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.

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.

Ozone exposure and pulmonary effects in panel and human clinical studies: Considerations for design and interpretation.

A wealth of literature exists regarding the pulmonary effects of ozone, a photochemical pollutant produced by the reaction of nitrogen oxide and volatile organic precursors in the presence of sunlight. This paper focuses on epidemiological panel studies and human clinical studies of ozone exposure, and discusses issues specific to this pollutant that may influence study design and interpretation as well as other, broader considerations relevant to ozone-health research. The issues are discussed using examples drawn from the wider literature. The recent panel and clinical literature is also reviewed. Health outcomes considered include lung function, symptoms, and pulmonary inflammation. Issues discussed include adversity, reversibility, adaptation, variability in ozone exposure metric used and health outcomes evaluated, co-pollutants in panel studies, influence of temperature in panel studies, and multiple comparisons. Improvements in and standardization of panel study approaches are recommended to facilitate comparisons between studies as well as meta-analyses. Additional clinical studies at or near the current National Ambient Air Quality Standard (NAAQS) of 70 ppb are recommended, as are clinical studies in sensitive subpopulations such as asthmatics. IMPLICATIONS: The pulmonary health impacts of ozone exposure have been well documented using both epidemiological and chamber study designs. However, there are a number of specific methodological and related issues that should be considered when interpreting the results of these studies and planning additional research, including the standardization of exposure and health metrics to facilitate comparisons among studies.

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.

Potential Occupational Exposures and Health Risks Associated with Biomass-Based Power Generation.

Biomass is increasingly being used for power generation; however, assessment of potential occupational health and safety (OH&S) concerns related to usage of biomass fuels in combustion-based generation remains limited. We reviewed the available literature on known and potential OH&S issues associated with biomass-based fuel usage for electricity generation at the utility scale. We considered three potential exposure scenarios--pre-combustion exposure to material associated with the fuel, exposure to combustion products, and post-combustion exposure to ash and residues. Testing of dust, fungal and bacterial levels at two power stations was also undertaken. Results indicated that dust concentrations within biomass plants can be extremely variable, with peak levels in some areas exceeding occupational exposure limits for wood dust and general inhalable dust. Fungal spore types, identified as common environmental species, were higher than in outdoor air. Our review suggests that pre-combustion risks, including bioaerosols and biogenic organics, should be considered further. Combustion and post-combustion risks appear similar to current fossil-based combustion. In light of limited available information, additional studies at power plants utilizing a variety of technologies and biomass fuels are recommended.

Assessment of the mutagenic potential of Cr(VI) in the oral mucosa of Big Blue® transgenic F344 rats.

Exposure to high concentrations of hexavalent chromium [Cr(VI)] in drinking water was associated with an increased incidence of oral tumors in F344 rats in a 2-year cancer bioassay conducted by the National Toxicology Program. These tumors primarily occurred at 180 ppm Cr(VI) and appeared to originate from the gingival mucosa surrounding the upper molar teeth. To investigate whether these tumors could have resulted from a mutagenic mode of action (MOA), a transgenic mutation assay based on OECD Test Guideline 488 was conducted in Big Blue(®) TgF344 rats. The mutagenic oral carcinogen 4-nitroquinoline-1-oxide (4-NQO) served as a positive control. Mutant frequency was measured in the inner gingiva with adjacent palate, and outer gingiva with adjacent buccal tissue. Exposure to 10 ppm 4-NQO in drinking water for 28 days increased mutant frequency in the cII transgene significantly, from 39.1 ± 7.5 × 10(-6) to 688 ± 250 × 10(-6) in the gingival/buccal region, and from 49.8 ± 17.8 × 10(-6) to 1818 ± 362 × 10(-6) in the gingival/palate region. Exposure to 180 ppm Cr(VI) in drinking water for 28 days did not significantly increase the mutant frequency in the gingival/buccal (44.4 ± 25.4 × 10(-6)) or the gingival/palate (57.8 ± 9.1 × 10(-6)) regions relative to controls. These data indicate that high (∼180,000 times expected human exposure), tumorigenic concentrations of Cr(VI) did not significantly increase mutations in the gingival epithelium, and suggest that Cr(VI) does not act by a mutagenic MOA in the rat oral cavity.

A robust method for assessing chemically induced mutagenic effects in the oral cavity of transgenic Big Blue® rats.

The Big Blue® (BB) in vivo mutation assay uses transgenic rodents to measure treatment-induced mutations in virtually any tissue. The BB assay can be conducted in rats or mice and is ideal for investigating tissue-specific mutagenic mode of action of tumor induction. Some tissues such as oral mucosa have not been thoroughly studied. Due to the small quantity and cartilaginous nature of oral cavity tissues, development of special prosection and DNA isolation methods was required to permit robust analysis of mutations in these tissues. Improved surgical methods permitted collection of adequate and reproducible quantities of tissue (∼45 mg gingiva/buccal and ∼30 mg gingiva/palate). Optimized DNA isolation methods included use of liquid nitrogen pulverization, homogenization, nuclei pelleting, digestion, and phenol/chloroform extraction, to yield sufficient quantities of DNA from these tissues. In preliminary optimization work, mutant frequency (MF) in tongue and gingiva was increased in rats exposed to the promutagen, benzo[a]pyrene, and the direct mutagen, N-ethyl-N-nitrosourea. The oral cavity carcinogen, 4-nitroquinoline-1-oxide (4-NQO; 10 ppm in drinking water; 28 days), was qualified as a positive control for mutagenesis in oral tissues since it caused significant increases in cII MFs in gingiva/palate (50.2-fold) and gingiva/buccal tissues (21.3-fold), but not in liver or bone marrow (0.9- and 1.4-fold, respectively). These results are consistent with the observation that 4-NQO primarily induces tumors in oral cavity. Results also demonstrate the utility of the BB rat mutation assay and optimized methods for investigation of oral cavity mutagenicity, and by extension, analysis of other small and cartilaginous tissues.

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.

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.

The health significance of gas- and particle-phase terpene oxidation products: a review.

The reactions between terpenes and ozone (or other oxidants) produce a wide variety of both gas- and particle-phase products. Terpenes are biogenic volatile organic compounds (VOCs) that are also contained in many consumer products. Ozone is present indoors since it infiltrates into the indoor environment and is emitted by some office and consumer equipment. Some of the gaseous products formed are irritating to biological tissues, while the condensed-phase products have received attention due to their contribution to ambient fine particulate matter (PM2.5) and its respective health significance. Despite common scientific questions, the indoor and ambient air research communities have tended to operate in isolation regarding this topic. This review critically evaluates the literature related to terpene oxidation products and attempts to synthesize results of indoor and ambient air studies to better understand the health significance of these materials and identify knowledge gaps. The review documents the results of a literature search covering terpene oxidation chemistry, epidemiological, toxicological, and controlled human exposure studies, as well as health studies focused more generically on secondary organic aerosol (SOA). The literature shows a clear role for gas-phase terpene oxidation products in adverse airway effects at high concentrations; however, whether these effects occur at more environmentally relevant levels is unclear. The evidence for toxicity of particle-phase products is less conclusive. Knowledge gaps and future research needs are outlined, and include the need for more consistency in study designs, incorporation of reaction product measurements into epidemiological studies conducted in both indoor and ambient settings, and more focused research on the toxicity of SOA, especially SOA of biogenic origin.

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.

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.

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.

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.

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.

Altered heart rate variability in spontaneously hypertensive rats is associated with specific particulate matter components in Detroit, Michigan.

BACKGROUND: Exposure to fine particulate matter [aerodynamic diameter ≤ 2.5 µm (PM2.5)] is linked to adverse cardiopulmonary health effects; however, the responsible constituents are not well defined. OBJECTIVE: We used a rat model to investigate linkages between cardiac effects of concentrated ambient particle (CAP) constituents and source factors using a unique, highly time-resolved data set. METHODS: Spontaneously hypertensive rats inhaled Detroit Michigan, CAPs during summer or winter (2005-2006) for 13 consecutive days. Electrocardiogram data were recorded continuously, and heart rate (HR) and heart rate variability (HRV) metrics were derived. Extensive CAP characterization, including use of a Semicontinuous Elements in Aerosol Sampler (SEAS), was performed, and positive matrix factorization was applied to investigate source factors. RESULTS: Mean CAP exposure concentrations were 518 µg/m(3) and 357 µg/m(3) in the summer and winter, respectively. Significant reductions in the standard deviation of the normal-to-normal intervals (SDNN) in the summer were strongly associated with cement/lime, iron/steel, and gasoline/diesel factors, whereas associations with the sludge factor and components were less consistent. In winter, increases in HR were associated with a refinery factor and its components. CAP-associated HR decreases in winter were linked to sludge incineration, cement/lime, and coal/secondary sulfate factors and most of their associated components. Specific relationships for increased root mean square of the standard deviation of successive normal-to-normal intervals (RMSSD) in winter were difficult to determine because of lack of consistency between factors and associated constituents. CONCLUSIONS: Our results indicate that specific modulation of cardiac function in Detroit was most strongly linked to local industrial sources. Findings also highlight the need to consider both factor analytical results and component-specific results when interpreting findings.

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.

A comparison of vascular effects from complex and individual air pollutants indicates a role for monoxide gases and volatile hydrocarbons.

BACKGROUND: Emerging evidence suggests that the systemic vasculature may be a target of inhaled pollutants of vehicular origin. We have identified several murine markers of vascular toxicity that appear sensitive to inhalation exposures to combustion emissions. OBJECTIVE: We sought to examine the relative impact of various pollutant atmospheres and specific individual components on these markers of altered vascular transcription and lipid peroxidation. METHODS: Apolipoprotein E knockout (ApoE(-/-)) mice were exposed to whole combustion emissions (gasoline, diesel, coal, hardwood), biogenically derived secondary organic aerosols (SOAs), or prominent combustion-source gases [nitric oxide (NO), NO(2), carbon monoxide (CO)] for 6 hr/day for 7 days. Aortas were assayed for transcriptional alterations of endothelin-1 (ET-1), matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-2 (TIMP-2), and heme oxygenase-1 (HO-1), along with measures of vascular lipid peroxides (LPOs) and gelatinase activity. RESULTS: We noted transcriptional alterations with exposures to gasoline and diesel emissions. Interestingly, ET-1 and MMP-9 transcriptional effects could be recreated by exposure to CO and NO, but not NO(2) or SOAs. Gelatinase activity aligned with levels of volatile hydrocarbons and also monoxide gases. Neither gases nor particles induced vascular LPO despite potent effects from whole vehicular emissions. CONCLUSIONS: In this head-to-head comparison of the effects of several pollutants and pollutant mixtures, we found an important contribution to vascular toxicity from readily bioavailable monoxide gases and possibly from volatile hydrocarbons. These data support a role for traffic-related pollutants in driving cardiopulmonary morbidity and mortality.