This test is most useful if any of these apply to you.
Cadmium is one of the most stubborn environmental toxins your body deals with. Once it gets in through food, water, or tobacco smoke, it can sit in your kidneys for decades, with a half-life measured in years rather than days. A single blood test tells you about recent exposure. A full 24-hour urine collection tells you something far more useful for prevention: how much has quietly accumulated inside you.
Cd (cadmium) in urine is not something your body makes. It is a heavy metal you have picked up from your environment, and how much shows up in your urine each day reflects both what has built up in your kidneys and how slowly your body is releasing it. If you smoke, ate a lot of leafy greens grown in cadmium-rich soil, or worked around metals, this test can reveal a burden you would never spot on a standard chemistry panel.
When cadmium enters your bloodstream, most of it binds to a small protein called metallothionein that shuttles it to your liver, and then slowly to your kidneys. The kidneys filter this bound form, reabsorb it in the tubules (the tiny straw-like structures that fine-tune urine), and store the metal in the outer layer of the kidney called the renal cortex. Only a tiny fraction leaks out into your urine each day, but that fraction is roughly proportional to how much has built up inside.
That slow release is why a 24-hour urine reading is such a useful window into cumulative exposure. In one Japanese population study, cadmium had a biological half-life in urine of about 13.6 years in men and 13.9 years in women after exposure stopped. Other toxicokinetic models place the half-life anywhere from roughly 11.6 years up to 15 to 45 years depending on the population and modeling approach, so the figure is best thought of as many years rather than a single fixed number. Either way, the number you see today reflects decisions and exposures from years back, not what you ate yesterday. It is also worth noting that at low environmental exposures, some researchers argue urinary cadmium is influenced by urinary flow, recent exposure, and low-level proteinuria as well as true body burden.
Your kidneys are the main organ cadmium harms. It quietly damages the proximal tubule cells, which are responsible for reabsorbing small proteins from urine. A comprehensive 2023 review concluded that clinically relevant kidney damage begins at urinary cadmium levels commonly seen in industrialized countries, with the observed adverse effect level for glomerular dysfunction landing at a very small concentration (adjusted for how concentrated your urine is).
In an area of Thailand with soil contamination, higher cadmium excretion tracked directly with albuminuria (protein leaking into urine) and reduced eGFR (a measure of how well kidneys filter blood). Occupational studies have shown that early tubular injury markers such as beta2-microglobulin, N-acetyl-beta-D-glucosaminidase, and retinol-binding protein rise before conventional kidney tests move. In benchmark-dose studies of Japanese and Chinese populations, thresholds for detectable kidney effects have been described.
Cadmium is not just a kidney problem. A 2024 systematic review and meta-analysis found that cadmium exposure, measured in urine or blood, was associated with higher cardiovascular disease risk. When urinary cadmium was the exposure marker, risk climbed roughly in a straight line at low exposures before the curve flattened at higher levels.
In a cohort of 10,713 Taiwanese adults, those in the highest quartile of urinary cadmium had roughly 2.6 times the risk of cardiovascular death and 1.7 times the risk of death from any cause compared with the lowest quartile. In older Australian women, each roughly 2.7-fold increase in urinary cadmium was tied to 36% higher risk of death from heart failure. The signal for isolated heart attacks in never-smokers is more mixed, which suggests cadmium is one input among several rather than a standalone predictor.
The International Agency for Research on Cancer has classified cadmium as a Group 1 human carcinogen since 1993. In a Belgian prospective cohort followed for a median of 17.2 years, each doubling of 24-hour urinary cadmium excretion was associated with about 31% higher risk of overall cancer and 70% higher risk of lung cancer. Living in a high-exposure area quadrupled lung cancer risk compared with a low-exposure area.
The picture varies by cancer site. A dose-response meta-analysis of breast cancer found no association when urinary cadmium was the exposure metric, even though a modest link appeared for dietary cadmium intake. This is a reminder that cadmium touches different tissues in different ways, and urinary levels do not automatically translate into risk for every cancer type.
A 2021 meta-analysis found moderate-certainty evidence for a positive association between urinary cadmium and both diabetes and prediabetes. Comparing higher versus lower exposure, urinary cadmium was associated with about 21% higher risk of type 2 diabetes and 41% higher risk of prediabetes. Prediabetes risk climbed with cadmium exposure until it reached a plateau.
Higher urinary cadmium consistently tracks with worse long-term outcomes. In a prospective cohort of postmenopausal Swedish women, those in the highest third of urinary cadmium had 20% higher risk of fractures and 38% higher risk of death from any cause compared with the lowest third. The exposure was long-term and low-level. This finding matters because cadmium can weaken bone through both direct effects and by disrupting how the body handles calcium and vitamin D.
A single urine reading tells you where you are today, not whether cadmium is climbing or falling in your body over time. Even 24-hour urine cadmium has moderate within-person stability, with intraclass correlation (a measure of how consistent repeated readings are, where 1.0 would be perfectly stable) around 0.50 to 0.85 depending on the population and time frame. In practical terms, if you make lifestyle changes such as quitting smoking or reducing exposure, one follow-up reading may not fully capture the trajectory.
No major medical society has published a formal retesting schedule for this test, so what follows is a practical expert-opinion approach rather than guideline-level guidance. Get a baseline, then consider retesting in 6 to 12 months if you are actively addressing an exposure source. After that, annual monitoring is reasonable if you have any known risk factor such as smoking history, occupational exposure, kidney disease, or living in an area with known soil or water contamination. Trends over years are more meaningful than any single value, because cadmium leaves the body so slowly that shifts happen on that timescale.
If your 24-hour urine cadmium comes back higher than expected, the first step is to confirm with a repeat 24-hour collection, ideally paired with kidney function testing. High cadmium alongside preserved kidney function points to accumulated exposure. High cadmium alongside proteinuria or reduced eGFR suggests the kidneys may be leaking cadmium because of injury, which changes the meaning of the number.
Companion tests worth considering include eGFR calculated from both creatinine and cystatin C for a fuller picture of kidney filtration, a urine albumin-to-creatinine ratio to check for early kidney damage, and other heavy metals like lead, mercury, and arsenic since environmental exposures often travel together. If levels are markedly elevated or you have occupational exposure, consulting an occupational medicine specialist or nephrologist is reasonable. Chelation therapy is not routinely recommended for chronic low-level exposure and should only be considered under specialist supervision.
Cadmium in urine is more nuanced than most lab numbers. A few situations can make a single reading misleading in ways that matter for how you interpret it.
Evidence-backed interventions that affect your Cadmium level
Cadmium is best interpreted alongside these tests.
Cadmium is included in these pre-built panels.