Blood Spot + Dried Urine ICPMS Toxic and Essential Elements

Mercury circulates predominantly as methylmercury bound to haemoglobin cysteine residues following dietary seafood intake, and as inorganic mercury after vapour inhalation or dental amalgam exposure. Blood mercury reflects recent exposure over the past few months and correlates with body burden in chronic low-level exposure, whereas urine captures inorganic mercury excretion.

Blood mercury is the primary marker for methylmercury from fish and shellfish, which crosses the blood–brain barrier and accumulates in the central nervous system. Elevated concentrations may signal neurotoxic risk, particularly in pregnant women and children, and prompt dietary counselling or source identification.

Lead in blood resides chiefly in erythrocytes, where it inhibits haem biosynthesis and mimics calcium in biochemical processes. Blood lead represents recent exposure (weeks to a few months) plus a component mobilised from bone, the principal long-term reservoir. After acute exposure ends, blood levels decline with a half-life of roughly 30 days.

Blood lead is the standard biomarker for occupational and environmental lead exposure. Even low concentrations are associated with neurocognitive effects in children and cardiovascular and renal sequelae in adults, so any detectable elevation warrants source investigation and remediation.

Cadmium is absorbed from tobacco smoke and certain foods, then binds to metallothionein in erythrocytes and distributes to liver and kidney. Blood cadmium reflects recent exposure (weeks to months), whereas urinary cadmium is a better index of cumulative body burden and renal accumulation.

Blood cadmium is used to monitor recent occupational or tobacco exposure and to assess acute intake. Chronic cadmium accumulation damages proximal renal tubules and bone, but body burden is better gauged by urine; blood and urine cadmium together provide short- and long-term exposure windows.

Inorganic arsenic is methylated in the liver to monomethylarsonic and dimethylarsinic acids, which are rapidly excreted in urine. Urinary arsenic reflects recent intake (past few days) of inorganic arsenic from water, soil, or food, plus organic arsenicals (arsenobetaine, arsenocholine) from seafood, which are non-toxic but contribute to total urinary arsenic.

Urinary arsenic is the primary biomarker for inorganic arsenic exposure, linked to cancer, cardiovascular disease, and diabetes. Speciation is essential — total arsenic without speciation can be elevated by recent seafood, leading to false-positive toxicity concerns. Dried-urine ICPMS typically measures total arsenic; practitioners should correlate with dietary history.

Selenium is incorporated into selenoproteins — glutathione peroxidases, thioredoxin reductases, and iodothyronine deiodinases — that govern redox homeostasis and thyroid hormone metabolism. Whole-blood or serum selenium reflects recent intake and tissue status; erythrocyte selenium integrates over the lifespan of the cell.

Blood selenium is used to assess adequacy in populations at risk of deficiency (low-selenium soils, restrictive diets) and to monitor repletion. Both deficiency and excess (selenosis, >400 µg/L) carry risk, so selenium sits within a relatively narrow optimal window.

Zinc circulates predominantly in erythrocytes bound to carbonic anhydrase and in plasma loosely associated with albumin. Plasma zinc is homeostatically regulated and falls during acute inflammation (negative acute-phase reactant) and with hypoalbuminaemia, limiting its sensitivity as a status marker; whole-blood or dried-spot zinc offers a broader integrative window.

Zinc status is notoriously difficult to assess biochemically. Low blood zinc may reflect true deficiency, acute-phase responses, or laboratory variation. Practitioners interpret zinc alongside clinical signs (dysgeusia, poor wound healing, immune dysfunction), dietary intake, and interfering factors rather than relying on a single concentration.

Most circulating copper is incorporated into caeruloplasmin, an acute-phase protein synthesised in the liver; a small fraction circulates loosely bound to albumin and amino acids. Plasma copper rises with oestrogen (pregnancy, oral contraceptives) and inflammation and falls in Wilson disease (impaired caeruloplasmin synthesis) and severe malnutrition.

Blood copper is used to screen for Wilson disease (low total copper, low caeruloplasmin, high free copper) and to assess deficiency in malabsorption or excessive zinc supplementation, which antagonises copper absorption. Isolated copper without caeruloplasmin or free-copper calculation has limited diagnostic specificity.

Magnesium is predominantly intracellular; serum or plasma represents <1 % of total body stores and is homeostatically defended, so normal blood magnesium does not exclude tissue depletion. Dried-blood-spot magnesium reflects the cellular fraction to some extent, offering a closer approximation to tissue status than serum alone.

Blood magnesium is insensitive for detecting marginal deficiency but is useful for identifying overt hypomagnesaemia in hospitalised or at-risk patients (diuretics, proton-pump inhibitors, alcohol use, gastrointestinal losses). Functional practitioners may order additional markers (ionised magnesium, red-cell magnesium) when clinical suspicion is high despite a normal result.

Iodine is concentrated by the thyroid for thyroid-hormone synthesis; excess is rapidly excreted in urine, so urinary iodine reflects very recent dietary intake (past day or two). Because of high day-to-day variability, a single spot-urine iodine is an imprecise marker of individual status, though it is the standard method for population surveillance.

Urinary iodine is used to screen for deficiency or excess in populations and to guide iodine supplementation in pregnancy. In individuals, it must be interpreted cautiously — a low value on one occasion may not reflect chronic deficiency, and very high values can occur after iodine-containing contrast or supplement loading.

Chromium circulates at trace concentrations and was historically proposed to potentiate insulin signalling, though the biochemical basis and clinical relevance of chromium deficiency in humans remain controversial. Blood chromium can be elevated by occupational exposure (welding, pigment manufacturing) or contamination during sample collection.

Blood chromium is rarely measured in routine practice. It may be included in comprehensive toxic and essential panels to screen for occupational hexavalent-chromium exposure or, in the functional-medicine context, to assess putative trivalent-chromium status, though evidence for clinically meaningful deficiency states is limited.

Molybdenum is a cofactor for several oxidoreductases (sulphite oxidase, xanthine oxidase, aldehyde oxidase). Deficiency is exceedingly rare outside total parenteral nutrition without supplementation. Blood molybdenum reflects recent intake and is influenced by geographical soil content and dietary legume and grain consumption.

Molybdenum measurement is largely exploratory in clinical practice, included in comprehensive trace-element panels to complete the essential-element picture. Deficiency presentations are so rare that low values should prompt specimen and assay verification before clinical action.