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      Air Pollution and Emergency Department Visits for Suicide Attempts in Vancouver, Canada

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          Abstract

          Background:

          Comorbidity of depression, heart disease, and migraine has been observed in clinical practice, while ambient air pollution has been identified among different risk factors for these health conditions. Suicide attempts and ideations as the result of depression may be linked to air pollution exposure. Therefore the effects of ambient air pollution on emergency department (ED) visits for suicide attempts were investigated.

          Methods:

          Emergency visit data were collected in a hospital in Vancouver, Canada. The generalized linear mixed models technique was applied in the analysis of these data. A natural hierarchical structure of the data was used to define the clusters, with days nested in a 3-level structure (day of week, month, year). Poisson models were fitted to the clustered counts of ED visits with a single air pollutant, temperature and relative humidity. In addition, the case-crossover methodology was used with the same data for comparison. The analysis was performed by gender (all, males, females) and month (all: January–December, warm: April–September, cold: October–March).

          Results:

          Both hierarchical and case-crossover methods confirmed positive and statistically significant associations among carbon monoxide (CO), nitrogen dioxide (NO 2), sulphur dioxide (SO 2), and particulate matter (PM 10) for all suicide attempts in the cold period. The largest increase was observed for males in the cold period for a 1-day lagged exposure to NO 2, with an excess risk of 23.9% (95% CI: 7.8, 42.4) and odds ratio of 1.21 (95% CI: 1.03, 1.41). In warm months the associations were not statistically significant, and the highest positive value was obtained for ozone lagged by 1 day.

          Conclusion:

          The results indicate a potential association between air pollution and emergency department visits for suicide attempts.

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          Most cited references26

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          Case-crossover analyses of air pollution exposure data: referent selection strategies and their implications for bias.

          The case-crossover design has been widely used to study the association between short-term air pollution exposure and the risk of an acute adverse health event. The design uses cases only; for each individual case, exposure just before the event is compared with exposure at other control (or "referent") times. Time-invariant confounders are controlled by making within-subject comparisons. Even more important in the air pollution setting is that time-varying confounders can also be controlled by design by matching referents to the index time. The referent selection strategy is important for reasons in addition to control of confounding. The case-crossover design makes the implicit assumption that there is no trend in exposure across the referent times. In addition, the statistical method that is used-conditional logistic regression-is unbiased only with certain referent strategies. We review here the case-crossover literature in the air pollution context, focusing on key issues regarding referent selection. We conclude with a set of recommendations for choosing a referent strategy with air pollution exposure data. Specifically, we advocate the time-stratified approach to referent selection because it ensures unbiased conditional logistic regression estimates, avoids bias resulting from time trend in the exposure series, and can be tailored to match on specific time-varying confounders.
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            Translocation of ultrafine insoluble iridium particles from lung epithelium to extrapulmonary organs is size dependent but very low.

            Recently it was speculated that ultrafine particles may translocate from deposition sites in the lungs to systemic circulation. This could lead to accumulation and potentially adverse reactions in critical organs such as liver, heart, and even brain, consistent with the hypothesis that ultrafine insoluble particles may play a role in the onset of cardiovascular diseases, as growing evidence from epidemiological studies suggests. Ultrafine (192)Ir radio-labeled iridium particles (15 and 80 nm count median diameter) generated by spark discharging were inhaled by young adult, healthy, male WKY rats ventilated for 1 h via an endotracheal tube. After exposure, excreta were collected quantitatively. At time points ranging from 6 h to 7 d, rats were sacrificed, and a complete balance of (192)Ir activity retained in the body and cleared by excretion was determined gamma spectroscopically. Thoracic deposition fractions of inhaled 15- and 80-nm (192)Ir particles were 0.49 and 0.28, respectively. Both batches of ultrafine iridium particles proved to be insoluble (<1% in 7 d). During wk 1 after inhalation particles were predominantly cleared via airways into the gastrointestinal tract and feces. This cleared fraction includes particles deposited in the alveolar region. Additionally, minute particle translocation of <1% of the deposited particles into secondary organs such as liver, spleen, heart, and brain was measured after systemic uptake from the lungs. The translocated fraction of the 80-nm particles was about an order of magnitude less than that of 15-nm particles. In additional studies, the biokinetics of ultrafine particles and soluble (192)Ir was studied after administration by either gavage or intratracheal instillation or intravenous injection. They confirmed the low solubility of the particles and proved that (1) particles were neither dissolved nor absorbed from the gut, (2) systemically circulating particles were rapidly and quantitatively accumulated in the liver and spleen and retained there, and (3) soluble (192)Ir instilled in the lungs was rapidly excreted via urine with little retention in the lungs and other organs. This study indicates that only a rather small fraction of ultrafine#10; iridium particles has access from peripheral lungs to systemic circulation and extrapulmonary organs. Therefore, the hypothesis that systemic access of ultrafine insoluble particles may generally induce adverse reactions in the cardiovascular system and liver leading to the onset of cardiovascular diseases needs additional detailed and differentiated consideration.
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              Particulate matter in polluted air may increase biomarkers of inflammation in mouse brain.

              The etiology of neurodegenerative disorders is at present unknown. However, many of these disorders are associated with an increase in oxidative and inflammatory events. Although a small percentage of these disorders are familial cases linked to specific genetic defects, most are idiopathic. Thus, environmental factors are thought to play an important role in the onset and progression of such disorders. We have demonstrated that exposure (4 h, 5 days per week for 2 weeks) to concentrated airborne particulate matter increases inflammatory indices in brain of ovalbumin-sensitized BALB/c mice. Animals were divided into three exposure groups: filtered air (control), ultrafine particles, or fine and ultrafine particles. The levels of proinflammatory cytokines interleukin-1 alpha (IL-1alpha) and tumor necrosis factor alpha (TNF-alpha) were increased in brain tissue of mice exposed to particulate matter compared to that of control animals. Levels of the immune-related transcription factor NF-kappaB were also found to be substantially elevated in the brain of exposed groups compared with the control group. These data indicate that components of inhaled particulate matter may trigger a proinflammatory response in nervous tissue that could contribute to the pathophysiology of neurodegenerative diseases.
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                Author and article information

                Journal
                Environ Health Insights
                Environmental Health Insights
                Environmental Health Insights
                Libertas Academica
                1178-6302
                15 October 2010
                2010
                : 4
                : 79-86
                Affiliations
                [1 ]Population Studies Division, Health Canada, Ottawa, ON, Canada
                [2 ]Air Quality Assessment Section, Health Canada, Ottawa, ON, Canada
                [3 ]Department of Emergency Medicine, Providence Health Care and St. Paul’s Hospital, Vancouver, BC, Canada
                [4 ]Department of Emergency Medicine, University of Alberta, Edmonton, AB, Canada
                [5 ]School of Public Health, University of Alberta, Edmonton, AB, Canada
                Author notes
                Corresponding author email: mietek.szyszkowicz@ 123456hc-sc.gc.ca
                Article
                ehi-2010-079
                10.4137/EHI.S5662
                2978939
                21079694
                7afddd35-365c-4488-98b8-90c624de756c
                © 2010 the author(s), publisher and licensee Libertas Academica Ltd.

                This is an open access article. Unrestricted non-commercial use is permitted provided the original work is properly cited.

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                Categories
                Original Research

                Public health
                air pollution,relative humidity,emergency department,temperature,suicide attempt
                Public health
                air pollution, relative humidity, emergency department, temperature, suicide attempt

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