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The recent sampling conducted by EPA/ERT confirms earlier findings that show creosote, and its constituent PAHs, at elevated levels in the subsurface. As stated by ATSDR in a previous Health Consultation, if the creosote contamination is unearthed, it may pose an acute contact threat causing irritation and burning of the skin and eyes [4]. The ultraviolet rays of the sun may intensify the effects of the exposure.

Long-term exposure to creosote has been shown to induce skin cancer in animal studies, but evidence of cancer in humans is less definitive. Some studies of workers showed an association between long-term exposure to creosote and the development of skin cancer. However, other studies suggest there is no association between exposure to creosote and other coal tar products and cancer in humans [6]. Since creosote used for wood treatment contains a mixture of several carcinogenic PAHs, it is prudent to assume that there may be an increased risk of cancer associated with long-term exposure to creosote.

Non-cancerous adverse effects have also been associated with exposures to PAHs [7]. Mice fed high levels of the PAH, benzo(a)pyrene (B(a)P), during pregnancy had difficulty reproducing. Also, the offspring of mice fed high levels of B(a)P had an increased incidence of birth effects and decreased body weight [6]. There are no studies that indicate these effects occur in people, and the doses that cause these effects are considerably higher than those likely to be experienced through environmental exposures.

Exposure to PAHs in the soil is most likely to occur through incidental ingestion of soil or dust. Some dermal absorption of PAHs may occur through direct contact with skin. However, PAHs bind to organic matter in the soil, which decreases its bioavailability through skin absorption.

The following health evaluations are based on the highest concentrations of PAHs detected in on-site surface soils.

Non-cancer assessment:

The EPA and ATSDR have derived health-based guidelines for several PAHs. These guidelines are defined as estimates of a daily oral exposure of humans, including sensitive sub-populations, that are likely to be without an appreciable risk of deleterious effects (non-cancer). Such guidelines are not thresholds for toxicity, but are useful for screening to determine if more detailed evaluations are necessary. The EPA guidelines are referred to as a Reference Dose (RfD), and the ATSDR guidelines values are Minimal Risk Levels (MRLs).

Assuming a worst case scenario, a 3-4 year old child (weight-16 kg) ingesting 200 mg of soil per day while playing on the property with the swing set (total PAHs-758 ppm), the child would receive a dose of 0.0094 mg/kg/day. This dose is 10-100 times below any screening values used by ATSDR, and several thousand times lower than levels that have caused effects in animals.

Cancer Assessment:

Several PAHs have been shown to have a carcinogenic potential. The potencies of the individual PAHs vary, so mixtures of PAHs are evaluated by expressing their carcinogenic potential as B(a)P equivalents. The following two scenarios assess cancer risks for adults and children who are exposed to PAH mixtures.

1). 30-Year Exposure

The highest concentrations of PAHs at the site in B(a)P equivalents was 80.9 ppm [8]. This was derived from the surface soil sample that had a total PAH concentration of 504 ppm. Using standard default values to evaluate potential carcinogenic risk: 30 year exposure to 80.9 ppm soil B(a)P equivalents (50 milligrams of contaminated soil ingested per day, 70 kilogram body weight), a cancer risk of 1.8E-04 is calculated. Calculation - (80.9 milligrams/kilogram) x (1/70 kilograms) x (50 milligrams soil/day) x (1 kilogram/106 milligrams) x (30/70) years = 0.000025 mg/kg/day; multiply by Cancer Slope Factor (7.3 mg/kg/day)-1 = 1.8E-04 estimated cancer risk. This is equivalent to 1.8 excess cancers per 10,000 exposed individuals.

2). 6-Year Exposure to Child

Again using standard default values to evaluate the potential carcinogenic risk: A 6-year exposure of a child to 80.9 ppm soil B(a)P equivalents (200 milligrams of contaminated soil ingested per day, 15 kilogram body weight), a cancer risk of 6.7E-04 is calculated. Calculation - (80.9 milligrams/kilogram) x (1/15 kilograms) x (200 milligrams soil/day) x (1 kilogram/106 milligrams) x (6/70) years = 0.000092 mg/kg/day; multiply by Cancer Slope Factor (7.3 mg/kg/day)-1 = 6.7E-04 estimated cancer risk. This is equivalent to 6.7 excess cancers per 10,000 exposed individuals.

The cancer risks calculated above for the two scenarios are considered unacceptable for contamination left in place. However, these calculations are very conservative, and the actual risks are likely to be much lower. For example, the calculations assume (1) continuous exposure and does not take into account winter months when exposure to the soil is limited (2) assumes 100% absorption of the ingested PAHs, and (3) does not account for a vegetative cover (e.g. grass) that serves as a protective barrier to exposure.

The calculations made above were also based on only one surface soil sample per yard. Typically, several samples are required to assess a site. Further, since no visible creosote contamination has been noted at the surface, the sampling results may have been skewed by a piece of hardened creosote material, and may not be representative of the soil that is likely to be ingested. More surface soil data would provide a better indication of the extent of contamination, and the likelihood of exposure.

Groundwater Pathway:

Although PAHs bind to the soil and do not migrate via groundwater very readily, there is a potential for creosote and some of its volatile fractions to do so. The installation and sampling of groundwater wells will assess this potential exposure pathway.

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