factor is primarily hereditary predisposition to the disease. In Type II, the risk factorsinclude: persons over age 45, persons with a family history of the disease, persons who areoverweight, persons who do not exercise, persons with a low fiber or high fat diet, certain racial andethnic groups, and women who have previously had gestational diabetes [97].

For more information about diabetes, please see Appendix D.

  • Can exposure to the site contaminants affect an asthma condition?

Reply: Experts now believe that the vast majority of asthma prevalence is considered atopic (dueto an hereditary allergen). The most common indoor allergens are: dust mites; pet dander, salivaor urine; cockroach or rodent antigens; fungi and molds. Outdoor allergens are most often pollenand molds. Risk factors that have been associated with asthma in adults are thought to be exercise-induced asthma, stress-induced asthma, changes in air temperature, and occupational sensitizers.

Of the chemicals detected in the air near the site, the one with the greatest potential to affect anasthma condition is formaldehyde. High-level exposures to formaldehyde have induced adultasthma in some workers [73]. A recent study also found that exposures to more typicalconcentrations of formaldehyde in homes could increase the risk of allergic sensitization to commonaeroallergens in children, although the results were not statistically significant [98]. Finally,Kryzanowski et al. reported that children who lived in households with formaldehyde concentrationsgreater than 70 ug/m3 had greater prevalence of physician-diagnosed bronchitis or asthmacompared with children who lived in households with concentrations less than 70 ug/m3 [68]. Formaldehyde is not exclusively a "site contaminant" because it is an expected constituent of indoorair in homes with pressed wood products (e.g., manufactured homes) [68]. The averageconcentration of formaldehyde measured in the indoor air of homes near the site was 55 ug/m3.

For more information about asthma see Appendix D.

  • Can exposure to the site contaminants cause birth defects?

Reply: Currently, there are no exposures to contaminants from the site at levels of health concern. For each of the major exposure pathways at the site in the past, DHHS reviewed what is knownabout the susceptibility of young children and fetuses to the effects of the chemical. This includeda review of developmental effects as a result of exposures in utero (i.e., during pregnancy). For thedrinking water pathway, some of the chemicals, such as trichloroethene, have been associated withdevelopmental effects following in utero exposures [77]. Therefore, at the five residences alongWatson Corner Road with contaminated drinking water wells (lots 7, 9, 11, 17, and 18), pastexposures to chemicals had the potential to affect the developing fetus of any pregnant women livingthere before the wells were abandoned (between 1985 and 2000 depending on the well). For the soilgas to indoor air pathway, the chemicals of concern have only been associated with effects on afetus at high enough exposures to also have toxic effects on the mother. Indoor air concentrationsof this magnitude were not observed. However, there is uncertainty regarding past indoor airexposures because groundwater contamination near the buffer zone was higher in the past.

Please see sections V(A)(1)(viii) and V(A)(2)(x) for a more detailed discussion of child health issuesrelated to the major exposure pathways at the site.

  • Can exposure to the site contaminants cause kidney cancer?

Reply: Kidney cancer is one of the less common types of cancer and the exact cause for it isunknown. However, several risk factors that can clearly be attributed to an increased risk ofdeveloping this disease include: gender (kidney cancers occur more frequently in men as comparedto women) and smoking (smokers have double the risk of developing kidney cancer as compared tonon-smokers). Other risk factors that may be related to the development of kidney cancer are:genetic mutations through either a hereditary route or through later damage by a trigger such ascigarette smoke; people with tuberous sclerosis or von Hippel-Lindau syndrome; and persons onlong term dialysis. The incidence of kidney cancers also occurs more frequently in older adults andin persons who tend to have a diet high in fat [94]

Some chemicals on the site have been associated with a risk of developing kidney cancer. Specifically, the body of occupational studies on kidney cancer and exposure to TCE has foundthere to be a slightly elevated risk in workers who were exposed to high levels of the substance [99]. Overall, environmental studies on the general population are sparse and have not shown anystatistically significant results regarding proximity to waste sites and the development of kidneycancer [100,101].

Based on our review of the exposures at the site, the increased risks of developing kidney cancerfrom exposures at the site are low and are only relevant to the past residents of homes withcontaminated wells along Watson Corner Road (before 1985 for lots 9, 11, and 18; before 2000 forlot 7).

For more information about kidney cancers, see Appendix D.

  • Can exposure to site contaminants cause lupus?

Reply: Systemic lupus erythematosus (SLE) is one of several autoimmune diseases in which theimmune system attacks and damages the body's own tissues. Another similar autoimmune diseaseis systemic sclerosis (scleroderma). These diseases are four times more prevalent among womenthan among men. Sex hormones and genetics are thought to play important roles in thedevelopment of the disease. However, certain chemical exposures have produced pseudo-sclerodermatous conditions in some people, implying that environmental exposures may be anotherrisk factor for the disease. At this point, the only exposures that have demonstrated clearassociations with SLE or scleroderma are estrogen replacement therapy (females only), use of oralcontraceptives (females only), and inhalation of silica dust (males only). Associations betweenautoimmune disease and organic solvents, like those found at the Cardinal Landfill, have beeninvestigated several times but the results have been conflicting. Positive associations betweenchemical exposures and the disease have only been observed for people who use concentratedsolvent solutions at work [79,80,81].

Please see Appendix D for more information on SLE.

  • Has breast cancer been associated with chemicals from the Cardinal Landfill?

Reply:   Research has found that the following estrogen-related risk factors indicate a predispositionin women to developing breast cancer: early age at menarche (first menstruation), late age atmenopause (cease of menstrual cycle), higher socioeconomic status, and presence of a mutation inthe BRAC1 gene [105]. Other risk factors that have been linked to increased rates of breast cancerare lack of exercise, alcohol consumption, cigarette smoke (either direct or second-hand), andvitamin D deficiency [106]. Studies on women with breast cancer have found that only about halfof all cases of breast cancer can be attributed to the established estrogen-related risk factors. Therefore, researchers have suggested that, as in the immune diseases, environmental agents thatfunction as estrogens or act upon estrogens already in the body are a possible risk factor for breastcancer [106]. This type of contamination is not present at the Cardinal Landfill.

For more information about breast cancer, please see Appendix D.

  • Could seizure disorders be caused by exposures at the Cardinal Landfill?

Reply: There are two main types of seizure disorder groups, epileptic and non-epileptic seizures. The etiology (i.e., the causes or origins) of these diseases is complex. However, general risk factorsfor epilepsy are: familial and genetic factors, febrile seizures, traumatic brain injury, previouscentral nervous system infections, cerebrovascular disease, brain tumors, and developmentaldisabilities [102]. While the risk factors for non-epileptic seizures are largely unknown, physicalor sexual abuse, general head trauma, stress, alcohol abuse, illegal or prescription drug overdose,exposure to lead and carbon monoxide and hormonal changes associated with a woman's menstrualcycle have been implicated in studies on these types of disorders [103]. Therefore, it is unlikely thatexposures to chemicals at the Cardinal Landfill would result in seizure disorders.

For more information about seizure disorders, contact the Epilepsy Foundation of America(www.efa.org) or the National Institute of Neurological Disorders and Stroke(http://www.ninds.nih.gov/health_and_medical/pubs/seizures_and_epilepsy_htrm).

(2) Nature and Extent of Contamination

  • Is dioxin present or has it been tested for?

Reply: Dioxin has not been tested for on the site. DHHS and ATSDR [30, Appendix C] havedetermined that the medical conditions reported by residents near the site would not lead us torecommend dioxin testing at the site. As of August 2000, DES was continuing to reviewenvironmental and waste disposal information to confirm that such testing is not needed. Please seea longer discussion on this topic in section IV(C)(4).

  • What other chemicals are being created by combining the chemicals in the landfill?

Reply: Chlorinated solvents, such as those in the Cardinal Landfill, are broken down bymicroorganisms in the groundwater. Most of the breakdown products are less toxic than theoriginal solvents. However, two particular chemicals, vinyl chloride and 1,1-dichloroethene, aremore toxic than their precursors. These chemicals are detected by the standard analyticaltechniques and have been evaluated as part of this public health assessment.

  • Will a casement around the landfill help to contain the contamination?

Reply: DHHS is not involved with the remedy design for the site. Please contact DES at (603) 271-3503 to learn more about the proposed plans for the site..

  • Would ambient air 100 feet away from the landfill be contaminated at levels of health concern? Wind is mostly blowing away from the park (from the west).
  • Are the site contaminants airborne?

Reply: DHHS reviewed tests of ambient air quality in the mobile home park and determined thatthis exposure pathway does not pose a health risk to residents. Please see section V(A)(3) for moreinformation on this topic.

  • Is our drinking water being affected?
  • Is the town water supply at risk?

Reply: Currently, no drinking water supplies contain contamination at concentrations greater thanhealth comparison values. The mobile home park receives water from the Town of Farmingtonmunicipal supply. The well that supplied the park until 1995 was not affected by contamination atthe site. In the past, five drinking water wells serving homes along Watson Corner Road werecontaminated. All five of these wells have been abandoned. Also in the past (1983), one of the wellsserving the Town of Farmington municipal system (GP-2) was discovered to contain tracecontamination, and it was immediately removed from the drinking water supply.

  • Does this affect the new park or is it just the old park?

Reply: The homes in the mobile home park that were potentially affected by soil gas contaminationfrom the site were in the "old park". Two of the three homes have been moved and the third wasabandoned in February 1999. A buffer zone between the park and the landfill has been establishedfor both the "old" and "new" sections of the park.

(3) Future Exposures

  • How will the regulatory agencies deal with future chemical contamination from the landfill?

Reply: DES is working with Textron to devise a remedy for the contamination at the site. Forinformation on this process and on proposed plans for the site, we recommend that you contact DESat (603) 271-3503.

  • Please identify any and all potential future risks to residents at the Peaceful Pines Park.
  • What is the best way to protect the residents and employees of the Peaceful Pines Mobile Home Park?

Reply: There are two potential future risks for residents of the mobile home park: (1) movement ofcontaminated soil gas across the buffer zone, and (2) contamination of water in the swale areabetween the old and new sections of the park. DHHS has recommended monitoring to guard againstexposures by either of these pathways.

  • Will the contamination expand in size in the future?

Reply: The movement and growth of contaminant plumes in the soil gas and groundwater areuncertain. We have recommended frequent testing of these media so that any plume movementswould be detected.

(4) Access to Site

  • Will access to the site be adequately restricted, because there are lots of children in the park?

Reply: The site perimeter was completely fenced in December 1999. We also encourage parents towarn their children to stay off the site.

(5) Concerns about Pets and Plants

  • Are pets at risk?
  • Can site contaminants affect the health and growth of trees, shrubs and garden vegetables?

Reply: For the purpose of the public health assessment and consistent with its mandate, DHHS hasfocused on issues related to human health. In many cases, humans and animals react to exposuresto chemicals in different ways, so this evaluation of human health risks is not necessarily relevantto pets. We cannot speculate on the potential effects the contamination may have on trees orvegetables. However, DES' Biology Bureau at (603) 271-3503 may be able to provide informationon this topic.

(6) Site History

  • Please summarize the site history and what, if any, problems have arisen recently.
  • How long have people known about this problem?

Reply: Starting in the late 1960s, Textron and its antecedents began disposing hazardous wastesin the Cardinal Landfill. Following an inspection of the Textron facility in 1981, the State prohibitedthis practice. For the next 10 years (until 1991), Textron continued to use the landfill for non-hazardous wastes. A series of environmental investigations have been conducted at the site startingin 1982. The most recent studies have focused on contamination in soil gas. Please see sectionsII(A) and II(B) for a more detailed history of the site.

(7) Length of Process

  • Why has it taken so long for the landfill to be cleaned up?

Reply: Textron is responsible for the timely remediation of the site with oversight from DES. Moreinformation on the cleanup process at this site is available in Appendix H (Comment 20 fromRespondent #2).

  • Why does a health assessment take so long?

Reply: A public health assessment is a comprehensive review of all the public health issues relatedto a site. Given the long history and complex nature of the Cardinal Landfill site, several monthswere needed to gather and understand all the relevant information.

  • When will epidemiological studies be done?

Reply: DHHS and ATSDR do not plan to conduct a full-scale epidemiological study of thecommunity around the Cardinal Landfill. To determine the need for an epidemiological study,sufficient exposure and toxicological information must suggest that: (1) a relationship between theenvironmental hazards at a site and adverse health outcomes is biologically plausible, and (2) theexposure affects a large enough population for effects to be observed statistically. While there weresignificant exposures to VOCs in drinking water for five homes along Watson Corner Road, thenumber of people exposed by this pathway would not be enough to detect low to moderatetheoretical cancer risks. The same could be said for exposures to contaminants in the three mobilehomes that were evaluated as part of the soil gas to indoor air pathway. The remaining completedexposure pathways at the site were not expected to result in adverse health effects based on thelevels of contamination. Therefore, an epidemiological study of the community around this sitewould not be able to provide any more information about health impacts to the community.

(8) Legal Issues

  • What does closing the park mean? Eviction?
  • How does this affect property values?
  • What are notification/disclosure requirements for chemical hazards in real estate transactions?

Reply: In general, these questions are a private matter between the tenants of the park and the parkowners. Information on property values and notification/disclosure requirements can be obtainedfrom any licensed real estate agency.

  • Is this a Superfund site?

Reply: No. Please contact DES at (603) 271-3503 for more information on the Superfund programas it relates to this site.

(9) Textron Activities

  • Has Davidson (Textron) ceased discharging chemicals into the environment?

Reply: Textron stopped disposing hazardous wastes and non-hazardous wastes in the landfill in1981 and 1991, respectively. Textron still operates a plant in Farmington. DHHS has not reviewedTextron's practices at their Farmington facility.

  • Will the site be capped in the future? If so, how? And will it be contained?

Reply: Textron and DES are devising a remedy for the site. For more information on this subject,please contact DES at (603) 271-3503.

(10) Testing

  • Please provide a list of laboratories that test Indoor Air Quality. We would like winter testing done.

Reply: DHHS does not have a complete list of laboratories that we could provide, and we areprecluded from recommending individual contractors. However, in the local phone directory, underthe heading "Air Pollution Control", there is a listing of local and regional laboratories.

  • Why were only three homes tested for contamination? What about other homes nearby?

Reply: The three homes that were tested were the only ones where there recently was the potentialfor indoor air contamination. Soil gas testing in the rest of the park does not indicate a need foradditional indoor air tests in other homes.

  • How long and in what way will the site be monitored?

Reply: DHHS recommends continued monitoring of the groundwater, soil gas, and Cocheco River. We provide our recommendations to regulatory agencies and the responsible party, but have noauthority to require that they be implemented.

  • When will testing be done in the park?

Reply: Soil gas testing was done in the mobile home park in 1999 and 2000. The drinking waterwell that served the park until 1995 was tested nine times starting in 1982.

(11) Independent Review

  • Please complete a full and independent review of current contamination and hazards.

Reply: This was done by means of this public health assessment.

(12) Occupational Exposures

  • Would workers who installed the fence around the site in December 1999 have been at risk?

Reply: Occupational exposures to chemicals fall under the jurisdiction of the New Hampshire Department of Labor (DOL) and U.S. Occupational Safety and Health Administration (OSHA). This question has been forwarded to OSHA for their review. However, it should be noted that the major contamination on the site is in the groundwater and soil gas. Surface soil contamination is minor, and subsurface wastes were only placed in one section of the site. Based on the data that we have, we would not expect that short-duration contact with the soil would result in significant exposures to chemicals. Soil gas contamination is not expected to cause high exposures outdoors because of dilution and mixing in the atmosphere.



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  16. P
  17. Q
  18. R
  19. S
  20. T
  21. U
  22. V
  23. W
  24. X
  25. Y
  26. Z
  27. #