Smoke Research Articles

Effect of prednisone on woodsmoke-induced sputum inflammation in healthy volunteers: A randomized, placebo-controlled pilot study

Inhalation of biomass smoke is associated with adverse respiratory effects in those with chronic pulmonary conditions. There are few published data regarding the effects of anti-inflammatory interventions on these outcomes. Our aim was to assess the effects of postexposure prednisone on woodsmoke (WS)-induced sputum neutrophilia. We carried out a randomized, placebo-controlled, crossover pilot study assessing the effect of a postexposure dose of 60 mg prednisone on induced sputum inflammation after controlled exposure to WS (500 μg/m3 for 2 hours) in healthy adults who had been identified in a separate screening protocol as being "PMN responsive" to WS. Secondary end points were sputum cytokine level and mucociliary clearance as measured by γ-scintigraphy. A total of 11 subjects yielded complete data for the primary analysis. At 24 hours after WS exposure, there was a significant increase in sputum percentage of PMNs (%PMN) versus at baseline after placebo (median= 42% [IQR= 31%-53%]) (P= .02) but not after prednisone (median= 32% [IQR= 18%-40%]) (P= .09). Prednisone reduced Δ%PMN at 24 hours, but this difference did not reach statistical significance. However, for the 8 of 11 subjects who were PMN responsive after placebo, prednisone reduced Δ%PMN significantly (P= .05). Prednisone had no significant effects on sputum levels of IL-1β, IL-6, IL-8, or TNF-α. WS exposure tended to reduce mucociliary clearance in the placebo arm but not in the prednisone arm. Prednisone taken immediately after exposure to WS mitigated short-term increase in sputum %PMN among healthy volunteers selected for their underlying inflammatory responsiveness to WS. Our data support future studies assessing anti-inflammatory interventions and the role of mucus clearance in WS-induced respiratory health effects.

NRF2 protects lung epithelial cells from wood smoke particle toxicity

Wildfire smoke is a potential source of oxidative stress in lung epithelial tissue. The response to oxidative stress is controlled by the transcription factor NRF2, which is the central regulator of antioxidant gene expression. If wood smoke particle (WSP) exposure induces reactive oxygen species (ROS) in epithelial cells, then NRF2 may protect against pathological conditions resulting from increased oxidative stress through changes in gene expression. We used two lung epithelial cell lines to test this hypothesis in vitro: A549, which harbor a mutation resulting in constitutive activation of NRF2, and BEAS-2B, which show limited NRF2 activity under basal conditions, but high inducibility during oxidative stress. In BEAS-2B cells, WSP exposure leads to increased cellular ROS, activation of NRF2, and upregulation of the NRF2 target genes NQO1, GCLM, and SRXN1. WSP exposure also increased ROS in A549 cells, although NRF2 activation and antioxidant gene upregulation were less robust as both were basally high in this cell line. Overall, the degree of ROS induction by WSP across cell lines is dependent upon NRF2 activity, and a similar pattern was observed for WSP cytotoxicity. WSP also sensitized both cell lines to the ferroptosis inducer erastin in a manner that is correlated with NRF2 activity. Knockout of NRF2 in A549 resulted in higher WSP-induced ROS generation, cytotoxicity, and erastin sensitivity. Taken together, these results suggest that NRF2 serves as a protective factor against wood smoke induced ROS and oxidative stress in lung epithelial cells.

Exposure to mixture particulate contaminants in the air and the risk of oral cancer: An updated systematic review and meta-analysis

The mixture of contaminants in the air (e.g., PM2.5, smoke) is a part of air pollutants that has become a hot environmental issue. Previous epidemiological studies have reported the relationship between wood smoke and PM2.5 exposure and oral cancer, but findings have been inconsistent. Therefore, this work designed to find out the relationship between mixture contaminants in air exposure and oral cancer. Fourteen studies were included through research in three databases before February 2024. Before analysis, the Newcastle-Ottawa Scale was applied to examine the quality of all selected studies. Then, the meta-analysis was carried out by meta-regression analysis, sensitivity analysis and subgroup analysis. The results showed that exposure to PM2.5 may have a positive association with oral cancer (pooled OR = 1.13, 95 % confidence interval: 1.06, 1.20). In contrast, no significant association was found between indoor air pollution and oral cancer. However, the result of the subgroup analysis indicated there is a significant association of indoor air pollution and oral cancer in developing countries (pooled OR = 2.5, 95 % confidence interval: 1.7, 3.6). In addition, the heterogeneity among studies of indoor air pollution exposure and oral cancer may caused by studies carried out in developed countries according to the subgroup and meta-regression analyses. In conclusion, the studies about indoor air pollution exposure and oral cancer are discrepant. The effects of mixed air contaminants for people's health are not simple and more studies are demanded to find out it in the future.

Eucalyptus Wood Smoke Extract Elicits a Dose-Dependent Effect in Brain Endothelial Cells

The frequency, duration, and size of wildfires have been increasing, and the inhalation of wildfire smoke particles poses a significant risk to human health. Epidemiological studies have shown that wildfire smoke exposure is positively associated with cognitive and neurological dysfunctions. However, there is a significant gap in knowledge on how wildfire smoke exposure can affect the blood–brain barrier and cause molecular and cellular changes in the brain. Our study aims to determine the acute effect of smoldering eucalyptus wood smoke extract (WSE) on brain endothelial cells for potential neurotoxicity in vitro. Primary human brain microvascular endothelial cells (HBMEC) and immortalized human brain endothelial cell line (hCMEC/D3) were treated with different doses of WSE for 24 h. WSE treatment resulted in a dose-dependent increase in IL-8 in both HBMEC and hCMEC/D3. RNA-seq analyses showed a dose-dependent upregulation of genes involved in aryl hydrocarbon receptor (AhR) and nuclear factor erythroid 2-related factor 2 (NRF2) pathways and a decrease in tight junction markers in both HBMEC and hCMEC/D3. When comparing untreated controls, RNA-seq analyses showed that HBMEC have a higher expression of tight junction markers compared to hCMEC/D3. In summary, our study found that 24 h WSE treatment increases IL-8 production dose-dependently and decreases tight junction markers in both HBMEC and hCMEC/D3 that may be mediated through the AhR and NRF2 pathways, and HBMEC could be a better in vitro model for studying the effect of wood smoke extract or particles on brain endothelial cells.

Synergistic neurological threat from Сu and wood smoke particulate matter

Trace metal Cu and carbonaceous airborn particulate matter (PM) are dangerous neuropollutants. Here, the ability of Cu2+ to modulate the neurotoxicity caused by water-suspended wood smoke PM preparations (SPs) and vice versa was examined using presynaptic rat cortex nerve terminals. Interaction of Cu2+ and SPs, changes of particle size and surface properties were shown in the presence of Cu2+ using microscopy, DLS, and IR spectroscopy. In nerve terminals, Cu2+ and SPs per se elevated the ambient levels of excitatory and inhibitory neurotransmitters L-[14C]glutamate and [3H]GABA, respectively. During combined application, Cu2+ significantly enhanced a SPs-induced increase in the ambient levels of both neurotransmitters, thereby demonstrating a cumulative synergistic effect and significant interference in the neurotoxic threat associated with Cu2+and SPs. In fluorimetric measurements, Cu2+ and SPs also demonstrated cumulative synergistic effects on the membrane potential, mitochondrial potential, synaptic vesicle acidification and ROS generation. Therefore, synergistic effects of Cu2+ and SPs on the most crucial presynaptic characteristics and neurohazard of multiple pollutants through excitatory/inhibitory imbalance, disruption of the membrane and mitochondrial potential, vesicle acidification and ROS generation were revealed. Increased expansion and burden of neuropathology may result from underestimation of synergistic interference of the neurotoxic effects of Cu2+ and carbonaceous smoke PM.

Pear Wood Pyrolysis Influences Quality and Levels of Polycyclic Aromatic Hydrocarbons in Liquid Smoke

Limu smoked chicken is a traditional Chinese delicacy; however, polycyclic aromatic hydrocarbons (PAHs) are generated during the smoking process. We developed a pyrolysis process for pear wood liquid smoke with minimal PAH generation. Pear wood liquid smoke products were prepared under different pyrolysis conditions in a self-made pyrolysis reactor, and the total phenol, carbonyl compound, total acid, and PAH contents and PAH toxicity risk were evaluated. With increasing temperatures, the toxicity equivalent ΣPAH of the smoke liquid reached 3.004 μg/kg. With increasing particle sizes, the total phenol content reached 1.6 mg/mL; the phenol content was 5.95 mg/mL. With increasing particle sizes, the toxicity equivalent ΣPAHs of the smoke liquor reached 2.441 μg/kg. The optimal parameters for treating pear wood smoke liquid in the thermal reaction device were a pyrolysis temperature of pear wood of >350 °C, particle size of S2, and sucrose content of 8%.

Systematic review and meta-analysis of studies of wood smoke exposure and nasopharyngeal

Systematic review and meta-analysis of studies of wood smoke exposure and nasopharyngeal

The mortality burden of wood smoke PM2.5 in Australia

The mortality burden of wood smoke PM2.5 in Australia

Reducing exposure to residential wood smoke in Australia: health equity, environmental justice, and implementation challenges and opportunities

Reducing exposure to residential wood smoke in Australia: health equity, environmental justice, and implementation challenges and opportunities

Examining public preferences for wood smoke mitigation policies in the sub-Arctic

Outdoor air pollution is a significant problem worldwide. Policies developed to mitigate air pollution require support from local residents to be successful. While some research has examined various social and psychological metrics associated with support for some types of pollution mitigation, less is known about what variables are critical in resident support for different types of policies that help mitigate air pollution associated with woodsmoke. This research examined the extent that perceived health and economic risks, perceived uncertainties in measuring air quality and estimating risks, trust in government, and affect relate to support for three different types of outdoor wood smoke mitigation policies in Alaska. Using a multiple regression analysis of data obtained from a mail-based survey (n = 442), we characterized local affective associations with wood burning, economic concerns and health risks around heat options, perceived uncertainties, and levels of trust in government. The research identified several social and psychological variables that were important in understanding support for air pollution policies associated with wood smoke. Significantly, we found that perceived economic risk of not taking actions to mitigate outdoor air pollution from wood smoke was related to support for all three policy options. Trust in local government was positively correlated to support for education and regulatory policies, and perceived uncertainty was inversely related to support for regulations. The research also confirmed other known findings with respect to variables associated with support for air pollution regulation policies including perceived health risks and affect.

Neuroinflammation is dependent on sex and ovarian hormone presence following acute woodsmoke exposure

Woodsmoke (WS) exposure is associated with significant health-related sequelae. Different populations can potentially exhibit varying susceptibility, based on endocrine phenotypes, to WS and investigating neurological impacts following inhaled WS is a growing area of research. In this study, a whole-body inhalation chamber was used to expose both male and female C57BL/6 mice (n = 8 per group) to either control filtered air (FA) or acute WS (0.861 ± 0.210 mg/m3) for 4 h/d for 2 days. Neuroinflammatory and lipid-based biological markers were then assessed. In a second set of studies, female mice were divided into two groups: one group was ovariectomized (OVX) to simulate an ovarian hormone-deficient state (surgical menopause), and the other underwent Sham surgery as controls, to mechanistically assess the impact of ovarian hormone presence on neuroinflammation following FA and acute WS exposure to simulate an acute wildfire episode. There was a statistically significant impact of sex (P ≤ 0.05) and statistically significant interactions between sex and treatment in IL-1β, CXCL-1, TGF-β, and IL-6 brain relative gene expression. Hippocampal and cortex genes also exhibited significant changes in acute WS-exposed Sham and OVX mice, particularly in TGF-β (hippocampus) and CCL-2 and CXCL-1 (cortex). Cortex GFAP optical density (OD) showed a notable elevation in male mice exposed to acute WS, compared to the control FA. Sham and OVX females demonstrated differential GFAP expression, depending on brain region. Overall, targeted lipidomics in phosphatidylcholine (PC) and phosphatidylethanolamine (PE) serum and brain lipids demonstrated more significant changes between control FA and acute WS exposure in female mice, compared to males. In summary, male and female mice show distinct neuroinflammatory markers in response to acute WS exposure. Furthermore, ovarian hormone deficiency may impact the neuroinflammatory response following an acute WS event.

Factors related to mortality in patients with chronic obstructive pulmonary disease in Colombian population

Introduction. Data in low- and middle-income countries on mortality and its related risk factors in patients with chronic obstructive pulmonary disease are limited. Objective. To identify the incidence of death and its relationship with variables in a Colombian population during 12 months of follow-up. Materials and methods. We carried out a retrospective study in subjects diagnosed with chronic obstructive pulmonary disease in a third-level hospital in Colombia. Odds ratios were calculated using multivariable logistic regression analysis with the outcome variable “mortality at 12 months”. Results. We included 524 patients, 18.1% (95 / 524) died. The average age was 69.7 (SD = 8.92), and 59.2% (310 / 524) were women. The variables associated with mortality were age (OR = 6.54; 95% CI = 3.65-11.36; p < 0.001), years of exposure to wood smoke (OR = 4.59; 95% CI = 1.64-2.82; p = 0.002), chronic heart failure (OR = 1.81; 95% CI = 1.13-2.91; p = 0.014), cerebrovascular disease (OR = 3.35; 95% CI = 1.04-10.75; p = 0.032), and chronic kidney disease (OR = 6.96; 95% CI = 1.15-41.67; p=0.015). When adjusting the variables in the multivariate analysis, only an association was found for sex (OR = 1.55; 95% CI = 0.95-2.54; p = 0.008) and age (OR = 5.94; 95% CI = 3.3-10.69; p < 0.001). Conclusion. Age, years of exposure to wood smoke, chronic heart failure, and cerebrovascular and chronic kidney disease were the clinical variables associated with a fatal outcome. However, age and sex were the only variables related to mortality when adjusted for confounding factors.

Atmospheric concentrations and potential sources of dioxin-like contaminants to Acadia National Park

Acadia National Park (ANP) is located on Mt. Desert Island, ME on the U.S. Atlantic coast. ANP is routinely a top-ten most popular National Park with over four million visits in 2022. The overall contribution and negative effects of long-range atmospheric transport and local sources of dioxin-like contaminants endangering natural and wildlife resources is unknown. Dioxin-like (DL) contaminants polychlorinated dibenzo-p-dioxins (∑PCDD) and polychlorinated dibenzofurans (∑PCDF), non-ortho coplanar PCBs (∑CP4), and polychlorinated naphthalenes (∑PCNs) were measured at the McFarland Hill air monitoring station (44.37⁰N, 68.26⁰W). On a mass/volume basis, total PCNs averaged 90.9 % (788 fg/m3) of DL contaminants measured annually, with 92.9 % of the collected total in the vapor-phase. Alternatively, total dioxin/furans (∑PCDD/Fs) represented 71.6 % of the total toxic equivalence (∑TEQ) (1.018 fg-TEQ/m3), with 69.7 % in the particulate-phase. Maximum concentrations measured for individual sampling events for ∑PCDD/F, ∑CP4, and ∑PCN were 159 (winter), 139 (summer), and 2100 (autumn), fg/m3 respectively. Whereas the maximum ∑TEQ concentrations for individual sampling events for ∑PCDD/F, ∑CP4, and ∑PCN were 2.8 (autumn), 0.38 (summer), and 0.71 (autumn), fg-TEQ/m3 respectively. Pearson correlations were calculated for ∑PCDD/Fs and ∑PCN particulate/vapor-phase air concentrations and PM2.5 wood smoke “indicator” species. The most significant correlations were observed in autumn for particulate-phase ∑PCDD/Fs suggesting a relationship between visitation-generated combustion sources (campfires and/or waste burning) or climate-change mediated forest fires. Significant Clausius-Clapeyron (C–C) correlations observed for particulate-phase ∑PCDDs (r2 = 0.567) as ambient temperatures decreased suggests a connection between localized domestic heating sources or visitor-based burning of wood/trash resources. Alternatively, highly significant C–C vapor-phase ∑CP4-PCBs correlations (r2 = 0.815) implies that the majority of ∑CP4-PCB loading to ANP is from long-range atmospheric transport processes. Based on these findings, Acadia National Park should be classified as a remote site with minor depositional impacts from ∑PCDD/Fs, ∑CP4-PCBs, and ∑PCN atmospheric transport or local diffuse sources.

Systemic immunological responses are dependent on sex and ovarian hormone presence following acute inhaled woodsmoke exposure

BackgroundRural regions of the western United States have experienced a noticeable surge in both the frequency and severity of acute wildfire events, which brings significant challenges to both public safety and environmental conservation efforts, with impacts felt globally. Identifying factors contributing to immune dysfunction, including endocrinological phenotypes, is essential to understanding how hormones may influence toxicological susceptibility.MethodsThis exploratory study utilized male and female C57BL/6 mice as in vivo models to investigate distinct responses to acute woodsmoke (WS) exposure with a focus on sex-based differences. In a second set of investigations, two groups were established within the female mouse cohort. In one group, mice experienced ovariectomy (OVX) to simulate an ovarian hormone-deficient state similar to surgical menopause, while the other group received Sham surgery as controls, to investigate the mechanistic role of ovarian hormone presence in driving immune dysregulation following acute WS exposure. Each experimental cohort followed a consecutive 2-day protocol with daily 4-h exposure intervals under two conditions: control HEPA-filtered air (FA) and acute WS to simulate an acute wildfire episode.ResultsMetals analysis of WS particulate matter (PM) revealed significantly increased levels of 63Cu, 182W, 208Pb, and 238U, compared to filtered air (FA) controls, providing insights into the specific metal components most impacted by the changing dynamics of wildfire occurrences in the region. Male and female mice exhibited diverse patterns in lung mRNA cytokine expression following WS exposure, with males showing downregulation and females displaying upregulation, notably for IL-1β, TNF-α, CXCL-1, CCL-5, TGF-β, and IL-6. After acute WS exposure, there were notable differences in the responses of macrophages, neutrophils, and bronchoalveolar lavage (BAL) cytokines IL-10, IL-6, IL-1β, and TNF-α. Significant diverse alterations were observed in BAL cytokines, specifically IL-1β, IL-10, IL-6, and TNF-α, as well as in the populations of immune cells, such as macrophages and polymorphonuclear leukocytes, in both Sham and OVX mice, following acute WS exposure. These findings elucidated the profound influence of hormonal changes on inflammatory outcomes, delineating substantial sex-related differences in immune activation and revealing altered immune responses in OVX mice due to ovarian hormone deficiency. In addition, the flow cytometry analysis highlighted the complex interaction between OVX surgery, acute WS exposure, and their collective impact on immune cell populations within the hematopoietic bone marrow niche.ConclusionsIn summary, both male and female mice, alongside females subjected to OVX and those who had sham surgery, exhibit significant variations in the expression of proinflammatory cytokines, chemokines, lung mRNA gene expression, and related functional networks linked to signaling pathways. These differences potentially act as mediators of sex-specific and hormonal influences in the systemic inflammatory response to acute WS exposure during a wildfire event. Understanding the regulatory roles of genes expressed differentially under environmental stressors holds considerable implications, aiding in identifying sex-specific therapeutic targets for addressing acute lung inflammation and injury.

A mouse model of wildfire smoke-induced health effects: sex differences in acute and sustained effects of inhalation exposures

Due to climate change, wildfires have increased in intensity and duration. While wildfires threaten lives directly, the smoke has more far-reaching adverse health impacts. During an extreme 2017 wildfire event, residents of Seeley Lake, Montana were exposed to unusually high levels of wood smoke (WS) causing sustained effects on lung function (decreased FEV1/FVC). Objective: The present study utilized an animal model of WS exposure to research cellular and molecular mechanisms of the resulting health effects. Methods: Mice were exposed to inhaled WS utilizing locally harvested wood to recapitulate community exposures. WS was generated at a rate resulting in a 5 mg/m3 PM2.5 exposure for five days. Results: This exposure resulted in a similar 0.28 mg/m2 particle deposition (lung surface area) in mice that was calculated for human exposure. As with the community observations, there was a significant effect on lung function, increased resistance, and decreased compliance, that was more pronounced in males at an extended (2 months) timepoint and males were more affected than females: ex vivo assays illustrated changes to alveolar macrophage functions (increased TNFα secretion and decreased efferocytosis). Female mice had significantly elevated IL-33 levels in lungs, however, pretreatment of male mice with IL-33 resulted in an abrogation of the observed WS effects, suggesting a dose-dependent role of IL-33. Additionally, there were greater immunotoxic effects in male mice. Discussion: These findings replicated the outcomes in humans and suggest that IL-33 is involved in a mechanism of the adverse effects of WS exposures that inform on potential sex differences.

Exposure to fine particulate matter 2.5 from wood combustion smoke causes vascular changes in placenta and reduce fetal size

During gestation, maternal blood flow to the umbilical cord and placenta increases, facilitating efficient nutrient absorption, waste elimination, and effective gas exchange for the developing fetus. However, the effects of exposure to wood smoke during this period on these processes are unknown. We hypothesize that exposure to PM2.5, primarily sourced from wood combustion for home heating, affects placental vascular morphophysiology and fetal size. We used exposure chambers that received either filtered or unfiltered air. Female rats were exposed to PM2.5 during pre-gestational and/or gestational stages. Twenty-one days post-fertilization, placentas were collected via cesarean section. In these placentas, oxygen diffusion capacity was measured, and the expression of angiogenic factors was analyzed using qPCR and immunohistochemistry. In groups exposed to PM2.5 during pre-gestational and/or gestational stages, a decrease in fetal weight, crown-rump length, theoretical and specific diffusion capacity, and an increase in HIF-1α expression were observed. In groups exposed exclusively to PM2.5 during the pre-gestational stage, there was an increase in the expression of placental genes Flt-1, Kdr, and PIGF. Additionally, in the placental labyrinth region, the expression of angiogenic factors was elevated. Changes in angiogenesis and angiogenic factors reflect adaptations to hypoxia, impacting fetal growth and oxygen supply. In conclusion, this study demonstrates that exposure to PM2.5, emitted from wood smoke, in both pre-gestational and gestational stages, affects fetal development and placental health. This underscores the importance of addressing air pollution in areas with high levels of wood smoke, which poses a significant health risk to pregnant women and their fetuses.

Seasonal extreme temperatures and short-term fine particulate matter increases pediatric respiratory healthcare encounters in a sparsely populated region of the intermountain western United States

BackgroundWestern Montana, USA, experiences complex air pollution patterns with predominant exposure sources from summer wildfire smoke and winter wood smoke. In addition, climate change related temperatures events are becoming more extreme and expected to contribute to increases in hospital admissions for a range of health outcomes. Evaluating while accounting for these exposures (air pollution and temperature) that often occur simultaneously and may act synergistically on health is becoming more important.MethodsWe explored short-term exposure to air pollution on children’s respiratory health outcomes and how extreme temperature or seasonal period modify the risk of air pollution-associated healthcare events. The main outcome measure included individual-based address located respiratory-related healthcare visits for three categories: asthma, lower respiratory tract infections (LRTI), and upper respiratory tract infections (URTI) across western Montana for ages 0–17 from 2017–2020. We used a time-stratified, case-crossover analysis with distributed lag models to identify sensitive exposure windows of fine particulate matter (PM2.5) lagged from 0 (same-day) to 14 prior-days modified by temperature or season.ResultsFor asthma, increases of 1 µg/m3 in PM2.5 exposure 7–13 days prior a healthcare visit date was associated with increased odds that were magnified during median to colder temperatures and winter periods. For LRTIs, 1 µg/m3 increases during 12 days of cumulative PM2.5 with peak exposure periods between 6–12 days before healthcare visit date was associated with elevated LRTI events, also heightened in median to colder temperatures but no seasonal effect was observed. For URTIs, 1 unit increases during 13 days of cumulative PM2.5 with peak exposure periods between 4–10 days prior event date was associated with greater risk for URTIs visits that were intensified during median to hotter temperatures and spring to summer periods.ConclusionsDelayed, short-term exposure increases of PM2.5 were associated with elevated odds of all three pediatric respiratory healthcare visit categories in a sparsely population area of the inter-Rocky Mountains, USA. PM2.5 in colder temperatures tended to increase instances of asthma and LRTIs, while PM2.5 during hotter periods increased URTIs.

The effect of liquid smoked flavourings and wood smoke on the quality of smoked mackerel fillets during chilled storage

This study was undertaken to evaluate the effects of liquid smoked flavourings and wood smoke on the sensory, color, texture, and lipid stability of smoked mackerel fillets for four weeks chilled storage. Fish fillets were smoked by two methods: (1) immersed in brine (1:1) containing 100 g/L NaCl at 0-5 °C for 3 hours, allowed to drain at room temperature (~20 °C) for 2 hours and smoked directly with wood smoke in a smoking chamber at 25 °C for 3 hours; (2) immersed in brine (1:1) containing 5 mL/L commercial liquid smoke flavourings and 60 g/L NaCl for 16 hours at 0-5 °C then dried at 25 °C for 2 hours in an oven. Smoked samples were then vacuum packed and stored chilled at -1 °C for one week, followed by 4±1°C for three weeks. The quality changes in sensory, color, texture, and lipid stability were observed after 0, 1, 2, 3 and 4 weeks of storage. The results showed that, smoked mackerel using commercial liquid smoked flavourings was higher in rancid flavour, lightness, redness, and yellowness but had less bitter odour and was softer than the wood smoked mackerel. The lipid oxidation was higher after the wood smoke process but was however rather stable during the chilled storage. In contrast, lipid oxidation in the liquid smoked products increased significantly during chilled storage. Keywords: Atlantic mackerel (Scomber scombrus), color, liquid smoked flavouring, lipid quality, sensory, texture, wood smoke

Repeated exposure to eucalyptus wood smoke alters pulmonary gene and metabolic profiles in male Long-Evans rats.

Exposure to wildfire smoke is associated with both acute and chronic cardiopulmonary illnesses, which are of special concern for wildland firefighters who experience repeated exposure to wood smoke. It is necessary to better understand the underlying pathophysiology by which wood smoke exposure increases pulmonary disease burdens in this population. We hypothesize that wood smoke exposure produces pulmonary dysfunction, lung inflammation, and gene expression profiles associated with future pulmonary complications. Male Long-Evans rats were intermittently exposed to smoldering eucalyptus wood smoke at 2 concentrations, low (11.0 ± 1.89 mg/m3) and high (23.7 ± 0.077 mg/m3), over a 2-week period. Whole-body plethysmography was measured intermittently throughout. Lung tissue and lavage fluid were collected 24 h after the final exposure for transcriptomics and metabolomics. Increasing smoke exposure upregulated neutrophils and select cytokines in the bronchoalveolar lavage fluid. In total, 3446 genes were differentially expressed in the lungs of rats in the high smoke exposure and only 1 gene in the low smoke exposure (Cd151). Genes altered in the high smoke group reflected changes to the Eukaryotic Initiation Factor 2 stress and oxidative stress responses, which mirrored metabolomics analyses. xMWAS-integrated analysis revealed that smoke exposure significantly altered pathways associated with oxidative stress, lung morphogenesis, and tumor proliferation pathways. These results indicate that intermittent, 2-week exposure to eucalyptus wood smoke leads to transcriptomic and metabolic changes in the lung that may predict future lung disease development. Collectively, these findings provide insight into cellular signaling pathways that may contribute to the chronic pulmonary conditions observed in wildland firefighters.

Binary Logistic Regression Analysis in Determining Risk Factors of Acute Respiratory Infection (IRA) on Under-Five Children

Acute Respiratory Infection (ARI) is a prevalent ailment and stands as one of the primary causes of mortality among children under the age of five. As reported by the Ministry of Health of the Republic of Indonesia, ARI predominantly affects children aged one to four years, with an incidence rate of 13.7%. Binary logistic regression is utilized to predict the likelihood of ARI occurrences in children under five, employing a linear combination of log-odds pertaining to suspected contributory factors. This study aims to evaluate the risk factors associated with ARI and develop an optimal logistic regression model by analyzing data from 166 participants who visited the Tarus regional health center between July 21 and September 1, 2023. Factors considered in this research as predictors for ARI (dependent variable ) include Immunization Status (X1), exposure to cigarette smoke at residence (X2), exposure to wood smoke at residence (X3), exclusive breastfeeding (X4), and nutritional status (X5). The final analysis revealed that incomplete immunization, exposure to cigarette smoke, and exposure to wood smoke at residence significantly heighten the risk of ARI. The most fitting logistic model obtained was expressed as logit (π_ijk)=-1.1051+1.2297X1+0.8709X2+1.31085X3.