Objectives Two spa workers reported such symptoms as fever, shivering, palpitation, arthralgia, and diarrhea after performing seaweed massages on clients at a spa center. This study was carried out to determine whether the symptoms were related to exposure to endotoxin. Methods Personal and stationary air sampling for the measurement of airborne endotoxin was carried out at the spa during the preparation of a bath and the following seaweed massage. In addition, the impact of storage time on the concentration of endotoxin in the seaweed was investigated. Results The measurements confirmed exposure to aerosolized endotoxin at the spa (11 ng/m 2 and 22 ng/m 3 ). The endotoxin concentration in the stored seaweed increased as the storage time increased, from 360 ng/g seaweed for fresh seaweed to 33100 ng/g seaweed for seaweed stored for >20 weeks. Conclusions Organic dust toxic syndrome was diagnosed for two workers who performed seaweed massages at a spa center at which aerosolized endotoxin was measured. In order to minimize entotoxin exposure during massages, it is important to use fresh seaweed or seaweed kept well cooled for no more than 2–3 weeks.
I denna studie har olika metoder for analys av partikulara polycykliska aromatiska kolvaten (PAH) efter provtagning pa filter utvarderats. Tva metoder for ultraljudsextraktion, ett traditionellt ul ...
Associations between air pollution and chronic kidney disease (CKD) have been reported, but studies at low exposure levels and relevant exposure time windows are still warranted. This study investigated clinical CKD at low air pollution levels in the Swedish Malmö Diet and Cancer Cohort in different exposure time windows.This study included 30,396 individuals, aged 45-74 at enrollment 1991-1996. Individual annual average residential outdoor PM2.5, PM10, nitrogen oxides (NOx), and black carbon (BC) were assigned using dispersion models from enrollment to 2016. Diagnoses of incident CKD were retrieved from national registries. Cox proportional hazards models were used to obtain hazard ratios (HRs) for CKD in relation to three time-dependent exposure time windows: exposure at concurrent year (lag 0), mean exposure in the 1-5 or 6-10 preceding years (lag 1-5 and lag 6-10), and baseline exposure.During the study period, the average annual residential exposures were 16 μg/m3 for PM10, 11 μg/m3 for PM2.5, 26 μg/m3 for NOx, and 0.97 μg/m3 for BC. For lag 1-5 and lag 6-10 exposure, significantly elevated HRs for incident CKD were found for total PM10:1.13 (95% CI: 1.01-1.26) and 1.22 (1.06-1.41); NOx: 1.19 (1.07-1.33) and 1.13 (1.02-1.25) and BC: 1.12 (1.03-1.22) and 1.11 (1.02-1.21) per interquartile range increase in exposure. For total PM2.5 the positive associations of 1.12 (0.97-1.31) and 1.16 (0.98-1.36) were not significant. For baseline or lag 0 exposure there were significant associations only for NOx and BC, not for PM.Residential exposure to outdoor air pollution was associated with increased risk of incident CKD at relatively low exposure levels. Average long-term exposure was more clearly associated with CKD than current exposure or exposure at recruitment. Our findings imply that the health effects of low-level air pollution on CKD are considerable.
The aim of this study was to measure the exposure to total dust, polycyclic aromatic hydrocarbons (PAHs), and nitrogen dioxide (NO2) of kitchen workers in four different types of restaurants in Sweden (Large scale, European, Fast food, and Asian). One hundred full work-shift (8 h) personal exposure samples were taken from 36 workers in 21 commercial kitchens. Most workers were sampled three times. Mass concentration of total dust was determined using standard gravimetric methods; the filters were analyzed for their content of particulate PAHs. Gas-phase PAHs were sampled using adsorbent tubes (XAD-II) placed after the filter and analyzed with high-resolution gas chromatography/low-resolution mass spectrometry. NO2 was measured using passive dosimeters. Stationary measurements in the kitchen were made in parallel with the personal sampling. Group geometric mean concentrations for personal exposure to total dust ranged from 77 µg m−3 (Fast food) to 320 µg m−3 (European kitchens). Individual exposure samples of total dust ranged from ~40 to 3900 µg m−3. In the Large-scale and European kitchens, the time spent frying was identified as a determinant increasing personal exposure to total dust. The within-worker variance dominated the exposure variability of total dust in Large-scale and European kitchens, whereas between-worker variance dominated in Fast food and Asian kitchens. Exposure to total PAHs was statistically significantly higher for workers in the Asian kitchens. Also, exposure to NO2 was higher in the Asian kitchens, which all used gas stoves for cooking. The stationary measurements of total dust showed lower levels than personal exposures for most kitchens, whereas for PAHs, stationary levels were closer to personal exposure levels for all kitchen types. The results of this study increase the knowledge about exposure to air pollutants for kitchen workers of restaurant types that are common in Sweden and the rest of Europe. Personal sampling is essential for an accurate exposure assessment, and the large day-to-day variability in exposure levels points to the importance of repeated sampling.
IntroductionSome restaurants use wood-fired ovens for cooking and baking, e.g. pizzerias. The aim was to measure exposure to fine particles for the workers and in the restaurants.MethodsMeasurements were performed at seven restaurants (2 days, 8 hr). The ovens were located in a working area in the restaurants. Personal exposure to fine particles (PM2.5) and particulate polycyclic aromatic hydrocarbons (PAHs) were measured on two workers at each restaurant. PM2.5 was collected on teflon filter. Mass concentration was determined gravimetrically and analyzed for PAHs using GC-MS in SIR mode. One of the workers also wore a personal sampler for black carbon (BC), MicroAeth Model AE51. Stationary sampling equipment were placed near the oven and near the dining tables. In addition, size-fractioned particle samples (five size ranges including >2.5, 1.0-2.5, 0.50-1.0, 0.25-0.50, and < 0.25 µm) were collected near the oven using a Sioutas Cascade Impactor. Particle number concentration (PNC), 10-1000 nm, was measured with a Condensation Particle Counter (CPC3007).ResultsMedian personal exposure to PM2.5 and B(a)P for 26 workers were 27 µg/m3 (range: 13-76 µg/m3) and 0.13 ng/m3 (range: 0.01-2.6 ng/m3), respectively. Stationary levels were similar to personal exposure. No significant difference was found between concentrations near the ovens and the dining area. The majority of the B(a)P (>95%) was found in the two finer stages (0.25-0.50, and <0.25 µm). Out of that, in average 78% was found in the finest stage. Median BC exposure varied between 0.5 and 4.1 µg/m3 and was higher during lunch and evening rush hours. The PNC varied across a wide range between the restaurants, with means from about 20 000 up to 170 000 part/cm3.ConclusionsThe exposure to B(a)P were well below OEL. Almost all B(a)P was associated with PM0.25. Particles generated from the wood-fired ovens gave rise to high number concentrations; however, the measured particles mass concentrations were low.
Trichloramine is a disinfection by-product in chlorinated swimming pools. It can evaporate into the air and irritate eyes and airways among swimmers and pool workers. This study aimed to evaluate airborne concentrations of trichloramine in different types of indoor swimming pools. Altogether, 72 swimming pools across Sweden were included; 36 exercise pools, 16 instruction pools, seven adventure pools, and 13 rehabilitation pools. In total, 167 sampling sessions were performed with the majority (N = 91) conducted in public exercise pools. Repeated sampling sessions on different days were performed within all pool categories. Airborne trichloramine was measured stationary by the poolside using active sampling on quartz filters. In total, 434 air samples were collected. The geometric mean (GM) concentration of trichloramine for the exercise pools was 0.12 mg/m3 (range GMpool: 0.02–0.29 mg/m3) and for about 30% the GMpool exceeded the Swedish public health guideline value (0.2 mg/m3). The geometric mean for instruction pools was 0.18 mg/m3 and for adventure pools 0.20 mg/m3. Trichloramine concentrations were statistically significantly lower in rehabilitation pools (GM: 0.03 mg/m3) compared with the other pool categories. A statistically significant effect of time of the day for sampling was found for the exercise and instruction pools, with higher trichloramine levels during evenings compared with mornings and afternoons. For the rehabilitation pools, trichloramine was significantly higher during the cold season compared with the warm season. Variability in trichloramine concentrations was attributed to between-pool as well as within-pool variances. The within-pool variability encourages a repeated sampling strategy to capture the variation between different days. These findings have implications for exposure assessment in epidemiological studies as well as for indoor air quality monitoring. Trichloramine can cause acute irritative effects at elevated levels, and since trichloramine concentrations may differ depending on the time of the day it is recommended that full-day stationary measurements are supplemented with short-term samplings to capture these variations.
Context: Urban particulate air pollution is associated with cardiovascular diseases and mortality, possibly mediated through systemic inflammation and increased blood viscosity.Objectives: To examine short-term effects of exposure to urban air pollution on blood biomarkers for systemic inflammation and coagulation in a panel of healthy adults living in Gothenburg, Sweden.Materials and methods: The 16 volunteers, all non-smokers, median age 35 years, were called for blood sampling the morning after a day with high levels of urban particulate matter (PM10 > 30 µg/m3) or a day with low levels (PM10 < 15 µg/m3 and NO2 < 35 µg/m3). Associations between exposure to air pollution and each biomarker (C-reactive protein, fibrinogen, serum amyloid A, coagulation factor VIII, plasminogen activator inhibitor-1, p-selectin, soluble intercellular adhesion molecule-1, soluble vascular adhesion molecule-1, Clara cell protein 16 and surfactant protein D) were examined using a linear mixed-effects model.Results: In total, 12 sampling sessions were performed, six after high-pollution and six after low-pollution days, over 21 months. The ratio of air pollution levels between high- and low-pollution days was five for PM10 (median: 49 and 10 µg/m3) and two for NO2 (median: 47 and 24 µg/m3). No significant increase in blood levels of any of the biomarkers were seen after days with high air pollution levels compared with low levels.Conclusion: Biomarkers of inflammation and coagulation were not found to be significantly increased in the mornings after days with elevated levels of urban air pollution compared with low levels when performing repeated blood samplings in healthy volunteers.
Short-term controlled exposure to diesel exhaust (DE) in chamber studies have shown mixed results on lung and systemic effects. There is a paucity of studies on well-characterized real-life DE exposure in humans. In the present study, 29 healthy volunteers were exposed to DE while sitting as passengers in diesel-powered trains. Exposure in electric trains was used as control scenario. Each train scenario consisted of three consecutive days (6 h/day) ending with biomarker samplings. Combustion-derived air pollutants were considerably higher in the passenger carriages of diesel trains compared with electric trains. The concentrations of black carbon and ultrafine particles were 8.5 μg/m3 and 1.2–1.8 × 105 particles/cm3 higher, respectively, in diesel as compared to electric trains. Net increases of NOx and NO2 concentrations were 317 μg/m3 and 36 μg/m3. Exposure to DE was associated with reduced lung function and increased levels of DNA strand breaks in peripheral blood mononuclear cells (PBMCs), whereas there were unaltered levels of oxidatively damaged DNA, soluble cell adhesion molecules, acute phase proteins in blood and urinary excretion of metabolites of polycyclic aromatic hydrocarbons. Also the microvascular function was unaltered. An increase in the low frequency of heart rate variability measures was observed, whereas time-domain measures were unaltered. Exposure to DE inside diesel-powered trains for 3 days was associated with reduced lung function and systemic effects in terms of altered heart rate variability and increased levels of DNA strand breaks in PBMCs compared with electric trains. ClinicalTrials.Gov ( NCT03104387 ). Registered on March 23rd 2017
Increasing epidemiological and experimental evidence suggests that particle exposure is an environmental risk factor for chronic kidney disease (CKD). However, only a few case-control studies have investigated this association in an occupational setting. Hence, our objective was to investigate associations between particle exposure and CKD in a large cohort of Swedish construction workers.
