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Background Cardiovascular toxicity as a consequence of nicotine from conventional tobacco cigarette smoking is well documented. However, little is known about the cardiovascular consequences of nicotine e-vaping. We review the literature and report a case series of three cases of major adverse cardiovascular clinical effects post nicotine e-vaping. Case summary Three patients with known peripheral arterial disease who switched from heavy cigarette smoking consumption to a high-intensity dose of nicotine e-vaping all developed further arterial complications within 6–30 months. Discussion With the recent epidemic of e-vaping in young individuals and the national outbreak of e-vaping use-associated lung injury (EVALI), the dangers of e-vaping are now coming to light. The pulmonary effects are now well described, and this paper highlights three new cases of cardiovascular toxicity associated with e-vaping. The potential role of nicotine e-vaping and the risk of coronavirus disease-2019 (COVID-19) will also be discussed.

Related the extremely transmittable abilities of SARS-CoV-2,a harmonious virus to the bat CoV, gets transmitted by three principal processes-- the inhalation of droplets from the SARS-CoV-2 infected person, contacting to the person, and by the surfaces and materials defiled with the virus. Whereupon bat Coronavirus is mostly like the pandemic causing virus SARS-CoV-2, bats are often deliberated and figured out as a possible primary host although no intermediate has not been defined yet in the wherewithal of transmission. The Spike Glycoprotein plays an important role in the case of penetration with the assistance of the ACE2 receptor and the Receptor Binding Domain. In the human body, infiltrating the nucleic acid into host cells, SARS-CoV-2 attacks one cell and one by one into the whole human body; therefore, infected cases are found symptomatic and asymptomatic considering the immune power. Patients with cardiovascular disease or diabetes proceed with their treatment with ACE2 often; therefore, there might be a high chance of getting infected. Whereas the SARS-CoV-2 infects the blood and then lungs, Antigens improvement can be better in order to avoid high-complicated effects. Currently, no vaccination or no accurate cure and treatment has not been defined. An explanation with analysis on SARS-CoV-2 has been performed from the aspect of virology, immunology and molecular biology. Several relevant figures have been included hereby in order to a better understanding of the very concept.

Lung surface is the first line of contact between inhaled carbon nanomaterials, CNMs, and the organism, so this is the place where pulmonary health effects begin. The paper analyzes the influence of several CNMs (single- and multi-walled nanotubes with various surface area: 90–1,280 m2/g and aspect ratio: 8–3,750) on the surface-active properties of the lung surfactant, LS, model (Survanta). Effects of CNM concentration (0.1–1 mg/ml) and surface oscillation rate were determined using the oscillating drop method at simulated breathing conditions (2–10 s per cycle, 37 °C). Based on the values of apparent elasticity and viscosity of the interfacial region, new parameters: Sε and Sμ were proposed to evaluate potential effect of particles on the LS at various breathing rates. Some of tested CNMs (e.g., COOH- functionalized short nanotubes) significantly influenced the surfactant dynamics, while the other had weaker effects even at high particle concentration. Analysis of changes in Sε and Sμ provides a new way to evaluate of a possible disturbance of the basic functions of LS. The results show that the expected pulmonary effects caused by inhaled CNMs at variable breathing rate depend not only on particle concentration (inhaled dose) but also on their size, structure and surface properties.

Recently, there has been a rise in the incidence of E-cigarette/Vaping-Associated Lung Injury (EVALI) in the United States, mostly involving tetrahydrocannabinol. Current treatment strategies for EVALI are aimed at controlling the inflammatory and infectious causes, in addition to supportive care. Although most patients improve with supportive measures, the long-term pulmonary effects of this illness are still not well defined. This report describes a case of EVALI resulting in progressive, irreversible destruction of the lung parenchyma that was treated with double lung transplantation.

In the present study, the suitability and sensitivity of different in vitro toxicity endpoints were determined to evaluate and distinguish the specific contributions of polycyclic aromatic carbon (PAC) mixtures from various sites in Toronto (Canada), to pulmonary toxicity. Air samples were collected for two-month periods from April 2014 to March 2015 from one location, and from August 2016 to August 2017 from multiple locations reflecting different geographical areas in Toronto, and the Greater Toronto Area, with varying source emissions including background, traffic, urban, industrial and residential sites. Relative concentrations of PACs and their derivatives in these air samples were characterised. In vitro cytotoxicity, pro-inflammatory, and oxidative stress assays were employed to assess the acute pulmonary effects of urban-air-derived air pollutants. In addition, global transcriptional profiling was utilized to understand how these chemical mixtures exert their harmful effects. Lastly, the transcriptomic data and the chemical profiles for each site and season were used to relate the biological response back to individual constituents. Site-specific responses could not be derived; however, the Spring season was identified as the most responsive through benchmark concentration analysis. A combination of correlational analysis and principal component analysis revealed that nitrated and oxygenated polycyclic aromatic hydrocarbons (PAHs) drive the response at lower concentrations while specific PAHs drive the response at the highest concentration tested. Unsubstituted PAHs are the current targets for analysis as priority pollutants. The present study highlights the importance of by-products of PAH degradation in the assessment of risk. The study also demonstrates the usefulness of in vitro toxicity assays to derive meaningful data in support of risk assessment.

Physical inactivity has caused serious effects on the health of the population, having an impact on the quality of life and the cost of healthcare for many countries. This has motivated government and private institutions to promote regular physical activity, which, paradoxically, can involve health risks when it is carried out in areas with poor air quality. This review collects information from studies conducted on healthy humans related to the pulmonary effects caused by the practice of physical activity when there is poor air quality. In addition, several challenges related to the technological and educational areas, as well as to applied and basic research, have been identified to facilitate the rational practice of exercise in poor air quality conditions.

Exposure to wildfire smoke continues to be a growing threat to public health, yet the chemical components in wildfire smoke that primarily drive toxicity and associated disease are largely unknown. This study utilized a suite of computational approaches to identify groups of chemicals induced by variable biomass burn conditions that were associated with biological responses in the mouse lung, including pulmonary immune response and injury markers. Smoke condensate samples were collected and characterized, resulting in chemical distribution information for 86 constituents across ten different exposures. Mixtures-relevant statistical methods included (i) a chemical clustering and data-reduction method, weighted chemical co-expression network analysis (WCCNA), (ii) a quantile g-computation approach to address the joint effect of multiple chemicals in different groupings, and (iii) a correlation analysis to compare mixtures modeling results against individual chemical relationships. Seven chemical groups were identified using WCCNA based on co-occurrence showing both positive and negative relationships with biological responses. A group containing methoxyphenols (e.g., coniferyl aldehyde, eugenol, guaiacol, and vanillin) displayed highly significant, negative relationships with several biological esponses, including cytokines and lung injury markers. This group was further shown through quantile g-computation methods to associate with reduced biological responses. Specifically, mixtures modeling based on all chemicals excluding those in the methoxyphenol group demonstrated more significant, positive relationships with several biological responses; whereas mixtures modeling based on just those in the methoxyphenol group demonstrated significant negative relationships with several biological responses, suggesting potential protective effects. Mixtures-based analyses also identified other groups consisting of inorganic elements and ionic constituents showing positive relationships with several biological responses, including markers of inflammation. Many of the effects identified through mixtures modeling in this analysis were not captured through individual chemical analyses. Together, this study demonstrates the utility of mixtures-based approaches to identify potential drivers and inhibitors of toxicity relevant to wildfire exposures., Graphical Abstract

An investigation into the potential toxicological effects of fracking sand dust (FSD), collected from unconventional gas drilling sites, has been undertaken, along with characterization of their chemical and biophysical properties. Using intratracheal instillation of nine FSDs in rats and a whole body 4-d inhalation model for one of the FSDs, i.e., FSD 8, and related in vivo and in vitro experiments, the effects of nine FSDs on the respiratory, cardiovascular and immune systems, brain and kidney were reported in the preceding eight tandem papers. Here, a summary is given of the key observations made in the organ systems reported in the individual studies. The major finding that inhaled FSD 8 elicits responses in extra-pulmonary organ systems is unexpected, as is the observation that the pulmonary effects of inhaled FSD 8 are attenuated relative to forms of crystalline silica more frequently used in animal studies, i.e., MIN-U-SIL® 5. An attempt is made to understand the basis for the extra-pulmonary toxicity and comparatively attenuated pulmonary toxicity of FSD 8.

The release of catecholamines is preceded by glucocorticoids during a stress response. We have shown that ozone-induced pulmonary responses are mediated through the activation of stress hormone receptors. To examine the interdependence of beta-adrenergic (βAR) and glucocorticoid receptors (GR), we inhibited βAR while inducing GR or inhibited GR while inducing βAR and examined ozone-induced stress-response. Twelve-week-old male Wistar-Kyoto rats were pretreated daily with saline or propranolol (PROP; βAR-antagonist; 10 mg/kg-i.p.; starting 7-days prior to exposure) followed-by saline or dexamethasone sulfate (DEX; GR-agonist; 0.02 mg/kg-i.p.; starting 1-day prior to exposure) and exposed to air or 0.8-ppm ozone (4hr/dayx2-days). In a second experiment, rats were similarly pretreated with corn-oil or mifepristone (MIFE; GR-antagonist, 30 mg/kg-s.c.) followed by saline or clenbuterol (CLEN; β(2)AR-agonist; 0.02 mg/kg-i.p.) and exposed. DEX and PROP+DEX decreased adrenal, spleen and thymus weights in all rats. DEX and MIFE decreased and increased corticosterone, respectively. Ozone-induced protein leakage, inflammation and IL-6 increases were inhibited by PROP or PROP+DEX and exacerbated by CLEN or CLEN+MIFE. DEX and ozone induced while MIFE reversed lymphopenia (MIFE>CLEN+MIFE). DEX exacerbated while PROP, MIFE or CLEN+MIFE inhibited ozone-induced hyperglycemia and glucose intolerance. Ozone inhibited glucose-mediated insulin release. In summary, 1) activating βAR, even with GR inhibition, exacerbated and inhibiting βAR, even with GR activation, attenuated ozone-induced pulmonary effects; and 2) activating GR exacerbated ozone systemic effects, but with βAR inhibition, this exacerbation was less remarkable. These data suggest the independent roles of βAR in pulmonary and dependent roles of βAR and GR in systemic effects of ozone.

Purpose This experimental sepsis model created with Escherichia coli aimed to investigate the histopathological effects of two different doses of ozone combined with antibiotherapy on lung tissue. Methods Rats were divided into 5 groups. Then sepsis was induced intraperitoneally in the first 4 groups. The 1st group was treated with cefepime, the 2nd and 3rd groups were treated with cefepime combined with ozone at a dose of 0.6 mg/kg and 1.1 mg/kg. Lung tissue sections were stained with hematoxylin-eosin and assessed under light microscope and scored between 0-4 in terms of histopathological findings. Results In the comparisons between Group 1 and Group 4 in terms of cellular damage (p=0.030), inflammation (p=0.000) and overall score (p=0.007), statistically significant positive effects were observed in favor of Group 1. In the comparisons of Groups 2 and 3 with Group 4, only positive effects were observed in terms of inflammation (p=0.020, p=0.012, respectively). Conclusion Although negative histopathological effects of ozone on tissue injury were detected, it was noteworthy that the increase in the ozone dose reduced the number of damaged parameters.

A wealth of literature exists regarding the pulmonary effects of ozone, a photochemical pollutant produced by the reaction of nitrogen oxide and volatile organic precursors in the presence of sunlight. This paper focuses on epidemiological panel studies and human clinical studies of ozone exposure, and discusses issues specific to this pollutant that may influence study design and interpretation as well as other, broader considerations relevant to ozone-health research. The issues are discussed using examples drawn from the wider literature. The recent panel and clinical literature is also reviewed. Health outcomes considered include lung function, symptoms, and pulmonary inflammation. Issues discussed include adversity, reversibility, adaptation, variability in ozone exposure metric used and health outcomes evaluated, co-pollutants in panel studies, influence of temperature in panel studies, and multiple comparisons. Improvements in and standardization of panel study approaches are recommended to facilitate comparisons between studies as well as meta-analyses. Additional clinical studies at or near the current National Ambient Air Quality Standard (NAAQS) of 70 ppb are recommended, as are clinical studies in sensitive subpopulations such as asthmatics.The pulmonary health impacts of ozone exposure have been well documented using both epidemiological and chamber study designs. However, there are a number of specific methodological and related issues that should be considered when interpreting the results of these studies and planning additional research, including the standardization of exposure and health metrics to facilitate comparisons among studies.

Background: Being exposed to cooking fumes, kitchen workers are occupationally at risk of multiple respiratory hazards. No conclusive evidence exists as to whether occupational exposure to these fumes is associated with acute and chronic pulmonary effects and symptoms of respiratory diseases. Objective: To quantify the exposure levels and evaluate possible chronic and acute pulmonary effects associated with exposure to cooking fumes. Methods: In this cross-sectional study, 60 kitchen workers exposed to cooking fumes and 60 unexposed employees were investigated. The prevalence of respiratory symptoms among these groups was determined through completion of a standard questionnaire. Pulmonary function parameters were also measured before and after participants' work shift. Moreover, air samples were collected and analyzed to quantify their aldehyde, particle, and volatile organic contents. Results: The mean airborne concentrations of formaldehyde, acetaldehyde, and acrolein was 0.45 (SD 0.41), 0.13 (0.1), and 1.56 (0.41) mg/m 3 , respectively. The mean atmospheric concentrations of PM 1 , PM 2.5 , PM 7 , PM 10 , and total volatile organic compounds (TVOCs) was 3.31 (2.6), 12.21 (5.9), 44.16 (16.6), 57 (21.55) μg/m 3 , and 1.31 (1.11) mg/m 3 , respectively. All respiratory symptoms were significantly (p

Introduction Year after year, we spend an increasing amount of time in a sitting position. Often, we sit with poor posture, as indicated by numerous pain syndromes within the musculoskeletal system. Several reports confirm that body posture and the amount of time spent in a seated position have extensive implications for our health. Previous studies and a literature review suggest there is limited knowledge regarding an ergonomic sitting position. Objective The aim of the study was to analyze the research relating to a proper sitting position and the consequences of incorrect sitting posture. A database search was conducted in Science Direct, Scopus, PubMed, Medline, and Google Scholar. Selection was made on the basis of titles, the abstracts and full texts of the studies. No limits were applied to the date of publication. Conclusions Incorrect sitting posture contributes to many disorders, especially in the cervical and lumbar spine. It also determines the work of the respiratory system. Most authors suggest that maintenance of the physiological curvature of the spine is crucial for the biomechanics of the sitting position, as well as the location of the head and position of the pelvis. It raises awareness of work-related hazards and the introduction of education on the principles of proper seating. It is necessary to draw attention to the risks associated with work performed in a sitting posture, and education on the principles of ergonomical sitting.

Background: Ozone increases IL-33 in the lungs, and obesity augments the pulmonary effects of acute ozone exposure. Objectives: We assessed the role of IL-33 in the augmented effects of ozone observed in obese mice. Methods: Lean wildtype and obese db/db mice were pretreated with antibodies blocking the IL-33 receptor, ST2, and then exposed to ozone (2 ppm for 3 hr). Airway responsiveness was assessed, bronchoalveolar lavage (BAL) was performed, and lung cells harvested for flow cytometry 24 hr later. Effects of ozone were also assessed in obese and lean mice deficient in γδ T cells and their wildtype controls. Results and Discussion: Ozone caused greater increases in BAL IL-33, neutrophils, and airway responsiveness in obese than lean mice. Anti-ST2 reduced ozone-induced airway hyperresponsiveness and inflammation in obese mice but had no effect in lean mice. Obesity also augmented ozone-induced increases in BAL CXCL1 and IL-6, and in BAL type 2 cytokines, whereas anti-ST2 treatment reduced these cytokines. In obese mice, ozone increased lung IL-13+ innate lymphoid cells type 2 (ILC2) and IL-13+ γδ T cells. Ozone increased ST2+ γδ T cells, indicating that these cells can be targets of IL-33, and γδ T cell deficiency reduced obesity-related increases in the response to ozone, including increases in type 2 cytokines. Conclusions: Our data indicate that IL-33 contributes to augmented responses to ozone in obese mice. Obesity and ozone also interacted to promote type 2 cytokine production in γδ T cells and ILC2 in the lungs, which may contribute to the observed effects of IL-33. Citation: Mathews JA, Krishnamoorthy N, Kasahara DI, Cho Y, Wurmbrand AP, Ribeiro L, Smith D, Umetsu D, Levy BD, Shore SA. 2017. IL-33 drives augmented responses to ozone in obese mice. Environ Health Perspect 125:246–253; http://dx.doi.org/10.1289/EHP272

We studied if the pulmonary and systemic toxicity of nanofibrillated celluloses can be reduced by carboxylation. Nanofibrillated celluloses administered at 6 or 18 mu g to mice by intratracheal instillation were: 1) FINE NFC, 2-20 mu m in length, 2-15 nm in width, 2) AS (-COOH), carboxylated, 0.5-10 mu m in length, 4-10 nm in width, containing the biocide BIM MC4901 and 3) BIOCID FINE NFC: as (1) but containing BIM MC4901. FINE NFC administration increased neutrophil influx in BAL and induced SAA3 in plasma. AS (-COOH) produced lower neutrophil influx and systemic SAA3 levels than FINE NFC. Results obtained with BIOCID FINE NFC suggested that BIM MC4901 biocide did not explain the lowered response. Increased DNA damage levels were observed across materials, doses and time points. In conclusion, carboxylation of nanofibrillated cellulose was associated with reduced pulmonary and systemic toxicity, suggesting involvement of OH groups in the inflammatory and acute phase responses.

Background The provision of guidance in ventilator therapy by continuous monitoring of regional lung ventilation, aeration and respiratory system mechanics is the main clinical benefit of electrical impedance tomography (EIT). A new application was recently described in critically ill patients undergoing diagnostic bronchoalveolar lavage (BAL) with the intention of using EIT to identify the region where sampling was performed. Increased electrical bioimpedance was reported after fluid instillation. To verify the accuracy of these findings, contradicting the current EIT knowledge, we have systematically analysed chest EIT data acquired under controlled experimental conditions in animals undergoing a large number of BAL procedures. Methods One hundred thirteen BAL procedures were performed in 13 newborn piglets positioned both supine and prone. EIT data was obtained at 13 images before, during and after each BAL. The data was analysed at three time points: (1) after disconnection from the ventilator before the fluid instillation and by the ends of fluid (2) instillation and (3) recovery by suction and compared with the baseline measurements before the procedure. Functional EIT images were generated, and changes in pixel electrical bioimpedance were calculated relative to baseline. The data was examined in the whole image and in three (ventral, middle, dorsal) regions-of-interest per lung. Results Compared with the baseline phase, chest electrical bioimpedance fell after the disconnection from the ventilator in all animals in both postures during all procedures. The fluid instillation further decreased electrical bioimpedance. During fluid recovery, electrical bioimpedance increased, but not to baseline values. All effects were highly significant (p

Hydraulic fracturing (“fracking”) is used in unconventional gas drilling to allow for the free flow of natural gas from rock. Sand in fracking fluid is pumped into the well bore under high pressure to enter and stabilize fissures in the rock. In the process of manipulating the sand on site, respirable dust (fracking sand dust, FSD) is generated. Inhalation of FSD is a potential hazard to workers inasmuch as respirable crystalline silica causes silicosis, and levels of FSD at drilling work sites have exceeded occupational exposure limits set by OSHA. In the absence of any information about its potential toxicity, a comprehensive rat animal model was designed to investigate the bioactivities of several FSDs in comparison to MIN-U-SIL® 5, a respirable α-quartz reference dust used in previous animal models of silicosis, in several organ systems (Fedan, J.S., Toxicol Appl Pharmacol. 00, 000–000, 2020). The present report, part of the larger investigation, describes: 1) a comparison of the physico-chemical properties of nine FSDs, collected at drilling sites, and MIN-U-SIL® 5, a reference silica dust, and 2) a comparison of the pulmonary inflammatory responses to intratracheal instillation of the nine FSDs and MIN-U-SIL® 5. Our findings indicate that, in many respects, the physico-chemical characteristics, and the biological effects of the FSDs and MIN-U-SIL® 5 after intratracheal instillation, have distinct differences.

Nicotine is a highly addictive principal component of both tobacco and electronic cigarette that is readily absorbed in blood. Nicotine-containing electronic cigarettes are promoted as a safe alternative to cigarette smoking. However, the isolated effects of inhaled nicotine are largely unknown. Here we report a novel rat model of aerosolized nicotine with a particle size (~1 μm) in the respirable diameter range. Acute nicotine inhalation caused increased pulmonary edema and lung injury as measured by enhanced bronchoalveolar lavage fluid protein, IgM, lung wet-to-dry weight ratio, and high-mobility group box 1 (HMGB1) protein and decreased lung E-cadherin protein. Immunohistochemical analysis revealed congested blood vessels and increased neutrophil infiltration. Lung myeloperoxidase mRNA and protein increased in the nicotine-exposed rats. Complete blood counts also showed an increase in neutrophils, white blood cells, eosinophils, and basophils. Arterial blood gas measurements showed an increase in lactate. Lungs of nicotine-inhaling animals revealed increased mRNA levels of IL-1A and CXCL1. There was also an increase in IL-1α protein. In in vitro air-liquid interface cultures of airway epithelial cells, there was a dose dependent increase in HMGB1 release with nicotine treatment. Air-liquid cultures exposed to nicotine also resulted in a dose-dependent loss of barrier as measured by transepithelial electrical resistance and a decrease in E-cadherin expression. Nicotine also caused a dose-dependent increase in epithelial cell death and an increase in caspase-3/7 activities. These results show that the nicotine content of electronic cigarettes may have adverse pulmonary and systemic effects.

Background Cigarette smoke exposure can affect pulmonary lipid homeostasis and cause a progressive increase in pulmonary antibodies against oxidized low-density lipoproteins (OxLDL). Similarly, increased anti-OxLDL antibodies are observed in atherosclerosis, a pathology also tightly associated with smoking and lipid homeostasis disruption. Several immunization strategies against oxidized lipid species to help with their clearance have been shown to reduce the formation of atherosclerotic lesions. Since oxidized lipids are generated during cigarette smoke exposure, we investigated the impact of a prophylactic immunization protocol against OxLDL on the pulmonary effects of cigarette smoke exposure in mice. Methods Mice were immunized systemically with a mixture of human OxLDL (antigen source) and AddaVax (adjuvant) or PBS alone prior to the initiation of acute (2 week) or sub-chronic (8 weeks) cigarette smoke exposure protocols. Anti-OxLDL antibodies were measured in the bronchoalveolar lavage (BAL) fluid and serum by direct ELISA. Pulmonary impacts of cigarette smoke exposure and OxLDL immunization were assessed by measuring BAL inflammatory cells, lung functions, and changes in lung structure and gene levels of matrix/matrix-related genes. Results Immunization to OxLDL led to a marked increase in circulating and pulmonary antibodies against OxLDL that persisted during cigarette smoke exposure. OxLDL immunization did not exacerbate or reduce the inflammatory response following acute or sub-chronic exposure to cigarette smoke. OxLDL immunization alone had effects similar to cigarette smoke exposure on lung functions but OxLDL immunization and cigarette smoke exposure had no additive effects on these parameters. No obvious changes in lung histology, airspace or levels of matrix and matrix-related genes were caused by OxLDL immunization compared to vehicle treatment. Conclusions Overall, this study shows for the first time that a prophylactic immunization protocol against OxLDL can potentially have detrimental effects lung functions, without having additive effects over cigarette smoke exposure. This work sheds light on a complex dynamic between anti-OxLDL antibodies and the pulmonary response to cigarette smoke exposure.

BACKGROUND: Silicosis is the most frequently occurring pneumoconiosis.AIM: Measurement of serum levels of Angiotensin converting enzyme (ACE), Copper (Cu) and Ceruloplasmin (Cp) in cement workers occupationally exposed to silica dust as biomarkers of exposure rather than biomarkers of effect for silicosis.METHODS: Plain chest X-ray & pulmonary functions were done for 30 silicotic and 42 non-silicotic workers and 42 controls. CT scan was done for the exposed groups. Serum levels of Cu, Cp and ACE were estimated.RESULTS: The results showed a higher significant difference between the exposed groups and controls, and between the two exposed groups regarding the mean levels of all measured biochemical parameters. The pulmonary functions were significantly lower among silicotic workers than controls and non-silicotic groups. There was a significant positive correlation between duration of employment and serum ACE and Cu.CONCLUSION: Since respirable dust exposure-linked lung fibrosis disease is non-curable, the biochemical parameters (Cu, ACE and Cp) can be used as exposure biomarkers to silica dust, providing a better way for early diagnosis of this deadly disease. Down regulating the inflammatory responses could potentially reduce the adverse clinical pulmonary effects of air pollution.

The National Aeronautics and Space Administration has announced a plan to establish a manned colony on the surface of the moon, and our country, Japan, has declared its participation. The surface of the moon is covered with soil called lunar regolith, which includes fine particles. It is possible that humans will inhale lunar regolith if it is brought into the spaceship. Therefore, an evaluation of the pulmonary effects caused by lunar regolith is important for exploration of the moon. In the present study, we examine the cellular effects of lunar regolith simulant, whose components are similar to those of lunar regolith. We focused on the chemical component and particle size in particular. The regolith simulant was fractionated to < 10 μm, < 25 μm and 10-25 μm by gravitational sedimentation in suspensions. We also examined the cellular effects of fine regolith simulant whose primary particle size is 5.10 μm. These regolith simulants were applied to human lung carcinoma A549 cells at concentrations of 0.1 and 1.0 mg/ml. Cytotoxicity, oxidative stress and immune response were examined after 24 h exposure. Cell membrane damage, mitochondrial dysfunction and induction of Interleukin-8 (IL-8) were observed at the concentration of 1.0 mg/ml. The cellular effects of the regolith simulant at the concentration of 0.1 mg/ml were small, as compared with crystalline silica as a positive control. Secretion of IL-1β and tumor necrosis factor-α (TNF-α) was observed at the concentration of 1.0 mg/ml, but induction of gene expression was not observed at 24 h after exposure. Induction of cellular oxidative stress was small. Although the cellular effects tended to be stronger in the < 10 μm particles, there was no remarkable difference. These results suggest that the chemical components and particle size have little relationship to the cellular effects of lunar regolith simulant such as cell membrane damage, induction of oxidative stress and proinflammatory effect.

Engineered nanomaterials are currently under review for their potential toxicity; however, their use in consumer/commercial products has continued to outpace risk assessments. In vitro methods may be utilized as tools to improve the efficiency of risk assessment approaches. We propose a framework to compare relationships between previously published in vitro and in vivo toxicity assessments of cadmium-selenium containing quantum dots (QDs) using benchmark dose (BMD) and dosimetric assessment methods. Although data were limited this approach was useful for identifying sensitive assays and strains. In vitro studies assessed effects of QDs in three pulmonary cell types across two mouse strains. Significant dose-response effects were modeled and a standardized method of BMD analysis was performed as a function of both exposure dose and dosimetric dose. In vivo studies assessed pulmonary effects of QD exposure across eight mouse strains. BMD analysis served as a basis for relative comparison with in vitro studies. We found consistent responses in common endpoints between in vitro and in vivo studies. Strain sensitivity was consistent between in vitro and in vivo studies, showing A/J mice more sensitive to QDs. Cell types were found to differentially take up QDs. Dosimetric adjustments identified similar sensitivity among cell types. Thus, BMD analysis can be used as an effective tool to compare the sensitivity of different strains, cell types, and assays to QDs. These methods allow for in vitro assays to be used to predict in vivo responses, improve the efficiency of in vivo studies, and allow for prioritization of nanomaterial assessments. This article is categorized under: Toxicology and Regulatory Issues in Nanomedicine > Toxicology of Nanomaterials Toxicology and Regulatory Issues in Nanomedicine > Regulatory and Policy Issues in Nanomedicine.

Airborne particulate matter (PM) is associated with adverse cardiorespiratory effects. To better understand source-orientated PM toxicity, a comparative study of the biological effects of fine PM (diameter≤2.5μm, PM2.5) collected during the winter season from Shanxi Province, China, and the Central Valley, California, United States, was conducted. The overarching hypothesis for this study was to test whether the chemical composition of PM on an equal mass basis from two urban areas, one in China and one in California, can lead to significantly different effects of acute toxicity and inflammation in the lungs of healthy young mice. Male, 8-week old BALB/C mice received a single 50μg dose of vehicle, Taiyuan PM or Sacramento PM by oropharyngeal aspiration and were sacrificed 24h later. Bronchoalveolar lavage, ELISA and histopathology were performed along with chemical analysis of PM composition. Sacramento PM had a greater proportion of oxidized organic material, significantly increased neutrophil numbers and elevated CXCL-1 and TNF-α protein levels compared to the Taiyuan PM. The findings suggest that Sacramento PM2.5 was associated with a greater inflammatory response compared to that of Taiyuan PM2.5 that may be due to a higher oxidice. Male, 8-week old BALB/C mice received a single 50μg dose of vehicle, Taiyuan PM or Sacramento PM by oropharyngeal aspiration and were sacrificed 24h later. Bronchoalveolar lavage, ELISA and histopathology were performed along with chemical analysis of PM composition. Sacramento PM had a greater proportion of oxidized organic material, significantly increased neutrophil numbers and elevated CXCL-1 and TNF-α protein levels compared to the Taiyuan PM. The findings suggest that Sacramento PM2.5 was associated with a greater inflammatory response compared to that of Taiyuan PM2.5 that may be due to a higher oxidized state of organic carbon and copper content.

Background There is a fundamental gap of knowledge on the health effects caused by the interaction of engineered nanomaterials (ENM) with the gastro-intestinal tract (GIT). This is partly due to the incomplete knowledge of the complex physical and chemical transformations that ENM undergo in the GIT, and partly to the widespread belief that GIT health effects of ENM are much less relevant than pulmonary effects. However, recent experimental findings, considering the role of new players in gut physiology (e.g. the microbiota), shed light on several outcomes of the interaction ENM/GIT. Along with this new information, there is growing direct and indirect evidence that not only ingested ENM, but also inhaled ENM may impact on the GIT. This fact, which may have relevant implications in occupational setting, has never been taken into consideration. This review paper summarizes the opinions and findings of a multidisciplinary team of experts, focusing on two main aspects of the issue: 1) ENM interactions within the GIT and their possible consequences, and 2) relevance of gastro-intestinal effects of inhaled ENMs. Under point 1, we analyzed how luminal gut-constituents, including mucus, may influence the adherence of ENM to cell surfaces in a size-dependent manner, and how intestinal permeability may be affected by different physico-chemical characteristics of ENM. Cytotoxic, oxidative, genotoxic and inflammatory effects on different GIT cells, as well as effects on microbiota, are also discussed. Concerning point 2, recent studies highlight the relevance of gastro-intestinal handling of inhaled ENM, showing significant excretion with feces of inhaled ENM and supporting the hypothesis that GIT should be considered an important target of extrapulmonary effects of inhaled ENM. Conclusions In spite of recent insights on the relevance of the GIT as a target for toxic effects of nanoparticles, there is still a major gap in knowledge regarding the impact of the direct versus indirect oral exposure. This fact probably applies also to larger particles and dictates careful consideration in workers, who carry the highest risk of exposure to particulate matter.

Demand for silver engineered nanomaterials (ENMs) is increasing rapidly in optoelectronic and in health and medical applications due to their antibacterial, thermal, electrical conductive, and other properties. The continued commercial up-scaling of ENM production and application needs to be accompanied by an understanding of the occupational health, public safety and environmental implications of these materials. There have been numerous in vitro studies and some in vivo studies of ENM toxicity but their results are frequently inconclusive. Some of the variability between studies has arisen due to a lack of consistency between experimental models, since small differences between test materials can markedly alter their behaviour. In addition, the propensity for the physicochemistry of silver ENMs to alter, sometimes quite radically, depending on the environment they encounter, can profoundly alter their bioreactivity. Consequently, it is important to accurately characterise the materials before use, at the point of exposure and at the nanomaterial-tissue, or “nanobio”, interface, to be able to appreciate their environmental impact. This paper reviews current literature on the pulmonary effects of silver nanomaterials. We focus our review on describing whether, and by which mechanisms, the chemistry and structure of these materials can be linked to their bioreactivity in the respiratory system. In particular, the mechanisms by which the physicochemical properties (e.g., aggregation state, morphology and chemistry) of silver nanomaterials change in various biological milieu (i.e., relevant proteins, lipids and other molecules, and biofluids, such as lung surfactant) and affect subsequent interactions with and within cells will be discussed, in the context not only of what is measured but also of what can be visualized.

Habitual smoking of marijuana is associated with multiple respiratory symptoms such as cough, sputum production, and wheezing .These symptoms are not significantly different from those exhibited by tobacco smokers. Furthermore, endobronchial biopsies of habitual smokers of marijuana and /or tobacco have shown that both marijuana and cigarette smoking cause significant bronchial mucosal histopathology and that these effects are additive. Although marijuana smokers have minimal changes in pulmonary function studies as compared to tobacco smokers, they may develop bullous disease and spontaneous pneumothoraces. The relationship between marijuana smoking and lung cancer remains unclear due to design limitations of the studies published so far. These findings should warn individuals that marijuana smoking may result in serious short-term and long-term respiratory complications, and habitual marijuana use should be viewed with caution. The medical literature so far does not support routine evaluation by pulmonary function tests or imaging studies; until more definitive data is available, we do not recommend the regular use of these tests in the evaluation of habitual marijuana smokers.

Background: Few studies have been performed on pulmonary effects of air pollution in the elderly—a vulnerable population with low reserve capacity—and mechanisms and susceptibility factors for potential effects are unclear. Objectives: We evaluated the lag structure of air pollutant associations with lung function and potential effect modification by DNA methylation (< or ≥ median) at 26 individual CpG sites in nine candidate genes in a well-characterized cohort of elderly men. Methods: We measured forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1), and blood DNA methylation one to four times between 1999 and 2009 in 776 men from the Normative Aging Study. Air pollution was measured at fixed monitors 4 hr to 28 days before lung function tests. We used linear mixed-effects models to estimate the main effects of air pollutants and effect modification by DNA methylation. Results: An interquartile range (IQR) increase in subchronic exposure (3 to 28 days cumulated), but not in acute exposure (during the previous 4 hr, or the current or previous day), to black carbon, total and nontraffic particles with aerodynamic diameter ≤ 2.5 μm (PM2.5), carbon monoxide, and nitrogen dioxide was associated with a 1–5% decrease in FVC and FEV1 (p < 0.05). Slope estimates were greater for FVC than FEV1, and increased with cumulative exposure. The estimates slopes for air pollutants (28 days cumulated) were higher in participants with low (< median) methylation in TLR2 at position 2 and position 5 and high (≥ median) methylation in GCR. Conclusions: Subchronic exposure to traffic-related pollutants was associated with significantly reduced lung function in the elderly; nontraffic pollutants (particles, ozone) had weaker associations. Epigenetic mechanisms related to inflammation and immunity may influence these associations. Citation: Lepeule J, Bind MAC, Baccarelli AA, Koutrakis P, Tarantini L, Litonjua A, Sparrow D, Vokonas P, Schwartz JD. 2014. Epigenetic influences on associations between air pollutants and lung function in elderly men: the Normative Aging Study. Environ Health Perspect 122:566–572; http://dx.doi.org/10.1289/ehp.1206458

A substantial disparity in asthma prevalence and morbidity among urban children compared with their nonurban counterparts has been recognized for more than two decades. Because of the nature of urban neighborhoods, pest allergens, such as cockroach and mouse, are present in high concentrations in US urban housing and have both repeatedly been linked to asthma morbidity in sensitized children. In addition, there is a growing body of evidence demonstrating that concentrations of many pollutants are higher indoors than outdoors in both US and European urban communities and that exposures to indoor pollutants such as particulate matter (PM) and nitrogen dioxide (NO2 ) are independently associated with symptoms in children with asthma. Although environmental interventions are challenging to implement, when they reduce relevant indoor allergen and pollutant exposures, they are associated with clear improvements in asthma. Other modifiable risk factors in urban childhood asthma that have emerged include dietary and nutritional factors. Overweight and obese children, for example, may be more susceptible to the pulmonary effects of pollutant exposure. Insufficiency of vitamin D and folate has also emerged as modifiable risk factors for asthma morbidity in children. The identification of these modifiable risk factors for urban childhood asthma morbidity offers a ripe opportunity for intervention.

Objective To evaluate the impact of a district hospital intervention focused on enhancing healthcare provider capacity to address leading causes of neonatal death: birth asphyxia, infection and prematurity. Methods The neonatal quality improvement initiative was launched at two intervention referral district hospitals in Ghana. Local Health and Demographic Surveillance Systems were enlisted to enhance recording of neonatal and infant deaths in the community and at the facility. After baseline site assessments, a team of local paediatric experts conducted three clinical trainings on-site at each intervention hospital. Assessments were conducted to evaluate participant knowledge before and after participation in training modules. Monthly mentorship visits provided additional training to support the adoption of essential early neonatal care practices. Results In the first year of implementation, the initiative provided focused clinical training to 278 participants. A comparison of pre- and post-training test results demonstrates significant improvement in provider knowledge (73% vs. 89% correct, P

Few studies were made regarding the pulmonary effects of exposure to volcanogenic air pollution, representing an unrecognized health risk for humans inhabiting non-eruptive volcanically active areas (10% of world human population). We tested the hypothesis whether chronic exposure to air pollution of volcanogenic origin causes lung injury, using wild mice (Mus musculus) as model. Lung injury was determined using histological morphometric parameters, inflammatory status (InfS) and the amount of black silver deposits (BSD). Mice exposed to volcanogenic air pollution have decreased percentage of alveolar space, alveolar perimeter and lung structural functionality (LSF) ratio and, increased alveolar septal thickness, amount of BSD and InfS. For the first time it is evidenced that non-eruptive active volcanism has a high potential to cause lung injury. This study also highlights the usefulness of M. musculus as bioindicator species, and of the developed biomarker of effect LSF ratio, for future animal and/or human biomonitoring programs.

Ethnopharmacological relevance Artemisia afra (Asteraceae) is a traditional medicinal plant frequently used in steam inhalation form to treat respiratory conditions. Aim of the study Quantify luteolin content in Artemisia afra dried crude and aqueous extract. Evaluate the pulmonary effects of Artemisia afra steam inhalation, nebulized Artemisia afra extract and luteolin in isolated perfused lungs (IPL). Evaluate the pulmonary disposition of intravenously administered luteolin. Materials and methods HPLC was used to quantify luteolin in Artemisia afra extracts. A modified version of the IPL was used to determine the effects of Artemisia afra steam inhalation, nebulized luteolin, and nebulized aqueous leaf extract on lung function, as well as the pulmonary disposition of IV luteolin. Results Artemisia afra extract contained significantly higher luteolin levels than the crude dried leaves. Inhaled Artemisia afra steam, and nebulized luteolin, and Artemisia afra extract and IV luteolin produced significant dose-dependent improvements in lung function, with nebulized Artemisia afra producing the greatest improvements. Nebulisation with Artemisia afra extract yielded higher quantities of luteolin than luteolin nebulisation. Conclusion Results verify the traditional use of inhalation of Artemisia afra steam, although nebulized luteolin and aqueous extract are better alternatives. Luteolin significantly contributes to the bronchodilatory effects of Artemisia afra.

Ozone-initiated monoterpene reaction products have been hypothesized to cause eye and airway complaints in office environments and some have been proposed to cause skin irritation and sensitization. The respiratory effects of 60 min exposures to five common oxidation products from abundant terpenoids (e.g. limonene), used as solvent and fragrance in common household products or present in skin lipids (e.g. squalene), were studied in a head out mouse bioassay. This allowed determination of acute upper airway (sensory) irritation, airflow limitation in the conducting airways, and pulmonary irritation in the alveolar region. Derived human reference values (RFs) for sensory irritation were 1.3, 0.16 and 0.3 ppm, respectively, for 4-acetyl-1-methylcyclohexene ( 0.2 ppm) [corrected], 3-isopropenyl-6-oxo-heptanal (IPOH), and 6-methyl-5-heptene-2-one (6-MHO). Derived RFs for airflow limitation were 0.8, 0.45, 0.03, and 0.5 ppm, respectively, for dihydrocarvone (DHC), 0.2 ppm [corrected], 4-oxo-pentanal (0.3 ppm) [corrected], and 6-MHO. Pulmonary irritation was unobserved as a critical effect. The RFs indicate that the oxidation products would not contribute substantially to sensory irritation in eyes and upper airways in office environments. Reported concentrations in offices of 6-MHO and 0.3 ppm [corrected]would not result in airflow limitation. However, based upon the RFs for IPOH and 0.3 ppm [corrected], precautionary actions should be considered that disfavor their formation in excess.

International audience; In spite of the great promises that the development of nanotechnologies can offer, concerns regarding potential adverse health effects of occupational exposure to nanoparticle (NP) is raised. We recently identified metal oxide NP in lung tissue sections of welders, located inside macrophages infiltrated in fibrous regions. This suggests a role of these NP in the lung alterations observed in welders. We therefore designed a study aimed to investigate the pulmonary effects, in mice, of repeated exposure to NP administered at occupationally relevant doses. We therefore chose four metal oxide NPs representative of those found in the welder’s lungs: Fe2O3, Fe3O4, MnFe2O4 and CrOOH. These NPs were administered weekly for up to 3 months at two different doses: 5 μg, chosen as occupationally relevant to welding activity, and 50 μg, chosen as occupationally relevant to the context of an NP-manufacturing facility. Our results show that 3 month-repeated exposures to 5 μg NP induced limited pulmonary effects, characterized by the development of a mild peribronchiolar fibrosis observed for MnFe2O4 and CrOOH NP only. This fibrotic event was further extended in terms of intensity and localization after the repeated administration of 50 μg NP: all but Fe2O3 NP induced the development of peribronchiolar, perivascular and alveolar fibrosis, together with an interstitial inflammation. Our data demonstrate for the first time a potential risk for respiratory health posed by repeated exposure to NP at occupationally relevant doses. Given these results, the development of occupational exposure limits (OELs) specifically dedicated to NP exposure might therefore be an important issue to address.

With rapid increasing usage of smart phones, social concerns have arisen about the possible effects of elec-tromagnetic fields emitted from wideband code division multiple access(WCDMA) mobile phones on human health.The number of people with self-reported electromagnetic hypersensitivity(EHS) who complain of various subjectivesymptoms such as headache, insomnia etc. has also recently increased. However, it is unclear whether EHS resultsfrom physiological or other origins. In this double-blinded study, we investigated physiological changes such as heartrate, respiration rate, and heart rate variability with real and sham exposures for 15 EHS and 17 non-EHS personsusing a module inside a dummy phone. Experiment was conducted using a WCDMA module with average powerof 24 dBm at 1950 MHz with the specific absorption rate of 1.57 W/kg using a headphone for 32 min. As a conclusion,WCDMA RF exposure did not have any effects on the physiological variables in either group. Key words: Smart phones, EHS, WCDMA, Physiological effects, Double-blinded

Objective To compare the performance of the new WHO (2007) diagnostic algorithm for pulmonary tuberculosis (PTB) in high HIV prevalent settings (WHO07) to the WHO 2003 guidelines used by the Ugandan National Tuberculosis Program (UgWHO03). Methods A prospective observational cohort design was used at Reach Out Mbuya Parish HIV/AIDS Initiative, an urban slum community-based AIDS Service Organisation (ASO) and Kayunga Rural District Government Hospital. Newly diagnosed and enrolled HIV-infected patients were assessed for PTB. Research staff interviewed patients and staff and observed operational constraints. Results WHO07 reduced the time to diagnosis of smear-negative PTB with increased sensitivity compared with the UgWHO03 at both sites. Time to diagnosis of smear-negative PTB was significantly shorter at the urban ASO than at the rural ASO (12.4 vs. 28.5 days, P = 0.003). Diagnostic specificity and sensitivity [95% confidence intervals (CIs)] for smear-negative PTB were higher at the rural hospital compared with the urban ASO: [98% (93–100%) vs. 86% (77–92%), P = 0.001] and [95% (72–100%) vs. 90% (54–99%), P > 0.05], respectively. Common barriers to implementation of algorithms included failure by patients to attend follow-up appointments and poor adherence by healthcare workers to algorithms. Conclusion At both sites, WHO07 expedited diagnosis of smear-negative PTB with increased diagnostic accuracy compared with the UgWHO03. The WHO07 expedited diagnosis more at the urban ASO but with more diagnostic accuracy at the rural hospital. Barriers to implementation should be taken into account when operationalising these guidelines for TB diagnosis in resource-limited settings. Objectif: Comparer les performances de nouvel algorithme de l’OMS (2007) pour le diagnostic de la tuberculose pulmonaire (TBP) dans les zones a forte prevalence du VIH (WHO07) aux directives de l’OMS 2003 utilisees par le Programme National Ougandais de la Tuberculose (UgWHO03). Methodes: Une etude de cohorte observationnelle prospective a ete utilisee dans l’Initiative Reach Out VIH/SIDA de la paroisse de Mbuya, un Service d’Organisation contre le SIDA (ASO) en milieu urbain communautaire de bidonville et a l’Hopital Rural Gouvernemental du District de Kayunga. Les personnes nouvellement diagnostiquees avec le VIH et inscrites, ont eteevaluees pour la TBP. Le personnel de recherche a interviewe les patients et le personnel, et a observe les contraintes operationnelles. Resultats: WHO07 permet une reduction de la duree du diagnostic de PTB a frottis negatif avec une sensibilite accrue par rapport a UgWHO03 sur les deux sites. La duree pour le diagnostic de PTB a frottis negatif etait significativement plus courte dans le milieu urbain ASO que dans le milieu rural ASO (12,4 jours, comparea 28,5 jours, p = 0,003). La specificite et la sensibilite diagnostiques [intervalle de confiance 95% (IC)] pour la PTB a frottis negatif etaient plus elevees a l’Hopital Rural que dans la zone urbaine ASO: [98% (93–100%) contre 86% (77–92%), P = 0,001] et [95% (72–100%) contre 90% (54–99%), P > 0,05], respectivement. Les obstacles courants a l’implementation des algorithmes comprennent: les rendez-vous manques par les patients lors du suivi et le non respect des algorithmes par les agents des soins de sante. Conclusion: Sur les deux sites, WHO07 a permis une acceleration du diagnostic de la PTB a frottis negatif avec une precision diagnostique accrue par rapport a UgWHO03. WHO07 a plus accelere le diagnostic dans la zone urbaine ASO, mais avec une precision diagnostic plus elevee a l’Hopital Rural. Les obstacles a l’implementation devraient etre pris en compte lors de l’application des directives pour le diagnostic de la TB dans les pays a ressources limitees. Objetivo: Comparar el desempeno del nuevo algoritmo de diagnostico de la OMS (2007) para tuberculosis pulmonar (TBP) en emplazamientos con una alta prevalencia del VIH (WHO07) con respecto a las guias de la OMS del 2003 utilizadas por el Programa Nacional de Tuberculosis de Uganda (UgWHO03). Metodos: Se utilizo un diseno observacional de cohortes prospectivo en la Iniciativa Reach Out Mbuya Parish para el VIH/SIDA, una Organizacion de Servicios para el SIDA (OSS) urbana, y basada en la comunidad de y el Hospital Distrital Rural de Kayunga. Los pacientes recientemente diagnosticados fueron examinados en busca de TB pulmonar (TBP). El personal investigador entrevisto a los pacientes y al personal sanitario, y observo las limitaciones operativas. Resultados: En ambos emplazamientos WHO07 redujo el tiempo hasta el diagnostico de la TBP con baciloscopia negativa con una mayor sensibilidad que la UgWHO03. El tiempo hasta el diagnostico de la TBP con baciloscopia negativa era significativamente mas corto en la OSS urbana que en la OSS rural (12.4 versus 28.5 dias, P = 0.003). La especificidad y sensibilidad diagnostica [IC 95%] para la TBP con baciloscopia negativa eran mayores en el hospital rural comparadas con la OSS urbana: [98% (93–100%) versus 86% (77–92%), P = 0.001] y [95% (72–100%) versus 90% (54–99%), P > 0.05] respectivamente. Las barreras mas comunes para la implementacion de los algoritmos incluian el fallo de los pacientes para atender a las visitas de seguimiento y una adherencia pobre de los sanitarios a la hora de utilizar los algoritmos. Conclusion: En ambos emplazamientos, el WHO07 facilito el diagnostico de la TBP con baciloscopia negativa con mayor precision, comparado con la UgWHO03. El WHO07 acelero el diagnostico en la OSS rural, pero con una mayor precision diagnostica en el hospital rural. Las barreras para la implementacion deberian tomarse en cuenta al operativizar estas guias para el diagnostico de la TB en emplazamientos con pocos recursos.

to the editor: In a recent issue of the American Journal of Physiology-Lung Cellular and Molecular Physiology , we read with great interest the review article by Chun et al. ([2][1]) about potential pulmonary effects of electronic cigarettes (ECs). This is a timely topic, and the authors do a

Pinewood (Pinus ssp.) is widely used for furniture and building purposes. However, despite its widespread use, information on possible human sensory irritations and pulmonary effects caused by exposure to volatile organic compounds (VOC) emitted from pinewood is sparse. For this purpose, (1) sensory irritation of eyes, nose and throat, (2) lung function parameters (FVC, FEV1), (3) exhaled nitrogen oxide (NO) concentration, (4) eye blink frequency, and (5) sensory evaluation (using the SD method) were investigated before, after, and partly during exposure of human volunteers to emissions from pinewood panels. Fifteen healthy nonsmokers were exposed for 2 h under controlled conditions to VOCs emitted from pinewood panels in a 48 m3 test chamber. VOC concentrations were about 5 mg/ m3 (loading rate, 1 m2/m3), 8 mg/m3 (loading rate, 2 m2/m3), and 13 mg/m3 (loading rate, 3 m2/m3), respectively. Terpene and aldehyde exposure concentrations ranged from about 3.50 ± 0.51 mg/m3 and 0.07 ± 0.008 mg/m3, 5.00 ± 0.95 mg/ m3, and 0.20 ± 0.02 mg/m3 or 9.51 ± 1.10 mg/m3 and 0.21 ± 0.04 mg/m3 for loading rates of 1, 2, and 3 m2/m3, respectively. The emissions consisted predominantly of a-pinene and ?3-carene. No concentration-dependent effects before or after exposure to the emissions were measured with respect to sensory irritation, pulmonary function, exhaled NO, and eye blink frequency. Only the odor of the emissions was perceived by the study subjects, rated as being closer to "pleasant" than to "unpleasant". In conclusion, the results of our study suggest that short-term exposure to high VOC concentrations, even up to 13 mg/m3, released from pinewood does not elicit sensory irritation or pulmonary effects in healthy humans under controlled conditions.