[Methods of development of a data bank on ecologic and hygienic characteristics of chemical environmental pollutants].
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Databases, Factual↗
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The fish gill: site of action and model for toxic effects of environmental pollutants.
The gill epithelium is the site of gas exchange, ionic regulation, acid-base balance, and nitrogenous waste excretion by fishes. The last three processes are controlled by passive and active transport of various solutes across the epithelium. Various environmental pollutants (e.g., heavy metals, acid rain, and organic xenobiotics) have been found to affect the morphology of the gill epithelium. Associated with these morphological pathologies, one finds alterations in blood ionic levels, as well as gill Na,K-activated ATPase activity and ionic fluxes. Such physiological disturbances may underly the toxicities of these pollutants. In addition, the epithelial transport steps which are affected in the fish gill model resemble those described in the human gut and kidney, sites of action of a variety of environmental toxins.
Animals↗
Fluoride concentration in superficial enamel layers of permanent teeth in children residing in areas with different levels of environmental pollution with fluorine compounds.
The concentration of fluoride in superficial layers of enamel of permanent teeth was studied in 14-year-old children residing in Szczecin and Bialystok-two cities differing regarding the level of environmental fluorine pollution. It was found that higher environmental pollution with fluorine favors the accumulation of this element in superficial layers of enamel in the form of structural fluoride. Total and structural fluoride concentration decreased with layer depth.
Child↗
Environmental pollutants and breast cancer.
Breast cancer is the most common cancer in women and the leading cause of cancer death among women 35-54 years of age. Rising incidence, increased risk among migrants to higher risk regions, and poor prediction of individual risk have prompted a search for additional modifiable factors. Risk factors for breast cancer include reproductive characteristics associated with estrogen and other hormones, pharmaceutical hormones, and activities such as alcohol use and lack of exercise that affect hormone levels. As a result, investigation of hormonally active compounds in commercial products and pollution is a priority. Compounds that cause mammary tumors in animals are additional priorities. Animal models provide insight into possible mechanisms for effects of environmental pollutants on breast cancer and identify chemical exposures to target in epidemiologic studies. Although few epidemiologic studies have been conducted for chemical exposures, occupational studies show associations between breast cancer and exposure to certain organic solvents and polycyclic aromatic hydrocarbons (PAHs). Population-based studies have been limited to a few organochlorine compounds and PAHs and have been mostly negative. A variety of challenges in studies of breast cancer and the environment may have contributed to negative findings. Lack of exposure assessment tools and few hypothesis-generating toxicologic studies limit the scope of epidemiologic studies. Issues of timing with respect to latency and periods of breast vulnerability, and individual differences in susceptibility pose other challenges. Substantial work is needed in exposure assessment, toxicology, and susceptibility before we can expect a pay-off from large epidemiologic studies of breast cancer and environment.
Alcohol Drinking↗
Congenital cleft deformities in Rivers state of Nigeria: is there any association with environmental pollution?
Thirty-nine children with congenital cleft deformities seen at the University of Port Harcourt Teaching Hospital over a four-year period (1984-87) were studied. The majority (69%) of the children came from PHALGA, OTELGA and ALGA, the areas of the state with a high concentration of oil wells, gas flares and a petroleum refinery. There is yet no proof that there is a cause and effect relationship between the deformities and the industrial pollution but attention has been drawn to the association, which may be real or apparent. Further prospective studies are indicated. Apart from the possible role of environmental pollution, other epidemiological factors discussed include parental age, socioeconomic class of the families and the significance of the absence of positive family history of cleft deformities in all the cases studied.
Adolescent↗
Retrospective biomonitoring: a hundred years of environmental pollution at selected areas in Slovakia.
Tetrade analyses of Calluna vulgaris from herbarium specimens showed significant differences in the frequency of aborted pollen tetrads over the last 100 years within various parts of Slovakia. Specifically, we observed changes in the dynamics of pollution peaking in the year 1965 in heavily polluted industrial area of an aluminium factory in Ziar nad Hronom.
Calluna↗
[Preschool children's health in towns with different levels of environmental pollution].
A total of 3497 preschool children residing in the towns having with different man-made burden were examined. The study showed that most children referred to Health Groups 2 and 3. In the town with higher environmental pollution there were a larger proportion of children with dysfunctions of different organs and systems and higher incidence of diseases, including respiratory allergoses, etc.
Age Factors↗
The susceptibility of the fetus and child to chemical pollutants. Environmental exposures and biologic considerations of the adolescent in relation to chemical pollutants.
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Adolescent↗
Histopathological effects of environmental pollutants beta-HCH and methyl mercury on reproductive organs in freshwater fish.
From various environmental pollutants studied so far, specific effects on the reproductive system of small fish species Poecilia reticulata (guppy) and Oryzias latipes (medaka) were noted in the case of beta-hexachlorocyclohexane (induction of vitellogenesis and hermaphroditism, both indicative of estrogenic activity; 32 micrograms/l) and methyl mercury (impaired spermatogenesis; 1.8 micrograms/l). The latter effect was attributed to a disturbance of mitosis.
Animals↗
Content of 8-oxodG in chromosomal DNA of Sparus aurata fish as biomarker of oxidative stress and environmental pollution.
The 8-oxodG content has been measured in chromosomal DNA of gilthead seabream (Sparus aurata) by HPLC-EC. Susceptibility of different tissues to oxidative DNA damage was studied by exposing fish to model pollutants. Cu(II), paraquat (PQ) and malathion failed to promote DNA oxidation in liver, while dieldrin significantly increased the 8-oxodG content in this organ, but not in gills or blood. After PQ exposure, fish liver showed high levels of glucose-6-P dehydrogenase (G-6PDH) and GSSG reductase activities. The increased antioxidant status and the lack of a specific transport system could explain the lack of susceptibility of liver to DNA oxidative damage induced by PQ. Increased levels of 8-oxodG were detected in the gills of PQ-exposed fish after 8 and 24 h. In contrast, after 48 h exposed fish contained lower 8-oxodG levels than controls. The existence of a PQ transport system in this O2-rich organ and the lack of a significant increase in antioxidant defenses would explain the sensitivity of gills to DNA damage promoted by PQ. Elimination of this soluble chemical and the putative induction of DNA-repair enzymes specific for oxidative damages could explain the drop of 8-oxodG levels at longer times. Fish exposed to moderate levels of urban and industrial pollution showed significantly high 8-oxodG content in hepatic DNA. We conclude that 8-oxodG determination in chromosomal DNA by HPLC-EC is a potentially useful biomarker of environmental pollution, although its response is still somewhat lower than that of other well-established biomarkers of oxidative stress.
8-Hydroxy-2'-Deoxyguanosine↗
Breast cancer, oestrogens and environmental pollutants: a re-evaluation from a mixture perspective.
The continuing rise in breast cancer incidence rates in almost all Western countries cannot be explained entirely in terms of known risk factors of the disease process. Additional determinants need to be examined, among them exposure to environmental pollutants. With the demonstration that elevated levels of endogenous sex hormones and the use of hormones for the relief of menopausal symptoms are associated with the disease, the oestrogen hypothesis of breast cancer has received further empirical support. This has led to heightened concerns about the possible involvement of oestrogen-like pollutants, such as p,p'-Dichlorodiphenyldichloroethane (DDE). Case-control studies assessing whether women with breast cancer have elevated burdens of p,p'-DDE have produced results not suggestive of a link with cancer risks. However, possible effects of p,p'-DDE and other pollutants cannot be seen in isolation from sex hormones also present in serum. In view of the low potency of p,p'-DDE, and its low levels in serum, it seems unlikely that the chemical on its own will add significantly to the action of sex hormones. However, chemical analyses show that numerous pollutants with oestrogen-like effect profiles can be found in human tissues. Thus, the oestrogen hypothesis of breast cancer should be extended to encompass the multitude of these agents. Viewed from such a perspective, a putative role of organochlorines and other agents in breast cancer should not be dismissed prematurely. Instead, breast cancer epidemiology should face the reality of combined exposures and should take account of recent evidence from in vitro models demonstrating that a large number of oestrogen-like pollutants, all present at low levels, can act together to add to the internal oestrogenic load.
Breast Neoplasms↗
Effect of environmental pollutants on the C-reactive protein of a freshwater major carp, Catla catla.
C-reactive proteins (CRP) have been affinity purified to electrophoretic homogeneity from the sera of major carp, Catla catla before and after exposure to environmental pollutants. Exposure to these pollutants elevate the levels of circulating CRPs to 2.8-3.5 times the normal values. Kinetic studies of metal intoxication indicate that a unique molecular variant of CRP is present in the serum at the peak level of acute phase induction, and this variant coexists with normal CRPs. Carbohydrate analysis and lectin binding reveals that these CRPs are glycoproteins differing significantly in total carbohydrate contents. Their electrophoretic mobilities in native gel are different but become identical on desialylation and deglycosylation implying that the molecular variants vary in the glycan parts. All these forms of CRP contain two nonidentical subunits of Mr 22 and 29 kDa. Examination of their immunological crossreactivity demonstrate their similarity in overall molecular topology but their differences in the quantitative extent of binding are reflected.
Animals↗
[Chief toxic effects associated with environmental pollution in Poland based on health status indices of the general population].
Poor health status of general population in Poland together with existing trends were discussed on the basis of health indices and in comparison with other European countries. Examples of health effects related to environmental pollution in Poland were presented, and some vital preventive activities for improving the situation were proposed.
Adolescent↗
Generation of SO3.- and OH radicals in SO3(2-) reactions with inorganic environmental pollutants and its implications to SO3(2-) toxicity.
Electron spin resonance (ESR) spin trapping and high performance liquid chromatography (HPLC) with electron chemical detection were utilized to investigate the generation of free radicals in reactions of sulfite (SO3(2-)) with inorganic environmental pollutants. The spin trap used was 5,5-dimethyl-1-pyrroline N-oxide (DMPO). Incubation of SO3(2-) with nitrite (NO2-) generated sulfur trioxide anion radical (SO3.-), whose yield approached saturation levels in approximately four minutes. Fe2+ promoted SO3.- formation. Molecular oxygen was required for radical generation. This was demonstrated by experiments carried out in an argon environment as well as by oxygen consumption measurements. Transition metal ions, CrO4(2-), VO2+, Fe3+, Mn2+, Ni2+, and Fe2+ enhanced SO3.- generation from SO3(2-) either through direct SO3(2-) oxidation by metal ions or by metal ions-catalyzed SO3(2-) oxidation by molecular oxygen. Incubation of SO3(2-) with H2O2 generated both SO3.- and .OH radicals as verified by spin trapping competition measurements using ethanol and formate as .OH radical scavengers. HPLC measurements showed that .OH radicals generated by reaction of SO3(2-) with H2O2 caused 2'-deoxyguanine hydroxylation to generate 8-hydroxy-2'-deoxyguanine, a DNA damage marker. The implications of SO3.- and .OH radical formation in relation to SO3(2-) toxicity are discussed.
8-Hydroxy-2'-Deoxyguanosine↗
[Cytogenetic aberrations in somatic cells of children living in areas with various levels of environmental pollution].
Micronuclear test was used to carry out genetic screening in somatic cells of children from different St. Petersburg districts with varying ecologic conditions. Preschool children from districts with high anthropogenic load (soil, air) revealed significant increase of epitheliocyte number in mouth mucosa. Girls appeared to be more sensitive to unfavourable environmental effects than boys. Mean values of cells with micronuclei in ecologically safe districts were 0.38 and 0.66% in pre- and school children, respectively. The study performed showed a possibility to use micronuclei count in the mouth mucosa investigating genetic effects of environmental pollution.
Adolescent↗
[Environmental pollution with heavy metals and their level in blood fractions among the population of the Taimyr autonomous district].
The studies proved higher nickel, lead and copper content of soil, ground lichens, berries, mushrooms and blood of healthy residents of Taimyr autonomous county settlements varying in ecologic jeopardy degree. Findings also are microelements disbalance in biologic materials due to excessive intake. Higher copper, nickel and lead content in RBC appears long-standing and correlates with degree of environmental pollution, being a marker of antropogenous pollution.
Adolescent↗
[The characteristics of the development of postvaccinal diphtheria immunity in children under elevated technogenic environmental pollution in the region near the Dnieper River].
Condition was studied of collective specific immunity against diphtheria in vaccinated children who ranged from 2 to 15 years old, living in the industrial region of Pridneprovye, with special reference for the degree of the technogenous environmental pollution. To determine specific cellular sensibilization to diphtherial antigen. LAIT was used for the first time. The studies made showed that in a region under health-hazard conditions lower level of antitoxic antidiphtherial immunity occurs more frequently than in non-polluted areas (twice as much of the values), which fact suggests that technologeous pollution may have a suppressive effect on formation of postvaccinal immunity. Apart from measuring the level of specific antibodies for control of the formation of the immune responsiveness to be monitored you may use LAIT and measure levels of R-proteins.
Adolescent↗
Mammary carcinogenesis and molecular analysis of in vivo cII gene mutations in the mammary tissue of female transgenic rats treated with the environmental pollutant 6-nitrochrysene.
We determined the mutant fractions (MF) and mutational specificities in the cII gene in histologically confirmed normal, non-involved and tumor mammary tissues of female transgenic (Big Blue F344 x Sprague-Dawley)F1 rats treated with the environmental pollutant 6-nitrochrysene (6-NC). At 30 days of age, three groups were set up for oral treatment with 6-NC dissolved in trioctanoin, or trioctanoin alone once a week for 8 weeks. Two dose levels of 6-NC (100 and 200 micromol/rat) were selected on the basis of our previous carcinogenicity bioassays with CD rats. The rats were decapitated 32 weeks after the last carcinogen dose. Both incidence and multiplicity of mammary adenocarcinomas were significantly elevated in the high dose (36%, 0.57, P < 0.01) group but at the low dose these outcomes (16%, 0.23, P < 0.1) were not significantly different from those of control rats (3%, 0.03). The MF in normal, non-involved and tumor tissues from the mammary glands of 6-NC-treated rats were comparable. At the high and low doses, respectively (4.8 +/- 2.0, 3.2 +/- 2.1) the MF of 6-NC-treated rats, were significantly higher (P < 0.05) than that observed in control rats (1.2 +/- 0.6). Control mutants consisted primarily of GC --> AT transitions, whereas 6-NC-induced mutants were comprised of several major classes of mutations with GC --> TA, GC --> CG, AT --> GC and AT --> TA as the most prevalent. Further studies indicated that the structures of 6-NC-DNA adducts in the mammary tissue are consistent with the mutational specificities. This is the first report that defines the relationship between carcinogenesis and mutagenesis, as well as between structures of 6-NC-DNA adducts and mutation characteristics in the target organ in vivo.
Adenocarcinoma↗