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Charge carrier transport and trapping was investigated in organic solar cell structures consisting of poly-3-hexylthiophene blended with the fullerene derivative [6,6]-phenyl-C61-butyric acid methyl ester in 6:5 weight ratio. The analysed devices having solar efficiency of 3.7 per cent were produced in the inverted layer sequence. The fill factor of the IV characteristics was as high as 68 per cent. It was demonstrated that despite of such relatively high fill factor carrier trapping is effectively involved in the charge transport phenomena. The density of the trapping states was evaluated to be up to 10(20) division by 7 x 10(21) cm(-3) and their activation energy was about 0.18 eV. At such high densities these states may probably act as transport states, limiting carrier mobility. The results were analyzed by taking into account carrier thermal generation from traps as well their mobility variation according to the Gaussian disorder model. The mobility parameters obtained by both methods demonstrated good coincidence.

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The most potent carcinogen of the cyclopenta[a]phenanthrene series, 15, 16-dihydro-11-methylcyclopenta[a]phenanthren-17-one and its non-carcinogenic, unmethylated parent compound, were compared for their abilities to induce micronuclei in epidermal keratinocytes after application onto the dorsal skin of Skh/HR-1 hairless mice. Although both substances were shown to be mutagenic in vitro, only the 11-methyl derivative has been proven to initiate cancer in TO and Sencar mouse strains. In the present study, only the 11-methyl derivative was active as a cancer initiator in Skh/HR-1 mice. For studying micronucleus induction, a preliminary experiment was conducted to establish doses of both chemicals that allowed cell survival. Subsequently, micronucleus induction in epidermal keratinocytes was shown to agree with the cancer-initiating potential of the two compounds. Only the carcinogenic derivative induced a statistically significant increase in micronuclei, over the range 10-100 nmol. This is considerably lower than the dose of approximately 1600 nmol commonly used to initiate skin cancer in mice, but is comparable to the active dose range for skin micronucleus induction by benzo[a]pyrene, a chemical of equivalent carcinogenic potency.

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Toxaphene is genotoxic in mammalian cell systems and also inhibits cell replication. It was therefore used to investigate possible masking of SCE induction due to cell-cycle delay. In this study, toxaphene-treated Chinese hamster lung (Don) cells exhibited a dose-dependent decrease in cell-cycle progression compared with untreated cells. At high, nontoxic toxaphene levels (15 micrograms/ml), cell cycling also slowed as the toxaphene treatment time was increased. Toxaphene induced significantly higher numbers of SCEs in treated cells, demonstrating a dose- and treatment time-relationship. Slopes of dose-response curves were 0.29, 0.43 and 0.77 SCE/micrograms toxaphene for 20.5 h, 24.5 h and 28.5 h incubation, respectively. There were no changes in SCE values in control cultures even when slower dividing cells were sampled e.g. at longer incubation times. Thus, higher SCE values in Chinese hamster cells were not associated per se with slower or more delayed cells. The results demonstrate that longer toxaphene treatment times were not necessary for obtaining sufficient harlequin-stained cells for SCE analysis, but that higher numbers of SCEs occurred in slower dividing cells, following prolonged incubation of cultures treated with toxaphene.

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Welding fumes generated by manual metal arc welding (MMAW) with an automatic welding machine were extracted with water and both the soluble and insoluble fractions were investigated for mitotic delay and for sister chromatid exchange (SCE) induction in cultured Chinese hamster lung (Don) cells. Five flux-coated electrodes of varying composition were chosen as representative of those available. In general, water-soluble and water-insoluble fractions induced SCE in proportion to their chromium(VI) content, and any contribution from chromium(III), fluorides, nickel, manganese or other fume constituents was minor. However, mitotic delay could not be explained in terms of the chromium(VI) concentration alone. This indicated that other components of both the soluble and insoluble fractions of the fumes were capable of inducing mitotic delay. The activity of insoluble fume fractions, either in mitotic delay- or in SCE-induction, was markedly less than that of soluble fractions. This was presumably because of the lower, though still significant, bioavailability of 'insoluble' components of the fume particles.

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Studies were undertaken with individuals fed fried bacon meals to determine whether fruit or vegetables, ingested along with bacon, modified uptake and subsequent excretion of bacon mutagen(s). Urinary mutagenic activity was significant in those who had consumed bacon or mixed bacon/vegetable or bacon/fruit meals within the previous 2 to 3 hr period. Although urine activity varied by a factor of 4 among 15 subjects who consumed different meals, there was no evidence from this investigation that fruit or vegetables contributed to the inherent variability in total urinary mutagenic activity. However, some differences in excretion kinetics may be attributable to vegetable or fruit supplements in mixed meals.

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The mutagenicity of 24 metal salts was investigated in plate incorporation and fluctuation assays with Salmonella TA strains or Escherichia coli WP2 uvrA pKm 101. Chromate(VI) and selenate(VI) ions were found to be mutagenic in plate incorporation assays employing conventional media. On the other hand, cadmium(II), beryllium(II), chromate(VI), and metavanadate(V) ions were detected in conventional fluctuation assays, indicating the importance of this technique in detection of metal mutagens. Modified culture media, with trimetaphosphate ions in place of orthophosphate as the sole phosphate source for bacterial growth, were also used in this study. The media modifications prevented precipitation of metals such as nickel and cadmium as their insoluble phosphates, and allowed detection of the mutagenicity of metavanadate ions in plate incorporation assays. However, the fluctuation technique using standard media was shown to detect a wider range of mutagenic metal ions than tests with modified media. It is notable that metaarsenite(III), arsenate(V), and nickel(II) ions were not found to be mutagenic in any of the assays although they are known to be carcinogenic and are mutagenic in other test systems. Their lack of mutagenicity in the modified media indicates that precipitation of these ions as orthophosphates is not the reason for their lack of activity in standard bacterial assays.

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After treatment with potassium chromate at concentrations causing ultramicroscopic cellular lesions, a significant proportion (up to 75%) of TA100 colonies fail to replicate on fresh minimal plates containing biotin. This suggests that chromium(VI) may not always induce his- reversion to his+ in Salmonella TA100. The terms 'false' or phenotypic reversion have been used to distinguish such instances from 'true' or genotypic reversion, where progeny his+ cells readily grow on biotin replica plates. Results of the present study indicate that the majority of chromate-exposed colonies, initially scored as his-, are identifiable as his+ after 24 h culture on nutrient agar. Moreover, chromate exerts a cytostatic effect on TA100 since early colony development is suppressed at high chromate concentrations. A gradual chemical reduction of chromium(VI) ions by normal media compounds is probably responsible for the re-emergence of colony growth during prolonged incubation of test plates. Thus, temporary growth inhibition at high chromate concentration appears to be responsible for most of the non-replicating colonies detected in mutagenicity assays of chromium(VI).

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Mutagens detected with Salmonella typhimurium strain TA 98 in the presence of liver S9 mix were extracted from potato slices, but not pure potato starch, after frying in oil. No mutagenic activity was detected using strain TA 100, in the presence or absence of S9 mix with either fried potato slices or potato starch. Mutagenic activity was detected at frying temperatures of 140 degrees C and above. The mutagenic activity was limited to the outer portion of the fried potato slices and increased with frying time and temperature. Mutagenic activity ratios for extraction with both (NH4)2SO4/NH4OH and Na2SO4/NaOH were similar.

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The mutagenicity of 2-ethylhexyl p-methoxycinnamate was demonstrated when 25 sunscreen ingredients were tested in the Salmonella/microsome assay. This substance also increased the frequency of sex-linked recessive lethals in Drosophila melanogaster. A trace contaminant may be implicated because many samples were obtained from several sources and the results were batch-related.

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Mutagenic activity has been demonstrated in urine of human subjects after ingestion of fried pork or bacon. Activity was detected with Salmonella strains TA1538 and TA98 particularly, in the presence of liver homogenate S9, and was not enhanced by prior incubation of urine with beta-glucuronidase. Chemical and biological characteristics of the urine activity closely resemble those found in extracts of fried pork and bacon which also increase the frequency of sex-linked recessive mutations in Drosophila melanogaster. Microwave-cooked meat neither contained extractable mutagenic activity, nor contributed to urinary mutagenicity, possible due to the paucity of browning reactions in meat cooked under these conditions. If the urine and meat factors are chemically identical, then approximately one-third of the food activity is recovered from the urine. These results show that mutagenic factors, generated during cooking of pork and bacon, are ingested and absorbed and are subject to urinary clearance in biologically detectable quantities. It is possible that the potential for genetic toxicity in humans of these and related factors has been underestimated.

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