Smoking and Asthma

Article Figures & Data

Table 1.

Examples of Mechanisms of Smoking and Airway Damage in Asthma

Mechanisms	References
Toxin direct to the bronchial epithelium, causing oxidative damage	5
Release of proinflammatory mediators and increased epithelial permeability	6
Proinflammatory mediators and cytokines involved
Interleukin-8	7–9, 10
Lipopolysaccharides	11
Leukotriene B4	7, 10
Prostaglandin E₂	12
Angiopoietin-2	13
Eotaxin-1	14

Table 2.

In Utero Exposure to Secondhand Smoke, Resulting in Asthma

Results of Exposure	References
Offspring are 1.8 times more likely to develop asthma and a lifetime history of wheezing	47, 48
Children diagnosed with early-onset asthma have more persistent deficits in lung function	49
Other effects	50–57
Significant reductions in forced expiratory flow
Suppression of alveolarization, functional residual capacity, and tidal flow volume

Table 3.

Effects of Secondhand Smoke (SHS) on Children with Asthma

Effects	References
Maternal exposure seems to be the most significant of SHS exposure, which may be because of the child’s close proximity to the mother	30, 67–69
The association between parental SHS exposure and asthma becomes less strong after adolescence into adulthood, which may be because the child is spending less time at home	70
Asthmatic children exposed to multiple household smokers face a 4.5-fold increase risk for respiratory illness related absences from school	71
Perinatal deficits in lung function are persistent and may increase during adolescence in the presence of parental SHS	72, 73
SHS is associated with increased asthma severity and is more likely to be diagnosed as moderate to severe asthma	42, 74
SHS is associated with worsening of lung function as evidence of decline in peak expiratory flow, and increase in symptoms and bronchodilator use in asthmatic children exposed to SHS	42, 58, 75
Household smoking increases the frequency of asthma attacks, number of visits to an emergency department, and risk of intubation	76

Table 4.

Effects of Smoking and Secondhand Smoke (SHS) on Response to Corticosteroids

Effects	References
It is unknown if there is a synergistic effect of smoking and asthma on airway mucosal permeability; however, this could contribute to increased clearance of inhaled corticosteroids from the airways of asthmatic smokers	91
Chronic hypersecretion of mucus is caused by cigarette smoking in patients with asthma, and this could impede the ability of inhaled corticosteroids to bind to GRs in the airways	92
S₂-agonists increase the nuclear localization of GRs, which may potentiate the effects of corticosteroids	93
Cigarette smoke leads to increased numbers of neutrophils and CD8+ lymphocytes and decreased numbers of eosinophils in the airways, which may contribute to corticosteroid resistance	91
Nitric oxide in cigarette smoke has been shown to decrease the binding affinity of glucocorticoid receptors (GR) in vitro; it remains to be seen whether or not nitric oxide shows the same effect in vivo ⁹⁴	94
Other proposed mechanisms include overexpression of proinflammatory transcription factors such as NF-κβ, activator protein-1, and signal transduction-activated factor	95, 96
HDAC activity is necessary for corticosteroids to fully suppress cytokine production, and smokers have decreased HDAC activity in alveolar macrophages, which could lead to corticosteroid resistance	97
The p38 mitogen-activated protein kinase signaling pathway may be activated in asthmatic smokers which phosphorylates GRs and decreases corticosteroid affinity	98