Protecting Workers Exposed to Lead-based Paint Hazards
A Report to Congress
 

DHHS (NIOSH) PUBLICATION NO. 98-112
JANUARY 1997

Chapter 1
Health Effects of Lead Exposure and Occupational Exposure Criteria

Introduction
Neurotoxic Effects
Hematologic and Renal Effects
Reproductive and Developmental Effects
Cardiovascular Effects
Carcinogenic Effects
Occupational Exposure Criteria
Conclusions
References

The health effects of lead have been previously extensively reviewed by the federal public health agencies: Agency for Toxic Substances and Disease Registry (ATSDR), Centers for Disease Control and Prevention (CDC), National Institute for Occupational Safety and Health (NIOSH)^1,2,3. There are thousands of scientific articles on the adverse health effects of lead in either children or adults. This chapter is a synopsis of the cardinal adverse health effects of lead in adults.

Lead is a bluish-gray metal used since ancient times because of its useful properties, such as low melting point, pliability, and resistance to corrosion. The ancient Romans and Greeks first discovered its toxic effects. Hippocrates (370 B.C.) attributed a severe case of colic in a worker who extracted metals to lead exposure, and Pliny the Elder (A.D. 23–79) wrote that workers painting ships with native ceruse (white lead) wore loose bags over their faces to avoid breathing noxious dust⁴. Lead is ubiquitous in older American homes and lead exposures in the workplace are common because of the widespread use, during the past century, of lead compounds in paints, gasoline, and industry.

Human lead exposure occurs when dust and fumes are inhaled and when lead is ingested via lead-contaminated hands, food, water, cigarettes, and clothing. Lead entering the respiratory and digestive systems is released to the blood and distributed throughout the body. More than 90 percent of total body burden of lead is accumulated in the bones, where it is stored for decades. Lead in bones may be released into the blood and re-exposes organ systems long after the original environmental exposure. This process can also expose the fetus to lead in pregnant women.

There are several biological indices of lead exposure. Lead concentrations in blood, urine, teeth, and hair can be used as biological indicators of lead exposure. Recent advances in the measurement of skeletal bone lead levels more accurately measure cumulative lead exposure and the total body burden of lead. At present, however, the best available method for monitoring biological exposure to lead is measurement of the blood lead level (BLL). The severity of symptoms associated with lead exposure generally increases as the BLL increases (see Table 1.1). No such relationship between symptoms and the other indices of lead exposure have been as well established.

A recent national survey found that the geometric mean BLL for the United States adult population (ages 20 to 74 yrs) declined significantly between 1976 and 1991, from 13.1 to 3.0 micrograms per deciliter (µg/dL)⁵. This decline was largely the result of stricter federal regulations and changes in regulated industries which reduced workplace exposures and the lead content of gasoline, paint, drinking water, and soldered food containers. To protect workers from lead poisoning, the Occupational Safety and Health Administration (OSHA) promulgated a lead standard for general industry in 1978 and an interim lead standard for the construction industry in 1993. More than 90 percent of adults now have a BLL <10 µg/dL, and more than 98 percent have a BLL < 15 µg/dL.

Although much progress has been made in reducing lead exposures, exposures in the workplace continue to be a significant public health problem. Even with the federal regulations, thousands of adult elevated BLLs 25 µg/dL are reported each year to NIOSH by states participating in a NIOSH surveillance program (see Chapter 2 for a more complete discussion). Elimination of worker BLLs greater than or equal to 25 µg/dL by the year 2000 is a health goal of the United States⁶.

The toxic nature of lead is well documented. The most important aspects of lead toxicity are its effects on the central nervous system, which may be irreversible; however, lead affects all organs and functions of the body to varying degrees. The frequency and severity of symptoms among exposed workers depend upon the level of exposure. A summary of the lowest-observed-effect levels for key lead-induced health effects in adults is presented in Table 1.1.

The remainder of this chapter summarizes the NIOSH evaluation of the scientific literature regarding health effects of high- and low-level lead exposures and occupational exposure limits. In preparing this section, NIOSH consulted with the National Institute of Environmental Health Sciences.

Table 1.1
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NEUROTOXIC EFFECTS

One of the major targets of lead toxicity in adults is the nervous system, including the central and peripheral nervous systems. Lead damages the blood-brain barrier and, subsequently, brain tissues. Severe exposures resulting in BLLs > 80 µg/dL may cause coma, encephalopathy, or death. Historically, the most severe damage to the peripheral nervous system from high, chronic, workplace exposures to lead (two or more times higher than the current OSHA Permissible Exposure Limits [PEL] of 50 µg/m³) resulted in local paralysis described as "wrist drop" or "foot drop." Because of the improved control of occupational lead exposures in recent decades, such overt symptoms of lead toxicity are rare today in the United States. Occupational lead exposures allowable under the current OSHA lead standards will not produce these obvious neurologic clinical symptoms; however, lead exposures permissible under the OSHA standards may be harmful to the central nervous system. Workers with BLLs of 40 to 50 µg/dL may experience fatigue, irritability, insomnia, headaches, and subtle evidence of mental and intellectual decline^8,9. BLLs as low as 30 to 40 µg/dL decrease motor nerve conduction velocity in workers, although these lead exposure levels are not associated with clinical symptoms¹⁰. These subclinical symptoms represent early stages of neurologic damage to the central and peripheral nervous system.

HEMATOLOGIC AND RENAL EFFECTS

Anemia is one of the most characteristic symptoms of high and prolonged exposures to lead associated with BLLs > 80 µg/dL. This anemia results from the damaging effects of lead on the formation and functioning of red blood cells. Lead inhibits the synthesis of heme (the nonprotein, iron-containing component of hemoglobin) and damages the ion transport system in red blood cell membranes. Measurement of protoporphyrin (free or zinc protoporphyrin [ZPP]) concentration in red blood cells can be a good indicator of inhibition of heme synthesis by lead. There are, however, other causes (e.g., iron deficiency) of elevated protoporphyrin levels. Effects on heme synthesis can be observed at BLLs below 15 µg/dL, but the clinical significance of these effects at low BLLs is undetermined11. As part of the medical evaluation for lead-exposed workers, OSHA requires measurement of blood lead and ZPP levels, hemoglobin and hematocrit determinations, red cell indices, and examination of the peripheral blood smears to evaluate red blood cell morphology.

Chronic high exposure to lead, above the OSHA PEL, may cause chronic nephropathy and, in extreme cases, kidney failure. There is substantially less evidence of kidney disease at lower exposures to lead¹².

REPRODUCTIVE AND DEVELOPMENTAL EFFECTS

Historical studies indicate that high exposures to lead produce stillbirths and miscarriages¹³. Several studies conducted in the United States and abroad indicated that exposures to lower concentrations of lead, with BLLs at or below 15 µg/dL may result in adverse pregnancy outcomes, such as shortened time of gestation and decreased fetal mental development and growth^14,15.

The developing nervous system of the fetus is particularly vulnerable to lead toxicity. Neurological toxicity is observed in children of exposed female workers as a result of the ability of lead to cross the placental barrier and to cause neurological impairment in the fetus¹⁶. A special concern for pregnant women is that some of the bone lead accumulation is released into the blood during pregnancy. Several studies conducted concurrently in the United States and other countries provided evidence that even low maternal exposures to lead, resulting in BLLs as low as 10 µg/dL, produce intellectual and behavioral deficits in children^{17, 18,19}.

BLLs of 60 µg/dL may be associated with male infertility²⁰. Studies in male workers indicate that exposures to lead resulting in BLLs as low as 40 µg/dL may cause decreased sperm count and abnormal sperm morphology^21,22. Several reports indicate that decreased sperm quality and hormonal changes can occur among male workers exposed to lead with BLLs of 30 to 40 µg/dL^23,24.

In promulgating its general industry lead standard in 1978, OSHA recognized that children of lead-exposed workers are more likely to have birth defects, mental retardation, behavioral disorders or to die during the first year, and that these effects could occur at parental BLLs below the 50 µg/dL BLL allowed under the standard²⁵. At that time, OSHA determined it was not feasible to establish a lead standard that would protect workers from all physiologic changes, symptoms, and reproductive effects in men and women. As a result, OSHA said that men or women planning to have children should be advised to limit their BLLs less than or equal to 30 µg/dL. Subsequently, at least several large corporations developed "fetal protection" policies that excluded all fertile women from lead-exposed jobs, which were often high-paying. In March 1991, the U.S. Supreme Court (UAW, et al. v. Johnson Controls, Inc.) banned employers from barring women from hazardous jobs, finding that fetal protection policies constitute illegal sex discrimination in violation of the Civil Rights Act.

CARDIOVASCULAR EFFECTS

Chronic high exposures to lead that existed earlier in this century were associated with an increased incidence of hypertension and cardiovascular disease²⁶. Today these severe effects of lead exposure are rarely observed in the United States²⁷. Several studies reported modest increases in blood pressure among workers exposed to concentrations of lead allowable under the OSHA lead standards.^28,29 Studies conducted in the general population, where lead exposures are much lower, have also indicated that increased BLLs are associated with small increases in blood pressure. This relationship appears to extend to BLLs below 10 µg/dL^30,31,32,33. A recent study suggests that long-term lead exposure, as measured by the bone lead level, is an independent predictor of development of hypertension in men in the general population³⁴.

CARCINOGENIC EFFECTS

Lead has been shown to be an animal carcinogen. Animal studies clearly indicate that some lead compounds ingested or administered by subcutaneous or intraperitoneal injection, in quantities approaching the maximally tolerated dose, cause cancers in rodents.^35,36

Several studies have examined the relationship between workers' lead exposure and the occurrence of cancer among these workers^37,38,39. Results from two recent studies indicate that lead may increase the risk of cancer among workers exposed to high levels of lead.^40,41

The International Agency for Research on Cancer (IARC) has designated lead and inorganic lead compounds as possibly carcinogenic to humans (Group 2B), based on evidence for carcinogenicity in animals⁴². The American Conference of Governmental Industrial Hygienists (ACGIH) has designated lead as an animal carcinogen, indicating that lead has been shown to be carcinogenic in animals⁴³.

OCCUPATIONAL EXPOSURE CRITERIA

Under the OSHA general industry lead standard (29 CFR 1910.1025), the PEL for personal exposure to airborne inorganic lead is 50 micrograms per cubic meter (µg/m³) as an 8-hour time-weighted average (TWA). Maintaining the concentration of airborne particles of lead in the work environment below the PEL represents a preventive measure intended to protect workers from excessive exposure, which OSHA defines as a BLL > 40 µg/dL. The OSHA general industry lead standard requires lowering the PEL for shifts longer than 8 hours, medical monitoring for employees exposed to airborne lead at or above the action level of 30 µg/m³, medical removal of employees whose average BLL is 50 µg/dL or greater, and pay retention for medically removed workers. Medically removed workers cannot return to jobs involving lead exposure until their BLL is below 40 µg/dL.

In the 1978 general industry standard, OSHA advised that men or women planning to have children should limit their exposure to maintain a BLL less than 30 µg/dL. At that time, OSHA said that feasibility constraints prevented it from establishing a lead standard that would prevent all physiologic changes, reproductive effects, and mild signs and symptoms in exposed workers⁴⁴. As required by Title X of the Residential Lead-Based Paint Hazard Reduction Act, in 1993 OSHA provided an equivalent level of protection to construction workers in an interim final rule for lead in the construction industry (29 CFR 1926.62). OSHA did not reexamine the feasibility of reducing the 1978 exposure limits for lead in this interim rule.

ACGIH has recommended that worker lead exposures be kept below 50 µg/m³ (as an 8-hour TWA), with worker BLLs to be kept less than or equal to 30 µg/dL. To protect lead-exposed workers, a World Health Organization study group recommended a biological exposure limit of 40 µg/dL in 1980, and further recommended that BLLs in women of reproductive ages should not exceed 30 µg/dL⁴⁵. In 1991, the U.S. Department of Health and Human Services established a national goal to eliminate, by the year 2000, all occupational lead exposures that result in BLLs greater than 25 µg/dL⁴⁶.

CONCLUSIONS

Research studies on lead toxicity in humans indicate that current OSHA standards should prevent the most severe symptoms of lead poisoning, but these standards do not protect workers and their developing children from all of the adverse effects of lead. In recognition of this problem, voluntary standards and public health goals have established lower exposure limits for workers exposed to lead, which offer increased protection for workers and their children.

REFERENCES

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2. CDC [1991]. Preventing lead poisoning in young children. Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control.

3. NIOSH [1978]. Criteria for a recommended standard: Occupational exposure to inorganic lead, revised criteria—1978. Cincinnati, OH: U.S. Department of Health, Education, and Welfare, Public Health Service, Center for Disease Control, National Institute for Occupational Safety and Health, DHEW (NIOSH) Publication No. 78–158.

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6. CDC [1994]. Adult blood lead epidemiology and surveillance—United States, fourth quarter 1994. Centers for Disease Control and Prevention. MMWR 44(14):286–287.

7. Feldman RG, Hayes MK, Younes R, Aldrich FD [1977]. Lead neuropathy in adults and children. Arch Neurol 34:481–488.

8. Mantere P, Hanninen H, Hernberg S, Luukkonen R [1984]. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Scand J Work Environ Health 10:43–50.

9. Hogstedt C, Hane M, Agrell A, Bodin L [1983]. Neuropsychological test results and symptoms among workers with well-defined long-term exposure to lead. Br J Ind Med 40:99–105.

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12. Goyer RA [1989]. Mechanisms of lead and cadmium nephrotoxicity. Toxicology Letters 46:153–162.

13. Rom W [1976]. Effects of lead on the female and reproduction: a review. Mt. Sinai J Med 43:542–552.

14. Andrews KW, Savitz DA, Hertz-Picciotto I [1994]. Prenatal lead exposure in relation to gestational age and birth weight: A review of epidemiologic studies. Am J Ind Med 26:13–32.

15. Schwartz J [1994]. Low-level lead exposure and children's IQ: a meta analysis and search for a threshold. Environ Res 65:42–55.

16. Zi-quiang C, Qi-ing C, Chin-chin P. Jia-yian Q [1985]. Peripheral nerve conduction velocity in workers occupationally exposed to lead. Scand J Work Environ Health 11(4):26–28.

17. Goyer RA [1990]. Transplacental transport of lead. Environ Health Perspect 89:101–105.

18. Mushak P., Davis JM, Crocetti AF, Grant LD [1989]. Prenatal and postnatal effects of low-level lead exposure: integrated summary of a report to the U.S. Congress on childhood lead poisoning. Environ Res 50:11–36.

19. Moore MR [1980]. Prenatal exposure to lead and mental retardation. In: H.L. Needleman, Ed. Low Level Lead Exposure: The Clinical Implications of Current Research. New York, NY: Raven Press, pp. 53–65.

20. Fisher-Fischbein J, Fischbein A, Melnick HD, Bardin W [1987]. Correlation between biochemical indicators of lead exposure and semen quality in a lead-poisoned firearms instructor. JAMA 257(6):803–805.

21. Lancranjan I, Popescu HI, Gavanescu O, Klepsch I, Serbanescu M [1975]. Reproductive ability of workmen occupationally exposed to lead. Arch Environ Health 30:396–401.

22. Alexander BH, Checkoway H, van Netten C, Muller CH, Ewers TG, Kaufman JD, Mueller BA, Vaughan TL, Faustman EM [1996]. Semen quality of men employed at a lead smelter. Occup Environ Med 53:411–416.

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24. Ng TP, Goh HH, Ng YL, Ong HY, Ong CN, Chia KS, Chia SE, Jeyaratnam J [1991]. Male endocrine functions in workers with moderate exposure to lead. Br J Ind Med 48:485–491.

25. OSHA [1978]. 43 Fed. Reg. No. 220. Occupational Safety and Health Administration: Final standard for occupational exposure to lead, supplementary information, health effects, pp. 52952–53014.

26. Dingwall–Fordyce I, Lane RE [1963]. A follow-up study of lead workers. Br J Ind Med 20:313–315.

27. Schwartz J [1991]. Lead, blood pressure, and cardiovascular disease in men and women. Environ Health Perspect 91:71–75.

28. Sharp DS, Osteloh J, Becker CE, Bernard B, Smith AH, Fisher JM, Syme SL, Holman BL, Johnston T [1988]. Blood pressure and blood lead concentration in bus drivers. Environ Health Perspect 78:131–137.

29. Weiss ST, Munoz A, Stein A, Sparrow D, Speizer FE [1988]. The relationship of blood lead to systolic blood pressure in a longitudinal study of policemen. Environ Health Perspect 78:53–56.

30. Pocock SJ, Shaper AG, Ashby D, Delves HT, Clayton BE [1988]. The relationship between blood lead, blood pressure, stroke, and heart attacks in middle-aged British men. Environ Hlth Perspect 78:23–30.

31. Pirkle JL, Schwartz J, Landis JR, Harlan WR [1985]. The relationship between blood lead levels and blood pressure and its cardiovascular risk implications. Am J Epidemiol 121(2):246–258.

32. Hertz-Picciotto I, Croft J [1993]. Review of the relation between blood lead and blood pressure. Epidemiologic Reviews 15(2):352.

33. Schwartz J [1995]. Lead, blood pressure and cardiovascular disease in men. Environ Hlth 50.

34. Hu H, Aro A, Payton M, Korrick S, Sparrow D, Weiss ST, and Rotnitzky A [1996]. The relationship of bone and blood lead to hypertension—the normative aging study. JAMA 275(15): 1171–1176.

35. Azar A, Trochimowicz HJ, Maxfield ME [1973]. Review of lead studies in animals carried out at Haskell laboratory—2-year feeding study and response to hemorrhage study. Proceedings of the International Symposium Environmental Health Aspects of Lead. Amsterdam, Netherlands: Commission of the European Communities and U.S. Environmental Protection Agency, pp. 199–210.

36. Zawirska B, Medras K [1968]. Tumoren und störungen des porphyrinstoffwechsels bei ratten mit chronischer experimenteller bleiintoxikation (in German). Zbl Allg Path Bd 111:1–11.

37. Lilis R [1981]. Long-term occupational lead exposure, chronic nephropathy, and renal cancer: a case report. Am J Ind Med 2:293–297.

38. Cantor KP, Sontag JM, Heid MF [1986]. Patterns of mortality among plumbers and pipefitters. Am J Ind Med 10:73–89.

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40. Anttila A, Heikkilä P, Nykyri E, Kauppinen T, Hernberg S, Hemminki K [1995]. Excess lung cancer among workers exposed to lead. Scan J Work Environ Health 21:460–469.

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42. IARC [1987]. IARC monographs on the evaluation of carcinogenic risks to humans. Overall evaluations of carcinogenicity: an updating of IARC monographs volumes 1 to 42. United Kingdom: World Health Organization, International Agency for Research on Cancer. Supplement 7, pp.230–232.

43. ACGIH [1995]. 1995–1996 Threshold limit values for chemical substances and physical agents and biological exposure indices. Cincinnati, OH: American Conference of Governmental Industrial Hygienists.

44. OSHA [1978]. 43 Fed. Reg. No. 220. Occupational Safety and Health Administration: Final standard for occupational exposure to lead, supplementary information, health effects, pp. 52954–52955.

45. WHO [1980]. Recommended health-based limits in occupational exposure to heavy metals. Report of a WHO Study Group. Geneva: World Health Organization. Technical Report Series No. 647.

46. DHHS [1990]. Healthy People 2000: national health promotion and disease objectives. Washington, DC: U.S. Department of Health and Human Services, Public Health Service, DHHS Publication No. (PHS) 91–50212.

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