Sorted By Test Name - Mayo Medical Laboratories

NICOS
82509
most toxic chemicals known to man. Ni(CO)(4) is absorbed after inhalation, readily crosses all biological
membranes, and noncompetitively inhibits ATP-ase and RNA polymerase. Ni(CO)(4) binds avidly to
hemoglobin with resultant inability to take up oxygen. The affinity for hemoglobin is higher than carbon
monoxide. The binding to hemoglobin is the main transport mechanism for spreading Ni(CO)(4)
throughout the body. Urine is the specimen of choice for the determination of Ni exposure via inhalation.
Patients undergoing dialysis are exposed to Ni and accumulate Ni in blood and other organs; there appear
to be no adverse health affects from this exposure. Hypernickelemia has been observed in patients
undergoing renal dialysis. At the present time, this is considered to be an incidental finding as no
correlation with toxic events has been identified. Routine monitoring of patients undergoing dialysis is
currently not recommended. Breathing dust high in Ni content has been associated with development of
neoplasms of the respiratory system and nasal sinuses. Most reactions to Ni are localized skin sensitivity
and allergic skin disorders that occur on contact with Ni-containing alloys. These reactions do not
correlate to urine concentrations; patients experiencing skin sensitivity reactions to Ni are likely to have
normal Ni excretion.
Useful For: Urine nickel is the test of choice for detecting nickel toxicity in patients exposed to nickel
carbonyl.
Interpretation: Values > or =7 mcg/g creatinine represent possible environmental or occupational
exposure. Nickel (Ni) concentrations >50 mcg/g creatinine are of concern, suggesting excessive exposure.
Clinical concern about Ni toxicity should be limited to patients with potential for exposure to toxic Ni
compounds such as nickel carbonyl. Hypernickelemia, in the absence of exposure to that specific form of
Ni, may be an incidental finding or could be due to specimen contamination.
Reference Values:
0.0-6.0 mcg/g Creatinine
Reference values apply to all ages.
Clinical References: 1. Moreno ME, Acosta-Saavedra LC, Mez-Figueroa D, et al: Biomonitoring of
metal in children living in a mine tailings zone in Southern Mexico: A pilot study. Int J Hyg Environ
Health 2010;213:252-258 2. Schulz C, Angerer J, Ewers U, et al: Revised and new reference values for
environmental pollutants in urine or blood of children in Germany derived from the German
Environmental Survey on Children 2003-2006 (GerES IV). Int J Hyg Environ Health 2009;212:637-647
Nicotine and Metabolites, Serum
Clinical Information: Tobacco use is the leading cause of death in the United States. Nicotine,
coadministered in tobacco products such as cigarettes, pipe, cigar, or chew, is an addicting substance that
causes individuals to continue use of tobacco despite concerted efforts to quit. Nicotine stimulates
dopamine release and increases dopamine concentration in the nucleus accumbens, a mechanism that is
thought to be the basis for addiction for drugs of abuse. Nicotine-dependent patients use tobacco products
to achieve a peak serum nicotine value of 30 ng/mL to 50 ng/mL, the concentration at which the nicotine
high is maximized. Nicotine is metabolized in the liver to cotinine. Cotinine accumulates in serum in
proportion to dose and hepatic metabolism (which is genetically determined); most tobacco users
accumulate cotinine in the range of 200 ng/mL to 800 ng/mL. Serum concentrations of nicotine and
metabolites in these ranges indicate the patient is using tobacco or is receiving high-dose nicotine patch
therapy. Nicotine is rapidly metabolized, exhibiting an elimination half-life of 2 hours. Cotinine exhibits
an apparent elimination half-life of 15 hours. Heavy tobacco users who abstain from tobacco for 2 weeks
exhibit serum nicotine values