Dataset Information

Validation of Miniaturized Particulate-Matter Real-Time Samplers for Characterizing Personal Polycyclic Aromatic Hydrocarbon Exposure.

ABSTRACT: This study validates the analysis of polycyclic aromatic hydrocarbons (PAHs) in microgram levels of particulate matter (PM) collected on filters by two low-flow rate, real-time monitors, microPEM™ and microAeth®. Particle-associated PAHs were analyzed by a coupling of a gas chromatograph to a sensitive, atmospheric-pressure laser ionization-mass spectrometer. Air particulate samples were collected over the course of one or two days in the living room of a fourth-floor apartment in New York City. Three types of samplers, the two aforementioned personal samplers and a high-flow rate pump (4 liters per minute), were operated side by side, and three samples of each type were collected during each sampling period. Intrasampler agreement as measured by relative standard deviation (RSD) was within 1% to 18%. After background subtraction, total PAH measured by all three sampler types had good agreement (R=0.99). This ability to accurately characterize personal PAH exposure in archived filters collected by these real-time samplers could provide additional important PAH exposure information that can benefit many environmental health studies using these monitors.

SUBMITTER: Yan B

PROVIDER: S-EPMC6039126 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Validation of Miniaturized Particulate-Matter Real-Time Samplers for Characterizing Personal Polycyclic Aromatic Hydrocarbon Exposure.

Yan Beizhan B Pitiranggon Masha M Ross James J Arthen-Engeland Thomas T Stelter Andreas A Chillrud Steven N SN

Journal of analytical & bioanalytical techniques 20180411 2

This study validates the analysis of polycyclic aromatic hydrocarbons (PAHs) in microgram levels of particulate matter (PM) collected on filters by two low-flow rate, real-time monitors, microPEM™ and microAeth<sup>®</sup>. Particle-associated PAHs were analyzed by a coupling of a gas chromatograph to a sensitive, atmospheric-pressure laser ionization-mass spectrometer. Air particulate samples were collected over the course of one or two days in the living room of a fourth-floor apartment in New ...[more]

PMID: 30002947

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Project description:BackgroundNowadays, effects of fine particulate matter (PM2.5) are well-documented and related to oxidative stress and pro-inflammatory response. Nevertheless, epidemiological studies show that PM2.5 exposure is correlated with an increase of pulmonary cancers and the remodeling of the airway epithelium involving the regulation of cell death processes. Here, we investigated the components of Parisian PM2.5 involved in either the induction or the inhibition of cell death quantified by different parameters of apoptosis and delineated the mechanism underlying this effect.ResultsIn this study, we showed that low levels of Parisian PM2.5 are not cytotoxic for three different cell lines and primary cultures of human bronchial epithelial cells. Conversely, a 4 hour-pretreatment with PM2.5 prevent mitochondria-driven apoptosis triggered by broad spectrum inducers (A23187, staurosporine and oligomycin) by reducing the mitochondrial transmembrane potential loss, the subsequent ROS production, phosphatidylserine externalization, plasma membrane permeabilization and typical morphological outcomes (cell size decrease, massive chromatin and nuclear condensation, formation of apoptotic bodies). The use of recombinant EGF and specific inhibitor led us to rule out the involvement of the classical EGFR signaling pathway as well as the proinflammatory cytokines secretion. Experiments performed with different compounds of PM2.5 suggest that endotoxins as well as carbon black do not participate to the antiapoptotic effect of PM2.5. Instead, the water-soluble fraction, washed particles and organic compounds such as polycyclic aromatic hydrocarbons (PAH) could mimic this antiapoptotic activity. Finally, the activation or silencing of the aryl hydrocarbon receptor (AhR) showed that it is involved into the molecular mechanism of the antiapoptotic effect of PM2.5 at the mitochondrial checkpoint of apoptosis.ConclusionsThe PM2.5-antiapoptotic effect in addition to the well-documented inflammatory response might explain the maintenance of a prolonged inflammation state induced after pollution exposure and might delay repair processes of injured tissues.

Project description:Relative importance of multiple indoor and outdoor venues on personal exposure concentrations to pro-carcinogenic polycyclic aromatic hydrocarbons (c-PAHs) remains poorly understood. This is particularly challenging because many c-PAHs share sources and occur as a complex mixture. Accurate and precise apportionment of personal exposure according to exposure venues could aid in the understanding of human health effects due to a given source. Here, we partitioned indoor and personal exposure concentrations to seven c-PAHs and pyrene according to the indoor- and outdoor-origins.A simultaneous, integrated monitoring of personal, indoor and outdoor concentrations of nine PAHs was conducted in 75 homes for a consecutive 48-hour period across a two-year period in Kraków, Poland. Due to few known indoor sources for chrysene, we used this PAH species as a tracer for infiltration of outdoor PAHs. Personal and indoor concentrations of seven c-PAHs and pyrene were apportioned to home indoor, non-home indoor and outdoor origins.Using Chrysenein/Chryseneout as proxy for an infiltration factor, Finf, infiltrated PAHs of outdoor origin are overall higher in concentration than those emitted from the indoor origin. Average contribution by the outdoor sources on B[a]A, B[b]F, and B[k]F were 92%, 79%, and 78% across all seasons, respectively. In contrast, in homes where a household member smoked, average contributions by the outdoor sources on B[ghi]P, B[a]P, D[ah]A, and IP were lower (i.e., 67%, 65%, 67%, and 66%, respectively). Season-averaged contributions by the outdoor sources on personal exposure to B[a]A, B[b]F, and B[k]F were 92%, 74%, and 77%, respectively. On the other hand, season-averaged home indoor source contributions on personal exposure to B[a]A, B[b]F, and B[k]F were estimated at 6%, 15%, and 19%, respectively. Similar contributions by season-averaged home indoor sources on personal exposure were estimated at 28% for B[ghi]P, 31% for B[a]P, 25% for D[ah]A, and 28% for IP.Of the seven c-PAHs, B[a]A, B[b]F, and B[k]F are enriched in indoor and personal exposure concentrations from the outdoor coal-combustion. B[ghi]P, B[a]P, D[a,h]A, and IP, PAHs with some of the highest carcinogenic and mutagenic potencies, are considerably enriched by cigarette smoke in addition to the outdoor sources.

Project description:BackgroundObserved seasonal differences in particulate matter (PM) associations with human health may be due to their composition and to toxicity-related seasonal interactions.ObjectivesWe assessed seasonality in PM composition and in vitro PM pro-inflammatory potential using multiple PM samples.MethodsWe collected 90 weekly PM10 and PM2.5 samples during the rainy-warm and dry-cold seasons in five urban areas with different pollution sources. The elements, polycyclic aromatic hydrocarbons (PAHs), and endotoxins identified in the samples were subjected to principal component analysis (PCA). We tested the potential of the PM to induce tumor necrosis factor alpha (TNFα) and interleukin 6 (IL-6) secretion in cultured human monocytes (THP-1), and we modeled pro-inflammatory responses using the component scores.ResultsPM composition varied by size and by season. PCA identified two main components that varied by season. Combustion-related constituents (e.g., vanadium, benzo[a]pyrene, benzo[a]anthracene) mainly comprised component 1 (C1). Soil-related constituents (e.g., endotoxins, silicon, aluminum) mainly comprised component 2 (C2). PM from the rainy-warm season was high in C2. PM (particularly PM2.5) from the dry-cold season was rich in C1. Elevated levels of cytokine production were associated with PM10 and C2 (rainy-warm season), whereas reduced levels of cytokine production were associated with PM2.5 and C1 (dry-cold season). TNFα secretion was increased following exposure to PM with high (vs. low) C2 content, but TNFα secretion in response to PM was decreased following exposure to samples containing ≥ 0.1% of C1-related PAHs, regardless of C2 content. The results of the IL-6 assays suggested more complex interactions between PM components and particle size.ConclusionsVariations in PM soil and PAH content underlie seasonal and PM size-related patterns in TNFα secretion. These results suggest that the mixture of components in PM explains some seasonal differences in associations between health outcomes and PM in epidemiologic studies.CitationManzano-León N, Serrano-Lomelin J, Sánchez BN, Quintana-Belmares R, Vega E, Vázquez-López I, Rojas-Bracho L, López-Villegas MT, Vadillo-Ortega F, De Vizcaya-Ruiz A, Rosas Perez I, O'Neill MS, Osornio-Vargas AR. 2016. TNFα and IL-6 responses to particulate matter in vitro: variation according to PM size, season, and polycyclic aromatic hydrocarbon and soil content. Environ Health Perspect 124:406-412; http://dx.doi.org/10.1289/ehp.1409287.

Project description:BackgroundExposure to polycyclic aromatic hydrocarbon (PAH) has been linked to various adverse health outcomes. Personal PAH exposures are usually measured by personal monitoring or biomarkers, which are costly and impractical for a large population. Modeling is a cost-effective alternative to characterize personal PAH exposure although challenges exist because the PAH exposure can be highly variable between locations and individuals in non-occupational settings. In this study we developed models to estimate personal inhalation exposures to particle-bound PAH (PB-PAH) using data from global positioning system (GPS) time-activity tracking data, traffic activity, and questionnaire information.MethodsWe conducted real-time (1-min interval) personal PB-PAH exposure sampling coupled with GPS tracking in 28 non-smoking women for one to three sessions and one to nine days each session from August 2009 to November 2010 in Los Angeles and Orange Counties, California. Each subject filled out a baseline questionnaire and environmental and behavior questionnaires on their typical activities in the previous three months. A validated model was used to classify major time-activity patterns (indoor, in-vehicle, and other) based on the raw GPS data. Multiple-linear regression and mixed effect models were developed to estimate averaged daily and subject-level PB-PAH exposures. The covariates we examined included day of week and time of day, GPS-based time-activity and GPS speed, traffic- and roadway-related parameters, meteorological variables (i.e. temperature, wind speed, relative humidity), and socio-demographic variables and occupational exposures from the questionnaire.ResultsWe measured personal PB-PAH exposures for 180?days with more than 6 h of valid data on each day. The adjusted R2 of the model was 0.58 for personal daily exposures, 0.61 for subject-level personal exposures, and 0.75 for subject-level micro-environmental exposures. The amount of time in vehicle (averaging 4.5% of total sampling time) explained 48% of the variance in daily personal PB-PAH exposure and 39% of the variance in subject-level exposure. The other major predictors of PB-PAH exposures included length-weighted traffic count, work-related exposures, and percent of weekday time.ConclusionWe successfully developed regression models to estimate PB-PAH exposures based on GPS-tracking data, traffic data, and simple questionnaire information. Time in vehicle was the most important determinant of personal PB-PAH exposure in this population. We demonstrated the importance of coupling real-time exposure measures with GPS time-activity tracking in personal air pollution exposure assessment.

Dataset Information

Validation of Miniaturized Particulate-Matter Real-Time Samplers for Characterizing Personal Polycyclic Aromatic Hydrocarbon Exposure.

Publications

Validation of Miniaturized Particulate-Matter Real-Time Samplers for Characterizing Personal Polycyclic Aromatic Hydrocarbon Exposure.

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