[Catecholamine provision and the morphofunctional characteristics of the lymph nodes with different special purposes in acute benzpyrene poisoning]. / Katekholaminobespechenie i morfofunktsional'naia kharakteristika limfaticheskikh uzlov razlichnoi spetsializatsii v usloviiakh ostroi intoksikatsii benzpirenom.

Using fluorescent histochemical methods of catecholamines detection microfluorometry, morphometry, and classical cytological technique the catecholamine level, the density of adrenergic nerve fibers and cytological composition of the lymph nodes of different localization were studied in rats in health and after intraperitoneal injection of benz(a)pyrene. It has been revealed that exposure to benzpyren leads to decrease of catecholamine level and of the density of adrenergic innervation of abdominal lymph nodes and is accompanied with structural changes (decrease of corticomedullary index as a result of augmentation of the area of medullary sinuses and medullary cords) and cytological content of these organs (increase of plasmocyte counts in medullary cords). The degree of structural reconstructions depends on the primary status of organs and its typological characteristics. Catecholamine-depending reconstruction of the lymph nodes is connected with the place and method of toxic agent injection.

Bladder cancer in the aluminium industry.

The incidence of bladder cancer is unusually high in aluminium smelter workers. An epidemiological study showed that workers in Soderberg potrooms are at highest risk for bladder cancer, the adjusted overall relative risk being 2.39 (1.34-4.28). Exposure to polycyclic aromatic hydrocarbons, of which benz(a)pyrene (BaP) served as an indicator, seems to be the causative factor. The relative risk was evaluated at 12.38 for workers with 20 or more equivalent years of BaP exposure. Cigarette smoking contributed significantly to the appearance of bladder cancer in the population studied. There is a synergistic effect when cigarette smoking and BaP exposure are combined; the numbers in our population are too small to determine whether this interaction effect is multiplicative or additive. It is concluded that bladder cancer is associated with aluminium smelting (primarily with the Soderberg process).

Data from short-term tests on motor vehicle exhausts.

The mutagenicity of motor vehicle exhausts has been studied by using Salmonella typhimurium strains TA 98 and TA 100. Acetone extracts of the particulate phase and the gas phase have been tested in the presence and absence of a metabolizing system (S9). The particulate phases from medium- and heavy-duty diesel vehicles were tested. The vehicles were driven according to a modified 13 mode test, and the particulate phase was sampled at mode 6 (maximum load and intermediate engine speed) and mode 12 (10% load and rated speed). In mode 6 all vehicles gave approximately the same mutagenicity in strain TA 98 (50,000-90,000 revertants/kW-hr) as well as in TA 100 (200,000-360,000 revertants/kW-hr). A higher mutagenic effect, in some cases up to 10 times, was seen with mode 12.Light-duty vehicles of different year models were tested using different fuel/engine combinations. The vehicles were driven according to FTP 72 or ECE driving cycle. Cold starts at two different temperature levels, approx. 0 degrees C and 23 degrees C, respectively, were also compared. Based on the mutagenicity of the particulate extracts (given as revertants per km), the light-duty vehicles could be divided into three main groups. The first group, the high mutagenicity group, giving 100,000-700,000 revertants/km, consists only of diesel cars. In the medium mutagenicity group, giving between 20,000 and 100,000 revertants/km, different gasoline fuels are placed, i.e., leaded and lead-free gasoline as well as alcohol/gasoline fuels. Two other fuels, methanol (M95) and propane (LPG), constitute the low mutagenicity group, giving less than 20,000 revertants/km. Fuels from the medium effect group will produce a particulate phase with low mutagenicity if the vehicle is equipped with a three way catalyst with closed loop, or fuel injection. The cold start temperature did not change this classification, since all samples gave a somewhat higher mutagenic effect at the low temperature. With the ECE driving cycle, much lower mutagenicity was noted with the diesel cars than in the tests with the FTP-72 driving cycle, at least with tester strain TA 98. On strain TA 100 the diesel exhaust samples still showed a much higher mutagenicity than other samples. Acetone extracts of the gas phase from diesel and gasoline exhaust (trapped in ice/water condensers and CO(2)/ethanol condensers) also gave mutagenic effects. The contribution of the gas phase to the mutagenic effects seems to be more important in the absence of S9 and more important in the case of gasoline exhausts.

Embryotoxic effects of benzo[a]pyrene, chrysene, and 7,12-dimethylbenz[a]anthracene in petroleum hydrocarbon mixtures in mallard ducks.

Studies with different avian species have revealed that surface applications of microliter amounts of some crude and fuel oils that coat less than 10% of the egg surface result in considerable reduction in hatching with teratogenicity and stunted growth. Other studies have shown that the embryotoxicity is dependent on the aromatic hydrocarbon content, further suggesting that the toxicity is due to causes other than asphyxia. In the present study the effects of three polycyclic aromatic hydrocarbons identified in petroleum were examined on mallard (Anas platyrhynchos) embryo development. Addition of benzo[a]pyrene (BaP), chrysene, or 7,12-dimethylbenz[a]anthracene (DMBA) to a synthetic petroleum hydrocarbon mixture of known composition and relatively low embryotoxicity resulted in embryotoxicity that was enhanced or equal to that of crude oil when 10 microliter was applied externally to eggs at 72 h of development. The order of ability to enhance embryotoxicity was DMBA greater than BaP greater than chrysene. The temporal pattern of embryonic death was similar to that reported after exposure to crude oil, with additional mortality occurring after outgrowth of the chorioallantois. Retarded growth, as reflected by embryonic body weight, crown-rump length, and bill length, was accompanied by teratogenicity. Abnormal embryos exhibited extreme stunting; eye, brain, and bill defects; and incomplete ossification. Gas chromatographic-mass spectral analysis of externally treated eggs showed the passage of aromatic hydrocarbons including chrysene through the shell and shell membranes to the developing embryos. These findings suggest that the presence of polycyclic aromatic hydrocarbons in petroleum, including BaP, chrysene, and DMBA, significantly enhances the overall embryotoxicity in avian species.

Diesel exhaust - an occupational carcinogen?

The existence of polycyclic aromatic hydrocarbons (PAH) in the particulate phase of diesel engine exhaust has raised concern about a carcinogenic effect in workers exposed to exhaust from diesel engines. Some of the PAH are carcinogenic following inhalation by experimental animals and are associated with excess cancer mortality in some occupational exposures. Studies of occupational exposure to diesel exhaust show concentrations of PAH are above ambient levels but below the very high levels in occupations with demonstrated excess cancer mortality. A critical review of the epidemiologic evidence on the carcinogenicity of workplace exposure to diesel engine exhaust is suggestive of a carcinogenic effect but the existing data are sparse and contradictory. Further epidemiologic studies of this question are needed.

Diet and cancer.

Differences in food intake patterns are positively correlated with differences in the incidence of various cancers in world populations. It is postulated here that dietary factors play a vital role in the genesis of several major neoplasms, specifically gastric and colon carcinomas. In addition to the food consumed, such variables as total caloric intake, nutrtional excess or deficit, exposure to carcinogens and consumption of alcohol also increase the risk of cancer. Through recognition of these factors and subsequent long-term manipulation of diet, it should be possible to reduce cancer morbidity and mortality.