Objectives: We summarized information on the environmental behavior, biokinetics, and toxicology of ²¹⁰Po and identified the need for future research.

Methods: Potential linkages between environmental exposure to ²¹⁰Po and human health effects were identified in a literature review.

Discussion: ²¹⁰Po accumulates in the ovaries where it kills primary oocytes at low doses. Because of its radiosensitivity and tendency to concentrate ²¹⁰Po, the ovary may be the critical organ in determining the lowest injurious dose for ²¹⁰Po. ²¹⁰Po also accumulates in the yolk sac of the embryo and in the fetal and placental tissues. Low-level exposure to ²¹⁰Po may have subtle, long-term biological effects because of its tropism towards reproductive and embryonic and fetal tissues where exposure to a single alpha particle may kill or damage critical cells. ²¹⁰Po is present in cigarettes and maternal smoking has several effects that appear consistent with the toxicology of ²¹⁰Po.

²¹⁰Po is one of the most toxic substances known because of its intense radioactivity, with 1 µg of ²¹⁰Po having an activity of 1.66 × 10⁸ Bq. After the death of Alexander Litvinenko from ²¹⁰Po poisoning in 2006, several papers were published that addressed the diagnosis, treatment, and toxicity of acute ²¹⁰Po poisoning (Harrison et al. 2007; Jefferson et al. 2009; Scott 2007) and the need for medical toxicology expertise about ²¹⁰Po because of its potential use in radiation terrorism events (Nemhauser 2010). The estimated acute lethal dose from oral ingestion for an adult if untreated is 10–30 µg (Jefferson et al. 2009), and as little as 1 µg might be lethal to the most radiosensitive members of the population (Scott 2007).

As an alpha-particle–emitting decay product of radium-226 (²²⁶Ra), ²¹⁰Po is classified as a Group 1 human carcinogen [International Agency for Research on Cancer (IARC) 2001]. Numerous epidemiological studies, which were reviewed by Canu et al. (2011), have investigated associations between exposure to members of the uranium-238 (²³⁸U) decay series in drinking water and cancers such as leukemia (e.g., Hoffmann et al. 1993; Lyman et al. 1985; Raaschou-Nielsen et al. 2008). Because ²¹⁰Po is the last radioactive member of the ²³⁸U decay series, a common feature of all these studies is the presence of ²¹⁰Po in the environment, even if it was not measured. Because ²¹⁰Po is a human carcinogen and because information on environmental exposure to it is poorly known, we reviewed the literature on ²¹⁰Po.

In this paper, we summarize relatively unknown and disparate information on the environmental behavior, biokinetics, and toxicology of ²¹⁰Po and suggest supportive research that could help guide future investigations.

The main source of ²¹⁰Po in the atmosphere and oceans is from the emanation of radon gas from surficial sediments to the atmosphere where it is spread by diffusion and winds (Parfenov 1974; Persson and Holm 2011). In addition, high ²¹⁰Po can be introduced into the atmosphere in volcanic emissions because of the high volatility of ²¹⁰Po compared with ²¹⁰Pb (Kim et al. 2011). Radon’s decay products, ²¹⁰Pb and ²¹⁰Po, have strong affinities for particles and become widely distributed on the earth’s surface as the ²¹⁰Pb and ²¹⁰Po that are formed from decay of radon in the atmosphere adsorb to aerosol particles and fall onto the land or sea.

²¹⁰Po activities exceeding 1 Bq/L have been found in private wells in Florida and Nevada and public supply wells in Louisiana and Maryland (Seiler et al. 2011). ²¹⁰Po in groundwater is normally < 30 mBq/L because it strongly adsorbs to aquifer materials (Harada et al. 1989). In typical aquifer sediments, however, ²¹⁰Po concentrations are high enough that geochemical and microbial processes that mobilize only a small percentage of the ²¹⁰Po that is present can yield groundwater with ²¹⁰Po concentrations that greatly exceed safe levels in drinking water. Wells with high ²¹⁰Po in Florida are typically shallow wells located in the central part of the state (Harada et al. 1989) where the ultimate source of the ²¹⁰Po is uranium-rich phosphate rock in the aquifers and phosphogypsum waste products from mining operations (Cherrier et al. 1995). U concentrations in aquifer sediments near contaminated wells in Nevada range from 1.4 to 4.5 mg/kg (Seiler et al. 2011) and are typical of the western United States (Figure 1). U concentrations in sediments near contaminated wells in Maryland and Louisiana have not been described.

Following exposure to ²¹⁰Po, much more ²¹⁰Po is excreted in feces than in urine (Moroz and Parfenov 1972). Renal excretion of ²¹⁰Po is slow compared with other elements because it binds strongly to hemoglobin and plasma proteins and is not filtered by the kidneys (Thomas et al. 2001). ²¹⁰Po is also excreted through the cutaneous glands and the hair (Moroz and Parfenov 1972) and in milk (Parfenov 1974). In an experiment that used a lactating goat, Schreckhise and Watters (1969) estimated the transfer coefficient (percent intake by the goat per liter of milk produced) for ²¹⁰Po was 0.18%.

Hunt and Rumney (2007) examined the retention of ²¹⁰Po from consuming shellfish and concluded its biological half-life was about 40 days, which is consistent with the International Commission on Radiological Protection (ICRP 1993) value of 50 days. On the other hand, Thomas et al. (2001) concluded that the biological half-life of ²¹⁰Po in humans following consumption of caribou meat is > 100 days and that once absorbed ²¹⁰Po is excreted very slowly if at all. Assuming that the biological half-life is 50 days, then the effective half-life in humans would be about 37 days.

Biodistribution. The tissue distribution of ²¹⁰Po across mammalian species is broadly similar (Thomas et al. 2001). ²¹⁰Po concentrations in the bones of farm animals are 2–3 orders of magnitude greater than in the muscles (Parfenov 1974). Average relative ²¹⁰Po activities in the liver, kidney, and muscle were 19, 13, and 1, respectively, in caribou and 24, 19, and 1, respectively, in wolves (Thomas et al. 1994). In adult female baboons, the highest concentrations of injected ²¹⁰Po were found in the liver and kidney, and the lowest were in the muscle, skeleton, and brain (Fellman et al. 1994).

Ingested ²¹⁰Po in humans is initially concentrated in red blood cells, followed by the liver, kidneys, bone marrow, gastrointestinal tract, and gonads (Jefferson et al. 2009). Once absorbed into the blood, about 30% goes to the liver, 10% to red bone marrow, 10% to the kidney, 5% to the spleen, and the remainder to the body in general (Thomas et al. 2001). Average wet weight ²¹⁰Po concentrations for nonsmokers were 0.055, 0.53, and 0.48 Bq/kg in skeletal muscle, liver, and kidney, respectively (Parfenov 1974). Based on reported measurements of ²¹⁰Po in the various organs and the weights of the organs in the standard reference person, the total ²¹⁰Po content of the human body was estimated to be about 20 Bq (Parfenov 1974).

Median wet weight ²¹⁰Po concentrations from cattle in an uncontaminated agricultural area in Germany were 1.2 Bq/kg in the liver and 6.6 Bq/kg in the kidney (Bunzl et al. 1979). In northern Poland with background levels of radioactivity, Skwarzec and Prucnal (2007) found that the average wet weight ²¹⁰Po concentrations in deer from these areas were 0.16 Bq/kg in muscle, 1.08 Bq/kg in liver, and 1.58 Bq/kg in kidney. Levels for animals from contaminated areas can be significantly higher. In the Arctic, lichens accumulate large amounts of ²¹⁰Po from the atmosphere and are the main winter forage for caribou (Thomas et al. 2001). In Canadian caribou that consume the lichens, ²¹⁰Po concentrations ranged from 9 to 40 Bq/kg in meat and from 90 to 620 Bq/kg in liver and kidney (Thomas et al. 2001). In cattle raised in an area in New Mexico that was frequently flooded by untreated effluent from a nearby uranium mine, Lapham et al. (1989) found that the average wet weight ²¹⁰Po concentrations were 3.4, 56, and 65 Bq/kg in muscle, liver, and kidney, respectively.

In general, testes and ovaries contain elevated ²¹⁰Po concentrations compared with most other tissues. An assessment of ²¹⁰Po biokinetics suggested that transfer coefficients to the testes and ovaries are 0.1% and 0.05% per day, respectively, for ²¹⁰Po in blood plasma that originated from the gastrointestinal tract or from systemic tissues returning to the blood (Leggett and Eckerman 2001). ²¹⁰Po in the ovaries accumulates preferentially in the cells of the follicular epithelium and in the connective tissue cells of the corpora lutea (Moroz and Parfenov 1972). Ten days after injecting 925,000 Bq/kg into mice, Finkel et al. (1953) found that the ²¹⁰Po concentrations in the ovaries were very high and caused severe damage to the ovaries. At 10 days, concentrations in the ovary were exceeded only by concentrations in the spleen; however, within 120 days after the injection, ²¹⁰Po concentrations in the ovaries had decreased and had become undetectable.

Published values for ²¹⁰Po concentration in cow’s milk ranged from 3.3 to 18.5 mBq/L and were > 1 order of magnitude lower than in meat (Parfenov 1974). Concentrations can be much higher in milk from areas known to be contaminated. For example, the geometric mean ²¹⁰Po concentration in milk samples from cattle raised in a uranium-mining district in India was 1.08 Bq/L (Giri et al. 2010), with a maximum of 2.94 Bq/L.

After injecting ²¹⁰Po into pregnant rats and guinea pigs, Haines et al. (1995) reported that fetal and placental tissues contained about 3–4% of the injected ²¹⁰Po in rats and about 10% in guinea pigs. The authors also observed that at birth each rat pup had about 0.1% of the injected ²¹⁰Po and that on day 57 each guinea pig fetus contained 0.6%. The highest concentrations of ²¹⁰Po, about 4% of the injected ²¹⁰Po per gram, were measured in the yolk sacs of the embryonic rats during their hematopoietic stage (Haines et al. 1995). The data suggest that the placenta acts as a barrier against movement of ²¹⁰Po from mother to fetus. In one population of caribou in Canada, fetal ²¹⁰Po averaged 62% of the ²¹⁰Pb and 41% in a second population of caribou (Thomas et al. 1994). We calculated that within the caribou gestation period of 230 days, it would take 204 and 117 days, respectively, in these two populations, for the decay of ²¹⁰Pb to generate this much ²¹⁰Po. Thus, decay of fetal ²¹⁰Pb could have provided all or most of the of the measured fetal ²¹⁰Po in the caribou. Paquet et al. (1998) found that approximately 0.7–1% of ²¹⁰Po injected into pregnant baboons at 5 months was present in the fetus 7 days later, which indicates that small amounts of ²¹⁰Po do pass through the placenta. Söremark and Hunt (1966) found that the autoradiographs of mice 4 days after being injected with ²¹⁰Po showed ²¹⁰Po was present in the placenta but not in the fetus; however, by the fifth day, ²¹⁰Po was detected in the fetus. By this time, the placenta was showing damage, which suggests that ²¹⁰Po transport across the placenta may change with dose and time.

²¹⁰Po is a known human carcinogen (IARC 2001), and its carcinogenicity to animals has been demonstrated by numerous animal studies (reviewed by Moroz and Parfenov 1972). Exposure of the lungs to ²¹⁰Po alone is capable of causing lung cancer in rats and hamsters (Little and O’Toole 1974; Yuile et al. 1967). Injecting ²¹⁰Po into CF-1 female mice caused an increased incidence of lymphomas and soft-tissue and malignant-bone tumors (Finkel and Hirsch 1950). At a dose of 33.3 Bq/g body weight, 42% of autopsied mice had developed lymphomas within 250 days of injection compared with 21% of the controls.

Injected ²¹⁰Po was taken up by the ovaries in mice and localized primarily in the follicle cells, whereas in the uterus it was distributed diffusely through the myometrium (Samuels 1966). Significant killing of primary oocytes occurred after exposure to as little as 0.037 Bq/g body weight ²¹⁰Po, with higher doses killing almost all the oocytes and causing gross distortion of the ovarian architecture. Radioautographs led Samuels (1966) to conclude that ²¹⁰Po appears to concentrate in the ovary in such a manner that it selectively irradiated the oocytes. Finkel et al. (1953) concluded that the ovary may be the critical organ in determining the lowest injurious dose for ²¹⁰Po because of its radiosensitivity and tendency to concentrate ²¹⁰Po.

For alpha radiation, substantial doses of radiation (0.5–1.3 Gy) are delivered to individual cells that are traversed by a single alpha particle no matter how low the dose to the whole body (Lorimore et al. 1998; Purnell et al. 1999). Alpha particles traversing the nucleus of HeLa cells produced a track averaging 10 µm, with an average of 22 double-strand chromosomal breaks (DSBs) (Aten et al. 2004). Breaks found at distant locations can subsequently be brought together and form chromosomal translocations (Aten et al. 2004). Alpha emitters can induce DNA lesions in stem cells that result in the transmission of chromosomal instability to their progeny (Kadhim et al. 1992), and even a single alpha particle can induce long-term chromosomal instability in primary human T lymphocytes (Kadhim et al. 2001). Chromosomal translocation and aneuploidy are a hallmark of the childhood leukemias regardless of specific histology (Szczepański et al. 2010). Because ²¹⁰Po is an alpha emitter, toxicological investigations on the cellular and molecular effects of alpha radiation using other alpha emitters likely will also apply to ²¹⁰Po. Irrespective of their source, alpha particles produce the same patterns of secondary ionizations and localized damage to biological molecules (IARC 2001), thus the important difference between different alpha emitters would be in what tissues they preferentially accumulate in, and thus what tissues are preferentially irradiated.

Direct ingestion of ²¹⁰Po-contaminated water. It is unusual to find ²¹⁰Po activities greater than approximately 30 mBq/L in groundwater because it is rapidly adsorbed onto particles (Harada et al. 1989); however, in some geochemical settings, much higher levels of ²¹⁰Po are found (Seiler et al. 2011). Exposure to contaminated drinking water is particularly insidious because it may be chronic and unrecognized, especially in rural areas where the population relies on private wells that are unregulated and not tested for radioactivity. Analyses for the presence of ²¹⁰Po in drinking water are rarely made, and ²¹⁰Po is not measured directly to determine compliance with drinking-water standards for public supply wells in the United States. In the United States, compliance is assessed indirectly by analyzing the U activity and the gross alpha radioactivity (GAR), a measure of emitted alpha radiation that does not identify the specific isotopes involved. The water samples are evaporated to dryness, which drives off radon gas, and the standard is violated if the GAR of the sample exceeds the U activity by 0.55 Bq [U.S. Environmental Protection Agency (EPA) 2000].

²¹⁰Po activities in private wells in Lahontan Valley, Nevada, were measured at levels as high as 6.59 Bq/L (Seiler 2011), and these private wells serve hundreds to thousands of people in areas where ²¹⁰Po commonly exceeds 0.5 Bq/L. In one well, the ²¹⁰Po activity was stable in measurements made six half-lives (830 days) apart (Seiler 2012), which suggests users of contaminated wells in Lahontan Valley have been exposed to ²¹⁰Po since the wells were drilled. Several wells with high ²¹⁰Po in West Central Florida were used as household drinking-water sources or for lowering groundwater levels near phosphate mines (Burnett et al. 1988). One intensively studied well in Hillsborough County, Florida, with ²¹⁰Po activities ranging between 9.6 Bq/L and 95 Bq/L (Burnett et al. 1988) was a private well used by several families as their main source of drinking water until the ²¹⁰Po contamination was discovered. Contaminated municipal wells have served large numbers of people for more than a decade before the contamination was discovered. For example, a municipal well in service since 1992 provided water for 95 houses in a subdivision in Charles County, Maryland, and was discovered to contain 1.7 Bq/L ²¹⁰Po in 2004 (Outola et al. 2008). The presence of ²¹⁰Po was not discovered earlier because before 2002 it took about 1 year before samples were analyzed (Outola et al. 2008), during which time ²¹⁰Po was being lost through radioactive decay.

The residents of parts of Lahontan Valley, where ²¹⁰Po in private wells exceeds 0.5 Bq/L, can potentially be exposed to substantial doses of radioactivity. Using the dose conversion factor of 1.2 × 10^–3 mSv/Bq for ²¹⁰Po 1 year after ingestion (ICRP 2010), the annual effective dose would be > 0.4 mSv/year for adults who consumed 2 L/day of water from wells with > 0.5 Bq/L of ²¹⁰Po. For adults using the well with 6.59 Bq/L of ²¹⁰Po, the annual effective dose would be almost 6 mSv/year. For comparison, the World Health Organization (WHO 2006) concluded that no deleterious radiological health effects are expected from consumption of drinking water if the committed effective dose (i.e., the total effective dose received over a lifetime), does not exceed 0.1 mSv/year.

Effective dose coefficients are higher for infants than for adults, in part because the fraction of ²¹⁰Po absorbed from the alimentary tract into the blood, f1, is assumed to be 100% for a child < 1 year of age, and 50% for older ages (ICRP 2010). For a 3-month-old child, the effective dose coefficient is 2.6 × 10^–2 mSv/Bq for ²¹⁰Po 1 year after ingestion, and for a 1-year-old child, it is 8.8 × 10^–3 mSv/Bq (ICRP 2010). For a 3-month-old child who consumed 1 L/day of well water used to prepare infant formula, the annual effective dose would be almost 5 mSv/year for well water that contained 0.5 Bq/L of ²¹⁰Po and about 60 mSv/year for well water that contained 6.59 Bq/L of ²¹⁰Po. For a 3-month-old child, the committed equivalent dose coefficient is 5.7 × 10^–3 mSv/Bq for the ovary, 8.1 × 10^–2 mSv/Bq for red bone marrow, and 2.2 × 10^–1 mSv/Bq for the spleen (ICRP 2010). Therefore, a 3-month-old child who consumed 1 L/day of well water that contained 0.5 Bq/L of ²¹⁰Po would receive doses to the ovary, red bone marrow, and spleen of about about 1, 15, and 40 mSv/year, respectively.

Direct ingestion of ²¹⁰Po-contaminated food. A review of food-chain transport of ²¹⁰Po concluded that the greatest sources of ingested ²¹⁰Po were found in populations with large dietary complements of seafood (Japan) or caribou and reindeer muscle and organs (Arctic) (Watson 1985). In shellfish and crustaceans, Lee et al. (2009) reported ²¹⁰Po concentrations ranging from 19.1 to 33 Bq/kg in Korea, and Carvalho (1995) reported levels from 49 to 152 Bq/kg in Portugal. Because all marine organisms accumulate ²¹⁰Po in high concentrations due to its solubility in seawater and its affinity to organic matter, seafood is a notable source of ²¹⁰Po in the human diet (Alam and Mohamed 2011).

Cigarette smoking has several effects that appear consistent with exposure to ²¹⁰Po. A 60% increase in the risk of infertility among smokers may be related to ovarian toxicity (Augood et al. 1998). Cigarette smoking appears to significantly reduce ovarian reserves in women (El-Nemr et al. 1998), and Tuttle et al. (2009) found that the ovaries of mice that had been exposed to cigarette smoke were on average 20% smaller and had significantly fewer follicles. These outcomes appear similar to those described by Samuels (1966) for mice exposed to ²¹⁰Po. Cigarette smoking also significantly increases a woman’s risk of developing mucinous ovarian cancer (Gram et al. 2011; Jordan et al. 2006). This may be linked to exposure to ²¹⁰Po, which is known to accumulate in the ovary (Finkel et al. 1953).

²¹⁰Po is equally plausible as a leukemogen in children. Epidemiologic studies on atomic bomb survivors indicated that young children were much more sensitive to radiation-induced leukemia than were adults (Little 2003). ²¹⁰Po accumulates in several tissues with the capacity for hematopoiesis, including the fetal yolk sac and bone marrow and liver in mature animals as explained above. Both ALL and acute myelocytic leukemia (AML) in children are known to originate in the fetus, as demonstrated by the presence of cells with leukemia clone-specific mutations present at birth in children who later contract the disease (Wiemels 2008). Indirect evidence for the fetal origin of childhood ALL stems from the immature nature of immunoglobulin rearrangements as well as lack of evidence for recombinase activating gene-induced alterations at chromosomal translocations (Steenbergen et al. 1994; Wasserman et al. 1992). These translocations as well as chromosomal deletions and aneuploidy are the characteristic hallmark of childhood ALL (Greaves and Wiemels 2003; Mullighan et al. 2007). Translocations are the primary method of dosimetry of ionizing radiation exposure (Tucker 2008). Ionizing radiation from sources such as alpha particles has the capacity to both break DNA, a precursor to translocations and deletions (Cohen-Jonathan et al. 1999), and to elicit mitotic catastrophe, a type of cell death that occurs during mitosis (Castedo et al. 2004). Cells that fail to execute apoptosis in response to mitotic failure are likely to divide asymmetrically, with the consequent generation of aneuploid cells (Castedo et al. 2004). It is notable that up to 35% of childhood leukemias exhibit “high hyperdiploidy,” which is defined as having five or more extra chromosomes; this cytogenetic feature is known to occur after a single mitotic failure in utero (Gruhn et al. 2008; Paulsson et al. 2005).

Little is specifically known about the effects of ²¹⁰Po exposure to the embryo and fetus, however, fetal exposure could cause failure of implantation or miscarriage or major malfunctions (Jefferson et al. 2009), as well an increased incidence of chromosomal breaks and translocations resulting in childhood cancer. At particular stages of development a future tissue, or stem cells for many cell lineages, can be represented by one or a few cells, and alpha irradiation may cause mutagenic effects in these cells that is later manifested as cancer (Goodhead 1991). The distribution of ²¹⁰Po to the ovaries and the embryo (Finkel et al. 1953; Haines et al. 1995; Samuels 1966) and the potential for a single alpha particle traversing a stem cell to induce chromosomal instability (Kadhim et al. 2001) suggests that even low-level alpha-particle irradiation to reproductive or embryonic cells may have significant downstream effects. New, basic, biological, and toxicological research is needed on ²¹⁰Po because of its potential to kill or damage critical reproductive, embryonic, or hematopoietic cells at low doses. New research is needed on transplacental transfer of ²¹⁰Po and the effects of low-level exposure to the embryo, fetus, and infant because the high degree of cell kinetics needed for normal growth of embryonic and hematopoietic cells and other tissues in the fetus and child imparts a high sensitivity to children from environmental insults such as ionizing radiation from ²¹⁰Po.

²¹⁰Po may be involved in leukemogenesis by exposing the hematopoietic stem cells in the embryonic yolk sac and fetal spleen, liver, and bone marrow to alpha-particle radiation. The placenta provides at least a partial barrier to transfer of ²¹⁰Po; however, ²¹⁰Pb readily passes the placenta (Goyer 1990). Fetal ²¹⁰Pb is incorporated into bone and ²¹⁰Pb-supported ²¹⁰Po could irradiate hematopoietic stem cells in fetal marrow. ²¹⁰Po remains in place following decay of calcified ²¹⁰Pb (James et al. 2004), and up to 80% of the marrow in lumbar vertebrae would be within range of alpha particles from ²¹⁰Po on bone surfaces because bone-marrow spaces are small in the fetus (Purnell et al. 1999). Maternal ²¹⁰Po that passes the placenta, or ²¹⁰Pb-supported ²¹⁰Po in soft tissues, could migrate in the blood to the fetal liver or spleen and potentially expose hematopoietic stem cells. Fat is present in adult but not fetal bone marrow and, being fat soluble, inhaled or ingested radon could accumulate in fat in adult marrow and expose it to alpha-particle irradiation from the radon itself or its daughters ²¹⁸Po and ²¹⁴Po (Richardson et al. 1991). New research is needed on toxicological and health effects of adult and embryonic and fetal exposure to Po isotopes, regardless of whether the exposure originates from ingestion of ²¹⁰Po itself or its radionuclide grandparents radon and ²¹⁰Pb. The emergence of exquisitely sensitive modern leukemia mouse models should be used to explore mechanisms of carcinogenesis by ²¹⁰Po and ²¹⁰Pb administered by appropriate routes and doses. Such models are currently used primarily to explore genetic pathways but increasingly are being made available for environmental research.

The linkage between smoking and female infertility (Augood et al. 1998) and the smaller size and reduced number of follicles in the ovaries of mice exposed to cigarette smoke (Tuttle et al. 2009) appear similar to outcomes described by Samuels (1966) for mice where primary oocytes were killed at low ²¹⁰Po doses and the structure of the ovaries affected at higher doses. An unrecognized outcome for women exposed to environmental ²¹⁰Po may be subfertility. Dose calculations together with a cell-survival function for primary oocytes could be used to estimate doses to the ovary and provide information on the expected level of killing of reproductive cells by environmental levels of ²¹⁰Po. A single alpha particle can induce bystander effects in a population of cells, thus the sensitivity of primary oocytes to low doses of ²¹⁰Po noted by Samuels (1966) may be the result of bystander effects. There may be tissue-specific differences in bystander responses, and research is needed on the susceptibility of reproductive and embryonic cells to bystander signals.

Numerous epidemiological studies reviewed by Canu et al. (2011) have investigated associations between cancers, including leukemia, and ingestion of naturally radioactive water. Even if exposure to ²¹⁰Po was not occurring, ²¹⁰Po must have been present in the environment at these studies because ²³⁸U, ²²⁶Ra, and radon ultimately decay to ²¹⁰Po. Future investigations of natural radioactivity should consider the possibility that exposure to ²¹⁰Po is occurring.

Residents of the subdivision in Charles County, Maryland (Outola et al. 2008), and rural areas of Lahontan Valley, Nevada (Seiler 2012), were exposed to levels of ²¹⁰Po exceeding 1.5 Bq/L in their drinking water for decades before it was discovered. If the ²¹⁰Po activity exceeds 0.55 Bq/L, then the GAR standard for ²¹⁰Po would be exceeded (U.S. EPA 2000). Hence, even levels that meet the current drinking-water standard could expose the public to more ²¹⁰Po than they would receive if they were smokers. The occurrence of ²¹⁰Po concentrations in groundwater > 0.55 Bq/L is currently assumed to be extremely rare, but this rarity may be an artifact of groundwater seldom being directly tested for ²¹⁰Po. Furthermore, the standard test for GAR (U.S. EPA 2000) may not adequately identify samples with ²¹⁰Po concentrations that exceed safety thresholds. The recommended procedure allows quarterly samples to be composited as long as they are analyzed within 1 year of the first sample being collected (U.S. EPA 2000). However, during this 1-year period, > 60% of the ²¹⁰Po in the composited samples can be lost by radioactive decay before analysis. Furthermore, sample heating during the analytical procedure for gross alpha radioactivity can drive off volatile radionuclides such as ²¹⁰Po (Arndt and West 2008). Research on the environmental occurrence of ²¹⁰Po and ²¹⁰Pb is needed, particularly in drinking water, because of potential health effects at low levels. Development of new, less expensive, analyses for ²¹⁰Po and ²¹⁰Pb is needed because of the potential that current screening tests for them do not adequately protect public health.

In uncontaminated settings, only about 14% of the human body burden is due to direct ingestion of ²¹⁰Po; the remainder is indirectly due to ingestion of ²¹⁰Pb. Nonetheless, exposure to ²¹⁰Po through drinking water may be more widespread than currently assumed and a comprehensive national reconnaissance is needed to determine what levels of ²¹⁰Po and ²¹⁰Pb the U.S. population is being exposed to in its drinking water. ²¹⁰Po concentrations in typical aquifer sediments are high enough that mobilization of only a small percentage of the ²¹⁰Po present in the sediments could yield water with sufficient ²¹⁰Po to affect the health of people drinking the water. For adults and infants using wells with 0.5 Bq/L of ²¹⁰Po, which would meet the current U.S. drinking-water standard, the annual effective dose would exceed the limit of 0.1 mSv/year recommended by the WHO (2006). Private wells used in rural areas and wells used for stockwater are unregulated, and even gross ²¹⁰Po contamination of one of these wells would almost never be detected.