10
Surface Lead

This chapter summarizes relevant toxicologic data on lead poisoning in adult humans. Selected chemical and physical properties and toxicokinetic and mechanism-of-action data are also presented. The committee could not recommend surface-lead exposure guidance levels, but it did endorse the monitoring of submariner blood lead concentrations to determine whether surface lead contamination onboard submarines is resulting in appreciable exposure of crews. Blood lead concentrations in the context of occupational lead exposures are therefore discussed. Adequacy of available data for defining submarine surface-lead exposure levels and research needed to define more clearly the issue of potential lead exposure among submariners are also outlined.

PHYSICAL AND CHEMICAL PROPERTIES

Elemental lead is a member of periodic table group IVB. Common commercially important forms of inorganic lead include elemental lead, lead acetate, lead azide, lead bromide, lead chloride, lead chromate, lead fluoroborate, lead iodide, lead molybdenum chromate, lead nitrate, lead oxide, lead phosphate, lead styphnate, lead sulfate, and lead sulfide. Metallic lead is a blue-grey material that is solid at room temperature. Physicochemical properties of lead are presented in Table 10-1.

OCCURRENCE AND USE

Lead is a ubiquitous element in the environment and biologic systems (Goyer 1996). Exposure to lead can occur from ingestion (for example, through the consumption of contaminated food, water, or soil), inhalation, and, in the



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10 Surface Lead This chapter summarizes relevant toxicologic data on lead poisoning in adult humans. Selected chemical and physical properties and toxicokinetic and mechanism-of-action data are also presented. The committee could not recom- mend surface-lead exposure guidance levels, but it did endorse the monitoring of submariner blood lead concentrations to determine whether surface lead con- tamination onboard submarines is resulting in appreciable exposure of crews. Blood lead concentrations in the context of occupational lead exposures are therefore discussed. Adequacy of available data for defining submarine surface- lead exposure levels and research needed to define more clearly the issue of potential lead exposure among submariners are also outlined. PHYSICAL AND CHEMICAL PROPERTIES Elemental lead is a member of periodic table group IVB. Common com- mercially important forms of inorganic lead include elemental lead, lead acetate, lead azide, lead bromide, lead chloride, lead chromate, lead fluoroborate, lead iodide, lead molybdenum chromate, lead nitrate, lead oxide, lead phosphate, lead styphnate, lead sulfate, and lead sulfide. Metallic lead is a blue-grey mate- rial that is solid at room temperature. Physicochemical properties of lead are presented in Table 10-1. OCCURRENCE AND USE Lead is a ubiquitous element in the environment and biologic systems (Goyer 1996). Exposure to lead can occur from ingestion (for example, through the consumption of contaminated food, water, or soil), inhalation, and, in the 214

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Surface Lead 215 TABLE 10-1 Selected Physical and Chemical Data on Elemental Lead Synonyms and trade names NA CAS registry number 7439-92-1 Molecular formula Pb Atomic weight 207.2 Boiling point 1,740EC Melting point 327.4EC Flash point NA 11.34 g/cm3 at 20°C Density Vapor pressure 1.77 mm Hg at 1000EC Solubility Salts have variable solubility in water; elemental lead is soluble in hot or concentrated mineral acids Abbreviations: NA, not applicable or not available Source: Data from Budavari et al. 1989. case of organic forms of lead, dermal absorption (Bolger et al. 1996). Histori- cally, elemental lead has been an important component of solder, brass, bronze, and other alloys. Lead is found in electric-cable insulation, and the oxide is found in some paints, inks, glass, crystal, plastics, textiles, and ceramics. At least half the elemental lead used worldwide is in lead-acid batteries (ATDSR 1999). Lead is present in stainless steel—such as that used in food-handling equipment and surfaces—as an unintentional contaminant at not more than 0.1% by weight (Precision Specialty Metals 2003; Nucor 2007). A variety of occupa- tions are associated with lead exposure, including those involved in lead smelt- ing, battery manufacturing, firing ranges, welding, construction, and demolition. Occupational exposure is often the most significant source of exposure of adults (Shannon 1998). SUMMARY OF TOXICITY The toxicology, epidemiology, and clinical presentation of lead intoxica- tion have been reviewed (EPA 1986; ATSDR 1999). Lead is a cumulative poi- son that is poisonous in all forms, its elimination from the body is slow, and consequences of exposure are varied and can be severe (Gosselin et al. 1984). Generally, only 5-10% of ingested lead is absorbed from the adult human gas- trointestinal tract. Lead may dissolve to an appreciable degree in the acid envi- ronment of the stomach, greatly increasing its absorption. Absorption of lead from the gastrointestinal tract is facilitated by the same mucosal transport pro- teins that mediate calcium transport (Fullmer 1992). Smaller lead particles are more readily absorbed from the gastrointestinal tract. In the blood, about 95% of

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216 Exposure Guidance Levels for Selected Submarine Contaminants the lead is associated with the red blood cells (RBCs), so measurement of blood lead concentrations is preferred to measurement in serum or plasma. Lead has a half-life of about 30 days in adult blood. Once absorbed, it readily passes mem- brane barriers, such as the blood-brain barrier. Distribution is primarily to the kidney cortex, liver, and bone; bone contains up to about 90-98% of the total body lead burden. Lead is excreted by the kidney, but the elimination rate var- ies, depending on the tissue that absorbed the lead. Lead perturbs multiple enzyme systems, especially ones that contain sulf- hydryl groups or are zinc-dependent. Signs of lead toxicosis are generally asso- ciated with the nervous, hematologic, and urinary systems (Table 10-2). Blood lead concentration has proved to be a valuable biomarker of exposure. The U.S. Environmental Protection Agency (56 Fed. Reg. 26460[1991]) summarized key aspects of the relationship between circulating lead concentration and adverse health effects (see Table 10-2). Although a valuable indicator of exposure, blood lead concentration does not indicate the length of exposure or the total amount of lead deposited in the body. Effects in Humans Sufficient data on the toxicity of lead were available to allow the commit- tee to focus strictly on the human clinical literature. One of the best character- ized and most sensitive adverse effects of lead is inhibition of the serum enzyme delta aminolevulinic acid (ALA) dehydratase (Godwin 2001). Lead-induced inhibition of ALA dehydratase can result in increased elimination of ALA in the urine. Determination of urinary ALA excretion has some merit as a diagnostic test for lead poisoning; however, urinary ALA may be unreliable when the daily intake of lead is small. Lead also inhibits ferrochelatase, an enzyme in the heme- biosynthesis pathway. Inhibition of this enzyme results in decreased heme pro- duction and accumulation of protoporphyrin in the RBCs of poisoned people (Godwin 2001). Adverse effects on the nervous system also occur after acute or chronic lead poisoning. Fulminant encephalopathy, wrist drop, and peripheral neuritis are signs of neurotoxicity (plumbism) in adults. Neurologic manifestations of plumbism occur when blood lead concentrations approach or exceed 100-120 µg/dL. Encephalopathy can quickly progress, people going from full conscious- ness to convulsions and terminal coma within hours. Reduced sensory and mo- tor nerve-conduction velocities can be observed when blood lead concentrations exceed 40-70 µg/dL (Araki et al. 2000; Triebig et al. 1984). There is no clear evidence, however, that adult blood lead concentrations under 30 µg/dL impairs peripheral nerve function (Araki et al. 2000).

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Surface Lead 217 TABLE 10-2 Blood Lead Concentrations and Associated Observed Effects in Exposed Men Observed Effect Blood Lead Cardiovascular, Concentration Hematologic, Heme Reproductive (µg/dL) Synthesis Nervous System Renal System System 100-120 — Encephalopathy Chronic — nephropathy 80 Frank anemia — — — 60 — — — — 50 — Subencephalopathic — Altered signs testicular function 40 Increased urinary Peripheral — — ALA and neuropathy coproporphyrins 30 Increased blood — — — pressure 25-30 Increased — — — protoporphyrin concentrations 15-20 — — — — <10 ALA dehydratase — — — inhibition Abbreviation: ALA, delta-aminolevulinic acid. Sources: Adapted from 56 Fed. Reg. 26460 (1991); Shannon 1998. Hypertension has been associated with acute and chronic occupational lead exposure. Overall, the effect of increased blood lead concentration on blood pressure is still the subject of debate because many studies demonstrating an association failed to account for the influence of tobacco-smoking or ethanol consumption (Staessen et al. 1995). Another common criticism of the studies concerns the relatively small numbers of men in each group (under 100), and not all the clinical investigations have confirmed the association. Surveys of 7,371 British men 40-59 years old found that alcohol consumption, body-mass index (BMI), and tobacco-smoking had a greater influence than blood lead on systolic blood pressure (Pocock et al. 1988). Policemen (n = 89) with blood lead concentrations of 30 µg/dL or higher had a significant increase in systolic pres- sure even after adjustment for tobacco-smoking, BMI, and age (Weiss et al. 1988). In another study that adjusted for potential confounders, systolic blood pressure of 53 male lead workers (blood lead concentrations, 44-51 µg/dL) was

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218 Exposure Guidance Levels for Selected Submarine Contaminants significantly higher than that of 52 workers without lead exposure (blood lead concentrations, under 20 µg/dL) (de Kort et al. 1987). Lead-exposed construc- tion workers developed clinical hypertension when blood lead concentrations increased from 48-50 to 85-120 µg/dL (Pollock and Ibels 1986; Marino et al. 1989). After controlling for exercise, tobacco and alcohol consumption, age, and educational level, Parkinson et al. (1987) could not detect a significant as- sociation between increases in diastolic or systolic blood pressure and blood lead concentrations in 270 white male lead-battery plant workers (blood lead concentration, 40 ± 13 µg/dL) and 158 similar males (blood lead concentration, 7 ± 5 µg/dL) who did not work with lead. Pirkle et al. (1985) suggested that a relationship of blood lead concentration to blood pressure was more evident at lower than at higher blood lead concentrations. Overall, there is suggestive evi- dence of an increase of 1.0-2.0 mm Hg in systolic blood pressure and 0.6 mm Hg in diastolic pressure associated with a doubling of blood lead concentration (Staessen et al. 1995; Victery et al. 1985). Staessen et al. (1995) concluded that increased blood pressure associated with increased low-level lead exposure was “unlikely to entail any public health implication in terms of hypertension-related complications.” Excessive urinary lead concentrations (100 to over 250 µg/dL) in a group of retired lead workers were associated with a significant excess risk of cerebrovascular accident (Dingwall-Fordyce and Lane 1963). Lead is also a recognized nephrotoxin. Two distinct renal syndromes are associated with excessive lead exposure, one acute and temporary and the sec- ond chronic and progressive (Gosselin et al. 1984). Acute plumbism can result in reversible impairment of proximal tubular function (Tepper 1963). Prolonged lead-induced damage to the human kidney is associated with interstitial fibrosis with atrophy and dilation of the tubules. It is difficult to relate current blood lead concentrations to reduced kidney function because they do not necessarily correlate with past lead exposures. Duration of lead exposure is an important determinant of potential renal toxicity (Lilis et al. 1968), and relatively low blood lead concentrations in an affected person may reflect a long interval be- tween the last lead exposure and when blood lead concentrations were meas- ured. In general, the risk of chronic nephropathy is increased when blood lead concentrations are over 60 µg/dL (ATSDR 1999). Renal biopsy of men with pyelonephritis and blood lead concentrations of 70-138 µg/dL found diffuse interstitial or peritubular fibrosis, sclerotic and obliterated glomeruli, proximal tubular degeneration characterized by mito- chondrial swelling, and deposition of eosinophilic dense-staining granular inclu- sion bodies (Pollock and Ibels 1986). Renal biopsy of 12 men with blood lead concentrations between 40 and over 80 µg/dL found characteristic focal intersti- tial nephritis (Wedeen et al. 1979).

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Surface Lead 219 Male Reproductive Toxicity At blood lead concentrations of 66 µg/dL or higher, lead can act directly on the testes, as evidenced by reduced testosterone synthesis and induction of peritubular testicular fibrosis (Braunstein et al. 1978; Cullen et al. 1984; Ro- damilans et al. 1988a,b). Although a number of laboratory animal models have documented the gametotoxic consequences of acute and chronic lead exposure (Stowe and Goyer 1971; EPA 1986), only data relevant to men and the adverse effects of lead on human male fertility are considered here. Lin and associates (1996) found reduced fertility in 4,256 adult males who were occupationally exposed to lead and had blood lead concentrations of 25 µg/dL or higher, compared with 5,148 matched controls. Although Lin et al. (1996) concluded that men with the highest cumulative exposure had the great- est reductions in fertility, the study failed to account for contraception use or marital status. Gennart et al. (1992) found that fertility decreased with duration of lead exposure in a group of 74 male lead factory workers (mean age, 39 years) who had a mean blood lead concentration of 46 µg/dL. However, the fact that no independent assessment of the worker’s wives was carried out by the authors reduces confidence in that finding. Others (Coste et al. 1991; Bonde and Kolstad 1997) failed to document any associations between blood lead concen- trations of less than 40 to 60 µg/dL or 39 µg/dL and live-birth rates per couple among 229 French and 1,349 Danish battery workers, respectively. Ng et al. (1991) studied circulating testosterone, prolactin, lutenizing hor- mone (LH), and follicle stimulating hormone (FSH) in 122 lead-battery workers (mean blood lead concentration, 35 µg/dL) compared with 49 controls (blood lead concentration, 8.3 µg/dL). Smokers displayed reduced prolactin concentra- tions, and workers aged 40 years old or older had reduced testosterone concen- trations. Among lead workers, circulating LH and FSH were increased. Among 150 lead workers examined by Lancranjan et al. (1975), a reduc- tion in sperm vitality (asthenospermia) was associated with blood lead concen- trations of 53-74 µg/dL. At least five studies (Alexander et al. 1996; Assennato et al. 1987; Chowdhury et al. 1986; Lerda 1992; Wildt et al. 1983) have docu- mented significant reductions in sperm count and increased numbers of abnor- mal sperm in men with blood lead concentrations of 40 µg/dL or higher. Genotoxicity Lead-exposed workers with blood lead concentrations of 28.2 to 65.5 µg/dL had an increased incidence of micronuclei in peripheral lymphocyte and clastogenic and aneugenic effects in peripheral lymphocytes (Palus et al. 2003). An increased number of chromatin defects were observed in sperm collected from men with blood lead concentrations of 45 µg/dL or higher (Bonde et al. 2002).

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220 Exposure Guidance Levels for Selected Submarine Contaminants Carcinogenicity The International Agency for Research on Cancer (IARC 1987) consid- ered the results of bioassays of parenteral and oral lead (for example, lead ace- tate and lead phosphate) as sufficient evidence of carcinogenicity in animals. At least two groups have published the results of mortality analyses of U.S. work- ers in lead smelters and battery plants (Cooper et al. 1986; Selevan et al. 1984). There was a nonsignificant increase in respiratory tract cancer (36.9 cases ex- pected compared with 41 observed), but excess renal cancers (2.9 expected and six observed) and bladder cancers (4.2 expected and six observed) were seen in those employed in smelters (Selevan et al. 1984). There was a significant excess of stomach cancers (20.2 expected and 34 observed) and respiratory tract can- cers (93.5 expected and 116 observed) in lead workers (Cooper et al. 1986). However, the smelter and battery-plant workers were also exposed to other car- cinogenic materials and processes. IARC (1987) considered the evidence of human carcinogenicity of inorganic lead inadequate. TOXICOKINETIC CONSIDERATIONS Depending on the physical characteristics of a particular lead-containing material, substantial differences in relative bioavailability can exist. The bioavailability of lead is a function of its chemical form, route of exposure, and physical state. The bioavailability of the lead in lead-acid batteries, cable cover- ings, ammunition, solder, caulking, paint, and dust depends in large part on par- ticle size. Percutaneous uptake of lead acetate through intact skin of human volun- teers was negligible (0-0.3%) (Moore et al. 1980). Deposition of inhaled lead also depends on particle size. Particles depos- ited in the upper airway are cleared and swallowed. As particle size increases from less than 0.05 µm to 0.05-0.5 µm, the fraction deposited in lung declines from 34-60% to 10-30% (Booker et al. 1969; Chamberlain et al. 1975; Gross 1981; Hursh and Mercer 1970; Morrow et al. 1980). As particle size increases, impaction and sedimentation increase; 28-70% deposition rates were seen in metal scrap yard and lead-battery plant workers (Mehani 1966). Uptake of in- haled lead also depends on the inhalable fraction of the material. Lead absorption from the gastrointestinal tract is influenced by diet, age, particle size, dose, and calcium and iron nutritional status. Most adults absorb about 7-15% of the soluble lead found in foods. Chemical forms that predomi- nate under alkaline conditions (for example, lead carbonate) are more soluble in gastric contents and are more readily absorbed from the stomach than less solu- ble forms (for example, lead sulfate). Uptake from the gastrointestinal tract oc- curs primarily in the duodenum (Mushak 1993). Absorption of soluble lead (consumed as either the nitrate or the acetate) was increased in fasting adults

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Surface Lead 221 compared with the amount that was absorbed when the same dose was con- sumed with food (4-8%) (Rabinowitz et al. 1980; James et al. 1985). Fractional lead absorption from metallic particles in the rat gastrointestinal tract decreased as particle size increased from 5 µm to 200 µm in mean diameter (Barltrop and Meek 1979). Gastrointestinal absorption of lead (consumed as the acetate) by adult volunteers was reduced from 63% of the ingested dose to 10% when the same quantity was consumed with calcium or phosphate salts (Heard and Cham- berlain 1982). Bioavailability can differ among white lead (basic lead carbonate), red lead (Pb3O4), basic lead sulfate, or lead chromate. The small size of ingested lead sulfate particles contributed to a higher relative absorption from the rat gas- trointestinal tract (164%) than lead acetate, but absorption of lead from lead chromate particles of similar size was 56% less than from lead acetate (Barltrop and Meek 1975). The pharmacokinetics of lead in healthy people can be described by using a three-compartment model (Rabinowitz et al. 1976). Elimination from the first compartment (blood) has a half-time of about 35 days. Nearly all (90-99%) cir- culating lead is found in RBCs complexed with hemoglobin (Hb); the remainder is bound to albumin and gamma-globulin. Because lead binding to Hb is capac- ity-limited, the plasma lead fraction increases as blood lead increases. In career lead employees with blood lead concentrations of 55-60 µg/dL, circulating lead concentrations declined to 40-50 µg/dL within 4-6 weeks of work cessation, but further reductions over the next 18 months were imperceptible (O’Flaherty 1986). The second compartment—represented by bile, hair, nails, saliva, sweat, digestive secretions, and soft tissues—has a similar elimination half-time. Soft- tissue lead exists primarily bound to cytosolic proteins, including metal- lothionein and high-affinity cytosolic binding proteins. The latter are thought to be associated with the formation of intranuclear inclusion bodies in the epithe- lium of the renal proximal tubule (Moore and Goyer 1974). A third (deep) human compartment—consisting of mineralized structures, including bone and teeth—contains the greatest fraction of the lead body bur- den. The lead elimination half-time from bone is 2-3 decades. Trabecular bone has a relatively rapid turnover and faster lead elimination than cortical bone. Lead in bone can contribute about 50% of current blood lead (Goyer 1996). Some 17% of blood lead in excess of 50 µg/dL found in macaques originated from bone lead that had accumulated over 11 years of lead exposure (O’Flaherty et al. 1998). Voluntary ingestion of lead at 0.3-3.0 mg/day (as lead acetate in drinking water) for 16-208 weeks by adults was followed by fecal elimination of over 90% of the administered dose (Kehoe 1987). Lead is excreted in urine, and uri- nary lead concentration has been used to gauge occupational lead exposure (bio- logical exposure index, 150 µg/g of creatinine) (ACGIH 1994), but the rate of urinary lead elimination is not proportional to blood lead concentration.

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222 Exposure Guidance Levels for Selected Submarine Contaminants Using a physiologically based pharmacokinetic lead model applied to a 20-year-old man employed 40 h/week with occupational lead exposure for 10 years and accounting for dietary and drinking-water lead exposure, O’Flaherty (1993) found that blood lead tripled over that period. For a 45-year-old man having blood lead of 55-60 μg/dL after 25 years of employment and exposure to lead at 84 μg/m3 in workplace air, only 4% of total skeletal lead had been elimi- nated 18 months after removal from work, and 26% of bone lead was removed after 10 years (O’Flaherty 1993). MAXIMAL INORGANIC SURFACE LEAD CONCENTRATIONS FROM OTHER ORGANIZATIONS A number of organizations have promulgated or otherwise established maximal surface lead concentrations (Table 10-3). COMMITTEE RECOMMENDATIONS The civilian occupational regulations cited in Table 10-3 reflect common work practices associated with the lead industry. They include physically sepa- rate eating areas, clothing-changing areas to prevent cross-contamination, sepa- rate shower facilities, vacuuming, downdraft booths, specific cleaning methods, and enforceable limits on eating, drinking, tobacco-smoking and tobacco- chewing, and other hand-to-mouth behaviors. The civilian workplace practices are not practical for submariners that reside, work, eat, and sleep in an enclosed and isolated environment. TABLE 10-3 Selected Maximal Surface Lead Concentrations Organization Type of Level/Activity Maximum Concentration Reference State of Welding, cutting, 0.06% dry weight 8 CCR 1532.1 California scraping, sanding, surface coating DOL Surfaces All surfaces shall be 1910.1025(h)(1) maintained as free as practicable of accumulations of lead 40 μg/ft2 HUD-EPA Residential floors 24 CFR 35.1350 NSF Residential food-zone 0.06% lead NSF/ANSI 51-2002 materials Abbreviations: ANSI, American National Standards Institute; DOL, Department of La- bor; EPA, Environmental Protection Agency; HUD, Department of Housing and Urban Development; NSF, National Sanitation Foundation

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Surface Lead 223 Sufficient information concerning the likely human exposures arising from surface lead contamination onboard a submarine was not provided to the committee. An increase in blood lead concentration due to ingestion of a con- taminated material, such as dusts found on surfaces, depends on the rate at which the contaminant is ingested (µg/g per day), the concentration of lead in the contaminant (µg/g), and a coefficient relating lead ingestion from a con- taminant to blood lead concentration (µg/dL per µg/day) (Stern 1996). Addi- tional consideration of inhalation exposure may also be required if the source of the lead on the contaminated surface is airborne. Thus, data needed to derive a surface lead concentration include characterization of crew exposure, exposure routes, sources of concern, physical and chemical forms, particle size, and bioavailability of the lead onboard the submarine. Lacking such data, the com- mittee could not develop useful surface lead exposure concentrations. The committee endorses monitoring of submariner blood lead concentrations to de- termine whether surface lead contamination onboard submarines is resulting in appreciable crew exposure. Occupational-lead risk characterizations are based predominantly on monitoring of blood lead concentrations in workers. The identification of a blood lead value that will protect submariners during their military careers is a prerequisite of any recommendation concerning lead limits for surface or air- borne lead-containing paint, dust, or other materials. It is important to determine whether submariner urinary lead, zinc protoporphyrin, or blood lead values are higher than background concentrations for U.S. adults (Pirkle et al. 1994). Blood lead screening values and promulgated blood-lead worker-removal regu- lations are available from a number of sources (ACGIH 2003; CDC 1991; Title 8 California Code of Regulations Section 1532.1). Wipe sampling and other techniques to assess surface contamination on work surfaces can provide useful information about worksite lead hazards. A few surface-contamination concentration guidelines have been published, but typical concentration limits must be established for a specific task (OSHA 1999). DATA ADEQUACY AND RESEARCH NEEDS No data were available to the committee on the physical nature, chemical identity, routes of exposure, or bioavailability of the surface lead materials of concern. To carry out submarine-specific lead health-risk analyses, data con- cerning generation, location, dispersion, and extent of onboard lead contamina- tion, including the lead concentration in submarine drinking water, must be available. Available methods for site-specific human health risk assessment for lead-containing dust require rigorous estimates of the quantity of dust ingested daily. In the present circumstance, it appears unlikely that published estimates of lead house-dust exposure (Clark et al. 1995; Wang et al. 1995) could be applied with confidence to a submarine.

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224 Exposure Guidance Levels for Selected Submarine Contaminants No data concerning inhalation exposure to lead onboard a submarine were available. Submarine air is one source that could contribute to a submariner’s blood lead concentration (Snee 1981). It is well known that factors other than air lead influence blood lead concentration (Bishop and Hill 1983). No data concerning urinary lead or blood lead concentrations of subma- riners were available to the committee. Thus, it is not clear whether significant exposure of the crew to lead occurs. Individual blood lead concentration is gen- erally correlated with the duration of exposure and how much time has passed since termination of exposure (O’Flaherty et al. 1982). At the outset, however, it must be recognized that individual submariner blood lead concentrations reflect not only the combined occupational and residential lead exposures as a result of active duty but environmental lead exposures while the submariners are not en- gaged in submarine operations (O’Flaherty 1993). Lead-exposed people who have higher rates of hand-to-mouth behavior often have higher lead intake; in- dividual hand-to-mouth lead exposure patterns can result in higher blood lead concentrations in those people than in people who do not eat or smoke in the same lead-containing environment. It is important to establish whether submariner blood lead concentrations differ from those of civilian adults and active military personnel not engaged in submarine operations who live in the United States. One potential avenue that the committee highly recommends and that could assist in the definition of sub- marine-associated lead exposure is determination of crew urinary lead or blood lead concentrations before submarine deployment followed by identical meas- urements on completion of typical tours of duty. If individual submariners with increased blood lead concentrations are identified, identification of the lead sources during deployment or as a result of on-shore activity (such as pottery and hobbies) is necessary. REFERENCES ACGIH (American Conference of Governmental Industrial Hygienists). 1994. P. 59 in 1994-1995 Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. American Conference of Governmental Indus- trial Hygienists, Cincinnati, OH. ACGIH (American Conference of Governmental Industrial Hygienists). 2003. P. 91 in TLVs® and BEIs® Based on the Documentation of the Threshold Limit Values for Chemical Substances and Physical Agents & Biological Exposure Indices. American Conference of Governmental Industrial Hygienists, Cincinnati, OH. Alexander, B.H., H. Checkoway, C. van Netten, C.H. Muller, T.G. Ewers, J.D. Kaufman, B.A. Muller, T.I. Vaughan, and E.M. Faustman. 1996. Semen quality of men em- ployed at a lead smelter. Occup. Environ. Med. 53(6):411-416. Araki, S., H. Sato, K. Yokoyama, and K. Murata. 2000. Subclinical neurophysiological effects of lead: A review on peripheral, central, and autonomic nervous system ef- fects in lead workers. Am. J. Ind. Med. 37(2):193-204.

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