Occupational Lead Poisoning

KEVIN C. STAUDINGER, M.D., M.P.H., Baptist Health Centers, Inc., Birmingham, Alabama

VICTOR S. ROTH, M.D., M.P.H., University of Alabama at Birmingham School of Medicine, Birmingham,
Alabama

Am Fam Physician. 1998 Feb 15;57(4):719-726.

  See related patient information handout on coronary artery disease

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The continued occurrence of occupational lead overexposure and lead poisoning in the United States
remains a serious problem despite awareness of its adverse health effects. Lead exposure is
arguably the oldest known occupational health hazard. It is a particularly insidious hazard with the
potential for causing irreversible health effects, including hypotension, central nervous system
problems, anemia and diminished hearing acuity before it is clinically recognized. Scientific evidence
of subclinical lead toxicity continues to accumulate, making further reduction in workplace exposure,
regular screening, and earlier diagnosis and treatment of critical importance in the prevention of this
occupational hazard. For the most part, the diagnosis of lead poisoning in the adult worker is based
on the integration of data obtained from the history, a physical examination, laboratory tests and
tests of specific organ function. A blood lead level of 40 μg per dL (1.95 μmol per L) or greater
requires medical intervention; a level of 60 μg per dL (2.90 μmol per L) or three consecutive
measurements averaging 50 μg per dL (2.40 μmol per L) or higher indicate the necessity for
employee removal. The decision to initiate chelation therapy is not based on specific blood lead
levels but depends on the severity of clinical symptoms.

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 μg per dL (1.20 μmol 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

View/Print Table
TABLE 1
Major Occupations and Industries Associated with Lead Overexposure

Battery manufacturing

Chemical industry

Construction workers

Demolition workers

Firing-range instructors

Foundry workers

Gas-station attendants

Gasoline additives production

 Jewelers

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TABLE 2
OSHA Lead Standards for Air and Blood

FOCUS LEVEL COMMENTS

Air 50 μg per m3 Permissible exposure limit (PEL): the employer shall

assure that no employee is exposed to lead at
concentrations >50 μg per m3 of air averaged over an
8-hour period.

Air 30 μg per m3 Action level: initiate medical surveillance for all

employees exposed to levels above 30 μg per m3 for
more than 30 days per year (regardless of respiratory
protection).

Blood ≥60 μg per dL (2.90 μmol per Medical removal from exposure
L) or average of last three
levels is ≥50 μg per dL (2.40
μmol per L)

Adapted with permission from Occupational exposure to lead: final standard. U.S. Department of Labor,
Occupational Safety and Health Administration. Federal Regist 1978; no. 29 CFR 1910.1025.

For workers in the United States who are covered by the OSHA lead standard, a detailed medical
examination is delineated under specific conditions3  (Table 3). Any general industry worker (i.e., battery,
foundry, smelting, mining, glass, ceramics) found to have a single blood lead level of 60 μg per dL (2.90
μmol per L) or greater, or an average blood lead level of 50 μg per dL (2.40 μmol per L) or greater must
be removed from the high-exposure job (termed “medical removal protection”). The “removed” worker
should subsequently receive more frequent medical evaluation and blood testing (Table 4). A worker is
not allowed to return to a job with the potential for high lead exposure until his or her blood lead level
has fallen below 40 μg per dL (1.95 μmol per L) on two successive tests.6

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TABLE 3
Medical Examination of Lead-Exposed Workers

Detailed medical and occupational history

Particular attention directed to lead exposure history (occupational and nonoccupational);

personal and workplace hygiene; history of gastrointestinal, hematologic, renal, reproductive
and neurologic disorders

Physical examination

Particular attention directed to neurologic and hematologic abnormalities; pulmonary status

should be evaluated in workers required to wear respiratory protective devices.

Blood pressure measurement

Blood testing

Blood lead level

Zinc protoporphyrin or free erythrocyte protoporphyrin level

View/Print Table
TABLE 4
OSHA Blood Lead Guidelines

A. Blood lead levels requiring employee removal. (Level must be confirmed with second follow-up
level within 2 weeks of first report.)

1. ≥60 μg per dL (2.90 μmol per L) or average of last three samples or all blood samples over
previous 6 months (whichever is a longer time period) is 50 μg per dL (2.40 μmol per L) or
greater unless last blood sample is 40 μg per dL (1.95 μmol per L) or less
 B. Frequency with which employees exposed to action level of lead (30 μg per m3 TWA) must have
blood lead level checked. Zinc protoporphyrin test is also strongly recommended at each occasion
that a blood lead level is obtained:

1. Last blood lead level is less than 40 μg per dL (1.95 μmol per L)

a. Every 6 months

2. Last blood level is between 40 μg per dL (1.95 μmol per L) and level requiring medical

A physician may also remove a worker with a lower blood lead level if risk of health impairment is
suspected and may restrict the worker from return to exposure until medically approved.3 To prevent
workers with elevated blood levels from being economically penalized during medical removal
protection, the OSHA standard requires that these workers must continue to receive their full rate of pay
(termed “pay rate retention”) while temporarily working in a less hazardous job.6

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 μm) lead fumes or lead-containing dust particles in the work-room atmosphere. Consequently, no
simple rule of thumb exists for categorizing different occupations into “more” or “less” hazardous
classifications, alathough 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

Toxicology
ABSORPTION

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

DISTRIBUTION

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

EXCRETION

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 toxicity6  (Table 5). 9

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TABLE 5
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 abdominal pain Diffuse abdominal pain Abdominal colic

Lethargy Weight loss Lead lines

Loss of libido Oliguria

Constipation

Adapted from Case studies in environmental medicine: lead toxicity Atlanta: Agency for Toxic

CHRONIC INORGANIC LEAD TOXICITY

Chronic toxicity is an insidious illness with protean manifestations.3,6 Symptoms may include
arthralgias, headache, weakness, depression, loss of libido, impotence and vague gastrointestinal
difficulties. Late effects may include chronic renal failure, hypertension, gout and chronic
encephalopathy.6

ORGAN SYSTEM DYSFUNCTION

Lead toxicity can be manifested clinically in multiple organs. Specific organ system dysfunction
includes the central and peripheral nervous system, and renal, hematologic, gastrointestinal and
reproductive systems. Figure 1 provides a summary of the organ-specific effects associated with the
lowest observable lead levels in the adult worker and, for comparison, in children.9

View/Print Figure
FIGURE 1.
Effects of inorganic lead on children and adults (lowest observable adverse-effect levels).
Diagnosis
Arriving at a diagnosis of lead poisoning in an adult requires a high index of suspicion and a careful
history. The infrequency of classic diagnostic signs and the nonspecific nature of the symptoms
frequently contribute to misdiagnosis.8

The diagnosis of inorganic lead intoxication in adults requires the demonstration of excess lead
absorption, documentation of impairment in an organ system consistent with the effects of lead, and
exclusion of other causes of disease. At present, the blood level concentration is the single best
indicator of recent, acutely elevated lead absorption (Table 6). This level provides good information on
lead absorption in persons with relatively brief exposure, such as construction workers or new entrants
into the lead industry. The blood lead level rises rapidly within hours after an acute exposure and
remains elevated for several weeks.6

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TABLE 6
Interpretation of Adult Worker Blood Lead Levels

TEST VALUE INTERPRETATION

≤9 μg per dL Unexposed or “normal”

10 to 40 μg per dL Acceptable levels for long-term

exposure; retest in 6 months

40 to 50 μg per dL (1.95 to 2.40 μmol per L) Close observation and follow-up

indicated; retest in 2 months

≥50 μg per dL (2.40 μmol per L) on average of last three Removal from exposure; retest within
or ≥60 μg per dL (2.90 μmol per L) 1 month

Adapted with permission from Occupational exposure to lead: final standard. U.S. Department of Labor,
Occupational Safety and Health Administration. Fed Regist 1978;no. 29 CFR 1910.1025.

Several attempts have been made over the years to relate blood lead levels to adverse health effects. It
is not possible to determine a precise blood lead level below which symptoms never occur or a blood
lead level at which symptoms are always reported. Individual susceptibility should always be
recognized.5 Moreover, exposure to lead does not protect the worker from incurring other, unrelated
diseases with signs and symptoms similar to those occurring in lead toxicity.

A zinc protoporphyrin or free erythrocyte protoporphyrin level reflects the toxic effect of lead on the
erythrocytic enzyme ferrochelatase. Zinc protoporphyrin levels usually begin to rise in adults when the
blood lead level exceeds 30 to 40 μg per dL (1.45 to 1.95 μmol per L). Once elevated, zinc protoporphyrin
levels tend to remain above background level for several months. Since the zinc protoporphyrin level
remains elevated long after exposure has ceased and the blood lead level has fallen, this test does not
discriminate between recent and past exposure. It is only of ancillary value in evaluating occupational
lead exposure.6  However, by obtaining both a blood lead level and a zinc protoporphyrin level, sufficient
information is provided to quantitate the severity of the effect due to lead toxicity and the approximate
chronology of the lead exposure (Table 7).2

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TABLE 7
Common Interpretation of Erythrocyte Protoporphyrin Levels

TEST VALUE INTERPRETATION

Up to 80 Normal range for adults

μg per dL

80 to 250 Typical range for occupationally lead–exposed adults whose blood lead levels
μg per dL range from 20 to 40 μg per dL (0.95 to 1.95 μmol per L)

250 to 500 High range for lead-exposed adults (blood lead levels range from 40 to 55 μg per
μg per dL dL [1.95 to 2.65 μmol per L])

>500 μg Excessive, indicating heavy exposure or extreme sensitivity to lead; symptoms

per dL likely

Adapted with permission from Saryan LA, Zenz C. Lead and its compounds. In: Zenz C, Dickerson OB,
Hovarth EP, eds. Occupational medicine. 3d ed. St. Louis: Mosby, 1994:506–41.

A most difficult task is to either establish or exclude past lead exposure as the etiology of a current
disease. Beyond several years since the last known lead exposure, the decision may be difficult,
especially when all functional tests are now normal. One way to show a relationship between past lead
exposure and present illness is to demonstrate an abnormally high body burden of lead. This is best
done by measuring the excretion of lead in urine after provocation with edetate calcium disodium
(calcium EDTA; Calcium Disodium Versenate) or another chelating agent. This is a reliable way to
demonstrate an increased body burden with previous high-level exposures. However, it is important to
recognize that this test indicates only past lead exposure, not past lead poisoning.2

In the future, the x-ray fluorescence method of analyzing lead content of bone may replace the EDTA
chelation challenge as the gold standard of cumulative absorption. The measurement of bone lead
content by x-ray fluorescence offers a noninvasive, relatively rapid approach to the assessment of body
lead burden, with minimal radiation exposure (approximately one-tenth the radiation of a dental x-ray.)6
As x-ray fluorescence becomes more readily available, its safety, specificity and simplicity should make
it an important alternative to chelation testing for the monitoring of lead burden for workers with
documented chronic exposure.10

The clinical symptoms previously discussed are an important aid in diagnosis and should always be
explored. Since many of the neurologic and gastrointestinal symptoms are non-specific, unless the
examining physician is aware of the history of lead exposure, the diagnosis of lead toxicity may be
easily overlooked. With improved control of the work environment resulting in lower levels of lead
exposure, occupational lead poisoning is now usually characterized by subtle, nonspecific symptoms.
Therefore, the diagnosis is typically made using laboratory tests along with a careful clinical evaluation.5

Treatment
In all cases of suspected lead intoxication in adults, the first step in management should be removal of
the individual from the exposure.3,5,6  A physician who believes his or her patient has occupational lead
poisoning should report the case to the local health department. Currently, 27 states require laboratory
reporting of elevated lead levels under the Adult Blood Lead Epidemiology and Surveillance (ABLES)
program administered by NIOSH (Table 8).Whether discontinuation of exposure is sufficient treatment
or chelation therapy should be administered depends on the blood lead concentration, the severity of
clinical symptoms, the biochemical and hematologic abnormalities, and the nature of the exposure. It is
not recommended that specific blood lead concentrations be used to determine when treatment with a
chelating agent is indicated. As a general rule, however, such a level is usually well above 80 μg per dL
(3.85 μmol per L), which is also the level frequently associated with more severe symptoms.5 The
primary indication for treatment of adults is brief, high-level exposure causing acute manifestations.3

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TABLE 8
27 States in the ABLES Program
 Alabama

Arizona

California

Connecticut

Iowa

Maine

Maryland

Massachusetts

Michigan

The use of chelation is not generally indicated in cases of long-term occupational exposure. The OSHA
Lead Standard specifically prohibits “prophylactic” chelation for the prevention of elevated blood lead
levels.2 In prophylactic chelation, chelating or similarly acting drugs are used routinely to prevent
elevated blood levels in workers who are occupationally exposed to lead or to lower blood lead levels to
predesignated concentrations thought to be safe.11 In patients with ongoing lead exposure, chelation
therapy is not considered appropriate medical treatment.12 Chronic administration of oral agents to
workers who continue to be exposed to unacceptably high levels in their workplace is a technique that
has been used by employers in the past and is considered inappropriate.6

The OSHA standard allows the use of “therapeutic” or “diagnostic” chelation only if administered under
the supervision of a licensed physician in a clinical setting in conjunction with thorough and appropriate
medical monitoring.11 When treatment with a chelating agent is indicated, edetate calcium disodium is
often the drug of choice. Dimercaprol (BAL in Oil) and penicillamine (Cuprimine), popular agents in the
past, are used less frequently today.5

The role of the new oral agent succimer (Chemet) in the treatment of adults has not been determined; it
is currently approved by the U.S. Food and Drug Administration for treatment in children only.13
Although isolated reports document effectiveness of succimer in treating adults, no clinical trials with
this agent for treatment of adult lead toxicity have been reported.14 The efficacy of chelating agents in
treating patients with subtle neurologic and renal abnormalities has not yet been fully studied13 and is
therefore not indicated.

It is essential to remember that the chelating agents themselves may have significant adverse effects,
which represent a risk apart from the lead toxicity. Treatment with these agents usually represents a
failure in preventing lead overexposure of the patient and should initiate investigation of other workers
at risk. Physicians contemplating chelation therapy for treatment of lead poisoning are advised to
consult with colleagues experienced with use of up-to-date treatment protocols in view of the lack of
clear and consistent guidelines addressing the issue of when to chelate in such cases.12

Prevention
The first line of defense in the elimination of occupational lead poisoning is primary prevention—actions
taken to prevent overexposure. Primary prevention is best achieved through the use of engineering
controls, personal protective equipment and good work practices (Table 9). The family physician can
have the greatest impact on prevention through worker education and instruction in proper personal
hygiene techniques.

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TABLE 9
Primary Prevention of Lead Poisoning

Engineering controls

Substitution of less hazardous material

Isolation via containment structure

Ventilation via local exhaust system

Personal protective equipment

Respirator utilization

Work practices
 Housekeeping activities to remove lead dust accumulation

Personal hygiene practices

Following identification of a case of lead poisoning, preventive strategies should begin as worker
removal and possible treatment are initiated. A single case of occupational lead poisoning may
represent a “sentinel health event,” thereby serving as a warning of potential overexposure of other
workers. With the assistance of industrial hygiene experts, the patient's workplace should be
investigated for possible additional cases and causes. State health departments should be notified with
possible referral to an occupational medicine specialist if questions remain regarding treatment
protocol, worker disposition and work-place evaluation. Excellent resources that can assist the family
physician in understanding these decisions are readily available and are listed in Table 10.

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TABLE 10
World Wide Web Resources for Information on Lead Poisoning

Code of Federal Regulations http://law.house.gov/cfr.htm

Duke University Occupational and http://dukeoccmed.mc.duke.edu/

Environmental Medicine (http://dukeoccmed.mc.duke.edu/)

CDC Homepage http://www.cdc.gov/ (http://www.cdc.gov/)

OSHA Regulations http://www.osha.gov/SLTC/lead/

(http://www.osha.gov/SLTC/lead/)

EPA Homepage http://www.epa.gov/ (http://www.epa.gov/)

NIOSH Homepage http://www.cdc.gov/niosh/homepage.html

(http://www.cdc.gov/niosh/homepage.html)

Envirolink http://envirolink.org (http://envirolink.org)

The Authors show all author info

KEVIN C. STAUDINGER, . ., . . ., 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....

Figure 1 adapted with permission from Case studies in environmental medicine: lead toxicity. Atlanta:
Agency for Toxic Substances and Disease Registry, 1992.

REFERENCES show all references

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

Each year members of a different family practice department develop articles for “Problem-Oriented
Diagnosis.” This series is coordinated by the Department of Family and Community Medicine at the
University of Alabama at Birmingam. Guest editors of the series are T. Michael Harrington, M.D., and Myra
A. Crawford, Ph.D.

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