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Sökning: WFRF:(Bryngelsson Ing Liss)

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21.
  • Graff, Pål, et al. (författare)
  • Sarcoidosis and silica dust exposure among men in Sweden : a case-control study
  • 2020
  • Ingår i: BMJ Open. - : BMJ Publishing Group Ltd. - 2044-6055. ; 10:9
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To determine whether occupational exposure to silica dust is associated with an increased risk of developing sarcoidosis.DESIGN: Case-control study of all individuals between 20 and 65 years of age diagnosed with sarcoidosis (D86) in Sweden between 2007 and 2016. Controls were matched to cases (2:1) based on age, sex and county at the time of diagnosis. A Job Exposure Matrix was used to estimate the occupational silica exposure of all cases and controls.SETTING: Medical and occupational data from the National Outpatient Register were used to implement a case-control analysis, while the two controls used for each case were selected from the National Register of the Total Population. Information about occupation and time of employment were collected from the Swedish Occupational Register.PARTICIPANTS: All men and women aged 20-65 years old who were diagnosed sarcoidosis (D86) from 2007 to 2016 were included and assigned two controls.MAIN OUTCOMES: Silica dust exposure correlates with an increased risk of developing sarcoidosis in men.RESULTS: The prevalence of silica exposure at work was statistically significantly higher among male cases than controls (OR 1.27, 95% CI 1.13 to 1.43). For men of an age of 35 years or younger the correlation seems to be stronger (OR 1.48, 95% CI 1.1 to 1.87) than in older men (OR 1.21, 95% CI 1.05 to 1.39). For men older than 35 with exposure to silica the prevalence of sarcoidosis increased with the exposure time, with an OR of 1.44 (95% CI 1.04 to 2.00) for exposure of more than 10 years.CONCLUSIONS: Occupational exposure to silica dust seems to increase the risk of sarcoidosis among men between 20 and 65 years of age. The risk is higher among exposed men 35 years or younger and older men with longer exposure (>6 years).
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22.
  • Hagström, Katja, 1975-, et al. (författare)
  • Exposure to wood dust, resin acids and volatile organic compounds during production of wood pellets
  • 2008
  • Ingår i: Journal of Occupational and Environmental Hygiene. - Philadelphia, PA : Taylor and Francis. - 1545-9624 .- 1545-9632. ; 5:5, s. 296-304
  • Tidskriftsartikel (refereegranskat)abstract
    • The main aim of this study was to investigate exposure to airborne substances that are potentially harmful to health during the production of wood pellets, including wood dust, monoterpenes, and resin acids, and as an indicator of diesel exhaust nitrogen dioxide. In addition, area measurements were taken to assess background exposure levels of these substances, volatile organic compounds (VOCs), and carbon monoxide. Measurements were taken at four wood pellet production plants from May 2004 to April 2005. Forty-four workers participated in the study, and a total of 68 personal measurements were taken to determine personal exposure to wood dust (inhalable and total dust), resin acids, monoterpenes, and nitrogen dioxide. In addition, 42 measurements of nitrogen dioxide and 71 measurements of total dust, resin acids, monoterpenes, VOCs, and carbon monoxide were taken to quantify their indoor area concentrations. Personal exposure levels to wood dust were high, and a third of the measured levels of inhalable dust exceeded the Swedish occupational exposure limit (OEL) of 2 mg/m3. Parallel measurements of inhalable and total dust indicated that the former were, on average, 3.2 times higher than the latter. The data indicate that workers at the plants are exposed to significant amounts of the resin acid 7-oxodehydroabietic acid in the air, an observation that has not been recorded previously at wood processing and handling plants. The study also found evidence of exposure to dehydroabietic acid, and exposure levels for resin acids approached 74% of the British OEL for colophony, set at 50 microg/m3. Personal exposure levels to monoterpenes and nitrogen dioxide were low. Area sampling measurements indicated that aldehydes and terpenes were the most abundant VOCs, suggesting that measuring personal exposure to aldehydes might be of interest. Carbon monoxide levels were under the detection limit in all area measurements. High wood dust exposure levels are likely to have implications for worker health; therefore, it is important to reduce exposure to wood dust in this industry.
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23.
  • Hagström, Katja, 1975-, et al. (författare)
  • Preschool children´s exposure to metals via measurements of hand deposition
  • 2019
  • Ingår i: Abstract Book, Monday.
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • Background: Since we spend most of our time indoors the indoor environment can lead to exposure to substances like metals. Small children are often more exposed than adults, for instance due to their hand-to-mouth behaviour. Since some metals can have adverse health effects in children the aim of this study was to investigate indoor exposure to metals on children’s hands in preschools.Method: In the study, 60 children at 8 preschools in two cities in Sweden participated. Metals on the hands were sampled at two different periods (winter and spring) giving a total of 109 samples. During sampling, both hands were wiped using hand-wipes soaked in 1 % HNO3, and sampling was done after two hours of indoor activities. The following metals were analyzed using ICP-MS; beryllium, magnesium, aluminium, vanadium, chromium, manganese, iron, cobalt, nickel, copper, zinc, arsenic, molybdenum, silver, cadmium, antimony, barium, thallium and lead. Results All samples were above limit of quantification (LOQ) except for beryllium and molybdenum (4 %Conclusion: Metals linked to severe health effects like cadmium, arsenic and lead as well as a range of other metals could be detected on children’s hands. These findings indicate an exposure to metals for children both via dermal uptake and oral intake due to hand-to-mouth transfer, but potential contributions to the body burden are unknown. Higher levels were seen during spring and in one of the cities, possible explanations to these observations needs to be looked into more closely.
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24.
  • Hedbrant, Alexander, 1987-, et al. (författare)
  • Effects on white blood cell counts and the NLRP3 inflammasome due to dust and cobalt exposure in the hard metal industry
  • 2022
  • Ingår i: Biomarkers. - : Taylor & Francis. - 1354-750X .- 1366-5804. ; , s. 60-70
  • Tidskriftsartikel (refereegranskat)abstract
    • INTRODUCTION: In light of potential negative health effects of cobalt exposure, a characterization of inflammatory mechanisms in exposed individuals is warranted. The current study investigated cobalt exposure in the Swedish hard metal industry and its relationship to inflammatory markers, including NLRP3 inflammasome activation and white blood cell (WBC) counts.MATERIAL AND METHODS: Inhalable cobalt and dust exposures, and systemic cobalt levels, were determined for 72 workers in the hard metal industry and linear regression models were applied to correlate exposure to markers of inflammasome activation and WBC counts.RESULTS: Mean exposures to inhalable dust (0.11 mg/m3) and cobalt (0.0034 mg/m3) were below the Swedish occupational exposure limits, and these low exposures did not correlate with any investigated outcomes. Instead, cobalt blood levels significantly correlated with a ca 10% decrease in IL-18 plasma levels per 10 nM cobalt increase. Furthermore, pre-shift cobalt blood and/or urine levels significantly correlated with some WBC measures, including decreased neutrophil-to-lymphocyte ratio, increased lymphocyte-to-monocyte ratio, and lymphocyte counts.CONCLUSION: The low inhalable particle exposures had no impact on WBC counts and inflammasome activation. Instead, systemic cobalt levels, which also include skin exposure, demonstrated possible suppressive effects on inflammatory responses in cobalt-exposed individuals in the hard metal industry.
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25.
  • Hedbrant, Alexander, 1987-, et al. (författare)
  • Quartz Dust Exposure Affects NLRP3 Inflammasome Activation and Plasma Levels of IL-18 and IL-1Ra in Iron Foundry Workers
  • 2020
  • Ingår i: Mediators of Inflammation. - : Hindawi Publishing Corporation. - 0962-9351 .- 1466-1861.
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose: To study the association between inhalation of particulate matter or quartz in Swedish iron foundries and the effects on NLRP3 inflammasome activation. Methods: Particle exposure measurements were performed during an eight-hour work day for 85 foundry workers at three Swedish iron foundries. Personal sampling was used for measurement of respirable quartz and dust and stationary measurements to obtain exposure measurements for inhalable dust and PM10. The NLRP3 inflammasome markers, interleukin- (IL-) 1β and IL-18, and inhibitors IL-1 receptor antagonist (IL-1Ra) and IL-18 binding protein (IL-18BP) were measured in plasma. Inflammasome activation was measured by caspase-1 enzymatic activity in monocytes in whole blood by flow cytometry, and expression of inflammasome-related genes was quantified using real-time PCR. Multiple linear regression analysis was used to investigate associations between PM exposures and inflammatory markers. Sex, age, smoking, current infection, BMI, and single nucleotide polymorphism in the inflammasome regulating genes CARD8 (C10X) and NLRP3 (Q705K) were included as covariates. Results: The average exposure levels of respirable dust and quartz were 0.85 and 0.052 mg/m3, respectively. A significant exposure-response was found for respirable dust and IL-18 and for inhalable dust and IL-1Ra. Whole blood, drawn from study participants, was stimulated ex vivo with inflammasome priming stimuli LPS or Pam3CSK4, resulting in a 47% and 49% increase in caspase-1 enzymatic activity in monocytes. This increase in caspase-1 activity was significantly attenuated in the higher exposure groups for most PM exposure measures. Conclusions: The results indicate that exposure levels of PM in the iron foundry environment can affect the NLRP3 inflammasome and systemic inflammation.
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26.
  • Johansson, Niclas, et al. (författare)
  • Effects on blood parameters from hand-arm vibrations exposure
  • 2023
  • Ingår i: Toxicology and industrial health. - : Sage Publications. - 0748-2337 .- 1477-0393. ; 39:6, s. 291-297
  • Tidskriftsartikel (refereegranskat)abstract
    • Vibration exposure from handheld tools can affect the hands with neurological symptoms and vibration-induced Raynaud's phenomenon (VRP). The underlying pathophysiological mechanisms are not fully known, however, changes in the composition of blood parameters may contribute to VRP with an increase in blood viscosity and inflammatory response. The aim of this study was to examine the effect on blood parameters in capillary blood from fingers that had been exposed to a vibrating hand-held tool. This study involved nine healthy participants who had been exposed to vibration and an unexposed control group of six participants. Capillary blood samples were collected before and after vibration exposure for the exposed group, and repeated samples also from the control group. The exposed groups were exposed to vibration for a 15-min period or until they reached a 5.0 m/s2 vibration dose. Analysis of blood status and differential counting of leucocytes was performed on the capillary blood samples. The results of the blood samples showed an increase in mean value for erythrocyte volume fraction (EVF), hemoglobin, red blood cell count, white blood cell count and neutrophils, as well as a decrease of mean cell volume, mean cell hemoglobin, and mean cell hemoglobin concentration. The increase of EVF and neutrophils was statistically significant for samples taken from the index finger but not the little finger. Even though the study was small it showed that an acute vibration exposure to the hands might increase EVF and neutrophilic granulocytes levels in the capillary blood taken from index fingers.
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27.
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28.
  • Klasson, Maria, 1977-, et al. (författare)
  • Biological monitoring of dermal and air exposure to cobalt at a Swedish hard metal production plant : does dermal exposure contribute to uptake?
  • 2017
  • Ingår i: Contact Dermatitis. - : John Wiley & Sons. - 0105-1873 .- 1600-0536. ; 77:4, s. 201-207
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Occupational exposure to cobalt is well established in hard metal manufacture. Cobalt is known to cause contact allergy, asthma, hard metal lung disease, and lung cancer. The relationship between skin exposure and uptake determined in blood has not been extensively investigated.Objective: To examine whether skin and inhalable air exposure to cobalt contributes to uptake, determined as cobalt in blood, in a hard metal manufacturing factory.Methods: The amount of cobalt on the skin found with an acid wash technique, the air concentrations of inhalable cobalt and cobalt blood concentrations were determined and correlated in exposed workers.Results: We found a significant rank correlation for cobalt concentrations on the skin, in inhalable air, and in blood (0.376-0.498). Multiple linear regression showed significant regression coefficients for cobalt skin exposure and blood (B = 0.01, p < 0.05) and for inhalable cobalt in air and blood (B = 49.1, p < 0.001). According to our model based on data from the regression analyses, a twofold increase in skin exposure levels at different air concentrations caused a 3 - 14% increase in blood levels.Conclusions: Our data suggest that skin exposure to cobalt in the hard metal industry could affect the total uptake at the same order of magnitude as air exposure.
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29.
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30.
  • Klasson, Maria, 1977-, et al. (författare)
  • Dermal exposure to cobalt studied in vitro in keratinocytes : effects of cobalt exposure on inflammasome activated cytokines, and mRNA response
  • 2021
  • Ingår i: Biomarkers. - : Taylor & Francis. - 1354-750X .- 1366-5804. ; 26:8, s. 674-684
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Cobalt is a dermal sensitizer, and keratinocytes respond to cobalt exposure by releasing proinflammatory mediators, regulating the immune response.OBJECTIVE: To determine the effect of cobalt on the inflammasome associated cytokine- and gene expression in cultured human keratinocytes (HaCaT). Cultivation in low- or high calcium conditions model separate differentiation states of keratinocytes in the skin.METHOD: HaCaT cells in two different states of differentiation were exposed to cobalt chloride and caspase-1 activity as well as the production of IL-1 beta, IL-18 and gene expression of IL1B, IL18, NLRP3, CASP1, and PYCARD was quantified. RESULTS: High cobalt chloride exposure mediated significant increase in caspase-1 activity, cytokine levels, and IL1B and NLRP3 expression with a corresponding regulatory decrease for CASP1 and PYCARD expression. No difference between high- and low calcium culturing conditions modelling differentiation states was detected.CONCLUSIONS: Our data suggest that HaCaT cells respond with inflammmasome associated activity upon cobalt exposure in a concentration-dependent manner. These mechanisms could be of importance for the understanding of the pathophysiology behind allergic sensitization to dermal cobalt exposure.
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