Anne Korpi
University of Eastern Finland
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Featured researches published by Anne Korpi.
Critical Reviews in Toxicology | 2009
Anne Korpi; Jill Järnberg; Anna-Liisa Pasanen
Microbial volatile organic compounds (MVOCs) are a variety of compounds formed in the metabolism of fungi and bacteria. Of more than 200 compounds identified as MVOCs in laboratory experiments, none can be regarded as exclusively of microbial origin or as specific for certain microbial species. Thus, the recognition of microbially contaminated areas by MVOC measurements is not successful with current methods. In this review, the basic physical and chemical properties of 96 typical MVOCs have been summarised. Of these, toxicological and exposure data were gathered for the 15 MVOCs most often analysed and reported in buildings with moisture and microbial damage. The most obvious health effect of MVOC exposure is eye and upper-airway irritation. However, in human experimental exposure studies, symptoms of irritation have appeared at MVOC concentrations several orders of magnitude higher than those measured indoors (single MVOC levels in indoor environments have ranged from a few ng/m3 up to 1 mg/m3). This is also supported by dose-dependent sensory-irritation response, as determined by the American Society for Testing and Materials mouse bioassay. On the other hand, the toxicological database is poor even for the 15 examined MVOCs. There may be more potent compounds and other endpoints not yet evaluated
Archives of Environmental Health | 1999
Anne Korpi; Jukka-Pekka Kasanen; Yves Alarie; Veli-Matti Kosma; Anna-Liisa Pasanen
The authors investigated the ability/potencies of 3 microbial volatile organic compounds and a mixture of 5 microbial volatile organic compounds to cause eye and upper respiratory tract irritation (i.e., sensory irritation), with an animal bioassay. The authors estimated potencies by determining the concentration capable of decreasing the respiratory frequency of mice by 50% (i.e., the RD50 value). The RD50 values for 1-octen-3-ol, 3-octanol, and 3-octanone were 182 mg/m3 (35 ppm), 1359 mg/m3 (256 ppm), and 17586 mg/m3 (3360 ppm), respectively. Recommended indoor air levels calculated from the individual RD50 values for 1-octen-3-ol, 3-octanol, and 3-octanone were 100, 1000, and 13000 microg/m3, respectively-values considerably higher than the reported measured indoor air levels for these compounds. The RD50 value for a mixture of 5 microbial volatile organic compounds was also determined and found to be 3.6 times lower than estimated from the fractional concentrations and the respective RD50s of the individual components. The data support the conclusion that a variety of microbial volatile organic compounds may have some synergistic effects for the sensory irritation response, which constrains the interpretation and application of recommended indoor air levels of individual microbial volatile organic compounds. The results also showed that if a particular component of a mixture was much more potent than the other components, it may dominate the sensory irritation effect. With respect to irritation symptoms reported in moldy houses, the results of this study indicate that the contribution of microbial volatile organic compounds to these symptoms seems less than previously supposed.
Environment International | 1998
Anna-Liisa Pasanen; Anne Korpi; Jukka-Pekka Kasanen; Pertti Pasanen
Abstract The effect of microbial growth in building materials on airborne levels of volatile organic compounds (VOCs) was demonstrated by theoretically calculating indoor air concentrations of selected VOCs for rooms with and without microbial contamination. The recommended indoor air level for individual VOCs was also estimated on the basis of their sensory irritation potency. Furthermore, the irritation potency for the mixtures of certain compounds (microbial volatile metabolites, MVOCs) at airborne concentrations measured in problem buildings was evaluated. The theoretical airborne concentrations of certain compounds, which are generally regarded as MVOCs, were estimated to be only about 1% higher in the biocontaminated rooms than in those with moist sterile materials. In fact, no individual VOCs indicated exclusively microbial contamination, but they could also be emitted even from sterile, moist constructions. Exposure to mixtures of the selected non-reactive VOCs at the theoretical airborne concentrations would not result in sensory irritation in humans, and, thus, microbial growth in constructions should not increase the probability of irritating symptoms considerably. The data on MVOC concentrations measured in some problem buildings also supported this idea. Irritation would be expected when the airborne concentrations of single non-reactive compounds approach a level of hundreds of μg/m3 or mg/m3.
International Biodeterioration & Biodegradation | 1997
Anne Korpi; Anna-Liisa Pasanen; Pertti Pasanen; Pentti Kalliokoski
Microbial growth and production of carbon dioxide (CO2) and microbial volatile organic compounds (MVOC) were investigated in house dust. According to CO2 measurements, the metabolic activity increased after 11 days at 84–86% air relative humidity (RH) and after 3 days at 96–98% RH. Within 25 days, the concentration of fungal spores in house dust increased to about 45-fold at 84–86% RH resulting mainly from the growth of Aspergillus, Eurotium and Penicillium. At 96–98% RH, the proliferations were on average 1370- and 240-fold for fungi and bacteria, respectively. The dominating fungal genera were Aspergillus and Penicillium. The MVOC composition revealed that microbes can utilize, for example, fatty acids and possibly aldehydes as carbon source resulting in the production of MVOC such as methyl ketones and alcohols. The main MVOC produced by microbes in house dust were 2-pentanone, 2-hexanone, 2-heptanone, limonene, 2-methylfuran, formaldehyde, acrolein and nonanal. Also, 3-octanone, 2-ethyl-1-hexanol, 1-octen-3-ol, 3-methyl-1-butanol, 3-methyl-2-butanol, camphene and α-pinene can be considered to derive from microbial metabolism to some extent.
Environment International | 1997
Pertti Pasanen; Anne Korpi; Pentti Kalliokoski; Anna-Liisa Pasanen
Abstract The ability of A. versicolor to grow and produce volatile metabolites, carbon dioxide, and microbial volatile organic compounds (MVOC) in house dust, was investigated. First, signs of metabolic activity were detected after 7 d at relative humidity (RH) of air of 84–86% and after 2 d at RH of 96–98%. Within four weeks, the concentration of A. versicolor spores increased almost 100 fold at the lower RH and over 600 fold at the higher RH. However, after the fast rising at the beginning of the incubation, CO 2 concentration became steady probably because of the depletion of favourable carbon sources. MVOC were analyzed by gas chromatography with thermal desorption and mass selective detector and high pressure liquid chromatography. The results revealed that A. versicolor can utilize various hydrocarbons and fatty acids in house dust. Some MVOC were also formed as a result of the biosynthesis of amino acids. The main MVOC were 2-ethyl-1-hexanol, 1-octen-3-ol, 3-octanone, 2-heptanone, 2-pentanone, 2-hexanone, and 2-methylfuran. The last three compounds have not been presented earlier as volatile metabolites of this fungus.
Toxicology Letters | 2009
J. Naarala; Anne Korpi
The effects of four phthalates, i.e., di-2-ethylhexyl phthalate (DEHP), butyl benzyl phthalate (BBP), dibutyl phthalate (DBP) and diisobutyl phthalate (DIBP) on necrotic and apoptotic cell death, and production of reactive oxygen species (ROS) were studied on mouse macrophage cell line RAW 264.7. All the phthalates caused negligible and non-dose-dependent ROS production compared to control experiment. DEHP and BBP did not cause significant necrotic nor apoptotic cell death at any of the studied doses. Both DIBP and DBP caused dose-dependent necrotic cell death at the two highest concentrations (100 microM and 1 mM). Both doses (500 microM and 1 mM) of DIBP increased apoptosis by 31- and 60-fold, respectively, whereas the increase in apoptotic cell death caused by DBP was only two and fourfold, that however, was not statistically significant. In conclusion, DIBP caused a substantially different apoptotic cell death effect on murine macrophages from the three other phthalates, and this effect was not related to ROS production. Thus, toxicological and health risks of DIBP and DBP should be assessed separately in the future.
Annals of Occupational Hygiene | 2011
Christina Rosenberg; Mervi Hämeilä; Jarkko Tornaeus; Kirsi Säkkinen; Katriina Puttonen; Anne Korpi; Mirja Kiilunen; Markku Linnainmaa; Antti Hesso
Waste electrical and electronic equipment (WEEE) contains various hazardous substances such as flame retardants (FRs). Inhalation exposures to many FRs simultaneously among WEEE recycling site workers have been little studied previously. The breathing zone airborne concentrations of five brominated FR compounds tetrabromobisphenol-A (TBBP-A), decabromodiphenylethane (DBDPE), hexabromocyclododecane, 1,2-bis(2,4,6-tribromophenoxy)ethane, hexabromobenzene, and one chlorinated FR (Dechlorane Plus®) were measured at four electronics recycling sites in two consecutive years. In addition, concentrations of polybrominated diphenyl ethers (PBDEs) and polybrominated biphenyls were measured. The three most abundant FRs in personal air samples were PBDEs (comprising mostly of deca-BDE), TBBP-A, and DBDPE, with mean concentrations ranging from 21 to 2320 ng m(-)(3), from 8.7 to 430 ng m(-3), and from 3.5 to 360 ng m(-3), respectively. At two of the sites, the emission control actions (such as improvements in ventilation and its maintenance and changes in cleaning habits) proved successful, the mean levels of FRs in personal samples being 10-68 and 14-79% of those from the previous year or alternatively below the limit of quantification. At the two remaining sites, the reductions in FR exposures were less consistent. The concentrations reported may pose a health hazard to the workers, although evaluation of the association between FR exposure and adverse health effects is hampered by lacking occupational exposure limits. Therefore, the exposures should be minimized by adequate control measures and maintaining good occupational hygiene practice.
Mediators of Inflammation | 2003
Anne Korpi; Jukka-Pekka Kasanen; Veli-Matti Kosma; R. Rylander; Anna-Liisa Pasanen
Airway irritation effects after single and repeated inhalation exposures to aerosols of beta-glucan (grifolan) were investigated in mice. In addition, the effects on serum total immunoglobulin E (IgE) production and histopathological inflammation in the respiratory tract were studied. The beta-glucan aerosols provoked slight sensory irritation in the airways, but the response was not concentration dependent at the levels studied. Slight pulmonary irritation was observed after repeated exposures. No effect was found on the serum total IgE levels, and no signs of inflammation were seen in the airways 6 h after the final exposure. The results suggest that, irrespective of previous fungal sensitization of the animals, inhaled beta-glucan may cause symptoms of respiratory tract irritation but without apparent inflammation. Respiratory tract irritation reported after inhalation of fungi may not be entirely attributed to beta-glucan.
Inhalation Toxicology | 2002
Anne Korpi; Jukka-Pekka Kasanen; P. Raunio; Veli-Matti Kosma; T. Virtanen; Anna-Liisa Pasanen
Acute effects on the upper and lower respiratory tract due to inhalation exposure to Stachybotrys chartarum (Sc) extract were investigated in mice. In addition, the capacity of the Sc exposure to activate immune system and cause inflammation in the respiratory tract was studied. The inhalation of Sc extract aerosols was observed to provoke sensory irritation in the airways of both naive and Sc -immunized mice. In contrast, exposure to aerosolized ovalbumin or phosphate buffered saline did not cause this effect. Exposure to Sc twice a week for 3 wk increased significantly the serum total immunoglobulin E (IgE) levels in BALB/ c mice immunized with Sc as well as in nonimmunized mice. A slight presence of inflammatory cells was observed in the alveoli 3 days after the last exposure to Sc. In conclusion, Sc extract has the capacity to provoke sensory irritation in the murine airways and to activate the murine immune system.
Nanotoxicology | 2015
Maija Leppänen; Anne Korpi; Santtu Mikkonen; Pasi Yli-Pirilä; Maili Lehto; Lea Pylkkänen; Henrik Wolff; Veli-Matti Kosma; Harri Alenius; Jorma Joutsensaari; Pertti Pasanen
Abstract The wide use of nanotechnology is here to stay. However, the knowledge on the health effects of different engineered nanomaterials (ENMs) is lacking. In this study, irritation and inflammation potential of commercially available silica-coated TiO2 ENMs (10 × 40 nm, rutile) were studied. Single exposure (30 min) at mass concentrations 5, 10, 20 and 30 mg/m3, and repeated exposure (altogether 16 h, 1 h/day, 4 days/week for 4 weeks) at mass concentration of 30 mg/m3 to silica-coated TiO2 induced first phase of pulmonary irritation (P1), which was seen as rapid, shallow breathing. During repeated exposures, P1 effect was partly evolved into more intense pulmonary irritation. Also sensory irritation was observed at the beginning of both single and repeated exposure periods, and the effect intensified during repeated exposures. Airflow limitation started to develop during repeated exposures. Repeated exposure to silica-coated TiO2 ENMs induced also pulmonary inflammation: inflammatory cells infiltrated in peribronchial and perivascular areas of the lungs, neutrophils were found in BAL fluids, and the number of CD3 and CD4 positive T cells increased significantly. In line with these results, pulmonary mRNA expression of chemokines CXCL1, CXCL5 and CXCL9 was enhanced. Also expression of mRNA levels of proinflammatory cytokines TNF-α and IL-6 was elevated after repeated exposures. Taken together, these results indicated that silica-coated TiO2 ENMs induce pulmonary and sensory irritation after single and repeated exposure, and airflow limitation and pulmonary inflammation after repeated exposure.