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Air pollution and circulating biomarkers of oxidative stress
Abstract and Figures
Chemical components of air pollutant exposures that induce oxidative stress and subsequent inflammation may be partly responsible for associations of cardiovascular morbidity and mortality with airborne particulate matter and combustion-related pollutant gasses. However, epidemiologic evidence regarding this is limited. An exposure-assessment approach is to measure the oxidative potential of particle mixtures because it is likely that hundreds of correlated chemicals are involved in overall effects of air pollution on health. Oxidative potential likely depends on particle composition and size distribution, especially ultrafine particle concentration, and on transition metals and certain semivolatile and volatile organic chemicals. For health effects, measuring systemic oxidative stress in the blood is one feasible approach, but there is no universal biomarker of oxidative stress and there are many potential target molecules (lipids, proteins, DNA, nitric oxide, etc.), which may be more or less suitable for specific study goals. Concurrent with the measurement of oxidative stress, it is important to measure gene and/or protein expression of endogenous antioxidant enzymes because they can modify relations between oxidative stress biomarkers and air pollutants. Conversely, the expression and activities of these enzymes are modified by oxidative stress. This interplay will likely determine the observed effects of air pollutants on systemic inflammatory and thrombotic mediators and related clinical outcomes. Studies are needed to assess the reliability and validity of oxidative stress biomarkers, evaluate differences in associations between oxidative stress biomarkers and various pollutant measurements (mass, chemical components, and oxidative potential), and evaluate impacts of antioxidant responses on these relations.
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... A low or acute exposure level to air pollutants may increase the activity of SOD system in the early phase to reduce oxidative damage, while chronic exposure, or highly toxic fine or ultrafine air particles, may lead to the halt of endogenous antioxidant responses [24]. For this reason, a progressive decrease in the activity of the enzymatic SOD system could be observed with chronic exposure to pollution, possibly leading to some endogenous antioxidant responses, such as as NF-E2-related factor-2 (Nrf2), Nuclear factor-κB (NF-κB), NAD(P)H quinone oxidoreductase 1 (Nqo1), glutamate-cysteine ligase modifier subunit (Gclm), activation protein-1 (AP-1), and CREB-binding proteins (CBPs), which are regulated and influenced by redox status and involved in the transcriptional regulation of a wide range of genes that are involved in oxidative stress and cellular response mechanisms [28][29][30]. ...
... Many studies confirm the generation of reactive oxygen and nitrogen species in epithelial cells of the airway, with macrophages that are within the lung being reviewed extensively as well [32,33], particularly in subjects with previous chronic diseases [30]. The pathway that reactive oxygen species are involved in and that causes oxidative stress is responsible for acute and chronic lung inflammation [30,33]. ...
... Many studies confirm the generation of reactive oxygen and nitrogen species in epithelial cells of the airway, with macrophages that are within the lung being reviewed extensively as well [32,33], particularly in subjects with previous chronic diseases [30]. The pathway that reactive oxygen species are involved in and that causes oxidative stress is responsible for acute and chronic lung inflammation [30,33]. The results of some studies suggest that oxidative stress, inflammation, and tissue damage are directly correlated with exposure to fine or ultrafine air particles [28,33,34]. ...
Recent studies revealed that the high production of reactive oxidative species due to exposure to fine or ultrafine particles are involved in many chronic respiratory disorders. However, the poor standard of clinical data in sub-Saharan countries makes the assessment of our knowledge on the health impacts of air pollution in urban cities very difficult. Objective: The aim of this study was to evaluate the distribution of respiratory disorders associated with exposure to fine and ul-trafine air particles through the changes of some oxidative stress biomarkers among motorbike drivers from two cities of Cameroon. Methods: A cross-sectional survey using a standardized questionnaire was conducted in 2019 on 191 motorcycle drivers (MDs) working in Douala and Dschang. Then, the activities of superoxide dismutase (SOD) and the level of malondialdehyde (MDA) were measured using colorimetric methods. The data of participants, after being clustered in Microsoft Excel, were analyzed and statistically compared using SPSS 20 software. Results: The motorbike drivers recruited from both cities were from 21 to 40 years old, with a mean age of 29.93 (±0.82). The distribution of respiratory disorders, such as a runny nose, cold, dry cough, chest discomfort, and breathlessness, was significantly increased among MDs in Douala. According to the results of biological assays, SOD and MDA were significantly greater among the MDs recruited in Douala compared to those of Dschang. The change in these oxidative stress markers was significantly positively correlated with the mobilization of monocytes and negatively correlated with neutrophils, showing the onset and progression of subjacent inflammatory reactions, and it seemed to be significantly influenced by the location MDs lived in. Conclusions: Through this study, we have confirmed the evidence supporting that the onset and progression of oxidative stress is caused by the long-term exposure to fine or ultrafine air particles among working people living in urban cities. Further studies should be conducted to provide evidence for the cellular damage and dysfunction related to the chronic exposure to fine particulate matter (PM) in the air among working people in the metropolitan sub-Saharan Africa context. Citation: Tiekwe, J.E.; Ongbayokolak, N.; Dabou, S.; Natheu, K.C.; Goka, M.S.; Nya Biapa , P.C.; Annesi-Maesano, I.; Telefo, P.B. Respiratory Symptoms and Changes of Oxidative Stress Markers among Motorbike Drivers Chronically Exposed to Fine and Ultrafine Air Particles: A Case Study of Douala and Dschang, Cameroon.
... Glutathione peroxidase (GPx) is an antioxidant enzyme that helps to protect cells from oxidative damage by scavenging harmful reactive oxygen species (ROS). GPx activity is also commonly used to measure oxidative stress indirectly, and increased GPx activity may suggest an upregulation of the antioxidant system to combat increased ROS production [47]. Consistently with the antecedents, we found a time-dependent increase in the GPx activity in animals exposed to PM 2.5 on day 28 compared to day 14. ...
PM2.5 and arsenic are two of the most hazardous substances for humans that coexist worldwide. Independently, they might cause multiple organ damage. However, the combined effect of PM2.5 and arsenic has not been studied. Here, we used an animal model of simultaneous exposure to arsenic and PM2.5. Adult Wistar rats were exposed to PM2.5, As, or PM2.5 + As and their corresponding control groups. After 7, 14, and 28 days of exposure, the animals were euthanized and serum, lungs, kidneys, and hearts were collected. Analysis performed showed high levels of lung inflammation in all experimental groups, with an additive effect in the coexposed group. Besides, we observed cartilaginous metaplasia in the hearts of all exposed animals. The levels of creatine kinase, CK-MB, and lactate dehydrogenase increased in experimental groups. Tissue alterations might be related to oxidative stress through increased GPx and NADPH oxidase activity. The findings of this study suggest that exposure to arsenic, PM2.5, or coexposure induces high levels of oxidative stress, which might be associated with lung inflammation and heart damage. These findings highlight the importance of reducing exposure to these pollutants to protect human health.
... Several potential mechanisms could explain these associations. As chemical components of air pollution, CO, NO 2 , O 3 , SO 2 , and PM 2.5 share a common biological pathway known to induce oxidative stress and inflammation, which are recognised as AMD risk factors [34,35]. Moreover, animal studies have demonstrated that PM 2.5 can impair microvascular function [36]. ...
Background
Several epidemiological studies have investigated the association between ambient air pollution and age-related macular degeneration (AMD). However, a consensus has not yet been reached. Our meta-analysis aimed to clarify this association.
Methods
Databases, including PubMed, EMBASE, and Web of Science, were searched for relevant studies from 01 January 2000 to 30 January 2024. English-language, peer-reviewed studies using cross-sectional, prospective, or retrospective cohorts and case–control studies exploring this relationship were included. Two authors independently extracted data and assessed study quality. A random-effects model was used to calculate pooled covariate-adjusted odds ratios. Heterogeneity across studies was also tested.
Results
We identified 358 relevant studies, of which eight were included in the meta-analysis. Four studies evaluated the association between particulate matter less than 2.5 μm in diameter (PM2.5) and AMD, and three studies explored the relationship between nitrogen dioxide (NO2) or ozone (O3) and AMD. The pooled odds ratios were 1.16 (95% confidence interval [CI]: 1.11–1.21), 1.17 (95% CI: 1.09–1.25), and 1.06 (95% CI: 1.05–1.07), respectively.
Conclusion
Current evidence suggests a concomitant positive but not causal relationship between PM2.5, NO2, or O3 and AMD risk.
... An in vitro cell study on gasoline exhaust particles showed that ultrafine particles present in gasoline exhaust also induced significant oxidative stress, lipid peroxidation, and cell inflammation [17]. In summary, the primary mechanism may involve the induction of inflammation and oxidative stress [18,19], with reactive oxygen species (ROS) generated by oxidative stress leading to the release of vascular permeability factor/vascular endothelial growth factor A, which affects the permeability of intercellular adhesion junctions [20]. Subsequently, particles may pass through the vascular endothelial-calcium-VE-cadherin network and enter the circulatory system [21], potentially affecting lipid metabolism in the human body. ...
Limited knowledge exists regarding gasoline and diesel exhaust effects on lipid metabolism. This study collected gasoline and diesel exhaust under actual driving conditions and conducted inhalation exposure on male young and middle-aged C57BL/6J mice for 4 h/day for 5 days to simulate commuting exposure intensity. Additionally, PM2.5 from actual roadways, representing gasoline and diesel vehicles, was generated for exposure to human umbilical vein endothelial cells (HUVECs) and normal liver cells (LO2) for 24, 48, and 72 h to further investigate exhaust particle toxicity. Results showed that diesel exhaust reduced total cholesterol and low-density lipoprotein cholesterol levels in young mice, indicating disrupted lipid metabolism. Aspartate aminotransferase and alanine aminotransferase levels increased by 53.7% and 21.7%, respectively, suggesting potential liver injury. Diesel exhaust exposure decreased superoxide dismutase and increased glutathione peroxidase levels. Cell viability decreased, and reactive oxygen species levels increased in HUVECs and LO2 following exposure to exhaust particles, with dose- and time-dependent effects. Diesel exhaust particles exhibited more severe inhibition of cell proliferation and oxidative damage compared to gasoline exhaust particles. These findings provide novel evidence of the risk of disrupted lipid metabolism due to gasoline and diesel exhaust, emphasizing the toxicity of diesel exhaust.
... The period of in utero and early post natal is critical in the development of organs system, including respiratory and immune systems (Esplugues et al. 2011;Lu et al. 2021). Therefore, potential harmful effects of toxic pollutions during pregnancy might result in longlasting impaired capacity to fight infections and increased risk of allergic manifestations later in life (Lu et al. 2021;Delfino et al. 2011). ...
Objective
There is limited study from low-and-middle income countries on the effect of perinatal exposure to air pollution and the risk of infection in infant. We assessed the association between perinatal exposure to traffic related air pollution and the risk of infection in infant during their first six months of life.
Methods
A prospective cohort study was performed in Jakarta, March 2016–September 2020 among 298 mother-infant pairs. PM2.5, soot, NOx, and NO2 concentrations were assessed using land use regression models (LUR) at individual level. Repeated interviewer-administered questionnaires were used to obtain data on infection at 1, 2, 4 and 6 months of age. The infections were categorized as upper respiratory tract (runny nose, cough, wheezing or shortness of breath), lower respiratory tract (pneumonia, bronchiolitis) or gastrointestinal tract infection. Logistic regression models adjusted for covariates were used to assess the association between perinatal exposure to air pollution and the risk of infection in the first six months of life.
Results
The average concentrations of PM2.5 and NO2 were much higher than the WHO recommended levels. Upper respiratory tract infections (URTI) were much more common in the first six months of life than diagnosed lower respiratory tract or gastro-intestinal infections (35.6%, 3.5% and 5.8% respectively). Perinatal exposure to PM2.5 and soot suggested increase cumulative risk of upper respiratory tract infection (URTI) in the first 6 months of life per IQR increase with adjusted OR of 1.50 (95% CI 0.91; 2.47) and 1.14 (95% CI 0.79; 1.64), respectively. Soot was significantly associated with the risk of URTI at 4–6 months age interval (aOR of 1.45, 95%CI 1.02; 2.09). All air pollutants were also positively associated with lower respiratory tract infection, but all CIs include unity because of relatively small samples. Adjusted odds ratios for gastrointestinal infections were close to unity.
Conclusion
Our study adds to the evidence that perinatal exposure to fine particles is associated with respiratory tract infection in infants in a low-middle income country.
... Certain pollutants, like heavy metals and air contaminants, can create oxidative stress by promoting the generation of ROS. This stimulation activates signalling pathways sensitive to redox signals, impacting cell survival, programmed cell death (apoptosis), and inflammation (Sierra-Vargas et al., 2023;Bhattacharyya et al., 2014;Delfino et al., 2011). Certain chemicals, known as endocrine-disrupting chemicals (EDCs), could imitate or inhibit body hormones. ...
This study investigates the intricate interplay between environmental pollutants and exosomes, shedding light on a novel paradigm in environmental health and disease. Cellular stress, induced by environmental toxicants or disease, significantly impacts the production and composition of exosomes, crucial mediators of intercellular communication. The heat shock response (HSR) and unfolded protein response (UPR) pathways, activated during cellular stress, profoundly influence exosome generation, cargo sorting, and function, shaping intercellular communication and stress responses. Environmental pollutants, particularly lipophilic ones, directly interact with exosome lipid bilayers, potentially affecting membrane stability, release, and cellular uptake. The study reveals that exposure to environmental contaminants induces significant changes in exosomal proteins, miRNAs, and lipids, impacting cellular function and health. Understanding the impact of environmental pollutants on exosomal cargo holds promise for biomarkers of exposure, enabling non-invasive sample collection and real-time insights into ongoing cellular responses. This research explores the potential of exosomal biomarkers for early detection of health effects, assessing treatment efficacy, and population-wide screening. Overcoming challenges requires advanced isolation techniques, standardized protocols, and machine learning for data analysis. Integration with omics technologies enhances comprehensive molecular analysis, offering a holistic understanding of the complex regulatory network influenced by environmental pollutants. The study underscores the capability of xosomes in circulation as promising biomarkers for assessing environmental exposure and systemic health effects, contributing to advancements in environmental health research and disease prevention.
... In this work, we profile the single-cell morphological changes after exposure to various PM mixtures to quantify cellular responses and identify cellular properties that are associated with cellular susceptibility to pollutants. Three major and novel findings of this work include the following: First, we identified that although there is a common transcriptomic response to PM in the activation of the P450 family cytochromes, as shown previously (15,61), the degree of pathway remodeling is dependent on the PM composition and concentration of exposure. Second, we show cell morphology is a strong indicator of response to differential PM exposure. ...
Particulate matter (PM) is a ubiquitous component of air pollution that is epidemiologically linked to human pulmonary diseases. PM chemical composition varies widely, and the development of high-throughput experimental techniques enables direct profiling of cellular effects using compositionally unique PM mixtures. Here, we show that in a human bronchial epithelial cell model, exposure to three chemically distinct PM mixtures drive unique cell viability patterns, transcriptional remodeling, and the emergence of distinct morphological subtypes. Specifically, PM mixtures modulate cell viability, DNA damage responses, and induce the remodeling of gene expression associated with cell morphology, extracellular matrix organization, and cellular motility. Profiling cellular responses showed that cell morphologies change in a PM composition-dependent manner. Finally, we observed that PM mixtures with higher cadmium content induced increased DNA damage and drove redistribution among morphological subtypes. Our results demonstrate that quantitative measurement of individual cellular morphologies provides a robust, high-throughput approach to gauge the effects of environmental stressors on biological systems and score cellular susceptibilities to pollution.
Air pollution causes a huge number of fatalities every year around the world. It has been suggested that air pollution contributes to approximately 8.8 million extra deaths worldwide every year, and about 40–80% of these deaths have been linked to various cardiovascular diseases (CVD). Recent epidemiological studies have provided extensive evidence linking air pollution with a wide variety of adverse health conditions and diseases pertaining to respiratory and cardiovascular systems, especially among vulnerable demographic groups such as the children, the elderly, and those with preexisting compromised cardiopulmonary conditions such as asthma. These adverse effects predominantly include reduced functionality of the lung, chronic respiratory and cardiovascular inflammation, chronic obstructive pulmonary disease (COPD), stroke and heart attacks, and lung cancer. All these effects have been associated with exposure to at least one major air pollutant that is routinely found in the ambient air in large cities around the world. These air pollutants include suspended particulate matter (PM), ozone (O3), nitrogen oxides (NOx), sulphur dioxide (SO2), carbon monoxide (CO), volatile organic carbon compounds including polyaromatic hydrocarbons (PAHs), and trace metals such as lead (Pb) (Cohen et al. 2017). Although each of these air pollutants can induce serious health implications for humans, exposure to fine (diameter ≤ 2.5 μm) and ultrafine (diameter ≤ 0.1 μm) particles are believed to be the leading cause of cardiorespiratory illnesses in the developing world. However, the current understanding of the health effects of PM is limited, and most of the epidemiological evidence of linking adverse health effects to PM exposure is not conclusive. Moreover, the cellular and molecular mechanisms by which PM, exclusively and in mixture with other air pollutants, elicit toxic effects in humans are yet to be fully understood. Nevertheless, the use of conventional biochemical and novel molecular biomarker assessments can provide important insights into the cellular perturbations that lead to the onset of adverse health effects during chronic exposure to air pollutants. Furthermore, the advent of next generation, systems biology molecular techniques (e.g., omics technologies) provides exciting new avenues to study the effects of air pollution on human health. These new tools can provide new knowledge on the interactions of air pollutants with genes, proteins and other biomolecules that are currently unknown, and thus, develop a more holistic and in-depth mechanistic understanding of the toxicity of these pollutants. Ultimately, this advanced understanding can then be used to develop toxicity models that can predict potential future adverse health outcomes early during exposure, enabling preventive interactions and implementation of effective mitigation strategies.
Air pollution is nowadays a complex problem due to industrial prosperity. Among the chemical industry,oil refineries have been identified as major emitters of a wide range of pollutants, the workers of the oilrefinery are exposed to a great variety of toxic compounds. Air pollution is the main environmental causeof human disease and death. Therefore, it is necessary to develop early warning signals or biomarkersthat convincingly reflect adverse biological responses towards anthropogenic environmental toxinseven at minute concentrations. This work aims to study the effects of exposure to the air pollution of oilrefinery, on the parameter blood, TNF-a, antioxidant glutathione peroxidase(GPx), and oxidative stressmalondialdehyde (MDA), in workers of the oil refinery. Results showed that exposure to air pollutionin the oil refinery lead to( a significant increase in levels Hb, WBC, Lymphocyte, TNF-a, and MDA,decrease levels of GPx) P<0.05. And non –significant in( RBC, HCT, Neutrophils ) P>0.05 in workers,compared to healthy control.
Oxidative stress is defined as an excessive bioavailability of Reactive Oxygen Species (ROS) due to imbalance of generation of ROS and antioxidant defense systems. ROS produced by vascular cells (endothelial cells, vascular smooth muscle cells, and adventitial fibroblasts) are implicated as possible underlying pathogenic mechanism in a progression of cardiovascular diseases such as ischemic heart disease (angina pectoris), atherosclerosis, hyperlipidemia, cardiac arrhythmia and hypertension. Lipid peroxidation is a major oxidative effect in which lipids after combination with oxygen through peroxyl radical formation, leads to lipid hydroperoxidation with membrane disruption and form highly cytotoxic products, leading to cardiovascular diseases mainly ischemic heart diseases like angina pectoris. Another oxidative process is an imbalance of reduced production of NO (Nitric Oxide) or increased production of reactive oxygen species (ROS), mainly by superoxides (O2 •) in vascular cells that promotes atherosclerosis and hypertension. In cardiac arrhythmia, cardiac mitochondria and NADPH oxidase are involved. ROS weakly couples cardiac mitochondria under oxidative stress conditions and leads to development of fatal ventricular arrthymia and when ROS oxidize Low Density Lipoprotein to O-LDL (Oxidized LDL) it leads to hyperlipidemia. This review focuses on how oxidative stress play role in promotion of various cardiovascular diseases.
Malondialdehyde (MDA) is one of the most frequently used indicators of lipid peroxidation. To generate reliable reference intervals for plasma malondialdehyde (P-MDA), a reference sample group was established in Funen, Denmark. The group consisted of 213 individuals (107 men, 106 women), ages 20–79 years. P-MDA was measured in EDTA-treated plasma after derivatization by thiobarbituric acid (TBA) and separation on HPLC. UV detection was performed at 532 nm. A reference interval was calculated as recommended by IFCC with REFVAL 3.42. The estimated reference limits (0.025 and 0.975 fractals) for the group were 0.36 and 1.24 μmol/L. The data were analyzed for gender- and age-related differences. Analysis of variance showed no interaction between gender and age, but separate analyses showed an independent effect of gender (P = 0.03), but not of age (P = 0.11). Daily smokers had a slightly higher average concentration of P-MDA than nonsmokers (P = 0.05), and P-MDA correlated with daily exposure to cigarette smoke (r = 0.162; P = 0.03). A positive correlation was also demonstrated between P-MDA and weekly alcohol consumption (r = 0.153; P = 0.03). Within-subject and day-to-day variations of P-MDA indicated that the potential of P-MDA as a biomarker for individuals is questionable. However, on a group basis, the present data support that P-MDA may be a potential biomarker for oxidative stress.
The hypothesis that oxidative modification of low density lipoprotein (LDL) might be a critically important step in atherogenesis grew out of the recognition that cholesterol accumulation in foam cells could not be due to uptake of native LDL by way of the LDL receptor. First of all, patients who totally lack LDL receptors nevertheless develop foam cell-rich lesions much like the lesions in hypercholesterolemic subjects with normal LDL receptors [1]. Second, neither cultured monocyte/macrophages [2] nor cultured smooth muscle cells [3] can be forced to accumulate any appreciable amounts of cholesterol ester by incubation with even very high concentrations of native LDL. This led to a search for alternative forms of LDL and alternative lipoprotein receptors. Chemically acetylated LDL (AcLDL) was the first modified form demonstrated to be taken up sufficiently rapidly by monocyte/macrophages to lead to cholesterol accumulation [2]. The uptake occurred by way of a new receptor, the AcLDL receptor, quite distinct from the native LDL receptor. Unlike the native LDL receptor, the acetyl LDL receptor does not downregulate as the cell cholesterol content increases, which allows the progressive accumulation of sterol. However, there is no evidence for generation of AcLDL in vivo. Oxidized LDL (OxLDL) was shown to be an alternative ligand for the AcLDL receptor and to cause accumulation of cholesterol esters in monocyte/macrophages [4]. Over the past decade a large body of evidence has accumulated demonstrating that oxidation of LDL does indeed take place in vivo and that this process may be playing a significant role in atherogenesis, at least in animal models [5,6]. If this hypothesis is valid with respect to the human disease, it would have important implications for intervention to slow the progression of atherosclerosis. Consequently there has been intense interest in the oxidation of LDL and the factors that contribute to it.
1. Oxygen is a toxic gas - an introductionto oxygen toxicity and reactive species 2. The chemistry of free radicals and related 'reactive species' 3. Antioxidant defences Endogenous and Diet Derived 4. Cellular responses to oxidative stress: adaptation, damage, repair, senescence and death 5. Measurement of reactive species 6. Reactive species can pose special problems needing special solutions. Some examples. 7. Reactive species can be useful some more examples 8. Reactive species can be poisonous: their role in toxicology 9. Reactive species and disease: fact, fiction or filibuster? 10. Ageing, nutrition, disease, and therapy: A role for antioxidants?
Quasi-ultrafine particulate matter (PM0.25) and its components were measured in indoor and outdoor environments at four retirement communities in the Los Angeles basin, California, as part of the Cardiovascular Health and Air Pollution Study (CHAPS). The present work focuses on the identification and quantification of the sources, characterization of organic constituents and indoor and outdoor relationships of quasi-ultrafine PM. To the contrary to n-alkanes and n-alkanoic acids, the average indoor/outdoor ratio of most of the measured PAHs, hopanes and steranes were close to or slightly lower than 1, and indoor-outdoor correlation coefficients (R) were always positive and for most of these components moderate to strong (median R was 0.60 for PAHs and 0.74 for hopanes and steranes). This suggests that indoor PAHs, hopanes and steranes were mainly from outdoor origin, whereas indoor n-alkanes and n-alkanoic acids were significantly influenced by indoor sources. The Chemical Mass Balance (CMB) model was applied to both indoor and outdoor speciated chemical measurements of quasi-ultrafine PM. Vehicular sources had the highest contribution to PM0.25 among the apportioned sources for both indoor and outdoor particles at all sites (on average 24-47%). The contribution of mobile sources to indoor levels was similar to their corresponding outdoor estimates, thus indicating the high penetration of these sources indoors.