Background
Air pollution is a mixture of gaseous and particulate pollutants emitted from multiple sources. During transport in the atmosphere, emissions undergo photochemical reactions that may render them more harmful.
Objectives
The aim of this study was to investigate the toxicity of primary and secondary traffic particles.
Methods
Sprague‐Dawley rats were exposed to either: fresh primary particles from a tunnel plenum (P); secondary organic aerosol formed from photochemical oxidation of primary gases after filtration of primary particles (SOA); photochemically aged primary particles plus secondary organic aerosol (P + SOA); or filtered clean air. In each exposure, pollutant gases were removed using a non‐selective denuder.
Animals were exposed for 5 hours/day, with varying numbers of days of exposure. Outcomes included breathing pattern, in‐vivo chemiluminescence (IVCL), broncho‐alveolar lavage, and complete blood count.
Results
Mass concentration was ~50μg/m3. Respiratory data showed many changes with each exposure type. All produced decreases in tidal/minute volumes and inspiratory/expiratory flows. There were mild inflammatory changes in BAL, with increased neutrophils for SOA and P+SOA and lymphocytes for P and P+SOA, without changes in total protein, β‐NAG or IVCL.
Conclusions
All exposures produced changes compared to filtered air; overall toxicity, P+SOA>P>SOA.
Validation of gene-chip microarray results is one of the challenges in genomic studies. The successful use of a custom-designed 96-well polymerase chain reaction (PCR) array to study the unexpected inflammatory effect of environmental titanium dioxide (TiO2) particles on the lungs of pregnant mice, with similar results not seen in control mice, is reported. In our approach, selection of candidate genes for the custom PCR array was informed by prior gene-chip microarray profiling. Results demonstrated multiple upregulation of genes in the lungs of pregnant but not control mice produced by TiO2 exposure. Customized PCR array is a flexible tool that offers the ability to combine the “blind” genome-wide scan with a hypothesis-driven approach, by including both the “candidate” genes for validation positively identified by the microarray and biologically relevant “suspects” that failed to be found in the genomic data. Compared to conventional gene-by-gene qPCR or manufacturer-preset pathway kits, this technique provides a cost-effective and time-saving method of analysis and allows for a strong, easily detectable signal. Genes with confirmed differential expression were further used for pathway analysis and indicated involvement in several biologically relevant pathways including allergy mediator signaling in dendritic cells. Finally, an analytical network was created that will inform further mechanistic studies. The dual purpose of the work was to demonstrate that the novel custom PCR array is a convenient approach to validate the microarray results, and to obtain biologically significant data on TiO2-induced inflammation by following the PCR array with pathway analysis, which provided feasible hypotheses to support future experimental studies.
BACKGROUND
Associations between exposure to fine particulate matter (PM2.5) and blood pressure (BP) have been inconsistent in epidemiologic studies.
OBJECTIVES
We used a unique exposure system to separate traffic‐derived PM2.5 into primary and secondary components to measure effects on BP.
METHODS
Sprague Dawley rats were repeatedly exposed to primary only (P), secondary organic aerosol only (SOA), a combination of the two (P+SOA) or filtered air for 5‐hours/day for 3 weeks. Exposure dose was ~50 μg/m3. BP was measured continuously using implanted telemetry. Mixed effects models were used to compare responses of systolic (SBP), diastolic blood pressure (DBP) and heart rate (HR).
RESULTS
Exposure to P increased and maintained an effect on SBP and DBP across weeks showing a significant dose response. SOA exposure on the first day resulted in a significant increase in both SBP and DBP (p=.001, p=.0003) becoming strongly negative by week 3. With P+SOA, significant increases in SBP and DBP of 13 mmHg were observed on the first day of exposure (p=.04, p=.0015) which was maintained through week 1 for SBP and through week 2 for DBP. Sham exposures in the SOA and P+SOA groups after 3 weeks showed compensatory decreases in both SBP and DBP. No exposure had a significant effect on HR.
CONCLUSIONS
Both primary and secondary traffic derived aerosols can substantially increase SBP and DBP but these increases are eventually lost.
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