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Reich Farm Health Assessment
(Dover Township) Toms River, New Jersey
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Public Health Implications
The public health implications of the completed exposure pathways in the past will now be considered. Several contaminants were confirmed to be present in water from private wells and community water supply wells at
levels above health-based comparison values. (See the appendix for definitions and uses of comparison values.) The NJDHSS and the ATDSR have further evaluated the public health significance of past exposures to these
contaminants through an examination of relevant toxicologic and epidemiologic information. In addition, this section will include a brief summary of the findings of an analysis of childhood cancer incidence data for
Dover Township.
Childhood Cancer Incidence in Dover Township
The NJDHSS and the ATSDR reviewed cancer incidence data in the period 1979 to 1995 for Dover Township, as part of the Public Health Response Plan. Findings are fully described in a separate Public Health Consultation
by the NJDHSS and the ATSDR (NJDHSS/ATSDR, 1997). Dover Township was the only municipality in Ocean County in which overall childhood cancer incidence (ages up to 19 years) was statistically elevated. Ninety cases were
observed in the 17-year period, compared to 67 that would have been expected if childhood cancer rates were the same in the township as in the entire State of New Jersey. Leukemia incidence was elevated in Dover Township,
particularly in females under the age of five years. In the Toms River section of the township, overall childhood cancer was elevated (24 observed vs. 14 expected). Both leukemia and brain/central nervous system cancers
were elevated, with the excess occurring primarily in female children under age five.
Toxicologic and Epidemiologic Evaluation
Before actions were taken in the mid-1970s to interrupt the private well exposure pathway, it is clear that many wells in the Pleasant Plains section of Dover Township were contaminated with organic chemicals, as evidenced
by the TOC, CCE, CC14/IR and "phenol" analytical results from the 1970s. However, the specific compounds and the levels that persons were exposed to through the use of water from their private wells is not known, although
complaints of abnormal tastes and odors indicate substantial contamination levels. Much uncertainty exists as to the public health significance of past exposures through consumption of contaminated private well water.
In 1986, one private well (RW-7), located just up-gradient from the RF-site, had levels of PCE, carbon tetrachloride and bromoform exceeding, but similar to, the health-based comparison values. A toxicological evaluation of
these contaminants, taken on an individual basis, would not indicate that an adverse health effect (carcinogenic or non-carcinogenic) is likely from past exposure to persons consuming water from RW-7 (ATSDR, 1990; ATSDR,
1994a; ATSDR, 1997a).
As seen from Tables 6 and 7, several contaminants have been detected in untreated raw water samples from the TRWC community water supply wells. Those contaminants detected at or above health-based comparison values include
TCE, PCE, 1,2-dichloroethane, benzene and N-nitrosodiphenylamine. In addition, persons were exposed in the past through this pathway to SAN trimer and possibly other organic constituents of unknown composition and toxicological
significance. With the exception of TCE in well #26 in 1990 (33 µg/1), the levels of the contaminants detected are generally only slightly above their respective health-based comparison values. However, it is important to note
that this measured level is not reflective of the actual concentration a household in the TRWC distribution system would receive because of the installation of the air stripping treatment to remove VOCs in 1988, the blending of
water from several wells at the Parkway well field, and the mixing of water within the distribution system from other well fields. For these reasons, a toxicological evaluation of the known contaminants, taken on an individual
basis, would not indicate that an adverse health effect (carcinogenic or non-carcinogenic) is likely from past exposures to persons consuming well water from the Parkway well field (ATSDR, 1989; ATSDR, 1994b; ATSDR, 1997a; ATSDR,
1997b; ATSDR, 1997c).
It should be noted that toxicologic evaluations of individual chemicals do not take into account the potential for adverse health effects from the combined exposure to mixtures of these contaminants, although research on the
toxicity of mixtures indicates that adverse health effects are unlikely when the mixture components are present at levels well below their individual toxicologic thresholds (Bond et al., 1997; Groton et al., 1997; Seed et al.,
1995; and Yang et al., 1989). Because documented contaminant levels indicate that the exposures were well below their respective individual toxicologic thresholds, the toxicological evidence suggests that exposures to combinations
of known contaminants detected in private wells and in untreated water from the Parkway well field are not likely to lead to adverse health effects.
However, it is clear from the previous discussions in the Environmental Contamination and Pathways Analysis sections that the water from private wells and the Parkway well field, and subsequently individual households using the water
from the system, were contaminated with organic contaminants of an undetermined nature and level in the past. Therefore, much uncertainty exists as to the public health significance of past exposures through consumption of contaminated
water. In order to help evaluate the public health significance of human exposure pathways associated with community water supply wells, the ATSDR is developing a model of the UWTR/TRWC water system which will enable a more accurate
evaluation of the patterns of distribution associated with the wells. The ATSDR and the NJDHSS will use this model in further public health evaluations of water sources from various points of entry in the distribution system.
The public health significance of the pathway associated with exposure to SAN trimer cannot be fully evaluated at this time (ATSDR, 1997e). However, there are some preliminary toxicological information regarding the toxicity of the
SAN trimer. In 1996, when the SAN trimer was first recognized to be present in the community water supply, nothing was known about the toxicology of this material. Since that time, UCC has sponsored genetic toxicology assays and
short-term toxicologic testing. SAN trimer was found to be mutagenic in two strains of Salmonella and induced chromosomal aberrations in Chinese hamster ovary (CHO) cells, but there was no evidence of mutagenicity in two other assays.
The lethal single dose (LD50 ) was estimated to be 440 and 590 mg/kg in male and female rats. A two-week repeat dosing study showed that daily dose of 300 mg/kg were lethal to rats, while doses of 150 mg/kg resulted in a variety of
toxic effects including lethargy, tremors, anemia, and increased liver weight. No adverse effects were observed at 75 mg/kg under the conditions of this test.
No determination about the toxicity of long-term exposure to lower levels of SAN trimer can be made from this limited set of data from these short-term, very high dose studies. Plans for further toxicological testing are being coordinated
by the USEPA and a working group of scientists from the National Institute of Environmental Health Sciences, ATSDR, NJDEP, and NJDHSS, with input from UCC and a consultant to the OCHD. The results of these on-going toxicological studies
may provide additional information to further the understanding of the public health implications of past exposures to this contaminant through consumption of community or private water supplies.
The available analyses of water from private and public water samples indicates that VOCs (primarily TCE and PCE) were the most consistently detected contaminants. For this reason and because of the uncertainty in the historical levels of
contamination of private wells and the Parkway well field, a discussion of the current scientific knowledge regarding the public health implications ofthese contaminants is presented below.
Effects of TCE and PCE in Adults
The effects of exposure to TCE and PCE have been evaluated in scientific studies for their possible impact upon adult human health. TCE and PCE are classified as probable human carcinogens by the International Agency for Research on Cancer
(IARC, 1995) based on the weight of evidence from laboratory animal experiments and limited human epidemiologic studies.
Laboratory animals have been exposed to these chemicals via contaminated air, drinking water, and food. The results of these studies indicate that the nervous system and liver, and to a lesser degree the kidney and heart, are the primary
organs of adult animals affected by these VOCs (ATSDR, 1997a; ATSDR, 1997c). Following long-term, high level exposure, TCE has been shown to produce liver cancer in mice and kidney and testicular tumors in rats (ATSDR, 1997c; IARC, 1995).
Chronic, high level PCE exposure produces liver cancer in mice and kidney tumors and mononuclear cell leukemia in rats (ATSDR, 1997a; IARC, 1995). The exposure levels needed to cause these adverse impacts in laboratory animals are many
times higher than exposure levels that could have occurred through the use of contaminated drinking water (ATSDR, 1997a; ATSDR, 1997c).
Epidemiological studies of occupationally-exposed workers suggest an association between long-term inhalation exposure to high levels of TCE and increased risk of liver and biliary tract cancer and non -Hodgkin's lymphoma (IARC, 1995; ATSDR,
1997c). Increased risks of esophageal cancer, cervical cancer, and non-Hodgkin's lymphoma have been observed in workers exposed to high levels of PCE (LARC, 1995; ATSDR, 1997a). Participants in the ATSDR TCE Exposure Subregistry (approximately
4,300 individuals with exposure to TCE in drinking at levels ranging from 2 to 19,000 µg/1 for as long as 18 years) have reported a variety of health problems at rates above national averages (ATSDR, 1993b). However, only the rate for strokes
was reported to increase with increasing concentration of TCE in drinking water. Results from the Subregistry have not documented any increased occurrence of cancer in the study population (ATSDR, 1993b).
Effects of TCE and PCE in Children and the Fetus
Children may be particularly susceptible to the toxic effects of chemicals; fetuses may also be sensitive to toxic effects if the chemicals can cross the placental barriers Recent epidemiologic studies suggest that fetal exposure to VOCs in
drinking water could result in adverse health effects. The NSDHSS evaluated the effects of VOCs in drinking water on birth outcomes in an area of northern New Jersey (Bove et al., 1995). This exploratory study found that maternal residence
during pregnancy in areas with TCE-contaminated drinking water was associated with an increased risk of birth defects ofthc neural tube and oral cleft. Exposure to PCE during pregnancy was associated with an increased risk of oral cleft defects.
The authors concluded that their study by itself cannot determine whether the drinking water contaminants caused the reported adverse birth outcomes.
A recent ATSDR study of exposure to VOCs in drinking water and occurrence of adverse pregnancy outcomes was conducted for residents of the U.S. Marine Corps Base at Camp LeJeune, North Carolina (ATSDR, 1997d). The researchers reported a
significantly decreased mean birth weight and increased small for gestational age babies for two potentially susceptible subgroups: infants of mothers older than 35 years of age and infants of mothers with histories of fetal death. However,
length of exposures to VOCs was not known for the entire period during which pregnancy outcomes were evaluated. Therefore, this study provides limited evidence for a causal relationship between exposure to VOCs and the reproductive and
developmental effects evaluated.
A study of childhood leukemia conducted in Woburn, Massachusetts, concluded that the incidence of childhood leukemia was associated with the mother's potential for exposure to water from specific wells contaminated with TCE and PCE,
particularly for exposure during pregnancy (MDPH, 1997). The study did not find any association between the development of childhood leukemia and the child's exposure to contaminated water after birth. The Woburn study should be interpreted
with caution, however, since small numbers of study subjects led to imprecise estimates of risk. A study by the NJDHSS found a statistically elevated rate of childhood leukemia in towns served by community water supplies contaminated with TCE
and PCE in the years 1979 to 1987 (before current drinking water regulations had been implemented), compared to towns without a history of such contamination (Cohn et al., 1994). Overall, the associations drawn from these limited epidemiological
data in humans are suggestive, yet inconclusive, that exposure to these VOCs through drinking water may cause birth defects or childhood leukemia in children exposed while a fetus. ATSDR and others are conducting or sponsoring research to clarify
this possible relationship.
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