Blood biomarkers for occupational hand-arm vibration exposure.

Hand-arm vibration is a common occupational exposure that causes neurological impairment, myalgia, and vibration-induced Raynaud's phenomena or vibration white fingers (VWF). The pathological mechanism is largely unknown, though several mechanisms have been proposed, involving both immunological vascular damage and defective neural responses. The aim of this study was to test whether the substances interleukin-33 (IL-33), macrophage-derived chemokine (MDC), interleukin-10 (IL-10), endothelin-1 (ET-1), C-C motif chemokine ligand 20 (CCL20), calcitonin, and thromboxane (TXA2) changed before and after occupational hand-arm vibration exposure. 38 full-time shift workers exposed to hand-arm vibration were recruited. All the participants underwent medical examinations regarding symptoms of Raynaud's phenomena. In 29 of the participants, the concentration of IL-33, MDC, IL-10, ET-1, CCL20, calcitonin, and TXA2 was measured before and after a workday. There was a significant increase in ET-1 and calcitonin concentration and a decrease in the CCL20 concentration after the work shift in all participants. In the group suffering from VWF, but not in the non-VWF group, MDC was statistically significantly lower before the work shift (p = .023). The VWF group also showed a significant increase in MDC after the work shift. Exposure to occupational hand-arm vibration is associated with changes in ET-1, calcitonin, and MDC concentration in subjects suffering from vibration white fingers, suggesting a role of these biomarkers in the pathophysiology of this condition.

Self-reported symptoms in Swedish hairdressers and association with exposure to volatile organic compounds (VOCs), including aldehydes.

BACKGROUND: Working as a hairdresser involves combined exposure to multiple chemicals in hair treatment products that may induce symptoms in airways and skin. METHODS: In this cross-sectional study, perceived symptoms among Swedish hairdressers at 10 hair salons were surveyed through a questionnaire. Associations with personal exposure to volatile organic compounds (VOCs), including aldehydes, and their corresponding hazard index (HI), based on the estimated risk for non-cancer health effects, were examined. The prevalence of four out of 11 symptoms was compared to available reference datasets from two other studies of office workers and school staff. RESULTS: All 11 surveyed symptoms were reported among the hairdressers (n = 38). For the whole study group, the most prevalent symptoms were dripping nose (n = 7) and headache (n = 7), followed by eczema (n = 6), stuffed nose (n = 5), cough (n = 5) and discomfort with strong odors (n = 5). Significant relationships between exposure and symptoms were scarce. The exception was total VOC (TVOC) exposure adjusted to worked years in the profession; a difference was observed for any symptom between hairdressers in the group with 20 + years compared to 0-5 years in the profession (logistic regression, OR 0.03, 95% CI 0.001-0.70). Out of the four symptoms available for comparison, the prevalence of headache and cough was significantly higher in hairdressers than in controls (OR 5.18, 95% CI 1.86-13.43 and OR 4.68, 95% CI 1.17-16.07, respectively). CONCLUSIONS: Adverse health effects related to occupation was common among the hairdressers, implying a need for exposure control measures in hair salons. Symptoms of headache and cough were more frequently reported by hairdressers than staff in offices and schools. A healthy worker effect among the hairdressers was indicated in the group with 20 + years compared to 0-5 years in the profession. Significant relationships between measured exposure and symptoms were scarce but gave information about advantages and disadvantages of the different exposure measures. The study design could be improved by increasing the size of the study population, using a better match of reference data and increasing the applicability and representability over time of the measured exposure.

Effects on blood parameters from hand-arm vibrations exposure.

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.

Effects on white blood cell counts and the NLRP3 inflammasome due to dust and cobalt exposure in the hard metal industry.

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. MATERIALS 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.

Contact allergy to haptens in the Swedish baseline series: Results from the Swedish Patch Test Register (2010 to 2017).

BACKGROUND: Allergic contact dermatitis has considerable public health impact and causative haptens vary over time. OBJECTIVES: To report the prevalence of contact allergy to allergens in the Swedish baseline series 2010 to 2017, as registered in the Swedish Patch Test Register. METHODS: Results and demographic information for patients tested with the Swedish baseline series in 2010 to 2017 were analysed. RESULTS: Data for 21 663 individuals (females 69%) were included. Females had significantly more positive patch tests (54% vs 40%). The reaction prevalence rates were highest for nickel sulfate (20.7%), fragrance mix I (7.1%), Myroxylon pereirae (6.9%), potassium dichromate (6.9%), cobalt chloride (6.8%), methylchloroisothiazolinone/methylisothiazolinone (MCI/MI; 6.4%), MI (3.7%), colophonium (3.5%), fragrance mix II (3.2%), and formaldehyde (3.2%). Myroxylon pereirae reaction prevalence increased from 5% in 2010 to 9% in 2017 and that for methyldibromo glutaronitrile from 3.1% to 4.6%. MCI/MI and MI reactions decreased in prevalence after 2014. Nickel reaction prevalence decreased among females aged 10 to 19 years. CONCLUSIONS: Nickel remains the most common sensitizing agent, with reaction prevalence decreasing among females younger than 20 years. The changes in MCI/MI and MI reaction prevalence mirrored those in Europe. The register can reveal changes in contact allergy prevalence over time among patients patch tested in Sweden.

Dermal exposure to cobalt studied in vitro in keratinocytes - effects of cobalt exposure on inflammasome activated cytokines, and mRNA response.

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-1ß, 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.

Inflammatory and coagulatory markers and exposure to different size fractions of particle mass, number and surface area air concentrations in the Swedish hard metal industry, in particular to cobalt.

PURPOSE: To study the relationship between inhalation of airborne particles and cobalt in the Swedish hard metal industry and markers of inflammation and coagulation in blood. METHODS: Personal sampling of inhalable cobalt and dust were performed for subjects in two Swedish hard metal plants. Stationary measurements were used to study concentrations of inhalable, respirable, and total dust and cobalt, PM10 and PM2.5, the particle surface area and the particle number concentrations. The inflammatory markers CC16, TNF, IL-6, IL-8, IL-10, SAA and CRP, and the coagulatory markers FVIII, vWF, fibrinogen, PAI-1 and D-dimer were measured. A complete sampling was performed on the second or third day of a working week following a work-free weekend, and additional sampling was taken on the fourth or fifth day. The mixed model analysis was used, including covariates. RESULTS: The average air concentrations of inhalable dust and cobalt were 0.11 mg/m3 and 0.003 mg/m3, respectively. For some mass-based exposure measures of cobalt and total dust, statistically significant increased levels of FVIII, vWF and CC16 were found. CONCLUSIONS: The observed relationships between particle exposure and coagulatory biomarkers may indicate an increased risk of cardiovascular disease.

Quartz Dust Exposure Affects NLRP3 Inflammasome Activation and Plasma Levels of IL-18 and IL-1Ra in Iron Foundry Workers.

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-) 1ß 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.

The incidence of Cushing's disease: a nationwide Swedish study.

BACKGROUND: Studies on the incidence of Cushing's disease (CD) are few and usually limited by a small number of patients. The aim of this study was to assess the annual incidence in a nationwide cohort of patients with presumed CD in Sweden. METHODS: Patients registered with a diagnostic code for Cushing's syndrome (CS) or CD, between 1987 and 2013 were identified in the Swedish National Patient Registry. The CD diagnosis was validated by reviewing clinical, biochemical, imaging, and histopathological data. RESULTS: Of 1317 patients identified, 534 (41%) had confirmed CD. One-hundred-and-fifty-six (12%) patients had other forms of CS, 41 (3%) had probable but unconfirmed CD, and 334 (25%) had diagnoses unrelated to CS. The mean (95% confidence interval) annual incidence between 1987 and 2013 of confirmed CD was 1.6 (1.4-1.8) cases per million. 1987-1995, 1996-2004, and 2005-2013, the mean annual incidence was 1.5 (1.1-1.8), 1.4 (1.0-1.7) and 2.0 (1.7-2.3) cases per million, respectively. During the last time period the incidence was higher than during the first and second time periods (P < 0.05). CONCLUSION: The incidence of CD in Sweden (1.6 cases per million) is in agreement with most previous reports. A higher incidence between 2005 and 2013 compared to 1987-2004 was noticed. Whether this reflects a truly increased incidence of the disease, or simply an increased awareness, earlier recognition, and earlier diagnosis can, however, not be answered. This study also illustrates the importance of validation of the diagnosis of CD in epidemiological research.

Inflammatory and coagulatory markers and exposure to different size fractions of particle mass, number and surface area air concentrations in Swedish iron foundries, in particular respirable quartz.

PURPOSE: To study the relationship between inhalation of airborne particles and quartz in Swedish iron foundries and markers of inflammation and coagulation in blood. METHODS: Personal sampling of respirable dust and quartz was performed for 85 subjects in three Swedish iron foundries. Stationary measurements were used to study the concentrations of respirable dust and quartz, inhalable and total dust, PM10 and PM2.5, as well as the particle surface area and the particle number concentrations. Markers of inflammation, namely interleukins (IL-1ß, IL-6, IL-8, IL-10 and IL-12), C-reactive protein, and serum amyloid A (SAA) were measured in plasma or serum, together with markers of coagulation including fibrinogen, factor VIII (FVIII), von Willebrand factor and D-dimer. Complete sampling was performed on the second or third day of a working week after a work-free weekend, and follow-up samples were collected 2 days later. A mixed model analysis was performed including sex, age, smoking, infections, blood group, sampling day and BMI as covariates. RESULTS: The average 8-h time-weighted average air concentrations of respirable dust and quartz were 0.85 mg/m3 and 0.052 mg/m3, respectively. Participants in high-exposure groups with respect to some of the measured particle types exhibited significantly elevated levels of SAA, fibrinogen and FVIII. CONCLUSIONS: These observed relationships between particle exposure and inflammatory markers may indicate an increased risk of cardiovascular disease among foundry workers with high particulate exposure.

Adult onset asthma in non-allergic women working in dampness damaged buildings: A retrospective cohort study.

BACKGROUND: There is still no consensus about the association between working in dampness-damaged buildings and new onset of asthma among adults. The purpose of this study was to assess asthma in the staff of two psychiatric clinics where some premises were suffering from dampness. METHODS: A 20-year retrospective cohort study was performed using questionnaires. RESULTS: Incidence rate ratios (IRR) for asthma were non-significantly elevated (IRR = 2.3) among exposed individuals. The risk was greater among females (IRR = 3.5, 95% CI 1.0-16). IRR for non-atopic women was 8.8 (95% CI 1.4-196). Adjusting for smoking habits weakened the risks marginally (IRR = 7.3, 95% CI 1.1-167). The number of male participants was too low to draw conclusion regarding the risk for men. CONCLUSION: The results suggest that working in dampness-damaged buildings might be a possible health hazard. This finding is most pronounced in non-atopic females.

Occupational exposure to trichloramine and trihalomethanes: adverse health effects among personnel in habilitation and rehabilitation swimming pools.

Personnel in swimming pool facilities typically experience ocular, nasal, and respiratory symptoms due to water chlorination and consequent exposure to disinfection by-products in the air. The aim of the study was to investigate exposure to trichloramine and trihalomethanes (chloroform, bromodichloromethane, dibromochloromethane, and bromoform) from the perspective of adverse health effects on the personnel at Swedish habilitation and rehabilitation swimming pools. The study included 10 habilitation and rehabilitation swimming pool facilities in nine Swedish cities. The study population comprised 24 exposed swimming pool workers and 50 unexposed office workers. Personal and stationary measurements of trichloramine and trihalomethanes in air were performed at all the facilities. Questionnaires were distributed to exposed workers and referents. Spirometry, fraction of exhaled nitric oxide (FENO), and peak expiratory flow (PEF) were measured. Personal and stationary measurements yielded trichloramine levels of 1-76 µg/m3 (average: 19 µg/m3) and 1-140 µg/m3 (average: 23 µg/m3), respectively. A slightly higher, but not significant, prevalence of reported eye- and throat-related symptoms occurred among the exposed workers than among the referents. A significantly increased risk of at least one ocular symptom was attributed to trichloramine exposure above the median (20 µg/m3). Lung function (FVC and FEV1) was in the normal range according to the Swedish reference materials, and no significant change in lung function before and after shift could be established between the groups. Average FENO values were in the normal range in both groups, but the difference in the values between the exposed workers and referents showed a significant increase after shift. Hourly registered PEF values during the day of the investigation did not show any unusual individual variability. In conclusion, the increased risk of developing at least one ocular symptom at personal trichloramine concentrations over 20 µg/m3 combined with an increase in the difference in FENO during the work shift of the exposed workers should not be neglected as an increased risk of respiratory inflammation in the habilitation and rehabilitation swimming pool environment.

Time trends of mortality in patients with non-functioning pituitary adenoma: a Swedish nationwide study.

PURPOSE: Patients with non-functioning pituitary adenomas (NFPA), especially women, have increased mortality. The aim of this study was to investigate whether mortality in NFPA patients has changed during the last two decades. METHODS: This was a nationwide population-based study including 2795 patients (1502 men, 1293 women) diagnosed with NFPA between 1997 and 2011. Patients were identified and followed in Swedish National Health Registries. Standardized mortality ratios (SMRs) with 95 % confidence intervals were calculated for three time periods at first NFPA diagnosis using the general population as reference. RESULTS: Mean (±SD) age at NFPA diagnosis was 58.9 ± 16.8 years. Mean (range) follow-up time was 8.3 (0-18) years, resulting in 20,517 patient-years at risk. Surgical treatment and radiotherapy were used in 53 and 5 %, respectively. The prevalence of hypopituitarism was 64 % during the first time period of diagnosis and then declined gradually during the study period (P value for trend <0.0001). The use of pituitary surgery and radiotherapy remained stable. In women, mortality was increased for patients diagnosed between 1997 and 2006 but not for those diagnosed between 2007 and 2011. The SMR in men remained stable throughout the study and did not differ from the general population. During the last time period, 2007-2011, the SMR between men and women did not differ. CONCLUSIONS: While mortality in men with NFPA remains normal and stable during the last two decades, mortality in women has declined. Decreasing prevalence of pituitary insufficiency may be a plausible explanation for this positive development.

Biological monitoring of dermal and air exposure to cobalt at a Swedish hard metal production plant: does dermal exposure contribute to uptake?

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.

Occupational Exposure to Cobalt and Tungsten in the Swedish Hard Metal Industry: Air Concentrations of Particle Mass, Number, and Surface Area.

Exposure to cobalt in the hard metal industry entails severe adverse health effects, including lung cancer and hard metal fibrosis. The main aim of this study was to determine exposure air concentration levels of cobalt and tungsten for risk assessment and dose-response analysis in our medical investigations in a Swedish hard metal plant. We also present mass-based, particle surface area, and particle number air concentrations from stationary sampling and investigate the possibility of using these data as proxies for exposure measures in our study. Personal exposure full-shift measurements were performed for inhalable and total dust, cobalt, and tungsten, including personal real-time continuous monitoring of dust. Stationary measurements of inhalable and total dust, PM2.5, and PM10 was also performed and cobalt and tungsten levels were determined, as were air concentration of particle number and particle surface area of fine particles. The personal exposure levels of inhalable dust were consistently low (AM 0.15mg m(-3), range <0.023-3.0mg m(-3)) and below the present Swedish occupational exposure limit (OEL) of 10mg m(-3) The cobalt levels were low as well (AM 0.0030mg m(-3), range 0.000028-0.056mg m(-3)) and only 6% of the samples exceeded the Swedish OEL of 0.02mg m(-3) For continuous personal monitoring of dust exposure, the peaks ranged from 0.001 to 83mg m(-3) by work task. Stationary measurements showed lower average levels both for inhalable and total dust and cobalt. The particle number concentration of fine particles (AM 3000 p·cm(-3)) showed the highest levels at the departments of powder production, pressing and storage, and for the particle surface area concentrations (AM 7.6 µm(2)·cm(-3)) similar results were found. Correlating cobalt mass-based exposure measurements to cobalt stationary mass-based, particle area, and particle number concentrations by rank and department showed significant correlations for all measures except for particle number. Linear regression analysis of the same data showed statistically significant regression coefficients only for the mass-based aerosol measures. Similar results were seen for rank correlation in the stationary rig, and linear regression analysis implied significant correlation for mass-based and particle surface area measures. The mass-based air concentration levels of cobalt and tungsten in the hard metal plant in our study were low compared to Swedish OELs. Particle number and particle surface area concentrations were in the same order of magnitude as for other industrial settings. Regression analysis implied the use of stationary determined mass-based and particle surface area aerosol concentration as proxies for various exposure measures in our study.

Inflammatory markers and exposure to airborne particles among workers in a Swedish pulp and paper mill.

PURPOSE: To study the relationship between exposure to airborne particles in a pulp and paper mill and markers of inflammation and coagulation in blood. METHODS: Personal sampling of inhalable dust was performed for 72 subjects working in a Swedish pulp and paper mill. Stationary measurements were used to study concentrations of total dust, respirable dust, PM10 and PM2.5, the particle surface area and the particle number concentrations. Markers of inflammation, interleukins (IL-1b, IL-6, IL-8, and IL-10), C-reactive protein (CRP), serum amyloid A (SAA), and fibrinogen and markers of coagulation factor VIII, von Willebrand, plasminogen activator inhibitor, and D-dimer were measured in plasma or serum. Sampling was performed on the last day of the work free period of 5 days, before and after the shift the first day of work and after the shifts the second and third day. In a mixed model analysis, the relationship between particulate exposures and inflammatory markers was determined. Sex, age, smoking, and BMI were included as covariates. RESULTS: The average 8-h time-weighted average (TWA) air concentration levels of inhalable dust were 0.30 mg/m(3), range 0.005-3.3 mg/m(3). The proxies for average 8-h TWAs of respirable dust were 0.045 mg/m(3). Significant and consistent positive relations were found between several exposure metrics (PM 10, total and inhalable dust) and CRP, SAA and fibrinogen taken post-shift, suggesting a dose-effect relationship. CONCLUSION: This study supports a relationship between occupational particle exposure and established inflammatory markers, which may indicate an increased risk of cardiovascular disease.

Occupational Exposure to Trichloramine and Trihalomethanes in Swedish Indoor Swimming Pools: Evaluation of Personal and Stationary Monitoring.

INTRODUCTION: Chlorination is a method commonly used to keep indoor swimming pool water free from pathogens. However, chlorination of swimming pools produces several potentially hazardous by-products as the chlorine reacts with nitrogen containing organic matter. Up till now, exposure assessments in indoor swimming pools have relied on stationary measurements at the poolside, used as a proxy for personal exposure. However, measurements at fixed locations are known to differ from personal exposure. METHODS: Eight public swimming pool facilities in four Swedish cities were included in this survey. Personal and stationary sampling was performed during day or evening shift. Samplers were placed at different fixed positions around the pool facilities, at ~1.5 m above the floor level and 0-1 m from the poolside. In total, 52 personal and 110 stationary samples of trichloramine and 51 personal and 109 stationary samples of trihalomethanes, were collected. RESULTS: The average concentration of trichloramine for personal sampling was 71 µg m(-3), ranging from 1 to 240 µg m(-3) and for stationary samples 179 µg m(-3), ranging from 1 to 640 µg m(-3). The air concentrations of chloroform were well below the occupational exposure limit (OEL). For the linear regression analysis and prediction of personal exposure to trichloramine from stationary sampling, only data from personal that spent >50% of their workday in the pool area were included. The linear regression analysis showed a correlation coefficient (r2) of 0.693 and a significant regression coefficient ß of 0.621; (95% CI = 0.329-0.912, P = 0.001). CONCLUSION: The trichloramine exposure levels determined in this study were well below the recommended air concentration level of 500 µg m(-3); a WHO reference value based on stationary sampling. Our regression data suggest a relation between personal exposure and area sampling of 1:2, implying an OEL of 250 µg m(-3) based on personal sampling.

All-cause mortality in 272,186 patients hospitalized with incident atrial fibrillation 1995-2008: a Swedish nationwide long-term case-control study.

AIMS: To evaluate long-term all-cause risk of mortality in women and men hospitalized for the first time with atrial fibrillation (AF) compared with matched controls. METHODS AND RESULTS: A total of 272 186 patients (44% women) ≤ 85 years at the time of hospitalization with incidental AF 1995-2008 and 544 344 matched controls free of in-hospital diagnosis of AF were identified. Patients were followed via record linkage of the Swedish National Patient Registry and the Cause of Death Registry. Using Cox regression models, the long-term relative all-cause mortality risk, adjusted for concomitant diseases, in women vs. controls was 2.15, 1.72, and 1.44 (P < 0.001) in the age categories ≤ 65, 65-74, and 75-85 years, respectively. The corresponding figures for men were 1.76, 1.36, and 1.24 (P < 0.001). Among concomitant diseases, neoplasm, chronic renal failure, and chronic obstructive pulmonary disease contributed most to the increased all-cause mortality vs. controls. In patients with AF as the primary diagnosis, the relative risk of mortality was 1.63, 1.46, and 1.28 (P < 0.001) in women and 1.45, 1.17, and 1.10 (P < 0.001) in men. CONCLUSION: Atrial fibrillation was an independent risk factor of all-cause mortality in patients with incident AF. The concomitant diseases that contributed most were found outside the thromboembolic risk scores. The highest relative risk of mortality was seen in women and in the youngest patients compared with controls, and the differences between genders in each age category were statistically significant.

Occupational Dust Exposure as a Risk Factor for Developing Lung Function Impairment.

OBJECTIVE: Dust exposure is high in several industries. We investigated associations of exposure in paper mills, wood pellet plants, and iron foundries with lung function impairment. METHODS: Respirable silica, inhalable paper dust, or inhalable wood dust were collected as personal samples and spirometry was performed. Multiple linear regression analyzed associations with FEV 1 %pred and FVC%pred. RESULTS: Wood pellet workers with high exposure to inhalable dust had lower FEV 1 %pred (95% CI) (-9.4 [-16 to -2.6]) and FVC%pred (-9.8 [-15 to -4.0]) compared with lowest exposure level. Workers at paper mills and foundries had no dose-dependent association but lower FEV 1 %pred and FVC%pred than in workers at wood pellets plants. CONCLUSIONS: Increased exposure to inhalable wood dust is associated with decreased lung function. Foundry and paper mill workers have generally lower lung function than wood pellet workers. Spirometry should be considered in workers in industries with airborne particulate matter pollution.

The risk for ophthalmological conditions in ulcerative colitis: A population-based case-control study. Is silica dust-exposure associated with inflammatory eye disease?

PURPOSE: To study the risk for eye diseases in individuals with Ulcerative Colitis (UC), and to assess whether silica dust-exposure could contribute to the development of inflammatory eye diseases. METHODS: A case-control study was conducted using a patient register processed by the National Board of Health and Welfare (NBHW) and Statistics Sweden. Cases were diagnosed with UC between 2007 and 2016. Matching was done with two random controls having the same age, sex and county of residence, without a systemic inflammatory disease. Using a job-exposure matrix, cases and controls were assessed for work-related silica dust exposure. The risk for eye disease was estimated by Cox regression analysis with calculation of Hazard Ratio (HR). RESULTS: A total of 58 989 individuals were included, comprising 19 663 cases and 39 326 controls. The sex distribution was similar. Overall, individuals with UC had an increased risk for eye disease, specified in ICD 10 chapter VII (H00-H59) with HR 1.25 (CI 1.20-1.32). The highest HR on block-level for cases was 1.52 (CI 1.36-1.70), (H15-H22), which includes episcleritis, keratitis and anterior uveitis. The risk for ocular disease was higher in silica dust-exposed than non-exposed with a HR of 1.44 (CI 1.16-1.78) and 1.25 (CI 1.19-1.31), respectively. Among cases, the risk for iridocyclitis (H20) was further elevated by silica dust exposure, with HR of 3.84 (CI 1.64-8.97) in exposed compared to 1.94 (1.57-2.41) in non-exposed. CONCLUSION: UC is associated with an increased risk for eye diseases, including inflammatory conditions. Our findings highlight that silica dust-exposure may be of importance in the pathogenesis of uveitis.