Environmental pollution
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Environmental pollution · Nov 2017
Phthalate and non-phthalate plasticizers in indoor dust from childcare facilities, salons, and homes across the USA.
The quality of indoor environment has received considerable attention owing to the declining outdoor human activities and the associated public health issues. The prolonged exposure of children in childcare facilities or the occupational exposure of adults to indoor environmental triggers can be a culprit of the pathophysiology of several commonly observed idiopathic syndromes. In this study, concentrations of potentially toxic plasticizers (phthalates as well as non-phthalates) were investigated in 28 dust samples collected from three different indoor environments across the USA. ⋯ The observed concentrations of these replacement non-phthalate plasticizer were as high as di-(2-ethylhexyl) phthalate, the most frequently detected phthalate plasticizer at highest concentration worldwide, in most of indoor dust samples. The estimated daily intakes of total phthalates (n = 7) by children and toddlers through indoor dust in childcare facilities were 1.6 times higher than the non-phthalate plasticizers (n = 3), whereas estimated daily intake of total non-phthalates for all age groups at homes were 1.9 times higher than the phthalate plasticizers. This study reveals, for the first time, a more elevated (∼3 folds) occupational intake of phthalate and non-phthalate plasticizers through the indoor dust at salons (214 and 285 ng/kg-bw/day, respectively) than at homes in the USA.
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Environmental pollution · Oct 2017
Integrative characterization of chronic cigarette smoke-induced cardiopulmonary comorbidities in a mouse model.
Cigarette smoke-triggered inflammatory cascades and consequent tissue damage are the main causes of chronic obstructive pulmonary disease (COPD). There is no effective therapy and the key mediators of COPD are not identified due to the lack of translational animal models with complex characterization. This integrative chronic study investigated cardiopulmonary pathophysiological alterations and mechanisms with functional, morphological and biochemical techniques in a 6-month-long cigarette smoke exposure mouse model. ⋯ These parameters together with the tricuspid annular plane systolic excursion (TAPSE) decreased again after 5-6 months. Soluble intercellular adhesion molecule-1 (sICAM-1) significantly increased in the heart homogenates at month 6, while other inflammatory cytokines were undetectable. This is the first study demonstrating smoking duration-dependent, complex cardiopulmonary alterations characteristic to COPD, in which inflammatory cytokine cascades and MMP-2/9 might be responsible for pulmonary destruction and sICAM-1 for heart dysfunction.
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Environmental pollution · Jun 2017
Personal exposure to fine particulate matter, lung function and serum club cell secretory protein (Clara).
The underlying mechanisms about the association between ambient fine particulate matter (PM2.5) and lung function were unclear. Few epidemiological studies have evaluated the potential mediating effects of serum club cell secretory protein (Clara) (CC16), a biomarker of pulmonary epithelium integrity. ⋯ Acute exposure to PM2.5 might induce an immediate decrease in lung function by virtue of the loss of pulmonary epithelium integrity.
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Environmental pollution · May 2017
Association between chronic exposure to air pollution and mortality in the acute respiratory distress syndrome.
The impact of chronic exposure to air pollution and outcomes in the acute respiratory distress syndrome (ARDS) is unknown. The Nationwide Inpatient Sample (NIS) from 2011 was utilized for this analysis. The NIS is a national database that captures 20% of all US in-patient hospitalizations from 47 states. ⋯ Similarly, for each increase in particulate matter exposure by 10 μg/m3, the OR for death was 1.08 (95% CI 1.02-1.16, p < 0.01). Chronic exposure to both ozone and particulate matter pollution is associated with higher rates of mortality in ARDS. These preliminary findings need to be confirmed by further detailed studies.
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Environmental pollution · May 2017
Urban air pollution and meteorological factors affect emergency department visits of elderly patients with chronic obstructive pulmonary disease in Taiwan.
Both air pollution and meteorological factors in metropolitan areas increased emergency department (ED) visits from people with chronic obstructive pulmonary disease (COPD). Few studies investigated the associations between air pollution, meteorological factors, and COPD-related health disorders in Asian countries. This study aimed to investigate the relationship between the environmental factors and COPD-associated ED visits of susceptible elderly population in the largest Taiwanese metropolitan area (Taipei area, including Taipei city and New Taipei city) between 2000 and 2013. ⋯ Additionally, either O3 or SO2 combined with other air pollutants increased the risk of elderly COPD-associated ED visits in the days of high relative humidity and air pressure difference, respectively. This study showed that joint effect of urban air pollution and meteorological factors contributed to the COPD-associated ED visits of the susceptible elderly population in the largest metropolitan area in Taiwan. Government authorities should review existing air pollution policies, and strengthen health education propaganda to ensure the health of the susceptible elderly population.