How To Avoid Asthma Triggers

You must be aware of asthma triggers in order to help avoid them. If you or anyone you know or love struggles with asthma, you know how critical it is to avoid any kind of trigger that would spur on an attack.

You can take your preventative medicine, of course, but as soon as you enter a dusty room or even go outside, allergens are inhaled and your airways may constrict, causing another attack.

Many people with asthma keep an inhaler with them to prepare for going outside or into the workplace. But we cannot control these environments, unfortunately.

On a better note, you can prevent asthma triggers in your own home! The main triggers in your average household are dust mites, molds, and pollens.

Dust mites may be the most common asthma trigger at home. How can you protect yourself? Wash your bedding in hot water every week and make sure your pillows and bedding don't contain feathering. Non carpeted floors are great because they are easily cleaned. If you don't have hardwood floors, vacuum more often with an allergen proof vacuum bag. MAKE SURE TO WEAR A MASK WHILE VACUUMING! Remember to keep clean air filters installed for your heating and air and cover air ducts with cheesecloth for extra protection. Remember what I said about washing your bedsheets in hot water? Do the same for your curtains every week! This may seem tedious, but it's worth it to have a dust-free home! And, as usual, keep surfaces and lampshades cleaned. Don't forget to wear that mask!

What about asthma triggers caused by mildew? How do you keep it from growing in your home? Where do we encounter mildew the most at home? Bathrooms! Clean your bathrooms regularly using cleaners that kill and prevent mold. If you feel like taking a hot shower, make sure to open the bathroom door or window to air it out. Nothing causes mildew more than too much humidity. Do you have a bathroom rug? After that hot bath or shower, make sure to immediately remove it and set it outside to air out and dry. Have a rug in front of the toilet? Get rid of it. Make sure to air our the damp and humid areas of your home regularly. Buy a dehumidifier if needed! Keep household plants OUT of the bedroom.

Lastly, remember to avoid those pollens. They may be difficult to avoid completely, but there are a couple of things you can do to cut down on exposure to them. Limit your exposure to the outdoors in the morning as the pollen counts are highest in the early morn. This is especially the case when the weather is warm and dry. Most importantly, and you may already have figured this one out, keep your windows shut.

Most people with asthma don't have pets. For those of you who do, make sure to restrict your pet's living area in the home. Once you find a main dwelling area for your pet, make sure to pull up any carpet if there is any. Do not allow it in the bedroom, and if possible, keep the pet outside. Like those bedsheets and curtains, put on your mask and wash your dog or cat weekly in hot water (not too hot!!!). If you are visiting a friend or relative's house and they are indoor pet owners, avoid long visits. Exposure to the pets should be kept to a minimum or completely avoided. And, as usual, take your medicine before entering the home.

These procedures may seem tedious, but once you make it a habit to follow them, the decrease of asthma triggers will give your system a break from excessive stressors in your living space. In addition, there's nothing like having a clean environment to come home to! Breathe easy, my friends and take care!

Allergic Rhinitis

Allergic airway illnesses such as allergic rhinitis and asthma are characterized by local muscle damage and organ dysfunction within the upper and reduced respiratory tract arising from an abnormal hypersensitivity immune response to usually harmless and ubiquitous environmental allergens. Allergens that cause airway disease are predominantly seasonal tree, grass, and weed pollens or perennial inhalants (eg, home dust mite antigen, cockroach, mold, animal dander, and some occupational protein antigens).

Sensitized illness is a typical trigger of pediatric and adult acute and chronic neck muscles problems. Both sensitized rhinitis and asthma account for substantial morbidity, and atopic disorders have increased in prevalence more than the past few decades. In a Danish survey, the prevalence of skin test-positive sensitized rhinitis in persons 15-41 years of age elevated from 12.9% in 1990 to 22.5% in 1998.

Allergic rhinitis is discussed right here like a model for the pathophysiology of IgE-mediated sensitized neck muscles disease. Sensitized rhinitis implies the existence of kind I (IgE-mediated) instant hypersensitivity to environmental allergens that impact the upper respiratory mucosa directly.

Particles bigger than 5 繕m are filtered nearly totally by the nasal mucosa. Because most pollen grains are a minimum of this big, couple of intact particles would be expected to penetrate the reduced airway when the nose is working normally. The sensitized or atopic state is characterized by an inherited tendency to generate IgE antibodies to specific environmental allergens and the physiologic responses that ensue from inflammatory mediators released after the interaction of allergen with mast cell-bound IgE.

The clinical presentation of sensitized rhinitis includes nasal, ocular, and palatal pruritus, paroxysmal sneezing, rhinorrhea, and nasal congestion. A individual or family history of other allergic illnesses such as asthma or atopic dermatitis supports a diagnosis of allergy. Proof of sinus eosinophilia or basophilia by sinus smear or scraping may assistance the diagnosis also.

Confirmation of sensitized rhinitis demands the demonstration of specific IgE antibodies to common allergens by in vitro checks such as the radioallergosorbent test or in vivo (skin) testing in individuals with a background of signs and symptoms with relevant exposures. Inflammatory changes within the airways are recognized as critical functions of both sensitized rhinitis and chronic asthma.

Cross-linking of surface-bound IgE by antigen activates tissue mast tissue and basophils, inducing the immediate discharge of preformed mediators and also the synthesis of newly generated mediators. Mast cells and basophils also have the ability to synthesize and discharge proinflammatory cytokines, growth and regulatory elements that interact in complex networks.

The interaction of mediators with numerous target organs and cells from the neck muscles can induce a biphasic allergic response: an early phase mediated chiefly by release of histamine and other stored mediators (tryptase, chymase, heparin, chondroitin sulfate, and TNF), whereas late-phase occasions are induced following generation of arachidonic acid metabolites (leukotrienes and prostaglandins), platelet-activating aspect and de novo cytokine synthesis.

The early-phase response occurs within minutes following coverage to an antigen. After intranasal challenge or ambient exposure to applicable allergen, the sensitized affected person begins sneezing and develops an improve in nasal secretions. After approximately five minutes, the affected person develops mucosal swelling primary to reduced airflow.

These alterations are secondary towards the outcomes of vasoactive and smooth muscle constrictive mediators, including histamine, N--p-tosyl-L-arginine methylester-esterase (TAME), leukotrienes, prostaglandin D2 (PGD2), and kinins and kininogens from mast tissue and basophils. Histologically, the early response is characterized by vascular permeability, vasodilatation, muscle edema, and a mild cellular infiltrate of mainly granulocytes.

The late-phase sensitized response may adhere to the early-phase response (dual reaction) or might occur as an isolated event. Late-phase reactions begin 2-4 hours following preliminary exposure to antigen, reach maximal activity at 6-12 hours, and usually resolve inside 12-24 several hours. If the exposure is regular or ongoing, however, the inflammatory response becomes chronic.

The late-phase response is characterized by erythema, induration, heat, burning, and itching and microscopically by a substantial cellular influx of mainly eosinophils and mononuclear tissue. Changes consistent with airway remodeling and muscle hyperreactivity might also happen.

Mediators from the early-phase response-except for PGD2-reappear throughout the late-phase response within the absence of antigen rechallenge. Absence of PGD2, an exclusive product of mast cellular discharge, within the presence of continued histamine release suggests that basophils and not mast cells are an important source of mediators within the late-phase response.

There is an earlier accumulation of neutrophils and eosinophils, with later accumulation of activated T cells, synthesizing TH2 cytokines. Inflammatory cells infiltrating tissues within the late response might additional elaborate cytokines and histamine-releasing elements that might perpetuate the late-phase reaction, leading to sustained hyperresponsiveness, mucus hypersecretion, IgE production, eosinophilia, and disruption of the focus on tissue (eg, bronchi, epidermis, or sinus mucosa).

There's powerful circumstantial evidence that eosinophils are key proinflammatory tissue in sensitized neck muscles illness. Eosinophils are frequently discovered in secretions in the nasal mucosa of patients with allergic rhinitis and within the sputum of asthmatics.

Items of activated eosinophils such as main fundamental protein and eosinophilic cationic protein, that are destructive to airway epithelial muscle and predispose to persistent airway reactivity, have also been localized to the airways of individuals with allergic illness.

The recruitment of eosinophils along with other inflammatory cells to the airway is largely a item of activated chemokines and adhesion molecules. You will find two subfamilies of chemokines, which differ within the tissue they largely attract and in the chromosome area of their genes. The C-C chemokines, such as RANTES, MCP-1, MCP-3, and eotaxin, are situated on chromosome segment 7q11-q21 and selectively recruit eosinophils.

Leukocytes attach to vascular endothelial cells via receptor-ligand interaction of cellular surface area adhesion molecules from the integrin, selectin, and immunoglobulin supergene family. The interaction of these adhesion molecules and their counterreceptors mediates a sequence of occasions that consists of margination of leukocytes along the walls of the microvasculature, adhesion of leukocytes towards the epithelium, transmigration of leukocytes through vessel walls, and migration along a chemotactic gradient to achieve muscle compartments.

Each chemokine manufacturing and adhesion molecule expression are upregulated by soluble inflammatory mediators. For example, endothelial cellular adhesion molecule receptors, ICAM-1, VCAM-1, and E-selectin, are upregulated by IL-1, TNF, and LPS. The clinical manifestations of sensitized airway illness arise in the interaction of mast cell and basophil mediators with target organs of the upper and lower airway.

The signs and symptoms of sensitized rhinitis look instantly after coverage to some applicable allergen (early-phase reaction), although numerous patients experience long-term and recurrent signs and symptoms on the basis from the late-phase inflammatory response. Issues of severe or untreated sensitized rhinitis consist of sinusitis, auditory tube dysfunction, dysosmia, sleep disturbances, asthma attack exacerbations, and chronic mouth breathing.

Patients with allergic rhinitis develop chronic or episodic paroxysmal sneezing; sinus, ocular, or palatal pruritus; and watery rhinorrhea triggered by coverage to some specific allergen. Individuals might demonstrate indicators of chronic pruritus from the upper neck muscles, including a horizontal nasal crease from regular nose rubbing ("allergic salute") and palatal "clicking" from rubbing the itching palate using the tongue. Numerous muscle mast tissue are located close to terminal sensory nerve endings.

Pruritus and sneezing are caused by histamine-mediated stimulation of those C fibers. Mucus hypersecretion outcomes largely from excitation of parasympathetic-cholinergic pathways. Early-phase signs and symptoms are greatest treated with avoidance of applicable allergens and oral or topical antihistamines, which competitively antagonize H1 receptor sites in focus on tissues.

Anti-inflammatory treatment can reduce mobile inflammation during the late stage, providing a lot more efficient symptom relief than antihistamines alone. Allergen immunotherapy (hyposensitization) has shown effectiveness in decreasing symptoms and airway inflammation by inhibiting each early- and late-phase allergic responses.

Diverse mechanisms of immunotherapy are already observed, such as reduction of seasonal raises in IL-4 and allergen-specific IgE, induction of allergen-specific IgG1 and IgG4 (blocking antibodies), modulation of T-cell cytokine synthesis by enhancing TH1 and inhibiting TH2 responses, upregulation of Treg and downregulation of eosinophilic and basophilic inflammatory responses to allergen.

One trial found that immunotherapy administered to patients with grass-pollen allergy for 3-4 many years induced prolonged clinical remission accompanied by a persistent alteration in immunologic reactivity that included sustained reductions in the past due skin response and associated T-cell infiltration and IL-4 mRNA expression.

Symptoms of sinus obstruction might turn out to be chronic like a outcome of continual late-phase allergic mechanisms. Sinus mucous membranes might look pale blue and boggy. Kids frequently show signs of obligate mouth breathing, including lengthy facies, narrow maxillae, flattened malar eminences, marked overbite, and high-arched palates (so-called adenoid facies).

These signs and symptoms are not mediated by histamine and are, therefore, poorly responsive to antihistamine therapy. Oral sympathomimetics that induce vasoconstriction by stimulation of -adrenergic receptors are frequently used in conjunction with antihistamines to treat nasal congestion.

Topical decongestants may be used to relieve acute congestion but have restricted value in individuals with long-term sensitized rhinitis because regular use outcomes in rebound vasodilation (rhinitis medicamentosa). The phenomenon of heightened sinus sensitivity to decreased levels of allergen after initial exposures towards the allergen is called priming.

Clinically, priming may be observed in individuals who produce elevated symptoms late within the pollen season compared with early within the season. Late-phase inflammation induces a state of sinus neck muscles hyperresponsiveness to each irritants and allergens in patients with long-term allergic rhinitis and asthma attack.

Airway hyperreactivity can trigger heightened sensitivity to each environmental irritants such as tobacco smoke and noxious odors as nicely as to allergens such as pollens. You will find no standardized clinical tools to accurately assess late-phase hyperresponsiveness in allergic rhinitis as you will find for asthma attack (methacholine or histamine bronchoprovocation challenge).

Genetic markers for bronchial neck muscles hyperresponsiveness, however, are already identified. It also seems that late-phase cellular infiltration and eosinophil by-products might inflict neck muscles epithelial damage, which in turn can predispose to upper and reduced airways hyperreactivity. Accumulating evidence supports a relationship between sensitized rhinitis and asthma attack.

Numerous individuals with rhinitis alone demonstrate nonspecific bronchial hyperresponsiveness, and prospective research recommend that sinus allergy may be a predisposing risk aspect for developing asthma. Treatment of individuals with allergic rhinitis may outcome in improvement of asthma signs and symptoms, airway caliber, and bronchial hyperresponsiveness to methacholine and exercise.

Lastly, mechanistic research of airway physiology have demonstrated that nasal illness might influence pulmonary function via each direct and indirect mechanisms. This kind of mechanisms might consist of the existence of the nasal-bronchial reflex (with sinus stimulation leading to bronchial constriction), postnasal drip of inflammatory tissue and mediators from the nose into the lower airways, absorption of inflammatory cells and mediators into the systemic circulation and ultimately to the lung, and nasal blockage and subsequent mouth breathing, which may facilitate the entry of asthmagenic triggers towards the reduced neck muscles.

This really is the primary tool for the confirmation of suspected allergic illness. In vivo skin diagnostic tests with allergens suspected of leading to hypersensitivity constitutes an indirect bioassay for that presence of allergen-specific IgE on muscle mast tissue or basophils. Percutaneous or intradermal administration of dilute concentrations of specific antigens elicits an immediate wheal-and-flare reaction inside a sensitized individual.

This response marks a "local anaphylaxis" resulting from the controlled release of mediators from activated mast cells. Good skin check outcomes to airborne allergens, combined having a background and examination suggestive of allergy, strongly implicate the allergen as a cause of the patient's symptoms. Damaging epidermis test outcomes with an unconvincing allergy background argue strongly against an allergic origin.

Main benefits to skin testing include simplicity, rapidity of performance, and low price. In vitro tests supply quantitative assays of allergen-specific IgE within the serum. In these assays, affected person serum is reacted initially with antigen bound to a solid-phase material after which labeled with a radioactive or enzyme-linked anti-IgE antibody.

These immunoallergosorbent tests display a 70-80% correlation with epidermis testing to pollens, dust mites, and danders and are helpful in patients receiving long-term antihistamine treatment who are unable to undergo skin diagnostic tests and in patients with extensive dermatitis. Serous otitis media and sinusitis are main comorbidities in patients with sensitized rhinitis.

Each conditions happen secondarily to the obstructed nasal passages and sinus ostia in individuals with long-term allergic or nonallergic rhinitis. Issues of long-term rhinitis should be regarded in individuals with protracted rhinitis unresponsive to therapy, refractory asthma, or continual bronchitis. Serous otitis results from auditory tube obstruction by mucosal edema and hypersecretion.

Children with serous otitis media can present with conductive hearing loss, delayed speech, and recurrent otitis media connected with long-term sinus obstruction. Sinusitis might be acute, subacute, or long-term depending on the duration of signs and symptoms. Obstruction of osteomeatal drainage in individuals with long-term rhinitis predisposes to bacterial infection in the sinus cavities.

Individuals manifest signs and symptoms of persistent sinus discharge, cough, sinus discomfort, and nasal obstruction. Examination may reveal long-term otitis media, infraorbital edema, inflamed sinus mucosa, and purulent sinus discharge. Radiographic diagnosis by x-ray film or computed tomographic (CT) scan reveals sinus opacification, membrane thickening, or the presence of an air-fluid degree.

Effective treatment of infectious issues of long-term rhinitis demands antibiotics, systemic antihistamine and decongestants, and possibly intranasal or systemic corticosteroids.

Asthma Attack Symptoms

The symptoms of asthma vary greatly among individuals; and at times, attacks can vary, even for the same person. Your ability to recognize the early signs and symptoms that initially appear prior to an attack is critical if you wish to avoid an emergency room visit. When you notice these signs, you should heed the advice of your Doctor and follow a professionally directed action plan.

Before a full-blown asthma attack, there are usually early signs and symptoms you should be able to easily recognize. Irritation of the nose and throat, thirst, and the increased need to urinate are all common symptoms that may occur before an asthma attack. Each person has his or her own peculiar pattern of early symptoms, and most often, these symptoms progress to a severe respiratory distress episode if not properly treated.

The classic symptoms of an actual attack include coughing, wheezing, and shortness of breath. Wheezing when exhaling is very common during an attack. Often the attack begins with wheezing and rapid breathing and, as respiratory airways constrict and tighten, all breathing muscles become visibly active.

Some people first experience this chest tightness or pain. Chest pain occurs in about 75% of asthmatics; it can be very severe and its intensity is unrelated to the severity of the attack itself. The neck muscles may tense and talking may become difficult or impossible. The end of an attack is often marked by a cough that produces a thick, stringy mucus. After an acute attack, inflammation can persist for a few days up to several weeks. This inflammation is most often left untreated since it is usually symptomless. But, it is this asymptomatic inflammation that must be treated in order to prevent long term respiratory damage or relapse.

The most common asthmatic symptoms are:

Shortness of breath (dyspnea)
If you experience breathlessness after laughing or speaking long sentences, you could have asthma. In rare instances, you may find that you feel the need to inhale before you have finished breathing out.

Wheezing
This is the whistling sound sometimes heard when you breathe. It indicates airway narrowing and it could be present on inhalation or exhalation. (Please recognize that not all asthmatics wheeze and not all wheezing indicates an asthmatic condition.)

Exercise induced breathlessness
If physical exertion (playing a sport, walking up a flight of stairs, rapid physical exertion, etc.) makes you short of breath, then this could be an indication of asthma.

Tight chested feeling
This sensation feels like a tight band across your chest - like an elastic band or a heavy weight resting on your chest. Your ability to fully inhale is limited and, in advanced situations, painful. Sometimes this tightness is exacerbated in cold weather.

Excessive mucus production
Gurgling or rattling during inhalation or exhalation plus coughing up a lot of white frothy mucus is common in asthmatic individuals. Sometimes this mucous will be thick in consistency and yellow or green in color.

Cough
A recurring, irritating cough is frequently a sign of asthma. This persistent cough usually occurs in the cool air, at night, or after exercise.

Chest pain
When air is trapped in the airways due to inflammation, the surrounding membrane stretches, and causes pain. Advanced cases can often lead to complicated situations involving conditions similar to emphysema.

Nasal Congestion and drainage Nasal congestion and a runny nose are often accompanying features of asthma. Rhinitis (inflammation of the nasal passages) is often called asthma of the nose.

Disturbed Sleep Patterns
An inability to sleep due to snoring or repeated awakening during the night could be an asthma symptom. Other conditions also display this condition, so this symptom alone should not be considered conclusive.

Lethargy
Feeling very tired is quite usual for asthmatics. It is often the result of interrupted sleep patterns, diminished oxygen supply to the blood and availability to the body tissues, plus the build up of muscular lactic acid which results in generalized muscle fatigue.

The Early Warning Signs:
Even mild asthmatics can have severe attacks and therefore it is important to recognize the early signs so that you can take appropriate action.

• Your reliever (puffer) is no longer as effective and you need to use it more frequently than every 3-4 hours.


• The wheeze improves or even disappears but there is no improvement in your ability to breathe.


• You have real difficulty in speaking complete sentences without stopping to take a breath.


• You start to turn a blue to gray color, especially around the lips and fingertips. This is a condition called cyanosis and indicates that you have insufficient oxygen levels in your circulating blood.


• You become anxious to the point of being frightened.


• Thinking clearly becomes difficult.


• Every breath becomes increasingly difficult.

The best advice we could possibly give you is, Never ignore an asthma attack in the hope that it will get better or go away. If problems persist, seek qualified medical attention and follow a professionally directed recovery and treatment plan.

10 Simple and Natural Home Remedies For Asthma

Asthma is a long-term disease that has already affected millions of people all around the world. It is generally caused by allergies to certain substances such as dust, gases, smoke, pollens, foods, animal dander, cold weather, environmental changes, etc. Coughing, wheezing, difficulty in breathing, and tightness in chest are some of the major symptoms of this disease.

One must control asthma as it is a life-threatening and serious disease. Although asthma is a chronic disease, it is treatable. Read this article to find the best natural home remedies for asthma. These natural remedies help reduce the severity of the disease and relieve the various symptoms associated with it. These home remedies are very simple and one can easily follow them in the comfort of their home.

Asthma Home Remedies

* The first thing you need to do is to know various allergens that may trigger the symptoms, and try to avoid them.

* Take one teaspoon turmeric (haldi) powder two times a day along with warm water. This is an effective home remedies for asthma.

* Prepare a decoction by boiling equal quantities of ginger (adrak), holy basil (tulsi) and black pepper (kali mirch). Take this mixed with half a teaspoon of honey.

* Another useful home remedy for asthma is honey and ginger juice. Take one teaspoon of honey along with few drops of fresh ginger (adrak) juice on an empty stomach in the morning.

* Boil some carom seeds (ajwain) in water. Inhale the fumes produced by this hot solution. This helps relieve chest congestion.

* Carom seeds (ajwain) are also beneficial in reducing the excessive production of phlegm. Take carom seeds in the form of powder twice daily, or prepare a decoction and take it warm. This remedy is taken especially in bronchial asthma, when phlegm remains stuck in the bronchioles.

* The smoke that is obtained by burning asafoetida (hing) can be inhaled to get relief from spasms of bronchial asthma.

* Boil two or three cloves of garlic (lahsun) to a glassful of milk for five minutes. Drink hot to get relief from asthmatic symptoms.

* Another simple home remedy for asthma is mint. It is well known for its property of decreasing phlegm. Crush fresh mint leaves to extract its juice. Add equal amount of ginger (adrak) juice in mint juice. Take 8-10 ml of this mixture two times a day, along with honey.

* Holy basil (tulsi) is a valuable herb known for its anti-asthmatic properties. Crush few fresh leaves of holy basil and extract the juice. Mix basil juice with few drops of ginger (adrak) juice and some honey.

Copyright © Ryan Mutt, All Rights Reserved. If you want to use this article on your website or in your ezine, make all the urls (links) active.

Flameless Candles and Other Tips for Asthma Sufferers

All kinds of everyday things can provoke asthma attacks, and what triggers an attack in some people won't have any effect on someone else. Indoor air pollution is one of the most common causes of an asthma attack, so understanding the possible triggers can make the home a more pleasant, safe and relaxing place.

While we're all aware of outdoor pollution, unless something smells bad in the house we don't necessarily associate breathing difficulties with poor air quality indoors.

Common household elements that create indoor pollution are:

• Perfumes


• Hair Spray


• Air Fresheners


• Pet Dander


• Smoke or Fumes from candles


• Dust Mites

Why Indoor Pollution is Bad for Asthma

Small liquid, or solid, airborne particles are easily breathed into the lungs, and in people with asthma this causes extreme irritation in the delicate lung tissue. This in turn causes a restriction of the airways that leads to coughing or wheezing, a feeling of tightness in the chest and difficulty in breathing. Allergic reactions to common household products can also trigger asthmatic attacks, particularly in children.

Practical Steps to Reduce Indoor Air Pollution

The first step towards creating cleaner, less harmful indoor air is to remove those items that you know are irritants. If you're not sure what's triggering an asthma attack in your home you may need to experiment a little, removing or reducing use of one irritant at a time and watching for improvement in the sufferer.

Candles

Many people are surprised to find they're allergic to the fumes given off by burning candles. It may be the compounds used in the manufacturing of the candle, or it may be perfume, whether it's an added scent or the natural scent particles in the wax. Either way, the answer is to switch to flameless candles so you can still enjoy the ambiance but carry on breathing at the same time. As an added bonus, flameless candles are much safer in the home, especially where there are children or pets.

Perfumes and Air Fresheners

These commonly trigger asthma attacks, with some people reporting that plug-in air fresheners are particularly risky. Try running the air conditioning to freshen the air in the home, or open a window and let in fresh air unless the pollen outside will make matters worse. Avoid wearing perfume or, if you can tolerate a little, try spraying it only on wrists or behind knees so you don't directly inhale the fumes.

Dust Mites

Keep house dust down by using a damp cloth rather than spray polish on sealed surfaces. Use mattress and pillow protectors to keep beds and linen dust and mite-free. Use non-aerosol cleaners for wood or shiny furniture.

Asthma can be debilitating and frightening for children and adults alike. Once triggers are known it's easier to keep attacks to a minimum, and simple solutions such as using flameless candles or non-perfumed cleaning products are a small price to pay for easier breathing.

The True Cost of Dust Mite Feces in the Workplace

Dust mites are an allergy sufferer's worst nightmare. Each year 40 pounds of dust is generated in every 1500 square feet of space. Approximately 42,000 of these little bugs live in just one ounce of dust. 100,000 dust mites can live in a square yard of carpet. They feed on human skin scales, pollen, fungi, bacteria and animal dander. Dust mites do not drink free water, but absorb water from the air and the environment.

Dust mites are most closely related to spiders and ticks. They have eight hairy legs, no eyes, no antennae, and a tough, translucent shell giving a "fearsome appearance." They are about.01 inches (250 - 300 microns) in size and cannot be seen with the naked eye. People are not allergic to dust mites per se. People are allergic to dust mite feces and body fragments which are components of dust. These particles are so small they can become airborne and inhaled when dust is disturbed.

The allergens originating from dust mite feces and body parts are the second leading cause of allergies, behind pollen, and are significant triggers of asthma attacks. Estimates are that dust mite feces and body parts may be a factor in 50 to 80 % of asthma cases, as well as in countless cases of eczema, hay fever, and other allergic ailments. Symptoms associated with dust mite allergies include sneezing, itchy, watery eyes, nasal stuffiness, runny nose, stuffy ears, respiratory problems, eczema and asthma.

Asthma is a chronic pulmonary condition in which the airways become blocked or narrowed when stimulated by allergens or other environmental triggers. Sufferers experience difficulty breathing; they cough, wheeze, and have shortness of breath. Allergic asthma is the most common form, affecting more than 10 million Americans - half of all asthma sufferers. It is triggered year-round by the inhalation of allergens such as dust mites, pet dander, pollen, and mold. These allergens trigger the antibody immunoglobulin E (IgE), which is a key component of the cascade that causes the symptoms that result in lost productivity at work.

Asthma is a rapidly growing public health problem. According to the Centers for Disease Control and Prevention, about 23 million people have asthma. 12 million people report having an asthma attack in the past year. Asthma accounts for nearly 17 million physician office and hospital visits and nearly 2 million emergency department visits each year. Annual expenditures for health and lost productivity at work due to asthma are estimated at nearly $20 billion, according to the National Heart Lung and Blood Institute.

Work-aggravated asthma, the occupational form of allergic asthma, can exacerbate the symptoms of existing asthmatic conditions, further decreasing employee productivity. From 5 to 25 % of newly diagnosed cases of adult asthma and aggravation of previously diagnosed asthma in adults are related to the work environment. The Asthma and Allergy Foundation of America ("AAFA") reports that every day-

• 40,000 people miss school or work because of some form of asthma
• 30,000 people have an asthma attack
• 1,000 people are admitted to the hospital
• 14 people die from an asthma attack.

According to the AAFA, the annual cost of asthma is estimated to be nearly $18 billion. For adults, asthma is the fourth leading cause of work absenteeism, resulting in nearly 15 million missed or lost workdays each year and a total cost to employers of nearly $3 billion in lost productivity.

According to the EPA, dust mites and other allergy symptom triggers can be reduced, although not eliminated through regular cleaning. The most powerful weapon against dust mites is frequent dusting and vacuuming of the work space. The EPA recommends that the work space should be dusted with a damp cloth before the area is vacuumed so the dust has time to settle on the floor, where it can be picked up by the vacuum. Damp dusting reduces airborne particles by 93 percent compared with dry dusting. Since fiber-filled surfaces collect the most dust mite food, they have the highest concentrations of dust mites and their waste products. In the workplace, these bugs are most at home in upholstered furniture, rugs, carpets, draperies and curtains. Frequent, thorough vacuuming of carpets, furniture, textiles and other furnishings such as draperies will help keep populations low. Vacuums with highly efficient particle absorbing (HEPA) filters are able to trap at least 99.97 percent of particles of .3 microns in size.

By: Jim Van Eman

Asthma Eating Habits - They Are Killing You

Bad Asthma Eating Habits

It's no secret that most people these days tend to have poor diets but when it comes to asthma we really should be watching what we eat after all it affects us asthmatics a whole lot more than the average person. When you have asthma you will usually be breathing in double the amount of oxygen than a normal person does and as a result asthma symptoms begin to develop. You will need to watch your diet closely because it affects your weight which in turn affects your breathing all this has a sever impact on your asthma if you are not eating the correct foods.

You should never eat before going to sleep as an asthmatic. This fills your stomach and causes you to sleep deeper, the deeper you sleep the greater chance of you inhaling more oxygen than on a normal night, it also will make you pick up weight a lot faster when you eat a few hours just before sleep, you should aim to eat around 4-5 hours before sleep. Eating before you sleep also creates heat in your body. Asthmatics should always sleep in a cool room, not to warm and not to cool.

When you body is too warm, it will then try to cool itself down when you are asleep, one way that your body tries to accomplish this is through deeper breathing and like i said you cannot breathe deeply when you are an asthmatic, the result would be that you have to use your inhaler.

You can naturally reduce your asthma by simply eating healthy rich raw foods such as vegetables, fruits, nuts and seeds. Your diet should contain dates as dates tend to help people with asthma and at all costs avoid anything which is processed, these tend to be the fast foods that so many people have incorporated into their daily diets as well as most tins foods.

For the most part avoid chocolate and anything that contains high dairy. If you eat foods they should be warm and not too cold. I'm sure by now you know that by eating high dairy enriched foods closes your chest such as ice cream, ice cream is also cold and as a result your chest will begin to start wheezing if you eat loads of ice cream.

You should incorporate a good exercise program into your daily life, this will help keep any excess weight off of you and also help your breathing, one of the best forms of exercise tends to be swimming as this helps asthmatics regulate their breathing pattern.