Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prolonged exposure to formaldehyde induces in the rabbit lung reactional and dystrophic changes involving the intrapulmonary bronchi, the bronchioli and the lung tissue. These changes are represented by bronchial cell hyperplasia with hypermucigenesis, extrusion of bronchial cells, bronchiolar hypermucigenesis, parcellary squamous metaplasia or necrobiosis of epithelia, thickening of bronchial and bronchiolar walls by subepithelial cell accumulations, destruction of musculo-elastic structures with stenosis or ectasia; the vascular reactions are hyperhaemic and proliferative with an obstructive and fibrous tendency; the parenchymal lesions are atelectasias, intralobular emphysema, and cellular thickening of alveolar walls and interlobular areas. The acid phosphatase, Tween-60-esterase, naphthol-AS-D-acetate-esterase, proline-oxidase and hydroxyproline-2-epimerase activities are increasing, while the leucyl-aminopeptidase and beta-glucuronidase ones are decreasing. The qualitative observations are completed and sustained by quanitative studies of mucous cell kinetics, of cell accumulations and differentiations.
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PMID:Experimental chronic obstructive lung disease. I. Bronchopulmonary changes induced in rabbits by prolonged exposure to formaldehyde. 15 Dec 23

The volumes of 78 adult human lungs at necropsy after fixation with intrabronchial 10% formaldehyde at a transpulmonary pressure of 25 cm of water (VL) were similar to their total lung capacity (TLC) as assessed radiologically (VX). Corrected for stature, VL and VX did not increase with age in non-emphsematous lungs, nor did the radio of VL to VX (VL/VX) change with age. VL and VX relative to body length increased with emphysema, and the increase even occurred in lungs from men with trivial or equivocal amounts of emphysema. Thus alteration of the mechanical properties of the lung may precede the appearance of obvious emphysema. VL/VX was not affected by the presence or severity of emphysema. The right lung formed 53% of VL with a range of 49-58% in apparently normal lungs. The amount of air in 13 human lungs at necropsy averaged 61% of TLC with a wide variation, indicating that this is not a useful point at which to measure lung dimensions. It is concluded that the volume of lungs fixed with formaldehyde at a transpulmonary pressure of 25 cmH2O closely approximates to total lung capacity.
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PMID:Post-mortem lung volumes. 54 11

We conducted a follow-up study to evaluate mortality among 14,861 workers employed in five facilities producing or using phenol and formaldehyde. More than 360,000 person-years of follow-up accrued. Mortality rates from all causes of death combined were similar to those in the general U.S. population. We observed excesses of cancer of the esophagus, cancer of the kidney, and Hodgkin's disease among workers exposed to phenol, but none of these excesses showed a dose-response relation with exposure to phenol. Excess lung cancer mortality (SMR = 1.2) showed no consistent pattern by any exposure index. Workers exposed to phenol had lower mortality ratios for cancer of the buccal cavity and pharynx, cancer of the stomach, cancer of the brain, arteriosclerotic heart disease, emphysema, disease of the digestive system, and cirrhosis of the liver. Of these, arteriosclerotic heart disease, emphysema, and cirrhosis of the liver were inversely related to duration of phenol exposure and to cumulative phenol exposure levels. Although these inverse associations may be due to chance or uncontrolled confounders, the ability of phenol to interfere with the generation of oxidants in experimental systems suggests that the pattern may have biologic plausibility.
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PMID:Mortality among industrial workers exposed to phenol. 205

We compared the jobs, estimates of exposures, and mortality experience of short-term (less than or equal to 1 year) and long-term (greater than 1 year) workers from nine plants producing formaldehyde or formaldehyde products. There were few jobs that were filled solely or primarily by newly hired workers. The estimated median level of formaldehyde exposure experienced by short-term workers on their first job was nearly identical to that for long-term workers, although short-term workers were more likely to be in jobs exposed to particulates than were long-term workers. As duration of employment increased, there was little change in the average estimated exposure level of formaldehyde, but the likelihood of being exposed to particulates decreased. Short-term workers had greater risks than long-term workers of dying from diseases of the circulatory system, arteriosclerotic heart disease, emphysema, diseases of the digestive system, cirrhosis of the liver, motor vehicle accidents, suicide and malignant neoplasms, particularly cancers of the stomach, colon, lung, prostate, and brain.
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PMID:Comparison of jobs, exposures, and mortality risks for short-term and long-term workers. 240 25

Wood dust is a well known nasal carcinogen in man, as formaldehyde is in rats. In certain occupational environments, combined exposure to wood dust and formaldehyde is common. Little is known about the effects of this combination. A pilot study was performed on four groups of Sprague-Dawley rats: one exposed to wood dust (25 mg/m3), another to formaldehyde (12.4 ppm) and a third to both wood dust and formaldehyde; the fourth group served a control group. After 104 weeks of exposure the nose and lungs were examined histologically. One well differentiated squamous cell carcinoma was found in the formaldehyde group. Squamous cell metaplasia was found significantly more often among the formaldehyde-exposed rats. Squamous cell metaplasia with dysplasia was most frequently observed, however, in the group exposed to both formaldehyde and wood dust. There were also significantly more rats with pulmonary emphysema in the groups exposed to wood dust than in the other groups.
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PMID:Histological changes in the nasal mucosa in rats after long-term exposure to formaldehyde and wood dust. 281 42

A retrospective cohort study was performed on a group of 664 male workers employed for at least one month during the period 1942-1979 in a chemical factory. Both established and suspected carcinogens had been handled in the plant, primarily piperazine, but also urethane, ethylene oxide, formaldehyde, and organic solvents. A significantly increased mortality, compared with the regional death rate, was observed in the cohort. The increase was mainly due to violent deaths and cardiovascular diseases. No rise in death rates was observed for asthma, bronchitis or emphysema, in spite of other evidence of a high risk of occupational asthma, due to exposure to piperazine. A statistically significant increase in cancer morbidity was observed for malignant lymphoma/myelomatosis when an induction latency time of at least 10 years was used. Furthermore, an increase in bronchial cancer was noted, but it was statistically significant only when an induction-latency time of at least 15 years was used. A case-referent study within the cohort did not reveal any significant association between any specific chemical exposure and cancer morbidity.
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PMID:Mortality and cancer morbidity among workers in a chemical factory. 382 3

In the final phase of the mortality study of workers at an automotive iron foundry, a subset (N = 3929) of the original cohort of 8147 men, consisting of those exposed to formaldehyde during the period from January 1960 through May 1987, was analyzed. In addition to the external US population, an internal population (N = 2032), consisting of men who had worked in the same foundry during the same time period but not in formaldehyde-exposed jobs, was also used as a referent. Follow-up continued through December 31, 1989. Smoking status was ascertained for 65.4% of the exposed and for 55.1% of the unexposed cohorts. Detailed work histories and evaluation of occupational exposures by an industrial hygienist enabled us to categorize cumulative formaldehyde and silica exposures. Standardized mortality ratios were used to compare the mortality experience of the exposed cohort with the US population and, because of concerns about the healthy worker effect, with an occupational referent population. Relative risks for race, formaldehyde exposure status, smoking status, and silica exposure level were estimated by fitting a Poisson regression model to four causes of death: cancers of the buccal cavity and pharynx, lung cancer, diseases of the respiratory system, and emphysema. No association between formaldehyde exposure and deaths from malignant or nonmalignant diseases of the respiratory system was found. Cigarette smoking and silica exposure were found to be significantly associated with deaths attributed to lung cancer and disease of the respiratory system.
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PMID:Mortality of iron foundry workers: IV. Analysis of a subcohort exposed to formaldehyde. 755 67

Tobacco is one of the major toxic agents in our civilization. The extent and severity of the current smoking epidemics are due to the use of industrial cigarettes: their smoke, less irritant than that of cigars and pipe, can be inhaled intensively with rapid absorption of all toxic compounds. Tobacco smoke is composed of a gas phase (CO2, CO, CNH, etc.) and a particle phase (a very fine aerosol) in which more than 4000 substances have been identified. The main toxic compounds in tobacco are Co, nicotine and tars. CO binds to haemoglobin to form COHb, a major factor of hypoxia and vascular accidents. Within a few seconds, nicotine reaches the brain where it binds to specific receptors, which explains its psycho-active effects (psychological dependence) and the induction of physical dependence. This dual dependence is responsible for the failures and relapses observed in attempted withdrawals. Furthermore, nicotine stimulates the sympathetic system with hypersecretion of catecholamines resulting in vascular complications. Tars contain carcinogenic substances, such as aromatic hydrocarbons, which exert local effects on the respiratory tract and systemic effects since they are absorbed by the lungs; this explains the remote neoplasias such as cancer of the bladder. Tars also contain irritant agents (acrolein, formaldehyde, etc.) and oxidative substances responsible for chronic bronchitis and emphysema. Thus, all organs and tissues can be damaged by the toxic compounds that are present in tobacco and, in particular, in tobacco smoke.
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PMID:[Toxicology of tobacco]. 823 55

The histologic changes in the respiratory tracts of chickens were evaluated after hatchery fumigation with 40% formaldehyde vapors and vaccination against infectious bronchitis virus with live attenuated vaccine (Massachusetts serotype). One-day-old chickens were housed in four isolation units in controlled environmental conditions, fed and watered ad libitum, and separated into four groups: 1) fumigated and vaccinated birds (FV group); 2) nonfumigated and vaccinated birds (NFV group); 3) fumigated and nonvaccinated birds (FNV group); and 4) control group (C group). All birds were tested to be free from Mycoplasma gallisepticum and Mycoplasma synoviae. After necropsy on the first, eighth, and twenty-sixth days after birth, samples from tracheal upper portion and lungs were conventionally processed for light, scanning, and transmission electron microscopy. Tissue response was monitored by microscopic examination of trachea and lung. On the first day of observation, fumigated and vaccinated birds (FV group) showed extensively damaged tracheal epithelium with exfoliated areas and some active glands with electrodense granules, and in the lung, the primary bronchi epithelium had disorganized cilia and abundant lymphocytes, with emphysematous areas in tertiary bronchus. On day 8 after vaccination, cubical and cylindrical tracheal cell proliferation was observed, and on day 26, ciliated columnar epithelium was almost regenerated with heterophil corion infiltration, and hyaline cartilage nodules appeared in parabronchi. The nonfumigated and vaccinated birds (NFV) revealed less injury on the epithelial surface and a more rapid response to epithelial regeneration than the in only fumigated animals (FNV). The control group did not show remarkable morphologic changes. Postvaccinal and fumigation effects on the upper respiratory tract were temporary, whereas in lungs, increased emphysema, cartilage nodules in the interchange zone, and general lymphocyte infiltration had caused intensive injury.
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PMID:Morphologic observations on respiratory tracts of chickens after hatchery infectious bronchitis vaccination and formaldehyde fumigation. 1100 97

Cigarette smoking is associated with chronic obstructive pulmonary disease (COPD)--a term encompassing chronic lung inflammation, chronic bronchitis and emphysema. Goblet cell hyperplasia is a characteristic feature of the lung epithelium in COPD patients contributing to the overproduction of airway mucus, including mucin MUC5AC. Using an in vitro model of differentiated lung epithelium we have investigated morphological and cellular changes in response to interleukin (IL)-13 (2.5-20 ng/ml), cigarette smoke total particulate matter (TPM; 0.31-20 microg/ml) and three mainstream cigarette smoke constituents: acrolein, formaldehyde and acetaldehyde (all at 0.001-1 microM) over 28 days during differentiation (agents replaced daily Monday-Friday). Control cultures of human bronchial epithelial cells (HBECs) underwent mucociliary differentiation producing a columnar epithelium containing goblet, ciliated and basal cells. Non-cytotoxic doses of IL-13 induced a significant increase in the percentage of MUC5AC positive cells. Using both flow cytometry and immunocytochemical techniques for identification of MUC5AC positive cells, TPM treatment induced an increase in MUC5AC positive cells, becoming maximal at 5 microg/ml. Acrolein treatment also increased the percentage of MUC5AC positive cells. However, formaldehyde or acetaldehyde had little effect. This study demonstrates that lung toxicants can induce a profound effect on cellular differentiation in an in vitro model of the human lung epithelium.
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PMID:Cigarette smoke total particulate matter increases mucous secreting cell numbers in vitro: a potential model of goblet cell hyperplasia. 2006 Apr 63


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