Smoke Research Articles

Unveiling Spatial Patterns of Exposure and Risk Perception to Air Pollution: A Case Study in Chilean Patagonia

Wood smoke pollution has emerged as a major public health issue in southern Chile. This paper endeavors to find evidence of environmental inequity by looking into the spatial associations between sociodemographic characteristics, exposures, and risk perception to air pollution. We integrate primary georeferenced survey data with estimates of excess outdoor exposure to wood smoke in Coyhaique, one of the most polluted cities in Latin America. Our findings reveal that certain social groups are disproportionately exposed to PM2.5. People of low-socioeconomic status, living in households with older adults and users of wood-burning stoves tend to spend more days per year with unhealthy air pollution levels. The results yield a modest but statistically significant relationship between PM2.5 levels and risk perception. Sociodemographic factors are also important predictors of air pollution risk perception. We discuss the implications in terms of environmental injustice patterns and public awareness campaigns.

Association of social determinants with the severity of congenital heart disease.

Congenital heart diseases are the most prevalent congenital malformations and cause greater morbi-mortality in newborns and infants. The aim of this study was to analyze the social determinants in families with children with the severity of congenital heart disease. Analytical cross-sectional study in 140 families of children with congenital heart disease to whom a structured survey was applied addressing topics related to family structure, health, economic conditions, exposure factors, and other social conditions relevant to the study, during 1 year. In all, 53.7% of the studied population belonged to low socioeconomic levels. No association was found between the severity of the heart disease and the presence of pathological antecedents in the parents. The families resided in urban areas. Also, 28.3% of the mothers had four or fewer prenatal controls during pregnancy. Only 22% of heart diseases were diagnosed during pregnancy. It was found that exposure to cigarette and wood smoke during pregnancy, in addition to low socioeconomic status, was associated with greater severity of heart disease (RACHS-1 and STS-Score), when evaluated by pathophysiological groups (cyanotic/non-cyanotic/single ventricle). Exposure to cigarette smoke, wood smoke during pregnancy, and low socioeconomic status turned out to be social determinants associated with the severity of heart disease analyzed by pathophysiological groups. The social component has not been well characterized as a cause of congenital heart disease, especially in countries like ours, where the existence of gaps and social inequities have a high impact. The findings of this study could have an impact on public health to the extent that policies are implemented to reduce exposure to cigarettes, especially during pregnancy. Knowledge of these changes and their measurement in this type of pathology could open the door to the creation of policies aimed at their prevention, focusing on the local risk factors found, which can impact the disease.

Development of a screening protocol to identify persons who are responsive to wood smoke particle-induced airway inflammation with pilot assessment of GSTM1 genotype and asthma status as response modifiers

Background We are currently screening human volunteers to determine their sputum polymorphonuclear neutrophil (PMN) response 6- and 24-hours following initiation of exposure to wood smoke particles (WSP). Inflammatory responders (≥10% increase in %PMN) are identified for their subsequent participation in mitigation studies against WSP-induced airways inflammation. In this report we compared responder status (N = 52) at both 6 and 24 hr time points to refine/expand its classification, assessed the impact of the GSTM1 genotype, asthma status and sex on responder status, and explored whether sputum soluble phase markers of inflammation correlate with PMN responsiveness to WSP. Results Six-hour responders tended to be 24-hour responders and vice versa, but 24-hour responders also had significantly increased IL-1beta, IL-6, IL-8 at 24 hours post WSP exposure. The GSTM1 null genotype significantly (p < 0.05) enhanced the %PMN response by 24% in the 24-hour responders and not at all in the 6 hours responders. Asthma status enhanced the 24 hour %PMN response in the 6- and 24-hour responders. In the entire cohort (not stratified by responder status), we found a significant, but very small decrease in FVC and systolic blood pressure immediately following WSP exposure and sputum %PMNs were significantly increased and associated with sputum inflammatory markers (IL-1beta, IL-6, IL-8, and PMN/mg) at 24 but not 6 hours post exposure. Blood endpoints in the entire cohort showed a significant increase in %PMN and PMN/mg at 6 but not 24 hours. Sex had no effect on %PMN response. Conclusions The 24-hour time point was more informative than the 6-hour time point in optimally and expansively defining airway inflammatory responsiveness to WSP exposure. GSTM1 and asthma status are significant effect modifiers of this response. These study design and subject parameters should be considered before enrolling volunteers for proof-of-concept WSP mitigation studies.

Effects of Wood Smoke Exposure and Associated Factors on Respiratory Parameters of Pygmies Involved in the Smoking of Game Meat in the Congo/Brazzaville

Effects of Wood Smoke Exposure and Associated Factors on Respiratory Parameters of Pygmies Involved in the Smoking of Game Meat in the Congo/Brazzaville

Wood smoke particulate matter (WSPM2.5) induces pyroptosis through both Caspase-1/IL-1β/IL-18 and ATP/P2Y-dependent mechanisms in human bronchial epithelial cells

Emerging evidences have linked the air pollution particulate matters, especially the fine particulate matter PM2.5, to the disease development of chronic obstructive pulmonary disease (COPD). Our previous studies reported that biofuel PM2.5 can induce devastated damage of human bronchial epithelial cells, this study aims to further investigate the underlying molecular mechanisms how biofuel PM2.5 induces bronchial epithelial cell death and dysfunction. In this study, biofuel PM2.5 extracted from wood smoke (WSPM2.5) was used according to our previous publication. A 16-HBE cell line was used as the cell model. Results showed that: Firstly, WSPM2.5 induced significant pyroptosis in 16-HBE cells, reflected by the typical changes including elevated release of lactate dehydrogenase release (LDH) and activated activity and expression of Caspase-1/IL-1β/IL-18 signaling pathway. Then, specific inhibitors for both Caspases (Z-VAD-FMK) and Caspase-1 (VX-765), as well as specific siRNA knockdown of IL-1β all effectively attenuated the WSPM2.5-induced upregulation of downstream inflammatory cytokines and chemokines (IL-6, IL-8, CXCL-1, CXCL-2, etc), respectively. Notably, WSPM2.5 caused a novel increase of intracellular-to-extracellular ATP secretion, which could also contribute to the WSPM2.5-induced pyroptosis and inflammation by activating the Caspase-1/IL-1β/IL-18 signaling pathway through possible autocrine and/or paracrine mechanisms. Antagonism of ATP (Apyrase) or specific siRNA knockdown against ATP receptors (P2Y2 and P2Y7) both significantly inhibited the WSPM2.5-induced pyroptosis and inflammation. These results add up to the current knowledge and bring up novel insights that WSPM2.5 could induce significant pyroptosis and inflammation of human bronchial epithelial cells, through both a classic NLRP3/Caspase-1/IL-1β-dependent and a novel ATP/P2Y-dependent mechanisms.

Effect of combined treatment including Litsea cubeba essential oil and wood smoke on Aspergillus niger development and consumer acceptability of dried catfish (Ariidae)

SummaryDried fish exports generate massive revenue. These exports are in highest demand in the world market. However, dried fish can quickly become spoiled by mould. This creates foul odours that may affect consumer acceptance. Dried fish requires natural antimicrobial agents to improve shelf life. This study aimed to control mould growth and improve the organoleptic properties of dried fish using Litsea cubeba oil vapour in combination with wood smoke. In addition, to understand consumer acceptability, the treated dried fish was used to test consumer brain responses using electroencephalography (EEG). The participants who were able to eat dried fish preferred smoked food and had no history of allergies to dried fish, and essential oils were selected for this test. The combined treatment of the L. cubeba oil vapour at ≥60 μL and smoke for 30 s completely controlled the growth of A. niger at least 6 Log10 CFU g−1 and extended the shelf life of dried fish to 7 days at 30 ± 2 °C compared with the control (3 days). The panellists preferred the dried fish treated with the combined treatment more than the untreated fish (P &lt; 0.05). The consumption (smelling, eating and swallowing) of the treated fish by the participants increased the alpha wave activity in their brains to increase the activation of the neural circuits for attention, working memory, active stage and sensory‐motor integration. These findings can be helpful for smoke‐dried fish product development and dried fish preservation.

PM2.5 Pollution Levels and Chemical Components at Teahouses along the Poon Hill Trek in Nepal

Unhealthy levels of fine particulate matter (PM2.5) from the local burning of solid fuels, and from regional transport of pollutants, remain a major public health problem in the Himalayan foothill villages in Nepal. Teahouses (i.e., mountain lodges) along popular hiking trails in the lower Himalayas commonly use wood as the primary energy source for heating; however, little is known about teahouse air quality. The purpose of this study was to characterize the levels and chemical constituents of indoor and ambient PM2.5 at three villages along the Poon Hill circuit trek in the Annapurna Conservation Area in Nepal. A convenience sample of five PM2.5 measurements was collected with portable MicroPEM V.3.2A exposure monitors. Filters were analyzed for black and brown carbon using integrating sphere optical transmittance and 33 elemental constituents using energy-dispersive X-ray fluorescence. Median indoor PM2.5 over the sampling period was 41.3 µg/m3, whereas median ambient PM2.5 over the sampling period was 34.7 µg/m3. Chemical species associated with wood smoke, such as potassium (GM = 0.88 µg/m3), predominated. High indoor and ambient PM2.5 levels may pose a significant occupational health risk to teahouse workers, who may experience chronic exposures during trekking seasons. Our findings warrant additional research to characterize teahouse air pollution exposures more fully and to evaluate intervention measures.

Nonparametric methods for clustered data in pre-post intervention design

In pre-post factorial designs involving clustered units, parametric methods such as generalized linear mixed effects models are used to handle within subject correlations. However, the distributional and parametric model assumptions in these methods are not always satisfied, especially so with modern data sets, and are often difficult to verify in practice. Often times, the assumptions may not even be realistic when data are measured in a non-metric scale as commonly happens, for example, in Quality-of-Life outcomes. In this article, nonparametric effect-size measures for clustered data in factorial designs with pre-post measurements will be introduced. In our setup, the pre and post occasions may also be viewed as two treatment conditions. Arbitrary dependence among observations within a cluster and across treatment groups is allowed. The effect-size estimators along with their asymptotic properties for computing confidence intervals and performing hypotheses tests are investigated. The proposed methods handle within-cluster as well as between-cluster treatment assignments seamlessly. The methods are shown to be effective in finite samples using simulation studies and they have high powers, especially in situations with multiple forms of clustering. Applications are illustrated with data from a three-arm Randomized Trial of Indoor Wood Smoke reduction.

Driver mutations and air pollution in advanced non-small cell lung cancer (NSCLC) at two reference hospitals in Mexico City.

e20545 Background: Currently, precision medicine has allowed the classification of NSCLC according to the profile of driver mutations and the development of highly effective treatments. There is evidence to support the relationship between outdoor air pollution, particularly particulate matter (PM) in outdoor air, with lung cancer incidence and mortality. Smoking is a negative predictor of EGFR mutation, but the effect of air pollution has not been stablished. Methods: We perform a retrospective study in two referral hospitals in Mexico City between 2015 to 2020 to determinate the frequency of key driver mutations in patients with advanced NSCLC and the relation with smoking habit, wood smoke exposure and pollution indexes (PM2.5, PM10, SO2, O3, NO2) according to their place of residence. We used WHO air quality thresholds for air pollutants to classify cases with high or low exposure. Results: A total of 1277 cases were analyzed. The median age at diagnosis was 66 years (range 18-97 years), 53% were females and 49.6% had history of smoking habit. According to histology, 61.6% of cases corresponded to adenocarcinoma, 11.7% were squamous, 1.3% large cell, and 25.4% indeterminate. Wood smoke was assessed in 83.1% of cases and 28.5% had exposure history. Air pollutants were measured in half of cases, high level of exposure for PM2.5, PM10, NO2 and SO2 occurred in 63.2%, 30.8%, 15.6%, 53.4%, respectively. EGFR, ALK and KRAS mutations were evaluated in 85%, 16.7% and 8.6% of patients, respectively. The presence of these mutations was: EGFR 17.1%, ALK 11.1%, and KRAS 16.5%. Patients with EGFR-positive NSCLC were more frequently female (65.1% vs 34.9%, OR 1.8 95%CI 1.4-2.5, p &lt; 0.001) and had no history of tobacco use (35% vs 65%, OR 0.49 95%CI 0.36-0.67, p &lt; 0.001). Wood smoke was not statistically significant. High exposure to PM2.5 was most common in patients with non-mutated EGFR NSCLC (65.3% vs 34.7%, OR 1.7 95%CI 1.2-2.5, p = 0.006). Relationship with other air pollutants were not statistically significant. ALK-positive NSCLC patients tend to be females (68% vs 32%, p = 0.07) and had no history of smoking habit (20.8% vs 79.2% OR 0.28 95%CI 0.1-0.78, p = 0.01). High exposure to SO2 was common (78.6% vs 21.4% p = 0.05). Association in KRAS-positive NSCLS patients were not found. Conclusions: A low rate of key driver mutations assessment was found in this Mexican cohort. Clinical profile of NSCLC EGFR positive is according with previous reports in the literature. Exposure to PM2.5 and SO2 were found associated with EGFR and ALK status in this retrospective study and are hypothesis generating information.

Gastroschisis at the León University Hospital, Nicaragua

Abstract Objective: The prevalence of midline birth defects, such as gastroschisis, has increased worldwide, over the last few decades. This study aims to explore the prevalence, maternal epidemiological characteristics, and natural history of neonates affected by gastroschisis at the University Hospital of León city, Nicaragua. Methods: Data were collected from the birth defect surveillance system of the Hospital Oscar Danilo Rosales (HEODRA). The analysis included all pregnancies that had gastroschisis complications between January 1 and December 31, 2020. The prevalence of gastroschisis was calculated according to maternal age. The mothers were interviewed, and the clinical records of the newborns were reviewed. Results: Among the 4,460 deliveries included in this study, four cases of gastroschisis were identified, including three live births and one stillbirth. The gastroschisis rate was 8.9 per 10,000 live births (95% confidence interval [CI]: 0.18–17.8). The prevalence among mothers younger than 20 years and those older than 20 years was 26.4 (95% CI: –3.43 to 56.25) and 3.01 (95% CI: 2.89–8.90)/10,000 births, respectively. Mothers of gastroschisis-affected fetuses were of rural origin (n = 3), had normal body mass indexes (n = 3), were exposed to tobacco and wood smoke (n = 2), and one was exposed to pesticides during the periconceptional period. Primary closure of the gastroschisis was performed on one patient, and complex gastroschisis for intestinal perforation was observed in another patient. The mean hospitalization duration was 33 days, and two patients were discharged alive. Conclusions: Gastroschisis was a significant birth defect among children delivered at HEODRA in 2020. Its prevalence in Nicaragua was higher than that in other countries in the region. All complicated pregnancies were young women with unplanned pregnancies, from rural areas, with exposure to secondhand smoke, and without vitamin supplements before or during the first trimester of pregnancy. Only 67% of infants survived after hospital discharge.

Linking Switzerland's PM&amp;lt;sub&amp;gt;10&amp;lt;/sub&amp;gt; and PM&amp;lt;sub&amp;gt;2.5&amp;lt;/sub&amp;gt; oxidative potential (OP) with emission sources

Abstract. Particulate matter (PM) is the air pollutant that causes the greatest deleterious health effects across the world, so PM is routinely monitored within air quality networks, usually in respect to PM mass or number in different size fractions. However, such measurements do not provide information on the biological toxicity of PM. Oxidative potential (OP) is a complementary metric that aims to classify PM in respect to its oxidising ability in the lungs and is being increasingly reported due to its assumed relevance concerning human health. Between June 2018 and May 2019, an intensive filter-based PM sampling campaign was conducted across Switzerland in five locations, which involved the quantification of a large number of PM constituents and the OP for both PM10 and PM2.5. OP was quantified by three assays: ascorbic acid (AA), dithiothreitol (DTT), and dichlorofluorescein (DCFH). OPv (OP by air volume) was found to be variable over time and space: Bern-Bollwerk, an urban-traffic sampling site, had the greatest levels of OPv among the Swiss sites (especially when considering OPvAA), with more rural locations such as Payerne experiencing a lower OPv. However, urban-background and suburban sites experienced a significant OPv enhancement, as did the rural Magadino-Cadenazzo site during wintertime because of high levels of wood smoke. The mean OP ranges for the sampling period were 0.4–4.1 nmolmin-1m-3, 0.6–3.0 nmolmin-1m-3, and 0.3–0.7 nmol H2O2 m−3 for OPvAA, OPvDTT, and OPvDCFH, respectively. A source allocation method using positive matrix factorisation (PMF) models indicated that although all PM10 and PM2.5 sources that were identified contributed to OPv, the anthropogenic road traffic and wood combustion sources had the greatest OPm potency (OP per PM mass) on average. A dimensionality reduction procedure coupled to multiple linear regression modelling consistently identified a handful of metals usually associated with non-exhaust emissions, namely copper, zinc, iron, tin, antimony, manganese, and cadmium, as well as three specific wood-burning-sourced organic tracers – levoglucosan, mannosan, and galactosan (or their metal substitutes: rubidium and potassium), as the most important PM components to explain and predict OPv. The combination of a metal and a wood-burning-specific tracer led to the best-performing linear models to explain OPv. Interestingly, within the non-exhaust and wood combustion emission groups, the exact choice of component was not critical; the models simply required a variable representing the emission source or process to be present. This analysis strongly suggests that anthropogenic and locally emitting road traffic and wood burning sources should be prioritised, targeted, and controlled to gain the most efficacious decrease in OPv and presumably biological harm reductions in Switzerland.

Environmental and Processing Contaminants from Pahs and Furan

Maintaining an adequate, safe food supply has been a major goal of the Federal Government since 1906, when the first Federal food and drug law was signed into law. Historically, chemicals such as salt, sugar, and wood smoke have been used to preserve foods. Modern food technology relies extensively on the use of chemicals not only for preservation but also to produce appealing colors, flavors, aromas, and textures. Most developed countries now have food laws designed to permit the use of such chemicals in food under conditions judged to be safe. These chemicals are not considered adulterants or contaminants and are classed as intentional additives. Other chemicals may enter food as a result of their use in food production, handling, or processing. Such substances maybe legally permitted if they are unavoidable under good manufacturing practices and if the amounts involved are considered safe. These chemicals are classed as incidental additives. The presence of both these classes of chemicals in food is controlled by regulation.

Identification of aroma-active compounds in Cheddar cheese imparted by wood smoke

Cheddar cheese is the most popular cheese in the United States, and the demand for specialty categories of cheese, such as smoked cheese, are rising. The objective of this study was to characterize the flavor differences among Cheddar cheeses smoked with hickory, cherry, or apple woods, and to identify important aroma-active compounds contributing to these differences. First, the aroma-active compound profiles of hickory, cherry, and apple wood smokes were analyzed by solid-phase microextraction (SPME) gas chromatography-olfactometry (GCO) and gas chromatography-mass spectrometry (GC-MS). Subsequently, commercial Cheddar cheeses smoked with hickory, cherry, or apple woods, as well as an unsmoked control, were evaluated by a trained sensory panel and by SPME GCO and GC-MS to identify aroma-active compounds. Selected compounds were quantified with external standard curves. Seventy-eight aroma-active compounds were identified in wood smokes. Compounds included phenolics, carbonyls, and furans. The trained panel identified distinct sensory attributes and intensities among the 3 cheeses exposed to different wood smokes (P < 0.05). Hickory smoked cheeses had the highest intensities of flavors associated with characteristic "smokiness" including smoke aroma, overall smoke flavor intensity, and meaty, smoky flavor. Cherry wood smoked cheeses were distinguished by the presence of a fruity flavor. Apple wood smoked cheeses were characterized by the presence of a waxy, green flavor. Ninety-nine aroma-active compounds were identified in smoked cheeses. Phenol, guaiacol, 4-methylguaiacol, and syringol were identified as the most important compounds contributing to characteristic "smokiness." Benzyl alcohol contributed to the fruity flavor in cherry wood smoked cheeses, and 2-methyl-2-butenal and 2-ethylfuran were responsible for the waxy, green flavor identified in apple wood smoked cheeses. These smoke flavor compounds, in addition to diacetyl and acetoin, were deemed important to the flavor of cheeses in this study. Results from this study identified volatile aroma-active compounds contributing to differences in sensory perception among Cheddar cheeses smoked with different wood sources.

Assessment of peak expiratory flow rate and other cardiometabolic parameters of meat roasters (Mai suya) in Kano Nigeria

Occupational exposure to wood smoke and oil fumes is an important cause of respiratory problems. Meat roasting exposes workers to hazard of wood smoke and oil fumes. The aim of this study was to assess peak expiratory flow rate (PEFR) and other cardiometabolic parameters of meat roasters (Mai suya) in Kano, Nigeria. A total of 105 participants consisting of 55 meat roasters and 50 controls were recruited. All participants were assessed for PEFR, pulse rate, oxygen saturation, blood pressure, weight, height, and body mass index (BMI) according to standard protocols. Data were analyzed using SPSS version 23.0 and p value ≤ 0.05 was considered statistically significant. Mean age of the meat roasters and controls was 30.64±10.28 and 23.68±3.15 years. Meat roasters had statistically significant lower PEFR (243±85.35 vs 377.40±64.93 mL/min; p = 0.01), elevated diastolic pressure (81.91±6.64 vs 78.36±4.59 mmHg; p = 0.01), mean arterial pressure (94.12±7.96 vs 90.75±4.88 mmHg; p = 0.01) and BMI (19.53±2.40 vs 18.49±2.08 kg/m2; p = 0.02) compared to the controls. Number of years of working as meat roaster was positively correlated with systolic pressure (r = 0.67, p = 0.01), diastolic pressure (r = 0.41, p = 0.01), mean arterial pressure (r = 0.60, p = 0.01), BMI (r = 0.37, p = 0.01), and pulse rate (r = 0.46, p = 0.01). Meat roasting is associated with impaired lung function and altered blood pressure. Routine assessment of lung function and use of safety equipment should be encouraged among meat roasters.

Chronic Exposure to the Combination of Cigarette Smoke and Morphine Decreases CD4+ Regulatory T Cell Numbers by Reprogramming the Treg Cell Transcriptome.

There is a high incidence of tobacco use among intravenous opioid drug users. It is well established that opioids and tobacco smoke induce a degree of immune activation, and recent work suggests that the combination of these drugs promotes further activation of the immune system. Our approach involved the treatment of wild-type mice with cigarette smoke (SM) for a period of eight weeks, and the chronic continuous administration of morphine (M) via mini-pumps for the final four weeks. In an effort to examine the responses of CD4+CD25highCD127low regulatory T (Treg) cells, the major immune suppressive cell type, to the combined chronic administration of SM and M, we determined the frequency of these cells in the spleen, lymph nodes and lungs. Flow cytometric analyses showed that SM and M individually, and the combination (SM + M) have differential effects on the numbers of Treg in the spleen, lymph node, and lung. Either SM or M alone increased Treg cell numbers in the spleen, but SM+M did not. Furthermore, SM + M decreased Treg cell numbers in the lymph node and lung. We then performed RNA-Seq on Treg cells from mice treated with SM, M, or SM + M, and we found that the S + M induced a number of significant changes in the transcriptome, that were not as apparent following treatment with either SM or M alone. This included an activation of TWEAK, PI3K/AKT and OXPHOS pathways and a shift to Th17 immunity. Our results have provided novel insights on tissue Treg cell changes, which we suggest are the result of transcriptomic reprogramming induced by SM, M, and SM + M, respectively. We believe these results may lead to the identification of novel therapeutic targets for suppressing smoke and opioid induced Treg cell impairment.

Investigation of Different Winemaking Protocols to Mitigate Smoke Taint Character in Wine.

There is an increase in the levels of volatile phenols in wine made with smoke-impacted grapes. These compounds are present in wood smoke resulting from the pyrolysis (thermal decomposition) of lignin and at high levels give overpowering smoky and ashy characters to a wine. This research aimed to compare all the suggested wine mitigation strategies that evolved from prior research using smoke-impacted grapes under identical winemaking conditions except for the parameter under investigation. Cabernet Sauvignon grapes were received from three areas with varying amounts of smoke exposure in Northern California. Gas chromatography combined with mass spectrometry (GC-MS) and descriptive analyses were performed to correlate the volatile phenol composition to smoke taint characteristics. The winemaking variables investigated were the use of different fermentation yeasts, oak additions, and fermentation temperatures. Among other attributes, smokiness and ashy aftertaste were significantly different among the wines, showing a clear difference between the wines made from smoke-impacted fruit and the control wines made from non-impacted fruit. Findings indicate that mitigation strategies during red wine fermentation have a limited impact on the extraction of smoke-taint markers and the expression of smoke-taint sensory characteristics.

Ambient sampling of real-world residential wood combustion plumes

ABSTRACT Wood smoke contains large quantities of carbonaceous aerosols known to increase climate forcing and be detrimental to human health. This paper reports the findings from our ambient sampling of fresh residential wood combustion (RWC) plumes in two heating seasons (2015–2016, 2016–2017) in Upstate New York. An Aethalometer (AE33) and a pDR-1500 were employed to monitor residential wood smoke plumes in Ithaca, NY through a hybrid mobile-stationary method. Fresh wood smoke plumes were captured and characterized at 13 different RWC sources in the city, all without significant influence from other combustion sources or atmospheric aging. Wood smoke absorption Ångström exponent (AAE) was estimated using both a one-component model, AAEWB, and a two-component model, AAEBrC (assuming AAEBC = 1.0). Consistent with the recent laboratory studies, our results show that AAEs were highly variable for residential wood smoke for the same source and across different sources, with AAEWB values ranging from 1.3 to 5.0 and AAEBrC values ranging from 2.2 to 7.4. This finding challenges the use of using a single AAE wood smoke value within the range of 1 to 2.5 for source apportionment studies. Furthermore, the PM2.5/BC ratio measured using optical instruments was demonstrated to be potentially useful to characterize burning conditions. Different wood smoke sources can be distinguished by their PM2.5/BC ratio, which range between 15 and 150. This shows promise as an in-situ, cost-effective, ambient sampling-based method to characterize wood burning conditions. Implications: There are two main implications from this paper. First, the large variability in wood smoke absorption Ångström exponent (AAE) values revealed from our real-world, ambient sampling of residential wood combustion plumes indicated that it is not appropriate to use a single AAE wood smoke value for source apportionment studies. Second, the PM2.5/BC ratio has been shown to serve as a promising in-situ, cost-effective, ambient sampling-based indicator to characterize wood burning conditions. This has the potential to greatly reduce the costs of insitu wood smoke surveillance.

Effects of Wood Smoke Constituents on Mucin Gene Expression in Mice and Human Airway Epithelial Cells and on Nasal Epithelia of Subjects with a Susceptibility Gene Variant in Tp53.

Background:Exposure to wood smoke (WS) increases the risk for chronic bronchitis more than exposure to cigarette smoke (CS), but the underlying mechanisms are unclear.Objective:The effect of WS and CS on mucous cell hyperplasia in mice and in human primary airway epithelial cells (AECs) was compared with replicate the findings in human cohorts. Responsible WS constituents were identified to better delineate the pathway involved, and the role of a tumor protein p53 (Tp53) gene polymorphism was investigated.Methods:Mice and primary human AECs were exposed to WS or CS and the signaling receptor and pathway were identified using short hairpin structures, small molecule inhibitors, and Western analyses. Mass spectrometric analysis was used to identify active WS constituents. The role of a gene variant in Tp53 that modifies proline to arginine was examined using nasal brushings from study participants in the Lovelace Smokers Cohort, primary human AECs, and mice with a modified Tp53 gene.Results:WS at 25-fold lower concentration than CS increased mucin expression more efficiently in mice and in human AECs in a p53 pathway-dependent manner. Study participants who were homozygous for p53 arginine compared with the proline variant showed higher mucin 5AC (MUC5AC) mRNA levels in nasal brushings if they reported WS exposure. The WS constituent, oxalate, increased MUC5AC levels similar to the whole WS extract, especially in primary human AECs homozygous for p53 arginine, and in mice with a modified Tp53 gene. Further, the anion exchange protein, SLC26A9, when reduced, enhanced WS- and oxalate-induced mucin expression.Discussion:The potency of WS compared with CS in inducing mucin expression may explain the increased risk for chronic bronchitis in participants exposed to WS. Identification of the responsible compounds could help estimate the risk of pollutants in causing chronic bronchitis in susceptible individuals and provide strategies to improve management of lung diseases. https://doi.org/10.1289/EHP9446

Wood smoke exposure affects lung aging, quality of life, and all-cause mortality in New Mexican smokers

BackgroundThe role of wood smoke (WS) exposure in the etiology of chronic obstructive pulmonary disease (COPD), lung cancer (LC), and mortality remains elusive in adults from countries with low ambient levels of combustion-emitted particulate matter. This study aims to delineate the impact of WS exposure on lung health and mortality in adults age 40 and older who ever smoked.MethodsWe assessed health impact of self-reported “ever WS exposure for over a year” in the Lovelace Smokers Cohort using both objective measures (i.e., lung function decline, LC incidence, and deaths) and two health related quality-of-life questionnaires (i.e., lung disease-specific St. George's Respiratory Questionnaire [SGRQ] and the generic 36-item short-form health survey).ResultsCompared to subjects without WS exposure, subjects with WS exposure had a more rapid decline of FEV1 (− 4.3 ml/s, P = 0.025) and FEV1/FVC ratio (− 0.093%, P = 0.015), but not of FVC (− 2.4 ml, P = 0.30). Age modified the impacts of WS exposure on lung function decline. WS exposure impaired all health domains with the increase in SGRQ scores exceeding the minimal clinically important difference. WS exposure increased hazard for incidence of LC and death of all-cause, cardiopulmonary diseases, and cancers by > 50% and shortened the lifespan by 3.5 year. We found no evidence for differential misclassification or confounding from socioeconomic status for the health effects of WS exposure.ConclusionsWe identified epidemiological evidence supporting WS exposure as an independent etiological factor for the development of COPD through accelerating lung function decline in an obstructive pattern. Time-to-event analyses of LC incidence and cancer-specific mortality provide human evidence supporting the carcinogenicity of WS exposure.

Measurement of gas-phase OH radical oxidation and film thickness of organic films at the air–water interface using material extracted from urban, remote and wood smoke aerosol

The presence of an organic film on a cloud droplet or aqueous aerosol particle has the potential to alter the chemical, optical and physical properties of the droplet or particle.