Blowin’ in the Wind

Why are allergies so bad in Texas? What causes an allergic reaction? How do you choose an allergist? And what’s the best treatment: drugs or shots? The Answers, my friend, are Blowin’ in the Wind.

April 1997By Comments

I HAVE A CONFESSION TO MAKE: IN the thirty years I’ve lived in Texas, I’ve acquired a taste for greasy Tex-Mex and developed a passable drawl, but I’ve yet to suffer from the state’s unofficial disease: allergies.

This is a happy situation, of course, but there’s a fine line between pride and gloating, so it’s not something I advertise—not normally, and certainly not on this day, a Wednesday in late January, when I’m hanging around the Allergy Clinic on the sixth floor of the old Parkland Memorial Hospital building in Dallas. The forty to fifty patients who arrived here beginning at seven-thirty this morning are in no mood to hear about my good fortune: They’ve come for skin tests and immunotherapy shots and consultations with allergists about antihistamines and corticosteroid nasal sprays. They are not seasonal sufferers, but rather what might be called the hard core of Texas’ allergic subculture. For them, allergies are a perennial nemesis—and potentially deadly.

Theresa Floyd, for example, has been plagued by asthma and rhinitis (more commonly known as hay fever) since her childhood in Lubbock. “I was sensitive to everything,” the fifty-year-old says while awaiting a nurse in a treatment room. “Not just the typical stuff like ragweed and mountain cedar, but sunflowers and poinsettias. I started getting shots when I was in the first grade.” Nine years ago, after numerous near-fatal asthma attacks, Floyd sought care from the allergists at Parkland, and she has been coming regularly to the clinic ever since. She’s here today for her weekly immunotherapy shots for allergies to grasses and trees and to talk with a doctor about her cold—hardly the sort of thing that would send most of us to the hospital, but an emergency situation for a chronic multiple-allergy sufferer. “I don’t tempt fate,” she says. “A year and a half ago I was out raking leaves in the yard. Apparently, the mold from them got to me, because when I got inside, all I could do was lie down. I had one of those shutdown attacks of asthma. Fortunately, I was able to call EMS in time. I was in a coma for two days. I consider this a disability. I can’t run. I can’t laugh hard. I can’t even cry.”

While the vast majority of the state’s allergy sufferers can’t lay claim to that degree of pathology, grumbling and whining alone would suggest that most of us are tormented to one degree or another. In truth, all we know is that our allergy-afflicted population exceeds the national rate of 15 to 20 percent. “At any given time, you’d have to say that more people here are probably suffering from allergies than in, say, Maine,” says Donald Kennerly, an associate professor of internal medicine at the University of Texas Southwestern Medical Center in Dallas and the medical director of Parkland’s allergy and asthma clinics. “If you’re genetically predisposed, you’re going to have them here, whereas in Maine, the predisposition might never be triggered.”

More than anything else, what makes Texas the allergy capital of the United States is the pollens of two plants: ragweed and mountain cedar. The former, a member of the composite family, is found in other regions of the nation, but it is a particular problem in Texas, notably the Metroplex, in the fall. The latter, a juniper, is indigenous to much of Texas—especially Central Texas; it discharges its pollen from late fall to late winter. Mountain cedar is known to allergists as a kind of sarin gas of allergens—a pollen so potent that the allergic reaction to it is known as cedar fever. “No question about it: Mountain cedar makes allergies a year-round disease in Texas,” says Austin allergist William Howland. “For most people who move here having never had an allergy problem, it’s usually the culprit.”

Beyond the pollens, though, there are other reasons for our ignominious distinction. For one thing, Texas’ location in the center of the country means it is fertile ground for the allergen-producing plants of both the West and the East coasts. For another, our generally temperate climate allows for generous growing seasons for those plants but few of the hard freezes that stymie pollination, so allergens are airborne during all seasons and are more plentiful here than anywhere else. In the northeast, for example, allergens “available to the host” (as allergists put it) are airborne, at worst, from March to September. In Texas the nasty stuff is with us practically every month of the year, and it’s supplemented by mold spores, which flourish in the moist clay soil that runs through the center of the state. This toxic cloud is carried by strong winds all over Texas, exposing more of us more often to multiple allergens; while the average Northerner becomes allergic to only two substances, Texans can be susceptible to more than a dozen. If the winds don’t get you, the humidity will: Muggy temperatures encourage the growth of fungi and molds, whose spores are devastating to the allergy-prone. Texas’ rapid urbanization exacerbates the problem because construction stirs resting allergens, and industrial pollution—though not an allergen itself—worsens respiratory allergies. Add to these outdoor allergens the long list of indoor irritants, such as dust and dust mites, and you have an environment in which high doses of allergens fill the air nearly 365 days a year.

How Allergies Work

ONE OF THE CRUELEST BIOLOGICAL IRONIES IS that allergies are caused by the human immune system, the very thing in our bodies that’s supposed to keep us free of disease. In evolutionary terms, the immune system developed to distinguish between the self and the non-self—to provide the necessary biochemical armaments to protect the former and block, repel, or destroy the noxious elements of the latter. The precise immunological mechanism that causes allergies originally evolved, scientists believe, to intercept and destroy foraging parasites; today, its main function is to play war games with essentially harmless pollens and dust. An allergic reaction is, in essence, a case of mistaken identity: If you’re allergy-prone, pollens, dust, and mold spores that enter your body are misidentified as harmful, thus setting off the kind of symptoms you might endure if you were infected by a bacterium or a virus. A bit of dust or pollen in your respiratory tract might ordinarily cause you to sneeze or cough; but if you’re allergic, your hyperreactive immune system orders up the full complement of disease-fighting weaponry to combat what is really an innocuous intruder.

With airborne allergies, the source of this friendly fire overreaction is the antibody immunoglobulin E (IgE). Unlike other antibodies in the immune system’s arsenal, IgE binds readily with the mast and basophil cells found in your stomach and in the lining of your upper and lower respiratory tracts. When triggered properly, these cells produce histamine and other chemical mediators, which in turn stimulate the receptors in your body tissue and induce allergic symptoms in your nose, lungs, eyes, and stomach: Your blood vessels dilate, causing �uid to leak through their walls; your mucous membrane secretes at a greater rate than normal; and your body tissue in�ames and swells. The symptoms are so severe because histamine is an especially strong antagonist—so strong that if enough of it were released throughout your body, it could cause a sometimes fatal allergic reaction called anaphylactic shock.

IgE’s misguided responses manifest themselves through the receptors on either end of its molecule: One intercepts and binds with the incoming allergen, while the other attaches to the mast cell, instigating the allergic response. In allergy-prone people, the receptors are specific and have a great memory: Once it is sensitized to a particular allergen—that is, once the genetically loaded gun is cocked—the IgE—mast cell apparatus is thereafter at-the-ready to fire whenever it spots the same allergen trespassing. And the system can easily accommodate multiple sensitivities, since mast cells can bind with literally thousands of different allergen-specific IgE antibodies. The more allergy-prone the person and/or allergen-laced the environment, the more likely it is for multiple allergies to develop.

The duration, frequency, and intensity of allergic reactions vary: Some people are seasonally allergic, meaning their misery lasts only as long as specific plants pollinate; others are perennially allergic, either allergic to several allergens that predominate at different times of the year (such as ragweed and cedar) or hypersensitive to allergens that pervade the air year-round (such as fungus, mold, and dust). The classic allergic response, however, comes in several phases. First is the early nasal response, which arrives within moments of inhaling an allergen and involves an itchy nose, sneezing, and congestion; it reaches its apex quickly and gradually abates within an hour or two. Next is the quiescent phase, two hours in which the IgE—mast cell gun reloads itself with histamine and other nasty mediators. In the late nasal response, the mast cells discharge more histamine, while basophil cells fire their own mediators and recruit in�ammatory cells such as eosinophils and neutrophils to join the fray. These in�ammatory agents in turn secrete their own mediators, creating in short order a kind of riot in the nasal and bronchial passageways that can last up to twelve hours after exposure.

For many allergy sufferers, this is it—the full extent of their agony. But for others, the agony has just begun. In addition to the above-mentioned phases, they must endure a hyperresponsive phase, in which the respiratory system becomes so primed with histamine and other mediators that it reacts symptomatically in response to lower volumes of an allergen than that initially inciting the allergic response. Worse, the punch-drunk respiratory tract begins responding to all manner of non-allergic stimuli, everything from aerosol sprays and newsprint to bright lights. Some allergics also suffer a delayed nasal response days after their contact with the allergen. This is what drives most allergy sufferers to distraction. “My cedar fever could last for weeks,” says 44-year-old Austinite Robin Howard Moore, who suffered near year-round rhinitis for a good ten years. “I probably missed only a few days of work because of it, but when it set in, I was truly sick.”

Indeed, while allergic rhinitis is frequently bum-rapped as some sort of ritualistic hypochondria, there’s no disputing its real-life impact. Hay fever causes 28 million days of restricted activity in the U.S., plus 5 million lost work days, 3 million absences from school, and 5 million days of required bed rest each year. That adds up to $200 million in lost wages and $500 million in health care expenditures.

What Allergies Are—And Aren’t

AS UBIQUITOUS AS ALLERGENS MUST seem to the besieged multiple-allergy sufferer who lives in the Hill Country—the epicenter of the corridor of misery that runs through the center of Texas—fewer substances are capable of producing an actual allergic reaction than you’d think. We know this because allergists tell us so.

Don’t laugh: The study and treatment of allergies is a real medical discipline with hard science behind it. Coined soon after the turn of the century, the word “allergy” initially meant any “altered reactivity” by the body. By the twenties, European scientists had narrowed the definition to reactions involving antibodies and antigens. Still, little scientific evidence supported the so-called immunologic theory of allergy until IgE was discovered in 1967: The antibody provided a hook on which to hang allergic diagnoses and treatment—a way of seeing allergies as a specific set of reactions to a specific set of substances governed by specific immunological machinery.

Simply put, a hay fever allergen is a substance that is (a) easily carried by the wind and small enough to be inhaled, (b) chemically composed in such a way that it triggers IgE antibodies, and (c) readily available to human hosts. The second criterion, the IgE response, is critical to distinguishing true allergies from hypersensitivities to mundane airborne irritants ranging from cigarette smoke to perfume. In most cases, the symptoms are similar—runny nose, watery and/or itchy eyes, chest congestion, asthma—but the pathology is different. While allergies proceed from the IgE—mast cell apparatus, sensitivities (or adverse reactions) tend to be neurologically based: An irritant antagonizes the nerve endings in your nose, which relay a message to your brain, which, in turn, relays back instructions to the tissues in your nose to begin running or swelling. Repeated exposures to the agent can turn the response into a kind of re�ex that looks very much like an allergy—but it is not. While this may seem a distinction without a difference, it becomes extremely important when you’re seeking treatment, since true allergies can be treated medically, whereas sensitivities to environmental irritants generally must be managed by avoidance.

By and large, the instigators of allergic rhinitis are pollens of trees, grasses, and weeds. There are some seven hundred species of trees native to North America, of which only 65 or so consistently cause allergies. In Texas the heavy hitters among trees—which discharge their pollen primarily in the spring—are oak, elm, cottonwood, mesquite, and hackberry. In the summer, when grass pollens fill the air, the most common allergy instigators are Bermuda and Johnson grass (Saint Augustine, the other common Texas lawn grass, doesn’t produce airborne pollen). Autumn is weed season, and in these parts, the chief offender is ragweed; it is also the season for the pollen of the oddly named cedar elm tree, which is rarely found in other parts of the nation. And in winter, of course, while noses around the rest of the nation are mostly getting a break from assault-by-pollen, those of allergic Texans are assaulted by the fearsome mountain cedar.

The bad guys vary from region to region: Though fall ragweed and winter mountain cedar infest nearly all parts of the state, the former is miasmic in North Texas, while the latter especially cripples the Hill Country. West Texas, which is arid, is plagued by tumbleweed and sagebrush. Oddly enough, humid Houston tends to have less of a pollen problem than North or Central Texas, though its mold spores are legion. “There are regions in the Midwest that will show as high an incidence of pollens as Texas during certain seasons, but their window of exposure closes a lot more quickly,” says Fort Worth physician Lazarus Loeb, who has been treating allergies for nearly forty years and is considered the unofficial dean of Texas allergists. “You don’t get a break here, and the mold just adds to the irritation.”

What it is about the chemical composition of, say, mountain cedar pollen that causes the IgE antibodies to mistake it for a dangerous trespasser is largely a scientific mystery. Most allergists believe it has something to do with the protein at the core of most plant pollen and how it is read (or misread) by the immune system. Or a particular pollen may become a menace simply because of its degree of availability to the human respiratory system. Whatever the case, scientists have been able to figure out what conditions are most conducive to allergen invasion. In general, late afternoon to evening is the worst time for allergy sufferers because offending pollens, which have gradually risen well above our noses in the atmosphere in the heat of the day, begin descending with the setting sun and lower temperatures. Likewise, warm, dry, and windy days are always worse than cold, humid, or rainy ones: On damp days, pollen absorbs the moisture and becomes heavier and less aerodynamic; a good rain can literally wash pollen from the air.

None of these environmental vagaries, however, affects indoor antigens, which cause their own share of grief. Dust and dust mites, for instance, are proof to many allergy sufferers that their af�iction must be the handiwork of the devil: Neither can be completely eliminated from a house or apartment even by the most obsessive cleaner. And because dust is not a single substance but an amalgam of many—including animal dander, dried insect droppings, and mold spores—a hypersensitive person can be allergic to it on several levels. About the only break Texans get from indoor allergens is an inadvertent one: At the height of the summer’s heat, when we run our air conditioners 24 hours a day, the inside of our homes becomes so dry that the dust mites, molds, and fungi wither and die.

How to Treat Allergies

ESPECIALLY IN AN ALLERGY-FRIENDLY state like Texas, it’s tempting to chalk up your repeated or protracted nasal or bronchial problems to allergies. In fact, 60 percent of rhinitis is caused by non-allergic pathologies: a deviated nasal septum, overuse of nose drops, a persistent virus, and the like. So before you embark on a time-consuming or costly course of treatment, it’s best to first consult with your primary-care physician or an ear, nose, and throat specialist. If they rule out these other possible causes, they can give you an allergy skin test to confirm your suspicions. Once the diagnosis is made, your allergy can be treated in several ways.

Avoidance The most obvious and effective remedy is to stay away from offending allergens. Obviously, outdoor pollens, molds, and fungi are hard to avoid unless you move to another region. But allergists say you can diminish your allergic response by keeping your distance from parks and other areas where multiple pollens are found and by remaining indoors as much as possible during the pollen-rich late afternoon and evening.

Once inside, you can do a lot to sanitize your environment. Allergists say that aside from wet-mopping and dusting frequently and washing your sheets and pillow cases in hot water, you should focus on the rooms where you spend most of your time—the bedroom, for example—and on items that serve as good nests for mites—say, carpeting. According to allergist Peter Boggs, the author of Sneezing Your Head Off?, one of the best things you can do if you’re particularly susceptible to dust and dust mites is rip the carpeting out of your bedroom. Yet another way to purify your indoor atmosphere is with an air-filtration system: It’s more expensive, but it can be remarkably effective in weeding allergens out of the air. Fans, by contrast, only provide the illusion of clearing the air; they actually increase your exposure to allergens by stirring them up, though they’re extremely good at drying out dark, damp areas where molds grow.

Avoidance tends to be an underused allergy treatment because in a lot of cases it’s impossible: You may be able to get your house under control, but then you find yourself deluged with allergens at the office. That’s when you turn to…

Drugs There are four types of medications designed to treat allergy symptoms: antihistamines, decongestants, antitussives, and expectorants. Each addresses some but not all of the common symptoms, and even then the relief is only temporary, and the underlying cause of the symptoms remains unchanged. You can also develop a tolerance to many of the medications rather quickly—in the case of nose drops, for instance, it can be a matter of a few days—and all of them pack possible unpleasant side effects, including, ironically, a potential allergic reaction. Yet symptom-first medications are an important component of allergy treatment because so many of us suffer only occasional or minor symptoms, and they work well enough at simply stopping the snif�ing and unblocking the nasal passages.

The best way to determine which of the hundreds of allergy drugs are for you is to talk to an experienced allergist. Beyond that, any prudent patient-consumer should consider the following when seeking either prescription or over-the-counter medications:

Antihistamines are for runny noses, sneezing, postnasal drip, watery eyes, and itchy noses and throats. Antihistamines suppress or block altogether the release of histamine from mast cells during an allergic reaction. Histamine, you’ll recall, is what provokes allergic symptoms through receptors located in nasal and bronchial tissue. Antihistamines compete for the receptors most responsible for allergic symptoms; when they occupy the receptors, the receptors, which can handle only one agent at a time, are forced to ignore the histamine. No receptor response; no symptoms.

Not all antihistamines are created equal. To begin with, there are “old” antihistamines, which cause drowsiness, and “new” antihistamines, which don’t. The latter are available by prescription only and are wildly popular, yet they may or may not be safe: The U.S. Food and Drug Administration recently determined that one such antihistamine, Seldane, has potentially life-threatening side effects when taken in combination with some antibiotic and antifungal drugs. Of course, the old antihistamines can cause cardiovascular irregularities too, as well as gastrointestinal problems and allergic reactions (including hives, eczema, shock, and swelling of the limbs, skin, and voice box). But there are at least seven chemical classes of antihistamines, and the extent of the side effects varies from class to class. It’s worth asking your doctor or pharmacist which ones cause the fewest unintended consequences; they will likely tell you that the antihistamines that provide sustained relief and not much drowsiness are those containing brompheniramine, chlorpheniramine, and clemastine—for example, Dimetane Extentabs, Tavist-1, and Chlor-Trimeton Repetabs.

Decongestants combat congestion and the swelling of air passages. They open the nose by constricting blood vessels that have been made to dilate and ooze by the release of histamine. Their side effects tend to be insomnia, higher blood pressure, nervousness, and difficulty urinating. Some topical decongestants, such as nose drops, can also cause rebound swelling in your nasal passages if you overuse them—that is, if you consistently use more of the drops than the lowest recommended dosage, if you use them for more than three to five days, or if you continue to use them when they aren’t working. There is no such rebound effect in systemic decongestants—that is, capsules and pills—and those that contain the generic substance pseudoephedrin (Sudafed) have less of an effect on your blood pressure, but the other side effects remain.

Start with topical decongestants; then, if they don’t work, move on to systemic decongestants. The reason for this is that the side effects of topical decongestants tend to be less invasive on the whole than those of systemic decongestants. So if your problem is primarily nasal congestion, try an over-the-counter spray such as Afrin regular or menthol sprays or Allerest 12-Hour Spray before trying capsules or pills. If the sprays don’t work, the best capsule decongestants are sustained-release products like Sudafed 12-Hour and Afrinol tablets. Such products are also more convenient, as they call for doses twice a day rather than four or six times.

Antitussives and expectorants are for coughing. The former are designed to stop a cough; the latter loosen mucus and bring up phlegm.

Combination drugs aren’t necessarily better. Many are available both by prescription and over the counter, a market-driven response to the fact that most allergy sufferers sustain multiple symptoms. Yet allergists say drugs that promise to suppress all symptoms can increase the chances of an unintended side effect—so it’s always best to treat the main symptom with the appropriate medication. If the problem is a runny nose, stick with antihistamines; if it’s sinus swelling, stay with decongestants. And if you decide to use a combination product, limit the possibility of side effects by making sure it contains only one antihistamine and one decongestant.

Contrary to popular belief, many over-the-counter medications are just as strong as the prescription varieties. Yet even though you don’t need a prescription, you still have to heed the dosage guidelines. As with any medication: When it’s not working, stop taking it.

Also contrary to popular belief, over-the-counter medications can be as expensive as prescription drugs. For example, the prescription antihistamine Extendryl costs $13 for thirty capsules at my neighborhood Eckerd Drugs; over-the-counter Drixoral costs between $15 and $17 for thirty capsules.

If the first line of defense doesn’t work, ask your doctor about corticosteroid or cromolyn sodium sprays. These products don’t act as quickly as over-the-counter decongestant sprays, but they can provide more sustained relief because they address both histamine activity and the chronic in�ammation that accompanies long-term allergies. For many allergy sufferers, the real problem is the ongoing tenderness and hypersensitivity of their nasal and bronchial passages. They’re sensitive not only to specific allergens but also to a wide host of other irritants. When administered on a regular basis, corticosteroid and cromolyn sodium sprays can reduce the number of in�ammatory cells swimming about in the mucosa and diminish the hypersensitivity of nasal nerves.

And if that doesn’t work—or even if it does, but you want a more global allergy treatment—there’s only one thing to do: Forget about going after the symptoms and go after the cause.

Immunotherapy Allergy shots have always had a bad name. At best, they’re seen by much of the public as overpriced placebos for an essentially incurable condition; at worst, they’re the latter-day witchcraft of quacks. As it has with the rest of allergy science, respect for immunotherapy as a safe, effective treatment for allergies has come slowly and uncertainly. Over time, skeptics have tried such questionable approaches as homeopathy, detoxification, autogenous urine therapy, neutralization therapy, and vitamin and nutrient supplements. Yet if administered properly by an allergist and adhered to prudently and patiently by the allergy sufferer, immunotherapy can yield a higher success rate than any of these alternatives—more than 70 percent, according to UT-Southwestern’s Kennerly, who not only administers the treatment but has undergone it himself.

Immunotherapy starts with allergy skin testing, a procedure in which doctors use plastic probes to gently scratch tiny doses of the extracts of as many as fifty antigens (such as pollens, grasses, weeds, molds, dust) into the skin on your back. After a fifteen- to twenty-minute wait, the allergist inspects the scratch sites for reddening and swelling known as �are and wheal reactions; the antigens that cause them become the basis of treatment.

If the offending allergens are, say, the pollens of certain trees, you’re placed on a weekly protocol of shots containing the extract of those pollens—the idea being that you’ll develop a resistance to the allergy. The initial dosages are small and highly diluted, so the therapy itself doesn’t cause an allergic reaction. As your system displays more tolerance, the size and potency of the doses are increased over a three- to six-month period, until you’re ready to receive a so-called maintenance dose, whose concentration is about 10,000 times as strong as the initial dose. “This is generally the dose that can produce the therapeutic results we want and can also be tolerated by the patient,” says Kennerly. By this time, your symptoms should be much improved or in remission. If so, the maintenance dose is adhered to from then on, with shots scaled back to twice a month, then once a month. “The whole process generally will take about three years,” Kennerly says. “There’s a lot of art to it, as well as science. Sometimes a person can be so sensitive that it takes much longer than the three to six months to establish the maintenance dose. In my case, that alone took about two years. It just depends on your specific sensitivity. It is a gradual process of the immune system building a kind of tolerance to the allergen.”

The inner scientific workings of immunotherapy aren’t completely clear, but allergists know a bit about what happens when your tolerance develops. When you receive a shot of the extract of the offending allergen, your immune system begins to produce more and more of the IgE antibody until the supply, in essence, begins to wane. At the same time the remaining IgE antibodies are gradually retrained not to initiate the allergic response. In a sense, the immune system, guilty of a well-intentioned error to begin with, makes amends by policing itself.

Of course, allergy shots aren’t for everyone. “In general,” says Kennerly, “they tend to work better on highly allergic individuals like me. Lesser degrees of sensitivity don’t get as good a response.” In any case, someone looking for such relief should be careful in selecting an allergist, he says, because some doctors may practice according to outdated treatment paradigms that dictate you don’t “dose up” a patient quickly or intensely. “We’ve only really known for about fifteen years that aggressive high-dosing is what works,” he says. “The cautious approach puts the patient through a lot of trouble for nothing.” Case in point: Jim Hicks, a Dallas labor and employment lawyer who began receiving immunotherapy shots from one doctor in the late eighties but didn’t really begin to feel improvement until 1994, when he switched to an allergist who favored the high-dose protocol. “I breezed through that fall of 1995, which was awful for pollen,” says Hicks, who was especially sensitive to fall pigweed. “Whatever he did, it sure has worked. It used to be that I really only had a ten-month year. This therapy has given me back two months. I can go hunting again in the fall.”

In addition to being symptom-effective, immunotherapy can be cost-effective as well. “Compared to what you might pay for antihistamine and corticosteroidal nasal sprays over a lifetime, it can actually represent a savings,” Kennerly says. Typically, immunotherapy shots run from between $5 and $20 apiece, not counting the fee for a visit to your doctor’s office. But because the number of shots required each month can be gradually decreased, and at some point the treatment ends altogether, immunotherapy still saves you money in the long run.

For his part, eight years after beginning immunotherapy, Kennerly still takes a monthly maintenance dose “as an insurance policy.” But he rarely needs to take an antihistamine or a decongestant. “It isn’t an absolute cure,” he says, “but it can send an allergy into complete remission.”

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