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Query: UMLS:C0149514 (bronchitis)
 6,902 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chlorine bleach or sodium hypochlorite can inactivate common indoor allergens. In this cross-sectional study we evaluated to what extent regular house cleaning with bleach can influence the risks of respiratory and allergic diseases in children. We studied a group of 234 schoolchildren aged 10-13 yr among whom 78 children were living in a house cleaned with bleach at least once per week. Children examination included a questionnaire, an exercise-induced bronchoconstriction test and the measurement of exhaled nitric oxide (NO) and of serum total and aeroallergen-specific immunoglobulin (Ig)E, Clara cell protein (CC16) and surfactant-associated protein D (SP-D). Children living in a house regularly cleaned with bleach were less likely to have asthma (OR, 0.10; CI, 0.02-0.51), eczema (OR, 0.22; CI, 0.06-0.79) and of being sensitized to indoor aeroallergens (OR, 0.53; CI, 0.27-1.02), especially house dust mite (OR, 0.43; CI, 0.19-0.99). These protective effects were independent of gender, ethnicity, previous respiratory infections, total serum IgE level and of family history of allergic diseases. They were however abolished by parental smoking, which also interacted with the use of bleach to increase the risk of recurrent bronchitis (OR, 2.03; CI, 1.12-3.66). House cleaning with bleach had effect neither on the sensitization to pollen allergens, nor on the levels of exhaled NO and of serum CC16 and SP-D. House cleaning with chlorine bleach appears to protect children from the risks of asthma and of sensitization to indoor allergens while increasing the risk of recurrent bronchitis through apparently an interaction with parental smoking. As chlorine bleach is one of the most effective cleaning agent to be found, these observations argue against the idea conveyed by the hygiene hypothesis that cleanliness per se increases the risk of asthma and allergy.
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PMID:House cleaning with chlorine bleach and the risks of allergic and respiratory diseases in children. 1729 96

The arylhydrocarbon receptor (AhR) is known for its ability to bind aromatic-containing compounds, which starts a molecular cascade involving the induction of cytochrome P450s and inflammatory cytokines. Our hypothesis is that many inhaled environmental toxicant components activate these inflammatory pathways via an initial binding to the AhR. To test this possibility, we treated Clara cell-derived NCI-H441 cells with the AhR agonist, 2,3,7,8-tetrachlordibenzo-p-dioxin (TCDD), and demonstrated that AhR activation increased the expression of both cytochrome P450 s and inflammatory markers. We also found increased mucin 5AC production with TCDD treatment. Similar results were observed in NCI-H441 cells treated with urban dust particles. Mucin 5AC expression was highly correlated with increased-expression cyclooxygenase-2 and IL-1beta, thus implicating these two inflammatory markers as possible conduits for AhR-mediated mucin production. We hypothesize that this increase in mucin 5AC production is a result of inflammation-induced differentiation of our epithelial cell to a mucin-producing cell. This theory is supported by morphological changes observed in the cells, as well as decreased expression of Clara cell secretory protein (CC10). In an in vivo C57BL/6 mouse model, TCDD increased expression of inflammatory cytokines, mucin 5AC, and a number of matrix metalloproteases in whole-lung samples. These changes were not seen in mice in which AhR signaling was repressed. These markers from the whole-lung samples have been correlated to onset of bronchitis, asthma, small airways disease, and fibrosis, and their increased expression further implicates AhR activation in producing the molecular environment for the development of lung injury to occur.
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PMID:Arylhydrocarbon receptor activation in NCI-H441 cells and C57BL/6 mice: possible mechanisms for lung dysfunction. 1937 48