Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.

Particulate matter (PM) is one of the most studied and problematic pollutants due to its toxicity and relati­vely high concentrations. This thesis aims to clarify the main sources and exposures of PM in Tallinn and Tartu, study the associations with health effects, and estimate the extent of those effects with health impact assessment (HIA). It appeared that the main sources of particulate air pollution in Tallinn (the capital of Estonia) and Tartu (the second largest city of Estonia) are local heating and traffic, inclu­ding road dust. In addition to local emissions, particulate levels are affected by transboundary pollution. If the transboundary air masses originated from the Eastern European areas, the concentration as well as the oxidative capacity of fine particles was significantly higher in urban background air in Tartu compared to air masses coming from Scandinavian areas (Paper I). During the last 15 years, traffic increase has been very fast in Tartu. However, due to the improvement in vehicle technology during this period, there has been only a slight increase in concentration of exhaust particles (Paper II). Nevertheless, a greater increase in road dust emissions was detected. A statistically significant relationship between long-term exposure to those traffic induced par­tic­les and cardiac disease in the RHINE (Respiratory Health in Northern Europe) Tartu cohort was shown (Paper III). However, no significant associations with respira­tory health were found. The HIA in Tallinn demonstrated 296 (95% CI = 76–528) premature deaths annually, because of PM (Paper IV). The average decrease in life expectancy was predicted to be 0.64 (95% CI 0.17–1.10) years. However, among risk groups it can be higher. In addi­tion, several cardiovascular hospitalizations are related. The costs to society be­cause of health effects reach up to €150 million annually (95% CI = 40–260) from pre­mature deaths and hospitali­zation constitute an additional €0.3 million (95% CI = 0.2–0.4). The special HIA scenario, when more pollution fuel peat will be used in boiler houses was analysed as well (Paper V). It indicated that peat bur­ning would result in up to 55.5 YLL per year within the population of Tartu. However, the health effects of pollution from current traffic, local heating, and industry are at least 28 times bigger. In conclusion, exposure to PM cause considerable health effects in the form of cardio­pulmo­nary diseases in main Estonian cities.

<p> </p><p>Introduction:<strong> </strong>Significant changes in the global ecosystem, together with a potential shortfall in oil resources, have stimulated intense interest in the development of other sources of energy, and most particularly biofuels since these are basically considered to be less harmful to human health than petroleum-based fuels. However, information about the impact of biofuel-derived vehicle emissions on human health is limited and incomplete<strong>. </strong></p><p> </p><p>Aim of the study:<em><strong> </strong></em>To identify those biofuels that are less detrimental to human health on the basis of published results from toxicological and chemical studies of vehicle emission products.</p><p> </p><p>Tasks of the study: To review systematically all conventional and alternative fuels used in internal combustion engines, to identify all known toxic emission products formed by such fuels, to review their toxic effects on human health, and to analyse the data collected in order to develop conclusions concerning the possible health benefits deriving from the use of alternative fuels.</p><p> </p><p>Materials and methods: In order to fulfil the requirements of a complete, comprehensive and up-to-date review of the toxic effects of automotive exhaust, an extensive search of official scientific data sources has been performed. Relevant publications were retrieved from public domain databases with a toxicological focus such as Toxcenter and CAplus, as well as from the websites of the US<em> </em><em><em>Environmental Protection Agency</em></em><em> </em>and the US <em><em>Agency for Toxic Substances and Disease Registry</em></em><em><strong>.</strong></em><strong> </strong>Keywords<strong> </strong>employed in the literature search were: petrol, gasoline, diesel exhaust, emission, biofuel, biogas, biodiesel, bioethanol, bioalcohol, toxicity, methanol and ethanol. A total of 295 references were initially selected relating to the period 1962 to 2008, and 142 of these presented titles and abstracts that met the main inclusion criteria, i.e. describing toxicological and epidemiological studies in humans. In cases where eligible studies relating to the goals and tasks of the review were limited or not available, some <em>in vitro</em> or <em>in vivo</em> toxicological studies involving animal models were included.</p><p> </p><p>Results:<strong> </strong>In comparison with petroleum diesel, the emissions derived from biodiesel contain less particulate matter, carbon monoxide, total hydrocarbons and other toxic compounds including vapour-phase C1-C12 hydrocarbons, aldehydes and ketones (up to C8), selected semi-volatile and particle-phase polycyclic aromatic hydrocarbons (PAHs). Whilst sulphur-containing compounds appear to be undetectable in biodiesel, nitrogen oxide and a soluble organic fraction comprising unregulated pollutants including the “aggregated toxics” (i.e., formaldehyde, acetaldehyde, acrolein, benzene, 1,3-butadiene, ethylbenzene, <em>n</em>-hexane, naphthalene, styrene, toluene and xylene) are present at elevated levels. Toxicological studies have shown that the mutagenicity of exhaust particles from biodiesel is normally lower than those obtained from petroleum diesel, however, rapeseed oil-derived biodiesel exhibits toxic effects that are 4-fold greater than petroleum diesel. Such enhanced toxicity is probably caused by the presence of carbonyl compounds and unburnt fuel. The toxicity of highly volatile components of biofuel exhaust has not yet been evaluated accurately. A substantial portion of these compounds was apparently lost in the process of preparing the test samples used for the assays (during the evaporation). The overall recoveries of these compounds have not been evaluated and the accuracy of the sample preparation method has not been validated. Hence, it could be that the cytotoxic effect of biodiesel exhaust is higher than that reported. Moreover, compared with fossil diesel, fuel derived from rapeseed oil emits particulate matter with increased mutagenic effects. Epidemiological investigations of the effects of biofuels on humans are very sparse but have revealed dose-dependent respiratory symptoms following exposure to rapeseed oil biodiesel, although the observed differences between this fuel and petroleum diesel are not significant. Such data, however, give rise to serious concerns about the future usage of this plant material as a replacement for established diesel fuels. Combustion of alcohol-based fuels leads to a reduced formation of photochemical smog in comparison with gasoline or diesel, however, the emission of aldehydes (officially classified as carcinogenic or potentially carcinogenic) is several times higher. The toxicity of the exhaust emissions of gasoline-fuelled engines is generally significantly greater than that of alcohol-burning engines. However, some harmful effects from ethanol blends might be expected, such as enhanced emissions of carcinogenic PAHs and increased ozone-related toxicity associated with the high level of aldehydes emitted. The use of ethanol–diesel fuel blends gives rise to increases in regulated exhaust emissions and, possibly, to greater emissions of aldehydes and unburnt hydrocarbons. The most promising fuels, in terms of reduced toxicity and genotoxicity of exhaust emissions, are methanol-containing blends. However, the emission from these fuels still contains formaldehyde, which is a carcinogen. The use of biogas can significantly reduce emissions of total PAHs and formaldehyde and, consequently, the risk of lung toxicity. On the other hand, the emissions of particulate matter by compressed natural gas, and the mutagenic potencies of the exhaust, are similar to those associated with gasoline and diesel fuels<strong>. </strong></p><p> </p><p>Conclusions: The use of biofuel is currently viewed very favourably and there are suggestions that the exhaust emissions from such fuel are less likely to present risks to human health in comparison with gasoline and diesel emissions. However, the expectation of a reduction in health effects based on the chemical composition of biodiesel exhaust is far from reality. Thus, although toxicological evidence relating to the effects of biofuels on humans is sparse, it is already apparent that emissions from the combustion of biofuel and blends thereof with petroleum-based fuels are toxic. In addition to the regulated toxic compounds, such as total hydrocarbons, carbon monoxide, nitrogen oxides, particulate matter and polycyclic aromatic hydrocarbons, biofuel emissions contain significant amounts of various other harmful substances that are not regulated, e.g. carbonyls (including formaldehyde, acetaldehyde, benzene, 3-butadiene, acrolein, etc.). Whilst biofuels may be potentially less damaging to human health than petroleum fuels, considerable harmful effects must still be expected. Substitution of conventional fuel by biofuel decreases the concentration of regulated toxic pollutants in vehicle exhaust, but increases the concentration of some unregulated toxic pollutants emitted from on-road engines. Generally, the toxicity of biofuels decreases in the order biodiesel>biogas>ethanol>=methanol. In this respect, methanol produced by the oxidation of biogas appears to represent an alternative fuel that exhibits the least potential for damage to human health, however, this alcohol represents a source of formaldehyde pollution and is carcinogenic.</p><p>.</p><p> </p>

In 1974 Random House published a popular and controversial book entitled Why Your Child is Hyperactive. The author, San Francisco allergist Ben F. Feingold, claimed that hyperactivity was caused by food additives and was best prevented and treated with a diet, subsequently dubbed the 'Feingold diet', free of such substances. Reaction to the idea was swift. The media and parents found Feingold's environmentally-based theory intriguing, as it provided an aetiological explanation for hyperactivity that was both sensible and topical. The medical community, in contrast, was suspicious and designed double-blind trials to test his theory. The dominant perception emerging out of these tests was that Feingold's hypothesis was incorrect and, soon after Feingold's death in 1982, medical and media attention faded away. Drawing on unpublished archival material, medical literature, popular media sources and oral history interviews, this thesis explores the rise and fall of the Feingold diet. It examines the origins of Feingold's idea, the manner in which his theory was disseminated to the medical community and the broader public, and analyses how physicians and patients evaluated whether or not Feingold's hypothesis was correct. Aiming to contribute to the histories of allergy, psychiatry and nutrition, the thesis contends that social factors, rather than scientific testing, were largely responsible for the fate of the Feingold diet. Some of these factors include Feingold's methods and approach to describing and promoting his diet, the professional and economic interests of medical practitioners and the food, chemical and pharmaceutical industries, and the difficulties inherent in following the diet. From a broader historiographical perspective, the history of the Feingold diet suggests that in order to understand how medical controversies are resolved it is essential to analyse the historical context within which they emerge.

Background Exhaustion disorder (ED) is a common mental and behavioural disorder which often leads to severe negative consequences for the individual and the society. Natural environments have positive effects on mental, physiological and attentional recovery in stressed persons, which encouraged us to test if forest visits could improve recovery from ED. The main objective of the thesis was to study if visits to different kinds of forest environments have positive health effects on patients suffering from ED, and if forest visits can be utilized for rehabilitation. Methods Participants in the MiniRest study (n=20) and the Pilot study (n=6) (Papers I and II) were recruited from the Stress Rehabilitation Clinic (SRC) at the University Hospital in Umeå.  Participants in the randomised controlled study, ForRest (n=99) and the Interview study (n=19) (Papers III and IV) were recruited from both the SRC and the Swedish Social Insurance Agency in Umeå. The MiniRest study involved only female ED patients and focused on immediate mental, physiological and attention capacity effects in one urban and three forest environments. The Pilot study investigated the practical arrangements for the forthcoming ForRest study. Participants in the ForRest study were randomised into either a three-month forest rehabilitation group; A (forest visits twice a week/4 hours per day) or to a control condition; B. Both groups received Cognitive Behavioural Rehabilitation (CBR) at 24 occasions/once a week after the three-month study period. Preferences for forest environments, mental state and attention capacity were studied for group A only. Psychological health measurements and sick leave data were compared between the groups after (i) the forest rehabilitation and (ii) the CBR. The Interview study was conducted according to grounded theory methodology and consisted of 19 participants from group A to explore personal experiences from the forest rehabilitation. Data collection was implemented through questionnaires, medical records, physiological measurements, and interviews. Results Exposure to forest environments was associated with higher preference, more favourable mental state and physiological responses, and increased attention capacity compared to an urban environment (Paper I). Open and accessible forest environments were preferred (Papers I, II and III). Recovery from ED was found in both groups in the ForRest study, but there were no differences between the groups over time. In group A, positive effects on mental state and attention capacity were found during the forest visits. An interaction effect was found with more positive effects on mental state during spring compared to autumn (Paper III). Solitude, feelings of freedom and no demands were important for finding peace of mind during the forest visits. Moreover, easier access to peace of mind, reflective thinking and positive feelings were reported as the forest rehabilitation progressed (Papers II and IV). Conclusions Forest visits have restorative effects for ED patients through enhanced mental well-being, easier access to peace of mind, beneficial physiological reactions and increased attention capacity which support the use of forest environments in rehabilitation. However, forest rehabilitation tested in a randomised controlled trial did not improve recovery from ED. Potentially rehabilitation with CBR and forest visits integrated could be more effective and should be further investigated in nature-assisted rehabilitation for ED patients.

Arsenic is a well-known lung carcinogen in humans. In 2006, IARC upgraded inorganic lead as a possible human carcinogen (2A). The aim of this thesis has been to evaluate the lung cancer mortality and incidence in long-term exposed primary lead smelter workers and also to estimate present exposures to arsenic and lead in relation to those occurring in the past. The basic cohort (N=3832 workers; hired before 1967 and followed up from 1950-1981; SMR comparisons with general and local reference populations) showed an excess of deaths for total mortality, malignant neoplasms (e.g. lung and stomach cancer), ischaemic heart diseases, and cerebrovascular diseases compared to the general population. In a subcohort of lead workers (N=437; regular blood lead sampling since 1950) only the raised SMR for lung cancer (162) was sustained. In a follow-up study of the basic cohort (N=3979), a subcohort of lead exposed workers (N=1992) was formed. The expected mortality in 1955-1987 and cancer incidence in 1958-1987 were calculated relative to county rates. A cumulative blood lead index (CBLI) was used for dose-response analyses. The lung cancer incidence was raised in the total cohort (SIR 2.8; 95 % CI 2.1 3.8). A higher lung cancer risk was observed in workers hired before 1950 (SIR 3.6; 95 % CI 2.6-5.0). The increased lung cancer risks were further elevated in the subcohort of lead exposed workers, especially in the highest exposed subgroup (SIR 5.1; 95 % 2.0-10.5; latency period of 15 y). No excesses of other malignancies were observed. The increased relative risks for lung cancer may have been caused by interactions between inorganic lead and other substances at the smelter, e.g. arsenic. To further analyze the effects from inorganic lead, two subcohorts of workers at the lead departments were formed from the original cohort (N=3979), one of 710 workers and the other of 383 workers. The lung cancer incidence was raised in both subcohorts (Lead subcohort 1; SIR 2.4; 95 % CI 1.2-4.5; Lead subcohort 2; SIR 3.6; 95 % CI 1.2-8.3). Among the 10 workers that had developed lung cancer in lead subcohort 1 all but one had a considerable exposure also to arsenic. Thus, a possible interaction effect between lead and arsenic may explain the increased lung cancer risks. To further elucidate the impact from lead and arsenic a case control study was undertaken. In the basic cohort (N=3979), 46 male workers had contracted respiratory malignancies. They were compared with 141 agematched male referents from the primary smelter by conditional logistic regression analysis using smoking habits, cumulative blood lead and air arsenic exposure as predictor variables. The lung cancer cases showed a significantly higher smoking rate than referents (Odds ratio, OR = 4.0; 95 % CI 1.6-10.1; p=0.003). When restricted to smokers, the cumulative arsenic air exposure index, but not the lead exposure indices, were significantly higher among the cases (OR=1.07; 95 % CI 1.02-1.11; p = 0.005). Accordingly, cumulative arsenic exposure and smoking were identified as significant risk factors for the development of lung cancer in the final analyses, while lead exposure was not a significant risk factor. However, inorganic lead still may play a minor role in the multifactorial genesis of lung cancer. These studies describe risks from exposures occurring from time periods before 1950 up to 1981. Because of the long latency period for lung cancer, exposures after 1970 probably have had limited impact on the reported results. Compared to the levels in the early 1970´s present exposures to arsenic are lower by a factor of ten or more and risks probably correspondingly lower.

Background: Ambient air pollution is associated with adverse health effects, but the sources and components, which cause these effects is still incompletely understood. The aim of this thesis was to investigate the pulmonary effects of a variety of common air pollutants, including diesel exhaust, biomass smoke, and road tunnel and subway station environments. Healthy non-smoking volunteers were exposed in random order to the specific air pollutants and air/control, during intermittent exercise, followed by bronchoscopy. Methods and results: In study I, exposures were performed with diesel exhaust (DE) generated at transient engine load and air for 1 hour with bronchoscopy at 6 hours post-exposure. Immunohistochemical analyses of bronchial mucosal biopsies showed that DE exposure significantly increased the endothelial adhesion molecule expression of p-selectin and VCAM-1, together with increased bronchoalveolar lavage (BAL) eosinophils. In study II, the subjects were exposed for 1 hour to DE generated during idling with bronchoscopy at 6 hours. The bronchial mucosal biopsies showed significant increases in neutrophils, mast cells and lymphocytes together with bronchial wash neutrophils. Additionally, DE exposure significantly increased the nuclear translocation of the aryl hydrocarbon receptor (AhR) and phosphorylated c-jun in the bronchial epithelium. In contrast, the phase II enzyme NAD(P)H-quinone oxidoreductase 1 (NQO1) decreased after DE. In study III, the 2-hour exposures took place in a road tunnel with bronchoscopy 14 hours later. The road tunnel exposure significantly increased the total numbers of lymphocytes and alveolar macrophages in BAL, whereas NK cell and CD56+/T cell numbers significantly decreased. Additionally, the nuclear expression of phosphorylated c-jun in the bronchial epithelium was significantly increased after road tunnel exposure. In study IV, the subjects were exposed to metal-rich particulate aerosol for 2 hours at a subway station with bronchial biopsy and BAL sampling at 14 hours. The subway exposure significantly increased the concentration of glutathione disulphide (GSSG) in BAL, with no airway inflammatory responses. In contrast, the number of neutrophils in the bronchial mucosa and the nuclear expression of phosphorylated c-jun in the bronchial epithelium tended to decrease after the subway exposure. In study V, the exposure to biomass smoke lasted 3 hours. Bronchoscopy was conducted 24 hours post exposure. The investigated biomass combustion emissions resulted in a significant increase in total glutathione and reduced glutathione in BAL, without any evident acute airway inflammatory responses.     Conclusion: The present thesis presents data from exposures of healthy subjects to a variety of common air pollutants, as compared with an air reference. Oxidative as well as bronchial mucosal and bronchoalveolar responses differed between these air pollutants, with the most pronounced airway effects seen after exposure to diesel exhaust. This may be due to differences in pulmonary deposition, physicochemical characteristics, toxicological pathways and potency. Additional studies will assist in addressing dose-response and time kinetic aspects of the airway responses.

Physicians are familiar with organophosphates (OPs) as a classic, though obscure, cause of cholinergic poisoning. Many opportunities for human exposure existsixty million pounds of OPs are applied as insecticides to sixty million acres of U.S. land each year, and, until recently, over one-fifth of Americans used these chemicals in their homes. Most physicians, however, still know little about the dangers that these pesticides pose to the developing nervous system. By the late 1980s, toxicologists increasingly recognized that toxicants such as lead and mercury, even at doses well-below the level required to cause symptomatic poisoning, could induce subtle, yet permanent, neurological deficits if the exposure occurred during critical periods of brain development. In the early 1990s, scientists and regulators began to realize that developmental neurotoxicity (DNT), as this phenomenon was called, could also result from OPs. In 1996 Congress passed the Food Quality Protection Act (FQPA), marking a major turning point in the regulation of hazardous chemicals. Prior to the FQPA, the Environmental Protection Agency (EPA) based its calculations of pesticide risk on adults and largely neglected the increased susceptibility of infants and children. The new law took a precautionary stance, protecting the vulnerable neural and physical development of the fetus and child with the inclusion of a 10-X safety factor, and shifting the burden of proof from health advocates to the pesticide manufacturers. The ensuing ten-year battle between health groups, pesticide manufacturers, and the EPA over the laws enforcement now provides an instructive lesson into the complex scientific, political, and economic world of environmental health, and serves as a relatively successful example of effective policy improving public health.

Diss. (sammanfattning) Uppsala : Uppsala universitet, 2005. / Härtill 4 uppsatser.

Sunlight is recognized as one of the most important environmental factors that influence human health. There is strong evidence in the scientific literature that adequate exposure to sunlight is associated with many physical and mental health benefits, including reduced overall mortality, prevention of many deadly forms of cancer, as well as a number of metabolic, cardiovascular, autoimmune, infectious and neuropsychatric diseases. Vitamin D deficiency, which is mainly due to insufficient exposure to sunlight, is now one of the most common medical conditions, estimated to affect more than a billion people worldwide. Health professionals, patients and the general public should receive more evidence-based information about the many health benefits of sunlight, and how to use it in prevention and treatment of disease.