Health Testing

Consult with your primary care physician or pediatrician before taking action. Pediatricians can contact 1-877-KIDCHEM (NW Pediatric Environmental Safety Unit) for more information about testing.


The Oregon Health Authority (OHA) currently recommends spot urine samples to measure exposure to cadmium and arsenic.

For testing chronic cadmium exposure, the CDC has different guidelines and states, “The best screening and diagnostic test for chronic cadmium exposure is a 24-hour urinary cadmium level, normalized to creatinine excretion.” For arsenic exposure, the CDC states, “The best specimen is a 24-hour urine collection for arsenic and creatinine as it more accurately reflects the true amount of arsenic excretion.” It’s important to note that this test recommended by the CDC may not be accurate in young children, please check with your pediatrician.

There are many methods of testing for toxic metals, including blood, hair, nails, and other specimens. Cadmium sequesters in organ tissues (lung, liver, kidneys). Getting organ tissue levels tested is not usually feasible. There are indirect ways to measure renal problems associated with cadmium exposure. Urinary beta-2 microglobulin can be an indicator of renal dysfunction in those who have kidney problems as a result of being chronically exposed to cadmium.

Naturopathic doctors often have experience in testing for cadmium, arsenic and other heavy metals. Some of the methods used by naturopathic practitioners are controversial. Some of these methods are effective at removing cadmium and other heavy metals, but there may be associated risk with removing and mobilizing such toxic metals.

If you are concerned about your or your child’s cadmium, arsenic, or other metal exposure, it’s important that you find a doctor that you trust. Ask your doctor about the risks and benefits of testing methods and treatment.

Oregon Health Authority (OHA) Testing Recommendations

Below is a PDF of the OHA Testing recommendations:

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Symptoms of Chronic Cadmium Toxicity

Respiratory Effects

Most studies have associated chronic occupational exposure to cadmium fumes and dusts with increased risk of chronic obstructive lung disease and emphysema, but some studies reported no such association (Hendrick 1996; ATSDR 1999). Study limitations, such as small sample size, lack of suitable cohorts, and failure to control for smoking and other confounding effects, render the association uncertain.

There are also reports that respiratory effects caused by occupational exposure can reverse themselves if exposure stops (ATSDR 1999).

Studies have examined the role of cadmium in the development of chronic obstructive pulmonary disease (COPD) in smokers (ATSDR 1999). The most recent (Mannino et al. 2004) study showed that current and former smokers had higher body burdens of cadmium than non-smokers and that within smokers, the body burden of cadmium was related to lung injury related to smoking. The authors conclude that cadmium might be important in the development of tobacco related lung disease.

Chronic cadmium inhalation is also suspected to be a possible cause of lung cancer (Sorhan and Esmen 2004; Verougstratete et al. 2003). Other respiratory effects of chronic occupational exposure to cadmium include chronic rhinitis, destruction of the olfactory epithelium with subsequent anosmia as well as the development of bronchitis (ATSDR 1999; Drebler 2002).

Cardiovascular Effects

In animals, chronic ingestion of cadmium causes increased systolic blood pressure in the absence of significant renal disease. Such pressor effects have been linked to depressed blood and tissue levels of atrial natriuretic peptide, increased blood levels of aldosterone, and retention of sodium and water (ATSDR 1999). This led to a hypothesis that cadmium exposure in humans might be related to hypertension.

Several studies have looked at this topic. The Cadmibel study, a prospective population study looking at the health effects of low-level environmental exposure to cadmium in the general population, found no effect of cadmium on the blood pressure of study subjects (Stassen J et al. 1991). A recent follow-up of the original Cadmibel cohort, the PheeCad study found the same result (Staessen J et al. 1999).

However, recent studies (Navas-Acien et al. 2004, 2005) have examined the contribution of cadmium and some other heavy metals to the development of peripheral artery disease. These studies found an association with cadmium exposure and the development of peripheral artery disease. In fact, the effect of smoking on peripheral artery disease decreased after adjustment for cadmium levels suggesting that the effect of smoking on the development of peripheral artery disease may be partially mediated by cadmium.

Renal Effects

The kidney is the principal organ targeted by chronic exposure to cadmium. Cadmium nephrotoxicity may follow chronic inhalation or ingestion. Data from human studies suggest a latency period of approximately 10 years before clinical onset of renal damage, depending on intensity of exposure. However, subtle alterations of renal function have been described after acute exposure in animals, and there are rare reports of renal cortical necrosis after acute high-dose exposure in humans.

Classically, chronic cadmium exposure is associated with progressive renal tubular dysfunction. The first sign of renal abnormalities occur at 2 μg/g creatinine and are microscopic tubular proteinuria – the biomarkers are β2-microglobulin, ά1-microglobulin. At urinary cadmium levels of 4 μg/gCr, enzymes such as N-acetyl-B-glucosaminidase (NAG) are elevated in urine and signs of glomerular damage including increased albumin in the urine and a decrease in glomerular filtration rate are seen. In the final stages of cadmium nephropathy, glycosuria, wasting of calcium and phosphate, and altered calcium metabolism with secondary effects on the skeleton of osteoporosis and osteomalacia are seen (Roels et al.1999; Jarup et al. 2000).

Some experts believe the microproteinuria related to cadmium exposure is not invariably progressive and the level at which cadmium-induced nephropathy becomes progressive and irreversible, even after termination of exposure occurs at urinary cadmium levels of >4 ug Cd/g c reatinine or at values of B2-microgloburia of > 1,000 µg/g creatinine (Ikeda et al. 2005; Kobayashi et al. 2006). Other experts believe that the renal tubular dysfunction associated with cadmium is irreversible (Iwata et al. 1993). Cadmium nephropathy is an important determinant of mortality in cadmium workers.

Toxic effects on the kidney are dose-related (Mueller et al. 1992). For workers, the risk of clinical nephropathy increases significantly with total airborne exposures greater than 300 mg/m3, urine cadmium levels greater than 10 µg/g creatinine, and renal cortex levels greater than 200 ppm (Roels et al. 1999).

Early signs of renal damage have been reported in members of the general population at urine levels between 2-4 nmol/mmol creatinine. A number of studies over the years have looked at the effects of cadmium on the kidney in the environmentally exposed including:

  • Cadmibel (Buchet et al. 1990)
  • Japan (Ikeda et al. 2003, 2005, 2006; Kobayashi et al. 2006)
  • OSCAR (Jarup et al. 2000)
  • Sweden
  • United States (Noonan et al. 2002)

These studies have found that even very low-levels of cadmium may have adverse effects on the kidney. WHO currently states that 200 μg/g levels wet weight in kidney causes adverse changes in 10% of the population (Satoh et al. 2002). In the past, several studies of occupationally and environmentally exposed populations have shown that the threshold for renal damage occurred at urinary cadmium levels of 2-4 nmol/mmol creatinine (Buchet et al. 1990); however, the OSCAR study found that those with a urine cadmium level of 1 nmol/mmol creatinine had a threefold risk of increased ά-1 microglobulin (Jarup et al. 2000). However, at this time, it is not known if these early subclinical changes in kidney biomarkers associated with low levels of environmental cadmium exposure have any correlation with continued decline in renal function to clinical levels of concern (Noonan et al. 2002).

Much work is underway to define the “critical renal concentration” at which cadmium-induced renal damage occurs. Recent studies in Japan estimate that the lifetime tolerable dose of cadmium is 2.0 grams for both men and women (Trzcinka-Ochocka et al. 2004; Watanabe et al.2004). There is a very low margin of safety between reaching the critical renal concentration and body burdens found in smokers (Satarug and Moore 2004). Recent work also suggests that exposed children might be a susceptible population (Trzcinka-Ochocka et al. 2004).

At moderate, usual occupational levels of exposure, increased excretion of high-molecular-weight proteins, such as albumin and transferrin, are early signs of glomerular damage from cadmium. Once begun, the glomerular damage is believed to be irreversible and the degree of damage is dose-dependent (Jarup 2002). The glomerular filtration rate (GFR) declines slowly but progressively, suggesting that cadmium accelerates the normal age-related decline in renal function. Clinical uremia is rare, but decreased filtration reserve capacity can be demonstrated in cadmium workers with normal baseline GFR and serum creatinine. Cadmium exposure may also potentiate the development of glomerulopathy in diabetic populations (Buchet et al. 1990).

Sufficient cadmium exposure can also lead to decreased GFR and chronic renal failure manifested by:

  • aminoaciduria
  • glucosuria
  • hypercalcuria
  • hyperphosphaturia
  • polyuria
  • reduced buffering capacity for acids (Jarup 2002)

Kidney stones are more common in cadmium-exposed populations, especially in exposed workers. Lifetime prevalence rates of 18%to 44% have been found, compared to rates less than 5% in control populations. Stone formation probably results from cadmium-induced renal damage leading to hypercalciuria and hyperphosphaturia, but other contributing factors may include uric aciduria, reduced urinary citrate, and renal tubular acidosis.

Skeletal Lesions

Although cadmium accumulates in bone, the bone disease that results from excessive cadmium exposure is believed to be secondary to changes in calcium metabolism due to cadmium-induced renal damage (ATSDR 1999). Clinically significant bone lesions usually occur late in severe chronic cadmium poisoning and include pseudofractures and other effects of osteomalacia and osteoporosis. Pseudofractures are spontaneous fractures that follow the distribution of stress in normal skeleton or occur at sites where major arteries cross the bone and cause mechanical stress through pulsation.

The OSCAR study in Sweden examined whether environmental cadmium exposure could be a risk factor for reduced mineral density in bone (Jarup et al. 2000; Alfven et al. 2002, 2004). The study authors found a negative correlation between urinary cadmium and bone density. Skeletal effects appear to be secondary to increased urinary calcium and phosphorus losses due to cadmium-induced renal effects (Jarup et al.2000). These effects are compounded by inhibition of renal hydroxylation of vitamin D, which eventually leads to a deficiency of its active form (Nogawa et al. 2004). Some investigators believe cadmium also exerts an inhibitory effect on calcium absorption from the gastrointestinal tract. Enhanced secretion of prostaglandin E2 may also contribute to bone resorption.

“Itai-itai” Disease

“Itai-itai” or ouch-ouch diseas was first described in post-menopausal Japanese women exposed to excessive levels of cadmium over their lifetimes. The women were exposed through their diet because the region of Japan in which they resided was contaminated with cadmium (Ikeda et al. 2000; Watanabe et al. 2000).

Symptoms and signs of “itai-itai” disease include:

  • Severe osteoporosis and osteomalacia with simultaneous severe renal dysfunction
  • Normochromic anemia and low blood pressure (Alfven et al. 2002; Nogawa et al. 2004)

Average urinary cadmium level in these patients is 20-30 ìg/g-creatinine of cadmium in urine (Ezaki et al. 2003).

Developmental Effects

In animals, cadmium crosses the placenta, and large parenteral doses during early gestation cause birth defects. During later pregnancy, doses greater than 2.5 mg/kg cause severe placental damage and fetal death.

Cadmium has not been reported to induce birth defects in infants of women occupationally exposed to cadmium. However, there are reports that women in Japan with higher urinary cadmium levels have increased rates of preterm delivery than mothers with lower levels. These mothers also had infants with birth weights that were lower than those of newborns of unexposed women but this difference was felt to be due to the increased incidence of early deliveries (Nishijo et al. 2002). However, other studies have not shown cadmium to cause pre-term labor (Zhang et al. 2004). At this time, the evidence of cadmium’s effects on pregnancy is inconsistent and requires further investigation.


Symptoms of Arsenic Toxicity

Skin lesions and peripheral neuropathy are the most suggestive effects of chronic arsenic exposure (via inhalation or ingestion). Their presence should result in an aggressive search for this etiology. In addition, neuropathy can occur insidiously in chronic toxicity without other apparent symptoms. However, careful evaluation usually reveals signs of multi organ and multi system involvement such as

  • anemia
  • leukopenia
  • elevated liver function tests

Lung cancer and skin cancer are serious long-term concerns in cases of chronic arsenic exposure.


The information about cadmium and arsenic is from the CDC and is not subject to copyright law.