Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

4.0K
Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
4.0K
Asthma-II: Pathophysiology and Classification01:26

Asthma-II: Pathophysiology and Classification

3.9K
Asthma is a prevalent chronic respiratory condition marked by inflammation and hyperresponsiveness of the airways. Its pathophysiology involves complex interactions among inflammatory pathways, immune responses, and neural mechanisms.
Additionally, environmental and genetic factors play crucial roles in determining an individual's susceptibility to asthma and the severity of their condition.
Critical processes in asthma pathophysiology include:
3.9K
Asthma-I: Introduction01:29

Asthma-I: Introduction

3.3K
Asthma is a chronic respiratory ailment that requires careful management due to its varying symptoms and influencing factors. It is characterized by airway inflammation, bronchial hyperresponsiveness, and reversible airflow obstruction, leading to symptoms like wheezing, shortness of breath, chest tightness, and coughing. The symptom frequency and intensity may vary considerably over time. It is also linked to immune system responses to allergens and irritants, highlighting the complex...
3.3K
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

278
Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
278
Asthma: Pathogenesis and Management01:20

Asthma: Pathogenesis and Management

1.1K
Asthma is a chronic pulmonary condition involving inflammation of the airways, hyper-reactivity, and reversible obstruction of the airways. This condition can significantly impact a person's quality of life, making breathing difficult and leading to distressing symptoms.
Asthma is classified as allergic and non-allergic. Allergens such as dust mites, pollen, and pet dander trigger allergic asthma, while factors like cold air, intense emotions, or exercise can induce non-allergic asthma.
1.1K
COPD: Pathogenesis and Clinical Features01:20

COPD: Pathogenesis and Clinical Features

1.7K
Chronic obstructive pulmonary disease (COPD) is a group of lung conditions that progressively worsen over time, including chronic bronchitis and emphysema. This cluster of diseases collectively leads to a gradual and irreversible decline in lung function over time.
The primary cause for the onset of COPD is cigarette smoking and exposure to air pollution. These hazardous factors initiate a chain reaction within the lungs, resulting in chronic inflammation, damage to the airways, and a...
1.7K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

From pre-tumor to tumor: Decoding the endoscopic-pathologic spectrum of neoplastic lesions in autoimmune gastritis.

iScience·2026
Same author

The Role of Ammonia in Particle Toxicity.

Journal of the American College of Cardiology·2026
Same author

Occupational Exposures in the Culinary Underbelly: Air Pollution in Restaurants.

Environmental science & technology·2026
Same author

High-throughput, organ-scale 3D tubule tracking using TubuleMAP.

Research square·2026
Same author

Exposure to electronic cigarette aerosols triggers alterations in genomic DNA methylation that impacts cancer pathways in mice.

Inhalation toxicology·2026
Same author

Harnessing diverse tRNAs and AI-guided mining for compact and efficient plant multiplex genome editing.

Trends in biotechnology·2026

Related Experiment Video

Updated: Dec 21, 2025

Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model
07:35

Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model

Published on: December 10, 2021

2.3K

World Trade Center Dust induces airway inflammation while promoting aortic endothelial dysfunction.

Michelle Hernandez1, Andrea Harrington1, Yanqin Ma1

  • 1Department of Environmental Medicine, New York University School of Medicine, New York, NY 10010, USA.

Toxicology and Applied Pharmacology
|May 20, 2020
PubMed
Summary

World Trade Center (WTC) particulate matter (WTCPM) exposure caused respiratory inflammation and aortic dysfunction in mice. These findings suggest WTCPM may contribute to chronic health issues in exposed populations.

Keywords:
Endothelial cell dysfunctionInhalation toxicologyIntranasal instillationParticulate matter exposurePulmonary inflammationWorld trade center dust

More Related Videos

Fundus Photography as a Convenient Tool to Study Microvascular Responses to Cardiovascular Disease Risk Factors in Epidemiological Studies
10:11

Fundus Photography as a Convenient Tool to Study Microvascular Responses to Cardiovascular Disease Risk Factors in Epidemiological Studies

Published on: October 22, 2014

19.5K
Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
14:48

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Published on: March 21, 2021

5.4K

Related Experiment Videos

Last Updated: Dec 21, 2025

Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model
07:35

Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model

Published on: December 10, 2021

2.3K
Fundus Photography as a Convenient Tool to Study Microvascular Responses to Cardiovascular Disease Risk Factors in Epidemiological Studies
10:11

Fundus Photography as a Convenient Tool to Study Microvascular Responses to Cardiovascular Disease Risk Factors in Epidemiological Studies

Published on: October 22, 2014

19.5K
Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
14:48

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Published on: March 21, 2021

5.4K

Area of Science:

  • Environmental Health
  • Toxicology
  • Immunology

Background:

  • Respiratory ailments are a significant public health concern for World Trade Center (WTC) responders and residents.
  • Inhalation exposure to WTC particulate matter (WTCPM) is hypothesized to induce these respiratory conditions.
  • Understanding the inflammatory potential of WTCPM is crucial for assessing health risks.

Purpose of the Study:

  • To investigate the inflammatory potential of WTC particulate matter (WTCPM).
  • To examine the effects of WTCPM on respiratory and endothelial tissues using in vitro and in vivo models.
  • To correlate WTCPM exposure with observed health effects in WTC-exposed human populations.

Main Methods:

  • In vitro studies using BEAS-2B pulmonary epithelial and THP-1 macrophage cells.
  • In vivo intranasal (IN) exposure model in C57BL/6 mice.
  • Analysis of inflammatory markers, NO2- levels, and aortic function via myography.

Main Results:

  • WTCPM exposure correlated with increased cytotoxicity and NO2- production in vitro.
  • In vivo studies showed elevated inflammatory markers, including neutrophil influx and cytokine levels.
  • Significant homeostatic deviations and aortic dysfunction were observed in exposed mice.

Conclusions:

  • WTC particulate matter (WTCPM) exposure induces significant respiratory and systemic inflammation.
  • Observed effects in mice resemble those in WTC-exposed human populations, suggesting a causal link.
  • Chronic alteration of homeostatic balances due to WTCPM may lead to long-term pathological states.