PUBLIC HEALTH ASSESSMENT

Plutonium 239 in Sewage Sludge
Used as a Soil or Soil Amendment in the Livermore Community

LAWRENCE LIVERMORE NATIONAL LABORATORY, MAIN SITE (U.S. DOE)
LIVERMORE, ALAMEDA COUNTY, CALIFORNIA


SECTION 4: PUBLIC HEALTH IMPLICATIONS

One hundred millirem per year (mrem/yr; above background) is the effective dose limit established for the general population by the International Commission on Radiological Protection (ICRP 1991; from ATSDR 1999) and used by ATSDR as the minimal risk level (MRL; ATSDR 1999b). An MRL is defined as "An estimate of daily human exposure to a dose of radiation or chemical that is likely to be without appreciable risk of adverse non-cancerous (8) effects over a specified period of time." The US EPA suggests that levels of 15 mrem/year or less (EDE) are protective of human health. The State of California uses an acceptable dose limit of 100 mrem/year for members of the public (Wong 2003).

Figure 5 shows the average Pu 239 soil concentrations that would be required to produce annual doses of 15, 25, and 100 mrem/year. The soil concentrations are derived from the RESRAD model output and also may be derived from linear extrapolation of the 0.31 mrem/year dose from a soil concentration of 2.5 pCi/g. In order to produce an annual dose of 15 mrem/year (considered to be health protective by the US EPA; EPA 1997), a residential yard would have to have an average Pu 239 concentration of more than 122 pCi/g. Similarly, to produce an annual dose of 25 mrem/year, a residential yard would have to have an average Pu 239 concentration of more than 204 pCi/g. A Pu 239 soil concentration of more than 816 pCi/g (average) would be required to produce an annual dose of 100 mrem/year (above background), which is considered health protective by the ATSDR and the ICRP (and is the dose limit used by the State of California).

These dose estimates and associated soil concentrations are derived using health protective assumptions for all exposure factors and durations. The estimated doses from these soil Pu 239 concentrations include ingestion of water and soil, inhalation of dust, ingestion of food grown in the soil, and direct external radiation. The intake rates and exposure durations for each of those routes of exposure are based on health-protective assumptions from the EPA exposure factor handbook or RESRAD default conditions as listed in the preceding section and Appendix 4.

Combining the above soil concentration-dose results with the LWRP gross alpha concentrations indicates that if the sludge was contaminated at a gross alpha concentration of 250 pCi/g, and that 108 truck loads of sludge were added to a 1/2 acre yard, the resulting dose would be less than the ATSDR MRL of 100 mrem/year. Although such an exposure scenario is possible, it is very unlikely. One or two truck loads of sludge at a concentration of 100 pCi/g, added to a yard would add a dose of 0.1 to 0.2 mrem/year to the natural background terrestrial dose of ~44 mrem/year (NCRP 1987). (9) Excess doses (above background) in the range of 0.1 to 0.2 mrem/year cannot be discriminated from natural background doses for the San Francisco area). The following sections will present a brief discussion of the toxicology of plutonium and the levels of radiation exposure that have been shown to produce cancer or other adverse health effects.

Pu 239 (and/or Pu 240) soil concentrations that produce annual radiological doses of 15, 25 and 100 mrem/year. Soil concentrations are derived from RESRAD soil guidance values for each dose and assume average concentrations over an entire area or residential yard. An average Pu 239 soil concentration of 122 pCi/g over an entire residential yard is required to produce an annual dose of 15 mrem/year. An average concentration of 204 pCi/g Pu 239 is required to produce an annual dose of 25 mrem/year, and an average concentration of 816 pCi/g will produce an annual dose of 100 mrem/year (above background).
Figure 5. Pu 239 (and/or Pu 240) soil concentrations that produce annual radiological doses of 15, 25 and 100 mrem/year. Soil concentrations are derived from RESRAD soil guidance values for each dose and assume average concentrations over an entire area or residential yard. An average Pu 239 soil concentration of 122 pCi/g over an entire residential yard is required to produce an annual dose of 15 mrem/year. An average concentration of 204 pCi/g Pu 239 is required to produce an annual dose of 25 mrem/year, and an average concentration of 816 pCi/g will produce an annual dose of 100 mrem/year (above background).

Toxicology of Pu 239/240

Plutonium is a silvery-white radioactive metal that is a solid under normal conditions. Produced in a nuclear reactor by the conversion of uranium, plutonium is found in the environment as the result of fallout from atmospheric nuclear testing. The most common forms of plutonium (isotopes) are plutonium 238 and plutonium 239, abbreviated Pu 238 and Pu 239. Because plutonium is a radioactive element, it constantly undergoes changes called "radioactive decays." In this decay process, energy is released and a new radioactive product is formed. Most plutonium is found in nature combined with other substances, for example, plutonium dioxide (plutonium with oxygen) or plutonium nitrate (plutonium with nitrogen and oxygen) (ATSDR, 1990). As the contaminant of concern for the sewage sludge release is Pu 239, the remainder of this section will only deal with Pu 239. Pu 239 is an alpha emitter and a gamma emitter. The energy released by the radioactive decays may cause damage to cells or the surrounding tissues. In order for damage to occur, the radiation must either be absorbed by the surrounding cells or some of the energy as the radiation passes through the cell must be transferred to the cell and the surrounding medium (Johns and Cunningham, 1983).

Plutonium enters the body mainly through two pathways, inhalation and ingestion. Studies have shown that plutonium is not absorbed through the skin; however, it can enter the body via cuts and wounds (ATSDR, 1990). For all pathways, the Pu leaves the body mostly by feces and urine. Any plutonium that is not eliminated is absorbed by the body where it deposits in the organs. The most common organs for deposition following ingestion include the bone surfaces (skeleton) and liver. The lung, however, is the most impacted organ following inhalation (ICRP, 1989). As a result of these intakes, the plutonium generally stays in the body for decades and continues to expose the surrounding tissues to radiation.

The intake of plutonium may eventually increase your chance of developing cancer, but it would be several years before such cancer effects became apparent, especially at extremely low exposures. The experimental evidence regarding cancer induction at low dose exposures is inconclusive, and studies of some human populations who have been exposed to low levels of plutonium have not definitely shown an increase in cancer. However, in laboratory animals, plutonium has been shown to cause both cancers and other damage, and might affect the ability to resist disease by reducing the immune response (ATSDR, 1990). The International Agency for Research on Cancer (IARC) states, "Dose-response relationships have been demonstrated for cancers of the lung, liver, and bone in both men and women exposed to a broad range of doses", and thus IARC has classified plutonium as carcinogenic to humans (Group 1).

Plutonium is not easily absorbed into the body. The International Commission on Radiation Protection (ICRP) has reviewed the literature and recommends that an absorption coefficient of 0.5% (infants) or 0.05% (adults) be used for ingestion. In the case of inhalation, the ICRP recommends an absorption coefficient of 0.1% (infants) and 0.01% (adults) for plutonium with very low solubility in the lung. The absorption coefficient is the fractional uptake of a radionuclide that would be absorbed into blood without radiological decay. The low values of these coefficients mean that 99.5% to 99.9% of the plutonium ingested or inhaled is not absorbed by the body. Of the amount transferred to the blood, less than 25% would be transferred to the skeleton and another 25% or less would be transferred to the liver (ICRP, 1989). In other words, if one were to ingest a picocurie of Pu 239, the amount that could be transferred to the skeleton or liver for possible deposition into the organs of interest is 0.00125 pCi for infants and 0.000125 pCi for adults. For an adult with a body weight of 70 kilograms (154 pounds), this is about 1.8 10-9 pCi/g body weight.

We do not know if plutonium deposited in the human body causes birth defects or affects the ability to have children. If plutonium can reach these sensitive target tissues, radioactivity from plutonium may produce these effects. A number of studies have documented levels of exposure that have caused no adverse health effects. Conversely, other studies have documented high levels of exposure that have caused adverse health effects. However, no information from peer-reviewed studies in humans or in animals has identified the specific level of exposure to plutonium in air, food, or water above which may result in harmful effects (ATSDR, 1990).

ATSDR also reported in its Toxicological Profile for Plutonium, a peer-reviewed analysis of the existing data, the following synopsis of the health effects of plutonium on humans (ATSDR 1990). Information on health effects in humans is very limited largely because exposed populations are small. Epidemiological studies of people who have been occupationally exposed by inhalation to plutonium have evaluated end points such as mortality, cancer, and systemic effects following chronic exposure. No information on health effects in humans after acute or intermediate exposure to plutonium was located. Nonetheless, the following observations were made in the toxicological profile:

  1. No deaths in humans specifically associated with plutonium have been reported following acute plutonium exposure;


  2. Neither deaths due to respiratory disease nor reduced respiratory function have been reported among the occupationally exposed cohorts;


  3. No acute hematological effects were observed among human volunteers given a single injection of plutonium, but no follow-up study was conducted to assess the possibility of delayed effects;


  4. Adverse hepatic effects associated with plutonium exposure have not been reported in humans;


  5. Adverse musculoskeletal effects associated with plutonium exposure have not been reported in humans


  6. Adverse gastrointestinal effects associated with plutonium exposure have not been reported in humans;


  7. No reports exist showing an adverse immunological effects associated with plutonium exposure in humans;


  8. With regards to genetic damage, epidemiological studies do not provide evidence that plutonium produces genetic damage in humans. In particular, the data from persons involved in the Manhattan project after a 30-year follow-up have been negative; and


  9. In workers with long-term exposure to plutonium (including workers at Los Alamos National Laboratory, Rocky Flats Nuclear Weapons Plant, or Hanford Weapons Plant and the cohort involved in the original Manhattan project at Los Alamos) no studies have demonstrated an unequivocal association between exposure to plutonium and cancer mortality 30 or more years after the exposures occurred.

Animal studies, however, have shown effects of plutonium exposure. For example, in dogs exposed to plutonium via inhalation, cancer and immunological effects were observed at a concentration of 1 pCi/g-animal weight (for an 8 kg dog, the dose would be 8,000 pCi). In mice, adverse health effects on the respiratory system were not observed following inhalation that resulted in a body burden of plutonium equivalent to 3 pCi/g-mouse weight. These exposures were over 2 weeks or less (ATSDR, 1990).

Rats given plutonium via ingestion over 2 weeks period had no adverse health effects with as much as 100 pCi/g body weight. The lowest observed effect level was approximately 300,000 pCi/g (ATSDR, 1990). These results indicate a significant difference in the dose effect from inhalation and ingestion. An inhaled dose is much more radiotoxic than an ingested dose. These factors are accounted for in the dose conversion factors and included in the RESRAD analysis (ANL, 2000).

Health effects associated with exposure to ionizing radiation

Exposure to radiation is expressed as two generic types, acute and chronic exposures. By definition, ATSDR considers acute exposures as exposures having a duration of less than 2 weeks; whereas, chronic exposures occur over a year or more (ATSDR, 1990, 1999).

The adverse health effects from acute exposures to radiation have been well defined as a result of the atomic bomb survivors, medical exposures and other medical accidents. The issues for this document are those health effects associated with chronic exposures to ionizing radiation. These health effects are more difficult to define, characterize, and discuss. ATSDR experience at sites contaminated with radioactive materials shows that chronic exposures are incremental in comparison to background. In the United States, background consists of naturally occurring radon (54%), terrestrial and cosmic radiation (8% each), and internal (11%). The remainder (19%) is associated with medical exposures and consumer products(ATSDR 1999). The typical average background radiation in the United States is 3.6 mSv (360 millirem) per year. Average external terrestrial (radionuclides in soil) background radiation exposures for the San Francisco area are about 44 mrem/year with a 95th percentile value of about 80 mrem/year (NCRP 1987).

Health Effects from background radiation

There have never been any peer-reviewed studies to show that background levels of radiation are harmful. In fact, there are portions of the globe where the background is higher than the typical area in the United States. According to the United Nations, the background can vary from below 1 mSv (100 millirem) to above 6.4 mSv (640 millirem) per year or more. For example, for an area in China where elevated levels of natural background radiation are found, studies have shown a significant increase in chromosomal aberrations, but there have been no observed increases in adverse health effects (over the 20 or more years this area has been studied). Other areas in the world where there are high background radiation levels include India, Brazil, and Iran. The area in Iran, Ramsar, has verified doses as high as 130 mSv per year (13,000 millirem) (10).

Incremental exposures above background radiation

Many studies have attempted to show a cause and effect from low-level chronic radiation exposure. In these studies, low dose has been defined as any dose less than 10 mSv (1,000 mrem). No studies exist for exposures or doses below this limit. For many of these low dose epidemiological studies, researchers used the standard mortality ratio (SMR) to estimate adverse health effects. The SMR is defined as the ratio of observed deaths in a population to the expected number of deaths as derived from rates in a standard population with adjustment of age and possibly other factors such as sex or race (Society for Risk Analysis). An SMR less than 1 indicates no causality or association.

An English study of over 95,000 radiation workers whose collective dose from external radiation is about 3200 man Sv (3200/95000 = 34 mSv or 3,400 mrem) only took into account external radiation exposure and dose. The results showed the standard mortality ratio for all cancers was less than 1 (Kendall et.al. 1992).

A later study by Cardis and coworkers included 95,000 nuclear industry workers in the United States, Canada, and the United Kingdom. The study participants were monitored for external radiation exposure (mostly gamma) and were employed for at least 6 months. In all, there were 15,825 deaths, of which 3976 were from cancer. The authors found no evidence of a dose response or mortality association from all causes or from all cancers. Of the cancer types, only leukemia (except for chronic lymphocytic and multiple myeloma) showed a significant association with cumulative external radiation dose (Cardis et.al. 1995). From the cardis paper - "The combined analysis of the data for the workers demonstrated a significant (P=0.046) association between mortality from leukemia excluding CCL and radiation dose in a population receiving protracted low-dose-rate exposures." They also state "The observed association between radiation dose and mortality from leukemia excluding CCL appeared to be restricted to myeloid leukemia, particularly CML ...."

In a cohort study to determine if children were at risk of developing leukemia or other cancers before 25 years of age, Roman and coworkers included 39,557 children of male nuclear industry workers and 8883 of female workers. The study suggested that the incidence of cancer and leukemia among children of nuclear industry employees is similar to that in the general population. The SMR for all cancers and leukemias for each sex of the worker was less than 1 (Roman et.al. 1999).

Special Consideration of Women and Children

The effect of radiation on humans, in general, has been well studied. However, there are few studies, especially with plutonium exposure, that are specific for women or children. In estimating radiological doses, the ICRP calculates dose conversion factors based on 6 age groups: 0 to 12 months; 1 to 2 years; 2 to 7 years; 7 to 12 years; 12 to 17 years; and more than 17 years in the cases of adult exposures. In some cases, such as the factors for plutonium, the adult exposures are calculated for 25 years or more (up to 70 years for this assessment) using the age-specific dose conversion factors. Other exposure factors include exposure durations, body and organ weights time periods, body and organ weights, and intake rates that represent childhood exposures. Consequently, the dose assessment methodology, following the intake of radioactive materials by the general population, is representative of children and adults. Also an age-adjusted soil ingestion rate is used to account for childhood soil intake, which may be larger than adult intakes (EPA 1999). Food intake rates are based on the larger long-term adult rates which is health protective for children. Therefore, the ICRP methodology and the exposure factors used in this assessment are health protective for men, women, and children.

Plutonium Doses of Public Health Concern

In order to determine whether the potential exposures to Pu-contaminated sludge presents a public health hazard, ATSDR compared the estimated doses with benchmarks or screening doses that are derived from dose levels known to produce adverse health effects. For ionizing radiation, which includes plutonium and its decay products, ATSDR has developed minimal risk levels (MRLs) that cover brief exposures (acute, or less than 14 days) and longer term exposures (chronic, or more than a year).

An MRL is an estimate of the daily human exposure to a hazardous substance that is likely to be without appreciable risk of adverse non-cancer health effects over a specified duration of exposure. The MRL is derived from exposure levels observed to produce adverse effects, with uncertainties (or safety factors) incorporated into the value.  Thus, MRLs are intended only to serve as a screening tool to help public health professionals decide which release situations require more extensive evaluation.  While estimated exposure dose levels below an MRL are not likely to produce non-cancer adverse effects, exposure estimates above an MRL do not mean that adverse effects will occur. ATSDR then evaluates the potential for adverse health effects in an exposed community by comparing levels known to produce adverse effects to the estimated site-related doses. This margin of exposure (MOE) approach, along with an evaluation of  available epidemiologic, toxicologic, and medical data, is used by health assessors as part of the public health determination to reach qualitative (rather than quantitative) decisions about hazards posed by site-specific conditions of exposure.

On the basis of an extensive review of the health studies and documented health effects from radiological exposures, ATSDR established an MRL of 400 mrem for acute duration (14 days or less) of external exposure (11) (ATSDR 1999) to ionizing radiation. The acute MRL is based on external dose levels that did not produce behavioral and/or neurological effects on the developing human embryo and fetus. Similarly, a chronic duration (a year or more) of external exposure MRL of 100 mrem/year (above background) has been established based on radiation doses that have not produced observable detrimental health effects in humans. Thus, the ATSDR acute and chronic MRLs for ionizing radiation (including tritium) are based on doses with No Observed Adverse Effect Levels (NOAELs). While ATSDR MRLs typically include only non-cancer health effects, all the studies on which the chronic MRL for ionizing radiation are based included cancer as the specific end-point.  Consequently, the chronic MRL for ionizing radiation is considered protective for both cancer and non-cancer health effects.

Similarly, ATSDR also evaluates the potential for cancer risk by first comparing the estimated dose levels to a theoretical risk level, usually the dose level associated with a 10-6 risk (one in a million) as defined by other governmental agencies.  ATSDR designates these screening levels as Cancer Risk Evaluation Guides (CREGs). As with the non-cancer approach, levels less than 10-6 require no further evaluation, while estimated dose levels that exceed the 10-6 value are evaluated further. The potential for observing adverse effects is made on the basis of dose evaluation (an MOE approach), rather than on the basis of theoretical risk calculations. (See below discussion on dose-based qualitative approaches for health assessment versus risk-based, quantiative approaches used by regulatory agencies).

In contrast to the dose-based health assessments conducted by ATSDR, the United States Environmental Protection Agency (EPA) develops regulations based on risk and policy decisions. To accommodate proper evaluation of the dose and risk issues associated with radiation exposure, it is necessary to clearly define the terms dose and risk. The International Society for Risk Analysis (www.sra.org) defines risk as "The potential for realization of unwanted, adverse consequences to human life, health, property, or the environment; estimation of risk is usually based on the expected value of the conditional probability of the event occurring times the consequence of the event given that it has occurred." As defined, risk is a statistical concept, and the threshold for acceptable risk, which is not based on observable adverse health effects, is simply a policy statement. Risk Assessments are useful in determining safe regulatory limits. The regulatory limits have extra safety factors built into them and may in fact be orders of magnitude below levels at which adverse effects have been documented to occur in humans. Risk assessments are useful in providing comparative risk discussions for purposes of prioritizing cleanup.

ATSDR defines dose as "The amount of a substance to which a person may be exposed, usually on a daily basis. Dose is often explained as "amount of substance(s) per body weight per day". Doses are the basis for determining levels of exposure that may cause adverse health effects and may be directly related to the assessment of public health. As noted, ATSDR uses risk assessment procedures as a screening tool in its evaluation, including MOE approaches along with the consideration of health effects data (epidemiologic, toxicologic, and medical) to reach conclusions about the potential for adverse effects being observed in the community.

More specifically, ATSDR uses radiation doses instead of risk in its public health documents for various reasons. Among these are the facts that dose coefficients are based on a more exact science; that is, the doses are based on physical constants and primary principles of physics such as energy absorption. Health effects resulting from radiation doses are based on a "weight-of-evidence" approach. ATSDR, in preparing its public health documents, also relies on site-specific parameters such as demographics, realistic land uses, and other pertinent data related to the site. Using dose coefficients and modifying the coefficients for chemical forms and particle sizes, which are not typically done for risk assessments, allows ATSDR to develop health-protective, albeit realistic, values for the dose assessments as they pertain to public health documents.

Similarly, radiation health studies use dose because there is a long history of research in which health outcomes were evaluated relative to the radiation dose and not on the numerical estimation of risk. ATSDR also recognizes there are uncertainties in these dose coefficients; however, those uncertainties are addressed by the use of health protective safety factors. Risk calculations include those uncertainties plus additional uncertainty associated with the risk estimation model. Consequently, the derivation of quantitative risk is much more uncertain that the underlying dose-based assessment.

The uncertainty in the dose effects lies within the middle ranges of exposure. Adverse health effects have been conclusively demonstrated for exposures greater than 10,000 mrem/year (ATSDR 1999). Numerous studies have also demonstrated that no adverse health effects have been documented for doses less than 360 mrem/year (ATSDR 1999). The ATSDR minimal risk level (MRL) for ionizing radiation is based on numerous evaluations of health effects from exposures to background and occupational levels of radiation. "The annual dose of 3.6 mSv per year (360 mrem/year) has not been associated with adverse health effects or increases in the incidence of cancers in humans or animals." (ATSDR 1999). Consequently, 360 mrem/year is defined as a "No Observed Adverse Effect Level" (NOAEL). The derived MRL, which is further reduced by a factor of 3 to account for human variability (and conservatively rounded down from 120 mrem/year to 100 mrem/year), is protective of human health.

The science associated with risk is based on a model that, at low doses typically associated with small multiples of background, cannot be proven. ATSDR also realizes that every action, radiation dose, or activity has an associated risk. However, because no adverse health effects have been observed at doses considerably higher than 100 mrem/year (above background), there is no public health basis for using highly uncertain, risk-based screening values. Acute exposures to plutonium via the inhalation, ingestion, and dermal pathways described in this health assessment that resulted in cumulative doses of less than 400 mrem or in chronic exposures less than 100 mrem/year (above background and averaged over 5 years) are unlikely to produce any adverse health effects and therefore are below levels of public health concern.

Adequacy of Available Data for Public Health Determination

The data underlying this public health assessment, as with all analytical data, have limitations involving sampling and measurement procedures. The most significant limitation is the lack of direct Pu 239 analyses of processed sludge following the 1964 and 1967 release events that may have been distributed to the Livermore community. (12) This limitation is resolved through the use of gross alpha data from both processed sludge and digester sludge. Available data indicate that gross alpha measurements will overestimate Pu 239 concentrations and that digester sludge concentrations will overestimate processed sludge concentrations. Consequently, use of digester sludge gross alpha concentrations is a health protective proxy for Pu 239 concentrations in processed sludge.

The use of the health protective gross alpha measurements presents another limitation. Because these values overestimate the processed sludge concentrations, they do not allow for direct evaluation of actual sludge concentrations. We only know that processed sludge Pu 239 concentrations are lower than the digester gross alpha values, we do not know how much lower. This limitation is not a problem as long as the Pu 239 doses calculated from the maximum, overestimated gross alpha concentrations are below levels of health concern. As the preceding sections indicate that the doses calculated from maximum gross alpha concentrations are below levels of health concern, this uncertainty in the available data does not present a significant problem in the use or evaluation of the available data.

Total reliance on the state-collected and analyzed digester gross alpha data set could also present several data limitations. There are several gaps in this data during the period 1960 to 1963, as well as after 1969 (Figure 3). However, during the period of those data gaps, sewer effluent and annual release data from LLNL are available. These data, which accurately track the CDHS digester gross alpha measurements during all other time periods, indicate that there were no significant Pu 239 (or gross alpha) releases during the time of the digester gross alpha data gaps.

Prior to May 1963, the state-collected digester gross alpha concentrations were reported as wet weight analyses (vs. dried weight analyses for all later time periods). (13) Although the difference in analytical methods may affect the absolute data values, the overall trends in the data indicate that the relative magnitudes are similar.

The 1964-65 time period includes the highest reported digester gross alpha concentration (297 pCi/g) as analyzed by CDPH. LLNL sewer effluent and annual release values during this same time period do indicate a release event(s), but not of the same magnitude as the May-June 1967 event. Processed sludge gross alpha concentrations for 1965 (~8-12 months following the digester gross alpha spike) reached 60 pCi/g (6 month average). These are the highest processed sludge gross alpha concentrations. The fact that digester sludge gross alpha concentrations for the 1964 and 1967 events were of similar magnitude (297 pCi/g vs. 258 pCi/g, respectively) suggests that processed sludge gross alpha concentrations following the 1967 release were also of a similar magnitude.

Community members have also expressed a concern that all of the data underlying this evaluation consist of gross alpha or Pu 239 concentrations averaged over different time periods. Digester concentrations are presented as monthly averages; processed sludge, LLNL sewer effluent, and annual release data are reported as 6 or 12 month average values (14). The basis of this concern seems to be that the 6 or 12 month average values may miss short term events or spikes in the Pu 239 concentrations. This apparent limitation is resolved by the mixing or averaging that occurs in the sewage treatment process.

Figure 6 shows the gross alpha concentrations from daily samples collected and analyzed by LLNL. These daily measurements have recently been recalculated from historic monitoring data records (McConachie 2003) and monthly averages of the daily values are included in Appendix 5. Maxima of the daily samples are about 4 times greater than the monthly composite samples analyzed by CDPH (Figure 3; Appendix 5). However, due to the mixing and dilution that occurs during the treatment process, the resulting processed sludge will not have similar short term Pu 239 concentration peaks.

Sewage treatment and sludge production is an averaging process. Material is added to and pumped from the digesters with an approximate processing duration of 1 month (see Appendix 2; also confirmed by J. Dupont, former LWRP plant manager, personal communication with M. Evans, ATSDR, 2002). Sludge from the digesters is added to the lagoons or drying beds over periods of 1 to 5 years. Processed, dried sludge is milled or ground before distribution resulting in further mixing. Thus, the production of sludge represents a mixing or averaging process over a period of at least one to several years. The use of 6 or 12 month average concentrations to represent this processed sludge will not result in the loss of useful information. Because of the mixing inherent in the sewage treatment system, short term releases to the sewer system will not occur as short term spikes in the Pu 239 concentration of processed sludge.

The validity of all of the historical data has also been questioned because current quality control and data management practices were not utilized for the collection and analysis of historical monitoring data. There have been many improvements in the analytical and data management procedures underlying environmental monitoring programs from those of the 1960s. The direction of these improvements is the reliable and accurate determination of very low contaminant concentrations. This public health evaluation of Pu 239 or gross alpha concentrations is based on determination of the maximum concentrations. These maximum concentrations are well within the basic limitations of the historic gas flow proportional counting technique used to measure gross alpha concentrations.

The overall utility of the historical data is indicated by the convergent and similar trends of the different data types. The similar patterns of digester sludge, LLNL sewer effluent, dried sludge, and annual release data over time (Figure 3) show similar peaks and declines, albeit with some time lags. The time lags are a necessary artifact of the treatment process and the duration of the time lags are appropriate to the sewage processing timeframe. In other words, digester gross alpha concentrations go up when effluent concentrations from LLNL indicate they should go up. Gross alpha concentrations in processed sludge go up 8 to 12 months after digester concentrations go up.

There is some inherent uncertainty in all monitoring or sampling data. This is because the measurement of the contaminant concentration in a very small "sample" is assumed to represent the contaminant concentration of the entire volume or mass of media of concern. Some community members have expressed a desire for additional soil sampling throughout the Livermore community to determine the Pu 239 concentrations in any areas where sludge from LWRP may have been distributed. Such sampling would be subject to the same types of uncertainty, with respect to sampling and analysis procedures, as past sampling. Further, the passage of more than 30 years following placement of any sludge from the 1967 release would make determination of appropriate locations to sample highly uncertain and increase the amount of dilution with non-contaminated soils.

Daily (and later weekly) measurements of gross alpha concentrations in LWRP digesters 1 and 2 in 1967 by LLNL (data from McConachie 2003). Note that the daily samples record higher concentrations than the monthly composites analyzed by CDPH (Figure 3).
Figure 6. Daily (and later weekly) measurements of gross alpha concentrations in LWRP digesters 1 and 2 in 1967 by LLNL (data from McConachie 2003). Note that the daily samples record higher concentrations than the monthly composites analyzed by CDPH (Figure 3).

Exposure and Health Evaluation

The purpose of this PHA is to evaluate the public health implications of the historical distribution of Pu-contaminated sludge to the Livermore community by answering three specific questions: 1) What concentrations of Pu 239 in sludge would produce doses of public health concern? 2) Were the concentrations of Pu 239 in the sludge distributed to the public by LWRP greater than the levels of potential health concern? 3) Do the available data provide an adequate basis for this exposure assessment and the resulting public health conclusions? The ATSDR MRL or 100 mrem/year is used as a basis for determining radiological doses of public health concern. No adverse health effects have ever been documented from radiological doses of 100 mrem/year or less (above background).

With regard to question 1, a soil (100 percent sludge cover) Pu 239 concentration of 816 pCi/g (averaged over entire area) is required to produce a dose of 100 mrem/year, as calculated using RESRAD. This calculation includes health-protective exposure factors and includes ingestion of soil and garden crops, inhalation of dust, and external exposure. This calculation also assumes that the contaminated area covers an area of acre to a depth of 2 meters, of the area is unvegetated (bare soil), and of the resident's food is grown on the contaminated area. Considering that about 65% of the total dose comes from food crops grown in the residential yard and that of all fruits, grains, and vegetables consumed are from the home garden, this is a very health protective assumption underlying the dose calculations. Further, because it would take 108 pick-up truck loads of sludge to cover a 1/2 acre lot (3 inch depth), such an exposure scenario, although possible, is very unlikely.

A nearly complete historical record of LWRP gross alpha concentrations for the period of 1960 through 1973 indicates that maximum digester sludge concentrations (as analyzed by CDPH) were less than 300 pCi/g. The digester sludge values show two distinct peaks corresponding with the 1964 and 1967 release episodes (297 pCi/g and 258 pCi/g, respectively). Gross alpha concentrations of LLNL effluent into the Livermore sewer system show the same peaks and provide supplementary data for those periods during which digester concentrations were not collected or analyzed. Collectively, the state analyzed digester sludge data and the LLNL analyzed effluent data indicate that the 1964 and 1967 release episodes represent the worst-case sludge concentrations.

As the concentrations of Pu 239 in processed sewage sludge following the 1964 episode of maximum digester sludge concentration were less than 816 pCi/g, it follows that the maximum Pu 239 concentrations in sludge were below levels of health concern. Although sludge concentrations following the 1967 event are not available, processed sludge gross alpha concentrations following the 297 pCi/g digester sludge values were approximately 60 pCi/g. This indicates that digester sludge gross alpha concentrations are considerably reduced during the treatment process. As processed sludge is further milled and mixed before disposal, it is expected that processed sludge concentrations would have been additionally reduced before distribution to the public.

Several areas where contaminated sludge was placed have been sampled for Pu 239 concentrations. These areas include Big Trees Park, residential yards of LLNL employees, and a test garden on the LLNL facility. Maximum Pu 239 concentrations of these locations were less than 2 pCi/g. Although the initial sludge concentration of most of these areas is unknown, sludge and soil sampling at the LLNL test garden indicated that sludge Pu 239 concentrations are reduced by a factor of more than 5 in the resulting soil. This indicates that tilling and mixing of applied sludge will additionally reduce residential soil Pu 239 concentrations.

Assuming that the available gross alpha concentrations in LWRP sludge and LLNL sewer effluent are a reasonable substitute for direct Pu 239 measurements, the available data clearly indicate that the Pu 239-contaminated sludge does not result in radiological doses of public health concern. Monthly nuclide specific and gross alpha monitoring data for 1973 indicate that gross alpha concentrations overestimate Pu 239 concentrations. Consequently, the use of gross alpha concentrations as a proxy for Pu 239 concentrations is a health protective assumption.

No single data set is adequate for making the above public health determinations. There is not a consistent time series of processed sludge Pu 239 or gross alpha concentrations. Similarly, there are gaps in the digester sludge measurements, and the LLNL effluent data do not provide specific levels of sludge contamination. However, collectively, the available data do provide an adequate basis for the public health assessment. The trends in the different data values support and reinforce the individual data sets. As the different data sets supplement each other, gaps in any one data source do not present a critical lack of information. Additionally, the health protective assumptions used in calculating doses provide additional certainty for the health conclusions. Consequently, the available data provide an adequate basis for public health assessment.

The data evaluated in this public health assessment clearly indicate that, although Pu 239-contaminated sludge was distributed to the Livermore community, the resulting radiological doses were below levels of public health concern. Some community members have doubts about the adequacy of the available data as a basis for the public health determination. They have recommended the collection of additional information on the historic distribution of contaminated sludge and soil sampling of areas determined to have received such sludge. As there is no public health basis for such sampling and the proposed sample results would be inconclusive, ATSDR is not currently recommending additional soil sampling.


SECTION 5. CONCLUSIONS, RECOMMENDATIONS, AND PUBLIC HEALTH ACTION PLAN

Conclusions

Pu 239 (including coincidentally measured Pu 240) was historically released from LLNL to the Livermore sewer system as both low level chronic releases and as higher concentration short-term episodes. Release episodes of particular concern occurred in 1964 and 1967. The sewage effluent from LLNL is both monitored and regulated and available data indicates that the historical releases, including the 1964 and 1967 episodes did not exceed permitted release concentrations.

Processed sludge from the LWRP was historically distributed to the Livermore community for use as a soil amendment or additive. There has been considerable community concern that exposure to the Pu 239-contaminated sewage sludge could result in radiological doses of health concern. These community health concerns have been exacerbated by the lack of direct measurements of Pu 239 concentrations in the processed sludge and some uncertainty about the specific distribution of sludge following the 1964 and 1967 releases. Historical monitoring involved measurement of gross alpha concentrations rather than nuclide-specific Pu 239 measurements.

The following conclusions are based on our current knowledge of radiation health effects and the data reviewed and evaluated in this health assessment:

  1. Pu 239 from LLNL was released to the Livermore sewer system and resulted in the contamination of LWRP sludge which may have been distributed to the Livermore community resulting in areas with Pu 239 soil concentrations above background.


  2. Using health protective exposure assumptions, radiological doses from maximum measured concentrations of any distributed sludge are below levels of health concern. This evaluation assumes that digester sludge gross alpha concentrations represent Pu 239 concentrations and that digester sludge is spread uniformly over an entire residential yard. Pu 239 concentrations of processed sludge distributed to the Livermore community are calculated to be more than 10 times lower than digester sludge concentrations.


  3. The available data and evaluations provide an adequate basis for these public health conclusions. Any additional sampling data will be subject to the same types of uncertainties as existing historical data.

Based on the above conclusions, the historic distribution of Pu-contaminated sewage sludge is determined to be no apparent public health hazard. This determination means that while exposure may have occurred, or may still be occurring, the resulting doses are unlikely to cause cancer, other illnesses, or death.

Recommendations

As the potential maximum radiological doses from exposures to Pu 239-contaminated sludge are below levels of health concern, ATSDR has no recommendations concerning additional soil sampling in areas of known or unknown sludge distribution. However, because the community may still have unresolved community concerns about this issue, ATSDR offers the following recommendations:

  1. Develop and present educational materials, based on the information included in this public health assessment, to the Livermore.


  2. Continue current monitoring of Pu 239 (and other contaminant) concentrations in LLNL effluent and the LWRP sewage treatment system (as stipulated by existing discharge permit requirements).

Public Health Action Plan

  1. ATSDR will prepare and distribute audience-specific educational materials based on the information presented in this PHA and other LLNL-specific ATSDR documents. ATSDR will conduct additional public availability sessions or make presentations at other community meetings to address community health concerns related to LLNL.


  2. LLNL will continue current radiological monitoring, as stipulated in current discharge and operating permits, to ensure that future plutonium (and other radionuclide) releases are below levels of public health concern.

REFERENCES

ANL 2001. RESRAD Version 6, Users Manual and Software, Argonne National Laboratory, ANL/EAD-04, Argonne IL.

ATSDR 1990. Toxicological Profile for Plutonium. Atlanta: US Department of Health and Human Services, 1 Agency for Toxic Substances and Disease Registry, Atlanta, GA, 1990.

ATSDR 1999a. Health Consultation, Plutonium Contamination in Big Trees Park, Lawrence Livermore National Laboratory, U.S. Department of Health and Human Services, Agency for Toxic Substances and Disease Registry, Atlanta, GA, May 17, 1999.

ATSDR 1999b. Toxicological Profile for Ionizing Radiation. Atlanta: US Department of Health and Human Services. Agency for Toxic Substances and Disease Registry, Atlanta, GA, September, 1999.

ATSDR 2000. Health Consultation, Big Trees Park 1998 Sampling, Lawrence Livermore National Laboratory, U.S. Department of Health and Human Services, Agency for Toxic Substances and Disease Registry, Atlanta, GA, January 10, 2000.

Balke, B. 1993. Plutonium Discharges to the Sanitary Sewer: Health Impacts at the Livermore Water Reclamation Plant. Lawrence Livermore National Laboratory, Environmental Protection Department, LLNL, Univ. of California, Livermore CA, April 16, 1993.

Cardis et.al. 1995. Cardis E, Gilbert ES, Carpenter L, Howe G, Kato I, Armstrong BK, Beral V, Cowper G, Douglas A, Fix J, et al. (1995). Effects of low doses and low dose rates of external ionizing radiation: cancer mortality among nuclear industry workers in three countries. Radiation research 142:117-132.

CDHS 1960-1969. Data sheets entitled Gross Radioactivity in Sewage Samples: 1960-1969, Published in the Radiological Health News, California Department of Health Services, Radiological Health Branch.

CDHS 2001. Health Consultation, Community Health Concerns, Lawrence Livermore National Laboratory. Prepared by California Department of Health Services, Oakland CA, April 30, 2001.

CDHS 2002. Proposed Process to Address the Historic Distribution of Sewage Sludge Containing Plutonium Releases from the Lawrence Livermore National Laboratory. Environmental Health Investigations Branch, California Department of Health Services, Oakland CA. November 2002.

DOE 1992. U.S. Department of Energy (DOE), 1992. Final Environmental Impact Statement and Environmental Impact Report for Continued Operation of the Lawrence Livermore National Laboratory and Sandia National Laboratories, Livermore. U.S. Department of Energy and University of California, DOE/EIS-0157. August 1992.

Eisenbud M and Gesell T, 1997. Environmental Radioactivity from Natural, Industrial, and Military Sources, 4th Edition. Academic Press, San Diego CA.

EPA 2002. Soil Screening Guidance for Radionuclides, U.S. Environmental Protection Agency website, http://risk.lsd.ornl.gov/rad_start.shtml, October, 2002.

EPA 1999. Exposure Factors Handbook. Washington DC: Environmental Protection Agency, EPA/600/C-99/001; 1999 February.

EPA 1997. Memorandum: Clarification of the Role of Applicable, or Relevant and Appropriate Requirements in Establishing Preliminary Remediation Goals Under CERCLA, From Timothy Fields, Acting Assistant Administrator, Office of Solid Waste and Emergency Response No. 9200.4-23, U.S. Environmental Protection Agency, Washington, D.C., August 22, 1997.

EPA 1994. Environmental Protection Agency (1994). Estimating Radiogenic Cancer Risks. EPA 402-R-93-076.

GAO 1994. United States General Accounting Office (1994). Report to the Chairman, Committee on Governmental Affairs, U.S. Senate. Nuclear Health and Safety: Consensus on Acceptable Radiation Risk to the Public Is Lacking. GAO/WED-94-190.

GAO 2000. United States General Accounting Office (2000). GAO Report to the Honorable Pete Domenici, U.S. Senate. June 2000 Radiation Standards: Scientific Basis Inconclusive, and EPA and NRC Disagreement Continues. GAO/RCED-00-152.

ICRP 1979. Limits for intakes of radionuclides by workers. International Commission on Radiological Protection, Publication 30, Part 1. Pergamon Press, New York.

ICRP 1989. Age-dependent doses to members of the public from the intake of radionuclides: Part I. International Commission on Radiological Protection Publication 56, Pergamon Press, New York.

ICRP 1991. International Commission on Radiological Protection (1991).1990 Recommendations of the International Commission on Radiological Protection. ICRP Publication 60.

ICRP 1993. Age-dependent doses to members of the public from the intake of radionuclides: Part 2 Ingestion dose coefficients. International Commission on Radiological Protection Publication 67, Pergamon Press, New York.

ICRP 1996. Age-dependent doses to members of the public from the intake of radionuclides: Part 5 Compilation of Ingestion and Inhalation dose coefficients. International Commission on Radiological Protection Publication 72, Pergamon Press, New York.

Johns, HE and Cunningham JR (1983). Physics of Radiology 4th edition. Springfield, Illinois: Charles C. Thomas.

Kendall et.al. 1992. Kendall GM, Muirhead CR, MacGibbon BH, O'Hagan JA, Conquest AJ, Goodill AA, Butland BK, Fell TP, Jackson DA, Webb MA, et al. (1992) . Mortality and occupational exposure to radiation: first analysis of the National Registry for Radiation Workers BMJ Jan 25;304(6821):220-225.

LLL 1972. Environmental Levels of Radioactivity in the Vicinity of the Lawrence Livermore Laboratory January through December 1971. P. Gudiksen et.al., Lawrence Livermore Laboratory, Livermore CA, UCRL 51242, June 14, 1972.

LLL 1973. Environmental Levels of Radioactivity in the Vicinity of the Lawrence Livermore Laboratory 1972 Annual Report. P. Gudiksen et.al., Lawrence Livermore Laboratory, Livermore CA, UCRL 51333, March 7, 1973.

LLL 1974. Environmental Levels of Radioactivity in the Vicinity of the Lawrence Livermore Laboratory 1973 Annual Report. W. Silver et.al., Lawrence Livermore Laboratory, Livermore CA, UCRL 51547, March 4, 1974.

LLNL 1990. CERCLA Remedial Investigations Report for the LLNL Livermore Site. Lawrence Livermore National Laboratory, University of California, Environmental Restoration Division, UCAR-10299, Livermore CA, May 1990.

LRL 1960-1970. LRL Environmental Report(s), Semi-annual and annual summaries, prepared by the Lawrence Radiation Laboratory for the US Atomic Energy Commission and submitted to the California State Department of Public Health, Bureau of Radiological Health, Berkeley CA.

MacQueen, D, et.al. 2002. Livermore Big Trees Park: 1998 Results. Lawrence Livermore National Laboratory, Environmental Protection Department UCRL-ID-143311, Univ. of CA, Livermore, CA, May 2002.

McConachie 2003. William McConachie, Environmental Chemist, LLNL personal communication (Facsimile transmission and e-mail) to Mark Evans, ATSDR. Data sheets from historic sewage samples, January 28, 2003.

Myers DS, et al. 1976. Evaluation of the Use of Sludge Containing Plutonium as a Soil Conditioner for Food Crops. In: Proceedings of the Symposium on Transuranium Nuclides in the Environment, San Francisco CA, November 17-21, 1975, International Atomic Energy Agency, Vienna, 1976.

NAS 1995. Management and Disposition of Excess Weapons Plutonium, Reactor-Related Options. National Academy of Sciences, Committee on International Security and Arms Control, National Academy Press, Washington, D.C., 1995.

NCRP 1987. Exposure of the Population of the United States and Canada from Natural Background Radiation. National Council on Radiation Protection and Measurements, NCRP Report No. 94, Bethesda MD, December 30, 1987.

NCRP 1993. Risk estimates for radiation protection. National Council on Radiation Protection and Measurements, NCRP Report 115, 1993, Bethesda, Maryland.

NCRP 1997. Uncertainties in Fatal Cancer Risk Estimates Used in Radiation Protection. National Council on Radiation Protection and Measurements, NCRP Report 126, 1997, Bethesda, Maryland.

NCRP 2001. Evaluation of the linear-nonthreshold dose-response model for ionizing radiation. National Council on Radiation Protection and Measurement. NCRP Report 136, Bethesda, Maryland.

NRC 1990. Health Effects of Exposure to low levels of Ionizing Radiation. National Research Council, Washington, DC, National Academy Press.

Roman et.al. 1999. Roman E, Doyle P, Maconochie N, Davies G, Smith PG, Beral V. (1999). Cancer in children of nuclear industry employees: report on children aged under 25 years from nuclear industry family study. BMJ. 1999 May 29;318(7196):1443-1450.

Wei L et al., 1986. Recent Advances of Health Survey in High Background Areas in Yangjiang, China. In: Proceedings of the International Symposium on Biological Effects of Low Level Radiation: p. 1-17.

Wong 2003. Wong, Jeffrey, California Department of Health Services, Radiation Health Branch, e-mail to Mark Evans, ATSDR, RE: sludge pha, January 10, 2003.


PREPARERS OF REPORT

Mark W. Evans, Ph.D.
Environmental Geologist
Federal Facilities Assessment Branch
Division of Health Assessment and Consultation

Paul A. Charp, Ph.D.
Senior Health Physicist
Federal Facilities Assessment Branch
Division of Health Assessment and Consultation


Reviewers of Report

Burt J. Cooper, M.S.
Supervisory Environmental Health Scientist
Energy Section Chief,
Federal Facilities Assessment Branch
Division of Health Assessment and Consultation

Sandra G. Isaacs
Chief,
Federal Facilities Assessment Branch
Division of Health Assessment and Consultation


Regional Representative

William Nelson
Senior Regional Representative
Regional Services, Region IX
Office of Regional Operations


APPENDIX 1: GLOSSARY OF TECHNICAL TERMS

Absorption:
How a chemical enters a person's blood after the chemical has been swallowed, has come into contact with the skin, or has been breathed in.


Acute Exposure:
Contact with a chemical that happens once or only for a limited period of time. ATSDR defines acute exposures as those that might last up to 14 days.


Additive Effect:
A response to a chemical mixture, or combination of substances, that might be expected if the known effects of individual chemicals, seen at specific doses, were added together.


Adverse Health Effect:
A change in body function or the structures of cells that can lead to disease or health problems.


Antagonistic Effect:
A response to a mixture of chemicals or combination of substances that is less than might be expected if the known effects of individual chemicals, seen at specific doses, were added together.


ATSDR:
The Agency for Toxic Substances and Disease Registry. ATSDR is a federal health agency in Atlanta, Georgia that deals with hazardous substance and waste site issues. ATSDR gives people information about harmful chemicals in their environment and tells people how to protect themselves from coming into contact with chemicals.


Background Level:
An average or expected amount of a chemical in a specific environment. Or, amounts of chemicals that occur naturally in a specific environment.


Biota:
Used in public health, things that humans would eat - including animals, fish and plants.


Cancer:
A group of diseases which occur when cells in the body become abnormal and grow, or multiply, out of control.


Carcinogen:
Any substance shown to cause tumors or cancer in experimental studies.


CERCLA:
See Comprehensive Environmental Response, Compensation, and Liability Act.


Chronic Exposure:
A contact with a substance or chemical that happens over a long period of time. ATSDR considers exposures of more than one year to be chronic.


Committed Dose Equivalent (HT50):
The dose equivalent to organs or tissues of reference (T) that will be received from an intake of radioactive material by an individual during the 50-year period following the intake.


Committed Effective Dose:
The International Commission on Radiological Protection (ICRP) term for committed effective dose equivalent. (See Committed Effective Dose Equivalent.)


Committed Effective Dose Equivalent (HE50):
The sum of the products of the weighting factors applicable to each of the body organs or tissues that are irradiated and the committed dose equivalent to the organs or tissues (HE50 = WTHT50). The committed effective dose equivalent is used in radiation safety because it implicitly includes the relative carcinogenic sensitivity of the various tissues.


Completed Exposure Pathway:
See Exposure Pathway.


Comparison Value (CVs):
Concentrations or the amount of substances in air, water, food, and soil that are unlikely, upon exposure, to cause adverse health effects. Comparison values are used by health assessors to select which substances and environmental media (air, water, food and soil) need additional evaluation while health concerns or effects are investigated.


Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA):
CERCLA was put into place in 1980. It is also known as Superfund. This act concerns releases of hazardous substances into the environment, and the cleanup of these substances and hazardous waste sites. ATSDR was created by this act and is responsible for looking into the health issues related to hazardous waste sites.


Concern:
A belief or worry that chemicals in the environment might cause harm to people.


Concentration:
How much or the amount of a substance present in a certain amount of soil, water, air, or food.


Contaminant:
See Environmental Contaminant.


Curie (Ci):
The quantity of radioactive material in which 37 billion transformations occur per second, which is approximately the activity of 1 gram of radium.


Delayed Health Effect:
A disease or injury that happens as a result of exposures that may have occurred far in the past.


Dermal Contact:
A chemical getting onto your skin. (see Route of Exposure).


Dose:
The amount of a substance to which a person may be exposed, usually on a daily basis. Dose is often explained as "amount of substance(s) per body weight per day". For radioactive materials or radiation, dose denotes the quantity of radiation or energy absorbed per unit body mass and is a generic term for absorbed dose, dose equivalent, effective dose equivalent, committed dose equivalent, committed effective dose equivalent, or total effective dose.


Dose Equivalent (DE):
A quantity used in radiation protection. It expresses all radiations on a common scale for calculating the dose for purposes of radiation safety. It is the product of the absorbed dose in rad or gray and a quality factor, whose value depends on the radiation. (The unit of dose equivalent is the rem. In SI units, the dose equivalent is the sievert, which equals 100 rem.)


Dose / Response:
The relationship between the amount of exposure (dose) and the change in body function or health that result.


Duration:
The amount of time (days, months, years) that a person is exposed to a chemical.


Effective Dose Equivalent:
The dose equivalent to organs and tissues of reference that will be received from an intake of radioactive material by an individual following the intake. Individual internal organ doses and the external dose are summed to determine the whole body dose.


Environmental Contaminant:
A substance (chemical) that gets into a system (person, animal, or the environment) in amounts higher than that found in Background Level, or what would be expected.


Environmental Media:
Usually refers to the air, water, and soil in which chemcials of interest are found. Sometimes refers to the plants and animals that are eaten by humans. Environmental Media is the second part of an Exposure Pathway.


U.S. Environmental Protection Agency (EPA):
The federal agency that develops and enforces environmental laws to protect the environment and the public's health.


Epidemiology:
The study of the different factors that determine how often, in how many people, and in which people will disease occur.


Exposure:
Coming into contact with a chemical substance. (For the three ways people can come in contact with substances, see Route of Exposure.)


Exposure Assessment:
The process of finding the ways people come in contact with chemicals, how often and how long they come in contact with chemicals, and the amounts of chemicals with which they come in contact.


Exposure Factors:
Variables, such as frequency, duration, inhalation/ingestion rates that determine how much or how often a person is exposed to an environmental contaminant.


Exposure Pathway:
A description of the way that a chemical moves from its source (where it began) to where and how people can come into contact with (or get exposed to) the chemical.

ATSDR defines an exposure pathway as having 5 parts:
1. Source of contamination,
2. Environmental Media and Transport Mechanism,
3. Point of Exposure,
4. Route of Exposure, and
5. Receptor Population.

When all 5 parts of an exposure pathway are present, it is called a Completed Exposure Pathway. Each of these 5 terms is defined in this Glossary.


Frequency:
How often a person is exposed to a chemical over time; for example, every day, once a week, twice a month.


Gray:
The international unit of absorbed radiation dose. One Gray (Gy) equals 100 rad.


Hazardous Waste:
Substances that have been released or thrown away into the environment and, under certain conditions, could be harmful to people who come into contact with them.


Health Effect:
ATSDR deals only with Adverse Health Effects (see definition in this Glossary).


Indeterminate Public Health Hazard:
The category is used in Public Health Assessment documents for sites where important information is lacking (missing or has not yet been gathered) about site-related chemical exposures.


Ingestion:
Swallowing something, as in eating or drinking. It is a way a chemical can enter your body (See Route of Exposure).


Inhalation:
Breathing. It is a way a chemical can enter your body (See Route of Exposure).


LOAEL:
Lowest Observed Adverse Effect Level. The lowest dose of a chemical in a study, or group of studies, that has caused harmful health effects in people or animals.


Malignancy:
See Cancer.


MRL:
Minimal Risk Level. An estimate of daily human exposure - by a specified route and length of time -- to a dose of chemical that is likely to be without a measurable risk of adverse, noncancerous effects. An MRL should not be used as a predictor of adverse health effects.


NPL:
The National Priorities List. (Which is part of Superfund.) A list kept by the U.S. Environmental Protection Agency (EPA) of the most serious, uncontrolled or abandoned hazardous waste sites in the country. An NPL site needs to be cleaned up or is being looked at to see if people can be exposed to chemicals from the site.


NOAEL:
No Observed Adverse Effect Level. The highest dose of a chemical in a study, or group of studies, that did not cause harmful health effects in people or animals.


No Apparent Public Health Hazard:
The category is used in ATSDR's Public Health Assessment documents for sites where exposure to site-related chemicals may have occurred in the past or is still occurring but the exposures are not at levels expected to cause adverse health effects.


No Public Health Hazard:
The category is used in ATSDR's Public Health Assessment documents for sites where there is evidence of an absence of exposure to site-related chemicals.


PHA:
Public Health Assessment. A report or document that looks at chemicals at a hazardous waste site and tells if people could be harmed from coming into contact with those chemicals. The PHA also tells if possible further public health actions are needed.


Point of Exposure:
The place where someone can come into contact with a contaminated environmental medium (air, water, food or soil). For examples: the area of a playground that has contaminated dirt, a contaminated spring used for drinking water, the location where fruits or vegetables are grown in contaminated soil, or the backyard area where someone might breathe contaminated air.


Population:
A group of people in a certain area; or the number of people in a that have similar exposure factors.


Public Health Assessment(s):
See PHA.


Public Health Hazard:
The category is used in PHAs for sites that have certain physical features or evidence of chronic, site-related chemical exposure that could result in adverse health effects.


Public Health Hazard Criteria:
PHA categories given to a site which tell whether people could be harmed by conditions present at the site. Each are defined in the Glossary. The categories are:
- Urgent Public Health Hazard
- Public Health Hazard
- Indeterminate Public Health Hazard
- No Apparent Public Health Hazard
- No Public Health Hazard


Rad:
The special unit of absorbed dose. One rad is equal to an absorbed dose of 0.01 Gray.


Receptor Population:
People who live or work in the path of one or more chemicals, and who could come into contact with them (See Exposure Pathway).


Reference Dose (RfD):
An estimate, with safety factors (see safety factor) built in, of the daily, life-time exposure of human populations to a possible hazard that is not likely to cause harm to the person.


Rem:
A unit of radiation dose equivalent. The dose equivalent in rem is numerically equal to the absorbed dose in rad multiplied by a quality factor. A mrem is 1e-3 Rem.


Route of Exposure:
The way a chemical can get into a person's body. There are three exposure routes:
- breathing (also called inhalation),
- eating or drinking (also called ingestion), and
- or getting something on the skin (also called dermal contact).


Safety Factor:
Also called Uncertainty Factor. When scientists don't have enough information to decide if an exposure will cause harm to people, they use "safety factors" and formulas in place of the information that is not known. These factors and formulas can help determine the amount of a chemical that is not likely to cause harm to people.


Sample:
A small number of items or people chosen from a larger population that is used to characterize the entire population (See Population).


Sievert:
The SI unit of any of the quantities expressed as dose equivalent. The dose equivalent in sieverts equals the absorbed dose in gray multiplied by the quality factor (1 Sv = 100 rem; 1 microsievert = 1E-06 sieverts).


Source (of Contamination):
The place where a chemical comes from, such as a landfill, pond, creek, incinerator, tank, or drum. Contaminant source is the first part of an Exposure Pathway.


Special Populations:
People who may be more sensitive to chemical exposures because of certain factors such as age, a disease they already have, occupation, sex, or certain behaviors (like cigarette smoking). Children, pregnant women, and older people are often considered special populations.


Statistics:
A branch of the math process of collecting, looking at, and summarizing data or information.


Survey:
A way to collect information or data from a group of people (population). Surveys can be done by phone, mail, or in person. ATSDR cannot do surveys of more than nine people without approval from the U.S. Department of Health and Human Services.


Synergistic effect:
A health effect from an exposure to more than one chemical, where one of the chemicals worsens the effect of another chemical. The combined effect of the chemicals acting together are greater than the effects of the chemicals acting by themselves.


Total Effective Dose Equivalent (TEDE):
The sum of the effective deep dose equivalent from external exposures and the committed effective dose equivalent from internal exposures.


Toxic:
Harmful. Any substance or chemical can be toxic at a certain dose (amount). The dose is what determines the potential harm of a chemical and whether it would cause someone to get sick.


Toxicology:
The study of the harmful effects of chemicals on humans or animals.


Tumor:
Abnormal growth of tissue or cells that have formed a lump or mass.


Uncertainty Factor:
See Safety Factor.


Urgent Public Health Hazard:
This category is used in ATSDR's Public Health Assessment documents for sites that have certain physical features or evidence of short-term (less than 1 year), site-related chemical exposure that could result in adverse health effects and require quick intervention to stop people from being exposed.

APPENDIX 2: 1967 ASSESSMENT OF PU 239 RELEASE

Letter and Attachment concerning "Summary Hazards Analysis- PU-AM Release to Sanitary Sewer" from D.C. Sewell, Associate Director, LRL, to E.C. Shute, Manager, San Francisco Operations Office, U.S. Atomic Energy Commission, August 22, 1967.

Click here to view Appendix 2 in PDF format (PDF, 824KB)

8 Although the standard definition of an ATSDR MRL specifies only non-cancerous health effects, the MRL for ionizing radiation includes cancerous health effects (ATSDR 1999b). Also, although the ATSDR MRL is specific to external radiation, the ICRP effective dose limit does not specify either external or internal exposure and will be used as a screening level dose for the internal exposure evaluated in this study.
9 The 95th percentile of external terrestrial background radiation doses for the San Francisco area is ~80 mrem/year (based on data from NCRP 1987).
10 Several data sources were used in developing this section include internet searches and the Health Physics Journal and United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) reports.
11 Although the ATSDR MRLs for ionizing radiation are specific to external exposure, the value of 100 mrem/year is consistent with those for either external or internal exposures promulgated by the US Nuclear Regulatory Commission, the National Commission on Radiation Protection, and the International Commission on Radiation Protection (as referenced in ATSDR 1999).
12 Due to construction activities at LWRP during the 1965 to 1967 timeframe, it is unlikely that any sludge was distributed to the public (CDHS 2002). As a 1964 release to the sewer system would not show up in processed sludge until 1965, it is unlikely that any sludge from the 1964 release was distributed to the public.
13 The "Radiological Health News" of July 1964 contained the following statement: "A correction should be made in the data on sewage sludge. Beginning May 1963 all sewage sludge has been reported in picocuries per gram of dry sludge. Before that date it was reported in picocuries per gram of wet sludge. The footnote should be so corrected." (Wong 2003).
14 During the period of concern in the 1960s, the LLNL monitoring data were collected and analyzed on a monthly basis. However, these data were only reported as 6 or 12- month average values.

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