# What Intrinsic Prism Tests Source page: https://intrinsicprism.com/what-we-test In our dated comparison of 11 tests, Intrinsic Prism is the only one that lists heavy metals, mycotoxins, environmental chemicals, glyphosate, PFAS and detox genetics in one order. [See the comparison](https://intrinsicprism.com/learn/compare-toxin-tests) · [All marker guides](https://intrinsicprism.com/learn/markers) ## Mycotoxins 29 Screens for toxins produced by indoor and food-associated molds, including aflatoxins, ochratoxin A, trichothecenes, and other clinically relevant compounds that can affect immune, neurologic, gut, and inflammatory pathways. [Mold toxicity test](https://intrinsicprism.com/tests/mold-mycotoxin-test) *Mold-related toxins* ### Aflatoxin B1 (AFB1) Aflatoxins · Urine Aflatoxin B1 is a potent mycotoxin made chiefly by Aspergillus molds that can contaminate peanuts, corn, tree nuts, spices, and poorly stored grains in warm, humid conditions. It is measured to investigate recent aflatoxin exposure. High or sustained intake can injure the liver and AFB1 is a recognized human carcinogenic hazard; a urine result depends on timing and method and cannot diagnose aflatoxicosis or identify one source. [Read the Aflatoxin guide →](https://intrinsicprism.com/learn/markers/aflatoxin-urine-test) ### Aflatoxin B2 (AFB2) Aflatoxins · Urine Aflatoxin B2 is a less potent aflatoxin that commonly accompanies AFB1 when Aspergillus-contaminated corn, peanuts, nuts, spices, or animal feed are stored under hot, damp conditions. Testing helps characterize the aflatoxin mixture reaching the body. It has liver-toxic and genotoxic concern, though evidence is stronger for AFB1; urine reflects a limited exposure window and a detected amount does not establish illness, dose, or the responsible food. [Read the Aflatoxin guide →](https://intrinsicprism.com/learn/markers/aflatoxin-urine-test) ### Aflatoxin G1 Aflatoxins · Urine Aflatoxin G1 is produced mainly by certain Aspergillus species and may occur in mold-damaged grains, corn, peanuts, tree nuts, seeds, and spices. Urine testing is intended to add compound-specific context when aflatoxin exposure is suspected. Like other aflatoxins it can damage liver cells and is genotoxic in experimental systems, but individual risk depends on dose and duration; one urine concentration cannot prove a particular food, building, or health effect. [Read the Aflatoxin guide →](https://intrinsicprism.com/learn/markers/aflatoxin-urine-test) ### Aflatoxin G2 Aflatoxins · Urine Aflatoxin G2 is a naturally occurring Aspergillus mycotoxin usually found with G1 and B-series aflatoxins in improperly dried or stored grains, nuts, seeds, corn, and spices. Measuring it helps define the pattern of recent aflatoxin exposure rather than relying on a class total. G2 is generally less potent than G1 or B1 but retains liver and genotoxic concern; urinary detection alone cannot establish harmful dose, chronic burden, or source. [Read the Aflatoxin guide →](https://intrinsicprism.com/learn/markers/aflatoxin-urine-test) ### Aflatoxin M1 Aflatoxins · Urine Aflatoxin M1 is a hydroxylated metabolite formed after people or animals process AFB1; it can also enter the diet through milk from animals fed contaminated feed. Urine measurement can therefore reflect recent AFB1 intake and metabolism rather than direct mold growth in the body. It remains genotoxic and has carcinogenic concern, although less potent than AFB1; timing, diet, liver metabolism, and hydration limit interpretation of a single result. [Read the Aflatoxin guide →](https://intrinsicprism.com/learn/markers/aflatoxin-urine-test) ### Chaetoglobosin A (CHA) Other mycotoxins · Urine Chaetoglobosin A is a fungal secondary metabolite produced by Chaetomium and some related molds, organisms reported in damp cellulose-rich materials such as drywall, paper, wood, and settled dust, as well as some foods. It is measured as an exploratory marker of possible fungal-metabolite exposure. Laboratory studies show cytoskeletal and cell-toxic effects, but human exposure thresholds and urinary clinical interpretation are poorly established; detection does not prove a moldy building caused symptoms. ### Citrinin (CTN) Other mycotoxins · Urine Citrinin is a Penicillium, Aspergillus, and Monascus mycotoxin found in some stored grains, rice, cereals, spices, and red-yeast-rice products. Urine testing may help assess recent dietary exposure to citrinin or its metabolites. Kidney toxicity is the principal concern from animal and food-safety evidence, with possible additive effects alongside ochratoxin A; a spot result varies with intake and clearance and cannot diagnose kidney injury or locate the source. [Read the Citrinin guide →](https://intrinsicprism.com/learn/markers/citrinin-urine-test) ### Dihydrocitrinone Other mycotoxins · Urine Dihydrocitrinone is a major human urinary metabolite of citrinin, not a mold toxin ordinarily encountered as a separate product. Its presence can indicate that citrinin from contaminated grains, rice, spices, or red-yeast-rice products was absorbed and metabolized. It is measured because it may be a more abundant exposure biomarker than parent citrinin. Toxic concern belongs mainly to citrinin, especially kidney effects; timing and metabolism prevent conversion of one value into a health diagnosis. ### Enniatin B1 (ENN B1) Other mycotoxins · Urine Enniatin B1 is an ionophoric mycotoxin made by Fusarium species that commonly infect wheat, barley, oats, corn, and other cereals before harvest or during storage. Measuring it can document exposure to an emerging Fusarium toxin that may accompany better-known grain mycotoxins. Cell and animal studies show membrane, mitochondrial, and cytotoxic effects, but human dose-response evidence remains limited; a urine detection does not establish that symptoms were caused by ENN B1. ### Fumonisins B1 Other mycotoxins · Urine Fumonisins B1 is the predominant and best-studied fumonisin, produced mainly by Fusarium molds on corn and corn-based foods and sometimes other grains. Urine testing is used to examine recent dietary exposure and the fumonisin mixture. Fumonisins disrupt sphingolipid metabolism; high exposure is associated with liver and kidney toxicity in animals and population-level disease concerns. One result is timing- and diet-dependent and cannot diagnose injury or prove a particular food source. ### Fumonisins B2 Other mycotoxins · Urine Fumonisins B2 is a related fumonisin that usually occurs at lower levels than B1, produced mainly by Fusarium molds on corn and corn-based foods and sometimes other grains. Urine testing is used to examine recent dietary exposure and the fumonisin mixture. Fumonisins disrupt sphingolipid metabolism; high exposure is associated with liver and kidney toxicity in animals and population-level disease concerns. One result is timing- and diet-dependent and cannot diagnose injury or prove a particular food source. ### Fumonisins B3 Other mycotoxins · Urine Fumonisins B3 is a less abundant member of the fumonisin B series, produced mainly by Fusarium molds on corn and corn-based foods and sometimes other grains. Urine testing is used to examine recent dietary exposure and the fumonisin mixture. Fumonisins disrupt sphingolipid metabolism; high exposure is associated with liver and kidney toxicity in animals and population-level disease concerns. One result is timing- and diet-dependent and cannot diagnose injury or prove a particular food source. ### Gliotoxin Other mycotoxins · Urine Gliotoxin is a sulfur-containing fungal metabolite produced by Aspergillus fumigatus and some other fungi found in compost, decaying vegetation, dust, and damp environments. It is measured experimentally to investigate fungal-metabolite exposure or biologic context. Laboratory studies show immunosuppressive, oxidative, and cell-toxic activity, and it also functions as a virulence factor during invasive aspergillosis; however, urine testing is not an established diagnosis of indoor-mold exposure or fungal infection. ### Mycophenolic Acid Other mycotoxins · Urine Mycophenolic acid is a fungal metabolite produced by Penicillium species, including molds that can grow on damp building materials and spoiled foods; it is also the active immunosuppressant generated by prescription mycophenolate medicines. Measurement may help distinguish environmental or medication-related exposure context. It inhibits lymphocyte proliferation and can suppress immunity at pharmacologic doses, but a result requires medication review and method context and cannot by itself attribute exposure to mold or predict toxicity. ### Ochratoxin A (OTA) Other mycotoxins · Urine Ochratoxin A is produced by Aspergillus and Penicillium molds and can contaminate cereals, coffee, dried fruit, wine, cocoa, spices, pork products, and poorly stored foods. It is measured to investigate dietary mycotoxin exposure because it can persist longer than many other mycotoxins. Kidney toxicity is the central concern, with immunotoxic and carcinogenic-hazard questions also studied; a urine value does not establish source, chronic dose, or kidney disease. [Read the Ochratoxin A guide →](https://intrinsicprism.com/learn/markers/ochratoxin-a-urine-test) ### Patulin Other mycotoxins · Urine Patulin is a Penicillium and Aspergillus mycotoxin most associated with moldy apples, apple juice, cider, and damaged fruit products. Urine testing is intended to provide evidence of recent exposure, although validated human biomonitoring interpretation is limited. High experimental doses can cause gastrointestinal, immune, and cellular toxicity, prompting strict food limits; processing and timing strongly affect exposure, and a detected urinary amount cannot diagnose poisoning or identify a specific beverage. [Read the Patulin guide →](https://intrinsicprism.com/learn/markers/patulin-urine-test) ### Sterigmatocystin (STC) Other mycotoxins · Urine Sterigmatocystin is an Aspergillus mycotoxin and biosynthetic precursor of aflatoxin B1. It has been detected in mold-damaged grains, cheese, spices, animal feed, indoor dust, and damp building materials. Measuring it can broaden assessment beyond regulated aflatoxins when food or indoor exposure is plausible. It is genotoxic and a carcinogenic hazard in animals, but human exposure data and urinary reference ranges are limited; detection cannot establish causation or disease. ### Zearalenone (ZEN) Other mycotoxins · Urine Zearalenone is an estrogenic Fusarium mycotoxin that commonly contaminates corn, wheat, barley, oats, sorghum, and animal feed, especially after wet growing or storage conditions. Urine measurement can indicate recent dietary exposure and metabolism. Its main concern is hormonal and reproductive activity demonstrated strongly in animals, while human effects at typical dietary levels remain less certain; a spot result cannot determine the food source, cumulative dose, or an endocrine diagnosis. [Read the Zearalenone guide →](https://intrinsicprism.com/learn/markers/zearalenone-urine-test) ### Deoxynivalenol (DON) Trichothecenes · Urine Deoxynivalenol, also called vomitoxin, is a type B trichothecene made by Fusarium molds on wheat, corn, barley, oats, and related cereal foods. Urine testing is used to estimate recent dietary exposure, often through DON metabolites. High intake can cause nausea, vomiting, reduced appetite, and immune effects, while chronic low-dose implications remain under study. Rapid clearance, meal timing, and urine dilution mean one value cannot diagnose toxicity or identify one grain product. ### Diacetoxyscirpenol (DAS) Trichothecenes · Urine Diacetoxyscirpenol is a type A trichothecene produced by Fusarium species and reported in contaminated grains, corn, cereals, and animal feed. It is measured to extend surveillance beyond DON and T-2 toxin when mixed Fusarium exposure is possible. Trichothecenes inhibit protein synthesis and sufficiently high DAS exposure can injure gastrointestinal, blood-forming, and immune tissues. Human biomonitoring data are sparse, so a urinary detection cannot establish dose, symptoms, or source. ### Nivalenol (NIV) Trichothecenes · Urine Nivalenol is a type B Fusarium trichothecene that may contaminate wheat, barley, corn, oats, and cereal products, often alongside deoxynivalenol. Measuring NIV helps characterize mixed grain-mycotoxin exposure rather than assuming all trichothecene burden is DON. It inhibits protein synthesis and has gastrointestinal, immune, and blood-cell toxicity in experimental studies; human thresholds and urinary reference data are limited, and a single result cannot diagnose a clinical effect. ### Roridin A Trichothecenes · Urine Roridin A is a macrocyclic trichothecene reported from Myrothecium and related fungi. Water-damaged cellulose materials, settled dust, and contaminated agricultural material are plausible contexts. Measurement is exploratory and aims to distinguish this compound within a mixed trichothecene profile. Macrocyclic trichothecenes potently inhibit protein synthesis and can damage cells in laboratory and animal studies, but validated human urine reference ranges and exposure-response relationships are lacking; detection does not prove a building source, inhaled dose, or cause of symptoms. ### Roridin E Trichothecenes · Urine Roridin E is a macrocyclic trichothecene produced by Myrothecium and some other molds. Water-damaged cellulose materials, settled dust, and contaminated agricultural material are plausible contexts. Measurement is exploratory and aims to distinguish this compound within a mixed trichothecene profile. Macrocyclic trichothecenes potently inhibit protein synthesis and can damage cells in laboratory and animal studies, but validated human urine reference ranges and exposure-response relationships are lacking; detection does not prove a building source, inhaled dose, or cause of symptoms. ### Roridin L2 Trichothecenes · Urine Roridin L2 is a less-studied macrocyclic trichothecene associated with fungal cultures. Water-damaged cellulose materials, settled dust, and contaminated agricultural material are plausible contexts. Measurement is exploratory and aims to distinguish this compound within a mixed trichothecene profile. Macrocyclic trichothecenes potently inhibit protein synthesis and can damage cells in laboratory and animal studies, but validated human urine reference ranges and exposure-response relationships are lacking; detection does not prove a building source, inhaled dose, or cause of symptoms. ### Satratoxin G Trichothecenes · Urine Satratoxin G is a macrocyclic trichothecene strongly associated with Stachybotrys chartarum. Water-damaged cellulose materials, settled dust, and contaminated agricultural material are plausible contexts. Measurement is exploratory and aims to distinguish this compound within a mixed trichothecene profile. Macrocyclic trichothecenes potently inhibit protein synthesis and can damage cells in laboratory and animal studies, but validated human urine reference ranges and exposure-response relationships are lacking; detection does not prove a building source, inhaled dose, or cause of symptoms. ### Satratoxin H Trichothecenes · Urine Satratoxin H is a related Stachybotrys macrocyclic trichothecene. Water-damaged cellulose materials, settled dust, and contaminated agricultural material are plausible contexts. Measurement is exploratory and aims to distinguish this compound within a mixed trichothecene profile. Macrocyclic trichothecenes potently inhibit protein synthesis and can damage cells in laboratory and animal studies, but validated human urine reference ranges and exposure-response relationships are lacking; detection does not prove a building source, inhaled dose, or cause of symptoms. ### T-2 Toxin Trichothecenes · Urine T-2 toxin is a potent type A trichothecene produced by Fusarium molds on oats, barley, wheat, corn, and animal feed, especially under cool, wet conditions. Urine testing may document recent dietary exposure or metabolites within a broader Fusarium profile. It inhibits protein synthesis and at high doses can injure skin, gastrointestinal, immune, and blood-forming tissues. Human exposure is usually food-related, and one urinary result cannot diagnose toxicity or identify the contaminated item. ### Verrucarin A Trichothecenes · Urine Verrucarin A is a macrocyclic trichothecene produced by Myrothecium and related fungi. Water-damaged cellulose materials, settled dust, and contaminated agricultural material are plausible contexts. Measurement is exploratory and aims to distinguish this compound within a mixed trichothecene profile. Macrocyclic trichothecenes potently inhibit protein synthesis and can damage cells in laboratory and animal studies, but validated human urine reference ranges and exposure-response relationships are lacking; detection does not prove a building source, inhaled dose, or cause of symptoms. ### Verrucarin J Trichothecenes · Urine Verrucarin J is a related macrocyclic trichothecene found in fungal cultures. Water-damaged cellulose materials, settled dust, and contaminated agricultural material are plausible contexts. Measurement is exploratory and aims to distinguish this compound within a mixed trichothecene profile. Macrocyclic trichothecenes potently inhibit protein synthesis and can damage cells in laboratory and animal studies, but validated human urine reference ranges and exposure-response relationships are lacking; detection does not prove a building source, inhaled dose, or cause of symptoms. ## Heavy Metals 20 Measures urinary excretion of toxic and potentially disruptive metals. Results help identify exposures that may affect neurologic, cardiovascular, kidney, thyroid, immune, and mitochondrial health. [Heavy metal test kit](https://intrinsicprism.com/tests/heavy-metal-test) *Metals burden* ### Aluminum Heavy metals and elements · Urine Aluminum is a widely used light metal. Sources include food additives, cookware, antacids, drinking water, dust, welding, mining, and metal production. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. nervous-system, lung, and bone effects are concerns at sufficiently high occupational or medically relevant exposure. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Aluminum guide →](https://intrinsicprism.com/learn/markers/aluminum-urine-test) ### Antimony Heavy metals and elements · Urine Antimony is a metalloid used in flame retardants, alloys, batteries, and plastics. Sources include industrial dust, smelting, brake materials, contaminated air or water, and some consumer products. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. lung, heart, gastrointestinal, and skin effects are reported with substantial exposure. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Antimony guide →](https://intrinsicprism.com/learn/markers/antimony-urine-test) ### Arsenic Heavy metals and elements · Urine Arsenic is a naturally occurring metalloid present in several chemical forms. Sources include groundwater, rice and some foods, treated wood, mining, smelting, and pesticides used historically. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. inorganic arsenic can damage skin, nerves, cardiovascular systems and is a human carcinogenic hazard. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Arsenic guide →](https://intrinsicprism.com/learn/markers/arsenic-urine-test) ### Barium Heavy metals and elements · Urine Barium is an alkaline-earth metal whose soluble salts differ greatly from insoluble barium sulfate. Sources include drinking water, soils, ceramics, drilling work, fireworks, and medical barium contrast. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. high soluble-barium exposure can disturb potassium, muscles, heart rhythm, and blood pressure. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Barium guide →](https://intrinsicprism.com/learn/markers/barium-urine-test) ### Beryllium Heavy metals and elements · Urine Beryllium is a lightweight metal used in aerospace, electronics, nuclear, ceramic, and specialty alloys. Sources include machining, grinding, recycling, smelting, and workplace dust; consumer exposure is usually low. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. inhalation can cause sensitization, chronic beryllium lung disease, and lung-cancer hazard. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Beryllium guide →](https://intrinsicprism.com/learn/markers/beryllium-urine-test) ### Bismuth Heavy metals and elements · Urine Bismuth is a heavy element used in stomach medicines, cosmetics, pigments, alloys, and some industrial processes. Sources include bismuth-containing medicines are often the most relevant source, alongside occupational dust. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. very high or prolonged exposure can affect the nervous system and kidneys, although typical medicinal use is usually well tolerated. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. ### Cadmium Heavy metals and elements · Urine Cadmium is a toxic metal used in batteries, pigments, plating, and some alloys. Sources include tobacco smoke, certain foods, contaminated soil, welding, smelting, battery work, and industrial dust. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. cadmium accumulates in kidneys and can harm kidney, bone, lung, and cardiovascular health; it is carcinogenic by inhalation. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Cadmium guide →](https://intrinsicprism.com/learn/markers/cadmium-urine-test) ### Cesium Heavy metals and elements · Urine Cesium is an alkali metal occurring naturally in trace amounts, distinct from radioactive cesium isotopes. Sources include food, water, soil, mining, electronics, drilling fluids, and specialized industrial work. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. stable cesium is generally less toxic than many heavy metals, while high doses can disturb potassium handling and heart rhythm. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Cesium guide →](https://intrinsicprism.com/learn/markers/cesium-urine-test) ### Gadolinium Heavy metals and elements · Urine Gadolinium is a rare-earth element mainly encountered clinically in gadolinium-based MRI contrast agents. Sources include prior contrast-enhanced MRI is the key source; specialized electronics and industrial work are less common sources. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. retention can occur after contrast, and severe fibrosis risk is chiefly associated with certain agents in advanced kidney impairment. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Gadolinium guide →](https://intrinsicprism.com/learn/markers/gadolinium-urine-test) ### Lead Heavy metals and elements · Urine Lead is a cumulative toxic metal with no known beneficial biologic role. Sources include old paint and dust, plumbing, contaminated soil or water, batteries, firing ranges, renovation, imported products, and occupational work. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. lead can harm brain development, nerves, blood, kidneys, blood pressure, and reproduction, especially in children and pregnancy. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Lead guide →](https://intrinsicprism.com/learn/markers/lead-urine-test) ### Mercury Heavy metals and elements · Urine Mercury is a metal occurring as elemental, inorganic, and organic forms with different toxicology. Sources include large predatory fish, dental or industrial settings, mining, broken devices, combustion, and contaminated workplaces. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. mercury can damage the nervous system and kidneys, with fetal neurodevelopment especially sensitive to methylmercury. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Mercury guide →](https://intrinsicprism.com/learn/markers/mercury-urine-test) ### Nickel Heavy metals and elements · Urine Nickel is a metal used in stainless steel, alloys, batteries, plating, coins, and jewelry. Sources include food, tobacco, metal work, welding, refining, dust, and skin contact with nickel-containing products. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. nickel commonly causes allergic dermatitis; inhaled occupational compounds can injure lungs and carry carcinogenic hazard. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Nickel guide →](https://intrinsicprism.com/learn/markers/nickel-urine-test) ### Palladium Heavy metals and elements · Urine Palladium is a platinum-group metal used in vehicle catalysts, electronics, dentistry, jewelry, and chemical processing. Sources include traffic and industrial dust, catalyst work, dental materials, and jewelry are possible sources. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. sensitization and skin or respiratory allergy are the best-described concerns, while systemic human toxicity data are limited. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Palladium guide →](https://intrinsicprism.com/learn/markers/palladium-urine-test) ### Platinum Heavy metals and elements · Urine Platinum is a platinum-group metal used in catalysts, jewelry, electronics, industry, and platinum-based chemotherapy. Sources include catalyst production, refining, traffic dust, jewelry, dental materials, or cancer treatment can contribute. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. soluble platinum salts can cause occupational allergy and asthma; chemotherapy compounds have distinct kidney, nerve, and blood toxicity. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Platinum guide →](https://intrinsicprism.com/learn/markers/platinum-urine-test) ### Tellurium Heavy metals and elements · Urine Tellurium is a rare metalloid used in solar panels, semiconductors, alloys, rubber, and metal refining. Sources include electronics and mining work, industrial dust, and uncommon dietary background are plausible sources. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. high exposure can irritate airways and cause garlic-like breath, gastrointestinal, neurologic, or liver effects; human data remain limited. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. ### Thallium Heavy metals and elements · Urine Thallium is a highly toxic metal formerly used in pesticides and now used in electronics, optics, and specialized industry. Sources include smelting, cement, coal combustion, contaminated food or water, and occupational processes can contribute. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. acute or substantial exposure can cause painful neuropathy, hair loss, gastrointestinal illness, and multi-organ injury. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Thallium guide →](https://intrinsicprism.com/learn/markers/thallium-urine-test) ### Thorium Heavy metals and elements · Urine Thorium is a naturally occurring radioactive metal found in some mineral sands and specialized alloys. Sources include mining, milling, welding electrodes, legacy products, soil, and occupational dust are typical contexts. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. internalized radioactive thorium can irradiate tissues over time; inhalation and ingestion risk depend on isotope, solubility, and dose. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Thorium guide →](https://intrinsicprism.com/learn/markers/thorium-urine-test) ### Tin Heavy metals and elements · Urine Tin is an element encountered as inorganic tin or more toxic organotin compounds. Sources include canned foods, alloys, solder, dust, marine coatings, PVC stabilizers, and industrial or hobby work can contribute. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. inorganic tin is generally poorly absorbed, while high doses or organotins can affect gastrointestinal, neurologic, immune, or liver systems. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Tin guide →](https://intrinsicprism.com/learn/markers/tin-urine-test) ### Tungsten Heavy metals and elements · Urine Tungsten is a dense metal used in hard-metal tools, electronics, munitions, welding, and high-temperature alloys. Sources include machining, grinding, mining, contaminated dust or water, and occupational hard-metal work are possible sources. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. human systemic toxicity is incompletely characterized; workplace mixtures, especially tungsten carbide with cobalt, can injure lungs. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Tungsten guide →](https://intrinsicprism.com/learn/markers/tungsten-urine-test) ### Uranium Heavy metals and elements · Urine Uranium is a naturally occurring radioactive heavy metal whose chemical kidney toxicity can be more immediate than its radiation hazard. Sources include groundwater, phosphate fertilizers, mining, milling, military materials, and contaminated soil or dust can contribute. Urine measurement reflects excretion, but body-burden meaning varies by form, timing, kidney function, and collection. sufficient soluble uranium exposure can damage kidneys; radiologic risk depends on isotope, route, dose, and duration. One value needs exposure history and suitable references; it cannot diagnose poisoning or identify the source. [Read the Uranium guide →](https://intrinsicprism.com/learn/markers/uranium-urine-test) ## Environmental Toxins 38 Captures common modern exposures from plastics, pesticides, herbicides, solvents, preservatives, antimicrobial agents, and volatile organic compounds, with interpretation tied to source reduction and detox support. [Plastic chemicals test guide](https://intrinsicprism.com/learn/microplastics-plastic-chemicals-test) [Pesticide test guide](https://intrinsicprism.com/learn/pesticide-exposure-test) *Everyday exposures* ### 4-Nonylphenol Environmental phenols · Urine 4-Nonylphenol is a parent alkylphenol associated with breakdown of nonylphenol ethoxylate surfactants used in industrial detergents, cleaners, paints, textiles, and some pesticide formulations; contaminated water and food can contribute. Urinary measurement indicates relatively recent exposure, not stored body burden. Experimental endocrine and aquatic toxicity concerns motivate monitoring, but one urine value cannot identify a source, predict disease, or establish an individual health effect. ### Bisphenol A (BPA) Environmental phenols · Urine Bisphenol A is a parent industrial chemical used in polycarbonate plastics and epoxy resins, including some food-can linings, reusable containers, thermal paper, and other consumer materials. Urinary BPA mainly reflects recent exposure and is measured to support source-reduction decisions. Endocrine, reproductive, metabolic, and developmental effects remain active research areas; a spot urine result varies with timing and hydration and does not by itself diagnose toxicity or disease. [Read the Bisphenol A guide →](https://intrinsicprism.com/learn/markers/bisphenol-a-urine-test) ### Triclosan (TCS) Environmental phenols · Urine Triclosan is a parent antimicrobial chemical formerly common in soaps and still found in some toothpastes, cosmetics, textiles, plastics, and other treated products. Urinary triclosan is used to characterize recent contact or ingestion. Laboratory and observational studies have raised endocrine, thyroid, microbiome, and antimicrobial-resistance questions, but clinical meaning at typical concentrations is uncertain; a single result cannot determine the product responsible or prove that harm has occurred. [Read the Triclosan guide →](https://intrinsicprism.com/learn/markers/triclosan-urine-test) ### 2,4-Dichlorophenoxyacetic Acid (2,4-D) Herbicides · Urine 2,4-D is a parent chlorophenoxy herbicide used on lawns, turf, rights-of-way, and agricultural crops; exposure may follow spray drift, treated vegetation, contaminated dust, or occupational handling. Urinary 2,4-D is a short-term exposure marker useful for comparing exposure patterns. High exposures can cause neurologic and other toxicity, while evidence at environmental levels is more limited; timing, hydration, and recent application strongly affect a spot result. [Read the 2,4-Dichlorophenoxyacetic Acid guide →](https://intrinsicprism.com/learn/markers/2-4-dichlorophenoxyacetic-acid-urine-test) ### Atrazine Herbicides · Urine Atrazine is a parent triazine herbicide used mainly on corn, sorghum, and sugarcane, with potential exposure through agricultural work, spray drift, and contaminated surface or drinking water. Measuring urine can document recent internal exposure and guide investigation of water or workplace sources. Reproductive and endocrine findings in animals and ecological effects drive concern, but human evidence and dose relevance are uncertain; one result cannot predict an individual outcome. [Read the Atrazine guide →](https://intrinsicprism.com/learn/markers/atrazine-urine-test) ### Atrazine mercapturate Herbicides · Urine Atrazine mercapturate is a glutathione-derived urinary exposure metabolite of atrazine, not the herbicide applied to fields. It can reflect recent contact with atrazine from agricultural work, spray drift, treated crops, or contaminated water and is often more practical to measure than the short-lived parent compound. It does not identify the route or dose, and health concerns belong chiefly to atrazine exposure; metabolism, collection timing, and hydration limit individual interpretation. [Read the Atrazine mercapturate guide →](https://intrinsicprism.com/learn/markers/atrazine-urine-test) ### Glyphosate Herbicides · Urine Glyphosate is a parent broad-spectrum herbicide used in agriculture, landscaping, rights-of-way, and home weed control; residues in food, water, dust, and occupational spray contact may contribute. Urinary measurement is intended to document recent exposure rather than cumulative storage. Agencies continue to evaluate carcinogenicity and other possible effects, with differing hazard interpretations; a detected amount does not establish unsafe dose, source, causation, or an individual health diagnosis. [Read the Glyphosate guide →](https://intrinsicprism.com/learn/glyphosate-urine-test) ### Tiglylglycine (TG) Mitochondrial marker · Urine Tiglylglycine is an endogenous acylglycine metabolite, not an environmental toxicant or a specific exposure metabolite. It arises during isoleucine-related mitochondrial metabolism and can increase with certain inherited organic-acid disorders or metabolic stress; diet, fasting, illness, and specimen handling may influence it. Measurement may provide metabolic context, but it does not identify a product, water, air, or occupational source and should not be interpreted alone as evidence of toxin exposure or mitochondrial disease. ### Diphenyl Phosphate (DPP) Other markers · Urine Diphenyl phosphate is commonly a urinary metabolite of triphenyl phosphate and related aryl organophosphate esters used as flame retardants and plasticizers in electronics, furniture foam, building materials, nail products, and indoor dust; it can also occur directly. Measuring DPP helps assess recent exposure but is not specific to one parent product. Toxicologic studies raise developmental, endocrine, reproductive, and neurologic questions, yet a spot urine level cannot establish dose or harm. ### N-acetyl-S-(2-carbamoylethyl)-cysteine Other markers · Urine N-acetyl-S-(2-carbamoylethyl)-cysteine is a mercapturic-acid exposure metabolite of acrylamide, not acrylamide itself. Acrylamide exposure can come from tobacco smoke, occupational polymer or grouting work, and carbohydrate-rich foods cooked at high temperatures, such as fries, chips, and coffee. Urinary measurement captures recent intake; acrylamide has neurotoxicity and carcinogenicity concerns at sufficient exposure, but this metabolite varies with metabolism and cannot identify source or predict individual risk. ### Perchlorate (PERC) Other markers · Urine Perchlorate is a parent inorganic anion associated with rocket propellants, explosives, fireworks, some fertilizers, contaminated drinking water, and foods irrigated with affected water. Urinary perchlorate reflects recent intake and is measured because perchlorate can competitively inhibit thyroid iodide uptake. Susceptibility depends on dose, iodine status, pregnancy, and age; one spot urine concentration is highly time- and dilution-dependent and cannot by itself demonstrate thyroid injury or locate the exposure source. [Read the Perchlorate guide →](https://intrinsicprism.com/learn/markers/perchlorate-urine-test) ### Butylparaben Parabens · Urine Butylparaben is a parent paraben preservative used in some cosmetics, personal-care products, pharmaceuticals, and occasionally foods, although use patterns vary by market. Urinary measurement generally reflects recent absorbed exposure and conjugated metabolites. Parabens have weak estrogenic activity in experimental systems, prompting reproductive and developmental research, but evidence of clinical harm at usual human exposures is uncertain; a single urine value is transient and cannot identify a specific product or diagnose endocrine dysfunction. [Read the Parabens guide →](https://intrinsicprism.com/learn/markers/parabens-urine-test) ### Ethylparaben Parabens · Urine Ethylparaben is a parent preservative that may be present in cosmetics, lotions, toiletries, medicines, and certain processed foods. Urinary ethylparaben is measured as a marker of recent aggregate exposure, often dominated by personal-care use rather than long-term accumulation. Experimental endocrine activity has motivated monitoring, but potency is low and human health implications at common exposures remain unsettled; product use, collection timing, metabolism, and urine dilution can substantially change a spot result. [Read the Parabens guide →](https://intrinsicprism.com/learn/markers/parabens-urine-test) ### Methylparaben Parabens · Urine Methylparaben is a parent antimicrobial preservative widely used in cosmetics, skin and hair products, pharmaceuticals, and some foods. Because it is metabolized and excreted relatively quickly, urine testing mainly reflects recent use or ingestion and can help prioritize avoidable sources. Laboratory studies report weak hormonal activity, but a measured concentration does not establish endocrine disruption or disease in a person; frequent product use and urine dilution strongly influence the result. [Read the Parabens guide →](https://intrinsicprism.com/learn/markers/parabens-urine-test) ### Propylparaben Parabens · Urine Propylparaben is a parent preservative found in some cosmetics, personal-care products, medicines, and foods, sometimes combined with other parabens. Urinary propylparaben is a recent-exposure biomarker useful for examining aggregate contact and possible product substitutions. Experimental reproductive and endocrine findings warrant study, but human evidence at typical exposure is limited and a spot result cannot prove adverse effect; timing, metabolism, formulation, and hydration complicate comparisons. [Read the Parabens guide →](https://intrinsicprism.com/learn/markers/parabens-urine-test) ### 2,2-bis(4-Chlorophenyl) acetic acid (DDA) Pesticides · Urine 2,2-bis(4-chlorophenyl)acetic acid, also called DDA, is a breakdown metabolite associated with DDT-related compounds rather than a currently applied parent pesticide. Exposure may reflect legacy residues in soil and dust, contaminated foods—especially fatty animal foods—or occupational contact in regions where DDT remains used. Measurement can indicate historical organochlorine exposure, but matrices and persistence matter; one urinary value has uncertain specificity and cannot establish dose, timing, or health injury. [Read the Pesticide test guide →](https://intrinsicprism.com/learn/pesticide-exposure-test) ### 3-Phenoxybenzoic Acid (3PBA) Pesticides · Urine 3-Phenoxybenzoic acid is a nonspecific urinary metabolite of several pyrethroid insecticides, not one identifiable pesticide. Household pest treatments, pet products, mosquito control, agricultural residues, indoor dust, and occupational spraying can contribute. It is measured to estimate recent pyrethroid-class exposure, but it cannot reveal which parent chemical or route was responsible. Pyrethroids can affect the nervous system at sufficient doses; usual spot levels do not by themselves predict symptoms or disease. [Read the Pesticide test guide →](https://intrinsicprism.com/learn/pesticide-exposure-test) ### Diethyl phosphate (DEP) Pesticides · Urine Diethyl phosphate is a nonspecific dialkyl-phosphate urinary metabolite of multiple organophosphate insecticides and may also arise from preformed environmental degradation products. Food residues, home or agricultural spraying, contaminated dust, and occupational handling can contribute. DEP is measured for recent class-level exposure, not to identify a particular pesticide. Organophosphates can inhibit cholinesterase at sufficient dose, but DEP itself does not reconstruct dose reliably and one spot result cannot establish toxicity. [Read the Pesticide test guide →](https://intrinsicprism.com/learn/pesticide-exposure-test) ### Diethyldithiophosphate (DEDTP) Pesticides · Urine Diethyldithiophosphate is a nonspecific urinary dialkyl-phosphate metabolite associated with certain organophosphate pesticides containing diethyl groups. Possible sources include treated produce, residential pest control, agricultural drift, and mixing or applying pesticides at work. Measurement supports recent class-level biomonitoring, yet environmental DEDTP can sometimes be absorbed directly and no single parent can be inferred. Acute organophosphate toxicity is dose-dependent; this result alone cannot diagnose cholinesterase inhibition or forecast chronic effects. [Read the Pesticide test guide →](https://intrinsicprism.com/learn/pesticide-exposure-test) ### Diethylthiophosphate (DETP) Pesticides · Urine Diethylthiophosphate is a nonspecific urinary metabolite shared by several diethyl organophosphate insecticides, not a unique fingerprint for one formulation. Diet, household insecticides, agricultural work or drift, and contaminated dust are plausible contributors. It is measured to characterize recent organophosphate-class exposure. Although sufficiently high parent-pesticide exposure can produce neurologic toxicity through cholinesterase inhibition, DETP levels are affected by preformed metabolites, timing, and dilution and do not alone demonstrate harmful dose. [Read the Pesticide test guide →](https://intrinsicprism.com/learn/pesticide-exposure-test) ### Dimethyl phosphate (DMP) Pesticides · Urine Dimethyl phosphate is a nonspecific dialkyl-phosphate metabolite of numerous dimethyl organophosphate pesticides and can also exist as an environmental breakdown product. Treated foods, home pest products, farm work, spray drift, and dust may contribute. Urine testing is useful for recent population-level exposure assessment but cannot name the parent pesticide. Parent compounds can cause cholinesterase-related toxicity at sufficient exposure; a DMP spot result cannot distinguish active pesticide from degradation product or diagnose poisoning. [Read the Pesticide test guide →](https://intrinsicprism.com/learn/pesticide-exposure-test) ### Dimethyldithiophosphate (DMDTP) Pesticides · Urine Dimethyldithiophosphate is a nonspecific urinary metabolite associated with several dimethyl organophosphate insecticides. Potential exposure comes from pesticide residues on food, agricultural spraying, indoor pest control, contaminated dust, or occupational mixing and application. It is measured as a recent class-level biomarker, but direct intake of environmental metabolites and rapid clearance limit source attribution. Health concern centers on adequately high parent-pesticide exposure; DMDTP alone does not quantify cholinesterase inhibition or prove clinical toxicity. [Read the Pesticide test guide →](https://intrinsicprism.com/learn/pesticide-exposure-test) ### Dimethylthiophosphate (DMTP) Pesticides · Urine Dimethylthiophosphate is a nonspecific urinary dialkyl-phosphate metabolite formed from multiple dimethyl organophosphate pesticides. Common pathways include diet, residential or agricultural insecticide use, spray drift, and occupational contact. Measuring DMTP helps characterize recent aggregate exposure but cannot determine the exact pesticide, route, or biologically active dose. Organophosphate neurotoxicity is recognized at sufficient exposure, yet hydration, collection timing, metabolism, and ingestion of preformed DMTP make individual interpretation cautious. [Read the Pesticide test guide →](https://intrinsicprism.com/learn/pesticide-exposure-test) ### Mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) Phthalates · Urine MEHHP is an oxidative urinary exposure metabolite of di(2-ethylhexyl) phthalate, or DEHP, rather than a commercial ingredient itself. DEHP has been used in flexible PVC, flooring, tubing, medical devices, packaging, and other plastics; food contact and indoor dust can contribute. MEHHP is measured because it is often a robust recent-exposure marker. Reproductive, developmental, and endocrine concerns motivate monitoring, but one urine level cannot predict an individual effect or long-term burden. [Read the Phthalates guide →](https://intrinsicprism.com/learn/markers/phthalates-urine-test) ### Mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP) Phthalates · Urine MEOHP is an oxidative urinary metabolite of DEHP and is not ordinarily a product ingredient. Exposure to its parent may occur from flexible vinyl materials, food processing or packaging, medical tubing and bags, building materials, and indoor dust. Measuring MEOHP helps estimate recent DEHP exposure, often alongside other DEHP metabolites. Animal and human studies raise reproductive, developmental, and metabolic concerns, but a spot concentration varies with timing and dilution and is not a diagnosis. [Read the Phthalates guide →](https://intrinsicprism.com/learn/markers/phthalates-urine-test) ### Mono-2-ethylhexyl phthalate (MEHP) Phthalates · Urine MEHP is the primary monoester exposure metabolite of DEHP, though it can undergo further oxidation and has a shorter urinary window than oxidative metabolites. Parent DEHP sources include flexible PVC, medical equipment, flooring, packaging, and contaminated food or dust. MEHP is measured to assess recent exposure and metabolism. DEHP-related reproductive and developmental concerns support monitoring, but contamination, timing, hydration, and interindividual metabolism limit conclusions from a single result. [Read the Phthalates guide →](https://intrinsicprism.com/learn/markers/phthalates-urine-test) ### Mono-ethyl phthalate (MEP) Phthalates · Urine Mono-ethyl phthalate is the principal urinary exposure metabolite of diethyl phthalate, a solvent and fragrance carrier used in some perfumes, cosmetics, personal-care products, plastics, and coatings. MEP is measured to estimate recent aggregate exposure, often driven by product use. Phthalate endocrine and reproductive effects are researched, but risks differ among parent compounds and doses; one spot MEP value cannot identify a product, establish cumulative burden, or prove an adverse health effect. [Read the Phthalates guide →](https://intrinsicprism.com/learn/markers/phthalates-urine-test) ### 2-Hydroxyethyl Mercapturic Acid (HEMA) Volatile organic compounds · Urine 2-Hydroxyethyl mercapturic acid is a nonspecific urinary exposure metabolite linked to ethylene oxide, vinyl chloride, and acrylonitrile, and it may have endogenous or other contributions. Tobacco smoke, combustion, sterilization or chemical workplaces, and polluted air are plausible sources. It is measured for recent VOC exposure, but cannot identify one parent. Those parent chemicals carry neurologic or carcinogenic concerns at sufficient exposure; HEMA alone does not establish dose, source, or disease. [Read the VOC exposure guide →](https://intrinsicprism.com/learn/benzene-voc-exposure-test) ### 2-Hydroxyisobutyric Acid (2HIB) Volatile organic compounds · Urine 2-Hydroxyisobutyric acid is a small organic acid that can arise endogenously and has been studied as a nonspecific urinary marker of tert-butyl compounds, including fuel oxygenates and industrial solvents; it is not a unique toxicant fingerprint. Gasoline vapors, polluted air, contaminated water, and occupational fuel or chemical contact are possible contributors. Measurement may provide exposure context, but diet and metabolism can influence it, so a single value cannot identify a source or predict harm. [Read the VOC exposure guide →](https://intrinsicprism.com/learn/benzene-voc-exposure-test) ### 2-Methylhippuric Acid (2MHA) Volatile organic compounds · Urine 2-Methylhippuric acid is a urinary exposure metabolite of o-xylene, not xylene itself. Xylene exposure can occur from paints, thinners, adhesives, fuels, printing, laboratories, tobacco smoke, polluted air, and occupational solvent use. Measuring 2MHA helps assess recent o-xylene uptake. High xylene exposure can affect the nervous system and irritate eyes and airways, but rapid clearance, coexposures, timing, and dilution prevent one result from predicting individual health effects. [Read the VOC exposure guide →](https://intrinsicprism.com/learn/benzene-voc-exposure-test) ### 3-Methylhippuric Acid (3MHA) Volatile organic compounds · Urine 3-Methylhippuric acid is a urinary exposure metabolite primarily associated with m-xylene. Likely sources include solvent-based paints and coatings, printing and cleaning products, gasoline, vehicle exhaust, cigarette smoke, indoor air, and workplace handling. It is measured to document recent uptake rather than cumulative storage. Xylene can cause acute irritation and central-nervous-system effects at high levels, but collection timing, mixed isomers, metabolism, and hydration limit interpretation of an isolated value. [Read the VOC exposure guide →](https://intrinsicprism.com/learn/benzene-voc-exposure-test) ### 4-Methylhippuric Acid (4MHA) Volatile organic compounds · Urine 4-Methylhippuric acid is a urinary exposure metabolite of p-xylene. Paints, lacquers, adhesives, printing operations, fuels, traffic emissions, tobacco smoke, and industrial solvent work may contribute. Urinary 4MHA is intended to indicate recent p-xylene uptake, although some laboratory methods report 3MHA and 4MHA together. Sufficient xylene exposure can cause neurologic and irritant effects; a single value cannot reconstruct air concentration, separate all sources, or establish disease. [Read the VOC exposure guide →](https://intrinsicprism.com/learn/benzene-voc-exposure-test) ### N-Acetyl-(2-cyanoethyl)-cysteine (NACE) Volatile organic compounds · Urine N-acetyl-(2-cyanoethyl)-cysteine is a mercapturic-acid exposure metabolite of acrylonitrile, rather than the parent volatile chemical. Tobacco smoke is an important source; plastics, synthetic rubber, resins, combustion emissions, and occupational acrylonitrile work can also contribute. Urinary measurement captures recent exposure. Acrylonitrile can cause acute neurologic and respiratory toxicity and is a carcinogenic hazard, but metabolite timing, smoking, and metabolism mean one result cannot quantify risk or prove harm. [Read the VOC exposure guide →](https://intrinsicprism.com/learn/benzene-voc-exposure-test) ### N-Acetyl-(2-hydroxypropyl)-cysteine (NAHP) Volatile organic compounds · Urine N-acetyl-(2-hydroxypropyl)-cysteine is a mercapturic-acid exposure metabolite of propylene oxide, not the parent epoxide. Propylene oxide is used in polyurethane production, fumigation and sterilization applications, and chemical manufacturing; workplace air and combustion-related exposures may contribute. Urinary measurement reflects recent uptake. The parent is irritating, mutagenic in experimental systems, and considered a carcinogenic hazard, but this biomarker cannot identify route, reconstruct dose, or predict an individual outcome. [Read the VOC exposure guide →](https://intrinsicprism.com/learn/benzene-voc-exposure-test) ### N-Acetyl-(3,4-dihydroxybutyl)-cysteine Volatile organic compounds · Urine N-acetyl-(3,4-dihydroxybutyl)-cysteine is a urinary mercapturic-acid exposure metabolite of 1,3-butadiene. Major sources include tobacco smoke, motor-vehicle exhaust, fires and combustion, synthetic-rubber production, and other occupational petrochemical settings. It is measured because the parent gas is short-lived and difficult to assess after exposure. 1,3-Butadiene is a recognized carcinogenic hazard, but biomarker concentration depends on timing and metabolism and does not by itself quantify cancer risk. [Read the VOC exposure guide →](https://intrinsicprism.com/learn/benzene-voc-exposure-test) ### N-Acetyl-(propyl)-cysteine (NAPR) Volatile organic compounds · Urine N-acetyl-(n-propyl)-cysteine is a urinary mercapturic-acid exposure metabolite of 1-bromopropane, not a general marker for every propyl compound. Sources include vapor-degreasing, dry-cleaning or spot-cleaning solvents, spray adhesives, and occupational manufacturing use. Measurement can document recent uptake. High workplace exposure has been associated with neurologic and reproductive toxicity concerns, but a spot urine value cannot reconstruct inhaled dose, distinguish every possible contributor, or diagnose injury. [Read the VOC exposure guide →](https://intrinsicprism.com/learn/benzene-voc-exposure-test) ### N-acetyl phenyl cysteine (NAP) Volatile organic compounds · Urine N-acetyl phenyl cysteine, often called phenylmercapturic acid, is a urinary exposure metabolite associated with benzene but is relatively nonspecific and may be affected by other aromatic sources. Tobacco smoke, gasoline and vehicle emissions, fires, polluted air, and petroleum or chemical work are plausible contributors. It is measured for recent exposure context. Benzene is a hematotoxic carcinogenic hazard, yet low-level NAP lacks the specificity needed to diagnose benzene toxicity or quantify cancer risk. [Read the VOC exposure guide →](https://intrinsicprism.com/learn/benzene-voc-exposure-test) ### Phenyl glyoxylic Acid (PGO) Volatile organic compounds · Urine Phenylglyoxylic acid is a nonspecific urinary exposure metabolite of ethylbenzene and styrene. Sources include tobacco smoke, fuels and traffic emissions, solvent-based products, plastics and fiberglass manufacturing, resins, paints, and occupational air. Measuring it can support recent aromatic-VOC exposure assessment, usually alongside other metabolites. High parent exposures can affect the nervous system and hearing, and styrene has carcinogenic-hazard concerns; this metabolite alone cannot identify the parent, dose, or clinical effect. [Read the VOC exposure guide →](https://intrinsicprism.com/learn/benzene-voc-exposure-test) ## PFAS Chemicals 21 Measures per- and polyfluoroalkyl substances associated with stain-resistant, non-stick, waterproof, food-packaging, and industrial exposures. Results help prioritize exposure reduction and clinical follow-up. [PFAS test guide](https://intrinsicprism.com/learn/pfas-test-at-home) *Forever chemicals* ### GenX/HPFO-DA PFAS compounds · Blood / serum GenX/HPFO-DA refers to hexafluoropropylene oxide dimer acid, a parent PFAS used as a processing-aid replacement for PFOA in fluoropolymer manufacture. Communities near facilities may encounter it in surface or drinking water; occupational and contaminated-food pathways are also possible. Serum measurement evaluates internal exposure, although this compound may clear faster than some legacy PFAS. Animal liver, immune, developmental, and cancer findings raise concern, but human outcome data are limited and one value is not diagnostic. ### 9-chlorohexadecafluoro-3-oxanonane-1-sulfonate PFAS compounds · Blood / serum 9-chlorohexadecafluoro-3-oxanonane-1-sulfonate, often called 9Cl-PFESA or a major F-53B component, is a parent chlorinated ether PFAS used notably as a mist suppressant in chrome plating. Occupational contact and industrially contaminated water, food, or sediment are plausible sources, especially near plating activity. Serum testing can document exposure to this persistent alternative. Toxicology and human data are sparse; thyroid and bioaccumulation findings warrant caution, not individualized disease prediction. ### Dodecafluoro-3H-4,8-dioxanoate (NaDONA) PFAS compounds · Blood / serum NaDONA is the sodium salt of ADONA, a parent ether PFAS introduced as a processing aid in fluoropolymer production. Exposure evidence points mainly to occupational settings and communities affected by industrial releases into surface or drinking water, with possible food-chain transfer. Serum measurement helps detect this replacement PFAS, but population data are limited. Experimental liver and developmental findings prompt concern; toxicokinetics and human dose-response remain uncertain, so a single result cannot establish harm. ### Perfluoro-[1,2-13C2] octanoic acid (M2PFOA) PFAS compounds · Blood / serum Perfluoro-[1,2-13C2]octanoic acid is a carbon-13-labeled PFOA analytical standard, not an environmental toxicant expected from cookware, water, food, air, or work. Laboratories add a known amount during isotope-dilution mass spectrometry to correct for recovery and instrument response and to quantify native PFOA accurately. It should be recorded as a quality-control reagent rather than interpreted as patient exposure; any reported patient concentration requires clarification with the laboratory and cannot carry PFOA health-risk meaning. ### Perfluoro-1-[1,2,3,4-13C4] octanesulfonic acid PFAS compounds · Blood / serum Perfluoro-1-[1,2,3,4-13C4]octanesulfonic acid is a carbon-13-labeled PFOS analytical internal standard, not a naturally occurring exposure marker or environmental toxicant. A laboratory deliberately adds it to serum preparations so mass spectrometry can compensate for sample loss, matrix effects, and response variation while measuring native PFOS. It has no consumer-product, food, water, air, or occupational source in the patient; a patient-facing numeric result would indicate reporting or panel-design confusion requiring laboratory review. ### Perfluoro-1-heptane sulfonic acid (PFHpS) PFAS compounds · Blood / serum PFHpS is a parent seven-carbon perfluoroalkyl sulfonic acid and may occur as an impurity, degradation product, or component of historical fluorochemical and firefighting-foam releases. Contaminated drinking water, seafood or other food, dust, and occupational contact can contribute. Serum testing documents internal exposure because sulfonates can persist, but PFHpS-specific toxicology and epidemiology are limited. Class-level liver, lipid, thyroid, immune, and developmental concerns do not make one result diagnostic. ### Perfluoro-n-[1,2-13C2] decanoic acid (MPFDA) PFAS compounds · Blood / serum Perfluoro-n-[1,2-13C2]decanoic acid is a carbon-13-labeled PFDA analytical internal standard, not native PFDA acquired from products or pollution. Laboratories spike it at a known concentration into samples for isotope-dilution mass spectrometry, improving correction for extraction recovery and matrix effects when quantifying unlabeled PFDA. It therefore has no meaningful patient food, water, air, consumer, or occupational source. A patient result should be queried with the laboratory, not interpreted as toxic exposure or health risk. ### Perfluoro-n-[1,2-13C2] hexanoic acid PFAS compounds · Blood / serum Perfluoro-n-[1,2-13C2]hexanoic acid is a carbon-13-labeled PFHxA analytical standard rather than an environmental contaminant being sought in the patient. It is intentionally added during isotope-dilution LC-MS/MS to track recovery, matrix suppression, and instrument response while native PFHxA is quantified. There is no plausible consumer-product, food, water, air, or workplace exposure pathway for this labeled reagent outside laboratory handling. Any patient-facing value requires laboratory clarification and has no standalone toxicologic interpretation. ### Perfluorobutanoic acid (PFBA) PFAS compounds · Blood / serum PFBA is a parent short-chain perfluorocarboxylic acid used or formed in fluorochemical manufacturing and as a breakdown product of precursor PFAS. Industrially affected drinking water, food, indoor dust, air, and occupational settings may contribute. Blood measurement can indicate exposure, but PFBA is eliminated faster than long-chain PFAS, making serum a relatively insensitive snapshot. PFBA-specific human health evidence is limited; class concerns justify source review, not diagnosis from a single concentration. ### Perfluorodecanoic acid (PFDeA) PFAS compounds · Blood / serum PFDeA, commonly abbreviated PFDA, is a parent long-chain perfluorocarboxylic acid associated with fluorochemical production, stain- and grease-resistant treatments, firefighting foams, and degradation of precursor compounds. Contaminated water, seafood and other foods, dust, and occupational contact can contribute. Serum measurement reflects internal burden over a longer window than urine. Liver, lipid, immune, thyroid, reproductive, and developmental concerns are studied, but PFDA-specific human evidence is limited and one value is not diagnostic. ### Perfluorododecanoic acid (PFDoA) PFAS compounds · Blood / serum PFDoA is a parent long-chain perfluorocarboxylic acid that may originate from fluorochemical manufacturing, treated materials, firefighting-foam contamination, and breakdown of fluorinated precursors. Diet—particularly contaminated seafood—water, dust, and occupational contact can contribute. Serum testing is used because long-chain PFAS can bind proteins and persist. Experimental liver, developmental, and reproductive findings support caution, but PFDoA-specific human studies are sparse; detection does not establish a harmful dose or individual disease. ### Perfluoroheptanoic acid (PFHpA) PFAS compounds · Blood / serum PFHpA is a parent seven-carbon perfluorocarboxylic acid used or produced in fluorochemical processes and formed from precursor degradation. Potential sources include contaminated drinking water, food, food-contact materials, indoor dust, air near facilities, and occupational work. Serum measurement indicates exposure, although PFHpA generally clears faster than longer-chain PFAS and a single sample may miss past peaks. Compound-specific health evidence is limited; broader PFAS concerns warrant source evaluation without assuming disease causation. ### Perfluorohexane Sulfonic Acid (PFHxS) PFAS compounds · Blood / serum PFHxS is a parent long-chain perfluoroalkyl sulfonic acid historically used in firefighting foams, stain-resistant treatments, carpet and textile applications, and industrial surfactants. Drinking water near contaminated sites, food, dust, and occupational exposure can contribute. Serum measurement is informative because PFHxS can remain in humans for years. Epidemiologic evidence links some PFAS exposures with lipid, thyroid, immune, and developmental changes, but associations do not prove causation and one level is not diagnostic. ### Perfluorohexanoic acid (PFHxA) PFAS compounds · Blood / serum PFHxA is a parent short-chain perfluorocarboxylic acid used in or produced by fluorochemical applications and precursor breakdown. Contaminated water, food packaging, treated textiles, indoor dust, air near manufacturing, and occupational contact may contribute. Serum testing can document current internal exposure, but PFHxA is generally cleared more rapidly than PFOA, so blood may underrepresent intermittent exposure. PFHxA-specific human toxicology is incomplete; detection supports exposure review, not a prediction of illness. ### Perfluorononanoic acid (PFNA) PFAS compounds · Blood / serum PFNA is a parent long-chain perfluorocarboxylic acid associated with fluoropolymer manufacture, emissions, treated materials, and degradation of precursor PFAS. Contaminated drinking water, seafood and other foods, household dust, and occupational settings may contribute. Serum measurement reflects persistent internal exposure. Human and animal studies support concern about liver, lipid, immune, thyroid, reproductive, and developmental outcomes across PFAS, but PFNA-specific dose-response remains uncertain and an individual result cannot diagnose disease. [Read the Perfluorononanoic acid guide →](https://intrinsicprism.com/learn/markers/perfluorononanoic-acid-blood-test) ### Perfluorooctane sulfonic acid (PFOS) PFAS compounds · Blood / serum PFOS is a parent, highly persistent perfluoroalkyl sulfonic acid formerly used widely in firefighting foams, stain and water repellents, carpet and paper treatments, metal plating, and industrial surfactants. Drinking water, fish and other foods, dust, and occupational contact remain sources despite phaseouts. Serum PFOS estimates longer-term internal burden. Studies associate exposure with cholesterol, immune-response, thyroid, reproductive, developmental, and cancer outcomes, but risk depends on dose and context; one result is not diagnostic. [Read the Perfluorooctane sulfonic acid guide →](https://intrinsicprism.com/learn/markers/perfluorooctane-sulfonic-acid-blood-test) ### Perfluorooctanoic acid (PFOA) PFAS compounds · Blood / serum PFOA is a parent, persistent perfluorocarboxylic acid historically used as a processing aid for fluoropolymers used in nonstick, stain-resistant, chemical-resistant, and industrial products. Contaminated drinking water, food, dust, and occupational exposure can contribute long after production reductions. Serum measurement estimates internal burden. Evidence supports associations with cholesterol changes, immune effects, pregnancy-related outcomes, liver effects, and kidney or testicular cancer, but a concentration alone cannot predict an individual outcome. [Read the Perfluorooctanoic acid guide →](https://intrinsicprism.com/learn/markers/perfluorooctanoic-acid-blood-test) ### Perfluoropentanoic acid (PFPeA) PFAS compounds · Blood / serum PFPeA is a parent short-chain perfluorocarboxylic acid used or generated in fluorochemical production and through degradation of fluorinated precursors. Exposure may occur through industrially affected water, food, food-contact materials, indoor dust, air, and certain workplaces. Blood testing can confirm current internal exposure, but relatively rapid clearance makes a serum value sensitive to timing. PFPeA-specific health data are sparse; class-level persistence and toxicity concerns justify source reduction without treating detection as a diagnosis. ### Perfluorotetradecanoic acid (PFTeDA) PFAS compounds · Blood / serum PFTeDA is a parent very-long-chain perfluorocarboxylic acid associated with fluorochemical products, precursor degradation, and environmental food-chain contamination. Seafood and other foods may be important pathways, alongside polluted water, dust, and occupational contact. Serum measurement seeks persistent, protein-bound internal exposure, though analytical detection can be uncommon. Compound-specific human evidence is very limited; animal and broader PFAS findings raise liver, developmental, and reproductive questions, but one detected level cannot establish health injury. ### Perfluorotridecanoic acid (PFTrDA) PFAS compounds · Blood / serum PFTrDA is a parent very-long-chain perfluorocarboxylic acid that can arise from fluorochemical manufacture and degradation of precursor substances, then accumulate in environmental food webs. Contaminated seafood, other foods, water, household dust, and occupational contact are plausible routes. Serum testing evaluates persistent internal exposure. Human toxicology for PFTrDA itself is sparse, so concerns are extrapolated partly from animal and PFAS-class evidence; detection cannot identify the source or predict an individual disease. ### Perfluoroundecanoic acid (PFUnA) PFAS compounds · Blood / serum PFUnA is a parent long-chain perfluorocarboxylic acid associated with fluorochemical production, precursor degradation, treated materials, and environmental food-chain contamination. Seafood and other foods, contaminated water, dust, and occupational settings may contribute. Serum measurement is useful because long-chain PFAS bind proteins and can persist. Experimental liver and developmental findings and broader PFAS epidemiology support caution, but PFUnA-specific human evidence is limited; one concentration cannot establish source, harmful dose, or disease. ## Toxin Genetics 25 Assesses selected genetic variants involved in biotransformation, antioxidant defense, methylation, metal handling, and DNA repair so protocols can account for detox capacity, not just exposure levels. *Detox capacity* ### SULT1A1 (rs1042157) Detox and repair variants · DNA SULT1A1 adds sulfate groups to hormones, medicines, and many xenobiotics, usually aiding solubility and clearance. rs1042157 lies in the gene’s 3′ untranslated region and has been studied for effects on SULT1A1 expression or enzyme activity. It may therefore contextualize exposure-biomarker handling, but this SNP is not an exposure, diagnosis, or deterministic prediction; without the reported genotype, no allele effect can be assigned. ### CYP1A2 (rs762551) Detox and repair variants · DNA CYP1A2 is a liver cytochrome P450 enzyme that oxidizes caffeine, medicines, and some combustion-derived compounds. rs762551 has been studied in relation to inducible CYP1A2 activity and caffeine metabolism, with findings influenced by smoking and other exposures. It may help frame differences in biomarker kinetics, but the SNP is not an exposure, diagnosis, or deterministic prediction; because genotype is unspecified, no allele effect is assigned. ### GSTP1 (rs1871042) Detox and repair variants · DNA GSTP1 conjugates glutathione to electrophilic compounds and also participates in cellular stress signaling. rs1871042 is an intronic GSTP1 locus studied as a common genetic marker in association analyses, although direct functional evidence is limited. It can provide background for interpreting oxidative-stress or exposure biomarkers; this SNP is not an exposure, diagnosis, or deterministic prediction, and no allele effect is assigned without the genotype. ### GPx4 (rs713041) Detox and repair variants · DNA GPX4 is a selenium-dependent antioxidant enzyme that reduces membrane-lipid hydroperoxides and restrains ferroptotic cell damage. rs713041 is a GPX4 coding/3′-UTR locus studied in relation to selenoprotein expression, selenium biology, and oxidative-stress-associated outcomes. It may contextualize redox biomarkers alongside exposure measurements, but the SNP is not an exposure, diagnosis, or deterministic prediction; genotype is not provided, so no allele-specific effect is assigned. ### COMT (rs4680) Detox and repair variants · DNA COMT methylates catecholamines, catechol estrogens, and other catechol compounds using S-adenosylmethionine. The widely studied missense locus rs4680 has been examined for differences in COMT stability and activity and for numerous neurobehavioral and metabolic traits. It may contextualize methylation-related handling when exposure biomarkers are reviewed, but this SNP is not an exposure, diagnosis, or deterministic prediction; without a specified genotype, no allele effect is assigned. ### EPHX1 (rs2234922, rs1051741) Detox and repair variants · DNA EPHX1 converts reactive epoxide intermediates from drugs and environmental chemicals into less reactive diols, though pathway context can alter net effects. rs2234922 and rs1051741 have been studied as EPHX1 coding variants in relation to microsomal epoxide-hydrolase activity and xenobiotic-response phenotypes. They may contextualize metabolite patterns, but these SNPs are not an exposure, diagnosis, or deterministic prediction; absent genotypes, no allele effects are assigned. ### EPHX2 (rs751141) Detox and repair variants · DNA EPHX2 encodes soluble epoxide hydrolase, which converts signaling epoxides—including epoxyeicosatrienoic acids—into corresponding diols and helps regulate vascular and inflammatory pathways. rs751141 is a missense locus studied in relation to enzyme function and cardiovascular, lipid, and inflammatory traits. It may provide physiological context for exposure-associated inflammation, but this SNP is not an exposure, diagnosis, or deterministic prediction; without genotype, no allele effect is assigned. ### UGT2B15 (rs1902023) Detox and repair variants · DNA UGT2B15 attaches glucuronic acid to steroid hormones, drugs, and other lipophilic substrates, supporting phase-II elimination. The missense locus rs1902023 has been studied in relation to UGT2B15 activity, drug glucuronidation, and hormone-related phenotypes. It may contextualize why biomarker clearance differs between people, but this SNP is not an exposure, diagnosis, or deterministic prediction; because genotype is unspecified, no allele effect is assigned. ### CYP1A1 (rs1048943) Detox and repair variants · DNA CYP1A1 is an inducible cytochrome P450 enzyme that oxidizes polycyclic aromatic hydrocarbons and other aryl-hydrocarbon-receptor substrates, sometimes forming reactive intermediates. rs1048943 is a missense variant studied in relation to CYP1A1 catalytic activity and susceptibility in smoking- or pollution-associated disease studies. It may contextualize internal dose, but this SNP is not an exposure, diagnosis, or deterministic prediction; no allele effect is assigned without genotype. ### CYP1B1 (rs1056836) Detox and repair variants · DNA CYP1B1 oxidizes estrogens, polycyclic aromatic hydrocarbons, and other xenobiotic substrates and can generate both clearance products and reactive metabolites. rs1056836 is a missense locus studied for altered catalytic properties and associations with hormone- and exposure-related outcomes. It may help interpret biomarker patterns within pathway context, but the SNP is not an exposure, diagnosis, or deterministic prediction; because genotype is unknown, no allele effect is assigned. ### GSTP1 (rs1695, rs1138272) Detox and repair variants · DNA GSTP1 uses glutathione to conjugate electrophiles and contributes to defense against products of oxidative stress. rs1695 and rs1138272 are missense loci studied for substrate-dependent differences in GSTP1 activity and in gene–environment association studies involving smoke, pollution, and treatment response. They may contextualize exposure-biomarker processing, but these SNPs are not an exposure, diagnosis, or deterministic prediction; without genotypes, no allele effects are assigned. ### MT1A (rs11076161) Detox and repair variants · DNA MT1A encodes a cysteine-rich metallothionein that binds metal ions and participates in metal homeostasis and protection from oxidative stress. rs11076161 is an intronic locus studied in relation to metal-burden biomarkers and susceptibility phenotypes in exposed populations. It may add host-response context to measured metals, but this SNP is not an exposure, diagnosis, or deterministic prediction; no allele effect can be assigned because genotype is unspecified. ### GPx1 (rs1050450) Detox and repair variants · DNA GPX1 is a selenium-dependent enzyme that reduces hydrogen peroxide and organic hydroperoxides using glutathione. The missense locus rs1050450 has been studied in relation to GPX1 activity, selenium status, oxidative stress, and cardiometabolic or cancer outcomes, with inconsistent context-dependent associations. It may contextualize redox biomarkers accompanying toxin measurements, but this SNP is not an exposure, diagnosis, or deterministic prediction; without genotype, no allele-specific effect is assigned. ### ITGB3 (rs2056131) Detox and repair variants · DNA ITGB3 forms integrin receptors involved in platelet aggregation, cell adhesion, and signaling between cells and extracellular matrix. rs2056131 is an intronic ITGB3 locus cataloged and examined in association studies, but evidence directly connecting it to toxin handling is limited. It may offer secondary vascular or inflammatory context rather than detoxification capacity; the SNP is not an exposure, diagnosis, or deterministic prediction, and no allele effect is assigned without genotype. ### XRCC4 (rs28383151, rs3734091) Detox and repair variants · DNA XRCC4 is a core scaffold for non-homologous end joining, the pathway that repairs DNA double-strand breaks. rs28383151 and rs3734091 have been studied in relation to DNA-repair capacity and cancer susceptibility; rs3734091 has also appeared in research on aflatoxin-B1-related hepatocellular carcinoma. They may contextualize vulnerability to genotoxic exposures, but these SNPs are not an exposure, diagnosis, or deterministic prediction; absent genotypes, no allele effects are assigned. ### XRCC1 (rs25487) Detox and repair variants · DNA XRCC1 organizes enzymes in base-excision and single-strand-break repair, pathways that correct oxidative and alkylation-related DNA damage. The missense locus rs25487 has been widely studied in relation to DNA-damage biomarkers and cancer risk, including studies of tobacco, occupational, and other environmental exposures, with mixed results. It may contextualize genotoxic-response biomarkers, but this SNP is not an exposure, diagnosis, or deterministic prediction; no allele effect is assigned without genotype. ### XRCC3 (rs861539) Detox and repair variants · DNA XRCC3 supports homologous-recombination repair of DNA double-strand breaks and helps maintain chromosome stability. The missense locus rs861539 has been studied in relation to DNA-repair phenotypes and susceptibility to cancers or chromosome damage, including investigations involving environmental and occupational exposures; findings vary across populations. It may contextualize damage-response biomarkers, but this SNP is not an exposure, diagnosis, or deterministic prediction; genotype is unspecified, so no allele effect is assigned. ### XRCC7 (rs7003908) Detox and repair variants · DNA XRCC7, the historical name for PRKDC, encodes DNA-PKcs, a key kinase in non-homologous end joining and cellular responses to DNA double-strand breaks. rs7003908 is an intronic locus studied in association with DNA-repair-related cancer susceptibility and treatment outcomes. It may contextualize resilience to genotoxic stress, but the SNP is not an exposure, diagnosis, or deterministic prediction; without a reported genotype, no allele effect is assigned. ### XPD (rs13181) Detox and repair variants · DNA XPD, now officially ERCC2, is a helicase within TFIIH that supports nucleotide-excision repair and transcription. The missense locus rs13181 has been extensively studied in relation to repair capacity, bulky-DNA-adduct burden, and cancer susceptibility in smoking or occupational-exposure settings, with heterogeneous findings. It may contextualize genotoxic exposure biomarkers, but this SNP is not an exposure, diagnosis, or deterministic prediction; genotype is not specified, so no allele effect is assigned. ### XPC (rs2228001) Detox and repair variants · DNA XPC helps recognize bulky, helix-distorting DNA lesions and initiates global-genome nucleotide-excision repair. The missense locus rs2228001 has been studied in relation to DNA-repair capacity, DNA-adduct or chromosome-damage measures, and susceptibility in tobacco, ultraviolet, and occupational-exposure research; results are not uniform. It may contextualize damage-response biomarkers, but this SNP is not an exposure, diagnosis, or deterministic prediction; without genotype, no allele-specific effect is assigned. No matching markers found.