Dataset Information

Inflammatory Cytokines and White Blood Cell Counts Response to Environmental Levels of Diesel Exhaust and Ozone Inhalation Exposures.

ABSTRACT: Epidemiological observations of urban inhalation exposures to diesel exhaust (DE) and ozone (O3) have shown pre-clinical cardiopulmonary responses in humans. Identifying the key biological mechanisms that initiate these health bioindicators is difficult due to variability in environmental exposure in time and from person to person. Previously, environmentally controlled human exposure chambers have been used to study DE and O3 dose-response patterns separately, but investigation of co-exposures has not been performed under controlled conditions. Because a mixture is a more realistic exposure scenario for the general public, in this study we investigate the relationships of urban levels of urban-level DE exposure (300 ?g/m3), O3 (0.3 ppm), DE + O3 co-exposure, and innate immune system responses. Fifteen healthy human volunteers were studied for changes in ten inflammatory cytokines (interleukins 1?, 2, 4, 5, 8, 10, 12p70 and 13, IFN-?, and TNF-?) and counts of three white blood cell types (lymphocytes, monocytes, and neutrophils) following controlled exposures to DE, O3, and DE+O3. The results show subtle cytokines responses to the diesel-only and ozone-only exposures, and that a more complex (possibly synergistic) relationship exists in the combination of these two exposures with suppression of IL-5, IL-12p70, IFN-?, and TNF-? that persists up to 22-hours for IFN-? and TNF-?. The white blood cell differential counts showed significant monocyte and lymphocyte decreases and neutrophil increases following the DE + O3 exposure; lymphocytes and neutrophils changes also persist for at least 22-hours. Because human studies must be conducted under strict safety protocols at environmental levels, these effects are subtle and are generally only seen with detailed statistical analysis. This study indicates that the observed associations between environmental exposures and cardiopulmonary effects are possibly mediated by inflammatory response mechanisms.

SUBMITTER: Stiegel MA

PROVIDER: S-EPMC4825980 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

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Inflammatory Cytokines and White Blood Cell Counts Response to Environmental Levels of Diesel Exhaust and Ozone Inhalation Exposures.

Stiegel Matthew A MA Pleil Joachim D JD Sobus Jon R JR Madden Michael C MC

PloS one 20160408 4

Epidemiological observations of urban inhalation exposures to diesel exhaust (DE) and ozone (O3) have shown pre-clinical cardiopulmonary responses in humans. Identifying the key biological mechanisms that initiate these health bioindicators is difficult due to variability in environmental exposure in time and from person to person. Previously, environmentally controlled human exposure chambers have been used to study DE and O3 dose-response patterns separately, but investigation of co-exposures ...[more]

PMID: 27058360

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Project description:The potential effects of combinations of dilute whole diesel exhaust (DE) and ozone (O?), each a common component of ambient airborne pollutant mixtures, on lung function were examined. Healthy young human volunteers were exposed for 2 hr to pollutants while exercising (~50 L/min) intermittently on two consecutive days. Day 1 exposures were either to filtered air, DE (300 ?g/m³), O? (0.300 ppm), or the combination of both pollutants. On Day 2 all exposures were to O? (0.300 ppm), and Day 3 served as a followup observation day. Lung function was assessed by spirometry just prior to, immediately after, and up to 4 hr post-exposure on each exposure day. Functional pulmonary responses to the pollutants were also characterized based on stratification by glutathione S-transferase mu 1 (GSTM1) genotype. On Day 1, exposure to air or DE did not change FEV1 or FVC in the subject population (n?=?15). The co-exposure to O? and DE decreased FEV1 (17.6%) to a greater extent than O? alone (9.9%). To test for synergistic exposure effects, i.e., in a greater than additive fashion, FEV1 changes post individual O? and DE exposures were summed together and compared to the combined DE and O? exposure; the p value was 0.057. On Day 2, subjects who received DE exposure on Day 1 had a larger FEV1 decrement (14.7%) immediately after the O? exposure than the individuals' matched response following a Day 1 air exposure (10.9%). GSTM1 genotype did not affect the magnitude of lung function changes in a significant fashion. These data suggest that altered respiratory responses to the combination of O? and DE exposure can be observed showing a greater than additive manner. In addition, O?-induced lung function decrements are greater with a prior exposure to DE compared to a prior exposure to filtered air. Based on the joint occurrence of these pollutants in the ambient environment, the potential exists for interactions in more than an additive fashion affecting lung physiological processes.

Project description:Diesel exhaust (DE) contains a variety of toxic air pollutants, including diesel particulate matter (DPM) and gaseous contaminants (e.g., carbon monoxide (CO)). DPM is dominated by fine (PM2.5) and ultrafine particles (UFP), and can be representatively determined by its thermal-optical refractory as elemental carbon (EC) or light-absorbing characteristics as black carbon (BC). The currently accepted reference method for sampling and analysis of occupational exposure to DPM is the National Institute for Occupational Safety and Health (NIOSH) Method 5040. However, this method cannot provide in-situ short-term measurements of DPM. Thus, real-time monitors are gaining attention to better examine DE exposures in occupational settings. However, real-time monitors are subject to changing environmental conditions. Field measurements have reported interferences in optical sensors and subsequent real-time readings, under conditions of high humidity and abrupt temperature changes. To begin dealing with these issues, we completed a controlled study to evaluate five real-time monitors: Airtec real-time DPM/EC Monitor, TSI SidePak Personal Aerosol Monitor AM510 (PM2.5), TSI Condensation Particle Counter 3007, microAeth AE51 BC Aethalometer, and Langan T15n CO Measurer. Tests were conducted under different temperatures (55, 70, and 80°F), relative humidity (10, 40, and 80%), and DPM concentrations (50 and 200 ?g/m(3)) in a controlled exposure facility. The 2-hr averaged EC measurements from the Airtec instrument showed relatively good agreement with NIOSH Method 5040 (R(2) = 0.84; slope = 1.17±0.06; N = 27) and reported ?17% higher EC concentrations than the NIOSH reference method. Temperature, relative humidity, and DPM levels did not significantly affect relative differences in 2-hr averaged EC concentrations obtained by the Airtec instrument vs. the NIOSH method (p < 0.05). Multiple linear regression analyses, based on 1-min averaged data, suggested combined effects of up to 5% from relative humidity and temperature on real-time measurements. The overall deviations of these real-time monitors from the NIOSH method results were ?20%. However, simultaneous monitoring of temperature and relative humidity is recommended in field investigations to understand and correct for environmental impacts on real-time monitoring data.

Project description:BackgroundRecent epidemiological studies indicate early-life exposure to pollution particulate is associated with adverse neurodevelopmental outcomes. The need is arising to evaluate the risks conferred by individual components and sources of air pollution to provide a framework for the regulation of the most relevant components for public health protection. Previous studies in rodent models have shown diesel particulate matter has neurotoxic potential and could be a health concern for neurodevelopment. The present study shows an evaluation of pathological and protracted behavioral alterations following neonatal exposure to aerosolized diesel exhaust particles (NIST SRM 1650b). The particular behavioral focus was on temporal control learning, a broad and fundamental cognitive domain in which reward delivery is contingent on a fixed interval schedule. For this purpose, C57BL/6?J mice were exposed to aerosolized NIST SRM 1650b, a well-characterized diesel particulate material, from postnatal days 4-7 and 10-13, for four hours per day. Pathological features, including glial fibrillary-acidic protein, myelin basic protein expression in the corpus callosum, and ventriculomegaly, as well as learning alterations were measured to determine the extent to which NIST SRM 1650b would induce developmental neurotoxicity.ResultsTwenty-four hours following exposure significant increases in glial-fibrillary acidic protein (GFAP) in the corpus callosum and cortex of exposed male mice were present. Additionally, the body weights of juvenile and early adult diesel particle exposed males were lower than controls, although the difference was not statistically significant. No treatment-related differences in males or females on overall locomotor activity or temporal learning during adulthood were observed in response to diesel particulate exposure.ConclusionWhile some sex and regional-specific pathological alterations in GFAP immunoreactivity suggestive of an inflammatory reaction to SRM 1650b were observed, the lack of protracted behavioral and pathological deficits suggests further clarity is needed on the developmental effects of diesel emissions prior to enacting regulatory guidelines.

Dataset Information

Inflammatory Cytokines and White Blood Cell Counts Response to Environmental Levels of Diesel Exhaust and Ozone Inhalation Exposures.

Publications

Inflammatory Cytokines and White Blood Cell Counts Response to Environmental Levels of Diesel Exhaust and Ozone Inhalation Exposures.

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