Association between air pollution and asthma admission among children in Hong Kong

OBJECTIVE: To examine the association of air pollutants with hospital admission for childhood asthma in Hong Kong. METHODS: Data on hospital admissions for asthma, influenza and total hospital admissions in children aged < or =18 years at all Hospital Authority hospitals during 1997-2002 were obtained. Data on daily mean concentrations of particles with aerodynamic diameter <10 microm (i. e. PM10) and <2.5 microm (i. e. PM2.5), nitrogen dioxide (NO2), sulphur dioxide (SO2), and ozone (O3) and data on meteorological variables were associated with asthma hospital admissions using Poisson's regression with generalized additive models for correction of yearly trend, temperature, humidity, day-of-week effect, holiday, influenza admissions and total hospital admission. The possibility of a lag effect of each pollutant and the interaction of different pollutants were also examined. RESULTS: The association between asthma admission with change of NO2, PM10, PM2.5 and O3 levels remained significant after adjustment for multi-pollutants effect and confounding variables, with increase in asthma admission rate of 5.64% (3.21-8.14) at lag 3 for NO2, 3.67% (1.52-5.86) at lag 4 for PM10, 3.24% (0.93-5.60) at lag 4 for PM2.5 and 2.63% (0.64-4.67) at lag 2 for O3. Effect of SO2 was lost after adjustment. CONCLUSION: Ambient levels of PM10, PM2.5) NO2 and O3 are associated with childhood asthma hospital admission in Hong Kong.     

Effects of air pollution on asthma hospitalization rates in different age groups in Hong Kong

AIMS: To assess the relationship between levels of ambient air pollutants and hospitalization rates for asthma in Hong Kong (HK). METHODS: This is a retrospective ecological study. Data of daily emergency hospital admissions to 15 major hospitals in HK for asthma and indices of air pollutants [sulphur dioxide (SO(2)), nitrogen dioxide (NO(2)), ozone (O(3)), particulates with an aerodynamic diameter of <10 microm particulate matter (PM(10)) and 2.5 microm (PM(2.5))] and meteorological variables from January 2000 to December 2005 were obtained from several government departments. Analysis was performed by the generalized additive models with Poisson distribution. The effects of time trend, season, other cyclical factors, temperature and humidity were adjusted. Autocorrelation and overdispersion were corrected. RESULTS: Altogether, 69 716 admissions were assessed. Significant associations were found between hospital admissions for asthma and levels of NO(2), O(3), PM(10) and PM(2.5). The relative risks (RR) for hospitalization for every 10 microg/m(3) increase in NO(2), O(3), PM(10) and PM(2.5) were 1.028, 1.034, 1.019 and 1.021, respectively, at a lag day that ranged from cumulative lag 0-4 to 0-5. In a multi-pollutant model, O(3) was significantly associated with increased admissions for asthma. The younger age group (0-14 years) tended to have a higher RR for each 10 microg/m(3) increase in pollutants than those aged 15-65 years. The elderly (aged >/=65 years) had a shorter 'best' lag time to develop asthma exacerbation following exposure to pollutants than those aged <65 years. CONCLUSION: Adverse effects of ambient concentrations of air pollutants on hospitalization rates for asthma are evident. Measures to improve air quality in HK are urgently needed.     

Air pollution and daily mortality in Inchon, Korea.

The association between total daily mortality and air pollution was investigated for a 1-year period (January 1995 to December 1995) in Inchon, Korea. The purpose of this study was to evaluate the relative importance of particulate and gaseous air pollution as predictors of daily mortality. Concentration of total suspended particulates (TSP), inhalable particles (PM10), and gaseous pollutants, such as sulfur dioxide, nitrogen dioxide, ozone, carbon monoxide, were measured daily during the study period. A generalized additive model was used to regress daily death counts on each air pollutant, controlling for time trend and meteorologic influences such as temperature or relative humidity. Total mortality was found to increase 1.2% (95% CI: 0.2 to 2.2%) for each 10 microg/m3 increase in 6-day moving average of TSP, and 1.2% (95% CI 0.2 to 2.1%) for each 10 microg/m3 increase in 5-day moving average of PM10. The association is similar in magnitude to associations between particulate air pollution and mortality found in several other communities in America and Europe. Associations with gaseous pollutants were all statistically insignificant in the generalized additive model. The relative risk of death increased at particulate levels that were well below the current Korean Ambient Air Quality Standard.     

Atmospheric pollution and the prevalence of asthma: study among schoolchildren of 2 areas in Rio de Janeiro, Brazil.

BACKGROUND: Air pollutants have been associated with the exacerbation of respiratory diseases. They may intensify the inflammatory allergic response and airways reactivity to inhaled allergens. However, it is still not clear if air pollution contributes to the increased prevalence of asthma. OBJECTIVE: To investigate if different levels of air pollution exposure can be related to differences in the prevalence of asthma. METHODS: The International Study of Asthma and Allergies in Childhood (ISAAC) protocol was used to determine and compare the prevalence of asthma among schoolchildren in 2 cities of the metropolitan region of Rio de Janeiro, Brazil, Duque de Caxias (DC) and Seropédica (SR), which have different levels of atmospheric pollution. The research involved 4,064 students aged 13 to 14 years from 49 schools in DC and 1,129 from 17 schools in SR. Air pollution was evaluated by the concentration of inhalable particulate matter (PM10). RESULTS: ISAAC's written questionnaire was answered by 4,040 students aged 13 to 14 years in DC and 1,080 in SR. Between 1998 and 2000, the PM10 annual arithmetic mean was 124 microg/m3 in DC and 35 microg/m3 in SR (acceptable level is up to 50 microg/m3). The prevalence of wheezing ever was 35.1% in DC and 29.9% in SR (P = .001), and the prevalence of wheezing in the last 12 months was 19.0% in DC and 15.0% in SR (P = .002). In DC, 14.5% of the adolescents presented 1 to 3 crises of wheezing in the last year, whereas in SR only 11.0% presented 1 to 3 crises (P = .003). CONCLUSIONS: In this study, the prevalence of asthma in adolescents was directly related to atmospheric pollution.     

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.     

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.     

Do levels of airborne grass pollen influence asthma hospital admissions?

Background The effects of environmental factors and ambient concentrations of grass pollen on allergic asthma are yet to be established.
Objective We sought to estimate the independent effects of grass pollen concentrations in the air over Melbourne on asthma hospital admissions for the 1992–1993 pollen season.
Methods Daily grass pollen concentrations were monitored over a 24-h period at three stations in Melbourne. The outcome variable was defined as all-age asthma hospital admissions with ICD9-493 codes. The ambient air pollutants were average daily measures of ozone, nitrogen dioxide and sulphur dioxide, and the airborne particle index representing fine particulate pollution. Semi-parametric Poisson regression models were used to estimate these effects, adjusted for air temperature, humidity, wind speed, rainfall, day-of-the-week effects and seasonal variation.
Results Grass pollen was a strong independent non-linear predictor of asthma hospital admissions in a multi-pollutant model ( P =0.01). Our data suggest that grass pollen had an increasing effect on asthma hospital admissions up to a threshold of 30 grains/m³, and that the effect remains stable thereafter.
Conclusion Our findings suggest that grass pollen levels influence asthma hospital admissions. High grass pollen days, currently defined as more than 50 grains/m³, are days when most sensitive individuals will experience allergic symptoms. However, some asthmatic patients may be at a significant risk even when airborne grass pollen levels are below this level. Patients with pollen allergies and asthma would be advised to take additional preventive medication at lower ambient concentrations.     

Combined effects of aerobiological pollutants, chemical pollutants and meteorological conditions on asthma admissions and A & E attendances in Derbyshire UK, 1993–96.

BACKGROUND: The effect of outdoor aeroallergen exposure in asthma may be enhanced by air pollutants, including ozone, nitrogen dioxide and particulates, and by certain weather conditions. It is not yet established whether these interactions are important in determining asthma morbidity at the population level. OBJECTIVE: We have investigated the joint effects of aeroallergens, rainfall, thunderstorms and outdoor air pollutants on daily asthma admissions and Accident and Emergency (A & E) attendance using routinely collected data between 1993 and 1996 from Derby in central England. METHODS: Daily counts during the aeroallergen season of grass and birch pollen, basidiospores, Didymella, Alternaria and Cladosporium, maximum 1 hour ozone and nitrogen dioxide and daily average black smoke measurements, all made in the vicinity of the city centre, were categorized in tertiles. Rainfall was classified as dry, light ( 2 mm). The modifying effect of outdoor pollutant levels, and rainfall or the occurrence of a thunderstorm, upon the effects of individual aeroallergens on asthma admissions and A & E attendance were investigated by fitting appropriate interactions in log linear autoregression models with adjustment for potential confounders. RESULTS: We found a significant interaction between the effects of grass pollen and weather conditions upon A & E attendance, such that the increase with grass pollen count was most marked on days of light rainfall (adjusted rate ratio for >/= 50 vs < 10 grains/m3 at lag 2 days = 2.1, 95% CI 1.4, 3.3). Asthma admissions increased with Cladosporium count. We found no statistically significant interactions between effects of any individual aeroallergen and outdoor air pollutant upon either measure of asthma morbidity. CONCLUSIONS: Rainfall and thunderstorms are important effect modifiers in the relation between grass pollen and measures of acute asthma morbidity. Interactions between ambient levels of aeroallergens and chemical pollutants in the Derby area do not play a major role in determining asthma admissions and A & E attendance.     

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.     

Exposure to air pollution during different gestational phases contributes to risks of low birth weight

BACKGROUND: Although there have been growing concerns about the adverse effects of air pollution on birth outcomes, little is known about which specific exposure times of specific pollutants contribute to low birth weight (LBW). METHODS: We evaluated the relationships between LBW and air pollution exposure levels in Seoul, Korea. Using the air pollution data, we estimated the exposure during each trimester and also during each month of pregnancy on the basis of the gestational age and birth date of each newborn. Generalized additive logistic regression analyses were conducted considering infant sex, birth order, maternal age, parental education level, time trend, and gestational age. RESULTS: The monthly analyses suggested that the risks for LBW tended to increase with carbon monoxide (CO) exposure between months 2-5 of pregnancy, with exposure to particles <10 micro m (PM(10)) in months 2 and 4, and for sulphur dioxide (SO(2)) and nitrogen dioxide (NO(2)) exposure between months 3-5. CONCLUSIONS: This study suggests that exposure to CO, PM(10,) SO(2) and NO(2) during early to mid pregnancy contribute to risks for LBW.     

Excess hospital admissions for pneumonia, chronic obstructive pulmonary disease, and heart failure during influenza seasons in Hong Kong

It is widely held that Southern China is a hypothetical influenza epicentre for the emergence of pandemic influenza viruses. However, influenza is perceived as a relatively unimportant infection in this part of the world compared with western countries. Hong Kong is situated within the hypothetical epicentre and serves as a sentinel post for the region. In a retrospective study, the influenza-associated excess hospitalisations in a regional hospital for pneumonia, chronic obstructive pulmonary disease (COPD), heart failure, and asthma in persons aged > or = 65 years from 1998 to 2001 were each estimated by a model taking into consideration the confounding effect of other respiratory viral infections, seasonal factors, time trends, and weather and pollution indices. In the regression models, influenza activity is an independent significant factor affecting admission rates for pneumonia, COPD, and heart failure but not that for asthma. The variations in hospital admissions for pneumonia, COPD, and heart failure explained by influenza activity were 38.9, 7.5, and 45.6%, respectively. The adjusted rates of excess influenza-associated hospital admissions for the three diagnoses combined amounted to 58.5, 20.0, 29.2, and 13.4 per 10,000 populations aged > or = 65 years in 1998, 1999, 2000, and 2001, respectively. In conclusion, influenza activity is associated significant excess hospital admissions among elderly aged 65 or above in Hong Kong, comparable to the data reported in Western countries. The findings support a wider application of annual influenza vaccination in this region.     

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.     

Fine particulate air pollution and mortality in 20 U.S. cities, 1987-1994

BACKGROUND: Air pollution in cities has been linked to increased rates of mortality and morbidity in developed and developing countries. Although these findings have helped lead to a tightening of air-quality standards, their validity with respect to public health has been questioned. METHODS: We assessed the effects of five major outdoor-air pollutants on daily mortality rates in 20 of the largest cities and metropolitan areas in the United States from 1987 to 1994. The pollutants were particulate matter that is less than 10 microm in aerodynamic diameter (PM10), ozone, carbon monoxide, sulfur dioxide, and nitrogen dioxide. We used a two-stage analytic approach that pooled data from multiple locations. RESULTS: After taking into account potential confounding by other pollutants, we found consistent evidence that the level of PM10 is associated with the rate of death from all causes and from cardiovascular and respiratory illnesses. The estimated increase in the relative rate of death from all causes was 0.51 percent (95 percent posterior interval, 0.07 to 0.93 percent) for each increase in the PM10 level of 10 microg per cubic meter. The estimated increase in the relative rate of death from cardiovascular and respiratory causes was 0.68 percent (95 percent posterior interval, 0.20 to 1.16 percent) for each increase in the PM10 level of 10 microg per cubic meter. There was weaker evidence that increases in ozone levels increased the relative rates of death during the summer, when ozone levels are highest, but not during the winter. Levels of the other pollutants were not significantly related to the mortality rate. CONCLUSIONS: There is consistent evidence that the levels of fine particulate matter in the air are associated with the risk of death from all causes and from cardiovascular and respiratory illnesses. These findings strengthen the rationale for controlling the levels of respirable particles in outdoor air.     

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.     

Residential outdoor air pollution and allergen sensitization in schoolchildren in Oslo, Norway

BACKGROUND: Epidemiological studies that have investigated the association between air pollution and atopy have found inconsistent results. Furthermore, often exposure to outdoor air pollution has had limited quality, and more individual exposure is needed. OBJECTIVE: To investigate the relations between early and lifetime exposure to residential outdoor air pollution and allergen sensitization in 9-10-year-old children in Oslo, Norway. METHODS: Sensitization to common allergens was measured by skin prick tests (SPTs), which were performed in 2244 children who had lived in Oslo since birth. Several definitions of positive SPT were used. Information on potential confounding variables was collected by a parental questionnaire. Exposure to outdoor air pollution was assessed by the EPISODE dispersion model, which calculates hourly concentrations of nitrogen dioxide (NO2), particulate matter (PM) with aerodynamic diameter <10 microm (PM10) and <2.5 microm (PM2.5), respectively. RESULTS: We found no associations between long-term air pollution exposure and sensitization to any allergen, any indoor or any pollen allergen. However, lifetime air pollution exposure was associated with sensitization to the house dust mite Dermatophagoides farinae. One interquartile increase of lifetime exposure to NO2, PM10 and PM2.5 was associated with 1.88 (adjusted odds ratio) (1.02, 3.47) [95% confidence interval (CI)], 1.61 (0.96, 2.72) and 1.46 (0.96, 2.22), respectively, for D. farinae. Lifetime exposure was also associated with sensitization to cat in a subpopulation. Both associations diminished after adjusting for a contextual socio-economic factor. CONCLUSION: Long-term exposure to traffic-related pollutants was generally not associated with allergen sensitization in 9-10-year-old Oslo children. However, lifetime exposure was associated with sensitization to D. farinae, and with sensitization to cat in a subpopulation, which may be explained by socio-economic confounding or multiple comparisons. The air pollution levels in Oslo may be too low to reveal associations with sensitization.     

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.     

Analysis of the relationships between environmental factors (aeroallergens, air pollution, and weather) and asthma emergency admissions to a hospital in Mexico City

There have been several studies of the relationships between environmental factors, particularly air pollution, and attacks of asthma. Most of these studies have ignored the potential confounding effects of aeroallergens such as pollens and fungal spores. We report a statistical analysis of the relationships between emergency admissions for asthma to a hospital in Mexico City and daily average airborne concentrations of pollen, fungal spores, air pollutants (O₃, NO₃, SO₃. and particulates) and weather factors. Asthma admissions had a seasonal pattern with more during the wet season (May-October) than the dry season (November-April). There were few statistical associations between asthma admissions and air pollutants for the three age groups studied (children under 15 years, adults, and seniors [adults over 59 years]) in either season. Grass pollen was associated with child and adult admissions for both the wet and dry seasons, and fungal spores were associated with child admissions during both the wet and dry seasons. The analysis was done with environmental data averaged over the day of admission and the 2 previous days. Our results suggest that aeroallergens may be statistically associated more strongly with asthma hospital admissions than air pollutants and may act as confounding factors in epidemiologic studies.     

Genetic and epigenetic influence on the response to environmental particulate matter

Ambient air pollution, including particulate matter (PM) and gaseous pollutants, represents important environmental exposures that adversely affect human health. Because of their heritable and reversible nature, epigenetic modifications provide a plausible link between the environment and alterations in gene expression that might lead to disease. Epidemiologic evidence supports that environmental exposures in childhood affect susceptibility to disease later in life, supporting the belief that epigenetic changes can affect ongoing development and promote disease long after the environmental exposure has ceased. Indeed, allergic disorders often have their roots in early childhood, and early exposure to PM has been strongly associated with the subsequent development of asthma. The purpose of this review is to summarize recent findings on the genetic and epigenetic regulation of responses to ambient air pollutants, specifically respirable PM, and their association with the development of allergic disorders. Understanding these epigenetic biomarkers and how they integrate with genetic influences to translate the biologic effect of particulate exposure is critical to developing novel preventative and therapeutic strategies for allergic disorders.     

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.