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PUBLIC HEALTH ASSESSMENT

PSC RESOURCES
PALMER, HAMPDEN COUNTY, MASSACHUSETTS


APPENDIX A. Tables


Table 1. Maximum Ambient Air Chemical Concentrations (µg/m3)

PSC Resources, Inc., Palmer, MA


Compound
Preexcavation
During Excavation
Comparison Values

Upwind Downwind Upwind Downwind
acetone 2.5 5.6 14 11 30,800
benzene ND 1.2 1.6 2.5 0.1
ethyl benzene ND 1.2 1.7 60 1300
chloroethane ND ND ND 6.9 10,000
2-butanone ND ND 6.1 4.5 1000
1,1-dichloroethane ND ND ND 6.7 520 (EPA)
4-methyl-2-pentanone ND ND ND 19 n/a
methylene chloride 15 25 10 53 3
1,1,1-trichloroethane 6.1 5.8 4.7 30 3800
trichloroethene ND ND ND 16 0.6
tetrachloroethene ND ND 3.2 21 2
xylenes 1.2 1.4 ND 19 217
toluene 2.4 2.8 3.6 16 3760

units in µg/m3
ND not detected
NA not available
data taken from Table 4-22 (HMM 1992).
EPA= taken from U.S. Region 3 guidance (no ATSDR value available)


Table 2. Wetland and Quabog River Sediment
Semivolatile, PCB, and Inorganic Compounds (ppm)


Chemical Wetland River Background Comparison
Value

naphthalene 24 0.34 n/a 3100
4-chloro-3-methylphenol 0.12 n/a n/a
2-methylnaphthalene 0.78 0.48 n/a n/a
acenaphthylene 5 0.13 0.005 4700
acenaphthene 0.071 0.2 0.006 3000
dibenzofuran 0.12 0.066 n/a n/a
fluorene 0.18 0.12 0.01 2000
pentachlorophenol ND 0.96 n/a 6
phenanthrene 26 1.1 0.14 n/a
anthracene 5.5 0.2 0.013 20,000
di-n-butylphthalate 0.98 0.94 n/a 30,000
fluoranthene 16 1.5 166 2000
pyrene 39 1.9 147 2000
butylbenzylphthalate 0.16 n/a 10,000
benzo(a)anthracene 7 0.76 59 1
chyrsene 6 0.82 0.64 100
bis(2-ethylhexyl)phthalate 11 0.42 n/a 50
benzo(b)fluoranthene 9.8 0.79 62 1
benzo(k)fluoranthene 9.3 0.8 26 10
benzo(a)pyrene 9.1 0.73 1.3 0.1
indeno(1,2,30cd)pyrene 5.5 0.71 61 n/a
dibenz(a,h)anthracene 1.1 0.089 n/a
benzo(g,h,i)perylene 7.4 0.62 47 n/a
PCBs 32 0.71 10
arsenic 21.8 17 20
beryllium 0.81 0.4 0.2
cadmium 25.3 2 40
chromium 72 29 300
lead 7970 99 400
manganese 1400 300 7000
mercury 1.1 0.3 2
nickel 80.8 17 1000

Background values for PAH compounds from ATSDR 1993.
Background values for inorganic compounds from MDEP 1995.


TABLE 3. Bladder Cancer Incidence, 1982-1992
Palmer, Massachusetts


Total Male Female

1982-1986 Obs Exp SIR CI Obs Exp SIR CI Obs Exp SIR CI

CT 8101 14 5.9 237* 129-398 12 4.2 289* 149-505 2 1.8 114 NC
CT 8102 3 3.0 99 NC 3 2.2 134 NC 0 0.7 0 NC
CT 8103 1 3.0 26 NC 1 2.9 35 NC 0 0.9 0 NC
PALMER 18 12.8 141 84-223 16 9.3 172 98-279 2 3.5 57 NC

1987-1992
CT 8101 8 6.6 121 52-238 8 4.7 171 74-337 0 1.9 0 NC
CT 8102 4 3.4 118 NC 3 2.5 119 NC 1 0.9 115 NC
CT 8103 7 4.3 162 65-335 6 3.2 187 68-408 1 1.1 90 NC
PALMER 19 14.3 133 80-208 17 10.4 163 95-261 2 1.7 118 NC

SIR standardized incidence ratio; calculated based on the exact number of expected cases; expected cases presented here are rounded to the nearest tenth
Obs observed number of cases Exp expected number of cases
CI 95-percent confidence interval for SIR NC not calculated when observed number of cases is less than 5
* indicates statistical significance
Data source is Massachusetts Cancer Registry, Bureau of Health Statistics, Research, and Evaluation, Massachusetts Department of Public Health


TABLE 4. Kidney Cancer Incidence, 1982-1992,
Palmer, Massachusetts


Total Male Female

1982-1986 Obs Exp SIR CI Obs Exp SIR CI Obs Exp SIR CI

CT 8101 1 2.4 41 NC 1 1.4 72 NC 0 1.0 0 NC
CT 8102 0 1.2 0 NC 0 0.8 0 NC 0 0.5 0 NC
CT 8103 0 1.6 0 NC 0 0.9 0 NC 0 0.6 0 NC
PALMER 2 5.2 38 NC 1 3.1 32 NC 1 2.1 47 NC

1987-1992
CT 8101 9 4.0 226* 103-429 5 2.3 213 69-497 4 1.6 246 NC
CT 8102 5 2.1 244 77-556 2 1.3 156 NC 3 0.8 389 NC
CT 8103 1 2.6 39 NC 1 1.6 63 NC 0 0.9 9 NC
PALMER 15 8.6 174 98-288 9 5.3 171 78-325 6 3.4 177 64-384

SIR standardized incidence ratio; calculated based on the exact number of expected cases; expected cases presented here are rounded to the nearest tenth
Obs observed number of cases Exp expected number of cases
CI 95-percent confidence interval for SIR NC not calculated when observed number of cases is less than 5
* indicates statistical significance

Data source is Massachusetts Cancer Registry, Bureau of Health Statistics, Research, and Evaluation, Massachusetts Department of Public Health


TABLE 5. Lung Cancer Incidence, 1982-1992
Palmer, Massachusetts


Total Male Female

1982-1986 Obs Exp SIR CI Obs Exp SIR CI Obs Exp SIR CI

CT 8101 28 18.9 148 98-214 21 12.2 172* 106-263 7 6.8 103 41-212
CT 8102 9 9.9 91 42-173 6 6.6 91 33-198 3 3.3 91 NC
CT 8103 10 12.5 80 38-147 7 8.2 85 34-175 3 4.2 71 NC
PALMER 47 41.2 114 84-152 34 27.0 126 87-176 13 14.3 91 48-156

1987-1992
CT 8101 27 24.8 109 72-159 16 14.4 111 63-180 11 10.3 107 53-191
CT 8102 12 12.8 94 49-164 7 7.9 89 36-183 5 5.0 101 33-236
CT 8103 14 16.1 87 48-146 8 9.9 81 35-160 6 6.3 95 35-207
PALMER 53 53.5 99 74-129 31 32.3 96 65-136 22 21.6 102 64-154

SIR standardized incidence ratio; calculated based on the exact number of expected cases; expected cases presented here are rounded to the nearest tenth
Obs observed number of cases Exp expected number of cases
CI 95-percent confidence interval for SIR NC not calculated when observed number of cases is less than 5
* indicates statistical significance
Data source is Massachusetts Cancer Registry, Bureau of Health Statistics, Research, and Evaluation, Massachusetts Department of Public Health



TABLE 6. Cancer Incidence, 1982-1992, Palmer, Massachusetts


Total Male Female

1982-1986 Obs Exp SIR CI Obs Exp SIR CI Obs Exp SIR CI

leukemia 10 5.6 180 86-331 7 3.1 229 92-472 3 2.5 119 NC
liver 1 1.4 74 NC 0 0.9 0 NC 1 0.5 215 NC
stomach 12 7.0 171 88-299 7 4.2 167 67-344 5 2.8 177 57-413

1987-1992
leukemia 7 6.3 112 45-231 3 3.5 85 NC 4 2.7 150 NC
liver 2 2.0 100 NC 2 1.4 145 NC 0 NC 0 NC
stomach 10 7.4 136 65-250 6 4.4 135 49-294 4 2.9 139 NC

SIR standardized incidence ratio; calculated based on the exact number of expected cases; expected cases presented here are rounded to the nearest tenth
Obs observed number of cases Exp expected number of cases
CI 95-percent confidence interval for SIR NC not calculated when observed number of cases is less than 5
* indicates statistical significance
Data source is Massachusetts Cancer Reigstry, Bureau of Health Statistics, Research, and Evaluation, Massachusetts Department of Public Health


TABLE 7. Cancer Incidence, 1982-1992, Monson, Massachusetts


Total Male Female

1982-1986 Obs Exp SIR CI Obs Exp SIR CI Obs Exp SIR CI
bladder 6 6.7 90 33-196 5 4.9 102 33-238 1 1.7 57 NC
kidney 2 2.9 70 NC 1 1.8 57 NC 1 1.1 90 NC
leukemia 4 3.0 131 NC 3 1.7 174 NC 1 1.3 76 NC
liver 0 0.7 0 NC 0 0.5 0 NC 0 0.2 0 NC
lung 28 22.4 125 83-181 22 14.9 148 93-224 6 7.6 79 29-172
stomach 3 3.6 83 NC 2 2.2 89 NC 1 1.4 74 NC

1987-1992
bladder 8 7.5 107 46-211 7 5.5 127 51-262 1 2.0 51 NC
kidney 4 4.7 85 NC 3 2.9 102 NC 1 1.8 57 NC
leukemia 6 3.4 175 64-381 4 2.0 198 NC 2 1.4 141 NC

1982-1986 (cont'd) Total Male Female
Obs Exp SIR CI Obs Exp SIR CI Obs Exp SIR CI
liver 0 1.1 0 NC 0 0.8 0 NC 0 0.3 0 NC
lung 33 28.9 114 78-160 21 17.6 119 74-182 12 11.2 107 55-187
stomach 3 3.8 80 NC 3 2.4 127 NC 0 1.4 0 NC

SIR standardized incidence ratio; calculated based on the exact number of expected cases; expected cases presented here are rounded to the nearest tenth
Obs observed number of cases Exp expected number of cases
CI 95-percent confidence interval for SIR NC not calculated when observed number of cases is less than 5
* indicates statistical significance
Data source is Massachusetts Cancer Reigstry, Bureau of Health Statistics, Research, and Evaluation, Massachusetts Department of Public Health



APPENDIX B
GENERAL DISCUSSION ON ETIOLOGY OF SELECTED CANCER TYPES

Leukemia

Leukemia is an "umbrella" term representing a group of cancers involving cells of blood-forming organs. There are four major subtypes into which most histologic types of leukemia can be categorized: acute lymphoid leukemia (ALL); chronic lymphoid leukemia (CLL); chronic myeloid leukemia (CML); and acute myeloid leukemia (AML). Epidemiologic research over the past twenty-five years has revealed patterns of incidence and risk factors which vary for each subtype. For this reason, leukemia incidence was evaluated according to cell type. While there are known and suspected risk factors for each subtype, leukemia cases are relatively rare, and despite a large body of research, risk factors that have been identified for different leukemia subtypes only account for a small percentage of cases.

Acute lymphoid leukemia occurs predominantly in children. Incidence rates drop off among middle aged people, and increase again among older individuals (ACS 1995). The known risk factors for ALL are ionizing radiation and benzene exposure. Suspected risk factors are genetic, viral, environmental, and occupational. Studies of associations between leukemia and chromosomal aberrations such as Down syndrome have related ALL to a genetic etiology (Isselbacher and Braunwald 1994). Other research has supported viral factors. An increased risk of childhood ALL has been associated with exposure to several chemicals and possible paternal occupational exposure to hydrocarbons (Linet 1985).

Chronic lymphoid leukemia is chiefly an adult disease; 90% of cases occur in people over 50 years old. CLL is the most common type of leukemia in the United States and occurs more often in males than females (ACS 1990). Adult T cell leukemia is a type of CLL caused by a virus, Human T-Cell Leukemia/Lymphoma Virus-I (HTLV-I) (Isselbacher and Braunwald 1994). The only known risk factor for other types of CLL is exposure to benzene. No association has been found between CLL and exposure to ionizing radiation (Linet 1985, Isselbacher and Braunwald 1994). Studies showing strong patterns of incidence in families suggest a genetic etiology. An association between CLL and autoimmune diseases suggests that immunologic factors may play an important role. Several viruses linked with leukemia in animals have been shown to cross species barriers; research suggests that human proximity to sick farm animals and pets may increase the risk of CLL (Schottenfeld and Fraumeni 1982). Rubber workers, and particularly tire builders, have a higher incidence of CLL. Exposure to some chemical wastes in the environment may also be a risk factor (Schottenfeld and Fraumeni 1982).

AML may occur in children up to the age of 19, with incidence increasing rapidly beyond age 20. The known risk factors for AML are similar to those for ALL: exposure to ionizing radiation and benzene (Linet 1985). Recent studies suggest that viral and genetic factors play a less important role in the development of AML than in ALL and CLL. Suspected risk factors for AML include occupational and environmental exposures and certain drug therapies, such as chloramphenicol and phenylbutazone (Linet 1985). Suspected chemical exposures include petroleum products and organic solvents. AML as a secondary malignancy is increasing among people who have previously had non-Hodgkin's lymphoma, multiple myeloma, breast cancer, ovarian cancer, and lung cancer. A high risk of secondary AML in people who have had Hodgkin's lymphoma has also been documented. The question remains whether secondary AML is a result of chemotherapy and/or radiation treatment for a previous cancer, or whether secondary AML occurs as part of the natural history of the previous cancer, because improved cancer therapy may have lengthened survival time (Linet 1985). Cigarette smoking has been identified as a possible risk factor in the development of AML (Siegel 1993).

Of all the leukemias, CML is among the least understood. CML is an acquired genetic disorder, characterized by the presence of the Philadelphia chromosome. CML can occur at any age, but is most often observed in people between 30-50 years old. The only known risk factor is exposure to ionizing radiation, based on studies of atomic bomb survivors (Isselbacher and Braunwald 1994). Occupational exposure to benzene has also been associated with the development of CML, however a causal relationship has not been established. Exposure to other chemical agents in the work place or environment is suspected in this disease (Linet 1985). Cigarette smoking is also suspected in the development of CML, however the association is weak at best (Siegel 1993). Current research has suggested that heredity and immunologic factors do not appear to be important in the development of CML (Linet 1985).

Hairy cell leukemia is an uncommon type of leukemia which is predominantly seen in males at an average of 55. Although very little is known about the etiology of this disease, hairy cell leukemia has an excellent survival rate because of a new and relatively non-toxic treatment. The majority of cases experience complete remission and live more than ten years after diagnosis (Tierney and McPhee 1995).

Liver cancer

Liver cancer incidence rates display a small peak during childhood, and then steadily increase with advancing age, and are greatest in the 85 and older age group. Three major etiologic factors are thought to be associated with the development of liver cancer or hepatocellular carcinoma, the predominant type of primary liver cancer occurring in about 75-95 percent of the cases. These factors include the hepatitis B virus, alcohol consumption and related cirrhosis. Sixty to ninety percent of liver cancers occur in association with cirrhosis, but the relationship is not completely understood (Page and Asire 1985). Exposure to aflatoxins, which are found in regions of the world where food storage and handling techniques are not optimal, is also associated with the development of liver cancer. A weak association has been found for oral contraceptive use and other benign liver masses (Schottenfeld and Fraumeni 1982).

Stomach cancer

Stomach cancer incidence rises steadily from about the age of 20 and reaches a peak in the 95 year and over age category. Males are nearly 2.5 times more likely than females to develop stomach cancer. The relationship between diet and stomach cancer has been extensively researched. Long-term ingestion of uncooked pickled vegetables, salty sauces, and dried, salted fish has been associated with a higher risk, while no association has been established with unprocessed raw vegetables and raw fish (Schottenfeld and Fraumeni 1982, Isselbacher and Braunwald 1994). This relationship has focused attention on food preparation methods, with implications indicating dietary nitrate sources; dry salted foods contain nitrates. Nitrates may be converted to nitrites, which are carcinogenic, by bacteria present in unrefrigerated, partially decayed foods. Such bacteria may be introduced through the ingestion of the partially decayed foods often consumed by lower socioeconomic classes (Isselbacher and Braunwald 1994). The substantial decrease in stomach cancer from its high incidence in the 1930s to the lower incidence of the present may have been influenced by the development of effective food preservation techniques, namely refrigeration. Conditions such as pernicious anemia and gastritis are also associated with a high risk of stomach cancer, as well as a history of gastric surgery (Schottenfeld and Fraumeni 1982).

Occupational exposure to asbestos also has been implicated as a risk factor in the development of stomach cancer (Schottenfeld and Fraumeni 1982).

REFERENCES FOR APPENDIX B

ACS. 1995. Cancer Facts & Figures - 1995. Atlanta: American Cancer Society.

Isselbacher, K.J., E. Braunwald, et.al. 1994. Harrison's Principles of Internal Medicine, Thirteenth Edition. McGraw-Hill, Inc.

Linet, M. 1985. The leukemias: epidemiologic aspects. Oxford: Oxford University Press.

Page, H.S., and A.J. Asire. 1985. Cancer rates and risks. 3rd ed. Washington, D.C.: national Institutes of Health, Publication No. 85-691.

Schottenfeld, D., and J.F. Fraumeni. 1982. Cancer epidemiology and prevention. Philadelphia: W.B. Saunders and Company.

Siegel, M. 1993. Smoking and leukemia: evaluation of a causal hypothesis. Amer J Epidem 138(1):1-9.

Tierney, L.Jr., S. McPhee, M. Papadakis. 1995. Current Medical Diagnosis and Treatment. 34th ed. Norwalk, CT: Appleton and Lange.


Appendix C
Responsiveness Summary

SUMMARY OF PUBLIC COMMENTS AND AGENCY RESPONSES

This responsiveness summary addresses comments that were received by MDPH and/or ATSDR during the public comment period for the PSC Resources NPL site. This period was from October 8, 1993 to November 5, 1993. The Agency received written commentary from the United States Environmental Protection Agency (USEPA) and these comments are addressed in the following section.

COMMENTS FROM FEDERAL OFFICIALS

COMMENT 1: EPA questions the relevance of a private well survey in the area since the contamination plume does not extend to residential areas.

ATSDR/MDPH Response: We recommended in the public comment release of the PSC Resources Health Assessment that an extensive private well survey be conducted in the area around the site. Residential housing is located immediately across the site on Water Street and citizen concern was voiced regarding the possibility of being exposed to site-related groundwater contaminants. If groundwater contaminants were migrating from the site toward this housing, exposure could occur by using contaminated water for drinking, cooking, bathing or laundering purposes. In order to address this citizen concern, we needed to determine either that on-site contaminants were not migrating through groundwater toward residential housing on Water Street or that there were no private wells in use in this area.

No complete well survey was conducted in the area around the site. The remedial investigation conducted in January of 1992, however, indicated the presence of one private well in Monson approximately one half mile northwest of the site. There is no mention in the investigation of whether private wells exist near the site in Palmer. To further pursue the possibility of the existence of private wells on Water Street, we contacted the Palmer Water Department, who informed us that the residences on Water Street have been served with municipal water for the past 30 years but that the possibility exists that private wells could also be situated on these properties. We then contacted the Palmer Board of Health, which indicated that there are no private water wells in existence on Water Street. Based on this information, there are no indications that there are private water wells on the properties across from the site on Water Street. If this information is accurate, there is no longer a need for a well survey in the area, and it appears unlikely that residents in the area have been or are currently exposed to site-related groundwater contaminants.

COMMENT 2: In response to the concern over future ingestion of contaminated ground water in the area near the site, EPA indicates that institutional controls on ground water use were put in place when the Record of Decision (ROD) was signed on September 15, 1992. This, EPA believes should alleviate any concern for future exposure to ground water contamination emanating from the site.

ATSDR/MDPH response: The Health Assessment was updated to reflect the reduced possibility of exposure to site-related groundwater contamination by restricting use of these waters until clean-up levels in the area have been achieved.

COMMENT 3: EPA questions the concern regarding exposure to wetlands and lagoon contaminants given the upgrade of security around the site which was done in 1992.

ATSDR/MDPH response: The Health Assessment has been revised accordingly to reflect this security upgrade.

COMMENT 4: In response to the recommendation in the Health Assessment for surface soil monitoring on the athletic field north of the site, EPA believes that the monitoring done to date was adequate to establish that soil levels on the field do not pose a health risk. EPA states that monitoring of the areas surrounding the site will be conducted during the remedial process in order to ensure that the cleanup will not affect these areas.

ATSDR/MDPH response: ATSDR and MDPH support EPA's proposed monitoring of surrounding soils during the remedial process.

COMMENT 5: EPA believes that the fish sampling and analysis was adequate to establish that consumption of fish caught near the site does not pose a health risk.

ATSDR/MDPH response: We do not believe that the fish data were adequate to evaluate human health risks. The data reflected whole-body concentrations rather than edible-tissue concentrations, which are most relevant and applicable to evaluating the potential for human health effects. We believe this remains as a data gap, not only in terms of chemical concentrations in fish tissue but also in terms of information on the extent of possible consumption of fish from the Quaboag River or what fish species may be consumed.

COMMENT 6: EPA indicates that the Health Assessment does not contain current information regarding the remedial decisions for the site.

ATSDR/MDPH response: The MDPH is appreciative of USEPA for apprising us of current developments regarding the status of the site's remediation and the Health Assessment has been revised accordingly.

Additional Agency Comments Subsequent to Revisions

ATSDR/MDPH revised the draft health assessment subsequent to the public comment period. The revised draft was distributed to state and federal environmental regulatory agencies for another opportunity to provide comments. The Massachusetts Department of Environmental Protection (MDEP) and the U.S. Environmental Protection Agency (EPA) provided comments.

COMMENT: MDEP supplied a number of comments requesting that information regarding the 1992 Record of Decision, site maps, and achievement of remedial work be incorporated into the paper. In addition, comments were supplied requesting clarification of facts, grammar, and syntzx.

ATSDR/MDPH Response: These comments were incorporated.

COMMENT: EPA supplied a number of comments requesting that information regarding the 1992 Record of Decision, the Consent Decree, and site maps be incorporated into the paper. In addition, comments were supplied requesting clarification of facts, grammar, and syntax.

ATSDR/MDPH Response: These comments were incorporated.

COMMENT: MDEP noted, "Pg 15,A. Pathways Analysis, Paragraph 2, the first sentence should read: 'To determine possible exposure by individuals to contaminants onsite, the factors influencing human exposure were evaluated. It is not evident if migration has or is occurring.'"

ATSDR/MDPH Response: The sentence to which the commenter refers was meant to be a general statement about evaluating exposures. For clarification, the sentence now reads: "To determine whether individuals are possibly exposed to contaminants, the factors influencing human exposure were evaluated."

COMMENT: EPA noted: "Pages 8-14; A figure should be provided showing where each of the various onsite versus offsite areas are and the samples from those areas. I did not confirm the data cited from the RI because it was not possible to determine which samples were being referenced in each section, I believe, however, that the areas refered as "off=property" areas are still within EPA's site boundary. This should be clarified."

ATSDR/MDPH Response: No figure was added that specifically delineated "onsite" and "offsite" areas or the sampling obtained from those areas. Instead, definitions were provided to more clearly describe the property boundaries (e.g., the EPA study area included "property" and non-property" areas). In addition, 2 figures (Figure 2 and Figue 3) were added to describe the general features of the surrounding area, as well as site-specific buildings and features.


CERTIFICATION

The Public Health Assessment for PSC Resources was prepared by the Massachusetts Department of Public Health under a cooperative agreement with the Agency for Toxic Substances and Disease Registry (ATSDR). It is in accordance with approved methodology and procedures existing at the time the Health Consultation was initiated.

Tina Forrester
Technical Project Officer, SPS, SSAB, DHAC

The Division of Health Assessment and Consultation, ATSDR, has reviewed this Health Consultation and concurs with its findings.

Richard Gillig
Chief, SPS, SSAB, DHAC, ATSDR


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