Related Experiment Video
Updated: Mar 13, 2026

Noninvasive Sampling of Mucosal Lining Fluid for the Quantification of In Vivo Upper Airway Immune-mediator Levels
Published on: August 7, 2017
Maternal smoking in pregnancy and its influence on childhood asthma
1Dept of Pediatrics and Adolescent Medicine, Teaching Hospital Wilhelminenspital of the Medical University of Vienna, Vienna, Austria.
Insights
Maternal smoking during pregnancy (MSP) significantly increases a child's risk of developing asthma. These effects, including epigenetic changes, can impact health across generations.
Area of Science:
- Environmental Health
- Pediatric Pulmonology
- Reproductive Health
Background:
- Maternal smoking during pregnancy (MSP) is a major risk factor for adverse pregnancy outcomes and childhood asthma.
- Understanding the long-term respiratory health consequences of MSP is crucial for public health initiatives.
Approach:
- This review synthesizes current research on the multifaceted effects of MSP on respiratory health from infancy through adolescence.
- It examines direct fetal damage, immune system alterations, and epigenetic modifications induced by maternal smoking.
Key Points:
- Nicotine directly harms fetal lung development, growth, and neuronal differentiation, while also impairing placental function.
- MSP exposure increases infection rates and modulates airway hyperreactivity, reducing lung function and elevating asthma morbidity.
- Epigenetic effects of cigarette smoke exposure can lead to transgenerational detrimental health impacts.
Conclusions:
- A causal link between MSP and asthma development is well-established, posing a significant, intergenerational health challenge.
- The high prevalence of MSP and its epigenetic consequences amplify the danger, contributing substantially to the global rise in asthma.
Abstract:
Maternal smoking in pregnancy (MSP) is a large modifiable risk factor for pregnancy related mortality and morbidity and also the most important known modifiable risk factor for asthma. This review summarises the effects of MSP throughout infancy, childhood and adolescence with regards to asthma (development and severity). Firstly, the direct damage caused by nicotine on fetal lung development, fetal growth and neuronal differentiation is discussed, as well as the indirect effects of nicotine on placental functioning. Secondly, the effects of MSP on later immune functioning resulting in increased infection rate are summarised and details are given on the effects of MSP modulating airway hyperreactivity, reducing lung function and therefore increasing asthma morbidity. Furthermore, epigenetic effects are increasingly being recognised. These can also result in transgenerational detrimental effects induced by cigarette smoke. In summary, the causal relationship between MSP and asthma development is well documented and presents a major health problem for generations to come. The high prevalence of MSP is alarming and epigenetic effects of nicotine on immune functioning potentiate this danger. A considerable part of the increase in asthma prevalence worldwide is due to MSP.
Related Concept Videos
Asthma-I: Introduction
Asthma: Pathogenesis and Management
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.
Upper Respiratory Drugs: Antitussives, Expectorants, and Mucolytics
Antitussives include codeine, dextromethorphan (Robitussin), and benzonatate (Tessalon). Codeine and dextromethorphan exert their effects centrally by suppressing the cough reflex center in the medulla. Benzonatate operates peripherally within the respiratory tract by...
Asthma-II: Pathophysiology and Classification
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:
Asthma-III: Symptoms and Complications
Classification of Asthma
Chronic Obstructive Pulmonary Disease-II: Pathophysiology
Chronic Inflammation

