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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Building-related illness ranges from mild rhinitis to potentially life-threatening hypersensitivity pneumonitis and legionellosis. Sick-building syndrome, consisting of headache, mucous membrane irritation, and fatigue, may be present in 30% of all office workers. Hypersensitivity pneumonitis, asthma, and legionellosis are less common, and it is difficult from existing studies to estimate the incidence of these more severe illnesses. There are even fewer data on an illness now being called multiple chemical sensitivity and its relationship to indoor environments. New studies are needed to estimate the frequency of all building-associated illnesses, and case definitions for these disorders must be delineated.
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PMID:Severity of health effects associated with building-related illness. 182 80

Outbreaks of acute illness among office workers have been reported with increasing frequency during the past 10-15 years. In the majority of cases, hazardous levels of airborne contaminants have not been found. Generally, health complaints have involved mucous membrane and respiratory tract irritation and nonspecific symptoms such as headache and fatigue. Except for rare examples of hypersensitivity pneumonitis related to microbiologic antigens, there have been no reports of serious morbidity or permanent sequelae. However, the anxiety, lost work time, decreased productivity and resources spent in investigating complaints has been substantial. NIOSH has reported on 446 Health Hazards Evaluations that were done in response to indoor air complaints. This data base is the source of most of the published accounts of building-related illness. Their results are summarized here with a discussion of common pollutants (tobacco smoke, formaldehyde, other organic volatiles), and the limitations of the available industrial hygiene and epidemiologic data. There has been one large scale epidemiologic survey of symptoms among office workers. The results associate risk of symptoms to building design and characteristics of the heating/air-conditioning systems, consistent with the NIOSH experience. Building construction since the 1970s has utilized energy conservation measures such as improved insulation, reduced air exchange, and construction without opening windows. These buildings are considered "airtight" and are commonly involved in episodes of building-associated illness in which no specific etiologic agent can be identified. After increasing the percentage of air exchange or correcting specific deficiencies found in the heating/air-conditioning systems, the health complaints often resolve, hence, the term "tight building syndrome" or "sick building syndrome."(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sick building syndrome: acute illness among office workers--the role of building ventilation, airborne contaminants and work stress. 219 1

Organic dust toxic syndrome is a term recently coined to describe a noninfectious, febrile illness associated with chills, malaise, myalgia, a dry cough, dyspnea, headache and nausea which occurs after heavy organic dust exposure. Organic dust toxic syndrome shares many clinical features with acute farmer's lung and other forms of hypersensitivity pneumonitis, including the presence of increased numbers of neutrophils in bronchoalveolar lavage. However, organic dust toxic syndrome differs from acute hypersensitivity pneumonitis in several respects: the chest X-ray does not show infiltrates, severe hypoxemia does not occur, prior sensitization to antigens in the organic dust is not required and there are no known sequelae of physiological significance, such as the recurrent attacks and the pulmonary fibrosis which may be seen with chronic hypersensitivity pneumonitis. Organic dust toxic syndrome is thought to be much more common than farmer's lung. It is important for clinical and investigational purposes that organic dust toxic syndrome be distinguished from acute farmer's lung.
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PMID:Organic dust toxic syndrome: an acute febrile reaction to organic dust exposure distinct from hypersensitivity pneumonitis. 226 97

Symptoms consistent with hypersensitivity pneumonitis (HP) occurred in 26 of 50 employees working in a localized area of a large factory. This area was served by a single heating-cooling unit utilizing a water humidification system. The illness consisted of flu-like symptoms with fever, chills, headache, cough, dyspnea. Most of the subjects affected demonstrated precipitating antibodies to a variety of organisms associated with HP, and inhalation challenge with water from the humidification system resulted in the reproduction of symptoms in one employee with a history suggestive of HP. Removal of the humidification system has resulted in a "cure" in that symptoms have not recurred during a one year followup period since the removal.
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PMID:Humidifier lung. An outbreak in office workers. 676 70

To study the clinical and physiologic manifestations of the grain fever syndrome and the potentially pathogenic role of complement activation, 12 subjects (six grain workers and six healthy non-grain workers) underwent inhalation provocations with airborne grain dust. The clinical response was characterized by facial warmth, headache, malaise, myalgias, feverish sensation, chilliness, throat and tracheal burning sensation, chest tightness, dyspnea, cough, and expectoration. Fever developed in four grain workers and two controls. Leukocytosis, ranging between 11,700 and 24,300 leukocytes/mm3 with left shift, developed in five grain workers and five controls. There was no evidence of complement activation by the classical or alternate pathway. None of the subjects had serum precipitins to grain dust. The pulmonary response was characterized by a decrease in FEV1, FVC, MMF, Vmax50, and Vmax75, with significant rise in pulmonary resistance and consistent change in dynamic compliance but without changes in static compliance or diffusing capacity. Hence, grain dust inhalation induced diffuse airways obstruction without detectable parenchymal reaction. The airways response to high concentrations of grain dust inhalation were unrelated to the presence of immediate skin hypersensitivity. Although we cannot exclude the etiopathogenetic role of an immunologic reaction to grain dust, our data do not support the hypothesis that the grain fever syndrome is a precipitin-mediated allergic pneumonitis. More likely, the manifestations of grain fever probably reflect the host reaction to grain dust bacterial endotoxins and/or nonallergic mediator release by grain or grain dust constituents.
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PMID:Grain fever syndrome induced by inhalation of airborne grain dust. 707 83

Since August, 1978, an epidemic characterised by respiratory symptoms and fever spread rapidly in a restricted area near Tampere, Finland. Four months later over half of the adult population reported intermittent or constant symptoms. The most frequent symptoms were cough, dyspnoea, chills, fever, headaches, muscle pain and aching of joints. The symptoms appeared to be associated with exposure to water vapour derived from tap water. Consequently this disease, which resembled extrinsic allergic alveolitis, was given the name 'bathing fever' for lack of any prevailing diagnosis. In clinical provocation tests lung diffusion capacity usually decreased, the leucocyte count increased, and a slight rise in body temperature was observed. Despite many efforts the specific causative agent in the tap water has not been identified. Neither massive chlorination of the water nor changing the sand filter of the water-works had any significant effect on the quality of the water. Therefore the source of water supply was changed in April, 1979. The symptoms have subsequently disappeared. Present knowledge about bathing fever suggests that, though rare, it may be typical of the Scandinavian type of climate.
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PMID:Bathing fever epidemic of unknown aetiology in Finland. 744 43

A 18-year-old woman presented to our hospital complaining of an acute onset of progressive dyspnea with nonproductive cough and high fever. The patient was in her usual good health until the previous day, when she started to develop symptoms 8 hours after taking aspirin for a headache. The chest roentgenogram revealed Kerley's lines (A and B), perivascular cuffing and hilar haze with bilateral pleural effusions. Body temperature was 38 degrees C and PaO2 was 48 torr. Infectious diseases and extrinsic allergic alveolitis were excluded. The lymphocyte stimulating test was negative for aspirin. Acute eosinophilic pneumonia was strongly suggested by bronchoalveolar lavage showing a marked increase in eosinophils without peripheral eosinophilia. By the seventh hospital day all clinical and radiographic signs were improved without steroid therapy. Most cases of acute eosinophilic pneumonia reported previously showed diffuse infiltrative shadows on the chest roentgenogram. The present case had interesting radiographic findings which suggested interstitial pulmonary edema.
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PMID:[A case of acute eosinophilic pneumonia with Kerley's lines (A and B) on chest X-ray]. 823 Aug 83

Increasingly recognized as a potential public health problem since the outbreak of Legionnaire's disease in Philadelphia in 1976, polluted indoor air has been associated with health problems that include asthma, sick building syndrome, multiple chemical sensitivity, and hypersensitivity pneumonitis. Symptoms are often nonspecific and include headache, eye and throat irritation, chest tightness and shortness of breath, and fatigue. Air-borne contaminants include commonly used chemicals, vehicular exhaust, microbial organisms, fibrous glass particles, and dust. Identified causes include defective building design and construction, aging of buildings and their ventilation systems, poor climate control, inattention to building maintenance. A major contributory factor is the explosion in the use of chemicals in building construction and furnishing materials over the past four decades. Organizational issues and psychological variables often contribute to the problem and hinder its resolution. This article describes the health problems related to poor indoor air quality and offers solutions.
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PMID:The indoor air we breathe. 976 64

Moulds are responsible for diseases in humans through the three pathogenetic mechanisms of infection, allergy, and toxicity. Fungal infection is especially a risk factor for immunodeficient patients, but it occurs in immunocompetent patients as well. Fungal allergy is manifested as bronchial asthma, hypersensitivity pneumonitis, allergic bronchopulmonary aspergillosis, or allergic fungal sinusitis. Mycotoxicosis is almost exclusively the result of ingestion of mould-contaminated foodstuffs. In each case there is specificity for the etiologic mould. There is controversy regarding the ability of indoor airborne mould spores to cause human disease through non-specific toxicity via the inhalation route. Pulmonary mycotoxicosis is an established, although rare, occupational disease of farmers who inhale enormous quantities of mycotoxins, endotoxins, and other toxic chemicals from contaminated silage. Other conditions attributed to indoor airborne mycotoxin are unproven. These include infantile pulmonary hemosiderosis, epistaxis, 'toxic encephalopathy', immune dysregulation and a variety of subjective complaints without objective signs of pathology such as fatigue, headache, dyspnea, gastrointestinal distress, neuromuscular and skeletal complaints, etc. Non-specific irritation from moulds via the inhalation route is also a controversial subject that remains unproven. Published studies alleging an epidemiologic causal relationship are unconvincing.
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PMID:Sick Building Syndrome: is mould the cause? 1925 24

Inhalation of agricultural dusts causes inflammatory reactions and symptoms such as headache, fever, and malaise, which can progress to chronic airway inflammation and associated diseases, e.g. asthma, chronic bronchitis, chronic obstructive pulmonary disease, and hypersensitivity pneumonitis. Although in many agricultural environments feed particles are the major constituent of these dusts, the inflammatory responses that they provoke are likely attributable to particle-associated bacteria, archaebacteria, fungi, and viruses. In this study, we performed shotgun pyrosequencing metagenomic analyses of DNA from dusts from swine confinement facilities or grain elevators, with comparisons to dusts from pet-free households. DNA sequence alignment showed that 19% or 62% of shotgun pyrosequencing metagenomic DNA sequence reads from swine facility or household dusts, respectively, were of swine or human origin, respectively. In contrast only 2% of such reads from grain elevator dust were of mammalian origin. These metagenomic shotgun reads of mammalian origin were excluded from our analyses of agricultural dust microbiota. The ten most prevalent bacterial taxa identified in swine facility compared to grain elevator or household dust were comprised of 75%, 16%, and 42% gram-positive organisms, respectively. Four of the top five swine facility dust genera were assignable (Clostridium, Lactobacillus, Ruminococcus, and Eubacterium, ranging from 4% to 19% relative abundance). The relative abundances of these four genera were lower in dust from grain elevators or pet-free households. These analyses also highlighted the predominance in swine facility dust of Firmicutes (70%) at the phylum level, Clostridia (44%) at the Class level, and Clostridiales at the Order level (41%). In summary, shotgun pyrosequencing metagenomic analyses of agricultural dusts show that they differ qualitatively and quantitatively at the level of microbial taxa present, and that the bioinformatic analyses used for such studies must be carefully designed to avoid the potential contribution of non-microbial DNA, e.g. from resident mammals.
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PMID:Shotgun pyrosequencing metagenomic analyses of dusts from swine confinement and grain facilities. 2474 47


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