5.4 Human health blra criteria

To understand the rationale for selecting sample sites, the sampler must have a basic understanding of risk assessment criteria. The following components of a risk assessment are normally part of all risk assessment discussions—even if those discussions are ulti­mately negative declarations—"we do not have to worry about that."

5.5 Toxicity assessment

The toxicity assessment weighs available evidence that COPCs may cause adverse health effects in exposed humans or other biota. The assessment estimates the extent of potential chemical exposure and the increased likelihood and/or severity of adverse effects. The toxicity assessment at the site location is accomplished in two steps:

1. Chemical hazard identification determines whether potential chemical exposure causes an increased incidence or severity of an adverse health or environmental effect. Toxicological data for COPCs are reviewed, and toxicological profiles are prepared for the COPCs.

2. The dose-response evaluation consists of quantitatively evaluating the toxicity information. Then the relationship between the chemical dose and the resultant incidence/severity of adverse health or environmental effects are reviewed.

The risk characterization portion of the BLRA estimates the likelihood of adverse effects occurring under the exposure scenarios. For the chemicals identified (except lead) the toxicity values have been derived by the U.S. EPA and are summarized in the Integrated Risk Information System (IRIS) database.

The EPA has not developed a reference dose (RfD) or carcinogenic potency slope fac­tor (SF) for elemental lead. The EPA considers lead a special case because lead is ubiquitous in all media; therefore, human exposure comes from multiple sources. Thus most people would exceed an RfD level under "background" conditions. The EPA Office of Solid Waste and Emergency Response (OSWER) has released a directive on BLRA and cleanup of resi­dential soil lead. This directive recommends that soil lead levels less than 400 ppm are con­sidered safe for residential use. The EPA action level (SDWA) for lead in drinking water is 15 |xg/l. An RfD, 1 X 10~⁷ mg/kg/day, has been provided for tetraethyl lead, formerly a common additive for gasolines in the U.S. The current accepted site usage levels for lead are evaluated in concert with the surrounding area soil levels.

For noncarcinogens, an RfD is established by the EPA as a result of hazard identifica­tion and dose-response evaluation. The RfD is an estimate of an exposure level judged likely to be without an appreciable risk of adverse health effects over a specified time of exposure. A critical study (or studies) in which a dose causing an adverse effect is identi­fied at a lower level of exposure as either having no effect or minimal effect—yields the RfD. Chronic RfDs reflect a level of exposure that would not result in adverse effects when experienced for 7 years to a lifetime (Baseline Risk Assessment Guidance for Superfund [RAGS] Part A). If the RfD is expressed as an administered dose, dermal toxicity values are derived by adjusting the oral toxicity value (i.e., multiplying by a chemical absorp­tion factor).

The noncarcinogenic effects potential is evaluated by comparing the chemical intake with an RfD. This ratio is referred to as a hazard quotient (HQ). The HQ assumes that

below a certain level of exposure, even sensitive populations will not experience adverse effects. Based on this assumption, if exposure is equivalent to or less than the RfD and the HQ is 1.0 or less, a hazard is not likely to exist. If the HQ exceeds 1.0, a hazard may exist.

For carcinogens a cancer SF and a weight-of-evidence classification are the toxicity val­ues used in the characterization of potential human carcinogenic risks. The relationship relating exposure level to the probability of developing cancer (i.e., the incidence) is expressed as a cancer SF.

The SF is a plausible upper-bound estimate of the probability of developing cancer per unit intake of a chemical over a lifetime. SFs are expressed as (mg/kg-day)"¹. If the SF is expressed as an administered dose, a dermal toxicity value is derived by adjusting the oral toxicity value (i.e., dividing by the chemical absorption factor).

The potential for carcinogenic effects is estimated by multiplying a chemical's SF by the lifetime average daily chemical intake. Exposure to carcinogens resulting in an increased carcinogenic risk of 1 X 10~⁶ or greater may be cause for potential concern and may indi­cate the need for remedial action.

The risk of developing cancer as a result of exposure to carcinogens can also be expressed as a unit risk. This toxicity value represents a risk per unit concentration in the particular medium contacted. Unit risks reflect risks resulting from continuous lifetime exposures. Unit risks are expressed as (jjig/m³)"¹ for inhalation exposures or (ixg/1)"¹ for oral exposures. A unit risk in the range of 1 X 10~⁴ to 1 X 10~⁶ implies that an individual has between a 1 in 10,000 and a 1 in 1,000,000 chance of developing cancer in excess of a background incidence if exposed to 1 |xg/m³ air or 1 |xg/l water of a carcinogenic chemical for a lifetime.

The carcinogenic potential of a chemical is classified into one of the following groups according to the weight of evidence from epidemiological and animal studies:

• A—human carcinogen

• Б1—probable human carcinogen (limited evidence of carcinogenicity in humans)

• B2—probable human carcinogen (sufficient evidence in animals with inadequate evidence in humans)

• С—possible human carcinogen (limited evidence of carcinogenicity in animals or lack of human data)

• D—not classifiable as a human carcinogen

• E—evidence of noncarcinogenicity in humans