Related Experiment Video

Updated: Jun 5, 2026

Cigarette Smoke Exposure in Mice using a Whole-Body Inhalation System
06:07

Cigarette Smoke Exposure in Mice using a Whole-Body Inhalation System

Published on: October 22, 2020

Prenatal exposure to polycyclic aromatic hydrocarbons, environmental tobacco smoke and asthma

Maria José Rosa1, Kyung Hwa Jung, Matthew S Perzanowski

  • 1Division of Pulmonary, Allergy, Critical Care Medicine, Department of Medicine, Columbia University College of Physicians and Surgeons, NY 10032, USA. mr2805@columbia.edu

Respiratory Medicine
|December 18, 2010
PubMed

Insights

Combined prenatal exposure to polycyclic aromatic hydrocarbons (PAH) and environmental tobacco smoke (ETS) is linked to childhood asthma. PAH or ETS exposure alone did not show a significant association with asthma or seroatopy at age 5-6 years.

Area of Science:

  • Environmental Health
  • Pediatric Respiratory Health
  • Toxicology

Background:

  • Previous research linked prenatal polycyclic aromatic hydrocarbons (PAH) and postnatal environmental tobacco smoke (ETS) to early respiratory symptoms.
  • This study investigated the long-term effects of combined prenatal PAH and ETS exposure on asthma and seroatopy in children aged 5-6 years.

Purpose of the Study:

  • To determine if combined prenatal exposure to PAH and ETS increases the risk of asthma and seroatopy.
  • To assess the independent effects of PAH and ETS exposure on these outcomes.

Main Methods:

  • Prenatal PAH exposure was quantified using personal air monitoring.
  • Environmental tobacco smoke (ETS) exposure, respiratory symptoms, and asthma were assessed via questionnaires.
  • Immunoglobulin E (IgE) levels were measured using Immunocap assays.

Main Results:

  • A significant interaction was found between prenatal PAH and prenatal ETS exposure concerning asthma risk (p < 0.05).
  • Prenatal PAH exposure showed a positive, nonsignificant association with asthma in children exposed to prenatal ETS.
  • No significant association was observed between prenatal PAH exposure alone and asthma or IgE levels at age 5-6.

Conclusions:

  • Combined prenatal exposure to PAH and ETS is associated with an increased risk of asthma at age 5-6.
  • Exposure to PAH or ETS alone was not significantly linked to asthma or seroatopy.
  • Further research is needed to understand the distinct impacts of prenatal ETS exposure on these associations.
Abstract

More Related Videos

Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure08:17

Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure

Published on: August 25, 2017

Related Concept Videos

Asthma-I: Introduction01:29

Asthma-I: Introduction

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...
Asthma I: Introduction01:28

Asthma I: Introduction

Asthma is a chronic inflammatory disorder of the airways characterized by variable airflow obstruction and heightened bronchial responsiveness to a wide range of triggers. The underlying inflammation leads to airway swelling, mucus hypersecretion, and smooth muscle constriction, all of which narrow the airway lumen and impede airflow. Clinically, asthma presents with recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing, symptoms that typically vary in intensity and...
Chronic Obstructive Pulmonary Disease I: Introduction01:23

Chronic Obstructive Pulmonary Disease I: Introduction

Chronic obstructive pulmonary disease is a common, preventable, and treatable respiratory disorder characterized by persistent symptoms and progressive airflow limitation. This limitation results from a combination of small-airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema), both driven by chronic inflammation from exposure to harmful particles or gases.The disease includes two main pathological entities: emphysema, marked by destruction of alveolar walls and...
Asthma-II: Pathophysiology and Classification01:26

Asthma-II: Pathophysiology and Classification

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:
Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features01:24

Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...
Asthma: Pathogenesis and Management01:20

Asthma: Pathogenesis and Management

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.