Environmental Causes of Asthma

2018 ◽  
Vol 39 (01) ◽  
pp. 012-018 ◽  
Author(s):  
Donald Cockcroft

AbstractEnvironmental factors which cause asthma are those that induce airway inflammation with eosinophils (more common) or neutrophils along with airway hyperresponsiveness (AHR). The most common of these (indeed the most common cause of asthma) are IgE-mediated inhalant allergen exposures. Allergen-induced AHR and inflammation are both associated with the allergen-induced late asthmatic response (LAR). Although allergens were previously recognized only as causes of symptoms and bronchoconstriction in asthmatics, we now appreciate them as causes of the fundamental pathophysiologic features of asthma. Low-molecular-weight chemical sensitizers, causes of occupational asthma, also cause asthma in a manner analogous to allergen. Acute irritant-induced asthma (reactive airways dysfunction syndrome) following a very heavy irritant exposure and chronic irritant-induced asthma following repeated high exposures can also induce persistent or permanent changes (inflammation and AHR) consistent with asthma. Textile dust exposure produces a different form of airway disease (byssinosis) which is less frequently observed currently. Environmental exposure to tobacco smoke facilitates the development of asthma in children. Personal smoking and environmental air pollution have an inconsistent and likely generally small effect in causing asthma.

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Jen-Chieh Chang ◽  
Lin Wang ◽  
Rong-Fu Chen ◽  
Chieh-An Liu

Atopic asthma is a complex disease associated with IgE-mediated immune reactions. Numerous genome-wide studies identified more than 100 genes in 22 chromosomes associated with atopic asthma, and different genetic backgrounds in different environments could modulate susceptibility to atopic asthma. Current knowledge emphasizes the effect of tobacco smoke on the development of childhood asthma. This suggests that asthma, although heritable, is significantly affected by gene-gene and gene-environment interactions. Evidence has recently shown that molecular mechanism of a complex disease may be limited to not only DNA sequence differences, but also gene-environmental interactions for epigenetic difference. This paper reviews and summarizes how gene-gene and gene-environment interactions affect IgE production and the development of atopic asthma in prenatal and childhood stages. Based on the mechanisms responsible for perinatal gene-environment interactions on IgE production and development of asthma, we formulate several potential strategies to prevent the development of asthma in the perinatal stage.


1998 ◽  
Vol 7 (3) ◽  
pp. 217-220 ◽  
Author(s):  
U. Westin ◽  
E. Lundberg ◽  
K. Ohlsson

The secretory leukocyte protease inhibitor (SLPI) is a low-molecular-weight inhibitor of proteases, such as elastase and cathepsin G which are released from leukocytes during phagocytosis. The purpose of this study was to determine whether or not SLPI is able to inhibit IgE-mediated histamine release. Nasal mucosa from 11 test subjects without atopic disposition was used for thisin vitrostudy. We found that SLPI inhibited histamine release in a dose-dependent way but was without influence on the spontaneous release.


ESC CardioMed ◽  
2018 ◽  
pp. 3099-3101
Author(s):  
Thomas Münzel ◽  
Sanjay Rajagopalan ◽  
Mette Sørenson ◽  
Dave Newby ◽  
Robert D. Brook

Cardiovascular disease represents the result of underlying genetic predisposition and lifetime exposure to multiple environmental factors. The past century has seen a revolution in our understanding of the importance of modifiable risk factors such as diet, exercise, and smoking. Exposure to environmental pollutants, be it in the air, water, or physical environment, is increasingly recognized as a silent, yet important determinant of cardiovascular disease. The cardiovascular system is highly vulnerable to a variety of environmental insults, including tobacco smoke, solvents, pesticides, and other inhaled or ingested pollutants, as well as extremes in noise and temperature. While our understanding of multiple environmental factors continues to evolve, it is estimated that environmental air pollution and noise pollution alone contribute a substantial burden attributable to environmental factors as we currently understand them.


2007 ◽  
Vol 144 (1) ◽  
pp. 10-22 ◽  
Author(s):  
Elide A. Pastorello ◽  
Laura Farioli ◽  
Amedeo Conti ◽  
Valerio Pravettoni ◽  
Simona Bonomi ◽  
...  

2008 ◽  
Vol 139 (2_suppl) ◽  
pp. P96-P96
Author(s):  
Peter C Belafsky ◽  
Debbie A. Mouadeb ◽  
Kent Pinkerton ◽  
Martin A Birchall ◽  
Thomas Konia

Problem Environmental factors such as second hand smoke and allergens are known to play an important part in the development of lower airway disease, specifically asthma. The effect of these common exposures on the larynx has been neglected. The purpose of this investigation was to investigate the effects of environmental tobacco smoke (ETS) and allergens on laryngeal mucosa. Methods Seventeen guinea pigs were exposed by inhalation to: 1) air and saline, 2) air and house dust mite allergen (HDMA), 3) ETS and saline 4) HDMA and ETS. Exposures began at 3 weeks of age and lasted 10 weeks. Histology was evaluated in different subsets of the larynx for eosinophils and mucin, markers of inflammation. Results Eosinophils in the supraglottis were elevated in the air/HDMA and ETS/HDMA groups (p<0.05). Animals exposed to HDMA were 4 times more likely to have > 10 eosinophils per HPF in the supraglottis than control animals (95% CI = 0.74, 20). Trends towards mucin hypersecretion in the subglottis of the ETS/air and ETS/HDMA groups were noted. Animals exposed to ETS and HDMA were 3.8 times more likely to have 25% of the subglottic epithelium stain PAS positive for mucin (95% CI = .59, 23.66). Conclusion The data suggest that environmental tobacco smoke and inhaled allergens contribute to the pathogenesis of laryngeal inflammation. Significance Environmental tobacco smoke and allergen exposure may play a role in the development of chronic laryngitis.


1988 ◽  
Vol 42b ◽  
pp. 690-696 ◽  
Author(s):  
Karl-Axel Persson ◽  
Sven Berg ◽  
Margareta Törnqvist ◽  
Gian-Paolo Scalia-Tomba ◽  
Lars Ehrenberg ◽  
...  

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