Controlled human exposures to wood smoke: a synthesis of the evidence

Schwartz, Carley; Bølling, Anette Kocbach; Carlsten, Christopher

doi:10.1186/s12989-020-00375-x

Cited by 31 publications

(31 citation statements)

References 45 publications

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“…The observational studies include studies focusing on wildfire smoke and also on household biomass smoke that can be important sources of evidence of an association with cardiovascular risk [ 47 ]. The experimental studies using wood smoke, are more likely to capture acute pathophysiological changes associated with wood smoke exposure, compared to the observational studies that are based on healthcare data such as hospitalizations and ED visits for acute cardiovascular symptoms [ 138 ]. In this review, we will systematically examine the evidence from these studies on the association between cardiovascular health impacts and wildfire smoke (including biomass smoke and wood smoke) exposure and their possible underlying mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Cardiovascular health impacts of wildfire smoke exposure

et al. 2021

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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.

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Section: Introductionmentioning

confidence: 99%

Cardiovascular health impacts of wildfire smoke exposure

et al. 2021

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“…Exposure to wildfire smoke also results in similar increased expression of inflammatory markers [19], in common with Covid19 and urban air pollution. Wildfire smoke health pathways are proposed to be similar to pathways for anthropogenic pollution or wood cooking and heating smoke [20]. Currently, there is a paucity of detailed mechanistic and long-term studies despite research showing significant health impacts from short-term wildfire smoke exposure [4,20].…”

Section: Discussionmentioning

confidence: 99%

“…Wildfire smoke health pathways are proposed to be similar to pathways for anthropogenic pollution or wood cooking and heating smoke [20]. Currently, there is a paucity of detailed mechanistic and long-term studies despite research showing significant health impacts from short-term wildfire smoke exposure [4,20]. Nevertheless, long-term health impacts are expected by analogy with air pollution health impacts that persist on lung-clearance timescales, i.e., months or longer.…”

Section: Discussionmentioning

confidence: 99%

Wildfire Smoke Exposure: Covid19 Comorbidity?

Leifer

Kleinman

Blake

et al. 2021

JoR

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Air pollution, particularly fine and ultrafine particulate matter aerosols, underlies a wide range of communicable and non-communicable disease affecting many systems including the cardiopulmonary and immune systems, and arises primarily from transportation and industry. A number of air pollution driven diseases also are Covid19 comorbidities. Thus, a number of studies on air pollution exposure, particularly particulate matter, strongly indicate air pollution is an important underlying factor in Covid19 transmission, severity, and mortality. This suggests that air pollution from natural sources, particularly wildfires, could play a role in the Covid19 pandemic. We tested this hypothesis on three wildfire smoke events in Orange County, CA, each of which was followed by Covid19 case increases after an approximately one-week lag. This lag was consistent with combined incubation time and testing/reporting times. Moreover, the three events suggest a dose dependency. The wildfire comorbidity hypothesis implies that at-risk-populations should reduce smoke exposure from wildfires, as well as indoors from biomass burning for heating, cooking, and aesthetic purposes.

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“…These WSP are composed of a heterogeneous mix of compounds including fine and coarse particulate matter, heavy metals, poly-aromatic hydrocarbons (PAHs) and volatile organic compounds (VOCs), which depend on the source of combustible material, similar to bona fide wildfire pollution (15). Experimental WSP inhalation in healthy individuals recruits inflammatory cells, stimulates oxidative damage and impairs immune responses to viral infections (17)(18)(19). WSP exposure in cell culture models causes cytotoxicity, genotoxicity, cellular stress, formation of reactive oxygen species (ROS), and increased expression of pro-inflammatory cytokines (16,20,21).…”

Section: Introductionmentioning

confidence: 99%

Genomics-based deconvolution of multiplexed transcriptional responses to wood smoke particles defines rapid AHR signaling dynamics

Gupta

Sanford

et al. 2021

Preprint

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Transcriptional responses to wildfire smoke, an increasingly important cause of human morbidity, are poorly understood. Here, using a combination of precision nuclear run-on sequencing (PRO-seq) and the assay for transposase-accessible chromatin using sequencing (ATAC-seq), we identify rapid and dynamic changes in transcription and chromatin structure in Beas-2B airway epithelial cells after exposure to wood smoke particles (WSP). By comparing 30 and 120 minutes of WSP exposure, we defined three distinct temporal patterns of transcriptional induction and chromatin responses to WSP. Whereas transcription of canonical targets of the aryl hydrocarbon receptor (AHR), such as CYP1A1 and AHRR, was robustly increased after 30 minutes of WSP exposure, transcription of these genes and associated enhancers returned to near baseline at 120 minutes. ChIP-qPCR assays and AHR knockdown confirmed a role for AHR in regulating these transcriptional responses, and we applied bioinformatics approaches to identify novel AHR-regulated pathways and targets including the DNA methyltransferase, DNMT3L, and its interacting factor, SPOCD1. Our analysis also defined a role for NFkB as a primary transcriptional effector of WSP-induced changes in gene expression. The kinetics of AHR- and NFkB-regulated responses to WSP were distinguishable based on the timing of both transcriptional responses and chromatin remodeling, with induction of several cytokines implicated in maintaining the NFkB response. In aggregate, our data establish a direct and primary role for AHR in mediating airway epithelial responses to WSP and identify crosstalk between AHR and NFkB signaling in controlling pro-inflammatory gene expression.

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Controlled human exposures to wood smoke: a synthesis of the evidence

Cited by 31 publications

References 45 publications

Cardiovascular health impacts of wildfire smoke exposure

Cardiovascular health impacts of wildfire smoke exposure

Wildfire Smoke Exposure: Covid19 Comorbidity?

Genomics-based deconvolution of multiplexed transcriptional responses to wood smoke particles defines rapid AHR signaling dynamics

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