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Background: Both tobacco smoking and atopy increase the risk of adult‐onset asthma. We studied if there are differences in the effects of smoking on the risks of atopic and non‐atopic adult‐onset asthma, and if gender modifies these effects. Methods: The Finnish Environment and Asthma Study (FEAS) includes 521 incident cases of adult‐onset asthma and 932 population‐based controls, aged 21 to 63 years, recruited from a geographically defined area of Pirkanmaa, South Finland. Asthma was defined based on symptoms and lung function measurements, atopy by IgE antibodies to common aeroallergens and smoking by the study questionnaire. Results: Altogether 212 cases were atopic, and 251 cases were non‐atopic. Regular smoking increased the risk of atopic asthma (adjusted OR 1.24, 95% CI 0.83–1.85), this effect was seen in women (aOR 1.77, 1.06–2.95) but not in men (aOR 0.75, 0.39–1.45). Among regular smokers, the amount smoked was lowest among women with atopic asthma. Recent quitting of smoking was related to increased risk of both atopic (aOR 4.91, 2.26–10.65) and non‐atopic (aOR 4.37, 1.87–10.21) asthma. Having quitted smoking over a year ago was related to increased risk of non‐atopic asthma (aOR 1.57, 1.08–2.28), mainly in men (aOR 2.03, 1.06–3.88). Conclusions: In women, rather small amounts of regular smoking increase the risk of atopic asthma. However, for non‐atopic asthma, the smoking induced risk continues for longer after quitting, especially in men. In conclusion, the effects of smoking on the risks of atopic and non‐atopic asthma differ, and gender modifies these effects. [ABSTRACT FROM AUTHOR]

Background: Previous studies have suggested an increased risk of asthma related to indoor dampness problems, but their role in the etiology of Asthma-COPD Overlap Syndrome has not been studied. We utilized a population-based incident case–control study to assess potential effect of indoor dampness and molds at home and at work on development of ACOS. Methods: We recruited systematically all new cases of asthma diagnosed during a 2.5-year study period (1997–2000) and randomly selected controls from the source population of adults 21–63 years old and representing 500,000 persons-years in the Pirkanmaa Hospital District, South Finland. Exposure indicators included water damage, damp stains or paint peeling, visible mold, and mold odor, asked separately for home and workplace. The clinically diagnosed case series consisted of 521 adults with newly diagnosed asthma. Altogether 25 of them satisfied the criteria for ACOS-cases, i.e. FEV1/FVC < 0.70 in post-bronchodilator spirometry. The control series, including 932 controls, were from a random sample of source population, after excluding 76 (7.5%) controls with asthma. Results: In logistic regression analysis adjusting for confounders, the risk of ACOS was significantly related to presence of mold odor in the workplace (OR 3.43; 95% CI 1.04–11.29), but not to other dampness indicators. The fraction of ACOS attributable to workplace mold odor was 70.8% (95% CI 3.8–91.1%) among the exposed. The risk of ACOS was not related to mold exposures at home. Conclusions: Present results provide new evidence of the significant relation between workplace exposure to mold odor and adult-onset ACOS. [ABSTRACT FROM AUTHOR]

Background: We hypothesised that occupational exposures differently affect subtypes of adult-onset asthma., Objective: We investigated potential relations between occupation and three subtypes of adult asthma, namely atopic asthma, non-atopic asthma and asthma-COPD overlap syndrome (ACOS)., Methods: This is a population-based case-control study of incident asthma among working-age adults living in Pirkanmaa Hospital District in Southern Finland. The determinant of interest was occupation at the time of diagnosis of asthma or the job that the subject had quit due to respiratory symptoms. Asthma was divided into three mutually exclusive subtypes on the basis of any positive IgE antibody (atopic and non-atopic asthma) and presence of persistent airways obstruction in spirometry (ACOS). We applied unconditional logistic regression analysis to estimate adjusted OR (aOR), taking into account gender, age and smoking., Results: The following occupational groups showed significantly increased risk of atopic asthma: chemical industry workers (aOR 15.76, 95% CI 2.64 to 94.12), bakers and food processors (aOR 4.69, 95% CI 1.18 to 18.69), waiters (aOR 4.67, 95% CI 1.40 to 15.56) and those unemployed (aOR 3.06, 95% CI 1.52 to 6.17). The following occupations showed clearly increased risk of non-atopic asthma: metal workers (aOR 8.37, 95% CI 3.77 to 18.59) and farmers and other agricultural workers (aOR 2.36, 95% CI 1.10 to 5.06). Some occupational groups showed statistically significantly increased OR of ACOS: electrical and electronic production workers (aOR 30.6, 95% CI 6.10 to 153.35), fur and leather workers (aOR 16.41, 95% CI 1.25 to 215.85) and those retired (aOR 5.55, 95% CI 1.63 to 18.97)., Conclusions: Our results show that different occupations are associated with different subtypes of adult-onset asthma., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Introduction: Smoking increases the risk of asthma and reduces lung function among subjects with and without asthma. We assessed the effects of smoking on lung function reflecting both central and small airways among adults with newly onset asthma., Methods: In a population-based study, 521 (response rate 86%) working-aged adults with clinically defined newly diagnosed asthma answered a questionnaire on personal smoking and other factors potentially influencing lung function, and performed spirometry. We applied multiple linear regression analysis to estimate the relations between smoking and lung function adjusting for confounding., Results: Among asthmatics, FEV 1 level was reduced significantly, on average 208 mL, related to regular smoking (adjusted effect estimate -0.208, 95% CI -0.355 to -0.061) and 245 mL in relation to former smoking, that is, among those who quit less than a year ago (-0.245, 95% CI -0.485 to -0.004). In contrast, FEV 1 was not significantly related to occasional smoking or former smoking among those who quit over a year ago. Forced expiratory flow (FEF) levels (L/s) were also significantly reduced among regular smokers (FEF 25-75% : -0.372, 95% CI -0.607 to -0.137; FEF 50% : -0.476, 95% CI -0.750 to -0.202). An exposure-response pattern related to both daily smoking rate and lifetime cumulative smoking was seen both among men and women., Conclusions: This study provides new evidence that among working-aged adults with new asthma, regular smoking and former smoking reduce lung function levels with a dose-response pattern. The lung function parameters applied as outcomes reflect both larger and smaller airways., Competing Interests: Competing interests: None declared.

Rationale: Identification of the subpopulation especially susceptible to the adverse effects of second-hand smoke exposure (SHS) would be useful for preventive actions and interventions., Objectives: To investigate whether asthmatic heredity indicates susceptibility to the effects of SHS on the risk of adult-onset asthma., Methods: A population-based incident case-control study of clinically defined adult-onset asthma and randomly drawn control subjects (adults 21-63 yr old) from a geographically defined area in South Finland. After excluding current and ex-smokers there were 226 cases and 450 disease-free control subjects., Measurements and Main Results: Our outcome measure was new adult-onset asthma. Parental asthma and recent SHS had a synergistic effect on the risk of asthma, the adjusted odds ratio being 1.97 (95% confidence interval, 1.12-3.45) for SHS; 2.64 (1.65-4.24) for parental asthma; and 12.69 (3.44-46.91) for their joint effect (relative excess risk due interaction, 9.08 [-0.22 to 43.18]). Synergistic effect followed a dose-dependent pattern with both recent and cumulative SHS exposures, with relative excess risk due interaction for parental asthma and over 100 SHS cigarette-years of 6.17 (0.57-19.16)., Conclusions: This is the first study showing that individuals with asthmatic heredity have a considerably increased risk of adult-onset asthma when exposed to SHS. SHS exposure has dose-dependent synergism with family history of asthma, the joint effect being stronger with higher exposure levels. Avoiding SHS could be an important preventive measure for reducing the risk of adult-onset asthma among those with asthmatic heredity. Asking about family history of asthma is a useful tool for identifying these susceptible individuals in clinical and preventive settings.