Application of urine mutagenicity to monitor coal liquefaction workers

Urinary mutagenicity reflects systemic exposure to complex mixtures of genotoxic/ carcinogenic agents and is linked to tumor development. Coal combustion emissions (CCE) and diesel engine exhaust (DEE) are associated with cancers of the lung and other sites, but their influence on urinary mutagenicity is unclear. We investigated associations between exposure to CCE or DEE and urinary mutagenicity. In two separate cross-sectional studies of nonsmokers, organic extracts of urine were evaluated for mutagenicity levels using strain YG1041 in the Salmonella (Ames) mutagenicity assay. First, we compared levels among 10 female bituminous (smoky) coal users from Laibin, Xuanwei, China, and 10 female anthracite (smokeless) coal users. We estimated exposure-response relationships using indoor air concentrations of two

Section: Protection Agencycontrasting

confidence: 54%

Elevated urinary mutagenicity among those exposed to bituminous coal combustion emissions or diesel engine exhaust

Wong

Vermeulen

Dai

et al. 2021

“…These results agree with those obtained in our previous biological monitoring of workers exposed to this complex mixture [Pasquini et al, 19821 and also to the urinary mutagenicity data reported by some other authors for workers exposed to fossil fuels other than petroleum pitch, but containing polycyclic aromatic hydrocarbons [Recio et al, 1984;Heussener et al, 1985;De Meo et al, 1987).…”

Section: Discussionsupporting

confidence: 94%

“…Urine of smokers [Yamasaki and Ames, 1977;Aeshbacher and Chappius, 1981;Bos et al, 1984;Kado et al, 19851 and people exposed to certain working activities [Falck et al, 1980;Dolaraet al, 1981; Kriebel e t a ] . , 1983; Recio et al, 1984;Heussner et al, 1985;De Meo et al, 19871 and to cytostatic drugs (Bos et al, 1982) was found to be mutagenic. Frequently, faeces of humans and various animal species also appear to contain mutagenic substances [Bruce et al, 1977;Stich et al, 1980;Venitt, 1981;Mower et al, 1982;Willems and De Raat, 1985;Reddy and Sharrna, 19861. These data suggest that testing human excreta for muta-genicity may be a suitable method for biological monitoring of exposure to genotoxic chemicals.…”

Section: Introductionmentioning

confidence: 95%

Urine mutagenicity and biochemical parameters as markers of exposure to petroleum pitch using a rat model

Pasquini

Monarca

Sforzolini

et al. 1990

A petroleum pitch sample collected in a carbon electrode factory was studied using a series of in vivo assays for genotoxicity and enzymatic induction capability. Rats were treated with the petroleum derivative in three doses: 100, 50, and 10 mg/kg body weight. The treatment produced a rapid excretion of mutagenic substances in the urines of the first 24 hr only in rats treated with high doses (100 and 50 mg/kg). No faecal mutagenic activity was observed. Analyses of urinary thioethers showed that urinary metabolites derived from the compounds present in the pitch-sample at the lowest dose-administered (10 mg/kg) were eliminated primarily as cysteine conjugates. The pitch sample was found to be a good inducer of pulmonary and hepatic aryl hydrocarbon hydroxylase, especially after a 50 mg/kg dose. Urinary D-glucaric acid content was always statistically increased in treated animals compared with controls, confirming the enzymatic induction activity. Hepatic glutathione-S-transferase activity increased following treatment with 50 and 10 mg/kg doses.

“…Other at-risk exposures for colorectal adenoma, such as dietary intake of protein-rich meals cooked at high temperature (i.e., thermic amines with pan-fried meats) show that oral intake may contribute to an increase in urinary mutagenicity, but this assertion needs further confirmation [Murray et al, 2001;Pavanello et al, 2002b;Peters et al, 2003]. Published negative results [Moller and Dyhing, 1980;Recio et al, 1984;Reuterwall et al, 1991] were presumably due to the low sensitivity of most urinary mutagenicity assays [Clonfero et al, 1995] employing Salmonella strains that are not specifically engineered for the detection of heterocyclic amine exposures. Moreover, increments in urinary mutagenicity found in certain occupational or environmental studies are of doubtful significance due to the lack of control for confounding factors such as tobacco smoke [Pasquini et al, 1982;DeMeo et al, 1995;Sardas et al, 1997;Sorsa and Anderson, 1996] and diet [DeMeo et al, 1987;Heussener et al, 1985;Kriebel et al, 1983].…”

Section: Introductionmentioning

confidence: 89%

Mutagenic activity of overnight urine from healthy non‐smoking subjects

Pavanello

Lupi

Pulliero

et al. 2007

Urinary mutagenicity was evaluated in relation to environmental mutagen exposure (i.e., diet, indoor/outdoor activities, residential area etc.) on the day prior to sample collection, and also considering factors that contribute to the variability of Salmonella mutagenicity assay results. Overnight urine samples from 283 healthy non-smoking residents of northeast Italy (46% males, 20-62 years) were analyzed for mutagenicity on sensitive Salmonella typhimurium strain YG1024 with S9 mix employing the preincubation version of the plate incorporation assay (i.e., the Salmonella reverse mutation test). Urinary mutagenicity varied between 0.02 and 9.84 rev/ equiv. ml, and 7% of samples were positive (i.e., sample elicited a two-fold increase in revertants). There was an evident increase in mutagenicity in subjects with increased intake of mutagen-rich meals (n = 80) (P < 0.01 and positive urine 13% vs. 5%, P = 0.025). Indoor-exposed subjects (n = 65) also showed a higher percentage of positive urine (14% vs. 5%, P = 0.015). In particular, those subjects exposed to cooking fumes the previous evening (n = 28) revealed higher urinary mutagenicity (P = 0.035, positive urine 25% vs. 5%, P < 0.001) than non-indoor exposed. The sources of variability of the mutagenicity assay, mainly the histidine content of the urine concentrate (z = 4.06, P < 0.0001), and to a lesser extent bacterial inoculum size (z = 2.33, P = 0.019), also significantly influenced urinary mutagenicity values. In a linear multiple regression analysis, their effects were still significant (i.e., histidine content P = 0.026 and inoculum size P = 0.021), but the effects of diet, indoor exposure, and other environmental exposures (i.e., traffic and heating system exhausts, residential area) were not. It is concluded that the previous day's exposure to mutagen-rich meals and cooking fumes may influence the presence of mutagenic activity in the overnight urine of non-smoking subjects. This mutagenic activity, which remains in contact with bladder mucosa for several hours, could be considered risk factors for colorectal adenoma and possibly other cancers (i.e., bladder) in non-smokers. Accurate control of histidine content and bacterial inoculum size is strongly recommended when investigating the mutagenic activity of urine from non-smokers.