Allergen ยท Symptoms & Treatment
moderate Severity

Bluegrass Allergy: When America's Favorite Lawn Grass Is Making You Sick

Kentucky bluegrass (Poa pratensis) dominates northern US residential lawns and produces its peak pollen in June. A Pooideae sweet grass, it shares approximately 95% IgE cross-reactivity with timothy via Group 1 and Group 5 allergens, so a single timothy-based immunotherapy covers bluegrass exposure. Poa annua (annual bluegrass) flowers year-round in mild climates, extending the pollen window beyond the typical Mayโ€“July season for many patients.

moderatePeak: Mayโ€“JulyUpdated April 24, 2026

Free ยท 5 min ยท Insurance accepted

Reviewed by Dr. Chet Tharpe, M.D.
As seen inUSA TODAYMen's HealthCBSForbes
The numbers
Headline stat
0%
WILD STANDS IN US/CANADA
US prevalence
0โ€“30%
Americans affected
~0M
Peak season
Mayโ€“July
Peer-reviewed sources
0

Key facts

  • Kentucky bluegrass (Poa pratensis) covers approximately 90% of US and Canadian wild pasture stands, making it one of the most ubiquitous aeroallergen sources in North America.

    Bousquet J et al., Allergy, 2008

  • Bluegrass shares approximately 95% IgE cross-reactivity with timothy via conserved Group 1 (Phl p 1) and Group 5 (Phl p 5) allergen proteins across the Pooideae subfamily.

    Bousquet J et al., Allergy, 2008

  • Poa annua (annual bluegrass) can produce pollen year-round in mild coastal climates, extending the effective bluegrass season beyond the typical Mayโ€“July window.

    D'Amato G et al., Allergy, 2007

  • Approximately 30โ€“40% of patients with untreated allergic rhinitis develop asthma within 10 years โ€” grass pollen is among the most prevalent outdoor drivers of this progression.

    Bousquet J et al., Allergy, 2008

  • A single timothy-based sublingual immunotherapy tablet (Grastek or Oralair) provides clinical benefit against bluegrass due to complete Group 1/Group 5 cross-reactivity.

    Bousquet J et al., Allergy, 2008

01Overview

Kentucky bluegrass (Poa pratensis) is the most commercially important lawn grass in the United States.

If you live north of the transition zone โ€” anywhere from New England through the Midwest, the mid-Atlantic, or the Pacific Northwest โ€” the grass in your front yard is almost certainly bluegrass. It blankets roughly 90% of US and Canadian wild pasture stands as an aggressive naturalized species far beyond intentional planting. In residential settings, bluegrass is deliberately sown precisely because it produces the dense, lush, blue-green turf Americans associate with a well-kept lawn.

Bluegrass belongs to subfamily Pooideae โ€” the "sweet grass" group that includes timothy, ryegrass, fescue, orchard, and sweet vernal grass. All Pooideae grasses share a highly conserved set of Group 1 and Group 5 allergen proteins, creating approximately 95% IgE cross-reactivity across the subfamily. What this means clinically: if you are allergic to bluegrass, your immune system reacts to the same molecular targets it would if you were allergic to timothy, ryegrass, or fescue. The grass in your lawn and the grass in an Oregon pasture trigger the same IgE antibodies.

Bluegrass is also called "June grass" โ€” a name that reflects its peak pollen production in June across most of its US range. Its pollen season runs from May through July, with the June peak accounting for the highest airborne concentrations. Along with orchard grass, bluegrass accounts for more grass pollinosis in the eastern United States during the first half of the grass pollen season than all other grass species combined. That statistic reflects the dual dominance of these two species: one in cultivated lawns, one in naturalized pastures and roadsides, together making June the most symptomatic month for grass-allergic Americans in the eastern half of the country.

02Symptoms

Recognizing symptoms early helps you get the right treatment faster.

When to see a doctor

Bluegrass allergy symptoms are identical to those of other grass pollen allergies, consistent with the shared Group 1 and Group 5 allergen proteins driving cross-reactive IgE across all Pooideae grasses. **Upper respiratory symptoms (most common):** - Sneezing โ€” often in rapid, multiple-sneeze bursts - Runny nose (watery rhinorrhea) - Nasal congestion and pressure - Postnasal drip - Itchy nose and palate **Ocular symptoms:** - Itchy, watery, red eyes (allergic conjunctivitis) - Eyelid swelling - Light sensitivity during peak pollen days **Lower respiratory symptoms (in sensitized individuals):** - Cough from postnasal drip - Wheezing and chest tightness in pollen-triggered asthma - Worsening of pre-existing asthma during June peak **Skin symptoms:** - Urticaria (hives) from grass contact after mowing or outdoor activities - Contact dermatitis at skin contact points Symptom severity typically correlates with pollen count: light days (below 50 grains/mยณ) may produce minimal symptoms in mildly sensitized individuals, while high-count days (above 200 grains/mยณ) cause significant impairment even in moderately sensitive patients. The unique exposure dynamic for bluegrass-allergic patients is the lawn itself โ€” symptoms often spike after the individual or a neighbor mows, temporarily elevating local pollen concentrations far above ambient levels.

Grass pollen is a well-established trigger for allergic asthma, and bluegrass's June dominance in northern and eastern US makes it the primary grass trigger for asthma exacerbations during that month. Studies of grass-related asthma hospitalizations consistently show a June spike in the northeastern and midwestern United States that mirrors bluegrass and timothy pollen counts. For individuals with both allergic rhinitis and asthma, the nasobronchial reflex means nasal congestion from bluegrass pollen can directly increase lower airway reactivity, even when inhaled pollen load to the bronchi is relatively low. Poorly controlled rhinitis from bluegrass exposure is a recognized risk factor for asthma worsening. The key distinction between bluegrass and ryegrass (the other major Pooideae grass with a documented asthma association) is the thunderstorm asthma mechanism. Thunderstorm asthma โ€” where osmotic rupture of hydrated pollen grains releases thousands of ultra-fine starch granules โ€” is primarily documented with ryegrass, not bluegrass, because ryegrass pollen ruptures more readily under osmotic stress. Bluegrass contributes to the overall grass-pollen-asthma relationship through conventional sensitization rather than the thunderstorm asthma pathway specifically. Patients with asthma and confirmed grass sensitization should discuss controller medication adjustments before June with their allergist. The mowing trigger is especially relevant: exposure to freshly mowed grass โ€” which aerosolizes pollen mechanically in addition to ambient airborne counts โ€” is a well-documented asthma flare trigger for grass-allergic patients.

If left untreated

Left untreated, seasonal bluegrass allergy can progress and compound, with several clinically significant complications: **Rhinitis-to-asthma progression:** An estimated 30โ€“40% of patients with untreated allergic rhinitis develop asthma within 10 years. Grass pollen, as one of the most prevalent outdoor aeroallergens, is among the most common drivers of this progression. Annual June symptom peaks that go untreated represent repeated inflammatory priming of the lower airway. **Sinus complications:** Chronic nasal congestion from seasonal rhinitis promotes eustachian tube dysfunction, otitis media, and sinusitis. Patients who tolerate moderate grass allergy symptoms each June may develop recurrent sinus infections as a secondary consequence. **Sleep disruption and cognitive impairment:** During peak June pollen periods, even moderate allergic rhinitis significantly impairs sleep quality. Studies show grass pollen season is associated with measurable reductions in reaction time and concentration โ€” a phenomenon sometimes called "brain fog" that carries real-world consequences for academic and occupational performance. **Oral allergy syndrome:** Bluegrass-sensitized individuals may experience oral allergy syndrome (OAS) โ€” itching or swelling of the mouth and throat after eating certain raw foods. Grass cross-reactive foods include celery, melon (especially watermelon), tomato, orange, and peach. OAS symptoms typically resolve with cooking. **Expansion of sensitization:** Without treatment, chronic allergen exposure can trigger new sensitizations โ€” patients who start with grass allergy sometimes develop additional tree, weed, or mold sensitivities over subsequent seasons, expanding the severity and duration of their overall allergy burden.

03Why it happens

Bluegrass allergy is driven by wind-dispersed pollen from Poa pratensis and closely related Poa species. When a sensitized individual inhales bluegrass pollen, IgE antibodies on mast cells in the nose, eyes, and airways recognize the allergen proteins and trigger immediate hypersensitivity reactions: histamine release, prostaglandin production, and the cascade of symptoms that collectively constitute hay fever and allergic rhinitis.

The primary allergen proteins in bluegrass are Group 1 (a beta-expansin, equivalent to Phl p 1 in timothy) and Group 5 (equivalent to Phl p 5). These are the same allergen families that drive sensitization to timothy, ryegrass, fescue, orchard, and sweet vernal grass โ€” explaining why 95% of grass-allergic patients who react to timothy also react to bluegrass and vice versa. Unlike bermuda or bahia grass, bluegrass carries Group 5 allergens, placing it firmly in the Pooideae cross-reactivity network.

An important amplifier of bluegrass exposure is Poa annua โ€” annual bluegrass โ€” a close relative that flowers year-round in mild climates including the Gulf Coast, coastal California, and parts of the Pacific Northwest. While Poa pratensis has a defined Mayโ€“July season, Poa annua can produce pollen in any month with mild temperatures. This extends the effective "bluegrass" pollen window for many patients beyond what standard seasonal allergy calendars would suggest, potentially explaining late-winter or early-spring grass symptoms in southern or coastal populations.

Two further exposure amplifiers: first, approximately 90% of Poa pratensis stands in North America are wild pasture, meaning bluegrass pollen production extends far beyond residential lawns into roadsides, field margins, and open land adjacent to suburban areas. Second, bluegrass is not simply passively encountered โ€” millions of Americans actively maintain bluegrass lawns, mowing and disturbing pollen-laden grass weekly during peak season.

The Allergy Cascade

1.Exposure

Allergen contact

2.Detection

Immune recognition

3.IgE Response

Antibody production

4.Mast Cells

Histamine release

5.Symptoms

Allergic reaction

05Diagnosis

Confirming bluegrass allergy and distinguishing Pooideae sensitization from sour grass sensitization is clinically important, because the treatment strategy differs significantly. Standard diagnostic approaches include: **Skin prick testing (SPT):** A small amount of standardized bluegrass extract (or a grass pollen mix) is applied to the forearm via lancet. A wheal-and-flare reaction confirms IgE-mediated sensitization. SPT is fast (results in 15โ€“20 minutes) and highly sensitive for grass pollen. **Serum IgE testing:** Blood tests measure specific IgE antibodies to bluegrass (ImmunoCAP g8) or to grass mix panels. Because bluegrass is nearly completely cross-reactive with other Pooideae grasses, a grass mix or timothy-specific panel detects bluegrass sensitization with high accuracy. **Component-resolved diagnostics (CRD):** Molecular testing distinguishes Pooideae sensitization from sour grass sensitization โ€” the clinically critical distinction. Phl p 1 and Phl p 5 are the key biomarkers: a positive Phl p 5 confirms Pooideae sensitization (bluegrass, timothy, ryegrass, fescue, orchard, sweet vernal), while negative Phl p 5 with positive Cyn d 1 indicates primary bermuda sensitization that is NOT covered by Grastek or Oralair. Curex offers at-home component-resolved testing that can identify Phl p 1 and Phl p 5 positivity, distinguishing Pooideae sensitization โ€” including bluegrass โ€” from co-existing sour grass sensitivities. This is especially valuable for patients in climate transition zones where bluegrass (northern) and bermuda (southern) territories overlap. **Nasal provocation testing:** Occasionally used in research settings to confirm clinical relevance of sensitization, but not routinely performed in clinical allergy practice.

At-home testing

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Immunotherapy

The long-term solution to allergies

Instead of masking symptoms, immunotherapy retrains your immune system.

Immunotherapy is the only treatment that modifies the underlying allergic disease rather than suppressing symptoms. For bluegrass allergy โ€” a Pooideae sensitization โ€” two FDA-approved SLIT tablets and one custom drop approach are available: **Grastek (timothy grass SLIT tablet, 2800 BAU):** The most direct option. Because bluegrass and timothy share ~95% IgE cross-reactivity via Group 1 and Group 5 allergens, the timothy-based Grastek tablet effectively desensitizes bluegrass-allergic patients. FDA-approved for ages 5โ€“65, Grastek must be initiated at least 12 weeks before grass season to achieve pre-seasonal efficacy. Pivotal trials demonstrated 10โ€“34% total combined score reductions versus placebo, with sustained effects through year 4. First dose is administered in a clinical setting; subsequent doses are taken daily at home. **Oralair (5-grass SLIT tablet, 300 IR):** Contains timothy, orchard, bluegrass, ryegrass, and sweet vernal. The inclusion of bluegrass as an explicit component may offer a marginal advantage over single-grass Grastek for patients with high-density bluegrass-specific sensitization, though given 95% cross-reactivity, the clinical difference is modest. Ages 10โ€“65. **Subcutaneous immunotherapy (SCIT):** Weekly injections with grass extract remain an effective option. For Pooideae-only sensitized patients, a timothy-based extract adequately covers bluegrass. Patients with co-existing bermuda sensitization need separate vials. **Curex custom SLIT drops** at **$39/month** offer multi-allergen convenience: patients sensitized to bluegrass plus tree pollen, dust mites, or weed pollen can combine all their sensitivities into a single daily drop formula โ€” eliminating the need to coordinate multiple tablet regimens or injection schedules. A real-world Curex study of 2,897 patients on at-home sublingual immunotherapy (Tharpe et al., Frontiers in Allergy, 2026) found that clinically meaningful symptom improvement rose to 45% of patients by two years, quality-of-life improvement reached 90.7%, adherence exceeded 90%, and no anaphylaxis was reported. Desensitization to the grass in your own lawn is particularly meaningful for bluegrass-allergic patients, as it directly targets the allergen they encounter every week for months each year.

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Living with it

Living With Bluegrass Allergy

Bluegrass allergy presents a distinctive management challenge: unlike tree pollen (which comes from external environmental sources) or animal allergens (which can be avoided by limiting contact), the dominant exposure source for many bluegrass-allergic patients is the turf they choose to maintain in their own yard. The grass is not incidental โ€” it is cultivated and maintained by the patient, creating a degree of control that most other allergen scenarios do not offer. Practically, this means bluegrass-allergic individuals have more agency over their primary exposure source than patients with most other pollen allergies. Keeping the lawn short, delegating mowing, or progressively replacing lawn sections with non-allergenic alternatives are all genuinely effective strategies โ€” not just generic avoidance advice. For parents of children with bluegrass allergy, the June lawn is a particular challenge. Grass play is a significant part of childhood outdoor activity, and the same lawn that triggers allergy symptoms in a sensitized child is often central to their summer recreation. Practical approaches include scheduling high-activity outdoor play on days with lower pollen counts, bathing and changing clothes after lawn play, and ensuring indoor spaces provide a pollen-free recovery environment. Work and school performance can be significantly affected during the June peak. Bluegrass-allergic adults and students should plan around known high-pollen periods: important presentations, exams, and deadlines are better scheduled on overcast, rainy days when counts are lower. Pre-treating with antihistamines and INCS before known high-exposure events (outdoor graduation ceremonies, summer weddings) helps maintain function. Many patients with long-standing bluegrass allergy find that immunotherapy changes their relationship with the season. Moving from reactive symptom management to proactive desensitization โ€” knowing that this June will be less miserable than last June โ€” substantially improves quality of life and long-term compliance with treatment.

Long-term outlook

Untreated grass pollen allergy rarely resolves spontaneously in adults. Natural tolerance does not develop with repeated annual exposures โ€” most patients find that symptoms remain stable or gradually worsen over years, both in severity and in duration, as the allergy season seems to "expand" in both directions relative to what was originally a tight June window. With pharmacological management alone (antihistamines, INCS), symptoms are controlled each season but the underlying sensitization persists and often strengthens. Patients on suppressive medication frequently find they need incrementally higher doses or combination therapy over the years. Immunotherapy is the only intervention that alters the natural history of grass allergy. Clinical trials of grass SLIT tablets demonstrate: - Statistically significant reductions in symptom scores and medication use during grass season (10โ€“34% TCS reduction for Grastek) - Sustained effect through at least year 4, with some evidence of benefit extending to year 5 - Reduction in the risk of new sensitizations developing in monosensitized patients - In children with allergic rhinitis, a documented reduction in progression to asthma For bluegrass-specific allergy, the prognosis with treatment is excellent. The Pooideae cross-reactivity system works in the patient's favor: one well-characterized immunotherapy (timothy-based) desensitizes the immune response to bluegrass and five other common grass species simultaneously. Patients who complete a 3-year SLIT course consistently report meaningfully reduced June symptoms and reduced dependence on rescue medications. The most important prognostic factor is early treatment. Starting immunotherapy at the first recognition of grass allergy โ€” rather than after years of escalating symptoms and expanding sensitization โ€” produces the best long-term outcomes.

The 95% cross-reactivity between bluegrass and timothy is clinically consequential: patients with bluegrass lawn exposure do not need a separate bluegrass extract in their immunotherapy. A timothy-based SLIT or SCIT protocol covers the Group 1 and Group 5 proteins responsible for their symptoms, simplifying treatment while delivering the same clinical benefit.

Board-certified allergist (clinical reviewer for this article)
FAQ

Frequently Asked Questions

Functionally, yes โ€” for the purposes of diagnosis and treatment. Bluegrass (Poa pratensis) and timothy (Phleum pratense) both belong to the Pooideae subfamily and share approximately 95% IgE cross-reactivity through conserved Group 1 (beta-expansin) and Group 5 (ribonuclease-like) allergen proteins. A positive Phl p 5 test result (the key timothy biomarker) reliably identifies bluegrass sensitization, and timothy-based immunotherapy โ€” including the FDA-approved Grastek tablet and Oralair 5-grass tablet โ€” effectively desensitizes patients to bluegrass pollen as well. Where bluegrass and timothy differ is in their exposure profile: timothy is primarily a hay and pasture grass, while bluegrass is the dominant residential lawn grass in northern America. Most bluegrass-allergic patients encounter their allergen weekly in their own yard, while timothy exposure is more incidental. The clinical treatment pathway is identical, but bluegrass patients have greater avoidance options through lawn management.

Mowing bluegrass dramatically elevates local pollen concentrations in ways that ambient air monitoring doesn't capture. When grass is cut mechanically, pollen-laden anthers that would otherwise release their pollen gradually over hours are disrupted all at once, releasing concentrated pollen into the air immediately surrounding the mowing activity. Additionally, mowing aerosolizes pollen that has already settled on grass blades, re-suspending it. Studies show that ambient pollen counts can be 5โ€“10 times higher in the immediate vicinity of mowing activity compared to undisturbed lawn areas during the same weather conditions. The simplest protective steps: mow in the evening (natural pollen counts are lower in evening hours), wear an N95 mask and close-fitting goggles, and change clothes and shower immediately after finishing. If symptoms are severe enough that mowing is genuinely debilitating, delegating the task during peak season is a legitimate medical recommendation.

Isolated bluegrass sensitization without cross-reactivity to other Pooideae grasses is theoretically possible but clinically uncommon. Because all Pooideae grasses share approximately 95% IgE cross-reactivity, the vast majority of bluegrass-allergic patients simultaneously react to timothy, ryegrass, fescue, orchard, and sweet vernal grass. What patients often perceive as bluegrass-only allergy is actually Pooideae family allergy, with bluegrass being the dominant exposure source in their environment. True grass-monosensitization โ€” allergy limited to a single species โ€” does occasionally occur, but component-resolved diagnostics would be needed to confirm this. More clinically relevant is the possibility of being allergic to bluegrass (Pooideae, covered by Grastek) while ALSO being allergic to bermuda grass (Chloridoideae, NOT covered by Grastek) โ€” this dual sensitization requires separate immunotherapy extracts and is best identified through component testing.

In mild-winter climates, yes โ€” Poa annua can cause year-round or nearly year-round grass pollen exposure. Annual bluegrass (Poa annua) is a widespread weed closely related to Kentucky bluegrass (Poa pratensis) that flowers whenever temperatures remain above freezing. In coastal California, the Gulf Coast, Pacific Northwest lowlands, and similar mild-winter regions, Poa annua pollen has been detected in ambient air samples during every month of the year. Patients in these regions who appear to have year-round or winter-onset grass allergy โ€” rather than the typical Mayโ€“July season โ€” may be reacting to Poa annua rather than the expected spring/summer grasses. Allergy testing for grass pollen in mild-climate regions should account for the possibility of Poa annua as a year-round sensitizer. Standard grass pollen extracts used in skin testing and immunotherapy cover Poa annua through cross-reactivity with Poa pratensis.

Yes โ€” bluegrass allergy is covered by both FDA-approved grass SLIT tablets. Grastek is a single-grass tablet standardized to timothy (Phleum pratense, 2800 BAU), approved for ages 5โ€“65. Because bluegrass and timothy share approximately 95% IgE cross-reactivity through Group 1 and Group 5 allergens, Grastek effectively desensitizes bluegrass-sensitized patients. Oralair is a 5-grass tablet that explicitly includes bluegrass (Poa pratensis) as one of its components alongside timothy, orchard, ryegrass, and sweet vernal, approved for ages 10โ€“65. Both tablets must be initiated at least 12 weeks before grass season begins and administered daily. For patients with both grass and non-grass allergies โ€” tree pollen, dust mites, or weeds โ€” SLIT tablets treat only grass and require supplementary treatment for other sensitivities, while custom SLIT drops allow combination of multiple allergens in a single regimen.

Yes โ€” children as young as five years old are eligible for Grastek, the FDA-approved timothy-based sublingual immunotherapy tablet that covers bluegrass through cross-reactivity. Oralair, which explicitly includes bluegrass pollen, is approved for ages ten and up. Pediatric grass immunotherapy carries the same efficacy profile seen in adults, with an important added benefit: clinical trials show that grass SLIT in children with allergic rhinitis significantly reduces the rate of progression to asthma compared to those receiving only symptomatic medications. This disease-modifying effect on asthma development is one of the strongest arguments for starting immunotherapy early in pediatric patients rather than relying on long-term antihistamine and nasal steroid use. Parents concerned about the daily sublingual dosing routine should know that SLIT tablets are designed for unsupervised home use after the first dose, and most school-age children tolerate the regimen without difficulty.

Yes โ€” outdoor exercise during bluegrass pollen season significantly increases allergen exposure compared to quiet activity. During vigorous exercise, breathing rate increases three to five times above resting levels, and breathing shifts from nasal to oral โ€” bypassing the nasal filter and delivering larger quantities of pollen directly to the lower airways. This explains why grass-allergic individuals commonly report that jogging, cycling, or playing sports outdoors during May and June triggers more severe symptoms than equivalent time spent sitting outside. The nasobronchial reflex means that the added lower-airway pollen load during exercise can also worsen asthma in those with both conditions. Practical strategies include timing outdoor workouts for early morning (before 8 AM when pollen is lower), choosing post-rain days for intensity sessions, pre-treating with an antihistamine one hour before, and carrying a rescue bronchodilator if asthma is co-existing. Indoor exercise alternatives during peak June pollen periods are a legitimate clinical recommendation for highly sensitized individuals.

Evidence suggests yes. Research on airborne pollen trends across North America consistently shows that grass pollen seasons are beginning earlier and lasting longer as average temperatures rise and frost dates shift earlier in spring. A 2021 study analyzing pollen data across North American monitoring stations found that grass pollen seasons had lengthened by an average of several days per decade over the previous two to three decades. For bluegrass specifically, warmer springs allow Poa pratensis to initiate pollen production earlier than historical norms in the upper Midwest and Northeast, and milder autumns may extend the season for Poa annua in transitional climate zones. Elevated atmospheric CO2 also appears to increase the total pollen output per plant โ€” meaning not just longer seasons, but higher pollen concentrations during peak periods. Patients who feel their bluegrass allergy symptoms are worsening year over year even with consistent medication use may be experiencing real increases in pollen load, not simply treatment failure or sensitization deepening.

This content is for informational purposes only and does not constitute medical advice, diagnosis, or treatment. Always consult a qualified healthcare provider with questions about a medical condition. Content reviewed by board-certified allergists at Curex.

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