Building dampness and mold in European homes in relation to climate, building characteristics and socio-economic status: The European Community Respiratory Health Survey ECRHS II.

We studied dampness and mold in homes in relation to climate, building characteristics and socio-economic status (SES) across Europe, for 7127 homes in 22 centers. A subsample of 3118 homes was inspected. Multilevel analysis was applied, including age, gender, center, SES, climate, and building factors. Self-reported water damage (10%), damp spots (21%), and mold (16%) in past year were similar as observed data (19% dampness and 14% mold). Ambient temperature was associated with self-reported water damage (OR=1.63 per 10°C; 95% CI 1.02-2.63), damp spots (OR=2.95; 95% CI 1.98-4.39), and mold (OR=2.28; 95% CI 1.04-4.67). Precipitation was associated with water damage (OR=1.12 per 100 mm; 95% CI 1.02-1.23) and damp spots (OR=1.11; 95% CI 1.02-1.20). Ambient relative air humidity was not associated with indoor dampness and mold. Older buildings had more dampness and mold (P<.001). Manual workers reported less water damage (OR=0.69; 95% CI 0.53-0.89) but more mold (OR=1.27; 95% CI 1.03-1.55) as compared to managerial/professional workers. There were correlations between reported and observed data at center level (Spearman rho 0.61 for dampness and 0.73 for mold). In conclusion, high ambient temperature and precipitation and high building age can be risk factors for dampness and mold in homes in Europe.

Transport-related measures to mitigate climate change in Basel, Switzerland: A health-effectiveness comparison study.

BACKGROUND: Local strategies to reduce green-house gases (GHG) imply changes of non-climatic exposure patterns. OBJECTIVE: To assess the health impacts of locally relevant transport-related climate change policies in Basel, Switzerland. METHODS: We modelled change in mortality and morbidity for the year 2020 based on several locally relevant transport scenarios including all decided transport policies up to 2020, additional realistic and hypothesized traffic reductions, as well as ambitious diffusion levels of electric cars. The scenarios were compared to the reference condition in 2010 assumed as status quo. The changes in non-climatic population exposure included ambient air pollution, physical activity, and noise. As secondary outcome, changes in Disability-Adjusted Life Years (DALYs) were put into perspective with predicted changes of CO2 emissions and fuel consumption. RESULTS: Under the scenario that assumed a strict particle emissions standard in diesel cars and all planned transport measures, 3% of premature deaths could be prevented from projected PM2.5 exposure reduction. A traffic reduction scenario assuming more active trips provided only minor added health benefits for any of the changes in exposure considered. A hypothetical strong support to electric vehicles diffusion would have the largest health effectiveness given that the energy production in Basel comes from renewable sources. CONCLUSION: The planned local transport related GHG emission reduction policies in Basel are sensible for mitigating climate change and improving public health. In this context, the most effective policy remains increasing zero-emission vehicles.

Sleep fragmentation and sleep-disordered breathing in individuals living close to main roads: results from a population-based study.

BACKGROUND: Nighttime traffic noise is associated with sleep disturbances, but sleep fragmentation and sleep-disordered breathing (SDB) have not been demonstrated in individuals living near busy roads. METHODS: We asked 1383 participants to answer a health questionnaire and to undergo 24-h electrocardiogram (ECG). Nocturnal ECG records were used to calculate the very low frequency index (VLFI) interval, a surrogate marker of sleep fragmentation. Distances of participants' addresses to roadways were calculated using the VECTOR25© Swisstopo roads classification, a traffic noise proxy. Distances of homes within 100 or 50 m of major roads defined proximity to busy roads. Adjusted multivariate logistic regressions analyzed associations between the distance of home to main roads and VLFI or self-reported SDB. RESULTS: Distance of participants' homes to main roads was significantly associated with the VLFI in women (odds ratio [OR], 1.58 [confidence interval {CI}, 1.03-2.42]; P = .038) but not in men (OR, 1.35 [CI, 0.77-2.35]; P = .295). Women under hormonal replacement therapy (HRT) were at higher risk for increased VLFI when living close to main roads (OR, 2.10 [CI, 1.20-3.68]; P = .01) than untreated women (P = .584). Associations with self-reported SDB were not statistically relevant. CONCLUSIONS: In our large population, women living close to main roads were at significantly higher risk for sleep fragmentation than men. The 2-fold higher risk for menopausal women under HRT underscores the vulnerability of this group.

Interactions between SERPINA1 PiMZ genotype, occupational exposure and lung function decline.

OBJECTIVES: We evaluated interactions between SERPINA1 PiMZ genotype, associated with intermediate α1-antitrysin deficiency, with outdoor particulate matter ≤10 µm (PM10), and occupational exposure to vapours, dusts, gases and fumes (VGDF), and their effects on annual change in lung function. METHODS: Pre-bronchodilator spirometry was performed in 3739 adults of the Swiss Cohort Study on Air Pollution and Lung Disease in Adults (SAPALDIA) for whom SERPINA1 genotypes were available. At baseline in 1991, participants were aged 18-62 years; follow-up measurements were conducted from 2001 to 2003. In linear mixed regression models of annual change in lung function, multiplicative interactions were evaluated between PiMZ genotype (PiMM as reference) and change in PM10 (µg/m(3)), and VGDF exposure (high-level, low-level or no exposure as reference) during follow-up. RESULTS: Annual declines in forced expiratory flow at 25-75% of forced vital capacity (FEF25-75%) (-82 mL/s, 95% CI -125 to -39) and forced expiratory volume in 1 s over forced vital capacity (FEV1/FVC) (-0.3%, 95% CI -0.6% to 0.0%) in association with VGDF exposure were observed only in PiMZ carriers (Pinteraction<0.0001 and Pinteraction=0.03, respectively). A three-way interaction between PiMZ genotype, smoking and VGDF exposure was identified such that VGDF-associated FEF25-75% decline was observed only in ever smoking PiMZ carriers (Pinteraction=0.01). No interactions were identified between PiMZ genotype and outdoor PM10. CONCLUSIONS: SERPINA1 PiMZ genotype, in combination with smoking, modified the association between occupational VGDF exposure and longitudinal change in lung function, suggesting that interactions between these factors are relevant for lung function decline. These novel findings warrant replication in larger studies.

Agreement between spirometers: a challenge in the follow-up of patients and populations?

BACKGROUND: Long-term cohort studies and lung function laboratories are confronted with the need for replacement of spirometers. Lack of agreement between spirometers might affect the longitudinal comparison of data, notably when replacing conventional by portable spirometers. OBJECTIVES: To compare the handheld EasyOne (EO) with the conventional SensorMedics (SM) spirometer, and to analyze the interdevice reproducibility of EO spirometers. METHODS: In total, 82 volunteers completed spirometry sessions with 1 SM and 2 of 3 EO spirometers following a Latin square design. Analyses of differences in forced vital capacity (FVC), forced expiratory flow in 1 s (FEV1), FEV1/FVC and mean forced expiratory flow calculated between 25 and 75% of the FVC between spirometers used a mixed effect model with a random intercept for each subject and the effect of the device as fixed effect adjusted for sex, age, height and order of spirometer tested. Bland-Altman plots show the 95% limits of agreement. RESULTS: Comparisons between EO and SM showed relatively small mean differences of <3%, but systematically lower values for FVC and FEV1 in all EO devices. The 95% agreement exceeded the limits for FEV1 by 50 ml in 2 EO spirometers. The EO interdevice comparisons showed mean differences and limits of agreement within established thresholds, thus indicating fair accuracy when comparing devices. Repeats with the same spirometer did not result in statistically significant differences. CONCLUSIONS: This study suggests fair agreement between the handheld and the conventional spirometer. Differences slightly exceeding limits for FEV1 in 2 EO devices might be considered mostly irrelevant for clinical practice. However, the systematically lower FVC and FEV1 observed with EO may be significant for epidemiological studies, thus justifying inspection before replacing devices.

[What is the role of outdoor air pollution in asthma?]. / Quel est le rôle de la pollution atmosphérique dans l'asthme?

Strong scientific evidence has shown that ordinary peaks of outdoor air pollution worsen the symptoms and control of asthma. As for chronic exposure, elevated mean level of local, near-road air pollution may cause increased incidence of asthma among children, and probably also among adults. By contrast, while there is no doubt that air pollution worsens allergic inflammatory processes, it is not clearly established that it may increase allergic sensitization among the general population. In this regard, more research is needed, particularly on the effects of outdoor air pollution in the early periods of life.

Acute respiratory health effects of urban air pollutants in adults with different patterns of underlying respiratory disease.

OBJECTIVE: Whether underlying chronic respiratory diseases are susceptible factors for symptomatic episodes, which lead to primary-level care, in association with air pollutant exposures is unknown. We evaluated and compared association lag structures between daily ambient levels of nitrogen dioxide (NO(2)) and total suspended particulates (TSP) and respiratory symptom-related doctor visits in adults with different patterns of underlying chronic respiratory disease. METHODS: In a time-stratified case-crossover analysis nested within a diary panel study, 459 Swiss adult participants with asthma, chronic bronchitis, chronic obstructive pulmonary disease (COPD) and healthy participants recorded occurrence of respiratory-symptom related doctor visits (n = 1,048) in one to six four-week intervals over two years. For each disease subgroup, odds ratios (ORs) for doctor visit were estimated as a function of NO(2) or TSP concentrations (per 10 micrograms per cubic meter [µg/m(3)]) lagged between 0-13 days in a polynomial distributed lag model. RESULTS: Higher ORs for NO(2) in participants with COPD (OR: 1.17, 95%CI: 1.02-1.35) and asthma (OR: 1.15, 95%CI: 1.02-1.30) occurred at exposure lags of two and five days, respectively. Doctor visits increased by 9.1% (95%CI: 3.2-15.4%) and 4.2% (95%CI: 1.2-7.2%) over the first week following a 10 µg/m(3) increase in NO(2) concentration in the COPD and chronic bronchitis subgroups, respectively. The percent increase in the COPD subgroup was significantly greater (p <0.05) when compared with the healthy subgroup. Observed findings were similar for TSP. CONCLUSIONS: Respiratory problems leading to a doctor visit, associated with an increase in exposure to NO(2) and TSP, may have a faster dynamic in individuals with COPD.

Determinants of change in airway reactivity over 11 years in the SAPALDIA population study.

We investigated determinants of change in bronchial reactivity in the Swiss Cohort Study on Air Pollution and Lung Diseases in Adults (SAPALDIA), a population-based cohort with wide age range (29-72 yrs at follow-up). The role of sex, age, atopic status, smoking and body mass index (BMI) on percentage change in bronchial reactivity slope from the baseline value was analysed in 3,005 participants with methacholine tests in 1991 and 2002, and complete covariate data. Slope was defined as percentage decline in forced expiratory volume in 1 s from its maximal value per micromole of methacholine. Bronchial hyperreactivity prevalence fell from 14.3 to 12.5% during follow-up. Baseline age was nonlinearly associated with change in reactivity slope: participants aged <50 yrs experienced a decline and those above an increase during follow-up. Atopy was not associated with change, but accentuated the age pattern (p-value for interaction = 0.038). Smoking significantly increased slope by 21.2%, as did weight gain (2.7% increase per BMI unit). Compared with persistent smokers, those who ceased smoking before baseline or during follow-up experienced a significant decrease in slope (-27.7 and -23.9%, respectively). Differing, but not statistically different, age relationships and effect sizes for smoking and BMI between sexes were found. Mean bronchial reactivity increases after 50 yrs of age, possibly due to airway remodelling or ventilation-perfusion disturbances related to cumulative lifetime exposures.

Longitudinal change of prebronchodilator spirometric obstruction and health outcomes: results from the SAPALDIA cohort.

BACKGROUND: Understanding the prognostic meaning of early stages of chronic obstructive pulmonary disease (COPD) in the general population is relevant for discussions about underdiagnosis. To date, COPD prevalence and incidence have often been estimated using prebrochodilation spirometry instead of postbronchodilation spirometry. In the SAPALDIA (Swiss Study on Air Pollution and Lung Disease in Adults) cohort, time course, clinical relevance and determinants of severity stages of obstruction were investigated using prebronchodilator spirometry. METHODS: Incident obstruction was defined as an FEV(1)/FVC (forced expiratory volume in 1 s/forced vital capacity) ratio >or=0.70 at baseline and <0.70 at follow-up, and non-persistence was defined inversely. Determinants were assessed in 5490 adults with spirometry and respiratory symptom data in 1991 and 2002 using Poisson regression controlling for self-declared asthma and wheezing. Change in obstruction severity (defined analogously to the GOLD (Global Initiative for Chronic Obstructive Lung Disease) classification) over 11 years was related to shortness of breath and health service utilisation for respiratory problems by logistic models. RESULTS: The incidence rate of obstruction was 14.2 cases/1000 person years. 20.9% of obstructive cases (n = 113/540) were non-persistent. Age, smoking, chronic bronchitis and non-current asthma were determinants of incidence. After adjustment for asthma, only progressive stage I or persistent stage II obstruction was associated with shortness of breath (OR 1.71, 95% CI 0.83 to 3.54; OR 3.11, 95% CI 1.50 to 6.42, respectively) and health service utilisation for respiratory problems (OR 2.49, 95% CI 1.02 to 6.10; OR 4.17 95% CI 1.91 to 9.13, respectively) at follow-up. CONCLUSIONS: The observed non-persistence of obstruction suggests that prebronchodilation spirometry, as used in epidemiological studies, might misclassify COPD. Future epidemiological studies should consider both prebronchodilation and postbronchodilation measurements and take specific clinical factors related to asthma and COPD into consideration for estimation of disease burden and prediction of health outcomes.

What defines airflow obstruction in asthma?

Asthma guidelines from the Global Initiative for Asthma (GINA) and from the National Heart, Lung, and Blood Institute provide conflicting definitions of airflow obstruction, suggesting a fixed forced expiratory volume in 1 s (FEV(1))/forced vital capacity (FVC) cut-off point and the lower limit of normality (LLN), respectively. The LLN was recommended by the recent American Thoracic Society/European Respiratory Society guidelines on lung function testing. The problem in using fixed cut-off points is that they are set regardless of age and sex in an attempt to simplify diagnosis at the expense of misclassification. The sensitivity and specificity of fixed FEV(1)/FVC ratios of 0.70, 0.75 and 0.80 versus the LLN were evaluated in 815 subjects (aged 20-44 yrs) with a diagnosis of asthma within the framework of the European Community Respiratory Health Survey. In males, the 0.70 ratio showed 76.5% sensitivity and 100.0% specificity, the 0.75 ratio 100.0% sensitivity and 92.4% specificity, and the 0.80 ratio 100.0% sensitivity but 58.1% specificity. In females, the 0.70 ratio showed 57.3% sensitivity and 100.0% specificity, the 0.75 ratio 91.5% sensitivity and 95.9% specificity, and the 0.80 ratio 100.0% sensitivity but 72.9% specificity. The fixed cut-off points cause a lot of misidentification of airflow obstruction in young adults, with overestimation with the 0.80 ratio and underestimation with the 0.70 ratio. In conclusion, the GINA guidelines should change their criteria for defining airflow obstruction.

Size fractionate particulate matter, vehicle traffic, and case-specific daily mortality in Barcelona, Spain.

Recent epidemiological research suggests that short-term effects of particle matter (PM) in urban areas may preferentially be driven by fine fractions. Questions remain concerning the adversehealth effects of coarse particles generated by noncombustion, traffic-related processes and the mechanism of action of PM. Using a time-stratified case-crossover design, we investigated the association between three independent size fractions, coarse (PM10-2.5), intermodal (PM2.5-1), and very fine PMs (PM1), and three health outcomes, respiratory, cardiovascular, and cerebrovascular mortality in Barcelona, Spain, during the period of March 2003-December 2005. Using existing data, we examined the chemical composition of each fraction to explore the effects of PM from different sources and the mechanisms of action. We found that increased levels of PM, and PM10-2.5 were associated with increased levels of cardiovascular and cerebrovascular mortality at lag 1 and lag 2. At lag 1, the odds ratio (OR) for a 1 microg/m3 increase in PM1 was 1.028 [95% confidence interval (CI), 1.000-1.058] for cardiovascular mortality and 1.063 (95% CI, 1.004-1.124) for cerebrovascular mortality. At lag 1, the odds ratio per a 10 microg/ m3 increase of PM10-2.5 was 1.059 (95% CI, 1.026-1.094) for cardiovascular mortality and 1.098 (95% CI, 1.030-1.171) for cerebrovascular mortality. Association with respiratory mortality was only detected for PM2.5-1 at lag 2 (OR, 1.206 per a 10 microg/ m3 increase; 95% CI, 1.028-1.416). Chemical composition data showed that PM in Barcelona was generated in a large proportion by vehicle traffic. Vehicle traffic PM, generated by combustion and noncombustion processes, should be considered in air pollution mitigation strategies in urban areas.

Association between modelled traffic-related air pollution and asthma score in the ECRHS.

The aim of our analysis was to study the association between air pollution and asthma among adults. For this goal, a previously developed "asthma score" was used. Persons aged 25-44 yrs were randomly selected (1991-1993) and followed up (2000-2002) within the European Community Respiratory Health Survey (ECRHS I and II, respectively). The asthma score was defined from 0 to 5, based on the positive answers to the following symptoms reported for the last 12 months: wheeze/breathlessness, chest tightness, dyspnoea at rest, dyspnoea after exercise and woken by dyspnoea. Participants' home addresses were linked to outdoor modelled NO2 estimates for 2001. Negative binomial regression was used to model the asthma score. The score from ECRHS II was positively associated with NO2 (ratio of the mean asthma score (RMS) 1.23, 95% CI 1.09-1.38, for an increase of 10 microg x m(-3)). After excluding participants with asthma and symptoms at baseline, the association remained (RMS 1.25, 95% CI 1.05-1.51), and was particularly high among those reporting a high score in ECRHS II. The latter probably reflects incident cases of asthma. Our results suggest that traffic-related pollution causes asthma symptoms and possibly asthma incidence in adults. The asthma score offers an alternative with which to investigate the course and aetiology of asthma in adults.

Traffic-related air pollution correlates with adult-onset asthma among never-smokers.

BACKGROUND: Traffic-related pollution is associated with the onset of asthma in children. Its effect on adult-onset asthma is poorly investigated. The SAPALDIA cohort study was used to investigate associations between the 11-year change (1991-2002) in home outdoor traffic-related particulate matter up to 10 microm in diameter (TPM(10)) and the incidence of asthma. METHODS: Never-smokers without asthma at baseline aged 18-60 years in 1991 were eligible for inclusion in the study. Subjects reporting doctor-diagnosed asthma at follow-up were considered incident cases. TPM(10) at baseline and follow-up was predicted and interpolated to subjects' place of residence by dispersion models using emission and meteorological data. Cox proportional hazard models for time to asthma onset were adjusted (age, gender, baseline atopy, body mass index, bronchial reactivity, maternal allergies). RESULTS: Of 2725 never-smokers, 41 reported asthma onset in 2002. Home outdoor TPM(10) concentrations improved during the interval (mean -0.6; range -9 to +7.2; IQR 0.6 microg/m(3)). The incidence of asthma was associated with a change in TPM(10). The hazard ratio (1.30; 95% CI 1.05 to 1.61) per 1 microg/m(3) change in TPM(10) (IQR) was not sensitive to further adjustments (education, workplace exposure, passive smoking, parental asthma or allergies, random area effects, lung function or co-pollutants such as regional, secondary, total PM(10) or proximity to busy roads). CONCLUSION: The data suggest a role for traffic-related pollution in adult-onset asthma. Space, time and source-specific individual assignment of exposure to traffic-related pollution is a key strength of SAPALDIA. It may explain why findings were statistically significant despite the limited number of new cases. As traffic-related pollution prevails, the finding may be of substantial public health relevance.

Evidence based public health - the example of air pollution.

Evidence Based Medicine (EBM) has become a common paradigm in medicine. The notion that action should be based on scientific evidence also applies to public health. The assessment of evidence and the application of evidence based action is a challenge both in EBM and public health. The focus of this article is Evidence Based Public Health (EBPH). We use the issue of air pollution related health as an educational example for EBPH.

Air pollution and asthma severity in adults.

BACKGROUND/OBJECTIVES: There is evidence that exposure to air pollution affects asthma, but the effect of air pollution on asthma severity has not been addressed. The aim was to assess the relation between asthma severity during the past 12 months and home outdoor concentrations of air pollution. METHODS: Asthma severity over the past 12 months was assessed in two complementary ways among 328 adult asthmatics from the French Epidemiological study on the Genetics and Environment of Asthma (EGEA) examined between 1991 and 1995. The four-class severity score integrated clinical events and type of treatment. The five-level asthma score is based only on the occurrence of symptoms. Nitrogen dioxide (NO(2)), sulphur dioxide (SO(2)) and ozone (O(3)) concentrations were assigned to each residence using two different methods. The first was based on the closest monitor data from 1991 to 1995. The second consisted of spatial models that used geostatistical interpolations and then assigned air pollutants to the geo-coded residences (1998). RESULTS: Higher asthma severity score was significantly related to the 8-hour average of ozone during April-September (O(3)-8 h) and the number of days (O(3)-days) with 8-hour ozone averages above 110 microg.m(-3) (for a 36-day increase, equivalent to the interquartile range, in O(3)-days, odds ratio 2.22 (95% confidence interval 1.61 to 3.07) for one class difference in score). Adjustment for age, sex, smoking habits, occupational exposure, and educational level did not alter results. Asthma severity was unrelated to NO(2). Both exposure assessment methods and severity scores resulted in very similar findings. SO(2) correlated with severity but reached statistical significance only for the model-based assignment of exposure. CONCLUSIONS: The observed associations between asthma severity and air pollution, in particular O(3), support the hypothesis that air pollution at levels far below current standards increases asthma severity.

Total serum IgE levels are associated with ambient ozone concentration in asthmatic adults.

BACKGROUND: Effects of air pollution exposure on IgE-mediated response in asthmatics are poorly investigated. The aim was to examine the relationship between air pollution concentrations and total IgE levels in adult asthmatics. METHODS: The present study relates to the 369 asthmatic adults from the French Epidemiological study on Genetics and Environment of Asthma (EGEA), with availability of data on both total serum IgE measurements and air pollution concentrations. Geo-statistical models were performed on 4 x 4 km grids to assess individual outdoor air pollution exposure. Annual outdoor concentrations of ozone (O(3)), nitrogen dioxide (NO(2)), sulphur dioxide (SO(2)), and particulate matter smaller than 10 microm size (PM(10)), and concentrations of summer ozone were assigned to subject's home address. RESULTS: The geometric mean of total IgE was 161 IU/ml and the average of O(3) exposure was 44.9 +/- 9.5 microg/m(3). Ozone concentrations were positively related to total IgE levels and an increase of 10 microg/m(3) of O(3) resulted in an increase of 20.4% (95% CI = 3.0-40.7) in total IgE levels. Adjustment for age, gender, smoking habits and previous life in the countryside did not change the results, and an increase of 19.1% (2.4-38.6) in total IgE was observed with O(3). Negative associations observed between NO(2) and total IgE levels disappeared after including O(3) in the models. Neither SO(2) nor PM(10) were correlated with total IgE levels. CONCLUSIONS: Results suggest that O(3) or related ambient pollutants may up-regulate total IgE levels among asthmatic adults.