Research Report (Health Effects Institute)[JOURNAL]
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200 papers
Uptake and inflammatory effects of nanoparticles in a human vascular endothelial cell line.
Kennedy IM, Wilson D, Barakat AI … +1 more , HEI Health Review Committee
Res Rep Health Eff Inst · 2009 Jan · PMID 19552347
The mechanisms governing the correlation between exposure to nanoparticles and the increased incidence of cardiovascular disease remain unknown. Nanoparticles appear to cross the pulmonary epithelial barrier into the blo...
The mechanisms governing the correlation between exposure to nanoparticles and the increased incidence of cardiovascular disease remain unknown. Nanoparticles appear to cross the pulmonary epithelial barrier into the bloodstream, raising the possibility of direct contact with the vascular endothelium. Because endothelial inflammation is critical for the development of cardiovascular pathology, we hypothesized that direct exposure of human aortic endothelial cells (HAECs*) to nanoparticles induces an inflammatory response and that this response depends on the composition of the particles. To test this hypothesis, we incubated HAECs for 1 to 8 hours with different concentrations (0.001-50 microg/mL) of iron oxide (Fe2O3), yttrium oxide (Y2O3), cerium oxide (CeO2), and zinc oxide (ZnO) nanoparticles. Using real-time reverse transcriptase-polymerase chain reaction (RT-PCR), we subsequently measured messenger RNA (mRNA) levels of three markers of inflammation: intercellular cell adhesion molecule-1 (ICAM-1), interleukin-8 (IL-8), and monocyte chemotactic protein-1 (MCP-1). The particles were well characterized in terms of size, surface area, composition, and crystal structure. To determine the interactions of nanoparticles with HAECs, we used inductively coupled plasma-mass spectrometry (ICP-MS) to measure the concentration of internalized particles. Our data indicate that the delivery of nanoparticles to the HAEC surface and their uptake within the cells correlate directly with the concentration of particles in the cell culture medium. Transmission electron microscopy (TEM) revealed that the Fe2O3, Y2O3, and ZnO nanoparticles are internalized by HAECs and are often found within intracellular vesicles (the CeO2 particles were not imaged). Fe2O3 nanoparticles did not provoke an inflammatory response in HAECs at any of the concentrations tested, CeO2 particles elicited no response at low concentrations and a weak response above 10 microg/mL, and Y2O3 and ZnO nanoparticles elicited a pronounced inflammatory response above a threshold concentration of 10 microg/mL. We used fluorescent markers to identify the production of reactive oxygen species (ROS) in cells; the results showed that Y2O3 and ZnO particles at the highest concentrations may lead to the production of ROS. At the highest concentration, ZnO nanoparticles caused significant loss of cell adherence. These results demonstrate that inflammation in HAECs after acute exposure to metal oxide nanoparticles depends on the concentration and composition of the particles.
Health effects of real-world exposure to diesel exhaust in persons with asthma.
Zhang JJ, McCreanor JE, Cullinan P … +5 more , Chung KF, Ohman-Strickland P, Han IK, Järup L, Nieuwenhuijsen MJ
Res Rep Health Eff Inst · 2009 Feb · PMID 19449765
Many people, including people with asthma, experience short-term exposure to diesel exhaust (DE*) during daily activities. The health effects of such exposures, however, remain poorly understood. The present study utiliz...
Many people, including people with asthma, experience short-term exposure to diesel exhaust (DE*) during daily activities. The health effects of such exposures, however, remain poorly understood. The present study utilized a real-world setting to examine whether short-term DE exposure would (1) worsen asthma symptoms, (2) augment airway inflammation, or (3) increase oxidative stress burdens. The study also examined exposure-response relations for several DE components and the contribution of background asthma severity to individuals' respiratory responses to DE exposure. Sixty people participated in the study; 31 had mild asthma and 29 had moderate asthma. Each participant completed an exposure and a control session. During the exposure session, participants walked for 2 hours along a heavily trafficked city street where motor vehicle access was restricted to buses and official taxicabs. These vehicles were powered by diesel engines. During the control session, participants walked for the same duration and at the same speed in a public park where motor vehicle traffic was prohibited. The concentrations of elemental carbon (EC), NO2, ultrafine particles (UFP), and particulate matter less than or equal to 2.5 microm in aerodynamic diameter (PM2.5) during exposure sessions were, on average, 4.8, 4.0, 3.4, and 2.0 times higher, respectively, than during control sessions. Increases in asthma symptom score and in the daily use of asthma reliever medication within the 7-day measurement period after exposure were not significant. Some effects on lung function were statistically significant. Compared with control sessions, forced expiratory volume in the first second (FEV1) was reduced 3.0% to 4.1%, and forced vital capacity (FVC) was reduced 2.8% to 3.7% in the 5 hours immediately after the exposure sessions. Analyses of biomarkers showed that the exposure sessions led to a significant reduction in exhaled breath condensate (EBC) pH and to significant increases in induced sputum neutrophils and myeloperoxidase (MPO). The changes in lung function indices (FEV1, FVC, and forced expiratory flow during the middle half of the FVC [FEF25-75]) were most consistently associated with UFP and EC exposures, whereas the changes in EBC pH were most consistently associated with NO2 exposure. In addition, NO2 had a significant effect on bronchial reactivity and on the amount of interleukin-8 (IL-8) in induced sputum; it also modified the UFP effect on EBC pH and the EC effect on exhaled nitric oxide (eNO). However, our findings cannot be taken as demonstrating a causal association with any measured pollutant, because the measured pollutant concentrations may simply represent the entire roadside diesel-traffic exposure that comprises not only the pollutants measured in this study but also other pollutants in the complex DE mixture and resuspended coarse particles from road dust, engine debris, and tire debris. The effects of exposure appeared to be larger in the more severe asthmatic group for most outcomes measured. In conclusion, short-term exposure to urban roadside diesel traffic led to consistent and significant reductions in lung function, accompanied by airway acidification and neutrophilic inflammation. Our findings help to explain the epidemiologic evidence on diesel traffic health effects in persons with asthma.
Mechanisms of particulate matter toxicity in neonatal and young adult rat lungs.
Pinkerton KE, Zhou Y, Zhong C … +4 more , Smith KR, Teague SV, Kennedy IM, Ménache MG
Res Rep Health Eff Inst · 2008 Oct · PMID 19203021
Particulate matter (PM*) has been associated with a variety of adverse health effects, primarily involving the cardiovascular and respiratory systems. Researchers continue to investigate biologic mechanisms that may expl...
Particulate matter (PM*) has been associated with a variety of adverse health effects, primarily involving the cardiovascular and respiratory systems. Researchers continue to investigate biologic mechanisms that may explain how exposure to PM exacerbates or directly causes adverse effects. Particle composition may play a critical role in these effects. In this study we used a diffusion flame system to generate ultrafine iron, soot, and iron combined with soot particles and exposed young adult and neonatal rats to different compositions of these particles. Young adult rats inhaled all three PM compositions on three consecutive days for 6 hours per day. Exposure to soot PM at 250 microg/m3 or to iron PM at 57 microg/m3 demonstrated no adverse respiratory effects. However, we observed mild pulmonary stress when the iron concentration was increased to 90 microg/m3. The most striking effects resulted when the rats inhaled PM composed of iron (45 microg/m3) combined with soot particles (total mass 250 microg/m3). This type of exposure produced significant indicators of oxidative stress, signs of inflammation, and increases in the levels of cytochrome P450 isozymes in the lungs. Repeated three-day exposure of neonatal rats to soot and iron particles in the second and the fourth weeks of life produced significant oxidative stress (elevations in oxidized and reduced glutathione) and ferritin induction. Neonatal rats exposed to PM in the second week of life also had a subtle but significant cell proliferation reduction in the centriacinar regions of the lungs. These findings suggest that iron combined with soot PM can lead to changes in the respiratory tract not found with exposure to iron or soot PM alone at similar concentrations. Unique effects in the neonate suggest that age may play an important role in susceptibility to inhaled particles.
Black-pigmented material in airway macrophages from healthy children: association with lung function and modeled PM10.
Grigg J, Kulkarni N, Pierse N … +3 more , Rushton L, O'Callaghan C, Rutman A
Res Rep Health Eff Inst · 2008 Jun · PMID 18767287
Epidemiologic studies in children suggest that chronic inhalation of carbonaceous particulate matter < or = 10 pm in aerodynamic diameter (PM10) attenuates the normal growth of lung function. However, the relation betwee...
Epidemiologic studies in children suggest that chronic inhalation of carbonaceous particulate matter < or = 10 pm in aerodynamic diameter (PM10) attenuates the normal growth of lung function. However, the relation between markers of PM10 exposure and the quantity of particles entering the pediatric airway is unclear. Experimental studies have shown that particles entering the lower airway remain visible in the cytoplasm of airway macrophages (AMs) for several months. We hypothesized that particle loading of AMs, detected as black-pigmented material, reflects individual exposure of healthy children to PM10. In this study, we aimed to establish the relation between the median area of black material in AMs (measured as the two-dimensional area of black material ["black area"] per AM per child) and (1) lung function, and (2) level of primary PM10 at the child's home address as estimated by dispersion modeling (referred to as "modeled primary PM10"). We also performed a series of exploratory analyses assessing the association between the median black area in AMs and (1) variables that could modify individual exposure, and (2) airway inflammation. To achieve these aims, AMs were sampled using induced sputum from children in Leicestershire, United Kingdom, and lung function was determined by spirometry. Data from 64 of 116 children who provided adequate induced sputum samples were analyzed. The area of the black material in AMs was determined by an analysis of digitized light-microscopic images of 100 randomly chosen AMs per child. There was a significant inverse association between size of black area in AMs and lung function: each 1.0-microm2 increase in the area of the black material in AMs was associated with a 17.0% (95% confidence interval [CI], 5.6 to 28.4) reduction in forced expiratory volume in one second (FEV1), a 12.9% (95% CI, 0.9 to 24.8) reduction in forced vital capacity (FVC), and a 34.7% (95% CI, 11.3 to 58.1) reduction in forced expiratory flow between 25% and 75% of forced vital capacity (FEF25%-75%). These associations were not affected by bronchodilator treatment. There was also an association between modeled exposure to primary PM10 and area of black material in AMs: each 1.0-microg/m3 increase in primary PM10 was associated with an increase of 0.10 microm2 (95% CI, 0.01 to 0.18) in black area in AMs. There was no significant association between the median black area in AMs and age, height, weight, sex, activity level, and levels of neutrophilic airway inflammation in the induced sputum. We conclude that the median area of black material in AMs in children is a promising marker of individual exposure to carbonaceous PM10 and that our data strengthen the epidemiologic data suggesting that PM10 impairs the growth of lung function in children.
Relationships of Indoor, Outdoor, and Personal Air (RIOPA): part II. Analyses of concentrations of particulate matter species.
Turpin BJ, Weisel CP, Morandi M … +4 more , Colome S, Stock T, Eisenreich S, Buckley B
Res Rep Health Eff Inst · 2007 Aug · PMID 18064946
During the study Relationships of Indoor, Outdoor, and Personal Air (RIOPA*), 48-hour integrated indoor, outdoor, and personal air samples were collected between summer 1999 and spring 2001 in three different areas of th...
During the study Relationships of Indoor, Outdoor, and Personal Air (RIOPA*), 48-hour integrated indoor, outdoor, and personal air samples were collected between summer 1999 and spring 2001 in three different areas of the United States: Elizabeth NJ, Houston TX, and Los Angeles County CA. Air samples suitable for analyzing particulate matter 2.5 microm or smaller in aerodynamic diameter (PM2.5) were collected in 219 homes (twice in 169 homes). Indoor and outdoor air samples suitable for gas-phase and particle-phase organic analyses were collected in 152 homes (twice in 132 homes). Samples or subsets of samples were analyzed for PM2.5 mass, organic functional groups, elements, organic carbon (OC), elemental carbon (EC), gas-phase and particle-phase polycyclic aromatic hydrocarbons (PAHs), and chlordanes. Air exchange rate (AER), temperature, and relative humidity were measured for each residence; questionnaire data and time-activity information were collected from the participants. Median indoor, outdoor, and personal PM2.5 mass concentrations were 14.4, 15.5, and 31.4 microg/m3, respectively. Personal PM2.5 concentrations were significantly higher and more variable than indoor and outdoor concentrations. Several approaches were applied to quantify indoor PM2.5 of ambient (outdoor) and nonambient (indoor) origin, some using PM2.5 mass concentrations and others using PM2.5 species concentrations. PM of outdoor origin was estimated in three ways using increasingly accurate assumptions. Comparing estimates from the three approaches enabled us to quantify several types of errors that may be introduced when central-site PM concentrations are used as surrogate estimates for PM exposure. Estimates made using individual measurements produced broader distributions and higher means than those made using a single infiltration factor for all homes and days. The best estimate (produced by the robust regression approach) of the mean contribution of outdoor PM2.5 to the indoor mass concentration was 73% and to personal exposure was 26%. Possible implications of exposure error for epidemiologic assessments of PM are discussed below. Organic particulate matter was the major constituent of PM2.5 generated indoors. After correcting for artifacts, it constituted 48%, 55%, and 61% of PM2.5 mass inside study homes in Los Angeles, Elizabeth, and Houston, respectively. At least 40% but probably closer to 75% of this organic matter, on average, was emitted or formed indoors. Functional group analysis provided some insights into the composition and properties of the indoor-generated organic PM2.5. Chlordane, a very minor but mutagenic semivolatile organic mixture previously used as a termiticide, was found to be mostly of indoor origin. High emission rates were most frequently found in homes built from 1945 to 1959. Analysis of the change in gas-particle partitioning during transport of outdoor PAHs to indoor environments illustrated that chemical thermodynamics can alter the concentration and composition of outdoor PM as it is transported indoors. (This has been previously noted for nitrate [Lunden et al 2003].) In epidemiologic studies that rely on central-site monitoring data, such transformations may result in measurement error, and this possibility warrants further investigation.
An updated study of mortality among North American synthetic rubber industry workers.
Delzell E, Sathiakumar N, Graff J … +4 more , Macaluso M, Maldonado G, Matthews R, Health Effects Institute
Res Rep Health Eff Inst · 2006 Aug · PMID 17326338
This study evaluated mortality rates from leukemia and other diseases during the time period 1944 through 1998 among 17,924 men employed in the synthetic rubber industry. In this group, there were 6237 deaths, which is 1...
This study evaluated mortality rates from leukemia and other diseases during the time period 1944 through 1998 among 17,924 men employed in the synthetic rubber industry. In this group, there were 6237 deaths, which is 14% fewer than the 7242 deaths expected based on general population rates. Numbers of observed versus expected deaths (shown hereafter as observed/expected) were 1608/1741 for all cancers combined, including 71/61 for leukemia, 53/53 for non-Hodgkin lymphoma (NHL*), and 26/27 for multiple myeloma. The higher than expected number of deaths from leukemia (16% increase) was concentrated in workers paid hourly who had started work 20 to 29 years earlier, had worked 10 or more years in the industry, and had worked in subgroups employed in polymerization, coagulation, maintenance labor, and laboratory operations. The overall higher leukemia mortality rate, as well as the higher rate in the subgroup of hourly workers who had 20 or more years since hire and 10 or more years worked, was not limited to a particular form of leukemia. Cumulative exposure to 1,3-butadiene (BD) was associated positively with all leukemias, with chronic myelogenous leukemia and, to a lesser extent, with chronic lymphocytic leukemia (CLL). Exposure to styrene or to dimethyldithiocarbamate (DMDTC) also was associated positively with leukemia. Exposures to these two agents were correlated with exposure to BD; data were limited on the independent effects of each of the three chemicals on leukemia. After controlling for the effects of BD, we found no consistent exposure-response relation between either styrene or DMDTC and all leukemias, chronic myelogenous leukemia, or CLL. However, a positive association between any exposure to DMDTC and leukemia persisted. The data from this study indicate that employment in the synthetic rubber industry is related causally to leukemia. Uncertainty remains about the specific agent or agents responsible for the association. The carcinogenic mechanisms through which BD, styrene, or DMDTC could cause leukemia in humans have not been established, and epidemiologic support for a leukemogenic role is limited for these agents. Styrene and DMDTC were associated positively with NHL. External support for this relation has not been reported from other epidemiologic studies. The study did not find any clear relation between exposure to BD, styrene, or DMDTC and multiple myeloma. Some subgroups of subjects had more than the expected number deaths from colorectal cancer, prostate cancer, and other diseases. These increases did not appear to be related to occupational exposure in the industry.
Particulate air pollution and nonfatal cardiac events. Part II. Association of air pollution with confirmed arrhythmias recorded by implanted defibrillators.
Dockery DW, Luttmann-Gibson H, Rich DQ … +6 more , Link MS, Schwartz JD, Gold DR, Koutrakis P, Verrier RL, Mittleman MA
Res Rep Health Eff Inst · 2005 Jun · PMID 17153518
Implanted cardioverter defibrillators (ICDs) monitor patients for episodes of cardiac arrhythmias and can initiate a therapeutic intervention to restore normal heart rhythm. These devices also record dates, times, and el...
Implanted cardioverter defibrillators (ICDs) monitor patients for episodes of cardiac arrhythmias and can initiate a therapeutic intervention to restore normal heart rhythm. These devices also record dates, times, and electrograms of these episodes. We examined the effects of air pollution on the incidence of arrhythmias in 195 cardiac patients with ICD devices in the Boston metropolitan area between July 1995 and July 2002. Gaseous air pollutant and meteorologic data were measured on essentially all days, fine particle mass on 80% of the days, and black carbon (BC) on 61% of the days. Date and time of detected arrhythmias, intracardiac electrograms, and therapeutic interventions were downloaded during the patients' regular follow-up visits every 3 months on average. A cardiac electrophysiologist reviewed electrograms recorded before, during, and after the arrhythmias and categorized them into ventricular and supraventricular events. Risk of arrhythmias associated with air pollution was estimated using logistic regression with adjustments for season, temperature, relative humidity, day of the week, and patient. We found increased relative risks of ventricular arrhythmias (VAs) associated with an increase in 2-day mean concentrations for all air pollutants considered, although these associations were not statistically significant. The relative risks of supraventricular arrhythmias (SVAs) increased in association with 2-day mean concentrations for all air pollutants, and this association was significant only for sulfur dioxide (SO2) at 4 ppb (odds ratio [OR] = 1.33; 95% confidence interval [CI] = 1.04, 1.70). The positive associations of VAs and SVAs with particulate matter less than 2.5microm in aerodynamic diameter (PM2.5; also referred to as fine particles), carbon monoxide (CO), nitrogen dioxide (NO2), BC, and SO2 suggest a link with motor vehicle pollutants. We explored patient characteristics that may have identified subjects susceptible to the effects of air pollution. The association of air pollution with SVAs was blunted by regularly prescribed beta-blockers. We found stronger associations of air pollution with VAs for episodes within 3 days of a previous arrhythmia, suggesting that VAs were triggered by air pollution episodes in combination with other factors that raised the patient's underlying risk. Although ICDs are specifically designed to monitor and treat only VAs, these results suggest that air pollution may trigger both VAs and SVAs.
Particulate air pollution and nonfatal cardiac events. Part I. Air pollution, personal activities, and onset of myocardial infarction in a case-crossover study.
Peters A, von Klot S, Heier M … +6 more , Trentinaglia I, Cyrys J, Hörmann A, Hauptmann M, Wichmann HE, Löwel H
Res Rep Health Eff Inst · 2005 Jun · PMID 17153517
We conducted a prospective case-crossover study to assess the association of particulate air pollution with onset of nonfatal myocardial infarction (MI). Patients who had survived MIs between February 1999 and July 2001...
We conducted a prospective case-crossover study to assess the association of particulate air pollution with onset of nonfatal myocardial infarction (MI). Patients who had survived MIs between February 1999 and July 2001 were identified based on the Coronary Event Registry in Augsburg, Southern Germany. The study included 851 MI subjects with known date and time of MI who had survived the first 24 hours and had completed the Registry's standard interview. Of these subjects, 691 provided case and control information for subject-specific MI triggers collected by a diary assessing the 4 days before symptom onset. The exposures of interest were the total number concentration (TNC) of particles as an indicator for ultrafine particles and the mass of particles with an aerodynamic diameter no larger than 2.5 microm (PM2.5). We conducted conditional logistic regression analyses using different control-selection strategies in a case-crossover approach, and Poisson regression analyses of the time-series data.
Characterization of metals emitted from motor vehicles.
Schauer JJ, Lough GC, Shafer MM … +4 more , Christensen WF, Arndt MF, DeMinter JT, Park JS
Res Rep Health Eff Inst · 2006 Mar · PMID 16669575
A systematic approach was used to quantify the metals present in particulate matter emissions associated with on-road motor vehicles. Consistent sampling and chemical analysis techniques were used to determine the chemic...
A systematic approach was used to quantify the metals present in particulate matter emissions associated with on-road motor vehicles. Consistent sampling and chemical analysis techniques were used to determine the chemical composition of particulate matter less than 10 microm in aerodynamic diameter (PM10*) and particulate matter less than 2.5 microm in aerodynamic diameter (PM2.5), including analysis of trace metals by inductively coupled plasma mass spectrometry (ICP-MS). Four sources of metals were analyzed in emissions associated with motor vehicles: tailpipe emissions from gasoline- and diesel-powered vehicles, brake wear, tire wear, and resuspended road dust. Profiles for these sources were used in a chemical mass balance (CMB) model to quantify their relative contributions to the metal emissions measured in roadway tunnel tests in Milwaukee, Wisconsin. Roadway tunnel measurements were supplemented by parallel measurements of atmospheric particulate matter and associated metals at three urban locations: Milwaukee and Waukesha, Wisconsin, and Denver, Colorado. Ambient aerosol samples were collected every sixth day for one year and analyzed by the same chemical analysis techniques used for the source samples. The two Wisconsin sites were studied to assess the spatial differences, within one urban airshed, of trace metals present in atmospheric particulate matter. The measurements were evaluated to help understand source and seasonal trends in atmospheric concentrations of trace metals. ICP-MS methods have not been widely used in analyses of ambient aerosols for metals despite demonstrated advantages over traditional techniques. In a preliminary study, ICP-MS techniques were used to assess the leachability of trace metals present in atmospheric particulate matter samples and motor vehicle source samples in a synthetic lung fluid.
Characterization of particulate and gas exposures of sensitive subpopulations living in Baltimore and Boston.
Koutrakis P, Suh HH, Sarnat JA … +3 more , Brown KW, Coull BA, Schwartz J
Res Rep Health Eff Inst · 2005 Dec · PMID 16541849
Personal exposures to particulate and gaseous pollutants and corresponding ambient concentrations were measured for 56 subjects living in Baltimore, Maryland, and 43 subjects living in Boston, Massachusetts. The 3 Baltim...
Personal exposures to particulate and gaseous pollutants and corresponding ambient concentrations were measured for 56 subjects living in Baltimore, Maryland, and 43 subjects living in Boston, Massachusetts. The 3 Baltimore cohorts consisted of 20 healthy older adults (seniors), 21 children, and 15 individuals with physician-diagnosed chronic obstructive pulmonary disease (COPD*). The 2 Boston cohorts were 20 healthy seniors and 23 children. All children were 9 to 13 years of age; seniors were 65 years of age or older; and the COPD participants had moderate to severe physician-diagnosed COPD. Personal exposures to particulate matter with aerodynamic diameters less than 2.5 microm (PM2.5), sulfate (SO(4)2-), elemental carbon (EC), ozone (03), nitrogen dioxide (NO2), and sulfur dioxide (SO2) were measured simultaneously for 24 hours/day. All subjects were monitored for 8 to 12 consecutive days. The primary objectives of this study were (1) to characterize the personal particulate and gaseous exposures for individuals sensitive to PM health effects and (2) to assess the appropriateness of exposure assessment strategies for use in PM epidemiologic studies. Personal exposures to multiple pollutants and ambient concentrations were measured for subjects from each cohort from each location. Pollutant data were analyzed using correlation and mixed-model regression analyses. In Baltimore, personal PM2.5 exposures tended to be comparable to (and frequently lower than) corresponding ambient concentrations; in Boston, the personal exposures were frequently higher. Overall, personal exposures to the gaseous pollutants, especially O3 and SO2, were considerably lower than corresponding ambient concentrations because of the lack of indoor sources for these gases and their high removal rate on indoor surfaces. Further, the impact of ambient particles on personal exposure (the infiltration factor) and differences in infiltration factor by city, season, and cohort were investigated. No difference in infiltration factor was found among the cohorts, which suggests that all subjects were exposed to the same fraction of ambient PM2.5 for a given ambient concentration. In addition, the results show significant correlations between ambient PM2.5 concentrations and corresponding personal exposures over time and provide further indication that ambient gaseous pollutant concentrations may be better surrogates for personal PM2.5 exposures, especially personal exposures to PM2.5 of ambient origin, than their respective personal exposures. These results have important implications for PM health effects studies that use regression models including both ambient PM2.5 and gaseous pollutant concentrations as independent variables, because both parameters may be serving as surrogates for PM2.5 exposures.
Relationships of Indoor, Outdoor, and Personal Air (RIOPA). Part I. Collection methods and descriptive analyses.
Weisel CP, Zhang J, Turpin BJ … +20 more , Morandi MT, Colome S, Stock TH, Spektor DM, Korn L, Winer AM, Kwon J, Meng QY, Zhang L, Harrington R, Liu W, Reff A, Lee JH, Alimokhtari S, Mohan K, Shendell D, Jones J, Farrar L, Maberti S, Fan T
Res Rep Health Eff Inst · 2005 Nov · PMID 16454009
This study on the relationships of indoor, outdoor, and personal air (RIOPA) was undertaken to collect data for use in evaluating the contribution of outdoor sources of air toxics and particulate matter (PM) to personal...
This study on the relationships of indoor, outdoor, and personal air (RIOPA) was undertaken to collect data for use in evaluating the contribution of outdoor sources of air toxics and particulate matter (PM) to personal exposure. The study was not designed to obtain a population-based sample, but rather to provide matched indoor, outdoor, and personal concentrations in homes that varied in their proximity to outdoor pollution sources and had a wide range of air exchange rates (AERs). This design allowed examination of relations among indoor, outdoor, and personal concentrations of air toxics and PM across a wide range of environmental conditions; the resulting data set obtained for a wide range of environmental pollutants and AERs can be used to evaluate exposure models. Approximately 100 households with residents who do not smoke participated in each of three cities in distinct locations expected to have different climates and housing characteristics: Elizabeth, New Jersey; Houston, Texas; and Los Angeles County, California. Questionnaires were administered to characterize homes, neighborhoods, and personal activities that might affect exposures. The concentrations of a suite of volatile organic compounds (VOCs) and carbonyl compounds, as well as the fraction of airborne particulate matter with a mass median aerodynamic diameter < or = 2.5 microm (PM2.5), were measured during continuous 48-hour sessions in which indoor, outdoor, and personal air samples were collected simultaneously. During the same 48-hour period, the AER (exchanges/hr; x hr(-1)) was determined in each home, and carbonyl compounds were measured inside vehicle cabins driven by a subset of the participants. In most of the homes, measurements were made twice, during two different seasons, to obtain a wide distribution of AERs. This report presents in detail the data collection methods, quality control measures, and initial analyses of data distributions and relations among indoor, outdoor, and personal concentrations. The results show that indoor sources dominated personal and indoor air concentrations of many measured VOCs and carbonyl compounds. For several measured species, personal concentrations were higher than either indoor or outdoor concentrations, indicating the presence of some sources closely related to personal activities. For some species there were no significant indoor sources in the majority of the homes; thus indoor concentrations were mainly determined by outdoor concentrations in these homes. The range of distributions of air concentrations for the measured VOCs, formaldehyde and acetaldehyde, PM2.5, and AERs were generally consistent with values reported previously in the literature. Thus associations derived from or models based on this data set that may link the influence of outdoor sources with indoor air concentrations of air toxics and PM2.5 can be relevant to other urban settings. The simultaneous measurements of indoor concentrations, outdoor concentrations, AERs, and room volumes allowed the use of a mass balance model, under the steady-state approximation, to mechanistically examine the relative contributions of indoor and outdoor sources to measured indoor concentrations on a home-by-home basis. Estimated indoor source strengths for VOCs and carbonyl compounds varied widely from home to home, consistent with the indoor-outdoor concentration patterns, as shown in scatter plots. The indoor source estimations agreed with published values for PM2.5 and with the general understanding of sources of VOCs and carbonyl compounds. The source strengths reported here, derived from hundreds of homes, are an important contribution to the literature on exposure to air toxics. For the first time for many compounds, these estimates present a cohesive set of measurements across a range of air toxics in paired indoor, outdoor, and personal samples along with AER and questionnaire results that can be used for future analyses of indoor air quality. The estimation of outdoor contributions to measured indoor concentrations provides insights about the relative importance of indoor and outdoor sources in determining indoor concentrations, the main determinant of personal exposure for most of the measured compounds. In this report simple statistical tests mainly of the pooled data were used to analyze differences by sampling site, emission source type, season, home type, and home age. Paired adult-child personal concentrations within the same home were also compared using the pooled data set. These analyses generated some intriguing results that warrant more in-depth investigation in the future.
Particle size and composition related to adverse health effects in aged, sensitive rats.
Hahn FF, Barr EB, Ménache MG … +1 more , Seagrave J
Res Rep Health Eff Inst · 2005 Sep · PMID 16300222
Small increases in concentrations of ambient particulate matter (PM*) have been linked to adverse health effects, especially in older people and people with preexisting respiratory disease. Some epidemiologic studies hav...
Small increases in concentrations of ambient particulate matter (PM*) have been linked to adverse health effects, especially in older people and people with preexisting respiratory disease. Some epidemiologic studies have shown the association to be stronger with PM less than 2.5 microm in aerodynamic diameter (PM2.5) than with PM less than 10 microm in aerodynamic diameter (PM10). Some scientists and regulators suggest that 2.5 microm might be an arbitrary cutoff and that the effects might be more pronounced for PM less than 0.1 microm in aerodynamic diameter (ultrafine PM). Our first aim was to determine the relation between size of respirable particles and particle toxicity, as well as the health effects of short-term increases (spikes) in particle concentration against backgrounds of relatively low or high baseline exposures. Our second aim was to determine the effect of spikes in concentration of fine particles (0.7 microm in mass median aerodynamic diameter [MMAD]) and ultrafine particles (35 nm in count median diameter [CMD]) of disparate composition: vanadium pentoxide (V2O5) and carbon black. The relative toxicity of these particles was determined in aged rats with mild pulmonary inflammation induced by instilled endotoxin. Our third aim was to determine the influence of age (aged vs young adult) on particle-induced toxicity in these rats.
Effects of combined ozone and air pollution particle exposure in mice.
Kobzik L, Goldsmith CA, Ning YY … +6 more , Qin G, Morgan B, Imrich A, Lawrence J, Murthy GG, Catalano PJ
Res Rep Health Eff Inst · 2001 Dec · PMID 16220691
Epidemiologic studies indicate that ozone (O3*) and air pollution particles can exacerbate asthma symptoms. We investigated whether coexposure to inhaled particles and O3 causes a synergistic effect on airway responsiven...
Epidemiologic studies indicate that ozone (O3*) and air pollution particles can exacerbate asthma symptoms. We investigated whether coexposure to inhaled particles and O3 causes a synergistic effect on airway responsiveness and allergic inflammation in a murine (BALB/c) model of ovalbumin (OVA)-induced asthma. Half of the mice were sensitized by intraperitoneal injection of OVA and then exposed to OVA aerosol on 3 successive days to create the asthmatic phenotype; the other half were sensitized to OVA and exposed to phosphate-buffered saline (PBS) to create the nonasthmatic control group. On the same 3 days that the OVA or PBS challenge was administered, mice were further divided into groups that were exposed for 5 hours to concentrated ambient particles (CAPs; mass values ranging from 63 to 1,569 microg/m3 for 1 day's exposure), 0.3 ppm O3, both, or neither (n > or = 61 total mice per exposure group for all 12 experiments). Whole-body plethysmography was used to measure airway responsiveness after challenge with aerosolized methacholine (MCh). Enhanced pause (Penh), an index that closely correlates with pulmonary resistance (Hamelmann et al 1997), was measured daily in each mouse immediately after pollutant exposure and, for 7 of the 12 experiments (n > or = 36/exposure group), beginning 24 hours after the final OVA or PBS challenge. Using several complementary statistical models, we found that exposure to CAPs alone caused a small but significant increase in Penh in both normal and asthmatic mice immediately after exposure (an increase of approximately 1% per 100-microg/m3 increase in CAPs). No increase in Penh was found in animals exposed to O3 alone or to filtered air. Compared with control animals, no combination of exposure atmosphere plus asthma produced a synergistic effect on Penh. By 24 hours after the last OVA or PBS challenge, any enhanced response induced by pollutant exposure had declined to control levels. The pollutant exposures did not significantly increase airway inflammation (assessed by bronchoalveolar lavage [BAL] fluid analysis beginning 24 or 48 hours after the final OVA or PBS challenge). Because CAPs are a heterogeneous mixture of particles, elemental analysis was conducted and associations between specific elemental groupings (present in daily samples) and airway responsiveness were analyzed. This analysis showed that increased Penh in asthmatic mice exposed to CAPs plus O3 was associated with the AlSi fraction of CAPs. No such association was found in control mice or in asthmatic mice not exposed to O3. We conclude that CAPs exposure causes an immediate, short-lived (< 24-hour), small increase in airway responsiveness in mice and that changes in airway physiology are correlated with specific elements found within the particle mixture.
Personal, indoor, and outdoor exposures to PM2.5 and its components for groups of cardiovascular patients in Amsterdam and Helsinki.
Brunekreef B, Janssen NA, de Hartog JJ … +8 more , Oldenwening M, Meliefste K, Hoek G, Lanki T, Timonen KL, Vallius M, Pekkanen J, Van Grieken R
Res Rep Health Eff Inst · 2005 Jan · PMID 15916017
The aim of the investigation was to assess the relations between pairs of personal, indoor, and outdoor levels of fine particles and their components with respect to effects for older subjects with cardiovascular disease...
The aim of the investigation was to assess the relations between pairs of personal, indoor, and outdoor levels of fine particles and their components with respect to effects for older subjects with cardiovascular disease. In the framework of a study funded by the European Union (Exposure and Risk Assessment for Fine and Ultrafine Particles in Ambient Air; referred to as ULTRA)*, panel studies were conducted in Amsterdam (The Netherlands) and Helsinki (Finland). Concentrations of outdoor particulate matter 2.5 pm or smaller in aerodynamic diameter (PM2.5) were measured at a fixed site in each location. With HEI funding, each subject's personal and indoor PM2.5 exposure was measured every other week for 6 months during the 24-hour period preceding intensive health measurements. Particle reflectance was measured as a marker for diesel exhaust. Elemental content of more than 50% of the personal and indoor samples and all corresponding outdoor samples was measured using x-ray fluorescence (XRF). Ion content (sulfate, nitrate) was measured using chromatography. For Amsterdam, 337 personal and 409 indoor measurements were collected from 37 subjects; for Helsinki, 336 personal and 503 indoor measurements were collected from 47 subjects. Median personal, indoor, and outdoor PM2.5 concentrations were 13.6, 13.6, and 16.5 microg/m3 in Amsterdam and 9.2, 9.2, and 11.1 microg/m3 in Helsinki. In both cities, personal and indoor PM2.5 concentrations were lower than and highly correlated with outdoor concentrations (median correlation coefficient [R] 0.7-0.8). For most elements, personal and indoor concentrations were also highly correlated with outdoor concentrations. The highest correlations (median R > 0.9) were found for sulfur (S), sulfate, and particle reflectance (reported as the absorption coefficient). Reflectance was a useful proxy for elemental carbon (EC), but site-specific calibration with EC data is necessary. The findings of this study support using fixed-site measurements as a measure of exposure to PM in time-series studies linking the day-to-day variations in PM to the day-to-day variations in health endpoints, especially for components of PM that are generally associated with fine particles and have few indoor sources.
Neurogenic responses in rat lungs after nose-only exposure to diesel exhaust.
Witten ML, Wong SS, Sun NN … +5 more , Keith I, Kweon CB, Foster DE, Schauer JJ, Sherrill DL
Res Rep Health Eff Inst · 2005 Jan · PMID 15916011
Using an in-line, real-time, in vivo exposure system, we investigated whether acute adverse effects of diesel exhaust (DE*) exposure involve neurogenic inflammation in the lungs via sensory nerve C fibers. A total of 168...
Using an in-line, real-time, in vivo exposure system, we investigated whether acute adverse effects of diesel exhaust (DE*) exposure involve neurogenic inflammation in the lungs via sensory nerve C fibers. A total of 168 female F344 rats (175 g, 8 weeks old) were randomly assigned to pretreatment with capsaicin or saline to deplete C-fiber neurotransmitters. In a 2 x 3 factorial design, groups of animals were then exposed nose-only to a low level of DE (LDE, 35.3 microg/m3), a high level of DE (HDE, 632.9 microg/m3), or side-stream cigarette smoke (CS, 0.4 mg/m3). Two control groups were exposed whole body to filtered air in the animal room (fRA) or unfiltered air in the diesel engine room (eRA), respectively. DE was taken directly from a heavy-duty Cummins N14 research engine operated at 75% throttle (California Air Resources Board [CARB] 8, mode 6). Exposure to DE or air was 4 hours/day, 5 days/week, for 3 weeks. Exposure to CS was for 4 hours/day for 7 days. Involvement of neurogenic inflammation in the response to DE or CS was assessed via comparison of plasma extravasation, a sensitive endpoint of neurogenic inflammation, between rats with and without capsaicin pretreatment. Lung injury was assessed via analysis of proinflammatory cytokines, respiratory permeability, and histopathology. Moreover, whether DE exposure affected the molecular mechanisms of neurogenic inflammation was analyzed through quantification of substance P (SP) and its primary neurokinin-1 (NK1) receptor at the gene and protein levels and through neutral endopeptidase (NEP) activity. DE and CS exposure induced dose-dependent plasma extravasation, which may play an important role in initiating the associated lung inflammation and injury. Exposure of rats to DE affected the SP signaling pathway as indicated by overexpression of the NK1 receptor or reduction of SP in the lung tissue. DE exposure consistently inactivated tissue NEP, a key factor that switches neurogenic inflammation from its physiological and protective functions to a role that increases and perpetuates lung injury. The roles of these overlapping neurokininergic mechanisms in the initiation of DE-associated lung injury are plausible, and these changes may contribute to DE-associated respiratory disorders. Capsaicin rats followed the same trends as those of saline animals when exposed to DE or CS: capsaicin rats did not have significantly different plasma extravasation in the airways or lung parenchyma compared to their corresponding controls. Histopathology evaluation likewise demonstrated the same degree of tissue changes, such as edema and alveolar macrophage collection, in capsaicin and saline rats after the same level of DE exposure. In summary, our data suggest that neurokininergic mechanisms may have been involved in DE-induced inflammatory conditions in rat lung but that C fibers did not appear to be involved under these exposure conditions. We believe that time-course or protein knockdown/knockout animal studies are required to characterize further the role of neurokininergic mechanisms in DE-induced lung injury.
Effects of exposure to ultrafine carbon particles in healthy subjects and subjects with asthma.
Frampton MW, Utell MJ, Zareba W … +9 more , Oberdörster G, Cox C, Huang LS, Morrow PE, Lee FE, Chalupa D, Frasier LM, Speers DM, Stewart J
Res Rep Health Eff Inst · 2004 Dec · PMID 15768531
Increased levels of particulate air pollution are associated with increased respiratory and cardiovascular mortality and morbidity as well as worsening of asthma. Ultrafine particles (UFP; less than 0.1 microm in aerodyn...
Increased levels of particulate air pollution are associated with increased respiratory and cardiovascular mortality and morbidity as well as worsening of asthma. Ultrafine particles (UFP; less than 0.1 microm in aerodynamic diameter) may contribute to the health effects of particulate matter (PM) for a number of reasons. Compared with larger particles on a mass basis, UFP have a higher predicted pulmonary deposition, greater potential to induce pulmonary inflammation, larger surface area, and enhanced oxidant capacity. UFP also have the potential to cross the epithelium and enter the systemic circulation. We hypothesized that exposure to UFP causes airway inflammation in susceptible humans with activation of circulating leukocytes and vascular endothelium, a systemic acute phase response, and transient hypercoagulability. We further hypothesized that in people with asthma, UFP deposition would be increased and underlying airway inflammation enhanced. Our objectives were: to develop a system for controlled exposures of humans to UFP; to measure the pulmonary fractional deposition of UFP; to assess the effects of UFP exposure on blood leukocyte and endothelial adhesion molecule expression and activation, on airway nitric oxide (NO) production, on the systemic acute phase response, on blood coagulability, and on cardiac electrical activity and repolarization; and to evaluate these responses in both healthy subjects and people with asthma. We developed and validated a mouthpiece exposure system for human studies of carbon UFP and then conducted three clinical exposure studies: healthy subjects breathing filtered air and UFP (10 microg/m3) at rest (UPREST); healthy subjects breathing air and UFP (10 and 25 microg/m3) with intermittent exercise (UPDOSE); and subjects with mild asthma breathing air and UFP (10 microg/m3) with intermittent exercise (UPASTHMA). All exposures were for 2 hours on the mouthpiece system. Exposures were separated by at least 2 (UPREST and UPDOSE) or 3 (UPASTHMA) weeks. Prior to and at intervals after each exposure, we assessed symptoms, pulmonary function, blood markers of inflammation and coagulation, and airway NO production. Sputum inflammatory cells were assessed 21 hours after exposure. Continuous 12-lead electrocardiography (ECG) recordings were analyzed for changes in heart rate variability, repolarization, and arrhythmias. For healthy subjects, the fractional deposition of UFP at rest was 0.66 +/- 0.11 (mean +/- SD) by particle number, confirming the high deposition for UFP predicted by models. Deposition further increased during exercise (0.83 +/- 0.04). Asthmatic subjects showed higher UFP deposition than did healthy subjects when breathing at rest (0.76 +/- 0.05). During the UPREST protocol, there were no convincing effects for any outcome measures. Breathing 25 microg/m3 UFP with exercise (UPDOSE) was associated with reductions in blood monocytes and activation of T lymphocytes in healthy females. In asthmatic subjects (UPASTHMA), breathing 10 microg/m3 UFP was associated with reduced numbers of blood eosinophils and CD4+ T lymphocytes. In the UPDOSE group, monocyte expression of intercellular adhesion molecule-1 (ICAM-1) was reduced in a concentration-related manner (P = 0.001). In the UPASTHMA group, CD11b expression was reduced on monocytes and eosinophils, and ICAM-1 expression was reduced on polymorphonuclear leukocytes (PMNs). ECG analyses of UPDOSE subjects showed transient reductions in parasympathetic influence on heart rate variability and a reduced repolarization (QT) interval. In UPASTHMA subjects, ECG analyses showed decreased QT variability, but no effect on the QT interval. There were no significant effects in any of the studies on symptoms, pulmonary function, or markers of airway inflammation. We found no increases in soluble markers of systemic inflammation or coagulation. Our hypothesis that inhalation of carbon UFP causes pulmonary inflammation and an acute phase response was not confirmed. However, the observed subtle changes in leukocyte subsets and adhesion molecule expression are consistent with effects on vascular endothelial function. We also found effects on heart rate variability and on cardiac repolarization in healthy subjects. If confirmed, the finding that very low mass concentrations of particles have cardiovascular effects would have important implications for future PM regulatory strategies.
Time-series analysis of air pollution and mortality: a statistical review.
Dominici F
Res Rep Health Eff Inst · 2004 Dec · PMID 15757000
The Walter A Rosenblith New Investigator Award provided funding to explore new statistical approaches for air pollution research. This report reviews and summarizes the methodologic and substantive contributions to time-...
The Walter A Rosenblith New Investigator Award provided funding to explore new statistical approaches for air pollution research. This report reviews and summarizes the methodologic and substantive contributions to time-series analyses of air pollution and mortality that this award made possible. The review is organized according to the following general topics: (1) semiparametric methods for time-series analyses of air pollution and mortality; (2) explorations into the sensitivity of generalized additive models (GAMs*) applied to time-series data; (3) combining information in multisite time-series studies; (4) effects of misclassification of exposure; (5) mortality displacement; (6) shape of the concentration-response curve; and (7) ongoing projects and future directions. Appendix A includes abstracts of papers published as reports and in peer-reviewed journals.
Evaluation of a personal and microenvironmental aerosol speciation sampler (PMASS).
Geyh AS, Hering S, Kreisberg N … +1 more , John W
Res Rep Health Eff Inst · 2004 Nov · PMID 15675716
In this study, an all-aluminum sampler was reconfigured to a lighter weight by using plastic for structural components not contacted by aerosol. Because the sampler body was made of plastic, the aluminum size-selective c...
In this study, an all-aluminum sampler was reconfigured to a lighter weight by using plastic for structural components not contacted by aerosol. Because the sampler body was made of plastic, the aluminum size-selective cyclone inlet was redesigned into a separate, removable unit. The resulting personal and microenvironmental aerosol speciation sampler (PMASS*) is a small, compact sampler designed for assaying concentrations of each major chemical constituent of particulate matter less than or equal to 2.5 pm in aerodynamic diameter (PM2.5) as well as its mass. The sampler consists of a miniature cyclone inlet and two parallel sampling channels, each of which may accommodate a denuder, particle filter, and backup filter. One channel serves to measure mass and inorganic ions; the other, organic and elemental carbon. Six of these samplers were first evaluated in the laboratory to verify the 50% cutpoint of the redesigned cyclone inlet near the target flow rate of 4.0 L/min and to test the effect of sampler orientation, aerosol type, and flow rate on the 50% cutpoint. The six samplers were fabricated at two different times with slight modifications in construction that yielded slightly different 50% cutpoints. The units were then evaluated as microenvironmental samplers under field conditions against reference samplers in Fresno, California, and Baltimore, Maryland. Testing in Maryland also included deployment as a personal sampler. In the laboratory, the mean (+/- SD) 50% cutpoint at a 4.1 L/min flow rate was 2.52 +/- 0.08 pm. Sampler orientation did not affect performance of the cyclone. Small differences in penetration efficiency were found with different challenge aerosols. For flow rates between 3.1 and 4.9 L/min, the 50% cutpoint varied from 3.3 pm to 2.1 pm, respectively. As a microenvironmental sampler, the PMASS performed well against relevant reference samplers for elemental carbon, organic carbon, and nitrate measurements but not for mass measurements, for which the PMASS showed a significant bias of -34%. Precision estimates for PMASS elemental carbon, organic carbon, nitrate, and mass, respectively, were 6.8%, 9.0%, 11.9%, and 12.7% in Fresno and 6.6%, 8.7%, 13.6%, and 17.5% in Baltimore. For personal sampling, PMASS measurements of mass again showed a significant bias of -24% compared with the reference sampler. Precision estimates for the PMASS as a personal sampler for elemental carbon, organic carbon, nitrate, and mass were 8.1%, 19.3%, 19.1% and 24.2%, respectively. Sulfate data were not analyzable because of the large magnitude and variability of the sulfate blanks. Field testing revealed some deformation of components of the PMASS filter pack. These problems may have affected the integrity of the particle filter.
Uptake distribution of ozone in human lungs: intersubject variability in physiologic response.
Ultman JS, Ben-Jebria A, Arnold SF
Res Rep Health Eff Inst · 2004 Nov · PMID 15675715
The primary hypothesis of this study was that intersubject variation in uptake of inhaled ozone causes corresponding variation in the resulting physiologic response. The second hypothesis was that differences in breathin...
The primary hypothesis of this study was that intersubject variation in uptake of inhaled ozone causes corresponding variation in the resulting physiologic response. The second hypothesis was that differences in breathing pattern and lung anatomy induce differences in ozone uptake. Sixty healthy nonsmokers participated in three exposure protocols during which their minute ventilation was 30 L/min, corresponding to moderate exercise. For the intermittent bolus exposure to ozone (BO3*), we measured the penetration volume at which 50% of the bolus was taken up (VP50%). Before and after continuous clean air exposure (Ca) and continuous ozone exposure (CO3: 0.25 ppm ozone), we measured forced expiratory volume in 1 second (FEV1), calculated as the percent change after exposure relative to start of exposure [%FEV1]). We also measured the cross-sectional area of the peripheral lung (Ap) for carbon dioxide (CO2) diffusion, calculated as the percent change after exposure relative to start of exposure (%Ap). After the CO3 session, we also measured ozone uptake (as ozone uptake rate) and fractional ozone uptake efficiency. Uptake efficiency ranged from 0.70 to 0.98 among all subjects. It was inversely correlated with breathing frequency (P = 0.000) but was not correlated with conducting airways volume (P = 0.333). VP50% ranged from 67 to 135 mL among all subjects and was directly correlated with conducting airways volume (P = 0.000). These results indicate that overall ozone uptake was related to breathing frequency but not to airway size, whereas internal distribution of ozone shifted distally as airway size increased. Values of %FEV1 (mean +/- SD: -13.71 +/- 12.99) and %Ap (-7.80 +/- 9.34) were both significantly more negative (P = 0.000) in the CO3 session than in the Ca (control) session (-0.055 +/- 4.57 and 0.40 +/- 11.03, respectively). Ozone uptake rate correlated with individual %Ap (P = 0.008) but not with individual %FEV1 (P = 0.575). Nor were individual %Ap or %FEV1 correlated with VP50%. Therefore, ozone uptake did not explain intersubject differences in forced expiratory responses in this study, but it did partially explain differences in the cross-sectional area available for gas diffusion in the peripheral lung.
Field evaluation of nanofilm detectors for measuring acidic particles in indoor and outdoor air.
Cohen BS, Heikkinen MS, Hazi Y … +3 more , Gao H, Peters P, Lippmann M
Res Rep Health Eff Inst · 2004 Sep · PMID 15553489
This field evaluation study was conducted to assess new technology designed to measure number concentrations of strongly acidic ultrafine particles. Interest in these particles derives from their potential to cause adver...
This field evaluation study was conducted to assess new technology designed to measure number concentrations of strongly acidic ultrafine particles. Interest in these particles derives from their potential to cause adverse health effects. Current methods for counting and sizing airborne ultrafine particles cannot isolate those particles that are acidic. We hypothesized that the size-resolved number concentration of such particles to which people are exposed could be measured by newly developed iron nanofilm detectors on which sulfuric acid (H2SO4*) droplets produce distinctive ringed reaction sites visible by atomic force microscopy (AFM). We carried out field measurements using an array of samplers, with and without the iron nanofilm detectors, that allowed indirect comparison of particle number concentrations and size-resolved measures of acidity. The iron nanofilm detectors are silicon chips (5 mm x 5 mm x 0.6 mm) that are coated with iron by vapor deposition. The iron layer was 21.5 or 26 nm thick for the two batches used in these experiments. After exposure the detector surface was scanned topographically by AFM to view and enumerate the ringed acid reaction sites and deposited nonacidic particles. The number of reaction sites and particles per scan can be counted directly on the image displayed by AFM. Sizes can also be measured, but for this research we did not size particles collected in the field. The integrity of the surface of iron nanofilm detectors was monitored by laboratory analysis and by deploying blank detectors and detectors that had previously been exposed to H2SO4 calibration aerosols. The work established that the detectors could be used with confidence in temperate climates. Under extreme high humidity and high temperature, the surface film was liable to detach from the support, but remaining portions of the film still produced reliable data. Exposure to ambient gases in a filtered air canister during the field tests did not affect the film quality. Sampling sessions to obtain particle measurements were scheduled for two 1-week periods in each of the four seasons at a rural site in Tuxedo, New York. This schedule was selected to test outdoor performance of the iron nanofilm detectors under a variety of weather conditions. To seek possible artifacts caused by local source differences, we also sampled outdoors for two 1-week sessions during the winter in New York City. Indoor tests were conducted in the cafeteria at the Nelson Institute of Environmental Medicine (NIEM) in Tuxedo and in a residence in Newburgh, New York. For the outdoor tests we simultaneously deployed several particle samplers to obtain several measures: --the number concentration of acidic and total particles that penetrated the 100-nm cut size of a microorifice impactor (MOI) and were electrically precipitated in an electrostatic aerosol sampler (EAS) onto the iron nanofilm detectors; --the number concentrations of acidic and total particles estimated from detectors placed in a simple ultrafine diffusion monitor (UDM); --the size-fractionated mass concentration of strong acids in samples from the submicrometer collection stages of the MOI and from a polycarbonate filter, parallel to the EAS, that also collected particles penetrating the MOI's 100-nm cut size; and --the number concentration of all ambient particles with diameters of 300 nm or smaller, determined using a scanning mobility particle sizer (SMPS). In the results from these samplers, the mean number concentration of acidic particles ranged from about 100 to 1800/cm3, representing 10% to 88% of all ambient ultrafine particles for the different seasons and sites. The number concentration did not correlate with the acidic mass (hydrogen ion, or H+, content) for particles smaller than 100 nm in diameter. This was not surprising because a single 100-nm particle may contain the same acid volume as many smaller particles if they are pure acid droplets. The ambient concentrations of H+, sulfate (SO4(2-)), and ammonium (NH4+), collected on polycarbonate filters and measured as a function of particle size, were highest for particles with diameters between 280 and 530 nm, but the size distributions also suggested that a small peak of these ions existed in the particle size range below 88 nm. The H+ / SO4(2-) ratio was somewhat higher for particles below 88 nm, suggesting greater excess acidity for these small particles. Our continuous monitoring showed that airborne concentrations of ultrafine particles varied substantially with time. The iron nanofilm detectors provided a time-integrated number concentration over several days or weeks. The counts on the detectors were relatively low for some of the sampling sessions, resulting in high statistical errors in calculations. Nonetheless, agreement of the mean values was remarkably good for some of the measurements. In future tests, longer collection times and new technologies, such as improved particle-charging methods for electrical precipitation samplers, could provide more efficient collection of particles onto the detectors, higher counts, and lower count-associated uncertainties. In general, concentrations of ultrafine particles determined by AFM analysis of the detectors in the MOI-EAS and UDM appeared to underestimate the total number concentration as determined by comparison samplers. The ability to monitor airborne acidic particles provided by these iron nanofilm detectors enlarges the array of air quality variables that can be measured. This may help to resolve some of the outstanding questions related to causal relations between demonstrated health effects of ambient particles and particulate matter (PM) components.
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