High Exposure to Passive Tobacco Smoking and the Development of Asthma in an Adult Patient Who Had Never Smoked

Jerzyńska, Joanna; Stelmach, Iwona; Grzelewski, Tomasz; Stelmach, Włodzimierz; Krakowiak, Jan

doi:10.1164/ajrccm.182.3.433

Cited by 4 publications

(3 citation statements)

References 13 publications

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“…123,124,128 There is a comparable causal relationship between exposure to environmental tobacco smoke (ETS) and asthma in nonsmoking adults and children. 126,[132][133][134][135][136][137][138] Evidence also supports an association between ETS exposure and asthma exacerbation. 132 Bronchial hyperresponsiveness (BHR) is regarded as a hallmark feature of asthma and bronchoprovocation testing is performed to support its diagnosis.…”

Section: Asthmamentioning

confidence: 84%

Cigarette Smoke Particle-Induced Lung Injury and Iron Homeostasis

Ghio¹,

Pavlisko²,

Roggli³

et al. 2022

COPD

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It is proposed that the mechanistic basis for non-neoplastic lung injury with cigarette smoking is a disruption of iron homeostasis in cells after exposure to cigarette smoke particle (CSP). Following the complexation and sequestration of intracellular iron by CSP, the host response (eg, inflammation, mucus production, and fibrosis) attempts to reverse a functional metal deficiency. Clinical manifestations of this response can present as respiratory bronchiolitis, desquamative interstitial pneumonitis, pulmonary Langerhans' cell histiocytosis, asthma, pulmonary hypertension, chronic bronchitis, and pulmonary fibrosis. If the response is unsuccessful, the functional deficiency of iron progresses to irreversible cell death evident in emphysema and bronchiectasis. The subsequent clinical and pathological presentation is a continuum of lung injuries, which overlap and coexist with one another. Designating these non-neoplastic lung injuries after smoking as distinct disease processes fails to recognize shared relationships to each other and ultimately to CSP, as well as the common mechanistic pathway (ie, disruption of iron homeostasis).

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Section: Asthmamentioning

confidence: 84%

Cigarette Smoke Particle-Induced Lung Injury and Iron Homeostasis

Ghio¹,

Pavlisko²,

Roggli³

et al. 2022

COPD

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“…Many clinical studies found smoking has deleterious effects on lung function, such as a rapid reduction in forced expiratory volume in one second and reduced peak expiratory flow as well as lowered responsivity to routine asthma treatment (14,15). Moreover, asthmatic smokers are also more likely to develop severe asthma (16,17).…”

Section: Discussionmentioning

confidence: 99%

Expression and pathological significance of CC chemokine receptor 7 and its ligands in the airway of asthmatic rats exposed to cigarette smoke

Zhang¹,

Li²,

Zhang³

et al. 2018

J. Thorac. Dis

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Background: Cigarette smoking aggravates the symptoms of asthma, leading to the rapid decline of lung function. Dendritic cells (DCs) and lymphocytes are considered initiating and promoting factors for the airway inflammation reactions of asthma. In addition, activation of CC chemokine receptor 7 (CCR7) by chemokine (C-C motif) ligand (CCL) 19 and 21 promotes DCs and T cells migration to lymphoid tissues during inflammation. We aimed to examine how cigarette smoke affects the expression of CCR7 in the lungs of asthmatic rats and explore the signaling mechanism linking CCR7 expression to exacerbation of symptoms. Methods: Forty Wistar rats were randomized to four groups: control, asthma, smoke exposure, and asthma with smoke exposure groups. A rat asthma model was established by intraperitoneal ovalbumin injection. CCR7 expression was examined with immunohistochemistry and western blotting. The number of airway DCs was determined by OX62 immunohistochemistry. Interferon (INF)-γ, interleukin (IL)-4, CCL19, and CCL21 expression levels in blood and bronchioalveolar lavage fluid (BALF) were determined by enzymelinked immunosorbent assays (ELISAs). Results: Tissue CCR7 expression, peripheral blood and BALF CCL19 and CCL21 concentrations, and the number of airway DCs were significantly higher in the asthma with smoke exposure group than the asthma group (P<0.01). In addition, INF-γ expression was decreased and IL-4 increased in the asthma and asthma with smoke exposure groups compared with the control group (P<0.01), and in the asthma with smoke exposure group compared with the asthma group (P<0.01). Expression of CCR7 correlated negatively with INF-γ expression in peripheral blood and BALF (P<0.01), and positively with the airway DCs and IL-4 expression in the peripheral blood and BALF (P<0.01). Conclusions: Cigarette smoking may aggravate asthma symptoms by attenuating immunity, possibly through CCR7-mediated DCs aggregation in lung tissue.

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“… 2 Although the effects of tobacco smoking are broad and devastating, much smoking-related research has traditionally focused on the lung because the lung is considered to be the primary target organ affected. ETS exposure has been implicated as a cause of lung diseases such as lung cancer, 3 , 4 asthma 5 , 6 and COPD 7 , 8 among nonsmokers. In a recent systematic review and meta-analysis, it was also confirmed that the risk of developing these respiratory diseases caused by ETS exposure significantly increased.…”

Section: Introductionmentioning

confidence: 99%

Exposure to environmental tobacco smoke from husband more strongly impacts on the airway obstruction of nonsmoking women

Suyama

Kozu

Tanaka

et al. 2017

COPD

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BackgroundThe impact of airway obstruction of nonsmoking women caused by their husband’s smoking is unclear, despite the association between environmental tobacco smoke (ETS) exposure at home and obstructive pulmonary diseases among nonsmoking women. The aim of this study was to provide evidence that ETS exposure from the husband at home has a more significant influence on the airway obstruction of nonsmoking women than other housemates.Participants and methodsNonsmoking women aged 40 years or older were recruited from the health checkup during May 2015–December 2016, Japan. They answered structured questionnaires, including ETS exposure from their husbands and other housemates (parents, siblings and dependants), and performed spirometry. We categorized the women with any history of ETS exposure from housemates into three groups (A = husband, B = others and C = both of husband and others) and defined the control group as those with no ETS exposure from housemates.ResultsA total of 811 nonsmoking women completed questionnaires and spirometry. The proportion of nonsmoking women who had airway obstruction (forced expiratory volume in 1 second [FEV1]/forced vital capacity [FVC] <70%) among Group A (7.5%) was significantly higher than those in the control group (1.1%, p<0.01) and Group B (0.8%, p<0.01). The proportion of airway obstruction in Group C (6.4%) was also higher than that in the control group (p<0.05) and Group B (p<0.05). ETS exposure from husband (odds ratio [OR], 3.53; 95% confidence interval [CI], 1.48–8.42) remained strongly associated with airway obstruction after multiple logistic regression analysis, adjusting for age, housemate’s smoking habits, family history and ETS exposure in childhood and at work.ConclusionNonsmoking women who were exposed to ETS from their husband had the lowest FEV1/FVC, and a higher proportion of them had airway obstruction when compared to nonsmoking women who experienced ETS from housemates other than their husbands. The findings suggest that tobacco control in husbands is the most important measure to prevent airway obstruction of nonsmoking women at home.

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High Exposure to Passive Tobacco Smoking and the Development of Asthma in an Adult Patient Who Had Never Smoked

Cited by 4 publications

References 13 publications

Cigarette Smoke Particle-Induced Lung Injury and Iron Homeostasis

Cigarette Smoke Particle-Induced Lung Injury and Iron Homeostasis

Expression and pathological significance of CC chemokine receptor 7 and its ligands in the airway of asthmatic rats exposed to cigarette smoke

Exposure to environmental tobacco smoke from husband more strongly impacts on the airway obstruction of nonsmoking women

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