Mohammadian-Hafshejani et al. 2024 — Cadmium exposure and prostate cancer risk: systematic review and meta-analysis
This systematic review and dose-response meta-analysis pooled 16 observational studies to examine the relationship between cadmium exposure and prostate cancer incidence. Searches covered ISI Web of Science, Cochrane, Science Direct, Scopus, PubMed, and Google Scholar up to May 2022. The authors note that dietary exposure to cadmium is the primary route for most people, occurring through contaminated cereals, potatoes, vegetables, and drinking water. The pooled dose-response analysis found a modest and non-statistically significant positive association: odds ratios of 1.03 (95% CI 0.95–1.12), 1.12 (0.99–1.26), and 1.16 (0.79–1.70) for the second, third, and fourth quartiles of Cd exposure vs. the first quartile, respectively. Publication bias was not detected (Begg’s and Egger’s tests non-significant across quartiles). The authors conclude that Cd exposure leads to a non-significant increase in prostate cancer risk.
Key numbers
- Studies included: 16 (after screening from 794 initial records, 427 after deduplication)
- Exposure sources in included studies: dietary cadmium (toenail Cd as biomarker most commonly used), occupational exposure, environmental exposure
- Quartile 2 OR: 1.03 (95% CI 0.95–1.12)
- Quartile 3 OR: 1.12 (95% CI 0.99–1.26)
- Quartile 4 OR: 1.16 (95% CI 0.79–1.70)
- Cd half-life in human body: 10–30 years
- Primary cadmium accumulation organs: liver, kidneys, intestines; also salivary glands, prostate, cerebral cortex, testes, lungs, pancreas, and central nervous system
- Exposure assessment methods across included studies: toenail Cd (most common), urinary Cd, dietary recall, serum Cd
Methods (brief)
Systematic review and dose-response meta-analysis. Stata 15 used for pooled analysis. Included human observational studies (case-control, cohort, cross-sectional) on Cd exposure vs. prostate cancer. Heterogeneity assessed by I² statistic; funnel plots for publication bias. Meta-regression performed. Funded by Shahrekord University of Medical Sciences (grant 6395; ethical code IR.SKUMS.REC.1401.114).
Limitation: Evidence tier B (systematic review pooling observational data, no primary food-matrix concentration measurements). Cannot distinguish dietary vs. occupational exposure paths in all included studies. Quartile boundaries differ across included studies because each study defines quartiles based on its own distribution, complicating dose-response pooling.
Implications
Certification: This meta-analysis supports the existing evidence base linking dietary Cd exposure to potential carcinogenicity (prostate is a Cd-accumulating organ). The association is directionally positive but not statistically significant in this pooled analysis; does not contradict the literature direction. Relevant to HMT&C rationale for Cd limits.
Courses: Useful for illustrating the epidemiological challenge of quantifying cancer risk from dietary Cd at typical food-matrix concentrations: 16 studies, dose-response directionally positive, but wide confidence intervals at the highest exposure quartile (0.79–1.70).
App: No direct food-matrix concentration data. Provides health-endpoint context for dietary Cd exposure — prostate cancer signal is present but not statistically significant; compared to kidney and bone effects (more robustly established at lower Cd doses), prostate cancer is a secondary concern at typical dietary exposure levels.