Academic literature on the topic 'Environmental risk factors'
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Journal articles on the topic "Environmental risk factors"
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Nazarko, Linda. "Falls: environmental risk factors." British Journal of Healthcare Assistants 6, no. 3 (March 2012): 111–15. http://dx.doi.org/10.12968/bjha.2012.6.3.111.
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Dietert, Rodney R., Janice M. Dietert, and Jamie C. Dewitt. "Environmental risk factors for autism." Emerging Health Threats Journal 4, no. 1 (January 2011): 7111. http://dx.doi.org/10.3402/ehtj.v4i0.7111.
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Granieri, Enrico, and Ilaria Casetta. "Multiple sclerosis: environmental risk factors." Neurology Bulletin XXX, no. 1-2 (March 15, 1998): 40–42. http://dx.doi.org/10.17816/nb80848.
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Multiple sclerosis is a disease of unknown etiology characterized by inflammory demyelination of the brain and spinal cord. Epidemiological investigations play important role in study of multiple sclerosis. Geographical distribution of the disease has been described in terms of prevalence and incidence. The possible role of environmental factors as a cause of multiple sclerosis had been hypothesized with observation of unequal geographic distribution of the disease. More interesting, in terms of their biological significance, are attempts to identify associations between multiple sclerosis and situations or events wich could cause blood-brain barrier damages, such as trauma or toxic exposures.
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Dudkina, N. A. "Multiple sclerosis: environmental risk factors." Neurology Bulletin XXX, no. 1-2 (March 15, 1998): 42–43. http://dx.doi.org/10.17816/nb80849.
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The author represented materials on incidence of progressive muscular distrophy in the region of Tver. 168 patients were investigated with different forms of disease. The most frequent form of disease was Erbs athophy (in 60%); incidence of Duchennes and Landuzys forms was the same (in 20%). Compared with the Russias indices of incidence, significant prevailing of this pathology in the region of Tver was revealed.
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Sameroff, Arnold J. "Environmental Risk Factors in Infancy." Pediatrics 102, Supplement_E1 (November 1, 1998): 1287–92. http://dx.doi.org/10.1542/peds.102.se1.1287.
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Environment plays an important role in shaping development from the newborn period through adolescence. Many individual environmental risk factors may impinge on development (poverty, mental illness, minority status, and many others), but the most detrimental effects are caused when multiple risk factors act on a single infant. These effects were revealed by the Rochester Longitudinal Study, an ongoing comprehensive investigation of environmental risk factors, summa rized in this article.
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Goyer, R. A., S. Epstein, M. Bhattacharyya, K. S. Korach, and J. Pounds. "Environmental risk factors for osteoporosis." Environmental Health Perspectives 102, no. 4 (April 1994): 390–94. http://dx.doi.org/10.1289/ehp.94102390.
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Björkstén, Bengt. "Environmental risk factors for atopy." Clinical Reviews in Allergy & Immunology 15, no. 2 (June 1997): 125–43. http://dx.doi.org/10.1007/bf02826583.
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Opler, Mark, Joseph Charap, Astrea Greig, Victoria Stein, Stephanie Polito, and Dolores Malaspina. "Environmental Risk Factors and Schizophrenia." International Journal of Mental Health 42, no. 1 (April 2013): 23–32. http://dx.doi.org/10.2753/imh0020-7411420102.
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Najem, R., and A. Salem. "Youth Suicide: Environmental Risk Factors." Epidemiology 17, Suppl (November 2006): S409. http://dx.doi.org/10.1097/00001648-200611001-01091.
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Ahuja, Dr Ravindra, Dr Ruchi Thakur, and Dr Rajat Ahuja. "Identification of Maternal, Environmental and Hygienic Practices as Risk Factors for Diarrhoea." International Journal of Scientific Research 3, no. 7 (June 1, 2012): 390–92. http://dx.doi.org/10.15373/22778179/july2014/120.
Full textDissertations / Theses on the topic "Environmental risk factors"
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Schultz, Stephen T. "Environmental Risk Factors for Autistic Disorder." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2006. http://wwwlib.umi.com/cr/ucsd/fullcit?p3212023.
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Thesis (Ph. D.)--University of California, San Diego and San Diego State University, 2006.Title from first page of PDF file (viewed July 10, 2006). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
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Salzer, Jonatan. "Environmental risk factors for multiple sclerosis." Doctoral thesis, Umeå universitet, Klinisk neurovetenskap, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-64212.
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Background Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. It usually strikes during young adulthood, and 2.5 million individuals are estimated to have the disease worldwide. The causes of MS are not known, but several factors have been shown to be associated with the risk of the disease, including certain genes, vitamin D, smoking and Epstein- Barr virus infection. Little is known about how/if these factors interact. Methods Study I: The risk of MS by month of birth was investigated using MS cases from the Swedish MS registry and using general population controls. Studies II–V: We identified MS cases who had donated blood prior to disease onset, and MS cases whose mothers had donated blood during pregnancy, by cross-linking a database of MS cases, and a database of mothers of MS cases, to two local biobank cohorts. One of them consisted of blood samples collected during early pregnancy, and one with samples collected during health controls. Levels of 25(OH)D (25-hydroxyvitamin D), RBP (retinol binding protein, a surrogate marker for vitamin A), CRP (C- reactive protein), cotinine (a nicotine metabolite) and anti Epstein-Barr virus nuclear antigen-1 (EBNA-1) antibodies were measured in cases and matched controls. The risk of MS by categories of these exposures was estimated in bi- and multivariable matched logistic regression models. Results Subjects born in spring had a higher risk of MS, but no influence of early gestational levels of the measured risk factors on the risk of MS in the offspring was observed. In prospective samples from MS cases and controls, 25(OH)D levels ≥75 nmol/l, intermediate RBP levels, and elevated CRP levels in young were associated with a decreased risk of MS. Elevated cotinine levels (suggestive of smoking) and high antibody reactivity against EBNA-1 were associated with an increased risk of MS. All factors but RBP were more clearly associated with MS in young subjects. Conclusion All factors analyzed in prospectively collected samples were associated with the risk of MS, and taken together, the data indicate that the key etiopathological events that lead to MS occur before the age of 20–30. Study II provides support for trials exploring the primary preventive potential of oral vitamin D supplementation.
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Gartner, Coral Elizabeth. "Environmental risk factors for Parkinson's disease." Thesis, Queensland University of Technology, 2006. https://eprints.qut.edu.au/16393/1/Coral_Gartner_Thesis.pdf.
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Parkinson's disease (PD) is a progressive, degenerative, neurological disease. The progressive disability associated with PD results in substantial burdens for those with the condition, their families and society in terms of increased health resource use, earnings loss of affected individuals and family caregivers, poorer quality of life, caregiver burden, disrupted family relationships, decreased social and leisure activities, and deteriorating emotional well-being. Currently, no cure is available and the efficacy of available treatments, such as medication and surgical interventions, decreases with longer duration of the disease. Whilst the cause of PD is unknown, genetic and environmental factors are believed to contribute to its aetiology. Descriptive and analytical epidemiological studies have been conducted in a number of countries in an effort to elucidate the cause, or causes, of PD. Rural residency, farming, well water consumption, pesticide exposure, metals and solvents have been implicated as potential risk factors for PD in some previous epidemiological studies. However, there is substantial disagreement between the results of existing studies. Therefore, the role of environmental exposures in the aetiology of PD remains unclear.
The main component of this thesis consists of a case-control study that assessed the contribution of environmental exposures to the risk of developing PD. An existing, previously unanalysed, dataset from a local case-control study was analysed to inform the design of the new case-control study. The analysis results suggested that regular exposure to pesticides and head injury were important risk factors for PD. However, due to the substantial limitations of this existing study, further confirmation of these results was desirable with a more robustly designed epidemiological study. A new exposure measurement instrument (a structured interviewer-delivered questionnaire) was developed for the new case-control study to obtain data on demographic, lifestyle, environmental and medical factors. Prior to its use in the case-control study, the questionnaire was assessed for test-retest repeatability in a series of 32 PD cases and 29 healthy sex-, age- and residential suburb-matched electoral roll controls. High repeatability was demonstrated for lifestyle exposures, such as smoking and coffee/tea consumption (kappas 0.70-1.00). The majority of environmental exposures, including use of pesticides, solvents and exposure to metal dusts and fumes, also showed high repeatability (kappas >0.78).
A consecutive series of 163 PD case participants was recruited from a neurology clinic in Brisbane. One hundred and fifty-one (151) control participants were randomly selected from the Australian Commonwealth Electoral Roll and individually matched to the PD cases on age (± 2 years), sex and current residential suburb. Participants ranged in age from 40-89 years (mean age 67 years). Exposure data were collected in face-to-face interviews. Odds ratios and 95% confidence intervals were calculated using conditional logistic regression for matched sets in SAS version 9.1. Consistent with previous studies, ever having been a regular smoker or coffee drinker was inversely associated with PD with dose-response relationships evident for packyears smoked and number of cups of coffee drunk per day. Passive smoking from ever having lived with a smoker or worked in a smoky workplace was also inversely related to PD. Ever having been a regular tea drinker was associated with decreased odds of PD. Hobby gardening was inversely associated with PD. However, use of fungicides in the home garden or occupationally was associated with increased odds of PD. Exposure to welding fumes, cleaning solvents, or thinners occupationally was associated with increased odds of PD. Ever having resided in a rural or remote area was inversely associated with PD. Ever having resided on a farm was only associated with moderately increased odds of PD. Whilst the current study's results suggest that environmental exposures on their own are only modest contributors to overall PD risk, the possibility that interaction with genetic factors may additively or synergistically increase risk should be considered.
The results of this research support the theory that PD has a multifactorial aetiology and that environmental exposures are some of a number of factors to contribute to PD risk. There was also evidence of interaction between some factors (eg smoking and welding) to moderate PD risk.
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Gartner, Coral Elizabeth. "Environmental risk factors for Parkinson's disease." Queensland University of Technology, 2006. http://eprints.qut.edu.au/16393/.
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Parkinson's disease (PD) is a progressive, degenerative, neurological disease. The progressive disability associated with PD results in substantial burdens for those with the condition, their families and society in terms of increased health resource use, earnings loss of affected individuals and family caregivers, poorer quality of life, caregiver burden, disrupted family relationships, decreased social and leisure activities, and deteriorating emotional well-being. Currently, no cure is available and the efficacy of available treatments, such as medication and surgical interventions, decreases with longer duration of the disease. Whilst the cause of PD is unknown, genetic and environmental factors are believed to contribute to its aetiology. Descriptive and analytical epidemiological studies have been conducted in a number of countries in an effort to elucidate the cause, or causes, of PD. Rural residency, farming, well water consumption, pesticide exposure, metals and solvents have been implicated as potential risk factors for PD in some previous epidemiological studies. However, there is substantial disagreement between the results of existing studies. Therefore, the role of environmental exposures in the aetiology of PD remains unclear. The main component of this thesis consists of a case-control study that assessed the contribution of environmental exposures to the risk of developing PD. An existing, previously unanalysed, dataset from a local case-control study was analysed to inform the design of the new case-control study. The analysis results suggested that regular exposure to pesticides and head injury were important risk factors for PD. However, due to the substantial limitations of this existing study, further confirmation of these results was desirable with a more robustly designed epidemiological study. A new exposure measurement instrument (a structured interviewer-delivered questionnaire) was developed for the new case-control study to obtain data on demographic, lifestyle, environmental and medical factors. Prior to its use in the case-control study, the questionnaire was assessed for test-retest repeatability in a series of 32 PD cases and 29 healthy sex-, age- and residential suburb-matched electoral roll controls. High repeatability was demonstrated for lifestyle exposures, such as smoking and coffee/tea consumption (kappas 0.70-1.00). The majority of environmental exposures, including use of pesticides, solvents and exposure to metal dusts and fumes, also showed high repeatability (kappas >0.78). A consecutive series of 163 PD case participants was recruited from a neurology clinic in Brisbane. One hundred and fifty-one (151) control participants were randomly selected from the Australian Commonwealth Electoral Roll and individually matched to the PD cases on age (± 2 years), sex and current residential suburb. Participants ranged in age from 40-89 years (mean age 67 years). Exposure data were collected in face-to-face interviews. Odds ratios and 95% confidence intervals were calculated using conditional logistic regression for matched sets in SAS version 9.1. Consistent with previous studies, ever having been a regular smoker or coffee drinker was inversely associated with PD with dose-response relationships evident for packyears smoked and number of cups of coffee drunk per day. Passive smoking from ever having lived with a smoker or worked in a smoky workplace was also inversely related to PD. Ever having been a regular tea drinker was associated with decreased odds of PD. Hobby gardening was inversely associated with PD. However, use of fungicides in the home garden or occupationally was associated with increased odds of PD. Exposure to welding fumes, cleaning solvents, or thinners occupationally was associated with increased odds of PD. Ever having resided in a rural or remote area was inversely associated with PD. Ever having resided on a farm was only associated with moderately increased odds of PD. Whilst the current study's results suggest that environmental exposures on their own are only modest contributors to overall PD risk, the possibility that interaction with genetic factors may additively or synergistically increase risk should be considered. The results of this research support the theory that PD has a multifactorial aetiology and that environmental exposures are some of a number of factors to contribute to PD risk. There was also evidence of interaction between some factors (eg smoking and welding) to moderate PD risk.
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Brooks, Constance M. "Environmental risk factors and risky sexual behavior outcomes attitudes as a mediating factor /." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/4820.
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Thesis (Ph. D.)--University of Missouri-Columbia, 2007.The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on September 19, 2007) Vita. Includes bibliographical references.
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Yazdy, Mahsa Mirmiran. "Environmental and infectious risk factors for gastroschisis." Thesis, Boston University, 2013. https://hdl.handle.net/2144/12946.
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Thesis (Ph.D.)--Boston UniversityGastroschisis is a rare congenital malformation where loops of bowel are protruding from the abdominal wall of an infant. The prevalence of gastroschisis has been increasing over the past 20 years, particularly in younger women. However, as the number of studies on gastroschisis increases each year, it continues to remain unclear why the prevalence is increasing and why it disproportionately affects younger mothers. Previous research has suggested that environmental or infectious factors may be involved in the pathogenesis of gastroschisis. This dissertation aims to explore the possibility of these two factors in relation to gastroschisis. In study 1, clusters of gastroschisis were identified in space or the combination of space and time. Cases and controls came from the National Birth Defects Study (NBDPS) or for some study centers from the birth defects surveillance systems. Generalized additive models were used to create a continuous map surface of odds ratios (OR) by smoothing over latitude and longitude. Data from the NBDPS were used for the Arkansas, California, and Utah study centers and the highest adjusted ORs detected were 2.0, 1.3, and 2.4, respectively. In Massachusetts and Texas, where surveillance data were used, the highest adjusted ORs observed were 2.4 and 1.3, respectively, with only the latter state achieving statistical significance. Texas had sufficient data to assess the combination of space and time, which identified an increased risk (OR=2.9) in the center of Texas in 2003. The results of this study suggest that clusters of gastroschisis may exist and further exploration of environmental or behavioral factors are warranted. [TRUNCATED]
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Rios, Fernandez Paula. "Perinatal and environmental risk factors of childhood neuroblastoma." Thesis, Sorbonne Paris Cité, 2019. http://www.theses.fr/2019USPCB017.
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Contexte : Le neuroblastome est une tumeur embryonnaire qui se développe à partir du système nerveux sympathique. C’est la tumeur maligne solide extra-cérébrale la plus fréquente chez les enfants de moins d’un an. La cause du neuroblastome est encore inconnue dans la majorité des cas. Cependant, les caractéristiques embryonnaires de la tumeur ainsi que sa courte latence de survenue après la naissance suggèrent l’origine périnatale de ce cancer et l’importance d’étudier les expositions survenant pendant la grossesse et les premières années de vie de l’enfant. Dans ce travail de recherche, nous avons analysé le lien entre certains facteurs périnataux et des expositions pendant la grossesse et le risque neuroblastome chez l’enfant. Matériel et méthodes : les données sont issues des enquêtes ESCALE (2003-2004) et ESTELLE (2010-2011) menées par notre équipe de recherche. Les mères de 357 cas de neuroblastome issus du Registre National des Cancers de l’Enfant (RNCE) ainsi que 1753 témoins recrutés en population générale ont répondu à un entretien qui portait sur les caractéristiques périnatales de l’enfant, les expositions maternelles pendant la grossesse, antécédents médicaux familiaux et personnels de l’enfant ainsi que sur des variables contextuelles et socioéconomiques. La taille de notre échantillon a permis de réaliser des analyses stratifiées sur l’âge au diagnostic et le statut du proto-oncogène MYCN. Résultats : une première analyse sur l’association entre les caractéristiques périnatales et le risque de neuroblastome chez l’enfant a mis en évidence des associations positives avec la présence de malformations congénitales (OR 3.6 [95% CI 1.3–8.9] parmi les enfants de moins de 18 mois) et des altérations de la croissance fœtale tels que le retard de croissance intra-utérine ou la surcroissance fœtale (OR 1.4 [95% CI 1.0-2.0]) et (OR 1.5 [95% CI 1.1–2.2], respectivement). Le fait d’être allaité était inversement associé au risque de neuroblastome (OR 0.7 [95% CI 0.5–1.0]). Des associations inverses ont été également observées avec la supplémentation maternelle préconceptionnelle en acide folique (OR 0.5 [95% CI 0.3–0.9]). La difficulté pour concevoir ou l’utilisation d’assistance médicale à la procréation n’ont pas été associé au risque de neuroblastome dans notre étude. Dans une deuxième partie de ce travail, nous avons analysé les expositions maternelles domestiques et professionnelles aux pesticides pendant la grossesse. Nos résultats suggèrent que l’utilisation domestique de pesticides pendant la grossesse pourrait augmenter le risque de neuroblastome chez l’enfant (OR 1.5 [95% CI 1.2–1.9]). Des associations positives ont été observées avec l’utilisation d’insecticides seulement (OR 1.4 [95% CI 1.1–1.9]), ou en combinaison avec d’autres pesticides (OR 2.0 [95% CI 1.1–3.4]). L’exposition professionnelle de la mère pendant la grossesse était également associée au risque de neuroblastome. La troisième partie de ce travail a porté sur l’analyse du tabagisme parental et la consommation maternelle d’alcool pendant la grossesse. La consommation maternelle de tabac était plus fréquente chez les mères des cas (24.1%) par rapport aux mères des témoins (19.7%) ; (OR 1.3 [95%CI 0.9–1.7]; OR à partir d’une méta-analyse 1.1 [95%CI 1.0–1.3]. Conclusion : nos résultats portant sur les associations entre neuroblastome, surcroissance fœtale et malformations congénitales supportent l’hypothèse d’un rôle des altérations de l’embryogénèse dans la survenue des neuroblastomes de l’enfant. Ce travail contribue à l’évidence en faveur des associations entre neuroblastome et certaines expositions pendant la grossesse, notamment l’utilisation domestique de pesticides et le tabagisme maternelle. Nos résultats soulignent l’importance des recommandations visant à réduire l’exposition aux pesticides et le tabagisme maternel pendant la grossesse. [...]Background: Neuroblastoma is the most common extra-cranial tumor in children. Little is known about the etiology of neuroblastoma. The early age at onset and the embryonic nature suggest a role for perinatal exposures. In this work, we analyzed whether childhood neuroblastoma was associated with specific perinatal characteristics and environmental exposures around pregnancy. We assessed the following birth-related characteristics: gestational age, birth-weight and fetal growth, and the presence of congenital malformations. The maternal reproductive history before the index pregnancy and maternal intake of folic acid or vitamins/minerals before or during pregnancy was also assessed. With regards to environmental exposures related to parental habits, we focused on maternal use of household pesticides during pregnancy, parental smoking and maternal alcohol consumption. Methods: We conducted a pooled analysis of two French national-based case-control studies. The mothers of 357 neuroblastoma case and 1,783 control children younger than 6 years, frequency-matched by age and gender, completed a telephone interview that focused on sociodemographic and perinatal characteristics, childhood environment and parental lifestyle. Unconditional logistic regression was used to estimate pooled odds ratios (OR) and 95% confidence intervals (CIs), including matching variables, study of origin and potential confounders. A meta-analysis of our findings with those of previous studies was also conducted with regards to maternal smoking and alcohol consumption during pregnancy. We used random effects, precision-based weighting to calculate the summary OR including our results. Results: The first part of the thesis focused on perinatal characteristics. We observed that being born either small (OR 1.4 [95% CI 1.0-2.0]) or large (OR 1.5 [95% CI 1.1–2.2]) for gestational age and, among children younger than 18 months, having congenital malformations (OR 3.6 [95% CI 1.3–8.9]), were significantly associated with neuroblastoma. Inverse associations were observed with breastfeeding (OR 0.7 [95% CI 0.5–1.0]) and maternal use of any supplements containing folic acid, vitamins or minerals (OR 0.5 [95% CI 0.3–0.9]) during the preconception period. The second part of the thesis showed that maternal use of any type of household pesticide during pregnancy was associated with neuroblastoma (OR 1.5 [95% CI 1.2–1.9]). The most commonly used type of pesticides were insecticides and there was a positive association with their use alone (OR 1.4 [95% CI 1.1–1.9]) or with other pesticides (OR 2.0 [95% CI 1.1–3.4]). In the third part, our analyses showed that maternal smoking during pregnancy was slightly more often reported for the cases (24.1%) than for the controls (19.7%) (OR 1.3 [95% CI 0.9–1.7]; Paternal smoking in the year before child’s birth was not associated with neuroblastoma as independent exposure (OR 1.1 [95%CI 0.9–1.4] but the association was stronger when both parents reported having smoked during pregnancy (OR 1.5 [95% CI 1.1–2.1]. Finally, in a meta-analysis of maternal smoking and neuroblastoma the summary OR from meta-analysis was 1.1 [95% CI 1.0–1.3]. Conclusions: Our findings support the hypothesis of a defective embryogenesis in neuroblastoma since fetal growth anomalies and congenital malformations were associated with an increased risk of neuroblastoma. This work also adds to the evidence of an association between neuroblastoma and some exposures during pregnancy, such as maternal use of household pesticides and maternal smoking, which are additional reasons why to advise pregnant women to limit these exposures in this period. Further investigations are needed to clarify the role of folic acid supplementation and breastfeeding, given their potential importance in neuroblastoma prevention
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Dick, Smita. "Occupational and environmental risk factors for Parkinson's disease." Thesis, University of Aberdeen, 2005. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU201019.
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Case-control study or prevalent parkinsonism and PD cases in Grampian and Easter Ross, Scotland. Cases were defined using United Kingdom Parkinson's Disease Society Brain Bank clinical diagnostic criteria. Dementia, cerebrovascular and drug-induced cases were excluded. Age and gender-balanced controls were drawn from hospital outpatients and the community. Trained interviewers administered a questionnaire regarding lifestyle and occupation including solvent, pesticide and metal exposure (iron, copper, manganese). An occupational hygienist estimated metal exposures blind to disease status using a job exposure matrix modified by subjective exposure estimation. Lifetime occupational histories were classified by occupational (Dictionary of Occupational Titles) and industry (modified International Standard Industrial Classification. A follow-up postal study in Grampian enquired about tea and coffee consumption, anxiolytic, anti-depressant and hypnotic use and head injury. 202 cases and 420 controls were recruited between June 2000 and July 2002 (responsive rate 46.2%). Multiple logistic regression analyses showed first-degree family history of PD (OR 4.12, 95%CI 1.92-8.83) and pesticides ('high' exposure OR 1.69, 95% CI 1.06-2.69) were risk factors. Smoking was protective (OR 0.26, 95%CI 0.18-0.29) with an exposure-response relationship. Both occupational and industry coding systems showed non-significantly increased risks for 'agriculture'. The follow-up study response rate was 93% (149 cases, 305 controls). Tea and coffee consumption were not associated with PD. A positive association of use of psychoactive medication with PD was probably explained by their use after disease onset. A non-significantly increased association of head injury and PD was not supported by the follow-up postal study. First-degree family history of PD was associated with PD. Pesticide use was a risk factor for PD, whereas smoking was associated with reduced risk. The increased risk for agriculture may reflect pesticide use.
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Krug, Isabel. "Environmental risk factors and therapeutical implications in eating disorders." Doctoral thesis, Universitat de Barcelona, 2008. http://hdl.handle.net/10803/2546.
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The central scientific objective of this thesis was to take a broad multidisciplinary approach to make use of the full potential information to battle EDs, utilizing an interactive and translational approach running from basic science through to the clinic. In our studies we assessed a.) clinical factors and comorbidity [namely substance use in EDs (Studies 1 to 3)], b.) psychosocial, behavioural and environmental correlates of EDs (Studies 4 to 7) and c.) treatment effectiveness of specific forms of ED interventions (Studies 8 to 9). Our first line of investigation comprised Studies 1 to 3 and assessed the comorbidity of substance use in EDs. The results of these studies suggest that compared to healthy controls, substance use was higher in individuals with EDs (Studies 1 and 3), that the presence of a family history of alcohol dependence was associated with the comorbidity of EDs and substance use (Study 2) that substance use was particularly prevalent in patients with bulimic characteristics (Studies 1 to 3) and that EDs and substance abuse may represent expressions of a fundamental predisposition to addictive behaviour possibly related to the genetically influenced traits such as novelty seeking (Study 2). Furthermore, we revealed some significant differences for the specific forms of drugs in people with EDs (Studies 1 and 3), which emphasize the significance of assessing various drug types in EDs. Finally we also observed cross-cultural differences across various European countries in the prevalence of substance use in EDs and healthy controls (Study 3).
The second research area was labelled psychological, behavioural and environmental correlates of EDs. In our animal study (Study 4) we found that contextual conditioning of eating response was more effective when high than low density caloric food was used. This result indicates that animal models are useful for analyzing and identifying human-animal links in feeding related behaviours.
Studies 5 and 6 assessed which early individual and family eating patterns play a role in the development of EDs. Our findings agree with the growing body of research indicating that a variety of environmental and social factors are associated with dysfunctional individual and family eating patterns (e.g. food used as individualization, control and rules about food) during the first years of life and which if not detected on time could lead to a subsequent ED. Conversely, healthy eating (including eating breakfast) was negatively linked to the development of a subsequent ED. Only a few differences across ED subtypes were observed. Finally some cross-cultural differences also emerged (Study 6).
In Study 7 we compared anger expressions in individuals with EDs and healthy controls and explored the relation among ED symptoms, comorbid psychopathology, personality traits and impulsive behaviours. The results indicated that individuals with EDs obtained significantly higher scores than controls on maladaptive anger expressions. When different purging methods were assessed independently, the frequency of laxative use was associated with anger suppression. ED symptoms and specific personality traits were also positively associated to different anger expressions. At last, we observed that inappropriate anger expressions were related to self-harming behaviours.
Finally our last research line assessed the effectiveness of various treatments for EDs. In Study 8 we compared full and subthreshold BN in terms of personality, clinical characteristics and short-term response to a psychoeducational therapy. The results showed that full-BN and sub-BN share common psychopathological symptoms and personality traits. Furthermore, no differences in therapy outcome were observed in terms of general ED symptomatology and psychopathology. In Study 9 we described and assessed a non-symptom oriented CBT treatment in a congenitally blind women. A dramatic reduction in ED symptoms was observed after the maintaining and triggering factors had been reduced.
To conclude, relatively little research has been performed towards understanding the aetiology of EDs. The findings from our investigations represent a major enhancement in the state of the art of EDs, and lead to the development of a new overall etiological model of EDs. The model we propose is a general understanding of how various ED predisposing and precipitating factors might eventually lead to EDs, and maintain the course of a disorder. Future work should address the effects of genes, environment and gene-environment interaction on the development and maintenance of EDs. Of specific interest is the query of which of these factors are non-specifically related to mental disorders and which factors may be more explicit factors that predispose an individual to EDs and related states, but not to mental disorders in general. The answers to these questions should hopefully become perceptible in the next couple of years.
El objetivo principal de esta tesis ha sido el abordar los Trastornos de la alimentación (TCA) desde una aproximación multidisciplinar, que nos ayude a combatir los TCA desde una perspectiva traslacional, en la que confluyan investigaciones básicas y aplicadas. En nuestros estudios hemos analizado en profundidad los siguientes aspectos: a.) Factores clínicos y comorbilidad [especialmente abuso de sustancias en TCA] (Estudios 1 a 3); b.) Correlatos psicosociales, conductuales y ambientales en TCA (Estudios 4 a 7); y c.) Eficacia de tratamientos específicos en TCA (Estudios 8 a 9).
Nuestra primera línea de investigación (Estudios 1-3), ha estudiado la comorbilidad de abuso de sustancias en TCA. Los resultados de estos estudios sugieren que: a) abuso de sustancias es más prevalente en TCA que en sujetos de control (Estudios 1 y 3); b) la presencia abuso de sustancias en pacientes con TCA, está asociada a historia familiar previa de dependencia de alcohol (Estudio 2); c) abuso de sustancias es especialmente prevalente en pacientes con características bulímicas (Estudios 1 a 3); y d) que presencia de abuso de sustancias en TCA puede ser expresión de una predisposición a conductas adictivas, cuya susceptibilidad viene determinada por rasgos de personalidad específicos (búsqueda de sensaciones) (Estudio 2). Asimismo, encontramos aspectos diferenciales en TCA, en base al tipo de droga que consumen (Estudio 1 y 3), hecho que enfatiza la importancia de evaluar los distintos tipos de drogas utilizados por estos pacientes. Finalmente, encontramos diferencias culturales entre distintos países europeos, respecto a la prevalencia de abuso de sustancias en TCA, al ser comparados con grupos de control (estudio 3).
Como segunda área de investigación, nos centramos en aspectos psicológicos, conductuales y ambientales en TCA. En un estudio, realizado siguiendo un modelo animal (estudio 4), encontramos que el condicionamiento contextual de respuesta alimentaria es más efectivo cuando es utilizado un alimento con alta densidad calórica, que cuando se utiliza un alimento con baja densidad calórica. Estos resultados sugieren qué modelos animales son útiles a la hora de analizar e identificar asociaciones entre comportamiento en humanos y animales, respecto a su conducta alimentaria.
En los estudios 5 y 6 se analizaron en qué medida conductas alimentarias tempranas y patrones alimentarios en la familia, influyen en la aparición posterior de un TCA. Los resultados de estos estudios sugieren, en concordancia con un creciente volumen estudios recientes, la influencia que poseen aspectos ambientales y sociales en el desarrollo posterior de una conducta alimentaria anormal (p.e., control y reglas entorno a la alimentación). Por contrario, patrones alimentarios regulares (p.e., desayunar antes de ir al colegio) se encontró negativamente asociado (factor protector) a subsecuente desarrollo de un TCA. Asimismo, fueron encontradas limitadas diferencias entre subtipos diagnósticos, aunque algunas hacían referencia al contexto cultural (estudio 6).
En el estudio 7 comparamos la expresión de ira en sujetos con un TCA y un grupo control, y analizamos su asociación con sintomatología alimentaria, psicopatología general comórbida, rasgos de personalidad y conductas impulsivas. Nuestros resultados indicaron que pacientes con TCA manifestaban sentimientos de ira de forma más inadecuada que grupos control. Al analizar los distintos procedimientos de purga, la frecuencia de abuso de laxantes iba asociada a supresión de sentimientos de ira.
La sintomatología alimentaria y algunos rasgos de personalidad se asociaban a determinadas formas inadecuadas de expresión de sentimientos. Asimismo, observamos que una inadecuada expresión de sentimientos en TCA se asociaba con una mayor frecuencia de conductas autoagresivas.
Finalmente, en nuestra última línea de investigación analizamos la eficacia de distintos tipos de tratamiento en TCA. En el estudio 8 comparamos casos totales y parciales de Bulimia nerviosa, en base rasgos de personalidad, sintomáticas alimentaria, psicopatología general y respuesta a un tratamiento de carácter psicoeducativo. Los resultados indicaron que los casos totales y parciales de BN comparten similitudes sintomáticas, psicopatológicas y de personalidad. Asimismo, no se obtuvieron diferencias respecto a la respuesta al tratamiento entre ambos grupos de pacientes. En el estudio 9, describimos y evaluamos un tratamiento cognitivo-conductual no centrado en los síntomas alimentarios, en una paciente ciega. En este caso, fue constatada una drástica reducción de los síntomas alimentarios tras este tipo de tratamiento.
En conclusión, hasta el momento, existen escasas referencias en la literatura que sirvan para esclarecer los aspectos etiopatológicos implicados en TCA. Los resultados obtenidos en nuestras investigaciones ayudan sobre el conocimiento actual de TCA, y contribuyen al desarrollo de un nuevo modelo multimodal de entendimiento de éstos. El modelo que proponemos combina la interacción de diversos factores (predisponentes, precipitantes y mantenedores). Trabajos futuros deberían prestar atención a la relevancia que tienen factores genéticos, ambientales e interacción genes-ambiente, en el desarrollo y mantenimiento de los TCA. Un especial interés presenta la pregunta de cuáles de estos factores son específicos para trastornos mentales y cuáles los son para TCA de forma específica.
RESUM:
L'objectiu principal d'aquesta tesi ha estat l'abordar els Trastorns de la conducta alimentària (TCA) des d'una aproximació multidisciplinar, que ens ajudi a combatre'ls des d'una perspectiva traslacional, en la que conflueixin investigacions bàsiques i aplicades. En els nostres estudis hem analitzat en profunditat els següents aspectes: a.) Factors clínics i comorbilitat [especialment abús de substàncies en TCA] (Estudis 1 a 3); b.) Correlats psicosocials, conductuals i ambientals en TCA (Estudis 4 a 7); i c.) Eficàcia de tractaments específics en TCA (Estudis 8 a 9).
La nostra primera línia d'investigació (Estudis 1 a 3), ha estudiat la comorbilitat d'abús de substàncies en TCA. Els resultats d'aquests estudis suggereixen que: a) l'abús de substàncies és més prevalent en TCA que en subjectes control (Estudis 1 i 3); b) la presència d'abús de substàncies en pacients amb TCA, està associada a història familiar prèvia de dependència d'alcohol (Estudi 2); c) l'abús de substàncies és especialment prevalent en pacients amb característiques bulímiques (Estudis 1 a 3); i d) que la presència d'abús de substàncies en TCA pot ser expressió d'una predisposició a conductes addictives, la susceptibilitat de les quals ve determinada per trets de personalitat específics (recerca percaça de sensacions) (Estudi 2). Així mateix, trobem aspectes diferencials en TCA, en base al tipus de droga que consumeixen (Estudis 1 i 3), fet que emfatitza la importància d'avaluar els diferents tipus de drogues utilitzats per aquests pacients. Finalment trobem diferències culturals entre distints països europeus, respecte a la prevalença d'abús de substàncies en TCA, al ser comparats amb grups control (Estudi 3).
Com a segona àrea d'investigació, ens centrem en aspectes psicològics, conductuals i ambientals en TCA. En un estudi realitzat seguint un model animal (Estudi 4), trobem que el condicionament contextual de resposta alimentària és més efectiu quan s'utilitza un aliment amb alta densitat calòrica, que quan se'n utilitza un amb baixa densitat calòrica. Aquests resultats suggereixen que els models animals són útils a l'hora d'analitzar i identificar associacions entre comportament en humans i animals, respecte la seva conducta alimentària.
En els estudis 5 i 6 es varen analitzar fins a quin punt conductes alimentàries primerenques i patrons alimentaris en la família influeixen en l'aparició posterior d'un TCA. Els resultats d'aquests estudis suggereixen, en concordància amb un volum creixent d'estudis recents, la influència que tenen aspectes ambientals i socials en el desenvolupament posterior d'una conducta alimentària anormal (per exemple, control i normes entorn a l'alimentació). Tanmateix, patrons alimentaris regulars (per exemple, esmorzar abans d'anar a l'escola) estaven negativament associats (factor protector) al subseqüent desenvolupament d'un TCA. Així mateix, es varen trobar diferències limitades entre subtipus diagnòstics. Finalment, es varen trobar algunes diferències en relació al context sociocultural. (Estudi 6).
En l'estudi 7 vàrem comparar expressió d'ira en subjectes amb un TCA i un grup control, i vàrem analitzar la seva associació amb simptomatologia alimentària, psicopatologia general comòrbida, trets de personalitat i conductes impulsives. Els nostres resultats varen indicar que pacients amb TCA manifestaven sentiments d'ira de forma més inadequada que grups control. A l'analitzar els diferents procediments de purga, la freqüència d'abús de laxants anava associada a la supressió de sentiments d'ira.
La simptomatologia alimentària i determinats trets de personalitat, s'associaven a determinades formes inadequades d'expressió de sentiments. Així mateix, vàrem observar que una expressió inadequada de sentiments en TCA anava associada a una freqüència major de conductes autoagressives.
Finalment, en la nostra darrera línia d'investigació vàrem analitzar l'eficàcia de diferents tipus de tractament en TCA. En l'estudi 8 vàrem comparar casos totals i parcials de Bulímia nerviosa (BN), en base a trets de personalitat, simptomatologia alimentària, psicopatologia general i resposta a un tractament de caràcter psicoeducatiu. Els resultats varen indicar que els casos totals i parcials de BN, comparteixen similituds simptomatològiques, psicopatològiques i de personalitat. Així mateix, no es varen obtenir diferències respecte a la resposta del tractament entre ambdós grups de pacients. En l'estudi 9, vàrem descriure i avaluar un tractament cognitiu-conductual no centrat en els símptomes alimentaris, en una pacient cega. En aquest cas es va constatar una reducció dràstica dels símptomes alimentaris després d'aquest tipus de tractament.
Fins el moment, existeixen escasses referències en la literatura que serveixin per aclarir els aspectes etiopatogènics implicats en els TCAs.
Els resultats obtinguts en les nostres investigacions ajuden en el coneixement actual dels TCA i contribueixen al desenvolupament d'un nou model multimodal per la comprensió de la seva etiologia. El model que proposem combina la interacció de diversos factors (predisponents, precipitants i mantenidors). Els treballs futurs haurien de incidir en la rellevància que tenen els factors genètics, ambientals i la interacció d'ambdós, en el desenvolupament i manteniment dels TCA. És d'especial interès la qüestió de quins d'aquests factors són específics per trastorns mentals i quins ho són per TCA.
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Zumel, Marne María Ángela 1984. "Environmental factors and brain tumour risk in young people." Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/668182.
Full textAbstract:
Risk factors and diagnosis in young people have been little explored, despite brain tumours (BT) is one of the most frequent tumour type in children and adolescents. The purpose of this doctoral thesis is to study 1) the clinical characteristics and symptoms of BTs in young people, based on the international MOBI-Kids case-control study; 2) a systematic review (SR) of the literature on risk of BTs in young people in relation to environmental factors; 3) the BT risk in relation to chemicals present in drinking water and to heavy metals.
The analyses of clinical characteristics revealed that the vast majority of tumours were neuroepithelial (mostly gliomas), followed by embryonal tumours and meningiomas. Overall, the most frequent symptoms were headache, followed by focal neurological signs and symptoms, nausea/ vomiting and visual signs and symptoms, being a 4% of the cases asymptomatic. The average time of diagnosis tended to be short (median 1.42 months), though this varied according to tumour type, age and type of symptom.
I found many studies that showed an association between environmental factors (including tobacco smoke, pesticides and diet, among other exposures) and BT risk in the SR. Because of methodological limitations however, the evidence about the role of these factors in the aetiology of this disease is still uncertain.
Our analyses in relation to water chemicals showed ORs below 1 for exposures to THMs, and ORs above 1 for nitrate exposure, for both pre- and postnatal exposure periods, some statistically significant so. Our analyses of heavy metals showed ORs below 1for exposures to chromium. However, literature is scarce about this association.
Overall, this thesis served to fill a gap in knowledge concerning 1) the clinical characteristics of BT in young people, useful to both clinical practice and aetiological research; 2) causes of this disease; 3) the role of heavy metals and ubiquitous chemicals in water. Further research needs on the aetiology and prevention of BTs in young people are provided.Los factores de riesgo y el diagnóstico en los jóvenes han sido poco explorados, a pesar de que los tumores cerebrales (TC) son uno de los tipos de tumores más frecuentes en los niños y jóvenes. El propósito de esta tesis doctoral es el estudio de 1) de las características clínicas y los síntomas de los TC en los jóvenes, basados en el estudio internacional de casos y controles MOBI-Kids; 2) una revisión sistemática de la literatura sobre el riesgo de TC en jóvenes en relación con factores ambientales; 3) el riesgo de TC en relación con los productos químicos presentes en el agua potable y con los metales pesados. Los análisis de las características clínicas revelaron que la gran mayoría de los tumores eran neuroepiteliales (principalmente gliomas), seguidos de tumores embrionarios y meningiomas. En general, los síntomas más frecuentes fueron dolor de cabeza, seguido de signos y síntomas neurológicos focales, náuseas/ vómitos y problemas en la visión, siendo un 4% de los casos asintomáticos. El tiempo promedio de diagnóstico tendió a ser corto (mediana 1,42 meses), aunque esto varió según el tipo de tumor, la edad y el tipo de síntoma. Encontré muchos estudios que encontraron asociación entre los factores ambientales (incluido el humo del tabaco, los pesticidas y la dieta, entre otras exposiciones) y el riesgo de TC en la revisión sistemática. Sin embargo, debido a limitaciones metodológicas, la evidencia sobre el papel de estos factores en la etiología de esta enfermedad aún es incierta. Nuestros análisis en relación con los productos químicos del agua mostraron unos OR por debajo de 1 para exposiciones a THMs, y OR por encima de 1 para exposición a nitrato, tanto en períodos de exposición prenatales como postnatales, algunos estadísticamente significativos. Nuestros análisis de metales pesados mostraron ORs por debajo de 1 para la exposición al cromo. Sin embargo, la literatura es escasa sobre esta asociación. En general, esta tesis sirvió para llenar un vacío en el conocimiento sobre 1) las características clínicas de la TC en los jóvenes, útiles tanto para la práctica clínica como para la investigación etiológica; 2) causas de esta enfermedad; 3) el papel de los metales pesados y los químicos ubicuos en el agua. Se ha identificado la necesidad de realizar más investigaciones sobre la etiología y la prevención de las TC en los jóvenes.
Books on the topic "Environmental risk factors"
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D, Griffith Jack, and Cooke Christopher 1944-, eds. Environmental epidemiology and risk assessment. New York: Van Nostrand Reinhold, 1993.
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Richard, Cothern C., ed. Comparative environmental risk assessment. Boca Raton: Lewis Publishers, 1993.
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Cancer risk evaluation: Methods and trends. Weinheim: Wiley-Blackwell, 2011.
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M, Kenyon Elaina, ed. Air toxics and risk assessment. Chelsea, Mich: Lewis Publishers, 1991.
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McColl, R. Stephen. Biological safety factors in toxicological risk assessment: A report. Ottawa, Ont: Health and Welfare Canada, 1989.
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Society for Risk Analysis. Meeting. Risk analysis: Prospects and opportunities. New York: Plenum Press, 1992.
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McColl, R. Stephen. Biological safety factors in toxicological risk assessment: A report. Ottawa: Dept. of National Health and Welfare, 1989.
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Jack, Siemiatycki, ed. Risk factors for cancer in the workplace. Boca Raton: CRC Press, 1991.
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Vaughan, Elaine. Some factors influencing the nonexpert's perception and evaluation of environmental risks. New York: Garland Pub., 1990.
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Organization, World Health, ed. Making a difference: Indicators to improve children's environmental health. Geneva: World Health Organization, 2003.
Find full textBook chapters on the topic "Environmental risk factors"
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Gullone, Eleonora. "Environmental Risk Factors." In Animal Cruelty, Antisocial Behaviour, and Aggression, 58–77. London: Palgrave Macmillan UK, 2012. http://dx.doi.org/10.1057/9781137284549_7.
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Kirby, Brian, and Rosalind Hughes. "Other environmental risk factors." In Psoriasis, 39–44. Second edition. | Boca Raton, FL : CRC Press, Taylor & Francis Group, [2017] | Preceded by Psoriasis / Alan Menter, Benjamin Stoff. c2011.: CRC Press, 2017. http://dx.doi.org/10.1201/9781315119298-6.
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McGrath, John J., and Robin M. Murray. "Environmental Risk Factors for Schizophrenia." In Schizophrenia, 226–44. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444327298.ch11.
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Barnes, Jammie K., and Maureen D. Mayes. "Epidemiology and Environmental Risk Factors." In Scleroderma, 17–28. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-5774-0_4.
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Mathew, Leny, Elizabeth Kauffman, Rebecca Schmidt, Irva Hertz-Picciotto, and Kristen Lyall. "Environmental Risk Factors for Autism." In Encyclopedia of Autism Spectrum Disorders, 1–14. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-6435-8_102054-1.
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Mathew, Leny, Elizabeth Kauffman, Rebecca Schmidt, Irva Hertz-Picciotto, and Kristen Lyall. "Environmental Risk Factors for Autism." In Encyclopedia of Autism Spectrum Disorders, 1–14. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-6435-8_102054-2.
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Gattaz, W. F., W. L. Abrahão, and R. Foccacia. "Environmental risk factors of psychosis." In Risk and Protective Factors in Schizophrenia, 133–38. Heidelberg: Steinkopff, 2002. http://dx.doi.org/10.1007/978-3-642-57516-7_12.
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Xie, Lishi, and Gail S. Prins. "Environmental Factors in Cancer Risk." In Nutritional Oncology, 459–73. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9780429317385-21.
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Mathew, Leny, Elizabeth Kauffman, Rebecca Schmidt, Irva Hertz-Picciotto, and Kristen Lyall. "Environmental Risk Factors for Autism." In Encyclopedia of Autism Spectrum Disorders, 1796–809. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-91280-6_102054.
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Björkstén, B. "Environmental Risk Factors for Atopy." In New Trends in Allergy IV, 3–11. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60419-5_1.
Full textConference papers on the topic "Environmental risk factors"
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Kliucininkas, L., and D. Velykiene. "Environmental health damage factors assessment in brownfield redevelopment." In ENVIRONMENTAL HEALTH RISK 2009. Southampton, UK: WIT Press, 2009. http://dx.doi.org/10.2495/ehr090181.
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Bayo, J., S. Moreno-Grau, M. J. Martínez-García, J. M. Moreno, J. M. Angosto, J. J. Guillén-Pérez, L. García-Marcos, and J. Moreno-Clavel. "Contributions of risk factors to high lead and cadmium levels in deciduous teeth." In Environmental Health Risk 2001. Southampton, UK: WIT Press, 2001. http://dx.doi.org/10.2495/ehr010001.
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da Costa Neto, A., D. M. Bonotto, and F. L. A. Mesquita. "Geogenic factors affecting the selenium(IV) distribution in sediments from Madeira River basin, Brazil." In Environmental Health Risk 2003. Southampton, UK: WIT Press, 2003. http://dx.doi.org/10.2495/ehr030011.
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Okraszewska, Romanika, Kazimierz Jamroz, Marek Bauer, Krystian Birr, and Anna Gobis. "Identification of Risk Factors for Collisions Involving Cyclists Based on Gdansk Example." In Environmental Engineering. VGTU Technika, 2017. http://dx.doi.org/10.3846/enviro.2017.112.
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The role of pedestrian and bicycle traffic in Poland has growing trend. The comprehensive traffic study, conducted in Gdansk in 2016, has confirmed the increase in the number of cyclists and their share in the modal split. Therefore, it is particularly important to ensure the safety of this group of unprotected road users. Only in 2015 on the roads of Gdansk occurred 93 accidents (excluding collisions) involving cyclists. As a result, 101 people were injured, including nine seriously and 3 people killed. The study aim was to identify risk factors for collisions involving cyclists based on data of accidents reported to the police. The following factors were analysed: the conditions for the drivers on the road (speed limits of, surface conditions), conditions for cyclists (cycling infrastructure, traffic management), external conditions (time of the year, time of the day, weather conditions), conditions organizational (type of intersection, traffic light) as well as the social aspects – the behaviour of all users.
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Pierson, Duane L., Satish K. Mehta, Rebekah J. Bruce, and C. Mark Ott. "Role of Environmental Factors in Immunity and Infectious Disease Risk." In International Conference On Environmental Systems. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 2005. http://dx.doi.org/10.4271/2005-01-2763.
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Pak, Mingyu, and Miyoung Shin. "Developing disease risk prediction model based on environmental factors." In 2014 International Symposium on Consumer Electronics (ICSE). IEEE, 2014. http://dx.doi.org/10.1109/isce.2014.6884338.
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Mutiara, E., Syarifah, and L. D. Arde. "Risk Factors of Non-communicable Diseases in Medan City." In International Conference of Science, Technology, Engineering, Environmental and Ramification Researches. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0010081006210627.
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De Novellis, S., A. Pasculli, and S. Palermi. "Innovative modeling methodology for mapping of radon potential based on local relationships between indoor radon measurements and environmental geology factors." In RISK ANALYSIS 2014. Southampton, UK: WIT Press, 2014. http://dx.doi.org/10.2495/risk140101.
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Breen, Kevin C., and Zdenek Hejzlar. "Operator and Environmental Factors Associated with Off-Road Equipment Risk." In International Off-Highway & Powerplant Congress & Exposition. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 1992. http://dx.doi.org/10.4271/921711.
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Lee, C., A. O. Adegunsoye, J. Chung, R. Jablonski, I. Pan, S. Montner, R. Vij, and M. E. Strek. "Identification of Predisposing Environmental Risk Factors for Interstitial Lung Disease." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1454.
Full textReports on the topic "Environmental risk factors"
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Sexton, Donald W. Combat Related Environmental Risk Factors as Predictors of Self-Rated Health. Fort Belvoir, VA: Defense Technical Information Center, June 2008. http://dx.doi.org/10.21236/ada493592.
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Erdmann, C. A., G. Farren, K. Baltzell, T. Chew, C. Clarkson, R. Fleshman, C. Leary, et al. Breast cancer and personal environmental risk factors in Marin County - Pilot study. Office of Scientific and Technical Information (OSTI), February 2003. http://dx.doi.org/10.2172/812452.
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Strenge, D. L., and P. J. II Chamberlain. Evaluation of unit risk factors in support of the Hanford Remedial Action Environmental Impact Statement. Office of Scientific and Technical Information (OSTI), November 1994. http://dx.doi.org/10.2172/10196784.
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Mack, Thomas M. Genetic Abnormalities in Breast Cancer Tumors and Relationships to Environmental and Genetic Risk Factors Using Twins. Fort Belvoir, VA: Defense Technical Information Center, October 1995. http://dx.doi.org/10.21236/ada303152.
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Mack, Thomas M. Genetic Abnormalities in Breast Cancer Tumors and Relationships to environmental and Genetic Risk Factors Using Twins. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada393066.
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Kaya, S., T. J. Pultz, C. M. Mbogo, J. C. Beier, and E. Mushinzimana. The Use of Radar Remote Sensing for Identifying Environmental Factors Associated with Malaria Risk in Coastal Kenya. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2002. http://dx.doi.org/10.4095/219902.
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Rycroft, Taylor, Kerry Hamilton, Charles Haas, and Igor Linkov. A quantitative risk assessment method for synthetic biology products in the environment. Engineer Research and Development Center (U.S.), July 2021. http://dx.doi.org/10.21079/11681/41331.
Full textAbstract:
The need to prevent possible adverse environmental health impacts resulting from synthetic biology (SynBio) products is widely acknowledged in both the SynBio risk literature and the global regulatory community. However, discussions of potential risks of SynBio products have been largely speculative, and the attempts to characterize the risks of SynBio products have been non-uniform and entirely qualitative. As the discipline continues to accelerate, a standardized risk assessment framework will become critical for ensuring that the environmental risks of these products are characterized in a consistent, reliable, and objective manner that incorporates all SynBio-unique risk factors. Current established risk assessment frameworks fall short of the features required of this standard framework. To address this, we propose the Quantitative Risk Assessment Method for Synthetic Biology Products (QRASynBio) – an incremental build on established risk assessment methodologies that supplements traditional paradigms with the SynBio risk factors that are currently absent and necessitates quantitative analysis for more transparent and objective risk characterizations. The proposed framework facilitates defensible quantification of the environmental risks of SynBio products in both foreseeable and hypothetical use scenarios. Additionally, we show how the proposed method can promote increased experimental investigation into the likelihood of hazard and exposure parameters and highlight the parameters where uncertainty should be reduced, leading to more targeted risk research and more precise characterizations of risk.
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Adlakha, Deepi, Jane Clarke, Perla Mansour, and Mark Tully. Walk-along and cycle-along: Assessing the benefits of the Connswater Community Greenway in Belfast, UK. Property Research Trust, 2021. http://dx.doi.org/10.52915/ghcj1777.
Full textAbstract:
Physical inactivity is a risk factor for numerous chronic diseases, and a mounting global health problem. It is likely that the outdoor physical environment, together with social environmental factors, has a tendency to either promote or discourage physical activity, not least in cities and other urban areas. However, the evidence base on this is sparse, making it hard to identify the best policy interventions to make, at the local or city level. This study seeks to assess the impact of one such intervention, the Connswater Community Greenway CCG), in Belfast, in Northern Ireland, UK. To do that it uses innovative methodologies, ‘Walk-along’ and ‘Cycle-along’ that involve wearable sensors and video footages, to improve our understanding of the impact of the CCG on local residents. The findings suggest that four characteristics of the CCG affect people’s activity and the benefits that the CCG created. These are physical factors, social factors, policy factors and individual factors. Each of these has many elements, with different impacts on different people using the greenway.
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Ukkusuri, Satish, Lu Ling, Tho V. Le, and Wenbo Zhang. Performance of Right-Turn Lane Designs at Intersections. Purdue University, 2021. http://dx.doi.org/10.5703/1288284317277.
Full textAbstract:
Right-turn lane (RTL) crashes are among the most key contributors to intersection crashes in the US. Different right turn lanes based on their design, traffic volume, and location have varying levels of crash risk. Therefore, engineers and researchers have been looking for alternative ways to improve the safety and operations for right-turn traffic. This study investigates the traffic safety performance of the RTL in Indiana state based on multi-sources, including official crash reports, official database, and field study. To understand the RTL crashes' influencing factors, we introduce a random effect negative binomial model and log-linear model to estimate the impact of influencing factors on the crash frequency and severity and adopt the robustness test to verify the reliability of estimations. In addition to the environmental factors, spatial and temporal factors, intersection, and RTL geometric factors, we propose build environment factors such as the RTL geometrics and intersection characteristics to address the endogeneity issues, which is rarely addressed in the accident-related research literature. Last, we develop a case study with the help of the Indiana Department of Transportation (INDOT). The empirical analyses indicate that RTL crash frequency and severity is mainly influenced by turn radius, traffic control, and other intersection related factors such as right-turn type and speed limit, channelized type, and AADT, acceleration lane and AADT. In particular, the effects of these factors are different among counties and right turn lane roadway types.
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Seale, Maria, Natàlia Garcia-Reyero, R. Salter, and Alicia Ruvinsky. An epigenetic modeling approach for adaptive prognostics of engineered systems. Engineer Research and Development Center (U.S.), July 2021. http://dx.doi.org/10.21079/11681/41282.
Full textAbstract:
Prognostics and health management (PHM) frameworks are widely used in engineered systems, such as manufacturing equipment, aircraft, and vehicles, to improve reliability, maintainability, and safety. Prognostic information for impending failures and remaining useful life is essential to inform decision-making by enabling cost versus risk estimates of maintenance actions. These estimates are generally provided by physics-based or data-driven models developed on historical information. Although current models provide some predictive capabilities, the ability to represent individualized dynamic factors that affect system health is limited. To address these shortcomings, we examine the biological phenomenon of epigenetics. Epigenetics provides insight into how environmental factors affect genetic expression in an organism, providing system health information that can be useful for predictions of future state. The means by which environmental factors influence epigenetic modifications leading to observable traits can be correlated to circumstances affecting system health. In this paper, we investigate the general parallels between the biological effects of epigenetic changes on cellular DNA to the influences leading to either system degradation and compromise, or improved system health. We also review a variety of epigenetic computational models and concepts, and present a general modeling framework to support adaptive system prognostics.