Air pollution exposure: a novel environmental risk factor for interstitial lung disease?
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ABSTRACT:
SUBMITTER: Johannson KA
PROVIDER: S-EPMC4388120 | biostudies-other | 2015 Apr
REPOSITORIES: biostudies-other
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Project description:BACKGROUND:Ambient air pollution accelerates lung function decline among adults, however, there are limited data about its role in the development and progression of early stages of interstitial lung disease. AIMS:To evaluate associations of long-term exposure to traffic and ambient pollutants with odds of interstitial lung abnormalities (ILA) and progression of ILA on repeated imaging. METHODS:We ascertained ILA on chest CT obtained from 2618 Framingham participants from 2008 to 2011. Among 1846 participants who also completed a cardiac CT from 2002 to 2005, we determined interval ILA progression. We assigned distance from home address to major roadway, and the 5-year average of fine particulate matter (PM2.5), elemental carbon (EC, a traffic-related PM2.5 constituent) and ozone using spatio-temporal prediction models. Logistic regression models were adjusted for age, sex, body mass index, smoking status, packyears of smoking, household tobacco exposure, neighbourhood household value, primary occupation, cohort and date. RESULTS:Among 2618 participants with a chest CT, 176 (6.7%) had ILA, 1361 (52.0%) had no ILA, and the remainder were indeterminate. Among 1846 with a preceding cardiac CT, 118 (6.4%) had ILA with interval progression. In adjusted logistic regression models, an IQR difference in 5-year EC exposure of 0.14?µg/m3 was associated with a 1.27 (95% CI 1.04 to 1.55) times greater odds of ILA, and a 1.33 (95% CI 1.00 to 1.76) times greater odds of ILA progression. PM2.5 and O3 were not associated with ILA or ILA progression. CONCLUSIONS:Exposure to EC may increase risk of progressive ILA, however, associations with other measures of ambient pollution were inconclusive.
| S-EPMC7136036 | biostudies-literature
Project description:We studied whether ambient air pollution is associated with interstitial lung abnormalities (ILAs) and high attenuation areas (HAAs), which are qualitative and quantitative measurements of subclinical interstitial lung disease (ILD) on computed tomography (CT).We performed analyses of community-based dwellers enrolled in the Multi-Ethnic Study of Atherosclerosis (MESA) study. We used cohort-specific spatio-temporal models to estimate ambient pollution (fine particulate matter (PM2.5), nitrogen oxides (NOx), nitrogen dioxide (NO2) and ozone (O3)) at each home. A total of 5495 participants underwent serial assessment of HAAs by cardiac CT; 2671 participants were assessed for ILAs using full lung CT at the 10-year follow-up. We used multivariable logistic regression and linear mixed models adjusted for age, sex, ethnicity, education, tobacco use, scanner technology and study site.The odds of ILAs increased 1.77-fold per 40?ppb increment in NOx (95% CI 1.06 to 2.95, p?=?0.03). There was an overall trend towards an association between higher exposure to NOx and greater progression of HAAs (0.45% annual increase in HAAs per 40?ppb increment in NOx; 95% CI -0.02 to 0.92, p?=?0.06). Associations of ambient fine particulate matter (PM2.5), NOx and NO2 concentrations with progression of HAAs varied by race/ethnicity (p?=?0.002, 0.007, 0.04, respectively, for interaction) and were strongest among non-Hispanic white people.We conclude that ambient air pollution exposures were associated with subclinical ILD.
| S-EPMC5726423 | biostudies-literature
Project description: Not available
| S-EPMC7605178 | biostudies-literature
Project description:IntroductionThere is a growing body of evidence suggesting a causal relationship between interstitial lung disease (ILD) and air pollution, both for the development of the disease, and driving disease progression. We aim to provide a comprehensive literature review of the association between air pollution, and ILD, including idiopathic pulmonary fibrosis (IPF).MethodsWe systematically searched from six online database. Two independent authors (DL and CF) selected studies and critically appraised the risk of bias using the Newcastle-Ottawa Scale (NOS). Findings are presented through a narrative synthesis and meta-analysis. Meta-analyses were performed exclusively when there was a minimum of three studies examining identical pollutant-health outcome pairs, all evaluating equivalent increments in pollutant concentration, using a random effects model.Results24 observational studies conducted in 13 countries or regions were identified. Pollutants under investigation encompassed ozone (O3), nitrogen dioxide (NO2), Particulate matter with diameters of 10 micrometers or less (PM10) and 2.5 micrometers or less (PM2.5), sulfur dioxide (SO2), carbon monoxide (CO), nitric oxide (NO) and nitrogen oxides (NOx). We conducted meta-analyses to assess the estimated Risk Ratios (RRs) for acute exacerbations (AE)-IPF in relation to exposure to every 10 μg/m3 increment in air pollutant concentrations, including O3, NO2, PM10, and PM2.5. The meta-analysis revealed a significant association between the increased risk of AE-IPF in PM2.5, yielding RR 1.94 (95% CI 1.30-2.90; p = 0.001). Findings across all the included studies suggest that increased exposure to air pollutants may be linked to a range of health issues in individuals with ILDs.ConclusionA scarcity of available studies on the air pollutants and ILD relationship underscores the imperative for further comprehensive research in this domain. The available data suggest that reducing levels of PM2.5 in the atmosphere could potentially reduce AE frequency and severity in ILD patients.
| S-EPMC10827982 | biostudies-literature
Project description:Introduction and aimAir pollution, a major environmental threat to human health, contributes to the premature deaths of millions of people worldwide. Cooking with solid fuels, such as charcoal and wood, in low- and middle-income countries generates very high emissions of particulate matter within and near the household as a result of their inefficient combustion. Women are especially exposed, as they often perform the cooking. The purpose of this study was to assess the burden of disease attributable to household air pollution exposure from cooking among women in Adama, Ethiopia.MethodsAirQ+ software (WHO Regional Office for Europe, Copenhagen, Denmark) was used to assess the health impact of household air pollution by estimating the burden of disease (BoD) including Acute Lower Respiratory Infections (ALRI), Chronic Obstructive Pulmonary Disease (COPD), Ischemic Heart Disease (IHD), lung cancer, and stroke, among a cohort of women in Adama. Household air pollution exposure estimated by cooking fuel type was assessed through questionnaires.ResultsThree-quarters (75%) of Adama's population used solid fuel for cooking; with this, the household air pollution attributable mortality was estimated to be 50% (95% CI: 38-58%) due to ALRI, 50% (95% CI: 35-61%) due to COPD, 50% (95% CI: 27-58%) due to lung cancer, (95% CI: 23-48%) due to IHD, and (95% CI: 23-51%) due to stroke. The corresponding disability-adjusted life years (DALYs) per 100,000 women ranged between 6000 and 9000 per disease.ConclusionsThis health impact assessment illustrates that household air pollution due to solid fuel use among women in Adama leads to premature death and a substantial quantity of DALYs. Therefore, decreasing or eliminating solid fuel use for cooking purposes could prevent deaths and improve quality of life.
| S-EPMC8472573 | biostudies-literature
Project description: Not available
| S-EPMC11198409 | biostudies-literature
Project description:Few epidemiologic studies have evaluated the effects of air pollution on the risk of Parkinson disease (PD).We investigated the associations of long-term residential concentrations of ambient particulate matter (PM) < 10 ?m in diameter (PM10) and < 2.5 ?m in diameter (PM2.5) and nitrogen dioxide (NO2) in relation to PD risk.Our nested case-control analysis included 1,556 self-reported physician-diagnosed PD cases identified between 1995 and 2006 and 3,313 controls frequency-matched on age, sex, and race. We geocoded home addresses reported in 1995-1996 and estimated the average ambient concentrations of PM10, PM2.5, and NO2 using a national fine-scale geostatistical model incorporating roadway information and other geographic covariates. Air pollutant exposures were analyzed as both quintiles and continuous variables, adjusting for matching variables and potential confounders.We observed no statistically significant overall association between PM or NO2 exposures and PD risk. However, in preplanned subgroup analyses, a higher risk of PD was associated with higher exposure to PM10 (ORQ5 vs. Q1 = 1.65; 95% CI: 1.11, 2.45; p-trend = 0.02) among women, and with higher exposure to PM2.5 (ORQ5 vs. Q1 = 1.29; 95% CI: 0.94, 1.76; p-trend = 0.04) among never smokers. In post hoc analyses among female never smokers, both PM2.5 (ORQ5 vs. Q1 = 1.79; 95% CI: 1.01, 3.17; p-trend = 0.05) and PM10 (ORQ5 vs. Q1 = 2.34; 95% CI: 1.29, 4.26; p-trend = 0.01) showed positive associations with PD risk. Analyses based on continuous exposure variables generally showed similar but nonsignificant associations.Overall, we found limited evidence for an association between exposures to ambient PM10, PM2.5, or NO2 and PD risk. The suggestive evidence that exposures to PM2.5 and PM10 may increase PD risk among female never smokers warrants further investigation. Citation: Liu R, Young MT, Chen JC, Kaufman JD, Chen H. 2016. Ambient air pollution exposures and risk of Parkinson disease. Environ Health Perspect 124:1759-1765;?http://dx.doi.org/10.1289/EHP135.
| S-EPMC5089873 | biostudies-other
Project description:ImportancePsoriasis is a chronic inflammatory disease with a relapsing-remitting course. Selected environmental factors such as infections, stressful life events, or drugs may trigger disease flares. Whether air pollution could trigger psoriasis flares is still unknown.ObjectiveTo investigate whether short-term exposure to environmental air pollution is associated with psoriasis flares.Design, setting, and participantsThis observational study with both case-crossover and cross-sectional design retrospectively analyzed longitudinal data from September 2013 to January 2020 from patients with chronic plaque psoriasis consecutively attending the outpatient dermatologic clinic of the University Hospital of Verona. For the case-crossover analysis, patients were included who had at least 1 disease flare, defined as Psoriasis Area and Severity Index (PASI) increase of 5 or greater between 2 consecutive assessments in a time frame of 3 to 4 months. For the cross-sectional analysis, patients were included who received any systemic treatment for 6 or more months, with grade 2 or higher consecutive PASI assessment.Main outcomes and measuresWe compared the mean and cumulative (area under the curve) concentrations of several air pollutants (carbon monoxide, nitrogen dioxide, other nitrogen oxides, benzene, coarse particulate matter [PM; 2.5-10.0 μm in diameter, PM10] and fine PM [<2.5 μm in diameter, PM2.5]) in the 60 days preceding the psoriasis flare and the control visits.ResultsA total of 957 patients with plaque psoriasis with 4398 follow-up visits were included in the study. Patients had a mean (SD) age of 61 (15) years and 602 (62.9%) were men. More than 15 000 measurements of air pollutant concentration from the official, open-source bulletin of the Italian Institute for Environmental Protection and Research (ISPRA) were retrieved. Among the overall cohort, 369 (38.6%) patients with psoriasis flare were included in the case-crossover study. We found that concentrations of all pollutants were significantly higher in the 60 days before psoriasis flare (median PASI at the flare 12; IQR, 9-18) compared with the control visit (median PASI 1; IQR, 1-3, P < .001). In the cross-sectional analysis, exposure to mean PM10 over 20 μg/m3 and mean PM2.5 over 15 μg/m3 in the 60 days before assessment were associated with a higher risk of PASI 5 or greater point worsening (adjusted odds ratio [aOR], 1.55; 95% CI, 1.21-1.99; and aOR, 1.25; 95% CI, 1.0-1.57, respectively). Sensitivity analyses that stratified for trimester of evaluation, with various lag of exposure and adjusting for type of treatment, yielded similar results.Conclusions and relevanceThe findings of this case-crossover and cross-sectional study suggest that air pollution may be a trigger factor for psoriasis flare.
| S-EPMC8851365 | biostudies-literature
Project description:Environmental justice efforts in the United States seek to provide equal protection from environmental hazards, such as air pollution, to all groups, particularly among traditionally disadvantaged populations. To accomplish this objective, the U.S. EPA has previously required states to use an environmental justice screening tool as part of air quality planning decision-making. The generally utilized approach to assess potential areas of environmental justice concern relies on static comparisons of environmental and demographic information to identify areas where minority and low income populations experience elevated environmental exposures, but does not include any additional information that may inform the trade-offs that sub-populations of varying socio-demographic groups make when choosing where to reside in cities. In order to address this limitation, job accessibility (measured by a mobility index defining the number of jobs available within a set commuting time) was developed as a novel environmental justice indicator of environmental justice priority areas at the local level. This approach is modeled using real-world data in Allegheny County, PA (USA), and identifies areas with relatively high levels of outdoor air pollution and low access to jobs. While traditional tools tend to flag the poorest neighborhoods for environmental justice concerns, this new method offers a more refined analysis, targeting populations suffering from the highest environmental burden without the associated benefits of urban living.
| S-EPMC6024918 | biostudies-literature
Project description:ObjectiveMUC5B and TOLLIP single nucleotide polymorphisms (SNPs) and cigarette smoking were associated with rheumatoid arthritis-interstitial lung disease (RA-ILD) in a predominantly Northern European population. We evaluated whether RA-ILD is associated with these genetic variants and HLA-DRB1 shared epitope (SE) alleles in a large RA cohort stratified by race and smoking history.MethodsHLA-DRB1 SE alleles and MUC5B rs35705950 and TOLLIP rs5743890 SNPs were genotyped in U.S. veterans with RA. ILD was validated through medical record review. Genetic associations with ILD were assessed in logistic regression models overall and in subgroups defined by race and smoking status, with additive interactions assessed by the relative excess risk of interaction (RERI).ResultsOf 2,556 participants (88% male, 77% White), 238 (9.3%) had ILD. The MUC5B variant was associated with ILD (OR 2.25 [95% CI 1.69, 3.02]), whereas TOLLIP and HLA-DRB1 SE were not. The MUC5B variant was less frequent among Black/African American participants (5.8% vs. 22.6%), though its association with RA-ILD was numerically stronger (OR 4.23 [1.65, 10.86]) compared to all other participants (OR 2.32 [1.70, 3.16]). Those with the MUC5B variant and a smoking history had numerically higher odds of ILD (OR 4.18 [2.53, 6.93]) than non-smokers (OR 2.41 [1.16, 5.04]). Additive interactions between MUC5B-race and MUC5B-smoking were not statistically significant.ConclusionIn this large RA cohort, the MUC5B promoter variant was associated with >2-fold higher odds of RA-ILD. While this variant is less common among Black/African American patients, its presence in this population carried >4-fold higher odds of RA-ILD.
| S-EPMC10123759 | biostudies-literature