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Konrad Rydzynski

Publications and source records attributed to Konrad Rydzynski.

5 recordsLinked to original sources

Relation between sources of particulate air pollution and biological effect parameters in samples from four European cities: an exploratory study.

Given that there are widely different prevalence rates of respiratory allergies and asthma between the countries of Europe and that exposure to ambient particulate matter (PM) is substantial in urban environments throughout Europe, an EU project entitled "Respiratory Allergy and Inflammation Due to Ambient Particles" (RAIAP) was set up. The project focused on the role of physical and chemical composition of PM on release of cytokines of cells in vitro, on respiratory inflammation in vivo, and on adjuvant potency in allergy animal models. Coarse (2.5-10 microm) and fine (0.15-2.5 microm) particles were collected during the spring, summer and winter in Rome (I), Oslo (N), Lodz (PL), and Amsterdam (NL). Markers within the same model were often well correlated. Markers of inflammation in the in vitro and in vivo models also showed a high degree of correlation. In contrast, correlation between parameters in the different allergy models and between allergy and inflammation markers was generally poor. This suggests that various bioassays are needed to assess the potential hazard of PM. The present study also showed that by clustering chemical constituents of PM based on the overall response pattern in the bioassays, five distinct groups could be identified. The clusters of traffic, industrial combustion and/or incinerators (TICI), and combustion of black and brown coal/wood smoke (BBCW) were associated primarily with adjuvant activity for respiratory allergy, whereas clusters of crustal of material (CM) and sea spray (SS) are predominantly associated with measures for inflammation and acute toxicity. The cluster of secondary inorganic aerosol and long-range transport aerosol (SIALT) was exclusive associated with systemic allergy. The present study has shown that biological effect of PM can be linked to one or more PM emission sources and that this linkage requires a wide range of bioassays.

Air Pollutants↗

DNA damage in leukocytes of workers occupationally exposed to arsenic in copper smelters.

Inorganic arsenic (i-As) is a known human carcinogen; however, humans continue to be exposed to i-As in drinking water and in certain occupational settings. In this study, we used the Comet assay to evaluate DNA damage in the somatic cells of workers from three Polish copper smelters who were occupationally exposed to i-As. Blood samples were collected from 72 male workers and 83 unexposed male controls and used for the detection of DNA damage, oxidative DNA damage, and DNA damage after a 3-hr incubation in culture. Urine samples were collected to assess the level of exposure. The mean concentration of arsenic metabolites in urine [the sum of arsenite (AsIII), arsenate (AsV), monomethylarsenate (MMA) and dimethylarsenate (DMA)] and the concentrations of DMA (the main metabolite in urine) were higher in workers than in controls, but the differences were not statistically significant. By contrast, the level of DNA damage, expressed as the median tail moment, was significantly higher in the leukocytes of workers than in the controls. Comet assays conducted with formamidopyrimidine glycosylase (FPG) digestion to detect oxidative DNA damage indicated that oxidative lesions were present in leukocytes from both the exposed and control groups, but the levels of damage were significantly higher among the workers. Incubation of the cells in culture resulted in a significant reduction in the levels of DNA damage, especially among leukocytes from the workers, suggesting that the DNA damage was subject to repair. Our findings indicate that copper smelter workers have increased levels of DNA damage in somatic cells, suggesting a potential health risk for the workers. Although i-As was present in air samples from the smelters and in urine samples from workers, no clear association could be made between i-As exposure and the DNA damage.

Adult↗

Glutaraldehyde-induced occupational asthma: BALF components and BALF and serum Clara cell protein (CC16) changes due to specific inhalatory provocation test.

OBJECTIVES: The purpose of this study was to evaluate bronchoalveolar lavage fluid (BALF) components and Clara cell protein (CC16) concentration in serum and BALF in patients with glutaraldehyde (GA)-induced asthma, before and after a specific inhalatory provocation test (SIPT) with GA, in comparison to atopic asthmatics and healthy individuals. METHODS: Spirometry and bronchoalveolar lavage were performed before and after SIPT. The serum and BALF concentrations of CC16 and cytogram content in BALF were evaluated. RESULTS: In GA-sensitized asthmatics, the level of CC16 in BALF and serum was significantly lower at 24 h after SIPT in comparison with the values recorded prior to the experiment. There was a significant increase in the proportion of eosinophils, basophils and lymphocytes in BALF of GA-sensitized asthmatics obtained after SIPT. CONCLUSIONS: The determination of CC16 either in serum or in BALF is a non-invasive test to detect Clara cell damage.

Adult↗

Neurological and respiratory symptoms in shipyard welders exposed to manganese.

OBJECTIVE: The nervous system is the major target of the toxic effect of manganese (Mn) and its compounds in welding fumes. In humans, inhalation is the most frequent route of Mn access, therefore, the respiratory tract and lungs are usually involved in the process of translocation of inhaled noxius agent by blood to the brain. This study was performed to assess whether it is possible to use neurophysiological tests for the detection of early effects of exposure to low Mn concentrations. It is also known that irritating welding fumes affect distal bronchioles of nonciliated, epithelial Clara cells, which secret anti-inflammatory and immunossupresive Clara cell protein (CC16) into the respiratory tract. The examination of usefulness of CC16 as early pulmonary biomarker for neurophysiological abnormal results of welding fumes exposure was performed. MATERIALS AND METHODS: The study group comprised 59 welders employed at different workposts in a shipyard, matched for age and smoking habits with the control group composed of 23 mechanicians and electricians not exposed to welding fumes. Subjective neurological symptops (CNS), visual evoked potentials (VEP) and electroencephalography (EEG) were examined in welders and the relationships between Mn concentrations in the air, blood and urine as well as between cummulative exposure index (CEI) (Mn mg/m3 x years of exposure) were investigated. Effects of exposure were expressed in the form of biomarkers of the body burden, and CC16 as early pulmonary biomarker in welding exposure was examined by sensitive latex-immunoassay. RESULTS: Abnormal results of VEP and EEG and the lowest CC16 levels were found in the youngest welders exposed to welding fumes. Those changes were related to the highest Mn airborne levels (xg > 0.3 mg/m3) and high blood Mn concentrations (approximately 14.0 microg/dL). The highest values of correlation coefficients were found only in welders characterized by abnormal neurophysiological results, VEP (r = 0.83) and VEP and VEP+EEG (r = 0.82). The multiple linear regression analysis from all analyzed subgroups, indicated that those with only abnormal neurophysiological tests, VEP and EEG, showed the highest values of partial correlation. It also revealed partial correlation cofficiants between Mn in the air, CEI (Mn mg/m3 x years) and CC16, Mn-B and Mn-U in VEP and VEP+EEG groups. It was found that the highest partial correlations were between the magnitude of exposure--Mn mg/m3, CEI and Mn-B concentration (R2 = 0.72, R2 = 0.66) as well as between CC16 pulmonary biomarker effects and Mn-B concentration (R2 = 0.51). CONCLUSIONS: The subclinical effects revealed in neurological endpoints and abnormal results of neurophysiological tests, VEP and EEG, confirmed that those sensitive tests could be used for the detection of early effect of exposure to low manganese concentration. Inhibition of Clara cell protein secretion in younger welders not adapted to the Mn environment suppresses anti-inflammatory effect in the respiratory tract and probably enhances the absorption and thus the incidence of subclinical neurotoxic symptoms related to airborne Mn and Mn-B levels.

Adult↗

Occupational allergy as a challenge to developing countries.

A steady increase in the incidence of allergic diseases can be observed since 1950s. For such atopic diseases as bronchial asthma, pollinosis or atopic dermatitis, a significantly increased morbidity rate in the general population has been found. Strikingly enough, the highest prevalence of asthma and allergy was recorded in highly developed countries. It can thus be assumed that the high rate of asthma may be an attribute of the post-industrial societies. The prevalence of occupational allergies is thought to be in direct proportion to the rate with which allergies occur in the general population. In view of the changing environment and lifestyles in the developing countries, their communities are expected to be faced with similar negative epidemiological effects concerning allergies. To counteract the spreading of negative health effects, the following measures need to be undertaken: 1. Limitation of exposure to strong allergens. 2. Modification of the training curriculum for medical personnel and of health service infrastructure, according to new tasks and challenges. 3. Considering a possibility of introducing a system of surveillance over occupational allergies and asthma, like the Surveillance of Work-related and Occupational Respiratory Disease (SWORD) system implemented in UK. This system ensures effective cooperation between specialists in preventive medicine, occupational hygiene services and research workers dealing with occupational health that enables prompt response to emerging hazards.

Asthma↗