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Table 3 Characteristics of the studies reviewed

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