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Biomedical subjects

B Nemery

Publications and source records attributed to B Nemery.

At least 37 records · Page 2Linked to original sources
PubMed2002

The Coca-Cola incident in Belgium, June 1999.

The present paper describes the outbreak of health complaints that occurred in Belgium, in June 1999, among schoolchildren and members of the general public in relation to the consumption of Coca-Cola and other soft drinks. The outbreak took place in the wake of a major food crisis, caused by PCB/dioxin contamination of animal feed, that had erupted shortly before. The clinical features (absence of serious poisoning) and epidemiological characteristics of the Coca-Cola outbreak pointed to mass sociogenic illness, and no subsequent toxicological or other data have refuted this hypothesis.

Abdominal Pain↗
PubMed2002

Increased HLA-DR expression after exposure of human monocytic cells to air particulates.

BACKGROUND: The expression of HLA-DR on the cell membrane of antigen-presenting cells is of major importance for the induction of an allergic response in the airways. Environmental particulates are thought to play an important role in inducing or enhancing allergic sensitization, possibly by increasing the expression of HLA-DR on the cell membrane of antigen-presenting cells. In addition, these particulates may synergize with common sensitizing agents in inducing or enhancing HLA-DR and thus antigen presentation. OBJECTIVE: In this study, we investigated the potential of three particle types, namely carbon black, diesel exhaust particles and urban air particulates (0.1-1000 ng/cm(2)), to induce the expression of HLA-DR on differentiated THP-1 cells, taken as a model for alveolar macrophages. We also assessed the "adjuvant" potential of the particles on interferon (IFN)-gamma, a known enhancer of HLA-DR. RESULTS: By themselves, the particles (0.1-1000 ng/cm(2)) were not able to induce HLA-DR on the THP-1 cells after an incubation of 48 h. However, even at very low concentrations, carbon black (from 1 ng/cm(2) on) and diesel exhaust particles (from 0.1 ng/cm(2) on), interacted with IFN-gamma (100 U/mL) to enhance HLA-DR expression (up to 2.5-fold increase). CONCLUSION: This finding may reflect in vitro one of the mechanisms by which pollutant particles exert an "adjuvant" activity and may partially explain how exposure to particles can be related to the enhancement of allergic sensitization.

Air Pollution↗
PubMed2002

Asthma prevalence in children living in villages, cities and refugee camps in Palestine.

Previous studies have suggested that asthma prevalence is generally lower in the Middle East than in more developed countries. The aim of this study was to investigate the prevalence and severity of asthma and asthma symptoms in schoolchildren in the Ramallah District in Palestine. In the autumn of 2000, 3,382 schoolchildren aged 6-12 yrs were surveyed in 12 schools, using the International Study for Asthma and Allergies in Childhood (ISAAC)-phase III, parents-administered translated questionnaire. The crude prevalence rates for "wheezing-ever", "wheezing in the previous 12 months", and "physician-diagnosed asthma" were 17.1, 8.8 and 9.4% respectively, with urban areas having higher prevalence rates than rural areas. Within urban areas, refugee camps had higher prevalence rates than cities. Yet, within the rural areas, the 12-month prevalence was lower in the deprived villages than other residences. Place of residence remained significant for asthma and asthma symptoms, after adjusting for sex, age, and place of birth. To conclude, children from refugee camps appear to be at higher risk of asthma than children from neighbouring villages or cities. The prevalence of asthma and asthma symptoms in Palestine appears to be close to that of Jordan, but it is much lower than Israel, and lower than some other countries in the region, such as Kuwait and Saudi Arabia, and more developed countries. This initial study is a baseline for a study on lifestyle and environmental determinants for asthma among Palestinian children.

Adolescent↗
PubMed2001

Passage of intratracheally instilled ultrafine particles from the lung into the systemic circulation in hamster.

The mechanisms of particulate pollution-related cardiovascular morbidity and mortality are not well understood. We studied the passage of radioactively labeled ultrafine particles after their intratracheal instillation. Hamsters received a single intratracheal instillation of 100 microg albumin nanocolloid particles (nominal diameter < or = 80 nm) labeled with 100 microCi technetium-99m and were killed after 5, 15, 30, and 60 min. In blood, radioactivity, expressed as percentage of total body radioactivity per gram blood, amounted to 2.88 +/- 0.80%, 1.30 +/- 0.17%, 1.52 +/- 0.46%, and 0.21 +/- 0.06% at 5, 15, 30, and 60 min, respectively. Thin-layer chromatography showed only one peak of radioactivity corresponding to unaltered (99m)Tc-albumin nanocolloid. In the liver, radioactivity, expressed as percentage of total radioactivity per organ, amounted to 0.10 +/- 0.07%, 0.23 +/- 0.06%, 1.24 +/- 0.27%, and 0.06 +/- 0.02% at 5, 15, 30, and 60 min, respectively. Lower values were observed in the heart, spleen, kidneys, and brain. Dose dependence was assessed at 30 min following instillation of 10 microg and 1 microg (99m)Tc-albumin per animal (n = 3 at each dose), and values of the same relative magnitudes as after instillation of 100 microg were obtained. We conclude that a significant fraction of (99m)Tc-albumin, taken as a model of ultrafine particles, rapidly diffuses from the lungs into the systemic circulation.

Air Pollutants↗
PubMed2001

Polyanions protect against the in vitro pulmonary toxicity of polycationic paint components associated with the Ardystil syndrome.

The polycationic paint components of the Acramin F system have led to severe pulmonary disease in textile printing sprayers in Spain and Algeria (Ardystil syndrome). In order to elucidate the underlying mechanisms of the toxicity of these nitrogen-containing polymeric paint components, Acramin FWR (FWR), Acramin FWN (FWN), and Acrafix FHN (FHN), we have studied the effect of coincubation with polyanionic compounds, Sulodexide (heparin-like substance), DNA and poly-l-glutamic acid (of different lengths) in different pulmonary cell types. This study shows that the cytotoxicity of the three polycationic paint components FWR (a polyurea), FWN (a polyamide-amine), and FHN (a polyamine) is markedly decreased in the presence of the polyanions. It is concluded that the paint components FWR, FWN, and FHN execute their cytotoxicity at least partly by the abundant positive charges these molecules carry at physiological pH.

Adipates↗
PubMed2001

Genotoxic effects of carbon black particles, diesel exhaust particles, and urban air particulates and their extracts on a human alveolar epithelial cell line (A549) and a human monocytic cell line (THP-1).

The possible genotoxicity of small particulate matter has been under investigation for the last 10 years. Diesel exhaust particles (DEP) are considered as "probably carcinogenic" (IARC group 2A) and a number of studies show genotoxic effects of urban particulate matter (UPM). Carbon black (CB) is carcinogenic in rats. In this study the cytotoxic and genotoxic potency of these three particle types was investigated by exposing human cells (A549 and THP-1 cell lines) in vitro to CB, DEP (SRM 1650, NIST), and UPM (SRM 1648, NIST) for 48 hr. Cytotoxicity was assessed using the Alamar Blue assay, whereas genotoxicity was assessed using the single-cell gel electrophoresis (comet assay). The particles were characterized with regard to their mean diameter in tissue culture medium (CB 100 nm, DEP 400 nm, UPM 2 microm), their total carbon content (CB 99%, DEP 85%, UPM 15%), and their acid-soluble metal composition (UPM >> CB approximately DEP). The concentrations ranged from 16 ng/ml to 16 microg/ml for cytotoxicity tests and from 16 ng/ml to 1.6 microg/ml for genotoxicity tests. In both assays, paraquat was used as a reference chemical. The CB, DEP, and UPM particles showed no significant cytotoxicity. However, all three particles were able to cause significant DNA damage, although to a different extent in the two cell lines. The genotoxicity of washed particles and dichloromethane extracts was also investigated. In THP-1 cells CB washed particles and DEP extracts caused significant DNA damage. This difference in effect may be related to differences in size, structure, and composition of the particles. These results suggest that CB, DEP, and UPM are able to cause DNA damage and, therefore, may contribute to the causation of lung cancer. More detailed studies on influence of size, structure, and composition of the particles are needed.

Air Pollutants↗
PubMed2001

Recurrent flu-like illness with migrating pulmonary infiltrates of unknown aetiology.

Migrating pulmonary infiltrates present a difficult diagnostic and therapeutic challenge. We report on eight patients (mean age 51 years, range 32-78 years, with a prolonged history of migrating pulmonary infiltrates of unknown aetiology despite a very elaborate search for infectious causes, hypersensitivity pneumonitis or inhalation fever due to occupational or domestic exposure to fungi, or to other environmental causes, and for humoral or cellular immunological incompetence. These patients (one male, seven females) presented with recurrent episodes (mean 6, range 2-13) of a flu-like illness, often with cough, wheezing and pleuritic chest pain, but without systemic involvement. Previous medical histories were unremarkable. There was no relation with smoking habits, occupation, drug use or other possible exposures. Biochemical data were non-specific. There was no peripheral nor pulmonary eosinophilia; total IgE was normal, with negative RASTs and precipitins to a variety of antigens. Cultures and serological tests for bacteria, viruses, fungi, etc were non-contributory. Chest X-ray and computed tomography (CT) scan showed bilateral migratory pulmonary infiltrates, with a predilection for the middle and lower lung zones, often with a minor-to-moderate pleural effusion. Lung function tests were usually normal; at the most a slight decrease in diffusing capacity was noted in some patients. There was no or only a slight response to antimicrobials; systemic corticosteroids were not given. Further evolution was benign with patients being asymptomatic between the episodes. Despite elaborate investigations, the cause of these 'pneumonias' remains frustratingly unknown.

Adult↗
PubMed2001

Giant cell interstitial pneumonia (hard metal lung disease, cobalt lung).

Hard metal lung disease is a rare form of occupational lung disease that can occur in workers engaged in the manufacture, utilization, or maintenance of tools composed of hard metal [a material composed mainly of tungsten carbide (WC) and cobalt] or diamond-cobalt. Clinically, the condition resembles hypersensitivity pneumonitis, with subacute presentations and possible evolution to pulmonary fibrosis. However, this interstitial lung disease is uniquely characterized by the presence of bizarre ;;cannibalistic'' multinucleated giant cells in the alveoli and the bronchoalveolar lavage. A pathological diagnosis of giant cell interstitial pneumonitis (GIP) is, therefore, specific for hard metal lung disease, even though not all affected subjects exhibit this pathognomonic feature. Cobalt is the critical toxic component causing hard metal lung disease, hence also the term cobalt-lung. Hard metal lung disease is more likely to occur in poorly regulated workplaces, but its occurrence depends mainly on individual susceptibility, rather than on cumulative exposure, so that even young subjects may be affected.

Journal Article↗
PubMed2001

Acquiring symptoms in response to odors: a learning perspective on multiple chemical sensitivity.

In this chapter, a learning account is discussed as a potential explanation for the symptoms in multiple chemical sensitivity. Clinical evidence is scarce and anecdotal. A laboratory model provides more convincing results. After a few breathing trials containing CO2-enriched air as an unconditioned stimulus in a compound with harmless odor substances as conditioned stimuli, subjective symptoms are elicited and respiratory behavior is altered by the odors only. Also, mental images can become conditioned stimuli to trigger subjective symptoms. The learning effects cannot be explained by a response bias or by conditioned arousal, and they appear to involve basic associative processes that do not overlap with aware cognition of the relationship between the odors and the CO2 inhalation. Learned symptoms generalize to new odors and they can be eliminated in a Pavlovian extinction procedure. In accordance with clinical findings, neurotic subjects and psychiatric cases are more vulnerable to learning subjective symptoms in response to odors. Consistent with a learning account, cognitive-behavioral treatment techniques appear to produce beneficial results in clinical cases. Several criticisms and unresolved questions regarding the potential role of learning mechanisms are discussed.

Administration, Inhalation↗
PubMed2001

What happens to the manuscripts that have not been accepted for publication in Occupational and Environmental Medicine?

OBJECTIVES: To evaluate the fate of manuscripts rejected by Occupational and Environmental Medicine (OEM). METHODS: A Medline search was conducted, up to March 2001, to find out whether and where articles submitted to OEM in 1995, 1996, and 1997, but not accepted for publication, were published. The articles were matched by authors and title, sometimes using the abstract to help decide whether the published article was the one that had been previously submitted to OEM. RESULTS: Out of 405 manuscripts rejected (44% of those submitted), 218 articles (54%) were traced in 72 different journals, with more than half being published in seven other major journals dealing with occupational and environmental health (rather than in specialty journals). Most papers were published within 2 years of their initial submission to OEM. Only a small proportion (10%) were published in a journal with a higher impact factor than OEM (1.96 in 1999). CONCLUSION: More than half the articles rejected by OEM found their way into the scientific literature covered by Medline. This figure is comparable with the few available data from other journals. It would be interesting to know the fate of articles published by OEM before they were submitted to our journal.

Bibliometrics↗
PubMed2001

Surface of localized pleural plaques quantitated by computed tomography scanning: no relation with cumulative asbestos exposure and no effect on lung function.

To evaluate if there is a relation between the size of asbestos plaques and the level of past exposure and pulmonary function, we measured the surface of localized pleural plaques found on high-resolution (HR) CT scan, using a computerized video display unit-imaging system, in 73 workers (mean age, 43.5 yr) who had worked from 23 to 27 yr in an asbestos-cement factory. Their estimated cumulative exposure to asbestos ranged from 16.4 to 98.7 fiber-years/ ml (mean, 26.3 fiber-years/ml). Lung function measurements included lung volumes, maximal expiratory flows, and diffusing capacity. A control group of 21 workers was examined by the same procedures. Plaques were detected by CT in 51 (70%) asbestos-exposed subjects and in none of the control subjects. The average calculated plaque surface was 47.9 +/- 61.7 cm2 (median, 22.1 cm2; range, 0 to 278.4 cm2). There was no relation between plaque surface and cumulative asbestos exposure (p = 0.24). In the 51 subjects with pleural plaques, the surface of the pleural lesions was not related to cumulative asbestos exposure, or to smoking history or time since first exposure. Neither the presence nor the extent of the plaques was correlated with lung function parameters.

Asbestosis↗
PubMed2001

Observer variation in computed tomography of pleural lesions in subjects exposed to indoor asbestos.

To assess the reliability of computed tomography (CT) in detecting discrete pleural lesions, the interobserver and intra-observer variability in reading the conventional and high-resolution CT (HRCT) scans of 100 volunteers, who had worked for > or = 10 yrs in a building with known asbestos contamination, was evaluated. In the first session, pleural abnormalities were detected by a single radiologist (A1) in 13 subjects. In the second session, the scans were read again independently by the same radiologist (A2) and two other experienced radiologists (B, C). The final decision for the presence of pleural lesions was made in a final consensus reading. This gave a diagnosis of pleural abnormalities in 18 subjects, of whom eight (44%) had been detected by all three readers, five (28%) by two readers and four (22%) by only one reader; one scan, rated normal by all readers during the second session, was reconsidered because pleural abnormalities had been noted at the first reading (A1). The intra-observer agreement for reader A was good (kappa (kappa) 0.68) but the interobserver agreement between the readers was only fair to moderate (weighted kappa: A2-B=0.43, A2-C = 0.45, B-C = 0.26) in the second reading session. In conclusion, when looking for the prevalence of pleural lesions in indoor asbestos exposed subjects, the potential lack of consistency in reporting the presence of small pleural abnormalities must be borne in mind and strict precautions must be taken.

Adult↗
PubMed2001

Xenobiotic-metabolizing enzyme activities in primary cultures of rat type II pneumocytes and alveolar macrophages.

Because of the evidence for the involvement of xenobiotic bioactivation in pulmonary toxicity and carcinogenesis, it is important to improve our understanding of the xenobiotic-metabolizing enzymes in isolated and cultured specific pulmonary cell populations. Some phase I and phase II xenobiotic-metabolizing enzyme activities, reduced glutathione (GSH), and gamma-glutamyl transferase (gamma-GT) were studied in rat type II pneumocytes and alveolar macrophages cultured for up to 48 h and 3 h, respectively. In type II pneumocytes, 7-ethoxyresorufin activity was not detected. 7-Benzyloxyresorufin (BROD) and 7-pentoxyresorufin (PROD) O-dealkylation decreased at 24 h by 84 and 82%, respectively, and continued to decline over the next 24 h with no measurable PROD at 48 h. The activity of NADPH- and NADH-cytochrome c reductase at 48 h decreased by 31 and 67%, respectively. GST activity decreased by 25 and 42% at 24 and 48 h, respectively. A transient increase in DT-diaphorase activity was observed at 24 h (by 55%). GSH content and gamma-GT activity increased significantly with time in culture. In freshly isolated alveolar macrophages, BROD activity was the only cytochrome P450-dependent alkoxyresorufin-O-dealkylase activity measured. BROD activity decreased by 38% in 3-h-attached macrophages. There were no changes in NADPH- and NADH-cytochrome c reductase, GST, and DT-diaphorase. An increase of GSH (by 24%) was observed in attached macrophages. In conclusion, type II pneumocytes and to a lesser extent alveolar macrophages in primary cultures undergo changes in biotransformation-related enzyme activities and intracellular GSH level that may affect xenobiotic toxicity at different times in culture.

Animals↗