nitrogen-dioxide and Idiopathic-Pulmonary-Fibrosis

Air pollution affects clinical course and prognosis of idiopathic pulmonary fibrosis (IPF). However, the effect of individual exposure to air pollutants on disease progression is unclear. We aimed to identify the effect of individual exposure to nitrogen dioxide (NO. The serial lung function data of 946 IPF patients (mean age: 65.4 years, male: 80.9%) were analysed. Individual-level long-term exposures to NO. Overall, 547 patients (57.8%) experienced progression during a median follow-up of 1.0 year (interquartile range: 0.4-2.6 years). In the primary model, a 10-ppb increase in NO. Our data suggest that increased individual exposure to NO

Topics: Aged; Air Pollutants; Air Pollution; Disease Progression; Environmental Exposure; Humans; Idiopathic Pulmonary Fibrosis; Male; Nitrogen Dioxide; Particulate Matter

Air pollutants are considered as non-negligible risk factors of idiopathic pulmonary fibrosis (IPF). However, the relationship between long-term air pollution and the incidence of IPF is unknown. Our objective was to explore the associations of air pollutants with IPF risk and further assess the modification effect of genetic susceptibility.. We used land-use regression model estimated concentrations of nitrogen dioxide (NO. Among 433 738 participants from the UK Biobank, the incidence of IPF was 27.45 per 100 000 person-years during a median follow-up of 11.78 years. The adjusted hazard ratios of IPF for each interquartile range increase in NO. Long-term exposures to air pollutants may elevate the risk of incident IPF. There are additive effects of air pollutants and genetic susceptibility on IPF risk.

Topics: Air Pollutants; Air Pollution; Environmental Exposure; Genetic Predisposition to Disease; Humans; Idiopathic Pulmonary Fibrosis; Nitrogen Dioxide; Particulate Matter

Air pollution has a significant impact on the morbidity and mortality of various respiratory diseases. However, this has not been widely studied in diffuse interstitial lung diseases, specifically in idiopathic pulmonary fibrosis.. In this study we aimed to assess the relationship between four major air pollutants individually [carbon monoxide (CO), nitrogen dioxide (NO. We conducted an exploratory retrospective panel study from 2011 to 2020 in 69 patients with idiopathic pulmonary fibrosis from the pulmonary medicine department of a tertiary hospital. Based on their geocoded residential address, levels of each pollutant were estimated 1, 3, 6, 12, and 36 months prior to each event (chronic respiratory failure, hospital admission and mortality). Data was collected from the air quality monitoring stations of the Community of Madrid located <3.5 km (2.2 miles) from each patient's home.. The increase in average values of CO [OR 1.62 (1.11-2.36) and OR 1.84 (1.1-3.06)], NO. Air pollution is associated with an increase in the probability of developing chronic respiratory failure, hospitalization due to respiratory causes and mortality in patients with idiopathic pulmonary fibrosis.

Topics: Air Pollution; Hospitalization; Humans; Idiopathic Pulmonary Fibrosis; Nitrogen Dioxide; Respiratory Insufficiency; Retrospective Studies

The association between long-term air pollution exposure and the development of idiopathic pulmonary fibrosis (IPF) has been established, but the evidence regarding the effect of low levels of air pollution, especially ambient sulfur dioxide (SO. This study retrieved data from 402,042 participants who were free of IPF at baseline in the UK Biobank. The annual mean concentration of ambient SO. After a median follow-up of 11.78 years, 2562 cases of IPF were identified. The results indicated that each 1 μg/m. The study suggests that long-term exposure to ambient SO

Topics: Air Pollutants; Air Pollution; Environmental Exposure; Genetic Predisposition to Disease; Humans; Idiopathic Pulmonary Fibrosis; Incidence; Nitrogen Dioxide; Particulate Matter; Prospective Studies; Sulfur Dioxide

Urban air pollution is involved in the progress of idiopathic pulmonary fibrosis (IPF). Its potential role on the devastating event of Acute Exacerbation of IPF (AE-IPF) needs to be clarified. This study examined the association between long-term personal air pollution exposure and AE- IPF risk taking into consideration inflammatory mediators and telomere length (TL).. All consecutive IPF-patients referred to our Hospital from October 2013-June 2019 were included. AE-IPF events were recorded and inflammatory mediators and TL measured. Long-term personal air pollution exposures were assigned to each patient retrospectively, for O. 118 IPF patients (mean age 72 ± 8.3 years) were analyzed. We detected positive significant associations between AE-IPF and a 10 μg/m. Long-term personal exposure to increased concentrations of air pollutants is an independent risk factor of AE-IPF. Inflammatory mediators implicated in lung repair mechanisms are involved.

Topics: Aged; Aged, 80 and over; Air Pollutants; Air Pollution; Cytokines; Disease Progression; Environmental Exposure; Female; Humans; Idiopathic Pulmonary Fibrosis; Male; Middle Aged; Nitrogen Dioxide; Ozone; Particulate Matter; Risk Factors; Telomere

Ambient air pollution is associated with the prognosis of idiopathic pulmonary fibrosis (IPF) patients. We aimed to identify the impacts of individual exposure to particulate matter with a 50% cut-off aerodynamic diameter of 10 μm (PM

Topics: Aged; Air Pollutants; Air Pollution; Environmental Exposure; Humans; Idiopathic Pulmonary Fibrosis; Male; Nitrogen Dioxide; Particulate Matter

Acute exacerbations and worsening of idiopathic pulmonary fibrosis (IPF) have been associated with exposure to ozone (O

Topics: Adult; Air Pollutants; Air Pollution; Databases, Factual; Environmental Exposure; Environmental Monitoring; Female; Geography; Humans; Idiopathic Pulmonary Fibrosis; Incidence; Italy; Male; Middle Aged; Nitrogen Dioxide; Oxygen; Ozone; Particulate Matter; Risk Factors; Seasons

Acute exacerbations of idiopathic pulmonary fibrosis are associated with high mortality and are of unknown cause. The effect of air pollution on exacerbations of interstitial lung disease is unknown. This study aims to define the association of air pollution exposure with acute exacerbation of idiopathic pulmonary fibrosis. Patients with idiopathic pulmonary fibrosis and corresponding air pollution data were identified from a longitudinal cohort. Air pollution exposures were assigned to each patient for ozone, nitrogen dioxide, particulate matter, sulfur dioxide and carbon monoxide based on geo-coded residential addresses. Cox proportional hazards models were used to estimate the association of air pollution exposures and acute exacerbations. Acute exacerbation was significantly associated with antecedent 6-week increases in mean level, maximum level and number of exceedances above accepted standards of ozone (hazard ratio (HR) 1.57, 95% CI 1.09-2.24; HR 1.42, 95% CI 1.11-1.82; and HR 1.51, 95% CI 1.17-1.94, respectively) and nitrogen dioxide (HR 1.41, 95% CI 1.04-1.91; HR 1.27, 95% CI 1.01-1.59; and HR 1.20, 95% CI 1.10-1.31, respectively). Increased ozone and nitrogen dioxide exposure over the preceding 6 weeks was associated with an increased risk of acute exacerbation of idiopathic pulmonary fibrosis, suggesting that air pollution may contribute to the development of this clinically meaningful event.

Topics: Aged; Air Pollutants; Air Pollution; Carbon Monoxide; Female; Follow-Up Studies; Humans; Idiopathic Pulmonary Fibrosis; Longitudinal Studies; Male; Middle Aged; Nitrogen Dioxide; Ozone; Particulate Matter; Proportional Hazards Models; Republic of Korea; Risk Factors; Smoking; Sulfur Dioxide; Treatment Outcome