Tritium oxide

/SURVEILLANCE/ Earlier study of acute tritiated water intakes in humans has demonstrated that the dose contribution from metabolized organically bound tritium is less than 10% of the body water dose. To further demonstrate that the dose contribution from the organically bound tritium per unit intake of tritiated water is the same, regardless of whether the intake is acute (all at once) or chronic (spread over time), urine samples from six male radiation workers with chronic tritiated water intakes were collected and analyzed for tritium. These workers have a well-documented dose history and a well-controlled tritium bioassay database, providing assurance that their tritium intakes were in the form of tritiated water. Each month for a full calendar year, urine samples were collected from each exposed worker. The monthly concentration of tritiumin-urine for each exposed worker was no lower than 10+4 Bq/L but no higher than 10+5 Bq/L. These urine samples were analyzed for tritiated water and organically bound tritium to determine the ratio of these tritiated species in urine. The average ratio of tritiated water to organically bound tritium in urine for each exposed worker was 330 +/- 129 (range, 297-589). In calculating the dose to these workers, we assumed that, under steady-state conditions, the ratio of the specific activity of tritium ((3)H activity per gH) in the organic matter and water fractions of urine is representative of the ratio of the specific activity of tritium in the organic matter and water fractions of soft tissue. A mathematical model was developed and used to estimate the dose increase from the metabolized organically bound tritium based on the ratio of tritiated water to organically bound tritium in urine. The resulting average dose from the organically bound tritium was 6.9 +/- 3.1% (range, 4.7-9.9%) of the body water dose for the six male workers, and agrees well with the value obtained from our acute tritiated water intakes study in humans. The observed dose contribution from organically bound tritium, relative to body water dose, is in agreement with current recommendations of assigning 10% of total body water dose for organically bound tritium in soft tissues after tritiated water intakes.

/SURVEILLANCE/ In general, internal exposure from tritium at pressurized heavy water reactors (PHWRs) accounts for approx. 20-40 % of the total radiation dose. Tritium usually reaches the equilibrium concentration after a few hours inside the body and is then excreted from the body with an effective half-life in the order of 10 d. In this study, tritium metabolism was reviewed using its excretion rate in urine samples of workers at Korean PHWRs. The tritium concentration in workers' urine samples was also measured as a function of time after intake. On the basis of the monitoring results, changes in the tritium concentration inside the body were then analyzed.

/GENOTOXICITY/ The present study was carried out to evaluate the genotoxicity of tritium, administered as tritiated water, in peripheral blood human lymphocyte cultures. Sister-chromatid exchanges (SCE) and chromosome aberrations (CA) were scored as genetic endpoints. From our results we can conclude that beta-radiation from low concentrations of tritium was able to induce a significant increase in the frequency of CA, although it was ineffective in increasing the frequency of SCE.

/GENOTOXICITY/ Tritiated water (HTO) is a major toxic effluent from the nuclear power industry, that is released into the environment in large quantities. The low dose radiation effect and dose rate effect of HTO on human lymphocytes and bone marrow cells have not been well studied. The present study was therefore undertaken to investigate the HTO dose-response relationship for chromosomal aberrations in human lymphocytes and bone marrow cells at low in vitro radiation doses ranging from 0.1 to 1 Gy. Lymphocytes (G0 stage) and bone marrow cells were incubated for 10-150 min with HTO at a dose rate of 2 cGy/min (555 MBq/mL). The relative biological effectiveness (RBE) of HTO was calculated with respect to (60)Co gamma-rays for the induction of dicentric and centric ring chromosomes at low radiation doses. The RBE value for HTO beta-rays relative to (60)Co gamma-rays was 2.7 for lymphocytes and 3.1 for chromatid aberrations in bone marrow cells. Lymphocytes were also chronically exposed to HTO for 6.7-80 hr at dose rates of 0.5 cGy/min (138.5 MBq/mL) and 0.02 cGy/min (5.6 MBq/mL). There was a 71.5% decrease in the yield of dicentrics and centric rings at the dose rate of 0.02 cGy/min, indicating a clear dose rate effect of HTO. The RBE value for HTO relative to (137)Cs gamma-rays was 2.0 at a dose rate of 0.02 cGy/min, suggesting that low HTO dose rates produce no increase of the RBE values and that the values may be constant between 2 and 3 within these dose rates. These results should prove useful in assessment of the health risk for humans exposed to low levels of HTO.

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/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ A series of experiments was carried out using female (C57BL/6N x C3H/He)F1 mice (BCF1) to assess the carcinogenic effect of tritiated water (HTO) following a preliminary experiment in which the acute effect of HTO was studied in young female mice of C57BL/6L strain in an attempt to gain basic information on the long-term experiment, and the results were compared with those of fission spectrum neutrons and gamma-rays. The obtained findings are summarized as follows. 1) C57BL/6N mice receiving a single intraperitoneal (i.p.) injection of HTO, 7.4 x 10+8 Bq (20 mCi) or more, died of bone marrow failure within 20 days. 2) In long-term experiment, BCF1 mice given 1.4 x 10+8 Bq to 5.6 x 10+8 Bq developed solid tumors in a variety of tissues but with no obvious dose dependency. 3) The fractionated exposure of 7.4 x 10+8 Bq (1.9 x 10+8 each, at 7-day intervals) was highly effective in induction of malignant T-cell lymphomas (85%) with a shorter latency than that of a single exposure (15%). 4) A protracted irradiation of 0.27 Gy of (137)Cs, designed to simulate the decreasing absorption rate with time after a single i.p. injection of an equivalent dose of HTO resulted in a drastic reduction in induction rate of ovarian tumors as compared with that of an acute (60)Co gamma irradiation. 5) The carcinogenic potential of HTO, given as a single i.p. injection, was quite similar to that of acute(60)Co gamma ray irradiation at both 2.7 Gy and 0.27 Gy levels. On the other hand, the effect of HTO was slightly higher than that of protracted gamma-ray irradiation. 6) 252Cf fission neutrons was found to be more potent in tumor induction than gamma-rays or HTO beta-rays under the present experimental conditions.

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ The purpose of this study was to determine the carcinogenicity and retention of tritiated water (HTO) in mice. A two-part study was undertaken. In an HTO-incorporation study, both sexes of 12-day old C3H/HeN mice were i.p. injected with 3.70 MBq/pup of HTO and sacrificed 3 hr and 1, 3, 7, 14 days after HTO administration; in a carcinogenicity study, pups were given a single i.p. injection of HTO at doses of 0, 0.23, 0.92 and 3.70 MBq/mouse, and then observed for 14 months. The survival rates of both sexes slightly decreased upon increasing the HTO administered doses. The results indicated that the administration of HTO to infants led to a significant increase of liver tumors in male mice, but not in females. In female mice, ovarian tumors were observed for the high-dose group of injected HTO.

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Previously we reported hematopoietic death as an effect of tritiated water (HTO) in drinking water in the concentration range from 5.92 x 10+11 to 1.85 x 10+10 Bq/dm3. In the present study the effects of HTO in a lower concentration range from 9.25 x 10+9 Bq/dm3 (0.240 Gy/day) to 3.70 x 10+8 Bq/cudm (0.096 Gy/day) are reported. Female (C57BL/6N and C3H/He)F1 mice were maintained on drinking water containing various levels of HTO. Mice survived for > 150 days with a high incidence of tumor development (70 to 80%). In the dose-rate range from 9.25 x 10+9 Bq/cudm (0.240 Gy/day) to 1.85 x 10+9 Bq/cudm (0.048 Gy/day) the main cause of death was thymic lymphoma. However, at a dose-rate of 9.25 x 10+8 Bq/cudm (0.024 Gy/day) the incidence of thymic lymphoma sharply decreased, while the incidence of other tumors increased. The tumor type became more diverse at lower concentrations of HTO. The latent period of tumor development was shorter and the life-shortening effect was more marked by (3)H beta-irradiation in this study than b X- or gamma-irradiation reported in other investigations.

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ The carcinogenicity of (3)H administrated as tritiated water ((3)H2 O) was tested in mice by intraperitoneal injection or oral administration, and in rats by intraperitoneal injection producing thymic lymphoma and myeloid leukeamia in mice and mammary tumours [tumour type not specified] in rats.

For more Non-Human Toxicity Excerpts (Complete) data for Tritium oxide (30 total), please visit the HSDB record page.

In general, internal exposure from tritium at pressurized heavy water reactors (PHWRs) accounts for 20-40% of the total radiation dose. Tritium usually reaches equilibrium concentration after a few hours inside the body and is then excreted from the body with an effective half-life in the order of 10 d. In this study, tritium metabolism was reviewed using its excretion rate in urine samples of workers at Korean PHWRs. The tritium concentration in workers' urine samples was also measured as a function of time after intake. On the basis of the monitoring results, changes in the tritium concentration inside the body were then analyzed.

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/

/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/

/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Radioactives I, II, and III/

For more Antidote and Emergency Treatment (Complete) data for Tritium oxide (6 total), please visit the HSDB record page.