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Aim. To assess associations between occupational air pollution and respiratory health, especially in miners. Background. Indications of associations between occupational exposure or social economic status and respiratory health have been found in several population-based studies. However, there have been few longitudinal studies of the putative correlations, the effects of environmental and genetic factors have seldom been simultaneously studied, and studies of miners have generated conflicting results. Material and methods. Population-based Obstructive Lung Disease in Northern Sweden (OLIN) cohorts surveyed in 1986, 1992 and 1996, and two industry-based materials, were used in cross-sectional and longitudinal studies. Inflammatory markers were compared in sputa from miners after a vacation of at least four weeks, after repeated occupational exposures for at least three months, and controls. The mortality from silicosis was studied in 7729 miners with at least 1 year of exposure. Multivariate analyses were used to adjust for confounders. Results. Up to about 30-40% (etiologic fraction) of incident symptoms in persons both with and without a family history of asthma (FHA) could be explained by exposure to occupational air pollution. Low socio-economic status (SES) was associated with impaired respiratory health. Population attributable risks for most examined disorders were about 10%. Current and ex-miners had increased prevalence of recurrent wheeze, longstanding cough, physician-diagnosed chronic bronchitis, and a trend for increased sputum production. For physician-diagnosed chronic bronchitis a multiplicative interaction was found between exposure and smoking habits. Ex-miners that had been exposed for on average 13 years and whose exposure had ceased 16 years before the study had an increased prevalence of physician-diagnosed chronic bronchitis and chronic productive cough and a trend to increased use of asthma medicines. Miners exposed underground for 18 years, on average, to diesel exhaust (with 0.28 mg/m3 nitrogen dioxide and 27 μg/m3 elemental carbon on average, EC) and particles (3.2 mg/m3 inhalable dust on average) had signs of higher inflammatory activity in their airways, i.e. significantly higher frequencies of macrophages, neutrophils, and total cells compared with referents. The activity in miners was similar after a vacation of at least four weeks and after repeated exposures for three months. There were 58 deaths from silicosis (underlying and contributing cause of death) and a clear dose-response relationship. The data indicated an increased risk of severe silicosis after long-term exposure to 0.1 mg/m3 respirable quartz, the current maximum allowable concentration (MAC) in Sweden and many other countries. Conclusion. Occupational exposure to dust, gases, and fumes impaired respiratory health, accounting for up to 30-40% of some respiratory symptoms in the general population. Low socio-economic status was associated with impaired respiratory health. The complex profiles of dust and diesel exhaust substances found in mines may cause inflammatory reactions in their lungs and persistent respiratory symptoms in occupationally exposed miners. Long-term exposure to quartz at the present MAC level may cause severe silicosis.

Several epidemiological studies have revealed an association between particulate matter (PM) pollution and various health effects. Importantly, there is evidence to suggest that individuals with pre-existing respiratory disease, such as asthma, are more sensitive to elevated ground levels of particulate matter as compared to healthy subjects. Among the various sources of PM pollution, diesel powered vehicles have been identified as important contributors. The aim of this thesis was to investigate the airway effects of experimental chamber exposure to diesel exhaust (DE) in healthy and asthmatic subjects, focusing on airway responsiveness, airway inflammation and lung function. To achieve a comprehensive picture of the airway responses to DE, a number of different methods were used, including lung function measurements, methacholine inhalation tests, induced sputum and bronchoscopy. Each subject acted as his/her own control by being exposed both to filtered air and DE in a crossover design. Short term exposure to DE, at a particle concentration (PMi0) of 300 ug/m3, was associated with a clinically significant increase in bronchial hyperresponsiveness in asthmatic subjects. In accordance with the epidemiological data suggesting a 1-4 day lag effect for most health outcomes to PM pollution, the increase was detected one day after DE exposure, indicating a long lasting response to DE in asthmatic airways. Diesel exhaust induced a range of airway inflammatory changes as reflected in induced sputum, bronchoalveolar lavage and bronchial mucosal biopsies. In healthy subjects, DE exposure was associated with an increase in neutrophils and IL-6 in sputum, elevated levels of IL-8 and IL-6 in bronchial wash (BW), enhanced expression of IL-8 and GRO-a in the bronchial epithelium and with increases in P-selectin and VCAM-1 in the airway mucosa. In contrast, asthmatics responded with an increase in IL-6 in sputum and an enhanced expression of IL-10 in the bronchial epithelium following exposure DE. Thus, clear differences were identified between healthy and asthmatic subjects in the inflammatory response to DE. Airway epithelial cells constitute the first line of cellular defence towards inhaled air pollutants and increasing evidence suggests that these cells contribute markedly to the initiation of airway inflammatory responses. The bronchial epithelium was identified to have an important regulatory role in response to diesel exhaust, including the capacity to produce chemoattractant and immunoregulatory proteins associated with development of airway inflammation and bronchial hyperresponsiveness. Lung function measurements revealed that short-term exposure to DE induces an immediate bronchoconstrictive response in both healthy and asthmatic individuals, with significant increases in airway resistance (Raw) following DE exposure. This thesis also investigated the effects of a lower concentration of DE (PMio 100 ug/m3) than previously studied. It was shown that exposure to DE at a concentration corresponding to a PM level that may be encountered in busy traffic situations, was still associated with potentially adverse airway responses in healthy and asthmatic subjects. In summary, the results presented here indicate that short term exposure to diesel exhaust, at high ambient concentrations, has the potential to induce a range of biological events in the airways of healthy and asthmatic subjects. / <p>Diss. (sammanfattning) Umeå : Umeå universitet, 2002, härtill 4 uppsatser.</p> / digitalisering@umu

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Allergic airway disease, i.e. allergic rhinitis (AR) and asthma, is a common health problem. The prevalence is increasing in most countries of the world. Traffic-related air pollution has been found to induce and enhance allergic airway disease, but the underlying mechanisms are not known. Oxylipins are fatty acid metabolites, of which several have been linked to asthmatic airway inflammation. Oxylipin profiles have previously been investigated in bronchoalveolar lavage (BAL), mainly reflecting the peripheral lung, but not in bronchial wash (BW), which better reflect the proximal airways. The airway epithelium is covered by a respiratory tract lining fluid (RTLF) The RTLF contains antioxidants to protect from oxidative stress, which may be caused by exposure to air pollution. Previous studies have reported diminished levels of the antioxidant ascorbate (vitamin C) in the RTLF of patients with asthma. Little is known about the regulation of vitamin C in the lung. The aim of this thesis was to investigate airway inflammatory responses to diesel exhaust exposure in patients with AR and allergic asthma; to evaluate oxylipin profiles in different regions of the lung in patients with allergic asthma; and to study the distribution of vitamin C transporters in the airways of patients with allergic asthma. Diesel exhaust (PM10 100 μg/m3 for 2 h) induced a neutrophilic airway inflammation in healthy individuals evaluated 18 h after exposure. Patients with AR and asthma did not respond with an enhanced airway inflammation. However, a small increase in myeloperoxidase was found in BAL from patients with AR, as well as decreases in epithelial tryptase and BW stem cell factor. This indicates that other mechanisms than classical inflammation are responsible for the increased sensitivity to traffic-related air pollution in patients with allergic airway disease. Oxylipin baseline profiles differed between peripheral and proximal airways in both allergic asthmatics and healthy individuals. Total oxylipin concentrations, and five individual oxylipins, primarily from the lipoxygenase (LOX) pathway, were elevated in BW from asthmatics compared to healthy controls, supported by immunohistochemical staining of 15-LOX-1 in the bronchial epithelium. This suggests that lung compartment-specific sampling should be considered in future studies. Sodium dependent vitamin C transporter 2 (SVCT2) was, for the first time, found present in the human lung epithelium, localised mainly within goblet cells. A negative correlation between SVCT2+ goblet cells and vitamin C suggests that these cells may play a hitherto unknown function in ascorbate re-uptake and recycling at the air-lung interface.

Background Anthropogenic air pollution is a global health problem estimated to contribute to millions of premature deaths. Exposure to biomass smoke is common due to varying sources, such as wildfires, indoor cooking over open fires, and residential heating from wood stoves. In urban environments transportation and industry rely heavily on the combustion of fossil fuels yet environmental policies increasingly support a shift to renewable fuels such as biodiesel. It has not been investigated how either wood smoke or biodiesel exhaust affect human health in general or the cardiovascular system in particular. We hypothesized that wood smoke exposure would induce acute cardiovascular impairment via similar underlying mechanisms as have been established for petrodiesel exhaust exposure. We also hypothesized that replacing petrodiesel with biodiesel, as a blend or pure biodiesel, would generate an exhaust profile with a less harmful effect on the cardiovascular system than petrodiesel exhaust. Methods In four separate studies healthy non-smoking subjects were exposed to different air pollutants in controlled exposure chambers followed by clinical investigations of the cardiovascular system. All studies were performed as randomized controlled trials in a crossover fashion with each individual acting as her own control. In study I healthy volunteers were exposed to wood smoke at a target concentration of particulate matter (PM) 300 µg/m3 for three hours followed by measures of blood pressure, heart rate variability and central arterial stiffness. In study II subjects were exposed to wood smoke at a target concentration of PM 1000 µg/m3 for one hour followed by measures of thrombus formation using the Badimon technique and vasomotor function using forearm venous occlusion plethysmography. In study III subjects were exposed to petrodiesel exhaust and a 30% rapeseed methyl ester (RME30) biodiesel blend for one hour at a target concentration of PM 300 µg/m3. Following exposure, thrombus formation and vasomotor function were assessed as in study II. In study IV subjects were exposed to petrodiesel exhaust at a target concentration of PM 300 μg/m3for one hour and pure rapeseed methyl ester (RME100) exhaust generated at identical running conditions of the engine. Following exposure, thrombus formation and vasomotor function were assessed as in study II and III. Results In study I fourteen subjects (8 males) were exposed to wood smoke at P M 294±36 μg/m3. Compared to filtered air exposure, measures of central arterial stiffness were increased and heart rate variability was decreased following wood smoke exposure. No effect was seen on blood pressure. In study II sixteen males were exposed to wood smoke at PM 899±100 μg/m3. We found no evidence of increased thrombus formation or impaired vasomotor function following wood smoke exposure. In study III sixteen subjects (14 males) were exposed to petrodiesel exhaust (PM 314±27 µg/m3) and RME30 exhaust (PM 309±30 µg/m3). Thrombus formation and vasomotor function were equal following either exposure. In study IV nineteen males were exposed to petrodiesel exhaust (PM 310±34 µg/m3, 1.7±0.3 x105 particles/cm3) and RME100 exhaust (PM 165±16 µg/m3, 2.2±0.1 x105 particles/cm3). As in study III, thrombus formation and vasomotor function were identical following both exposures. Conclusions We have for the first time demonstrated that wood smoke exposure can increase central arterial stiffness and decrease heart rate variability in healthy subjects. We did not, however find evidence of increased thrombus formation and impaired vasomotor function following wood smoke exposure at a higher concentration for a shorter time period. We have, for the first time, demonstrated that exhaust from RME biodiesel induced acute adverse cardiovascular effects of increased thrombus formation and impaired vasomotor function in man. These effects are on par with those seen following exposure to petrodiesel exhaust, despite marked physicochemical differences of the exhaust characteristics.

Air pollution is a threat to the environment and human health. Freight trucking in particular is the main source of freight transportation emissions. Heavy-duty trucks emit large amounts of toxic air pollutants that cause serious diseases and harm public health. In addition, heavy-duty trucks emit great amounts of greenhouse gas (GHG), which is the leading cause of global warming. Despite increased environmental restrictions on air pollution and rising trucking greenhouse gas emissions in the past decades, no economic study has examined the potential GHG and air pollution reductions in the trucking sector and the associated private abatement costs to the industry. This study accounts for GHG emissions and toxic air pollutants in measuring and evaluating efficiency and productivity for the trucking industry in the 48 contiguous states. Moreover, the private costs of abatement to the industry were also estimated. When only GHG was incorporated in the production model, the results showed that each state could expand desirable output and reduce GHG by an average of 11 percent per year between 2000 and 2007. The Malmquist-Luenberger productivity indexes showed that omitting or ignoring GHG in trucking service production yielded biased estimates. On the other hand, due to increased environmental regulations, most of the toxic air pollutants decreased dramatically between 2002 and 2005. The analytical results showed that inefficiency decreased during this period. The private costs of abatement averaged $73 million per state in 2005. When GHG and six toxic air pollutants were incorporated in the production model, the estimated private abatement cost was $76 million per state, which was equivalent to 0.7 percent of the industry output in 2005.

Concentrations of diesel particulate matter (DPM) and polycyclic aromatic hydrocarbons (PAHs) in platinum mine environments are likely to be higher than in ambient air due to the use of diesel machinery in confined environments. PAHs may be present in gaseous or particulate phases each of which have different human health impacts due to their ultimate fate in the body. The sampling of both phases was made possible by means of small, portable denuder sampling devices consisting of two polydimethylsiloxane multi-channel traps connected in series and separated by a quartz fibre filter. Thermal desorption coupled with two dimensional gas chromatography with mass spectrometric detection (TD-GCxGC-ToFMS) was employed to analyse samples from three different platinum mines. The underground environments revealed that PAHs were predominantly found in the gaseous phase with naphthalene and mono-methylated derivatives being detected in the highest concentrations ranging from 0.15 – 8.73 μg.m-3. Similarly higher gas phase PAH loading was found in the Daspoort Tunnel. The particle bound PAHs underground were found in the highest concentrations at the Load Haul Dump (LHD) vehicle exhaust with dominance of fluoranthene and pyrene and concentrations ranged from 0.52-109.60 ng.m-3. This work highlighted the need to characterise both gaseous and particulate phases of PAHs in order to assess occupational exposure and demonstrated the successful application of these portable denuders in the mining environment. / Dissertation (MSc)--University of Pretoria, 2014. / tm2015 / Chemistry / MSc / Unrestricted

La pollution atmosphérique est un problème de santé publique majeur responsable en 2012 de 3,7 millions de décès prématurés dans le monde. La pollution de l’air, au même titre que les autres facteurs environnementaux (e.g., nutrition, stress) auxquels sont exposées les femmes enceintes, pourrait avoir un impact sur le développement foetal. L’objectif de ce travail était d’étudier les effets d’une exposition gestationnelle aux gaz d’échappement de moteur diesel, source majeure de la pollution atmosphérique, sur le développement foetoplacentaire en première (F1) et deuxième (F2) génération. Des lapines gestantes (F0) ont été exposées 2h/jour du 3e au 27e jour post-conception (jpc) à des niveaux de gaz d’échappement de moteur diesel mimant un pic de pollution aux particules fines de grandes villes européennes. L’exposition gestationnelle des lapines F0 entrainait des signes d’hypotrophie foetale (réduction de la longueur de la tête, de l’efficacité placentaire et hypoinsulinémie des foetus F1 à 28jpc) associés à un défaut de vascularisation placentaire et des dérégulations fonctionnelles du placenta identifiées par une analyse d’enrichissement de réseaux de gènes (GSEA) sur des données de transcriptomique (microarray dédié). Le transfert transplacentaire des nanoparticules inhalées a été démontré par microscopie électronique à transmission. En F2, la concentration plasmatique en triglycérides était réduite et la concentration plasmatique en cholestérol augmentée chez les foetus issus des lapines F1 exposées in utero. La biométrie foeto-placentaire et la structure du placenta n’ont pas été affectées. Les analyses GSEA du transcriptome placentaire F2 ont révélé des perturbations de réseaux de gènes impliqués dans la formation du protéasome et desexosomes et dans l’inflammation. Les modulations de profils en acides gras au niveau placentaire et fœtal suggèrent la mise en place de mécanismes adaptatifs anti-inflammatoires chez les F2. En conclusion, l’exposition gestationnelle chronique à des gaz d’échappement de moteur diesel induit des perturbations foeto-placentaires sur plusieurs générations. Ces données ont mis en évidence le risque lié aux nanoparticules émises par les moteurs diesel et qui ne sont soumises actuellement à aucune réglementation. / Atmospheric pollution is a major threat for human health, causing 3.7 million premature deaths worldwide in 2012. Air pollution, as well as other environmental factors (e.g., nutrition, stress) faced by pregnant women may affect fetal development. The objective of this work was to study the impact of gestational exposure to diesel engine exhaust (DE), a major source of air pollution, on the fetoplacental development in the first (F1) and second (F2) generation. Pregnant rabbits (F0) were exposed 2h/day from 3 to 27 days post-conception (dpc) at DE levels mimicking a pollution peak in major European cities. Gestational exposure of F0 females induced signs of fetal hypotrophia (reduced head length, placental efficiency and hypoinsulinemia in fetuses at 28 dpc) associated with placental vasculature failure and placental functional deregulations identified by gene set enrichment analysis (GSEA) on transcriptomic data (dedicated microarray). Transplacental transfer of inhaled nanoparticles was demonstrated by transmission electronic microscopy. In F2 generation, plasma triglyceride concentrations were reduced and plasma cholesterol concentration increased in fetuses of in utero exposed F1 rabbits. Placental biometry and structure were not affected. GSEA analysis of F2 placental transcriptome revealed disturbances in gene networks involved in formation of proteaome and exosome, in inflammation. Modulations of placental and fetal fatty acid profiles suggest anti-inflammatory adaptive mechanisms in F2 fetuses. In conclusion, chronic gestational exposure to diesel engine exhaust affects fetoplacental development over several generations. These data highlight health hazards caused by DE nanoparticles and currently not subject to regulation.

No description available.