The Toxin Test · Analyte Review
The complete panel
Seventy-seven
analytes,
explained
A plain-language guide to everything the DetoxU Toxin Test looks for — what each one is, where you meet it, what it does in the body, and why it earned a place on the panel.
77 analytes in 8 groups · tap a segment to filter
The panel
Metals & trace elements 18
Elements never break down. The body can’t destroy them — only store them, bind them, or clear them. That one fact shapes how every metals result is read.
Mycotoxins 30
Chemicals that molds make, not the mold itself. They outlast the organism, survive cooking, and reach most of us through food far more often than through a damp building.
Plastic-related compounds 4
The compounds most people mean by ‘endocrine disruptor’. Short-lived, found in nearly everyone, and more about when you were exposed than how much.
Parabens 4
Preservatives with a long safety record for acute toxicity and a weak estrogen-like activity — applied to skin, daily, for decades. Potency rises with chain length.
Pesticides & herbicides 8
Weed and insect killers, and the breakdown products your body makes from them. Detection usually means contact with a class of chemical, not a measured dose of the parent.
Solvent & VOC markers 9
Volatile chemicals leave the body within hours, so we measure what your body made of them. These reflect roughly the last one to two days — a snapshot, not a burden.
Industrial compounds 3
Three chemicals — from detergents, antimicrobials and flame retardants — that behave differently enough to sit on their own.
Organic acid marker 1
One analyte that isn’t a toxin at all: a marker of how your metabolism is coping.
Nothing on the panel matches . Try a source — coffee, receipts, well water, nail polish — or an analyte name.
Short codes are DetoxU panel abbreviations for quick reference, not official chemical nomenclature. * Available on request rather than reported by default.
Before you read a result
Detected is not the same as harmful
A surprising number of these — BPA, methylparaben, vomitoxin — turn up in nearly everyone surveyed. What matters is where your number sits against everyone else’s, and whether it moves when you change something.
The specimen decides what a number means
Urine shows what your body is clearing now. It says little about what’s stored in bone or brain, and for a few analytes — lead and beryllium among them — a different test is the clinical standard. We say so on each entry.
Timing is everything for the fast ones
Solvent, phthalate and paraben markers reflect the last day or two. A weekend of painting, a new perfume, a hospital stay: all of it shows. Note what you did the day before you collect, and read those markers as a snapshot.
A number can’t tell you where it came from
Ochratoxin from breakfast and ochratoxin from a damp wall look identical in urine. A result is a prompt to look at your food, water and home together — not a verdict on any one of them.
The Toxin Test
One specimen.
All seventy-seven.
Everything on this page is measured from a single at-home urine collection and reported back in the same plain language — what was found, how much, and how to read it. If a result raises a question this page doesn’t answer, write to us.
Questions and corrections welcome
Reference · all 77
Al AluminumMetals
Aluminum
Abundant, poorly absorbed, and the subject of a forty-year argument that isn’t over.
- What urine shows
- What’s being cleared now. Recent antacid use can dominate the number.
- Main sources
- Antacids and buffered aspirin above all; cookware and foil; antiperspirants; some food additives; treated drinking water; welding and smelting dust.
- The evidence
- Toxicity in kidney failure is established. The everyday link to Alzheimer’s is contested, with careful studies on both sides.
What it is
The most abundant metal in the earth’s crust, and one living systems never found a use for. There is no known biological role for aluminum in humans.
Where you meet it
Cookware and foil, antiperspirants, antacids and buffered aspirin, additives in processed cheese and baking powder, vaccine adjuvants, drinking water treated with aluminum sulfate, and industrial dust from smelting and welding. Regular antacid users swallow far more aluminum than drinking water ever contributes.
What it does in the body
Very little of what you swallow is absorbed — that’s the body’s main defense. What does get in binds a transport protein in the blood and tends to settle in the brain’s frontal cortex and hippocampus, and it interferes with how bone handles calcium and phosphate. The kidneys are the only meaningful exit, so when kidney function falls, the safety margin collapses.
Why it’s on the panel
Because exposure is nearly universal and almost entirely modifiable, and because the question people most want answered — does it matter? — deserves a real number rather than a slogan. The clearest human harm is in dialysis patients, where contaminated dialysate caused brain and bone disease. The everyday link to Alzheimer’s is unresolved: some drinking-water studies show an association, the largest prospective study found none overall, and a 2025 meta-analysis found aluminum accumulating in the hippocampus alongside amyloid changes. We present it as a live disagreement, because it is one.
Food & drinkHome & personal careMedicines & medicalWork & industry
Sb AntimonyMetals
Antimony
Arsenic’s chemical cousin, and the reason a warm bottle of water is worth asking about.
- What urine shows
- Recent exposure — days, not months.
- Main sources
- PET plastic bottles, especially stored warm or long; flame-retarded textiles and furnishings; metalwork and brake dust.
- The evidence
- Leaching from PET is well documented. Chronic low-dose effects in people are less clear. Antimony trioxide is IARC Group 2B — possibly carcinogenic.
What it is
A metalloid that sits next to arsenic on the periodic table and behaves like it. The trivalent form is considerably more toxic than the pentavalent.
Where you meet it
Antimony trioxide is the standard catalyst for making PET, the plastic in most water and soda bottles, and a flame-retardant helper in textiles and foam. It leaches from PET into water and juice, and the amount rises the longer and warmer the bottle sits. Brake pads, solder, ammunition and pigments add occupational exposure, and some antimony-based drugs treat parasitic infection.
What it does in the body
Trivalent antimony binds sulfur groups on proteins, disrupting enzymes that depend on them and taxing glutathione, the body’s main detox buffer. The heart is a target organ — which is why antimony drugs are given with heart monitoring. Breathing the dust irritates the airways and, over years, the lungs.
Why it’s on the panel
A persistently raised antimony in someone who doesn’t work with metal almost always points at a domestic habit — a case of bottled water stored in a hot car, a new flame-retarded mattress — and those are things you can change.
WaterHome & personal careWork & industryMedicines & medical
As ArsenicMetals
Arsenic
The most common false alarm on a metals panel — and one of the most important toxins in the world.
- What urine shows
- What’s being cleared now. A seafood meal can raise total arsenic for several days.
- Main sources
- Groundwater and private wells; rice and rice products; seafood (mostly a harmless organic form); older pressure-treated lumber.
- The evidence
- Very strong. Inorganic arsenic is a confirmed human carcinogen (IARC Group 1).
What it is
A metalloid whose inorganic forms are classified as carcinogenic to humans, and — counted by the number of people exposed — arguably the most important environmental toxicant on earth.
Where you meet it
Groundwater and private wells are the big one. Rice concentrates arsenic because flooded paddies mobilize it, and rice-based products carry it into infant foods. Seafood is dominated by arsenobetaine, an organic form the body excretes unchanged and that is essentially non-toxic; shellfish and seaweed carry proportionally more of the inorganic and sugar-bound forms. Older pressure-treated wood, historical pesticides and coal smoke round it out.
What it does in the body
The body converts inorganic arsenic into methylated forms for excretion, and makes reactive intermediates along the way. Long-term exposure is linked to skin changes, nerve damage, blood-vessel disease, diabetes and cancers of the skin, bladder, lung, liver and kidney. Newer work suggests some seafood arsenic compounds are also converted to those intermediates, so the old clean line between ‘toxic inorganic’ and ‘harmless organic’ is less absolute than it was taught.
Why it’s on the panel
Because well water isn’t routinely tested for it, and because a total-arsenic number without context is the best-documented misread on any panel. In one study, volunteers asked to avoid seafood for four days still had nearly half their urinary arsenic coming from fish — sometimes almost all of it.
WaterFood & drink
Ba BariumMetals
Barium
Two substances under one name, separated entirely by solubility.
- What urine shows
- Recent exposure.
- Main sources
- Groundwater near natural deposits or drilling; welding, brick and ceramic work; pigments and fireworks; a recent barium contrast scan.
- The evidence
- Acute poisoning is well described; chronic low-level effects in people are less studied.
What it is
An alkaline earth metal whose danger depends entirely on whether it dissolves. Barium sulfate is so insoluble it’s swallowed by the cupful as X-ray contrast. Soluble barium salts are another matter.
Where you meet it
Oil and gas drilling fluids, welding, brick and ceramic manufacture, pigments and fireworks, and groundwater near natural deposits or active drilling.
What it does in the body
Soluble barium blocks potassium channels, pushing potassium out of the bloodstream and into cells. The result is muscle weakness that can progress to paralysis and heart-rhythm problems — a redistribution of potassium rather than a true shortage.
Why it’s on the panel
A raised barium near active drilling is best read as a water-quality signal. It’s one of the analytes where the source is often a single well or a single job site.
WaterWork & industryMedicines & medical
Be BerylliumMetals
Beryllium
One of the few occupational diseases that’s genuinely written into your genes.
- What urine shows
- Exposure only. A level says nothing about whether the immune system has reacted.
- Main sources
- Aerospace and defense alloys, electronics, dental alloys, nuclear work, coal combustion. Almost entirely occupational.
- The evidence
- Strong. A confirmed human carcinogen (IARC Group 1); the genetics of sensitization are well replicated.
What it is
A light, extraordinarily strong metal, classified as carcinogenic to humans, and the cause of a lung disease that only some exposed people ever develop — largely depending on a single immune gene.
Where you meet it
Aerospace and defense alloys, electronics and semiconductor manufacture, dental alloys, nuclear applications and coal combustion. If you don’t work in one of those, exposure is unusual.
What it does in the body
In susceptible people the immune system treats beryllium as an antigen. Carriers of one variant of the HLA-DPB1 gene are several times more likely to develop chronic beryllium disease, a granulomatous attack on the lung that looks — on scans and under the microscope — almost exactly like sarcoidosis. Not everyone who becomes sensitized progresses to disease.
Why it’s on the panel
A urine level tells you about exposure, and that’s useful in itself. It can’t tell you whether you’re sensitized: that’s a separate blood test, the beryllium lymphocyte proliferation test, and it’s the one that matters clinically.
Work & industry
Bi BismuthMetals
Bismuth
Usually a medication history you haven’t given yet.
- What urine shows
- Recent exposure; clears over days.
- Main sources
- Over-the-counter stomach remedies containing bismuth subsalicylate; H. pylori therapy; pearlescent cosmetics.
- The evidence
- Toxicity is well described at sustained high doses; ordinary use is considered low-risk.
What it is
A heavy metal with an unusually benign reputation — often called the least toxic of the heavy metals — that is mostly, but not entirely, deserved.
Where you meet it
Almost always pharmaceutical. Bismuth subsalicylate is the active ingredient in common pink stomach remedies, and bismuth compounds are part of standard therapy for Helicobacter pylori. Cosmetics use bismuth oxychloride for a pearlescent finish.
What it does in the body
Absorption is poor and most of an oral dose passes straight through. What does get in goes to the kidney and, at high exposure, the brain. Sustained heavy use has caused a distinctive, reversible confusion-and-tremor syndrome, and kidney injury is the other concern.
Why it’s on the panel
Because people rarely think of an over-the-counter stomach remedy as a drug, and a surprising bismuth result is usually explained in one question.
Medicines & medicalHome & personal care
Cd CadmiumMetals
Cadmium
A half-life in the kidney measured in decades. The definition of a cumulative toxicant.
- What urine shows
- Accumulated kidney burden — one of the few urine results that reflects a lifetime, not a week.
- Main sources
- Tobacco smoke and diet above all; nickel-cadmium batteries, pigments, electroplating and metal recycling at work.
- The evidence
- Very strong. A confirmed human carcinogen (IARC Group 1); the kidney dose-response has been documented since the 1970s.
What it is
A confirmed human carcinogen with a biological half-life in the kidney of more than 25 years. Once it’s in, it stays.
Where you meet it
For most people, food and tobacco smoke. Crops take cadmium up from soil readily, so grains, leafy vegetables and shellfish are steady low-level sources, and smoking adds substantially on top. Nickel-cadmium batteries, pigments, electroplating and metal recycling supply the occupational exposure.
What it does in the body
In blood, cadmium rides on small proteins that get filtered by the kidney and then reabsorbed by the tubules — which is how it accumulates there. Over years it damages the tubules, causing a slow decline in filtration and leakage of small proteins into urine. It also disrupts calcium and vitamin D handling, weakening bone. Iron deficiency increases absorption, because cadmium uses the same transporter.
Why it’s on the panel
Because urine cadmium is one of the most meaningful numbers on the whole panel: it reflects decades of accumulated kidney burden rather than last week’s meals, and the two biggest levers — smoking and iron status — are both changeable.
Smoke, fuel & trafficFood & drinkWork & industry
Gd GadoliniumMetals
Gadolinium
Deposition is proven. The symptom story is not. Both are true at once.
- What urine shows
- Depends on when you last had contrast — days to months, longer with older linear agents.
- Main sources
- MRI contrast agents, essentially exclusively.
- The evidence
- Deposition in brain, bone and skin is established; the serious disease NSF is established in kidney failure. Symptoms in people with normal kidneys are contested.
What it is
A rare-earth metal with no biological role, injected on purpose as MRI contrast. Free gadolinium is toxic, so contrast agents cage it in a chelate until the kidneys clear it.
Where you meet it
MRI contrast, and essentially nothing else. Gadolinium-based agents have been in clinical use since 1988; older ‘linear’ agents deposit more than newer ‘macrocyclic’ ones.
What it does in the body
The established harm is nephrogenic systemic fibrosis, a rare and serious hardening of skin and organs seen in patients with severe kidney disease — now very rare thanks to screening. Separately, small amounts of gadolinium are known to deposit in brain, bone and skin even in people with normal kidneys, across every class of agent. Whether that deposition causes symptoms is the open question: some researchers describe a ‘gadolinium deposition disease’; radiology bodies use a more neutral label and note that no adverse effects have been established.
Why it’s on the panel
Because millions of people have had contrast MRIs, and many arrive either certain it harmed them or certain it couldn’t have. Neither position matches the evidence. A measured level, with the date of your last scan, is more useful than either.
Medicines & medical
Pb LeadMetals
Lead
Every time researchers look at a lower exposure level, they find effects.
- What urine shows
- What’s being cleared now. Blood lead is the standard for assessing exposure; most of the body’s lead sits in bone.
- Main sources
- Pre-1978 paint and its dust; lead pipes and solder; imported spices, ceramics, cosmetics and remedies; ammunition and shooting ranges; radiator, battery and stained-glass work.
- The evidence
- The most thoroughly studied environmental toxicant in history. Effects on children’s brains are documented at levels once considered safe.
What it is
The most studied environmental toxin in human history, and the one where every look at a lower exposure has found effects. Harm to young children’s developing brains is documented below levels that were once called safe.
Where you meet it
Dust from paint applied before 1978, lead service lines and old solder, imported spices, glazed ceramics, traditional cosmetics and remedies, ammunition and shooting ranges, and hobby or trade work with radiators, batteries and stained glass.
What it does in the body
Lead mimics calcium and zinc and slips into the systems that use them. Around 90 to 95 percent of an adult’s lead is stored in bone, where it lingers for decades; blood lead falls within weeks of an exposure ending, then declines slowly for years as bone releases it. Pregnancy and breastfeeding accelerate that release and pass lead to the baby, which is why calcium intake matters so much then. Iron deficiency increases absorption.
Why it’s on the panel
Because the sources are old, ordinary and fixable, and because no level of lead has been shown to be harmless.
Home & personal careWaterWork & industryFood & drink
Hg MercuryMetals
Mercury
Three different toxins under one name. Mixing them up is the commonest mistake.
- What urine shows
- Urine mostly reflects vapor and inorganic exposure; methylmercury from fish is better read in blood or hair.
- Main sources
- Predatory fish (methylmercury); dental amalgam and broken bulbs or thermometers (vapor); some skin-lightening creams and traditional remedies (inorganic salts).
- The evidence
- Strong across all three forms. Genetic differences in how people handle mercury are increasingly well documented.
What it is
Three toxicologically different substances that share a name: methylmercury from fish, elemental mercury vapor, and inorganic mercury salts. They enter, travel and harm differently.
Where you meet it
Methylmercury comes almost entirely from seafood, especially large predatory fish. Elemental vapor comes from dental amalgam, broken thermometers and fluorescent bulbs, and artisanal gold mining. Inorganic salts turn up in some skin-lightening creams and traditional remedies.
What it does in the body
Methylmercury and mercury vapor both cross into the brain and across the placenta; inorganic mercury does not. Vapor targets brain and kidney, inorganic compounds the kidney. Your genes matter more than most people realise: variation in glutathione, selenium and transport pathways means two people with identical intake can carry measurably different levels.
Why it’s on the panel
Because the fix depends on the form. A fish-eater and a person with a mouthful of old amalgam need different conversations, and the number alone doesn’t say which you are.
Food & drinkMedicines & medicalWork & industryHome & personal care
Pd PalladiumMetals
Palladium
Low systemic toxicity. The real issue is allergy.
- What urine shows
- Recent exposure.
- Main sources
- Dental alloys — crowns, bridges and partial dentures; white-gold jewelry; catalytic-converter dust near roads.
- The evidence
- Contact allergy and its cross-reaction with nickel are well described; systemic effects at environmental levels are low.
What it is
A platinum-group metal, increasingly common in the environment, and a meaningful contact allergen — especially in people already sensitive to nickel.
Where you meet it
Dental alloys are the major direct exposure: crowns, bridges and partial dentures. White-gold jewelry and electronics contribute, and catalytic converters have put palladium into roadside dust.
What it does in the body
Systemic toxicity from everyday exposure is low. The concern is sensitization: palladium cross-reacts strongly with nickel, so nickel-allergic people are often palladium-allergic too. In the mouth that shows up as lichen-like patches, burning, or inflamed tissue next to a metal restoration.
Why it’s on the panel
Because a raised palladium alongside unexplained mouth soreness and a set of metal dental work is a pattern worth acting on, and it’s easy to miss without the number.
Medicines & medicalHome & personal care
Pt PlatinumMetals
Platinum
Inert as a metal. Potently sensitizing as a salt.
- What urine shows
- Recent exposure — except after chemotherapy, where platinum persists for years.
- Main sources
- Platinum-based chemotherapy; refinery and catalyst work; jewelry; roadside dust.
- The evidence
- Occupational sensitization and chemotherapy toxicity are well established.
What it is
A noble metal — chemically unreactive as metal, and a potent sensitizer and cell poison in certain soluble complexes.
Where you meet it
Catalytic converters and roadside dust, jewelry, laboratory and industrial catalysis, and platinum-based chemotherapy such as cisplatin, carboplatin and oxaliplatin.
What it does in the body
Soluble platinum salts are among the most potent respiratory sensitizers known, causing asthma and rhinitis in refinery workers. Platinum chemotherapy works by cross-linking DNA; its toxic side is kidney damage, hearing loss and nerve damage, and platinum stays in the body for years after treatment ends.
Why it’s on the panel
Because in someone who has had platinum chemotherapy, a raised level is expected rather than alarming — and may be relevant to lingering neuropathy or hearing loss. In anyone else it points to a workplace.
Medicines & medicalWork & industry
Te TelluriumMetals
Tellurium
Rare, occupational, and betrayed by the breath.
- What urine shows
- Recent exposure, though the garlic odor can persist for months.
- Main sources
- Metallurgy, solar-panel manufacture, rubber vulcanization, thermoelectric devices.
- The evidence
- The clinical picture is well described; human data are limited because exposure is rare.
What it is
A rare metalloid related to selenium, and the source of one of toxicology’s more memorable clinical signs.
Where you meet it
Metallurgy, solar-panel manufacture, rubber vulcanization and thermoelectric devices. Exposure is overwhelmingly occupational and uncommon.
What it does in the body
The body converts tellurium to dimethyl telluride, which leaves through the lungs and skin and produces an intense garlic odor that can last for months after a single exposure. Tellurium also interferes with an enzyme in cholesterol synthesis, which is thought to underlie the nerve damage seen at higher exposures, since myelin depends on it.
Why it’s on the panel
Because it’s easy to rule in or out: garlic breath with no dietary explanation, in someone with an industrial history, is close to diagnostic on its own.
Work & industry
Sn TinMetals
Tin
Two entirely different stories under one name — and the total can’t tell them apart.
- What urine shows
- Recent exposure.
- Main sources
- Canned food, especially acidic foods in unlacquered cans (inorganic tin); PVC stabilizers, treated textiles and old marine paints (organotins).
- The evidence
- Inorganic tin: low toxicity, well established. Organotins: among the most potent endocrine disruptors known, with strong laboratory and wildlife evidence.
What it is
Inorganic tin is poorly absorbed and of low toxicity. Organotins — tin bonded to carbon — are among the most potent endocrine disruptors ever identified. A total tin result doesn’t distinguish them.
Where you meet it
Inorganic tin comes from canned food. Organotins such as tributyltin come from PVC stabilizers, antifungal treatments for textiles and wood, industrial catalysts and, historically, anti-fouling paint on boats.
What it does in the body
Tributyltin switches on the master receptors for fat-cell formation at vanishingly small concentrations — it’s the original ‘obesogen’, the compound that established that environmental chemicals can reprogram metabolism. It’s also strongly immunotoxic. Its effect on marine snails, where females developed male organs at parts-per-trillion levels, is the classic demonstration of endocrine disruption.
Why it’s on the panel
Because a raised tin in someone who eats a lot of canned food and a raised tin in someone who handles PVC stabilizers are two different conversations, and the panel is where that conversation starts.
Food & drinkHome & personal careWork & industry
Tl ThalliumMetals
Thallium
Painful neuropathy plus hair loss is thallium until proven otherwise.
- What urine shows
- Recent exposure.
- Main sources
- Coal combustion and cement manufacture; historic rodenticides; contaminated food, water or illicit drugs.
- The evidence
- Strong. Poisoning and its treatment are well described; long-term effects can persist for years.
What it is
Odorless, tasteless and highly toxic. Chemically it behaves like potassium, which is precisely the problem.
Where you meet it
Thallium rat poisons were once common and are now rare, but accidental and deliberate poisonings still occur. Industrial exposure tends to be low-level and chronic. Contaminated food and water are documented sources, as is contamination of illicit drugs. Coal burning and cement manufacture are the main environmental contributors.
What it does in the body
Thallium enters cells through potassium channels and competes with potassium in the pump that keeps every cell’s charge balanced. It sabotages energy metabolism, and mitochondrial damage is visible at autopsy. The classic sequence is stomach upset first, then severely painful nerve pain rising up the limbs within days, then hair loss at two to three weeks.
Why it’s on the panel
Because there is no benign low-level story for thallium, and because by the time the tell-tale hair loss appears, the window in which treatment prevents lasting nerve damage may already be closing. Even a modest elevation warrants a hunt for the source.
Work & industryFood & drinkWater
Th ThoriumMetals
Thorium
Radiological rather than chemical toxicity. A different category entirely.
- What urine shows
- Recent exposure.
- Main sources
- Naturally occurring radioactive material in mining, oil-and-gas scale and phosphate processing; old gas-lantern mantles and some welding rods.
- The evidence
- Historical evidence from Thorotrast is strong; everyday exposure data are thin.
What it is
A naturally occurring radioactive element whose harm comes from radiation, not chemistry.
Where you meet it
Naturally occurring radioactive material in mining, oil-and-gas pipe scale and phosphate processing. Older gas-lantern mantles, some welding rods, certain older optical glass, and monazite beach sands in a few coastal regions.
What it does in the body
Inhaled or injected thorium settles in lung, liver, spleen, bone marrow and bone and emits alpha radiation for the rest of the person’s life — its half-life is measured in billions of years, so it does not decay away in any meaningful sense. The historical evidence comes from Thorotrast, a thorium contrast agent used from the 1930s to the 1950s, which caused a striking excess of liver cancers and leukemia decades later.
Why it’s on the panel
Because a detectable thorium in someone without an industrial history is unusual enough to deserve a real exposure history.
Work & industry
W TungstenMetals
Tungsten
Reclassified from inert to emerging toxicant. The reference ranges are still catching up.
- What urine shows
- Recent exposure; some deposits in bone.
- Main sources
- Hard-metal tooling and cutting tools; drilling; munitions; welding; some orthopedic and dental hardware; groundwater near deposits.
- The evidence
- Emerging. Absorption and bone deposition are established; the health picture is still being worked out.
What it is
An extremely hard, high-melting metal, long considered biologically inert and now classed as an emerging toxicant of concern.
Where you meet it
Hard-metal tooling and cutting tools, drilling equipment, munitions, welding, electronics, some dental and orthopedic hardware, and groundwater near mineral deposits or industrial sites.
What it does in the body
Better methods showed tungsten is absorbed more readily than believed and deposits in bone, where it persists. It appears to interfere with enzymes that depend on molybdenum, its chemical near-twin, by sitting in the active site without doing the job. Cobalt–tungsten carbide dust causes ‘hard metal’ lung disease. A childhood leukemia cluster in Fallon, Nevada drew attention to tungsten in groundwater, though causation was never established.
Why it’s on the panel
Because the science is moving, and a raised level is best treated as a reason to find the source rather than as a well-characterized diagnosis.
Work & industryWater
U UraniumMetals
Uranium
The highest-yield finding on the panel, because the source is usually singular and fixable.
- What urine shows
- Recent exposure; long-term storage in bone.
- Main sources
- Private well water, especially over granite bedrock; phosphate fertilizers; mining, milling and munitions.
- The evidence
- Kidney toxicity at natural enrichment is chemical, not radiological, and well described.
What it is
A radioactive heavy metal whose most important harm at natural enrichment is chemical rather than radiological. Natural uranium poisons the kidney the way any heavy metal does, long before radiation becomes the issue.
Where you meet it
Private well water is the dominant source for the general public, particularly in regions with granite bedrock — and it isn’t part of standard water testing. Phosphate fertilizers carry it as a natural contaminant. Mining, milling and processing supply occupational exposure, and depleted-uranium munitions are a specific military exposure.
What it does in the body
Absorbed uranium circulates bound to bicarbonate, filters through the kidney and damages the proximal tubule — the same target as cadmium, with the same early signature of small proteins and amino acids leaking into urine. Bone is the long-term store.
Why it’s on the panel
Because a raised urinary uranium almost always has one source, that source is usually a well, and the right filter fixes it. Few findings on the panel are this actionable.
WaterWork & industryFood & drink
AFB1 Aflatoxin B1Mycotoxins
Aflatoxin B1
The most potent naturally occurring liver carcinogen known, and the reference compound for its class.
- What urine shows
- Recent intake — the last day or two.
- Main sources
- Peanuts, corn, tree nuts, cottonseed, dried figs and spices contaminated by Aspergillus molds.
- The evidence
- Very strong. A confirmed human carcinogen (IARC Group 1) and one of the best-characterized carcinogens in humans.
What it is
The most potent and most abundant of the aflatoxins, made by Aspergillus flavus and A. parasiticus. Contamination happens in the field under drought stress and in storage when moisture isn’t controlled.
Where you meet it
Peanuts and peanut products, corn and corn products, tree nuts, dried figs, cottonseed and spices — anything that can carry mold from field to shelf. Tropical and subtropical supply chains carry more.
What it does in the body
The liver’s own enzymes convert aflatoxin B1 into a reactive form that attaches to DNA. It leaves a characteristic mutation in the TP53 tumor-suppressor gene — so characteristic it’s used as a molecular fingerprint of aflatoxin exposure. The interaction with chronic hepatitis B is not additive: the two hit the same protective pathway from opposite directions, and the combined liver-cancer risk is far greater than the sum of each.
Why it’s on the panel
Because aflatoxin exposure is one of the few things on this panel with a clear, decades-old causal path to a specific cancer — and because knowing your hepatitis B status is the single fact that most changes what a result means.
Food & drink
AFB2 Aflatoxin B2Mycotoxins
Aflatoxin B2
The dihydro cousin. Travels with B1 and confirms the same source.
- What urine shows
- Recent intake.
- Main sources
- The same foods as aflatoxin B1.
- The evidence
- Congener-specific human data are limited; potency is lower than B1.
What it is
A close chemical variant of aflatoxin B1, produced by the same molds and found in the same foods. A saturated bond makes it less able to form the reactive intermediate that makes B1 so dangerous, so it’s considerably less potent.
Where you meet it
Wherever B1 is: peanuts, corn, tree nuts, dried fruit and spices.
What it does in the body
Less potent than B1 by the same mechanism, and usually present at lower levels than B1 in the same sample.
Why it’s on the panel
Its presence corroborates an Aspergillus source rather than adding a separate risk. It’s read alongside B1, not on its own.
Food & drink
AFG1 Aflatoxin G1Mycotoxins
Aflatoxin G1
Tells you which mold did it.
- What urine shows
- Recent intake.
- Main sources
- The same foods as B1; more associated with Aspergillus parasiticus.
- The evidence
- Carcinogenic but less potent than B1; human data on the G-series alone are limited.
What it is
Produced mainly by Aspergillus parasiticus rather than A. flavus. Carcinogenic, though less potent than B1.
Where you meet it
The same commodities as the B-series aflatoxins.
What it does in the body
The same mechanism as B1 at lower potency.
Why it’s on the panel
G1 alongside B1 helps identify which organism contaminated the crop, which matters for tracing a food source. It’s a source-attribution marker more than an independent risk.
Food & drink
AFG2 Aflatoxin G2Mycotoxins
Aflatoxin G2
The least potent of the four principal aflatoxins.
- What urine shows
- Recent intake.
- Main sources
- The same foods as the other aflatoxins.
- The evidence
- Rarely the dominant aflatoxin in a sample; lowest potency of the four.
What it is
The saturated counterpart of G1, following the same pattern as B2 relative to B1.
Where you meet it
Wherever the other aflatoxins are.
What it does in the body
The lowest potency of the four principal aflatoxins.
Why it’s on the panel
Completeness. It rounds out the exposure picture and rarely drives risk on its own.
Food & drink
AFM1 Aflatoxin M1Mycotoxins
Aflatoxin M1
Why dairy is its own exposure route — and why infants are the most exposed group.
- What urine shows
- Recent intake, plus your own conversion of ingested B1.
- Main sources
- Milk and dairy from animals fed contaminated feed. It survives pasteurization and concentrates in cheese.
- The evidence
- IARC Group 2B — possibly carcinogenic. Limits in milk are stricter than for B1 in other foods, because of infant exposure.
What it is
The form of aflatoxin B1 that a cow’s liver makes and excretes into milk after eating contaminated feed.
Where you meet it
Milk, cheese and other dairy. It survives pasteurization and concentrates in cheese. By intake per kilogram of body weight, infants and young children are the most exposed people.
What it does in the body
Carcinogenic, though less potent than the parent compound. It’s also what your own liver makes from any B1 you’ve eaten, so a urine M1 reflects both direct dairy intake and your own recent B1.
Why it’s on the panel
Because it’s a useful marker of recent aflatoxin exposure overall, and because dairy is a route most people don’t think to consider.
Food & drink
OTA Ochratoxin AMycotoxins
Ochratoxin A
A month-long half-life means one result reflects habitual intake, not one bad meal.
- What urine shows
- Habitual intake over weeks — the longest window of any mycotoxin here.
- Main sources
- Coffee, wine, beer, cereals, dried fruit, cocoa, spices and cured meats; also produced by molds in damp buildings.
- The evidence
- IARC Group 2B. Kidney toxicity is established in animals; the link to Balkan endemic nephropathy remains unresolved.
What it is
A kidney-toxic, immune-toxic mycotoxin from Aspergillus and Penicillium molds, and one of the most widely detected mycotoxins in human populations. It’s heat-stable enough that complete removal from food is practically impossible.
Where you meet it
Coffee, wine, beer, cereals and bread, dried fruit, cocoa, spices and cured meats. The molds that make it also grow in damp buildings.
What it does in the body
After absorption it binds tightly to albumin, which gives it an unusually long half-life — days to about a month. It concentrates in the kidney, where in animals it causes tumors and DNA damage. It has long been a candidate cause of Balkan endemic nephropathy, a slow kidney failure clustered in the Danube basin; a plant toxin, aristolochic acid, was later proposed instead, and the evidence for both is still live. Genetic differences in detox enzymes appear to influence who is affected.
Why it’s on the panel
Because it’s the analyte where the mycotoxin caveat bites hardest: coffee and wine alone will produce a detectable result in most people, so the question is always level and trend, not presence.
Food & drinkDamp & mold
CIT CitrininMycotoxins
Citrinin
Ask about red yeast rice. People rarely think to mention it.
- What urine shows
- Recent intake.
- Main sources
- Stored grains; red yeast rice supplements.
- The evidence
- Kidney toxicity is well described in animals; supplement contamination is documented and recurring.
What it is
A kidney-toxic mycotoxin from Penicillium, Aspergillus and Monascus molds.
Where you meet it
Stored grains, and — importantly — red yeast rice. The mold used to ferment red yeast rice supplements makes citrinin as a natural byproduct, and contamination of those supplements is a documented, recurring problem.
What it does in the body
Citrinin targets the kidney’s proximal tubule, disrupting mitochondria and making cell membranes leaky. It often occurs alongside ochratoxin A, and their kidney effects may add up.
Why it’s on the panel
Because the source is so often a supplement taken for cholesterol that nobody thought counted as a supplement.
Food & drinkHome & personal care
DH-CIT DihydrocitrinoneMycotoxins
Dihydrocitrinone
Often higher than the parent. Measuring citrinin alone undercounts exposure.
- What urine shows
- Recent intake.
- Main sources
- Your own metabolism of citrinin — same sources: stored grain and red yeast rice.
- The evidence
- Established as the main human urinary metabolite of citrinin.
What it is
The main form in which citrinin leaves the body in urine.
Where you meet it
Same sources as citrinin. This is what your body made of it.
What it does in the body
It’s a breakdown product rather than an added hazard, but it’s frequently present at higher concentration than citrinin itself.
Why it’s on the panel
Measuring both the parent and the metabolite makes citrinin detection considerably more sensitive. On its own, citrinin underestimates exposure.
Food & drinkHome & personal care
SATG Satratoxin GMycotoxins
Satratoxin G
The signature toxin of black mold — and the hardest one to read from urine.
- What urine shows
- Recent exposure; urine is not a validated measure of building exposure.
- Main sources
- Stachybotrys chartarum growing on wet cellulose — drywall paper, ceiling tile, cardboard.
- The evidence
- Toxicity and presence in damp buildings are well documented. Urine as a measure of building exposure is not validated by any regulator.
What it is
One of the two signature macrocyclic trichothecenes of Stachybotrys chartarum — the ‘black mold’ — produced when it grows on soaked cellulose.
Where you meet it
Water-damaged buildings: wet drywall paper, ceiling tile, cardboard and similar material after leaks or flooding.
What it does in the body
Trichothecenes bind the ribosome and halt protein synthesis, triggering a stress response that drives inflammation and cell death. Fast-dividing tissues — gut lining, bone marrow, immune cells — are hit first. The macrocyclic ring makes this family far more potent than simpler trichothecenes, and in animals satratoxins specifically damage the nerves of smell after inhalation, which is among the better mechanistic arguments for airway toxicity.
Why it’s on the panel
Because people who suspect a mold problem deserve a measurement rather than a guess — with an honest statement of its limits. The compound is real and the toxicology is real. What isn’t established is the leap from a urine number to a building as the source.
Damp & mold
SATH Satratoxin HMycotoxins
Satratoxin H
Usually the more abundant of the two satratoxins.
- What urine shows
- Recent exposure; urine is not a validated measure of building exposure.
- Main sources
- Stachybotrys chartarum on wet building materials.
- The evidence
- As for satratoxin G.
What it is
The companion satratoxin, sharing the mechanism, potency class and source of satratoxin G — and usually the more abundant of the two.
Where you meet it
Stachybotrys chartarum on wet building materials.
What it does in the body
The same ribosome-blocking mechanism and potency class as satratoxin G.
Why it’s on the panel
The pair is read together. Two satratoxins moving together is a more coherent signal than either alone.
Damp & mold
RORA Roridin AMycotoxins
Roridin A
The most studied of the roridins. Stachybotrys and its relatives.
- What urine shows
- Recent exposure; urine is not a validated measure of building exposure.
- Main sources
- Stachybotrys chartarum and Myrothecium molds on wet material.
- The evidence
- Mechanism and potency class are established; the urine biomarker is not validated.
What it is
A macrocyclic trichothecene produced by both Stachybotrys and Myrothecium species, sharing the satratoxins’ mechanism and potency class. The best studied of the three roridins here.
Where you meet it
Water-damaged buildings, and some plant-pathogen molds.
What it does in the body
Ribosome inhibition, as for the satratoxins.
Why it’s on the panel
Part of the Stachybotrys signature. Its value is in the pattern — several macrocyclic trichothecenes together — rather than in any one number.
Damp & mold
RORE Roridin EMycotoxins
Roridin E
Made by a plant pathogen too — so farm exposure is possible, not only indoor.
- What urine shows
- Recent exposure.
- Main sources
- Stachybotrys; also Myrothecium verrucaria, a plant pathogen.
- The evidence
- Mechanism established; human exposure data thin.
What it is
A macrocyclic trichothecene notable for being produced by Myrothecium verrucaria, a plant pathogen — which makes agricultural exposure plausible alongside indoor growth.
Where you meet it
Damp buildings, and farms or gardens with infected crops.
What it does in the body
As for the other macrocyclic trichothecenes.
Why it’s on the panel
It’s the one roridin where a building isn’t the only plausible source.
Damp & moldWork & industry
RORL2 Roridin L2Mycotoxins
Roridin L2
A less common congener. Rarely appears alone.
- What urine shows
- Recent exposure.
- Main sources
- Stachybotrys chartarum.
- The evidence
- Limited; read as part of the group.
What it is
A less common macrocyclic congener whose presence usually accompanies the other roridins and satratoxins.
Where you meet it
Water-damaged buildings.
What it does in the body
As for the other macrocyclic trichothecenes.
Why it’s on the panel
Pattern completeness for the Stachybotrys group.
Damp & mold
VERA Verrucarin AMycotoxins
Verrucarin A
Among the most cell-toxic trichothecenes ever characterized — active at nanomolar concentrations.
- What urine shows
- Recent exposure.
- Main sources
- Stachybotrys and Myrothecium verrucaria.
- The evidence
- Extremely potent in cells; demonstrated human harm at environmental levels is not established.
What it is
Among the most cell-toxic trichothecenes ever characterized — potent enough that it’s used as a reference cytotoxin in laboratory work.
Where you meet it
Water-damaged buildings and infected plant material. Remediation workers and anyone who has handled heavily colonized material get direct contact.
What it does in the body
Ribosome inhibition like the rest of the family, at very high potency. It’s also directly irritating to skin: contact with heavily colonized material causes inflammation independent of any systemic effect.
Why it’s on the panel
Because potency in a dish and demonstrated harm in people at environmental levels are two different things, and it’s worth holding both.
Damp & moldWork & industry
VERJ Verrucarin JMycotoxins
Verrucarin J
A close relative of verrucarin A.
- What urine shows
- Recent exposure.
- Main sources
- Stachybotrys and Myrothecium verrucaria.
- The evidence
- As for verrucarin A.
What it is
A structurally related congener of verrucarin A, sharing its source molds, mechanism and skin irritancy.
Where you meet it
As for verrucarin A.
What it does in the body
As for verrucarin A.
Why it’s on the panel
Read with verrucarin A and the rest of the macrocyclic group.
Damp & moldWork & industry
DON DeoxynivalenolMycotoxins
Deoxynivalenol
The most common mycotoxin in the world’s grain supply. Detection is expected, not exceptional.
- What urine shows
- Recent intake — the last day or two.
- Main sources
- Wheat, barley, oats, corn and everything made from them.
- The evidence
- Mechanism well characterized. IARC finds no evidence it causes cancer in humans; a colorectal signal is being watched.
What it is
Also called vomitoxin. Produced by Fusarium molds that cause head blight in wheat and barley. Wet weather at flowering drives contamination, so levels track the weather across whole growing regions.
Where you meet it
Wheat, barley, oats and corn, and everything made from them — bread, pasta, cereal, beer. In some surveys, average dietary intake in children exceeds the tolerable daily intake.
What it does in the body
The nickname is earned. DON switches on receptors in gut hormone cells that release the signals for nausea and fullness — which explains not only vomiting at high doses but reduced appetite and slowed growth at chronic low ones. It also weakens the tight junctions that seal the gut lining. One research group has reported an association with colorectal cancer risk; the international cancer agency has not found evidence of human carcinogenicity, so treat that as a signal to watch.
Why it’s on the panel
Because it’s in most people, most of the time, and the useful information is in the level and the trend rather than the fact of detection. For someone with heavy grain intake and a sensitive gut, the barrier effect is the most actionable finding.
Food & drink
NIV NivalenolMycotoxins
Nivalenol
DON’s relative — more toxic per molecule, usually at lower levels.
- What urine shows
- Recent intake.
- Main sources
- Grain; more common in Asian and European supplies than North American.
- The evidence
- More cytotoxic and immunotoxic than DON per molecule; dietary exposure is usually lower.
What it is
A close relative of deoxynivalenol made by the same Fusarium molds, with the same mechanism and target tissues.
Where you meet it
Grain — more often in Asian and European supply chains than North American ones. It usually appears alongside DON.
What it does in the body
More toxic to cells and to the immune system than DON on a per-molecule basis, but typically present at lower concentrations, so the two partly offset.
Why it’s on the panel
Read alongside DON. Nivalenol without DON is unusual on a North American diet and usually points to imported grain.
Food & drink
DAS DiacetoxyscirpenolMycotoxins
Diacetoxyscirpenol
Once investigated as chemotherapy — which tells you what it does to dividing cells.
- What urine shows
- Recent intake.
- Main sources
- Grain and animal feed contaminated by Fusarium.
- The evidence
- More potent than DON; human dietary exposure is generally lower.
What it is
A trichothecene from several Fusarium species, contaminating grain and animal feed.
Where you meet it
Grain and grain products.
What it does in the body
Gut and blood toxicity through the standard trichothecene mechanism. It was once investigated as a cancer drug, which is an efficient summary of its effect on rapidly dividing cells.
Why it’s on the panel
Dietary exposure is usually lower than DON, but higher potency closes some of that gap.
Food & drink
T-2 T-2 ToxinMycotoxins
T-2 Toxin
The trichothecene with the clearest human record — and it’s a bad one.
- What urine shows
- Recent intake.
- Main sources
- Grain left in the field over winter or stored wet — oats, barley, corn.
- The evidence
- The strongest human evidence of any trichothecene, from a mid-century outbreak of bone-marrow failure.
What it is
The most toxic of the non-macrocyclic trichothecenes.
Where you meet it
Grain overwintered in the field or stored wet — especially oats, barley and corn.
What it does in the body
Ribosome inhibition potent enough to cause organ failure. Bone marrow is the most sensitive target, and T-2 blisters skin on direct contact. The human record comes from alimentary toxic aleukia, an outbreak in the Soviet Union during and after the Second World War in communities that ate grain left in the fields over winter: stomach illness progressing to profound bone-marrow failure, with substantial mortality.
Why it’s on the panel
Because among the trichothecenes, T-2 has the strongest case for real blood and bone-marrow harm in people.
Food & drink
ZEN ZearalenoneMycotoxins
Zearalenone
Not a steroid, but it fits the estrogen receptor anyway.
- What urine shows
- Recent intake.
- Main sources
- Corn above all; also wheat, barley, sorghum and beer.
- The evidence
- IARC Group 3 — not classifiable. Livestock effects are firmly established; human data are suggestive.
What it is
A Fusarium toxin that isn’t structurally a steroid but happens to fit the estrogen receptor — one of the most potent naturally occurring estrogenic compounds in the food supply.
Where you meet it
Corn above all, then wheat, barley, sorghum and beer.
What it does in the body
Genuine estrogen-like activity through both estrogen receptors. In pigs, feed contamination causes a well-known reproductive syndrome at levels that aren’t hard to reach. In people, several studies have linked exposure to early breast development and early puberty in girls, though the evidence isn’t conclusive.
Why it’s on the panel
Because the metabolites matter more than the parent — and how your body converts zearalenone is the clinically interesting part. That’s why alpha- and beta-zearalenol are reported separately.
Food & drink
α-ZEL alpha-ZearalenolMycotoxins
alpha-Zearalenol
The body can make zearalenone more estrogenic, not less. This is the form doing the work.
- What urine shows
- Recent intake.
- Main sources
- Your own metabolism of zearalenone, from corn and grain.
- The evidence
- Roughly three to four times the estrogenic potency of zearalenone.
What it is
A reduced metabolite of zearalenone, several times more estrogenically potent than the parent.
Where you meet it
Not a food contaminant in its own right — it’s what your body makes from zearalenone.
What it does in the body
The enzyme that produces it means your handling of zearalenone can increase its hormonal activity rather than reduce it. Individual variation in this conversion is substantial and may explain why the same diet affects different people differently. In practical terms, alpha-zearalenol is doing most of the estrogenic work.
Why it’s on the panel
The ratio of alpha- to beta-zearalenol describes whether you amplify or dampen the estrogenic signal from your diet. That ratio is more informative than either value alone.
Food & drink
β-ZEL beta-ZearalenolMycotoxins
beta-Zearalenol
The dampening metabolite. Its value is as the denominator.
- What urine shows
- Recent intake.
- Main sources
- Your own metabolism of zearalenone.
- The evidence
- Considerably less estrogenic than the parent.
What it is
The other reduced metabolite of zearalenone, and considerably less estrogenic than the parent.
Where you meet it
Made in the body from dietary zearalenone.
What it does in the body
Weakly estrogenic. Its main significance is what it says about your metabolism.
Why it’s on the panel
It’s the denominator of the alpha-to-beta ratio, which describes whether a given person is amplifying or attenuating the estrogenic signal.
Food & drink
FB1 Fumonisin B1Mycotoxins
Fumonisin B1
A sphingolipid mimic. Its reach goes well beyond the gut.
- What urine shows
- Recent intake.
- Main sources
- Corn, almost exclusively — tortillas, masa, cornmeal, corn products.
- The evidence
- IARC Group 2B. The neural-tube-defect association comes from a population case-control study; the mechanism is well worked out.
What it is
The most abundant and most studied fumonisin, from Fusarium molds that live inside almost every corn plant on earth. Exposure tracks corn consumption directly.
Where you meet it
Corn and everything made from it: tortillas, masa, cornmeal, polenta, corn-based snacks.
What it does in the body
Fumonisins are structural mimics of sphinganine, the backbone of sphingolipids. They block the enzyme that builds ceramide, so sphinganine piles up. Reduced sphingolipid synthesis compromises certain membrane proteins, including the folate transporter, which gives a coherent route from contaminated corn to neural tube defects that doesn’t depend on how much folate you eat. Along the Texas–Mexico border in 1990–91, neural tube defects doubled among women in the same crop year that fumonisin poisoned livestock.
Why it’s on the panel
Because for a woman planning pregnancy with a high corn-masa intake, this is a modifiable exposure with a plausible mechanism and human data behind it — and folate supplements alone may not address it.
Food & drink
FB2 Fumonisin B2Mycotoxins
Fumonisin B2
Typically a quarter to a third of B1, with comparable toxicity per molecule.
- What urine shows
- Recent intake.
- Main sources
- Corn — the same Fusarium source as B1.
- The evidence
- Shares B1’s mechanism; usually the second most abundant congener.
What it is
Usually the second most abundant fumonisin, at roughly a quarter to a third of B1 levels, with similar per-molecule toxicity.
Where you meet it
Corn products.
What it does in the body
Shares B1’s ceramide-synthase mechanism.
Why it’s on the panel
Its presence confirms the same source and adds to the total fumonisin load. It’s read as part of the total rather than on its own.
Food & drink
FB3 Fumonisin B3Mycotoxins
Fumonisin B3
A minor congener, counted toward the total.
- What urine shows
- Recent intake.
- Main sources
- Corn.
- The evidence
- Shares the fumonisin mechanism; minor contributor.
What it is
A minor congener, usually present at low levels relative to B1 and B2.
Where you meet it
Corn products.
What it does in the body
Shares the fumonisin mechanism.
Why it’s on the panel
Completeness of the total fumonisin picture. See Fumonisin B1 for the substance.
Food & drink
STC SterigmatocystinMycotoxins
Sterigmatocystin
The aflatoxin precursor — and the most coherent indoor mycotoxin on the panel.
- What urine shows
- Recent exposure.
- Main sources
- Aspergillus versicolor, one of the commonest molds in water-damaged buildings; also grain, cheese and spices.
- The evidence
- IARC Group 2B. The building link is mechanistically coherent; the urine biomarker is not yet validated.
What it is
The molecule a mold makes on its way to making aflatoxin — the biosynthetic precursor.
Where you meet it
Grain, cheese and spices, and — critically — damp buildings, because Aspergillus versicolor is one of the most common molds found after water damage.
What it does in the body
Activated by the same liver enzymes as aflatoxin to a reactive form that attaches to DNA; less potent than aflatoxin B1, same mechanism.
Why it’s on the panel
Because of all the mycotoxins here, sterigmatocystin has the strongest claim to being a genuine indoor marker — its producer is so consistently present in damp buildings. That makes the building link more coherent; it doesn’t make a urine number a building diagnosis.
Damp & moldFood & drink
GTX GliotoxinMycotoxins
Gliotoxin
Context decides everything. Validated in invasive infection; contested as an environmental marker.
- What urine shows
- Recent exposure — and the molecule is unstable.
- Main sources
- Aspergillus fumigatus — ubiquitous in compost, soil and HVAC systems.
- The evidence
- Well established as a blood marker of invasive aspergillosis. As a urine marker of environmental exposure it is contested, partly because the molecule is chemically unstable.
What it is
An immune-suppressing toxin produced by Aspergillus fumigatus, and one of that organism’s main weapons when it infects people.
Where you meet it
Aspergillus fumigatus is everywhere: compost, soil, decaying leaves, and heating and air-conditioning systems.
What it does in the body
Gliotoxin reacts with proteins and generates reactive oxygen species, and it triggers self-destruction in the exact immune cells — neutrophils, macrophages, lymphocytes — that would otherwise clear the fungus. In short, it disarms the defense.
Why it’s on the panel
Because the same molecule means two different things in two settings. In invasive aspergillosis, blood gliotoxin correlates with disease and matters. As a urine marker of everyday mold exposure in a healthy person, it’s far less established — the compound breaks down readily and its stability in urine has been questioned.
Damp & moldHome & personal careWork & industry
MPA Mycophenolic acidMycotoxins
Mycophenolic acid
Check the medicine cabinet before reading anything.
- What urine shows
- Recent exposure.
- Main sources
- Penicillium molds in grain, silage, mold-ripened cheese and damp buildings — and the prescription drug mycophenolate mofetil.
- The evidence
- Very well characterized, because it’s a licensed drug.
What it is
A Penicillium metabolite that is also a prescription immunosuppressant used after organ transplant and in autoimmune disease.
Where you meet it
Penicillium molds in grain, silage, mold-ripened cheese and damp buildings. And, decisively, the medication mycophenolate mofetil.
What it does in the body
It blocks an enzyme lymphocytes uniquely depend on for building DNA, suppressing T and B cell proliferation with unusual selectivity. That’s why it works as a transplant drug, and why environmental exposure is worth noting.
Why it’s on the panel
Because it’s a clean, specific marker of Penicillium exposure — unless you take the drug, in which case the result is dramatic and says nothing about your environment.
Medicines & medicalFood & drinkDamp & mold
CHA Chaetoglobosin AMycotoxins
Chaetoglobosin A
An actin poison from a water-damage mold. Human data are thin.
- What urine shows
- Recent exposure.
- Main sources
- Chaetomium globosum on wet drywall and other cellulose.
- The evidence
- Mechanism established in cells; human exposure data are limited.
What it is
A cytochalasan toxin from Chaetomium globosum, a mold strongly associated with water-damaged buildings, often found growing alongside Stachybotrys.
Where you meet it
Wet drywall and cellulose-rich building material after leaks.
What it does in the body
Cytochalasans bind actin, the protein scaffolding cells use to divide, move and hold their shape, and stop it from assembling. Blocking it is broadly toxic to cells.
Why it’s on the panel
Its main value is as a corroborating signal when a building inspection has already found Chaetomium. On its own it’s a weak finding.
Damp & mold
ENB1 Enniatin B1Mycotoxins
Enniatin B1
Common exposure, incomplete risk assessment. No guidance value exists yet.
- What urine shows
- Recent intake.
- Main sources
- Wheat, barley, oats and rye, particularly from cooler northern climates.
- The evidence
- Emerging. Widespread in grain; no health-based guidance value in most jurisdictions.
What it is
An ‘emerging’ mycotoxin — a Fusarium compound that wasn’t routinely monitored until better methods revealed how common it is. Now found in a large share of European grain, usually alongside DON.
Where you meet it
Wheat, barley, oats and rye, especially from cooler northern growing regions.
What it does in the body
Enniatins are ionophores: they punch channels through membranes that let charged particles flow freely, collapsing the gradients cells depend on. Mitochondria are a particular target, which impairs energy production. They also interfere with some drug transporters.
Why it’s on the panel
Because it’s worth measuring and worth watching — and not yet worth alarming anyone about. There’s no established guidance value to compare a result against.
Food & drink
BPA-G Bisphenol APlastics
Bisphenol A
Bisphenol A glucuronide
The detoxified form — and the honest record of how much BPA came in.
- What urine shows
- Roughly the last day. Half-life about six hours.
- Main sources
- Canned food linings, polycarbonate plastics, thermal receipt paper, dental sealants.
- The evidence
- Detected in the large majority of people in every national survey; effects at membrane receptors are documented at low concentrations.
What it is
The form your liver turns BPA into for excretion. Attaching a sugar acid switches off its hormonal activity and marks it for urine. Free BPA clears so fast that this is the fraction worth measuring.
Where you meet it
Canned food is the largest dietary source for most people. Handling thermal receipts gives a real skin dose, and it rises sharply if you used hand sanitizer first, because the alcohol helps it through the skin. Polycarbonate containers, especially with hot liquid, and some dental sealants contribute.
What it does in the body
BPA binds classical estrogen receptors weakly but membrane-bound estrogen receptors strongly, triggering signals well below what the classical data would predict. It also has anti-androgen activity and interacts with thyroid hormone receptors.
Why it’s on the panel
Because detection is the population norm, and the finding worth acting on is a level well above the rest of the population — which nearly always points to a specific, changeable behavior.
Food & drinkHome & personal care
BPS Bisphenol SPlastics
Bisphenol S
‘BPA-free’ is a claim about one molecule, not about estrogenic activity.
- What urine shows
- Roughly the last day or two — possibly longer than BPA.
- Main sources
- Thermal receipt paper, where it is now the dominant developer; ‘BPA-free’ plastics; can linings.
- The evidence
- Comparable estrogenic activity to BPA in most test systems; more resistant to breakdown.
What it is
The most common replacement for BPA, and the reason a ‘BPA-free’ label deserves less confidence than it invites.
Where you meet it
Thermal receipt paper, where it has largely replaced BPA; ‘BPA-free’ plastics and can linings.
What it does in the body
BPS has comparable estrogenic activity to BPA in most test systems. It isn’t a safer molecule — it’s a different molecule with the same working part. Some evidence suggests it clears more slowly than BPA, meaning longer internal exposure per unit of intake.
Why it’s on the panel
Because this is the regrettable-substitution problem in a single analyte. If you switched to BPA-free products and your BPS is high, the substitution happened; the exposure didn’t stop.
Home & personal careFood & drink
DEP Diethyl phthalatePlastics
Diethyl phthalate
The fragrance phthalate — and the easiest exposure on the panel to actually reduce.
- What urine shows
- About a day.
- Main sources
- Fragrance — perfume, lotion, deodorant, hair products, anything with ‘fragrance’ or ‘parfum’ on the label.
- The evidence
- Well characterized. Unlike heavier phthalates it isn’t a strong anti-androgen; associations run toward oxidative stress and some neurodevelopmental endpoints.
What it is
A light phthalate used as a solvent and fixative for scent rather than as a plasticizer.
Where you meet it
Fragrance is the dominant source: DEP holds scent molecules and slows their evaporation. Under most regulations ‘fragrance’ is a trade secret that needn’t disclose its ingredients.
What it does in the body
Absorbed efficiently through skin, converted to its metabolite and excreted within about a day. It isn’t a strong anti-androgen like the heavier phthalates; its associations are with oxidative stress, inflammation and some behavioral and neurodevelopmental measures.
Why it’s on the panel
Because it’s the best teaching analyte on the panel. Switch to fragrance-free products and this number drops measurably within days — you get to see cause and effect on a retest. Build the habit here before tackling harder exposures.
Home & personal care
MEHP DEHP phthalatePlastics
DEHP phthalate
Mono(2-ethylhexyl) phthalate
The phthalate where the animal findings translated most directly to people.
- What urine shows
- About a day.
- Main sources
- Fatty foods that contacted PVC in processing or packaging; medical devices — IV bags, tubing, dialysis circuits; vinyl flooring and shower curtains.
- The evidence
- Strong. Anti-androgen effects in animals are echoed in human birth studies.
What it is
The main metabolite of DEHP, the high-molecular-weight phthalate of greatest toxicological concern.
Where you meet it
DEHP is what makes PVC flexible: vinyl flooring, shower curtains, food packaging and processing tubing, and medical devices — IV bags and tubing, blood bags, dialysis circuits, feeding tubes. Hospitalized patients, especially newborns in intensive care, can receive doses far above the general population.
What it does in the body
DEHP and MEHP are anti-androgens: they suppress testosterone production in the developing testis. In animals, exposure during pregnancy produces a consistent cluster of male reproductive effects, and human studies have linked maternal phthalate levels to a shortened androgen-dependent measurement in male infants — one of the most direct animal-to-human translations in this field. MEHP also activates receptors involved in fat and liver metabolism.
Why it’s on the panel
Because pregnancy is when this matters most, and the male reproductive tract is the target. Knowing your level before or during pregnancy is the point.
Food & drinkMedicines & medicalHome & personal care
MeP MethylparabenParabens
Methylparaben
The most used and the least potent. Detection is nearly universal.
- What urine shows
- About a day.
- Main sources
- Nearly all conventional cosmetics, lotions and shampoos; some foods and medicines.
- The evidence
- Weakly estrogenic — orders of magnitude weaker than estradiol; cleared quickly.
What it is
The most widely used paraben and the least estrogenically potent — several orders of magnitude weaker than the body’s own estradiol.
Where you meet it
Almost every conventional cosmetic, lotion and shampoo, plus some foods and pharmaceuticals as a preservative.
What it does in the body
Broken down quickly by enzymes in the skin and liver and excreted within a day.
Why it’s on the panel
Because it’s usually the most abundant paraben in urine simply because it’s the most used, and it sets the baseline for reading the longer-chain parabens, which are the ones that matter.
Home & personal careFood & drink
EtP EthylparabenParabens
Ethylparaben
Slightly more potent, usually paired with methylparaben.
- What urine shows
- About a day.
- Main sources
- The same products as methylparaben; also evaluated as a food preservative in some places.
- The evidence
- Slightly more potent than methylparaben; rapidly cleared.
What it is
Slightly more fat-soluble and slightly more potent than methylparaben, and usually used alongside it to broaden antimicrobial coverage.
Where you meet it
The same products as methylparaben.
What it does in the body
The same rapid metabolism and clearance.
Why it’s on the panel
The methyl–ethyl pair together indicates conventional personal-care product use rather than any specific exposure.
Home & personal careFood & drink
PrP PropylparabenParabens
Propylparaben
The point where regulatory attention begins.
- What urine shows
- About a day.
- Main sources
- Lotions, creams, sunscreens and many pharmaceuticals.
- The evidence
- Restricted in the EU in leave-on products for young children; potency meaningfully above the short-chain parabens.
What it is
Meaningfully more potent than the short-chain parabens, and the point at which regulators started restricting use.
Where you meet it
Lotions, creams, sunscreens and many medicines.
What it does in the body
Beyond estrogen-receptor binding, propylparaben has been reported to speed proliferation in estrogen-responsive cells and to affect ovarian function in animal studies.
Why it’s on the panel
Because this and butylparaben are the two parabens worth translating into a product swap. The short-chain pair usually isn’t.
Home & personal care
BuP ButylparabenParabens
Butylparaben
The most potent of the common parabens, and the most restricted.
- What urine shows
- About a day.
- Main sources
- Cosmetics.
- The evidence
- The paraben most consistently linked to reproductive effects in animals; accumulates more than shorter-chain parabens.
What it is
The most estrogenically potent of the commonly used parabens and the one carrying the most regulatory restriction.
Where you meet it
Cosmetics.
What it does in the body
The paraben most consistently associated with reproductive effects in animal studies, including reduced sperm production. Greater fat-solubility means more tissue accumulation than the shorter-chain compounds.
Why it’s on the panel
It’s the highest-yield paraben finding. For someone with a hormone-sensitive condition, this is the one to act on first.
Home & personal care
GLY GlyphosatePesticides
Glyphosate
The most politically charged molecule in modern toxicology. We present both sides.
- What urine shows
- Recent exposure; most is excreted unchanged within days.
- Main sources
- Glyphosate-tolerant crops; pre-harvest desiccation of wheat, oats, barley and legumes; lawn and garden use.
- The evidence
- IARC: probably carcinogenic (Group 2A). EPA and EFSA: unlikely to be carcinogenic at expected exposures. A direct expert disagreement.
What it is
The most heavily used herbicide in the world.
Where you meet it
Residue on glyphosate-tolerant crops and on wheat, oats, barley and legumes sprayed to dry them before harvest; home weedkillers; occupational application.
What it does in the body
Glyphosate blocks an enzyme in a pathway plants use to make amino acids and animals don’t have — the basis of its selectivity and the core of the safety argument. The counterpoints are that gut bacteria do have that pathway, raising microbiome questions, and that commercial formulations contain surfactants that are more toxic to cells than glyphosate alone.
Why it’s on the panel
Because a person who has heard only IARC will over-read a detectable result, and a person who has heard only the EPA will dismiss a real occupational exposure. In 2015 IARC classed glyphosate as probably carcinogenic, citing limited human evidence for non-Hodgkin lymphoma and strong mechanistic evidence. The EPA and European agencies reviewed the same data and concluded it’s unlikely to be carcinogenic at realistic exposures. Much of the gap is a hazard-versus-risk question — can it cause cancer under any conditions, versus does it at real-world doses — and the human signal that does exist comes from heavy, repeated occupational use, not dietary residue.
Food & drinkHome & personal careWork & industry
2,4-D 2,4-DPesticides
2,4-D
2,4-Dichlorophenoxyacetic acid
Not Agent Orange. That distinction is accuracy, not defense.
- What urine shows
- A couple of days; excreted largely unchanged.
- Main sources
- Lawn and turf ‘weed and feed’ products; agriculture, roadsides and forestry.
- The evidence
- IARC Group 2B — possibly carcinogenic — largely from farm-worker lymphoma studies complicated by other pesticides.
What it is
One of the oldest synthetic herbicides still in wide use, dating to the 1940s.
Where you meet it
Lawn and turf products above all, then agricultural, roadside and forestry spraying. Pets track it indoors, and children play on treated grass.
What it does in the body
It mimics a plant growth hormone. In people it’s absorbed and excreted largely unchanged. Its ‘possibly carcinogenic’ classification rests on studies of non-Hodgkin lymphoma in agricultural workers who were also exposed to other pesticides, and some evidence points to thyroid effects.
Why it’s on the panel
Because people ask about Agent Orange and deserve a straight answer: Agent Orange was a mixture of 2,4-D and 2,4,5-T, and the serious harms attributed to it trace to a dioxin contaminant of the 2,4,5-T half — not to 2,4-D. That’s not a defense of 2,4-D. It’s accuracy, and accuracy is what makes the rest of the picture credible.
Home & personal careWork & industry
ATZ AtrazinePesticides
Atrazine
Banned in the EU since 2004, still heavily used on US corn. Water is the route.
- What urine shows
- Clears quickly and appears inconsistently — see atrazine mercapturate.
- Main sources
- Drinking water, with seasonal spikes after spring application in corn-growing regions.
- The evidence
- The aromatase mechanism is well replicated. The widely publicized amphibian findings remain disputed.
What it is
A triazine herbicide heavily used on US corn and banned in the European Union since 2004, mainly over persistent groundwater contamination.
Where you meet it
Drinking water is the main route for most people. Atrazine moves readily through soil into ground and surface water, with spikes after spring application. Corn-growing regions have the highest levels.
What it does in the body
Its best-documented endocrine effect is switching on aromatase, the enzyme that converts androgens to estrogens — shifting hormone balance toward estrogen without binding an estrogen receptor itself. It also disrupts the signaling between brain and ovaries in animal studies. The famous frog studies reporting feminization at low doses remain scientifically disputed; the aromatase mechanism is the stronger part of the case.
Why it’s on the panel
Because if your water comes from a well in corn country, a single winter sample can miss the exposure entirely. Collecting after spring application tells you what a winter sample can’t.
WaterFood & drink
ATZ-M Atrazine mercapturatePesticides
Atrazine mercapturate
The more reliable of the two atrazine measurements.
- What urine shows
- Recent exposure.
- Main sources
- Your body’s processing of atrazine — same routes: drinking water in corn-growing regions.
- The evidence
- Established as the better urinary biomarker; parent atrazine alone underestimates exposure.
What it is
The metabolite your body makes when it processes atrazine through glutathione — and the more reliable of the two atrazine markers.
Where you meet it
Same sources as atrazine.
What it does in the body
Detection confirms the body handled atrazine through glutathione conjugation, its main detox route.
Why it’s on the panel
Because parent atrazine is cleared quickly and shows up inconsistently, measuring only the parent substantially underestimates exposure.
WaterFood & drink
3-PBA Pyrethroid markerPesticides
Pyrethroid marker
3-Phenoxybenzoic acid
One number covers the whole pyrethroid class — and can’t say which one.
- What urine shows
- Recent exposure — days.
- Main sources
- Household insecticides, pet flea and tick products, lice treatments, mosquito-control programs; indoor dust.
- The evidence
- Mammals are far less sensitive than insects. Human links to child behavior and sperm quality are suggestive, not definitive.
What it is
The common metabolite of most pyrethroid insecticides — permethrin, cypermethrin, deltamethrin and their relatives.
Where you meet it
Pyrethroids are now the dominant home insecticide class, having replaced organophosphates in most consumer products. Indoor use makes household dust a reservoir, and crawling children get a much bigger dose from it than adults do.
What it does in the body
Pyrethroids hold nerve sodium channels open, causing repetitive firing. Mammals are far less sensitive than insects thanks to faster metabolism and lower channel affinity — a genuine safety margin. Human studies have linked pyrethroid metabolites to attention and behavior measures in children and to sperm quality in men; the evidence is suggestive rather than definitive.
Why it’s on the panel
Because rising levels in a household usually trace to something specific — a pest-control visit, a pet treatment, a mosquito program — and that’s findable.
Home & personal careFood & drink
DEDTP Diethyl dithiophosphatePesticides
Diethyl dithiophosphate
O,O-Diethyl dithiophosphate
The diethyl marker — chlorpyrifos and diazinon.
- What urine shows
- Recent exposure.
- Main sources
- Dietary residue from diethyl organophosphates such as chlorpyrifos and diazinon.
- The evidence
- Prenatal organophosphate exposure is consistently linked to children’s neurodevelopment. The marker can also come from breakdown products already in food.
What it is
A metabolite of the diethyl organophosphates, most notably chlorpyrifos and diazinon.
Where you meet it
Chlorpyrifos was the most widely used home insecticide in the United States before it was restricted, and remains in agricultural use in many places, so dietary residue is the main route today.
What it does in the body
Organophosphates inhibit the enzyme that switches off acetylcholine at nerve junctions; acute poisoning is a cholinergic crisis. The chronic question is different, and it’s where the research has concentrated: prospective birth cohorts have repeatedly linked prenatal exposure to lower IQ, attention problems and altered brain structure in children — findings central to restricting chlorpyrifos at home.
Why it’s on the panel
Because the three organophosphate markers are read together as evidence of contact with the class.
Food & drinkHome & personal care
DMDTP Dimethyl dithiophosphatePesticides
Dimethyl dithiophosphate
O,O-Dimethyl dithiophosphate
The dimethyl marker — malathion and dimethoate.
- What urine shows
- Recent exposure.
- Main sources
- Dietary residue; mosquito-control spraying; some lice treatments.
- The evidence
- Malathion is among the less acutely toxic organophosphates to mammals; the shared class caveat applies.
What it is
A metabolite of the dimethyl organophosphates — malathion, dimethoate and relatives.
Where you meet it
Malathion is used in mosquito-control programs, agriculture and lice treatment. Detection usually reflects dietary residue or a recent spraying program nearby.
What it does in the body
The same class mechanism as the other organophosphates. Malathion is among the less acutely toxic to mammals, because human enzymes break it down efficiently.
Why it’s on the panel
Part of the three-marker organophosphate read.
Food & drinkHome & personal care
DMTP Dimethyl phosphorothioatePesticides
Dimethyl phosphorothioate
O,O-Dimethyl phosphorothioate
The second dimethyl route — measured to catch what the other misses.
- What urine shows
- Recent exposure.
- Main sources
- The same dimethyl organophosphates, via a different breakdown route.
- The evidence
- As for the other organophosphate markers.
What it is
Another dimethyl-class metabolite, produced by the same parent compounds through a different oxidation route.
Where you meet it
As for dimethyl dithiophosphate.
What it does in the body
The same class mechanism.
Why it’s on the panel
Some parent compounds favor one breakdown route over the other. Measuring both catches more exposure than either alone.
Food & drinkHome & personal care
2-MHA ortho-Xylene markerSolvents
ortho-Xylene marker
2-Methylhippuric acid
The ortho-xylene marker.
- What urine shows
- The last 24 to 48 hours.
- Main sources
- Paints, varnishes, adhesives, printing inks, degreasers and gasoline.
- The evidence
- Xylene’s nervous-system effects are well documented at high exposure.
What it is
The specific metabolite of ortho-xylene, one of the three forms of xylene in commercial solvent mixtures.
Where you meet it
Painting, printing, auto-body work, laboratory work, and any recent project with solvents, adhesives or gasoline.
What it does in the body
Xylene depresses the central nervous system at high exposure — headache, dizziness, poor coordination — and long-term occupational exposure has been linked to persistent effects on mood, memory and attention.
Why it’s on the panel
Because commercial xylene is a mixture of all three isomers, the three methylhippuric acids usually rise together; this is one leg of that tripod.
Work & industryHome & personal careSmoke, fuel & traffic
3-MHA meta-Xylene markerSolvents
meta-Xylene marker
3-Methylhippuric acid
The meta-xylene marker — usually the biggest of the three.
- What urine shows
- The last 24 to 48 hours.
- Main sources
- The same solvent products as the other xylene markers.
- The evidence
- The most sensitive of the three xylene markers.
What it is
The metabolite of meta-xylene, the most abundant isomer in commercial xylene — which makes this typically the highest of the three and the most sensitive indicator of xylene exposure overall.
Where you meet it
As for the other xylene markers.
What it does in the body
As for xylene generally.
Why it’s on the panel
The most sensitive of the three xylene markers.
Work & industryHome & personal careSmoke, fuel & traffic
4-MHA para-Xylene markerSolvents
para-Xylene marker
4-Methylhippuric acid
The para-xylene marker — confirms the picture rather than adding to it.
- What urine shows
- The last 24 to 48 hours.
- Main sources
- The same solvent products as the other xylene markers.
- The evidence
- A smaller share of commercial mixtures than the meta isomer.
What it is
The metabolite of para-xylene, a smaller share of commercial mixtures than the meta isomer.
Where you meet it
As for the other xylene markers.
What it does in the body
As for xylene.
Why it’s on the panel
Mainly confirmation of the xylene picture.
Work & industryHome & personal careSmoke, fuel & traffic
SPMA Benzene markerSolvents
Benzene marker
N-Acetyl-S-phenyl-L-cysteine
One of the best-validated occupational biomarkers in existence.
- What urine shows
- The last 24 to 48 hours.
- Main sources
- Gasoline and exhaust, tobacco smoke, attached garages, heavy traffic, some solvents.
- The evidence
- Very strong. Benzene is a confirmed human carcinogen (IARC Group 1) with no clearly identified safe threshold for leukemia risk.
What it is
Also called S-phenylmercapturic acid. It’s the fingerprint benzene leaves in urine, and benzene has an unambiguous causal link to acute myeloid leukemia.
Where you meet it
Gasoline vapor and vehicle exhaust, tobacco smoke including secondhand, an attached garage, heavy traffic, and some solvents and glues.
What it does in the body
The liver converts benzene into products that travel to the bone marrow, where they damage DNA and suppress the stem cells that make blood.
Why it’s on the panel
Because a raised result deserves both a source hunt and a complete blood count. Smokers and people exposed to secondhand smoke run substantially higher levels, and an attached garage is the residential source most often missed.
Smoke, fuel & trafficWork & industryHome & personal care
HEMA Ethylene oxide markerSolvents
Ethylene oxide marker
N-Acetyl-S-(2-hydroxyethyl)-L-cysteine
Sensitive, but not entirely specific.
- What urine shows
- The last 24 to 48 hours.
- Main sources
- Medical-device and spice sterilization; living near a sterilization facility; also vinyl chloride, acrylonitrile and tobacco smoke.
- The evidence
- Ethylene oxide is a confirmed human carcinogen (IARC Group 1). A small background is expected in everyone.
What it is
A marker of ethylene oxide — and also of vinyl chloride and acrylonitrile — so it’s read alongside the other markers in this group.
Where you meet it
Ethylene oxide sterilizes medical devices and spices, and communities near sterilization plants have been the subject of significant regulatory attention. Tobacco smoke contributes. A small amount is also made in the body from ethylene, so a low background is normal.
What it does in the body
Ethylene oxide alkylates DNA directly, without needing to be activated. It’s linked to blood and lymph cancers and to breast cancer.
Why it’s on the panel
Because residential proximity to a sterilization facility is a real exposure pathway that most people never think to check.
Work & industryHome & personal careSmoke, fuel & traffic
2HPMA Propylene oxide markerSolvents
Propylene oxide marker
N-Acetyl-S-(2-hydroxypropyl)-L-cysteine
Mostly occupational, with a dietary tail.
- What urine shows
- The last 24 to 48 hours.
- Main sources
- Polyurethane and propylene-glycol manufacture; fumigation of nuts, spices and cocoa.
- The evidence
- IARC Group 2B; a direct alkylating agent, less potent than ethylene oxide.
What it is
The marker of propylene oxide, an alkylating agent used to make polyurethane and propylene glycol, and as a fumigant for nuts, spices and cocoa.
Where you meet it
Mostly industrial, with a smaller dietary contribution from fumigated foods.
What it does in the body
A direct-acting DNA alkylator, less potent than ethylene oxide.
Why it’s on the panel
Worth a question about bulk nuts and spices in someone with no industrial exposure.
Work & industryFood & drink
CEMA Acrylonitrile markerSolvents
Acrylonitrile marker
N-Acetyl-S-(2-cyanoethyl)-L-cysteine
The most reliable objective smoking biomarker on the panel.
- What urine shows
- The last 24 to 48 hours.
- Main sources
- Tobacco combustion above all; acrylic fibers, ABS plastics and nitrile rubber manufacture.
- The evidence
- Acrylonitrile is classed as possibly carcinogenic; the smoking association is exceptionally clear.
What it is
The acrylonitrile marker — and in practice one of the most reliable tobacco-exposure biomarkers available.
Where you meet it
Tobacco smoke, decisively. Acrylic fiber, ABS plastic and nitrile rubber production add occupational exposure.
What it does in the body
Acrylonitrile is partly metabolized to cyanide, which contributes to its acute toxicity, and it’s classed as possibly carcinogenic to humans.
Why it’s on the panel
Because it separates smokers from non-smokers with unusual clarity — close to undetectable in true non-smokers, clearly raised in smokers, intermediate with heavy secondhand exposure. That makes it an honest check on the rest of the panel’s smoke-related markers.
Smoke, fuel & trafficWork & industry
PrMA Propyl halide markerSolvents
Propyl halide marker
N-Acetyl-S-propyl-L-cysteine
The least standardized marker in the group. Supporting information only.
- What urine shows
- The last 24 to 48 hours.
- Main sources
- Propyl halides and certain organosulfur compounds.
- The evidence
- Reference data are the thinnest in this group.
What it is
A less commonly measured mercapturic acid reflecting exposure to propyl halides and some organosulfur compounds.
Where you meet it
Mainly industrial.
What it does in the body
Little is established beyond its use as an exposure marker.
Why it’s on the panel
It’s supporting information within the overall solvent picture, not a stand-alone finding.
Work & industry
2-HIB MTBE markerSolvents
MTBE marker
2-Hydroxyisobutyric acid
Available on request — and not a clean marker of anything.
Available on request — not part of the standard panel report.
- What urine shows
- Recent exposure, mixed with your own metabolism.
- Main sources
- Well water near fuel storage or leaking underground tanks (MTBE); also made by your own metabolism and gut bacteria.
- The evidence
- Well known as an MTBE metabolite, but not specific to it.
What it is
Best known as a breakdown product of MTBE, the gasoline additive phased out in the United States after widespread groundwater contamination and still used in some countries.
Where you meet it
Well water near fuel storage or a leaking underground tank.
What it does in the body
The problem is that 2-HIB isn’t exclusively from outside. It also arises from the body’s own metabolism and from gut bacteria, and it appears as a marker in several unrelated metabolic contexts.
Why it’s on the panel
It’s available on request for people with a specific exposure concern — a well near a fuel site — because without that history it can’t be read as an MTBE finding.
WaterMade in the body
4-NP 4-NonylphenolIndustrial
4-Nonylphenol
Bioaccumulates — which makes it behave unlike the other plastics markers here.
- What urine shows
- Longer-term exposure — weeks to months, unlike bisphenols and phthalates.
- Main sources
- Industrial detergents and wetting agents; textile and paper processing; fish from contaminated watersheds; residues in clothing.
- The evidence
- A founding compound of endocrine-disruption science; binds the estrogen receptor more potently than BPA.
What it is
The persistent breakdown product of nonylphenol ethoxylate surfactants, and one of the compounds that helped establish the field of environmental endocrine disruption.
Where you meet it
Nonylphenol ethoxylates are industrial detergents and wetting agents. They degrade in wastewater treatment into nonylphenol, which is far more persistent and more estrogenic than the parent. It settles in river sediment and accumulates in fish; residues in clothing and textiles are a documented route. The EU has restricted it substantially; regulation elsewhere is looser.
What it does in the body
Fat-soluble and bioaccumulative — it behaves more like a persistent pollutant than a short-lived plasticizer, and it’s been detected in breast milk, placenta and fat tissue. The feminization of fish downstream of treatment plants, one of the founding observations of endocrine-disruption science, is attributed partly to this compound.
Why it’s on the panel
Because a raised level reflects longer-term exposure rather than yesterday’s habits — so the advice is different. A behavior change won’t show on retest in days.
Home & personal careFood & drinkWork & industry
TCS TriclosanIndustrial
Triclosan
Largely restricted since 2016 — so a raised result now points at a specific source.
- What urine shows
- Recent exposure.
- Main sources
- Toothpaste; treated textiles, plastics and cutting boards; some cosmetics.
- The evidence
- Thyroid effects in animals, microbiome effects and antimicrobial resistance are documented; the FDA removed it from consumer washes in 2016.
What it is
A synthetic antimicrobial that was in nearly everything for two decades and has been substantially restricted since.
Where you meet it
The FDA banned it from consumer antiseptic washes in 2016 after manufacturers couldn’t show it beat plain soap. It remains in some toothpaste — where it does have real evidence against gum disease — and in textiles, plastics, cutting boards and some cosmetics.
What it does in the body
Triclosan blocks a bacterial fatty-acid enzyme. In people the effects of interest are on thyroid hormone — reduced circulating thyroxine in animal studies, apparently through faster clearance — and on the microbiome, since a broad antimicrobial doesn’t distinguish good bacteria from bad. There’s also a legitimate antibiotic-resistance concern.
Why it’s on the panel
Because population levels have fallen since the restriction, a raised level now points at a specific ongoing source rather than general background — usually toothpaste, or a product at work. That makes it unusually actionable.
Home & personal care
DPhP Diphenyl phosphateIndustrial
Diphenyl phosphate
Dust is the exposure. Cleaning beats avoidance.
- What urine shows
- Recent exposure — hours to days.
- Main sources
- Household dust; furniture foam, electronics, vehicle interiors, hydraulic fluids; nail polish.
- The evidence
- Effects on thyroid and reproductive hormones and on fat-cell signaling are documented; the nail-polish route has been demonstrated directly in volunteers.
What it is
The urinary metabolite of triphenyl phosphate, an organophosphate ester used as both flame retardant and plasticizer — one of the replacements for the brominated flame retardants that were phased out, and another case of substitution outrunning safety assessment.
Where you meet it
Furniture foam, electronics casings, building materials, vehicle interiors, hydraulic fluids, and nail polish. Studies applying nail polish to volunteers measured a rise in urinary diphenyl phosphate within hours. For most people, household dust is the dominant route, because these additives aren’t chemically bound and migrate out over the life of the product.
What it does in the body
Associated with altered thyroid hormone levels, effects on reproductive hormones, and metabolic effects including activation of the master fat-cell switch — which places it in the obesogen conversation alongside tributyltin. It also inhibits an enzyme involved in drug metabolism.
Why it’s on the panel
Because the fix is cheap: dust is the lever. Wet-cleaning hard surfaces, a vacuum with a sealed HEPA system and washing hands before eating reduce exposure more than replacing the couch — because the exposure is what has already off-gassed into the home.
Home & personal care
TG TiglylglycineMetabolic
Tiglylglycine
The one analyte here that isn’t an environmental chemical.
- What urine shows
- A current read on how metabolism is coping.
- Main sources
- Your own metabolism — a byproduct when the breakdown of the amino acid isoleucine backs up.
- The evidence
- Established as a marker in mitochondrial disorders and one rare inherited enzyme deficiency; non-specific outside those.
What it is
A glycine conjugate produced when the breakdown of the amino acid isoleucine backs up — specifically when one mitochondrial enzyme can’t keep pace.
Where you meet it
You don’t meet it. Your body makes it.
What it does in the body
Because the isoleucine pathway depends on mitochondrial enzymes and adequate cofactors, a bottleneck spills tiglylglycine into urine. Elevations have been described in mitochondrial disorders and, dramatically, in a rare inherited enzyme deficiency.
Why it’s on the panel
Because a striking number of exposures on this panel converge on mitochondrial function, and this is a functional read on how that machinery is holding up. It’s non-specific — a general signal of metabolic strain rather than a pointer to any one toxin.
Made in the body