From: Cardiovascular health impacts of wildfire smoke exposure
Study type | Number of studies | Number of studies showing positive association | Major findings | Strength | Limitation |
---|---|---|---|---|---|
Epidemiological studies on wildfire smoke | 48 | 33 | Wildfire smoke exposure (most using PM2.5 or PM10 as exposure metric) is associated with increased morbidity and mortality of IHD, HF, CAD, CHD, and arrhythmia | Direct investigation on the cardiovascular effects of wildfire smoke exposure; relatively straightforward availability of hospitalization records and air quality (mainly PM) data | Exposure misclassification; limited causal inference; difficult to capture subclinical cardiovascular changes; failure to consider the effects of gases (O3, NO2, etc) and VOCs from wildfire smoke |
Epidemiological studies on household biomass smoke | 29 | 26 | Indoor biomass smoke exposure is associated with increased blood pressure, vascular dysfunction, circulating vascular markers, and cardiovascular morbidity and mortality | Study sites and length are not restricted to wildfire events; straightforward follow-up with subjects using household fuels; applicability of interventions; can study subclinical endpoints | Household biomass smoke is not equal to wildfire smoke; not ideal for causal inference, cannot account for real-world wildfire events |
Intervention / controlled human exposure studies | 15 | 11 | There are significant changes in vascular function, blood pressure, HRV, circulating cardiovascular and inflammatory markers | Controlled exposure and environmental conditions; potential for causal inference; detailed smoke characterization; randomization and cross-over design | Wood smoke does not equal wildfire smoke; cannot account for other environmental conditions in the real world wildfire events; exposure time is relatively short |
In vivo animal studies | 7 | 6 | At different extent, wood /peat smoke condensate cause cardiovascular dysfunction, and increase inflammatory and cardiovascular injury markers | Detailed wood smoke characterization; controlled dose and exposure duration; sound model to examine cardiovascular function; sound for mechanistic studies | Wood smoke does not equal wildfire smoke; difficult to generalize the information to human exposure; intratracheal aspiration as exposure method in some studies is different from inhalation |
In vitro studies | 9 | 8 | Wood smoke extract can induce cytotoxicity, oxidative stress and altered levels of inflammatory and vascular markers | Detailed wood smoke characterization; controlled dose and exposure duration; sound for mechanistic studies | Wood smoke does not equal wildfire smoke; difficult to generalize the information to human exposure |