Occupational particle exposure and chronic kidney disease: a cohort study in Swedish construction workers.

OBJECTIVES: 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. METHODS: We performed a retrospective cohort study in the Swedish Construction Workers' Cohort, recruited 1971-1993 (n=286 089). A job-exposure matrix was used to identify workers exposed to nine different particulate exposures, which were combined into three main categories (inorganic dust and fumes, wood dust and fibres). Incident CKD and start of renal replacement therapy (RRT) were obtained from validated national registries until 2021 and analysed using adjusted Cox proportional hazards models. RESULTS: Exposure to inorganic dust and fumes was associated with an increased risk of CKD and RRT during working age (adjusted HR for CKD at age <65 years 1.15, 95% CI 1.05 to 1.26). The elevated risk did not persist after retirement age. Exposure to cement dust, concrete dust and diesel exhaust was associated with CKD. Elevated HRs were also found for quartz dust and welding fumes. CONCLUSIONS: Workers exposed to inorganic particles seem to be at elevated risk of CKD and RRT. Our results are in line with previous evidence of renal effects of ambient air pollution and warrant further efforts to reduce occupational and ambient particle exposure.

Exposure to Air Pollution inside Electric and Diesel-Powered Passenger Trains.

Diesel-powered trains are used worldwide for passenger transport. The present study aimed to assess air pollution concentrations in passenger cars from diesel and electric trains. Personal exposure monitoring (6-7 h per day) was carried out for 49 days on diesel and 22 days on electric trains. Diesel trains had higher concentrations of all the assessed air pollution components. Average increases (and fold differences) in passenger cars of diesel trains compared with electric trains were for ultrafine particles 212 000 particles/cm3 (35-fold), black carbon 8.3 µg/m3 (6-fold), NO x 316 µg/m3 (8-fold), NO2 38 µg/m3 (3-fold), PM2.5 34 µg/m3 (2-fold), and benzo( a)pyrene 0.14 ng/m3 (6-fold). From time-series data, the pull and push movement modes, the engine in use, and the distance to the locomotive influenced the concentrations inside the diesel trains. In conclusion, concentrations of all air pollutants were significantly elevated in passenger cars in diesel trains compared to electric trains.

Health effects of exposure to diesel exhaust in diesel-powered trains.

BACKGROUND: 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. RESULTS: 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. CONCLUSION: 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. TRIAL REGISTRATION: ClinicalTrials.Gov ( NCT03104387 ). Registered on March 23rd 2017.

Urban air pollution and effects on biomarkers of systemic inflammation and coagulation: a panel study in healthy adults.

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.

Effects on airways of short-term exposure to two kinds of wood smoke in a chamber study of healthy humans.

INTRODUCTION: Air pollution causes respiratory symptoms and pulmonary disease. Airway inflammation may be involved in the mechanism also for cardiovascular disease. Wood smoke is a significant contributor to air pollution, with complex and varying composition. We examined airway effects of two kinds of wood smoke in a chamber study. MATERIALS AND METHODS: Thirteen subjects were exposed to filtered air and to wood smoke from the start-up phase and the burn-out phase of the wood-burning cycle. Levels of PM(2.5) were 295 µg/m(3) and 146 µg/m(3), number concentrations 140 000/cm(3) and 100 000/cm(3). Biomarkers in blood, breath and urine were measured before and on several occasions after exposure. Effects of wood smoke exposure were assessed adjusting for results with filtered air. RESULTS: After exposure to wood smoke from the start-up, but not the burn-out session, Clara cell protein 16 (CC16) increased in serum after 4 hours, and in urine the next morning. CC16 showed a clear diurnal variation. Fraction of exhaled nitric oxide (FENO) increased after wood smoke exposure from the burn-out phase, but partly due to a decrease after exposure to filtered air. No other airway markers increased. CONCLUSIONS: The results indicate that relatively low levels of wood smoke exposure induce effects on airways. Effects on airway epithelial permeability was shown for the start-up phase of wood burning, while FENO increased after the burn-out session. CC16 seems to be a sensitive marker of effects of air pollution both in serum and urine, but its function and the significance need to be clarified.

Associations between long-term exposure to low-level air pollution and risk of chronic kidney disease-findings from the Malmö Diet and Cancer cohort.

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

Acute effects after occupational endotoxin exposure at a spa.

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.

Exposure to Particles, Polycyclic Aromatic Hydrocarbons, and Nitrogen Dioxide in Swedish Restaurant Kitchen Workers.

AIMS: 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). METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Experimental wood smoke exposure in humans.

Experimental studies are used to evaluate effects of human exposure to diesel exhaust and concentrated ambient particles. This article describes a system for studying exposure of humans to wood smoke. Wood smoke was generated using a wood stove placed outside an exposure chamber that can hold at least 10 subjects. A partial flow of the generated wood smoke from the stove was mixed with filtered indoor air. Personal and stationary measurements were performed of PM2.5 and PM1 mass concentrations and various volatile organic compounds (VOCs): 1,3-butadiene, benzene, and aldehydes. In addition, particulate matter (PM) mass, number concentrations, and size distributions of particles (0.007-6.7 microm), as well as nitrous oxides, CO2, and CO, were measured online. Filters were analyzed for trace elements and black smoke. Polycyclic aromatic compounds, toluene, and xylenes were determined in stationary samples. Results of the first experiment showed no differences between personal and stationary measurements for particles or VOCs. Consequently, stationary measurements can be used to predict personal exposure. All PM mass (about 250 microg/m3) was in the PM1 fraction. Subjective symptoms were generally weak, while clear objective signs were found, for example, in biomarkers of inflammation. With careful control of the combustion process, relatively constant mass and number concentrations were obtained over each exposure session. By varying the combustion and dilution of the wood smoke, different exposure scenarios can be achieved and thus, knowledge about which of the properties of particles and gaseous compounds are crucial for the effects.

Determinants of personal exposure to some carcinogenic substances and nitrogen dioxide among the general population in five Swedish cities.

Environmental levels of airborne carcinogenic and related substances are comparatively better known than individual exposure and its determinants. We report on a personal monitoring program involving five Swedish urban populations. The aim of the program was to investigate personal exposure to benzene, 1,3-butadiene, formaldehyde, and nitrogen dioxide (NO2). The measurements were performed among 40 inhabitants during seven consecutive days, in one urban area each year, during 2000-2008. The estimated population exposure levels were 1.95 µg/m(3) for benzene, 0.56 µg/m(3) for 1,3-butadiene, 19.4 µg/m(3) for formaldehyde, and 14.1 µg/m(3) for NO2. Statistical analysis using a mixed-effects model revealed that time spent in traffic and time outdoors contributed to benzene and 1,3- butadiene exposure. For benzene, refueling a car was an additional determinant influencing the exposure level. Smoking or environmental tobacco smoke were significant determinants of exposure to NO2, benzene, and 1,3-butadiene. Those with a gas stove had higher NO2 exposure. Living in a single-family house increased the exposure to formaldehyde significantly. In a variance component model, the between-subject variance dominated for 1,3-butadiene and formaldehyde, whereas the between-city variance dominated for NO2. For benzene, the between-subject and between-cities variances were similar.

Variability of environmental exposure to fine particles, black smoke, and trace elements among a Swedish population.

Mixed-effects models were used to estimate within-person and between-person variance components, and some determinants of environmental exposure to particulate matter (PM(2.5)), black smoke (BS) and trace elements (Cl, K, Ca, Ti, Fe, Ni, Cu, Zn, and Pb) for personal measurements from 30 adult subjects in Gothenburg, Sweden. The within-person variance component dominated the total variability for all investigated compounds except for PM(2.5) and Zn (in which the variance components were about equal). Expressed as fold ranges containing 95% of the underlying distributions, the within-person variance component ranged between 5-fold and 39-fold (median: sixfold), whereas the between-person variance component was always

Exposure to fine particles (PM2.5 and PM1) and black smoke in the general population: personal, indoor, and outdoor levels.

Personal exposure to PM(2.5) and PM(1), together with indoor and residential outdoor levels, was measured in the general adult population (30 subjects, 23-51 years of age) of Gothenburg, Sweden. Simultaneously, urban background concentrations of PM(2.5) were monitored with an EPA WINS impactor. The 24-h samples were gravimetrically analyzed for mass concentration and black smoke (BS) using a smokestain reflectometer. Median levels of PM(2.5) were 8.4 microg/m(3) (personal), 8.6 microg/m(3) (indoor), 6.4 microg/m(3) (residential outdoor), and 5.6 microg/m(3) (urban background). Personal exposure to PM(1) was 5.4 microg/m(3), while PM(1) indoor and outdoor levels were 6.2 and 5.2 microg/m(3), respectively. In non-smokers, personal exposure to PM(2.5) was significantly higher than were residential outdoor levels. BS absorption coefficients were fairly similar for all microenvironments (0.4-0.5 10(-5) m(-1)). Personal exposure to particulate matter (PM) and BS was well correlated with indoor levels, and there was an acceptable agreement between personal exposure and urban background concentrations for PM(2.5) and BS(2.5) (r(s)=0.61 and 0.65, respectively). PM(1) made up a considerable amount (70-80%) of PM(2.5) in all microenvironments. Levels of BS were higher outdoors than indoors and higher during the fall compared with spring. The correlations between particle mass and BS for both PM(2.5) vs. BS(2.5) and PM(1) versus BS(1) were weak for all microenvironments including personal exposure. The urban background station provided a good estimate of residential outdoor levels of PM(2.5) and BS(2.5) within the city (r(s)=0.90 and 0.77, respectively). Outdoor levels were considerably affected by long-range transported air pollution, which was not found for personal exposure or indoor levels. The within-individual (day-to-day) variability dominated for personal exposure to both PM(2.5) and BS(2.5) in non-smokers.

Personal exposures and indoor, residential outdoor, and urban background levels of fine particle trace elements in the general population.

Personal exposures and indoor, residential outdoor, and urban background levels of PM(2.5) and PM(1) were measured simultaneously in Göteborg, Sweden. A total of 270 24 hour samples from 30 subjects were analyzed for elemental concentrations using X-ray fluorescence (XRF) spectroscopy. Personal exposures to PM(2.5) were significantly higher for Cl, Ca, Ti, and Fe compared with the other locations. For most elements, residential outdoor levels were significantly higher than urban background levels. Correlations between personal exposure and stationary measurements were moderate to high for Zn, Br, and Pb (r(s)= 0.47-0.81), while Ca and Cu showed low correlations. The penetration indoors from outdoors was 0.7, as calculated from S and Pb ratios. For the pairs of parallel PM(1) and PM(2.5) measurements, only Ca and Fe levels were significantly lower for PM(1) at all sites. Significant correlations were found between urban background mass concentrations and personal exposure levels for elements attributed to combustion processes (S, V, and Pb) and resuspended dust (Ti, Fe, and Zn), indicating that both sources could be relevant to health effects related to urban background mass. Air mass origin strongly affected the measured urban background concentrations of some elements (S, Cl, V, Ni, Br, and Pb). These findings were also seen for personal exposure (S, Cl, V, and Pb) and indoor levels (S, Cl, V, Ni, and Pb). No differences were seen for crustal elements. Air mass origin should be taken into account in the description and interpretation of time series studies of air pollution and health.