PubMed Health⌕ Search

Biomedical subjects

V Haufroid

Publications and source records attributed to V Haufroid.

24 records · Page 2Linked to original sources

Urinary cotinine as a tobacco-smoke exposure index: a minireview.

A minireview is presented concerning the use of cotinine as a tobacco-smoke exposure index. First, general considerations about methods for the determination of urinary cotinine are presented. Besides pure analytical aspects, this minireview considers major problems encountered in the establishment of threshold values that can be used to distinguish not only smokers from nonsmokers but also nonsmokers exposed or not exposed to environmental tobacco smoke (ETS). In addition, the use of urinary cotinine is illustrated in several situations where smoking status assessment is of interest. Such situations include evaluation of the impact of smoking cessation programs, monitoring of pregnancy and of other groups at risk, assessment of occupational exposure to industrial pollutants, validation of phase I clinical trials, and the control of life insurance candidates. The specific problem of ETS exposure assessment is briefly mentioned.

Biomarkers↗

Biological monitoring of vehicle mechanics and other workers exposed to low concentrations of benzene.

It has been suggested that the threshold limit value (TLV) for the time-weighted average (TWA), of benzene be lowered because of its possible leukemogenic effect at low exposure concentrations. This requires the development of new methods of biological monitoring. In this cross-sectional study the diagnostic power of blood and breath benzene and of urinary phenol, catechol, hydroquinone, S-phenylmercapturic acid, and muconic acid were compared in a population of 410 male workers exposed to benzene in garages, in two coke plants, and in a by-product plant. Benzene exposure was assessed by personal air sampling (charcoal tube and passive dosimeter). In all, 95% of the workers were exposed to less than 0.5 ppm benzene. According to the multiple regression equation, the muconic acid and S-phenylmercapturic acid concentrations detected in nonsmokers exposed to 0.5 ppm benzene were 0.3 mg/g and 6 micrograms/g, respectively (range 0.2-0.6 mg/g and 1.2-8.5 micrograms/g, respectively). With muconic acid very few false-positive test results were found, and this determination remained reliable even around a cutoff level of 0.1 ppm benzene. Moreover, the diagnostic power of this test proved to be good even when diluted or concentrated urine samples were not excluded. S-Phenylmercapturic acid (S-PMA) also performed fairly well. Blood and breath benzene as well as urinary phenol (PH) and hydroquinone (HQ) were clearly less suitable biomarkers than muconic acid (MA). Catechol (CA) was not associated with occupational benzene exposure. According to the results of biological monitoring, the skin resorption of benzene from gasoline or other fuels seems negligible. Correlation, multiple regression, and likelihood ratios consistently showed that MA and S-PMA concentrations were fairly good indicators of benzene exposure in the 0.1- to 1-ppm range, even in a population comprising both smokers and nonsmokers. PH, HQ, CA, and blood and breath benzene were less suitable, if at all, in the same exposure range.

Adult↗

Biological monitoring of workers exposed to low levels of 2-butoxyethanol.

OBJECTIVES: (1) To assess the value of urinary butoxyacetic acid (BAA) measurement for the monitoring of workers exposed to low concentration of 2-butoxyethanol (BE); (2) to evaluate the in vivo effect of low occupational BE exposure on the erythrocyte lineage; and (3) to test the possible influence of genetic polymorphism for cytochrome P450 2E1 (CYP 2E1) on urinary BAA excretion rate. METHODS: Thirty-one male workers exposed to BE in a beverage package production plant were examined according to their external (BE) and internal (BAA) solvent exposure. The effect of this exposure on erythrocyte lineage [red blood cell numeration (RBC), hemoglobin (Hb), hematocrit (Htc), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), haptoglobin (Hp), reticulocyte numeration (Ret) and osmotic resistance (OR)], hepatic [aspartate aminotransferase (GOT), alanine aminotransferase (GPT)] and renal [plasmatic creatinine, urinary retinol binding protein (RBP)] parameters was also investigated. DNA purified from whole blood was used for CYP 2E1 genotyping. RESULTS: Average airborne concentration of BE was 2.91 mg/m3 (0.59 ppm) with a standard deviation of 1.30 mg/m3 (0.27 ppm). There was a relatively good correlation between external and internal exposure estimated by measuring BAA in post-shift urine samples (average 10.4 mg/g creatinine; r = 0.55; P = 0.0012). Compared with a matched control group (n = 21) exposed workers had a statistically significant decrease (3.3%; P = 0.03) in Hct while MCHC was increased (2.1%; P = 0.02). No significant difference was observed either in other erythroid parameters or in hepatic and renal biomarkers. One exposed individual exhibited a mutant allele with increased cytochrome P450 oxidative activity which coincided with a very low urinary BAA excretion. CONCLUSIONS: Single determination of BAA in post-shift urine samples can be used to assess exposure to low levels of BE. A slight but significant effect on erythroid parameters suggesting membrane damage was observed in exposed workers. The influence of the genetic polymorphism for CYP 2E1 deserves further investigation for the interpretation of urinary BAA measurements.

Adult↗

Relationships between smoking habits, smoking-associated hematological changes, and urinary benzene metabolites.

It has been suggested that benzene metabolites might be good indicators of smoking. Moreover, benzene could stimulate the neutrophil lineage while depressing the lymphocytic and erythroid lineages, possibly by an interference with cytokines. The effect on the neutrophil lineage could explain the smokers' leukocytosis, the mechanism of which is presently unknown. Therefore, the usefulness of benzene metabolites as indicators of smoking was compared to that of cotinine and thiocyanate, and the relationships between benzene metabolites, the hematological parameters of smokers, and interleukin 1 alpha production were examined. The results show that benzene metabolites are not better indicators of smoking status than cotinine or thiocyanate. Furthermore, it seems unlikely that the smokers' leukocytosis is benzene induced.

Adult↗