Lead (Pb)

This synthesis draws on ATSDR, EFSA, JECFA, EPA IRIS, CDC, OEHHA, FDA Closer to Zero, mechanism reviews, and chapter-level textbook context from Ufelle & Barchowsky 2021. The complete citation list remains at the bottom of the page so first-time readers can get the main interpretation before the source trail.

Overview

Lead is a non-essential heavy metal and a pervasive environmental contaminant. It enters the human food system through atmospheric deposition from historical leaded gasoline use, soil contamination from leaded paint and industrial emissions, contact with legacy lead-containing food processing equipment and water distribution materials, and uptake by crops from contaminated soil (ATSDR 2020). The metal is absorbed at higher rates by children than by adults (5 to 15 percent in adults, with children retaining more of what they absorb), distributes to soft tissues in the short term and to bone over decades, and is excreted slowly through urine and faeces (ATSDR 2020). Blood lead has a half-life of approximately 30 days; bone lead has a half-life of 10 to 30 years and serves as an internal reservoir that releases lead during pregnancy, lactation, and bone resorption (ATSDR 2020).

The defining feature of lead’s regulatory framing is the absence of a demonstrated effect threshold for the most sensitive endpoint, developmental neurotoxicity in young children (EFSA 2010). JECFA withdrew its previous provisional tolerable weekly intake of 25 µg/kg b.w./week in 2010 (JECFA 73rd), EFSA concluded the same year that no PTWI is health-protective (EFSA 2010), EPA IRIS does not derive an oral reference dose (EPA IRIS Lead), and ATSDR does not derive Minimal Risk Levels for lead (ATSDR 2020). Operational US public-health action runs through CDC’s blood lead reference value of 3.5 µg/dL (CDC BLRV) and FDA’s Closer to Zero Interim Reference Levels (2.2 µg/day for children, 8.8 µg/day for women of childbearing age, derived from the BLRV with a 10x safety factor) (FDA CTZ 2025). California Proposition 65 lists lead under both cancer and reproductive-toxicity categories with separate quantitative implementation thresholds (OEHHA Prop 65).

At a glance

Three facts that matter most for a consumer trying to interpret lead exposure.

First, no major regulatory body has identified a safe blood lead level for children. Lead’s developmental neurotoxicity occurs at the lowest measurable blood concentrations, and effects on cognition, behavior, and brain development have been documented at blood lead levels well below the population threshold the CDC uses for screening (3.5 µg/dL) (EFSA 2010, CDC BLRV). The framing for lead is “minimize exposure as far as practicable,” not “stay below a specific number.” Unlike most environmental hazards, lead does not have a “safe daily dose” that consumers can target.

Second, children are at materially higher risk than adults. Children absorb a larger fraction of ingested lead, retain more of what they absorb, and are exposed during developmental windows when the brain is most susceptible to lead’s effects (ATSDR 2020). EFSA 2010 estimates that European children’s average dietary lead exposure (0.80 to 3.10 µg/kg body weight per day) already exceeds the developmental-neurotoxicity benchmark dose lower confidence limit of 0.50 µg/kg b.w./day across most of the country range; high-consumer European children exceed the BMDL by approximately 10-fold. Pregnancy is also a high-risk period because bone lead accumulated over a lifetime can mobilize during pregnancy and lactation, transferring to the fetus or nursing infant (ATSDR 2020).

Third, lead reaches the food supply through specific identifiable pathways that consumers can prioritize. Cereals are the dominant population-level dietary contributor (per EFSA 2010); root vegetables grown in contaminated soil are an FDA Closer to Zero target category (FDA CTZ 2025). Outside of food, dust and soil from older homes with deteriorating leaded paint, drinking water from lead service lines or lead-soldered plumbing, and traditional or imported cosmetics, lead-glazed ceramics, and certain herbal medicines are the meaningful non-dietary pathways for most consumers in jurisdictions where leaded gasoline has been phased out (ATSDR 2020).

Toxicology

Association of exposure to synthetic phenols and metal(loid)s with early puberty in Spanish girls: a multicentric case–control study reports urinary metal biomarkers and early-puberty associations in girls recruited across six Spanish hospitals during 2018–2022. The source keeps case and control summaries, detection frequencies and observational effect estimates separate. A single urine measurement and case–control sampling cannot establish exposure before puberty onset, causality, or a particular consumer-product source.

Lead is primarily a developmental neurotoxicant. The 2010 EFSA opinion identified developmental neurotoxicity in young children as the most sensitive critical endpoint, with a Benchmark Dose Lower Confidence Limit (BMDL01) of 12 µg/L blood lead, corresponding to a dietary intake of 0.50 µg/kg body weight per day. Cognitive deficits, behavioral abnormalities, and reduced IQ have been documented in cohort studies at blood lead levels below the BMDL, supporting the regulatory position that no safe level exists. The molecular mechanism of lead neurotoxicity operates through multiple pathways: substitution for divalent cations (Ca²⁺ and Zn²⁺) in zinc-finger transcription factors essential for brain development (Ordemann and Austin 2016), disruption of glutamatergic signaling through interference with NMDA, AMPA, and metabotropic glutamate receptors and the EAAT, VGLUT, and SNAT transporter families (Tamagno and Freeman 2025), induction of oxidative stress and excitotoxicity, and inhibition of DNA repair.

Cardiovascular effects are the second canonical adult endpoint. EFSA 2010 derived a BMDL01 of 36 µg/L blood lead for systolic blood pressure effects (1.50 µg/kg b.w./day dietary equivalent). Renal effects are the third canonical adult endpoint, with a BMDL10 of 15 µg/L for chronic kidney disease prevalence (0.63 µg/kg b.w./day dietary equivalent), comparable in dietary-equivalent terms to the developmental BMDL01 (EFSA 2010).

Hematological effects are mechanistically central to lead toxicity. Lead inhibits δ-aminolevulinic acid dehydratase (ALAD), an essential enzyme in heme biosynthesis; Huang et al. 2020 used Generalized Additive Models to detect the dose-response threshold for ALAD activity reduction in occupationally exposed workers, providing biomarker-level evidence of mechanistic effects at exposures below those producing clinical anemia. Additional documented endpoints include immunological effects, peripheral neuropathy in adults, and reproductive effects (the basis of California Prop 65 reproductive listing) (ATSDR 2020, OEHHA Prop 65).

Lead is classified by EPA as B2 (probable human carcinogen, animal evidence with inadequate human evidence) (EPA IRIS Lead) and by California Prop 65 as a chemical known to cause cancer (OEHHA Prop 65); quantitative cancer dose-response is not derived in the IRIS file because the developmental neurotoxicity endpoint is more sensitive and dominates regulatory action (EPA IRIS Lead).

Typical exposure routes

Dietary intake is one of several meaningful routes for the general population. Adult gastrointestinal absorption of ingested lead is approximately 5 to 15 percent, with adults retaining typically less than 5 percent of an ingested dose; children absorb a substantially higher fraction (often cited as 30 to 50 percent of the ingested dose) and retain more of what they absorb because of incomplete bone-deposition equilibrium (ATSDR 2020). Inhalation of airborne lead is operationally minor since the phase-out of leaded gasoline but remains relevant in occupational settings, in proximity to active smelting or battery manufacture, and from re-entrainment of historically deposited soil and dust (ATSDR 2020). Dust and soil ingestion is the dominant non-dietary route for young children (hand-to-mouth behavior, contaminated indoor dust from deteriorating leaded paint) (EFSA 2010, ATSDR 2020).

Bone lead accumulated over a lifetime is itself an internal exposure source: bone lead mobilizes during pregnancy, lactation, postmenopausal bone resorption, and any other period of accelerated bone turnover, providing endogenous lead exposure to the bloodstream and to the fetus or nursing infant (ATSDR 2020). This bone-mobilization effect is the reason that pre-pregnancy lead exposure remains relevant to fetal exposure decades after the original intake (ATSDR 2020).

Biological half-life and body burden accumulation

Lead distributes between three kinetic compartments with sharply different half-lives. Blood lead has a half-life of approximately 30 days; soft-tissue lead (liver, kidney, brain) has a half-life on the order of weeks to months; and bone lead has a half-life of 10 to 30 years (cortical bone slower than trabecular) (ATSDR 2020). Approximately 90 percent of total body lead burden in adults resides in bone (ATSDR 2020). Bone lead concentrations measured by K-shell X-ray fluorescence (KXRF) reflect cumulative lifetime exposure rather than recent intake, and are increasingly used in epidemiological studies of chronic lead effects (ATSDR 2020).

The kinetic implication for risk assessment is that blood lead at any given moment reflects a weighted combination of recent intake and bone-released endogenous exposure, with the bone fraction dominating in older adults and during physiological states of accelerated bone turnover (ATSDR 2020). This is mechanistically why the developmental window for fetal exposure includes the pre-conception lead body burden of the mother, not just her gestational dietary intake.

Food sources

EFSA 2010 identified cereal products as the dominant population-level dietary contributor to lead exposure across European Member States. Vegetables (root vegetables in particular for children) contribute substantially (EFSA 2010).

Adult dietary lead exposure across European populations ranges from 0.36 to 1.24 µg/kg b.w./day average, up to 2.43 in high consumers. Child dietary lead exposure ranges from 0.80 to 3.10 µg/kg b.w./day average, up to 5.51 in high consumers. Infant exposure ranges from 0.21 to 0.94 µg/kg b.w./day. The EFSA developmental-neurotoxicity BMDL01 of 0.50 µg/kg b.w./day is therefore exceeded by mean adult European exposure on the upper end of the country-specific range, by mean European child exposure across most of the range, and by high-consumer European child exposure by approximately 10-fold (EFSA 2010).

What this means for food choice

The framing for lead is different from the framing for most other dietary contaminants because there is no demonstrated safe blood lead level for children. Consumer guidance is therefore not “stay below a specific number” but rather “minimize exposure across all sources.” Cereals dominate population-level dietary lead because they are eaten in large volume; an adult who consumes a varied diet within EFSA’s average-consumer exposure range (0.36 to 1.24 µg/kg b.w./day) is already at 0.7 to 2.5 times the developmental-neurotoxicity dietary BMDL, and high-consumer children are at approximately 10-fold the BMDL. There is no consumer dietary choice that brings exposure below the BMDL while maintaining a normal diet.

The leverage points for individual consumers, in approximate order of impact:

For children specifically, the FDA Closer to Zero matrix-specific action levels (10 ppb in fruits, non-root vegetables, mixtures, yogurts, custards, and single-ingredient meats; 20 ppb in single-ingredient root vegetables; 20 ppb in dry infant cereals) define an enforcement-relevant federal guidance context for what FDA may regard as adulterated (FDA CTZ 2025; FDA 2025 Lead Action Levels for Processed Food Intended for Babies and Young Children). They are nonbinding recommendations, not statutory maximum levels. Choosing baby-food brands and products with documented testing programs that operate below these thresholds reduces exposure relative to the population mean.

For non-dietary lead, the dominant exposure pathways for most US consumers are deteriorating leaded paint and contaminated indoor dust in pre-1978 housing, drinking water from lead service lines or lead-soldered plumbing, and (where applicable) imported spices, traditional cosmetics, and lead-glazed ceramics (ATSDR 2020).

For pregnancy and pre-pregnancy planning, the bone-lead reservoir matters: lead body burden accumulated over decades mobilizes during pregnancy, lactation, and postmenopausal bone resorption (ATSDR 2020). Consumers planning pregnancy can reduce future fetal exposure by minimizing current lead intake but cannot meaningfully reduce existing bone burden in the short term (ATSDR 2020).

Regulatory limits

For the ppb-normalized Category 1 comparison table, see Category 1 Lead Benchmark Context.

What the reference values mean in practice

Lead is unusual among dietary contaminants in that the major regulatory bodies have explicitly declined to set a single tolerable intake level. JECFA withdrew its PTWI of 25 µg/kg b.w./week in 2010 (JECFA 73rd); EFSA reports BMDLs but does not set a TWI (EFSA 2010); EPA IRIS does not derive an oral RfD (EPA IRIS Lead); ATSDR does not derive MRLs (ATSDR 2020). The operational anchor is CDC’s blood lead reference value of 3.5 µg/dL, which is itself a population-percentile-based screening threshold, not a health-based safety threshold (CDC BLRV).

For a consumer trying to interpret these values: the CDC value defines “elevated relative to the US child population,” not “safe below this threshold.” A child below 3.5 µg/dL is not at zero risk; the BLRV simply identifies the top 2.5 percent of measured US children for public-health intervention (CDC BLRV). The FDA Interim Reference Level of 2.2 µg/day for children is the dietary translation of the CDC BLRV, derived with a 10x safety factor for variability in dietary-to-blood-lead conversion (FDA CTZ 2025).

The practical consumer position: there is no “safe daily lead intake” that a regulator has endorsed. Consumer action should focus on minimizing total lead exposure (dietary plus dust plus water plus other sources), with priority weighting toward children and pregnancy.

Testing

Blood lead concentration is the standard exposure biomarker for human health assessment, measured by graphite furnace atomic absorption spectrometry, ICP-MS, or LeadCare anodic stripping voltammetry (point-of-care) (ATSDR 2020). The CDC reference value of 3.5 µg/dL is denominated in whole blood (CDC BLRV). Bone lead measurement by K-shell X-ray fluorescence (KXRF) is used in research settings to assess cumulative lead body burden and is the most direct measurement of long-term exposure (ATSDR 2020). ALAD activity in red blood cells (Huang et al. 2020) is a sensitive biochemical biomarker of lead’s interference with heme biosynthesis, with detectable reduction at blood lead levels below clinical anemia thresholds.

Food and water lead concentrations are typically measured by ICP-MS, the method FDA’s Toxic Elements Program uses for the Closer to Zero data underlying the action levels (FDA TDS 2018-2020). Detection limits in the 0.001 to 0.1 µg/L range are achievable, sufficient for the 10 ppb level the CTZ guidance specifies as the smallest of the three baby-food action levels (FDA CTZ 2025).

Gut microbiome and lead

Lead exposure is associated with differences in gut communities in people and changes those communities in a mouse drinking-water experiment. A review also reports that selected microbes, when supplemented, reduced lead burden. That reverse direction is not a measured change in lead absorption from a food.

Lead and gut communities

Eggers and colleagues (Eggers et al. 2023) analyzed the PROGRESS birth cohort in Mexico City. Per WikiBiome source summary, DOI 10.3389/fmicb.2023.1193919, and the abstract on the Heavy Metal Index source record, this pilot included 123 children (74 male and 49 female). Maternal whole-blood lead was measured in the second and third trimesters. Stool at ages 9 to 11 was sequenced by metagenomics. Mean prenatal blood lead was 33.6 µg/L (standard error 2.1) in the second trimester and 34.9 µg/L (standard error 2.1) in the third. Weighted quantile sum regression gave beta -0.17 in both trimesters. The 95 percent confidence intervals were -0.46 to 0.11 and -0.44 to 0.10, so both intervals cross zero. Ruminococcus gnavus, Bifidobacterium longum, Alistipes indistinctus, Bacteroides caccae, and Bifidobacterium bifidum were above the importance threshold in 80 percent or more of repeated holdouts in both trimesters. This is an observational association. It does not show that prenatal lead caused those taxa to change.

Xiong and colleagues (Xiong et al. 2025) recruited 146 mother-infant pairs and measured elements in maternal hair. The article reports a cohort median hair lead of 0.20 µg/g. In the high-versus-low comparison in the same figure as the aluminum taxa (18 infants and 18 infants), higher maternal hair lead was associated with higher relative abundance of the Ruminococcus gnavus group, Erysipelatoclostridium, and Cutibacterium. The article does not give an administered lead dose, and that sentence does not separate lead from the other elements in the same hair. Hair lead is not a concentration in food.

Gao and colleagues (Gao et al. 2017) ran a mouse experiment. Per WikiBiome source summary, DOI 10.1021/acs.chemrestox.6b00401, female C57BL/6 mice about 7 weeks old, 5 per group, received 10 ppm lead chloride in drinking water for 13 weeks. The summary states that lead disturbed microbiome development, inhibited phylogenetic diversity, and reduced vitamin E (alpha-tocopherol and gamma-tocopherol), the primary bile acids cholic acid and ursodeoxycholic acid, cholesterol, and coprostanol. Ruminococcus and Oscillospira decreased. The measured endpoints are community and metabolite change, not lead absorption.

Microbes and lead handling

Ghosh and colleagues (Ghosh et al. 2024) is a review, not a new experiment. Per WikiBiome source summary, DOI 10.1530/MAH-23-0015, lead reduces colonic MUC2 and the tight-junction proteins ZO-1, claudin-1, and occludin. The same summary states that supplementing lead-intolerant gut microbes reduced lead burden. The taxa are named as Akkermansia muciniphila, Faecalibacterium prausnitzii, and O. ruminantium. The summary does not restate the host, the dose, or a percent change in lead absorption from a food. A supplemented-microbe result is not a lot assay.

Studies of lead and the gut microbiome

Brands, suppliers, and testing

Stool taxa are research context for how lead and gut communities are studied. They do not release a lot, and they are not a certificate of analysis. Brands, suppliers, and quality teams still measure lead in the ingredient or finished product by the method the specification names, commonly inductively coupled plasma mass spectrometry. A taxon shift in a mouse drinking-water study, or in a birth-cohort stool sample, does not pass or fail that lot.

What remains uncertain

The human results are associations. Eggers confidence intervals cross zero. A shorter WikiBiome note on DOI 10.3389/fmicb.2023.1193919 disagrees with the detailed summary on sample size and on whether sequencing was metagenomic; that conflict is not reconciled here. Gao did not measure lead uptake. Ghosh reports a review of supplementation, not an absorption factor for an ingredient. No study in this section gives a percent change in lead uptake from a food.

Historical context

The current regulatory consensus that no safe blood lead level exists for children rests on a multi-decade public-health record. Population-level blood lead concentrations in US children declined from a NHANES II (1976-1980) geometric mean of approximately 15 µg/dL to a NHANES 2015-2018 geometric mean below 1 µg/dL, with the CDC blood lead reference value declining in parallel from an earlier value of 10 µg/dL (1991-2012), to 5 µg/dL (2012-2021), to the current 3.5 µg/dL (CDC BLRV). Effects are now established at blood lead levels below 5 µg/dL, well within the range where most US children currently fall (CDC BLRV).

The corresponding regulatory conclusion, JECFA’s 2010 withdrawal of the PTWI and EFSA’s 2010 statement that no PTWI is health-protective (JECFA 73rd, EFSA 2010), is the cumulative position the wiki adopts for current lead content.

Vulnerable populations

If you are in one of these groups

For parents of children under age 6: pre-1978 housing (the cutoff year for lead-paint phase-out in the US), lead service lines, and lead-soldered plumbing are priority targets for testing and remediation (ATSDR 2020). Pediatric blood lead screening is part of standard well-child care in most US settings; children identified above the BLRV are followed clinically with environmental investigation (CDC BLRV).

For pregnant and potentially-pregnant women: bone lead body burden accumulated over a lifetime is the dominant fetal exposure source, and there is no short-term intervention that meaningfully reduces existing bone lead (ATSDR 2020). Pre-conception minimization of current intake is the operational lever. The California OEHHA Proposition 65 reproductive-toxicity MADL applies to consumer products sold in California and is the directly relevant California regulatory threshold; products carrying a Prop 65 reproductive-toxicity warning for lead are products that, at typical use, would exceed this level (OEHHA Prop 65).

For the immigrant and traditional-medicine consumer: certain imported spices (particularly turmeric and chili powders from some sources), traditional cosmetics (surma, kohl, kajal in some preparations), traditional medicines (ayurvedic, traditional Chinese, some Latin American), and lead-glazed ceramics in contact with acidic foods have produced documented elevated lead exposure cases in the US public-health literature (ATSDR 2020).

App-layer integration

Machine-readable takeaways from this synthesis for the Heavy Metal Index consumer app pipeline.

The reference-value scale for lead is qualitatively different from cadmium, mercury, or arsenic because no single tolerable-intake reference value exists. The app should not display a “percent of reference” for dietary lead in the way it does for cadmium; instead, the app should reference the FDA Closer to Zero matrix-specific action levels for products in the baby-food categories, the FDA IRL of 2.2 µg/day for children (with 10x safety factor flag noted), and the EFSA dietary BMDL01 of 0.50 µg/kg b.w./day for users wanting an explicit benchmark.

Pediatric multipliers for lead are amplified relative to cadmium because of higher absorption and longer retention in children (ATSDR 2020, EFSA 2010). Default app pediatric exposure multipliers: 1.6x adult per-kg for ages 0.5-12 (per the EFSA child:adult ratio finding) (EFSA 2010), and an additional GI absorption multiplier of approximately 3-5x for children to reflect the higher absorption fraction (ATSDR 2020).

Structured outputs for app consumption:

• Adult GI absorption: 5 to 15 percent (use midpoint 10 percent for default) (ATSDR 2020).
• Child GI absorption: 30 to 50 percent (use midpoint 40 percent for default in pediatric mode) (ATSDR 2020).
• Blood lead half-life: 30 days (ATSDR 2020).
• Bone lead half-life: 10 to 30 years (use 20 years for body-burden modeling) (ATSDR 2020).
• Bone fraction of total body lead (adults): approximately 90 percent (ATSDR 2020).
• Non-dietary exposure flags: pre-1978 housing (leaded paint, deteriorating dust), lead service lines (drinking water), traditional cosmetics, imported spices, lead-glazed ceramics (ATSDR 2020).

For consumer-facing risk communication, the app should never present “safe lead intake” or “safe blood lead level” framings. Acceptable framings: “your estimated weekly lead intake from these products is X µg, which is Y percent of the FDA Interim Reference Level for your age group” or “no consumer-protective blood lead threshold has been established; minimize total exposure as far as practicable.”

Open questions

Three load-bearing open questions for lead, surfaced by the current ingest:

First, the absence of a single international tolerable intake reference value is operationally awkward. JECFA withdrew the PTWI in 2010, EFSA reports BMDLs without setting a TWI, EPA IRIS is qualitative-only, ATSDR does not derive MRLs. Operational US action runs through CDC BLRV → FDA IRL → CTZ matrix-specific action levels, but this chain is not internationally harmonized. A practicability-based framing such as “lead exposure as far below typical as practicable” is methodologically coherent at the framing level but does not resolve to a single numeric anchor, because no agency currently provides one.

Second, the carcinogenicity classification (EPA B2, Prop 65 listed) is settled at the categorical level but not derived to a quantitative cancer slope factor. Whether dietary lead exposures contribute meaningfully to cancer risk at general-population levels remains an area where regulatory bodies have declined to derive quantitative dose-response, citing data limitations.

Third, the bone-lead-mobilization contribution to fetal and infant exposure is mechanistically established but not quantitatively integrated into FDA’s IRL framework. The IRL is anchored on dietary intake during the exposure window of interest, but for pregnant women a substantial fraction of fetal blood lead derives from maternal bone reserves accumulated decades earlier. How to incorporate this non-dietary contribution into intake-anchored frameworks for products marketed to pregnant women is an open methodological question.

Frequently asked questions

Chromium research: qualified source context

One Nilore, Islamabad soil characterization reported lead of 3.15 µg/g by bulk elemental analysis (Table 2). The source does not state a wet/dry basis or replicated uncertainty. This is a local soil result; it does not measure food occurrence or crop transfer. LABORATORY SCALE ELECTROKINETIC REMEDIATION OF HEXAVALENT CHROMIUM FROM CONTAMINATED SOIL

A chromium-plating overview describes a lead anode alloy containing tin (editorial p1779). This is equipment-composition context; the editorial does not measure lead release or lead in food. Special Issue: Hexavalent Chromium: Sources, Toxicity, and Remediation

Nahavand farm study: evidence limitations

A 150-farm Iranian environmental study measured lead in soil, irrigation water and whole above-ground biomass. Its wheat cadmium (Cd)–lead (Pb) association is +0.69 in prose and −0.084 in Figure 4. The source therefore supports qualified study context, with the conflicting coefficients kept distinct; it does not measure lead in isolated edible grains or roots (pp4–5,11–12). Soil–water–crop pathways of heavy metal contamination and human health risks in intensive smallholder farms of the Nahavand Plain, Iran

Controlled dermal lead-removal study

Esswein et al. evaluated removal of experimentally applied lead from skin. In a nine-volunteer evaluation, two serial post-cleaning handwipes recovered1.6–6.6µg Pb and the authors reported99.7–99.9% removal. These are controlled challenge and sampling endpoints, with initial loading and spill accounting; they do not establish blood-lead reduction or lead concentration in retail wipes (2011, Table3). Handwipe Method for Removing Lead from Skin

Plant-extract water-treatment experiment

A plant-extract water-treatment experiment reported residual lead in centrifuged liquid, including collard-green treatment at a mean 2.4 ppm (SD 0.015) and carrot treatment at 20.6 ppm (SD 0.61). These source-labelled aqueous values are not lead concentrations in the original plants. The lead-nitrate preparation basis and percentage-removal denominator remain unresolved, and several abstract/conclusion values conflict with the tables (Agwaramgbo et al. 2012, Tables 1–3). An Evaluation of Edible Plant Extracts for the Phytoremediation of Lead Contaminated Water

Arzew surface-soil survey

In 27 road-zone soils around Arzew, source-reported lead was mean 98.4 mg/kg, median 77.0 mg/kg, SD 51.85 mg/kg and range 45.6–220.5 mg/kg. The values refer to air-dried aqua-regia-extractable soil, not foods or measured human exposure; the paper’s traffic-source explanation remains an attributed interpretation (Boudia et al. 2019, Table 2). Spatial contamination and health risks of heavy metal(loid)s in surface soils from a petrochemical complex in the north-eastern region of Algeria

China imported pet foods: preprint evidence

In Du et al.’s pet-food preprint,39 of 93 products were classified Pb-positive, with positive-only mean 3.63 mg/kg and range 2.07–5.80 mg/kg (2024,Table 3). The source defines Pb positivity against a 2 mg/kg quantitation limit. These are China retail imported pet foods, and the same samples also appear in the later published version; they do not form a second cohort. Individual and Combined Contamination of the Heavy Metals in Commercial Cat and Dog Food

Dry dog-food formulation comparison

Kim et al.(2018) report lead median 0.091(range 0.032–1.621)mg/Mcal in 17 red-meat dry dog foods; poultry and fish medians were 0.037 and 0.049 mg/Mcal(Table 1). The Results and Figure 4 identify a red-meat versus poultry difference; fish differed significantly from neither. One lot per formulation and absent ingredient provenance limit causal interpretation. Evaluation of Arsenic, Cadmium, Lead and Mercury Contamination in Over-the-Counter Available Dry Dog Foods With Different Animal Ingredients (Red Meat, Poultry, and Fish)

Texas animal-feed survey

Texas fish-meal samples had lead mean 1.11 mg/kg, SD 0.86 and median 1.45 (N=38; Dai et al. 2016, Table 3). The same table reports a horse-feed median incompatible with its mean and SD; that cell remains an explicit source error without an inferred replacement. Results describe animal-feed inputs, not measured meat or milk transfer. Heavy Metal Contamination of Animal Feed in Texas

Banat soil–nettle–snail study

Nica et al. report a soil-to-nettle lead correlation of 0.76 (P<0.05) and a nonsignificant foot-to-hepatopancreas lead correlation of 0.39 (2012, Table 1). The study distinguishes dilute-acid-extractable soil from washed nettle and separately analyzed snail tissues. The broad narrative of food-chain depletion has site-specific exceptions; neither the correlations nor the dry-weight tissue charts establish edible wet-weight lead exposure. Bioaccumulative and conchological assessment of heavy metal transfer in a soil-plant-snail food chain

Ganga freshwater-fish study: qualified evidence

The Ganga study reports lead in separate freshwater-fish muscle, gill and liver groups. Its highest tabulated gill lead was 4.77 ± 0.34 µg/g in C. reba (Maurya et al. 2019, Table 4). The table’s wet-weight label conflicts with the dry-tissue methods. Inconsistent intake and hazard calculations do not support a consumption-safety conclusion from these measurements. Bioaccumulation and potential sources of heavy metal contamination in fish species in River Ganga basin: Possible human health risks evaluation

References

Works cited in this page’s text, in first-appearance order. See Sources for this page’s source inventory. Each title links to a source record with bibliographic details, reported findings, and document provenance.

1. Toxic Effects of Metals (Chapter 23), in Casarett & Doull’s Essentials of Toxicology, Fourth EditionUfelle AC and Barchowsky A · Casarett & Doull’s Essentials of Toxicology, Fourth Edition. McGraw Hill Education · 2021 · www.mhprofessional.comTextbook
2. Toxicological Profile for LeadAgency for Toxic Substances and Disease Registry · 2020 · doi.org/10.15620/cdc:95222Government
3. Scientific Opinion on Lead in FoodEFSA Panel on Contaminants in the Food Chain (CONTAM) · EFSA Journal 2010;8(4):1570 · 2010 · doi.org/10.2903/j.efsa.2010.1570Government
4. Lead (Addendum), 73rd Meeting of the Joint FAO/WHO Expert Committee on Food Additives — Safety Evaluation of Certain Food Additives and ContaminantsJoint FAO/WHO Expert Committee on Food Additives · WHO Technical Report Series 960 (2011); lead addendum in WHO Food Additives Series No. 64 · 2011 · www.who.intGovernment
5. Lead and Compounds (Inorganic) — IRIS Chemical Assessment SummaryU.S. Environmental Protection Agency, National Center for Environmental Assessment · U.S. Environmental Protection Agency, Integrated Risk Information System · 2004 · iris.epa.govGovernment
6. Blood Lead Reference Value (3.5 µg/dL)U.S. Centers for Disease Control and Prevention · 2021 · www.cdc.govGovernment
7. Action Levels for Lead in Processed Food Intended for Babies and Young Children: Guidance for IndustryU.S. Food and Drug Administration · U.S. Department of Health and Human Services, Food and Drug Administration, Human Foods Program · 2025 · www.fda.govGuidance
8. Lead and Lead Compounds — Proposition 65 Chemical ListingCalifornia Office of Environmental Health Hazard Assessment · oehha.ca.govGovernment
9. Association of exposure to synthetic phenols and metal(loid)s with early puberty in Spanish girls: a multicentric case–control studyOlivas-Martinez A, Escribano A, Riaño-Galán I, Torrebias M, Olmedo P, Gil F, et al. · European Journal of Pediatrics 185:295 · 2026 · doi.org/10.1007/s00431-026-06919-1Peer-reviewed
10. Lead neurotoxicity: exploring the potential impact of lead substitution in zinc-finger proteins on mental healthOrdemann JM and Austin RN · Metallomics, Issue 6, 2016 · 2016 · doi.org/10.1039/c5mt00300hPeer-reviewed
11. Glutamate-Mediated Neural Alterations in Lead Exposure: Mechanisms, Pathways, and PhenotypesTamagno WA and Freeman JL · Toxics 13(7):519 · 2025 · doi.org/10.3390/toxics13070519Peer-reviewed
12. Use of Generalized Additive Model to Detect the Threshold of delta-Aminolevulinic Acid Dehydratase Activity Reduced by Lead ExposureHuang CC, Yang CC, Liu TY, Dai CY, Wang CL, and Chuang HY · International Journal of Environmental Research and Public Health · 2020 · doi.org/10.3390/ijerph17165712Peer-reviewed
13. Total Diet Study Report: Fiscal Years 2018-2020 Elements DataU.S. Food and Drug Administration · 2022 · www.fda.govGovernment
14. Prenatal lead exposure is negatively associated with the gut microbiome in childhoodShoshannah Eggers, Vishal Midya, Moira Bixby, Chris Gennings, Libni A. Torres-Olascoaga, Ryan W. Walker, et al. · Frontiers in Microbiology · 2023 · doi.org/10.3389/fmicb.2023.1193919Peer-reviewed
15. Prenatal exposure to trace elements impacts mother-infant gut microbiome, metabolome and resistome during the first year of lifeShimao Xiong, Bing Xie, Naiyi Yin, Hongmei Zhu, Huimin Gao, Xue Xu, et al. · Nature Communications · 2025 · doi.org/10.1038/s41467-025-60508-8Peer-reviewed
16. Multi-Omics Reveals that Lead Exposure Disturbs Gut Microbiome Development, Key Metabolites and Metabolic PathwaysBei Gao, Liang Chi, Ridwan Mahbub, Xiaoming Bian, Pengcheng Tu, Hongyu Ru, et al. · Chemical Research in Toxicology, Vol. 30, No. 4, pp. 996-1005 · 2017 · doi.org/10.1021/acs.chemrestox.6b00401Peer-reviewed
17. Effects of heavy metals on gut barrier integrity and gut microbiotaSweta Ghosh, Syam P. Nukavarapu, and Venkatakrishna Rao Jala · Microbiota and Host 2(1):e230015 · 2024 · doi.org/10.1530/MAH-23-0015Peer-reviewed
18. LABORATORY SCALE ELECTROKINETIC REMEDIATION OF HEXAVALENT CHROMIUM FROM CONTAMINATED SOILM. Khalid, N. Ahmed, and R. M. Qureshi · The Nucleus 45(1–2):55–61 · 2008 · doi.org/10.71330/nucleus.45.01-2.998Peer-reviewed
19. Special Issue: Hexavalent Chromium: Sources, Toxicity, and RemediationBidyut Saha, Aziz Amine, and Francis Verpoort · Chemistry Africa5:1779–1780 · 2022 · doi.org/10.1007/s42250-022-00443-zEditorial
20. Soil–water–crop pathways of heavy metal contamination and human health risks in intensive smallholder farms of the Nahavand Plain, IranSaeed Sharafi, Maryam Sharafi, and Maryam Lorvand · Scientific Reports 16:9947 · 2026 · doi.org/10.1038/s41598-026-38637-xPeer-reviewed
21. Handwipe Method for Removing Lead from SkinEric J. Esswein, Mark F. Boeniger, and Kevin Ashley · Journal of ASTM International 8(5); reprinted in STP1533 pp67–81 · 2011 · doi.org/10.1520/JAI103527Peer-reviewed
22. An Evaluation of Edible Plant Extracts for the Phytoremediation of Lead Contaminated WaterLovell Agwaramgbo, Charne Thomas, Chardai Grays, Jessica Small, and Tajeve Young · Journal of Environmental Protection 3:722–730 · 2012 · doi.org/10.4236/jep.2012.38086Peer-reviewed
23. Spatial contamination and health risks of heavy metal(loid)s in surface soils from a petrochemical complex in the north-eastern region of AlgeriaHayat Boudia, Laurent Vassalo, Mohammed Hadjel, Pascale Prudent, and Jean-Luc Boudenne · International Journal of Environmental Science and Technology 16:4707–4718; HAL author-manuscript version read · 2019 · doi.org/10.1007/s13762-018-02195-1Peer-reviewed
24. Individual and Combined Contamination of the Heavy Metals in Commercial Cat and Dog FoodJiaying Du, Kerui Zhou, Han Jiang, Shen Hu, Wei Zhang, Qiang Zheng, et al. · Research Square, version1, posted8September2024 · 2024 · doi.org/10.21203/rs.3.rs-4838876/v1Preprint
25. Evaluation of Arsenic, Cadmium, Lead and Mercury Contamination in Over-the-Counter Available Dry Dog Foods With Different Animal Ingredients (Red Meat, Poultry, and Fish)Hyun-Tae Kim, John P. Loftus, Sabine Mann, and Joseph J. Wakshlag · Frontiers in Veterinary Science5:264 · 2018 · doi.org/10.3389/fvets.2018.00264Peer-reviewed
26. Heavy Metal Contamination of Animal Feed in TexasSusie Y. Dai, Ben Jones, Kyung-Min Lee, Wei Li, Lynn Post, and Timothy J. Herrman · Journal of Regulatory Science4(1):21–32 · 2016 · doi.org/10.21423/jrs-v04n01p021Peer-reviewed
27. Bioaccumulative and conchological assessment of heavy metal transfer in a soil-plant-snail food chainDragos V Nica, Marian Bura, Iosif Gergen, Monica Harmanescu, and Despina-Maria Bordean · Chemistry Central Journal 6:55 · 2012 · doi.org/10.1186/1752-153X-6-55Peer-reviewed
28. Bioaccumulation and potential sources of heavy metal contamination in fish species in River Ganga basin: Possible human health risks evaluationPradip Kumar Maurya, D. S. Malik, Krishna Kumar Yadav, Amit Kumar, Sandeep Kumar, and Hesam Kamyab · Toxicology Reports 6:472–481 · 2019 · doi.org/10.1016/j.toxrep.2019.05.012Peer-reviewed
29. Potential of Two Vegetable Plants in Reducing Lead Contamination in SoilMahayu Woro Lestari and Anis Rosyidah · Journal of Ecological Engineering 23(8):320–326 · 2022 · doi.org/10.12911/22998993/151092Peer-reviewed
30. Wastewater Irrigation and Accumulation of Heavy Metals in Vegetable Crops (Broccoli and Cauliflower)Bayan Rashid Rahim · Tikrit Journal for Agricultural Sciences 23(2):162–170 · 2023 · doi.org/10.25130/tjas.23.2.13Peer-reviewed
31. Effects of sewage water irrigation on heavy metals accumulation in vegetables in peri-urban areas of Faisalabad, PakistanMuhammad Abubakar, Basit Haider, Hadeeqa Arshad, Tufail Shah, Ameer Khan, Hummera Nawaz, et al. · Agricultural Research Reports 3(1):46–57 · 2025 · doi.org/10.54219/arr.03.1.2025.418Peer-reviewed
32. Assessment of the Level of Heavy Metals in Irrigation Water, Farm Soil, and Vegetables Grown in Gobbiya Dam, Bogoro Local Government Area Bauchi State, NigeriaJohn Joseph, Toma Buba, Jalo Enoch, and Ayuba Kaluri · Journal of Energy Technology and Environment 7(4):79–92 · 2025 · doi.org/10.37933/jete/7.4.2025.2568Peer-reviewed
33. Occurrence and Risk Assessment of Pesticides, Phthalates, and Heavy Metal Residues in Vegetables from Hydroponic and Conventional CultivationShanshan Chen, Chunxia Yao, Jiaxin Zhou, Haiyao Ma, Jing Jin, Weiguo Song, et al. · Foods 13, 1151 · 2024 · doi.org/10.3390/foods13081151Peer-reviewed
34. Study of Peculiarities of Accumulation of Heavy Metals and Arsenic in Medicinal Plant Raw Materials of Synanthropic Flora of Voronezh RegionNina Alekseevna Dyakova · Khimiya Rastitel’nogo Syr’ya 2:163–170 · 2023 · doi.org/10.14258/jcprm.20230211725Peer-reviewed
35. Yield Assessment of Beetroot and Potato, Cultivated on Ordinary Chernozem Contaminated with Heavy MetalsN. V. Gromakova · Vegetable Crops of Russia 5(38):74–75 · 2017 · doi.org/10.18619/2072-9146-2017-5-74-75Peer-reviewed
36. Removal of Heavy Metals from Industrial Sludge Using Soil Washing TechniqueJ. Sumalatha, B. P. Naveen, and R. K. Malik · Asian Journal of Water, Environment and Pollution 16(3):83–89 · 2019 · doi.org/10.3233/ajw190036Peer-reviewed
37. Bioaccessibility of Heavy Metals in Raw and Processed Alternanthera sessilis and Centella asiatica: An In vitro StudyThilini Kananke, Jagath Wansapala, and Anil Gunarathne · Nature Environment and Pollution Technology25(1):D1830 · 2026 · doi.org/10.46488/nept.2026.v25i01.d1830Peer-reviewed
38. HEAVY METALS ACCUMULATION IN SOIL AND CELERY ROOT (APIUM GRAVEOLENS L.) HARVESTED FROM THE POLLUTED AREAS IN SIBIU COUNTY, CENTRAL ROMANIABogdan Ștefan Oprea, Nicoleta Olimpia Vrînceanu, Dumitru-Marian Motelică, Georgiana Iuliana Plopeanu, Vera Carabulea, and Mihaela Costea · Annals of the University of Craiova—Agriculture,Montanology,Cadastre52(1):422–429 · 2022 · doi.org/10.52846/aamc.v52i1.1370Peer-reviewed
39. Levels of heavy metals concentrations in chocolates from Bwari market Abuja FCT, NigeriaEmmanuel Joy Enogbe and Agbaghare Daniel Enajeme · International Journal of Adulteration9:e2ijad3057 · 2025 · doi.org/10.54905/disssi.v9i10.e2ijad3057Peer-reviewed
40. Assessment of the Risk of Heavy Metals Accumulation in Vegetable CropsVladimir N. Bashkin and Rosa A. Galiulina · Issues of Risk Analysis 18(4): 48-65 · 2021 · doi.org/10.32686/1812-5220-2021-18-4-48-65Peer-reviewed
41. Application of principal component analysis in the pollution assessment with heavy metals of vegetable food chain in the old mining areasIosif Gergen and Monica Harmanescu · Chemistry Central Journal6:156 · 2012 · doi.org/10.1186/1752-153x-6-156Peer-reviewed

Sources

Source records associated with this topic. Inclusion does not establish that every finding applies to this product or ingredient. References above identify works cited in the text. Additional records await source or bibliographic review and are excluded from this list.

Recent source records are shown below. Browse the complete evidence table for all source records and their reported findings.

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Additional geographic and remediation evidence

Mahayu Woro Lestari, 2022. Lestari and Rosyidah compared lead accumulation and growth in two vegetable species grown in lead-amended soil and compost in Malang, Indonesia. Lead treatment reduced growth and the reported shoot-to-root translocation factors. The table supports a narrower interpretation than the paper’s broad phytoextraction conclusion: factors exceed one only in the controls. This is experimental remediation and soil-to-plant pathway evidence. It does not characterize unamended market vegetables, quantify field-scale lead removal, or establish the suitability of harvested biomass for food. Increased root retention under treatment must remain distinct from successful removal of lead from soil.

Bayan Rashid Rahim, 2023. Rahim measured lead, cadmium, iron and copper in dried edible broccoli and cauliflower heads grown under three irrigation regimes in Sulaymaniyah, Iraq. The tables preserve crop-specific differences: wastewater-irrigated broccoli had the largest listed values for the four metals, whereas cauliflower cadmium was greatest under alternating irrigation. The paired treatment summaries contribute source-native vegetable occurrence and irrigation-pathway evidence. The dried basis is not interchangeable with fresh vegetables. The experiment is site- and season-specific and does not characterize all river water, all Iraqi produce or long-term dietary exposure.

Muhammad Abubakar, 2025. Abubakar and colleagues measured seven metals in sewage water, soil, spinach and cauliflower at two peri-urban sites in Faisalabad, Pakistan. The paper reports substantial differences between the two crop/site combinations, but its design does not separate plant-species effects from location. Concentrations are retained with the source’s measurement and tissue limitations. These are localized paired environmental and crop measurements, with plant results routed as leafy-tissue evidence. They do not establish a cauliflower-head concentration, a fresh-weight concentration, or a causal reduction in biomass from metal exposure. Industrial source attribution is proposed by the authors, rather than measured by a source-apportionment experiment.

John Joseph, 2025. Joseph and colleagues measured seven metals in kenaf, chili pepper, tomato and spinach plant parts, with associated soil and irrigation water from Gobbiya Dam in Nigeria. The paper separates edible leaves or fruits from roots and stems. Its concentration tables are preserved independently of several inconsistent safety comparisons and a soil-index calculation that uses water standards. The organ-resolved dry-weight values support local occurrence and irrigation-pathway analysis. Roots, stems and non-edible leaves are retained as pathway context rather than assigned to edible-product distributions. Broad leafy-vegetable and herb/spice ingredient routes retain kenaf and chili identity in the structured record without substituting a named cultivar.

Shanshan Chen, 2024. Shanghai farm samples had lower reported lead and cadmium concentrations under hydroponic cultivation than conventional soil cultivation. The element-specific summaries combine four vegetables, while commodity-specific means combine lead with cadmium; neither split can be reconstructed into commodity-by-element concentrations from the preserved main paper. Supports a local cultivation-system comparison and the soil/irrigation pathway. It does not establish commodity-specific Pb or Cd distributions or universal hydroponic safety. Mixed-contaminant hazard indices include pesticides and phthalates; their interpretation remains source-reported.

Nina Alekseevna Dyakova, 2023. Dyakova compares nine elements in medicinal plant materials collected in disturbed and control environments in Russia’s Voronezh region during 2015–2020. The reported ranges preserve tissue and environmental setting; the paper also proposes regional background means across species. Supports geographic and tissue-specific contamination evidence for botanical raw materials and environmental attribution hypotheses. It does not measure finished supplements or isolate an individual polluter’s causal contribution.

N. V. Gromakova, 2017. A 2015 Rostov-region field experiment measured copper, zinc and lead in beetroot and potato grown on artificially metal-amended chernozem. Adding mineral fertilizer reduced several crop concentrations relative to the metal-only treatment, while yield responses differed between crops. Supports crop-specific agronomic mitigation and soil-to-crop transfer evidence. Artificially amended experimental crops are not a market-occurrence distribution. Paper limit comparisons remain secondary context.

J. Sumalatha, 2019. Column washing of Bangalore-area industrial sludge removed substantially more metals with hydrochloric acid plus EDTA than with distilled water. This is a remediation experiment relevant to sludge contamination pathways, with no measurements in food or a demonstrated safe land-application endpoint. Supports laboratory washing and contaminant-transport comparisons. Metal-rich leachate still requires management; the study does not establish agricultural reuse or field-scale safety.

Thilini Kananke, 2026. This Sri Lankan study compares elemental concentrations and simulated digestive release in two leafy vegetables across five growing areas. Raw, coconut-milk-cooked and coconut-oil-stir-fried portions were tested separately; lower in-vitro release does not establish lower human absorption or safe consumption. Supports region-specific leafy-vegetable occurrence and cooking/bioaccessibility comparisons. Processing effects are not uniform: for example Wellampitiya A. sessilis gastric Pb is 15.3% raw and 20.7% cooked. Coconut additions can change the matrix; an in-vitro endpoint is not in-vivo absorption.

Bogdan Ștefan Oprea, 2022. Celery roots and garden soils from 26 households in a historically polluted Romanian area showed wide cadmium and lead variation in 2021–2022. Soil results use dry weight, while edible celeriac results use fresh weight; these paired measurements preserve a legacy-contamination pathway without assigning sole liability to any facility. Supports historical industrial-burden and present edible-root occurrence evidence. Celery here is celeriac, not stalk celery; the product category is root/tuber vegetables. Geographic sampling is targeted to a polluted area and is not a national market sample.

Emmanuel Joy Enogbe, 2025. Two anonymous chocolate products from Bwari market contained measurable nickel, iron, copper, chromium and lead. Their reported sample concentrations are preserved independently of inconsistent dispersion, intake means and safety comparisons in the paper. Provides a small local occurrence observation with anonymous products. It cannot establish market prevalence, source attribution, or a no-risk conclusion. Total chromium (Cr) is not Cr(VI).

Vladimir N. Bashkin, 2021. Bashkin and Galiulina review vegetable-associated metal exposure assessment and microbial/agronomic risk-management approaches. Chinese and Russian case-study values are secondary reports; they remain traceable to the cited studies and are not counted as new independent occurrence samples. Supports exposure-method and remediation literature discovery. Bacterial effects can increase as well as decrease uptake depending on organism, metal and plant; the review does not establish a universal inoculant intervention. Secondary model outputs are not contemporary health or certification thresholds.

Iosif Gergen, 2012. Gergen and Harmanescu analyze metal contamination patterns across two historic Romanian mining areas and a reference area. Their PCA study reproduces vegetable concentrations and male hazard quotients from the earlier Harmanescu 2011 study; these remain linked secondary observations rather than additional independent samples. Supports legacy mining and tissue/region differences. Parsley root and leaf remain distinct, as do carrot root and leaf. The fresh-matter food table is retained with cohort linkage so that a reanalysis cannot inflate the evidence pool. Source THQ rankings are model results, not clinical outcomes.