Relationship of outdoor air quality to pediatric asthma exacerbations.

BACKGROUND: Although exposure to outdoor air pollutants has been shown to be associated with exacerbations of asthma, there are relatively few admissions for asthma to Cincinnati Children's Hospital, Cincinnati, OH during the summer months when air quality tends to be worst. OBJECTIVE: The objective of this study was to determine the relationship of outdoor air quality parameters to asthma exacerbations in children. METHODS: The number of emergency room visits and hospitalizations for asthma were determined by review of emergency department logs and the hospital computer database. Outdoor air concentrations of ozone, particulates of < 10 microm diameter (PM-10), pollens, and fungal spores were obtained from the Hamilton County Department of Environmental Services. Multiple regression analysis was performed, looking for relationships between the daily number of asthma visits and the air quality data for the same day and for 1 through 5 days before the visits. RESULTS: A significant association was found between the number of asthma visits and the daily pollen count (P = 0.014, SE = 0.001). The effect was stronger for visits 1, 2, and 3 days after the pollen count (P < 0.001 for pollen count lagged 3 days). High PM-10 counts were synergistic with the pollen count as a predictor of asthma visits. There was no association between asthma visits and the ozone concentration or fungal spore count. CONCLUSIONS: Exacerbations of asthma severe enough to require visits to the hospital were associated with elevated concentrations of airborne pollens and particulates, with a significant delayed effect. Ozone, in the concentrations measured here, was not a risk factor for severe asthma exacerbations in children.     

Roles of pollution in the prevalence and exacerbations of allergic diseases in Asia

The prevalence of asthma and allergic diseases has been found to be increasingly rapidly, especially in developing countries. Environmental factors have been found to be important contributors to the manifestations of allergic diseases. Air pollution has been extensively studied in different regions of the world. The levels of ambient air pollutants in many Asian countries are very high when compared with those in developed Western countries. However, the prevalence of asthma was relatively low across many Asian countries. Many studies have clearly documented that environmental air pollution is an important factor resulting in exacerbations of asthma. In particular, levels of traffic-related pollutants are increasing rapidly across many Asian countries in parallel with the level of urbanization and economic development. The loss of protective factors associated with a rural environment will further contribute to the adverse effect on patients with allergic diseases such as asthma. In this review the roles of air pollution were examined in relation to the inception and exacerbations of allergic diseases in Asia.     

GSTP1 is a hub gene for gene–air pollution interactions on childhood asthma

There is growing evidence that multiple genes and air pollutants are associated with asthma. By identifying the effect of air pollution on the general population, the effects of air pollution on childhood asthma can be better understood. We conducted the Taiwan Children Health Study (TCHS) to investigate the influence of gene–air pollution interactions on childhood asthma. Complete monitoring data for the ambient air pollutants were collected from Taiwan Environmental Protection Agency air monitoring stations. Our results show a significant two‐way gene–air pollution interaction between glutathione S‐transferase P (GSTP1) and PM₁₀ on the risk of childhood asthma. Interactions between GSTP1 and different types of air pollutants have a higher information gain than other gene–air pollutant combinations. Our study suggests that interaction between GSTP1 and PM₁₀ is the most influential gene–air pollution interaction model on childhood asthma. The different types of air pollution combined with the GSTP1 gene may alter the susceptibility to childhood asthma. It implies that GSTP1 is an important hub gene in the anti‐oxidative pathway that buffers the harmful effects of air pollution.     

Temporal relationship between air pollution and hospital admissions for asthmatic children in Hong Kong

BACKGROUND: Many epidemiological studies have shown positive association between respiratory health and current levels of outdoor air pollution in Europe and America. OBJECTIVE: The aim of this study was to investigate the association between air pollution and the number of childhood admissions for asthma in Hong Kong. METHODS: Daily counts of childhood admission for asthma to a large teaching Hospital were obtained from the computerized database for the period 1993-1994. A Poisson regression allowing for seasonal patterns and meteorological conditions was used to assess the associations between the number of Hospital admissions and the three pollutants: nitrogen dioxide, sulphur dioxide and inhalable particles (measured as PM10, particles < 10 microm in aerodynamic diameter). RESULTS: A total of 1217 children under 15 years of age were admitted for asthma during the study period. The calculated annual hospitalization rates were 283 and 178 per 100 000 for boys and girls, respectively. The mean PM10, NO2 and SO2 levels were 44.1 microg/m3, 43.3 microg/m3, and 12.2 microg/m3, respectively. Daily admission for asthma increased significantly with increasing ambient level of nitrogen dioxide (relative risk (RR) = 1.08 per 10 microg/m3 increase), sulphur dioxide (RR = 1.06) and inhalable particles (RR = 1.03). No association was found between hospital admission and humidity, temperature or atmospheric pressure. CONCLUSION: This is the first daily time series study of childhood admissions for asthma and air pollution in Hong Kong. The results support that current levels of air pollution contribute to the respiratory morbidity in asthmatic children in Hong Kong.     

The role of symptomatic colds in asthma exacerbations: Influence of outdoor allergens and air pollutants.

BACKGROUND: Both air pollutants and respiratory viral infections have been recognized to be important triggers of asthma exacerbations, but the possible interaction of these has not been assessed in an epidemiologic study. OBJECTIVE: In this study, we aimed to assess the possible associations of symptomatic colds with outdoor allergens and air pollutants in exacerbating asthma. METHODS: A total of 57 adults and children with asthma participated in a 1-year study in Vancouver, British Columbia. Diary cards recording symptoms of asthma and colds, medication usage, and peak expiratory flow rates were completed twice daily. Outdoor air pollutant levels and levels of pollen and fungal spores were measured. Levels were examined for associations with exacerbations of asthma with symptoms of a cold, as compared with asthma exacerbations with no cold symptoms and colds in the absence of asthma exacerbations. RESULTS: Of 130 asthma exacerbations, 47% were associated with cold symptoms (accounting for 44% of episodes of colds). Asthma exacerbations with colds were associated with higher levels of sulfur dioxide, and nitric oxide during March to November in comparison with asthma exacerbations without cold symptoms (P <.018). Cold-symptom days overall were more common in winter and were significantly associated with lower temperatures, lower ozone levels, and higher sulfur dioxide, nitrogen dioxide, nitrogen oxide (NO and NO(x)), and carbon monoxide levels. CONCLUSIONS: Asthma exacerbations are commonly associated with cold symptoms. These episodes are associated with higher levels of sulfur dioxide and nitrogen oxides from March to November in comparison with asthma exacerbations without cold symptoms.     

Winter air pollution and disease parameters in advanced chronic obstructive pulmonary disease panels residing in Denver, Colorado

BACKGROUND: Ambient pollution might worsen chronic obstructive pulmonary disease (COPD). OBJECTIVE: We explored the associations of pollution to pulmonary function, rescue medication, and symptoms over 2 winters in 2 panels of subjects with advanced COPD in Denver, Colorado. METHODS: Subjects measured lung function and recorded symptoms and rescue medications. Daily ambient pollution concentrations for particulate matter (PM(10) and PM(2.5)), carbon monoxide (CO), and nitrogen dioxide (NO(2)) were obtained for Denver. Estimated effects of pollution on outcomes were derived for the same day and 1 and 2 days after pollution measurements (lags 0, 1, and 2, respectively). RESULTS: Sixteen (mean age, 65.8 years; mean FEV 1 , 42.3% of predicted value) and 18 (mean age, 67.4 years; mean FEV 1 , 39.4% of predicted value) subjects participated in the first and second winters, respectively. There were no differences in demographic or disease characteristics between the 2 panels. In the first winter no detrimental associations were found. In the second winter, however, there were significant detrimental associations of CO in the morning and PM(10), CO, and NO(2) in the evening, increasing medication use at lag 0. Total symptom score increased at lag 0 with NO(2). The concentrations of particulates were increased in the second winter compared with in the first winter, and this winter was colder and more humid. CONCLUSIONS: In the second winter, subjects with severe COPD had worse lung function at lags 0 and 1 and increased rescue medication at lag 0 with increases in ambient air pollution. The effects of pollution varied between the 2 winters, perhaps related to levels of pollution and weather patterns. Significant effects were seen despite ambient pollution levels that conformed to US Environmental Protection Agency standards.     

Association of ambient air‐pollution levels with acute asthma exacerbation among children in Singapore

BACKGROUND: Air-pollution levels have been shown to be associated with increased morbidity of respiratory diseases. METHODS: Data for ambient air-pollutant levels, meteorologic factors, and hospitalization or emergency room (ER) visits for acute asthma in Singapore children over a 5-year period (1990-4) were obtained and analyzed for associations by time-series methods. RESULTS: Throughout this period, the annual mean and 24-h mean levels for sulfur dioxide (SO2), nitrogen dioxide (NO2), and total suspended particles (TSP) and maximum 1-h daily average for ozone were generally within the air-quality guidelines established by the World Health Organization (WHO). However, positive correlation between levels of each of these pollutants and daily ER visits for asthma was observed in children aged 3-12 years, but not among adolescents and young adults (13-21 years old). The association with SO2 and TSP persisted after standardization for meteorologic and temporal variables. An adjusted increase in 2.9 ER visits for every 20 microg/m3 increase in atmospheric SO2 levels, lagged by 1 day, was observed on days when levels were above 68 microg/m3. With TSP, an adjusted increase of 5.80 ER visits for every 20 microg/m3 increase in its daily atmospheric levels, lagged by 1 day, was observed on days with levels above 73 microg/m3. Similar results were also obtained after controlling for autocorrelation by time-series analysis. CONCLUSIONS: These associations were observed even though the overall levels of all pollutants were generally within the air-quality guidelines established by the WHO. These findings suggest that asthmatic children are susceptible to increased levels of air pollutants, particularly SO2 and TSP, although the ambient levels are generally within "acceptable" ranges.     

Environmental risk factors and allergic bronchial asthma

The prevalence of allergic respiratory diseases such as bronchial asthma has increased in recent years, especially in industrialized countries. A change in the genetic predisposition is an unlikely cause of the increase in allergic diseases because genetic changes in a population require several generations. Consequently, this increase may be explained by changes in environmental factors, including indoor and outdoor air pollution. Over the past two decades, there has been increasing interest in studies of air pollution and its effects on human health. Although the role played by outdoor pollutants in allergic sensitization of the airways has yet to be clarified, a body of evidence suggests that urbanization, with its high levels of vehicle emissions, and a westernized lifestyle are linked to the rising frequency of respiratory allergic diseases observed in most industrialized countries, and there is considerable evidence that asthmatic persons are at increased risk of developing asthma exacerbations with exposure to ozone, nitrogen dioxide, sulphur dioxide and inhalable particulate matter. However, it is not easy to evaluate the impact of air pollution on the timing of asthma exacerbations and on the prevalence of asthma in general. As concentrations of airborne allergens and air pollutants are frequently increased contemporaneously, an enhanced IgE-mediated response to aeroallergens and enhanced airway inflammation could account for the increasing frequency of allergic respiratory allergy and bronchial asthma. Pollinosis is frequently used to study the interrelationship between air pollution and respiratory allergy. Climatic factors (temperature, wind speed, humidity, thunderstorms, etc) can affect both components (biological and chemical) of this interaction. By attaching to the surface of pollen grains and of plant-derived particles of paucimicronic size, pollutants could modify not only the morphology of these antigen-carrying agents but also their allergenic potential. In addition, by inducing airway inflammation, which increases airway permeability, pollutants overcome the mucosal barrier and could be able to "prime" allergen-induced responses. There are also observations that a thunderstorm occurring during pollen season can induce severe asthma attacks in pollinosis patients. After rupture by thunderstorm, pollen grains may release part of their cytoplasmic content, including inhalable, allergen-carrying paucimicronic particles.     

Long-term exposure to background air pollution related to respiratory and allergic health in schoolchildren

BACKGROUND: The impact of air pollution on asthma and allergies still remains a debate. OBJECTIVE: Our cross-sectional study was intended to analyse the associations between long-term exposure to background air pollution and atopic and respiratory outcomes in a large population-based sample of schoolchildren. METHODS: Six thousand six hundred and seventy-two children aged 9-11 years recruited from 108 randomly schools in six French cities underwent a clinical examination including a skin prick test (SPT) to common allergens, exercise-induced bronchial reactivity (EIB) and skin examination for flexural dermatitis. The prevalence of asthma, allergic rhinitis (AR) and atopic dermatitis was assessed by a standardized health questionnaire completed by the parents. Three-year-averaged concentrations of air pollutants (NO2, SO2, PM10 and O3) were calculated at children' schools using measurements of background monitoring stations. RESULTS: After adjusting for confounders, EIB, lifetime asthma and lifetime AR were found to be positively related to an increase in the exposure to SO2, PM10 and O3. The adjusted odds ratios (aOR) per increase of 5 microg/m3 of SO2 was 1.39 (95% confidence interval (CI)=1.15-1.66) for EIB and 1.19 (1.00-1.41) for lifetime asthma. The aOR for lifetime AR per increase of 10 microg/m3 of PM10 was 1.32 (CI=1.04-1.68). Moreover, SPT positivity was associated with O3 (aOR=1.34; CI=1.24-1.46). Associations with past year symptoms were consistent, even if not always statistically significant. Results persisted in long-term resident (current address for at least 8 years) children. However, no consistent positive association was found with NO2. CONCLUSIONS: A moderate increase in long-term exposure to background ambient air pollution was associated with an increased prevalence of respiratory and atopic indicators in children.     

Air pollution and airway disease

Epidemiological and toxicological research continues to support a link between urban air pollution and an increased incidence and/or severity of airway disease. Detrimental effects of ozone (O₃), nitrogen dioxide (NO₂) and particulate matter (PM), as well as traffic‐related pollution as a whole, on respiratory symptoms and function are well documented. Not only do we have strong epidemiological evidence of a relationship between air pollution and exacerbation of asthma and respiratory morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD), but recent studies, particularly in urban areas, have suggested a role for pollutants in the development of both asthma and COPD. Similarly, while prevalence and severity of atopic conditions appear to be more common in urban compared with rural communities, evidence is emerging that traffic‐related pollutants may contribute to the development of allergy. Furthermore, numerous epidemiological and experimental studies suggest an association between exposure to NO₂, O₃, PM and combustion products of biomass fuels and an increased susceptibility to and morbidity from respiratory infection. Given the considerable contribution that traffic emissions make to urban air pollution researchers have sought to characterize the relative toxicity of traffic‐related PM pollutants. Recent advances in mechanisms implicated in the association of air pollutants and airway disease include epigenetic alteration of genes by combustion‐related pollutants and how polymorphisms in genes involved in antioxidant pathways and airway inflammation can modify responses to air pollution exposures. Other interesting epidemiological observations related to increased host susceptibility include a possible link between chronic PM exposure during childhood and vulnerability to COPD in adulthood, and that infants subjected to higher prenatal levels of air pollution may be at greater risk of developing respiratory conditions. While the characterization of pollutant components and sources promise to guide pollution control strategies, the identification of susceptible subpopulations will be necessary if targeted therapy/prevention of pollution‐induced respiratory diseases is to be developed. Cite this as: F. J. Kelly and J. C. Fussell, Clinical & Experimental Allergy, 2011 (41) 1059–1071.     

Air pollution and seasonal asthma during the pollen season. A cohort study in Puertollano and Ciudad Real (Spain)

BACKGROUND: Many studies have demonstrated a positive association between air pollutants and emergency visits for asthma. However, few studies have included pollen when analysing this relationship in mild-moderate asthmatic patients. OBJECTIVE: To determine the importance of the pollutants such as ozone (O(3)), particles (PM(10)), nitrogen dioxide (NO(2)) and sulphur dioxide (SO(2)) in the clinical course of mild-moderate pollen-allergic asthmatic patients from two Spanish towns in La Mancha: Puertollano (high pollution levels) and Ciudad Real (low pollution levels). METHODS: We used a Poisson regression model to study a cohort of 137 patients from Puertollano and Ciudad Real during two pollen seasons (2000-2001) and analysed the relationship between air pollutant and pollen levels and daily symptoms, the medication used and peak-flow measurements. RESULTS: The number of asthma symptoms and the mean values of the PM(10), SO(2) and NO(2) levels were higher in Puertollano than in Ciudad Real. In Puertollano, the risk of asthma increased by 6% with a 3-day lag for PM(10), by 8% with a 3-day lag for O(3), by 4% with a 1-day lag for SO(2) and by 15% with a 3-day lag for O(3) when its values exceeded the health threshold (P < 0.05). CONCLUSIONS: The air pollution levels in Puertollano were associated with an increased risk of asthma symptoms in pollen-allergic asthmatic patients com pared with a similar group from Ciudad Real.     

The role of particulate matter in exacerbation of atopic asthma

Increasing evidence shows that elevated levels of particulate matter (PM) can exacerbate existing asthma, while evidence that PM can promote the induction of asthma is limited. PM in ambient air has been associated with increased emergency room visits and medication use by asthmatics. Controlled human exposure studies of acid aerosols suggest increased responses among adolescent asthmatics. Increased ambient and indoor levels of bioaerosols (e.g., house dust mite, fungal spores, endotoxin) have been associated with exacerbation of asthma. Environmental Protection Agency (EPA) studies focus on the effects of exposing humans and animal models to a combination of various PM samples (e.g., diesel exhaust particles, oil fly ash) and allergens (e.g., house dust mite, ovalbumin). These research efforts to understand the mechanisms by which PM exposure can promote allergic sensitization and exacerbate existing asthma concentrate on the role of transition metals. Exposure of animal models to combined PM and allergen promotes allergic sensitization and increases allergic inflammation and airway hyperresponsiveness. Exposure of healthy human volunteers to emission source PM samples promotes inflammation and increased indices of oxidant formation correlating with the quantity of transition metals in the samples. Results of these studies suggest that transition metals in ambient PM promote the formation of reactive oxygen species and subsequent lung injury, inflammation, and airway hyperresponsiveness leading to airflow limitation and symptoms of asthma.     

Glutathione S-transferase P1 gene polymorphism and air pollution as interactive risk factors for childhood asthma

BACKGROUND: Polymorphisms at the glutathione S-transferase (GST) P1 locus were associated with asthma-related phenotypes and bronchial hyper-responsiveness. OBJECTIVE: This study investigated whether GSTP1 genotypes and outdoor air pollution were interactive risk factors on childhood asthma. METHODS: Four hundred and thirty-six subjects were recruited for oral mucosa samplings from 2853 fourth- to ninth-grade schoolchildren from three districts with different air pollution levels in southern Taiwan. PCR-based assays were performed by oral mucosa DNA to determine GSTP1 genotypes. We also conducted a nested case-control study comprising 61 asthmatic children and 95 controls confirmed by International Study of Asthma and Allergies in Childhood questionnaire results and methacholine challenge test. Multiple logistic regression was used to adjust for potential confounding factors. RESULTS: All participants were homozygous at the Ala-114 locus. Although only a marginally significant association existed between the frequency of homozygosity at the Ile-105 locus and asthma when air pollution was not considered, we found a significant gene-environmental interaction between GSTP1-105 alleles and air pollution after adjusting for confounders (P=0.035). Specifically, we found that compared with participants carrying any Val-105 allele in low air pollution, those who are Ile-105 homozygotes in high air pollution district had a significantly increased risk of asthma (adjusted odds ratio (AOR)=5.52, 95% confidence interval (CI)=1.64-21.25). Compared with participants carrying any Val-105 allele, in high air pollution district, children with Ile-105 homozygotes had a significantly increased risk of asthma (AOR=3.79, 95% CI=1.01-17.08), but those who carried two Ile-105 alleles in low or moderate air pollution districts did not show similar tendencies. The risk of asthma also revealed a clear dose-response relationship with outdoor air pollution in children with Ile-105 homozygotes. CONCLUSION: Our result suggests a gene-environmental interaction between GSTP1-105 genotypes and outdoor air pollution on childhood asthma.     

Allergy in severe asthma

It is well recognized that atopic sensitization is an important risk factor for asthma, both in adults and in children. However, the role of allergy in severe asthma is still under debate. The term ‘Severe Asthma’ encompasses a highly heterogeneous group of patients who require treatment on steps 4–5 of GINA guidelines to prevent their asthma from becoming ‘uncontrolled’, or whose disease remains ‘uncontrolled’ despite this therapy. Epidemiological studies on emergency room visits and hospital admissions for asthma suggest the important role of allergy in asthma exacerbations. In addition, allergic asthma in childhood is often associated with severe asthma in adulthood. A strong association exists between asthma exacerbations and respiratory viral infections, and interaction between viruses and allergy further increases the risk of asthma exacerbations. Furthermore, fungal allergy has been shown to play an important role in severe asthma. Other contributing factors include smoking, pollution and work‐related exposures. The ‘Allergy and Asthma Severity’ EAACI Task Force examined the current evidence and produced this position document on the role of allergy in severe asthma.     

The epidemiology and genetics of asthma risk associated with air pollution

The occurrence of asthma and allergic diseases has continued to increase in the United States and worldwide, despite general improvements in air quality over the past 40 years. This observation has led many to question whether air quality is truly a significant risk factor in the development and exacerbation of asthma and whether further improvement in air quality is likely to result in improved health outcomes. However, epidemiologic studies have shown that levels of pollutants of less than the current ambient air quality standards still result in exacerbations of asthma and are associated with other morbidities as well. Specific locations, such as living near a roadway, might pose a special exposure risk. Genetic factors almost certainly play a role in determining susceptibility to pollutants, such as including those involved with antioxidant defenses. The best studied of these in the context of air pollution risks are glutathione-S-transferase polymorphisms. Irrespective of whether pollutants contribute to the development of asthma or the well-documented increases in asthma results in more people having pollutant-induced disease, poor air quality in many places remains a significant problem for patients with asthma and allergic disease. A number of public health, pharmaceutical, and nutriceutical interventions might mitigate the effects of pollutant exposure and deserve further study.     

Atopic sensitization and respiratory symptoms among Polish and Swedish school children

Allergic sensitization and symptoms from the airways in relation to air pollution were compared in 10–12-year-old school children (n= 1113) from urban Konin in central Poland and both urban and rural parts of Sundsvall in northern Sweden. The measurements included parental questionnaires, skin-prick tests and serial peak flow measurements during 2 weeks with simultaneous monitoring of outdoor air pollutants. The skin-prick test technique was validated by IgE antibody determinations. The levels of common industrial pollutants, SO₂ and smoke particles were much higher in Konin than in urban Sundsvall and the levels of NO₂ were similar. Various respiratory symptoms were more often reported among school children in Konin (except for wheezing and diagnosed asthma). Multiple logistic regression analyses yielded the following increased odds ratios for children in Konin as compared with the reference group (rural Sundsvall): chest tightness and breathlessness 348 (95% confidence interval 2.08–5.82), exercise-induced coughing attacks 3.69 (95% confidence interval 1.68–8.10), recurrent episodes of common cold 2.79 (95% confidence interval 1.53–5.09) and prolonged cough 4–89 (95% confidence interval 2.59–9.23). In contrast, as compared with rural Sundsvall, the adjusted odds ratio for a positive skin-prick test was decreased in Konin, but increased in urban Sundsvall, 0.58 (95% confidence interval 0.37–0.91) and 1.67 (95% confidence interval 1.15–2.42) respectively. The study confirms that living in urban, as compared with rural areas, is associated with an increased prevalence of respiratory symptoms and sensitization to allergens. These differences could be explained by air pollution. Respiratory symptoms were more common in a similar urban group of Polish children who were exposed to even higher levels of air pollution. These children, however, had a much lower prevalence of sensitization to allergens, as compared with the Swedish children. This indicates that differences in lifestyle and standard of living between western Europe and a former socialist country influences the prevalence of atopy.     

Pollution and allergic airways disease

The incidence of allergic diseases has increased dramatically over recent years in most industrialized countries of the world. Air pollution from motor vehicles has been implicated as one of the factors that are responsible for this increase. Epidemiological studies carried out in different geographical regions in the world have shown a significant and consistent association between ambient levels of pollutants and increased asthma and rhinitis symptoms. Recent human and animal exposure studies, as well as laboratory-based studies, have demonstrated that diesel particles, ozone and nitrogen dioxide induce an inflammatory response that involves various inflammatory cells, mediators and adhesion molecules, which could contribute to worsening of the allergic disorders. The present review describes our current understanding of the mechanisms by which pollutants such as diesel exhaust and ozone enhance the underlying allergic inflammatory response, and possibly explain the associations between pollutants and increasing allergic diseases noted in epidemiological studies.     

Effects of ambient air pollution on symptom severity and medication use in children with asthma.

BACKGROUND: Exposure to air pollutants has been investigated as a possible cause of asthma attacks in children. OBJECTIVE: To investigate the short-term effects of air pollutants on a panel of 133 children with asthma who enrolled in the Childhood Asthma Management Program. METHODS: During screening, the children completed daily diary cards for an average of 58 days to indicate their medication use and asthma severity. We used ordinal logistic regression to compare the odds of a more serious relative to a less serious asthma attack, and we used a Poisson model to analyze medication use. In both analyses we accommodate dependence in the data and different periods of observation for study subjects. RESULTS: Our results indicate that a 10-microg/m3 increase in particulate matter less than or equal to 2.5 microm (PM2.5) lagged 1 day was associated with a 1.20 times increased odds of having a more serious asthma attack [95% confidence interval (CI), 1.05 to 1.37] and a 1.08-fold increase in medication use (95% CI, 1.01 to 1.15). A 10-microg/m3 increase in particulate matter less than or equal to 10 microm (PM10) increased the odds of a more serious asthma attack (odds ratio = 1.12; 95% CI, 1.04 to 1.22) and also increased medication use (relative risk = 1.05; 95% CI, 1.00 to 1.09). CONCLUSIONS: Increases in PM2.5 and PM10 are significantly associated with an increased risk of more severe asthma attacks and medication use in Seattle area children with asthma. We also found associations with carbon monoxide, but we believe that carbon monoxide is a marker for exposure to combustion byproducts.     

The relationship of air pollution to the prevalence of allergic diseases in Taichung and Chu-Shan in 2002.

This study was conducted in order to determine the relationship between air pollution and the varying prevalence of allergic diseases in the city of Taichung and the rural town of Chu-Shan. We used questionnaires to screen children aged from 7 to 15 years in Taichung and Chu-Shan and compared the results from these 2 areas with the factors related to air pollution. The study included 11,580 children in Taichung and 2621 children in Chu-Shan. In Taichung, the prevalence of asthma was 7.0%, of allergic rhinitis 27.6% and of atopic dermatitis 3.4%. In Chu-Shan, the prevalence of asthma was 5.6%, of allergic rhinitis 21.8% and of atopic dermatitis 3.3%. We also collected data on the concentration of air pollutants in the 2 areas over a 1-year period from January to December 2001 and compared the average annual concentrations of various pollutants. Compared with Chu-Shan, Taichung had higher air concentrations of nitric oxide (NO; 11.47 +/- 4.75 vs 5.07 +/- 2.81 ppb), carbon monoxide (CO; 0.78 +/- 0.19 vs 0.59 +/- 0.12 ppm), nitrogen dioxide (NO(2); 24.99 +/- 6.8 vs 21.45 +/- 7.87 ppb) and sulfur dioxide (SO(2); 2.58 +/- 1.0 vs 2.44 +/- 0.88 ppb). Student's t test results showed that CO and NO were related significantly to the prevalence of allergic disease (p<0.005). The prevalence of both asthma and allergic rhinitis is higher in Taichung than in Chu-Shan, a finding that could be related to higher levels of some air pollutants in the urban location.     

Effects of climate change on environmental factors in respiratory allergic diseases

A body of evidence suggests that major changes involving the atmosphere and the climate, including global warming induced by human activity, have an impact on the biosphere and the human environment. Studies on the effects of climate change on respiratory allergy are still lacking and current knowledge is provided by epidemiological and experimental studies on the relationship between asthma and environmental factors, such as meteorological variables, airborne allergens and air pollution. However, there is also considerable evidence that subjects affected by asthma are at an increased risk of developing obstructive airway exacerbations with exposure to gaseous and particulate components of air pollution. It is not easy to evaluate the impact of climate change and air pollution on the prevalence of asthma in general and on the timing of asthma exacerbations. However, the global rise in asthma prevalence and severity suggests that air pollution and climate changes could be contributing. Pollen allergy is frequently used to study the interrelationship between air pollution, rhinitis and bronchial asthma. Epidemiological studies have demonstrated that urbanization, high levels of vehicle emissions and westernized lifestyle are correlated to an increase in the frequency of pollen‐induced respiratory allergy, prevalent in people who live in urban areas compared with those who live in rural areas. Meteorological factors (temperature, wind speed, humidity, etc.) along with their climatological regimes (warm or cold anomalies and dry or wet periods, etc.), can affect both biological and chemical components of this interaction. In addition, by inducing airway inflammation, air pollution overcomes the mucosal barrier priming allergen‐induced responses. In conclusion, climate change might induce negative effects on respiratory allergic diseases. In particular, the increased length and severity of the pollen season, the higher occurrence of heavy precipitation events and the increasing frequency of urban air pollution episodes suggest that environmental risk factors will have a stronger effect in the following decades.