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The influence of cigarette smoking on concentrations of urinary benzene, a sensitive and specific biomarker proposed for biological monitoring of exposure to very low doses of benzene, was investigated in 24 filling-station attendants and 31 workers non occupationally exposed to benzene. Environmental monitoring was performed by personal passive samplers "Radiello", and a spot urine sample was collected at the end of the work shift, from all subjects, for the determination of urinary benzene. Exposure to benzene resulted significantly higher in filling-station attendants (mean 23.3 +/- 17.0 microg/m3; range 4.5-66.3 microg/m3) than in controls (mean 4.6 +/- 2.6 microg/m3; range < 3-11.5 microg/m3), while concentrations of urinary benzene did not show any significant difference between the two groups. Considering all subjects as a single group, it was observed that urinary benzene concentrations were positively correlated with the number of cigarettes smoked during the sampling time (rho = 0.38; p = 0.047) and with airborne benzene levels (rho = 0.32; p = 0.019), and negatively correlated with the time elapsed between the last smoked cigarette and urine collecting (rho = -0.40; p = 0.045). Multiple regression analysis confirmed the influence of cigarette smoking on urinary benzene concentrations. In conclusion, our study showed the validity of urinary benzene as a biomarker for biological monitoring of exposure to very low doses of benzene, although cigarette smoking determined a prevalent etiological role at the low environmental benzene concentrations observed.

S-Phenylmercapturic acid (PMA), a urinary metabolite which derives from the conjugation of benzene epoxide with glutathione, has been recently included in the list of the biological markers of benzene exposure. We have evaluated the urinary PMA levels in 145 workers exposed to benzene and in 87 subjects not occupationally exposed to the solvent (45 smokers and 42 non-smokers). In non-exposed persons, the background PMA excretion was nearly constant during one day (urine samples were collected in the morning, afternoon, and evening) and in smokers the mean PMA levels were higher than in non-smokers (9.6 vs 1.3 micrograms/g creatinine). This difference was presumably due to the extra-exposure to benzene (from cigarette smoke) in smokers compared with non-smokers, in fact a close relationship was found between PMA excretion and urinary benzene concentration (r = 0.86). Urine samples from workers exposed to benzene (airborne mean concentration = 0.52 ppm) showed higher mean levels of PMA (37.6 micrograms/g creatinine) than samples taken from not occupationally exposed subjects, both smokers and non-smokers. The mean biotransformation rate of benzene to PMA was 0.073%, with a large inter-individual variability (range = 0.002-0.21%). Also, statistical analysis of data revealed a clear bimodal distribution pattern of the conversion rate frequencies in the population examined: this is consistent with the hypothesis of the presence of "slow" and "fast" converters, due to the polymorphism of glutathione-S-transferase isozymes.

Objective: To test the hypothesis that heavy smoking may interfere with the variation in ambulatory blood pressure (ABP) and sympathetic nervous system in essential hypertension., Methods: We compared the office and 24-hour ABP of 48 untreated hypertensive smokers (> 20 cigarettes daily) with 90 non-smoking hypertensives matched for age, sex and body mass index. ABP was recorded using fully automatic SpaceLabs 90,207 units set to take a measurement every 15 minutes during the day (7.00 a.m.-10.00 p.m.) and every 20 minutes during the night (10.00 p.m.-7.00 a.m.). Urine collection for urinary sodium, potassium, epinephrine and norepinephrine excretion was performed during the 24-hour period of ABP monitoring. Catecholamines were measured by high pressure liquid chromatography., Results: The office blood pressure readings of the smoking and non-smoking groups were 156.7/103.4 and 156.5/103.9 mmHg respectively. During the day-time period, ambulatory systolic and diastolic blood pressure was significantly higher in the smokers (146 +/- 12 vs 140.4 +/- 13 mmHg, p < 0.02; 96.4 +/- 8.15 vs 93.1 +/- 10 mmHg, p < 0.05 respectively). This difference was greater among patients under the age of 50 (145.9 +/- 13 vs 136.6 +/- 11 mmHg, p < 0.001 and 97.1 +/- 8.7 vs 92.3 +/- 9.9 mmHg, p < 0.02). Blood pressure during the night-time period did not differ between the two groups (130.5/81.3 vs 126.3/79.5). No differences were detected among the groups as far as urinary catecholamine excretion is concerned., Conclusion: Our data suggest that among hypertensive subjects, smokers maintain a higher day-time ambulatory systolic and diastolic blood pressure than non-smokers, particularly in the younger patients, even though casual blood pressure is similar.

Vehicle exhausts are a well known source of aromatic hydrocarbon pollution in urban environments. The paper reports the results of environmental and biological monitoring of benzene exposure in traffic wardens carried out over a 5-hour workshift. Subjects (n = 131) were grouped according to smoking habits and job task as follows: group (A) 52 nonsmoking office workers, (B) 43 nonsmoking outdoor workers, subdivided into (B1) 36 working on foot and (B2) 7 cyclists; (C) 20 smokers office workers, (D) 16 smokers outdoor workers, subdivided into (D1) 11 working on foot and (D1) 5 cyclists. The median indoor environmental benzene concentration (26 micrograms/m3, n = 50) was significantly lower than the outdoor concentration (45 micrograms/m3, n = 43) (p < 0.01); median exposure value of cyclists was 78 micrograms/m3 (n = 12). For biological monitoring, urinary excretion of trans,transmuconic acid was determined in spot samples collected at 7:30 h (MAit) and 12:30 h (MAft). The MAftA median value (63 micrograms/l, range 2-242 micrograms/l) was not statistically different from MAftB (74 micrograms/l, range 15-216 micrograms/l), while the MAftB2 value of 96 micrograms/l was higher than both MAftB1 (71 micrograms/l) and MAftA. In group (B) there was a relationship between airborne benzene levels and MAftB excretion (y = 17.2 + 1.1x, r = 0.62, n = 35, p < 0.01). The influence of smoking on urinary MA excretion was studied by comparing the results obtained in all nonsmokers (AB) with smokers (CD). MAftCD (192 micrograms/l) was significantly higher than MAftAB (69 micrograms/l) (p < 0.01). In smokers, statistically significant relationships were observed between urinary excretion of MAft (y, microgram/l) and cotinine (x, microgram/l) (y = 83 + 0.08x, r = 0.73, n = 23, p < 0.01), and smoking (x, number cigarettes/day) (y = 87.4 + 4.4x, r = 0.53, n = 29, p < 0.01). Comparison between MAft and MAit median excretion values, calculated for each of the 6 exposure groups, showed that MAft was always higher than the corresponding MAit value. A rough estimate of the total dose of benzene ("index of exposure", EI) inhaled by each subject during the 5-hour working shift as a consequence of air pollution and smoking was also made. Considering the entire group of subjects, a significant association was observed between EI and MAft values (y = 43.4 + 0.39x, r = 0.65, n = 104, p < 0.01). Individual values of MA it were correlated with MAft according to the equation y = 43.6 + 0.82x (r = 0.62, n = 105; p < 0.01) and were also positively associated with EI values (y = 42.3 + 0.20x; r = 0.55; n = 74; p < 0.01). In conclusion, the results suggest that the measurement of urinary MA excretion is a poor indicator for assessing environmental benzene exposure at levels below 100 micrograms/m3, such as those seen in this study; MA can however be reliably used as a biomarker for higher exposures such as those, for example, due to smoking.

Indoor air is a complex mixture of chemicals and airborne particles. Volatile Organic Compounds (VOC), a broad class of chemicals including diverse compounds such as Aldehydes, Terpenes, Aromatic and Aliphatic Hydrocarbons and Halogenated Volatile Organics, are an important category of indoor air pollutants. The evaluation of exposure to low doses of Chloroform and Benzene through the measurement of Chloroform and Benzene in urine was performed. Results show that biological monitoring may be helpful in indoor environmental studies in non occupational situations.

It has long been known that occupational or environmental exposure to arsenic (As) may cause skin and lung cancer. Moreover, several epidemiological studies on populations exposed to inorganic As by ingestion indicate an increased risk for cancer at other sites and, particularly, for bladder cancer. We describe the case of a petrol chemical worker, who died of metastasized bladder cancer at the age of 52, after being employed for over 30 years in a hydrogen production unit. Analysis of the technological cycle and biological monitoring data revealed an excessive, prolonged exposure to arsenic trioxide (As2O3) vapours and fumes; a solution of this compound was utilized to absorb the CO2 produced by oxidation of the synthesis gas. Careful anamnesis indicated a prolonged contact between the carcinogen and the bladder mucosa, due to the presence of severe urethral stenosis with chronic urinary obstruction. It also appears likely that synergism between As exposure and smoking (5-10 cigarettes per day until 46 years) occurred. This case suggests the opportunity to extend to the occupational setting future epidemiological research on the relationship between inorganic As exposure and bladder cancer.

"Trans-placental" exposure to polycyclic aromatic hydrocarbons (PAHs) in newborn babies of mothers smoking during pregnancy was investigated and compared with that in newborn babies of non smoking mothers. PAHs intake was evaluated by measuring urinary levels of 1-hydroxypyrene, a pyrene metabolita and a biological index of exposure. 42 mothers-babies couples (31 smoking and 11 non smoking mothers) were examined. Urinary concentrations of 1-hydroxypyrene in 42 controls, 18 non smoking and 24 smoking women, were determined at the same time. Mean values of 1-hydroxypyrene in non smoking women in labour and their babies were 0.15 (SD 0.11) and 0.15 (SD 0.10) micrograms/g creatinine respectively. In controls the mean was 0.15 (SD 0.09) micrograms/g creat. Mean values of 0.23 (SD 0.17) and 0.20 (SD 0.15) micrograms/g creatinine were determined in smoking mothers and their newborn babies, whereas in smoking controls 1-hydroxypyrene was 0.42 (SD 0.45) micrograms/g creatinine. The highest levels of 1-hydroxypyrene were detected in smokers (both controls and women in labour). Babies of smoking mothers also showed a higher mean value of 1-hydroxypyrene than babies of non smokers. However the only statistically significant difference found was between smoking and non smoking controls.

Smoking habits were studied in a group of employees of a telephone company. The smokers were 34% of the subjects interviewed. The non-smokers said that they were bothered by other people smoking everywhere and also to a considerable extent at the workplace. Differences between smokers and non-smokers and between exposed and non-exposed non-smokers were studied by measuring expired CO and urinary cotinine. An expired CO concentration of 10 ppm discriminated between smokers and non-smokers. A mean urinary cotinine concentration of about 16 ng/mg was found in the exposed non-smokers, corresponding to the direct smoking of 1/10 of a cigarette per day. The search for the metabolic phenotype of destromethorphane, which was taken as an indicator of susceptibility to contract lung cancer due to IPA, showed that there were no differences between smokers and non-smokers since the rapid metabolizers, and therefore subjects potentially exposed to risk of lung cancer due to tobacco smoke, prevailed in both groups.

The sensitivity of 3 urinary mutagenicity tests was assayed: the plate test, the fluctuation test and the micropreincubation test, in order to assess their possible use in monitoring human exposure to polycyclic aromatic hydrocarbons (PAH). Urine samples from workers of an anode production plant exposed to coal tar and from psoriatic patients undergoing treatment with coal-tar ointments were tested for mutagenic activity on strain TA98 Salmonella typhimurium, in the presence of the microsome fraction and deconjugating enzymes. Parallelly, the urinary concentration of PAH metabolites or one of their trace metabolites, 1-hydroxypyrene, was determined. Increased levels of PAH metabolites were observed in the urine of anode production workers after a work shift compared with controls. Results of the plate test and the fluctuation test performed on urine of exposed subjects, both smokers and nonsmokers, showed mutagenicity values similar to the controls. Much higher 1-hydroxypyrene concentrations were found in the urine of psoriatic patients treated with coal tar than in post-shift urine of anode production workers. The urine of the former was also mutagenic in the 3 mutagenicity tests used. The minimum mean dose of PAH metabolites was calculated, expressed as quantity of 1-hydroxypyrene, that would give a mutagenic response in the 3 tests: the micropreincubation test was found to be about 100 times more sensitive than the plate test and about 30 times more sensitive than the fluctuation test. The theoretical minimum urinary concentration of 1-hydroxypyrene detectable by each test was determined: the micropreincubation test was 15 times more sensitive than the plate test and 7 times more sensitive than the fluctuation test.(ABSTRACT TRUNCATED AT 250 WORDS)