Direct solid sampling system for electrothermal vaporization and its application to the determination of chlorine in nanopowder samples by inductively coupled plasma optical emission spectroscopy.

An electrothermal vaporization (ETV) system using a tungsten boat furnace (TBF) sample cuvette was designed for the direct determination of chlorine in metallic nanopowders and fine powder samples with detection by inductively coupled plasma optical emission spectroscopy (ICP-OES). A portion of a powder or particle sample was placed into a small tungsten sample cuvette and weighed accurately. A modifier solution of aqueous or alcoholic potassium hydroxide was added to it. Then, the cuvette was positioned on the TBF incorporated into the ETV apparatus. The analyte was vaporized and introduced into the ICP optical emission spectrometer with a carrier gas stream of argon and hydrogen. The metal samples were analyzed by using an external calibration curve prepared from aqueous standard solutions. Few chemical species including analyte and some chlorine-free species were introduced into the ICP, because the analyte has been separated from the matrix before introduction. Under such dry plasma conditions, the energy of plasma discharge was focused on the excitation of chlorine atoms, and as a result, lower detection limits were achieved. A detection limit of 170 ng g(-1) of chlorine in solid metal samples was established when 60 mg sample was used. The relative standard deviation for 16 replicate measurements obtained with 100 ng chlorine was 8.7%. Approximately 30 batches could be vaporized per hour. The analytical results for various nanopowders (iron (III) oxide, copper, silver, and gold) and metallic fine powder samples (silver and gold) are described.

Microscopic analysis of the chromium content in the chromium-induced malignant and premalignant bronchial lesions of the rat.

OBJECTIVE: Our previous studies demonstrated that the frequency of gene instability in lung cancer of chromate workers was very high, but the frequencies of the p53 and ras gene mutations were low. To clarify the carcinogenesis of chromate in the lung, we established a chromate-induced cancer model in the rat proximal airway and examined the relationship between chromium accumulations and the chromium-induced cancer and premalignant bronchial lesions of the rat. METHODS: Fifteen male, bred, 12-week-old Jcl-Wister rats were used. A pellet of strontium chromate were inserted into the bronchus of the rats. The rats were sacrificed 9 months after the pellet was inserted. We pathologically examined the region of the bronchi to which the pellet was attached. We quantified the amount of chromium accumulation in the bronchial lesions using a microscopic X-ray fluorescence analyzer. RESULTS: Of the 15 rats, 1 rat had a lesion of squamous cell carcinoma (SCC), 7 rats had carcinoma in situ (CIS) or dysplasia, 8 rats had squamous metaplasia, and 5 rats had goblet cell hyperplasia. The amounts of chromium accumulation in normal epithelium (n=24), goblet cell hyperplasia (n=14), squamous metaplasia (n=8), and dysplasia plus CIS plus SCC (n=9) were 500+/-1354, 713+/-1062, 941+/-1328, and 3511+/-4473 (mean+/-SD) counts/s/mA, respectively. The amount of chromium accumulation was significantly increased according to the progression of malignant change of the bronchial epithelium (Spearman's correlation coefficient by ranks, rs=0.454, P<0.01). CONCLUSIONS: The amount of chromium accumulation was significantly increased according to the progression of malignant change of the bronchial epithelium. Examining the genetic alterations of histologic changes in this model was helpful in elucidating the process of carcinogenesis of chromium in the lung.

Quantitative analysis of trace bulk oxygen in silicon wafers using an inert gas fusion method.

This paper describes a method for removing oxide film from the surface of silicon wafers using an inert gas fusion impulse furnace and precise determination of bulk oxygen within the wafer. A silicon wafer was cut to about 0.35 g (6 x 13 x 2 mm) and dropped into a graphite crucible. The sample was then heated for 40 s at 1300 degrees C. The wafer's oxide film was reduced by carbon and removed as carbon monoxide. The treated silicon sample was taken out of the graphite crucible and maintained again with the holder of the oxygen analyzer. The graphite crucible was then heated to 2100 degrees C. The treated silicon sample was dropped into the heated graphite crucible and the trace bulk oxygen in the wafer was measured using the inert gas fusion infrared absorption method. The relative standard deviations of the oxygen in silicon wafer samples with the removed surface oxide film were determined to be 0.8% for 9.8 x 10(17) atoms/cm3, and 2.7% for 13.0 x 10(17) atoms/cm3.

Microscopic analysis of chromium accumulation in the bronchi and lung of chromate workers.

BACKGROUND: It is known that chromium is an inhaled carcinogen and an important risk factor in the development of lung carcinoma. METHODS: The authors used a microscopic X-ray fluorescence analyzer with transmitted X-ray mapping imaging (Horiba, Kyoto, Japan) to measure the accumulation of chromium in 10 resected lung tissue specimens and 90 biopsy specimens from chromate workers. RESULTS: The maximum chromium accumulation (mean +/- standard deviation) in 10 resected lung tissue specimens was 197 +/- 238 counts per second (cps)/mili ampere (mA) (range, 4-649 cps/mA). Chromium accumulation was scattered in six tissue specimens and diffuse in one specimen. Chromium accumulation in the proximal bronchi was less than in the bronchioles or subpleural regions of the lung. Chromium accumulation was detectable in 63 (70%) of 90 biopsy specimens, and the mean accumulation was 6.5 +/- 9.2 cps/mA (range, 0-46.5 cps/mA). Chromium detected in bronchial tissue specimens was deposited in the bronchial stroma but not in the epithelium. The maximum chromium accumulations in dysplasic (n = 3), squamous metaplastic (n = 10), and normal bronchial epithelia (n = 9) in chromate workers and in normal bronchial epithelia (n = 3) in non-chromate workers were 20.2 +/- 5.4, 18.3 +/- 12.2, 13.2 +/- 13.4, and 3.0 +/- 1.8 cps/mA, respectively. The amount of chromium accumulation significantly increased according to the progression of malignant change of the bronchial epithelium (P = 0.003). CONCLUSIONS: Previous studies found that lung carcinoma with chromate exposure exhibited a variety of genetic abnormalities. Considering genetic aberrations and chromium accumulation in these premalignant lesions is useful for elucidating the process of carcinogenesis in chromium-induced lung carcinoma.