Exposure to animals and the risk of allergic asthma: a population-based cross-sectional study in Finnish and Russian children

<p>Abstract</p> <p>Background</p> <p>There is little information on potential differences in animal exposure between Finland and Russia and particularly on the effects of animal exposure on asthma among Russian children. The aim of the study was to compare the pet and farm animal exposures and to assess the relations of pre- and postnatal animal exposures to the occurrence of allergic asthma in Finnish and Russian school children.</p> <p>Methods</p> <p>We conducted a population-based cross-sectional study in neighbour towns on either side of the Finnish-Russian border; Imatra in Finland and Svetogorsk in Russia. The study population consisted of 512 Finnish and 581 Russian school children aged 7–16 years (response rate 79%). Multivariate logistic regression analysis was used to estimate adjusted odds ratios (OR) and 95% confidence intervals (CI) related to each exposure.</p> <p>Results</p> <p>Current indoor exposure to pets was more frequent among school children in Svetogorsk than in Imatra (67.5% vs. 56.0%, P < 0.001). Finnish children were exposed more frequently to dogs, whereas Russian children to cats during childhood and to farm animals during pregnancy and infancy. The risk of self-reported allergic asthma was inversely related to indoor dog keeping ever in Finland (adjusted OR 0.35, 95% CI 0.13, 0.95), whereas in Russia the risk of allergic asthma was increased in relation to combined indoor cat exposure during infancy and currently (4.56, 1.10, 18.91). The risk of asthma was elevated in relation to contact to farm animals during pregnancy (Finland: 1.95, 0.69, 5.50; Russia: 1.90, 0.70, 5.17) and early life (Finland: 2.05, 0.78, 5.40; Russia: 1.21, 0.39, 3.73).</p> <p>Conclusion</p> <p>Exposure to pets and farm animals during childhood differed significantly between Finland and Russia. Our study provides evidence that early-life exposure to cats increases the risk of asthma whereas exposure to dogs is protective. Our findings suggest that intermittent fetal and early-life exposure to farm animals increases the risk of allergic asthma in urban children visiting farms.</p

Subtypes of Adult-Onset Asthma at the Time of Diagnosis: A Latent Class Analysis

Introduction: Only a few previous studies have investigated the subtypes of adult-onset asthma. No previous study has assessed whether these subtypes are different between men and women, or whether these subtypes have different risk factors. Methods: We applied latent class analyses to the Finnish Environment and Asthma Study population, including 520 new cases of adult-onset asthma. We formed subtypes separately between women and men and analyzed the following determinants as potential predictors for these subtypes: age, body mass index, smoking, and parental asthma. Results: Among women, the subtypes identified were: 1. Moderate asthma, 2. Cough-variant asthma, 3. Eosinophilic asthma, 4. Allergic asthma, and 5. Difficult asthma. Among men, the subtypes were: 1. Mild asthma, 2. Moderate asthma, 3. Allergic asthma, and 4. Difficult asthma. Three of the subtypes were similar among women and men: Moderate, Allergic, and Difficult asthma. In addition, women had two distinct subtypes: Cough-variant asthma, and Eosinophilic asthma. These subtypes had different risk factor profiles, e.g., heredity was important for Eosinophilic and Allergic asthma (RR for Both parents having asthma in Eosinophilic 3.55 (1.09 to 11.62)). Furthermore, smoking increased the risk of Moderate asthma among women (RR for former smoking 2.21 (1.19 to 4.11)) and Difficult asthma among men but had little influence on Allergic or Cough-variant asthma. Conclusion: This is an original investigation of the subtypes of adult-onset asthma identified at the time of diagnosis. These subtypes differ between women and men, and these subtypes have different risk factor profiles. These findings have both clinical and public health importance for the etiology, prognosis, and treatment of adult-onset asthma

The effect of sampling height on grass pollen concentrations in different urban environments in the Helsinki Metropolitan Area, Finland

Introduction It is important to study potential differences in pollen concentrations between sampling heights because of diverse outdoor and indoor activity of humans (exposure) at different height levels in urban environments. Previous studies have investigated the effect of height on pollen concentrations based on just one or a few sampling points. We studied the effect of sampling height on grass pollen concentrations in several urban environments with different levels of urbanity. Methods This study was conducted in the Helsinki Metropolitan Area, Finland, in 2013 during the pollen season of grasses. Pollen grains were monitored in eight different points in the morning and afternoon. Rotorod-type samplers were attached on sampling poles at the heights of 1.5 meters and 4 meters. Results Grass pollen concentrations were on average higher at the height of 1.5 meters (Helsinki mean 5.24 grains / m3; Espoo mean 75.71 grains / m3) compared to the height of 4 meters (Helsinki mean 3.84 grains / m3; Espoo mean 37.42 grains / m3) with a difference of 1.40 grains / m3 (95% CI -0.21 to 3.01) in Helsinki, and 38.29 grains / m3 (7.52 to 69.07) in Espoo, although not always statistically significant. This was detected both in the morning and in the afternoon. However, in the most urban sites the levels were lower at 1.5 meters compared to 4 meters, whereas in the least urban sites the concentrations were higher at 1.5 meters. In linear regression models with interaction terms, the modifying effect of urbanity on concentration-height relation was statistically significant in both cities. The effect of urbanity on pollen concentrations at both heights was stronger in less urban Espoo. Conclusions The present study provides evidence that height affects the abundance and distribution of grass pollen in urban environments, but this effect depends on the level of urbanity.Peer reviewe

Indoor dampness and molds and development of adult-onset asthma: a population-based incident case-control study.

Previous cross-sectional and prevalent case-control studies have suggested increased risk of asthma in adults related to dampness problems and molds in homes. We conducted a population-based incident case-control study to assess the effects of indoor dampness problems and molds at work and at home on development of asthma in adults. We recruited systematically all new cases of asthma during a 2.5-year study period (1997-2000) and randomly selected controls from a source population consisting of adults 21-63 years old living in the Pirkanmaa Hospital district, South Finland. The clinically diagnosed case series consisted of 521 adults with newly diagnosed asthma and the control series of 932 controls, after we excluded 76 (7.5%) controls with a history of asthma. In logistic regression analysis adjusting for confounders, the risk of asthma was related to the presence of visible mold and/or mold odor in the workplace (odds ratio, 1.54; 95% confidence interval, 1.01-2.32) but not to water damage or damp stains alone. We estimated the fraction of asthma attributable to workplace mold exposure to be 35.1% (95% confidence interval, 1.0-56.9%) among the exposed. Present results provide new evidence of the relation between workplace exposure to indoor molds and adult-onset asthma

How Exposure to Environmental Tobacco Smoke, Outdoor Air Pollutants, and Increased Pollen Burdens Influences the Incidence of Asthma

Asthma is a multifactorial airway disease that arises from a relatively common genetic background interphased with exposures to allergens and airborne irritants. The rapid rise in asthma over the past three decades in Western societies has been attributed to numerous diverse factors, including increased awareness of the disease, altered lifestyle and activity patterns, and ill-defined changes in environmental exposures. It is well accepted that persons with asthma are more sensitive than persons without asthma to air pollutants such as cigarette smoke, traffic emissions, and photochemical smog components. It has also been demonstrated that exposure to a mix of allergens and irritants can at times promote the development phase (induction) of the disease. Experimental evidence suggests that complex organic molecules from diesel exhaust may act as allergic adjuvants through the production of oxidative stress in airway cells. It also seems that climate change is increasing the abundance of aeroallergens such as pollen, which may result in greater incidence or severity of allergic diseases. In this review we illustrate how environmental tobacco smoke, outdoor air pollution, and climate change may act as environmental risk factors for the development of asthma and provide mechanistic explanations for how some of these effects can occur

Assessment of public health impact of work-related asthma

<p>Abstract</p> <p>Background</p> <p>Asthma is among the most common chronic diseases in working-aged populations and occupational exposures are important causal agents. Our aims were to evaluate the best methods to assess occurrence, public health impact, and burden to society related to occupational or work-related asthma and to achieve comparable estimates for different populations.</p> <p>Methods</p> <p>We addressed three central questions: <b>1: What is the best method to assess the occurrence of occupational asthma? </b>We evaluated: 1) assessment of the occurrence of occupational asthma <it>per se</it>, and 2) assessment of adult-onset asthma and the population attributable fractions due to specific occupational exposures. <b>2: What are the best methods to assess public health impact and burden to society related to occupational or work-related asthma? </b>We evaluated methods based on assessment of excess burden of disease due to specific occupational exposures. <b>3: How to achieve comparable estimates for different populations? </b>We evaluated comparability of estimates of occurrence and burden attributable to occupational asthma based on different methods.</p> <p>Results</p> <p>Assessment of the occurrence of occupational asthma <it>per se </it>can be used in countries with good coverage of the identification system for occupational asthma, i.e. countries with well-functioning occupational health services. Assessment based on adult-onset asthma and population attributable fractions due to specific occupational exposures is a good approach to estimate the occurrence of occupational asthma at the population level. For assessment of public health impact from work-related asthma we recommend assessing excess burden of disease due to specific occupational exposures, including excess incidence of asthma complemented by an assessment of disability from it. International comparability of estimates can be best achieved by methods based on population attributable fractions.</p> <p>Conclusions</p> <p>Public health impact assessment for occupational asthma is central in prevention and health policy planning and could be improved by purposeful development of methods for assessing health benefits from preventive actions. Registry-based methods are suitable for evaluating time-trends of occurrence at a given population but for international comparisons they face serious limitations. Assessment of excess burden of disease due to specific occupational exposure is a useful measure, when there is valid information on population exposure and attributable fractions.</p

Respiratory Infections Precede Adult-Onset Asthma

BACKGROUND: Respiratory infections in early life are associated with an increased risk of developing asthma but there is little evidence on the role of infections for onset of asthma in adults. The objective of this study was to assess the relation of the occurrence of respiratory infections in the past 12 months to adult-onset asthma in a population-based incident case-control study of adults 21-63 years of age. METHODS/PRINCIPAL FINDINGS: We recruited all new clinically diagnosed cases of asthma (n = 521) during a 2.5-year study period and randomly selected controls (n = 932) in a geographically defined area in South Finland. Information on respiratory infections was collected by a self-administered questionnaire. The diagnosis of asthma was based on symptoms and reversible airflow obstruction in lung function measurements. The risk of asthma onset was strongly increased in subjects who had experienced in the preceding 12 months lower respiratory tract infections (including acute bronchitis and pneumonia) with an adjusted odds ratio (OR) 7.18 (95% confidence interval [CI] 5.16-9.99), or upper respiratory tract infections (including common cold, sinusitis, tonsillitis, and otitis media) with an adjusted OR 2.26 (95% CI 1.72-2.97). Individuals with personal atopy and/or parental atopy were more susceptible to the effects of respiratory infections on asthma onset than non-atopic persons. CONCLUSIONS/SIGNIFICANCE: This study provides new evidence that recently experienced respiratory infections are a strong determinant for adult-onset asthma. Reducing such infections might prevent onset of asthma in adulthood, especially in individuals with atopy or hereditary propensity to it

Exposure to benzene at work and the risk of leukemia: a systematic review and meta-analysis

Background A substantial number of epidemiologic studies have provided estimates of the relation between exposure to benzene at work and the risk of leukemia, but the results have been heterogeneous. To bridge this gap in knowledge, we synthesized the existing epidemiologic evidence on the relation between occupational exposure to benzene and the risk of leukemia, including all types combined and the four main subgroups acute myeloid leukemia (AML), acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), and chronic myeloid leukemia (CML). Methods A systematic literature review was carried out using two databases 'Medline' and 'Embase' from 1950 through to July 2009. We selected articles which provided information that can be used to estimate the relation between benzene exposure and cancer risk (effect size). Results In total 15 studies were identified in the search, providing 16 effect estimates for the main analysis. The summary effect size for any leukemia from the fixed-effects model was 1.40 (95% CI, 1.23-1.57), but the study-specific estimates were strongly heterogeneous (I2 = 56.5%, Q stat = 34.47, p = 0.003). The random-effects model yielded a summary- effect size estimate of 1.72 (95% CI, 1.37-2.17). Effect estimates from 9 studies were based on cumulative exposures. In these studies the risk of leukemia increased with a dose-response pattern with a summary-effect estimate of 1.64 (95% CI, 1.13-2.39) for low (< 40 ppm-years), 1.90 (95% CI, 1.26-2.89) for medium (40-99.9 ppm-years), and 2.62 (95% CI, 1.57-4.39) for high exposure category (> 100 ppm-years). In a meta-regression, the trend was statistically significant (P = 0.015). Use of cumulative exposure eliminated heterogeneity. The risk of AML also increased from low (1.94, 95% CI, 0.95-3.95), medium (2.32, 95% CI, 0.91-5.94) to high exposure category (3.20, 95% CI, 1.09-9.45), but the trend was not statistically significant. Conclusions Our study provides consistent evidence that exposure to benzene at work increases the risk of leukemia with a dose-response pattern. There was some evidence of an increased risk of AML and CLL. The meta-analysis indicated a lack of association between benzene exposure and the risk of CML

Respiratory and skin health among glass microfiber production workers: a cross-sectional study

<p>Abstract</p> <p>Background</p> <p>Only a few studies have investigated non-malignant respiratory effects of glass microfibers and these have provided inconsistent results. Our objective was to assess the effects of exposure to glass microfibers on respiratory and skin symptoms, asthma and lung function.</p> <p>Methods</p> <p>A cross-sectional study of 102 workers from a microfiber factory (response rate 100%) and 76 office workers (73%) from four factories in Thailand was conducted. They answered a questionnaire on respiratory health, occupational exposures, and lifestyle factors, and performed spirometry. Measurements of respirable dust were available from 2004 and 2005.</p> <p>Results</p> <p>Workers exposed to glass microfibers experienced increased risk of cough (adjusted OR 2.04), wheezing (adjOR 2.20), breathlessness (adjOR 4.46), nasal (adjOR 2.13) and skin symptoms (adjOR 3.89) and ever asthma (adjOR 3.51), the risks of breathlessness (95%CI 1.68–11.86) and skin symptoms (1.70–8.90) remaining statistically significant after adjustment for confounders. There was an exposure-response relation between the risk of breathlessness and skin symptoms and increasing level of microfiber exposure. Workers exposed to sensitizing chemicals, including phenol-formaldehyde resin, experienced increased risk of cough (3.43, 1.20–9.87) and nasal symptoms (3.07, 1.05–9.00).</p> <p>Conclusion</p> <p>This study provides evidence that exposure to glass microfibers increases the risk of respiratory and skin symptoms, and has an exposure-response relation with breathlessness and skin symptoms. Exposure to sensitizing chemicals increased the risk of cough and nasal symptoms. The results suggest that occupational exposure to glass microfibers is related to non-malignant adverse health effects, and that implementing exposure control measures in these industries could protect the health of employees.</p