Vehicle Emissions
Motor Vehicles
Air Pollutants
Air Pollution
Pharmaceutical Vehicles
Positron-Emission Tomography
Otoacoustic Emissions, Spontaneous
Arizona
Environmental Illness
Diesel exhaust particles are taken up by human airway epithelial cells in vitro and alter cytokine production. (1/958)
The involvement of diesel exhaust particles (DEPs) in respiratory diseases was evaluated by studying their effects on two in vitro models of human airway epithelial cells. The cytotoxicity of DEPs, their phagocytosis, and the resulting immune response were investigated in a human bronchial epithelial cell line (16HBE14o-) as well as in human nasal epithelial cells in primary culture. DEP exposure induced a time- and dose-dependent membrane damage. Transmission electron microscopy showed that DEPs underwent endocytosis by epithelial cells and translocated through the epithelial cell sheet. Flow cytometric measurements allowed establishment of the time and dose dependency of this phagocytosis and its nonspecificity with different particles (DEPs, carbon black, and latex particles). DEPs also induced a time-dependent increase in interleukin-8, granulocyte-macrophage colony-stimulating factor, and interleukin-1beta release. This inflammatory response occurred later than phagocytosis, and its extent seems to depend on the content of adsorbed organic compounds because carbon black had no effect on cytokine release. Furthermore, exhaust gas posttreatments, which diminished the adsorbed organic compounds, reduced the DEP-induced increase in granulocyte-macrophage colony-stimulating factor release. These results suggest that DEPs could 1) be phagocytosed by airway epithelial cells and 2) induce a specific inflammatory response. (+info)Diesel exhaust particles induce NF-kappa B activation in human bronchial epithelial cells in vitro: importance in cytokine transcription. (2/958)
Fine particles derived from diesel engines (diesel exhaust particles, DEP) have attracted attention, since their density in industrial countries seems related to the increased prevalence of pulmonary diseases. Previous studies have suggested that DEP have a potential to directly activate airway epithelial cells to produce and release inflammatory cytokines and mediators, and thus facilitate inflammatory responses in the lung. To elucidate the molecular mechanisms of their action, we studied here IL-8 gene expression, one of the important cytokines in inflammatory responses, by Northern blot analysis and run-on transcription assay. Suspended DEP (1-50 microgram/ml) increased the steady state levels of IL-8 mRNA, which was suggested to be largely due to increased transcriptional rates. Electrophoretic mobility shift assay demonstrated that DEP induced increased binding to the specific motif of NF-kappa B, but not of transcription factor AP-1. The luciferase reporter gene assay using wild-type and mutated NF-kappa B-binding sequences showed that DEP-induced NF-kappa B activation was involved in IL-8 transcription. Finally, both N-acetylcysteine and pyrrolidine dithiocarbamate attenuated the action of DEP on IL-8 mRNA expression, suggesting that oxidant-mediated pathway might be involved in its processes. These results suggested that DEP activate NF-kappa B, which might be an important mechanism of its potential to increase the expression of inflammatory cytokines in vitro. (+info)Inhalation of diesel engine exhaust affects spermatogenesis in growing male rats. (3/958)
We conducted experiments to determine whether diesel engine exhaust affects reproductive endocrine function in growing rats. The rats were assigned to three groups: a group exposed to total diesel engine exhaust containing 5.63 mg/m3 particulate matter, 4.10 ppm nitrogen dioxide, and 8.10 ppm nitrogen oxide; a group exposed to filtered exhaust without particulate matter; and a group exposed to clean air. Dosing experiments were performed for 3 months beginning at birth (6 hr/day for 5 days/week). Serum levels of testosterone and estradiol were significantly higher in animals exposed to total diesel exhaust and filtered exhaust (p < 0.05 for each group) as compared to the controls. Follicle-stimulating hormone was significantly decreased in the two groups exposed to diesel exhaust as compared to the control group (p < 0.05). Luteinizing hormone was significantly decreased in the total exhaust-exposed group as compared to the control and filtered groups (p < 0.05). Although testis weight did not show any significant difference among the groups, sperm production and activity of testicular hyaluronidase were significantly reduced in both exhaust-exposed groups as compared to the control group. Histological examination showed decreased numbers of step 18 and 19 spermatids in stage VI, VII, and VIII tubules in the testes of both diesel exhaust-exposed groups. This study suggests that diesel exhaust stimulates hormonal secretion of the adrenal cortex, depresses gonadotropin-releasing-hormone, and inhibits spermatogenesis in rats. Because these effects were not inhibited by filtration, the gaseous phase of the exhaust appears to be more responsible than particulate matter for disrupting the endocrine system. (+info)Diesel exhaust exposure among adolescents in Harlem: a community-driven study. (4/958)
OBJECTIVES: This study sought individual-level data on diesel exhaust exposure and lung function among adolescents in Harlem as part of a community-driven research agenda. METHODS: High school students administered in-person surveys to seventh grade students to ascertain information on demographics, asthma history, and self-reported and maternal smoking. Urine samples were assayed for 1-hydroxypyrene (1-HP), a marker of diesel exhaust exposure, and cotinine, a marker of tobacco smoke exposure. Computer-assisted spirometry was used to measure lung function. RESULTS: Three quarters (76%) of the participating students had detectable levels of 1-HP. Three students (13%) had an FEF25-75 of less than or equal to 80% of their predicted measurements, and 4 students (17%) had results between 80% and 90% of the predicted value, all of which are suggestive of possible lung impairment. CONCLUSIONS: These data suggest that most adolescents in Harlem are exposed to detectable levels of diesel exhaust, a known exacerbator and possible cause of chronic lung disorders such as asthma. Community-driven research initiatives are important for empowering communities to make needed changes to improve their environments and health. (+info)Occupational exposure to diesel exhaust and lung cancer: a meta-analysis. (5/958)
OBJECTIVES: We undertook a meta-analysis of epidemiological studies investigating the relationship between occupational diesel exhaust exposure and lung cancer. METHODS: Thirty of 47 studies initially identified as potentially relevant met specified inclusion criteria. We extracted or calculated 39 independent estimates of relative risk and derived pooled estimates of risk for all studies and for numerous study subsets by using a random-effects model. We also examined interstudy heterogeneity by using linear metaregressions. RESULTS: There was substantial heterogeneity in the pooled risk estimates for all studies combined and for most subsets. Several factors consistent with higher study quality, however, contributed to increased pooled estimates of risk and lower heterogeneity, including (1) adjustment for confounding by cigarette smoking and other covariates, (2) having a lower likelihood of selection bias, and (3) having increased study power. CONCLUSION: This analysis provides quantitative support for prior qualitative reviews that have ascribed an etiologic role to occupational diesel exhaust exposure in lung cancer induction. Among study populations most likely to have had substantial exposure to diesel exhaust, the pooled smoking-adjusted relative risk was 1.47 (95% confidence interval = 1.29, 1.67). (+info)Enhancement of collagen-induced arthritis in mice by diesel exhaust particles. (6/958)
The present study was undertaken to investigate the effect of diesel exhaust particles (DEP) on collagen-induced arthritis (CIA), which is an experimental model of autoimmune disease, in mice. CIA was induced by s.c. injection of type II collagen (CII) emulsified with complete Freund's adjuvant into the base of the tail (day 0) followed by a booster injection on day 21. Varying doses of DEP were intranasally administered every 2 days from days 0 to 20. The results showed that administration of DEP enhanced both the incidence and the severity of CIA. The enhancement of the disease was associated with pronounced production of anti-CII IgG and IgG2a antibodies. Treatment with DEP also augmented proliferative responses of spleen cells to CII. There was marked secretion of interferon-gamma, interleukin (IL)-2, and IL-4 from the lymphoid cells in DEP-treated mice. Administration of DEP after onset of CIA was also effective in enhancing the severity of the disease as well as production of anti-CII IgG and IgG2a antibodies and secretion of interferon-gamma, IL-2, and IL-4. These results suggest that exposure to DEP may influence autoimmune disease. (+info)Changes in levels of 8-hydroxyguanine in DNA, its repair and OGG1 mRNA in rat lungs after intratracheal administration of diesel exhaust particles. (7/958)
Diesel exhaust particles (DEP), an environmental pollutant, are known to induce lung cancer in experimental animals. To clarify whether reactive oxygen species (ROS) are involved in its carcinogenic mechanism, we examined the levels of 8-hydroxyguanine (8-OH-Gua), its total repair and the repair enzyme OGG1 mRNA in female Fischer 344 rat lungs, as markers of the response to ROS, after DEP was intratracheally instilled. The 8-OH-Gua levels in both DEP-treated groups (2 and 4 mg) were increased during the 2-8 h following exposure to DEP. The 8-OH-Gua repair activities in the DEP-treated groups decreased during the period from 2 h to 2 days following DEP exposure and then recovered to the level of the control group at 5 days after exposure. OGG1 mRNA was induced in rats treated with 4 mg DEP for 5-7 days after administration. In conclusion, the 8-OH-Gua level in rat lung DNA increases markedly at an early phase after DEP exposure, by the generation of ROS and the inhibition of 8-OH-Gua repair activity, and induction of OGG1 mRNA is also a good marker of cellular oxidative stress during carcinogenesis. (+info)Generation of reactive oxygen species and 8-hydroxy-2'-deoxyguanosine formation from diesel exhaust particle components in L1210 cells. (8/958)
The generation of the reactive oxygen species during the interaction of diesel exhaust particles (DEP) with NADPH-cytochrome P450 reductase (P450 reductase) was investigated by electron spin resonance using the spin-trap 5,5'-dimethyl-1-pyrroline-N-oxide (DMPO). Addition of DEP extract to an incubation mixture of mouse lung microsomes in the presence of NADPH resulted in a time-dependent NADPH oxidation and acetylated-cytochrome c reduction. Using purified P450 reductase as the enzyme source, superoxide radicals which were detected as the spin adduct (DMPO-OOH) while metabolized by P450 reductase were dependent upon both DEP and enzyme concentrations. The ELISA method using a specific monoclonal antibody revealed that DEP produced 8-hydroxy-2'-deoxyguanosine (8-OHdG), which is formed from deoxyguanosine in DNA by hydroxyl radicals, in the culture medium of L1210 cells. Active oxygen scavengers such as superoxide dismutase and catalase effectively blocked the formation of 8-OHdG in culture medium, and deferoxamine, which inhibits hydroxyl radicals production by chelating iron, was also effective in inhibiting the DEP-produced 8-OHdG formation. These results indicate that DEP components produce 8-OHdG through the hydroxyl radical formation via superoxide by redox cycling of P450 reductase. (+info)'Vehicle Emissions' is not a term typically used in medical definitions. However, in a broader context, it refers to the gases and particles released into the atmosphere by vehicles such as cars, trucks, buses, and airplanes. The main pollutants found in vehicle emissions include carbon monoxide (CO), nitrogen oxides (NOx), particulate matter (PM), and volatile organic compounds (VOCs). Exposure to these pollutants can have negative health effects, including respiratory symptoms, cardiovascular disease, and cancer. Therefore, vehicle emissions are a significant public health concern.
I'm sorry for any confusion, but "Motor Vehicles" is not a term that typically has a medical definition. It is a general term used to describe vehicles that are powered by a motor or engine and are designed for land transportation. This would include cars, trucks, motorcycles, buses, and other similar types of vehicles.
However, in a legal context, a "motor vehicle" may have a specific definition that varies by jurisdiction. For example, in some places, the definition might only include vehicles that are intended for use on public roads, excluding things like golf carts or construction equipment.
If you're looking for a medical term related to motor vehicles, there are many that could apply, such as "motor vehicle accident," "whiplash injury," or "traumatic brain injury due to motor vehicle collision." But the term "motor vehicles" itself does not have a specific medical definition.
Air pollutants are substances or mixtures of substances present in the air that can have negative effects on human health, the environment, and climate. These pollutants can come from a variety of sources, including industrial processes, transportation, residential heating and cooking, agricultural activities, and natural events. Some common examples of air pollutants include particulate matter, nitrogen dioxide, sulfur dioxide, ozone, carbon monoxide, and volatile organic compounds (VOCs).
Air pollutants can cause a range of health effects, from respiratory irritation and coughing to more serious conditions such as bronchitis, asthma, and cancer. They can also contribute to climate change by reacting with other chemicals in the atmosphere to form harmful ground-level ozone and by directly absorbing or scattering sunlight, which can affect temperature and precipitation patterns.
Air quality standards and regulations have been established to limit the amount of air pollutants that can be released into the environment, and efforts are ongoing to reduce emissions and improve air quality worldwide.
Air pollution is defined as the contamination of air due to the presence of substances or harmful elements that exceed the acceptable limits. These pollutants can be in the form of solid particles, liquid droplets, gases, or a combination of these. They can be released from various sources, including industrial processes, vehicle emissions, burning of fossil fuels, and natural events like volcanic eruptions.
Exposure to air pollution can have significant impacts on human health, contributing to respiratory diseases, cardiovascular issues, and even premature death. It can also harm the environment, damaging crops, forests, and wildlife populations. Stringent regulations and measures are necessary to control and reduce air pollution levels, thereby protecting public health and the environment.
"Pharmaceutical vehicles" is not a standard term in medical or pharmaceutical sciences. However, I can provide some context based on the phrase's possible meaning. If by "pharmaceutical vehicles," you mean the carriers or delivery systems for drugs or medications, then the definition would be:
Pharmaceutical vehicles refer to various formulations, preparations, or technologies that facilitate and control the administration of a drug or therapeutic agent to its target site in the body. These can include different types of drug delivery systems such as tablets, capsules, liposomes, nanoparticles, transdermal patches, inhalers, injectables, and other innovative drug carrier technologies.
These pharmaceutical vehicles ensure that the active ingredients are safely and effectively transported to their intended site of action within the body, enhancing therapeutic efficacy while minimizing potential side effects.
Positron-Emission Tomography (PET) is a type of nuclear medicine imaging that uses small amounts of radioactive material, called a radiotracer, to produce detailed, three-dimensional images. This technique measures metabolic activity within the body, such as sugar metabolism, to help distinguish between healthy and diseased tissue, identify cancerous cells, or examine the function of organs.
During a PET scan, the patient is injected with a radiotracer, typically a sugar-based compound labeled with a positron-emitting radioisotope, such as fluorine-18 (^18^F). The radiotracer accumulates in cells that are metabolically active, like cancer cells. As the radiotracer decays, it emits positrons, which then collide with electrons in nearby tissue, producing gamma rays. A special camera, called a PET scanner, detects these gamma rays and uses this information to create detailed images of the body's internal structures and processes.
PET is often used in conjunction with computed tomography (CT) or magnetic resonance imaging (MRI) to provide both functional and anatomical information, allowing for more accurate diagnosis and treatment planning. Common applications include detecting cancer recurrence, staging and monitoring cancer, evaluating heart function, and assessing brain function in conditions like dementia and epilepsy.
Spontaneous otoacoustic emissions (SOAEs) are low-level sounds that are produced by the inner ear (cochlea) without any external stimulation. They can be recorded in a quiet room using specialized microphones placed inside the ear canal. SOAEs are thought to arise from the motion of the hair cells within the cochlea, which generate tiny currents in response to sound. These currents then cause the surrounding fluid and tissue to vibrate, producing sound waves that can be detected with a microphone.
SOAEs are typically present in individuals with normal hearing, although their presence or absence is not a definitive indicator of hearing ability. They tend to occur at specific frequencies and can vary from person to person. In some cases, SOAEs may be absent or reduced in individuals with hearing loss or damage to the hair cells in the cochlea.
It's worth noting that SOAEs are different from evoked otoacoustic emissions (EOAEs), which are sounds produced by the inner ear in response to external stimuli, such as clicks or tones. Both types of otoacoustic emissions are used in hearing tests and research to assess cochlear function and health.
I believe you are looking for a medical condition or term related to the state of Arizona. However, there is no specific medical condition or term named "Arizona." If you're looking for medical conditions or healthcare-related information specific to Arizona, I could provide some general statistics or facts about healthcare in Arizona. Please clarify if this is not what you were looking for.
Arizona has a diverse population and unique healthcare needs. Here are some key points related to healthcare in Arizona:
1. Chronic diseases: Arizona experiences high rates of chronic diseases, such as diabetes and cardiovascular disease, which can lead to various health complications if not managed properly.
2. Mental health: Access to mental health services is a concern in Arizona, with a significant portion of the population living in areas with mental health professional shortages.
3. Rural healthcare: Rural communities in Arizona often face challenges accessing quality healthcare due to provider shortages and longer travel distances to medical facilities.
4. COVID-19 pandemic: Like other states, Arizona has been affected by the COVID-19 pandemic, which has strained healthcare resources and highlighted existing health disparities among various populations.
5. Indigenous communities: Arizona is home to several indigenous communities, including the Navajo Nation, which faces significant health challenges, such as higher rates of diabetes, heart disease, and COVID-19 infections compared to the general population.
If you were looking for information on a specific medical condition or term related to Arizona, please provide more context so I can give a more accurate response.
Environmental Illness (EI) is a condition in which individuals report experiencing various symptoms that they believe are caused or worsened by exposure to specific environmental factors. These factors can include chemicals, allergens, pollutants, or other substances present in the air, water, or food. The symptoms of EI can vary widely and may include headaches, fatigue, difficulty concentrating, respiratory problems, skin irritations, and gastrointestinal issues.
It's important to note that while some people may be more sensitive than others to environmental factors, the term "Environmental Illness" is not recognized as a formal medical diagnosis by major medical organizations such as the American Medical Association or the World Health Organization. Instead, the symptoms of EI are often attributed to other conditions, such as allergies, asthma, or chemical sensitivities.
In some cases, individuals with EI may be diagnosed with a related condition called Multiple Chemical Sensitivity (MCS), which is characterized by heightened sensitivity to chemicals and other environmental factors. However, MCS is also not recognized as a formal medical diagnosis by many major medical organizations.
Overall, while some people may experience symptoms that they believe are caused by exposure to environmental factors, it's important to consult with a healthcare provider for an accurate diagnosis and treatment plan.
I'm sorry for any confusion, but "gasoline" is not a medical term. It is a petroleum-derived liquid used as fuel in internal combustion engines. If you have any questions about medical terms or concepts, I would be happy to help with those!