Wood smoke particles from different combustion phases induce similar pro-inflammatory effects in a co-culture of monocyte and pneumocyte cell lines

Background Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The pro-inflammatory potential of PM depends on the particles’ physical and chemical characteristics, which again depend on the emitting source. Wood combustion is a major source of ambient air pollution in Northern countries during the winter season. The overall aim of this study was therefore to investigate cellular responses to wood smoke particles (WSPs) collected from different phases of the combustion cycle, and from combustion at different temperatures. Results WSPs from different phases of the combustion cycle induced very similar effects on pro-inflammatory mediator release, cytotoxicity and cell number, whereas WSPs from medium-temperature combustion were more cytotoxic than WSPs from high-temperature incomplete combustion. Furthermore, comparisons of effects induced by native WSPs with the corresponding organic extracts and washed particles revealed that the organic fraction was the most important determinant for the WSP-induced effects. However, the responses induced by the organic fraction could generally not be linked to the content of the measured polycyclic aromatic hydrocarbons (PAHs), suggesting that also other organic compounds were involved. Conclusion The toxicity of WSPs seems to a large extent to be determined by stove type and combustion conditions, rather than the phase of the combustion cycle. Notably, this toxicity seems to strongly depend on the organic fraction, and it is probably associated with organic components other than the commonly measured unsubstituted PAHs

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

Background Exposure to particulate matter (PM) from wood combustion represents a global health risk, encompassing diverse exposure sources; indoor exposures due to cooking in developing countries, ambient PM exposures from residential wood combustion in developed countries, and the predicted increasing number of wildfires due to global warming. Although physicochemical properties of the PM, as well as the exposure levels vary considerably between these sources, controlled human exposure studies may provide valuable insight to the harmful effects of wood smoke (WS) exposures in general. However, no previous review has focused specifically on controlled human exposure studies to WS. Results The 22 publications identified, resulting from 12 controlled human studies, applied a range of combustion conditions, exposure levels and durations, and exercise components in their WS exposure. A range of airway, cardiovascular and systemic endpoints were assessed, including lung function and heart rate measures, inflammation and oxidative stress. However, the possibility for drawing general conclusions was precluded by the large variation in study design, resulting in differences in physicochemical properties of WS, effective dose, as well as included endpoints and time-points for analysis. Overall, there was most consistency in reported effects for airways, while oxidative stress, systemic inflammation and cardiovascular physiology did not show any clear patterns. Conclusion Based on the reviewed controlled human exposure studies, conclusions regarding effects of acute WS exposure on human health are premature. Thus, more carefully conducted human studies are needed. Future studies should pay particular attention to the applied WS exposure, to assure that both exposure levels and PM properties reflect the research question.Medicine, Faculty ofNon UBCMedicine, Department ofRespiratory Medicine, Division ofReviewedFacultyResearche

Particulate Matter 2.5 Exposure and Self-Reported Use of Wood Stoves and Other Indoor Combustion Sources in Urban Nonsmoking Homes in Norway.

Few studies have examined particulate matter (PM) exposure from self-reported use of wood stoves and other indoor combustion sources in urban settings in developed countries. We measured concentrations of indoor PM < 2.5 microns (PM2.5) for one week with the MicroPEM™ nephelometer in 36 households in the greater Oslo, Norway metropolitan area. We examined indoor PM2.5 levels in relation to use of wood stoves and other combustion sources during a 7 day monitoring period using mixed effects linear models with adjustment for ambient PM2.5 levels. Mean hourly indoor PM2.5 concentrations were higher (p = 0.04) for the 14 homes with wood stove use (15.6 μg/m3) than for the 22 homes without (12.6 μg/m3). Moreover, mean hourly PM2.5 was higher (p = 0.001) for use of wood stoves made before 1997 (6 homes, 20.2 μg/m3), when wood stove emission limits were instituted in Norway, compared to newer wood stoves (8 homes, 11.9 μg/m3) which had mean hourly values similar to control homes. Increased PM2.5 levels during diary-reported burning of candles was detected independently of concomitant wood stove use. These results suggest that self-reported use of wood stoves, particularly older stoves, and other combustion sources, such as candles, are associated with indoor PM2.5 measurements in an urban population from a high income country

Peroxisome proliferator-activated receptor gamma gene variants modify human airway and systemic responses to indoor dibutyl phthalate exposure

Abstract Background Single nucleotide polymorphisms (SNPs) of peroxisome proliferator-activated receptor gamma (PPAR-γ; gene: PPARG) and oxidative stress genes are associated with asthma risk. However, whether such variants modulate responses to dibutyl phthalate (DBP), a common plasticizer associated with increased asthma development, remains unknown. The purpose of this study is to investigate how SNPs in PPARG and oxidative stress genes, as represented by two separate genetic risk scores, modify the impact of DBP exposure on lung function and the airway and systemic response after an inhaled allergen challenge. Methods We conducted a double-blinded human crossover study with sixteen allergen-sensitized participants exposed for three hours to DBP and control air on distinct occasions separated by a 4-week washout. Each exposure was followed by an allergen inhalation challenge; subsequently, lung function was measured, and blood and bronchoalveolar lavage (BAL) were collected and analyzed for cell counts and allergen-specific immunoglobulin E (IgE). Genetic risk scores for PPAR-γ (P-GRS; weighted sum of PPARG SNPs rs10865710, rs709158, and rs3856806) and oxidative stress (OS-GRS; unweighted sum of 16 SNPs across multiple genes) were developed, and their ability to modify DBP effects were assessed using linear mixed-effects models. Results P-GRS and OS-GRS modified DBP effects on allergen-specific IgE in blood at 20 h (interaction effect [95% CI]: 1.43 [1.13 to 1.80], p = 0.005) and 3 h (0.99 [0.98 to 1], p = 0.03), respectively. P-GRS also modified DBP effects on Th2 cells in blood at 3 h (− 25.2 [− 47.7 to − 2.70], p = 0.03) and 20 h (− 39.1 [− 57.9 to − 20.3], p = 0.0005), and Th2 cells in BAL at 24 h (− 4.99 [− 8.97 to − 1.01], p = 0.02). An increasing P-GRS associated with reduced DBP effect on Th2 cells. Neither GRS significantly modified DBP effects on lung function parameters. Conclusions PPAR-γ variants modulated several airway and systemic immune responses to the ubiquitous chemical plasticizer DBP. Our results suggest that PPAR-γ variants may play a greater role than those in oxidative stress-related genes in airway allergic responses to DBP.Medicine, Faculty ofNon UBCMedical Genetics, Department ofMedicine, Department ofReviewedFacultyResearcherPostdoctoralGraduat