Background: Children's information about their parents' lifestyle is increasingly used in research, and it is crucial to assess its validity. Aim: To validate offspring's reports of parents' smoking status and examine predictors for discrepant answers. Methods: We studied 5678 offspring (18-51yrs) and one of their parents, n=4151 (38-65yrs) participating in the Respiratory Health in Northern Europe, Spain and Australia (RHINESSA) generation study. Information about parent's smoking status during offspring's childhood was obtained by questionnaires from parents and their offspring. We calculated sensitivity, specificity and Cohens Kappa for agreement (using parent's own report as the gold standard). We performed logistic regression to examine if offspring gender, age, education, asthma, or own smoking status predicted agreement. Results: The sensitivity for correct offspring report of parents smoking status during childhood (0-10yrs) was 0.83 (95% CI 0.82–0.85), specificity was 0.95 (95% CI 0.94–0.96) and a good agreement was seen (κ = 0.79, 95% CI 0.78–0.81). Similar results were seen for childhood defined as 0-18yrs. Logistic regression analysis showed that fewer discrepant answers were related to younger offspring age (<30yrs = odds ratio [OR] 0.66 (95% CI 0.51–0.86), 30-39yrs OR 0.70 (95% CI 0.54–0.90) reference ≥40yrs) and parents amount of smoking (≥10 cigarettes/day OR 0.56 (95% CI 0.44–0.71) reference <10). Offspring's gender, education, smoking or asthma status did not predict discrepant answers. Conclusion: Offspring quite correctly report their parents' smoking status during the offspring's childhood. In the absence of direct report, offspring's reports could be valuable.
Objectives Two spa workers reported such symptoms as fever, shivering, palpitation, arthralgia, and diarrhea after performing seaweed massages on clients at a spa center. This study was carried out to determine whether the symptoms were related to exposure to endotoxin. Methods Personal and stationary air sampling for the measurement of airborne endotoxin was carried out at the spa during the preparation of a bath and the following seaweed massage. In addition, the impact of storage time on the concentration of endotoxin in the seaweed was investigated. Results The measurements confirmed exposure to aerosolized endotoxin at the spa (11 ng/m 2 and 22 ng/m 3 ). The endotoxin concentration in the stored seaweed increased as the storage time increased, from 360 ng/g seaweed for fresh seaweed to 33100 ng/g seaweed for seaweed stored for >20 weeks. Conclusions Organic dust toxic syndrome was diagnosed for two workers who performed seaweed massages at a spa center at which aerosolized endotoxin was measured. In order to minimize entotoxin exposure during massages, it is important to use fresh seaweed or seaweed kept well cooled for no more than 2–3 weeks.
Selection bias is a systematic error in epidemiologic studies that may seriously distort true measures of associations between exposure and disease. Observational studies are highly susceptible to selection bias, and researchers should therefore always examine to what extent selection bias may be present in their material and what characterizes the bias in their material. In the present study we examined long-term participation and consequences of loss to follow-up in the studies Respiratory Health in Northern Europe (RHINE), Italian centers of European Community Respiratory Health Survey (I-ECRHS), and the Italian Study on Asthma in Young Adults (ISAYA).Logistic regression identified predictors for follow-up participation. Baseline prevalence of 9 respiratory symptoms (asthma attack, asthma medication, combined variable with asthma attack and/or asthma medication, wheeze, rhinitis, wheeze with dyspnea, wheeze without cold, waking with chest tightness, waking with dyspnea) and 9 exposure-outcome associations (predictors sex, age and smoking; outcomes wheeze, asthma and rhinitis) were compared between all baseline participants and long-term participants. Bias was measured as ratios of relative frequencies and ratios of odds ratios (ROR).Follow-up response rates after 10 years were 75% in RHINE, 64% in I-ECRHS and 53% in ISAYA. After 20 years of follow-up, response was 53% in RHINE and 49% in I-ECRHS. Female sex predicted long-term participation (in RHINE OR (95% CI) 1.30(1.22, 1.38); in I-ECRHS 1.29 (1.11, 1.50); and in ISAYA 1.42 (1.25, 1.61)), as did increasing age. Baseline prevalence of respiratory symptoms were lower among long-term participants (relative deviations compared to total baseline population 0-15% (RHINE), 0-48% (I-ECRHS), 3-20% (ISAYA)), except rhinitis which had a slightly higher prevalence. Most exposure-outcome associations did not differ between long-term participants and all baseline participants, except lower OR for rhinitis among ISAYA long-term participating smokers (relative deviation 17% (smokers) and 44% (10-20 pack years)).We found comparable patterns of long-term participation and loss to follow-up in RHINE, I-ECRHS and ISAYA. Baseline prevalence estimates for long-term participants were slightly lower than for the total baseline population, while exposure-outcome associations were mainly unchanged by loss to follow-up.
The aim of the present study was to investigate the remission rate of adult asthma in a general population sample in relation to age, sex, asthma symptoms, allergic rhinitis and smoking. A follow-up of the random population samples from the European Community Respiratory Health Survey in Northern Europe was conducted from 1999–2001 on 1,153 individuals (aged 26–53 yrs) with reported asthma. Remission was defined as no asthmatic symptoms in two consecutive years and no current use of asthma medication. Remission rates per 1,000 person-yrs were calculated and Cox regression models, adjusting for confounders, were used to estimate hazard ratios (HR) with 95% confidence intervals (CI). An average remission rate of 20.2 per 1,000 person-yrs was found. There was no significant difference according to sex; the remission rates were 21.7 and 17.8 per 1,000 person-yrs in females and males, respectively. An increased remission rate was observed among subjects who quit smoking during the observation period. Subjects not reporting any asthma symptom at baseline had an increased remission rate. In the Cox regression model, ex-smoking (HR 1.65, 95% CI 1.01–2.71) was associated with increased remission rate, and reporting any asthma symptom at baseline was associated with decreased remission rate (HR 0.7, 95% CI 0.40–0.90). In conclusion, the present prospective longitudinal study showed that quitting smoking and the presence of mild disease appeared to favour remission.
Highlights•Previous evidence suggests that menopause, or more specifically the associated lack of female sex steroids, is related to a decline in lung function.•This study investigated decline in lung function over 20 years in 275 users of hormone replacement therapy and 383 non-users from the general European public.•Taking exogenous female sex steroids for more than five years is related to a slower decline in respiratory function.AbstractObjectives: Menopause involves hypoestrogenism, which is associated with numerous detrimental effects, including on respiratory health. Hormone replacement therapy (HRT) is often used to improve symptoms of menopause. The effects of HRT on lung function decline, hence lung ageing, have not yet been investigated despite the recognized effects of HRT on other health outcomes.Study design: The population-based multi-centre European Community Respiratory Health Survey provided complete data for 275 oral HRT users at two time points, who were matched with 383 nonusers and analysed with a two-level linear mixed effects regression model.Main outcome measures: We studied whether HRT use was associated with the annual decline in forced vital capacity (FVC) and forced expiratory volume in one second (FEV1).Results: Lung function of women using oral HRT for more than five years declined less rapidly than that of nonusers. The adjusted difference in FVC decline was 5.6 mL/y (95%CI: 1.8 to 9.3, p = 0.01) for women who had taken HRT for six to ten years and 8.9 mL/y (3.5 to 14.2, p = 0.003) for those who had taken it for more than ten years. The adjusted difference in FEV1 decline was 4.4 mL/y (0.9 to 8.0, p = 0.02) with treatment from six to ten years and 5.3 mL/y (0.4 to 10.2, p = 0.048) with treatment for over ten years.Conclusions: In this longitudinal population-based study, the decline in lung function was less rapid in women who used HRT, following a dose-response pattern, and consistent when adjusting for potential confounding factors. This may signify that female sex hormones are of importance for lung ageing.
Very few studies have examined whether a long-term beneficial effect of physical activity on lung function can be influenced by living in polluted urban areas.We assessed whether annual average residential concentrations of nitrogen dioxide (NO2) and particulate matter with aerodynamic diameters < 2.5 μm (PM2.5) and <10 μm (PM10) modify the effect of physical activity on lung function among never- (N = 2801) and current (N = 1719) smokers in the multi-center European Community Respiratory Health Survey.Associations between repeated assessments (at 27-57 and 39-67 years) of being physically active (physical activity: ≥2 times and ≥1 h per week) and forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) were evaluated using adjusted mixed linear regression models. Models were conducted separately for never- and current smokers and stratified by residential long-term NO2, PM2.5 mass and PM10 mass concentrations (≤75th percentile (low/medium) versus >75th percentile (high)).Among current smokers, physical activity and lung function were positively associated regardless of air pollution levels. Among never-smokers, physical activity was associated with lung function in areas with low/medium NO2, PM2.5 mass and PM10 mass concentrations (e.g. mean difference in FVC between active and non-active subjects was 43.0 mL (13.6, 72.5), 49.5 mL (20.1, 78.8) and 49.7 mL (18.6, 80.7), respectively), but these associations were attenuated in high air pollution areas. Only the interaction term of physical activity and PM10 mass for FEV1 among never-smokers was significant (p-value = 0.03).Physical activity has beneficial effects on adult lung function in current smokers, irrespective of residential air pollution levels in Western Europe. Trends among never-smokers living in high air pollution areas are less clear.
A causal relationship between occupational exposures and the development of chronic bronchitis and COPD has been recognized, but there is limited evidence from prospective population-based studies. The ECRHS is a multicentre cohort study that has recently completed a second follow-up after a mean of 19 years. We examined the relationship between occupational exposures and group-level changes in chronic bronchitis symptoms using 3 time points. We used repeated questionnaire data from 9175 ECRHS participants in 29 study centres, 6754 (74%) of whom completed the second follow-up. Occupational exposures were assessed from job histories up to the first follow-up using the ALOHA Job-Exposure Matrix. Absolute annual change in prevalence of chronic cough and/or chronic phlegm was assessed using Generalized Estimating Equation models, fitted separately for each study centre and pooled using multivariate meta-analysis. Any high exposure to dusts, gases or fumes (14% of participants) was associated with increasing prevalence of cough or phlegm in men (0.087%/year, p=0.002), and decreasing prevalence of cough with phlegm in women (-0.039%/year, p<0.001). Heterogeneity between centre-level estimates was moderate (men: Ι2=46%, women: I2=26%). Smoking was a strong predictor of cough and phlegm, but did not modify the observed associations. Certain occupations were associated with increased, but others with decreased prevalence of symptoms, e.g. nurses (-0.039%/year, p=0.001). We conclude that occupational exposures may affect the prevalence of chronic bronchitis during two decades of follow-up. The direction of this effect depends on gender and specific occupation.
Background: We found that a father's overweight in puberty was associated with non-allergic asthma in his future offspring. Aim: We explored the associations of both fathers and their offsprings own weight gain throughout the lifespan with offspring non-allergic asthma. Methods: We analysed questionnaire data from 3018 adult offspring (age 18-50) and their 2153 fathers (age 39-66) participating in the RHINESSA/RHINE generation study in 10 ECRHS centres in North Europe, Spain and Australia. The associations of fathers9 and their offsprings weight gain was assessed by 9 body silhouettes (from lean to fat) self-reported for childhood, puberty and adult ages with non-allergic asthma in the offspring. It was analysed using a logistic regression model adjusted for parents and offspring variables, and cluster by family. Results: Non-allergic asthma was related to a weight gain of ≥2 body silhouettes from 8 years to puberty, both for fathers' weight gain (OR 1.69; 95% CI 1.05-2.72; adjusted for fathers asthma, offspring body mass index, smoking and education) and for their offspring weight gain (1.77 [1.12-2.79], adjusted for parents´ education, smoking and asthma, and fathers´ weight gain from age 8 to puberty). If the father was overweight at puberty, in addition to having gained weight, non-allergic asthma in the offspring was more than tripled (3.53[1.80-6.94]; weight gain and adjustment as given above). No effect of weight gain from puberty or within adulthood in fathers' or their offspring was observed. Conclusion: Non-allergic asthma was associated with weight gain from childhood to puberty. This was found both for personal weight gain and for having a father who gained weight.
Microbial exposures in homes of asthmatic adults have been rarely investigated; specificities and implications for respiratory health are not well understood. The objectives of this study were to investigate associations of microbial levels with asthma status, asthma symptoms, bronchial hyperresponsiveness (BHR), and atopy. Mattress dust samples of 199 asthmatics and 198 control subjects from 7 European countries participating in the European Community Respiratory Health Survey II study were analyzed for fungal and bacterial cell wall components and individual taxa. We observed trends for protective associations of higher levels of mostly bacterial markers. Increased levels of muramic acid, a cell wall component predominant in Gram-positive bacteria, tended to be inversely associated with asthma (OR's for different quartiles: II 0.71 [0.39-1.30], III 0.44 [0.23-0.82], and IV 0.60 [0.31-1.18] P for trend .07) and with asthma score (P for trend .06) and with atopy (P for trend .02). These associations were more pronounced in northern Europe. This study among adults across Europe supports a potential protective effect of Gram-positive bacteria in mattress dust and points out that this may be more pronounced in areas where microbial exposure levels are generally lower.
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