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Some studies suggest that genotoxic effects of combustion-related aerosols are induced by carcinogenic polycyclic aromatic hydrocarbons (c-PAHs) and their derivatives, which are part of the organic fraction of the particulate matter (PM) in ambient air. The proportion of the organic fraction in PM is known to vary with particle size. The ultrafine fraction is hypothesized to be the most important carrier of c-PAHs, since it possesses the highest specific surface area of PM. To test this hypothesis, the distribution of c-PAHs in organic extracts (EOMs) was compared for four size fractions of ambient-air aerosols: coarse (1

Burning charcoal is normally placed atop the tobacco to smoke the narghile waterpipe. We investigated the importance of charcoal as a toxicant source in the mainstream smoke, with particular attention to two well-known charcoal emissions: carbon monoxide (CO) and polyaromatic hydrocarbons (PAH). CO and PAH yields were compared when a waterpipe was machine smoked using charcoal and using an electrical heating element. The electrical heating element was designed to produce spatial and temporal temperature distributions similar to those measured using charcoal. With a popular type of ma'assel tobacco mixture, and using a smoking regimen consisting of 105 puffs of 530ml volume spaced 17s apart, it was found that approximately 90% of the CO and 75-92% of the 4- and 5-membered ring PAH compounds originated in the charcoal. Greater than 95% of the benzo(a)pyrene in the smoke was attributable to the charcoal. It was also found that the relative proportions of individual PAH species, the "PAH fingerprint", of the mainstream smoke were highly correlated to those extracted from the unburned charcoal (R(2)>0.94). In contrast, there was no correlation between the PAH fingerprint of the electrically heated and charcoal-heated conditions (R(2)<0.02). In addition to inhaling toxicants transferred from the tobacco, such as nicotine, "tar", and nitrosamines, waterpipe smokers thus also inhale large quantities of combustion-generated toxicants. This explains why, despite the generally low temperatures attained in the narghile tobacco, large quantities of CO and PAH have been found in the smoke.

Polynuclear aromatic hydrocarbons (PAHs) are natural constituents of transformer oils and are essential in prolonging transformer in-service lifetime. Issues concerning PAH carcinogenicity demand methods that provide qualitative and quantitative information on the PAH composition of new and in-service oils to allow informed operational decisions to be made. However, current analytical methods focus on PAH fingerprinting, as opposed to quantitative analysis and are also cumbersome, relying on the use of large (>100 ml) volumes of organic solvents, some of which are hazardous. This paper reports a method for the improved quantification of carcinogenic PAHs in transformer oils that is both simple and repeatable. The method uses commercially available solid-phase extraction columns and millilitre volumes of relatively non-hazardous solvents. Extraction efficiencies of > or =74% were obtained for the Environmental Protection Agency priority PAHs. The method has potential for automation and high-throughput analysis and thus is of interest to industries that use transformer oils.

Objective: To study the characteristics of occupational exposure of polycyclic aromatic hydrocarbons (PAHs) in coke oven workers., Methods: Samples were collected individually and PAHs concentration in the ambient air were assayed by high performance liquid chromatography (HPLC) and toxic equivalency factors (TEFs) were introduced to assess the carcinogenic potency., Results: The levels of PAHs occupational exposure in oven workers at topside was higher than at side oven and bottom oven (P < 0.05). Non-carcinogenic PAHs were more than 70% of total PAHs and benzo[a]pyrene accounted for 65.5% approximately 72.4% of total benzo[a]pyrene equivalents. Total occupational exposure level of PAHs in coke oven workers was positively related to the content of benzo[a]pyrene and pyrene, respectively (r(2) = 0.84, r(2) = 0.94, P < 0.05)., Conclusion: Coke oven workers were exposed to a high level of PAHs which possessed some extent of carcinogenic potency, and benzo[a]pyrene is the chief carcinogenic substance.

Historically our knowledge about the direct carcinogenic activity of cigarette smoke and its constituents grew from painting experiments on the skin of mice to produce papillomas and carcinomas. The neutral fraction of cigarette smoke condensate had most of the carcinogenic activity in this test and was rich in carcinogenic polycyclic aromatic hydrocarbons (PAHs), the most abundant by far being BP. However, the concentration of BP in the condensate was only about 2% the amount of pure BP required to cause skin tumors. In other fractions there were non-carcinogenic constituents that promoted tumor formation when applied repeatedly to mouse skin that had been initiated by a single subcarcinogenic application of BP. There were also constituents of cigarette smoke that acted as co-carcinogens when applied simultaneously with repeated applications of BP. BP was effective as an initiator at lower concentrations than as a complete carcinogen, and some non-carcinogenic PAHs in the condensate were also active initiators. It was concluded from these studies that cigarette smoke condensate is primarily a tumor-promoting and co-carcinogenic agent with weak activity as a complete carcinogen. A major effect of promoters, and possibly of co-carcinogens, is a diffuse hyperplasia which includes selective expansion of clones carrying endogenous mutations and/or mutations induced by PAHs and other carcinogens such as NNK. The induced mutations as well as damaged cells would occur throughout the exposed region and, along with the hyperplasia, increase the permissiveness of the cellular microenvironment for neoplastic expression of any potential tumor cell in its midst. Since neither the promoters nor co-carcinogens in tobacco smoke are known to interact directly with DNA, their effects can be considered epigenetic processes that act upon genetically altered cells. Examples are cited from studies of experimental skin carcinogenesis, smoking-induced histopathological changes in human lung and spontaneous transformation in cell culture to illustrate the genetic and epigenetic interactions of neoplastic development in general and their significance for smoking-induced lung cancer in particular. Certain dietary modifications that appear to be effective in moderating the promotional phase of animal and human carcinogenesis are suggested for trial in managing lung cancer.

The levels of 9 polycyclic aromatic hydrocarbons (PAHs) 6 of which carcinogenic were measured in the leaves of evergreen tree (Laurus nobilis) sampled in 13 locations in summer and winter in Tuscany, Italy. The carcinogenic PAH levels were correlated with the PAH air levels sampled at the same site. Samples from larger towns had higher PAH levels than those from medium and small towns. Leaves collected in the center of larger cities had higher carcinogenic PAH levels than samples from residential areas indicating that vehicular traffic is the main PAH source. Carcinogenic PAH levels in leaves collected in the winter in medium towns were considerably higher than expected, probably due to domestic heating. These findings demonstrate that air quality in terms of PAH contamination is not markedly different in towns of different size in Tuscany.

Immunoperoxidase methods using two antibodies were developed for detection and quantitation of DNA damage in single cells. A monoclonal antibody that recognizes 4-aminobiphenyl (4-ABP)-DNA adducts was initially tested on liver tissues of BALB/c mice treated with 4-ABP, then applied to the detection of adducts in oral mucosa and exfoliated urothelial cells of smokers and nonsmokers. Levels of 4-ABP-DNA in exfoliated urothelial cells were elevated in each of 20 smokers (mean relative staining intensity, 517 +/- 137) compared with age-, race-, and sex-matched nonsmokers (313 +/- 79; P < 0.0005). Significantly higher damage levels were also observed in oral mucosa cells of smokers compared with nonsmokers (552 +/- 157 versus 326 +/- 101; P < 0.0005). A polyclonal antiserum that recognizes benzo(a)pyrene and structurally related polycyclic aromatic hydrocarbon (PAH) diol epoxide-DNA adducts was also applied to the same study samples after validation by staining of 10T1/2 cells treated with (+/-)-trans-anti-benzo(a)pyrene diol epoxide. Smokers had higher levels of PAH-DNA damage in oral mucosa and exfoliated urothelial cells than nonsmokers (oral mucosa cells, 684 +/- 107 versus 370 +/- 83; P < 0.0005; urothelial cells, 689 +/- 72 versus 495 +/- 57; P < 0.0005). A similar 2-3-fold range in relative staining was found in smokers and nonsmokers for both 4-ABP- and PAH-DNA, suggesting the importance of individual differences in capacity to metabolize the carcinogens and/or repair damaged DNA. Significant correlations were found among the biomarkers in both cell types. This noninvasive method, requiring small numbers of cells and with a relatively low cost, will be useful for monitoring DNA damage in large-scale molecular epidemiology studies.

To evaluate the association between an indicator of carcinogen exposure (peripheral blood leukocyte DNA adducts of polycyclic aromatic hydrocarbons) and an early indicator of neoplastic transformation (sputum epithelial cell membrane antigens binding by monoclonal antibodies against small cell lung cancer and against nonsmall cell lung cancer), a survey of 350 coke-oven workers and 100 unexposed workers was planned. This paper reports a pilot investigation on a subgroup of 23 coke-oven workers and 8 unexposed controls. A "gas regulator" worker with positive tumor antigen binding was identified. Results show that smokers, subjects with decreased pulmonary function (forced expiratory volume in 1 sec/forced vital capacity% < 80), and those with morphological dysplasia of sputum cells have higher levels of DNA adducts. The gas regulators showed the highest values for adducts; however, no significant difference of adduct levels was found between the coke-oven group and unexposed controls.

This contribution describes methodological modifications and improvements that may contribute to inter-assay reproducibility and more accurate adduct quantification for 32P-postlabelling. Firstly, an anion-exchange chromatography procedure was developed to determine the amount of DNA used per assay and to check its purity, in particular to verify the absence of contaminating RNA. Secondly, calibration standards were prepared, in order to correct for differences in recovery. The modification levels of these standards were determined by synchronous fluorescence spectrophotometric analysis. Thirdly, the effect on adduct levels of exposure to light during postlabelling was investigated. Exposure of polyaromatic DNA adducts on a PEI-cellulose plate reduced the amounts of adducts detected considerably.

Methods for the detection of carcinogen-DNA adducts require both sensitivity and specificity. The 32P-postlabelling assay is highly sensitive but lacks adduct specificity. The strategy reported herein combines micropreparative techniques including HPLC and immunoaffinity chromatography (IAC) to enhance chemical specificity. The resultant assays have retained sensitivity for human DNA analysis. Combined HPLC and 32P-postlabelling has detected 7-methyldeoxyguanosine in human lung samples, while combined IAC and 32P-postlabelling has detected O6-methyldeoxyguanosine adducts in stomach tissue. The limits of detection are one adduct in 10(7) and 10(8) unmodified deoxyguanosine (dG), respectively. IAC was combined with 32P-postlabelling to detect polycyclic aromatic hydrocarbon (PAH)-DNA adducts in human lung. The detection limit was one adduct in 10(7) dG. Our laboratory has also employed synchronous fluorescence spectroscopy (SFS) for the detection of adducts formed from benzo[a]pyrene in human lung. Complex fluorescence matrices suggest the presence of other PAH-DNA adducts. Both the SFS assay and the 32P-postlabelling assay were applied to a series of human samples and a high correlation was found for adduct levels. The development of such assays using synthetic standards, internal standards, determination of calibration curves and validation with corroborating methods is required for chemically specific and sensitive adduct detection.

There has been significant recent progress toward the development of human carcinogen-DNA adduct biomonitoring methods. 32P-Postlabelling is a technique which has found wide application in human studies. 32P-Postlabelling involves enzymatic preparation and labelling of DNA samples, followed by chromatographic separation of carcinogen-nucleotide adducts from unadducted nucleotides. Thin-layer ion-exchange and high-performance liquid chromatography (HPLC) have been utilized. This paper critically reviews 32P-postlabelling methods for analysis of bulky, polyaromatic carcinogen-DNA adducts and details a strategy to optimize this technique for monitoring human samples. Development of a human carcinogen biomonitoring method requires that the biomarker meet certain criteria: that the biomarker be responsive to exposures known to increase human cancer risk, to reductions in those exposures, and to the influence of metabolic differences. In addition, reliable samples must be available by non-invasive means. The ability of 32P-postlabelling to meet these criteria is traced in the literature and discussed. Identification of specific carcinogen-DNA adducts is a difficult task due to the low (femtomole) levels in human target tissues. Because co-chromatography in thin-layer chromatography (TLC) is generally not considered to be proof of chemical identity, both synchronous fluorescence and HPLC in conjunction with 32P-postlabelling and TLC are used to confirm the identity of specific carcinogen-DNA adducts in human samples. Mass spectrometry is a highly specific method, the sensitivity of which has been improved to the point which may allow its use to confirm the identity of carcinogen-DNA adducts isolated by 32P-postlabelling and other methods. The literature relating to the use of mass spectral techniques in carcinogen-DNA adduct analysis is reviewed.

13C Nuclear magnetic resonance (13C-NMR) spectra were measured for polycyclic aromatic hydrocarbons (PAH) to examine the correlation between their chemical shift and carcinogenicity. We confirmed our previous proposition that the carcinogenicity of PAH molecules can be predicted from the value of the averaged 13C-NMR chemical shift. It was also found, using the averaged chemical shift as a parameter, that several quantum chemical indices for the intermediate states of the metabolic transformation are correlated with the carcinogenic activity of PAH. This indicates that the averaged chemical shift can be applied to investigate the metabolic transformation of carcinogenicity.

A method useful as a preconcentration technique for isolating mutagens and carcinogens is described. Cotton bearing covalently linked copper phthalocyanine trisulphonate as ligand (blue cotton) can adsorb selectively compounds having three or more fused rings. The adsorption takes place in aqueous media, involving 1:1 complex formation between the ligand and the polycyclic compound. The desorption can be done by elution with organic solvents, most effectively with methanol containing ammonia. As many important environmental mutagens and carcinogens are polycyclics, this adsorption is useful as a means of extracting this class of materials from crude samples such as food, urine and river waters. The use of copper phthalocyanine as a ligand for chromatographic supports has recently been initiated, yielding promising results for the effective separation of polycyclic aromatic compounds from each other.

South Indian food dishes, comprising several deep fried items have been proved to be mutagenic. Polycyclic aromatic hydrocarbons (PAHs) such as, benzo(a)pyrene, chrysene and dibenzanthracene, which are potent and proven carcinogens have been identified and quantified in several of the commonly consumed South Indian food dishes and food components. Most of the pyrolysed items contained PAHs in appreciable quantities. PAHs were detected in significant levels in salted, sundried and oil fried vegetables and fishes. Some of the raw and uncooked food components also revealed the presence of PAHs.

In the present study, data on the concentration of polycyclic aromatic hydrocarbons (PAH) in air samples from fish smokehouses (Nordholm et al. 1986) and meat smokehouses (Hansen et al. submitted for publication) were used to analyze the extent to which six different volatile PAH compounds could function as markers for the total concentration of six different carcinogenic particulate PAH compounds. Although a significant positive correlation was observed between the concentration of each of six volatile compounds and the total concentration of carcinogenic PAH compounds, a particularly good correlation was observed for phenanthrene, anthracene, fluoranthene and pyrene. Calculations of the sensitivity, specificity, positive predictive value and negative predictive value of these potential markers revealed that naphthalene and phenanthrene exhibited the highest sensitivity as markers for total carcinogenic PAH compounds in air samples from smokehouses, whereas fluoranthene and pyrene displayed the highest specificity. However, when the applicability of the six markers was tested on air samples from iron foundries, only naphthalene and pyrene were useful as markers for the carcinogenic compounds. The present study indicates that naphthalene and pyrene might function as markers for carcinogenic PAH compounds, that are present at low concentrations and are therefore difficult and time-consuming to measure directly.

Fetal tissue and placentas from 15 human spontaneous abortions were evaluated for DNA adducts of polycyclic aromatic hydrocarbons (PAHs), using a competitive enzyme-linked immunosorbent assay (ELISA) with fluorescent end-point detection. PAH-derived adducts were found in 43% of placentas, 27% of fetal liver samples and 42% of fetal lung specimens, thus confirming that the human fetus is a target for DNA damage. As there was only 60% concordance between placenta and fetal lung or liver on the presence or absence of detectable PAH adducts, the placenta was not a good surrogate for adduct formation in other fetal organs. PAH-derived adducts in fetal liver and lung presumably form as a result of transplacental exposure to environmental stimuli. Since none of the positive fetal samples were from women who reported smoking during pregnancy, cigarette smoke is, in this case, an unlikely candidate and the adducts detected must be due to some other common source(s) of hydrocarbon exposure. The high frequency of positive samples in our small series casts some doubt on whether fetal PAH-DNA adducts identify a population at increased risk for transplacental carcinogenesis.

Over a period of 2.5 yr, 221 different food items of a 'market basket' of 18-yr-old males were purchased every 3 months. In total, 10 market baskets were collected. The foodstuffs were prepared by normal methods and combined into 23 commodity groups. Homogenates were prepared from each commodity group, followed by analysis for 17 different polycyclic aromatic hydrocarbons (PAHs). All these compounds were detected. The most frequently occurring PAHs were benzo[b]fluoranthene, fluoranthene and benzo[k]fluoranthene, in 59, 48 and 46% of the samples, respectively. The highest concentration of a single PAH was 36 micrograms chrysene/kg in the commodity group 'sugar and sweets'. On the basis of concentrations found in the total diet samples the possible daily intakes of the various PAHs were calculated. The mean daily intake of the total PAH fraction analysed was between 5 micrograms/day (low estimate) and 17 micrograms/day (high estimate). The intake of the carcinogenic PAH fraction was roughly half these amounts. The largest contribution to the daily PAH intake came from sugar and sweets, cereals, oils, fats and nuts.

Animal experiments have shown that the carcinogenic activity of organic extracts of exhaust condensates is caused predominantly by PAHs containing 4-6 rings. The carcinogenic potency not only of PAH-containing extracts but also of the whole exhausts has often been estimated from their benzo[a]pyrene (BP) content. However, this simplified yardstick should not be applied for comparison of the carcinogenic potency of different types of PAH-containing exhausts. Epidemiological and experimental studies indicate that, for the induction of a certain tumour incidence, inhaled cigarette smoke contains about 100 times less BP and inhaled diesel exhaust contains about 1000 times less BP than the exhausts from coke ovens or heated tar pitch which yield the same results. This means that diesel exhaust and cigarette smoke contain--apart from PAHs--highly potent carcinogenic substances and/or they induce tumorigenic reactions which are very effective.

Experiments using various types of gas samplers showed that application of A phi A type fibrous material-containing filters for benzo(a)pyrene monitoring may result in significant underestimation of the carcinogen level in the air. The authors developed pulsed sampler using suspended layer of sorbent which proved most effective in catching benzo(a)pyrene in gaseous atmosphere. The unit allows simultaneous sampling of carcinogenic polycyclic aromatic hydrocarbons and N-nitroso compounds.

Monoclonal antibodies have been developed which recognize a number of carcinogen-DNA and protein adducts. These antibodies can be used in highly sensitive competitive enzyme linked immunosorbent assays (ELISA) to detect femtomole levels of adducts in human samples. With the most sensitive antibodies, DNA adducts in the range of 1/10(8) nucleotides can be measured. In addition, antibodies to DNA adducts can be used to investigate immunohistochemically the localization of adducts in specific cell and tissue types. Antibodies recognizing benzo(a)pyrene diol epoxide-DNA have been used to monitor adducts in white blood cell DNA of foundry workers and placental and white blood cell DNA of smokers and nonsmokers. Because of antibody crossreactivity with structurally related adducts of other polycyclic aromatic hydrocarbons, this assay is not specific for benzo(a)pyrene adducts. Antibodies to the stable guanine imidazole ring opened aflatoxin-B1-DNA adduct have been used to detect elevated levels of adducts in liver tissue from Taiwanese hepatocellular cancer patients. Monoclonal antibodies against 8-methoxypsoralen-DNA have been used to monitor adducts in psoriasis and cancer patients treated with psoralen plus UVA light. These patients have also served as model systems for the development of immunofluorescence methods for adduct detection. Immunohistochemical staining of skin biopsies from psoriasis patients demonstrated specific staining of epidermal cells. With further increases in sensitivity, this method should be applicable to the detection of adducts in other human tissues. Adduct detection in humans is now established as a viable method for determination of exposure to certain chemical carcinogens. However, the relationship of adduct measurements to individual risk requires further investigation.

The rapid development of the natural sciences and the technical progress during the last century have significantly changed our society and environment. During this period the average life expectancy for people in industrialized countries has doubled. A prolongation of life expectancy to this extent, due to for example, understanding of the relationship between various diseases and their corresponding causative agents, had never before occurred in mankind's history. It resulted in specific hygiene precautions. The recognition of such causal relationship was facilitated by the fact that infection diseases generally become apparent after a short incubation time, i.e. that an environmental situation causes health damage. At present, we are searching for origins of diseases of which the causal correlations with environmental influences are far more difficult to recognize than those of infection diseases, since long-term effects have to be observed. Do we have a situation similar to that which we had for infections at the end of the last century ? For diseases such as lung and larynx cancer, there are significant indications of carcinogenic compounds in the environment. Since both types of cancer are about 10 times more common among cigarette smokers who inhale than among non-smokers, a correlation to the risk factor "smoking" is beyond doubt. Living and working in larger cities or highly populated areas are additional factors which many enhance the lung cancer incidence ("urbanisation factor"). The air quality of these areas is supposed to be the reason for this effect. However, the present "bad air quality" at most doubles the disease incidence. A large number of epidemiological studies report on local differences of the incidence rates as well as significant increases or decreases of the mortality rates for some cancer diseases during comparatively short periods. A summary recently has been published by Misfeld (1). As an example, the mortality rate due to lung cancer for males in the F.R.G. has almost doubled during 1955-1975 from 36.5 per 100,000 to 65.9 per 100,000. This holds true for cancer of the rectum which increased from 8.8 per 100,000 to 18.9 per 100,000 during the same period. In contrast, mortality due to stomach cancer decreased from 59.3 to 36.6 per 100,000 and uterine cancer in females decreased from 16.6. to 8.5 per 100,000 (2). The pronounced changes in mortality rates cannot be explained by alterations of the genetic disposition during such a short period. Improved diagnostic and therapeutic techniques might explain decreases but not increases of mortality rates.(ABSTRACT TRUNCATED AT 400 WORDS)

The content of benz(a)pyrene (BP) in the soil of the agricultural regions of the USSR, away from the intense sources of industrial wastes ranges within 1-10 microgram/kg and depends on the soil type. In the vicinity of the industrial enterprises, the BP content in the soil may be tens thousand times higher. The baseline natural content of BP in the green parts of the vegetables constitutes 1-5 microgram/kg, while in the grain, seeds and fruit it is 10-100 times lower. In the vicinity of the sources of industrial wastes, the BP content in the green parts of the vegetables, in the grain, seeds and fruit was found to be drastically increased. There is a correlation between the BP content in the potato tubers and the soil where the potato is grown.

Polycyclic aromatic hydrocarbons (=PAH) emitted by two different vehicles were separated by gas chromatography and characterized by mass spectrometry after enrichment from exhaust gas condensate. Gasoline was investigated also using this technique. The quantities of PAH with boiling points higher than 338 degrees C contained in the exhaust gas were compared to those present in the fuel. About 150 different PAH have been characterized by mass spectrometry, 75 of these were identified by means of comparison with authentic samples. Six compounds of the PAH-group consisting of 4-7 rings, which are suspected of possessing carcinogenic activity, are described here for the first time. Structures of these hitherto unidentified PAH are proposed by means of MS and UV spectral informations (11H-cyclopenta(qrs)benzo(e)-pyrene, 10H-cyclopenta(mno)benzo(a)pyrene, benzo(ghi)cyclopenta(pqr)perylene, cyclopentenopyrene). According to the different PAH-profiles of the fuel and of the exhaust gas, it is concluded that the main part of the PAH emitted is produced de novo during the combustion in the engine and furthermore that the PAH contained in the fuel are combusted for the most part.

The criteria of a biological detection system discriminating carcinogenic and non-carcinogenic fractions of a mixture are discussed. Automobile exhaust gas condensate (in total 545.5 g) produced by a passenger car during the Europa driving cycle was separated into fractions with and without polycyclic aromatic hydrocarbons (PAH) by liquid-liquid distribution between methanol + water / cyclohexane and cyclohexane + nitromethane, respectively. This fractionation was chosen because of the general experience that PAH are highly potent carcinogens. To prove whether other non-PAH contribute to the total carcinogenic effect, these had to be separated from the PAH-containing fraction. Carbazol and acridine derivatives as well as aromatic amines remain predominantly in the PAH-free methanolic phase.

The authors have studied the electrochemical behavior of a series of carcinogenic and inactive heterocyclic compounds in anhydrous medium in the presence of a proton-donor. As anhydrous medium the authors used anhydrous dimethylformamide as proton-donor phenol. In the presence of proton-donor there had occurred on polarographic reduction of the employed carcinogenic heterocyclic compounds changes in the number of polarographic waves. Between the two original waves in these compounds there arose in the presence of phenol a new wave. In non-carcinogenic heterocyclic compounds such an effect of phenol was not noted. In the present paper the authors discuss the possible mechanism of electroreduction of carcinogenic and inactive heterocyclic compounds in anhydrous medium in the presence of a proton-donor.

The biological monitoring of exposure to carcinogens and mutagens has gained a lot of research interest recently. Biological monitoring data, in conjunction with environmental monitoring data, will provide information for the needed exposure assessment for directing preventive actions. For the reviewed carcinogens aromatic amines, benzene, ethylene oxide, aflatoxins, N-nitroso compounds, polynuclear aromatic hydrocarbons, and alkylating anticancer drugs, there are methods which are already routine in practice, whereas some promising methods are still used only for research purposes.

Coal tar and petroleum asphalt paints are among the products used as coatings for water pipes and storage tanks to retard corrosion. Formulations of these coatings were tested in the Ames mutagenesis and the mouse skin carcinogenesis bioassays. To test the mutagenicity of the paints, six doses ranging from 0.005 to 10 microliters per plate were assayed. In the mouse skin bioassay, doses of the coal tar paints ranging from 0.2 to 200 microliters were administered topically to 30 SENCAR mice per group. These initiating doses were followed by applications of 1.0 micrograms of 12-o-tetradecanoyl-phorbol-13-acetate (TPA) in 0.2 ml acetone topically, three times weekly for 20 weeks. Petroleum asphalt paints were tested in groups of 40 animals at 200 and 600 microliters doses. All coal tar paints showed mutagenic activity after metabolic activation with S-9, with the highest response being in strains TA 98 and TA 100. None of the petroleum asphalt paints gave mutagenic responses. Both types of coatings resulted in positive responses in the initiation/promotion study. The coal tar paints gave rise to 1000-1800 times the tumor response observed with petroleum asphalt products. One coal tar product was positive when tested as a complete carcinogen in the mouse at 2 microliters per application once weekly for 30 weeks, whereas the asphalt paint was negative at 100 times the dose. The biological responses to the products were greater than expected from their polycyclic aromatic hydrocarbon (PAH) content. These findings suggest that the hazard posed by these coatings may not be fully explained by their PAH contents.

Samples of raw waters from the Oława River, chlorinated raw water, raw water filtered through activated charcoal and treated and chlorinated water before and after ozonization were examined with the use of the Ames test for potential carcinogenic activity. Positive results were obtained for raw water with Salmonella typhimurium strains TA 98 and TA 1535 and for chlorinated raw water with strain TA 1537.

(1) The mean content in benzypyrene (bp) of human pulmonary tissue amounts to 0.2 mug./100 g. of dry substance. As in all other organ tissues, however, the content differs with the age of the individual: in infants, we find maximum concentrations, in the medium age groups the levels decline and rise once more with increasing age. (2) No increase in the 3,4-benzpyrene levels (average: 0.2 mug./100 g. of dry substance) will be found in tissues with high cellular proliferative activity, such as exocrine and endocrine glands (pancreas, testicles, thyroid gland, adrenals, mammary glands, as well as bone marrow). (3) In human adipose tissue, as well as in that of pork and beef, the 3,4-benzpyrene levels are found to be exceedingly low. With values of 0.1 mug./100 g, the average concentrations lie markedly below the organ tissue levels. Hence, this class of noxious substances in not stored in the adipose tissue. (4) Both in man and in animals (pig, fowl), the 3,4-benzyprene concentrations consistently exceed the average values during early postnatal life. (5) This relatively high concentration of bp in early infancy is due to exogenous factors and is not the expression of biogenous synthesis, as has been demonstrated in examinations of the environmentally influenced embryonic development of the chick. Throughout the entire development of the embryo within the hen's egg, the benzpyrene levels remain constant. Only when the chickens have been hatched out do the benzyprene levels rise significantly. Thus, the low 3,4-benzpyrene levels detected in all human and animal organ tissues prove to be the result of the interplay of exogenous environmental loading and individual capability of eliminating this substance.

Used gasoline engine oils are carcinogenic in mouse skin and mutagenic in Salmonella. The toxicity of fresh gasoline engine oils and that of fresh and used diesel engine oils are less well defined. The present studies examined the dermal carcinogenic potential of a series of fresh and used oils from both gasoline and diesel engines. The used oils represented a variety of operating conditions. The objective of the study was to assess the potential carcinogenic hazards associated with exposure to these materials. The majority of the used gasoline engine oils tested were carcinogenic although one oil, collected after a relatively short drainage interval, was inactive in the dermal carcinogenesis bioassay. Additionally, polycyclic aromatic hydrocarbon (PAH) concentrations were elevated in the used oils in comparison to the fresh oils. The fresh gasoline engine oils and both the fresh and used diesel engine oil samples were noncarcinogenic, and there was little evidence of elevated PAH levels in the used diesel engine oils. The carcinogenic potency of used oils from gasoline engines was related to drainage interval, but other factors such as contribution of the fuel due to blowby and driving cycle may also have been important. The used diesel engine oils were not carcinogenic even after extended use.

A previously developed method for the determination of polycyclic aromatic hydrocarbons (PAH) in purified petroleum products was applied to some fully-refined paraffin samples for cosmetic and medicinal uses of Italian Pharmacopoeia grade materials. The analytical procedure used provided identification and quantitative assay for ng/g amounts of two well-known carcinogenic PAH, namely benzo[a]pyrene and benzo[b]fluroanthene, together with five other none-carcinogenic PAH. The method is sensitive and reliable for routine analysis of PAH content in these paraffins and is compared with very rapid pharmocopoeial tests based on different criteria of quality. The data obtained showed a lack in agreement between PAH content in paraffin samples and the results of pharmacopoeial tests.

After the measurements of emissions from an oil oven and a gas oven (2) the investigation on room heaters was continued with a coal oven. This oven had a nominal power of 7 kW. The following pollutants were measured: polycyclic aromatics, benzene, the total gaseous hydrocarbons, soot/fly ash and NOx. Studies were made with anthrazit-nut brown-coal briquettes. Investigations and results are described in a research report (3). This paper presents a summary of the research report. The emissions of almost all measured pollutants were essential larger at the coal oven than those from the oil and the gas oven.

Twelve polynuclear aromatic hydrocarbons (PAH) were evaluated by chromatographic procedures using a HPLC-UV detector and a GC-FID detector. The PAH were evaluated in airborne particulate matter collected in La Plata, Argentina, over a period of 2 years (with sampling periods of approximately 4 months). The samples were size fractionated, and the PAH in each fraction determined. The analytical procedure used was as follows: extraction in benzene, concentration at room temperature, clean-up in a silica gel column and, finally, evaluation by chromatographic procedures. The extraction recovery was 76.2 +/- 5.8% for naphthalene and 96.0 +/- 6.2% for chrysene. Clean-up recovery was 87.8 +/- 7.15% for phenanthrene and 98.1 +/- 8.3% for anthracene. The largest PAH load was present in the smallest fractions. The smallest particles were carbonaceous in nature. The concentration peak was associated both with the total mass of airborne particulate matter and the reduction in amounts of coarse particles. The PAH distribution could not be correlated with characteristic physicochemical properties such as water solubility or the octanol-water distribution coefficient. The PAH load was greater in fall and winter than in spring and summer. This could be attributed to the reduction of photochemical processes during the cold seasons.

The quantity of phycyclic aromatic hydrocarbons (PAHs) in Hungarian foods and consumer goods were measured in more than 300 samples of food and other consumables. In more than 60% of the samples, pyrene, fluoranthene, benz(a)anthracene and benzo(g.h.i)perylene were detectable besides the highly carcinogenic benzo(a)pyrene (BaP). Investigational results and consumption data show that the average per man-year BaP intake with food in Hungary is 300-600 microgram.

Airborne particulate matter was collected on filters at various times in Duisburg, Duesseldorf, Muenster and in 2 rural areas. After extraction with organic solvents the extract was partly fractionated and analyzed for BaP and 7 other polycyclic aromatic hydrocarbons (PAH). The carcinogenicity was examined with the subcutaneous test using 7000 mice in total. The amount of extract required was relatively small. Extracts from suspended matter with a BaP content of 0.37 to 1.1 microgram BaP brought about tumour rates in the range of 30%. On account of the results the following can be concluded: 1. The total extract of atmospheric particulates results in definite dose-response relationship, when the part of the compounds not belonging to the PAH is rather low. 2. The PAH fractions derived from the suspended matter collected in different cities show the same carcinogenic potency, when they are adjusted to the same BaP level by means of concentration or dilution. 3. The PAH bear the most important share with respect to the carcinogenic potency of an extract from suspended matter. 4. Numerous compounds (polar substances) which are not classed with the PAH are carcinogenic to some extent, partly they are able to inhibit the carcinogenic effect. 5. The dose-response relationship of BaP is strongly leveled off in general when all the substances of an extract are present. That means when the dose of an extract is low, the importance of BaP becomes less. Therefore a fixed ratio concerning the effect of BaP within an extract cannot be given. It has to be examined in particular, which PAH and non-PAH are necessary to analyse in order to describe the carcinogenic effect due to an extract from airborne particulates. Much more attention is to be payed to the polar substances.

The contamination of foods is technologically induced by smoke gases (smoking, grilling, drying) and also due to environmental factors such as air and soil, soil conditioners, migration from plastics etc. The author presents and discusses the major problems concerning the accurate analysis of smallest amounts (micrograms/kg of food) of polycyclic aromatic hydrocarbons (PAH). Such problems occur in the separation from he matrix and the clean-up of the PAH, as well as in their identification and determination. Benzo[a]pyrene - under certain preconditions internationally accepted as the reference standard of PAH - is ingested by the GDR citizens in an order of magnitude ranging from 0.2 to 1.0 mg per annum; this corresponds to a daily intake varying within 0.5 and 2.5 micrograms. It is particularly difficult and as yet not possible to establish scientifically founded maximum tolerances for cancerogenic substances in foods which exclude a risk to man. The establishment of tolerances in the sense of a "socially acceptable level of risk" (which does not mean physiological safety) is recommended. Controlled tolerances would enable the legislator to aim at the optimum reduction or exclusion of the cancerogenic noxious agent in the framework of technical and economic possibilities.

The discharge of used motor oils in the environment poses public health problems because of the mutagenic/carcinogenic compounds in them. Among these hazardous chemicals, polycyclic aromatic hydrocarbons (PAH) are of particular interest since the carcinogenic properties of some of them are known. The authors have applied the Salmonella/microsome test, coupled with two preparation methods of samples, to motor oils of different brands, both before and after use in car petrol engines. A PAH determination method was also studied. The results showed the unused motor oils to be nonmutagenic and to contain traces of PAH, while the used motor oils of the samples taken according to both preparation methods were highly mutagenic and contained a much higher quantity of mutagenic/carcinogenic PAH.

Environmental monitoring of mutagenic/carcinogenic hazards associated with occupational exposure to bitumen fumes was performed during road paving operations. Bitumen samples were collected and analysed for polycyclic aromatic hydrocarbons (PAH) content by HPLC and for mutagenicity by the Ames test. The exposure of sixteen road workers to bitumen fumes was studied. Time-weighted average values of bitumen fumes were determined by personal samplers. PAH concentration in the air and the mutagenicity of airborne particulates were also analysed. The results showed that bitumen samples contained low levels of total PAH (microgram/g) and were not mutagenic. Environmental monitoring showed a low level of exposure to bitumen fumes, which were found to contain only trace levels of PAH and not to be mutagenic. The authors suggest that these workers' exposure to mutagenic/carcinogenic agents is low.