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Suggested Citation:"10 Surface Lead." National Research Council. 2008. Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants: Volume 2. Washington, DC: The National Academies Press. doi: 10.17226/12032.
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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 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

Suggested Citation:"10 Surface Lead." National Research Council. 2008. Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants: Volume 2. Washington, DC: The National Academies Press. doi: 10.17226/12032.
×

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

1,740°C

Melting point

327.4°C

Flash point

NA

Density

11.34 g/cm3 at 20°C

Vapor pressure

1.77 mm Hg at 1000°C

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). Historically, 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 occupations are associated with lead exposure, including those involved in lead smelting, 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 intoxication have been reviewed (EPA 1986; ATSDR 1999). Lead is a cumulative poison 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 gastrointestinal tract. Lead may dissolve to an appreciable degree in the acid environment of the stomach, greatly increasing its absorption. Absorption of lead from the gastrointestinal tract is facilitated by the same mucosal transport proteins that mediate calcium transport (Fullmer 1992). Smaller lead particles are more readily absorbed from the gastrointestinal tract. In the blood, about 95% of

Suggested Citation:"10 Surface Lead." National Research Council. 2008. Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants: Volume 2. Washington, DC: The National Academies Press. doi: 10.17226/12032.
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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 membrane 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 varies, depending on the tissue that absorbed the lead.

Lead perturbs multiple enzyme systems, especially ones that contain sulfhydryl groups or are zinc-dependent. Signs of lead toxicosis are generally associated 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 committee to focus strictly on the human clinical literature. One of the best characterized 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 hemebiosynthesis pathway. Inhibition of this enzyme results in decreased heme production 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 consciousness to convulsions and terminal coma within hours. Reduced sensory and motor 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).

Suggested Citation:"10 Surface Lead." National Research Council. 2008. Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants: Volume 2. Washington, DC: The National Academies Press. doi: 10.17226/12032.
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TABLE 10-2 Blood Lead Concentrations and Associated Observed Effects in Exposed Men

Blood Lead Concentration (µg/dL)

Observed Effect

Cardiovascular, Hematologic, Heme Synthesis

Nervous System

Renal System

Reproductive System

100-120

Encephalopathy

Chronic nephropathy

80

Frank anemia

60

50

Subencephalopathic signs

Altered testicular function

40

Increased urinary ALA and coproporphyrins

Peripheral neuropathy

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 pressure 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

Suggested Citation:"10 Surface Lead." National Research Council. 2008. Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants: Volume 2. Washington, DC: The National Academies Press. doi: 10.17226/12032.
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significantly higher than that of 52 workers without lead exposure (blood lead concentrations, under 20 µg/dL) (de Kort et al. 1987). Lead-exposed construction 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 association 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 evidence 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 second 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 between the last lead exposure and when blood lead concentrations were measured. 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 mitochondrial swelling, and deposition of eosinophilic dense-staining granular inclusion bodies (Pollock and Ibels 1986). Renal biopsy of 12 men with blood lead concentrations between 40 and over 80 µg/dL found characteristic focal interstitial nephritis (Wedeen et al. 1979).

Suggested Citation:"10 Surface Lead." National Research Council. 2008. Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants: Volume 2. Washington, DC: The National Academies Press. doi: 10.17226/12032.
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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; Rodamilans 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 greatest 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 concentrations 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 hormone (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 concentrations, and workers aged 40 years old or older had reduced testosterone concentrations. Among lead workers, circulating LH and FSH were increased.

Among 150 lead workers examined by Lancranjan et al. (1975), a reduction in sperm vitality (asthenospermia) was associated with blood lead concentrations 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 documented significant reductions in sperm count and increased numbers of abnormal 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).

Suggested Citation:"10 Surface Lead." National Research Council. 2008. Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants: Volume 2. Washington, DC: The National Academies Press. doi: 10.17226/12032.
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Carcinogenicity

The International Agency for Research on Cancer (IARC 1987) considered the results of bioassays of parenteral and oral lead (for example, lead acetate and lead phosphate) as sufficient evidence of carcinogenicity in animals. At least two groups have published the results of mortality analyses of U.S. workers 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 expected 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 cancers (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 carcinogenic 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 coverings, ammunition, solder, caulking, paint, and dust depends in large part on particle size.

Percutaneous uptake of lead acetate through intact skin of human volunteers was negligible (0-0.3%) (Moore et al. 1980).

Deposition of inhaled lead also depends on particle size. Particles deposited 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 inhaled 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 predominate under alkaline conditions (for example, lead carbonate) are more soluble in gastric contents and are more readily absorbed from the stomach than less soluble forms (for example, lead sulfate). Uptake from the gastrointestinal tract occurs primarily in the duodenum (Mushak 1993). Absorption of soluble lead (consumed as either the nitrate or the acetate) was increased in fasting adults

Suggested Citation:"10 Surface Lead." National Research Council. 2008. Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants: Volume 2. Washington, DC: The National Academies Press. doi: 10.17226/12032.
×

compared with the amount that was absorbed when the same dose was consumed 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 Chamberlain 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 gastrointestinal 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%) circulating lead is found in RBCs complexed with hemoglobin (Hb); the remainder is bound to albumin and gamma-globulin. Because lead binding to Hb is capacity-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 metallothionein and high-affinity cytosolic binding proteins. The latter are thought to be associated with the formation of intranuclear inclusion bodies in the epithelium 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 burden. 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 urinary lead concentration has been used to gauge occupational lead exposure (biological exposure index, 150 µg/g of creatinine) (ACGIH 1994), but the rate of urinary lead elimination is not proportional to blood lead concentration.

Suggested Citation:"10 Surface Lead." National Research Council. 2008. Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants: Volume 2. Washington, DC: The National Academies Press. doi: 10.17226/12032.
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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 eliminated 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 separate eating areas, clothing-changing areas to prevent cross-contamination, separate 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 California

Welding, cutting, scraping, sanding, surface coating

0.06% dry weight

8 CCR 1532.1

DOL

Surfaces

All surfaces shall be maintained as free as practicable of accumulations of lead

1910.1025(h)(1)

HUD-EPA

Residential floors

40 µg/ft2

24 CFR 35.1350

NSF

Residential food-zone materials

0.06% lead

NSF/ANSI 51-2002

Abbreviations: ANSI, American National Standards Institute; DOL, Department of Labor; EPA, Environmental Protection Agency; HUD, Department of Housing and Urban Development; NSF, National Sanitation Foundation

Suggested Citation:"10 Surface Lead." National Research Council. 2008. Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants: Volume 2. Washington, DC: The National Academies Press. doi: 10.17226/12032.
×

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 contaminated 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 contaminant to blood lead concentration (µg/dL per µg/day) (Stern 1996). Additional 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 committee could not develop useful surface lead exposure concentrations. The committee endorses monitoring of submariner blood lead concentrations to determine 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 airborne 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 regulations 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 concerning generation, location, dispersion, and extent of onboard lead contamination, 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.

Suggested Citation:"10 Surface Lead." National Research Council. 2008. Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants: Volume 2. Washington, DC: The National Academies Press. doi: 10.17226/12032.
×

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 submariners were available to the committee. Thus, it is not clear whether significant exposure of the crew to lead occurs. Individual blood lead concentration is generally 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 engaged in submarine operations (O’Flaherty 1993). Lead-exposed people who have higher rates of hand-to-mouth behavior often have higher lead intake; individual 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 submarine-associated lead exposure is determination of crew urinary lead or blood lead concentrations before submarine deployment followed by identical measurements 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.

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Suggested Citation:"10 Surface Lead." National Research Council. 2008. Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants: Volume 2. Washington, DC: The National Academies Press. doi: 10.17226/12032.
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Suggested Citation:"10 Surface Lead." National Research Council. 2008. Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants: Volume 2. Washington, DC: The National Academies Press. doi: 10.17226/12032.
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