ContextStudies from different geographical regions have assessed the relations between indoor dampness and mold problems and the risk of asthma, but the evidence has been inconclusive.ObjectiveTo assess the relations between indicators of indoor dampness and mold problems and the risk of developing new asthma, and to investigate whether such relations differ according to the type of exposure.Data sourcesA systematic literature search of PubMed database from 1990 through March 2012 and the reference lists of recent reviews and of relevant articles identified in our search.Study selectionCohort/longitudinal and incident case-control studies assessing the relation between mold/dampness and new asthma were included.Data extractionThree authors independently evaluated eligible articles and extracted relevant information using a structured form.SynthesisSixteen studies were included: 11 cohort and 5 incident case-control studies. The summary effect estimates (EE) based on the highest and lowest estimates for the relation between any exposure and onset of asthma were 1.50 (95% confidence interval [CI] 1.25–1.80, random-effects model, Q-statistic 38.74 (16), P = 0.001) and 1.31 (95% CI 1.09–1.58, random-effects model, Q-statistic 40.08 (16), P = 0.000), respectively. The summary effect estimates were significantly elevated for dampness (fixed-effects model: EE 1.33, 95% CI 1.12–1.56, Q-statistic 8.22 (9), P = 0.413), visible mold (random-effects model; EE 1.29, 95% CI 1.04–1.60, 30.30 (12), P = 0.001), and mold odor (random-effects model; EE 1.73, 95% CI 1.19–2.50, Q-statistics 14.85 (8), P = 0.038), but not for water damage (fixed-effects model; EE 1.12, 95% CI 0.98–1.27). Heterogeneity was observed in the study-specific effect estimates.ConclusionThe evidence indicates that dampness and molds in the home are determinants of developing asthma. The association of the presence of visible mold and especially mold odor to the risk of asthma points towards mold-related causal agents.
BackgroundFamily history of asthma and other allergic diseases have been linked to the risk of childhood asthma previously, but little is known about their effect on the age-of-onset and persistency of asthma until young adulthood.MethodsWe assessed the effect of the family history of asthma and allergic diseases on persistent vs. transient, and early- vs. late-onset persistent asthma in The Espoo Cohort Study 1991–2011, a population-based cohort study of 1623 subjects (follow-up rate 63.2%). The determinants were any family history (any parent or sibling); maternal; paternal; siblings only; parents only; and both siblings and parents. Analyses were conducted separately for asthma and allergic diseases while taking the other disease into account as a confounding factor. The outcomes were persistent, transient, early-onset persistent (<13 years) and late-onset persistent asthma. Adjusted risk ratios (RR) were calculated applying Poisson regression. Q-statistics were used to assess heterogeneity between RRs.ResultsFamily history was associated with the different subtypes but the magnitude of effect varied quantitatively. Any family history of asthma was a stronger determinant of persistent (adjusted RR = 2.82, 95% CI 1.99-4.00) than transient asthma (1.65, 1.03-2.65) (heterogeneity: P = 0.07) and on early-onset than late-onset persistent asthma. Also any family history of allergic diseases was a stronger determinant of persistent and early-onset asthma. The impact of paternal asthma continued to young adulthood (early-onset: 3.33, 1.57-7.06 vs. late-onset 2.04, 0.75-5.52) while the influence of maternal asthma decreased with age (Early-onset 3.94, 2.11-7.36 vs. Late-onset 0.88, 0.28-2.81). Paternal allergic diseases did not follow the pattern of paternal asthma, since they showed no association with late-onset asthma. Also the effect estimates for other subtypes were lower than in other hereditary groups (persistent 1.29, 0.75-2.22 vs. transient 1.20, 0.67-2.15 and early-onset 1.86, 0.95-3.64 vs. late-onset 0.64, 0.22-1.80).ConclusionsFamily history of asthma and allergic diseases are strong determinants of asthma, but the magnitude of effect varies according to the hereditary group so that some subtypes have a stronger hereditary component, and others may be more strongly related to environmental exposures. Our results provide useful information for assessing the prognosis of asthma based on a thorough family history.
BackgroundSeveral studies have assessed effects of short-term exposure to pollen on allergic and asthmatic manifestations. The evidence is inconclusive, and no meta-analysis has been published.ObjectiveTo synthesise the evidence on the relations between short-term pollen exposure and the risk of allergic and asthmatic manifestations.MethodsWe performed a systematic literature search of PubMed and Scopus databases up to the end of August 2018. In addition, we reviewed the reference lists of relevant articles. Two authors independently evaluated the eligible articles and extracted relevant information in a structured form. We calculated summary effect estimates (EE) based on the study-specific ORs and regression coefficients (β) by applying both fixed-effects and random-effects models.Results26 studies met the a priori eligibility criteria, and 12 of them provided sufficient information for the meta-analysis. The summary EE related to 10 grains per m³ increase in pollen exposure showed an 1% increase (EE 1.01, 95% CI 1.00 to 1.02) in the risk of lower respiratory symptoms and a 2% increase (EE 1.02, 95% CI 1.01 to 1.03) in the risk of any allergic or asthmatic symptom. Correspondingly, the risk of upper respiratory symptoms and ocular symptoms increased 7% (EE 1.07, 95% CI 1.04 to 1.09) and 11% (EE 1.11, 95% CI 1.05 to 1.17), respectively, in relation to such pollen exposure. Short-term exposure to pollen did not show any significant effect on daily lung function levels.ConclusionOur results provide new evidence that short-term pollen exposure significantly increases the risks of allergic and asthmatic symptoms.
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