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1.
Acta Chir Belg ; 108(3): 318-22, 2008.
Article in English | MEDLINE | ID: mdl-18710106

ABSTRACT

In order to provide some answers to the much debated subject of the consequences of the Chernobyl accident, this study attempts to measure the incidence of surgically removed thyroid cancers in Belgium ten years following the explosion. The analysis was made from the hospital discharge data between 1993 and 1998. It offers the advantage of national coverage in spite of certain validity limits. The results show an increase in surgically removed thyroid cancers, which is not, however, evident in the more susceptible younger generation who were involved at the time of the accident. Furthermore, the geographic distribution of the incidence is more marked in the south of the country, unaffected by the radioactive iodine contamination of 1986, which was more prevalent in the east of the country. The study of the type of surgery involved shows a rise in the proportion of total thyroidectomies. These findings are in favour of the hypothesis of a causal effect linking the increased incidence of thyroid cancers to medical practice and surgery in particular and not to the consequence of the possible contamination.


Subject(s)
Adenocarcinoma, Papillary/epidemiology , Chernobyl Nuclear Accident , Neoplasms, Radiation-Induced/epidemiology , Thyroid Neoplasms/epidemiology , Adenocarcinoma, Papillary/surgery , Adult , Belgium/epidemiology , Female , Follow-Up Studies , Humans , Incidence , Male , Middle Aged , Neoplasms, Radiation-Induced/surgery , Patient Discharge/statistics & numerical data , Thyroid Neoplasms/surgery , Time Factors
2.
Food Chem Toxicol ; 46(2): 527-36, 2008 Feb.
Article in English | MEDLINE | ID: mdl-17936466

ABSTRACT

We investigated whether inhaling peak concentrations of aldehydes several times daily is more damaging than semi-continuously inhaling low-dose aldehydes. We exposed Xpa-/-p53+/- knock-out mice either intermittently or semi-continuously to mixed acetaldehyde, formaldehyde, and acrolein. The intermittent regimen entailed exposure to the aldehydes 7 min every 45 min, 12 times/day, 5 days/week, corresponding to concentrations inhaled by smokers. Semi-continuously exposed animals received half the dose of aldehydes in 8h/day, 5 days/week. Some mice in each group were sacrificed after 13 weeks of exposure; the rest breathed clean air until the end of 1 year. Mice injected intratracheally with benzo[a]pyrene formed a positive control group. The nasal cavity, lungs, and any macroscopically abnormal organs of all mice were analysed histopathologically. After 13 weeks of exposure, the subacute, overall, histopathological changes induced by the inhalation differed noticeably between the intermittently and semi-continuously treated Xpa-/-p53+/- knock-out mice. After 13 weeks of mixed aldehyde exposure, atrophy of the olfactory epithelium generally appeared, but disappeared after 1 year (adaptation and/or recovery). Respiratory epithelial metaplasia of the olfactory epithelium occurred at a higher incidence at 1 year. Except for a significantly greater number of tumours observed in knock-out mice compared to wild mice (semi-continuous aldehyde exposure and controls), no differences between the semi-continuous and intermittent exposure groups were observed.


Subject(s)
Acetaldehyde/toxicity , Acrolein/toxicity , Disinfectants/toxicity , Formaldehyde/toxicity , Lung/drug effects , Olfactory Mucosa/drug effects , Smoke/adverse effects , Acetaldehyde/administration & dosage , Acetaldehyde/analysis , Acrolein/administration & dosage , Acrolein/analysis , Administration, Inhalation , Animals , Atmosphere Exposure Chambers , Disinfectants/administration & dosage , Disinfectants/analysis , Female , Formaldehyde/administration & dosage , Formaldehyde/analysis , Humans , Lung/pathology , Male , Metaplasia/chemically induced , Mice , Mice, Knockout , Olfactory Mucosa/pathology , Smoke/analysis , Species Specificity
3.
J Toxicol Environ Health A ; 70(3-4): 284-94, 2007 Feb 01.
Article in English | MEDLINE | ID: mdl-17365591

ABSTRACT

Little is known about antioxidant status, selenium status in particular, and lung response to NO2, which acts as a proinflammatory air pollutant. The effects of a low selenium diet (1.3 microg Se/d) with or without selenium supplementation were therefore studied in 128 Wistar rats, 2 mo old, male exposed to either acute (50 ppm, 30 min), intermittent subacute (5 ppm, 6 h/d, 5 d), intermittent long-term NO2 (1 ppm, 10 ppm, 6 h/d, 5 d/wk, 28 d), or normal atmospheric air (controls). Following sacrifice, measurements of lipid peroxidation (thiobarbituric acid-reactive substances, chemiluminescence), antioxidative protective enzymes (glutathione peroxidase [GPx], superoxide dismutase [SOD], glutathione S-transferase [GST], ceruloplasmin), lung damage (lactate dehydrogenase, alkaline and acid phosphatases), lung permeability (total protein, albumin), and inflammation (cell populations), along with the determination of new biomarkers such as CC16 (Clara-cell protein), were performed in serum and bronchoalveolar lavage fluid (BALF). While selenium-supplemented animals had increased GPx activity in serum prior to inhalation experiments, they also had decreased BALF CC16, blood SOD, and GST levels. Nevertheless, the protective role of normal selenium status with respect to NO2 lung toxicity was evident both for long-term and acute exposures, as the increase in BALF total proteins and corresponding decrease in serum (indicating increased lung permeability) was significantly more pronounced in selenium-deficient animals. During the various inhalation experiments, serum CC16 demonstrated its key role as an early marker of increased lung permeability. These findings corroborate the important role of selenium status in NO2 oxidative damage modulation, but also indicate, in view of its negative impact on CC16, a natural anti-inflammatory and immunosuppressor, that caution should be used prior to advocating selenium supplementation.


Subject(s)
Antioxidants/metabolism , Lung/drug effects , Nitrogen Dioxide/adverse effects , Permeability/drug effects , Selenium/pharmacology , Acid Phosphatase/metabolism , Air Pollutants/adverse effects , Alkaline Phosphatase/metabolism , Animals , Biomarkers/analysis , Biomarkers/blood , Bronchoalveolar Lavage Fluid/chemistry , Dietary Supplements , Dose-Response Relationship, Drug , Inhalation Exposure , L-Lactate Dehydrogenase/metabolism , Male , Rats , Rats, Wistar , Thiobarbituric Acid Reactive Substances/metabolism , Uteroglobin/metabolism
4.
Eur J Intern Med ; 14(5): 321-325, 2003 Aug.
Article in English | MEDLINE | ID: mdl-13678758

ABSTRACT

BACKGROUND: Thyroid nodules in patients with Graves' disease (GD) are common, and the incidence of coexisting thyroid carcinoma is a much debated subject, which is addressed in this study. METHODS: In order to determine the incidence rate of coexisting malignancy, a retrospective study was conducted on 103 patients who underwent surgery for GD between 1990 and 2000 at the Cliniques Universitaires Saint-Luc in Brussels, Belgium. The patients were classified into groups. Those in group I had a solitary palpable nodule (4.9%), those in group II multiple palpable nodules (12.6%), group IIIa had nodule(s) revealed by imaging techniques (incidentalomas: 17.5%), and group IIIb had diffuse non-nodular goiter (65%). RESULTS: Patients with nodules (groups I, II, and IIIa) were found to have significantly more thyroid carcinomas than those with diffuse non-nodular goiters (P=0.02), and the rate of malignancy was significantly increased when the nodules were palpable (groups I and II; P=0.03). Eight patients (7.8%) were diagnosed as having coexisting carcinomas, all but one being microcarcinomas. CONCLUSIONS: Well-differentiated papillary carcinomas are found to coexist with GD surgically treated (7.8%) and occur most frequently in GD with palpable nodular lesions (35%). Even though the majority (88%) of coexisting carcinomas are microcarcinomas, the presence of palpable nodules justifies further evaluation and follow-up.

5.
Biomarkers ; 7(1): 49-57, 2002.
Article in English | MEDLINE | ID: mdl-12101784

ABSTRACT

Current evidence suggests that the neurotoxic effects of lead may partially be mediated through interference with the dopaminergic system. The aim of this study was to assess the levels of two peripheral dopaminergic markers--serum prolactin (Pro-S) and urinary homovanillic acid (HVA-U)--in children living around two lead smelters, who are presumed to be exposed to high environmental lead pollution (n = 200), and compare their results with 200 age- and sex-matched controls living in an area unpolluted by heavy metals, giving a total of 400 children (200 boys and 200 girls). The influence of lead exposure on HVA-U and Pro-S was assessed by stepwise multiple regression, testing lead concentrations in blood (Pb-B), age, sex and area of residence as predictors. Though lead levels were significantly higher in boys and in the lead-polluted environment, mean Pb-B values were relatively low, indicating a low uptake of lead in the contaminated environment (39.5 micrograms l-1, range 4.6-165 micrograms l-1, n = 200), and no significant correlation could be found with either Pro-S or HVA-U. However, when the subgroup of 121 children with Pb-B levels above 50 micrograms l-1 were considered, a weak positive correlation was found between Pb-B and HVA-U (r2 = 0.04, p = 0.03), whilst in the even smaller subgroup of 15 children with Pb-B levels above 100 micrograms l-1, Pro-S appeared to be positively correlated with Pb-B, though the numbers of children were too small for the correlation to reach statistical significance (p = 0.095). These weak associations, probably not important in biological terms, indicate that Pro-S and HVA-U are not useful biomarkers at present exposure levels to lead in the environment. Nevertheless, the finding of subtle biochemical alterations in the dopaminergic system at Pb-B levels of around 100 micrograms l-1 supports the recommended setting of the action level at this value.


Subject(s)
Environmental Monitoring/methods , Homovanillic Acid/urine , Lead/toxicity , Prolactin/blood , Biomarkers , Child , Environmental Exposure , Female , Humans , Lead/blood
6.
J Pathol ; 145(2): 177-83, 1985 Feb.
Article in English | MEDLINE | ID: mdl-3973770

ABSTRACT

It has been suggested that macrophages in atherosclerotic plaques oxidize the lipid they contain, leading to necrosis in the plaque. Over 200 human aortic and coronary atherosclerotic plaques from 102 human necropsy subjects aged between 5 and 88 were, therefore, examined histologically for the presence of insoluble lipid (ceroid), thought to be a product of lipid oxidation. Ceroid was present in all the plaques but not in areas of diffuse intimal thickening. In early lesions the insoluble lipid was within membrane-bound vesicles in macrophage-like cells, many showing characteristic ring structures suggesting that membrane-associated oxidative systems might be responsible for rendering the lipid insoluble. Staining was increased by an oxidizing agent and abolished by a reducing agent. It is suggested that this distribution supports the concept of lipid oxidation by macrophages within the plaque.


Subject(s)
Arteriosclerosis/metabolism , Ceroid/metabolism , Pigments, Biological/metabolism , Adolescent , Adult , Aged , Arteriosclerosis/pathology , Child , Child, Preschool , Female , Humans , Macrophages/metabolism , Male , Microscopy, Electron , Middle Aged , Pinocytosis
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