Lab Library

Environmental Toxins

What interferes with minerals and vitamins. A deficiency gets investigated; the other half of the equation, something occupying the seat a nutrient was meant to sit in, usually does not. This panel names the six categories of that other half, what each test can and cannot report, and the halogens that compete with iodine. It covers 6 markers. This page explains what each one measures, what it does NOT measure, and which nutrients are known to move it.

Read this first: Every test here reports exposure or a recent load, not a diagnosis, and the body's own clearance pathways are the only mechanism this site describes. No product takes a toxin out of a body; the evidence supports reducing the exposure and giving the body's own pathways what they are built from.

The Library is open to read. Your own numbers after you join.

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What this is, and is not

A detectable glyphosate, a mycotoxin metabolite or a blood lead is a measurement of exposure. It is not a diagnosis, and a result inside a reference interval is not proof of a clean body: blood lead and mercury reflect recent exposure rather than what is stored, and most of these tests have no population reference at all. What the library does hold is the interference: which exposure moves which nutrient marker, in which direction, in which study.

The reading order

The frame is interference. Across 44 studies, lower blood or dietary zinc and iron were linked to higher cadmium in blood or urine, while the evidence for selenium, calcium and the vitamins was inconsistentHH-39120. Aflatoxin exposure was associated with lower hemoglobin and with vitamin A deficiency across ten observational studiesHH-80097. Lead at or above 5 micrograms per deciliter in children near e-waste sites was linked to impaired hemoglobin synthesis and poorer neurodevelopmentHH-346222. Selenium limits methylmercury's oxidative stress and bioaccumulationHH-126434, and in 36 lamp-factory workers exposed to mercury, lead and cadmium, selenium with vitamin E was associated with lower blood metal levels and better antioxidant markersHH-442780. For arsenic, vitamins, tea, glutathione, N-acetylcysteine and zinc reduced toxicity by raising antioxidant enzymes in human studiesHH-37889, and a folate-supplemented diet shifted arsenic toward its methylated, excretable form in humanized mice without lowering tissue arsenicHH-126266. Prenatal phthalate exposure may disrupt maternal and placental metabolism in ways micronutrient status could partly offset, a proposed mechanism rather than a trialHH-34998.

The endocrine half. Urinary bisphenol A was linked to altered thyroid hormone levels in adult men and women across 18 studiesHH-35477, and prenatal bisphenol exposure to altered child thyroid hormones in girls only across 11 cohortsHH-35571; higher DEHP phthalate exposure was linked to lower testosterone in men across 37 studies of 28,911 peopleHH-34515; PFAS compounds, legacy and newer, were associated with thyroid outcomesHH-114935 with the legacy compounds carrying the stronger effect in mother-child populationsHH-25948. These sit on this panel because a thyroid or hormone panel that does not ask the exposure question is reading only half the mechanism.

The six categories below are the brain's own testing guide, carried over without numbers because the guide has none. Where this site already holds a marker with a sourced range (lead, mercury, aluminum, PFAS, the whole-test entries), it is in the list above; everything else is what to ask for.

Halogens: bromide, fluoride, perchlorate and chlorine against iodine

Iodine is a halogen, and the other halogens compete for its doors. In molecular modeling, fluoride, chloride, bromide and perchlorate all bound thyroid peroxidase and the sodium-iodide symporter more strongly than iodide didHH-192173. Perchlorate competitively inhibits the sodium-iodide symporter, reducing thyroid hormone synthesis and potentially raising TSH, most in pregnant and iodine-deficient populationsHH-131240; its binding affinity for the symporter was re-estimated about 60 percent stronger than earlier figuresHH-131142; chronic low-dose perchlorate from food and water was linked to altered thyroid synthesis, especially with iodine insufficiency, and to worse infant neurodevelopment after prenatal exposureHH-131303; in pregnant women with borderline thyroid function, the highest maternal perchlorate levels carried three-fold higher odds of the child's IQ falling in the lowest decile at age threeHH-131980.

Bromide interferes with iodine metabolism by lowering thyroid iodide uptake and raising urinary iodide lossHH-192049, and potassium bromate was detected in every tested bread sample in one validated method study at 4.5 to 9.15 mg/kg, above the WHO and FDA limitHH-131489. Fluoride: a dose-response meta-analysis found TSH rising with drinking-water fluoride above roughly 2.5 mg/L and higher odds of goiter and low thyroid functionHH-151656; a systematic review found five of seven studies linking high fluoride exposure to altered thyroid function, with the overall evidence quality rated lowHH-131358; in a Canadian pregnancy cohort, each 0.5 mg/L of water fluoride was associated with 1.65-fold higher odds of primary hypothyroidismHH-151548; a review of the latest research reported the same correlation with TSH, strongest in pregnancyHH-363358. Chlorine's competition rests on the modeling row above; the library holds no human chlorine-thyroid trial, which is a gap on the search list, not a verdict.

What to measure. Urinary iodine is the population measure of iodine intake, and the Chinese cohort that followed deficient, more-than-adequate and excessive intake for five years found the lowest rates of thyroid dysfunction at a urinary iodine near 100 to 200 micrograms per liter, with both ends of the range raising themHH-2449; iodine and bromine can now be measured together in urine and serum by ICP-MS in a method built for population studiesHH-192176. Urinary perchlorate, bromide and fluoride are specialty measurements with no reference interval on this site; ask for them by name where the exposure questions (well water, bread, a pool, an agricultural area) make them plausible. The thyroid markers themselves (TSH, free T4, free T3, TPO antibodies) sit on the Thyroid panel.

What to ask for

Tests this panel names that the tool carries no sourced range for. Nothing here invents a number: read each against the reporting laboratory's own interval.

  • Urine mycotoxin panel (ochratoxin A, aflatoxins, trichothecenes, zearalenone, gliotoxin)

    Mycotoxin metabolites in a first-morning urine. Aflatoxin B1-lysine and ochratoxin A are the most studied blood biomarkers, and a high share of samples test positive worldwideHH-33339; in 447 urine samples from pregnant women in rural Bangladesh, 96 percent held detectable mycotoxinsHH-33317. The limit, from the field itself: missing reference standards and no reliable link yet between a urine level and dietary intakeHH-33358. Serum mycotoxin antibodies are the second route the guide names when urine is negative.

  • Urine glyphosate and AMPA

    Glyphosate and its metabolite in a random or first-morning urine. Biomonitoring found glyphosate in 99.8 percent of U.S. samples at a mean of 1.19 ng/mL, higher in males, children and agricultural workersHH-190256; across studies, urinary glyphosate ranged from 0.02 to 233 micrograms per literHH-282063; in 17 vineyard workers it was undetectable before a single application and measurable in all of them afterwardHH-27858. A randomized crossover trial of organic and conventional groceries in pregnancy is one of the few tests of whether diet changes the numberHH-27251.

  • Organic acids (urine)

    Metabolic byproducts reflecting mitochondrial function, neurotransmitter turnover, conjugation capacity and microbial metabolites. A review of this urine test describes eight compounds its authors propose as markers of toxic exposure, liver conjugation activity and glutathione statusHH-34012; in 392 people, organic acids linked to energy and conjugation pathways predicted autoimmune status with 66.7 to 74.9 percent accuracyHH-27544. A specialty test; no reference interval on this site.

  • Urine VOC metabolites (benzene, toluene, xylene, formaldehyde, ethylbenzene)

    Breakdown products of volatile organic compounds. Exposure to benzene, styrene and formaldehyde was associated with more DNA strand breaks in human white cells across the comet-assay literatureHH-329099; indoor particulate matter and VOCs from cooking, candles, cleaning products and building materials were linked to worse lung function across 69 studiesHH-28019; better ventilation and waiting over a year after a renovation lowered indoor exposureHH-28022.

  • Urine phthalates and bisphenols (DEHP metabolites, BPA, BPS, BPF)

    Plasticizer and plastic-monomer metabolites. Phthalate exposure was nearly double in non-pregnant and youth groups compared with pregnant adults across 216 studies, up to tenfold higher in the Middle East and South AsiaHH-35479; paired hair, nail and urine samples carried different dominant compounds with little correlation between them, so one sample type cannot stand in for anotherHH-32117; combined dietary exposure to BPA and its analogues can exceed safety thresholds even as BPA itself fallsHH-31143.

  • Cadmium (blood and urine) and speciated urine arsenic

    The two heavy metals this site has no entry for. Cadmium concentrates in the kidney and its urine level reflects cumulative burden; lower zinc and iron tracked with higher cadmium across 44 studiesHH-39120. Arsenic needs a speciated test that separates the toxic inorganic form from the harmless organic form in seafood; nutrients that raised antioxidant enzymes reduced its toxicity in human studiesHH-37889. Heavy-Metals.md records the mainstream position that provoked (post-chelation) urine testing is not validated; the unprovoked blood or urine test against a standard reference is the accepted approach.

  • Urinary iodine, perchlorate, bromide and fluoride

    The halogen set. Urinary iodine has the one sourced band on this page (lowest thyroid dysfunction near 100 to 200 micrograms per liter in the five-year Chinese cohort)HH-2449; the other three have no reference interval on this site and are named because the thyroid literature above says they compete.

Source: Labs/Panels/Environmental-Toxin-Panel.md (six categories), Labs/Toxicity/Heavy-Metals.md, Labs/Toxicity/Glyphosate.md, Labs/Toxicity/Mold-Mycotoxins.md, under Labs/Toxicity/DETOX-CLAIMS-POSITION.md; the halogen rows from wave-iodine-halogens-20260910 and the exposure wave of 2026-09-07. Every chip is a row of the library, approved, with the paper's own title on hover; a count is attention in this library, never a verdict.

The markers, and what they actually tell you

Each marker below carries its technical name, what it measures in plain language, the limits of what it can tell you, and the nutrients known to move it. Where a framework and mainstream practice disagree, both views are shown rather than one being hidden.

Toxic Elements & Halogens (the overlooked half)

Whether something is occupying the seat a nutrient was meant to sit in. This is a tier-one entry not because everyone needs a full toxic-element workup, but because almost nobody is offered one at all -- and a standard panel is silent on it. Deficiency gets investigated. The other half of the equation usually does not.

Typical range: There is no single number here. Blood lead and mercury reflect recent exposure rather than what is stored in tissue; a normal blood level does not rule out a body burden accumulated over years. Aluminium and glyphosate are not on any standard panel at all. That absence is the point of this entry -- it is a gap in the usual workup, not a result.

Nutrients that move it

  • Displacement is chemistry, not a hypothesissolid -- Elements that sit near each other on the periodic table share charge and size, and transport proteins select on charge and size. So the wrong element gets carried through the right door. This is established biochemistry with named machinery, not an association waiting for a trial. The sodium-iodide symporter is the thyroid's iodine door, and perchlorate, thiocyanate, nitrate and fluoride all compete at it (source: PMC6466022). DMT1, the divalent metal transporter, carries iron -- and also manganese, cadmium, cobalt and lead, because they present to it the same way (source: PMID 22736759). Metallothionein binds zinc and copper, and cadmium binds it harder and displaces them (source: PMC5486060, PMID 21462106).
  • Being deficient makes you absorb more of the wrong thingsolid -- This is the part that joins the two halves of the model. DMT1 is upregulated when iron is low -- the body opens the door wider because it needs iron (source: PMID 25753988) -- and the same widened door admits lead and cadmium. So deficiency does not merely sit alongside toxicity; it actively increases uptake of it. Sufficiency is therefore the first line of defence: iodine against the halogen group, and adequate iron, zinc, calcium and selenium across the metals.
  • Where to look if you suspect itemerging -- If exposure is plausible -- older housing, occupational contact, well water, heavy fish intake, dental history, agricultural proximity -- the honest move is to look at the whole set rather than one element, because they arrive together and compete together. Tier 3 on this page carries lead, mercury, aluminium and PFAS individually. Tissue-level elemental screening measures the whole panel at once rather than one at a time.

Food first: The protective pattern is unglamorous and consistent: sufficient minerals so there is no vacancy to fill, adequate protein for the conjugation pathways, sulphur-bearing vegetables such as brassicas, garlic and onions, and enough fibre to carry conjugated compounds out rather than allowing reabsorption. Iodine sufficiency specifically, because the halogen competition is at a single named door. Filtered water, and reducing the intake side wherever it is identifiable.

Read the studies on Toxic Elements & Halogens (the overlooked half)

Lead

The level of a toxic heavy metal with no known safe or beneficial level in the body, accumulating in bone and affecting the brain, kidneys, and cardiovascular system with chronic exposure.

Typical range: Standard: under 3.5 mcg/dL is the current CDC reference/action level for adults -- there is no optimal nonzero level; lower is always better.

Nutrients that move it

  • Calcium -- Competes with lead for absorption in the gut and for storage sites in bone; a randomized placebo-controlled trial in pregnant women found calcium supplementation reduced blood lead levels by about 11% compared to placebo.
  • Iron -- Iron deficiency increases intestinal lead absorption (the gut appears to substitute lead for iron when iron is scarce); iron repletion in iron-deficient individuals modestly lowers blood lead.
  • Vitamin C -- Observational data associates adequate vitamin C status with lower lead absorption, though dedicated high-quality RCT evidence is thinner than for calcium/iron.
  • Zinc -- Observational data associates adequate zinc status with lower lead absorption, though dedicated high-quality RCT evidence is thinner than for calcium/iron.

Food first: Ensure adequate dietary calcium, iron, and vitamin C, especially in children and pregnant women (the highest-risk groups for lead's neurodevelopmental effects).

When to see someone: Nutritional strategies reduce absorption of *ongoing* low-level exposure -- they do not treat significant lead toxicity, which requires medical evaluation and, in some cases, chelation therapy. Any meaningfully elevated lead level needs a source investigation, not just a supplement response.

Read the studies on Lead

Mercury

The level of a toxic heavy metal, most commonly elevated in adults from eating fish/seafood higher on the food chain.

Typical range: Standard: under 10 mcg/L (whole blood) is a commonly used general-population reference, though this varies by lab and by whether inorganic vs. methylmercury is being measured; there is no optimal nonzero level.

Nutrients that move it

  • Selenium -- Binds mercury (forming inert mercury selenide) and is a cofactor for antioxidant enzymes that counter mercury's oxidative damage; animal and cell studies show a clear protective relationship, but robust human RCT evidence that selenium supplementation reverses mercury toxicity in people is still limited.

Food first: Choose lower-mercury fish (salmon, sardines, shrimp, cod) over high-mercury species (swordfish, king mackerel, shark, bigeye tuna) to get omega-3 benefits without excess mercury load; adequate selenium intake is theoretically protective but shouldn't be a reason to eat high-mercury fish liberally.

When to see someone: Elevated mercury in pregnant women or young children warrants dietary source investigation and possibly medical guidance given fetal/childhood neurodevelopmental sensitivity; don't rely on selenium supplementation as a way to "offset" ongoing high-mercury fish consumption.

Read the studies on Mercury

Aluminum

Serum aluminum is the standard test, and what it means depends almost entirely on kidney function. With normal kidneys the body clears aluminum efficiently, so serum levels are usually low and not very informative about tissue burden. Urine aluminum reflects recent exposure and excretion capacity and is used in research protocols.

Typical range: There is no meaningful optimal level -- aluminum has no biological role. The marker becomes genuinely actionable in one specific population: people with impaired kidney function, especially dialysis patients, where aluminum is renally cleared and dialysis does not remove it efficiently. Periodic monitoring is standard of care there.

Nutrients that move it

  • Silicic acid (silicon-rich mineral water)emerging -- Silicon appears to reduce aluminum's bioavailability and promote urinary excretion, probably by forming a complex the body does not absorb. A 12-week pilot gave 15 Alzheimer's patients 1 litre a day of silicon-rich water; urinary aluminum excretion rose without affecting iron or copper, and body burden fell. It was small, uncontrolled and unblinded, and the authors framed it as a preliminary test of a hypothesis -- not a treatment.
  • Magnesiumcontested -- Magnesium and aluminum compete for some of the same intestinal transport sites, so adequate magnesium is sometimes proposed to reduce absorption. That is plausible chemistry and it is not backed by a dedicated human aluminum-reduction trial.
  • Adequate hydrationsolid -- The kidney is the main clearance route for absorbed aluminum, so anything supporting normal renal function supports clearance. This is normal physiology working as intended rather than a targeted intervention.

Food first: Silicon-rich mineral water, adequate magnesium, and enough fluid to support normal kidney function.

Read the studies on Aluminum

PFAS (per- and polyfluoroalkyl substances)

A serum or plasma panel that sums seven to nine individually measurable PFAS compounds -- PFOA, PFOS, PFHxS, PFNA, PFDA, PFUnDA and MeFOSAA -- rather than reporting "PFAS" as one number. There are thousands of these chemicals and only a handful can be measured and interpreted reliably. They are called forever chemicals because the carbon-fluorine bond barely breaks down, so they persist in the body for years.

Typical range: The National Academies (NASEM, 2022) published numeric action tiers, which is unusual for a toxin panel: under 2 ng/mL summed is usual standard of care; 2 to under 20 ng/mL means counselling on exposure reduction plus screening for dyslipidemia and pregnancy hypertension; 20 ng/mL and above adds thyroid testing, and kidney assessment over 45.

Nutrients that move it

  • Dietary fiberemerging -- An NHANES analysis of 6,482 adults found higher fiber intake associated with lower serum PFAS, plausibly because fiber binds bile acids and interrupts the recirculation that keeps PFAS in the body. This is a cross-sectional association, not a trial showing that adding fiber lowers an individual's level -- but it is low-risk and healthy regardless.
  • Blood or plasma donationsolid -- The strongest evidence of anything tried. A randomized trial of 285 Australian firefighters found plasma donation every 6 weeks lowered mean serum PFOS by 2.9 ng/mL versus 1.1 for whole-blood donation, still present 3 months after the trial. It works by physically removing the blood proteins PFAS binds to -- it is direct removal, not a detox mechanism.
  • Filtered drinking watersolid -- Activated carbon and reverse osmosis remove PFAS from water at the tap. This prevents FUTURE accumulation and does not lower what is already in the blood -- which makes it the most reliable lever available, and a different job from reducing existing burden.

Food first: Fiber-rich whole foods, filtered drinking water, and reduced exposure at source -- PFAS-free cookware and food packaging where practical, and care with fish from known-contaminated waters.

When to see someone: Any product marketed as a PFAS detox should be treated skeptically -- the evidence-backed list is short: donation, prescription bile-acid binders under supervision, dietary fiber, and removing the exposure source.

Read the studies on PFAS (per- and polyfluoroalkyl substances)

Whole-Blood / Hair Mineral Analysis (HTMA)

Cellular Six: Transform

This marker sits in Transform -- the cofactors enzymes need to turn fuel into usable energy.

Hair tissue mineral analysis (HTMA) measures mineral and trace-element concentrations in a hair sample, marketed as a window into longer-term tissue mineral status; the functional model sometimes references whole-blood or hair testing as a supplementary way to assess mineral patterns beyond a standard serum panel.

Typical range: No standardized reference ranges exist across labs; each commercial HTMA lab uses its own ranges and often its own proprietary "ratio" interpretive system.

How it is used clinically

HTMA's reliability is genuinely contested even outside the functional model specifically. **[CONTESTED]** A landmark study sent split samples from a single healthy volunteer to six US commercial hair-testing labs and found more than 10-fold differences in reported concentrations for 12 different minerals between labs. (cite: JAMA, 2001, PMID 11150111) More recent work confirms that intra- and inter-laboratory reliability for HTMA remains inconsistent and heavily dependent on which lab and methodology is used, and correlation between hair mineral levels and actual serum/tissue status is weak to moderate for most minerals (hair zinc versus serum zinc correlates only weakly, for example). (cite: PMC3582931) HTMA is on firmer ground for detecting toxic heavy metals (lead, mercury, cadmium, arsenic), where peer-reviewed and CDC/ATSDR biomonitoring methods have more established validity -- but using it to diagnose "metabolic types," mineral-ratio-based disease patterns, or to guide the functional model's specific mineral-dosing decisions is not supported by controlled clinical evidence.

What this framework claims

HTMA and mineral-ratio analysis are used by some the functional model-adjacent practitioners to infer "oxidation type," adrenal/thyroid patterns, and mineral dysregulation not visible on standard blood work.

Food first: N/A.

When to see someone: Don't make major supplementation decisions (especially involving iron, copper, or high-dose minerals) based solely on an HTMA result -- confirm with standard serum/blood testing, since HTMA's inter-lab reliability for general mineral status is weak.

Read the studies on Whole-Blood / Hair Mineral Analysis (HTMA)

What moves it

The levers the library records for this panel, positive and null findings side by side. Nothing here treats, prevents or reverses anything.

  • Reduce the exposure first

    The brain's own guide puts source reduction before anything else: filtered water, organic where glyphosate is the question, glass and steel over plastic, ventilation, fragrance-free products, a mold inspection where there was water damage. Waiting over a year after a renovation lowered indoor VOC exposureHH-28022; an organic-grocery week is the trial design that tests the glyphosate questionHH-27251.

  • Give the body's own pathways what they are built from

    The strongest claim in Labs/Toxicity/DETOX-CLAIMS-POSITION.md, measured against the library: glutathione, N-acetylcysteine, sulforaphane, adequate protein and fiber, hydration. In human arsenic exposure, vitamins, tea, glutathione, N-acetylcysteine and zinc reduced toxicity by raising antioxidant enzymesHH-37889; selenium with vitamin E in metal-exposed workers tracked with lower blood metalsHH-442780; folate shifted arsenic toward its methylated form in a humanized mouse modelHH-126266.

  • Mineral sufficiency closes the seat

    Lower zinc and iron, higher cadmiumHH-39120; the Heavy-Metals guide records the same for lead, where iron deficiency raises intestinal lead absorption. A full mineral panel is the exposure panel's other half, which is why the toxic-element entry on this site is tier one.

  • Sweat and movement, said exactly

    Sweat is a measured excretion route for several metals, a small human literature; movement supports circulation, lymph and the sweat that carries them. The position file is explicit that neither clears a body burden, and this site does not say they do.

What no one orders

The markers in this panel a standard visit rarely includes, and why each one changes what the rest of the panel means.

  • Urine glyphosate and AMPA

    Found in 99.8 percent of U.S. biomonitoring samples and on no standard panelHH-190256.

  • Urinary iodine with perchlorate, bromide and fluoride

    The halogen competition the thyroid literature describes; urinary iodine has a sourced band, the other three have none hereHH-2449HH-192176.

  • Cadmium and speciated arsenic

    The two metals this site has no entry for; lower zinc and iron tracked with higher cadmium across 44 studiesHH-39120; speciation keeps seafood arsenic from reading as toxicHH-37889.

A named door over markers the Library already holds. Other doors: Anemia, Liver, Neuro.

The network

What moves together in this panel

Every marker is a node in a network: it depends on cofactors, it is raised by some things and lowered by others, and it moves other markers in turn. Below, the Environmental Toxins markers the citation graph has reached, and the edges between them in this library. Open any marker on My Panel for its whole network.

The graph holds edges on 4 of these 6 markers; it has not reached Aluminum, Hair / Whole-Blood Mineral Analysis (whole test) yet.

  • Toxic Elements & Halogens screen (whole test) · 53 relationships in the graph, 50 of them rest on one study.
  • Lead · 24 relationships in the graph, 22 of them rest on one study.
  • Mercury · 18 relationships in the graph, 17 of them rest on one study.
  • PFAS (total or by compound) · 57 relationships in the graph, 52 of them rest on one study.

Edges between these markers

  • Mercury and Toxic Elements & Halogens screen (whole test) · 3 shared studiesHH-38352HH-38817HH-38818
  • Lead and Mercury · one shared studyHH-255215
  • Lead and Toxic Elements & Halogens screen (whole test) · one shared studyHH-26656

Counts are the number of approved studies in this library that recorded a claim, under the alias map the generator documents; a count is attention, not a verdict, and a pair on one study is a reading to check. The graph grows as the edge readers run.

The cofactors

What your Environmental Toxins panel leaves out

The standard numbers are only half of how a marker moves. The other half is its cofactors: the nutrients the body needs to make it, use it or clear it. A routine blood count, metabolic panel, lipid panel and TSH do not measure them. These are the tests that would, for the markers on this page.

  • Copper and ceruloplasmin · for copper, tied to Toxic Elements & Halogens screen, Mercury, Aluminum · listed on How to get measured (Walk-In Lab)
  • Ferritin and iron studies · for iron, tied to Toxic Elements & Halogens screen, Lead, Aluminum · listed on How to get measured (Labcorp OnDemand, Quest (questhealth.com), Walk-In Lab)
  • Magnesium (red-cell) · for magnesium, tied to Aluminum · listed on How to get measured (Labcorp OnDemand, Walk-In Lab)
  • Omega-3 Index · for omega-3 fats (epa, dha), tied to Mercury · ask for it by name; no direct-access page was read for it. See How to get measured.
  • Selenium · for selenium, tied to Toxic Elements & Halogens screen, Mercury · ask for it by name; no direct-access page was read for it. See How to get measured.
  • Zinc · for zinc, tied to Toxic Elements & Halogens screen, Lead, Mercury, Aluminum · listed on How to get measured (Walk-In Lab)

Derived from the cofactor rows in the library (a nutrient is listed when a study edge or at least 50 studies tie it to a marker here). Ordering links are lab testing only; ask your clinician what fits you.

How to get measured

The Environmental Toxins markers as a direct-access order in three sizes. Each card names what it covers, what it still misses, and the provider tests that carry it, with the price read on the provider's page and the date it was read.

Good is the minimum set, Better the fuller set, Best the most complete set this page can point at. The tiers are about coverage, not about which number matters most for you.

Good (the minimum set)

Blood lead and blood mercury

The two metals with a cheap single test and an entry on this site.

Covers: Lead · Mercury

Misses: No arsenic or cadmium, no aluminum, no PFAS, nothing in urine or hair.

Better (the fuller set)

The four-metal blood profile

Arsenic, cadmium, lead and mercury in one draw.

Covers: Toxic Elements & Halogens (the overlooked half) · Lead · Mercury

Misses: No aluminum, no PFAS, no halogens, no glyphosate.

Best (the most complete set)

Add the hair toxic and essential elements kit

43 elements in hair, aluminum among the 23 potentially toxic ones, read beside the blood values and never alone.

Covers: Aluminum · Whole-Blood / Hair Mineral Analysis (HTMA)

Misses: PFAS, urine glyphosate and AMPA, urinary iodine, perchlorate, bromide and fluoride: no direct-access page was read for any of them. Ask by name; several are specialty-laboratory tests.

What no one orders, and where it is ordered

  • Urine glyphosate and AMPA

    No direct-access provider on this page lists it. Ask for it by name; it may be a specialty-laboratory or clinic-ordered test.

  • Urinary iodine with perchlorate, bromide and fluoride

    No direct-access provider on this page lists it. Ask for it by name; it may be a specialty-laboratory or clinic-ordered test.

  • Cadmium and speciated arsenic

Which states

State law limits direct-access testing in some states (New York, New Jersey and Rhode Island are named by most providers; Hawaii, Arizona, Maryland and Massachusetts by some). Each provider's own line is quoted below, and the checkout is where it is enforced.

  • Walk-In Lab: Walk-In Lab's FAQ: not offered through Labcorp in NY, NJ, RI, MD and MA, and not through the other national lab network in AZ, NY, NJ and RI (paraphrased; the FAQ names both labs). source · +$6.00 per order physician fee, shown on every product page.
  • Labcorp OnDemand: "Available in all 50 states" to consumers 18 or older, on Labcorp's own page. source · No separate order fee was shown on the pages read.
  • A direct-access order is a lab test without a visit: the provider supplies the order, you are drawn at a Labcorp or Quest patient centre or collect at home, and the results go to you.
  • The Lab Atlas never sees a result unless you enter it yourself. Nothing here is sent to a provider and nothing comes back.
  • A result outside the interval is a conversation with a clinician, not a verdict. The panel pages say what each marker measures and what it cannot; this page only says where to get the number.
  • Every price was read on the provider's page on the date shown and carries its link. Prices move; the date is part of the number. Per-order fees are listed by provider and sit on top.

Every provider, every verified price and the map for every panel: How to get measured.

Food first, then fill the gaps

Every marker above lists the nutrients known to move it. Build a day around them first -- the Diet Builder shows which food groups you are consistently missing, inside the way you already eat.