## Abstract In an ongoing longitudinal study for tumor markers in breast cancer patients, levels of placental alkaline phos‐phatase (PAP) measured by RIA were found to be elevated in 34% of patients who smoked cigarettes as opposed to 5 % of non‐smoking subjects. A normal range was established (0‐2
Elevated levels of benzene-related compounds in the urine of cigarette smokers
✍ Scribed by C. N. Ong; B. L. Lee; C. Y. Shi; H. Y. Ong; H. P. Lee
- Publisher
- John Wiley and Sons
- Year
- 1994
- Tongue
- French
- Weight
- 417 KB
- Volume
- 59
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Benzene exposure causes leukemia and lymphomas. Recent epidemiological findings have also shown an association between cigarette smoking and an increased risk of leukemia. However, further evidence is required to document the biological plausibility of this association. In evaluating this link, it is important to note that cigarette smoke contains benzene and various pyrolytic compounds, among other carcinogens. This study aims to determine the uptake of benzene by measuring 3 benzene‐related compounds in cigarette smokers and non‐smokers. Urinary concentrations of catechol (CAT), hydroquinone (HQ), and trans,trans‐muconic acid (tt‐MA) were measured by high‐performance liquid chromatography (HPLC) with fluorimetric and UV detection, respectively. The results showed that these compounds were present in all urine samples. However, the concentrations were significantly higher in smokers than in non‐smokers. The mean level of urinary tt‐MA was 0.19 ± 0.09 mg/g creatinine for 46 male smokers and the corresponding value for 40 non‐smokers was 0.14 ± 0.07 mg/g creatinine. The mean concentrations of HQ and CAT were 0.81 ± 0.4 and 3.51 ± 2.6 mg/g creatinine for smokers, and 0.45 ± 0.4 and 1.94 ± 1.2 mg/g creatinine for non‐smokers, respectively. These results suggest that cigarette smoking is associated with a significant additional exposure to benzene and its related compounds. Furthermore, significant correlations were observed between the concentrations of cotinine, the metabolite of nicotine, and the above compounds. These findings suggest that the exposure originated from cigarette smoking.
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