Development of a Novel Simulation Reactor for Chronic Exposure to Atmospheric Particulate Matter.
ABSTRACT: Epidemiological studies have shown that air pollution is associated with the morbidity and mortality from cardiopulmonary diseases. Currently, limited experimental models are available to evaluate the physiological and cellular pathways activated by chronic multi-pollutant exposures. This manuscript describes an atmospheric simulation reactor (ASR) that was developed to investigate the health effects of air pollutants by permitting controlled chronic in vivo exposure of mice to combined particulate and gaseous pollutants. BALB/c mice were exposed for 1?hr/day for 3 consecutive days to secondary organic aerosol (SOA, a common particulate air pollutant) at 10-150??g/m3, SOA (30??g/m3)?+?ozone (65?ppb) or SOA?+?ozone (65?ppb)?+?nitrogen dioxide (NO2; 100?ppb). Daily exposure to SOA alone led to increased airway hyperresponsiveness (AHR) to methacholine with increasing SOA concentrations. Multi-pollutant exposure with ozone and/or NO2 in conjunction with a sub-toxic concentration of SOA resulted in additive effects on AHR to methacholine. Inflammatory cell recruitment to the airways was not observed in any of the exposure conditions. The ASR developed in this study allows us to evaluate the chronic health effects of relevant multi-pollutant exposures at 'real-life' levels under controlled conditions and permits repeated-exposure studies.
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:No study has evaluated the mutagenicity of atmospheres with a calculated air quality health index (AQHI). Thus, we generated in a UV-light-containing reaction chamber two simulated atmospheres (SAs) with similar AQHIs but different proportions of criteria pollutants and evaluated them for mutagenicity in three Salmonella strains at the air-agar interface. We continuously injected into the chamber gasoline, nitric oxide, and ammonium sulfate, as well as either ?-pinene to produce SA-PM, which had a high concentration of particulate matter (PM): 119 ppb ozone (O3), 321 ppb NO2, and 1007 ?g/m3 PM2.5; or isoprene to produce SA-O3, which had a high ozone (O3) concentration: 415 ppb O3, 633 ppb NO2, and 55 ?g/m3 PM2.5. Neither PM2.5 extracts, NO2, or O3 alone, nor nonphoto-oxidized mixtures were mutagenic or cytotoxic. Both photo-oxidized atmospheres were largely direct-acting base-substitution mutagens with similar mutagenic potencies in TA100 and TA104. The mutagenic potencies [(revertants/h)/(mgC/m3)] of SA-PM (4.3 ± 0.4) and SA-O3 (9.5 ± 1.3) in TA100 were significantly different ( P < 0.0001), but the mutation spectra were not ( P = 0.16), being ?54% C ? T and ?46% C ? A. Thus, the AQHI may have some predictive value for the mutagenicity of the gas phase of air.
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: 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:Disparities in exposure to air pollution by race-ethnicity and by socioeconomic status have been documented in the United States, but the impacts of declining transportation-related air pollutant emissions on disparities in exposure have not been studied in detail.This study was designed to estimate changes over time (2000 to 2010) in disparities in exposure to outdoor concentrations of a transportation-related air pollutant, nitrogen dioxide (NO2), in the United States.We combined annual average NO2 concentration estimates from a temporal land use regression model with Census demographic data to estimate outdoor exposures by race-ethnicity, socioeconomic characteristics (income, age, education), and by location (region, state, county, urban area) for the contiguous United States in 2000 and 2010.Estimated annual average NO2 concentrations decreased from 2000 to 2010 for all of the race-ethnicity and socioeconomic status groups, including a decrease from 17.6?ppb to 10.7?ppb (-6.9?ppb) in nonwhite [non-(white alone, non-Hispanic)] populations, and 12.6?ppb to 7.8?ppb (-4.7?ppb) in white (white alone, non-Hispanic) populations. In 2000 and 2010, disparities in NO2 concentrations were larger by race-ethnicity than by income. Although the national nonwhite-white mean NO2 concentration disparity decreased from a difference of 5.0?ppb in 2000 to 2.9?ppb in 2010, estimated mean NO2 concentrations remained 37% higher for nonwhites than whites in 2010 (40% higher in 2000), and nonwhites were 2.5 times more likely than whites to live in a block group with an average NO2 concentration above the WHO annual guideline in 2010 (3.0 times more likely in 2000).Findings suggest that absolute NO2 exposure disparities by race-ethnicity decreased from 2000 to 2010, but relative NO2 exposure disparities persisted, with higher NO2 concentrations for nonwhites than whites in 2010. https://doi.org/10.1289/EHP959.
Project description:Objective To investigate the relation between exposure to both air and noise pollution from road traffic and birth weight outcomes.Design Retrospective population based cohort study.Setting Greater London and surrounding counties up to the M25 motorway (2317 km2), UK, from 2006 to 2010.Participants 540?365 singleton term live births.Main outcome measures Term low birth weight (LBW), small for gestational age (SGA) at term, and term birth weight.Results Average air pollutant exposures across pregnancy were 41 ?g/m3 nitrogen dioxide (NO2), 73 ?g/m3 nitrogen oxides (NOx), 14 ?g/m3 particulate matter with aerodynamic diameter <2.5 ?m (PM2.5), 23 ?g/m3 particulate matter with aerodynamic diameter <10 ?m (PM10), and 32 ?g/m3 ozone (O3). Average daytime (LAeq,16hr) and night-time (Lnight) road traffic A-weighted noise levels were 58 dB and 53 dB respectively. Interquartile range increases in NO2, NOx, PM2.5, PM10, and source specific PM2.5 from traffic exhaust (PM2.5 traffic exhaust) and traffic non-exhaust (brake or tyre wear and resuspension) (PM2.5 traffic non-exhaust) were associated with 2% to 6% increased odds of term LBW, and 1% to 3% increased odds of term SGA. Air pollutant associations were robust to adjustment for road traffic noise. Trends of decreasing birth weight across increasing road traffic noise categories were observed, but were strongly attenuated when adjusted for primary traffic related air pollutants. Only PM2.5 traffic exhaust and PM2.5 were consistently associated with increased risk of term LBW after adjustment for each of the other air pollutants. It was estimated that 3% of term LBW cases in London are directly attributable to residential exposure to PM2.5>13.8 ?g/m3during pregnancy.Conclusions The findings suggest that air pollution from road traffic in London is adversely affecting fetal growth. The results suggest little evidence for an independent exposure-response effect of traffic related noise on birth weight outcomes.
Project description:Hypertensive disorders of pregnancy (HDP, including gestational hypertension, preeclampsia, and eclampsia) have a substantial public health impact. Maternal exposure to high levels of air pollution may trigger HDP, but this association remains unclear. The objective of our report is to assess and quantify the association between maternal exposures to criteria air pollutants (ozone, carbon monoxide, nitrogen dioxide, sulfur dioxide, and particulate matter ? 10, 2.5 ?m) on HDP risk. PubMed, EMBASE, MEDLINE, Current Contents, Global Health, and Cochrane were searched (last search: September, 2013). After a detailed screening of 270 studies, 10 studies were extracted. We conducted meta-analyses if a pollutant in a specific exposure window was reported by at least four studies. Using fixed- and random-effects models, odds ratios (ORs) and 95% CIs were calculated for each pollutant with specific increment of concentration. Increases in risks of HDP (OR per 10 ppb = 1.16; 95% CI, 1.03-1.30) and preeclampsia (OR per 10 ppb = 1.10; 95% CI, 1.03-1.17) were observed to be associated with exposure to NO2 during the entire pregnancy, and significant associations between HDP and exposure to CO (OR per 1 ppm = 1.79; 95% CI, 1.31-2.45) and O3 (OR per 10 ppb = 1.09; 95% CI, 1.05-1.13) during the first trimester were also observed. Our review suggests an association between ambient air pollution and HDP risk. Although the ORs were relatively low, the population-attributable fractions were not negligible given the ubiquitous nature of air pollution.
Project description:Nitrogen dioxide is a common air pollutant with growing evidence of health impacts independent of other common pollutants such as ozone and particulate matter. However, the worldwide distribution of NO2 exposure and associated impacts on health is still largely uncertain. To advance global exposure estimates we created a global nitrogen dioxide (NO2) land use regression model for 2011 using annual measurements from 5,220 air monitors in 58 countries. The model captured 54% of global NO2 variation, with a mean absolute error of 3.7 ppb. Regional performance varied from R2 = 0.42 (Africa) to 0.67 (South America). Repeated 10% cross-validation using bootstrap sampling (n = 10,000) demonstrated a robust performance with respect to air monitor sampling in North America, Europe, and Asia (adjusted R2 within 2%) but not for Africa and Oceania (adjusted R2 within 11%) where NO2 monitoring data are sparse. The final model included 10 variables that captured both between and within-city spatial gradients in NO2 concentrations. Variable contributions differed between continental regions, but major roads within 100 m and satellite-derived NO2 were consistently the strongest predictors. The resulting model can be used for global risk assessments and health studies, particularly in countries without existing NO2 monitoring data or models.
Project description:Evidence shows that exposure to air pollutants can increase blood pressure in the short and long term. Some studies show higher levels of hypertension prevalence in areas of high pollution. Few data exist on the association of air pollution with hypertension incidence. The purpose of the present study was to prospectively assess the associations of the traffic-related nitrogen dioxide (NO2) and of ozone with the incidence of hypertension in the Black Women's Health Study (BWHS), a large cohort study of African American women.We used Cox proportional hazards models to calculate hazard ratios (HRs) and 95% confidence intervals (CI) for hypertension associated with exposure to NO2 and ozone among 33,771 BWHS participants. NO2 and ozone levels at participant residential locations were estimated with validated models.From 1995 to 2011, 9,570 incident cases of hypertension occurred in a total of 348,154 person-years (median follow-up time, 11 years). The multivariable HRs per interquartile range of NO2 (9.7 ppb) and ozone (6.7 ppb) were 0.92 (95% CI = 0.86, 0.98) and 1.09 (95% CI = 1.00, 1.18).In this large cohort of African American women, higher ozone levels were associated with an increase in hypertension incidence. Higher NO2 levels were not associated with greater hypertension incidence; indeed, incidence was lower at higher NO2 levels.
Project description:Increasing experimental evidence has suggested air pollution as new risk factor for neurological disease. Although long-term exposure is reportedly related to neurological disease, information on association with short-term exposure is scarce. We examined the association of short-term exposure to particles <2.5??m (PM2.5), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3), and carbon monoxide (CO) with PD aggravation in Seoul from the National Health Insurance Service-National Sample Cohort, Korea during 2002-2013. PD aggravation cases were defined as emergency hospital admissions for primarily diagnosed PD and analyzed with a case-crossover analysis, designed for rare acute outcomes. Pollutants concentrations on case and control days were compared and effect modifications were explored. A unit increase in 8-day moving average of concentrations was significantly associated with PD aggravation. The association was consistent for PM2.5 (odds ratio [95% confidence interval]: 1.61 [1.14-2.29] per 10??g/m3), NO2 (2.35 [1.39-3.97] per 10?ppb), SO2 (1.54 [1.11-2.14] per 1?ppb), and CO (1.46 [1.05-2.04] per 0.1?ppm). The associations were stronger in women, patients aged 65-74 years, and cold season, but not significant. In conclusion, short-term air pollution exposure increased risk of PD aggravation, and may cause neurological disease progression in humans.