Association of short-term increases in ambient air pollution and timing of initial asthma diagnosis among Medicaid-enrolled children in a metropolitan area.
ABSTRACT: We investigated associations of short-term changes in ambient ozone (O3), fine particulate matter (PM2.5) and nitrogen dioxide (NO2) concentrations and the timing of new-onset asthma, using a large, high-risk population in an area with historically high ozone levels.The study population included 18,289 incident asthma cases identified among Medicaid-enrolled children in Harris County Texas between 2005-2007, using Medicaid Analytic Extract enrollment and claims files. We used a time-stratified case-crossover design and conditional logistic regression to assess the effect of increased short-term pollutant concentrations on the timing of asthma onset.Each 10 ppb increase in ozone was significantly associated with new-onset asthma during the warm season (May-October), with the strongest association seen when a 6-day cumulative average period was used as the exposure metric (odds ratio [OR]=1.05, 95% confidence interval [CI], 1.02-1.08). Similar results were seen for NO2 and PM2.5 (OR=1.07, 95% CI, 1.03-1.11 and OR=1.12, 95% CI, 1.03-1.22, respectively), and PM2.5 also had significant effects in the cold season (November-April), 5-day cumulative lag (OR=1.11. 95% CI, 1.00-1.22). Significantly increased ORs for O3 and NO2 during the warm season persisted in co-pollutant models including PM2.5. Race and age at diagnosis modified associations between ozone and onset of asthma.Our results indicate that among children in this low-income urban population who developed asthma, their initial date of diagnosis was more likely to occur following periods of higher short-term ambient pollutant levels.
Project description:BACKGROUND: Relatively few studies have been conducted of the association between air pollution and emergency department (ED) visits, and most of these have been based on a small number of visits, for a limited number of health conditions and pollutants, and only daily measures of exposure and response. METHODS: A time-series analysis was conducted on nearly 400,000 ED visits to 14 hospitals in seven Canadian cities during the 1990 s and early 2000s. Associations were examined between carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), sulfur dioxide (SO2), and particulate matter (PM 10 and PM2.5), and visits for angina/myocardial infarction, heart failure, dysrhythmia/conduction disturbance, asthma, chronic obstructive pulmonary disease (COPD), and respiratory infections. Daily and 3-hourly visit counts were modeled as quasi-Poisson and analyses controlled for effects of temporal cycles, weather, day of week and holidays. RESULTS: 24-hour average concentrations of CO and NO2 lag 0 days exhibited the most consistent associations with cardiac conditions (2.1% (95% CI, 0.0-4.2%) and 2.6% (95% CI, 0.2-5.0%) increase in visits for myocardial infarction/angina per 0.7 ppm CO and 18.4 ppb NO2 respectively; 3.8% (95% CI, 0.7-6.9%) and 4.7% (95% CI, 1.2-8.4%) increase in visits for heart failure). Ozone (lag 2 days) was most consistently associated with respiratory visits (3.2% (95% CI, 0.3-6.2%), and 3.7% (95% CI, -0.5-7.9%) increases in asthma and COPD visits respectively per 18.4 ppb). Associations tended to be of greater magnitude during the warm season (April - September). In particular, the associations of PM 10 and PM2.5 with asthma visits were respectively nearly three- and over fourfold larger vs. all year analyses (14.4% increase in visits, 95% CI, 0.2-30.7, per 20.6 microg/m3 PM 10 and 7.6% increase in visits, 95% CI, 5.1-10.1, per 8.2 microg/m3 PM2.5). No consistent associations were observed between three hour average pollutant concentrations and same-day three hour averages of ED visits. CONCLUSION: In this large multicenter analysis, daily average concentrations of CO and NO2 exhibited the most consistent associations with ED visits for cardiac conditions, while ozone exhibited the most consistent associations with visits for respiratory conditions. PM 10 and PM2.5 were strongly associated with asthma visits during the warm season.
Project description:We examined the association of long-term, daily 1-h maximum O3 (ozone) exposures on cause-specific mortality for 22.2 million US Medicare beneficiaries between 2000-2008. We modeled the association between O3 and mortality using age-gender-race stratified log-linear regression models, adjusted for state of residence. We examined confounding by (1) adjusting for PM2.5 (particles with aerodynamic diameters <2.5??m) and NO2 (nitrogen dioxide) exposures, temperature, and neighborhood-level characteristics and behaviors, and (2) decomposing O3 into its temporal and spatio-temporal components and comparing estimated risk ratios. We also examined sensitivity of our results to alternate exposure measures based on warm-season 8-h daily maximum and 24-h average exposures. We found increased risks from long-term O3 exposures to be strongest and most consistent for mortality from respiratory disease (1.030, 95% CI: 1.027, 1.034) (including COPD (chronic obstructive pulmonary disease)), CHF (congestive heart failure), and lung cancer (1.015, 95% CI: 1.010, 1.020), with no evidence of confounding by PM2.5, NO2, and temperature and with results similar across O3 exposure measures. While significant, associations between long-term O3 exposures and CVD (cardiovascular)-related mortality (1.005, 95% CI: 1.003, 1.007) were confounded by PM2.5 and varied with the exposure measure, with associations no longer significantly positive when warm-season 8-h maximum or 24-h average O3 was used to assess exposures. In this large study, we provide strong evidence that O3 exposure is associated with mortality from respiratory-related causes and for the first-time, lung cancer, but raise questions regarding O3-related impacts on CVD mortality. Our findings demonstrate the need to further identify potential confounders.
Project description:BACKGROUND:Social and environmental stressors may modify associations between environmental pollutants and asthma symptoms. We examined if neighborhood asthma prevalence (higher: HAPN vs. lower: LAPN), a surrogate for underlying risk factors for asthma, modified the relationship between pollutants and urgent asthma visits. METHODS:Through zip code, home addresses were linked to New York City Community Air Survey's land use regression model for street-level, annual average nitrogen dioxide (NO2), particulate matter (PM2.5), elemental carbon (EC), summer average ozone (O3), winter average sulfur dioxide (SO2) concentrations. Poisson regression models were fit to estimate the association (prevalence ratio, PR) between pollutant exposures and seeking urgent asthma care. RESULTS:All pollutants, except O3 were higher in HAPN than LAPN (P?<?0.01). Neighborhood asthma prevalence modified the relationship between pollutants and urgent asthma (P-interaction?<?0.01, for NO2 and SO3). Associations between pollutants and urgent asthma were observed only in LAPN (NO2: PR?=?1.38, P?=?0.01; SO3: PR?=?1.85, P?=?0.04). No association was observed between pollutants and urgent asthma among children in HAPN (P?>?0.05). CONCLUSIONS:Relationships between modeled street-level pollutants and urgent asthma were stronger in LAPN compared to HAPN. Social stressors that may be more prevalent in HAPN than LAPN, could play a greater role in asthma exacerbations in HAPN vs. pollutant exposure alone.
Project description:We investigated if greenness and air pollution exposure in parents' childhood affect offspring asthma and hay fever, and if effects were mediated through parental asthma, pregnancy greenness/pollution exposure, and offspring exposure. We analysed 1106 parents with 1949 offspring (mean age 35 and 6) from the Respiratory Health in Northern Europe, Spain and Australia (RHINESSA) generation study. Mean particulate matter (PM2.5 and PM10), nitrogen dioxide (NO2), black carbon (BC), ozone (O3) (µg/m3) and greenness (normalized difference vegetation index (NDVI)) were calculated for parents 0-18 years old and offspring 0-10 years old, and were categorised in tertiles. We performed logistic regression and mediation analyses for two-pollutant models (clustered by family and centre, stratified by parental lines, and adjusted for grandparental asthma and education). Maternal medium PM2.5 and PM10 exposure was associated with higher offspring asthma risk (odds ratio (OR) 2.23, 95%CI 1.32-3.78, OR 2.27, 95%CI 1.36-3.80), and paternal high BC exposure with lower asthma risk (OR 0.31, 95%CI 0.11-0.87). Hay fever risk increased for offspring of fathers with medium O3 exposure (OR 4.15, 95%CI 1.28-13.50) and mothers with high PM10 exposure (OR 2.66, 95%CI 1.19-5.91). The effect of maternal PM10 exposure on offspring asthma was direct, while for hay fever, it was mediated through exposures in pregnancy and offspring's own exposures. Paternal O3 exposure had a direct effect on offspring hay fever. To conclude, parental exposure to air pollution appears to influence the risk of asthma and allergies in future offspring.
Project description:Few studies examining the associations between long-term exposure to ambient air pollution and mortality have considered multiple pollutants when assessing changes in exposure due to residential mobility during follow-up.We investigated associations between cause-specific mortality and ambient concentrations of fine particulate matter (? 2.5 ?m; PM2.5), ozone (O3), and nitrogen dioxide (NO2) in a national cohort of about 2.5 million Canadians.We assigned estimates of annual concentrations of these pollutants to the residential postal codes of subjects for each year during 16 years of follow-up. Historical tax data allowed us to track subjects' residential postal code annually. We estimated hazard ratios (HRs) for each pollutant separately and adjusted for the other pollutants. We also estimated the product of the three HRs as a measure of the cumulative association with mortality for several causes of death for an increment of the mean minus the 5th percentile of each pollutant: 5.0 ?g/m3 for PM2.5, 9.5 ppb for O3, and 8.1 ppb for NO2.PM2.5, O3, and NO2 were associated with nonaccidental and cause-specific mortality in single-pollutant models. Exposure to PM2.5 alone was not sufficient to fully characterize the toxicity of the atmospheric mix or to fully explain the risk of mortality associated with exposure to ambient pollution. Assuming additive associations, the estimated HR for nonaccidental mortality corresponding to a change in exposure from the mean to the 5th percentile for all three pollutants together was 1.075 (95% CI: 1.067, 1.084). Accounting for residential mobility had only a limited impact on the association between mortality and PM2.5 and O3, but increased associations with NO2.In this large, national-level cohort, we found positive associations between several common causes of death and exposure to PM2.5, O3, and NO2.Crouse DL, Peters PA, Hystad P, Brook JR, van Donkelaar A, Martin RV, Villeneuve PJ, Jerrett M, Goldberg MS, Pope CA III, Brauer M, Brook RD, Robichaud A, Menard R, Burnett RT. 2015. Ambient PM2.5, O3, and NO2 exposures and associations with mortality over 16 years of follow-up in the Canadian Census Health and Environment Cohort (CanCHEC). Environ Health Perspect 123:1180-1186; http://dx.doi.org/10.1289/ehp.1409276.
Project description:BACKGROUND:Air pollution constitutes a significant stimulus of asthma exacerbations; however, the impacts of exposure to major air pollutants on asthma-related hospital admissions and emergency room visits (ERVs) have not been fully determined. OBJECTIVE:We sought to quantify the associations between short-term exposure to air pollutants [ozone (O3), carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and particulate matter ?10 ?m (PM10) and PM2.5] and the asthma-related emergency room visits (ERV) and hospitalizations. METHODS:Systematic computerized searches without language limitation were performed. Pooled relative risks (RRs) and 95% confidence intervals (95%CIs) were estimated using the random-effect models. Sensitivity analyses and subgroup analyses were also performed. RESULTS:After screening of 246 studies, 87 were included in our analyses. Air pollutants were associated with significantly increased risks of asthma ERVs and hospitalizations [O3: RR(95%CI), 1.009 (1.006, 1.011); I2 = 87.8%, population-attributable fraction (PAF) (95%CI): 0.8 (0.6, 1.1); CO: RR(95%CI), 1.045 (1.029, 1.061); I2 = 85.7%, PAF (95%CI): 4.3 (2.8, 5.7); NO2: RR(95%CI), 1.018 (1.014, 1.022); I2 = 87.6%, PAF (95%CI): 1.8 (1.4, 2.2); SO2: RR(95%CI), 1.011 (1.007, 1.015); I2 = 77.1%, PAF (95%CI): 1.1 (0.7, 1.5); PM10: RR(95%CI), 1.010 (1.008, 1.013); I2 = 69.1%, PAF (95%CI): 1.1 (0.8, 1.3); PM2.5: RR(95%CI), 1.023 (1.015, 1.031); I2 = 82.8%, PAF (95%CI): 2.3 (1.5, 3.1)]. Sensitivity analyses yielded compatible findings as compared with the overall analyses without publication bias. Stronger associations were found in hospitalized males, children and elderly patients in warm seasons with lag of 2 days or greater. CONCLUSION:Short-term exposures to air pollutants account for increased risks of asthma-related ERVs and hospitalizations that constitute a considerable healthcare utilization and socioeconomic burden.
Project description:Exposure to air pollutants has been related to preterm birth, but little evidence can be available for PM2.5, O3 and CO in China. This study aimed to investigate the short-term effect of exposure to air pollutants on risk preterm birth during 2014-2016 in Ningbo, China.We conducted a time-series study to evaluate the associations between daily preterm birth and major air pollutants (including PM2.5, PM10, SO2, NO2, O3 and CO) in Ningbo during 2014-2016. A General Additive Model extend Poisson regression was used to evaluate the relationship between preterm birth and air pollution with adjustment for time-trend, meteorological factors and day of the week (DOW). We also conducted a subgroup analysis by season and age.In this study, a total of 37,389 birth occurred between 2014 and 2016 from the Electronic Medical Records System of Ningbo Women and Children's Hospital, of which 5428 were verified as preterm birth. The single pollutant model suggested that lag effect of PM2.5, PM10, NO2 reached a peak at day 3 before delivery and day 6 for SO2, and no relationships were observed for O3 and preterm birth. Excess risks (95% confidence intervals) for an increase of IQR of air pollutant concentrations were 4.84 (95% CI: 1.77, 8.00) for PM2.5, 3.56 (95% CI: 0.07, 7.17) for PM10, 3.65 (95% CI: 0.86, 6.51) for SO2, 6.49 (95% CI: 1.86, 11.34) for NO2, -?0.90 (95% CI: -4.76, 3.11) for O3, and 3.36 (95% CI: 0.50, 6.30) for CO. Sensitivity analyses by exclusion of maternal age?<?18 or?>?35 years did not materially alter our results.This study indicates that short-term exposure to air pollutants (including PM2.5, PM10, SO2, NO2) are positively associated with risk of preterm birth in Ningbo, China.
Project description:Air quality is heavily influenced by weather conditions. In this study, we assessed the impact of long-term weather changes on air quality and health in the US during 1994-2012. We quantified past weather-related increases, or 'weather penalty', in ozone (O3) and fine particulate matter (PM2.5), and thereafter estimated the associated excess deaths. Using statistical regression methods, we derived the weather penalty as the additional increases in air pollution relative to trends assuming constant weather conditions (i.e., weather-adjusted trends). During our study period, temperature increased and wind speed decreased in most US regions. Nationally, weather-related 8 h max O3 increases were 0.18 ppb per year (95% CI: 0.06, 0.31) in the warm season (May-October) and 0.07 ppb per year (95% CI: 0.02, 0.13) in the cold season (November-April). The weather penalties on O3 were relatively larger than PM2.5 weather penalties, which were 0.056 µg m-3 per year (95% CI: 0.016, 0.096) in warm months and 0.027 µg m-3 per year (95% CI: 0.010, 0.043) in cold months. Weather penalties on O3 and PM2.5 were associated with 290 (95% CI: 80, 510) and 770 (95% CI: 190, 1350) excess annual deaths, respectively. Over a 19-year period, this amounts to 20 300 excess deaths (5600 from O3, 14 700 from PM2.5) attributable to the weather penalty on air quality.
Project description:BACKGROUND:Studies of effects of air pollution on gestational diabetes mellitus (GDM) have not been consistent, and there has been little investigation of effects of exposure preceding pregnancy. In previous studies, the temporal relationship between exposure and GDM onset has been difficult to establish. METHODS:Data were obtained for 239,574 pregnancies between 1999 and 2009 in a population-based health care system with comprehensive electronic medical records. Concentrations of ambient nitrogen dioxide (NO2), particulate matter (PM) ?2.5??m in aerodynamic diameter (PM2.5) and ?10??m (PM10), and ozone (O3) during preconception and the first trimester of pregnancy at the residential birth address were estimated from regulatory air monitoring stations. Odds ratios (ORs) of GDM diagnosed in the second and third trimesters in association with pollutant exposure were estimated using generalized estimating equation models adjusted for birth year, medical center service areas, maternal age, race/ethnicity, education, census-tract household income, and parity. RESULTS:In single-pollutant models, preconception NO2 was associated with increased risk of GDM (OR?=?1.10 per 10.4?ppb, 95% confidence interval [CI]: 1.07, 1.13). First trimester NO2 was weakly associated with GDM, and this was not statistically significant (OR?=?1.02 per 10.4?ppb, 95% CI: 0.99, 1.05). Preconception NO2 associations were robust in multi-pollutant models adjusted for first trimester NO2 with another co-pollutant from both exposure windows. In single-pollutant models, preconception PM2.5 and PM10 associations were associated with increased risk of GDM (OR?=?1.04 per 6.5??g/m3, 95% CI: 1.01, 1.06; OR?=?1.03 per 16.1??g/m3, 95% CI: 1.00, 1.06, respectively), but these effect estimates were not robust to adjustment for other pollutants. In single-pollutant models, preconception and first trimester O3 were associated with reduced risk of GDM (OR?=?0.94 per 15.7?ppb, 95% CI: 0.92, 0.95; OR?=?0.95 per 15.7?ppb, 95% CI: 0.94, 0.97), associations that were robust to adjustment for co-pollutants. CONCLUSIONS:Maternal exposure to NO2 during the preconception trimester may increase risk of GDM.
Project description:<h4>Background</h4>Although it is well established that air pollutants can exacerbate asthma, the link with new asthma onset in children is less clear.<h4>Objective</h4>We assessed the association between the onset of childhood asthma with both time of birth and time-varying exposures to outdoor air pollutants.<h4>Method</h4>An open cohort of children born in the province of Québec, Canada, was created using linked medical-administrative databases. New cases of asthma were defined as one hospital discharge with a diagnosis of asthma or two physician claims for asthma within a 2 year period. Annual ozone (O3) levels were estimated at the child's residence for all births 1999-2010, and nitrogen dioxide (NO2) levels during 1996-2006 were estimated for births on the Montreal Island. Satellite based concentrations of fine particles (PM2.5) were estimated at a 10 km × 10 km resolution and assigned to residential postal codes throughout the province (1996-2011). Hazard ratios (HRs) were assessed with Cox models for the exposure at the birth address and for the time-dependent exposure. We performed an indirect adjustment for secondhand smoke (SHS).<h4>Results</h4>We followed 1,183,865 children (7,752,083 person-years), of whom 162,752 became asthmatic. After controlling for sex and material and social deprivation, HRs for an interquartile range increase in exposure at the birth address to NO2 (5.45 ppb), O3 (3.22 ppb), and PM2.5 (6.50 ?g/m3) were 1.04 (95% CI: 1.02, 1.05), 1.11 (95% CI: 1.10, 1.12), and 1.31 (95% CI: 1.28, 1.33), respectively. Effects of O3 and PM2.5 estimated with time-varying Cox models were similar to those estimated using exposure at birth, whereas the effect of NO2 was slightly stronger (HR = 1.07; 95% CI: 1.05, 1.09).<h4>Conclusions</h4>Asthma onset in children appears to be associated with residential exposure to PM2.5, O3 and NO2.<h4>Citation</h4>Tétreault LF, Doucet M, Gamache P, Fournier M, Brand A, Kosatsky T, Smargiassi A. 2016. Childhood exposure to ambient air pollutants and the onset of asthma: an administrative cohort study in Québec. Environ Health Perspect 124:1276-1282;?http://dx.doi.org/10.1289/ehp.1509838.