Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242429 (sore throat)
 2,760 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possibility that air pollution exposure can extend the duration of respiratory symptoms was examined in a diary study of student nurses. This diary study has already shown associations between air pollution and incidence rates of respiratory symptoms. After individual risk factors and temperature were controlled for, photochemical oxidants were significantly (p less than .0001) associated with the duration of episodes of coughing, phlegm, and sore throat. Some heterogeneity of response to oxidants was seen; there was little effect on asthmatics, but the impact increased as family income increased. Plots of the mean duration of symptoms, by quintiles of oxidants, for which the other covariates were controlled, showed strong signs of a dose-response relationship for coughing and phlegm and moderate signs of a monotonic dose-response relationship for sore throat. The relationships continued for concentrations below the current ambient standard for ozone. Chest tightness or discomfort was significantly associated with sulfur dioxide (p = .016), but the effect seemed mainly restricted to asthmatics. However, evidence for a dose-dependent increase was weak.
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PMID:Air pollution and the duration of acute respiratory symptoms. 156 34

The relation of respiratory symptoms, pulmonary function, and abnormalities of chest radiographs to estimated exposures of borax dust has been investigated in a cross sectional study of 629 actively employed borax workers. Ninety three per cent of the eligible workers participated in the study and exposures ranged from 1.1 mg/m3 to 14.6 mg/m3. Symptoms of acute respiratory irritation such as dryness of the mouth, nose, or throat, dry cough, nose bleeds, sore throat, productive cough, shortness of breath, and chest tightness were related to exposures of 4.0 mg/m3 or more, and were infrequent at exposures of 1.1 mg/m3. Symptoms of persistent respiratory irritation meeting the definition of chronic simple bronchitis were related to exposure among non-smokers. Decrements in the FEV1 as a percentage of predicted were seen among smokers who had heavy cumulative borax exposures (greater than or equal to 80 mg/m3 years) but were not seen among less exposed smokers or among non-smokers. Radiographic abnormalities were uncommon and were not related to dust exposure. Borax dust appears to act as a simple respiratory irritant and perhaps causes small changes in the FEV1 among smokers who are heavily exposed.
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PMID:Respiratory effects of borax dust. 387 56

Seven repair technicians (RT, site A) repeatedly exposed to facsimile machine fume developed recurring sore throat, fever, lymphadenopathy, chest tightness, dry cough, and dyspnea. The fume concentration was low (0.6 mg/m3 of breathing-zone air) but it contained butyl methacrylate (BMA), a known skin sensitizer. Although chest radiographs were normal, three of the seven RT-A had lung crackles and spirometric abnormalities, and increased serum levels of immunoglobulins IgE or IgM. Symptoms and most other abnormalities improved when exposure to BMA was stopped. We later evaluated workers in two other sites (B and C). Six RT-B had daily contact with BMA fume (0.14 to 0.40 mg/m3 of air) at a field repair depot. Six administrative and six sales staff members (AS-B, SS-B) without regular fume exposure served as controls. All RT-B had elevated serum IgE levels (202+/-69 U/mL [SEM]; normal <41 U/mL). IgE and fume levels were positively correlated (r=0.83). four RT-B had lung crackles, but few symptoms and normal results of spirometry. The crackles cleared 8 weeks after substitution of a BMA-free paper, but IgE levels remained high (201+/-69). The nonexposed AS-B and SS-B had no crackles. Their IgE levels were normal (19+/-4 U/mL [SEM]; p<0.01). The crackles suggest BMA fume might have caused inflammation in terminal airways units. The significance of the IgE elevations is also uncertain since this class of antibodies is usually associated with asthma, not pneumonitis. In view of these uncertainties, BMA was eliminated from the facsimile transceiver process. Follow-up of group C workers (n=32) found no symptoms, lung crackles, or abnormal results of spirometry. However, IgE concentrations were elevated in 15 and remained so for 21 months, perhaps because of continuing exposure to residual low levels of BMA. These findings suggest that BMA-bearing facsimile fume caused increased IgE levels in RT at sites A, B, and C, and might have resulted in permanent lung injury if such exposure had continued.
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PMID:Pulmonary abnormalities and serum immunoglobulins in facsimile machine repair technicians exposed to butyl methacrylate fume. 863 24

Legionella pneumophila is the cause of Legionnaires' disease, and Pontiac fever, an influenza-like condition without pneumonia. We present a case of Pontiac fever after exposure to a hot tub contaminated with L pneumophila. A 37 y/o wf presented to the office with acute onset of sore throat, fever, headache, and myalgia. Patient was hospitalized 3 days later because of worsening shortness of air. Chest x-ray was normal. Patient was treated with 2 days of IV erythromycin and was discharged home on oral erythromycin. Her Legionella IFA was 1:16,384. Two days later, she developed chest tightness, pleuritic chest pain, and increasing shortness of air but did not have any cough or sputum production. She was re-hospitalized with a diagnosis of Pontiac fever and treated with IV erythromycin plus oral rifampin. A repeat chest x-ray remained normal. After a detailed epidemiologic history was obtained, it was noted that she became ill after using a hot tub, which her two children also used and they themselves developed a self limited illness. Water from the hot tub was positive for L pneumophila by DFA, culture, and PCR. Patient improved gradually with therapy and was discharged home. This report emphasizes the importance of a complete epidemiologic history in the diagnosis of respiratory infections. It also demonstrates that aquatic environment can be contaminated with Legionella and serve as a source of infection.
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PMID:Hot tub legionellosis. 885 93

Alocasia macrorrhiza (L) Schott and Endl is called Hai Yu, Tien Ho, Shan Yu, Kuan Yin Lien, Tu Chiao lien, Lao Hu Yu and Lang Du in Chinese. Its common English name is Giant Elephant's Ear. The toxic effects of A macrorrhiza arise from sapotoxin and include gastroenteritis and paralysis of the nerve centers. From 1985 to 1993 all individuals who called the Poison Control Center asking for information regarding macrorrhiza were included in this retrospective study. A questionnaire filled out by the Poison Control Center staff collected the demographic data of the victim, the reason for consumption, the prescribed part, clinical symptoms and signs of the victim, and medical outcome of poisonings. Among 27 cases of A macrorrhiza poisoning, the age was 1.5 to 68 y with 12 females and 15 males. One had skin contact and 1 had eye contact. In the 25 cases that consumed the plant leaf or tuber either raw or cooked, the primary symptom was in injected sore throat and the secondary symptom was numbness of the oral cavity. Some patients had salivation, dysphonia, abdominal pain, ulcers of the oral cavity, difficulty in swallowing, thoracodynia, chest tightness and swollen lips. We believe the presence of sapotoxin alone is not sufficient to explain the injected swollen and ulcerative lesions. Calcium oxalate is reported distributed in the entire plant and results in inflammation of the oral cavity and mucous membranes just as our patients had.
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PMID:Calcium oxalate is the main toxic component in clinical presentations of alocasis macrorrhiza (L) Schott and Endl poisonings. 955 63

Whereas human respiratory effects of brief ozone exposures are well documented, much less is known about the human health effects of mid- to long-term exposures. The authors' objective in this study was to determine whether lung function or respiratory symptom changes would occur over the course of a summer season among healthy young adults working outdoors in the presence of ozone. The authors studied 72 sophomore cadets from the U.S. Military Academy at West Point, New York, 21 of whom attended special summer training in Fort Dix, New Jersey, an area characterized by elevated ozone levels; the remaining cadets attended training in areas with moderate ozone levels (i.e., Fort Benning, Georgia; Fort Leonard Wood, Missouri; and Fort Sill, Oklahoma). The authors hypothesized that adverse respiratory outcomes, if any, would be more pronounced in the group exposed to higher ozone levels. Spirometry was performed and respiratory symptoms were assessed-both before and after the summer-in a clinic at West Point. Time spent outdoors during summer training averaged 11 hr/d. Both mean and peak ozone levels were higher at Fort Dix than at the three remaining sites. Regional levels of sulfur dioxide and particulate matter less than 10 microm in aerodynamic diameter were relatively low during the study. However, all cadets reported frequent exposure to dust, exhaust, and smoke in the course of their training. Averaged across all subjects, there was a statistically significant drop in forced expiratory volume in 1 sec of 44 ml (p = .035) over the summer. There were also significant increases in reports of cough, chest tightness, and sore throat at the follow-up clinic visit. A larger mean forced expiratory volume in 1 sec decline was observed at Fort Dix, where ozone exposures were the highest. The results of this study demonstrated a seasonal decline in respiratory function among healthy young adults working outdoors in the presence of ozone and particulate matter.
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PMID:Respiratory effects of seasonal exposures to ozone and particles. 1090 5

In response to worker and union representative concerns, the association between metalworking fluid exposure and respiratory symptoms was investigated in a cross-sectional survey, in a large automotive machining location. A self-administered respiratory symptom-screening questionnaire was sent to 2935 current employees. MWF exposure levels were assigned to respondents on a departmental basis based on average and "peak" area aerosol measurements. MWF exposure, years in the plant, and smoking status were regressed on presence or absence of daily or weekly respiratory symptoms, as well as upper and lower respiratory symptom groupings derived from principal components factor analysis. The response rate was 81 percent. Symptom prevalence was high: 29 percent of subjects reported weekly or daily phlegm; 23 percent, dry cough; 42 percent, runny or plugged nose. Average aerosol concentration in departments with exposure ranged from 0.02 to 0.84 mg/m(3), and peak levels from 0.02 to 2.85 mg/m(3). Average exposures ranging from 0.25 to 0.84 mg/m(3), as compared to exposures in the range of 0.02 to 0.09 mg/m(3), were statistically significantly associated with wheezing, chest tightness, sore throat, and hoarse throat, as well as with the upper respiratory symptom grouping. When peak exposure was included in the regression, it exerted a stronger effect than average exposure level on dry cough, phlegm, wheezing, fever/chills, and hoarse throat, as well as on upper and lower respiratory symptom groupings. These effects were independent of smoking status. Exposure-symptom trends for the average and peak departmental area concentration categories were statistically significant for the upper and lower respiratory symptom groupings and for most individual symptoms. We have observed an association of increasing upper and lower respiratory symptoms with estimated MWF exposure, measured independently, at average departmental aerosol concentrations well below the NIOSH recommended personal exposure level of 0.5 mg/m(3). The results have been used to prioritize exposure reduction efforts in the workplace.
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PMID:Investigating respiratory responses to metalworking fluid exposure. 1455 47

Historically, unpleasant odors have been considered warning signs or indicators of potential risks to human health but not necessarily direct triggers of health effects. However, citizen complaints to public health agencies suggest that odors may not simply serve as a warning of potential risks but that odor sensations themselves may cause health symptoms. Mal-odors emitted from large animal production facilities and wastewater treatment plants, for example, elicit complaints of eye, nose, and throat irritation, headache, nausea, diarrhea, hoarseness, sore throat, cough, chest tightness, nasal congestion, palpitations, shortness of breath, stress, drowsiness, and alterations in mood. There are at least three mechanisms by which ambient odors may produce health symptoms. First, symptoms can be induced by exposure to odorants (compounds with odor properties) at levels that also cause irritation or other toxicological effects. That is, irritation--rather than the odor--is the cause of the health symptoms, and odor (the sensation) simply serves as an exposure marker. Second, health symptoms from odorants at non-irritant concentrations can be due to innate (genetically coded) or learned aversions. Third, symptoms may be due to a co-pollutant (such as endotoxin) that is part of an odorant mixture. Objective biomarkers of health symptoms must be obtained, however, to determine if health complaints constitute health effects. One industry that is receiving much attention, worldwide, related to this subject is concentrated animal production agriculture. Sustainability of this industry will likely necessitate the development of new technologies to mitigate odorous aerial emissions. Examples of such "environmentally superior technologies" (EST) developed under the initiative sponsored through agreements between the Attorney General of North Carolina and Smithfield Foods and Premium Standard Farms are described.
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PMID:Science of odor as a potential health issue. 1564 42

The first pyrethroid pesticide, allethrin, was identified in 1949. Allethrin and other pyrethroids with a basic cyclopropane carboxylic ester structure are type I pyrethroids. The insecticidal activity of these synthetic pyrethroids was enhanced further by the addition of a cyano group to give alpha-cyano (type II) pyrethroids, such as cypermethrin. The finding of insecticidal activity in a group of phenylacetic 3-phenoxybenzyl esters, which lacked the cyclopropane ring but contained the alpha-cyano group (and hence were type II pyrethroids) led to the development of fenvalerate and related compounds. All pyrethroids can exist as at least four stereoisomers, each with different biological activities. They are marketed as racemic mixtures or as single isomers. In commercial formulations, the activity of pyrethroids is usually enhanced by the addition of a synergist such as piperonyl butoxide, which inhibits metabolic degradation of the active ingredient. Pyrethroids are used widely as insecticides both in the home and commercially, and in medicine for the topical treatment of scabies and headlice. In tropical countries mosquito nets are commonly soaked in solutions of deltamethrin as part of antimalarial strategies. Pyrethroids are some 2250 times more toxic to insects than mammals because insects have increased sodium channel sensitivity, smaller body size and lower body temperature. In addition, mammals are protected by poor dermal absorption and rapid metabolism to non-toxic metabolites. The mechanisms by which pyrethroids alone are toxic are complex and become more complicated when they are co-formulated with either piperonyl butoxide or an organophosphorus insecticide, or both, as these compounds inhibit pyrethroid metabolism. The main effects of pyrethroids are on sodium and chloride channels. Pyrethroids modify the gating characteristics of voltage-sensitive sodium channels to delay their closure. A protracted sodium influx (referred to as a sodium 'tail current') ensues which, if it is sufficiently large and/or long, lowers the action potential threshold and causes repetitive firing; this may be the mechanism causing paraesthesiae. At high pyrethroid concentrations, the sodium tail current may be sufficiently great to prevent further action potential generation and 'conduction block' ensues. Only low pyrethroid concentrations are necessary to modify sensory neurone function. Type II pyrethroids also decrease chloride currents through voltage-dependent chloride channels and this action probably contributes the most to the features of poisoning with type II pyrethroids. At relatively high concentrations, pyrethroids can also act on GABA-gated chloride channels, which may be responsible for the seizures seen with severe type II poisoning. Despite their extensive world-wide use, there are relatively few reports of human pyrethroid poisoning. Less than ten deaths have been reported from ingestion or following occupational exposure. Occupationally, the main route of pyrethroid absorption is through the skin. Inhalation is much less important but increases when pyrethroids are used in confined spaces. The main adverse effect of dermal exposure is paraesthesiae, presumably due to hyperactivity of cutaneous sensory nerve fibres. The face is affected most commonly and the paraesthesiae are exacerbated by sensory stimulation such as heat, sunlight, scratching, sweating or the application of water. Pyrethroid ingestion gives rise within minutes to a sore throat, nausea, vomiting and abdominal pain. There may be mouth ulceration, increased secretions and/or dysphagia. Systemic effects occur 4-48 hours after exposure. Dizziness, headache and fatigue are common, and palpitations, chest tightness and blurred vision less frequent. Coma and convulsions are the principal life-threatening features. Most patients recover within 6 days, although there were seven fatalities among 573 cases in one series and one among 48 cases in another. Management is supportive. As paraesthesiae usually resolve in 12-24 hours, specific treatment is not generally required, although topical application of dl-alpha tocopherol acetate (vitamin E) may reduce their severity.
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PMID:Poisoning due to pyrethroids. 1618 Sep 29

A previously healthy 16-year-old boy presented to the Emergency Department with a 2-day history of hoarseness, sore throat, and chest tightness. The physical examination was significant for diffuse neck and chest subcutaneous emphysema. A computed tomography (CT) scan of the neck and chest revealed pneumomediastinum after a plain chest X-ray study failed to uncover this finding. The patient reported that 5 days before presentation he forcefully inhaled helium gas directly from multiple party balloons in an attempt to alter his voice. The patient fully recovered over the next 2 days. Spontaneous pneumomediastinum developed in this patient with no underlying lung disease, presumably from air leakage secondary to the excessive elevation of intra-thoracic pressure due to repetitive inhalation of helium gas. Spontaneous pneumomediastinum remains largely underdiagnosed clinically, especially in young, healthy patients.
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PMID:Pneumomediastinum after inhalation of helium gas from party balloons. 2281 81


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