nitrogen-dioxide and Lung-Diseases

Air pollutants, especially fine dust, ozone, and nitrogen dioxide, pose a danger to health worldwide. In 2005, the World Health Organization (WHO), in order to protect public health, issued global recommendations for maximum levels of fine dust (10 μg/m3 for fine dust particles smaller than 2.5 μm [PM2.5]), ozone, and nitrogen dioxide. The recommended levels are regularly exceeded in many places in Germany.. This review is based on relevant publications retrieved by a selective search in PubMed and, in part, on an expert statement issued in the name of the International Society for Environmental Epidemiology (ISEE) and the European Respiratory Society (ERS).. Air pollutants affect the entire body, from the beginning of intrauterine development all the way to the end of life, causing premature death mainly through lung and heart disease. An epidemiological study has shown, for example, that mor- tality rises approximately 7% for every incremental long-term exposure to 5 μg/m3 PM2.5 (95% confidence interval: [2; 13]). Aside from lung and heart disease, the carcinogenic effect of fine dust is now well established. High fine-dust exposure has also been linked to metabolic diseases. For example, in a meta-analysis of cohort studies, the incidence of type 2 diabetes mellitus was found to be associated with elevated fine dust concentrations, with a 25% relative risk increase [10; 43] for every 10 µg/m3 of PM2.5. More recent studies have shown that these substances cause harm even in concentrations that are below the recommended limits.. It is very important for public health that the current EU standards for rkedly lowered so that health risks can be further reduced, in accordance with the recommendations of the WHO.

Topics: Air Pollution; Diabetes Mellitus, Type 2; Dust; Environmental Exposure; Germany; Heart Diseases; Humans; Lung Diseases; Nitrogen Dioxide; Ozone

Short-term exposure to NO₂ has been associated with adverse health effects and there is increasing concern that NO₂ is causally related to health effects, not merely a marker of traffic-generated pollution. No comprehensive meta-analysis of the time-series evidence on NO₂ has been published since 2007.. To quantitatively assess the evidence from epidemiological time-series studies published worldwide to determine whether and to what extent short-term exposure to NO₂ is associated with increased numbers of daily deaths and hospital admissions.. We conducted a quantitative systematic review of 204 time-series studies of NO₂ and daily mortality and hospital admissions for several diagnoses and ages, which were indexed in three bibliographic databases up to May 2011. We calculated random-effects estimates by different geographic regions and globally, and also tested for heterogeneity and small study bias.. Sufficient estimates for meta-analysis were available for 43 cause-specific and age-specific combinations of mortality or hospital admissions (25 for 24 h NO₂ and 18 of the same combinations for 1 h measures). For the all-age group, a 10 µg/m(3) increase in 24 h NO₂ was associated with increases in all-cause, cardiovascular and respiratory mortality (0.71% (95% CI 0.43% to 1.00%), 0.88% (0.63% to 1.13%) and 1.09% (0.75% to 1.42%), respectively), and with hospital admissions for respiratory (0.57% (0.33% to 0.82%)) and cardiovascular (0.66% (0.32% to 1.01%)) diseases. Evidence of heterogeneity between geographical region-specific estimates was identified in more than half of the combinations analysed.. Our review provides clear evidence of health effects associated with short-term exposure to NO₂ although further work is required to understand reasons for the regional heterogeneity observed. The growing literature, incorporating large multicentre studies and new evidence from less well-studied regions of the world, supports further quantitative review to assess the independence of NO₂ health effects from other air pollutants.

Topics: Air Pollutants; Air Pollution; Cardiovascular Diseases; Environmental Monitoring; Evaluation Studies as Topic; Hospitalization; Humans; Lung Diseases; Multicenter Studies as Topic; Nitrogen Dioxide; Particulate Matter; Time Factors

There is a growing understanding that chronic respiratory diseases in adults have their origins in early life. Adverse environmental exposures occurring in vulnerable periods during lung growth and development in the fetal period and in early childhood that alter lung structure and limit the growth in lung function may have lifelong consequences. Evidence is increasing that exposure to the ambient environment, including air pollutants, persistent toxic substances, water pollutants and respiratory viral infections, can inhibit lung function growth and predispose to chronic non-malignant lung diseases. These exposures generally interact with a genetic predisposition, and gene-environment interactions and epigenetic phenomena are attracting considerable study. An understanding of how ambient exposures impact on normal lung growth and development will aid in understanding of how chronic respiratory diseases of adults develop and may lead to new preventative strategies.

Topics: Adult; Air Pollutants; Arsenic; Child; Disease Susceptibility; Environmental Exposure; Female; Humans; Lung; Lung Diseases; Nitrogen Dioxide; Nutritional Status; Oxidative Stress; Ozone; Particulate Matter; Pregnancy; Prenatal Exposure Delayed Effects; Respiratory Tract Infections; Social Class; Sulfur Dioxide; Water Pollutants, Chemical

Topics: Air Pollutants; Air Pollution; Animals; Cardiovascular Diseases; Climate Change; Environmental Exposure; Humans; Inflammation; Life Expectancy; Lung Diseases; Nanoparticles; Nitrogen Dioxide; Occupational Diseases; Particle Size; Particulate Matter

There is large variation between individuals in their response to air pollutants. This review summarises the existing evidence that genetic factors influence the mechanisms of lung injury caused by air pollutants. Genetic association studies have compared the adverse effects of air pollutants between subjects with specific genotypes in biologically relevant genes. In human studies of ozone exposure, polymorphisms in oxidative stress genes (NQO1, GSTM1, GSTP1) modify respiratory symptoms, lung function, biomarkers and risk of asthma. Inflammatory gene polymorphisms (TNF) influence the lung function response to ozone, and the effect of different levels of ozone on the development of asthma. Polymorphisms in oxidative stress genes (GSTM1, GSTP1) alter the response to combined exposure to ragweed pollen and diesel exhaust particles. Importantly, polymorphisms in an oxidative stress gene (GSTM1) have predicted patients with asthma who benefit from antioxidant supplementation in Mexico City, which has chronically high ozone exposure. Genetic linkage studies of families have not been feasible for studying the effects of air pollution in humans, but some progress has been made with pedigrees of specially bred mice, in identifying chromosomal regions linked to effects of ozone or particles. A high priority now, in addition to avoiding exposure in the most susceptible people, is to clearly identify the most effective and safe chemopreventive agents for individuals who are genetically susceptible to the adverse effects of air pollution (eg, antioxidants to be taken during high ozone levels).

Topics: Air Pollution; Genetic Predisposition to Disease; Genetic Variation; Humans; Lung Diseases; Nitrogen Dioxide; Ozone; Particulate Matter; Phenotype; Polymorphism, Genetic; Respiration Disorders; Sulfur Dioxide

From as early as 1930 there has been evidence for effects on health of air pollution. Ozone, particulates and nitrogen dioxide are the most important pollutants today. The acute increase in air pollution leads to a significant raise in morbidity and mortality. Hospital admissions of patients with chronic obstructive pulmonary disease (COPD) or asthma are more frequent during these periods. Chronic exposure to pollution causes bronchitis, accelerated decline of lung function and impaired maturing of the lungs. Ozone and a residence in proximity to major roads seem to play a role in the development of asthma. A further important environmental factor is climate change, which has an impact on air pollution but also on distribution and quality of aero-allergens and the dissemination and transmission of respiratory pathogens.

Topics: Air Pollution; Asthma; Climate; Dust; Germany; Humans; Lung Diseases; Morbidity; Nitrogen Dioxide; Ozone; Pulmonary Disease, Chronic Obstructive

Around 50% of people, almost all in developing countries, rely on coal and biomass in the form of wood, dung and crop residues for domestic energy. These materials are typically burnt in simple stoves with very incomplete combustion. Consequently, women and young children are exposed to high levels of indoor air pollution every day. There is consistent evidence that indoor air pollution increases the risk of chronic obstructive pulmonary disease and of acute respiratory infections in childhood, the most important cause of death among children under 5 years of age in developing countries. Evidence also exists of associations with low birth weight, increased infant and perinatal mortality, pulmonary tuberculosis, nasopharyngeal and laryngeal cancer, cataract, and, specifically in respect of the use of coal, with lung cancer. Conflicting evidence exists with regard to asthma. All studies are observational and very few have measured exposure directly, while a substantial proportion have not dealt with confounding. As a result, risk estimates are poorly quantified and may be biased. Exposure to indoor air pollution may be responsible for nearly 2 million excess deaths in developing countries and for some 4% of the global burden of disease. Indoor air pollution is a major global public health threat requiring greatly increased efforts in the areas of research and policy-making. Research on its health effects should be strengthened, particularly in relation to tuberculosis and acute lower respiratory infections. A more systematic approach to the development and evaluation of interventions is desirable, with clearer recognition of the interrelationships between poverty and dependence on polluting fuels.

Topics: Adult; Air Pollution, Indoor; Carbon Monoxide; Child; Developing Countries; Female; Heating; Humans; Lung Diseases; Nitrogen Dioxide; Poverty; Public Health; Sulfur Dioxide

Topics: Air Pollutants; Air Pollution; Air Pollution, Indoor; Anhydrides; Asthma; Bronchitis; Chronic Disease; Environmental Illness; Global Health; Heart Diseases; Humans; Lung Diseases; Nitrogen Dioxide; Ozone; Risk Factors; Sulfur Compounds

Nitrogen dioxide exposure occurs in many civilian occupations as well as during military combat. Little interaction has occurred between the two communities in regards to the exchange of information about NO2 research. This presentation provides an overview of NO2 related epidemiology; available research models and issues of particular interest to both the civilian and military sectors; clinical presentations, prophylaxis and treatment; and pathophysiology and mechanisms of injury. Throughout the presentation civilian and military issues are contrasted when pertinent. The most significant difference between the civilian and military research requirements is the need for information on chronic (with and without intermittent peaks) for the former, and information on acute high-level NO2 research for the latter. Another military requirement is predicting not only injury but incapacitation. This requirement can be compared to the need of clinicians to measure impairment for patients seeking disability. Both communities are faced with the same challenges of selecting appropriate models, understanding dosimetry and its many variables, clarifying the fate of inhaled NO2, developing specific markers of injury, and elucidating the mechanisms of NO2 injury for the development of prophylactic and therapeutic agents. Further research is required in these areas and it is hoped that this symposium will be the first attempt to join civilian and military resources and expertise for future research cooperation and collaboration.

Topics: Animals; Humans; Lung; Lung Diseases; Military Personnel; Nitrogen Dioxide; Occupational Diseases; Occupational Exposure

Nitrogen dioxide (NO2) and ozone (O3) occur throughout the world as the primary pollutants of urban air. NO2 and O3 oxidize cell membrane lipids and proteins. Inflammatory agents are elaborated from the lung either as a direct result of oxidation or as a consequence of leukocytes recruited into the lung by injury. My hypothesis is that NO2 and O3 initiate or exacerbate chronic lung disease through an inflammatory mechanism which can be reduced by supplementation with greater amounts than those required to alleviate vitamin deficiency symptoms of vitamins C (ascorbic acid) and E (alpha-tocopherol). Children, whose lungs are developing, are the most likely group to benefit from supplementation with vitamins C and E because the adverse effects of inflammation on the developing lung are likely to be greater and the time of exposure is longer than in adults. This hypothesis is in accord with current human and experimental animal data and the chemistry of O3 and NO2 toxicity, and is supported by recent ecological epidemiological studies of persons supplementing their intake of vitamins C and E.

Topics: Air Pollutants; Animals; Chronic Disease; Humans; Lung Diseases; Nitrogen Dioxide; Oxidation-Reduction; Ozone; Stress, Physiological

As we increasingly recognize the complexity of the pollutants in indoor and outdoor microenvironments, a broad array of inhaled mixtures has assumed scientific, public health, and regulatory importance. Few adverse effects of environmental pollutants are specific, that is, uniquely associated with a single agent; the adverse effects that might be considered in an investigation of the consequences of exposure to an inhaled complex mixture are generally nonspecific. In the context of this paper, we will refer to binary mixtures as complex, though we realize that a more precise definition of complexity would restrict the term to mixtures of three or more constituents. Their causes potentially include not only pollutant exposures through the medium of inhaled air but other environmental agents, such as infectious organisms and radiation, and inherent characteristics of the exposed persons, such as atopy. We review the outcome measures that have been used in epidemiologic studies of the health effects of single pollutants and complex mixtures. Some of these outcome measures have been carefully standardized, whereas others need similar standardization and modification to improve sensitivity and specificity for investigating the health effects of air pollution.

Topics: Air Pollutants; Environmental Monitoring; Epidemiological Monitoring; Humans; Lung Diseases; Mortality; Neuropsychological Tests; Nitrogen Dioxide; Radon; Tobacco Smoke Pollution

Although the evidence for oxidative stress for air pollution in the human lung is fragmentary, the hypothesis that oxidative stress is an important, if not the sole, mechanism of toxicity of oxidizing air pollutants and tobacco smoke is compelling and growing. First, biochemical mechanisms have been worked out for oxidation of lung lipids by the gas phase of cigarette smoke, NO2 and O3. The oxidation of lung lipids can be prevented by both vitamins C and E. Vitamin C is more effective in preventing oxidation by NO2, and vitamin E is more effective against O3. Second, multiple species of experimental animals develop lung disease similar to human bronchitis and emphysema from exposure to NO2 and O3, respectively. The development of these diseases occurs over a near lifetime exposure when the levels of NO2 or O3 are at near ambient air pollution values. Third, isolated human cells are protected against oxidative damage from NO2 and O3 by both vitamins C and E. Fourth, the vitamin C level in the lung either declines on exposure to NO2 for short-term exposures or increases on chronic cigarette smoke exposure. The effects of cigarette smoking on serum vitamin C is apparently complex and may be related to the daily intake of vitamin C as well as smoking. Serum vitamin C levels may be poor indicators of lung demands when daily vitamin C intakes are above 100 mg/day. Fifth, vitamin C supplementation protects against the effects of ambient levels of air pollution in adults as measured by histamine challenge. An augmented response to histamine challenge may represent increased lung permeability brought about by air pollution. In experimental animal and human experiments, the amount of vitamin C or E that afforded protection was in excess of the current recommended dietary allowance. Although animal studies do not provide evidence for complete protection against NO2 or O3, they do illustrate that current recommended daily allowances are inadequate for maximum protection against air pollution levels to which over 100 million Americans are exposed. The problem of air pollution and its effects on humans is truly of global concern. Air pollution is not restricted to North America or Japan where it was first recognized, but is a major public health problem in Europe as well. When data are available, air pollution probably will be shown to be a major public health problem in all urban areas of the world.(ABSTRACT TRUNCATED AT 400 WORDS)

Topics: Air Pollution; Animals; Antioxidants; Humans; Lung Diseases; Nitrogen Dioxide; Ozone; Smoking; Tobacco Smoke Pollution; Vitamin E Deficiency; Vitamins

The database for the acute health effects of common outdoor air pollutants is rapidly increasing but important gaps still exist. Greater technical efforts and innovative studies are required to adequately characterize health effects and understand the underlying mechanisms of toxicity. Controlled human exposures provide relevant data about short-term effects and complement animal and epidemiologic investigations. Except for possibly nitrogen dioxide, the clinical data for ozone, sulfur dioxide, and particulates (H2SO4) at contemporary levels indicate potentially untoward or adverse physiologic or clinical responses in healthy individuals and sensitive groups such as children, adolescents, and asthmatic patients. Exercise, duration, and other exposure factors may potentiate pollutant effects on symptoms, lung function, nonspecific bronchial reactivity, mucociliary clearance, and BAL markers of inflammation. Continued animal, clinical, and epidemiologic research of both short- and long-term health effects is clearly needed to support or limit future regulatory decisions regarding the quality of outdoor air.

Topics: Air Pollutants; Air Pollution; Animals; Environmental Exposure; Humans; Lung Diseases; Nitrogen Dioxide; Ozone; Sulfur Dioxide

Topics: Adult; Air Pollution; Asbestos; Carbon Monoxide; Cardiovascular Diseases; Environmental Pollutants; Humans; Lung Diseases; Nitrogen Dioxide; Oxidants, Photochemical; Ozone; Peracetic Acid; Physical Exertion; Silicon Dioxide; Sulfur Dioxide

The highly pulmonary concentration of 1,2-dipalmitoyl-sn-glycerol-3-phosphorylcholine (dipalmitoyllecithin) and its implication as an important component of lung surfactant have promoted investigation of phospholipid metabolism in the lung. This review will set the contents including recent informations for better understanding of phospholipid metabolism of the lung in normal state (physiological significances of lung phospholipids, characteristics of phospholipids in lung tissue and alveolar washing, biosynthetic pathways of dipalmitoyllecithin, etc.) as well as in toxic states (pulmonary oxygen toxicity, etc.) and in diseased states (idiopathic respiratory distress syndrome, pulmonary alveolar proteinosis, etc.) Since our main concern has been to clarify the most important route for supplying dipalmitoyllecithin, this review will be focused upon the various biosynthetic pathways leading to the formation of different molecular species of lecithin and their potential significance in the normal, toxic, and diseased lungs.

Topics: Fetus; Humans; Lung; Lung Diseases; Nitrogen Dioxide; Oxygen; Ozone; Phosphatidylcholines; Phospholipids; Pulmonary Alveolar Proteinosis; Pulmonary Surfactants; Respiratory Distress Syndrome

Topics: Adolescent; Adult; Aged; Air Pollutants; Animals; Carbon Monoxide; Female; Haplorhini; Humans; Lung Diseases; Male; Mice; Microscopy, Electron, Scanning; Middle Aged; Nitrogen Dioxide; Oxidants, Photochemical; Oxygen; Ozone; Pulmonary Alveoli; Rats; Saimiri; Smog; Sulfur Dioxide

Topics: Air Pollutants; Bronchial Diseases; Chemical Phenomena; Chemistry; Environmental Exposure; Lung Diseases; Lung Diseases, Obstructive; Maximum Allowable Concentration; Nitrogen Dioxide; Nitrogen Oxides; Occupational Diseases; Smoking; Time Factors

Topics: Adaptation, Physiological; Age Factors; Amines; Animals; Body Weight; Bronchi; DNA; Free Radicals; Glucose; Humans; Lipid Metabolism; Lung; Lung Diseases; Nitrogen Dioxide; Oxygen; Ozone; Protein Biosynthesis; Pulmonary Alveoli; Species Specificity; Sulfhydryl Compounds; Vitamin E

Topics: Air Pollutants; Animals; Bacterial Infections; Child; Cilia; Dark Adaptation; Environmental Exposure; Evaluation Studies as Topic; Humans; Lung Diseases; Macrophages; Maximum Allowable Concentration; Mucous Membrane; Nitrogen Dioxide; Occupational Diseases; Phagocytosis; Pulmonary Alveoli; Respiration; Respiratory Tract Diseases; Smell; Time Factors; United States

Topics: Adult; Age Factors; alpha 1-Antitrypsin; alpha 1-Antitrypsin Deficiency; Alpha-Globulins; Animals; Antigen-Antibody Reactions; Cadmium; Collagen; Elastin; Environmental Exposure; Humans; Infant; Leukocytes; Lung; Lung Diseases; Macrophages; Microbial Collagenase; Nitrogen Dioxide; Ozone; Pancreatic Elastase; Peptide Hydrolases; Pulmonary Alveoli; Pulmonary Edema; Pulmonary Emphysema; Smoking

Topics: Acidosis; Animals; Brain; Diabetes Mellitus, Experimental; Diabetic Ketoacidosis; Electron Transport; Erythrocytes; Humans; Hypercapnia; Hypoxia; Liver; Lung Diseases; Macrophages; NAD; NADP; Nitrogen Dioxide; Oxidation-Reduction; Pulmonary Alveoli; Starvation

Topics: Air Pollution; Animals; Cell Membrane; Fatty Acids; Humans; L-Lactate Dehydrogenase; Lung; Lung Diseases; Muramidase; Nitrogen Dioxide; Oxidation-Reduction; Oxygen Consumption; Ozone; Phospholipids; Proteins; Pulmonary Emphysema; Surface Properties

Topics: Air Pollution; Arsenic Poisoning; Berylliosis; Cadmium Poisoning; Humans; Lung Diseases; Lung Diseases, Obstructive; Lung Neoplasms; Nitrogen Dioxide; Poisoning; Respiratory Tract Diseases; Solvents; Sulfur Dioxide

Topics: Air Pollution; Animals; Carbon Monoxide; Drug Synergism; Female; Humans; Lung Diseases; Male; Nitrogen Dioxide; Ozone; Sulfur Dioxide

Topics: Air Pollution; Animals; Blood Circulation; Bronchial Diseases; Lung Diseases; Nasal Mucosa; Nitrogen Dioxide; Nose Diseases; Ozone; Pulmonary Circulation; Pulmonary Edema; Respiratory Tract Diseases; Sulfoxides; Sulfur; Sulfur Dioxide

Chronic obstructive pulmonary disease (COPD), lung cancer (LC) and tuberculosis (TB) are common chronic lung diseases that generate a large disease burden and significant health care resource use in China. The aim of this study was to quantify spatial patterns and effects of air pollution and meteorological factors on hospitalization of COPD, LC and TB in Beijing. Daily counts of hospitalization for 2010 were obtained from the Beijing Urban Employees Basic Medical Insurance (UEBMI) system. Bayesian hierarchical Poisson regression models were applied to identify spatial patterns of hospitalization for COPD, LC and TB at the district level and explore associations with inhalable particulate matter (aerodynamic diameter <10 μm, PM

Topics: Air Pollutants; Air Pollution; Beijing; Environmental Exposure; Geography; Hospitalization; Humans; Humidity; Lung Diseases; Lung Neoplasms; Meteorological Concepts; Models, Statistical; Nitrogen Dioxide; Particulate Matter; Pulmonary Disease, Chronic Obstructive; Risk Factors; Seasons; Sulfur Dioxide; Temperature; Tuberculosis

Topics: Adult; Biomarkers; Environmental Pollutants; Humans; Infant, Newborn; Lung Diseases; Nitrogen Dioxide; Uteroglobin

On July 1st. We used interrupted time series (ITS) with segmented regression to identify any change in ambient concentrations of SO. Mean monthly concentrations of SO. Implementation of the shipping emission policy in Hong Kong successfully reduced ambient SO

Topics: Air Pollutants; Air Pollution; Cardiovascular Diseases; Commerce; Environmental Monitoring; Hong Kong; Humans; Lung Diseases; Nitrogen Dioxide; Ozone; Particulate Matter; Social Responsibility; Sulfur Dioxide

Chronic health effects of traffic-related air pollution, like nitrogen dioxide (NO. We evaluated the association between traffic-related NO. 140 adolescents provided repeated salivary cortisol samples throughout one day. We built a land use regression model to estimate chronic NO. In adolescents, we found that increased, chronic exposure to NO

Topics: Adolescent; Air Pollutants; Air Pollution; Asthma; Environmental Exposure; Environmental Monitoring; Female; Humans; Hydrocortisone; Lung Diseases; Male; Nitrogen Dioxide; Saliva

Air pollution is a growing concern in Korea because of transboundary air pollution from mainland China. A panel study was conducted to clarify the effects of air pollution on respiratory symptoms and health-related quality of life (HR-QoL) in outpatients with and without chronic obstructive pulmonary disease (COPD) in Korea.. Patients filled out a questionnaire including self-reported HR-QoL in February and were followed up in May and July. The study was conducted from 2013 to 2015, with different participants each year. Air quality parameters were applied in a generalized estimating equation as independent variables to predict factors affecting HR-QoL.. Lower physical fitness scores were associated with Asian sand dust events. Daily activity scores were worse when there were high concentrations of particulate matter (PM) less than 10 μm in diameter (PM. The results suggest that PM, NO

Topics: Adult; Aged; Air Pollutants; Chronic Disease; Dust; Female; Humans; Lung Diseases; Male; Middle Aged; Nitrogen Dioxide; Outpatients; Ozone; Particulate Matter; Quality of Life; Republic of Korea; Seasons; Self Report; Surveys and Questionnaires

Tunnel construction workers are exposed to particulate and gaseous air contaminants. Previous studies carried out in the 1990s showed that tunnel construction workers were at increased risk of both short-term and long-term lung function decline. Since then, efforts have been made to reduce exposure. The objective of the present study was to investigate if current exposure may still cause short-term lung function impairment.. Tunnel workers work 12 days consecutively, and then they are off for 9 days. Ninety tunnel workers and 51 referents were examined with spirometry and questionnaires before their work period started and again 11 days later. Personal exposure to particles and α-quartz in the thoracic aerosol subfraction, elemental carbon and organic carbon, oil mist, nitrogen dioxide and ammonia was assessed on two consecutive days between the two health examinations.. The geometric means air concentrations for particulate matter in the thoracic mass aerosol subfraction, α-quartz, oil mist, organic carbon and elemental carbon for all workers were 561, 63, 210, 146 and 35 μg/m(3), respectively. After 11 days of work, the mean forced expiratory volume in 1 s (FEV1) in healthy participants had declined 73 mL (SD 173), p<0.001 in the tunnel workers, compared to 3 mL (SD 21), p=0.9 in the referents. Also, forced vital capacity (FVC) had declined significantly. Declines in FVC and FEV1 were significantly associated with exposure to organic carbon.. In spite of reduced levels of exposure in modern tunnelling operations, a negative impact on lung function was still observed.

Topics: Adolescent; Adult; Air Pollutants, Occupational; Ammonia; Carbon; Construction Industry; Forced Expiratory Volume; Humans; Lung; Lung Diseases; Middle Aged; Nitrogen Dioxide; Occupational Diseases; Occupational Exposure; Oils; Particulate Matter; Quartz; Spirometry; Surveys and Questionnaires; Time Factors; Vital Capacity; Young Adult

This study was undertaken to determine whether there was an association between coarse particles (PM₂.₅-₁₀) levels and frequency of hospital admissions for respiratory diseases (RD) in Kaohsiung, Taiwan. Hospital admissions for RD including chronic obstructive pulmonary disease (COPD), asthma, and pneumonia, and ambient air pollution data levels for Kaohsiung were obtained for the period from 2006 to 2010. The relative risk of hospital admissions for RD was estimated using a case-crossover approach, controlling for weather variables, day of the week, seasonality, and long-term time trends. For the single pollutant model (without adjustment for other pollutants), increased rate of admissions for RD were significantly associated with higher coarse PM levels only on cool days (<25 °C), with a 10 µg/m³ elevation in PM₂.₅-₁₀ concentrations associated with a 3% (95% CI = 1%-5%) rise in COPD admissions, 4% (95% CI = 1%-7%) increase in asthma admissions, and 3% (95% CI = 2%-4%) rise in pneumonia admissions. No significant associations were found between coarse particle levels and the number of hospital admissions for RD on warm days. In the two-pollutant models, PM₂.₅-₁₀ levels remained significantly correlated with higher rate of RD admissions even controlling for sulfur dioxide, nitrogen dioxide, carbon monoxide, or ozone on cool days. This study provides evidence that higher levels of PM₂.₅-₁₀ enhance the risk of hospital admissions for RD on cool days.

Topics: Air Pollution; Asthma; Carbon Monoxide; Cities; Cross-Over Studies; Hospitalization; Humans; Lung Diseases; Nitrogen Dioxide; Ozone; Particulate Matter; Pneumonia; Pulmonary Disease, Chronic Obstructive; Risk; Sulfur Dioxide; Taiwan; Weather

This study was undertaken to determine whether there was a correlation between fine particles (PM2.5) levels and hospital admissions for respiratory diseases in Kaohsiung, Taiwan. Hospital admissions for respiratory diseases including pneumonia, asthma, and chronic obstructive pulmonary disease (COPD) and ambient air pollution data for Kaohsiung were obtained for the period 2006-2010. The relative risk (RR) of hospital admissions for respiratory diseases was estimated using a case-crossover approach, controlling for weather variables, day of the week, seasonality, and chronic time trends. For the single-pollutant model (without adjustment for other pollutants), increased number of admissions for respiratory diseases were significantly associated with higher PM2.5 levels only on cool days (<25°C), with an interquartile range rise associated with a 50 (95% CI% = 45-55%), 40% (95% CI = 25-58%), and 46% (95% CI = 36-57%) elevation in frequency of admissions for pneumonia, asthma, and COPD, respectively. In the two-pollutant models, PM2.5 levels remained significant even controlling for sulfur dioxide, nitrogen dioxide, carbon monoxide, or ozone on cool days. This study provides evidence that higher levels of PM2.5 increase the risk of hospital admissions for respiratory diseases in Taiwan.

Topics: Air Pollution; Carbon Monoxide; Cities; Cross-Over Studies; Hospitalization; Humans; Logistic Models; Lung Diseases; Nitrogen Dioxide; Ozone; Particulate Matter; Risk Factors; Sulfur Dioxide; Taiwan; Weather

Multiple-breath washout (MBW)-derived lung clearance index (LCI) is a sensitive measure of ventilation inhomogeneity in patients with cystic fibrosis (CF), but LCI measurement is time consuming. We systematically assessed ways to shorten LCI measurements. In 68 school-aged children (44 with mild CF lung disease) three standard nitrogen (N2) MBWs were applied. We assessed repeatability and diagnostic performance of (1) LCI measured earlier from three MBW runs and (2) LCI measured at complete MBW (1/40th of starting N2 concentration) from two runs only. Compared with the standard LCI from three complete MBW runs, the new LCI based on three N2MBW runs until 1/20th, or two complete runs until 1/40th, provided similar or better repeatability as well as sensitivity and specificity for CF lung disease. Alternative ways to measure LCI reduced test duration in children with CF by 30% and 41%, respectively. LCI measurements can be reliably shortened in children. These new MBW protocols may advance the transition of LCI from research into clinical settings.

Topics: Adolescent; Breath Tests; Child; Cystic Fibrosis; Exhalation; Female; Forced Expiratory Volume; Humans; Lung Diseases; Male; Nitrogen Dioxide; ROC Curve

In China, both the levels and patterns of outdoor air pollution have altered dramatically with the rapid economic development and urbanization over the past two decades. However, few studies have investigated the association of outdoor air pollution with respiratory mortality, especially in the high pollution range.. We conducted a retrospective cohort study of 9,941 residents aged ≥35 years old in Shenyang, China, to examine the association between outdoor air pollutants [particulate matter <10 µm in aerodynamic diameter (PM(10)), sulfur dioxide (SO(2)) and nitrogen dioxide (NO(2))] and mortality using 12 years of data.. We applied extended Cox proportional hazards modeling with time-dependent covariates to respiratory mortality. Analyses were also stratified by age, sex, educational level, smoking status, personal income, occupational exposure and body mass index (BMI) to examine the association of air pollution with mortality.. We found significant associations between PM(10) and NO(2) levels and respiratory disease mortality. Our analysis found a relative risk of 1.67 [95% confidence interval (CI) 1.60-1.74] and 2.97 (95% CI 2.69-3.27) for respiratory mortality per 10 µg/m(3) increase in PM(10) and NO(2), respectively. The effects of air pollution were more apparent in women than in men. Age, sex, educational level, smoking status, personal income, occupational exposure, BMI and exercise frequency influenced the relationship between outdoor PM(10) and NO(2) and mortality. For SO(2), only smoking, little regular exercise and BMI above 18.5 influenced the relationship with mortality.. These data contribute to the scientific literature on the long-term effects of air pollution for the high-exposure settings typical in developing countries.

Topics: Adult; Age Factors; Aged; Aged, 80 and over; Air Pollution; China; Cohort Studies; Environmental Exposure; Female; Humans; Lung Diseases; Male; Middle Aged; Nitrogen Dioxide; Particulate Matter; Proportional Hazards Models; Retrospective Studies; Sex Factors; Smoking; Socioeconomic Factors; Sulfur Dioxide

Investigators examined 5,654 children enrolled in the El Paso, Texas, public school district by questionnaire in 2001. Exposure measurements were first collected in the late fall of 1999. School-level and residence-level exposures to traffic-related air pollutants were estimated using a land use regression model. For 1,529 children with spirometry, overall geographic information system (GIS)-modeled residential levels of traffic-related ambient air pollution (calibrated to a 10-ppb increment in nitrogen dioxide levels) were associated with a 2.4% decrement in forced vital capacity (95% confidence interval (CI): -4.0, -0.7) after adjustment for demographic, anthropomorphic, and socioeconomic factors and spirometer/technician effects. After adjustment for these potential covariates, overall GIS-modeled residential levels of traffic-related ambient air pollution (calibrated to a 10-ppb increment in nitrogen dioxide levels) were associated with pulmonary function levels below 85% of those predicted for both forced vital capacity (odds ratio (OR) = 3.10, 95% CI: 1.65, 5.78) and forced expiratory volume in 1 second (OR = 2.35, 95% CI: 1.38, 4.01). For children attending schools at elevations above 1,170 m, a 10-ppb increment in modeled nitrogen dioxide levels was associated with current asthma (OR = 1.56, 95% CI: 1.08, 2.50) after adjustment for demographic, socioeconomic, and parental factors and random school effects. These results are consistent with previous studies in Europe and California that found adverse health outcomes in children associated with modeled traffic-related air pollutants.

Topics: Air Pollution; Child; Female; Geographic Information Systems; Humans; Logistic Models; Lung Diseases; Male; Motor Vehicles; Nitrogen Dioxide; Odds Ratio; Spirometry; Texas; Urban Population

Few case-crossover studies were conducted in China to investigate the acute health effects of air pollution. We conducted a time-stratified case-crossover analysis to examine the association between air pollution and daily mortality in Anshan, a heavily-polluted industrial city in northeastern China. Daily mortality, air pollution, and weather data in 2004-2006 in Anshan were collected. Time-stratified case-crossover approach was used to estimate the effect of air pollutants (PM(10), SO(2), NO(2) and CO) on total and cardiopulmonary mortality. Controls were selected as matched days of the week in the same month. Potential effect modifiers, such as gender and age, were also examined. We found significant associations between air pollution and daily mortality from cardiovascular diseases in Anshan. A 10μg/m(3) elevation of 2-day moving average (lag 01) concentration in PM(10), SO(2), NO(2) and CO corresponded to 0.67% (95% CI: 0.29%, 1.04%), 0.38% (95% CI: -0.06%, 0.83%), 2.11% (95% CI: 0.22%, 4.00%) and 0.04% (95% CI: 0.01%, 0.07%) increase of cardiovascular mortality. The associations for total and respiratory mortality were generally positive but statistically insignificant. The air pollution health effects were significantly modified by age, but not by gender. Conclusively, our study showed that short-term exposure to air pollution was associated with increased cardiovascular mortality in Anshan. These findings may have implications for local environmental and social policies.

Topics: Adolescent; Adult; Aged; Air Pollutants; Air Pollution; Carbon Monoxide; Cardiovascular Diseases; Child; Child, Preschool; China; Cities; Cross-Over Studies; Female; Humans; Lung Diseases; Male; Middle Aged; Nitrogen Dioxide; Particulate Matter; Sulfur Dioxide; Young Adult

Protein S-glutathionylation (PSSG) is a posttranslational modification that involves the conjugation of the small antioxidant molecule glutathione to cysteine residues and is emerging as a critical mechanism of redox-based signaling. PSSG levels increase under conditions of oxidative stress and are controlled by glutaredoxins (Grx) that, under physiological conditions, preferentially deglutathionylate cysteines and restore sulfhydryls. Both the occurrence and distribution of PSSG in tissues is unknown because of the labile nature of this oxidative event and the lack of specific reagents. The goal of this study was to establish and validate a protocol that enables detection of PSSG in situ, using the property of Grx to deglutathionylate cysteines. Using Grx1-catalyzed cysteine derivatization, we evaluated PSSG content in mice subjected to various models of lung injury and fibrosis. In control mice, PSSG was detectable primarily in the airway epithelium and alveolar macrophages. Exposure of mice to NO(2) resulted in enhanced PSSG levels in parenchymal regions, while exposure to O(2) resulted in minor detectable changes. Finally, bleomycin exposure resulted in marked increases in PSSG reactivity both in the bronchial epithelium as well as in parenchymal regions. Taken together, these findings demonstrate that Grx1-based cysteine derivatization is a powerful technique to specifically detect patterns of PSSG expression in lungs, and will enable investigations into regional changes in PSSG content in a variety of diseases.

Topics: Animals; Biocatalysis; Cysteine; Glutaredoxins; Glutathione; Histocytochemistry; Lung; Lung Diseases; Mice; Mice, Inbred C57BL; Microscopy, Confocal; Microscopy, Fluorescence; Nitrogen Dioxide; Oxidants, Photochemical; Oxidation-Reduction; Oxygen; Paraffin Embedding; Protein S

This study investigated the concentration-response relation between air pollution (nitrogen dioxide and particulate matter pollutants PM(10) and PM(2.5)) and cause-specific mortality. The population included all inhabitants of Oslo, Norway, aged 51-90 years on January 1, 1992 (n = 143,842) with follow-up of deaths from 1992 to 1998. An air dispersion model (AirQUIS; Norwegian Institute for Air Research (NILU), Oslo, Norway) was used to estimate levels of exposure in 1992-1995 in all 470 administrative neighborhoods. These data were linked to census, education, and death registries. A consistent effect on all causes of death was found for both sexes and age groups by all indicators of air pollution. The effects appeared to increase at nitrogen dioxide levels higher than 40 micro g/m(3) in the youngest age group and with a linear effect in the interval 20-60 micro g/m(3) for the oldest. An effect of all indicators on cardiovascular causes, lung cancer, and chronic obstructive pulmonary disease was also found in both age groups and sexes. The effects were particularly strong for chronic obstructive pulmonary disease, which appeared to have linear effects, whereas cardiovascular causes and lung cancer seemed to have threshold effects. Results show that vulnerable persons with chronic obstructive pulmonary disease and the elderly seem to be susceptible to air pollution at lower levels than the general population.

Topics: Aged; Aged, 80 and over; Air Pollution; Cardiovascular Diseases; Cause of Death; Female; Follow-Up Studies; Humans; Lung Diseases; Male; Middle Aged; Nitrogen Dioxide; Norway; Prognosis; Retrospective Studies; Risk Factors; Urban Population

Few, if any, published time series studies have evaluated the effects of particulate matter air exposures by combining hospital admissions with medical visit data for smaller populations. We investigated the relationship between daily particulate matter (<10 microm in aerometric diameter or PM10) exposures with admissions and medical visits (emergency room, urgent care, and family practice) for respiratory and cardiovascular disease in Pocatello and Chubbuck, Idaho (population about 60,000), from November 1994 through March 2000. Within generalized linear models, time, weather, influenza, and day-of-week effects were controlled. In single-pollutant models, respiratory disease admissions and visits increased (7.1-15.4% per 50 microg/m3 PM10) for each age group analyzed, with the highest increases in two groups, children and especially the elderly. Statistical analyses suggest that the results probably did not occur by chance. Sensitivity analyses did not provide strong evidence that the respiratory disease effect estimates were sensitive to reasonable changes in the final degrees of freedom choice for time and weather effects. No strong evidence of confounding by NO2 and SO2 was found from results of multi-pollutant models. Ozone and carbon monoxide data were not available to include multi-pollutant models, but evidence suggests that they were not a problem. Unexpectedly, evidence of an association between PM10 with cardiovascular disease was not found, possibly due to the lifestyles of the mostly Mormon study population. Successful time series analyses can be performed on smaller populations if diverse, centralized databases are available. Hospitals that offer urgent or other primary care services may be a rich source of data for researchers. Using data that potentially represented a wide-range of disease severity, the findings provide evidence that evaluating only hospital admissions or emergency room visit effects may underestimate the overall morbidity due to acute particulate matter exposures. Further work is planned to test this conclusion.

Topics: Adolescent; Adult; Age Factors; Aged; Air Pollutants; Air Pollution; Carbon Dioxide; Child; Cities; Heart Diseases; Hospitalization; Humans; Idaho; Infant; Infant, Newborn; Linear Models; Lung Diseases; Middle Aged; Models, Biological; Nitrogen Dioxide; Particulate Matter; Seasons; Time Factors

Although numerous epidemiologic studies now use models of intraurban exposure, there has been little systematic evaluation of the performance of different models.. In this present article we proposed a modeling framework for assessing exposure model performance and the role of spatial autocorrelation in the estimation of health effects.. We obtained data from an exposure measurement substudy of subjects from the Southern California Children's Health Study. We examined how the addition of spatial correlations to a previously described unified exposure and health outcome modeling framework affects estimates of exposure-response relationships using the substudy data. The methods proposed build upon the previous work, which developed measurement-error techniques to estimate long-term nitrogen dioxide exposure and its effect on lung function in children. In this present article, we further develop these methods by introducing between- and within-community spatial autocorrelation error terms to evaluate effects of air pollution on forced vital capacity. The analytical methods developed are set in a Bayesian framework where multistage models are fitted jointly, properly incorporating parameter estimation uncertainty at all levels of the modeling process.. Results suggest that the inclusion of residual spatial error terms improves the prediction of adverse health effects. These findings also demonstrate how residual spatial error may be used as a diagnostic for comparing exposure model performance.

Topics: Adolescent; Air Pollutants; Air Pollution; Bayes Theorem; California; Child; Environmental Monitoring; Epidemiological Monitoring; Humans; Lung Diseases; Models, Biological; Nitrogen Dioxide; Uncertainty; Vehicle Emissions; Vital Capacity

To examine the short-term health effects of air pollution on daily mortality in four Australian cities (Brisbane, Melbourne, Perth and Sydney), where more than 50% of Australians reside.. The study used a similar protocol to APHEA2 (Air Pollution and Health: A European Approach) study and derived single-city and pooled estimates.. The results derived from the different approaches for the 1996-99 period showed consistent results for different statistical models used. There were significant effects on total mortality, (RR = 1.0284 per 1 unit increase in nephelometry [10(-4).m(-1)], RR = 1.0011 per 1ppb increase in NO2), and on respiratory mortality (RR = 1.0022 per 1ppb increase in O3). No significant differences between cities were found, but the NO2 and particle effects may refer to the same impacts. Meta-analyses carried out for three cities yielded estimates for the increase in the daily total number of deaths of 0.2% (-0.8% to 1.2%) for a 10 microg/m3 increase in PM10 concentration, and 0.9% (-0.7% to 2.5%) for a 10 microg/m3 increase in PM2.5 concentration.. Air pollutants in Australian cities have significant effects on mortality.

Topics: Aged; Air Pollutants; Australia; Cardiovascular Diseases; Humans; Lung Diseases; Meta-Analysis as Topic; Mortality; Nitrogen Dioxide; Ozone; Urban Population

This paper examines the short-term health effects of air pollution on daily hospital admissions in Australian cities (those considered comprise more than 50% of the Australian population) for the period 1996-99.. The study used a similar protocol to overseas studies and derived single city and pooled estimates using different statistical approaches to assess the accuracy of the results.. There was little difference between the results derived from the different statistical approaches for cardiovascular admissions, while in those for respiratory admissions there were differences. For three of the four cities (for the other the results were positive but not significant), fine particles (measured by nephelometry - bsp) and nitrogen dioxide (NO2) have a significant impact on cardiovascular admissions (for total cardiac admissions, RR = 1.0856 for a one-unit increase in bsp (10(-4) x m(-1)), RR = 1.0023 for a 1 ppb increase in NO2). For three of the four cities (for the other, the results were negative and significant), fine particles, NO2 and ozone have a significant impact on respiratory admissions (for total elderly respiratory admissions, RR = 1.0552 per 1 unit (10(-4) x m(-1)) increase in bsp, RR = 1.0027 per 1ppb increase in NO2, RR = 10014 per 1 ppb increase in ozone for elderly asthma and COPD admissions). In all analyses the particle and NO2 impacts appear to be related.. Similar to overseas studies, air pollution has an impact on hospital admissions in Australian cities, but there can be significant differences between cities.

Topics: Adolescent; Adult; Age Distribution; Aged; Air Pollutants; Australia; Cardiovascular Diseases; Hospitalization; Humans; Lung Diseases; Middle Aged; Nitrogen Dioxide; Ozone; Urban Population

Daily variations in ambient particulate air pollution have been associated with respiratory mortality and morbidity.. To assess the associations between urinary concentration of lung Clara cell protein CC16, a marker for lung damage, and daily variation in fine and ultrafine particulate air pollution.. Spot urinary samples (n = 1249) were collected biweekly for six months in subjects with coronary heart disease in Amsterdam, Netherlands (n = 37), Erfurt, Germany (n = 47), and Helsinki, Finland (n = 47). Ambient particulate air pollution was monitored at a central site in each city.. The mean 24 hour number concentration of ultrafine particles was 17.3x10(3) cm(-3) in Amsterdam, 21.1x10(3) cm(-3) in Erfurt, and 17.0x10(3) cm(-3) in Helsinki. The mean 24 hour PM2.5 concentrations were 20, 23, and 13 microg/m3, respectively. Daily variation in ultrafine particle levels was not associated with CC16. In contrast, CC16 concentration seemed to increase with increasing levels of PM2.5 in Helsinki, especially among subjects with lung disorders. No clear associations were observed in Amsterdam and Erfurt. In Helsinki, the CC16 concentration increased by 20.2% (95% CI 6.9 to 33.5) per 10 microg/m3 increase in PM2.5 concentration (lag 2). The respective pooled effect estimate was 2.1% (95% CI -1.3 to 5.6).. The results suggest that exposure to particulate air pollution may lead to increased epithelial barrier permeability in lungs.

Topics: Aged; Air Pollutants; Biomarkers; Carbon Dioxide; Female; Humans; Lung Diseases; Male; Middle Aged; Nitrogen Dioxide; Particle Size; Respiratory Mucosa; Uteroglobin

Based on several severe air pollution episodes, a temporal correlation between high concentrations of particulate matter (PM) and SO2 pollution and acute increases in respiratory and cardiopulmonary mortality had been established in Vienna for the 1970's. After air pollution had decreased in Austria in the 1980's--as documented by data on SO2, and total suspended particles (TSP)--no such associations between day-to-day changes of SO2 and TSP and mortality have been documented any more, however, traffic related pollutants like fine particles and NO2 remained a problem. Therefore, short term effects of PM on lung function, morbidity and mortality were investigated in Vienna, Linz, Graz and a rural control area. Long-term exposure and chronic disease--even more important for public health--were studied in repeated cross-sectional, a mixed longitudinal and a birth cohort study on school children in the city of Linz. Lung function growth was found impaired from long-term exposure to air pollutants and improved in districts where ambient air pollution had decreased. Where only TSP and SO2 had decreased, no continuous improvement of small airway function was found and end-expiratory flow rates stayed impaired where NO2-reduction from technical improvements of cars and industry was counterbalanced by increase of motorized (diesel) traffic. Remaining acute effects of ambient air pollution in 2001 from PM, NO2 and co-pollutants found in a time series study also show that continuing efforts are necessary. Active surface of particles inhaled several hours to days before spirometry was found related to short-term reductions in forced vital capacity-FVC (p<0.01), forced expiratory volume in one second-FEV1 (p<0.01) and maximal expiratory flow rate at 50% of vital capacity-MEF50 (p<0.05). In pupils with asthma or previous airway obstruction 4-week-diaries proved that the following symptoms increased with acute exposure to higher active surface of particles: wheezing (p<0.01), dyspnea, cough when going to sleep, cough at night (p<0.05). Efforts to reduce exposure to fine particles from motor traffic and passive smoking have to be increased if we want to achieve full recovery of children from air pollution effects and best respiratory performance in adulthood. Surveillance seems to be necessary not only for particle mass but also for particle number and surface. Little is known on the mechanisms of irreversible long-term effects of PM such as myocardial infarction and can

Topics: Adult; Air Pollutants; Austria; Cause of Death; Child; Chronic Disease; Cohort Studies; Dust; Female; Forecasting; Humans; Longitudinal Studies; Lung Diseases; Male; Nitrogen Dioxide; Risk Assessment; Rural Population; Sulfur Dioxide; Urban Population

Surfactant synthesis and secretion has been shown to be impaired in type II cells from diseased lungs. The mechanism of surfactant lipid recycling, which is an important physiological process in surfactant treatment, was studied in type II cells isolated from injured lungs.. Different stages of lung injury were induced by exposing rats to 10 ppm nitrogen dioxide (NO(2)) for 3, 20, and 28 days. Type II cells were isolated from these lungs and recycling of (3)H-DPPC labelled surfactant-like liposomes was studied in vitro.. Uptake of liposomes (150 micro g/ml) for 20 minutes in the absence and presence of surfactant protein-A (SP-A, 5 micro g/ml) was higher in cells from NO(2) injured lungs (63-78%) than in control cells. There was no difference in liposome uptake between the groups with NO(2) exposure of different duration. After liposome uptake, most of the internalised label remained in the phosphatidylcholine (PC) fraction and increased with duration of exposure to NO(2). After 20 minutes internalisation, cells were allowed to resecrete lipids for a further 20 minute period. In cells from controls and from all stages of lung injury, liposomes that had been internalised in the presence of SP-A were resecreted to a greater extent than those internalised without SP-A. However, cells from lungs exposed to NO(2) resecreted less lipid than cells from control lungs. Again, there was no difference in resecretion between the groups with NO(2) exposure of different duration.. Type II cells from injured lungs internalise more surfactant-like liposomes than cells from controls, suggesting a putative therapeutic significance to cope with limited alveolar surfactant pools in lung injury.

Topics: Animals; Chromatography, Thin Layer; Liposomes; Lung Diseases; Male; Nitrogen Dioxide; Pulmonary Surfactants; Rats; Rats, Sprague-Dawley

The effect of exposure to irritant air pollutants on the development of allergic airway disease is poorly understood. This study examines the effects of the lower respiratory tract irritant, NO(2), on the outcome of ovalbumin (OVA)-induced allergic airway disease. Male and female C57Bl/6 mice were sensitized by weekly intraperitoneal (ip) OVA injections for 3 wk followed by daily 1-h OVA aerosol inhalation challenge for 3 or 10 d. Initially, mice were exposed daily for 3 d to air or 0.7 or 5 ppm NO(2) for 2 h following each OVA aerosol challenge. OVA exposure resulted in pronounced lower airway inflammation, as evidenced by a significant increase in bronchoalveolar lavage (BAL) total cellularity and eosinophil levels. BAL eosinophil levels were significantly lower in OVA-NO(2) compared to OVA-air animals. The reduction was similar at both NO(2) exposure concentrations. In a subsequent study, sensitized animals were exposed for 3 or 10 d to aerosolized OVA followed by air or 0.7 ppm NO(2). BAL eosinophils were again reduced at 3 d by OVA-NO(2) exposure compared to OVA-air mice. At 10 d the eosinophilia was virtually abolished. This reduction in OVA-induced cellular inflammation by NO(2) was confirmed by histopathological analysis. Contrary to expectations, exposure to NO(2) during the aerosol challenge to OVA dramatically diminished the outcome of allergic disease in lungs as measured by airway cellular inflammation.

Topics: Aerosols; Animals; Disease Models, Animal; Humans; Hypersensitivity; Inflammation; Inhalation Exposure; Lung Diseases; Mice; Mice, Inbred C57BL; Nitrogen Dioxide; Oxidants, Photochemical

Oxidant-induced lung injury is believed to be mediated by reactive oxygen species. Recovery from oxidant exposure has been associated with pulmonary inflammation. Inflammatory cell accumulation involves the synthesis of chemokines, including neutrophil chemoattractants such as macrophage inflammatory protein-2 (MIP-2) and monocyte chemoattractants such as monocyte chemoattractant protein-1 (MCP-1). Antioxidants are the first line of defense of lung cells against inhaled oxidants. Metallothionein (MT) can act as an antioxidant and free-radical scavenger. To better understand the pulmonary response associated with recovery from oxidant-mediated injury, we exposed mice to either 15 ppm nitrogen dioxide for 24 h, >99% oxygen for 72 h, or 1 ppm ozone for 24 h. Mice were examined at the end of exposure or after recovering in room air for 4 or 24 h. Neutrophils were elevated at the end of exposure and remained elevated through the postexposure period, whereas macrophage numbers were decreased at the end of exposure and remained below control levels at 4 and 24 h postexposure. MT, MIP-2, and MCP-1 mRNA levels were elevated at 4 h postexposure; however, after 24 h of recovery only MCP-1 remained elevated. These results indicate that MT, MIP-2, and MCP-1 mRNA levels responded similarly to recovery from nitrogen dioxide, oxygen, and ozone exposure. Monocyte accumulation was delayed as compared to neutrophils and was consistent with the timing of MIP-2 and MCP-1 expression. Peak expression of MT and MIP-2 preceded peak neutrophil accumulation. Consequently, the timing of MT, MIP-2, and MCP-1 expression may be important biological markers in assessing the state of injury and recovery associated with oxidant-mediated injury.

Topics: Administration, Inhalation; Animals; Bronchoalveolar Lavage; Bronchoalveolar Lavage Fluid; Chemokine CCL2; Chemokine CXCL2; Chemotactic Factors; In Situ Hybridization; Lung Diseases; Male; Metallothionein; Mice; Mice, Inbred C57BL; Monokines; Nitrogen Dioxide; Nuclease Protection Assays; Oxidants, Photochemical; Oxygen; Ozone; RNA, Messenger

To examine whether underground construction workers exposed to tunnelling pollutants over a follow up period of 8 years have an increased risk of decline in lung function and respiratory symptoms compared with reference subjects working outside the tunnel atmosphere, and relate the findings to job groups and cumulative exposure to dust and gases.. 96 Tunnel workers and a reference group of 249 other heavy construction workers were examined in 1991 and re-examined in 1999. Exposure measurements were carried out to estimate personal cumulative exposure to total dust, respirable dust, alpha-quartz, oil mist, and nitrogen dioxide. The subjects answered a questionnaire on respiratory symptoms and smoking habits, performed spirometry, and had chest radiographs taken. Radiological signs of silicosis were evaluated (International Labour Organisation (ILO) classification). Atopy was determined by a multiple radioallergosorbent test (RAST).. The mean exposure to respirable dust and alpha-quartz in tunnel workers varied from 1.2-3.6 mg/m3 (respirable dust) and 0.019-0.044 mg/m3 (alpha-quartz) depending on job task performed. Decrease in forced expiratory volume in 1 second (FEV1) was associated with cumulative exposure to respirable dust (p<0.001) and alpha-quartz (p=0.02). The multiple regression model predicted that in a worker 40 years of age, the annual decrease in FEV1 would be 25 ml in a non-exposed non-smoker, 35 ml in a non-exposed smoker, and 50-63 ml in a non-smoking tunnel worker (depending on job). Compared with the reference group the odds ratio for the occurrence of new respiratory symptoms during the follow up period was increased in the tunnel workers and associated with cumulative exposure to respirable dust.. Cumulative exposures to respirable dust and alpha-quartz are the most important risk factors for airflow limitation in underground heavy construction workers, and cumulative exposure to respirable dust is the most important risk factor for respiratory symptoms. The finding of accelerated decline in lung function in tunnel workers suggests that better control of exposures is needed.

Topics: Adult; Asthma; Case-Control Studies; Confined Spaces; Dust; Engineering; Forced Expiratory Volume; Healthy Worker Effect; Humans; Logistic Models; Longitudinal Studies; Lung Diseases; Maximal Midexpiratory Flow Rate; Middle Aged; Mineral Oil; Nitrogen Dioxide; Occupational Exposure; Odds Ratio; Quartz; Radioallergosorbent Test; Radiography; Silicosis; Smoking; Statistics, Nonparametric; Vital Capacity

Very few published studies have looked at the effects of air pollution on health in the primary care setting. As part of a large study to examine the association between air pollution and a number of health outcomes, the relationship between daily GP consultations for asthma and other lower respiratory diseases (LRD) and air pollution in London was investigated.. Time-series analysis of daily numbers of GP consultations controlling for time trends, seasonal factors, day of week cycles, influenza, weather, pollen levels, and serial correlation was performed. Consultation data were available from between 268 718 and 295 740 registered patients from 45-47 London practices contributing to the General Practice Research Database during 1992-4.. Positive associations, weakly significant and consistent across lags, were observed between asthma consultations and nitrogen dioxide (NO2) and carbon monoxide (CO) in children and particulate matter of less than 10 microm in diameter (PM10) in adults, and between other LRD consultations and sulphur dioxide (SO2) in children. A consistently negative association with ozone in children was observed in both disease categories. The effect estimates of most pollutants were much larger when analysed separately by season, particularly in the children: percentage change in asthma consultations during the warm season (April-September) for a 10-90th percentile increase in 24 hour NO2 lagged by one day = 13.2% (95% CI 5.6 to 21.3), with CO = 11.4% (95% CI 3.3 to 20.0), and with SO2 = 9.0% (95% CI 2.2 to 16.2). In adults the only association consistent over different lag periods was with PM10 = 9.2% (3.7 to 15.1). The associations of pollution and consultations for LRD were increased mainly in the winter months: percentage change in consultations by children in winter with NO2 = 7.2% (95% CI 2.8 to 11.6), CO = 6.2% (95% CI 2.3 to 10.2), and SO2 = 5.8% (95% CI 1.6 to 10.2).. There are associations between air pollution and daily consultations for asthma and other lower respiratory disease in London. The most significant associations were observed in children and the most important pollutants were NO2, CO, and SO2. In adults the only consistent association was with PM10.

Topics: Adolescent; Adult; Aged; Air Pollution; Asthma; Carbon Monoxide; Child; Child, Preschool; Databases, Factual; Family Practice; Humans; Infant; London; Lung Diseases; Middle Aged; Models, Statistical; Nitrogen Dioxide; Patient Acceptance of Health Care; Seasons; Sulfur Dioxide

Topics: Air Microbiology; Air Pollutants; Granuloma; Humans; Lung Diseases; Nitrogen Dioxide; Skating; Swimming

This study examined the effects of outdoor air pollutants in Sydney, Australia, on daily mortality.. Time-series analysis was performed on counts of daily mortality and major outdoor air pollutants (particulates, ozone, and nitrogen dioxide) in Sydney (1989 to 1993) with adjustment for seasonal and cyclical factors. Poisson regression was calculated with allowance for overdispersion and autocorrelation. The effects of lagging exposure by 0 to 2 days were assessed with single- and multiple-pollutant models.. An increase in daily mean particulate concentration from the 10th to the 90th centile was associated with an increase of 2.63% (95% confidence interval 0.87 to 4.41) in all-cause mortality and 2.68% (0.25 to 5.16) in cardiovascular mortality. An increase in daily maximum 1-hour ozone concentration from the 10th to the 90th centile was associated with an increase of 2.04% (0.37 to 3.73) in all-cause mortality and 2.52% (-0.25 to 5.38) in cardiovascular mortality. An increase in the daily mean nitrogen dioxide concentration from the 10th to the 90th centile was associated with an increase of 7.71% (-0.34 to 16.40) in respiratory mortality. Multiple-pollutant models suggest that the effects of particulates and ozone on all-cause and cardiovascular mortality, and of nitrogen dioxide on respiratory mortality, are independent of the effects of the other pollutants.. Current levels of air pollution in Sydney are associated with daily mortality.. The effects of outdoor air pollutants on mortality in Sydney, Australia, are examined over the period 1989-1993 using a time-series analysis. The results show a clear relation between levels of air pollution and all-cause, cardiovascular, and respiratory mortality.

Topics: Air Pollutants; Cardiovascular Diseases; Humans; Lung Diseases; Mortality; New South Wales; Nitrogen Dioxide; Poisson Distribution; Seasons; Urban Health

Home indoor and outdoor levels, and personal exposures to NO2 were determined for more than 500 subjects in a subpopulation of SAPALDIA by using passive samplers. The overall personal NO2 average was found to be 27 micrograms m-3, the overall indoor average 21 micrograms m-3 and the overall outdoor average 31 micrograms m-3. Personal NO2 levels ranged between the outdoor and indoor levels, with the exception of study areas with low NO2 concentrations. In the winter, the indoor/outdoor ratios were lower than in the summer. Outdoor NO2 levels were higher in winter. In some study areas, indoor NO2 levels were lower in the winter than in the summer due to reduced ventilation but this was not consistent. Personal NO2 concentrations were very similar during all seasons. Gas-cooking and smoking were important factors for elevated indoor and personal NO2 levels (contribution: 5 micrograms m-3, 2 micrograms m-3, respectively). Personal exposure to NO2 correlated best with the indoor NO2 concentrations.

Topics: Adult; Air Pollution, Indoor; Environmental Exposure; Environmental Monitoring; Epidemiological Monitoring; Follow-Up Studies; Fossil Fuels; Humans; Lung Diseases; Nitrogen Dioxide; Occupational Exposure; Oxidants, Photochemical; Regression Analysis; Seasons; Smoking; Switzerland; Ventilation

To examine possible associations between daily concentrations of urban air pollutants and hospital emergency admissions and mortality due to cardiac and pulmonary disease.. A time series study was conducted in the City of Edinburgh, which has a population of about 450,000. Poisson log linear regression models were used to investigate the relation of the daily event rate with daily air pollution concentrations of sulphur dioxide (SO2) and black smoke from 1981 to 1995, and of nitrogen dioxide (NO2), ozone (O3), carbon monoxide (CO), and particulate matter (PM10) from 1992 to 1995. Adjustments were made for seasonal and weekday variation, daily temperature, and wind speed.. The most significant findings were positive associations over the period 1981-95 between black smoke as a mean of the previous three days and daily all cause mortality in people aged > or = 65, and respiratory mortality also in this age group (3.9% increase in mortality for a 10 micrograms/m3 increment in black smoke). For hospital emergency admissions between 1992 and 1995 the two most significant findings (p < 0.05) were for cardiovascular admissions of people aged > or = 65 which showed a positive association with PM10 as a mean of the 3 previous days, and a negative association with O3 as a mean of the previous three days. Analyses of outcomes based on linkage with previous cardiorespiratory emergency admissions did not show substantially different results.. These data suggest that in the City of Edinburgh, after correction for confounders, there was a small but significant association between concentrations of black smoke and respiratory mortality in the older age group, probably attributable to higher pollution levels in the early part of the study period. There were also generally weak and variable associations between day to day changes in concentrations of urban air pollutants at a single central point and emergency hospital admission rates from cardiac and respiratory disease.

Topics: Adult; Aged; Air Pollutants; Carbon Monoxide; Heart Diseases; Humans; Longitudinal Studies; Lung Diseases; Middle Aged; Nitrogen Dioxide; Ozone; Scotland; Smoke; Sulfur Dioxide; Time Factors

The aim of the present study was to analyse the time response to nitric oxide (NO) dosing changes as well as the formation of nitrogen dioxide (NO2) with different ventilation systems, respirator settings and application sites during NO inhalation. The inspired NO and NO2 concentrations were continuously measured using chemiluminiscence within a dummy ventilatory system equipped with two different respirator systems (Siemens Servo 900c and Bear BP 2001). NO was either introduced into the afferent limb of the ventilatory circuit close to the endotracheal tube (site A) or into the so-called low pressure port of the Servo 900c respirator, far away from the endotracheal tube (site B). In addition, the decay of the inspired NO concentration after cessation of the NO gas flow was studied. This decay was considerably prolonged when NO was introduced at site B (time constants: tau = 7.19 min versus tau = 0.29 min). Within the concentration range studied (0-25 ppm NO) a linear correlation between the NO and NO2 concentration was found. At site A and an inspired oxygen concentration of > 0.95 NO2 formation amounts to 1.14% +/- 0.11% of the NO concentration. Using this value one can calculate the NO2 formation for a given NO dose. For example, when 40 ppm NO are applied, a concentration of 0.45 ppm NO2 can be expected, which is well below the relevant toxic concentrations. However, when NO was introduced at site B, NO2 formation was significantly increased to 1.61% +/- 0.16%. Passage of the ventilated gas through soda lime led only to a slight and insignificant reduction in NO2 concentration. The continuous flow respirator BP 2001 showed a significantly lower NO2 concentration when compared to the non-continuous flow respirator Servo 900c (0.64 +/- 0.11% vs.1.14 +/- 0.11%).. The application of NO close to the endotracheal tube is associated with a much faster response of the actual inspired NO concentration to dosing changes and shows the lowest NO2 formation. In order to avoid toxic NO2 concentrations, an upper limit of 40 ppm NO is recommended for continuous NO inhalation.

Topics: Analysis of Variance; Child; Humans; Infant; Intensive Care Units; Luminescent Measurements; Lung Diseases; Nitric Oxide; Nitrogen Dioxide; Regression Analysis; Respiratory Therapy; Ventilators, Mechanical

Topics: Animals; Disease Models, Animal; Dust; Lung Diseases; Nitrogen Dioxide; Rats; Rats, Inbred BN; Up-Regulation

To determine the number of states with laws monitoring toxic gases in ice arenas. To inform physicians who care for ice skaters of the dangers of carbon monoxide and nitrogen dioxide exposure in ice arenas.. Survey, literature review.. Health Departments of the 50 states and Washington D.C.. At risk are users of ice arenas. Vigorous exercise (hockey or competitive figure skating) and underlying pulmonary or cardiovascular disease increase the risk toxicity. Toxic gas concentration is determined by the amount of production from internal combustion engines, effectiveness and use of the ventilation system, and the "cold air pool" over the ice.. Number of states with laws regulating toxic gases in ice arenas.. Only two states (Minnesota and Rhode Island) have laws regulating toxic gases in indoor ice areas.. Physicians and the public are generally unaware of this problem. Toxic gas exposure in ice arenas is under recognized and underreported. The risks are not documented in journals generally seen by physicians who care for skaters. Conversion to electric ice resurfacing machines--the best solution--is not economically practical; legislation on the monitoring of toxic gas levels offers a reasonable alternative.

Topics: Air Pollutants; Air Pollution, Indoor; Carbon Monoxide; Environmental Exposure; Environmental Monitoring; Heart Diseases; Hockey; Humans; Lung Diseases; Minnesota; Nitrogen Dioxide; Physical Exertion; Poisons; Public Health Administration; Rhode Island; Risk Factors; Skating; Toxins, Biological; United States; Vehicle Emissions; Ventilation

Immune hypersensitivity to house dust mite antigen (HDM) is a frequent cause of respiratory allergy. The objective of this study was to determine whether exposure to NO2, a common indoor air pollutant, modulates immune responses to HDM and influences immune-mediated lung disease. Brown Norway rats were immunized ip with 100 micrograms semipurified antigen and Bordetella pertussis adjuvant and challenged 2 weeks later with an intratracheal injection of 50 micrograms of a crude antigen preparation. Exposure to 5 ppm NO2 for 3 hr after both immunization and challenge procedures resulted in significantly higher levels of antigen-specific serum IgE, local IgA, IgG, and IgE antibody than air controls, and increased numbers of inflammatory cells in the lungs. Lymphocyte responsiveness to antigen in the spleen and MLN was also significantly higher in NO2-exposed animals. These data show that exposure to a common air pollutant can upregulate specific immune responses and subsequent immune-mediated pulmonary inflammation.

Topics: Air Pollutants; Allergens; Animals; Bronchoalveolar Lavage Fluid; Dust; Enzyme-Linked Immunosorbent Assay; Female; Immunity; Immunoglobulin G; Immunoglobulins; Inflammation; Intubation, Intratracheal; Lung Diseases; Lymphocyte Activation; Mites; Nitrogen Dioxide; Rats; Rats, Inbred BN

Topics: Humans; Humidity; Lung Diseases; Nitric Oxide; Nitrogen Dioxide; Oxidation-Reduction; Temperature

Human inhalation exposures to relatively high mass concentrations of the oxidant gas nitrogen dioxide (NO2) can result in a variety of pulmonary disorders, including life-threatening pulmonary edema, pneumonia, and bronchiolitis obliterans. Inasmuch as most experimental studies to date have examined NO2-induced lung injury following exposures to near ambient or supra-ambient concentrations of NO2, e.g., < or = 50 ppm, little detailed information about the pulmonary injurious responses following the acute inhalation of higher NO2 concentrations that are more commensurate with some actual human exposure conditions is currently available. Described in this report are the results from a series of investigations in which various aspects of the inhalation toxicity of high concentrations of NO2 have been examined in laboratory rats. In the first component of our study, we characterized the kinetic course of development of lung injury following acute exposures to high concentrations of NO2 delivered over varying durations, and we assessed the relative importance of NO2 exposure concentration versus exposure time in producing lung injury. For a given exposure duration, the resulting severity of lung injury was found to generally scale proportionately with inhaled mass concentration, whereas for a given concentration of inhaled NO2, the magnitude of resulting injury was not directly proportional to exposure duration. Moreover, evidence was obtained that indicated exposure concentration is more important than exposure time when high concentrations of NO2 are inhaled. In a second component of our investigation, we assessed the pulmonary injurious response that occurs when NO2 is inhaled during very brief, 'high burst' exposures to very high concentrations of NO2. Such exposures resulted in significant lung injury, with the magnitude of such injury being directly proportional to exposure concentration. Comparisons of results obtained from this and the first component studies additionally revealed that brief exposures to the very high concentrations of NO2 are more hazardous than longer duration exposures to lower concentrations. In a third study series, we examined pre-exposure, exposure, and post-exposure modifiers of NO2-induced lung injury, including dietary taurine, minute ventilation, and post-exposure exercise. Results from these studies indicated: (i) dietary taurine does not protect the rat lung against high concentration NO2 exposure, (ii) the severity of acu

Topics: Administration, Inhalation; Animals; Disease Models, Animal; Dose-Response Relationship, Drug; Lung Diseases; Male; Nitrogen Dioxide; Permeability; Physical Conditioning, Animal; Pneumonia; Pulmonary Alveoli; Pulmonary Edema; Rats; Rats, Inbred F344; Respiration; Taurine; Time Factors

Lung mechanics, hemodynamics and blood chemistries were assessed in sheep (Ovis aries) before, and up to 24 h following, a 15-20 min exposure to either air (control) or approximately 500 ppm nitrogen dioxide (NO2). Histopathologic examinations of lung tissues were performed 24 h after exposure. Nose-only and lung-only routes of exposure were compared for effects on NO2 pathogenesis. Bronchoalveolar lavage fluids from air- and NO2-exposed sheep were analyzed for biochemical and cellular signs of NO2 insult. The influence of breathing pattern on NO2 dose was also assessed. Five hundred ppm NO2 exposure of intubated sheep (lung-only exposure) was marked by a statistically significant, albeit small, blood methemoglobin increase. The exposure induced an immediate tidal volume decrease, and an increase in both breathing rate and inspired minute ventilation. Pulmonary function, indexed by lung resistance and dynamic lung compliance, progressively deteriorated after exposure. Maximal lung resistance and dynamic lung compliance changes occurred at 24 h post exposure, concomitant with arterial hypoxemia. Bronchoalveolar lavage fluid epithelial cell number and total protein were significantly increased while macrophage number was significantly decreased within the 24 h post-exposure period. Histopathologic examination of lung tissue 24 h after NO2 revealed patchy edema, mild hemorrhage and polymorphonuclear and mononuclear leukocyte infiltration. The NO2 toxicologic profile was significantly attenuated when sheep were exposed to the gas through a face mask (nose-only exposure). Respiratory pattern was not significantly altered, lung mechanics changes were minimal, hypoxemia did not occur, and pathologic evidence of exudation was not apparent in nose-only, NO2-exposed sheep. The qualitative responses of this large animal species to high-level NO2 supports the concept of size dependent species sensitivity to NO2. In addition, when inspired minute ventilation was used as a dose-determinant, a linear relationship between NO2 dose and lung resistance was found. The importance of these findings, NO2 dose-determinants, and the utility of sheep as a large animal inhalation model are discussed.

Topics: Administration, Inhalation; Animals; Bronchoalveolar Lavage Fluid; Dose-Response Relationship, Drug; Female; Lung; Lung Diseases; Mouth Breathing; Nitrogen Dioxide; Nose; Pulmonary Circulation; Respiration; Sheep

1. In previous studies a rat inhalation model was developed to investigate the efficacy of treatment in acute NO2 intoxication. 2. Desferrioxamine was administered intravenously to study its effect on histological alterations in lung tissue in rats after acute NO2 exposure. 3. Twenty four hours after exposure to 175 ppm NO2 for 10 minutes the lung injury observed by light microscopy in the desferrioxamine treated rats was less pronounced than in the saline treated rats. 4. Desferrioxamine appeared to provide more protection with a dose of 100 mg kg-1 24 h-1 than with 200 mg kg-1 24 h-1.

Topics: Administration, Inhalation; Animals; Body Weight; Deferoxamine; Female; Injections, Intravenous; Lung; Lung Diseases; Nitrogen Dioxide; Organ Size; Rats; Rats, Wistar

The effect of ambient NO2 on lung function was investigated in a sample of 423 schoolchildren. At each of four locations NO2 was monitored continuously. Over a 6-month period from January to June 1990 two surveys were performed and spirometry recorded each time for each child. Linear regression was used to estimate the effect of NO2 for different time intervals preceding lung function testing. A decrease of NO2 between surveys was significantly associated with a higher forced vital capacity (FVC) at the second survey. For each microgram/m3 NO2 decrease the model predicted an increase in FVC of 1.5 ml [for the 2-hr mean (P < 0.05)] and 3.1 ml [for the 12-hr mean (P < 0.01)]. We conclude that even at NO2 levels below current air-quality standards children demonstrate significant changes in lung function.

Topics: Air Pollutants; Austria; Child; Dermatitis, Atopic; Female; Humans; Lung Diseases; Male; Models, Biological; Nitrogen Dioxide; Respiratory Function Tests; Vital Capacity

To investigate the potential for up to a near-lifetime exposure to high-ambient levels of nitrogen dioxide (NO2) to induce functional lung damage, groups of rats were exposed to air or a simulated urban profile of NO2 (0.5 ppm background, 1.5 ppm peak) for 1, 3, 13, 52, or 78 weeks. The dynamic, static, and diffusional characteristics of the lung were evaluated postexposure in anesthetized rats. Furthermore, for the 13-, 52-, and 78-week groups, additional animals were tested after a 6-, 26-, or 17-week period in filtered air, respectively. No significant NO2 differences between exposed and control animals were found for the nitrogen washout, compliance, lung volume, or diffusion capacity of carbon monoxide measurements. At 78 weeks, however, a reduction in delta FEF25%, an estimate of convexity in the later portion of the forced expiratory flow volume curve, was observed. Breathing patterns and mechanisms were also assessed postexposure in a parallel group of similarly exposed unanesthetized rats. These rats were examined during a filtered air, 4 and 8% carbon dioxide (CO2) challenge. In the unanesthetized rat, frequency of breathing was significantly decreased and tidal volume, expiratory resistance, and inspiratory and expiratory times tended to increase. For several of these variables, the largest response also occurred at 78 weeks and seemed to be exacerbated by CO2 challenge.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Air Pollutants; Animals; Electrocardiography; Lung Diseases; Male; Nitrogen Dioxide; Rats; Rats, Inbred F344; Respiratory Function Tests; Respiratory Mechanics

Topics: Acetylcysteine; Alveolitis, Extrinsic Allergic; Animals; Free Radical Scavengers; Humans; Lung; Lung Diseases; Nitrogen Dioxide; Ozone; Reactive Oxygen Species; Respiratory Burst; Smoking

Topics: Ascorbic Acid; Hockey; Humans; Lung Diseases; Nitrogen Dioxide

The goal of this study was to develop an early marker of lung injury that might change in response to exposure to a mobile source emission. Nitrogen dioxide (NO2)2 was chosen as an example of an atmospheric pollutant that is related to automobile emissions. Since reorganization of the connective tissue matrix of the lung occurs in response to injury, markers of connective tissue metabolism were selected as targets. Hydroxylysine became the marker of choice. It is an amino acid that is virtually exclusive to collagen, although it does occur in minimal amounts in other proteins. Furthermore, it is excreted in the urine, which makes it readily available for analysis using noninvasive techniques. Other markers evaluated as part of the study included angiotensin-converting enzyme as a marker of lung injury, desmosine as a marker of elastin degradation, and hydroxyproline as another marker of collagen metabolism. Male Fischer-344 rats were exposed in whole-body chambers to controlled concentrations of NO2 for various doses and periods of time. The concentrations of NO2 ranged from 0.5 to 30 parts per million (ppm); the rats were exposed for six hours per day for periods of two days to four weeks. Urine and bronchoalveolar lavage samples were collected and analyzed for the appropriate marker. In addition, pulmonary function studies and histologic examinations of the lungs were completed at selected time points. Urinary hydroxylysine concentration increased as a function of NO2 concentration during six-hour-per-day exposures for two days. This short-term exposure required relatively high doses to achieve significant changes in the hydroxylysine output. During one-week exposures to either 25 or 30 ppm NO2, there was an increase in urinary hydroxylysine associated with changes in lavage concentrations of angiotensin-converting enzyme and hydroxylysine. The lungs of these animals demonstrated histologic changes typical of oxidant injury. Four-week exposure protocols using 0.5 and 1 ppm NO2 were most interesting in terms of the sensitivity of the marker. There was minimal damage revealed by the histology and function studies, yet there were significant increases in the excretion of hydroxylysine. It appears that hydroxylysine can be indicative of exposure when other parameters are normal. It will require long-term follow-up of exposed rats to determine whether or not the change in marker concentration is predictive of damage. Hydroxylysine may be an excellent marker

Topics: Animals; Biomarkers; Bronchoalveolar Lavage Fluid; Desmosine; Hydroxylysine; Lung Diseases; Male; Nitrogen Dioxide; Peptidyl-Dipeptidase A; Rats; Rats, Inbred F344

It is well recognized that the oxidant gases ozone and nitrogen dioxide cause lung injury at high concentrations and, as such, are considered to be "hazardous" air pollutants. What is not known is the upper limit of their concentration in ambient air that can be tolerated without causing lung injury. This uncertainty is due, in major part, to a lack of sensitive and noninvasive tests that can identify the presence of early lung injury after exposure to oxidant gases. The hypothesis underlying the studies reported in this document was that the changes in cell populations that occur in the lung after oxidant lung injury are due to the local generation of lung-cell-specific growth factors, and that these factors should leak into the blood stream in sufficient quantities to allow their identification. Once identified, such factors could be used as early markers of oxidant injury. The question asked in the design of these studies was: "Is oxidant lung injury associated with the appearance in blood of factors that enhance lung cell growth, as tested in a cultured lung cell bioassay?" Groups of rats were exposed to either 1 ppm ozone, 85 percent oxygen, or air, and samples of plasma, lung washings, and lung tissue were collected at intervals over a two-week period. These samples were tested for their effect on the DNA synthesis of purified populations of three major lung cell types (pneumocyte, fibroblast, and endothelial cell) in culture. The concentrations of the two oxidant gases used in these studies were selected on the basis of their known effect on these cell types in the intact animal. The collected samples were tested either whole or after separation into various fractions, determined by the preference of the sample's constituents for an alkaline or acidic environment. This fractionation procedure was included because simple testing of crude samples may not always reveal the presence of biologically active material because both growth stimulators and growth inhibitors may be present in the same sample. The results from testing whole samples confirm that factors that enhance DNA synthesis by all three lung cell types do appear in blood and lavage after exposure to 1 ppm ozone or 85 percent oxygen. These factors appear to be distinct for each lung cell type, in that the timing of maximal activity in the collected samples differs for each cell type. The time at which they appear in blood bears a close temporal relationship with cellular changes reported to

Topics: Animals; Bronchoalveolar Lavage Fluid; Endothelium; Fibroblasts; Growth Substances; Lung Diseases; Male; Nitrogen Dioxide; Ozone; Phagocytes; Rats

A 52 year-old male farmer was admitted to our hospital because of cough, sputum and dyspnea on exertion. Chest X-ray showed pulmonary edema and arterial blood gas analysis showed hypoxemia. Silo-fillers' disease was diagnosed because he had allegedly inhaled yellowish gas in the silo. The day following steroid therapy, symptoms and pulmonary edema improved. Silo-fillers' disease is chemical pneumonitis due to exposure to the oxides of nitrogen which are produced in silos. Although reported cases of silo-fillers' disease in Japan are rare it should be kept in mind in areas involved with dairy farming.

Topics: Humans; Lung Diseases; Male; Methylprednisolone; Middle Aged; Nitrogen Dioxide; Prednisolone; Silo Filler's Disease

Between 1955 and 1987, 17 patients were examined at the Mayo Clinic shortly after exposure to silo gas. All exposures had occurred in conventional top-unloading silos. Acute lung injury occurred in 11 patients, 1 of whom died; early diffuse alveolar damage with hyaline membranes and hemorrhagic pulmonary edema and acute edema of the airways were found at autopsy. In one patient, hypoxemia and transient obstruction of the airways developed, but no pulmonary infiltrates were noted. One patient had symptoms for 5 weeks and diffuse confluent pulmonary infiltrates; many years later, chronic obstructive pulmonary disease developed (he had, however, been a heavy smoker before exposure). Bronchiolitis obliterans was not observed in the other patients, probably because of less severe exposure or early corticosteroid therapy. Prophylactic corticosteroid therapy is advised for workers who have been exposed to silo gas. The management of patients with established acute lung injury is reviewed. Previously unreported patterns of exposure to silo gas in conventional silos are described, and recommendations for avoiding exposure are suggested.

Topics: Acute Disease; Adolescent; Adrenal Cortex Hormones; Adult; Diagnosis, Differential; Humans; Lung Diseases; Lung Injury; Male; Middle Aged; Minnesota; Nitrogen Dioxide; Silo Filler's Disease

Topics: Adrenal Cortex Hormones; Bronchiolitis Obliterans; Death, Sudden; Humans; Lung Diseases; Male; Nitrogen Dioxide; Pulmonary Edema; Silo Filler's Disease

The sensitivity of different parameters for the determination of lung injury caused by nitrogen dioxide (NO2) was investigated. Male rats were exposed to concentrations of 0, 4, 10 or 25 ppm NO2 for 6 h/day, for 7, 14 or 21 days. Histopathology of the nasal cavity, larynx, trachea and lungs was compared with the changes in macrophage function and morphology. In addition several biochemical parameters were determined in lung lavages. Cytotoxic effects were investigated in primary cultures of rat and bovine alveolar macrophages, exposed to the same NO2-levels as in the in vivo exposure. Treatment-related histopathological changes were observed in the lungs. No differences between exposed and control animals were observed in the nasal cavity, larynx or trachea. The morphology of the lavaged alveolar macrophages was changed at all exposure concentrations on day 7, 14 and 21. An increase in the number of macrophages was found after exposure to 10 and 25 ppm NO2 on days 7, 14 and 21. The phagocytic capacity was diminished after 14 and 21 days exposure to 25 ppm and at both times exposure to 10 and 25 ppm increased the level of gamma-glutamyl transferase (GGT) in lavage fluids. Morphology of the macrophages and levels of GGT were found to be sensitive parameters of nitrogen dioxide toxicity. In vitro exposure of rat and bovine alveolar macrophages to comparable NO2-concentrations induced effects on phagocytosis similar to those observed for macrophages from exposed rats.

Topics: Administration, Inhalation; Alkaline Phosphatase; Animals; Body Weight; Bronchoalveolar Lavage Fluid; Cell Survival; gamma-Glutamyltransferase; L-Lactate Dehydrogenase; Lung Diseases; Macrophages; Male; Nitrogen Dioxide; Phagocytosis; Proteins; Rats; Rats, Inbred Strains

This study examined age-related differences in the physiological responses of rats to inhaled automotive emissions. Previous reports suggested that lung development of animals exposed to oxidant gases early in life might be impaired, or that developing lungs might be more susceptible than adult lungs to inhaled toxicants. There were no previous comparisons in developing and adult lungs of the effects of atmospheres containing particles. The hypothesis tested in this study was that rats exposed to chronically inhaled nitrogen dioxide (NO2) or diesel exhaust during lung development were more susceptible to lung injury than rats that were exposed to these atmospheres as adults. Rats were exposed either throughout the period of lung development or as adults, and health effects in the two groups were compared at the end of exposure. Rats were exposed seven hours per day, five days per week for six months to NO2 at 9.5 ppm, to whole diesel exhaust diluted to a soot concentration of 3.5 mg/m3, or to filtered air as controls. These concentrations were selected to produce mild effects in adults. The younger group (developing) was conceived in the exposure atmospheres and exposed during gestation and through the age of six months, and the older group (adult) was exposed between six and twelve months of age. Health effects were evaluated at the end of six months' exposure and some measurements were repeated six months after the cessation of exposure. Measurements included respiratory function, pulmonary immune responses, lung clearance of radiolabeled particles, airway fluid enzymes, protein and cytology, lung tissue collagen and proteinases, lung burdens of diesel soot, lung morphometry and histopathology. Nitrogen dioxide slightly reduced body weight and altered airway fluid enzymes of both age groups, with a greater number of statistically significant differences detectable in the enzyme levels of animals exposed as adults. Normal lung development, as reflected in the size and functional efficiency at adulthood, was not affected by NO2 in this study. Diesel exhaust altered the airway fluid constituents as well as lung tissue collagen and proteinases of both age groups. Particularly striking was an almost sixfold increase in the percentage of neutrophils, a class of highly phagocytic leukocytes, in the airway fluids of adults after six months of exposure. Exhaust-exposed adults had increased numbers of cells in pulmonary lymph nodes, delayed clearance of both dies

Topics: Administration, Inhalation; Age Factors; Animals; Embryonic and Fetal Development; Lung; Lung Diseases; Male; Nitrogen Dioxide; Rats; Rats, Inbred F344; Respiratory Function Tests; Vehicle Emissions

Nitrogen dioxide (NO2), a major oxidant constituent of vehicle emissions, is toxic to lung cells including endothelial cells. Since NO2 is a reactive free radical, one of the postulated mechanisms of NO2-induced pulmonary injury involves the peroxidation of membrane lipids. Therefore, this study evaluated the dose- and time-dependent effects of nitrogen dioxide exposure by measuring the biochemical and biophysical parameters, as well as the metabolic function, in porcine pulmonary artery and aortic endothelial cells in monolayer cultures. To evaluate the biochemical changes, the antioxidant enzyme GSH-reductase (GSH-red), GSH-peroxidase (GSH-per), and glucose-6-phosphate dehydrogenase (G6PDH) activities, as well as the lipid peroxide formation, glutathione (GSH) content, and lactate dehydrogenase (LDH) release were measured. Biophysical changes were measured by monitoring lipid fluidity in both the hydrophobic and hydrophilic regions of the plasma membrane. The uptake of 5-hydroxytryptamine (5-HT) was measured as a metabolic function of endothelial cells. Confluent porcine pulmonary artery and aortic endothelial cells were exposed to 3 or 5 ppm NO2 or air (control) for 3-24 hours. After 3-, 6-, or 12-hour exposures to 3 or 5 ppm NO2, the GSH-red and G6PDH activities, as well as the lipid peroxide formation and LDH release, were not different from those of controls in both pulmonary artery and aortic endothelial cells. Exposure of the cells to 3 or 5 ppm NO2 for 24 hours resulted in significant increases in GSH-red (p less than 0.05) and G6PDH (p less than 0.001) activities in both cell types. Exposure to 5 ppm NO2 for 24 hours significantly (p less than 0.05) increased lipid peroxide formation and increased (p less than 0.01) LDH release in both the pulmonary artery and aortic endothelial cells. GSH-per activity and GSH content in NO2-exposed pulmonary artery and aortic endothelial cells were not different from those of controls, irrespective of NO2 concentration and exposure time. Fluorescence spectroscopy was used to measure the membrane lipid fluidity. Membrane fluidity in the hydrophobic region was measured by 1,6-diphenyl-1, 3, 5-hexatriene (DPH), an aromatic hydrocarbon that partitions into the hydrophobic interior of the lipid bilayer.(ABSTRACT TRUNCATED AT 400 WORDS)

Topics: Animals; Aorta, Thoracic; Endothelium, Vascular; Glucosephosphate Dehydrogenase; Glutathione Peroxidase; Glutathione Reductase; Lung Diseases; Nitrogen Dioxide; Pulmonary Artery; Swine; Vehicle Emissions

Topics: Adult; Air Pollutants; Animals; Carbon Monoxide; Child; Formaldehyde; Humans; Lung Diseases; Nitrogen Dioxide; Ozone; Radon; Sulfur Dioxide

The pulmonary function of eight men and eight women (51 to 76 years of age), all non-smokers, was measured before and after 2-hr exposures to filtered air (FA) and 0.60 ppm nitrogen dioxide (NO2). The subjects alternated 20-min periods of rest and 20-min periods of cycle ergometer exercise at a work load predetermined to elicit a ventilatory minute volume (VE) of approximately 25 liter/min. Functional residual capacity was determined pre- and postexposure. Forced vital capacity was determined preexposure and 5 min after each exercise period. VE was measured during the last 2 min of each exercise period, and heart rate was monitored throughout each exposure. The pulmonary function data were evaluated as the percentage change from pre- to postexposure to partially remove the effect of differences between men and women in absolute lung volume. There were no statistically significant (P greater than 0.05) differences between the responses of men and women to FA or NO2 exposure. There were no significant (P greater than 0.05) changes in any variable consequent to FA or NO2 exposure. Our older subjects had responses to NO2 exposure similar to those of young adults, suggesting that, at least for healthy people, exposure to 0.60 ppm NO2 has little effect.

Topics: Aged; Female; Forced Expiratory Flow Rates; Forced Expiratory Volume; Humans; Lung; Lung Diseases; Male; Middle Aged; Nitrogen Dioxide; Physical Exertion; Vital Capacity

Short-time exposure to air pollutants and in particular to sulfur dioxide, nitrogen oxides and photochemical oxidants may cause respiratory symptoms similar to acute bronchial asthma. In healthy adults however the concentrations required to evoke significant bronchial obstruction lie still above the level of atmospheric air pollution usually observed in our country. In contrast patients with preexisting pulmonary diseases or with impaired bronchopulmonary defense mechanisms may show harmful reactions even at concentrations which actually occur in urban and rural atmospheres. In addition there is evidence of on increased prevalence of chronic obstructive pulmonary diseases in countries with high chemical pollution indicating that long-term exposure of ambient air pollution may cause chronic illness as well. Since air pollution is accepted to produce adverse health effects, emergent efforts are required to improve air quality in order to avoid further injuries in man.

Topics: Adult; Aged; Air Pollutants; Asthma; Bronchitis; Humans; Lung Diseases; Lung Diseases, Obstructive; Middle Aged; Nitric Oxide; Nitrogen Dioxide; Ozone; Risk; Smoking; Sulfur Dioxide; Switzerland

A study of the response of rat and hamster to nitrogen dioxide (NO2) under identical conditions has been undertaken. Exposure to 20 parts/IO6 NO2 for 24 h produced a mild cytotoxic effect on the terminal bronchiole and proximal alveoli in the rat, whereas the hamster developed a moderate to severe bronchiolitis and alveolitis. Electron microscopic examination of tissue sections showed accumulation of surfactant in lamellar bodies of the alveolar type II cell in the rat but not in the hamster, whereas in the hamster Clara cells were observed in mitosis. Increased levels of surfactant isolated from whole lung homogenates by sucrose gradient centrifugation were found in both rat and hamster. In contrast surfactant isolated from bronchiolo-alveolar lavage was increased only in the hamster. The results suggest that caution must be exercised in the choice of animal model in investigations aimed at the understanding of the toxicological effects of nitrogen dioxide in man.

Topics: Animals; Bronchi; Bronchitis; Cricetinae; Cytoplasm; Female; Leukocyte Count; Lung; Lung Diseases; Macrophages; Microscopy, Electron; Nitrogen Dioxide; Pulmonary Surfactants; Rats; Rats, Inbred Strains

Topics: Adrenal Cortex Hormones; Adult; Humans; Lung Diseases; Male; Nitrogen Dioxide; Respiratory Insufficiency; Silo Filler's Disease

Fire fighters' respiratory organs, circulatory system and muscular system are often exposed to considerable risks. In fact in addition to the most obvious external stress causes (heat, humidity, O2 decrement, CO2 increment, emotional stress) these workers use heavy equipments and carry people or things. Furthermore always present is the risk of poisoning by inhalation of toxic combustion gas of the fire atmosphere.

Topics: Acrolein; Adult; Burns, Inhalation; Carbon Dioxide; Carbon Monoxide; Cardiovascular Diseases; Cyanides; Fires; Humans; Hydrochloric Acid; Hydrogen Cyanide; Lung Diseases; Male; Middle Aged; Nitrogen Dioxide; Occupational Diseases; Smoke; Stress, Psychological

The histopathology of rat lung after exposure to high concentrations of mixed oxides of nitrogen (NOx) has been studied. Considerable damage was observed, which initially took the form of 'thickening' and 'blebbing' of the alveolar epithelium and disruption of type II pneumocytes. These early changes were attributed to the direct effect of the oxidant action of NOx. There then followed a latent period of approximately 6 h after which the development of oedema of the interstitium and alveolar septum was observed. Clinical observations and the results from light and electron microscopical examination suggested that the lung damage caused by exposure to 518 parts/10(6) NOx for 5 min was greater than that caused by 1435 parts/10(6) for 1 min. This was not supported by the findings from light microscopy where similar damage was observed at both dose levels. These results suggest that such exposures might pose a risk of lung damage to man.

Topics: Animals; Dose-Response Relationship, Drug; Lung; Lung Diseases; Male; Microscopy, Electron; Nitric Oxide; Nitrogen Dioxide; Nitrogen Oxides; Pulmonary Edema; Rats; Rats, Inbred Strains

Topics: Adult; Humans; Lung Diseases; Male; Nitrogen Dioxide

The pulmonary effects of NO2 were investigated in two animal species. Rats and guinea pigs aged from 5 to 60 days or more were exposed for 3 days either to 2 ppm or to 10 ppm NO2. Lung histology or superoxide dismutase (SOD) determination in alveolar macrophages was assessed in air and NO2-exposed animals. Results demonstrated that the lung histological alterations are different for both NO2-exposed species. Rats were more tolerant than guinea pigs, but rat and guinea pig newborns were less affected than adults. The enzyme response to NO2 exposure was similar in both species and a decrease in SOD activity was noted in animals of all ages. These observations support the conclusion that NO2 exposure leads to increased lung damage during the life span, but on the contrary, exposure to oxygen does not involve SOD induction. This suggests that the defense mechanisms against NO2 are different from those of O2.

Topics: Animals; Animals, Newborn; Guinea Pigs; Lung; Lung Diseases; Nitrogen Dioxide; Rats; Rats, Inbred Strains; Superoxide Dismutase

Topics: Adult; Drug Contamination; Humans; Lung Diseases; Male; Nitrogen Dioxide; Nitrous Oxide; Substance-Related Disorders

Topics: Age Factors; Animals; Biometry; Dose-Response Relationship, Drug; Female; Lung Diseases; Lung Volume Measurements; Microscopy, Electron; Nitrogen Dioxide; Pulmonary Alveoli; Rats

Topics: Animals; Antioxidants; Body Weight; Diet; DNA; Lipid Metabolism; Lung; Lung Diseases; Nitrogen Dioxide; Organ Size; Proteins; Rats; Rats, Inbred Strains; Vitamin E

Topics: Adult; Air Pollutants; Animals; Child; Environmental Exposure; Female; Humans; Infant, Newborn; Lung; Lung Diseases; Male; Nitric Oxide; Nitrogen Dioxide; Nitrogen Oxides; Rats; Risk

We studied the reparative process after inhalation exposure to 20 ppm of nitrogen dioxide (NO2) in the lungs of hemizygous blotchy male (Blo/g) and heterozygous blotchy female (Bio/+) mice. Age-matched siblings (C3Hf) without the blotchy gene at X-chromosome locus (+/y) and +/+) served as control animals. After exposure to NO2 for 28 days, there was a marked progression in the extent of emphysema in Blo/y mice associated with a significant decrease of internal surface area (p < 0.05) and an increase in the mean linear intercept (p < 0.005). In contrast, +/y, Blo/+, and +/+ mice showed mild airspace enlargement without decrease in internal surface area after similar exposures. Blo/y mice killed 1 month after cessation of NO2 exposure showed a persistent, mild chronic bronchiolitis that was more frequent and of greater severity than that present in control +/y mice. Alveolar macrophages in the Blo/y mice were larger than those in +/y, +/+, and Blo/+ mice both before and after exposure to NO2. Crystalloid inclusions were observed in the enlarged alveolar macrophages of the Blo/g mice only after exposure to NO2, but were not seen in control animals. These observations indicate that the pattern of lung injury and repair after subacute exposure to 20 ppm of NO2 in the Blo/y mouse differs from that present in age-matched siblings in that inherited abnormalities in alveolar macrophage function may exist in addition to the previously described alterations in connective tissue proteins. Both of these alterations may influence the development of emphysema in the blotchy male mouse.

Topics: Animals; Collagen Diseases; Female; Lung; Lung Diseases; Lung Volume Measurements; Macrophages; Male; Mice; Mice, Mutant Strains; Nitrogen Dioxide; Protein-Lysine 6-Oxidase; Pulmonary Alveoli; Pulmonary Emphysema

Topics: Accidents; Arizona; Humans; Lung Diseases; Military Medicine; Nitrogen Dioxide; Silo Filler's Disease; United States

Topics: Acid Phosphatase; Animals; Cricetinae; Female; Fructose-Bisphosphate Aldolase; L-Lactate Dehydrogenase; Leukocytes; Lipid Peroxides; Lung Diseases; Male; Mesocricetus; Nitrogen Dioxide; Oxygen Consumption

Topics: Animals; Antibody-Producing Cells; Colloids; Erythrocytes; Lung; Lung Compliance; Lung Diseases; Male; Nitrogen Dioxide; Rats; Sheep

Topics: Animals; Blood Cell Count; Dogs; Lung Diseases; Nitrogen Dioxide; Pulmonary Diffusing Capacity; Pulmonary Edema; Ventilation-Perfusion Ratio

Serial physiologic studies were performed to characterize both the immediate and delayed effects of a single occupational exposure to nitrogen dioxide in a nonsmoker. During the initial acute stage of pulmonary edema, the abnormal static pressure-volume curve and decreased static compliance corresponded to a reduction in pulmonary volume. During the delayed acute stage, elastic recoil and properties of resistance to flow were normal, but dynamic compliance was reduced and dependent on respiratory frequency, and oxygen transport was abnormal during exercise, which is consistent with dysfunction of the small airways.

Topics: Forced Expiratory Flow Rates; Forced Expiratory Volume; Humans; Lung Diseases; Male; Middle Aged; Nitrogen Dioxide; Occupational Diseases; Pulmonary Edema; Respiration Disorders; Total Lung Capacity; Vital Capacity

Twenty-three patients exposed to nitrogen dioxide in agriculture or industry were referred to the University of Wisconsin Medical Center. Eighteen experienced a transient upper respiratory tract syndrome; five developed pulmonary edema or bronchiolitis obliterans. This latter group responded to steroid therapy but all demonstrated evidence of persistent pulmonary dysfunction on follow-up studies. Combining our findings with those in the literature we concluded: (1) exposure to NO2 is more common than generally appreciated; (2) case fatality is high--29% for silo-filler's disease; (3) steroids are effective therapy and should be continued for at least eight weeks; (4) although the majority recover without significant sequelae, some individuals may develop persistent functional abnormalities; (5) there is no evidence that long-term exposure to low concentrations of NO2 leads to chronic airway obstruction; and, (6) NO2-induced pulmonary disease could be elminated with appropriate preventive measures.

Topics: Adult; Female; Humans; Lung Diseases; Male; Middle Aged; Nitrogen Dioxide; Occupational Diseases; Pneumonia; Prednisone; Pulmonary Edema; Radiography; Syndrome

The ultrastructural morphogenesis of pulmonary lesions was studied in cats exposed to either aerosols of feline calicivirus (FCV) or high concentrations of NO2. Both directly injured alveolar lining cells, particularly type I cells. Necrosis of pneumocytes attended by an acute exudative response in the air exchange tissues was evident from 0 through 24 hours after exposure of cats to NO2 and from 12 through 96 hours after infection with FCV. The reparative process following alveolar injury was characterized by regenerative hyperplasia of type II pneumocytes, proliferation of stromal cells, and infiltration of mononuclear cells. Differences in the lesions produced by NO2 and FCV also were encountered. Endothelial necrosis was detected only after NO2 injury, whereas a marked infiltration of neutrophils and immunocytes was observed only after FCV injury. The FCV/NO2 experimental system in cats is well suited for studies of diffuse alveolar damage of toxic and viral etiology.

Topics: Animals; Bronchi; Caliciviridae; Cats; Inflammation; Lung Diseases; Necrosis; Nitrogen Dioxide; Pulmonary Alveoli; Virus Diseases

Following exposure to an aerosol of 0.1% (.005 M) cadmium chloride, rat lungs were examined at 6 hours and 1, 2, 3, 4, 7, and 10 days. By light microscopy, damage was multifocal and centered about respiratory bronchioles. Ultrastructurally, there was Type 1 cell edema with frequent loss of surface plasma membranes during the first 24 hours. After 2 days, the number of Type 2 cells had markedly increased, and by 3 days the damaged alveoli were lined by plump cuboidal cells closely resembling Type 2 cells. By 4 days, these cells were flatter, the change being more marked by 7 days; by 10 days, the cells had regained the appearance of Type 1 cells through loss of osmiophilic bodies and superficial microvilli. We conclude that CdCl2 damages Type 1 cells, which are then replaced by proliferation of Type 2 cells. These cells lose their osmiophilic bodies and flatten out to replace the lost Type 1 cells, the process being almost complete by 10 days after the injury. This pattern resembles the injury caused by NO2, O3, and O2.

Topics: Aerosols; Animals; Cadmium; Epithelial Cells; Epithelium; Lung; Lung Diseases; Male; Nitrogen Dioxide; Oxygen; Ozone; Pulmonary Alveoli; Rats; Time Factors

Nitrogen dioxide poisoning was experimentally produced in dogs. PO2, PCO2 and pH were measured in poisoned animals and during treatment with hyperbaric oxygen (OHP) lung lesions in both groups were evaluated. It is concluded that OHP has a deleterious effect both in terms of mortality and pathological changes.

Topics: Animals; Carbon Dioxide; Dogs; Hydrogen-Ion Concentration; Hyperbaric Oxygenation; Lung Diseases; Nitrogen Dioxide; Oxygen

The effects of oxides of nitrogen inhalation are reported in a 21-year-old gardener exposed to silage gas. Initial nausea, cough and fever remitted, but respiratory failure developed 3 weeks later. Roentgenograms and lung function studies revealed pulmonary edema, volume restriction, and severely impaired gas exchange. Needle biopsy showed a nonspecific interstitial pneumonia. With steroid therapy all functional parameters except diffusing capacity returned to normal. Failure to inquire about non-occupational activities led to delayed diagnosis. A brief review of toxic effects of nitrogen oxides is presented.

Topics: Adrenal Cortex Hormones; Adult; Biopsy, Needle; Humans; Lung Diseases; Male; Nitrogen Dioxide; Radiography; Respiratory Function Tests; Silo Filler's Disease

Topics: Animals; Lung; Lung Diseases; Mice; Nitrogen Dioxide; Ozone

Topics: Accidents, Occupational; Adult; Follow-Up Studies; Humans; Lung Diseases; Male; Middle Aged; Nitrogen Dioxide; Phosgene; Poisoning; Pulmonary Edema; Respiratory Function Tests; Switzerland

Topics: Animals; Blood Cell Count; Body Weight; Carbon Monoxide; Dogs; Drug Synergism; Environmental Exposure; Female; Heart; Hemoglobinometry; Kidney; Lung; Lung Diseases; Nitrogen Dioxide; Organ Size; Pulmonary Diffusing Capacity; Respiratory Function Tests; Sulfur Dioxide; Sulfuric Acids; Time Factors

Topics: Animals; Bacteriolysis; Environmental Exposure; Lung; Lung Diseases; Male; Mice; Nitrogen Dioxide; Phosphorus Isotopes; Staphylococcal Infections; Staphylococcus; Time Factors

Topics: Animals; BCG Vaccine; Cell Migration Inhibition; Immunity, Cellular; Injections, Intravenous; Lung; Lung Diseases; Lymphocyte Activation; Macrophages; Nitrogen Dioxide; Occupational Medicine; Phagocytosis; Pulmonary Alveoli; Rabbits; Tuberculin Test

Topics: Aged; Agricultural Workers' Diseases; Blood; Carbon Dioxide; Chronic Disease; Follow-Up Studies; Humans; Hydrogen-Ion Concentration; Lung Diseases; Male; Middle Aged; Nitrogen Dioxide; Oxygen; Prednisone; Prognosis; Pulmonary Diffusing Capacity; Radiography; Silo Filler's Disease; Spirometry; Vital Capacity

Topics: Adult; Alloys; Animals; Bronchial Diseases; Environmental Exposure; Esterases; Humans; Lung Diseases; Male; Middle Aged; Nitrogen Dioxide; Occupational Diseases; Ozone; Trypsin Inhibitors; Welding

Topics: Adolescent; Agricultural Workers' Diseases; Denmark; Diagnosis, Differential; Farmer's Lung; Humans; Lung Diseases; Male; Nitrogen Dioxide; Silage; Silo Filler's Disease

Topics: Animals; Bronchitis; Chronic Disease; Cricetinae; Disease Models, Animal; Lung; Lung Diseases; Nitrogen Dioxide; Papain; Pneumonia; Pulmonary Emphysema; Respiratory Tract Diseases; Trachea

Topics: Agricultural Workers' Diseases; Fermentation; Humans; Lung Diseases; Male; Nitrogen Dioxide; Pulmonary Edema; Silage

Topics: Adult; Age Factors; Air Pollution; California; Environment, Controlled; Environmental Exposure; Environmental Health; Female; Histamine; Humans; Lung Diseases; Lung Diseases, Obstructive; Male; Middle Aged; Nitrogen Dioxide; Occupational Diseases; Sex Factors; Smoking; Sputum; Styrenes; Toluene; Urban Population

Topics: Air Pollution; Animals; Antioxidants; Chemical Phenomena; Chemistry; Fatty Acids; Linoleic Acids; Lung; Lung Diseases; Male; Nitrogen Dioxide; Oxidation-Reduction; Ozone; Rats; Vitamin E

Topics: Adult; Agricultural Workers' Diseases; Humans; Humidity; Lung Diseases; Male; Middle Aged; Nitrogen Dioxide; Poaceae; Silo Filler's Disease; Soil

Topics: Animals; Guinea Pigs; Hyperplasia; Lipids; Lung; Lung Diseases; Male; Methods; Microscopy, Electron; Nitrogen Dioxide; Pulmonary Alveoli

Topics: Animals; Basement Membrane; Bronchi; Collagen; Connective Tissue; Elastic Tissue; Fibroblasts; Lung; Lung Diseases; Microscopy, Electron; Muscle, Smooth; Nitrogen Dioxide; Pulmonary Alveoli; Rats

Topics: Adult; Agricultural Workers' Diseases; Airway Resistance; Bronchial Diseases; Carbon Dioxide; Follow-Up Studies; Humans; Hydrogen-Ion Concentration; Leukocytosis; Lung Compliance; Lung Diseases; Male; Nitrogen Dioxide; Oxygen; Pulmonary Edema; Radiography; Respiratory Function Tests; Silo Filler's Disease; Spirometry

Topics: Adrenal Glands; Adrenalectomy; Animals; Asphyxia; Bronchi; Carbon Dioxide; Cold Temperature; Dogs; Edema; Environmental Exposure; Female; Guinea Pigs; Lung; Lung Diseases; Male; Mice; Nitrogen Dioxide; Physical Exertion; Pneumonia; Pulmonary Alveoli; Rabbits; Rats; Species Specificity; Stress, Physiological

Topics: Air Pollution; Animals; Environmental Exposure; Humans; Lung Diseases; Nitrogen Dioxide; Occupational Diseases

Topics: Aerosols; Animals; Coal Mining; Collagen; Dust; Environmental Exposure; Gas Poisoning; Lung; Lung Diseases; Microscopy, Electron; Nitrogen Dioxide; Pneumoconiosis; Rats; Time Factors

Topics: Accidents; Adolescent; Cellulose; Female; Fires; Gas Poisoning; Glucocorticoids; Humans; Lung; Lung Diseases; Nitrogen Dioxide

Topics: Adolescent; Cellulose; Cerebral Palsy; Female; Fires; Gas Poisoning; Humans; Lung; Lung Diseases; Models, Structural; Nitro Compounds; Nitrogen; Nitrogen Dioxide; Nitrogen Oxides; Peroxides; Radiography, Thoracic

Topics: Aging; Animals; Body Weight; Bronchi; Elastic Tissue; Lung Diseases; Nitrogen Dioxide; Organ Size; Pulmonary Alveoli; Pulmonary Fibrosis; Rats; Staining and Labeling; Time Factors

Topics: Air Pollution; Animals; Environmental Exposure; Lung; Lung Diseases; Nitrogen Dioxide; Pulmonary Emphysema; Rats

Topics: Animals; Edema; Emphysema; Histological Techniques; Lung; Lung Diseases; Nitrogen Dioxide; Organ Size; Pulmonary Alveoli; Rats; Smoking

Topics: Agricultural Workers' Diseases; Carbon Monoxide; Carbon Monoxide Poisoning; Chromatography, Gas; Humans; Lung Diseases; Nitrogen Dioxide; Silo Filler's Disease

Topics: Animals; Body Weight; Bronchi; Environmental Exposure; Lung; Lung Diseases; Microscopy, Electron; Nitrogen Dioxide; Organ Size; Rats; Respiration

Topics: Animals; Bronchopneumonia; Dogs; Hemorrhage; Lung Diseases; Mucous Membrane; Nitric Oxide; Nitrogen Dioxide; Pulmonary Alveoli; Pulmonary Edema

Topics: Animals; Cattle; Cattle Diseases; Lung Diseases; Nitrogen Dioxide; Rumen

Topics: Air Pollution; Animals; Cytoplasmic Granules; Lung; Lung Diseases; Mast Cells; Nitrogen Dioxide; Rats

Topics: Adult; Aged; Anesthesia, Inhalation; Barbiturates; Bronchial Neoplasms; Catecholamines; Flavoring Agents; Halothane; Humans; Lung Diseases; Male; Mandelic Acids; Middle Aged; Neuroleptanalgesia; Nitrogen Dioxide; Pneumonectomy

Topics: Aerosols; Animals; Carbon; Drug Synergism; Environmental Exposure; Female; Guinea Pigs; Lung; Lung Diseases; Male; Nitrogen Dioxide; Phagocytosis

Topics: Animals; Cattle; Cattle Diseases; Lung Diseases; Nitrogen Dioxide

Topics: Adult; Agricultural Workers' Diseases; Humans; Lung Diseases; Male; Nitrogen Dioxide; Radiography

Topics: Agricultural Workers' Diseases; Ambroxol; Dust; Farmer's Lung; Gas Poisoning; Humans; Hypersensitivity; Lung Diseases; Nitrogen; Nitrogen Dioxide; Oxygen Inhalation Therapy; Oxytetracycline; Pathology; Penicillins; Pneumonia; Radiography, Thoracic; Silo Filler's Disease; Toxicology; Tuberculin Test

Topics: Air Pollution; Animals; Bronchial Diseases; Bronchitis; Bronchopneumonia; Dogs; Guinea Pigs; Lung; Lung Diseases; Mice; Nitrogen Dioxide; Pathology; Poisoning; Pulmonary Edema; Pulmonary Fibrosis; Rabbits; Rats; Research; Toxicology; Tracheitis

Topics: Humans; Lung Diseases; Nitrogen Dioxide; Nitrous Oxide; Occupational Diseases; Pneumonia; Silo Filler's Disease