Evaluation of health effects in Sequoyah Fuels Corporation workers from accidental exposure to uranium hexafluoride

Abstract

Urine bioassay ~easurements for uranium and medical laborato ry resu~ts were studied to determine whether there were any health effects from urcnium intake among a group of 31 workers exposed to uranium hexafluoride (UF6) and hydrolysis products following the accidental rupture of a 14-tun shipping cylinder in early 1986 at the Sequoyah FJels Corporation uranium conversion facility in Gore, Oklahoffid. Physiological indicators studied to detect kidney tissue damage inc "i uded tests for urinary protein, casts and cells, blood, specific gravity, and urine pH, blood urea nitrogen, and blood creatinine. We concluded after reviewing two years of follow-up medical data that none of the 31 workers sustained any observable health effects from exposure to uranium. The early excretion of uranium in urine showed more rapid systemic uptake of uranium from the lung than is assumed using the International Commission on Radiological Protection (ICRP) Publication 30 and Publication 54 models. The urinary excretion dota from these workers were USE" to develop an improved systemic recycling model for inhaled soluble uranium. We estimated initial intakes, clearance rates, kidney burdens, and resulting radiation doses to lungs, kidneys, and bone surfaces. Radiation dose limits and limits on intake, as recommended by the JCRP , were not exceeded. However, the NRC derived limit of 9.6 mg was exceeded by eight of the 31 workers. Maximum kidney concentrations in exposed workers ranged from 0.05 to 2.5 ~~ U/g kidney tissue. We found no toxicological effects on the kidneys of workers at these concentrations. Uranium urinalyses and medical laboratol'Y result s on Dlo od dnli lit' in c were studied to determine whether ~here were Jnv health eff ect s i n 3 1 \':orkcl's exposed to uranium hexafluoride (UF6) following-the acciden ta l r u~lu r e of d 14-ton shipping cylinde:r in early 1986 at a uranium convers io n facil ity in Gore, Oklahoma. The workers were likely exposed t o very hi gtl concent ' ,t(ia/;s of ai rborne uranium for short time periods. The mos t imp ort Jnt Sil()\'t •, t eli ll concern was inhalation of hydrofluoric acid (HF) with pos s ibl e l ung d lilldge and skin-exposure burns. The major long-term concern wa s kidney dd ll ldCJC in workers with significant intakes of uranium. Urinalyse s wet' e pe r forJ1!ed 0 11 workers to evaluate their health and kidney function. The data were also evaluated to estimate their initial intakes of ura~ium, resulting r adi ation doses to bone surfcces, kidneys, and lungs, and the resu It i ng (oIllmi tte d effective dose equivalent (a measure of risk to the whole body). ~he physiological indicators studied to detect kidney tissue damage by uranium poisoning included tests for urinary protein, casts and cells, urinary blood, specific gravity, pH of the urine, blood urea nitrogen, and blood creatinine. Physical examination and pulmonary function ' est res ults over a two-year follow-up period were also evaluated. We conclud ed fr om review of the medical records and laboratory results tha...

Uranium hexafluoride public risk

“…Studies at the Pacific NorthwestLaboratory(PNL) on urine data obtained from Sequoyah Fuels Corporationworkers after the 1986 UF6 rupture accident showed that a maximum likely kidney tissue concentrationof about 2.5 _g U per g of kidney tissue occurred in the highest-exposed workers. No _ong-termkidney tissue damage was observed at these concentrations,but there was some evidence of increasedurinary protein in the highest-exposed workers (Fisher et al 1990). The clinical laboratoryevidence from this study suggestedthat uranium concentrationsin kidneysof these workers may approached,but not exceed, the threshold for toxicity in humans.…”

Methods and Models of the Hanford Internal Dosimetry Program, PNNL-MA-860

“…The renal toxicity of uranium varies with the compound form, with toxicity increasing with chemical solubility (Morrow et al 1982). Based on work by Just (1984), Just and Emler (1984), and Fisher, Swint, and Kathren (1990), McGuire (1991) concluded that an acute intake of soluble uranium of 10 mg or less is unlikely to have any detectable (even transient) effects, and that a 40-mg intake (possibly as high as 100 mg) is likely to be below the level of any permanent effects. …”

“…Albuminuria is also an indicator of kidney damage. Leggett (1989) and Fisher, Swint, and Kathren (1990) have identified a number of other potentially useful tests. The decision to perform such tests is made by HEHF Occupational Medicine.…”

Proposed Standards for Acute Exposure to Low Enrichment Uranium for Compliance with 10 CFR 70.61

“…Data are available for a number of other cases with acute inhalation intakes estimated to be several tens of mg of uranium, all of whom showed minor transitory renal effects as evidenced by biomarkers in the urine, but all of whom recovered within days after exposure (Boback 1975;Fisher et al 1990;Kathren and Moore 1986). Also, Butterworth (1955) reported a case of voluntary experimental ingestion of 470 mg of uranium as uranyl nitrate by a male subject, with complete recovery from minor renal effects within 24 h.…”

“…Once again based on animal studies, the relatively insoluble compounds such as UO 2 , U 3 O 8 , and UF 4 exhibit a low order of chemical toxicity because they are poorly absorbed via the gut or respiratory tract, while the more soluble compounds of uranium such as Na 2 U 2 O, UO 2 (NO 3 ) 2 , and UO 4 are more quickly absorbed into the blood and therefore exhibit toxic effects in moderate doses (ATSDR 1999;Stannard 1988). UO 2 F 2 and UF 6 constitute a special case because they hydrolyze to yield HF which produces corrosive chemical effects (acid burns) on tissues independent of uranium chemical toxicity or enrichment (Tannenbaum and Silverstone 1951;Kathren and Moore 1986;Fisher et al 1990). …”