Dataset Information

Cigarette-related cadmium and environmental pollution exposure are reflected in airway ultrafine particle content.

ABSTRACT: Introduction:Particulate matter (PM) and cigarette-related cadmium exposure increases inflammation and smokers' susceptibility to developing lung diseases. The majority of inhaled metals are attached to the surface of ultrafine particles (UFPs). A low inhaled UFP content in exhaled breath condensate (EBC) reflects a high inflammatory status of airways. Methods:EBC was collected from 58 COPD patients and 40 healthy smokers and nonsmokers. Participants underwent spirometry, diffusion capacity, EBC and blood sampling. Environmental pollution data were collected from monitoring stations. UFPs were measured in EBC and serum, and cadmium content was quantified. Results:Subjects with low UFP concentrations in EBC (<0.18×108·mL-1) had been exposed to higher long-term PM2.5 levels versus subjects with high UFP concentrations in EBC (>0.18×108·mL-1) (21.9 µg·m-3 versus 17.4 µg·m-3, p?0.001). Long-term PM2.5 exposure levels correlated negatively with UFP concentrations in EBC and positively with UFP concentrations in serum (r=-0.54, p?0.001 and r=0.23, p=0.04, respectively). Healthy smokers had higher cadmium levels in EBC versus healthy nonsmokers and COPD patients (25.2 ppm versus 23.7 ppm and 23.3 ppm, p=0.02 and p=0.002, respectively). Subjects with low UFP concentrations in EBC also had low cadmium levels in EBC versus subjects with high UFP levels (22.8 ppm versus 24.2 ppm, p=0.004). Conclusions:Low UFP concentration in EBC is an indicator of high-level PM exposure. High cadmium levels in EBC among smokers and the association between cadmium and UFP content in EBC among COPD patients indicate cadmium lung toxicity.

SUBMITTER: Klein EF

PROVIDER: S-EPMC7487350 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Cigarette-related cadmium and environmental pollution exposure are reflected in airway ultrafine particle content.

Fireman Klein Einat E Adir Yochai Y Fireman Elizabeth E Kessel Aharon A

ERJ open research 20200701 3

<h4>Introduction</h4>Particulate matter (PM) and cigarette-related cadmium exposure increases inflammation and smokers' susceptibility to developing lung diseases. The majority of inhaled metals are attached to the surface of ultrafine particles (UFPs). A low inhaled UFP content in exhaled breath condensate (EBC) reflects a high inflammatory status of airways.<h4>Methods</h4>EBC was collected from 58 COPD patients and 40 healthy smokers and nonsmokers. Participants underwent spirometry, diffusio ...[more]

PMID: 32963996

Similar Datasets

Project description:Epidemiology studies have linked exposure to pollutant particles to increased cardiovascular mortality and morbidity, however, the mechanism remains unknown. In this study, we hypothesized that the ultrafine fraction of ambient pollutant particles would cause endothelial cells dysfunction. We profiled gene expression of human pulmonary artery endothelial cells (HPAEC) exposed to ultrafine Chapel Hill particles (UFP) (100μg/ml) or vehicle for 4h with Affymetrix HG U133 Plus 2.0 chips (N = 4 each). Using an unpaired t-test (p <0.01, 5% false discovery rate) we found 426 unique genes to be differentially expressed with 320 upregulated genes and 106 downregulated genes. Among these genes, we noted upregulation of genes related to coagulation-inflammation circuitry including tissue factor (F3), coagulation factor II receptor-like 2 (F2RL2, PAR3), interleukin (IL)-6 and IL-8. Upregulation of these genes were independently confirmed by RT-PCR and/or protein release. Genes related to the CXC chemokine family that have been implicated in the pathogenesis of vascular disease were upregulated, including MCP-1 (2.60 fold), IL-8 (2.47 fold), CXCL1 (1.41 fold), CXCL2 (1.95 fold), CXCL3 (2.28 fold) and CXCR4 (1.30 fold). In addition, genes related to clotting independent signaling of F3 were also differentially expressed, including FOS, JUN and NFKBIA. Treatment of HPAEC with UFP for 16 hours increased the release of IL6 and IL8 by 1.9-fold and 1.8-fold respectively. Pretreatment of HPAEC with a blocking antibody against F3 attenuated IL6 and IL8 release by 30% and 70% respectively. Thus using gene profiling, we uncovered that UFP may induce vascular endothelial cells to express genes related to clotting and angiogenesis. These results provide a novel hypothesis that PM may cause cardiovascular adverse health effects via induction of tissue factor in vascular endothelial cells which then triggers clotting dependent and independent downstream signaling. Keywords: particle treatment

Dataset Information

Cigarette-related cadmium and environmental pollution exposure are reflected in airway ultrafine particle content.

Publications

Cigarette-related cadmium and environmental pollution exposure are reflected in airway ultrafine particle content.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets