Effects Of Air Pollution Exposure Research Articles

Long-term Exposure to PM 10 and NO 2 in Association with Lung Volume and Airway Resistance in the MAAS Birth Cohort

Background: Findings from previous studies on the effects of air pollution exposure on lung function during childhood have been inconsistent. A common limitation has been the quality of exposure data used, and few studies have modeled exposure longitudinally throughout early life.Objectives: We sought to study the long-term effects of exposure to particulate matter with an aerodynamic diameter ≤ 10 μm (PM10) and to nitrogen dioxide (NO2) on specific airway resistance (sRaw) and forced expiratory volume in 1 sec (FEV1) before and after bronchodilator treatment. Subjects were from the Manchester Asthma and Allergy Study (MAAS) birth cohort (n = 1,185).Methods: Spirometry was performed during clinic visits at ages 3, 5, 8, and 11 years. Individual-level PM10 and NO2 exposures were estimated from birth to 11 years of age through a microenvironmental exposure model. Longitudinal and cross-sectional associations were estimated using generalized estimating equations and multivariable linear regression models.Results: Lifetime exposure to PM10 and NO2 was associated with significantly less growth in FEV1 (percent predicted) over time, both before (–1.37%; 95% CI: –2.52, –0.23 for a 1-unit increase in PM10 and –0.83%; 95% CI: –1.39, –0.28 for a 1-unit increase in NO2) and after bronchodilator treatment (–3.59%; 95% CI: –5.36, –1.83 and –1.20%; 95% CI: –1.97, –0.43, respectively). We found no association between lifetime exposure and sRaw over time. Cross-sectional analyses of detailed exposure estimates for the summer and winter before 11 years of age and lung function at 11 years indicated no significant associations.Conclusions: Long-term PM10 and NO2 exposures were associated with small but statistically significant reductions in lung volume growth in children of elementary-school age.Citation: Mölter A, Agius RM, de Vocht F, Lindley S, Gerrard W, Lowe L, Belgrave D, Custovic A, Simpson A. 2013. Long-term exposure to PM10 and NO2 in association with lung volume and airway resistance in the MAAS birth cohort. Environ Health Perspect 121:1232–1238. http://dx.doi.org/10.1289/ehp.1205961

Hypoxia Stress Test Reveals Exaggerated Cardiovascular Effects in Hypertensive Rats After Exposure to the Air Pollutant Acrolein

Exposure to air pollution increases the risk of cardiovascular morbidity and mortality, especially in susceptible populations. Despite increased risk, adverse responses are often delayed and require additional stress tests to reveal latent effects of exposure. The goal of this study was to use an episode of "transient hypoxia" as an extrinsic stressor to uncover latent susceptibility to environmental pollutants in a rodent model of hypertension. We hypothesized that exposure to acrolein, an unsaturated aldehyde and mucosal irritant found in cigarette smoke, diesel exhaust, and power plant emissions, would increase cardiopulmonary sensitivity to hypoxia, particularly in hypertensive rats. Spontaneously hypertensive and Wistar Kyoto (normotensive) rats, implanted with radiotelemeters, were exposed once for 3h to 3 ppm acrolein gas or filtered air in whole-body plethysmograph chambers and challenged with a 10% oxygen atmosphere (10min) 24h later. Acrolein exposure increased heart rate, blood pressure, breathing frequency, and minute volume in hypertensive rats and also increased the heart rate variability parameter LF, suggesting a potential role for increased sympathetic tone. Normotensive rats only had increased blood pressure during acrolein exposure. The hypoxia stress test after acrolein exposure revealed increased diastolic blood pressure only in hypertensive rats and increased minute volume and expiratory time only in normotensive rats. These results suggest that hypertension confers exaggerated sensitivity to air pollution and that the hypoxia stress test is a novel tool to reveal the potential latent effects of air pollution exposure.

Early-Life Exposure to Outdoor Air Pollution and Respiratory Health, Ear Infections, and Eczema in Infants from the INMA Study

Background: Prenatal and early-life periods may be critical windows for harmful effects of air pollution on infant health.Objectives: We studied the association of air pollution exposure during pregnancy and the first year of life with respiratory illnesses, ear infections, and eczema during the first 12–18 months of age in a Spanish birth cohort of 2,199 infants.Methods: We obtained parentally reported information on doctor-diagnosed lower respiratory tract infections (LRTI) and parental reports of wheezing, eczema, and ear infections. We estimated individual exposures to nitrogen dioxide (NO2) and benzene with temporally adjusted land use regression models. We used log-binomial regression models and a combined random-effects meta-analysis to estimate the effects of air pollution exposure on health outcomes across the four study locations.Results: A 10-µg/m3 increase in average NO2 during pregnancy was associated with LRTI [relative risk (RR) = 1.05; 95% CI: 0.98, 1.12] and ear infections (RR = 1.18; 95% CI: 0.98, 1.41). The RRs for an interquartile range (IQR) increase in NO2 were 1.08 (95% CI: 0.97, 1.21) for LRTI and 1.31 (95% CI: 0.97, 1.76) for ear infections. Compared with NO2, the association for an IQR increase in average benzene exposure was similar for LRTI (RR = 1.06; 95% CI: 0.94, 1.19) and slightly lower for ear infections (RR = 1.17; 95% CI: 0.93, 1.46). Associations were slightly stronger among infants whose mothers spent more time at home during pregnancy. Air pollution exposure during the first year was highly correlated with prenatal exposure, so we were unable to discern the relative importance of each exposure period.Conclusions: Our findings support the hypothesis that early-life exposure to ambient air pollution may increase the risk of upper and lower respiratory tract infections in infants.

Cardiovascular effects of particulate air pollution exposure: time course and underlying mechanisms

Air pollution is now recognized as an important independent risk factor for cardiovascular morbidity and mortality and may be responsible for up to 3 million premature deaths each year worldwide. The mechanisms underlying the observed effects are poorly understood but are likely to be multifactorial. Here, we review the acute and chronic effects of air pollution exposure on the cardiovascular system and discuss how these effects may explain the observed increases in cardiovascular morbidity and mortality.

Ambient Air Pollutants and Acute Case-Fatality of Cerebro-Cardiovascular Events: Takashima Stroke and AMI Registry, Japan (1988–2004)

Background: Apart from the conventional risk factors, cerebro-cardiovascular disease (CVD) are also reported to be associated with air pollution, thus lowering the level of exposure might contribute in prevention activities to reduce the associated adverse outcomes. Though few studies conducted in Japan have reported on the CVD mortality but none have explored the effect of air pollutant exposure on the acute case-fatality of CVD. We investigated the effects of air pollution exposure on acute case-fatality of stroke and acute myocardial infarction (AMI) in a setting where pollutant levels are rather low. Methods: We leveraged the data from the Takashima Stroke and AMI Registry, which covers a population of approximately 55,000 in Takashima County located in central Japan. The study period of 6,210 days (16 years, leap years also taken into account) were divided into quartiles of daily average pollutant concentration; suspended particulate matter (SPM), sulfur dioxide (SO₂), nitrogen dioxide (NO₂), and photochemical oxidants (Ox). The stroke and AMI events were categorized to corresponding quartiles based on the pollution levels of the onset day. To study the effects of air pollutants, we estimated the fatality rate ratio across quartiles of the pollutants where the lowest quartile served as the reference. Results: There were 307 (men: 153 and women: 154) fatal stroke cases within 28 days of onset among the 2,038 first ever stroke during 1988–2004. In the same period, there were 142 (men: 94 and women: 54) fatal AMI cases within 28 days of onset among the 429 first ever AMI events. The mean of the measured pollutant levels were as follows: SPM 26.9 µg/m³, SO₂ 3.9 ppb, NO₂ 16.0 ppb, and Ox 28.4 ppb. Among the pollutants, higher levels of NO₂ showed increased fatality risk. In multi-pollutant model, the highest quartile of NO₂ was associated with 60% higher stroke case-fatality risk in comparison to lowest quartile of NO₂. In the fully adjusted model the fatality-rate ratio was 1.65 (95% CI 1.06–2.57). This association was more prominent among stroke subtype of cerebral infarction. Other pollutant levels did not show any association with stroke or AMI case-fatality. Conclusion: We observed association between NO₂ levels, an index of traffic related air pollution, with the acute case-fatality of stroke, especially cerebral infarction in our study population. Further studies are needed in different regions to determine the association between ambient air pollutants and acute cardiovascular fatalities.

Genomics and the respiratory effects of air pollution exposure

Adverse health effects from air pollutants remain important, despite improvement in air quality in the past few decades. The exact mechanisms of lung injury from exposure to air pollutants are not yet fully understood. Studying the genome (e.g. single-nucleotide polymorphisms (SNP) ), epigenome (e.g. methylation of genes), transcriptome (mRNA expression) and microRNAome (microRNA expression) has the potential to improve our understanding of the adverse effects of air pollutants. Genome-wide association studies of SNP have detected SNP associated with respiratory phenotypes; however, to date, only candidate gene studies of air pollution exposure have been performed. Changes in epigenetic processes, such DNA methylation that leads to gene silencing without altering the DNA sequence, occur with air pollutant exposure, especially global and gene-specific methylation changes. Respiratory cell line and animal models demonstrate distinct gene expression signatures in the transcriptome, arising from exposure to particulate matter or ozone. Particulate matter and other environmental toxins alter expression of microRNA, which are short non-coding RNA that regulate gene expression. While it is clearly important to contain rising levels of air pollution, strategies also need to be developed to minimize the damaging effects of air pollutant exposure on the lung, especially for patients with chronic lung disease and for people at risk of future lung disease. Careful study of genomic responses will improve our understanding of mechanisms of lung injury from air pollution and enable future clinical testing of interventions against the toxic effects of air pollutants.

Neurobehavioral effects of exposure to traffic-related air pollution and transportation noise in primary schoolchildren

BackgroundChildren living close to roads are exposed to both traffic noise and traffic-related air pollution. There are indications that both exposures affect cognitive functioning. So far, the effects of both exposures have only been investigated separately. ObjectivesTo investigate the relationship between air pollution and transportation noise on the cognitive performance of primary schoolchildren in both the home and school setting. MethodsData acquired within RANCH from 553 children (aged 9–11 years) from 24 primary schools were analysed using multilevel modelling with adjustment for a range of socio-economic and life-style factors. ResultsExposure to NO2 (which is in urban areas an indicator for traffic-related air pollution) at school was statistically significantly associated with a decrease in the memory span length measured during DMST (χ2=6.8, df=1, p=0.01). This remained after additional adjustment for transportation noise. Statistically significant associations were observed between road and air traffic noise exposure at school and the number of errors made during the ‘arrow’ (χ2=7.5, df=1, p=0.006) and ‘switch’ (χ2=4.8, df=1, p=0.028) conditions of the SAT. This remained after adjustment for NO2. No effects of air pollution exposure or transportation noise exposure at home were observed. Combined exposure of air pollution and road traffic noise had a significant effect on the reaction times measured during the SRTT and the ‘block’ and the ‘arrow’ conditions of the SAT. ConclusionsOur results provide some support that prolonged exposure to traffic-related air pollution as well as to noise adversely affects cognitive functioning.

Variable Selection for High Dimensional Bayesian Density Estimation: Application to Human Exposure Simulation

SummaryNumerous studies have linked ambient air pollution and adverse health outcomes. Many studies of this nature relate outdoor pollution levels measured at a few monitoring stations with health outcomes. Recently, computational methods have been developed to model the distribution of personal exposures, rather than ambient concentration, and then relate the exposure distribution to the health outcome. Although these methods show great promise, they are limited by the computational demands of the exposure model. We propose a method to alleviate these computational burdens with the eventual goal of implementing a national study of the health effects of air pollution exposure. Our approach is to develop a statistical emulator for the exposure model, i.e. we use Bayesian density estimation to predict the conditional exposure distribution as a function of several variables, such as temperature, human activity and physical characteristics of the pollutant. This poses a challenging statistical problem because there are many predictors of the exposure distribution and density estimation is notoriously difficult in high dimensions. To overcome this challenge, we use stochastic search variable selection to identify a subset of the variables that have more than just additive effects on the mean of the exposure distribution. We apply our method to emulate an ozone exposure model in Philadelphia.

USE OF REMOTE SENSING ESTIMATES OF NO2 AND PM2.5 EXPOSURE IN A STUDY OF HOSPITAL AND EMERGENCY ROOM VISITS IN ONTARIO, CANADA

Background and Aims: Remote sensing (RS) offers an alternative to ground based air pollution monitoring that provides broad, cost-effective coverage. However, the use of RS estimates in epidemiological studies has not been thoroughly studied, especially for acute health effects. We examine the use of RS to estimate exposure in a case-crossover study of acute myocardial infarction (MI) and asthma hospital visits in Ontario, Canada. Methods: Daily estimates of NO2 and PM2.5 levels were developed by combining retrievals from the OMI, MODIS and MISR instruments with daily profiles from a chemical transport model for the summer of 2005 (June-September). For comparison, ground-based measurements were obtained from Environment Canada’s National Air Pollution Surveillance (NAPS) network. Hospitalization and emergency room visit data, including individual level data on main cause of admission/visit (ICD-10 code), age, sex, and three-digit postal code of home residence, were obtained from databases maintained by the Canadian Institutes for Health Research. Individual exposure was estimated by linkage of residential postal code centroid to the RS estimate (at approximately 10 km resolution) and the nearest NAPS station within 40km. We will use a case-crossover analysis with full-stratum bidirectional control selection as well as a sensitivity analysis with two-week bidirectional control selection to examine the acute health effects of air pollution exposure as estimated by both RS and ground-based methods. Results: There were 7,562 hospitalizations for MI and 26,962 emergency room visits for asthma in Ontario in the summer of 2005. Preliminary analyses show RS estimates were available for PM2.5 on 36% of days and for NO2 on 24% of days over this time period. RS estimates of PM2.5 were highly correlated with daily-average ground-based NAPS measurements (r=0.73), while daily NO2 measurements were moderately correlated (r=0.48). Conclusions: RS estimates of PM2.5 and NO2 are well correlated with ground-based measurements and offer a promising alternative for estimating exposure in a study of acute health effects.

EFFECTS OF METAL-RICH PARTICULATE MATTER EXPOSURE ON EXOSOME-ASSOCIATED MICRORNAS.

Background and Aims: Epidemiological studies have reported an increased risk for cardiovascular disease (CVD) in relation to exposure to metal-rich particulate matter. Cell-derived membrane vesicles (exosomes) are released in plasma and transfer microRNAs. Exosomes might mediate the effects of air pollution, since potentially they could be produced by the respiratory system, reach the systemic circulation and lead to the development of CVD. The aim of the present study was to identify effects of exposure to metal-rich particulate matter on exosomes-associated microRNAs expression in workers of an electric furnace steel plant with well characterized exposure. Methods: Plasma exosomes were isolated by ultracentrifuge from 55 steel workers on the first day of a workweek (baseline) and after three days of work (post-exposure). We measured the expression of the 88 most abundantly expressed and best characterized micro RNA sequences by SYBR green chemistry. The relative expression of miRNAs was measured by real-time PCR using SNORD48, SNORD47, SNORD44 and RNU6-2 as endogenous controls. Relative quantification of miRNA expression was calculated using the 2-ΔCt method. Paired t-tests were used to compare baseline and post-exposure samples. Results: Expression profiling of 88 human miRNAs extracted from baseline and paired post-exposure blood samples identified 6 miRNAs which showed significant differential expression between the two samples. Among the most notable changes were miR-302c and miR-128 which were up-regulated by 13.9-and 5.6-fold respectively (p<0.001), and miR-28-3p and let-7g which were up-regulated by 3.6-and 2.26-fold (p=0.01), miR-125a-5p and miR-181a that were up-regulated 3-and 1.7-fold (p<0.02). Conclusion: These results propose a new role for exosomes in mediating the effects of air pollution exposure on CVD risk. Our findings, if confirmed, could lead to the identification of potentially reversible alterations that might be also considered as potential target for new diagnostic and therapeutic interventions. This work was supported by ESSIA Regione Lombardia DGR VIII/10462 e PRIN -2007 2 S2HT8 area 06.

TRAFFIC-RELATED AIR POLLUTION AND ACUTE CHANGES IN HEART RATE VARIABILITY AND RESPIRATORY FUNCTION IN URBAN CYCLISTS

Background and Aims: Few studies have examined the acute health effects of air pollution exposures experienced while cycling in traffic. The aim of this study was to examine the relationship betwee...

MYOCARDIAL INFARCTION INCIDENCE AND ROAD TRAFFIC NOISE EXPOSURE,PISA (ITALY),2002-2006

Background and Aims: Evidence is growing on association between exposure to road traffic noise and health effects, in particular cardiovascular and myocardial infarction (MI). The ongoing study aims to evaluate the association between MI incidence and residential exposure to road traffic noise by a case control (CC) study, on current data. Methods: Mortality and hospitalization data (1998-2006) have been used to obtain cases of first MI incidence in 2002-2006 through a validated algorithm. Five controls will be matched to each case by gender, age and a deprivation index (DI), based on 2001 census. Residential address, residence length and geographical coordinates come from Municipality archives. Road traffic noise exposure have been estimated at the buildings façades from Pisa noise map built by Environmental Protection Agency of Tuscany Region according to new acoustic indicators and interim methods issued by European Directive 2009/49/CE. Results: The CC study is ongoing. 823 MI cases (age 35+ years) have been identified in 2002-2006 with the aim to analyze also the last- residence noise exposure length. Preliminary analyses of MI cases on residents, living in the same building (769 different buildings) on the same year, estimated incidence rates, direcly standardized by age and DI, computed by sex and night noise levels (<50dB; 50-54dB; 55+ dB). The rate ratios vs the lowest noise level were 1.14 at 50-54dB, 1.33 at 55+ dB among men while were respectively 1.12 and 1.06 among women. Conclusions: Preliminary results confirm, in men, the presence of an association between first MI occurrence and high leves of nocturnal traffic noise exposure at residence place. The ongoing CC study will consider the residence length and will try to evaluate the confoundig effect of air pollution exposure by means of traffic characterization (veichles number, pedestrian area, vicinity to airport,railway etc) in the road of residence.

Traffic-Related Air Pollution and Acute Changes in Heart Rate Variability and Respiratory Function in Urban Cyclists

Background: Few studies have examined the acute health effects of air pollution exposures experienced while cycling in traffic.Objectives: We conducted a crossover study to examine the relationship between traffic pollution and acute changes in heart rate variability. We also collected spirometry and exhaled nitric oxide measures.Methods: Forty-two healthy adults cycled for 1 hr on high- and low-traffic routes as well as indoors. Health measures were collected before cycling and 1–4 hr after the start of cycling. Ultrafine particles (UFPs; ≤ 0.1 μm in aerodynamic diameter), particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5), black carbon, and volatile organic compounds were measured along each cycling route, and ambient nitrogen dioxide (NO2) and ozone (O3) levels were recorded from a fixed-site monitor. Mixed-effects models were used to estimate associations between air pollutants and changes in health outcome measures relative to precycling baseline values.Results: An interquartile range increase in UFP levels (18,200/cm3) was associated with a significant decrease in high-frequency power 4 hr after the start of cycling [β = –224 msec2; 95% confidence interval (CI), –386 to –63 msec2]. Ambient NO2 levels were inversely associated with the standard deviation of normal-to-normal (NN) intervals (β = –10 msec; 95% CI, –20 to –0.34 msec) and positively associated with the ratio of low-frequency to high-frequency power (β = 1.4; 95% CI, 0.35 to 2.5) 2 hr after the start of cycling. We also observed significant inverse associations between ambient O3 levels and the root mean square of successive differences in adjacent NN intervals 3 hr after the start of cycling.Conclusions: Short-term exposures to traffic pollution may contribute to altered autonomic modulation of the heart in the hours immediately after cycling.

Air Pollution and Stillbirth: A Population-Based Case–Control Study in Taiwan

Background: There is limited evidence suggesting that prenatal exposure to ambient air pollutants may increase the risk of stillbirth, but previous epidemiological studies have not elaborated the most susceptible gestational period for the effects of air pollution exposure on stillbirth.Objectives: We estimated associations between exposure to ambient air pollutants and stillbirth, with special reference to the assessment of gestational periods when the fetus is most susceptible.Methods: We conducted a population-based case–control study in Taiwan. The case group consisted of 9,325 stillbirths, and the control group included 93,250 births randomly selected from 1,510,064 Taiwanese singleton newborns in 2001–2007. Adjusted logistic regression models were used to estimate odds ratios (ORs) per 10-ppb change for ozone and nitrogen dioxide, 1-ppb change for sulfur dioxide (SO2), 10-μg/m3 change for particulate matter with aerodynamic diameter ≤ 10 μm (PM10), and 100-ppb change for carbon monoxide during different gestational periods and according to term or preterm (< 37 weeks) birth status.Results: Stillbirth increased in association with a 1-ppb increase in first-trimester SO2 [adjusted OR = 1.02; 95% confidence interval (CI), 1.00–1.04], particularly among preterm births (adjusted OR = 1.04; 95% CI, 1.01–1.07). Stillbirth was also associated with a 10-μg/m3 increase in PM10 during the first (adjusted OR = 1.02; 95% CI, 1.00–1.05) and second (adjusted OR = 1.02; 95% CI, 1.00–1.04) month of gestation, and, as with SO2, associations appeared to be restricted to preterm births (first-trimester adjusted OR = 1.03; 95% CI, 1.00–1.07).Conclusion: The study provides evidence that exposure to outdoor air SO2 and PM10 may increase the risk of stillbirth, especially among preterm births, and that the most susceptible time periods for exposure are during the first trimester of gestation.

Traffic-related air pollution, preterm birth and term birth weight in the PIAMA birth cohort study

Background Maternal exposure to air pollution has been associated with adverse pregnancy outcomes. Few studies took into account the spatial and temporal variation of air pollution levels. Objectives To evaluate the impact of maternal exposure to traffic-related air pollution during pregnancy on preterm birth and term birth weight using a spatio-temporal exposure model. Methods We estimated maternal residential exposure to nitrogen dioxide (NO 2), particulate matter (PM 2.5) and soot during pregnancy (entire pregnancy, 1st trimester, and last month) for 3853 singleton births within the Dutch PIAMA prospective birth cohort study by means of temporally adjusted land-use regression models. Associations between air pollution concentrations and preterm birth and term birth weight were analyzed by means of logistic and linear regression models with and without adjustment for maternal physical, lifestyle, and socio-demographic characteristics. Results We found positive, statistically non-significant associations between exposure to soot during entire pregnancy and during the last month of pregnancy and preterm birth [adj. OR (95% CI) per interquartile range increase in exposure 1.08 (0.88–1.34) and 1.09 (0.93–1.27), respectively]. There was no indication of an adverse effect of air pollution exposure on term birth weight. Conclusions In this study, maternal exposure to traffic-related air pollution during pregnancy was not associated with term birth weight. There was a tendency towards an increased risk of preterm birth with increasing air pollution exposure, but statistical power was low.

Modelling air pollution for epidemiologic research – Part II: Predicting temporal variation through land use regression

Over recent years land use regression (LUR) has become a frequently used method in air pollution exposure studies, as it can model intra-urban variation in pollutant concentrations at a fine spatial scale. However, very few studies have used the LUR methodology to also model the temporal variation in air pollution exposure. The aim of this study is to estimate annual mean NO 2 and PM 10 concentrations from 1996 to 2008 for Greater Manchester using land use regression models. The results from these models will be used in the Manchester Asthma and Allergy Study (MAAS) birth cohort to determine health effects of air pollution exposure. The Greater Manchester LUR model for 2005 was recalibrated using interpolated and adjusted NO 2 and PM 10 concentrations as dependent variables for 1996-2008. In addition, temporally resolved variables were available for traffic intensity and PM 10 emissions. To validate the resulting LUR models, they were applied to the locations of automatic monitoring stations and the estimated concentrations were compared against measured concentrations. The 2005 LUR models were successfully recalibrated, providing individual models for each year from 1996 to 2008. When applied to the monitoring stations the mean prediction error (MPE) for NO 2 concentrations for all stations and years was -0.8 μg/m³ and the root mean squared error (RMSE) was 6.7 μg/m³. For PM 10 concentrations the MPE was 0.8 μg/m³ and the RMSE was 3.4 μg/m³. These results indicate that it is possible to model temporal variation in air pollution through LUR with relatively small prediction errors. It is likely that most previous LUR studies did not include temporal variation, because they were based on short term monitoring campaigns and did not have historic pollution data. The advantage of this study is that it uses data from an air dispersion model, which provided concentrations for 2005 and 2010, and therefore allowed extrapolation over a longer time period.

Drug consumption and air pollution: an overview

Acute respiratory symptoms are among the health effects of air pollution exposure. Studies over the past decades have linked respiratory drug use (consumption or sales) with changes in air pollution conditions. Twenty-one studies were analyzed to discuss whether increased levels of air pollution are associated with the use of medications for respiratory diseases. Epidemiological studies agree that variation in the drug use is related to air pollution exposure. In panel studies, although asthmatics are more sensitive to air pollution effects, the increase in drug use was comparable and similar to non-asthmatics. Ecological studies confirm a significant association in respiratory drug sales depending on the selected lags (that is the time elapsing between air pollution measurement and the resulting drug use). The results of a meta-analysis of two ecological studies showed an increase in risk for increase in daily mean concentration of some pollutant (10 µg m(-3) ). For Black Smoke RR=1.007 (95% CI 1.004-1.011) for lag 1, and RR=1.008 (95% CI 1.005-1.010) for lag 8. For Nitrogen dioxide, RR=1.008 (95% CI 1.005-1.012) for lag 8 and for Sulfur dioxide, RR=1.005 (95% CI 1.001-1.010) for lag 9. The analysis of drug use provides useful data for the evaluation of risks which derive from exposure to air pollution. More studies are needed to measure the effects of air pollution on respiratory medication use. Lags of up to 14 days have to be considered and the pollutants to be considered should include particulate matter and ozone.

The Inflammatory Bowel Diseases and Ambient Air Pollution: A Novel Association

OBJECTIVES:The inflammatory bowel diseases (IBDs) emerged after industrialization. We studied whether ambient air pollution levels were associated with the incidence of IBD.METHODS:The health improvement network (THIN) database in the United Kingdom was used to identify incident cases of Crohn's disease (n=367) or ulcerative colitis (n=591), and age- and sex-matched controls. Conditional logistic regression analyses assessed whether IBD patients were more likely to live in areas of higher ambient concentrations of nitrogen dioxide (NO2), sulfur dioxide (SO2), and particulate matter <10μm (PM10), as determined by using quintiles of concentrations, after adjusting for smoking, socioeconomic status, non-steroidal anti-inflammatory drugs (NSAIDs), and appendectomy. Stratified analyses investigated effects by age.RESULTS:Overall, NO2, SO2, and PM10 were not associated with the risk of IBD. However, individuals ≤23 years were more likely to be diagnosed with Crohn's disease if they lived in regions with NO2 concentrations within the upper three quintiles (odds ratio (OR)=2.31; 95% confidence interval (CI)=1.25–4.28), after adjusting for confounders. Among these Crohn's disease patients, the adjusted OR increased linearly across quintile levels for NO2 (P=0.02). Crohn's disease patients aged 44–57 years were less likely to live in regions of higher NO2 (OR=0.56; 95% CI=0.33–0.95) and PM10 (OR=0.48; 95% CI=0.29–0.80). Ulcerative colitis patients ≤25 years (OR=2.00; 95% CI=1.08–3.72) were more likely to live in regions of higher SO2; however, a dose–response effect was not observed.CONCLUSIONS:On the whole, air pollution exposure was not associated with the incidence of IBD. However, residential exposures to SO2 and NO2 may increase the risk of early-onset ulcerative colitis and Crohn's disease, respectively. Future studies are needed to explore the age-specific effects of air pollution exposure on IBD risk.

Ambient air pollution and respiratory health effects in mail carriers

Mail carriers represent an occupational group suffering from respiratory symptoms and lung function impairment. Although environmental conditions may play role, information on the effects of air pollution exposure in this population is lacking. The present study was conducted in Athens, Greece, in order to investigate the adverse effects of long-term air pollution exposure on respiratory outcomes in mail carriers. A total of 226 mail carriers and 73 office employees were enrolled. Information on respiratory symptoms, medical, occupational, residential and smoking history was obtained through a questionnaire. Flow-volume curves were performed in the workplace using a portable spirometer. Individualised personal exposure assessment has been applied based on long-term residential and occupational subject history linked with geographical air pollution distribution. Furthermore, personal measurements were obtained for forty-one mail carriers using NO(2) and O(3) passive samplers, assuming that current air pollution exposure is sufficiently representative of long-term, previous exposure to make a plausible link with current health status. The analysis based on exposures estimated on the basis of residential and work addresses showed that the most exposed to PM(10) postal workers have rhinitis at a higher rate (OR=1.67, 95% CI: 1.01-2.75). In mail carriers there is indication that those exposed to higher concentrations of Omicron(3) or PM(10) have a greater possibility to present rhinitis (OR=1.63, 95% CI: 0.93-2.88 and OR=1.70, 95% CI: 0.96-3.03, respectively). The effect of O(3) on rhinitis became even more apparent in the analysis based on exposures assessed by personal measurements (OR=6.74, 95% CI: 1.24-36.55). Exposure to NO(2) was significantly associated with decrements in lung function. For office employees the exposure to air pollutants was not associated to any adverse respiratory outcome. Our findings suggest that air pollution is a contributing factor for the occurrence of rhinitis and lung function impairment in mail carriers.

Preterm Birth and Ambient Air Pollution in Volta Redonda, Rio de Janeiro, Brazil

ISEE-0523 Background and Objective: Preterm birth (PTB) is related to some health outcomes such as pulmonary, ophthalmologic and neurologic morbidity, delayed psychomotor development and death. In recent years, several studies have examined the relationship between PTB and air pollution. This study investigated the association between prematurity and air pollution in Volta Redonda, an industrialized city in Rio de Janeiro/Brazil. Methods: In this population-based study we examined prematurity in relation to maternal exposure to outdoor air pollution, among 13,366 singleton births in Volta Redonda from 2003 to 2006. Birth and air monitoring data were obtained from governmental offices. We estimated maternal exposure to particulate matter with an aerodynamic diameter of ≤ 10 μm (PM10), sulfur dioxide (SO2) and ozone (O3) considering their daily arithmetic means concentrations. Date of birth was used to estimate maternal exposure to pollutants over each trimester of pregnancy. We estimated crude and adjusted effects of air pollution exposure on the risk of PTB using logistic regression models. Analyses were performed to single and multiple pollutants models to assess the robustness of each contaminant in the association. We adjusted models for potential confounders of preterm birth. Results: Statistical significant crude and adjusted odds ratios (OR) for PTB was observed to maternal exposure to SO2 during each trimester of pregnancy. Multiple pollutants model indicates the robustness of the relationship between maternal exposure to SO2 and PTB OR First trimester = 1.304; 95% CI: 1.145, 1.487; OR Second trimester = 1.310; 95% CI: 1.187, 1.446; OR Third trimester = 1.252; 95% CI: 1.1152, 1.360). Dose-response patterns were also observed for interquartile range in all three trimesters of pregnancy in their relation to maternal exposure to SO2. Conclusion: Results show that maternal exposure to sulfur dioxide may increase risk of preterm birth.