Skip directly to search Skip directly to A to Z list Skip directly to site content




Based on the ISA investigation sample results and TSEP/ATSDR site visit observations, contact with contaminated surface soil represents a completed exposure pathway to trespassers and workers who come on-site. Exposure to contaminated soil is the primary pathway of concern due to the elevated concentrations of metals (particularly lead) and PAHs, unrestricted site access, and adjacent residential properties (Table 3).

A potential surface water and sediment pathway exists because of possible migration of site contaminants from the site to Riverview Park Lake which is used for fishing and recreation. A potential air pathway also exists because, as surface soil is disturbed on the site, fugitive dust may be transported toward the residential area. These two potential pathways can not be evaluated due to a lack of available data.

The process of estimating the health risk associated with exposure to any contaminant involves two major steps: 1) estimating the amount of contaminant to which a person is or was exposed to and the length of exposure; and 2) comparing the exposure level for that particular contaminant to known toxicological and health outcome information. In general, people can be exposed to higher contaminant concentrations for a short period of time (acute exposure, 14 days or less) without adverse effects as compared to a longer time period (chronic exposure, 365 days or more).

Table 3.

Completed Exposure Pathway
Source of
Point of
Route of
surface soil surface soil on-site and nearby residences ingestion, inhalation, and dermal contact site trespassers, local residents, employees of nearby businesses, a homeless person living on the site past, current, future

Exposures can be estimated by using concentrations of the substance which have been measured in soil, air, or water and the amount of the media taken into the body and calculating an internal dose. A dose is the amount of a contaminant which is taken into the body through ingestion, inhalation, or dermal absorption. Doses are commonly expressed in terms of milligrams of contaminant per kilogram of body weight per day (mg/kg/day). Dose estimates are needed in order to estimate health risks.

This process of estimating health risks from contaminant exposure is complicated at the Diller Battery site by the fact that people have been exposed to a mixture of different contaminants for long periods of time during which no sampling occurred. Another important consideration when estimating health risk from contaminant exposure is that people differ in their susceptibility to exposures and the subsequent adverse health effects. For example, children are more susceptible to airborne and soil contamination because they tend to spend more time outdoors and have faster rates of respiration and soil ingestion as compared to adults. Also, people with pre-existing health conditions such as heart disease and asthma can be more susceptible to adverse health effects.

Human health effects resulting from lead exposure have largely been studied in occupational settings. Dose data for humans, generally expressed in terms of absorbed dose, are usually measured as levels of lead in blood. Dose-effect data, in terms of external exposure levels (mg/kg/day) by a single route of exposure, are not generally available for humans. No Minimal Risk Level (MRL) has been developed for lead because a threshold level has not yet been defined for the most sensitive effects in humans (i.e., neurotoxicity).4 An MRL is an estimate of daily human exposure to a contaminant that is likely to be without appreciable risk of noncancerous effects over a specified duration of exposure.

The Centers for Disease Control and Prevention considers children to have an elevated level if the amount of lead in the blood exceeds 10 g/dL. Exposure to low levels of lead has been shown to interfere with the mental development of children. Exposure to high levels of lead decrease intelligence quotient (IQ) scores and reduce the growth of young children. In adults, low lead exposure may decrease reaction time, adversely affect memory, increase blood pressure in middle-aged men (no data on this effect in women), cause anemia, and produce blood disorders. At high levels of exposure, lead can severely damage the brain and kidneys in adults and children. In addition, high levels of exposure to lead may cause spontaneous abortion of pregnant women and damage the male reproductive system. The effects of lead are the same regardless of whether it enters the body through inhalation or ingestion. EPA considers lead to be a B-2 carcinogen, meaning that lead may be considered as a probable human carcinogen (i.e., while sufficient animals studies have been documented, there is inadequate data on humans).

In general, lead in soil and dust appears to be responsible for blood levels in children increasing above background levels when the concentration in the soil or dust exceeds 500 mg/kg. However, no studies are available to indicate conclusively how much lead must be present in soil and dust before increased lead levels in the blood can be expected. It is highly probable that lead in on-site surface soil has been present since the late 1940s when Diller Battery began operation. On-site surface soil samples contained lead at concentrations as high as 8,660 mg/kg. Extended human exposure to soil-contaminated lead was likely due to lack of knowledge and unrestricted access to the site. Such a situation could pose a significant increased health risk, especially among children. Off-site surface soil samples contained lead at concentrations as high as 630 mg/kg. Off-site sampling was insufficient to determine the extent of contamination and human exposure. In particular, the residential properties north of the site did not grant permission to sample their yards.

The homeless person living on the site has a blood lead level of 16 g/dL which is higher than the mean level of 3.1 g/dL for persons 50-69 years of age.5 Nonetheless, no adverse health effects are likely to occur. However, some research has shown that several hematological health effects in adults can be observed at blood lead levels as low as 10 g/dL, and at levels of 30 g/dL, blood pressure can increase in males.6 Adults absorb 5 to 15 percent of ingested lead and usually retain less than 5 percent of what is absorbed. Children are known to have a greater absorption of lead than adults; an average absorption of 41.5 percent and 31.8 percent retention in infants. There is no data for blood lead levels in children who may visit or who live close to the site. Although no correlation can be made concerning this individual's blood lead level and possible exposures of others coming in contact with the site, it is unlikely that other people coming on-site less frequently will have exposures higher than this person.

When simultaneous exposure to multiple contaminants occurs, there is a potential for additive, synergetic, or antagonistic interactive effects. Interactions between arsenic and other metals have been investigated, but no clear evidence for toxicologically significant effects has been shown. For example, studies of rats exposed to arsenic, lead, and cadmium, alone or in combination, revealed mainly additive or sub-additive effects on body weight, hematological parameters, and enzymes of hemesynthesis.9,10 Similarly, studies of the tissue levels of arsenic in rats that were fed arsenic with or without lead or cadmium revealed only limited evidence of toxicokinetic interactions.7 These data do not suggest that arsenic toxicity is likely to be significantly influenced by concomitant exposure to other metals.

Although lead is the primary contaminant at the site, arsenic and PAHs were also found at concentrations exceeding their comparison values (see Tables 1 and 2). EPA classifies arsenic as a known human carcinogen. PAHs, benzo(a)pyrene, benzo(a)anthracene, indeno(1,2,3 c-d)pyrene, and benzo(b)fluoranthene, are classified as probable human carcinogens. Cancer effects could occur at lower exposure levels than noncancer effects for each exposure duration. Levels of chronic oral exposure associated with the carcinogenic effects of arsenic range from a risk of 1 in 10-4 to 10-7, as developed by EPA. An MRL of 3x10-4 mg/kg/day has been derived for chronic oral exposure to arsenic. Long-term incidental ingestion of contaminated soil at the site could pose an increase in cancer risk.7 An MRL of 0.1 mg/kg/day has been derived for acute oral exposure to benzo(a)pyrene. A chronic exposure MRL for benzo(a)pyrene has not been determined. No chronic MRLs have been derived for the other PAHs found at the site. PAHs could potentially pose a slight increase in cancer risk for long-term exposure, based on toxicity of benzo(a)pyrene.8

Because humans are usually exposed to PAHs in complex mixtures rather than to individual PAHs, it is important to understand their potential interactions. Several experiments have shown that most PAH mixtures are considerably less potent than individual PAHs. The interaction between noncarcinogenic and carcinogenic PAHs has been extensively examined in animals. It has been documented that a mixture of selected noncarcinogenic PAHs and carcinogenic benzo(a)pyrene reduced the carcinogenic potential of benzo(a)pyrene in animals.8 Interactions between PAHs and metals, such as lead and arsenic, have not been studied.


In a October 21, 1997 meeting between EPA, ATSDR, and TSEP, the EPA Remedial Project Manager stated that it is EPA's intention to have site remediation underway by the spring of 1998.11 With winter now approaching, the frequency and likelihood of exposure for people coming on-site should be reduced.

Next Section          Table of Contents The U.S. Government's Official Web PortalDepartment of Health and Human Services
Agency for Toxic Substances and Disease Registry, 4770 Buford Hwy NE, Atlanta, GA 30341
Contact CDC: 800-232-4636 / TTY: 888-232-6348

A-Z Index

  1. A
  2. B
  3. C
  4. D
  5. E
  6. F
  7. G
  8. H
  9. I
  10. J
  11. K
  12. L
  13. M
  14. N
  15. O
  16. P
  17. Q
  18. R
  19. S
  20. T
  21. U
  22. V
  23. W
  24. X
  25. Y
  26. Z
  27. #