In recent years, wildland fires have occurred more frequently and with increased intensity in many fire-prone areas. In addition to the direct life and economic losses attributable to wildfires, the emitted smoke is a major contributor to ambient air pollution, leading to significant public health impacts. Wildfire smoke is a complex mixture of particulate matter (PM), gases such as carbon monoxide, nitrogen oxide, and volatile and semi-volatile organic compounds. PM from wildfire smoke has a high content of elemental carbon and organic carbon, with lesser amounts of metal compounds. Epidemiological studies have consistently found an association between exposure to wildfire smoke (typically monitored as the PM concentration) and increased respiratory morbidity and mortality. However, previous reviews of the health effects of wildfire smoke exposure have not established a conclusive link between wildfire smoke exposure and adverse cardiovascular effects. In this review, we systematically evaluate published epidemiological observations, controlled clinical exposure studies, and toxicological studies focusing on evidence of wildfire smoke exposure and cardiovascular effects, and identify knowledge gaps. Improving exposure assessment and identifying sensitive cardiovascular endpoints will serve to better understand the association between exposure to wildfire smoke and cardiovascular effects and the mechanisms involved. Similarly, filling the knowledge gaps identified in this review will better define adverse cardiovascular health effects of exposure to wildfire smoke, thus informing risk assessments and potentially leading to the development of targeted interventional strategies to mitigate the health impacts of wildfire smoke.

Background: Exposure to air pollution is associated with elevated cardiovascular risk. Evidence shows that omega-3 polyunsaturated fatty acids (omega-3 PUFA) may attenuate the adverse cardiovascular effects of exposure to fine particulate matter (PM_2.5). However, it is unclear whether habitual dietary intake of omega-3 PUFA protects against the cardiovascular effects of short-term exposure to low-level ambient air pollution in healthy participants. In the present study, sixty-two adults with low or high dietary omega-3 PUFA intake were enrolled. Blood lipids, markers of vascular inflammation, coagulation and fibrinolysis, and heart rate variability (HRV) and repolarization were repeatedly assessed in 5 sessions separated by at least 7 days. This study was carried out in the Research Triangle area of North Carolina, USA between October 2016 and September 2019. Daily PM_2.5 and maximum 8-h ozone (O₃) concentrations were obtained from nearby air quality monitoring stations. Linear mixed-effects models were used to assess the associations between air pollutant concentrations and cardiovascular responses stratified by the omega-3 intake levels. Results: The average concentrations of ambient PM_2.5 and O₃ were well below the U.S. National Ambient Air Quality Standards during the study period. Significant associations between exposure to PM_2.5 and changes in total cholesterol, von Willebrand factor (vWF), tissue plasminogen activator, D-dimer, and very-low frequency HRV were observed in the low omega-3 group, but not in the high group. Similarly, O₃-associated adverse changes in cardiovascular biomarkers (total cholesterol, high-density lipoprotein, serum amyloid A, soluable intracellular adhesion molecule 1, and vWF) were mainly observed in the low omega-3 group. Lag-time-dependent biphasic changes were observed for some biomarkers. Conclusions: This study demonstrates associations between short-term exposure to PM_2.5 and O₃, at concentrations below regulatory standard, and subclinical cardiovascular responses, and that dietary omega-3 PUFA consumption may provide protection against such cardiovascular effects in healthy adults.

Rationale: Exposure to air pollution is associated with adverse respiratory effects. Polyunsaturated omega 3 (n-3) fatty acids (FAs) appear to attenuate the health effects of air pollution. Objectives: This panel study evaluated whether n-3 FA intake and blood levels of polyunsaturated omega 6 (n-6) FAs can modulate the associations between respiratory effects and short-term exposure to ambient air pollution in healthy adults. Methods: Sixty-two healthy adults were enrolled into either high or low n-3 FA groups on the basis of n-3 FA intake and erythrocyte n-3 FA concentrations. Low and high n-6 FA groups were dichotomized on the basis of blood n-6 FA levels. Participants underwent three to five testing sessions separated by at least 7 days. At each session, the forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), and plasma markers of inflammation (IL-6 [interleukin-6]) and oxidative stress (ox-LDL [oxidized low-density lipoprotein]) were measured. Associations between the ambient ozone and fine particulate matter (PM) (PM with an aerodynamic diameter ⩽2.5 μm [PM2.5]) levels and the lung function and blood markers were assessed by using mixed-effect models stratified by FA levels. Results: Average levels of ozone (40.8 ± 11.1 ppb) and PM2.5 (10.2 ± 4.1 μg/m3) were below national ambient air quality standards during the study period. FVC was positively associated with ozone at a lag of 0 days (lag0) in the high n-3 FA group, whereas the association was null in the low n-3 FA group (for an interquartile range increase in ozone of 1.8% [95% confidence interval (CI): 0.5% to 3.2%] vs. 0.0% [95% CI: −1.4% to 1.5%]); however, the association shifted to being negative at lag4 (−1.9% [95% CI: −3.2 to −0.5] vs. 0.2% [95% CI: −1.2% to 1.5%]) and lag5 (−1.2% [95% CI: −2.4% to 0.0%] vs. 0.9% [95% CI: −0.4% to 2.3%]). A similar pattern was observed in the low n-6 FA group compared with the high n-6 FA group (lag0: 1.7% [95% CI: 0.3% to 3.0%] vs. 0.5% [95% CI: −0.9% to 2.0%] and lag4: −1.4% [95% CI: −2.8% to 0.0%] vs. −0.5% [95% CI: −1.8% to 0.9%]). The associations between FEV1 and ozone and between FVC and PM2.5 also followed a similar pattern. Elevated ozone levels were associated with an immediate decrease in ox-LDL in the high n-3 FA group at lag0 (−12.3% [95% CI: −24.8% to 0.1%]), whereas there was no change in the low n-3 FA group (−7.5% [95% CI: −21.4% to 6.5%]) and there was a delayed increase in IL-6 in the high n-3 FA group compared with the low n-3 FA group (lag4: 66.9% [95% CI: 27.9% to 106.0%] vs. 8.9% [95% CI: −31.8% to 49.6%], lag5: 58.2% [95% CI: 22.4% to 94.1%] vs. −7.4% [95% CI: −48.8% to 34.0%], and lag6: 45.8% [95% CI: 8.7% to 82.9%] vs. −8.5% [95% CI: −49.7% to 32.6%]). Conclusions: We observed lag-dependent associations between short-term ambient air pollutants and lung function that were differentially modulated by n-3 and n-6 FAs, suggesting that n-3 and n-6 FAs counteract the respiratory response to low levels of ambient air pollution in healthy adults.Clinical trial registered with clinicaltrials.gov (NCT 02921048)

Nanomaterial science and design have shifted from generating single passive nanoparticles to more complex and adaptive multi-component nanohybrids. These adaptive nanohybrids (ANHs) are designed to simultaneously perform multiple functions, while actively responding to the surrounding environment. ANHs are engineered for use as drug delivery carriers, in tissue-engineered templates and scaffolds, adaptive clothing, smart surface coatings, electrical switches and in platforms for diversified functional applications. Such ANHs are composed of carbonaceous, metallic or polymeric materials with stimuli-responsive soft-layer coatings that enable them to perform such switchable functions. Since ANHs are engineered to dynamically transform under different exposure environments, evaluating their environmental behavior will likely require new approaches. Literature on polymer science has established a knowledge core on stimuli-responsive materials. However, translation of such knowledge to environmental health and safety (EHS) of these ANHs has not yet been realized. It is critical to investigate and categorize the potential hazards of ANHs, because exposure in an unintended or shifting environment could present uncertainty in EHS. This article presents a perspective on EHS evaluation of ANHs, proposes a principle to facilitate their identification for environmental evaluation, outlines a stimuli-based classification for ANHs and discusses emerging properties and dynamic aspects for systematic EHS evaluation.

Exposure to ambient air pollutants such as ozone (O₃) and particulate matter (PM) is associated with increased cardiovascular morbidity and rate of mortality, but the underlying biological mechanisms have yet to be described. Emerging evidence shows that extracellular vehicle (EV) microRNAs (miRNAs) may facilitate cell-to-cell and organ-to-organ communications and play a role in the air pollution-induced cardiovascular effects. This study aims to explore the association between air pollutant exposure and miRNA changes related to cardiovascular diseases. Using a panel study design, 14 participants with coronary artery diseases were enrolled in this study. Each participant had up to 10 clinical visits and their plasma samples were collected and measured for expression of miRNA-21 (miR-21), miR-126, miR-146, miR-150, and miR-155. Mixed effects models adjusted for temperature, humidity, and season were used to examine the association between miRNA levels and exposure to 8-hr O₃ or 24-hr PM_2.5 up to 4 days prior. Results demonstrated that miR-150 expression was positively associated with O₃ exposure at 1–4 days lag and 5day moving average while miR-155 expression tracked with O₃ exposure at lag 0. No significant association was found between miRNA expression and ambient PM_2.5 at any time point. β-blocker and diabetic medication usage significantly modified the correlation between O₃ exposure and miR-150 expression where the link was more prominent among non-users. In conclusion, evidence indicated an association between exposure to ambient O₃ and circulating levels of EV miR-150 and miR-155 was observed. These findings pointed to a future research direction involving miRNA-mediated mechanisms of O₃-induced cardiovascular effects.