Occupational lead poisoning

Occupational lead poisoning – includes patients handouts on lead and health

Kevin C. Stauding

Occupational lead poisoning has been a recognized health hazard for more than 2,000 years. Characteristic features of lead toxicity, including anemia, colic, neuropathy, nephropathy, sterility and coma, were noted by Hippocrates and Nikander in ancient times, as well as Ramazzini and Hamilton in the modern era.[1] Physicians have gained an extensive understanding of the causes, the clinical presentations and the means of preventing lead poisoning. However, it remains one of the most important occupational and environmental health problems.[2]

Lead serves no useful biologic function in the human body. Over the past several years, concern has increased over the health effects of low-level lead exposure and the “normal” body burden of lead. In the occupational setting, the present “no-effect” level for lead exposure is currently being reevaluated as more sensitive measures of the physiologic effects of lead are made available through clinical investigations.[3] Based on current knowledge of the health effects of lead in adults, the U.S. Public Health Service has declared a health objective for the year 2000: the elimination of all exposures that result in blood lead concentrations greater than 25 [micro]g per dL (1.20 [micro]mol per L) in workers.[4]

Occupational Exposure and the OSHA Lead Standard

Lead and lead compounds play a significant role in modern industry, with lead being the most widely used nonferrous metal.[5] A wide variety of industrial populations is at risk of occupational exposure to lead (Table 1). According to estimates made by the National Institute of Occupational Safety and Health (NIOSH), more than 3 million workers in the United States are potentially exposed to lead in the workplace. Occupational exposure to lead in general industry is regulated by the 1978 Occupational Safety and Health Administration (OSHA) Lead Standard. The general industry standard specifies permissible limits on airborne lead exposure, as well as blood lead levels (Table 2). A construction standard, recently extended to cover workers in the construction industry, has slight differences in detail. However, enforcement of both standards is inadequate, and significant occupational exposure remains widespread.[6]

TABLE 1 Major Occupations and Industries Associated with Lead Overexposure

Battery manufacturing Pigment manufacturing

Chemical industry Pipe fitters

Construction workers Plastics industry

Demolition workers Pottery workers

Firing-range instructors Printers

Foundry workers Radiator repair

Gas-station attendants Rubber industry

Gasoline additives Soldering of lead

production products

Jewelers Solid waste production

Lead miners Stained-glass makers

Lead smelters and Welders



OSHA Lead Standards for Air and Blood

Focus Level Comments

Air 50 [micro]g per ml Permissible exposure limit

(PEL): the employer shall

assure that no employee is

exposed to lead at

concentrations > 50 [micro]g

per ml of air averaged over

an 8-hour period.

Air 30 [micro]g per [m.sup.3] Action level: initiate medical

surveillance for all employees

exposed to levels above 30

[micro]g per [m.sup.3] for more

than 30 days per year

(regardless of respiratory


Blood [is greater than or Medical removal from exposure

equal to] 60

[micro]g per dL

(2.90 [micro]mol

per L) or average

of last three levels

is [is greater than

or equal to] 50 [micro]g

per dL (2.40 [micro]mol

per L)

The mere presence of lead in the workplace does not necessarily signify a potential risk of poisoning. Lead is considered a hazard in the workplace primarily depending on the, generation of respirable (below 5 [micro]m) lead fumes or lead-containing dust particles in the workroom atmosphere. Consequently, no simple rule of thumb exists for categorizing different occupations into “more” or “less” hazardous classifications, although experience has shown that some types of work are indeed more dangerous than others (Table 1). Determining the magnitude of risk in a particular work process should always include a review of the process itself (does potential exposure involve dust, fumes or aerosolized particles?), the adequacy of abatement employed (local and general ventilation) and the general hygienic level of the workplace itself.[2]



Lead is absorbed primarily through the respiratory and gastrointestinal systems, with the former being the more important route of entry in occupational exposures. Cutaneous absorption of inorganic lead is negligible. However, organic lead compounds, because of their lipid solubility, are readily absorbed through intact skin.[5]

Respiratory lead absorption is primarily dependent on particle size; solubility, respiratory volume and physiologic interindividual variation are less important factors. The percentage of inhaled lead reaching the bloodstream is estimated to be 30 to 40 percent.[2]

Gastrointestinal absorption of lead is lower in adults than in children, with an estimated 10 to 15 percent of lead in an adult’s diet absorbed gastrointestinally. The degree of lead absorption is increased considerably with fasting or in persons whose diet is deficient in calcium, iron, phosphorus or zinc.[5]


After lead is absorbed into the bloodstream, through either ingestion or inhalation, most of it is carried, bound, to erythrocytes. The freely diffusible plasma fraction is distributed extensively throughout tissues, reaching highest concentrations in bone, teeth, liver, lungs, kidneys, brain and spleen.[2] Lead in blood has an estimated half-life of 35 days, in soft tissue 40 days and in bone 20 to 30 years.[7] Inorganic lead does not undergo any metabolic transformation or digestion in the intestines, or detoxification in the liver.[5]

With chronic exposure over a long period of time, most absorbed lead ends up in bone. Lead, it appears, is substituted for calcium in the bone matrix. This is not known to cause any deleterious effect on bone itself Bone storage likely acts as a “sink,” protecting other organs while allowing chronic accumulation. The lead that accumulates in the bone ultimately provides a source for remobilization and continued toxicity after exposure ceases.[8] The total bodily content of lead is called the body burden; in a steady state, about 90 percent of the body burden is bound to bone.[2]


Although lead is excreted by several routes (including sweat and nails), only the renal and gastrointestinal pathways are of practical importance. In general, lead is excreted quite slowly from the body (with the biologic half-life estimated at 10 years). Since excretion is slow, accumulation in the body occurs easily.[2]

Clinical Effects In Adults

Acute Inorganic Lead Toxicity

Excessive occupational exposure to lead over a brief period of time can cause a syndrome of acute lead poisoning. Classic clinical findings in this syndrome include abdominal colic, constipation, fatigue and central nervous system dysfunction. With even greater doses, acute encephalopathy with coma and convulsions may occur. In milder exposures, headaches and personality changes may be the only signs of neurologic toxicity[6] (Table 5).[9]


General Signs and Symptoms of Lead Toxicity

Mild Moderate Severe

Myalgias Headache Encephalopathy

Irritability Tremor Motor neuropathy

Paresthesias Vomiting Seizures

Mild fatigue General fatigue Coma

Intermittent Diffuse abdominal pain Abdominal colic

abdominal pain Weight loss Lead lines

Lethargy Loss of libido Oliguria


[1.] Landrigan PJ, Silbergeld EK, Froines JR, Pfeffer RM. Lead in the modern workplace [Editorial]. Am i Public Health 1990;80:907-8.

[2.] Saryan LA, Zenz C. Lead and its compounds. In: Zenz C, Dickerson OB, Horvath EP Jr, eds. Occupational medicine. 3d ed. St. Louis: Mosby, 1994:506-41.

[3.] Lewis R. Metals. In: LaDou J, ed. Occupational medicine. Norwalk, Conn.: Appleton & Lange, 1990:306-10.

[4.] Kaufman JD, Burt J, Silverstein B. Occupational lead poisoning: can it be eliminated? Am J Industrial Med 1994;26:703-12.

[5.] Fischlbein A. Occupational and environmental lead exposure. In: Rom WN. Environmental and occupational medicine. 2d ed. Boston: Little, Brown, 1992:735-58.

[6.] Landrigan PJ. Lead. In: Rosenstock L, Cullen MR, eds. Textbook of clinical occupational and environmental medicine. Philadelphia: Saunders, 1994:745-54.

[7.] Grimsley EW, Adams-Mount L. Occupational lead intoxication: report of four cases. South Med J 1994;87:689-91.

[8.] Keogh JR Lead. In: Sullivan JB Jr, Krieger GR, eds. Hazardous materials toxicology: clinical principles of environmental health. Baltimore: Williams & Wilkins, 1992:834-44.

[9.] Case studies in environmental medicine: lead toxicity. Atlanta: Agency for Toxic Substances and Disease Registry, 1992.

[10.] Wedeen RP, Ty A, Udasin I, Favata EA, Jones KW. Clinical application of in vivo tibial K-XRF for monitoring lead stores. Arch Environ Health 1995;50(5):355-61.

[11.] Occupational exposure to lead: final standard. U.S. Department of Labor, Occupational Safety and Health Administration. Federal Regist 1978; no. 29 CFR 1910.1025.

[12.] Royce S, Rosenberg J. Chelation therapy in workers with lead exposure. West J Med 1993; 158:372-5.

[13.] Porru S, Alessio L. The use of chelating agents in occupational lead poisoning. Occup Med 1996;46:41-8.

[14.] Meggs WJ, Gerr F, Aly MH, Kierena T, Roberts DL, Shih R, et al. The treatment of lead poisoning from gunshot wounds with succimer (DMSA). J Toxicol Clin Toxicol 1994;32(4):377-85.

KEVIN C. STAUDINGER, M.D., M.P.H., is medical director of the Division of Occupational Medicine at Baptist Health Centers, Inc., Birmingham, Ala. He graduated from Tufts University School of Medicine, Boston, and earned a master of public health degree from the University of Alabama at Birmingham School of Public Health. Dr. Staudinger completed a residency in occupational and environmental medicine at the University of Alabama School of Medicine, Birmingham.

VICTOR S. ROTH, M.D., M.P.H., is an assistant professor in the Division of Occupational and Environmental Medicine in the Department of Family and Community Medicine at the University of Alabama School of Medicine. He graduated from the University of Cincinnati (Ohio) College of Medicine and earned a master of public health degree from the University of Michigan School of Public Health, Ann Arbor. Dr. Roth completed a residency in family medicine at the University of Maryland Hospital, Baltimore, and a residency in occupational medicine at the University of Michigan, Ann Arbor.

Address correspondence to Kevin C Staudinger M.D., M.P.H., Baptist Health Centers, Inc., OMC Princeton, 701 Princeton Ave., Birmingham, AL 36211. Reprints are not available from the authors.

COPYRIGHT 1998 American Academy of Family Physicians

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