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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

Medical examinations were performed in a group of 51 Polish farmers heavily exposed to flax dust during harvesting and scutching (threshing) and in a group of 50 healthy urban dwellers not exposed to organic dusts (controls). The examinations included: interview concerning the occurrence of respiratory disorders and work-related symptoms, physical examination, X-ray examination of chest, lung function tests, oxymetric examinations, determination of the concentration of cytokines (IL-1alpha IL-6, TNFalpha) in blood serum and allergological tests with microbial antigens associated with organic dust, comprising: skin prick test with 4 antigens, agar-gel precipitation test with 12 antigens and test for specific inhibition of leukocyte migration with 4 antigens. As many as 32 farmers (62.7%) reported the occurrence of work-related symptoms during harvesting, transporting and scutching of flax. The most common complaint was general weakness reported by 15 farmers (29.4%), followed by headache reported by 14 (27.5%), blocking of the nose - by 11 (21.6%), dry cough, shivering, and eyes itching - each by 10 (19.8%), chest tightness and hoarseness - each by 9 (17.6%). No control subjects reported these work-related symptoms. The mean spirometric values in the examined group of farmers were within a normal range and did not show a significant post-shift decline. In contrast, a significant post-shift decline of oxymetric values was found among flax farmers. The farmers showed a frequency of the positive early skin reactions to environmental allergens in the range of 0-19.6%, a frequency of positive precipitin reactions in a range of 0-56.9%, and frequency of positive reactions of leukocyte migration inhibition in a range of 7.8-21.6%. The members of the control group responded to the majority of allergens with a significantly lower frequency of positive results compared to the farmers. Elevated concentrations of IL-1alpha and IL-6, but not TNFalpha, were found in blood sera of flax farmers. In conclusion, farmers engaged in harvesting and scutching of flax represent a group of elevated professional risk because of high incidence of work-related symptoms and high frequency of allergic reactions to bacteria and fungi associated with organic dust.
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PMID:Effects of exposure to flax dust in Polish farmers: work-related symptoms and immunologic response to microbial antigens associated with dust. 1115 40

Almost every second trekker or climber develops two to three symptoms of the high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high altitude pulmonary edema. Essentially, acute mountain sickness is self-limiting and benign. Its symptoms are mild to moderate headache, loss of appetite, nausea, dizziness and insomnia. Nausea rarely progresses to vomiting, but if it does, this may anticipate a progression of the disease into the severe form of acute mountain sickness, called high altitude cerebral edema. Symptoms and signs of high altitude cerebral edema are severe headache, which is not relieved by acetaminophen, loss of movement coordination, ataxia and mental deterioration ending in coma. The mechanisms leading to acute mountain sickness are not very well understood; the loss of cerebral autoregulation and a vasogenic type of cerebral edema are being discussed. High altitude pulmonary edema presents in roughly twenty percent of the cases with mild symptoms of acute mountain sickness or even without any symptoms at all. Symptoms associated with high altitude pulmonary edema are incapacitating fatigue, chest tightness, dyspnoe at the minimal effort that advances to dyspnoe at rest and orthopnoe, and a dry non-productive cough that progresses to cough with pink frothy sputum due to hemoptysis. The hallmark of high altitude pulmonary edema is an exaggerated hypoxic pulmonary vasoconstriction. Successful prophylaxis and treatment of high altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary hypertension is crucial for the development of high altitude pulmonary edema. The primary treatment of high altitude illness consists in improving hypoxemia and acclimatization. For prophylaxis a slow ascent at a rate of 300 m/day is recommended, if symptoms persist, acetazolamide at a dose of 500 mg/day is effective. Mild acute mountain sickness may also be treated with the same dose acetazolamide. Glucocorticoids are the first line treatment of the malignant form of acute mountain sickness. Nifedipine is effective only for the prophylaxis and treatment of high altitude pulmonary edema.
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PMID:[Mountaineering and altitude sickness]. 1144 1

The use of alternative medicines is increasing world-wide and in Israel. These drugs, considered by the Ministry of Health as food supplements, are to be obtained at pharmacies and health stores and are being sold freely, without any professional advice. Many of the herbs are used by patients to treat psychiatric disorders. These herbs have a pharmacological activity, adverse effects and interactions with conventional drugs, which can produce changes in mood, cognition, and behavior. We present the most commonly used herbal drugs, and discuss their safety and efficacy in psychiatric practice. Hypericum--used as an antidepressant and as an antiviral medicine, was reported in 23 randomized clinical trials reviewed from the MEDLINE. It was found to be significantly more effective than placebo and had a similar level of effectiveness as standard antidepressants. Recent studies almost clearly prove that this herb, like most of the conventional antidepressants, can induce mania. Valerian--is used as an anti-anxiety drug, and reported to have sedative as well as antidepressant properties. In contrast to the significant improvement in sleep that was found with the use of valerian, compared to placebo, there are several reports on the valerian root toxicity. This includes nephrotoxicity, headaches, chest tightness, mydriasis, abdominal pain, and tremor of the hands and feet. Ginseng--another plant that is widely used as an aphrodisiac and a stimulant. It has been associated with the occurrence of vaginal bleeding, mastalgia, mental status changes and Stevens-Johnson syndrome after it's chronic administration. It has interactions with digoxin, phenelzine and warfarin. Ginkgo--in clinical trials the ginkgo extract has shown a significant improvement in symptoms such as memory loss, difficulties in concentration, fatigue, anxiety, and depressed mood. Long-term use has been associated with increased bleeding time and spontaneous hemorrhage. Ginkgo should be used cautiously in patients receiving aspirin, NSAIDs, anticoagulants or other platelet inhibitors. Health care professionals can no longer ignore the widespread use of alternative medicines and cannot continue with the "don't ask, don't tell" policy. Clinicians should ask the patients about their use of herbs in a non-judgmental way, and should document the patient's use of these drugs. Finally, we must be more aware of the side effects and the potential drug interactions of these herbs, and advise our patients to avoid long term use of these drugs due to lack of information regarding the safety of these medicines.
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PMID:[The safety of herbal medicines in the psychiatric practice]. 1154 87

Clinical findings for 38 community residents who complained of symptoms they attributed to exposure to air emissions from nearby fiber processing and polyurethane foam manufacturing facilities are reported. Common complaints included headache, mucosal irritation, shortness of breath, chest tightness, and wheezing. Airway hyperreactivity, measured by methacholine challenge, was observed in 8 individuals (22% of those tested), who also reported temporal relationships between exposure to visible emissions or odors and symptoms consistent with environmentally induced asthma. Six individuals (18.2%) had antibodies to at least 1 of the 3 common industrial diisocyanates. The number of individuals with antibodies to diisocyanates, coupled with the absence of other diisocyanate exposure, was highly suggestive of environmental exposure. The findings raised concern that some residents may have become sensitized to toluene diisocyanate.
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PMID:Clinical findings for residents near a polyurethane foam manufacturing plant. 1250 78

The 45(th) Annual Scientific Meeting of the American Headache Society focused on new areas of headache research: revised diagnostic criteria, increased the understanding of the pathogenesis of migraine and expansion of identified physiological changes in migraine beyond head pain to include cognitive, sleep and vestibular disturbances. A preview of the new International Headache Society criteria described changes in diagnostic categories, including special criteria for research. New definitions to categorise chronic daily headache, menstrual migraine and secondary headaches were the main highlights of the modified criteria. In addition, novel data on activation within trigeminovascular pathways expand the understanding of the pathogenesis of migraine. Identification of the ability of treatment to impact activation and sensitisation of peripheral and central neurons results in: an explanation for initial headache worsening and neck/chest tightness that commonly occur with triptans, a better understanding of the mechanisms of triptans, and a strong recommendation for early triptan intervention (within 20 min of headache onset). Application of matrix metalloproteinase models to migraine helps explain the ability of medications to cross the blood-brain barrier during a migraine episode, as well as describe possible ischaemia with repeated migraine (e.g., white matter abnormalities seen on magnetic resonance scanning). Improved classification of headache disorders, along with increased understanding of the physiology of migraine and mechanism of action of common treatments, should enhance future development and evaluation of effective headache therapy.
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PMID:45(th) Annual Scientific Meeting of the American Headache Society June 19 -22, 2003, Chicago, IL, USA. 1294 91

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

Several disease-modifying agents (DMAs) are approved for the treatment of multiple sclerosis, including three interferon (IFN)-beta products, glatiramer acetate and mitoxantrone. This article reviews the adverse event profiles of these DMAs based on the pivotal phase III trials, and provides practical guidelines for managing adverse effects. In general, the most common adverse events associated with IFN beta therapy are flu-like symptoms, including fever, chills and myalgias, and headache. The flu-like symptoms typically resolve within 24 hours and may be mitigated by over-the-counter anti-inflammatory agents. Adverse events related to glatiramer acetate therapy include injection-site reactions and a systemic reaction consisting of flushing, chest tightness, palpitation, anxiety or dyspnoea. The systemic reaction is transient (30 seconds to 30 minutes) and self-limited. Mitoxantrone may cause nausea, vomiting, alopecia, amenorrhoea and myelosuppression; isolated cases of acute leukaemia and dose-related cardiotoxicity have been reported in the literature. Longer-term tolerability data on mitoxantrone as a treatment for multiple sclerosis are needed. It is important for physicians to counsel patients on DMA-related adverse effects, most of which are transient and of mild-to-moderate severity. Various strategies that can be employed to prevent or manage these adverse effects and lessen their impact on the patient are discussed.
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PMID:US FDA-approved disease-modifying treatments for multiple sclerosis: review of adverse effect profiles. 1574 Jan 78

(1) The reference first-line drug therapy for migraine attacks in adolescents is a non specific analgesic such as paracetamol or a nonsteroidal antiinflammatory drug like ibuprofen. Two specific analgesics are authorised for use in this setting in France, namely ergotamine and dihydroergotamine. (2) Nasal sumatriptan is the first triptan to be licensed for this age group in France. (3) Evaluation data includes three flawed placebo-controlled trials. (4) Effects were modest at best. Only one of the three trials showed that sumatriptan was more likely than placebo to give complete pain relief within two hours. The three trials fail to show that sumatriptan is effective against symptoms such as nausea and vomiting, photophobia and phonophobia. (5) The principal known adverse effects of sumatriptan are chest tightness, flushing, and increased blood pressure. (6) In the only trial report containing relevant information, unpleasant taste was the only adverse effect more commonly associated with sumatriptan than with placebo. (7) Postmarketing follow-up revealed a number of serious adverse effects, including stroke, myocardial infarction and loss of vision. (8) The packs containing 6 or 12 spray vials carry a risk of overuse and self-induced headache. (9) In practice, sumatriptan must not be used to treat migraine attacks in adolescents.
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PMID:Nasal sumatriptan: new dosage. For adolescents with migraine: too little benefit. 1587 37

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


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