Impact of Tobacco Control Policy on Smoking and Exposure to Environmental Tobacco Smoke

The aim of the study was to evaluate the impact of the Finnish tobacco control measures for reduction of smoking. First, the trends and patterns in ever smoking among adult Finns in 1978 2001 as well as the associations of trends with the Tobacco Control Act in 1976 were examined. Secondly, the impact of the 1976 TCA on the proportion of ever daily smokers in different socioeconomic groups was studied. Thirdly, the impact of the 1995 TCAA on recent trends in the prevalence of daily smoking was evaluated by gender and employment status. Fourthly, the trends of exposure to environmental tobacco smoke (ETS) at workplaces and homes were investigated. The study is based on data of the Health Behaviour among the Finnish Adult Population surveys. Among Finnish men smoking initiation declined from earlier to later cohorts, whereas among women it increased in successive birth cohorts born before 1956. The lasting differences between birth cohorts as regards ever daily smoking reflected well the impact of measures to reduce smoking in Finland in 1976. Smoking initiation in the birth cohorts (born in 1961 or later) which were in critical age as regards the risk of smoking initiation when the TCA came into force was less common than could be expected according to the trends seen in the earlier birth cohorts. Marked socioeconomic differences were found in smoking in the different birth cohorts. Smoking was more prevalent in the lower socioeconomic groups than in the higher ones, and the differences were larger in the later birth cohorts compared to the earlier ones. The differences between the birth cohorts in ever daily smoking were compatible with the hypothetical impact of the TCA in almost all socioeconomic groups, except farmers. Among men the 1976 TCA appears to have had the greatest impact on white-collar employees. Among women the effect of the act was highly significant in all socioeconomic groups. However, female smoking prevalence continues to show wide socioeconomic disparities. Daily smoking decreased among employees after the 1995 TCAA, supporting the hypothesis of the lowering impact of the amendment on daily smoking due to increased smoking cessation. No parallel change in daily smoking was found in the population without direct expose to ETS legislation (farmers, students, housewives, pensioners or unemployed). Exposure to ETS decreased markedly among non-smokers at work after the 1995 TCAA. The 1976 TCA and the 1995 TCAA were useful in controlling smoking initiation and cessation, but their impact was not equal across the population groups. The results of this study strongly suggested that tobacco control policies markedly contribute to the decrease in smoking and in exposure to environmental tobacco smoke.

The effects of organic environmental toxicants on hard tissue formation in developing tooth : An in vitro study in mice

Dioxins are organic toxicants that are known to impair tooth development, especially dental hard tissue formation. The most toxic dioxin congener is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Further, clinical studies suggest that maternal smoking during pregnancy can affect child s tooth development. One of the main components of tobacco smoke is the group of non-halogenated polycyclic aromatic hydrocarbons (PAHs), a representative of which is 7,12-dimethylbenz[a]anthracene (DMBA). Tributyltin (TBT), an organic tin compound, has been shown to impair bone mineralization in experimental animals. In addition to exposure to organic toxicants, a well-established cause for enamel hypomineralization is excess fluoride intake. The principal aim of this thesis project was to examine in vitro if, in addition to dioxins, other organic environmental toxicants, like PAHs and organic tin compounds, have adverse effects on tooth development, specifically on formation and mineralization of the major dental hard tissues, the dentin and the enamel. The second aim was to investigate in vitro if fluoride could intensify the manifestation of the detrimental developmental dental effects elicited by TCDD. The study was conducted by culturing mandibular first and second molar tooth germs of E18 NMRI mouse embryos in a Trowell-type organ culture and exposing them to DMBA, TBT, and sodium fluoride (NaF) and/or TCDD at various concentrations during the secretory and mineralization stages of development. Specific methods used were HE-staining for studying cell and tissue morphology, BrdU-staining for cell proliferation, TUNEL-staining for apoptosis, and QPCR, in situ hybridization and immunohistochemistry for the expressions of selected genes associated with mineralization. This thesis work showed that DMBA, TBT, TCDD and NaF interfere with dentin and enamel formation of embryonic mouse tooth in vitro, and that fluoride can potentiate the harmful effect of TCDD. The results suggested that adverse effects of TBT involve altered expression of genes associated with mineralization, and that DMBA and TBT as well as NaF and TCDD together primarily affect dentin mineralization. Since amelogenesis does not start until mineralization of dentin begins, impaired enamel matrix secretion could be a secondary effect. Dioxins, PAHs and organotins are all liposoluble and can be transferred to the infant by breast-feeding. Since doses are usually very low, developmental toxicity on most of the organs is difficult to indentify clinically. However, tooth may act as an indicator of exposure, since the major dental hard tissues, the dentin and the enamel, are not replaced once they have been formed. Thus, disturbed dental hard tissue formation raises the question of more extensive developmental toxicity.

Polymorphic low penetrance genes and breast cancer : The role of genes involved in metabolism of xenobiotics, estrogens and reactive oxygen species

Various endogenous and exogenous factors have been reported to increase the risk of breast cancer. Many of those are related to prolonged lifetime exposure to estrogens. Furthermore, a positive family history of breast cancer and certain benign breast diseases are known to increase the risk of breast cancer. The role of lifestyle factors, such as use of alcohol and smoking has been an area of intensive study. Alcohol has been found to increase the risk of breast cancer, whereas the role of smoking has remained obscure. A multitude of enzymes are involved in the metabolism of estrogens and xenobiotics including the carcinogens found in tobacco smoke. Many of the metabolic enzymes exhibit genetic polymorphisms that can lead to inter-individual differences in their abilities to modify hazardous substrates. Therefore, in presence of a given chemical exposure, one subgroup of women may be more susceptible to breast carcinogenesis, since they carry unfavourable forms of the polymorphic genes involved in the metabolism of the chemical. In this work, polymorphic genes encoding for cytochrome P450 (CYP) 1A1 and 1B1, N-acetyl transferase 2 (NAT2), sulfotransferase 1A1 (SULT1A1), manganese superoxide dismutase (MnSOD) and vitamin D receptor (VDR) were investigated in relation to breast cancer susceptibility in a Finnish population. CYP1A1, CYP1B1 and SULT1A1 are involved in the metabolism of both estrogens and xenobiotics, whereas NAT2 is involved only in the latter. MnSOD is an antioxidant enzyme protecting cells from oxidative damage. VDR, in turn, mediates the effects of the active form of vitamin D (1,25(OH)2D3, calcitriol) on maintenance of calcium homeostasis and it has anti-proliferative effects in many cancer cells. A 1.3-fold (95% CIs 1.01-1.73) increased risk of breast cancer was seen among women who carried the NAT2 slow acetylator genotype and a 1.5-fold (95% CI 1.1-2.0) risk was found in women with a MnSOD variant A allele containing genotypes compared to women with the NAT2 rapid acetylator genotype or to those with the MnSOD VV genotype, respectively. Instead, women with the VDR a allele containing genotypes were found to be at a decreased risk for breast cancer (OR 0.73; 95% CI 0.54-0.98) compared to women with the AA genotype. No significant overall associations were found between SULT1A1 or CYP genotypes and breast cancer risk, whereas a combination of the CYP1B1 432Val allele containing genotypes with the NAT2 slow acetylator genotypes posed a 1.5-fold (95% CI 1.03-2.24) increased risk. Moreover, NAT2 slow acetylator genotype was found to be confined to women with an advanced stage of breast cancer (stages III and IV). Further evidence for the association of xenobiotic metabolising genes with breast cancer risk was found when active smoking was taken into account. Women who smoked less than 10 cigarettes/day and carried at least one CYP1B1 432Val variant allele, were at 3.1-fold (95% CI 1.32-7.12) risk of breast cancer compared to women who smoked the same amount but did not carry the variant allele. Furthermore, the risk was significantly increased with increasing number of the CYP1B1 432Val alleles (p for trend 0.005). In addition, women who smoked less than 5 pack-years and carried the NAT2 slow acetylator genotype were at a 2.6-fold (95% CI 1.01-6.48) increased risk of breast cancer compared to women who smoked the same amount but carried the NAT2 rapid acetylator genotype. Furthermore, the combination of the CYP1B1 432Val allele and the NAT2 slow acetylator genotype increased the risk of breast cancer by 2.5-fold (95% CI 1.11-5.45) among ever smokers. Instead, the MnSOD A allele was found to be a risk factor among postmenopausal long-term smokers (>15 years of smoking) (OR 5.1; 95% CI 1.4-18.4) or among postmenopausal women who had smoked more than 10 cigarettes/day (OR 5.5; 95% CI 1.3-23.4) compared to women who had similar smoking habits but carried the MnSOD V/V genotype. Similarly, within subgroups of postmenopausal women who were using oral contraceptives, hormone replacement therapy or alcohol, women carrying the MnSOD A allele genotypes seemed to be at increased risk of breast cancer compared to women with the MnSOD V/V genotype. A positive family history of breast cancer and high parity were shown to be inversely associated with breast cancer risk among women carrying the VDR ApaI a allele or among premenopausal women carrying the SULT1A1*2 allele, respectively.

Childhood otitis media - risk factors and surgical management

Background: Otitis media (OM) is one of the most common childhood diseases. Approximately every third child suffers from recurrent acute otitis media (RAOM), and 5% of all children have persistent middle ear effusion for months during their childhood. Despite numerous studies on the prevention and treatment of OM during the past decades, its management remains challenging and controversial. In this study, the effect of adenoidectomy on the risk for OM, the potential risk factors influencing the development of OM and the frequency of asthma among otitis-prone children were investigated. Subjects and methods: One prospective randomized trial and two retrospective studies were conducted. In the prospective trial, 217 children with RAOM or chronic otitis media with effusion (COME) were randomized to have tympanostomy with or without adenoidectomy. The age of the children at recruitment was between 1 and 4 years. RAOM was defined as having at least 3 episodes of AOM during the last 6 months or at least 5 episodes of AOM during the last 12 months. COME was defined as having persistent middle ear effusion for 2-3 months. The children were followed up for one year. In the first retrospective study, the frequency of childhood infections and allergy was evaluated by a questionnaire among 819 individuals. In the second retrospective study, data of asthma diagnosis were analysed from hospital discharge records of 1616 children who underwent adenoidectomy or had probing of the nasolacrimal duct. Results: In the prospective randomized study, adenoidectomy had no beneficial effect on the prevention of subsequent episodes of AOM. Parental smoking was found to be a significant risk factor for OM even after the insertion of tympanostomy tubes. The frequencies of exposure to tobacco smoke and day-care attendance at the time of randomization were similar among children with RAOM and COME. However, the frequencies of allergy to animal dust and pollen and parental asthma were lower among children with COME than those with RAOM. The questionnaire survey and the hospital discharge data revealed that children who had frequent episodes of OM had an increased risk for asthma. Conclusions: The first surgical intervention to treat an otitis-prone child younger than 4 years should not include adenoidectomy. Interventions to stop parental smoking could significantly reduce the risk for childhood RAOM. Whether an otitis-prone child develops COME or RAOM, seems to be influenced by genetic predisposition more strongly than by environmental risk factors. Children who suffer from repeated upper respiratory tract infections, like OM, may be at increased risk for developing asthma.

Kaupunkilaisen elinympäristöongelma : Käsitteellistämistavat ja puuttumisen mallit

The study analyses the reaction of urban residents to problems, i.e. disturbing factors, in their living environment, and also their ways of doing something about these problems. It is based on urban-sociological theory on everyday life in a modern metropolis. On this theoretical basis, problems in the urban living environment are analysed in terms of a policy of everyday interference: when urban citizens become aware of a problem in their environment, they face a pattern of behaviour where the norm is polite indifference and negative solidarity. They may feel they ought to do something about the problem, but at the same time, an implicit rule of urban life is not to interfere with other people s lives so they won t interfere with yours. For example, it is not that easy for someone disturbed by littering to complain directly to those who litter the streets. Or if you complain about tobacco smoke from the neighbour s balcony, your neighbours might get cross. Direct interference with a problem in the environment usually implies an encounter with a hitherto unknown counterpart and their possible counter-reaction. The risk is either to lose face or get into downright conflict. Therefore, an easier way may be to complain to the city authorities. The Helsinki City Environment Centre is currently working on solutions for all the various kinds of problems that occur in a dense urban structure. Various ways of conceptualising the problems in the living environment are analysed empirically using theme interviews made with citizens having contacted Helsinki City Environment Centre. A phenomenographic approach and a theory-based categorisation are applied on the analysis of the theme interviews. On the grounds of the analysis, the ways of conceptualising are determined by 1) the difficulty of interfering and convincing other people, which in practice means meddling in other people s business, 2) a territorial struggle for space and a place in a dense urban structure, 3) breaches of rules and norms for social routines in urban life, and 4) a crumbling of the urban identity and all that goes along with that. The analysis of the ways of conceptualisation is deepened using a cultural risk theory. The final outcome of the analysis is four types of behaviour among urban residents with regard to interference with everyday problems in the living environment. They have been called yard police , fence builder , park warden and environmental caretaker . The study combines an urban-sociological approach with the theoretical tradition of urban research and with research on municipal environmental policy.

Snoring and sleep apnea in children

Snoring is a primary and major clinical symptom of upper airway obstruction during sleep. Sleep-disordered breathing ranges from primary snoring to significant partial upper airway obstruction, and obstructive sleep apnea. Adult snoring and obstructive sleep apnea have been extensively studied, whereas less is known about these disorders in children. Snoring and more severe obstructive sleep apnea have been shown to have a harmful effect on the neurobehavioral development of children, but the mechanisms of this effect remains unknown. Furthermore, the correlation of this effect to objective sleep study parameters remains poor. This study evaluated the prevalence of snoring in preschool-aged children in Finland. Host and environmental risk factors, and neurobehavioral and neurocognitive symptoms of children suffering from snoring or obstructive sleep apnea were also investigated. The feasibility of acoustic rhinometry in young children was assessed. The prevalence and risk factors of snoring (I) were evaluated by a questionnaire. The random sample included 2100 children aged 1-6 years living in Helsinki. All 3- to 6-year-old children whose parents reported their child to snore always, often, or sometimes were categorized as snorers, and invited to participate to the clinical study (II-IV). Non-snoring children whose parents were willing to participate in the clinical study were invited to serve as controls. Children underwent a clinical ear-nose-throat examination. Emotional, behavioral, and cognitive performances were evaluated by Child Behavioral Checklist (CBCL), Wechsler Preschool and Primary Scale of Intelligence (WPPSI-R) and NEPSY-A Developmental Neuropsychological Assessment (NEPSY). Nasal volume was measured by acoustic rhinometry, and nasal resistance by rhinomanometry. Lateral and posteroanterior cephalometry were performed. A standard overnight ambulatory polysomnography was performed in the home environment. Twenty-six healthy children were tested in order to assess the feasibility of acoustic rhinometry in young children (V). Snoring was common in children; 6.3% of children snored always or often, whereas 81.3% snored never or occasionally. No differences were apparent between snorers and non-snorers regarding age, or gender. Pediatric snoring was associated with recurrent upper respiratory infections, otitis media, and allergic rhinitis. Exposure to parental tobacco smoke, especially maternal smoking, was more common among snorers. Rhinitis was more common among children who exposured to tobacco smoke. Overnight polysomnography (PSG) was performed on 87 children; 74% showed no signs of significant upper airway obstruction during sleep. Three children had obstructive apnea/hypopnea index (OAHI) greater than 5/h. Age, gender, or a previous adenoidectomy or tonsillectomy did not correlate with OAHI, whereas tonsillar size did correlate with OAHI. Relative body weight and obesity correlated with none of the PSG parameters. In cephalometry, no clear differences or correlations were found in PSG parameters or between snorers and non-snorers. No correlations were observed between acoustic rhinometry, rhinomanometry, and PSG parameters. Psychiatric symptoms were more frequent in the snoring group than in the nonsnoring group. In particular, anxious and depressed symptoms were more prevalent in the snoring group. Snoring children frequently scored lower in language functions. However, PSG parameters correlated poorly with neurocognitive test results in these children. This study and previous studies indicate that snoring without episodes of obstructive apnea or SpO2 desaturations may cause impairment in behavioral and neurocognitive functions. The mechanism of action remains unknown. Exposure to parental tobacco smoke is more common among snorers than non-snorers, emphasizing the importance of a smoke-free environment. Children tolerated acoustic rhinometry measurements well.

Upregulation and Functionality of Neuronal Nicotinic Acetylcholine Receptors

Cigarette smoking is, in developed countries, the leading cause of premature death. In tobacco smoke, the main addictive compound is nicotine, which in the brain binds to neuronal nicotinic acetylcholine receptors (neuronal nAChRs). These have been implicated in addiction, but also in several neurological disorders including Alzheimer's and Parkinson's diseases, Tourette's syndrome, attention-deficit hyperactivity disorder (ADHD), schizophrenia, pain, depression, and autosomal-dominant noctural frontal lobe epilepsy; all of which makes nAChRs an intriguing target of study. Chronic treatment with nicotine leads to an increase in the number of nAChRs (upregulation) in the brain and changes their functionality. Changes in the properties of nAChRs are likely to occur in smokers as well, since they are exposed to nicotine for long periods of time. Several nAChR subtypes likely play a role in the formation of nicotine addiction by participating in the release of dopamine in the striatum. The aim of this study was to clarify at cellular level the changes in nAChR characteristics resulting from chronic nicotine treatment. SH-SY5Y cells, endogenously several nAChR-expressing, and SH-EP1-h-alfa7 cells, transfected with the alfa 7 nAChR subunit gene were treated chronically with nicotine. The localisation of alfa 7 and beta2 subunits was studied with confocal and electron microscopy. Functionality of nAChRs was studied with calcium fluorometry. Effects of long-term treatment with opioid compounds on nAChRs were studied by means of ligand binding. Confocal microscopy showed that in SH-SY5Y cells, alfa7 and beta2 subunits formed clusters, unlike the case in SH-EP1-h alfa7 cells, where alfa7 nAChRs were distributed more diffusely. The majority of nAChR subunits localised on endoplasmic reticulum (ER). The isomers of methadone acted as agonists at alfa7 nAChRs. Acute morphine challenge also stimulated nAChRs. Chronic treatment with methadone or morphine led to an increased number of nAChRs. In animal studies, mice received nicotine for 7 weeks. Electron microscopical analysis of the localisation of nAChRs showed in the striatum that alfa7 and beta2 nAChR subunits localised synaptically, extrasynaptically, and intracellularly, with the majority localising extrasynaptically. Chronic nicotine treatment caused an increase in the number of nAChR subunits at all studied locations. These results suggest that the alfa7 nAChR and beta2 subunit-containing nAChRs respond to chronic nicotine treatment differently. This may indicate that the functional balance of various nAChR subtypes in control of the release of dopamine is altered as a result of chronic nicotine treatment. Compounds binding both to opioid and nACh receptors may be of clinical importance.

Interaction of alcohol and smoking in the pathogenesis of upper digestive tract cancers - possible chemoprevention with cysteine

Background: Alcohol consumption and smoking are the main causes of upper digestive tract cancers. These risk factors account for over 75% of all cases in developed countries. Epidemiological studies have shown that alcohol and tobacco interact in a multiplicative way to the cancer risk, but the pathogenetic mechanism behind this is poorly understood. Strong experimental and human genetic linkage data suggest that acetaldehyde is one of the major factors behind the carcinogenic effect. In the digestive tract, acetaldehyde is mainly formed by microbial metabolism of ethanol. Acetaldehyde is also a major constituent of tobacco smoke. Thus, acetaldehyde from both of these sources may have an interacting carcinogenic effect in the human upper digestive tract. Aims: The first aim of this thesis was to investigate acetaldehyde production and exposure in the human mouth resulting from alcohol ingestion and tobacco smoking in vivo. Secondly, specific L-cysteine products were prepared to examine their efficacy in the binding of salivary acetaldehyde in order to reduce the exposure of the upper digestive tract to acetaldehyde. Methods: Acetaldehyde levels in saliva were measured from human volunteers during alcohol metabolism, during tobacco smoking and during the combined use of alcohol and tobacco. The ability of L-cysteine to eliminate acetaldehyde during alcohol metabolism and tobacco smoking was also investigated with specifically developed tablets. Also the acetaldehyde production of Escherichia coli - an important member of the human microbiota - was measured in different conditions prevailing in the digestive tract. Results and conclusions: These studies established that smokers have significantly increased acetaldehyde exposure during ethanol consumption even when not actively smoking. Acetaldehyde exposure was dramatically further increased during active tobacco smoking. Thus, the elevated aerodigestive tract cancer risk observed in smokers and drinkers may be the result of the increased acetaldehyde exposure. Acetaldehyde produced in the oral cavity during ethanol challenge was significantly decreased by a buccal L-cysteine -releasing tablet. Also smoking-derived acetaldehyde could be totally removed by using a tablet containing L-cysteine. In conclusion, this thesis confirms the essential role of acetaldehyde in the pathogenesis of alcohol- and smoking-induced cancers. This thesis presents a novel experimental approach to decrease the local acetaldehyde exposure of the upper digestive tract with L-cysteine, with the eventual goal of reducting the prevalence of upper digestive tract cancers.

Genetic and environmental influences on human responses to odors

Olfaction, the sense of smell, has many important functions in humans. Human responses to odors show substantial individual variation. Olfactory receptor genes have been identified and other genes may also influence olfaction. However, the proportion of phenotypic variation in odor response due to genetic variation remains largely unknown. Little is also known about which genes modify specific responses to odors. This study aimed to elucidate genetic and environmental influences on human responses to odors. Individuals from Finnish families (n=146) and Australian (n=413), British (n=163), Danish (n=336), and Finnish (n=399) twins rated intensity and pleasantness of a set of 12 (families) or 6 (twins) odors and tried to identify the odors. In addition, the participants rated their own sense of smell and annoyance experienced with different environmental odors. The odor stimuli of a commercial smell test (The Brief Smell Identification Test; banana, chocolate, cinnamon, gasoline, lemon, onion, paint thinner, pineapple, rose, smoke, soap, and turpentine) were presented in the family study. Based on the results of the family study and a literature survey, a new set of odor stimuli (androstenone, chocolate, cinnamon, isovaleric acid, lemon, and turpentine) was designed for the twin studies. In the family sample, heritabilities of the traits were estimated and underlying genomic regions were searched using a genome-wide linkage scan. In the pooled twin sample, variation in the measured traits was decomposed into genetic and environmental components using quantitative genetic modeling. In addition, associations between nongenetic factors (e.g., sex, age, and smoking) and olfactory-related traits were explored. Suggestive evidence for a genetic linkage for pleasantness of cinnamon at a locus on chromosome 4q32.3 emerged from the family sample. High heritability for the pleasantness of cinnamon was found in the family but not the twin study. Heritability of perceived intensity of androstenone odor was determined to be ~30% in the twin sample. A strong genetic correlation between perceived intensity and pleasantness of androstenone, in the absence of any environmental correlation, indicated that only the genetic correlation explained the phenotypic correlation between the traits (r=-0.27) and that the traits were influenced by an overlapping set of genes. Self-rated olfactory function appeared to reflect the odor annoyance experienced rather than actual olfactory acuity or genetic involvement. Results from nongenetic analyses supported the speculated superiority of females' olfactory abilities, the age-related diminishing of olfactory acuity, and the influences of experience-dependent factors on odor responses. This was the first study to estimate heritabilities and perform linkage screens for individual odors. A genetic effect was detected for only a few responses to specific odors, suggesting the predominance of environmental effects in odor perceptions.

Texts "Con and Pro" : The Early Modern Medical Controversy over Tobacco

The habit of "drinking smoke" , meaning tobacco smoking, caused a true controversy in early modern England. The new substance was used both for its alleged therapeutic properties as well as its narcotic effects. The dispute over tobacco continues the line of written controversies which were an important means of communication in the sixteenth and seventeenth century Europe. The tobacco controversy is special among medical controversies because the recreational use of tobacco soon spread and outweighed its medicinal use, ultimately causing a social and cultural crisis in England. This study examines how language is used in polemic discourse and argumentation. The material consists of medical texts arguing for and against tobacco in early modern England. The texts were compiled into an electronic corpus of tobacco texts (1577 1670) representing different genres and styles of writing. With the help of the corpus, the tobacco controversy is described and analyzed in the context of early modern medicine. A variety of methods suitable for the study of conflict discourse were used to assess internal and external text variation. The linguistic features examined include personal pronouns, intertextuality, structural components, and statistically derived keywords. A common thread in the work is persuasive language use manifested, for example, in the form of emotive adjectives and the generic use of pronouns; the latter is especially pronounced in the dichotomy between us and them. Controversies have not been studied in this manner before but the methods applied have supplemented each other and proven their suitability in the study of conflictive discourse. These methods can also be applied to present-day materials.

Environmental change and human history in the Jabal Harun area, Jordan

The research is related to the Finnish Jabal Harun Project (FJHP), which is part of the research unit directed by Professor Jaakko Frösén. The project consists of two interrelated parts: the excavation of a Byzantine monastery/pilgrimage centre on Jabal Harun, and a multiperiod archaeological survey of the surrounding landscape. It is generally held that the Near Eastern landscape has been modified by millennia of human habitation and activity. Past climatic changes and human activities could be expected to have significantly changed also the landscape of the Jabal Harun area. Therefore it was considered that a study of erosion in the Jabal Harun area could shed light on the environmental and human history of the area. It was hoped that it would be possible to connect the results of the sedimentological studies either to wider climatic changes in the Near East, or to archaeologically observable periods of human activity and land use. As evidence of some archaeological periods is completely missing from the Jabal Harun area, it was also of interest whether catastrophic erosion or unfavourable environmental change, caused either by natural forces or by human agency, could explain the gaps in the archaeological record. Changes in climate and/or land-use were expected to be reflected in the sedimentary record. The field research, carried out as part of the FJHP survey fieldwork, included the mapping of wadi terraces and cleaning of sediment profiles which were recorded and sampled for laboratory analyses of facies and lithology. To obtain a chronology for the sedimentation and erosion phases also OSL (optically stimulated luminescence) dating samples were collected. The results were compared to the record of the Near Eastern palaeoclimate, and to data from geoarchaeological studies in central and southern Jordan. The picture of the environmental development was then compared to the human history in the area, based on archaeological evidence from the FJHP survey and the published archaeological research in the Petra region, and the question of the relationship between human activity and environmental change was critically discussed. Using the palaeoclimatic data and the results from geoarchaeological studies it was possible to outline the environmental development in the Jabal Harun area from the Pleistocene to the present.It is appears that there was a phase of accumulation of sediment before the Middle Palaeolithic period, possibly related to tectonic movement. This phase was later followed by erosion, tentatively suggested to have taken place during the Upper Palaeolithic. A period of wadi aggradation probably occurred during the Late Glacial and continued until the end of the Pleistocene, followed by significant channel degradation, attributed to increased rainfall during the Early Holocene. It seems that during the later Holocene channel incision has been dominant in the Jabal Harûn area although there have been also small-scale channel aggradation phases, two of which were OSL-dated to around 4000-3000 BP and 2400-2000 BP. As there is no evidence of tectonic movements in the Jabal Harun area after the early Pleistocene, it is suggested that climate change and human activity have been the major causes of environmental change in the area. At a brief glance it seems that many of the changes in the settlement and land use in the Jabal Harun area can be explained by climatic and environmental conditions. However, the responses of human societies to environmental change are dependent on many factors. Therefore an evaluation of the significance of environmental, cultural, socio-economic and political factors is needed to decide whether certain phenomena are environmentally induced. Comparison with the wider Petra region is also needed to judge whether the phenomena are characteristic of the Jabal Harun area only, or can they be connected to social, political and economic development over a wider area.

On the environmental genetics of depressive symptoms : Focus on two serotonergic genes

Depression is a complex psychiatric disorder influenced by several genes, environmental factors, and their interplay. Serotonin receptor 2A (HTR2A) and tryptophan hydroxylase 1 (TPH1) genes have been implicated in vulnerability to depression and other psychiatric disorders, but the results have been inconsistent. The present study examined whether these two genes moderated the influence of different depressogenic environmental factors on subthreshold depressive symptoms (assessed on a modified version of Beck s Depression Inventory, BDI) and depression-related temperament, i.e., harm avoidance (assessed on the Temperament and Character Inventory, TCI). The environmental factors included measures of childhood and adolescence exposure, i.e., maternal nurturance and parental socioeconomic status, and adulthood social circumstances, i.e., perceived social support and urban/rural residence. The participants were two randomly selected subsamples (n = 1246, n = 341) from the longitudinal population-based Cardiovascular Risk in Young Finns study (n = 3596). Childhood environmental factors were assessed when the participants were 3 to 18 years of age, and three years after the baseline. Adulthood environmental factors and outcome measures were assessed 17 and 21 years later when the participants were 21 to 39 years of age. The T102C polymorphism of the HTR2A gene moderated the association between childhood maternal nurturance and adulthood depressive symptoms, such that exposure to high maternal nurturance predicted low depressive symptoms among individuals carrying the T/T or T/C genotypes, but not among those carrying the C/C genotype. Likewise, high parental SES predicted low adulthood harm avoidance in individuals carrying the T/T or T/C genotype, but not in C/C-genotype carriers. Individuals carrying the T/T or T/C genotype were also sensitive to urban/rural residence, such that they had lower depressive symptoms in urban than in rural areas, whereas those carrying the C/C genotype were not sensitive to urban/rural residence difference. HTR2A did not moderate the influence of social support. TheA779C/A218C haplotype of the TPH1 gene was not involved in the association between childhood environment and adulthood outcomes. However, individuals carrying A alleles of the TPH1 haplotype were more vulnerable to the lack of adulthood social support in terms of high depressive symptoms than their counterparts carrying no A alleles. Furthermore, individuals living in remote rural areas and carrying the A/A haplotype had higher depressive symptoms than those carrying other genotypes of the TPH1. The findings suggest that the HTR2A and TPH1 genes may be involved in the development of depression by influencing individual s sensitivity to depressogenic environmental influences.

Nicotine Dependence and Smoking Behaviour : A genetic and epidemiological study

The worldwide health burden caused by the tobacco epidemic highlights the importance of study-ing determinants of smoking behaviour and key factors sustaining nicotine dependence. Despite vast-ranging preventive efforts, smoking remains one of the most deleterious health behaviours, and its genetic and environmental factors warrant continuous investigation. The heritability of smoking behaviour and nicotine dependence has been suggested to be relatively high. Earlier smoking behaviour, nicotine dependence, socio-economic position and demographic factors have all been shown to be associated with smoking cessation. This thesis aimed to examine various aspects of smoking behaviour and nicotine dependence from an epidemiological and genetic per-spective. Data for Studies I and IV were obtained from the Older Finnish Twin Cohort, a postal health sur-vey conducted in 1975, 1981 and 1990 on same-sexed pairs and in 1996-1997 on male-female adult pairs. The number of ever-smoking participants was 8941 in Study I and 3069 in Study IV. Data for Studies II and III came from the Family Study of Cigarette Smoking - Vulnerability to Nicotine Addiction. This study is linked to the Older Finnish Twin Cohort with new data collec-tion during 2001-2006 that focused on smoking twin pairs and their family members. The meas-ures included intensive telephone interviews, blood samples and additional postal questionnaires. The numbers of ever-smoking participants was 1370 in Study II and 529 in Study III. Study I examined whether a genetic component underlies smoking behaviour among Finnish adults. Genetic factors were important in the amount smoked and smoking cessation, with about half of the phenotypic differences explained by genetic variance. A novel finding was that genetic influences on amount smoked and smoking cessation were largely independent of genetic influ-ences on age at initiation. This result has implications for defining phenotypes in the search for genes underlying smoking behaviour. Furthermore, even if smoking initiation is postponed to a later age, potential vulnerability to subsequent nicotine dependence cannot be completely inhib-ited. Study II investigated the effect of genetic and environmental factors on nicotine dependence, as measured by the novel multidimensional Nicotine Dependence Syndrome Scale (NDSS). This scale was validated in the Finnish data. The NDSS correlated highly with other established nico-tine dependence scales (FTND and DSM-IV), suggesting that this new scale would be a feasible and valid measure for identifying nicotine-dependent smokers among the ever-smoking popula-tion. About one-third of the phenotypic variation in nicotine dependence in this sample was ex-plained by genetic influences. Study III aimed at identifying chromosomal regions harbouring genes that influence smoking be-haviour and nicotine dependence. Linkage analysis of family data revealed that for smoker and nicotine dependence phenotypes as well as for co-morbidity between nicotine dependence and alcohol use signals on specific chromosome regions (chromosomes 2q33, 5q12, 5q34 7q21, 7q31, 10q25, 11p15, 20p13) exist. Results further support the hypothesis that smoking behaviour phe-notypes have a genetic background. Study IV examined associations of smoking behaviour, socio-economic position and transition of marital status with smoking cessation. Indicators of socio-economic position were important pre-dictors of smoking cessation even when adjusted for previous smoking behaviour. Getting married was associated with an increased probability of cessation in men, a finding confirmed among dis-cordant twin pairs. Thus, having a partner appears to have a positive impact on smoking cessation. In conclusion, nicotine dependence and smoking behaviour demonstrate significant genetic liabil-ity, but also substantial environmental influences among Finnish adults. Smoking initiation should be prevented or at least postponed to a later age. Although genetic factors are important in nicotine dependence and smoking behaviour, societal actions still have a primary role in tobacco control and smoking prevalence. Future studies should examine the complex interactions between genetic and environmental factors in nicotine dependence.

Community forestry and environmental literacy in northern Thailand : Towards collaborative natural resource management and conservation

Conservation and sustainable management of tropical forests needs a holistic approach: in addition to ecological concerns, socio-economic issues including cultural aspects must be taken into consideration. An ability to adapt practices is a key to successful collaborative natural resource management. Achieving this requires local participation and understanding of local conceptions of the environment. This study examined these issues in the context of northern Thailand. Northern uplands are the home of much of the remaining natural forest in Thailand and several ethnic minority groups commonly referred to as hill tribes. The overall purpose of this study was to grasp a regional view of an ethnically diverse forested area and to elicit prospects to develop community forestry for conservation purposes and for securing people s livelihood. Conservation was a central goal of management as the forests in the area were largely designated as protected. The aim was to study local perceptions, objectives, values and practices of forest management, under the umbrella of the concept environmental literacy, as well as the effects of forest policy on community management goals and activities. Environmental literacy refers to holistic understanding of the environment. It was used as a tool to examine people s views, interests, knowledge and motivation associated to forests. The material for this study was gathered in six villages in Chiang Mai Province. Three minority groups were included in the study, the Karen, Hmong and Lawa, and also the Thai. Household and focus group interviews were conducted in the villages. In addition, officials at district, regional and national levels, workers of non-governmental organisations, and academics were interviewed, and some data were gathered from the students of a local school. The results showed that motivation for protecting the forests existed among each ethnic group studied. This was a result of culture and traditions evolved in the forest environment but also of a need to adapt to a changed situation and environment and to outside pressures. The consequences of deforestation were widely agreed on in the villages, and the impact of socio-economic changes on the forests and livelihood was also recognised. The forest was regarded as a source of livelihood providing land, products and services essential to the people inhabiting rural uplands. Traditions, fire control, cooperation, reforestation, separation of protected and utilisable areas, and rules were viewed as central for conservation. For the villagers, however, conservation meant sustainable use, whereas the government has tended to prefer strict restrictions on forest resource use. Thus, conflicts had arisen. Between communities, cooperation was more dominant than conflict. The results indicated that the heterogeneity of forest dwellers, although it has to be recognised, should not be overemphasised: ethnic diversity can be considered as no major obstacle for successful community forestry. Collaborative management is particularly important in protected areas in order to meet the conservation goals while providing opportunities for livelihood. Forest management needs more positive incentives and increased dialogue.