Developing air pollution concentration fields for health studies using multiple methods: Cross-comparison and evaluation.

Past air pollution epidemiological studies have used a wide range of methods to develop concentration fields for health analyses. The fields developed differ considerably among these methods. The reasons for these differences and comparisons of their strengths, as well as the limitations for estimating exposures, remains under-investigated. Here, we applied nine methods to develop fields of eight pollutants (carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3), fine particulate matter (PM2.5), and three speciated PM2.5 constituents including elemental carbon (EC), organic carbon (OC), and sulfate (SO4)) for the metropolitan Atlanta region for five years. The nine methods are Central Monitor (CM), Site Average (SA), Inverse Distance Weighting (IDW), Kriging (KRIG), Land Use Regression (LUR), satellite Aerosol Optical Depth (AOD), CMAQ model, CMAQ with kriging adjustment (CMAQ-KRIG), and CMAQ based data fusion (CMAQ-DF). Additionally, we applied an increasingly popular method, Random Forest (RF), and compared its results for NO2 and PM2.5 with other methods. For statistical evaluation, we focused our discussion on the temporal coefficient of determination, although other metrics are also calculated. Raw output from the CMAQ model contains modeling biases and errors, which are partially mitigated by fusing observational data in the CMAQ-KRIG and CMAQ-DF methods. Based on analyses that simulated model responses to more limited input data, the RF model is more robust and outperforms LUR for PM2.5. These results suggest RF may have potential in air pollution health studies, especially when limited measurement data are available. The RF method has several important weaknesses, including a relatively poor performance for NO2, diagnostic challenges, and computational intensiveness. The results of this study will help to improve our understanding of the strengths and weaknesses of different methods for estimating air pollutant exposures in epidemiological studies.

Influence of airborne particulates on respiratory tract deposition of inhaled toluene and naphthalene in the rat.

OBJECTIVE: Most studies report that inhaled volatile and semivolatile organic compounds (VOCs/SVOCs) tend to deposit in the upper respiratory tract, while ultrafine (or near ultrafine) particulate matter (PM) (∼100 nm) reaches the lower airways. The objective of this study was to determine whether carbon particle co-exposure carries VOCs/SVOCs deeper into the lungs where they are deposited. MATERIALS AND METHODS: Male Sprague-Dawley rats were exposed by inhalation (nose-only) to radiolabeled toluene (20 ppm) or naphthalene (20 ppm) on a single occasion for 1 h, with or without concurrent carbon particle exposure (∼5 mg/m3). The distribution of radiolabel deposited within the respiratory tract of each animal was determined after sacrifice. The extent of adsorption of toluene and naphthalene to airborne carbon particles under the exposure conditions of the study was also assessed. RESULTS: We found that in the absence of particles, the highest deposition of both naphthalene and toluene was observed in the upper respiratory tract. Co-exposure with carbon particles tended to increase naphthalene deposition slightly throughout the respiratory tract, whereas slight decreases in toluene deposition were observed. Few differences were statistically significant. Naphthalene showed greater adsorption to the particles compared to toluene, but overall the particle-adsorbed concentration of each of these compounds was a small fraction of the total inspired concentration. CONCLUSIONS: These studies imply that at the concentrations used for the exposures in this study, inhaled carbon particles do not substantially alter the deposition of naphthalene and toluene within the respiratory tract.

Assessment of the mutagenic potential of hexavalent chromium in the duodenum of big blue® rats.

A cancer bioassay on hexavalent chromium Cr(VI) in drinking water reported increased incidences of duodenal tumors in B6C3F1 mice at exposures of 30-180ppm, and oral cavity tumors in F344 rats at 180ppm. A subsequent transgenic rodent (TGR) in vivo mutation assay in Big Blue® TgF344 rats found that exposure to 180ppm Cr(VI) in drinking water for 28days did not increase cII transgene mutant frequency (MF) in the oral cavity (Thompson et al., 2015). Herein, we extend our analysis to the duodenum of these same TgF344 rats. At study termination, duodenum chromium levels were below either the limit of detection or quantification in control rats, but were 24.6±3.8µg/g in Cr(VI)-treated rats. The MF in control (23.2×10-6) and Cr(VI)-treated rats (22.7×10-6) were nearly identical. In contrast, the MF in the duodenum of rats exposed to 1-ethyl-1-nitrosourea for six days (study days 1, 2, 3, 12, 19, 26) increased 24-fold to 557×10-6. These findings indicate that mutagenicity is unlikely an early initiating event in Cr(VI)-induced intestinal carcinogenesis.

Health effects of carbon-containing particulate matter: focus on sources and recent research program results.

Air pollution is a complex mixture of gas-, vapor-, and particulate-phase materials comprised of inorganic and organic species. Many of these components have been associated with adverse health effects in epidemiological and toxicological studies, including a broad spectrum of carbonaceous atmospheric components. This paper reviews recent literature on the health impacts of organic aerosols, with a focus on specific sources of organic material; it is not intended to be a comprehensive review of all the available literature. Specific emission sources reviewed include engine emissions, wood/biomass combustion emissions, biogenic emissions and secondary organic aerosol (SOA), resuspended road dust, tire and brake wear, and cooking emissions. In addition, recent findings from large toxicological and epidemiological research programs are reviewed in the context of organic PM, including SPHERES, NPACT, NERC, ACES, and TERESA. A review of the extant literature suggests that there are clear health impacts from emissions containing carbon-containing PM, but difficulty remains in apportioning responses to certain groupings of carbonaceous materials, such as organic and elemental carbon, condensed and gas phases, and primary and secondary material. More focused epidemiological and toxicological studies, including increased characterization of organic materials, would increase understanding of this issue.

Carbon capture and sequestration: an exploratory inhalation toxicity assessment of amine-trapping solvents and their degradation products.

Carbon dioxide (CO2) absorption with aqueous amine solvents is a method of carbon capture and sequestration (CCS) from flue gases. One concern is the possible release of amine solvents and degradation products into the atmosphere, warranting evaluation of potential pulmonary effects from inhalation. The CCS amines monoethanolamine (MEA), methyldiethanolamine (MDEA), and piperazine (PIP) underwent oxidative and CO2-mediated degradation for 75 days. C57bl/6N mice were exposed for 7 days by inhalation of 25 ppm neat amine or equivalant concentration in the degraded mixture. The aqueous solutions were nebulized to create the inhalation atmospheres. Pulmonary response was measured by changes in inflammatory cells in bronchoalveolar lavage fluid and cytokine expression in lung tissue. Ames mutagenicity and CHO-K1 micronucleus assays were applied to assess genotoxicity. Chemical analysis of the test atmosphere and liquid revealed complex mixtures, including acids, aldehydes, and other compounds. Exposure to oxidatively degraded MEA increased (p < 0.05) total cells, neutrophils, and lymphocytes compared to control mice and caused inflammatory cytokine expression (statistical increase at p < 0.05). MEA and CO2-degraded MEA were the only atmospheres to show statistical (p < 0.05) increase in oxidative stress. CO2 degradation resulted in a different composition, less degradation, and lower observed toxicity (less magnitude and number of effects) with no genotoxicity. Overall, oxidative degradation of the amines studied resulted in enhanced toxicity (increased magnitude and number of effects) compared to the neat chemicals.

PM2.5-induced cardiovascular dysregulation in rats is associated with elemental carbon and temperature-resolved carbon subfractions.

BACKGROUND: We tested the hypothesis that cardiovascular responses to PM2.5 exposure will be enhanced in hypertensive rats and linked to specific carbonaceous pollutants in an urban industrial setting. METHODS: Spontaneously hypertensive rats were exposed by inhalation to concentrated PM2.5 in an industrial area of Dearborn, Michigan, for four consecutive summer days. Blood pressure (BP), heart rate (HR) and HR variability (HRV) metrics (SDNN, RMSSD) were assessed by radiotelemetry and compared to 1 h- and 8 h-averaged fluctuations in PM2.5 composition, with a focus on elemental and organic carbon (EC and OC, respectively), and temperature-resolved subfractions (EC1-EC5, PC (pyrolized carbon), and OC1-OC4), as well as other major and minor PM components. RESULTS: Mean HR and BP were increased, while HRV was decreased over 4 days of exposure. Using 1 h averages, EC (1 µg/m3 increase) was associated with increased HR of 11-32 bpm (4-11% increase), 1.2-1.5 ms (22-27%) decreases in SDNN, 3-14 mmHg (1.5-8%) increases in systolic BP, and 5-12 mmHg (4-9%) increases in diastolic BP. By comparison, associations with OC were negligible. Using 8 h averages, EC subfractions were linked with increased heart rate (EC1: 13 bpm; EC2, EC3, PC: <5 bpm) and SDNN (EC1> > EC2 > EC3, EC4, PC), but with decreased RMSSD (EC2, EC5 > EC3, EC4). Minimal effects were associated with OC and OC1. Associations between carbon subfractions and BP were negligible. Associations with non-carbonaceous components and trace elements were generally non-significant or of negligible effect size. CONCLUSIONS: These findings are the first to describe associations between acute cardiovascular responses and thermally resolved carbon subfractions. We report that cardiovascular responses to PM2.5 carbonaceous materials appear to be driven by EC and its EC1 fraction.

Childhood asthma acute primary care visits, traffic, and traffic-related pollutants.

UNLABELLED: Previous studies have found associations between traffic-related air pollution and asthma exacerbation in children, where exacerbations were measured according to emergency department visits and hospital admissions. Fewer studies have been undertaken that look at asthma exacerbations in a less severe primary care setting. Therefore, the authors sought to examine the associations between childhood asthma exacerbations, measured as acute visits to a primary care setting, and vehicular-traffic measures in a population of children aged 18 and under in the metropolitan Atlanta area. Statistical tests for differences of mean monthly visits for members with traffic measures above the median compared with below the median and for the upper quartile compared with the lower quartile were conducted. We also compared the odds of having one or more visits in a month for those who lived closer to a major roadway were compared with those who lived farther (greater than 300 m) from a major roadway. Poisson general linear modeling was used to determine associations between daily levels of acute visits for childhood asthma and traffic-related pollutants (zinc, EC [elemental carbon], and PM10 and PM2.5 [particulate matter with an aerodynamic diameter of < or = 10 and < or = 2.5 microm, respectively]) for different levels of traffic and distance measures. This analysis found that both larger traffic volumes and smaller distances to the nearest major roadway were positively and significantly associated with larger numbers of childhood asthma visits, when compared with less traffic and larger distances. Our findings point to motor vehicle traffic as an important contributor to childhood asthma exacerbations. IMPLICATIONS: Previous studies have found associations between traffic-related air pollution and asthma exacerbation in children. However, these studies were mainly conducted in emergency department or hospital admission settings; little is known regarding less acute health effects. This analysis of the association between vehicular traffic measures and childhood asthma in a primary care setting suggests that motor vehicle traffic is a contributor to less acute asthma episodes in children. The present analysis of traffic-related air pollutants and childhood asthma were less conclusive, likely due to methods limitations outlined in the paper. The implication is that further evidence of adverse respiratory health effects in children due to motor vehicle traffic can be found in a primary care setting and similar studies should be considered.

Evaluation of community response to wind turbine-related noise in western New York state.

As the boundaries of harvesting wind energy expand to meet the ever-increasing societal energy demands, the number and size of wind turbines being constructed rises. As part of a larger project to monitor sound in an operating wind park in western New York State, a cross-sectional survey was conducted among individuals living in and around the wind park to characterize the perception, level of annoyance, and self-reported health effects of residents. We conducted the study in a 126 MW wind park consisting of 84 turbines spanning approximately 19 square miles of farmland. Short-term outdoor and indoor sound level measurements were also performed at each dwelling in which a questionnaire was administered. To our knowledge, this study is the first to collect sound measurements at individual residences. There was no apparent exposure-response relationship between an individual's level of annoyance and the short duration sound measurements collected at the time of the survey. There was a correlation between an individual's concern regarding health effects and the prevalence of sleep disturbance and stress among the study population. The siting process is unique to each community with varying degrees of success. Additional sound level measurements inside and outside homes in larger cohorts in concert with detailed questionnaires would be useful in verifying those exposure-response relationships found in studies using calculated sound level data. Additional research should include a detailed investigation of sleep patterns and possible disturbance in those living in and near operating wind turbine projects.

The effects of α-pinene versus toluene-derived secondary organic aerosol exposure on the expression of markers associated with vascular disease.

To investigate the toxicological effects of biogenic- versus anthropogenic-source secondary organic aerosol (SOA) on the cardiovascular system, the Secondary Particulate Health Effects Research program irradiation chamber was used to expose atherosclerotic apolipoprotein E null (Apo E-/-) mice to SOA from the oxidation of either α-pinene or toluene for 7 days. SOA atmospheres were produced to yield 250-300 µg/m(3) of particulate matter and ratios of 10:1:1 α-pinene:nitrogen oxide (NOx):ammonia (NH3); 10:1:1:1 α-pinene:NOx:NH3:sulfur dioxide (SO2) or 10:1:1 toluene:NOx:NH3; and 10:1:1:1 toluene:NOx:NH3:SO2. Resulting effects on the cardiovascular system were assessed by measurement of vascular lipid peroxidation (thiobarbituric acid reactive substance (TBARS)), as well as quantification of heme-oxygenase (HO)-1, endothelin (ET)-1, and matrix metalloproteinase (MMP)-9 mRNA expression for comparison to previous program exposure results. Consistent with similar previous studies, vascular TBARS were not increased significantly with any acute SOA exposure. However, vascular HO-1, MMP-9, and ET-1 observed in Apo E-/- mice exposed to α-pinene + NOx + NH3 + SO2 increased statistically, while α-pinene + NOx + NH3 exposure to either toluene + NOx + NH3 or toluene +NOx + NH3 + SO2 resulted in a decreased expression of these vascular factors. Such findings suggest that the specific chemistry created by the presence or absence of acidic components may be important in SOA-mediated toxicity in the cardiovascular system and/or progression of cardiovascular disease.

Assessment of SARS-CoV-2 surrogate inactivation on surfaces and in air using UV and blue light-based intervention technologies.

The COVID-19 pandemic has created an urgent need to utilize existing and develop new intervention technologies for SARS-CoV-2 inactivation on surfaces and in the air. Ultraviolet (UV) technology has been shown to be an effective antimicrobial intervention. Here a study was conducted to determine the efficacy of commercially available UV and blue light-based devices for inactivating HCoV-229E, a surrogate of SARS-CoV-2. The results indicate that two UV devices designed for surface disinfection, with doses of 8.07 µJ/cm2 for the 254 nm device and 20.61 µJ/cm2 for the 275 nm device, were efficient in inactivating 4.94 logs of surface inoculated HCoV-229E. Additionally, a 222 nm UV device with intended ceiling-based operation was effective in inactivating 1.7 logs of the virus inoculated on surface, with a dose of 6 mJ/cm2. A ceiling-based device designed to emit blue light at 405 nm was found to produce 89% reduction in HCoV-229E inoculated on a surface for a dose of 78 J/cm2. Finally, the UV based 222 nm device was found to produce a 90% reduction in the concentration of airborne HCoV-229E, at a 55 µJ/cm2 dose. These results are indicative of the great potential of using UV based technology for the control of SARS-CoV-2.Implications: An important avenue of arresting COVID-19 and future pandemics caused by infectious pathogens is through environmental disinfection. To this effect, the study presented here evaluates commercially available UV and blue light based antimicrobial devices for their ability to kill the human coronavirus HCoV-229E, a surrogate of SARS-CoV-2, on surfaces and in air. The results indicate that two handheld UV devices produced complete inactivation of surface viral inoculum and a UVC ceiling based device produced 1 log reduction in HCoV-229E in air. These results imply the efficacy of UV technology as an antimicrobial tool, especially for rapid disinfection of indoor air.

Cardiopulmonary response to inhalation of secondary organic aerosol derived from gas-phase oxidation of toluene.

The biological response to inhalation of secondary organic aerosol (SOA) was determined in rodents exposed to SOA derived from the oxidation of toluene, a precursor emitted from anthropogenic sources. SOA atmospheres were produced to yield 300 µg·m(-3) of particulate matter (PM) plus accompanying gases. Whole-body exposures were conducted in mice to assess both pulmonary and cardiovascular effects. ApoE(-/-) mice were exposed for 7 days and measurements of TBARS and gene expression of heme-oxygenase-1 (HO-1), endothelin-1 (ET-1), and matrix metalloproteinase-9 (MMP-9) were made in aorta. Pulmonary inflammatory responses in both species were measured by bronchoalveolar lavage fluid (BALF) cell counts. No pulmonary inflammation was observed. A mild response was observed in mouse aorta for the upregulation of ET-1 and HO-1, with a trend for increased MMP-9 and TBARS, and. Overall, toluene-derived SOA revealed limited biological response compared with previous studies using this exposure protocol with other environmental pollutants.

Toxicological evaluation of realistic emission source aerosols (TERESA): summary and conclusions.

The toxicological evaluation of realistic emissions of source aerosols (TERESA) study seeks to delineate health effects of aerosols formed from emissions of particulate matter sources. This series of papers reports the findings of experiments using coal-fired power plants as the source of emissions and this paper summarizes the findings and knowledge acquired from these studies. Emissions were drawn directly from the stacks of three coal-fired power plants in the US, and photochemically aged in a mobile laboratory to simulate downwind power plant plume processing. The power plants used different sources of coal and had different emission controls. Exposure scenarios included primary particles, secondary particles and mixtures of these with common atmospheric constituents (α-pinene and ammonia). Extensive exposure characterization was carried out, and toxicological outcomes were evaluated in Sprague-Dawley rats exposed to different emission scenarios. Breathing pattern, pulmonary inflammatory responses, in vivo pulmonary and cardiac chemiluminescence and cardiac response in a model of acute myocardial infarction were assessed. The results showed no response or relatively mild responses to the inhaled aerosols studied; complex scenarios which included oxidized emissions and α-pinene to simulate biogenic secondary organic aerosol tended to induce more statistically significant responses than scenarios of oxidized and non-oxidized emissions alone. Relating adverse effects to specific components did not consistently identify a toxic constituent. These findings are consistent with most of the previously published studies using pure compounds to model secondary power plant emissions, but importantly add substantial complexity and thus have considerable merit in defining toxicological responses.

Toxicological evaluation of realistic emission source aerosols (TERESA): introduction and overview.

Determining the health impacts of sources and components of fine particulate matter (PM(2.5)) is an important scientific goal. PM(2.5) is a complex mixture of inorganic and organic constituents that are likely to differ in their potential to cause adverse health outcomes. The Toxicological Evaluation of Realistic Emissions of Source Aerosols (TERESA) study focused on two PM sources--coal-fired power plants and mobile sources--and sought to investigate the toxicological effects of exposure to emissions from these sources. The set of papers published here document the power plant experiments. TERESA attempted to delineate health effects of primary particles, secondary (aged) particles, and mixtures of these with common atmospheric constituents. TERESA involved withdrawal of emissions from the stacks of three coal-fired power plants in the United States. The emissions were aged and atmospherically transformed in a mobile laboratory simulating downwind power plant plume processing. Toxicological evaluations were carried out in laboratory rats exposed to different emission scenarios with extensive exposure characterization. The approach employed in TERESA was ambitious and innovative. Technical challenges included the development of stack sampling technology that prevented condensation of water vapor from the power plant exhaust during sampling and transfer, while minimizing losses of primary particles; development and optimization of a photochemical chamber to provide an aged aerosol for animal exposures; development and evaluation of a denuder system to remove excess gaseous components; and development of a mobile toxicology laboratory. This paper provides an overview of the conceptual framework, design, and methods employed in the study.

PM2.5-induced changes in cardiac function of hypertensive rats depend on wind direction and specific sources in Steubenville, Ohio.

BACKGROUND: Increases in particulate matter less than 2.5 µm (PM(2.5)) in ambient air is linked to acute cardiovascular morbidity and mortality. Specific components and potential emission sources of PM(2.5) responsible for adverse health effects of cardiovascular function are unclear. METHODS: Spontaneously hypertensive rats were implemented with radiotelemeters to record ECG responses during inhalation exposure to concentrated ambient particles (CAPs) for 13 consecutive days in Steubenville, OH. Changes in heart rate (HR) and its variability (HRV) were compared to PM(2.5) trace elements in 30-min time frames to capture acute physiological responses with real-time fluctuations in PM(2.5) composition. Using positive matrix factorization, six major source factors were identified: (i) coal/secondary, (ii) mobile sources, (iii) metal coating/processing, (iv) iron/steel manufacturing, (v) lead and (vi) incineration. RESULTS: Exposure-related changes in HR and HRV were dependant on winds predominately from either the northeast (NE) or southwest (SW). During SW winds, the metal processing factor was associated with increased HR, whereas factors of incineration, lead and iron/steel with NE winds were associated with decreased HR. Decreased SDNN was dominated during NE winds by the incinerator factor, and with SW winds by the metal factor. Metals and mobile source factors also had minor impacts on decreased SDNN with NE winds. Individual elemental components loaded onto these factors generally showed significant associations, although there were some discrepancies. CONCLUSIONS: Acute cardiovascular changes in response to ambient PM(2.5) exposure can be attributed to specific PM constituents and sources linked with incineration, metal processing, and iron/steel production.

Toxicological evaluation of realistic emission source aerosols (TERESA)--power plant studies: assessment of breathing pattern.

Our approach to study multi-pollutant aerosols isolates a single emissions source, evaluates the toxicity of primary and secondary particles derived from this source, and simulates chemical reactions that occur in the atmosphere after emission. Three U.S. coal-fired power plants utilizing different coals and with different emission controls were evaluated. Secondary organic aerosol (SOA) derived from α-pinene and/or ammonia was added in some experiments. Male Sprague-Dawley rats were exposed for 6 h to filtered air or different atmospheric mixtures. Scenarios studied at each plant included the following: primary particles (P); secondary (oxidized) particles (PO); oxidized particles + SOA (POS); and oxidized and neutralized particles + SOA (PONS); additional control scenarios were also studied. Continuous respiratory data were obtained during exposures using whole body plethysmography chambers. Of the 12 respiratory outcomes assessed, each had statistically significant changes at some plant and with some of the 4 scenarios. The most robust outcomes were found with exposure to the PO scenario (increased respiratory frequency with decreases in inspiratory and expiratory time); and the PONS scenario (decreased peak expiratory flow and expiratory flow at 50%). PONS findings were most strongly associated with ammonium, neutralized sulfate, and elemental carbon (EC) in univariate analyses, but only with EC in multivariate analyses. Control scenario O (oxidized without primary particles) had similar changes to PO. Adjusted R(2) analyses showed that scenario was a better predictor of respiratory responses than individual components, suggesting that the complex atmospheric mixture was responsible for respiratory effects.

Aged particles derived from emissions of coal-fired power plants: the TERESA field results.

The Toxicological Evaluation of Realistic Emissions Source Aerosols (TERESA) study was carried out at three US coal-fired power plants to investigate the potential toxicological effects of primary and photochemically aged (secondary) particles using in situ stack emissions. The exposure system designed successfully simulated chemical reactions that power plant emissions undergo in a plume during transport from the stack to receptor areas (e.g., urban areas). Test atmospheres developed for toxicological experiments included scenarios to simulate a sequence of atmospheric reactions that can occur in a plume: (1) primary emissions only; (2) H(2)SO(4) aerosol from oxidation of SO(2); (3) H(2)SO(4) aerosol neutralized by gas-phase NH(3); (4) neutralized H(2)SO(4) with secondary organic aerosol (SOA) formed by the reaction of α-pinene with O(3); and (5) three control scenarios excluding primary particles. The aged particle mass concentrations varied significantly from 43.8 to 257.1 µg/m(3) with respect to scenario and power plant. The highest was found when oxidized aerosols were neutralized by gas-phase NH(3) with added SOA. The mass concentration depended primarily on the ratio of SO(2) to NO(x) (particularly NO) emissions, which was determined mainly by coal composition and emissions controls. Particulate sulfate (H(2)SO(4) + neutralized sulfate) and organic carbon (OC) were major components of the aged particles with added SOA, whereas trace elements were present at very low concentrations. Physical and chemical properties of aged particles appear to be influenced by coal type, emissions controls and the particular atmospheric scenarios employed.

Review and analysis of personal-ambient ozone measurements.

Ambient ozone measurements are often used as surrogates for personal exposures. Due to the limited number of central ozone monitors and varying personal behavioral patterns, some level of variability between ambient and personal exposures is expected. Low-cost sensors and different ways to capture personal activity patterns are being developed as an effort to improve the accuracy of exposure assessment. However, it is still most common to use the traditional approach of using unadjusted ambient concentrations as surrogates for personal exposures. To our knowledge, there has not been a meta-analysis that summarizes the findings from studies that investigated the differences between personal and ambient ozone. We conducted a literature search in PubMed and Science Direct for peer-reviewed studies reporting at least one of the following in a numeric format: 1) personal-ambient measurements, 2) personal-ambient slopes, or 3) personal-ambient correlations to identify and summarize existing studies that investigated personal and ambient ozone concentrations. Twenty-two articles met inclusion criteria and were included in our review. Ambient concentrations almost always overestimated personal exposures. A meta-analysis of slopes showed an overall personal-ambient slope of 0.21 (95% CI: 0.15, 0.27) with high heterogeneity (97%) across studies. The correlations between personal and ambient ozone varied dramatically across subjects from a strong positive (0.77) to a moderate negative correlation (-0.43). Our study found that ambient measurements are not accurate representations of personal exposure, while the magnitude of exposure measurement error varied across studies. Different sources of ozone and how they contribute to true exposure levels for individuals in complementary ways need to be better addressed. The effort to better understand the impact of traditional exposure assessment on the risk estimates must be emphasized along with efforts to improve the current exposure assessment approaches to provide context for interpreting the results from ozone epidemiological studies. Implications: The traditional approach of using ambient ozone measurements as surrogates for personal exposures is likely to result in exposure misclassification, which is a well-recognized source of bias in epidemiological studies. There are efforts to characterize the differences between ambient and personal ozone measurements, though, to our knowledge, there has not been a meta-analysis that summarizes the findings of different studies. Better understanding of the pattern and magnitude of exposure error for ambient and personal ozone can provide directions for future studies and context for interpreting the results from ozone epidemiological studies.

Cardiopulmonary responses in spontaneously hypertensive and Wistar-Kyoto rats exposed to concentrated ambient particles from Detroit, Michigan.

Toxicological effects have been observed in rats exposed to concentrated ambient particles (CAPs) from different regions of the United States. The objective of this study was to evaluate the cardiopulmonary and systemic effects of CAPs in Detroit. The authors stationed a mobile concentrator at a location near major traffic and industrial sources. Spontaneously hypertensive (SH) and Wistar-Kyoto (WKY) rats were exposed to fine CAPs (diameter < 0.1-2.5 microm) 8 h/day for 13 consecutive days. Animals were implanted with telemeters, and electrocardiogram data were recorded continuously. Bronchoalveolar lavage (BAL) fluid and plasma were analyzed. Comprehensive exposure monitoring was conducted, including CAPs components. CAPs exposure concentrations were 103-918 microg/m(3) (mean = 502 microg/m(3)). The authors found no statistically significant differences in heart rate or SDNN (standard deviation of the normal-to-normal intervals), a measure of heart rate variability, between CAPs-exposed and control rats. The authors found significantly higher levels of C-reactive protein in the serum of CAPs-exposed SH rats compared with air-exposed animals. Protein in BAL fluid was elevated in WKY rats exposed to CAPs. Measurement of trace metals in lung tissue showed elevated concentrations of V, Sb, La, and Ce in CAPs-exposed SH animals versus controls. These elements are generally associated with oil combustion, oil refining, waste incineration, and traffic. Examination of wind rose data from the exposure period confirmed that the predominant wind direction was SSW, the direction of many of the aforementioned sources. These results indicate that ambient particles in Detroit can cause mild pulmonary and systemic changes in rats, and suggest the importance of local PM(2.5) sources in these effects.

Cardiopulmonary response to inhalation of biogenic secondary organic aerosol.

An irradiation chamber designed for reproducible generation of inhalation test atmospheres of secondary organic aerosol (SOA) was used to evaluate cardiopulmonary responses in rodents exposed to SOA derived from the oxidation of alpha-pinene. SOA atmospheres were produced with 10:1 ratios of alpha-pinene:nitrogen oxides (NO(x)) and 10:1:1 ratios of alpha-pinene:nitrogen oxides:sulfur dioxide (SO(2)). SOA atmospheres were produced to yield 200 microg m(-3) of particulate matter (PM). Exposures were conducted downstream of honeycomb denuders employed to remove the gas-phase precursors and reaction products. Nose-only exposures were conducted with both rats (pulmonary effects) and mice (pulmonary and cardiovascular effects). Composition of the atmospheres was optimized to ensure that the SOA generated resembled SOA observed in previous irradiation studies, and contained specific SOA compounds of interest (e.g., organosulfates) identified in ambient air. Pulmonary and cardiovascular toxicity were measured in two different rodent species. In situ chemiluminescence and thiobarbituric acid- reactive substances (TBARS) were used to evaluate oxidative reactions in the F344 rats. ApoE(-/-) mice were exposed for 7 days and measurements of TBARS and gene expression of heme oxygenase-1 (HO-1), endothelin-1 (ET-1), matrix metalloproteinase-9 (MMP-9) were made in aorta. Pulmonary inflammatory responses in both species were measured by bronchoalveolar lavage fluid (BALF) cell counts. No pulmonary inflammation was observed in either species. A mild response was observed in mouse aorta for the upregulation of HO-1 and MMP-9, but was not seen for ET-1. Overall, alpha-pinene-derived SOA, including SOA that included organosulfate compounds, revealed limited biological response after short-term inhalation exposures.

Oxidative stress, inflammation, and pulmonary function assessment in rats exposed to laboratory-generated pollutant mixtures.

Oxidative stress may mediate adverse health effects of many inhaled pollutants. Cardiopulmonary responses of Sprague-Dawley rats to inhalation of whole or filtered gasoline engine exhaust (GEE, FGEE); simulated downwind coal emission atmospheres (SDCAs) from two types of coal, each tested at two concentrations; and two concentrations of re-aerosolized paved road dust (RD) were evaluated. In situ chemiluminescence and thiobarbituric acid-reactive substances (TBARS) were used to evaluate oxidative reactions in the lungs, heart, and liver immediately following exposures. Pulmonary inflammatory responses were measured by bronchoalveolar lavage (BAL) cell counts. Respiratory function parameters during exposure were measured by plethysmography. Only GEE significantly enhanced in situ chemiluminescence (all three organs), but only exposure to the high RD concentration increased TBARS (hearts only). There was a weak trend toward increased macrophages recovered in lavage fluid from both SDCAs, and macrophages were significantly elevated by both FGEE and the lower concentration of RD. Respiratory function effects were small, though the effects of the Central Appalachian low-sulfur SDCA on enhanced pause and the effects of the Powder River Basin SCDA on tidal volume were significant. The discordance between the oxidative stress indicators may relate to the use of a single time point in the context of dynamic changes in compensatory mechanisms. These results further suggest that inflammatory responses measured by BAL cellularity may not always correlate with oxidative stress. Overall, the toxicological effects from exposure to these pollutant mixtures were subtle, but the results show differences in the effects of atmospheres having different physical/chemical characteristics.