Clinical Pharmacist and Master’s student in Clinical Pharmacy with research interests in pharmacovigilance, behavioral interventions in mental health, and AI applications in clinical decision support. Experience includes digital health research with Bloomsbury Health (London) and pharmacovigilance practice in patient support programs. Published work covers drug awareness among healthcare providers, postpartum depression management, and patient safety reporting. What was reviewed?
This review assessed evidence on cadmium in the maternal diet, synthesizing toxicokinetics, exposure sources, health-based guidance values, and risk characterization relevant to pregnancy and the postpartum period. The Committee on Toxicity evaluated prior EFSA and JECFA opinions, epidemiology, animal data, and UK monitoring surveys to determine whether habitual dietary exposures approach thresholds for renal, skeletal, carcinogenic, and developmental effects. Central to the analysis is EFSA’s tolerable weekly intake of 2.5 µg/kg bw, derived from renal tubular toxicity biomarkers, and how women of childbearing age compare to this benchmark under contemporary UK dietary patterns.
Who was reviewed?
Populations considered included pregnant and lactating women by extrapolation from UK women aged 16–49 years because national dietary datasets exclude pregnancy; this proxy was used to estimate cadmium intake from food and water. Specific maternal subgroups, smokers versus non-smokers, vegetarians, and ethnic cohorts, were examined where available, alongside birth cohorts from Sweden, China, Korea, and the US, evaluating placental transfer, cord blood levels, and infant neurobehavioral outcomes. The review also considered physiological states such as iron deficiency that increase cadmium absorption during pregnancy, thereby elevating maternal body burden and potential fetal exposure.
Most important findings
| Critical point | Details |
|---|---|
| Diet is the dominant non-occupational source | In non-smokers, ~90% of cadmium exposure arises from food; cereals, potatoes, bread, and rice drive intake, influenced by soil pH and phosphate fertilizers. Offal (kidney, liver) also contains elevated levels due to organ accumulation. |
| Smoking doubles internal dose | Tobacco leaves bioaccumulate cadmium; smokers and those exposed to second-hand smoke show substantially higher body burdens than non-smokers, and prior smoking contributes to maternal stores even after cessation. |
| Pregnancy increases absorption | Oral bioavailability is typically 1–10% but can rise to ~20% with iron deficiency; pregnancy-related iron demands and low zinc/calcium intakes enhance gastrointestinal uptake via DMT-1. |
| Long biological half-life drives cumulative risk | Cadmium binds metallothionein, accumulates in the kidney and liver, and exhibits a 10–35-year half-life, making lifetime dietary management important for maternal cohorts. |
| Renal toxicity underpins EFSA TWI | EFSA set a TWI of 2.5 µg/kg bw/week to keep urinary cadmium below 1 µg/g creatinine by age 50, based on β2-microglobulin as a tubular damage marker; EFSA retained this stricter value compared with JECFA’s PTMI. |
| UK exposure vs. TWI | Cadmium accumulates in the placenta, may disrupt steroidogenesis and 11-β-HSD2, and is associated in some cohorts with lower birth weight indices and adverse infant neurobehavioral profiles, though results are inconsistent across studies. |
| Reproductive/placental effects | Cadmium binds metallothionein, accumulates in the kidney and liver, and exhibits a 10–35-year half-life, making lifetime dietary management important for maternal cohorts. |
| Bone and cancer endpoints | Chronic exposure impairs vitamin D activation and calcium handling, increasing osteoporosis and fracture risk; IARC classifies cadmium as carcinogenic (Group 1) with strongest evidence for lung cancer, while oral carcinogenicity evidence remains limited. |
| Overall risk judgment | Among women of childbearing age, the mean total dietary exposure corresponds to ~22–58% of EFSA’s TWI; the 97.5th percentile approaches 58–100%, with miscellaneous cereals, potatoes, and bread contributing the most. Drinking water minimally affects totals. |
Key implications
For regulatory impacts, cadmium in the maternal diet supports maintaining EFSA’s TWI as the operative benchmark and prioritizing exposure mitigation in staple cereals and potatoes; for certification requirements, HTMC should require product-level cadmium testing aligned to portions that keep weekly intake below 2.5 µg/kg bw; for industry applications, procurement should favor low-Cd supply chains and soils with controlled pH and fertilizer inputs; research gaps include pregnancy-specific consumption data and longitudinal maternal biomarkers; practical recommendations include iron sufficiency screening, smoking cessation support, and risk-based guidance on high-cadmium foods during pregnancy.
Citation
Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment (COT). Statement on the potential risks from cadmium in the maternal diet. November 2022. Statement 05/22.
Cadmium is a persistent heavy metal that accumulates in kidneys and bones. Dietary sources include cereals, cocoa, shellfish and vegetables, while smokers and industrial workers receive higher exposures. Studies link cadmium to kidney dysfunction, bone fractures and cancer.
