Overview

Nickel (Ni) is a transition metal that occurs in the earth’s crust and is widely used in alloys, batteries, electronics and industrial processes. It can contaminate food crops and water, and it is released from consumer products and occupational sources. The European Food Safety Authority (EFSA) established a tolerable daily intake (TDI) of 3 μg/kg body weight for nickel but noted that this value is exceeded in toddlers, children and, in some cases, infants. ^[1] The Heavy Metal Tested & Certified (HMTC) program includes nickel in its top‑eight metals because of its ubiquity and the growing evidence that chronic exposure negatively affects cardiovascular, reproductive and developmental health.^[2]

Nickel (Ni)

Elemental nickel (atomic number 28) exists in metallic and ionic forms. Industrial production uses nickel in stainless steel, alloys, electroplating, pigments, and batteries. Nickel compounds include nickel sulfate (water‑soluble) and nickel oxide and sulfides (water‑insoluble). Although small amounts of nickel are essential in some microorganisms, there is no known nutritional requirement for humans pmc.ncbi.nlm.nih.gov. Nickel’s widespread use means it can leach into food, water, and consumer products. EFSA’s reassessment showed that dietary nickel intake from grains, nuts, legumes and chocolate is a primary exposure route for children.^[3] Nickel is also emitted from combustion, mining and smelting, leading to inhalation exposures.

Major Sources of Nickel Exposure

Nickel allergy is one of the most common causes of allergic contact dermatitis. Contact occurs when the skin touches nickel-containing objects; the rash and itching may appear up to 72 hours later. Systemic exposure via diet or implants can trigger more serious symptoms such as fatigue, headaches and swelling. Nickel exposure is a multifaceted public health concern due to its presence in food, consumer products, occupational settings, and the broader environment. Individuals may be exposed through ingestion, inhalation, or dermal contact, with both acute and chronic health effects. Below, the primary sources of nickel exposure and associated health outcomes are organized in two-column tables to provide clarity for clinicians, researchers, and industry stakeholders.

Source Category	Examples
Dietary sources	Nuts, beans and legumes; chocolate and cocoa; whole-grain bread and cereals; shellfish and seafood; soy products; tea; leafy vegetables
Consumer products	Jewelry (earrings, rings, watchbands); clothing fasteners (belt buckles, snaps, zippers); coins
Everyday items and medical devices	Cooking utensils; eyeglasses; dental braces; keys; razors; electronics; batteries.
Occupational sources	Stainless steel production; electroplating; welding; nickel refinery work
Environmental releases	Industrial emissions; waste incineration contaminating air, soil, and water

Exposure Route / Effect	Key Outcomes
Dermal contact	Nickel allergy is one of the most common causes of allergic contact dermatitis; rash and itching may appear up to 72 hours after exposure.
Systemic exposure (diet or implants)	May trigger more severe symptoms such as fatigue, headaches, and swelling.

Adverse Health Effects of Nickel

Nickel exposure is associated with a wide spectrum of adverse health effects, supported by both mechanistic toxicology and epidemiological data. The evidence demonstrates that nickel can trigger hypersensitivity reactions, genomic instability, organ damage, and developmental toxicity, with particular risks for pregnant women, children, and occupationally exposed populations. The tables below summarize the major health effects of nickel exposure, their underlying mechanisms, and epidemiological findings.

Health Effect	Evidence and Mechanisms
Allergic reactions and skin disorders	Nickel induces hypersensitivity reactions, causing allergic contact dermatitis in up to 20% of people in industrialized countries. ^[4]
Genomic damage and carcinogenicity	Narrative reviews report links between nickel exposure and genomic damage, renal disease, pulmonary fibrosis, and cancers of the lung and nasal cavities. Mechanisms include oxidative stress and mitochondrial dysfunction.^[5]
Cardiovascular and metabolic effects	Human NHANES studies show urinary nickel levels correlate with cardiovascular and metabolic disorders; animal studies confirm that nickel exposure damages the heart and liver through oxidative stress.^[6]
Developmental toxicity	Nickel crosses the placenta and accumulates in fetal tissues. In a cohort of 7,291 Chinese pregnant women, higher maternal urinary nickel levels were linked to shorter gestational age and preterm delivery. Animal studies show nickel(II) compounds act as potent transplacental carcinogens.^[7]
Congenital heart defects (CHDs)	A 2019 case-control study of 399 CHD cases and 490 controls found high maternal hair nickel levels increased CHD risk (aOR 2.672 for the highest tertile). ^[8] Placental nickel >0.2658 ng/mg raised the risk of non-septal heart defects by aOR 4.538. ^[9]
Reproductive and systemic toxicity	Nickel compounds cause neurotoxicity, genotoxicity, reproductive toxicity, nephrotoxicity, and immunotoxicity in animals.^[10] High dietary nickel chloride doses (>300 mg/kg) induce immunotoxicity, weight loss, gastrointestinal disease, and neurological damage.^[11]

Minimal Risk Levels (inhalation)

The U.S. Agency for Toxic Substances and Disease Registry (ATSDR) derived an acute inhalation minimal risk level (MRL) of 1×10−4 mg Ni/m³ for nickel based on bronchiole epithelial degeneration/hyperplasia in rats exposed to nickel sulfate.^[12] This MRL assumes a continuous exposure and includes uncertainty factors to protect sensitive populations.^[13]

Summary Table of Health Effects

Health Effect	Supporting Research (Author, Year, Journal)
Allergic contact dermatitis & systemic allergy	Cardio‑metabolic narrative review summarizing human data, noting that nickel is the leading cause of metal allergy and contact dermatitis affects up to 20 % of people. ^[14]
Genomic damage, renal disease, pulmonary fibrosis and cancers	Narrative review linking nickel exposure to genomic damage, renal disorders, pulmonary fibrosis and cancers of the lung and nasal cavities.^[15]
Cardiovascular toxicity and metabolic disease	NHANES analyses and animal studies reviewed by Liu et al. (2025) showing associations between urinary nickel levels and cardiovascular and metabolic disorders and demonstrating organ damage via oxidative stress.^[16]
Developmental toxicity & preterm birth	Prospective cohort study (2020) reporting that elevated maternal urinary nickel is associated with reduced gestational age and higher risk of preterm delivery; animal studies showing nickel crosses the placenta and acts as a trans‑placental carcinogen. ^[17]
Congenital heart defects (CHDs)	Case‑control study (Zhang et al., 2019) demonstrating increased CHD risk with higher maternal hair and placental nickel levels (aOR up to 4.538.^[18]
Neurotoxicity, reproductive toxicity & systemic effects	Studies compiled by Zhang et al. showing nickel and its compounds induce neurotoxicity, genotoxicity, reproductive toxicity and nephrotoxicity; dietary nickel chloride >300 mg/kg causes immunotoxicity and weight loss.^[19]
Respiratory toxicity & minimal risk levels	ATSDR 2024 MRL worksheet: acute inhalation MRL of 1×10−4 mg Ni/m³; critical effect is bronchiole epithelial degeneration/hyperplasia in rats.^[20]

Consumer Relevance Sidebar

Many everyday products and foods contain nickel:^[21][22]

Category	Examples

Jewelry and personal items

Bracelets, earrings, rings, watchbands, belt buckles, bra hooks, buttons, snaps, zippers, eyeglasses

Household and medical equipment

Cooking utensils, coins, keys, razors, dental braces, medical implants, electronic devices

High nickel foods

Beans and legumes, nuts, chocolate and cocoa, figs, prunes, raspberries, whole grain cereals, oats, shellfish, soy products, tea, leafy vegetables such as kale and spinach

Infant and toddler foods

Soy based infant formulas, cereals, chocolates; EFSA monitoring indicates some products can exceed new EU maximum levels

Regulatory Snapshot

The EFSA updated its risk assessment in 2020, setting a TDI for nickel of 3 μg/kg body weight but concluded that this intake is exceeded in toddlers and children.^[23] In response, the European Commission enacted Regulation (EU) 2024/1987, which establishes maximum nickel levels in nuts, vegetables, legumes, seaweed, chocolate and infant formulas; for example, peanuts may contain no more than 12 mg/kg and infant formula 0.1 mg/kg. These limits take effect in 2025–2026. ATSDR’s acute inhalation MRL (1×10−4 mg Ni/m³) sets a screening level for occupational and environmental air exposures. Despite these standards, EFSA notes that current monitoring data show exceedances, especially among young children.^[24]

Implications for the HMTC Program

Nickel’s omnipresence in foods, consumer products and the environment, combined with evidence of allergic, genotoxic, reproductive and developmental toxicity, underscores the need for rigorous regulation. HMTC’s As Low As Reasonably Achievable (ALARA) approach sets nickel limits below the EU maximum levels to protect infants, children and other vulnerable groups. The program requires third‑party laboratory testing of finished products and raw materials, transparent reporting and lot‑specific traceability. By obtaining HMTC certification, manufacturers can demonstrate proactive compliance with impending regulations, differentiate their products in the marketplace and build consumer trust.

Research Feed

September 23, 2025

What was studied? This study investigated the effects of prenatal heavy metal exposure and infant neurodevelopment, considering the adverse effects of multiple heavy metals—cadmium (Cd), nickel (Ni), mercury (Hg), and lead (Pb). Heavy metal levels were measured in maternal urine samples collected at the 12th week of gestation, while infant neurodevelopment was assessed at 40 days using the Bayley Scales of Infant and Toddler Development. The study applied multiple statistical approaches, including Generalized Additive Models (GAM), Multivariable Linear Regression (MLR) with restricted cubic splines (RCS), Bayesian Kernel Machine Regression (BKMR), and Weighted Quantile Sum (WQS) regression, to evaluate both individual and joint effects of these metals on early neurodevelopment. Who was studied? The study examined 400 mother-infant pairs recruited from a community-based birth cohort in Tarragona, Spain, between 2013 and 2017. Mothers were recruited during their initial prenatal visits, and urine samples were analyzed for metal concentrations using ICP-MS/MS with creatinine adjustment. Infants were assessed at 40 days old by trained psychologists, focusing on cognitive, language, and motor domains. The mothers had a mean age of 30.9 years, with most belonging to a low- or middle-socioeconomic class, and nearly 70% reported never smoking. Infants were almost evenly split between male and female, with 74.5% breastfed. Most important findings Cadmium was consistently associated with adverse neurodevelopmental outcomes. GAM and MLR analyses confirmed a negative linear association between Cd exposure and both cognitive and expressive language scores (β = −1.47 and β = −0.32, respectively, both statistically significant). Pb demonstrated a non-linear, inverted U-shaped relationship with language development, indicating risk at both low and high exposure levels. WQS regression revealed that mixtures of heavy metals were significantly associated with impaired expressive language development (β = −0.26, 95% CI = −0.44, −0.07), with Cd and Ni identified as the main contributors. BKMR analyses supported an overall negative trend for metal mixtures, though not statistically significant. Mercury exposure showed no consistent associations. Key implications The study highlights that prenatal heavy metal exposure and infant neurodevelopment are particularly negatively impacted by cadmium and nickel exposure, with expressive language being the most vulnerable domain. The findings underscore the limitations of focusing on single-metal exposures, as real-world scenarios typically involve complex mixtures. Importantly for a certification program such as Heavy Metal Tested and Certified (HMTC), the evidence supports the inclusion of cadmium and nickel within the Infant and Child Foods Standards alongside lead and mercury as priority metals for regulatory thresholds, given their demonstrable neurodevelopmental risks even at low levels of prenatal exposure. These results emphasize the urgency of establishing stricter heavy metal limits in foods consumed by pregnant women, since dietary intake is a major source of exposure. For industry, compliance with reduced heavy metal thresholds is not only protective of infant health but also scientifically justified by evidence linking prenatal exposure to cognitive and language deficits in early life. For regulators, the study validates the need for mixture-based risk assessment approaches, moving beyond single-metal evaluations to capture the cumulative effects on vulnerable populations. Citation Kou X, Palleja-Millan M, Canals J, Rivera Moreno V, Renzetti S, Arija V. Effects of prenatal exposure to multiple heavy metals on infant neurodevelopment: A multi-statistical approach. Environmental Pollution. 2025;367:125647. doi:10.1016/j.envpol.2025.125647.

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