Worker exposure to ultrafine particles during carbon black treatment
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
MetadataShow full item record
Other TitlesEKSPOZYCJA NA CZĄSTKI ULTRADROBNE U PRACOWNIKÓW ZATRUDNIONYCH PRZY OBRÓBCE SADZY TECHNICZNEJ
AbstractWstęp: Celem badania była ocena uwalniania do powietrza stanowisk pracy cząstek ultradrobnych podczas przesypu i pakowania sadzy technicznej. Materiał i metody: Ocena obejmowała wyniki pomiarów przeprowadzonych w zakładzie przesypu sadzy technicznej przed rozpoczęciem procesu przesypu, w czasie wykonywania i po zakończeniu procesu. Określono stężenie liczbowe cząstek o wymiarach z zakresu 10–1000 nm i 10–100 nm z wykorzystaniem kondensacyjnego licznika cząstek (condensation particle counter – CPC). Do oceny stężenia masowego cząstek użyto monitora stężenia aerozolu w powietrzu DustTrak II DRX aerosol concentration monitor. Oszacowano także stężenie powierzchniowe cząstek potencjalnie odkładających się w rejonie pęcherzykowym (alveolar – A) i tchawiczo-oskrzelowym (tracheo-bronchial – TB) człowieka, korzystając z monitora nanocząstek AeroTrak 9000. Wyniki: Średnie stężenie masowe cząstek podczas procesu było 6-krotnie wyższe w porównaniu z wartością przed jego rozpoczęciem. Zaobserwowano 3-krotny wzrost średniego stężenia liczbowego cząstek 10–1000 nm i cząstek 10–100 nm podczas wykonywania ww. czynności. Stężenie powierzchniowe cząstek potencjalnie zdeponowanych w rejonie pęcherzykowym (A) i w rejonie tchawiczo-oskrzelowym (TB) wzrosło 4-krotnie. Wnioski: Podczas przesypywania i pakowania sadzy odnotowano istotnie wyższe wartości każdego z analizowanych parametrów charakteryzujących narażenie na cząstki ultradrobne. The aim of the project was to assess the exposure of workers to ultrafine particles released during handling and packing of carbon black. The assessment included the results of the measurements performed in a carbon black handling plant before, during, and after work shift. Material and Methods: The number concentration of particles within the dimension range 10–1000 nm and 10–100 nm was assayed by a condensation particle counter (CPC). The mass concentration of particles was determined by a DustTrak II DRX aerosol concentration monitor. The surface area concentration of the particles potentially deposited in the alveolar (A) and tracheo-bronchial (TB) regions was estimated by an AeroTrak 9000 nanoparticle monitor. Results: An average mass concentration of particles during the process was 6-fold higher than that before its start, while a 3-fold increase in the average number concentration of particles within the dimension range 10–1000 nm and 10–100 nm was observed during the process. At the same time a 4-fold increase was found in the surface area concentration of the particles potentially deposited in the A and TB regions. Conclusions: During the process of carbon black handling and packing a significantly higher values of each of the analysed parameters, characterizing the exposure to ultrafine particles, were noted.
CitationMedycyna Pracy 2015;66(3):317–326
Sponsorsresearch project 5052/B/PO1/2010/38; research project 7PR/236215/2011 MARINA Managing Risks of NanoMATERIALS; IMP.3.8/2013
The following license files are associated with this item:
Showing items related by title, author, creator and subject.
Effects of nitrated-polycyclic aromatic hydrocarbons and diesel exhaust particle extracts on cell signalling related to apoptosis: possible implications for their mutagenic and carcinogenic effects.Landvik, Nina E.; Gorria, Morgane; Arlt, Volker M.; Asare, Nana; Solhaug, Anita; Lagadic-Gossmann, Dominique; Holme, Jorn A. (2007-03-07)Nitrated-polycyclic aromatic hydrocarbons (nitro-PAHs) and diesel exhaust particle extracts (DEPE) induced apoptosis in Hepa1c1c7 cells with the following potency: 1,3-dinitropyrene (1,3-DNP)>1-nitropyrene (1-NP) >> DEPE >> 1,8-dinitropyrene (1,8-DNP). The compounds induced cyp1a1, and activated various intracellular signalling pathways related to apoptosis. The CYP inhibitor alpha-naphthoflavone strongly reduced 1,3-DNP-induced cell death, whereas cell death induced by 1-NP was rather increased. Toxic 1,3-DNP and 1-NP were found to induce a concentration-dependent lipid peroxidation. 1,3-DNP caused pro-apoptotic events, including increased phosphorylation and accumulation of p53 in the nucleus, cleavage of bid and of caspases 8 and 3, down-regulation of bcl-x(L) and phosphorylation of p38 and JNK MAPK. Furthermore, 1,3-DNP increased the activation of survival signals including phosphorylation of Akt and inactivation (phosphorylation) of pro-apoptotic bad. Although less potent, rather similar effects were observed following exposure to DEPE, compared to 1-NP. The most important finding was that the most mutagenic and carcinogenic compound tested, 1,8-DNP, induced little (if any) cell death, despite the fact that this compound seemed to give the most DNA damage as judged by DNA adduct formation, increased phosphorylation of p53 and accumulation of cells in S-phase. Immunocytochemical studies revealed that the p53 protein did not accumulate into the nucleus suggesting that 1,8-DNP inactivated the pro-apoptotic function of the p53 protein by a non-mutagenic event. These results suggest that after exposure to 1,8-DNP more cells may survive with DNA damage, thereby increasing its mutagenic and carcinogenic potential.
Surface characteristics, copper release, and toxicity of nano- and micrometer-sized copper and copper(II) oxide particles: a cross-disciplinary study.Midander, Klara; Cronholm, Pontus; Karlsson, Hanna L.; Elihn, Karine; Moller, Lennart; Leygraf, Christofer; Wallinder, Inger Odnevall (2009-03)An interdisciplinary and multianalytical research effort is undertaken to assess the toxic aspects of thoroughly characterized nano- and micrometer-sized particles of oxidized metallic copper and copper(II) oxide in contact with cultivated lung cells, as well as copper release in relevant media. All particles, except micrometer-sized Cu, release more copper in serum-containing cell medium (supplemented Dulbecco's minimal essential medium) compared to identical exposures in phosphate-buffered saline. Sonication of particles for dispersion prior to exposure has a large effect on the initial copper release from Cu nanoparticles. A clear size-dependent effect is observed from both a copper release and a toxicity perspective. In agreement with greater released amounts of copper per quantity of particles from the nanometer-sized particles compared to the micrometer-sized particles, the nanometer particles cause a higher degree of DNA damage (single-strand breaks) and cause a significantly higher percentage of cell death compared to cytotoxicity induced by micrometer-sized particles. Cytotoxic effects related to the released copper fraction are found to be significantly lower than the effects related to particles. No DNA damage is induced by the released copper fraction.
Exposure to ultrafine particles from ambient air and oxidative stress-induced DNA damage.Brauner, Elvira Vaclavik; Forchhammer, Lykke; Moller, Peter; Simonsen, Jacob; Glasius, Marianne; Wahlin, Peter; Raaschou-Nielsen, Ole; Loft, Steffen (2007-08)BACKGROUND: Particulate matter, especially ultrafine particles (UFPs), may cause health effects through generation of oxidative stress, with resulting damage to DNA and other macromolecules. OBJECTIVE: We investigated oxidative damage to DNA and related repair capacity in peripheral blood mononuclear cells (PBMCs) during controlled exposure to urban air particles with assignment of number concentration (NC) to four size modes with average diameters of 12, 23, 57, and 212 nm. DESIGN: Twenty-nine healthy adults participated in a randomized, two-factor cross-over study with or without biking exercise for 180 min and with exposure to particles (NC 6169-15362/cm(3)) or filtered air (NC 91-542/cm(3)) for 24 hr. METHODS: The levels of DNA strand breaks (SBs), oxidized purines as formamidopyrimidine DNA glycolase (FPG) sites, and activity of 7,8-dihydro-8-oxoguanine-DNA glycosylase (OGG1) in PBMCs were measured by the Comet assay. mRNA levels of OGG1, nucleoside diphosphate linked moiety X-type motif 1 (NUDT1), and heme oxygenase-1 (HO1) were determined by real-time reverse transcriptase-polymerase chain reaction. RESULTS: Exposure to UFPs for 6 and 24 hr significantly increased the levels of SBs and FPG sites, with a further insignificant increase after physical exercise. The OGG1 activity and expression of OGG1, NUDT1, and HO1 were unaltered. There was a significant dose-response relationship between NC and DNA damage, with the 57-nm mode as the major contributor to effects. Concomitant exposure to ozone, nitrogen oxides, and carbon monoxide had no influence. CONCLUSION: Our results indicate that UFPs, especially the 57-nm soot fraction from vehicle emissions, causes systemic oxidative stress with damage to DNA and no apparent compensatory up-regulation of DNA repair within 24 hr.