Rapid analysis of nickel in urine by electrothermal atomic absorption spectrophotometry.

A method is described for analysis of nickel in urine, which involves dilution of urine with dilute nitric acid and direct quantitation of nickel by electrothermal atomic absorption spectrophotometry with Zeeman background correction. The detection limit for nickel is 0.5 micrograms per L of urine; the coefficient of variation of replicate determinations is 4 to 5 percent (within-run) and 6 percent (run-to-run). Recovery of nickel added to urine (20 micrograms per L) averages 99 +/- 5 percent (mean +/- SD). Analytical results agree closely with measurements by the International Union of Pure and Applied Chemistry (IUPAC) reference procedure (correlation coefficient = 0.99). Nickel concentrations in urine specimens from 34 non-exposed, healthy, adult persons living in Connecticut average 2.0 +/- 1.5 microgram per L (range = 0.5 to 6.0 micrograms per L). Urine nickel concentrations are directly correlated with urine creatinine concentrations and specific gravity measurements. Elevated concentrations of nickel are observed in urine specimens from nickel-exposed workers, including nickel electroplating workers (mean = 27 micrograms per L, range = 3.1 to 82 micrograms per L, N = 19) and nickel battery workers (mean = 32 micrograms per L, range = 2.8 to 103 micrograms per L, N = 7). This method is more rapid and convenient than previous techniques and is suitable for routine use in clinical and industrial laboratories.

Electrothermal atomic absorption spectrophotometry of nickel in tissue homogenates.

A method for analysis of Ni concentrations in tissues is described, which involves (a) tissue dissection with metal-free obsidian knives, (b) tissue homogenization in polyethylene bags by use of a "Stomacher" blender, (c) oxidative digestion with mixed nitric, sulfuric, and perchloric acids, and (d) quantitation of Ni by electrothermal atomic absorption spectrophotometry with Zeeman background correction. The detection limit for Ni in tissues is 10 ng per g, dry weight; the coefficient of variation ranges from 7 to 15 percent, depending on the tissue Ni concentration; the recovery of Ni added in concentration of 20 ng per g, dry weight, to kidney homogenates averages 101 +/- 8 percent (mean +/- SD). In control rats, Ni concentrations are highest in lung (102 +/- 39 ng per g, dry weight) and lowest in spleen (35 +/- 16 ng per g, dry wt.). In descending order of Ni concentrations, the tissues of control rats rank as follows: lung greater than heart greater than bone greater than kidney greater than brain greater than testis greater than fat greater than liver greater than spleen. In rats killed 24 h after sc injection of NiCl2 (0.125 mmol per kg, body weight) Ni concentrations are highest in kidney (17.7 +/- 2.5 micrograms per g, dry weight) and lowest in brain (0.38 +/- 0.14 micrograms per g, dry weight). In descending order of Ni concentrations, the tissues of NiCl2-treated rats rank as follows: kidney much greater than lung greater than spleen greater than testis greater than heart greater than fat greater than liver greater than bone greater than brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Nickel concentrations in serum of patients with acute myocardial infarction or unstable angina pectoris.

Nickel was measured, by electrothermal atomic absorption spectrophotometry, in sera from (a) 30 healthy adults, (b) 54 patients with acute myocardial infarction, (c) 33 patients with unstable angina pectoris without infarction, and (d) five patients with coronary atherosclerosis who developed cardiac ischemia during treadmill exercise. Mean (and SD) concentrations in Group a were 0.3 (0.3) microgram/L (range less than 0.05-1.1 microgram/L). Within 72 h after hospital admission, hypernickelemia (Ni greater than or equal to 1.2 microgram/L) was found in 41 patients of group b (76%) and in 16 patients of group c (48%). Hypernickelemia was found before and after exercise in one patient of Group d (20%). Peak values averaged 3.0 micrograms/L (range 0.4-21 micrograms/L) in Group b, 1.5 microgram/L (range less than 0.05-3.3 micrograms/L) in Group c. In Group b, the mean time interval between the peak values for creatine kinase activity and for nickel was 18 h. Serum nickel concentrations were unrelated to age, sex, time of day, cigarette smoking, medications, clinical complications, or outcome. Mechanisms and sources of release of nickel into the serum of patients with acute myocardial infarction or unstable angina pectoris are conjectural, but hypernickelemia may be related to the pathogenesis of ischemic myocardial injury.

Rapid analysis of nickel in serum and whole blood by electrothermal atomic absorption spectrophotometry.

A method is described for analysis of nickel in serum and heparinized blood. After the sample has been subjected to protein precipitation with nitric acid and heat, nickel in the protein-free extract is measured by electrothermal atomic absorption with Zeeman background correction. The method is more sensitive, rapid, and convenient than previous techniques, and less subject to nickel contamination. Nickel concentrations in serums from New Zealand rabbits (mean +/- SD) average 4.0 +/- 2.5 micrograms per L, range = 0.9 to 11.9, N = 30; these results agree with measurements by the International Union of Pure and Applied Chemistry (IUPAC) reference procedure ( corr . coef . = 0.98). The following values are reported for nickel concentrations in serum and whole blood from healthy adult persons living in central Connecticut: serum, 0.46 +/- 0.26 micrograms per L, range = 0.1 to 1.3, N = 39; whole blood, 1.26 +/- 0.33 micrograms per L, range = 0.6 to 1.8, N = 30. This method is suitable for routine use in clinical and industrial laboratories.