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Indoor Air Quality and Respiratory Morbidity in School-Aged Children With BPD

2019-10-03 07:54:46 | BioPortfolio

Summary

Investigators want to learn the role of indoor environmental exposures on respiratory symptoms, and, separately, on lung function deficits in school-aged children with bronchopulmonary dysplasia (BPD).

Description

Bronchopulmonary dysplasia (BPD) is the most common respiratory disease affecting children born prematurely and leads to long-term respiratory symptoms and lung function impairment throughout childhood. This study will, evaluate the contribution of indoor sources of respiratory irritants to respiratory health impairment in school-aged children with BPD. State-of-the-art measures of indoor air quality constituents will assess the relationship of nitrogen dioxide (NO2), particulate matter (PM2.5), as well as, concentrations of allergens (mold, mouse, cockroach, pet), endotoxin, air temperature and humidity with concurrently measured respiratory symptoms and lung function in a well-characterized cohort of children with BPD. This research will identify specific harmful components of the indoor environment associated with respiratory morbidity and poor lung function in children with BPD.

Investigators will ask the participants to come in for a one time clinic visit for undergoing procedures as well as answering questions regarding health and home environment. During the 1 year of participation there will also be 2 home assessment visits where investigators will take a sample of the home environment as well record home characteristics.

Study Design

Conditions

Bronchopulmonary Dysplasia

Location

Boston Childrens Hospital
Boston
Massachusetts
United States
02115

Status

Recruiting

Source

Boston Children’s Hospital

Results (where available)

View Results

Links

Published on BioPortfolio: 2019-10-03T07:54:46-0400

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PubMed Articles [362 Associated PubMed Articles listed on BioPortfolio]

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The study aimed to establish how granulocytes, monocytes and macrophages contribute to the development of bronchopulmonary dysplasia (BPD).

Bubbly and cystic appearance on chest radiograph of extremely preterm infants with bronchopulmonary dysplasia is associated with wheezing disorder.

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Extended course of prednisolone in infants with severe bronchopulmonary dysplasia.

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Bronchopulmonary Dysplasia Is Associated with Altered Brain Volumes and White Matter Microstructure in Preterm Infants.

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Medical and Biotech [MESH] Definitions

A chronic lung disease developed after OXYGEN INHALATION THERAPY or mechanical ventilation (VENTILATION, MECHANICAL) usually occurring in certain premature infants (INFANT, PREMATURE) or newborn infants with respiratory distress syndrome (RESPIRATORY DISTRESS SYNDROME, NEWBORN). Histologically, it is characterized by the unusual abnormalities of the bronchioles, such as METAPLASIA, decrease in alveolar number, and formation of CYSTS.

A disease of bone marked by thinning of the cortex and replacement of bone marrow by gritty fibrous tissue containing bony spicules, producing pain, disability, and gradually increasing deformity. Only one bone may be involved (FIBROUS DYSPLASIA, MONOSTOTIC) or several (FIBROUS DYSPLASIA, POLYOSTOTIC). (From Dorland, 28th ed)

A condition resulting from congenital malformations involving the brain. The syndrome of septo-optic dysplasia combines hypoplasia or agenesis of the SEPTUM PELLUCIDUM and the OPTIC NERVE. The extent of the abnormalities can vary. Septo-optic dysplasia is often associated with abnormalities of the hypothalamic and other diencephalic structures, and HYPOPITUITARISM.

A nutritional condition produced by a deficiency of VITAMIN E in the diet, characterized by posterior column and spinocerebellar tract abnormalities, areflexia, ophthalmoplegia, and disturbances of gait, proprioception, and vibration. In premature infants vitamin E deficiency is associated with hemolytic anemia, thrombocytosis, edema, intraventricular hemorrhage, and increasing risk of retrolental fibroplasia and bronchopulmonary dysplasia. An apparent inborn error of vitamin E metabolism, named familial isolated vitamin E deficiency, has recently been identified. (Cecil Textbook of Medicine, 19th ed, p1181)

An autosomal dominant form of ectodermal dysplasia which is due to mutations in the gene for the EDAR RECEPTOR.

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