- Ubiquitous fine particulate matter (PM2.5) exposures significantly impact global public health, yet little is known about the mechanisms causing these known adverse health effects. Oxidative stress due to PM2.5 associated chemical constituents, such as polycyclic aromatic hydrocarbons (PAHs), is a proposed possible mechanism for PM2.5 mediated health effects. Variations in the ability to induce oxidative stress have been previously identified in PM2.5 air filter samples and these variations may be attributed to the differing source contributions and thus chemical constituents of PM2.5. To test this hypothesis, PM2.5 filters collected at locations with differing predominant sources were assessed for oxidative potential, chemical composition, and developmental toxicity. Sampling locations included an outdoor rural park across seasons, two vehicular traffic influenced locations and 32 indoor homes in India. PM2.5 was extracted from filters via sonication in methanol. Aliquots of individual filter samples were removed to measure oxidative potential using the dithiothreitol (DTT) assay. Samples were then pooled by location for chemical analysis of PAHs (n=115) and elements (n=20). Pooled samples were also prepared for developmental toxicity testing in zebrafish starting at 6 hours post fertilization (hpf) to assess morphological and behavioral changes at 24 and 120 hpf. Significant variation in chemical constituents between locations of differing sources was observed. Significant differences in oxidative potential were observed between both individual filters and sample sites. Samples sites showed significantly different toxicities, inducing both morphological and behavioral effects in zebrafish at varying concentration ranges between sources. This research will ultimately lead to a greater understanding of health-relevant metrics for PM2.5 exposures and the potential impacts of various PM2.5 sources.
- Key Words: air pollution, particulate matter, toxicology, PAH