Interpretation

Arsenic:

Mayo Clinic uses the American Conference of Governmental Industrial Hygienists biological exposure index (BEI) as the reference value. The BEI is the sum of all the toxic species (inorganic arsenic plus methylated arsenic metabolites).

Physiologically, arsenic exists in a number of toxic and nontoxic forms. The total arsenic concentration reflects all the arsenic present in the sample regardless of species (eg, inorganic vs. methylated vs. organic arsenic). The measurement of urinary total arsenic levels is generally accepted as the most reliable indicator of recent arsenic exposure. However, if the total urine arsenic concentration is elevated, arsenic speciation must be performed to identify if it is a toxic form (eg, inorganic and methylated arsenic forms) or a relatively nontoxic organic form (eg, arsenobetaine and arsenocholine).

The inorganic toxic forms of arsenic (eg, As[III] and As[V]) are found in the urine shortly after ingestion, whereas the less toxic methylated forms, monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) are the species that predominate longer than 24 hours after ingestion. In general, urinary As(III) and As(V) concentrations peak in the urine at approximately 10 hours and return to normal 20 to 30 hours after ingestion. Urinary MMA and DMA concentrations normally peak at approximately 40 to 60 hours and return to baseline 6 to 20 days after ingestion.

This test can determine if a patient has been exposed to above-average levels of arsenic. It cannot predict whether the arsenic levels in their body will affect their health.

Cadmium:

In chronic cadmium exposure, the kidneys are the primary target organ. Urine concentrations of cadmium can be useful to assess long-term exposure and determine cadmium body burden.

Cadmium excretion above 3.0 mcg/g creatinine indicates significant exposure to cadmium. For occupational testing, the OSHA cadmium standard is below 3.0 mcg/g creatinine, and the BEI is 5 mcg/g creatinine.

Mercury:

The correlation between the levels of mercury excretion in the urine and the clinical symptoms is considered poor.

Previous thought indicated urine as a more appropriate marker of inorganic mercury because organic mercury represented only a small fraction of urinary mercury. Based on possible demethylation of methylmercury within the body, urine may represent a mixture of dietary methylmercury and inorganic mercury. Seafood consumption can contribute to urinary mercury levels (up to 30%),(1) which is consistent with the suggestion that due to demethylation processes in the human body, a certain proportion of urinary mercury can originate from dietary consumption of fish/seafood.(2)

Lead:

Measurements of urinary lead levels have been used to assess lead exposure. However, like blood lead, urinary lead excretion mainly reflects recent exposure and thus, shares many of the same limitations for assessing lead body burden or long-term exposure.(3,4)

Urinary lead concentration increases exponentially with blood lead and can exhibit relatively high intra-individual variability, even at similar blood lead concentrations.(5,6)