The reactions between terpenes and ozone (or other oxidants) produce a wide variety of both gas- and particle-phase products. Terpenes are biogenic volatile organic compounds (VOCs) that are also contained in many consumer products. Ozone is present indoors since it infiltrates into the indoor environment and is emitted by some office and consumer equipment. Some of the gaseous products formed are irritating to biological tissues, while the condensed-phase products have received attention due to their contribution to ambient fine particulate matter (PM2.5) and its respective health significance. Despite common scientific questions, the indoor and ambient air research communities have tended to operate in isolation regarding this topic. This review critically evaluates the literature related to terpene oxidation products and attempts to synthesize results of indoor and ambient air studies to better understand the health significance of these materials and identify knowledge gaps. The review documents the results of a literature search covering terpene oxidation chemistry, epidemiological, toxicological, and controlled human exposure studies, as well as health studies focused more generically on secondary organic aerosol (SOA). The literature shows a clear role for gas-phase terpene oxidation products in adverse airway effects at high concentrations; however, whether these effects occur at more environmentally relevant levels is unclear. The evidence for toxicity of particle-phase products is less conclusive. Knowledge gaps and future research needs are outlined, and include the need for more consistency in study designs, incorporation of reaction product measurements into epidemiological studies conducted in both indoor and ambient settings, and more focused research on the toxicity of SOA, especially SOA of biogenic origin.
Keywords: BAL; C-reactive protein; C/EBP; CCAAT/enhancer binding protein; CCL-2; CCL-5; CO-2; CRP; EC; EEP; EIP; ET-1; Enhanced Pause; GM-CSF; HO-1; Health; IL-1α; IL-1β; IL-6; IL-8; MAP kinase; MMP-9; NF-κB; NOS-1; OC; Oxidation; Ozone; PEF; PM; Penh; SOA; SOD; ST-segment depression; Secondary organic aerosol; TB; TE; TGF-β1; TI; TIMP-2; TNF-α; Terpene; Toxicology; VOC; VT; bronchoalveolar lavage; chemokine [C-C motif] ligand 2; chemokine [C-C motif] ligand 5; cyclooxygenase-2; depression of the flatline segment running along the baseline of an EKG tracing; elemental carbon; end expiratory pause; end inspiratory pause; endothelin-1; expiratory time; f; granulocyte-macrophage colony stimulating factor; heme oxygenase-1; inspiratory time; interleukin-1-alpha; interleukin-1-beta; interleukin-6; interleukin-8; matrix metalloproteinase 9; mitogen activated protein kinase; nitric oxide synthase-1; nuclear factor kappa beta; organic carbon; particulate matter; peak expiratory flow; respiratory frequency; sP-selectin; sTNF-RII; secondary organic aerosol; soluble platelet selectin; superoxide dismutase; tidal volume; time of brake; tissue inhibitor of metalloproteinase-2; transforming growth factor-beta 1; tumor necrosis factor alpha; tumor necrosis factor receptor II; volatile organic compound.
© 2013.