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Mechanistic research suggests that lifestyle and environmental factors impact respiratory health across generations by epigenetic changes transmitted through male germ cells. Evidence from studies on humans is very limited.We investigated multigeneration causal associations to estimate the causal effects of tobacco smoking on lung function within the paternal line. We analysed data from 383 adult offspring (age 18-47 years; 52.0% female) and their 274 fathers, who had participated in the European Community Respiratory Health Survey (ECRHS)/Respiratory Health in Northern Europe, Spain and Australia (RHINESSA) generation study and had provided valid measures of pre-bronchodilator lung function. Two counterfactual-based, multilevel mediation models were developed with: paternal grandmothers' smoking in pregnancy and fathers' smoking initiation in prepuberty as exposures; fathers' forced expiratory volume in 1 s (FEV 1 ) and forced vital capacity (FVC), or FEV 1 /FVC z-scores as potential mediators (proxies of unobserved biological mechanisms that are true mediators); and offspring's FEV 1 and FVC, or FEV 1 /FVC z-scores as outcomes. All effects were summarised as differences (Δ) in expected z-scores related to fathers' and grandmothers' smoking history.Fathers' smoking initiation in prepuberty had a negative direct effect on both offspring's FEV 1 (Δz-score -0.36, 95% CI -0.63- -0.10) and FVC (-0.50, 95% CI -0.80- -0.20) compared with fathers' never smoking. Paternal grandmothers' smoking in pregnancy had a negative direct effect on fathers' FEV 1 /FVC (-0.57, 95% CI -1.09- -0.05) and a negative indirect effect on offspring's FEV 1 /FVC (-0.12, 95% CI -0.21- -0.03) compared with grandmothers' not smoking before fathers' birth nor during fathers' childhood.Fathers' smoking in prepuberty and paternal grandmothers' smoking in pregnancy may cause lower lung function in offspring. Our results support the concept that lifestyle-related exposures during these susceptibility periods influence the health of future generations., Competing Interests: Conflict of interest: S. Accordini has nothing to disclose. Conflict of interest: L. Calciano has nothing to disclose. Conflict of interest: A. Johannessen has nothing to disclose. Conflict of interest: B. Benediktsdóttir has nothing to disclose. Conflict of interest: R.J. Bertelsen has nothing to disclose. Conflict of interest: L. Bråbäck has nothing to disclose. Conflict of interest: S.C. Dharmage has nothing to disclose. Conflict of interest: B. Forsberg has nothing to disclose. Conflict of interest: F. Gómez Real has nothing to disclose. Conflict of interest: J.W. Holloway reports grants from the European Union's Horizon 2020 research and innovation programme, and from the Research Council of Norway, during the conduct of the study. Conflict of interest: M. Holm has nothing to disclose. Conflict of interest: C. Janson has nothing to disclose. Conflict of interest: N.O. Jõgi has nothing to disclose. Conflict of interest: R. Jõgi reports grants from the Estonian Research Council (personal research grant number 562), during the conduct of the study; personal fees for consultancy and lectures from GSK, Boehringer and Novartis, personal fees for travel/accommodation/meeting expenses from GSK and Boehringer, outside the submitted work. Conflict of interest: A. Malinovschi has nothing to disclose. Conflict of interest: A. Marcon has nothing to disclose. Conflict of interest: J. Martínez-Moratalla Rovira has nothing to disclose. Conflict of interest: J.L. Sánchez-Ramos has nothing to disclose. Conflict of interest: V. Schlünssen has nothing to disclose. Conflict of interest: K. Torén has nothing to disclose. Conflict of interest: D. Jarvis reports grants from the European Union, during the conduct of the study. Conflict of interest: C. Svanes has nothing to disclose., (Copyright ©The authors 2021.)

We investigated the prevalence of chronic cough and its association with work ability and sick leave in the general population.Data were analysed from the Respiratory Health In Northern Europe (RHINE) III cohort (n=13 500), of which 11 252 participants had also participated in RHINE II 10 years earlier, a multicentre study in Northern Europe. Participants answered a questionnaire on chronic cough, employment factors, smoking and respiratory comorbidities.Nonproductive chronic cough was found in 7% and productive chronic cough in 9% of the participants. Participants with nonproductive cough were more often female and participants with productive cough were more often smokers and had a higher body mass index (BMI) than those without cough. Participants with chronic cough more often reported >7 days of sick leave in the preceding year than those without cough ("nonproductive cough" 21% and "productive cough" 24%; p<0.001 for comparisons with "no cough" 13%). This pattern was consistent after adjusting for age, sex, BMI, education level, smoking status and comorbidities. Participants with chronic cough at baseline reported lower work ability and more often had >7 days of sick leave at follow-up than those without cough. These associations remained significant after adjusting for cough at follow-up and other confounding factors.Chronic cough was found in around one in six participants and was associated with more sick leave. Chronic cough 10 years earlier was associated with lower work ability and sick leave at follow-up. These associations were not explained by studied comorbidities. This indication of negative effects on employment from chronic cough needs to be recognised., Competing Interests: Conflict of interest: A. Johannessen has nothing to disclose. Conflict of interest: M. Holm has nothing to disclose. Conflict of interest: B. Forsberg has nothing to disclose. Conflict of interest: V. Schlünssen has nothing to disclose. Conflict of interest: R. Jõgi has nothing to disclose. Conflict of interest: M. Clausen has nothing to disclose. Conflict of interest: E. Lindberg has nothing to disclose. Conflict of interest: A. Malinovschi has nothing to disclose. Conflict of interest: Ö.I. Emilsson has nothing to disclose. Conflict of interest: H. Johansson has nothing to disclose., (Copyright ©ERS 2021.)

Both protective and adverse effects of indoor microbial exposure on asthma have been reported, but mostly in children. To date, no study in adults has used non-targeted methods for detection of indoor bacteria followed by quantitative confirmation.A cross-sectional study of 198 asthmatic and 199 controls was conducted within the European Community Respiratory Health Survey (ECRHS) II. DNA was extracted from mattress dust for bacterial analysis using denaturing gradient gel electrophoresis (DGGE). Selected bands were sequenced and associations with asthma confirmed with four quantitative PCR (qPCR) assays.15 out of 37 bands detected with DGGE, which had at least a suggestive association (p<0.25) with asthma, were sequenced. Of the four targeted qPCRs, Clostridium cluster XI confirmed the protective association with asthma. The association was dose dependent (aOR 0.43 (95% CI 0.22-0.84) for the fourth versus first quartile, p for trend 0.009) and independent of other microbial markers. Few significant associations were observed for the three other qPCRs used.In this large international study, the level of Clostridium cluster XI was independently associated with a lower risk of prevalent asthma. Results suggest the importance of environmental bacteria also in adult asthma, but need to be confirmed in future studies., Competing Interests: Conflict of interest: Disclosures can be found alongside this article at erj.ersjournals.com, (Copyright ©ERS 2018.)

Activity-related breathlessness is twice as common among females as males in the general population and is associated with adverse health outcomes. We tested whether this sex difference is explained by the lower absolute forced expiratory volume in 1 s (FEV 1 ) or forced vital capacity (FVC) in females.This was a cross-sectional analysis of 3250 subjects (51% female) aged 38-67 years across 13 countries in the population-based third European Community Respiratory Health Survey. Activity-related breathlessness was measured using the modified Medical Research Council (mMRC) scale. Associations with mMRC were analysed using ordered logistic regression clustering on centre, adjusting for post-bronchodilator spirometry, body mass index, pack-years smoking, cardiopulmonary diseases, depression and level of exercise.Activity-related breathlessness (mMRC ≥1) was twice as common in females (27%) as in males (14%) (odds ratio (OR) 2.21, 95% CI 1.79-2.72). The sex difference was not reduced when controlling for FEV 1 % predicted (OR 2.33), but disappeared when controlling for absolute FEV 1 (OR 0.89, 95% CI 0.69-1.14). Absolute FEV 1 explained 98-100% of the sex difference adjusting for confounders. The effect was similar within males and females, when using FVC instead of FEV 1 and in healthy never-smokers.The markedly more severe activity-related breathlessness among females in the general population is explained by their smaller spirometric lung volumes., Competing Interests: Conflict of interest: Disclosures can be found alongside this article at erj.ersjournals.com, (Copyright ©ERS 2017.)

The American Thoracic Society has previously published statements on what constitutes an adverse effect on health of air pollution in 1985 and 2000. We set out to update and broaden these past statements that focused primarily on effects on the respiratory system. Since then, many studies have documented effects of air pollution on other organ systems, such as on the cardiovascular and central nervous systems. In addition, many new biomarkers of effects have been developed and applied in air pollution studies.This current report seeks to integrate the latest science into a general framework for interpreting the adversity of the human health effects of air pollution. Rather than trying to provide a catalogue of what is and what is not an adverse effect of air pollution, we propose a set of considerations that can be applied in forming judgments of the adversity of not only currently documented, but also emerging and future effects of air pollution on human health. These considerations are illustrated by the inclusion of examples for different types of health effects of air pollution., (Copyright ©ERS 2017.)

Climate change policies have stimulated a shift towards renewable energy sources such as biomass. The economic crisis of 2008 has also increased the practice of household biomass burning as it is often cheaper than using oil, gas or electricity for heating. As a result, household biomass combustion is becoming an important source of air pollutants in the European Union.This position paper discusses the contribution of biomass combustion to pollution levels in Europe, and the emerging evidence on the adverse health effects of biomass combustion products.Epidemiological studies in the developed world have documented associations between indoor and outdoor exposure to biomass combustion products and a range of adverse health effects. A conservative estimate of the current contribution of biomass smoke to premature mortality in Europe amounts to at least 40 000 deaths per year.We conclude that emissions from current biomass combustion products negatively affect respiratory and, possibly, cardiovascular health in Europe. Biomass combustion emissions, in contrast to emissions from most other sources of air pollution, are increasing. More needs to be done to further document the health effects of biomass combustion in Europe, and to reduce emissions of harmful biomass combustion products to protect public health., (Copyright ©ERS 2015.)

Welding-related asthma is well recognised but less is known about rhinitis in relation to welding. The aim here, was to study associations between welding, rhinitis and asthma in a general population sample, and factors influencing selection into and out of a welding occupation.Adult-onset asthma and non-infectious rhinitis were investigated in the international multicentre population-based Respiratory Health in Northern Europe (RHINE) study, including 16,191 responders aged 26-54 years. Ever welding (n=2181), welding >25% of working time (n=747), and welding in stainless steel >6 months (n=173) were assessed by questionnaire. Subjects with rhinitis or asthma onset when aged <18 years were excluded. Incidence rates for asthma and rhinitis were calculated from year of disease onset, and start and end of welding job. Cox's proportional hazard models adjusting for age, sex, parental education and study centre, and Kaplan-Meier curves were used.Rhinitis incidence was higher among welders (hazard ratio (HR) 1.4, 95% CI 1.3-1.6), consistent in men and women, and across centres (pheterogeneity=0.4). In men, asthma incidence was higher among welders (HR 1.4, 95% CI 1.04-1.97). Quitting welding was indicated higher after adult-onset rhinitis (HR 1.1, 95% CI 1.0-1.3). Adult-onset rhinitis and asthma was higher among welders, consistent across population samples from Northern Europe. No pre-employment selection was found, whereas selection out of welding jobs was suggested., (Copyright ©ERS 2015.)

The chronic impact of ambient air pollutants on lung function in adults is not fully understood. The objective of this study was to investigate the association of long-term exposure to ambient air pollution with lung function in adult participants from five cohorts in the European Study of Cohorts for Air Pollution Effects (ESCAPE). Residential exposure to nitrogen oxides (NO₂, NOx) and particulate matter (PM) was modelled and traffic indicators were assessed in a standardised manner. The spirometric parameters forced expiratory volume in 1 s (FEV₁) and forced vital capacity (FVC) from 7613 subjects were considered as outcomes. Cohort-specific results were combined using meta-analysis. We did not observe an association of air pollution with longitudinal change in lung function, but we observed that a 10 μg·m(-3) increase in NO₂ exposure was associated with lower levels of FEV₁ (-14.0 mL, 95% CI -25.8 to -2.1) and FVC (-14.9 mL, 95% CI -28.7 to -1.1). An increase of 10 μg·m(-3) in PM10, but not other PM metrics (PM2.5, coarse fraction of PM, PM absorbance), was associated with a lower level of FEV₁ (-44.6 mL, 95% CI -85.4 to -3.8) and FVC (-59.0 mL, 95% CI -112.3 to -5.6). The associations were particularly strong in obese persons. This study adds to the evidence for an adverse association of ambient air pollution with lung function in adults at very low levels in Europe., (Copyright ©ERS 2015.)

The role of air pollution in chronic obstructive pulmonary disease (COPD) remains uncertain. The aim was to assess the impact of chronic exposure to air pollution on COPD in four cohorts using the standardised ESCAPE exposure estimates. Annual average particulate matter (PM), nitrogen oxides (NOx) and road traffic exposure were assigned to home addresses using land-use regression models. COPD was defined by NHANES reference equation (forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) less than the lower limit of normal) and the Global Initiative for Chronic Obstructive Lung Disease criterion (FEV1/FVC <0.70) and categorised by severity in non-asthmatics. We included 6550 subjects with assigned NOx and 3692 with PM measures. COPD was not associated with NO2 or PM10 in any individual cohort. In meta-analyses only NO2, NOx, PM10 and the traffic indicators were positively, although not significantly, associated with COPD. The only statistically significant associations were seen in females (COPD prevalence using GOLD: OR 1.57, 95% CI 1.11-2.23; and incidence: OR 1.79, 95% CI 1.21-2.68). None of the principal results were statistically significant, the weak positive associations of exposure with COPD and the significant subgroup findings need to be evaluated in further well standardised cohorts followed up for longer time, and with time-matched exposure assignments., (©ERS 2014.)

Recent epidemiological research suggests that near road traffic-related pollution may cause chronic disease, as well as exacerbation of related pathologies, implying that the entire "chronic disease progression" should be attributed to air pollution, no matter what the proximate cause was. We estimated the burden of childhood asthma attributable to air pollution in 10 European cities by calculating the number of cases of 1) asthma caused by near road traffic-related pollution, and 2) acute asthma events related to urban air pollution levels. We then expanded our approach to include coronary heart diseases in adults. Derivation of attributable cases required combining concentration-response function between exposures and the respective health outcome of interest (obtained from published literature), an estimate of the distribution of selected exposures in the target population, and information about the frequency of the assessed morbidities. Exposure to roads with high vehicle traffic, a proxy for near road traffic-related pollution, accounted for 14% of all asthma cases. When a causal relationship between near road traffic-related pollution and asthma is assumed, 15% of all episodes of asthma symptoms were attributable to air pollution. Without this assumption, only 2% of asthma symptoms were attributable to air pollution. Similar patterns were found for coronary heart diseases in older adults. Pollutants along busy roads are responsible for a large and preventable share of chronic disease and related acute exacerbations in European urban areas.

Ozone is a highly oxidative pollutant formed from precursors in the presence of sunlight, associated with respiratory morbidity and mortality. All else being equal, concentrations of ground-level ozone are expected to increase due to climate change. Ozone-related health impacts under a changing climate are projected using emission scenarios, models and epidemiological data. European ozone concentrations are modelled with the model of atmospheric transport and chemistry (MATCH)-RCA3 (50×50 km). Projections from two climate models, ECHAM4 and HadCM3, are applied under greenhouse gas emission scenarios A2 and A1B, respectively. We applied a European-wide exposure-response function to gridded population data and country-specific baseline mortality and morbidity. Comparing the current situation (1990-2009) with the baseline period (1961-1990), the largest increase in ozone-associated mortality and morbidity due to climate change (4-5%) have occurred in Belgium, Ireland, the Netherlands and the UK. Comparing the baseline period and the future periods (2021-2050 and 2041-2060), much larger increases in ozone-related mortality and morbidity are projected for Belgium, France, Spain and Portugal, with the impact being stronger using the climate projection from ECHAM4 (A2). However, in Nordic and Baltic countries the same magnitude of decrease is projected. The current study suggests that projected effects of climate change on ozone concentrations could differentially influence mortality and morbidity across Europe.

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.

Climate change will affect individuals with pre-existing respiratory disease, but the extent of the effect remains unclear. The present position statement was developed on behalf of the European Respiratory Society in order to identify areas of concern arising from climate change for individuals with respiratory disease, healthcare workers in the respiratory sector and policy makers. The statement was developed following a 2-day workshop held in Leuven (Belgium) in March 2008. Key areas of concern for the respiratory community arising from climate change are discussed and recommendations made to address gaps in knowledge. The most important recommendation was the development of more accurate predictive models for predicting the impact of climate change on respiratory health. Respiratory healthcare workers also have an advocatory role in persuading governments and the European Union to maintain awareness and appropriate actions with respect to climate change, and these areas are also discussed in the position statement.

Few studies have investigated the relationship between vehicle exhaust and the new onset of asthma among adults. The aim of the present prospective cohort study was to investigate the relationship between the cumulative incidence of asthma and onset of asthma among adults and vehicle exhaust concentrations at home. Participants from three Swedish cities included in the Respiratory Health in Northern Europe cohort constituted the study population. Exposure at each participant's home was calculated using dispersion models. We also used <50 m distance to nearest major road as a more simple indicator of exposure. The adjusted model included 3,609 participants, of which 107 were classified as onset cases and 55 as true incident cases of asthma. There was a positive association between asthma onset (odds ratio (OR) per 10 microg x m(-3) 1.46, 95% confidence interval (CI) 1.07-1.99) and incident asthma (OR per 10 microg x m(-3) 1.54, 95% CI 1.00-2.36) and the levels of nitrogen dioxide (NO(2)), which remained statistically significant after adjusting for potential confounders. The relationship between asthma and NO(2) was not significantly modified by sex, hay fever or wheeze. The risk of developing asthma was also significantly related to living close to a major road. The current study suggests that elevated levels of vehicle exhaust outside the home increase the risk of onset and incident asthma among adults.

The present study aimed to investigate how the heat-related increase in deaths in summer and the extent of mortality displacement depend on influenza and other categories of mortality in the previous winter, which when low leaves a greater pool of susceptible individuals. Mortality data from Stockholm, Sweden, from 1990-2002 were stratified into a summer period and a winter period. A Poisson regression model was established for the daily mortality in the summer, with temperature and confounders as explanatory variables. In addition, indicators of total, respiratory, cardiovascular and influenza mortality of the winter period were incorporated as effect modifiers in the summer model, and lagged effects in strata defined by indicators were studied. A high rate of respiratory as well as cardiovascular mortality in winter reduced the heat effect the following summer, and influenza mortality tended to do so as well. The cumulative effect per degrees C increase was 0.79% below and 0.88% [corrected] above a threshold (21.3 degrees C) after a winter with low cardiovascular and respiratory mortality, but modified with -0.29% [corrected] below and -0.04% [corrected] above the threshold after a winter with high cardiovascular and respiratory mortality. The current study shows that high respiratory, cardiovascular and influenza mortality in winter leads to lower temperature effects in the following summer. It also suggests that persons for whom influenza may be fatal are often also susceptible to heat and this subgroup might, therefore, not benefit as much as expected from influenza vaccinations.

The objective of this case-control study was to evaluate whether traffic-related air pollution exposure at home increases the risk of asthma in adults and to compare two commonly used exposure variables and differences between urban and rural living. Incident cases of asthma and matched controls of subjects aged 20-60 yrs were recruited in Luleå, Sweden. In total 203 cases and 203 controls were enrolled in the study. Exposure was estimated by traffic flow and measured levels of outdoor nitrogen dioxide (NO2) in the surrounding environment of each home, respectively. The relationship between measured levels of NO2 and traffic flow was studied using linear regression. The results indicated a nonsignificant tendency between living in a home close to a high traffic flow and an increased risk of asthma. The association between asthma and measured NO2 was weak and not significant, but the skin-prick test result acted as an effect modifier with a borderline significant association among positives. The correlation between traffic flow and outdoor NO2 was low. The results suggest that living close to high traffic flows might increase the asthma incidence in adults, while the tendency for nitrogen dioxide was only seen among atopics. Traffic flow and nitrogen dioxide had a lower than expected correlation.

The short-term effects of nitrogen dioxide (NO(2)) on total, cardiovascular and respiratory mortality in 30 European cities participating in the Air Pollution on Health: a European Approach (APHEA)-2 project were investigated. The association was examined using hierarchical models implemented in two stages. In the first stage, data from each city were analysed separately, whereas in the second stage, the city-specific air pollution estimates were regressed on city-specific covariates to obtain overall estimates and to explore sources of possible heterogeneity. A significant association of NO(2) with total, cardiovascular and respiratory mortality was found, with stronger effects on cause-specific mortality. There was evidence of confounding in respiratory mortality with black smoke and sulphur dioxide. The effect of NO(2) on total and cardiovascular mortality was observed mainly in western and southern European cities, and was larger when smoking prevalence was lower and household gas consumption was higher. The effect of NO(2) on respiratory mortality was higher in cities with a larger proportion of elderly persons in the population and higher levels of particulate matter with a 50% cut-off aerodynamic diameter of 10 mum. The results of this large study are consistent with an independent effect of nitrogen dioxide on mortality, but the role of nitrogen dioxide as a surrogate of other unmeasured pollutants cannot be completely ruled out.

Studies on health effects of airborne particulate matter (PM) have traditionally focused on particles <10 microm in diameter (PM10) or particles <2.5 microm in diameter (PM2.5). The coarse fraction of PM10, particles >2.5 microm, has only been studied recently. These particles have different sources and composition compared with PM2.5. This paper is based on a systematic review of studies that have analysed fine and coarse PM jointly and examines the epidemiological evidence for effects of coarse particles on health. Time series studies relating ambient PM to mortality have in some places provided evidence of an independent effect of coarse PM on daily mortality, but in most urban areas, the evidence is stronger for fine particles. The few long-term studies of effects of coarse PM on survival do not provide any evidence of association. In studies of chronic obstructive pulmonary disease, asthma and respiratory admissions, coarse PM has a stronger or as strong short-term effect as fine PM, suggesting that coarse PM may lead to adverse responses in the lungs triggering processes leading to hospital admissions. There is also support for an association between coarse PM and cardiovascular admissions. It is concluded that special consideration should be given to studying and regulating coarse particles separately from fine particles.

The annual incidence of asthma in adults in northern Sweden has been estimated at 2.3 per thousand population. Risk factors for incident asthma among adults were studied in a case-referent study based on incident cases of asthma during 1995-1999. The healthcare providers reported suspected cases of incident asthma. After clinical examination, 309 (65% female) of 473 reported subjects were included. Inclusion criteria were a history of incident asthma (onset <12 months) and verified bronchial variability. Referents were randomly selected and stratified by age, sex and area of residence. The significant risk factors were hay fever, a family history of asthma, ex-smoking status and elevated body mass index (25.0-29.9 and > or =30). The risk factor pattern was similar for females and males, and increased body mass index was a significant risk factor for both males and females, as well as for allergic and nonallergic subjects. In conclusion, in addition to hay fever, a family history of asthma, allergic sensitisation and ex-smoking status, increased body mass index was a significant risk factor for incident asthma independent of sex and allergic status.

The objective of this longitudinal study was to estimate the incidence rate of asthma, and to compare the incidence between subjects with or without baseline reporting of certain respiratory symptoms. A follow-up of the random population samples in the European Respiratory Health Survey (ECRHS) in Sweden, Norway, Denmark, Iceland and Estonia was conducted in 1999-2001, in a population aged 30-54 yrs at follow-up (n=14,731). Asthma was defined as reporting either asthma or physician-diagnosed asthma, and a reported year when asthma symptoms were first noticed. Incidence rates, incidence rate ratios and hazard ratios were calculated with 95% confidence intervals. The incidence rate of asthma was 2.2 cases per 1,000 person-yrs. The incidence was higher among females (2.9 cases.1,000 person-yrs(-1)) than among males (1.5 cases.1,000 person-yrs(-1)). When subjects with baseline reporting of wheezing were excluded, the incidence rate decreased to 1.7 cases.1,000 person-yrs(-1), with a further decrease to 1.5 cases.1,000 person-yrs(-1) after exclusion of subjects with wheezing, nocturnal dyspnoea, chest tightness and cough. There was a strong association between onset of asthma and wheezing at baseline. In this prospective, population-based study, the incidence rate of asthma in the whole population sample ranged 1.5-2.2.1,000 person-yrs(-1), with a higher incidence range among females. The incidence was dependent on the extent to which subjects with respiratory symptoms were excluded from follow-up. Hence, for comparability between studies, the exclusion criteria in the follow-up population must be stated.

Several studies have identified obesity as a risk factor for asthma in both children and adults. An increased prevalence of asthma in subjects with gastro-oesophageal reflux (GOR) and obstructive sleep apnoea syndrome has also been reported. The aim of this investigation was to study obesity, nocturnal GOR and snoring as independent risk factors for onset of asthma and respiratory symptoms in a Nordic population. In a 5-10 yr follow-up study of the European Community Respiratory Health Survey in Iceland, Norway, Denmark, Sweden and Estonia, a postal questionnaire was sent to previous respondents. A total of 16,191 participants responded to the questionnaire. Reported onset of asthma, wheeze and night-time symptoms as well as nocturnal GOR and habitual snoring increased in prevalence along with the increase in body mass index (BMI). After adjusting for nocturnal GOR, habitual snoring and other confounders, obesity (BMI >30) remained significantly related to the onset of asthma, wheeze and night-time symptoms. Nocturnal GOR was independently related to the onset of asthma and in addition, both nocturnal GOR and habitual snoring were independently related to onset of wheeze and night-time symptoms. This study adds evidence to an independent relationship between obesity, nocturnal gastro-oesophageal reflux and habitual snoring and the onset of asthma and respiratory symptoms in adults.

Exposure to ozone (O3) impairs lung function, induces airway inflammation and alters epithelial permeability. Whilst impaired lung function and neutrophilia have been observed at relatively low concentrations, altered lung epithelial permeability is only seen after high-dose challenges. The appearance of Clara cell protein (CC16) in serum has been proposed as a sensitive marker of lung epithelial injury. Here, the use of CC16 as an injury biomarker was evaluated under a controlled exposure to O3 and the relationship between this marker of lung injury and early lung function decrements was investigated. Subjects (n=22) were exposed on two separate occasions to 0.2 parts per million O3 and filtered air for 2 h. Blood samples were drawn and lung function assessed at 2 h pre-exposure, immediately before and immediately after exposure as well as 2 and 4 h postexposure. O3 increased CC16 serum concentrations at 2 h (12.0+/-4.5 versus 8.4+/-3.1 microg x L(-1)) and 4 h postexposure (11.7+/-5.0 versus 7.9+/-2.6 microg x L(-1)) compared with air concentrations. Archived samples from O3 studies utilising the same design indicated that this increase was sustained for up to 6 h postexposure (9.1+/-2.6 versus 7.1+/-1.7 microg x L(-1)) with concentrations returning to baseline by 18 h (7.7+/-2.9 versus 6.6+/-1.7 microg x L(-1)). In these studies, the increased plasma CC16 concentration was noted in the absence of increases in traditional markers of epithelial permeability. No association was observed between increased CC16 concentrations and lung function changes. To conclude, Clara cell protein represents a sensitive and noninvasive biomarker for ozone-induced lung epithelial damage that may have important uses in assessing the health effects of air pollutants in future epidemiological and field studies.

The ability of particles with a 50% cut-off aerodynamic diameter of 10 microm (PM10) to cause respiratory health effects possibly depends on their composition. This study evaluated whether the soluble elemental concentrations in PM10 were related to acute respiratory health effects. The Pollution Effects on Asthmatic Children in Europe (PEACE) study is a multicentre study of the acute effects of PM10 and other air pollution components on the respiratory health of children with chronic respiratory symptoms in urban and suburban panels. Children, 1208, divided among 17 panels were followed for > or =2 months. Exposure to air pollution was monitored on a daily basis. Health status was monitored by twice daily peak expiratory flow (PEF) measurements and a symptom diary. Median concentrations of iron ranged 105-1,110 ng x m(-3) in the urban and 32-517 ng x m(-3) in the suburban locations. The daily concentrations of most elements were not associated with daily variation in PEF, prevalence of respiratory symptoms or bronchodilator use. Silicon and iron concentrations tended to be negatively associated with PEF, and positively associated with the prevalence of phlegm. In two pollutant models, PM10 effect-estimates on phlegm prevalence were reduced and lost significance, whereas the effect-estimates of iron or silicon remained essentially unchanged. The effects of silicon and iron could not be separated. In conclusion, this study provides only weak support for the hypothesis that daily fluctuations in soluble elemental concentrations in ambient particulate matter are responsible for acute health effects.

This study aimed to investigate the association between daily air pollution levels and the occurrence of acute respiratory signs and symptoms among people with asthma or asthma-like problems. Thirty eight subjects in the southern Swedish city of Landskrona kept a daily diary for 10 weeks. The daily prevalence of symptoms, supplementary bronchodilator use and peak flow deviations were compared with measurements of environmental nitrogen dioxide (NO2), sulphur dioxide, temperature and humidity in the city. The occurrence of severe asthma, both during the day and during the evening, was significantly positively associated with the concurrent 24 h average concentration of NO2, which never exceeded 72 microg x m(-3). A correlation of borderline significance was found between the use of on-demand medication and the NO2 level. However, peak flow deviations were not associated with air pollution or weather conditions, which may be explained by the beneficial effect of bronchodilators used by 28 of the subjects. The results of this study confirm those of some earlier studies and suggest that aggravation of asthma is related to daily variations in air quality, as indicated by relatively low ambient concentrations of nitrogen dioxide. These results also indicate that it may be appropriate to examine severe asthma symptoms separately.

We wanted to assess relations between the daily occurrence of asthma symptoms and fluctuations of air pollution concentrations and meteorological conditions. In a panel of 31 asthmatic patients residing in the town of Piteå in northern Sweden, severe symptoms of shortness of breath, wheeze, cough and phlegm were recorded in an asthma diary together with suspected causes. Sulphur dioxide, nitrogen dioxide, black smoke, relative humidity and temperature were used to evaluate the relationship to the environment. By using multivariate analyses, we found that daily variations in the particulate pollution levels, indicated by black smoke levels below the criteria limits, had significant effects on the risk of developing severe symptoms of shortness of breath. This association was stronger among 10 subjects, who had at least five incident days with severe shortness of breath. Meteorological conditions were not significant in the multivariate models. Cough and phlegm did not show significant relationships to any environmental condition that was evaluated. Only one-third of the subjects reported, at least once during the study, symptoms believed to be related to air pollutants, although we found significant correlations between the pollution levels and the frequency of pollution-related symptoms. We conclude that an association has been established for black smoke as pollutant and shortness of breath as respiratory symptom, and that in certain asthmatics, effects were occurring at lower particulate levels than suggested previously.