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
Pollen of common ragweed (Ambrosia artemisiifolia L.): Illumina-based de novo sequencing and differential transcript expression upon elevated NO2/O3.
Common ragweed (Ambrosia artemisiifolia L.) is a highly allergenic annual ruderal plant and native to Northern America, but now also spreading across Europe. Air pollution and climate change will not only affect plant growth, pollen production and duration of the whole pollen season, but also the amount of allergenic encoding transcripts and proteins of the pollen. The objective of this study was to get a better understanding of transcriptional changes in ragweed pollen upon NO2 and O3 fumigation. ⋯ Moreover transcripts encoding allergen known from other plants could be identified. The transcriptional changes in ragweed pollen upon elevated NO2 fumigation indicates that air pollution will alter the transcriptome of the pollen. The changed levels of allergenic encoding transcripts may have an influence on the total allergenic potential of ragweed pollen.