Blood Metals Panel

Lead is a toxic heavy metal with no physiological role. It binds to sulfhydryl groups in enzymes and structural proteins, interfering with haem synthesis, mitochondrial function, and cellular signalling. Blood lead reflects recent or ongoing exposure; more than 95% circulates bound to erythrocytes, with a blood half-life of approximately 30 days. Bone stores can remobilise during physiological stress, pregnancy, or periods of increased bone turnover.

Blood lead is the standard marker for recent lead exposure and is used to screen occupational and environmental exposure, guide chelation decisions, and monitor workers in lead industries. Chronic low-level exposure is associated with neurodevelopmental deficits in children and cardiovascular, renal, and neurocognitive effects in adults. No safe threshold has been established for children.

Blood mercury reflects primarily organic (methylmercury) exposure from fish and seafood, with a half-life of approximately 50 days. Methylmercury crosses the blood-brain barrier and placenta readily, posing neurotoxic risk. Inorganic mercury from dental amalgam or occupational sources contributes minimally to whole-blood levels but may be seen in plasma or serum fractions.

Blood mercury is ordered to assess dietary or occupational exposure and to evaluate neurological symptoms, tremor, or suspected toxicity. Elevated levels in pregnant or reproductive-age women guide dietary counselling to reduce foetal methylmercury exposure, which is associated with neurodevelopmental impairment.

Cadmium is a nephrotoxic and carcinogenic metal absorbed via inhalation (tobacco smoke, occupational dust) and diet (shellfish, offal, some grains). Blood cadmium reflects recent exposure with a half-life of several months, while urinary cadmium integrates long-term body burden. Cadmium binds metallothionein in erythrocytes and accumulates in renal tubules.

Blood cadmium is used to monitor recent occupational or smoking-related exposure. Chronic accumulation causes proximal tubular dysfunction (Fanconi syndrome), bone demineralisation (itai-itai disease in severe cases), and is a class I carcinogen. Practitioners order it in battery workers, smelters, and heavy smokers, or when investigating unexplained proteinuria.

Blood arsenic has a very short half-life (hours for inorganic arsenic) and reflects only acute or very recent exposure. Inorganic arsenic is metabolised to methylated forms and excreted in urine; organic arsenicals from seafood (arsenobetaine) are non-toxic and rapidly cleared. Blood total arsenic can be misleading without speciation or a concurrent urine sample.

Blood arsenic is rarely the preferred specimen for chronic exposure assessment — urine arsenic with speciation is more informative. Blood measurement is useful in acute poisoning or to confirm very recent high-level exposure. Chronic inorganic arsenic exposure causes skin changes, peripheral neuropathy, vascular disease, and increased cancer risk.

Aluminium is ubiquitous in the environment but poorly absorbed from the gastrointestinal tract in healthy individuals. Blood aluminium reflects recent exposure and is elevated in renal failure, where diminished clearance permits accumulation, and in patients receiving aluminium-containing antacids or parenteral nutrition. Aluminium binds transferrin and distributes to bone and brain.

Blood aluminium is ordered primarily in dialysis patients, where chronic elevation can cause dialysis encephalopathy, osteomalacia, and microcytic anaemia unresponsive to iron. It is also used to investigate occupational exposure in welders and smelters, or following high-dose antacid use in renal patients.

Chromium exists in trivalent (Cr³⁺) and hexavalent (Cr⁶⁺) forms. Trivalent chromium is an essential trace element involved in glucose and lipid metabolism, while hexavalent chromium is a recognised carcinogen. Blood chromium is not routinely measured for nutritional assessment; elevations reflect occupational exposure (welding, chrome plating) or contamination.

Blood chromium is ordered to assess hexavalent chromium exposure in industrial workers, where inhalation can cause lung cancer and dermatitis. Interpretation is complicated by contamination risk during collection and the inability of routine assays to distinguish Cr³⁺ from Cr⁶⁺. Nutritional chromium status is not reliably assessed by blood level.

Manganese is an essential trace element, a cofactor for superoxide dismutase and other metalloenzymes. It is tightly regulated by biliary excretion; whole-blood levels reflect recent intake and occupational inhalation. Chronic excessive exposure — especially via inhalation in welders and miners — causes accumulation in the basal ganglia and a Parkinsonian syndrome (manganism).

Blood manganese is ordered to investigate suspected neurotoxicity in workers with high inhalation exposure (welding fume, mining, battery manufacture) or in patients on long-term parenteral nutrition. Elevated levels correlate poorly with body burden because excretion is so tightly regulated, so neuroimaging (MRI T1 hyperintensity in the globus pallidus) often adds diagnostic value.

Copper is an essential trace element, incorporated into caeruloplasmin (the main plasma copper-binding protein) and enzymes including cytochrome c oxidase and superoxide dismutase. Whole-blood or serum copper reflects both caeruloplasmin-bound and free (exchangeable) copper. Free copper rises in Wilson disease and can be neurotoxic and hepatotoxic.

Blood copper, interpreted with caeruloplasmin and 24-hour urinary copper, is central to the diagnosis of Wilson disease (low total copper, low caeruloplasmin, high free copper, high urinary copper) and to monitoring copper deficiency in malabsorption, prolonged parenteral nutrition, or zinc overload. Copper deficiency causes microcytic or sideroblastic anaemia, neutropaenia, and myelopathy.

Zinc is an essential trace element required for more than 300 enzymes, immune function, wound healing, and DNA synthesis. Most circulating zinc is bound to albumin; inflammatory states lower serum zinc by redistributing it into tissues, so interpretation requires correlating with acute-phase markers. Whole-blood zinc includes an intracellular pool and is less influenced by inflammation.

Blood zinc is ordered to diagnose deficiency (acrodermatitis enteropathica, malabsorption, prolonged parenteral nutrition, chronic diarrhoea) and to monitor repletion. Deficiency impairs immune function, delays wound healing, and causes taste disturbance and dermatitis. Excess zinc, often from supplementation, causes copper deficiency by competitive inhibition of intestinal absorption.