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Nowadays, exposure to lead is one of the global human health concerns and therefore it is considered as one of the most important toxic ele­ments.


Lead applications are various by playing special roles in industries, including smelting, battery manufacturing, and mining (1,2) as well as in agricultural fertilizers and pesticide (3). On the other hand, industrialization discharging into rivers has led to polluting water bodies (1). Moreover, lead pollution of soils as a result of contaminated water bodies and exhaust product of leaded gasoline used in urban areas have had serious environmental effects (4,5).

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The lead entrance into bloodstream is less commonly through the skin and mucosa and only organic lead gets absorbed through these routes (8, 9). However, the main lead absorption occurs via gastrointestinal and respiratory tracts. The latter route absorbs the most amount of lead (30-70%), by being four times higher in adults, whereas the gastrointestinal absorption in children increases up to five times compared to adults. Overall, iron deficiency, low dietary calcium, and fasting promote lead absorption (8).


After absorption lead gets bound to various soft and hard tissues, such as hair dense, bone, teeth (hard tissue) and brain, spleen, kidney, bone marrow, lungs (soft tissue) and the rest is excreted with urine, feces, and sweating )7). About 99% of the circulating lead is bound to red blood cells for about 30-35 days then it spreads out into the soft tissues over the next 4-6 weeks. The remaining 1% of the absorbed lead is found in serum and plasma. lead is stored in the bones (95%), these are the primary lead pool. As a result of long lead half-life, patients suffer from lead toxicity in bones even after the removal of any external source of lead, and therefore bones are considered as the primary reservoir of lead content (9).

The hypothalamus pituitary thyroid (HPT) axis controls thyroid function through thyrotropin releasing hormone (TRH), thyroid stimulating hormone (TSH), and the Thyroid hormones such as thyroxine (T4) and triiodothyronine (T3). Most of the time, T4 and T3 are bound to thyroxine-binding globulin, transthyretin, and albumin, and only less than 1% of circulating T4 and T3 are unbound and active. In peripheral tissues, type 1 and type 2 deiodinases convert T4 to T3; in turn it binds thyroid receptors ? and ? and initiates target gene expression (10). What results in clinical or subclinical thyroid diseases include disruption of TH synthesis, transport, deiodination, and metabolism (10). Environmental chemicals, such as lead, might change TH levels via several mechanisms, including TH-binding proteins, disruption of iodine transport, thyroid peroxidase, deiodinases, and receptor binding (11).

Lead is an environmental chemical that affects the hypothalamic-pituitary axis resulting in blunted TSH, FSH/LH, and GH responses to TRH, GNRH, and GHRH stimulation. It can also affect Thyroid hormone kinetics. (ref)

Thyroid hormones activity can be damaged by thyroid axis defection and T4 metabolism alteration as well as by protein binding (12).

Lead, as a divalent cation, can interfere with enzymes and structural proteins and more importantly with heme production resulting in reduction of the heme body pool. Another markers for lead toxicity include inhibition of the enzyme delta aminolevulinic acid dehydratase (delta-ALAD; ALAD) and the accumulation of aminolevulinic acid (ALA) in urinary excretion (14). When delta-ALAD prevents ALA from being converted to porphobilinogen reduction in heme synthesis occurs contributing to the fatigue and anemia seen in chronic lead toxicity. Furthermore, increased circulating levels of ALA leads to decreased GABA release in the central nervous system (CNS) causing behavioral disorders (15).

Previous studies on various populations have shown strong relationships between the ALAD2 allele and increased blood and bone lead levels (16).


Ferrochelatase, which catalyses terminal step in the biosynthesis of heme also gets impaired by lead (18) resulting in decreased red blood cell counts and eventually anemia (ref). Blood hemoglobin levels change as a result of exposure to 50 ?g/dl of lead in adults (18).


Observation of basophilic stippling and premature erythrocyte hemolysis in the blood smear are the hematologic signs of lead poisoning (ref).

Finally, lead toxicity changes calcitropic hormones’ homeostasis and it increases skeletal disorder risk (12).

Now, it is well accepted that lead (Pb) has many toxic influ­ences on the health of humans. Several studies have been conducted on occupational exposure and biologic evaluation of lead in Iranian workers, but few studies have been carried out on the effects of lead on thyroid parameters and blood parameters.


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