Search

Background: Road-traffic noise may influence the development of cardiovascular events such as stroke and myocardial infarction, but etiological mechanisms remain unclear. This study aimed to assess the relationship between long-term road-traffic noise exposure and coronary atherosclerosis in Sweden., Methods: In the Swedish CArdioPulmonary bioImage Study (SCAPIS) cohort, including 30,154 subjects aged 50-65 years, recruited between 2013 and 2018, coronary atherosclerosis was measured based on computer tomography (CT) scans as coronary artery calcium score, segment involvement score (SIS), and non-calcified plaques (NCP) at enrollment. Based on modified Nordic model, road-traffic noise exposure was modeled for 2000, 2013, and 2018 with interpolation for intermediate years. We investigated the association between time-weighted long-term exposure to road-traffic noise (L den ) and the prevalence of atherosclerosis using ordinal logistic regression models adjusting for potential socioeconomic, behavioral, and environmental confounders, including air pollution., Results: No clear associations were found between road-traffic noise and coronary atherosclerosis. The odds ratio for coronary artery calcium score was 1.00 (95% confidence interval [CI] = 0.96, 1.04), SIS 0.99 (0.96, 1.03), and NCP 0.98 (0.90, 1.03) per interquartile range (9.4 dB L den ) for road-traffic noise exposure during 10 years before enrollment. No consistent associations were observed in site-specific analyses or using shorter exposure periods. Furthermore, exposure-response analyses revealed no clear trends, and there were no strong interactions between road-traffic noise and cardiovascular risk factors in relation to the atherosclerosis markers., Conclusions: Long-term exposure to road-traffic noise was not linked to coronary atherosclerosis or calcification in relatively healthy, middle-aged populations in Sweden., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report., (Copyright © 2024 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)

Background and Aims: Despite firm evidence for an association between long-term ambient air pollution exposure and cardiovascular morbidity and mortality, results from epidemiological studies on the association between air pollution exposure and atherosclerosis have not been consistent. We investigated associations between long-term low-level air pollution exposure and coronary atherosclerosis., Methods: We performed a cross-sectional analysis in the large Swedish CArdioPulmonary bioImaging Study (SCAPIS, n = 30 154), a random general population sample. Concentrations of total and locally emitted particulate matter <2.5 μm (PM 2.5 ), <10 μm (PM 10 ), and nitrogen oxides (NO x ) at the residential address were modelled using high-resolution dispersion models. We estimated associations between air pollution exposures and segment involvement score (SIS), coronary artery calcification score (CACS), number of non-calcified plaques (NCP), and number of significant stenoses, using ordinal regression models extensively adjusted for potential confounders., Results: Median 10-year average PM 2.5 exposure was 6.2 μg/m 3 (range 3.5-13.4 μg/m 3 ). 51 % of participants were women and 51 % were never-smokers. None of the assessed pollutants were associated with a higher SIS or CACS. Exposure to PM 2.5 was associated with NCP (adjusted OR 1.34, 95 % CI 1.13, 1.58, per 2.05 μg/m 3 ). Associations with significant stenoses were inconsistent., Conclusions: In this large, middle-aged general population sample with low exposure levels, air pollution was not associated with measures of total burden of coronary atherosclerosis. However, PM 2.5 appeared to be associated with a higher prevalence of non-calcified plaques. The results suggest that increased risk of early-stage atherosclerosis or rupture, but not increased total atherosclerotic burden, may be a pathway for long-term air pollution effects on cardiovascular disease., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: Available evidence suggests a link between exposure to transportation noise and an increased risk of obesity. We aimed to assess exposure-response functions for long-term residential exposure to road traffic, railway and aircraft noise, and markers of obesity., Methods: Our cross-sectional study is based on pooled data from 11 Nordic cohorts, including up to 162,639 individuals with either measured (69.2%) or self-reported obesity data. Residential exposure to transportation noise was estimated as a time-weighted average L den 5 years before recruitment. Adjusted linear and logistic regression models were fitted to assess beta coefficients and odds ratios (OR) with 95% confidence intervals (CI) for body mass index, overweight, and obesity, as well as for waist circumference and central obesity. Furthermore, natural splines were fitted to assess the shape of the exposure-response functions., Results: For road traffic noise, the OR for obesity was 1.06 (95% CI = 1.03, 1.08) and for central obesity 1.03 (95% CI = 1.01, 1.05) per 10 dB L den . Thresholds were observed at around 50-55 and 55-60 dB L den , respectively, above which there was an approximate 10% risk increase per 10 dB L den increment for both outcomes. However, linear associations only occurred in participants with measured obesity markers and were strongly influenced by the largest cohort. Similar risk estimates as for road traffic noise were found for railway noise, with no clear thresholds. For aircraft noise, results were uncertain due to the low number of exposed participants., Conclusion: Our results support an association between road traffic and railway noise and obesity., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report., (Copyright © 2024 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)

In this study, the long-term mortality effects associated with exposure to PM 10 (particles with an aerodynamic diameter smaller than or equal to 10 µm), PM 2.5 (particles with an aerodynamic diameter smaller than or equal to 2.5 µm), BC (black carbon), and NO x (nitrogen oxides) were analyzed in a cohort in southern Sweden during the period from 1991 to 2016. Participants (those residing in Malmö, Sweden, born between 1923 and 1950) were randomly recruited from 1991 to 1996. At enrollment, 30,438 participants underwent a health screening, which consisted of questionnaires about lifestyle and diet, a clinical examination, and blood sampling. Mortality data were retrieved from the Swedish National Cause of Death Register. The modeled concentrations of PM 10 , PM 2.5 , BC, and NO x at the cohort participants' home addresses were used to assess air pollution exposure. Cox proportional hazard models were used to estimate the associations between long-term exposure to PM 10 , PM 2.5 , BC, and NO x and the time until death among the participants during the period from 1991 to 2016. The hazard ratios (HRs) associated with an interquartile range (IQR) increase in each air pollutant were calculated based on the exposure lag windows of the same year (lag0), 1-5 years (lag1-5), and 6-10 years (lag6-10). Three models were used with varying adjustments for possible confounders including both single-pollutant estimates and two-pollutant estimates. With adjustments for all covariates, the HRs for PM 10 , PM 2.5 , BC, and NO x in the single-pollutant models at lag1-5 were 1.06 (95% CI: 1.02-1.11), 1.01 (95% CI: 0.95-1.08), 1.07 (95% CI: 1.04-1.11), and 1.11 (95% CI: 1.07-1.16) per IQR increase, respectively. The HRs, in most cases, decreased with the inclusion of a larger number of covariates in the models. The most robust associations were shown for NO x , with statistically significant positive HRs in all the models. An overall conclusion is that road traffic-related pollutants had a significant association with mortality in the cohort.

Air pollution is a major contributor to the global burden of disease and has been linked to several diseases and conditions, including cardiovascular disease. The biological mechanisms are related to inflammation and increased coagulability, factors that play an important role in the pathogenesis of venous thromboembolism (VTE, i.e., deep vein thrombosis or pulmonary embolism). This study investigates if long-term exposure to air pollution is associated with increased VTE incidence. The study followed 29 408 participants from the Malmö Diet and Cancer (MDC) cohort, which consists of adults aged 44-74 recruited in Malmö, Sweden between 1991 and 1996. For each participant, annual mean residential exposures to particulate matter <2.5 μg (PM 2.5 ) and <10 μg (PM 10 ), nitrogen oxides (NO x ) and black carbon (BC) from 1990 up to 2016 were calculated. Associations with VTE were analysed using Cox proportional hazard models for air pollution in the year of the VTE event (lag0) and the mean of the prior 1-10 years (lag1-10). Annual air pollution exposures for the full follow-up period had the following means: 10.8 μg/m 3 for PM 2.5 , 15.8 μg/m 3 for PM 10 , 27.7 μg/m 3 for NO x , and 0.96 μg/m 3 for BC. The mean follow-up period was 19.5 years, with 1418 incident VTE events recorded during this period. Exposure to lag1-10 PM 2.5 was associated with an increased risk of VTE (HR 1.17 (95%CI 1.01-1.37)) per interquartile range (IQR) of 1.2 μg/m 3 increase in PM 2.5 exposure. No significant associations were found between other pollutants or lag0 PM 2.5 and incident VTE. When VTE was divided into specific diagnoses, associations with lag1-10 PM 2.5 exposure were similarly positive for deep vein thrombosis but not for pulmonary embolism. Results persisted in sensitivity analyses and in multi-pollutant models. Long-term exposure to moderate concentrations of ambient PM 2.5 was associated with increased risks of VTE in the general population in Sweden., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Environmental noise is an important environmental exposure that can affect health. An association between transportation noise and breast cancer incidence has been suggested, although current evidence is limited. We investigated the pooled association between long-term exposure to transportation noise and breast cancer incidence., Methods: Pooled data from eight Nordic cohorts provided a study population of 111,492 women. Road, railway, and aircraft noise were modelled at residential addresses. Breast cancer incidence (all, estrogen receptor (ER) positive, and ER negative) was derived from cancer registries. Hazard ratios (HR) were estimated using Cox Proportional Hazards Models, adjusting main models for sociodemographic and lifestyle variables together with long-term exposure to air pollution., Results: A total of 93,859 women were included in the analyses, of whom 5,875 developed breast cancer. The median (5th-95th percentile) 5-year residential road traffic noise was 54.8 (40.0-67.8) dB Lden, and among those exposed, the median railway noise was 51.0 (41.2-65.8) dB Lden. We observed a pooled HR for breast cancer (95 % confidence interval (CI)) of 1.03 (0.99-1.06) per 10 dB increase in 5-year mean exposure to road traffic noise, and 1.03 (95 % CI: 0.96-1.11) for railway noise, after adjustment for lifestyle and sociodemographic covariates. HRs remained unchanged in analyses with further adjustment for PM 2.5 and attenuated when adjusted for NO 2 (HRs from 1.02 to 1.01), in analyses using the same sample. For aircraft noise, no association was observed. The associations did not vary by ER status for any noise source. In analyses using <60 dB as a cutoff, we found HRs of 1.08 (0.99-1.18) for road traffic and 1.19 (0.95-1.49) for railway noise., Conclusions: We found weak associations between road and railway noise and breast cancer risk. More high-quality prospective studies are needed, particularly among those exposed to railway and aircraft noise before conclusions regarding noise as a risk factor for breast cancer can be made., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background Colon cancer incidence is rising globally, and factors pertaining to urbanization have been proposed involved in this development. Traffic noise may increase colon cancer risk by causing sleep disturbance and stress, thereby inducing known colon cancer risk-factors, e.g. obesity, diabetes, physical inactivity, and alcohol consumption, but few studies have examined this. Objectives The objective of this study was to investigate the association between traffic noise and colon cancer (all, proximal, distal) in a pooled population of 11 Nordic cohorts, totaling 155,203 persons. Methods We identified residential address history and estimated road, railway, and aircraft noise, as well as air pollution, for all addresses, using similar exposure models across cohorts. Colon cancer cases were identified through national registries. We analyzed data using Cox Proportional Hazards Models, adjusting main models for harmonized sociodemographic and lifestyle data. Results During follow-up (median 18.8 years), 2757 colon cancer cases developed. We found a hazard ratio (HR) of 1.05 (95% confidence interval (CI): 0.99-1.10) per 10-dB higher 5-year mean time-weighted road traffic noise. In sub-type analyses, the association seemed confined to distal colon cancer: HR 1.06 (95% CI: 0.98-1.14). Railway and aircraft noise was not associated with colon cancer, albeit there was some indication in sub-type analyses that railway noise may also be associated with distal colon cancer. In interaction-analyses, the association between road traffic noise and colon cancer was strongest among obese persons and those with high NO 2 -exposure. Discussion A prominent study strength is the large population with harmonized data across eleven cohorts, and the complete address-history during follow-up. However, each cohort estimated noise independently, and only at the most exposed façade, which may introduce exposure misclassification. Despite this, the results of this pooled study suggest that traffic noise may be a risk factor for colon cancer, especially of distal origin., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: Air pollution is associated with cardiovascular morbidity and mortality, but its role in the development of congestive heart failure (CHF) and the role of different pollution sources in cardiovascular disease remain uncertain., Methods: Participants were enrolled in the Malmö Diet and Cancer cohort in 1991-1996 with information on lifestyle and clinical indicators of cardiovascular disease. The cohort participants were followed through registers until 2016. Annual total and local source-specific concentrations of particulate matter less than 10 μm and 2.5 μm (PM 10 and PM 2.5 ), black carbon (BC), and nitrogen oxides (NO x ) from traffic, residential heating, and industry were assigned to each participant's address throughout the study period. Cox proportional hazards models adjusted for possible confounders was used to estimate associations between air pollution 1-5 years prior to outcomes of incident CHF, fatal myocardial infarction (MI), major adverse coronary events (MACE), and ischemic stroke., Results: Air pollution exposure levels (mean annual exposures to PM 2.5 of 11 μg/m 3 and NO x of 26 μg/m 3 ) within the cohort were moderate in terms of environmental standards. After adjusting for confounders, we observed statistically significant associations between NO x and CHF (hazard ratio [HR] 1.11, 95% confidence interval [CI] 1.01-1.22) and NO x and fatal MI (HR 1.10, 95%CI 1.01-1.20) per interquartile range (IQR) of 9.6 μg/m 3 . In fully adjusted models, the estimates were similar, but the precision worse. In stratified analyses, the associations were stronger in males, ever-smokers, older participants, and those with baseline carotid artery plaques. Locally emitted and traffic-related air pollutants generally showed positive associations with CHF and fatal MI. There were no associations between air pollution and MACE or stroke., Discussion/conclusion: In an area with low to moderate air pollution exposure, we observed significant associations of long-term residential NO x with increased risk of incident CHF and fatal MI, but not with coronary events and stroke., (Copyright © 2022. Published by Elsevier Inc.)

Introduction: Air pollution is associated with increased risk of cardiovascular disease, possibly through chronic systemic inflammation that promotes the progression of atherosclerosis and the risk of cardiovascular events. This study aimed to investigate the associations between air pollution and established biomarkers of inflammation and cardiovascular disease., Methods: The Cardiovascular Subcohort of the Malmö Diet and Cancer cohort includes 6103 participants from the general population of Malmö, Sweden. The participants were recruited 1991-1994. Annual mean residential exposure to particulate matter < 2.5 and < 10 μm (PM 2.5 and PM 10 ), and nitrogen oxides (NO x ) at year of recruitment were assigned from dispersion models. Blood samples collected at recruitment, including blood cell counts, and biomarkers (lymphocyte- and neutrophil counts, C-reactive protein (CRP), soluble urokinase-type plasminogen activator receptor (suPAR), lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ), ceruloplasmin, orosomucoid, haptoglobin, complement-C3, and alpha-1-antitrypsin) were analyzed. Multiple linear regression models were used to investigate the cross-sectional associations between air pollutants and biomarkers., Results: The mean annual exposure levels in the cohort were only slightly or moderately above the new WHO guidelines of 5 μg/m 3 PM 2.5 (10.5 μg/m 3 PM 2.5 ). Residential PM 2.5 exposure was associated with increased levels of ceruloplasmin, orosomucoid, C3, alpha-1-antitrypsin, haptoglobin, Lp-PLA 2 and the neutrophil-lymphocyte ratio. Ceruloplasmin, orosomucoid, C3 and alpha-1-antitrypsin were also positively associated with PM 10 . There were no associations between air pollutants and suPAR, leukocyte counts or CRP. The associations between particles and biomarkers were still significant after removing outliers and adjustment for CRP levels. The associations were more prominent in smokers., Conclusion: Long-term residential exposure to moderate levels of particulate air pollution was associated with several biomarkers of inflammation and cardiovascular disease. This supports inflammation as a mechanism behind the association between air pollution and cardiovascular disease., (© 2022. The Author(s).)

Long-term air pollution exposure increases the risk for cardiovascular disease, but little is known about the temporal relationships between exposure and health outcomes. This study aims to estimate the exposure-lag response between air pollution exposure and risk for ischemic heart disease (IHD) and stroke incidence by applying distributed lag non-linear models (DLNMs). Annual mean concentrations of particles with aerodynamic diameter less than 2.5 µm (PM 2.5 ) and black carbon (BC) were estimated for participants in five Swedish cohorts using dispersion models. Simultaneous estimates of exposure lags 1-10 years using DLNMs were compared with separate year specific (single lag) estimates and estimates for lag 1-5- and 6-10-years using moving average exposure. The DLNM estimated no exposure lag-response between PM 2.5 total, BC, and IHD. However, for PM 2.5 from local sources, a 20% risk increase per 1 µg/m 3 for 1-year lag was estimated. A risk increase for stroke was suggested in relation to lags 2-4-year PM 2.5 and BC, and also lags 8-9-years BC. No associations were shown in single lag models. Increased risk estimates for stroke in relation to lag 1-5- and 6-10-years BC moving averages were observed. Estimates generally supported a greater contribution to increased risk from exposure windows closer in time to incident IHD and incident stroke.

Background: Transportation noise is increasingly acknowledged as a cardiovascular risk factor, but the evidence base for an association with stroke is sparse., Objective: We aimed to investigate the association between transportation noise and stroke incidence in a large Scandinavian population., Methods: We harmonized and pooled data from nine Scandinavian cohorts (seven Swedish, two Danish), totaling 135,951 participants. We identified residential address history and estimated road, railway, and aircraft noise for all addresses. Information on stroke incidence was acquired through linkage to national patient and mortality registries. We analyzed data using Cox proportional hazards models, including socioeconomic and lifestyle confounders, and air pollution., Results: During follow-up ( median = 19.5 y ), 11,056 stroke cases were identified. Road traffic noise ( L den ) was associated with risk of stroke, with a hazard ratio (HR) of 1.06 [95% confidence interval (CI): 1.03, 1.08] per 10-dB higher 5-y mean time-weighted exposure in analyses adjusted for individual- and area-level socioeconomic covariates. The association was approximately linear and persisted after adjustment for air pollution [particulate matter (PM) with an aerodynamic diameter of ≤ 2.5 μ m ( PM 2.5 ) and NO 2 ]. Stroke was associated with moderate levels of 5-y aircraft noise exposure (40-50 vs. ≤ 40  dB ) ( HR = 1.12 ; 95% CI: 0.99, 1.27), but not with higher exposure ( ≥ 50  dB , HR = 0.94 ; 95% CI: 0.79, 1.11). Railway noise was not associated with stroke., Discussion: In this pooled study, road traffic noise was associated with a higher risk of stroke. This finding supports road traffic noise as an important cardiovascular risk factor that should be included when estimating the burden of disease due to traffic noise. https://doi.org/10.1289/EHP8949.

Background: Long-term exposure to air pollution increases the risk of cardiovascular morbidity and mortality, but the mechanisms are not fully known. Current evidence suggests that air pollution exposure contributes to the development of atherosclerosis. There are few studies investigating associations between air pollution and carotid plaques, a well-known precursor of cardiovascular disease., Methods: A Swedish population-based cohort (aged 45-64 years at recruitment) was randomly selected from the Malmö Diet and Cancer study between 1991 and 1994, of which 6103 participants underwent ultrasound examination of the right carotid artery to determine carotid plaque presence and carotid intima media thickness (CIMT). Participants were assigned individual residential air pollution exposure (source-specific PM 2.5 , PM 10 , NO x , BC) at recruitment from Gaussian dispersion models. Logistic and linear regression models, adjusted for potential confounders and cardiovascular risk factors, were used to investigate associations between air pollutants and prevalence of carotid plaques, and CIMT, respectively., Results: The prevalence of carotid plaques was 35%. The mean levels of PM 2.5 and PM 10 at recruitment were 11 and 14 μg/m 3 , most of which was due to long range transport. The exposure contrast within the cohort was relatively low. PM 2.5 exposure was associated with carotid plaques in a model including age and sex only (OR 1.10 (95% CI 1.01-1.20) per 1 μg/m 3 ), but after adjustment for cardiovascular risk factors and socioeconomic status (SES) the association was weak and not significant (OR 1.05 (95% CI 0.96-1.16) per 1 μg/m 3 ). The pattern was similar for PM 10 and NO x exposure. Associations between air pollutants and plaques were slightly stronger for long-term residents and in younger participants with hypertension. There was no clear linear trend between air pollution exposure and plaque prevalence. Non-significant slightly positive associations were seen between air pollution exposures and CIMT., Conclusions: In this large, well-controlled cross-sectional study at low exposure levels we found no significant associations between air pollution exposures and subclinical atherosclerosis in the carotid arteries, after adjusting for cardiovascular risk factors and SES. Further epidemiological studies of air pollution and intermediate outcomes are needed to explain the link between air pollution and cardiovascular events., (Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.)

Air pollution is responsible for one in eight premature deaths worldwide, and thereby a major threat to human health. Health impact assessments of hypothetic changes in air pollution concentrations can be used as a mean of assessing the health impacts of policy, plans and projects, and support decision-makers in choices to prevent disease. The aim of this study was to estimate health impacts attributable to a hypothetical decrease in air pollution concentrations in the city of Malmö in Southern Sweden corresponding to a policy on-road transportations without tail-pipe emissions in the municipality. We used air pollution data modelled for each of the 326,092 inhabitants in Malmö by a Gaussian dispersion model combined with an emission database with >40,000 sources. The dispersion model calculates Nitrogen Oxides (NO x ) (later transformed into Nitrogen Dioxide (NO 2 )) and particulate matter with an aerodynamic diameter < 2.5 μg/m 3 (PM 2.5 ) with high spatial and temporal resolution (85 m and 1 h, respectively). The average individual reduction was 5.1 (ranging from 0.6 to 11.8) μg/m 3 in NO 2, which would prevent 55 (2% of all deaths) to 93 (4%) deaths annually, depending on dose-response function used. Furthermore, we estimate that the NO 2 reduction would result in 21 (6%) fewer cases of incident asthma in children, 95 (10%) fewer children with bronchitis every year, 30 (1%) fewer hospital admissions for respiratory disease, 87(4%) fewer dementia cases, and 11(11%) fewer cases of preeclampsia every year. The average reduction in PM 2.5 of 0.6 (ranging from 0.1 till 1.7) μg/m 3 would mean that 2729 (0.3%) work days would not be lost due to sick-days and that there would be 16,472 fewer restricted activity days (0.3%) that year had all on-road transportations been without tail-pipe emissions. Even though the estimates are sensitive to the dose-response functions used and to exposure misclassification errors, even the most conservative estimate of the number of prevented deaths is 7 times larger than the annual traffic fatalities in Malmö, indicating a substantial possibility to reduce the health burden attributed to tail-pipe emissions in the study area., (Copyright © 2018. Published by Elsevier Ltd.)

A new type of isocyanate sampler has been used to investigate aging aerosols generated during thermal degradation of polyurethane (PUR). The sampler consists of a denuder connected in series with a three-stage cascade impactor and a filter. The denuder collects gas-phase isocyanates. The three impactor stages had cut-off diameters (d(50)) of 2.5, 1.0 and 0.5 mum, respectively. The end filter collects particles <0.5 mum. For derivatization of isocyanates in the sampler, di-n-butylamine mixed with an equimolar amount of acetic acid was used for impregnation of the sampler stages. Consecutive sampling using three denuder-impactor samplers was performed in a test chamber, with a total sampling time of 9 min. Analysis of air samples was performed using liquid chromatography-mass spectrometry (LC-MS)/MS. Particle size measurements were performed using a scanning mobility particle sizer (SMPS). A time-dependent behavior was observed for aromatic diisocyanates during aging of the aerosol. Thermal degradation of different PUR materials showed different distribution of isocyanates between gas and particles. Aromatic diisocyanates (toluene diisocyanate (TDI) and methylene diphenyl diisocyanate) were initially in gas phase and associated to very small particles. After a few minutes most of these isocyanates were associated with particles <1 mum. Monoisocyanates and hexamethylene diisocyanate (HDI) were not found to be associated with particles.

Isocyanates in the workplace atmosphere are typically present both in gas and particle phase. The health effects of exposure to isocyanates in gas phase and different particle size fractions are likely to be different due to their ability to reach different parts in the respiratory system. To reveal more details regarding the exposure to isocyanate aerosols, a denuder-impactor (DI) sampler for airborne isocyanates was designed. The sampler consists of a channel-plate denuder for collection of gaseous isocyanates, in series with three-cascade impactor stages with cut-off diameters (d(50)) of 2.5, 1.0 and 0.5 mum. An end filter was connected in series after the impactor for collection of particles smaller than 0.5 mum. The denuder, impactor plates and the end filter were impregnated with a mixture of di-n-butylamine (DBA) and acetic acid for derivatization of the isocyanates. During sampling, the reagent on the impactor plates and the end filter is continuously refreshed, due to the DBA release from the impregnated denuder plates. This secures efficient derivatization of all isocyanate particles. The airflow through the sampler was 5 l min(-1). After sampling, the samples containing the different size fractions were analyzed using liquid chromatography-mass spectrometry (LC-MS)/MS. The DBA impregnation was stable in the sampler for at least 1 week. After sampling, the DBA derivatives were stable for at least 3 weeks. Air sampling was performed in a test chamber (300 l). Isocyanate aerosols studied were thermal degradation products of different polyurethane polymers, spraying of isocyanate coating compounds and pure gas-phase isocyanates. Sampling with impinger flasks, containing DBA in toluene, with a glass fiber filter in series was used as a reference method. The DI sampler showed good compliance with the reference method, regarding total air levels. For the different aerosols studied, vast differences were revealed in the distribution of isocyanate in gas and different particle size fractions. The opportunity to obtain detailed information regarding the distribution of isocyanates in aerosols in addition to the total air levels make the DI sampler a valuable tool for studies of possible health effects in the different parts of the airways.

The aim of this study was to investigate if the uptake of N-methyl-2-pyrrolidone (NMP), a widely used industrial chemical, increases after exposure to NMP in humid air compared to dry air. NMP has been described to be an airway irritant and a developmentally toxic compound. Six male volunteers were exposed to NMP, three at the time, for 8h in an exposure chamber. They were each exposed on four different occasions to air levels of 0 and 20mg NMP/m(3) in dry and humid air. Blood and urine were sampled before, during and up to 5 days after the end of the 8-h exposure. Plasma and urine were analysed for NMP and its metabolites, using liquid chromatography-tandem mass spectrometry. There was no statistically significant increase in the total cumulated excretion of NMP and its metabolites in urine after exposure in humid air as compared to dry air. Furthermore, there were no differences in the levels of peak concentrations in either plasma or urine. Also, no differences were found in AUC between the exposures. However, there were large individual differences, especially for the exposure in humid air. A not previously identified metabolite in human, 2-pyrrolidone (2-P), was identified. The results do not support a significantly higher absorption of NMP at exposure in humid air as compared to dry air. However, the large individual differences support the use of biological monitoring for assessment of NMP exposure. In addition, 2-P was confirmed to be an NMP metabolite in humans. This may be of importance for the developmental toxicity of NMP since 2-P have been described to be a reproductively toxic substance.

Isocyanates constitute a group of highly reactive chemicals used on a large scale for the production of flexible polyurethane (PUR) foam. Exposure to isocyanates is known to produce irritation of the mucous membranes and the eyes. Isocyanates also have strong sensitizing properties and may cause occupational asthma. It is therefore important to monitor isocyanate emissions at workplaces. To obtain information for the improvement of isocyanate samplers and for health risk assessments of exposure, the emitted aerosol from two types of flexible PUR foam subjected to thermal degradation was characterized. Particle size distribution and toluene diisocyanate (TDI) concentration in the emitted aerosols were measured. Thermal degradation of flexible PUR foam at temperatures from 250 to 300 degrees C produced an aerosol with a geometric mean particle diameter of 30-50 nm. Between 5% and 9% of the PUR foam was emitted as TDI, and 2% to 6% of TDI monomers were found in the particle phase under the experimental conditions used. The 2,6-TDI isomer was more abundant in the gas phase than in the particle phase.

A methodology for workplace air monitoring of aromatic and aliphatic, mono- and polyisocyanates by derivatisation with di-n-butylamine (DBA) is presented. Air sampling was performed using midget impinger flasks containing 10 ml of 0.01 mol l(-1) DBA in toluene and a glass-fibre filter in series after the impinger flask, thereby providing the possibility of collecting and derivatising isocyanates in both the gas and particle phases. Quantification was made by LC-MS, monitoring the molecular ions [MH]+. Air samples taken with this method in car repair shops showed that many different isocyanates are formed during thermal decomposition of polyurethane (PUR) coatings. In addition to isocyanates such as hexamethylene (HDI), isophorone (IPDI), toluene (TDI) and methylenediphenyl diisocyanate (MDI), monoisocyanates such as methyl (MIC), ethyl (EIC), propyl (PIC), butyl (BIC) and phenyl isocyanate (PhI) were found. In many air samples the aliphatic monoisocyanates dominated. During cutting and welding operations, the highest levels of isocyanates were observed. In a single air sample from a welding operation in a car repair shop, the highest concentrations found were: MIC, 290; EIC, 60; PIC, 20; BIC, 9; PhI, 27; HDI, 105; IPDI, 39; MDI, 4; and 2,4-TDI and 2,6-TDI 140 microg m(-3). Monitoring the particle size distribution and concentration during grinding, welding and cutting operations showed that ultrafine particles (< 0.1 microm) were formed at high concentrations. Isocyanates with low volatility were mainly found in the particle phase, but isocyanates with a relatively high volatility such as TDI, were found in both the particle and gas phases.

A method is presented for the determination of isocyanates in polymeric methylenediphenyl diisocyanate (MDI) and related compounds formed during the thermal decomposition of polyurethane (PUR). Derivatization of isocyanates was performed in impinger flasks containing dibutylamine (DBA) with the formation of urea derivatives. Compounds containing amine groups were then derivatized with ethyl chloroformate (ET to give urethane derivatives. Reversed-phase liquid chromatography, with a gradient flow rate of 40 milligrams min-1 and mass spectrometry in the electrospray mode monitoring positive ions was studied. Injection volumes of up to 10 milligrams of the sample were made possible by using column focusing. 1,5-Naphthyldiisocyanate-DBA and 1,5-naphthyldiamine-ET derivatives were used as internal standards. Virtually linear calibration curves were obtained for 4,4'-MDI-DBA and 4,4'-methylenediphenyldiamine-ET (MDA-ET) and the correlation coefficients were 0.9952-0.9964 (n = 14). The precision for five injections of samples spiked with 4,4'-MDA-ET, and 4,4'-MDI-DBA ar concentrations of 50 nmol ml-1 was 2.76 and 2.55%, respectively. The instrumental detection limit, defined as three times the noise, was 4 fmol of MDI-DBA and 50 fmol of MDA-ET injected. In chromatograms of polymeric MDI derivatized with diethylamine, dipropylamine and DBA, the presence of several structural isomers and analogues in polymeric MDI was demonstrated. In the chromatograms of thermal decomposition products of MDI-PUR, in addition to isocyanates, related amino isocyanates and amines were also observed.