Inflammatory markers and lung function in relation to indoor and ambient air pollution.

Ambient air pollution causes a range of adverse health effects, whereas effects of indoor sources of air pollution are not well described in high-income countries. We compared hazards of ambient air pollution and indoor sources with respect to important biomarkers of cardiorespiratory effects in terms of lung function and systemic inflammation in a middle-aged Danish cohort. Our cohort comprised 5199 men and women aged 49-63 years at the recruitment during April 2009 to March 2011, with information on exposure to second-hand smoke (SHS) and use of candles, wood stove, kerosene heater and gas cooker as well as relevant covariates.

Role of microbiota-derived lipopolysaccharide in adipose tissue inflammation, adipocyte size and pyroptosis during obesity.

It has been established that ingestion of a high-fat diet increases the blood levels of lipopolysaccharides (LPS) from Gram-negative bacteria in the gut. Obesity is characterised by low-grade systemic and adipose tissue inflammation. This is suggested to be implicated in the metabolic syndrome and obesity.

Exposure to ultrafine particles, intracellular production of reactive oxygen species in leukocytes and altered levels of endothelial progenitor cells.

Exposure to particles in the fine and ultrafine size range has been linked to induction of low-grade systemic inflammation, oxidative stress and development of cardiovascular diseases. Declining levels of endothelial progenitor cells within systemic circulation have likewise been linked to progression of cardiovascular diseases. The objective was to determine if exposure to fine and ultrafine particles from indoor and outdoor sources, assessed by personal and residential indoor monitoring, is associated with altered levels of endothelial progenitor cells, and whether such effects are related to leukocyte-mediated oxidative stress.

Applications of the comet assay in particle toxicology: air pollution and engineered nanomaterials exposure.

Exposure to ambient air particles is associated with elevated levels of DNA strand breaks (SBs) and endonuclease III, formamidopyrimidine DNA glycosylase (FPG) and oxoguanine DNA glycosylase-sensitive sites in cell cultures, animals and humans. In both animals and cell cultures, increases in SB and in oxidatively damaged DNA are seen after exposure to a range of engineered nanomaterials (ENMs), including carbon black, carbon nanotubes, fullerene C60, ZnO, silver and gold. Exposure to TiO2 has generated mixed data with regard to SB and oxidatively damaged DNA in cell cultures.

Vascular and lung function related to ultrafine and fine particles exposure assessed by personal and indoor monitoring: a cross-sectional study.

Background: Exposure to ambient air particulate matter (PM) has been linked to decline in pulmonary function and cardiovascular events possibly through inflammation. Little is known about individual exposure to ultrafine particles (UFP) inside and outside modern homes and associated health-related effects.

Methods: Associations between vascular and lung function, inflammation markers and exposure in terms of particle number concentration (PNC; d = 10-300 nm) were studied in a cross-sectional design with personal and home indoor monitoring in the Western Copenhagen Area, Denmark.

Role of oxidative stress in carbon nanotube-generated health effects.

The development of products containing carbon nanotubes (CNTs) is a major achievement of nanotechnology, although concerns regarding risk of toxic effects linger if the hazards associated with these materials are not thoroughly investigated. Exposure to CNTs has been associated with depletion of antioxidants, increased intracellular production of reactive oxygen species and pro-inflammatory signaling in cultured cells with primary function in the immune system as well as epithelial, endothelial and stromal cells. Pre-treatment with antioxidants has been shown to attenuate these effects, indicating a dependency of oxidative stress on cellular responses to CNT exposure.

Measurement of oxidative damage to DNA in nanomaterial exposed cells and animals.

Increased levels of oxidatively damaged DNA have been documented in studies of metal, metal oxide, carbon-based and ceramic engineered nanomaterials (ENMs). In particular, 8-oxo-7,8-dihydroguanine-2'-deoxyguanosine (8-oxodG) is widely assessed as a DNA nucleobase oxidation product, measured by chromatographic assays, antibody-based methods or the comet assay with DNA repair enzymes. However, spurious oxidation of DNA has been a problem in certain studies applying chromatographic assays, yielding high baseline levels of 8-oxodG.

Interaction between filaggrin null mutations and tobacco smoking in relation to asthma.

Background: The mechanisms underlying the association between filaggrin (FLG) deficiency and asthma are not known. It has been hypothesized that FLG deficiency leads to enhanced percutaneous exposure to environmental substances that might trigger immune responses. We hypothesized that interactions between FLG deficiency and environmental exposures play a role in asthma development.

The relationship of glutathione-S-transferases copy number variation and indoor air pollution to symptoms and markers of respiratory disease.

Introduction: Exposure to particulate matter (PM) may induce inflammation and oxidative stress in the airways. Carriers of null polymorphisms of glutathione S-transferases (GSTs), which detoxify reactive oxygen species, may be particularly susceptible to the effects of PM.

Objectives: To investigate whether deletions of GSTM1 and GSTT1 modify the potential effects of exposure to indoor sources of PM on symptoms and objective markers of respiratory disease.

Association of indoor air pollution with rhinitis symptoms, atopy and nitric oxide levels in exhaled air.

Background: Exposure to particulate matter (PM) outdoors can induce airway inflammation and exacerbation of asthma in adults. However, there is limited knowledge about the effects of exposure to indoor PM. The aim of this study was to investigate the association of exposure to indoor sources of PM with rhinitis symptoms, atopy and nitric oxide in exhaled air (FeNO) as a measure of airway inflammation.

Indoor exposure to environmental cigarette smoke, but not other inhaled particulates associates with respiratory symptoms and diminished lung function in adults.

Background And Objective: Exposure to particulate matter (PM) can induce airway inflammation and exacerbation of asthma. However, there is limited knowledge about the effects of exposure to indoor sources of PM. We investigated the associations between self-reported exposure to indoor sources of PM and lower airway symptoms and lung function.

Effects of alcohol consumption on the allergen-specific immune response in mice.

Background: There is evidence that chronic alcohol consumption impairs the T-helper 1 (Th1) lymphocyte-regulated cell-mediated immune response possibly favoring a Th2 deviation of the immune response. Moreover, a few epidemiological studies have linked alcohol consumption to allergen-specific IgE sensitization.

Objective: To investigate the effects of alcohol consumption on the allergen-specific immune response in mice.

Maternal employment in child-care institutions and the risk of infant wheeze and atopic dermatitis in the offspring.

It has been proposed that exposure to infections and microbes protects against atopic diseases, but epidemiological data has so far been conflicting. We hypothesized that maternal exposure to infections and microbes before or during pregnancy would be of particular importance. To test this hypothesis, we studied the incidence of wheezing and atopic dermatitis (AD) in infants of mothers employed in child-care institutions - and thus presumably being highly exposed to infections and microbes - compared with infants of mothers not so employed.

A built-in co-carcinogenic effect due to viruses involved in latent or persistent infections.

A new hypothesis for some cancers, which combines the chromosomal instability theories with a co-carcinogenic effect of viruses causing latent or persistent infection, is presented. The hypothesis incorporates the multi-step model of cancer and that pre-cancerous cells reach a state of chromosomal instability. Because of chromosomal instability, the genome of these cell lines will lead to changes from generation to generation and will face a remarkable selection pressure both from lost traits, apoptosis, and from the immune system.

A reformulation of the hygiene hypothesis: maternal infectious diseases confer protection against asthma in the infant.

Epidemiological studies have shown an inverse relationship between allergic respiratory diseases and the number of siblings. It was hypothesized that the lower prevalence of allergic respiratory diseases in large sibships was due to cross-infections between siblings. According to this hygiene hypothesis the increase in the prevalence of atopic diseases is caused by a decrease in the exposure to infections.