Page 89 - JSOM Spring 2018

Epidemiology include sleep disturbance, anorexia, decreased libido, head-
In the late 1970s, the US national geometric mean BLL was ache, myalgia, arthralgia, difficulty concentrating, and confu-
12.8μg/dL. As of 2004, that BLL was lower, 1.43μg/dL (95% sion. High doses over short duration with BLL higher than
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confidence interval [CI], 1.36–1.50), largely due to the removal 80μg/dL may cause convulsions, seizure, encephalopathy, and
of leaded additives in automotive fuel. ABLES data have dem- coma.
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onstrated a decreasing national prevalence of BLLs of at least
25μg/dL, from 14.0 per 100,000 in 1994 to 5.2 in 2013. Simi- Physical findings are limited but may include a bluish pigmen-
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larly, data provided by the National Health and Nutrition Ex- tation of the gum–tooth line that results from an interaction
amination Survey (NHANES) showed a decrease in adults with between lead and gingival bacteria. However, this finding is
BLL of at least 10μg/dL, from 3.1% in the early 1990s to 0.7% not a sensitive indicator. Presentation may include a peripheral
less than a decade later. The ABLES data also demonstrate motor neuropathy that begins in the wrist and finger exten-
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higher prevalence of elevated BLL in men and non-Hispanic sors, and develops secondarily to lead-induced axonal degen-
blacks. Minimal data are available to determine the preva- eration. However, this finding is not specific. 25
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lence of lead toxicity in Department of Defense (DoD) or SOF
personnel. However, an Army Occupational Health Program Complete blood cell (CBC) count may demonstrate anemia
Surveillance Report indicated that the percentage of screened with corresponding deficits in hemoglobin concentration,
employees who had “abnormal” BLLs was as high as 5%. 3 mean corpuscular volume, mean corpuscular hemoglobin, and
erythrocyte count. The causes of anemia are multifactorial but
Absorption and Distribution have been associated with changes in erythrocyte structure,
Lead provides no benefit to the human body and is only a erythrocyte survival, heme synthesis, and renal production of
source of harm. Respiratory and gastrointestinal absorption erythropoietin. Blood smear may display basophilic stippling
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can reach 50% of the aerosolized or ingested dose. Once ab- that results from inclusions of aggregated ribosomes, though
sorbed, greater than 95% of lead is initially bound to erythro- this finding is neither sensitive nor specific. Blood smear or
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cytes (i.e., red blood cells), with the remainder in plasma. Lead other laboratory tests may indicate frank hemolysis associated
is first distributed throughout soft tissues, including the central with deficient erythrocyte pyrimidine 5’-nucleotidase. 27
and peripheral nervous systems, renal system, and the repro-
ductive system. Blood lead is excreted primarily in the urine Subclinical Health Outcomes
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and has a half-life of approximately 30 days. However, greater Chronic lead toxicity with levels lower than 40μg/dL will
than 90% of blood lead is eventually deposited in bone, where likely present asymptomatically or with mild, nonspecific
the half-life can reach 19 years. Bone lead may be redistrib- findings. However, over time, significant damage can occur
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uted into soft tissues in the event of trauma, fracture, or other to the renal, cardiovascular, nervous, and reproductive sys-
causes for bone resorption, such as pregnancy or cancer. tems. Current medical and scientific consensus is that lead
exposure causing adverse health effects begins at a BLL of
Mechanism of Toxicity 5μg/dL for female reproductive outcomes and 10μg/dL for
Lead occurs as the pure metal or combined in organic and other maladies.
inorganic compounds. When ionized, lead is a divalent cation
and can replace calcium or other metals in biologic systems. Cumulative lead exposure causes chronic kidney disease and
Lead ion (Pb ) has high affinity for sulfhydryl groups. This nephropathy. Many studies have demonstrated direct corre-
2+
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causes inhibition of multiple enzymes that have active-site sulf- lations between BLL and increased serum creatinine, reduced
hydryls, disrupting crucial pathways including heme synthesis creatinine clearance, and reduced glomerular filtration rate. Pa-
and mitochondrial respiration. Lead can inhibit pyrimidine tients with hypertension and diabetes are particularly suscep-
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5’-nucleotidase, causing degradation of ribosomal ribonucleic tible to the renal effects of lead. A cross-sectional analysis of
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acid. Lead is associated with global reduction of deoxyribo- men in the Normative Aging Study (n = 744) demonstrated that
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nucleic acid methylation and shortening of telomeres, in- a 10μg/dL increase in blood lead corresponded with a 10.4mL/
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creasing the risk of future genetic damage. In addition, lead min decrease in creatinine clearance. The National Toxicol-
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exposure generates reactive oxygen species in coronary endo- ogy Program has concluded that adverse effects on renal func-
thelial and vascular smooth muscle cells, potentiating a wide tion in adults are associated with BLL less than 10μg/dL. 30
variety of cellular and tissue damage. 23
Lead behaves as a vasopressor through previously described
Clinical Manifestations mechanisms, and thorough review has suggested a causal re-
Clinical manifestations of lead poisoning can vary from indi- lationship of lead exposure with hypertension. The impli-
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vidual to individual and may correlate poorly with the dose, cations of increased blood pressure for cardiovascular and
duration, and timing of exposure. High doses and acute expo- cerebrovascular mortality are well established, and the involve-
sures may provoke a dose-dependent clinical syndrome that ment of lead has been further elucidated in studies of general
correlates with BLL and can be treated if identified early, pre- population cohorts. A cross-sectional study of the Second Na-
venting disability. However, chronic and lower-dose exposures tional Health and Nutrition Examination Survey (NHANES II)
induce an array of negative health outcomes that are difficult found that people with blood lead levels of 20μg/dL to 29μg/dL
to identify and may produce devastating long-term health had a 39% increase in mortality from circulatory system dis-
consequences. ease (relative risk, 1.39; 95% CI, 1.01–1.91; n = 4,292) com-
pared with persons with lead levels less than 10μg/dL. Further
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Symptoms of acute lead poisoning usually become evident at longitudinal evaluation of adults age 40 years or older in the
around 40μg/dL BLL; nonspecific findings classically include NHANES III cohort (n = 9,757) found the relative risk of car-
abdominal pain (or “lead colic”), constipation, fatigue, and diovascular mortality to be 1.59 (95% CI, 1.21–1.94) in per-
central nervous system dysfunction. Additional findings may sons with BLL at least 10μg/dL (median, 11.8μg/dL) compared
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Lead Exposure in the Special Operations Shooter | 83