moderate Severity

White Goosefoot Allergy: A Major Late-Summer Weed Pollen Trigger

White goosefoot (Chenopodium album), also called lamb's quarters, is a globally distributed weed and a significant late-summer aeroallergen. Its pollen is a major cause of seasonal allergic rhinitis from July through October, particularly in the Midwest and Great Plains. The primary allergen, Che a 1, is a profilin that cross-reacts broadly with other weed, grass, and tree pollens. Evidence-based management combines antihistamines, intranasal corticosteroids, and sublingual immunotherapy for long-term desensitization.

moderatePeak: Jul–OctUpdated July 13, 2026

Free · 5 min · Insurance accepted

Reviewed by Dr. Chet Tharpe, M.D.
As seen inUSA TODAYMen's HealthCBSForbes
The numbers
Headline stat
Che a 0
PRIMARY ALLERGEN
US prevalence
0–30%
Peak season
Jul–Oct
Symptoms tracked
0
Treatment paths
0
01Overview

What Is White Goosefoot Allergy?

White goosefoot allergy is an IgE-mediated hypersensitivity reaction to the pollen of Chenopodium album, one of the most widespread and abundant weed species on Earth.

Known commonly as lamb's quarters, pigweed (though this name is shared with Amaranthus), or fat hen, this plant is a member of the Amaranthaceae family and produces enormous quantities of lightweight, wind-dispersed pollen from midsummer through early autumn. It is a dominant weed in agricultural fields, roadsides, and disturbed urban soils across all 50 US states, making it a clinically significant aeroallergen for a substantial portion of the atopic population.

Unlike the more famous ragweed, which dominates allergy discourse in the eastern US, white goosefoot is a major driver of late-summer hay fever in the Midwest, Great Plains, and Intermountain West — regions where it often outcompetes ragweed in both biomass and pollen production. Its primary allergen, Che a 1, is a profilin, a pan-allergen that cross-reacts with profilins from virtually all other pollens and many plant foods, meaning patients sensitized to white goosefoot often test positive to multiple unrelated pollens.

02Symptoms

Symptoms of White Goosefoot Pollen Allergy

Recognizing symptoms early helps you get the right treatment faster.

Sneezing

moderate

Paroxysmal sneezing triggered by inhaled goosefoot pollen is a hallmark of IgE-mediated weed pollinosis, often occurring in bursts during peak pollen hours.

Nasal congestion

moderate

Mucosal edema from histamine and leukotriene release causes nasal blockage, often worse in the morning when pollen counts are highest.

Clear rhinorrhea

mild

Watery nasal discharge is a direct result of increased vascular permeability driven by mast cell mediators in the nasal mucosa.

Ocular itching and tearing

moderate

Allergic conjunctivitis with intense itch, redness, and watery discharge is common; goosefoot pollen grains readily contact the conjunctival surface.

Palatal and pharyngeal itch

mild

Deep itching of the soft palate and throat is a characteristic feature of pollen allergy, often described as an 'itch that can't be scratched.'

Postnasal drip and cough

mild

Excess mucus production draining into the pharynx can trigger a chronic dry cough, particularly at night, and may be mistaken for a lingering cold.

Fatigue and irritability

mild

Poor sleep quality from nighttime nasal congestion, combined with the systemic effects of chronic allergic inflammation, commonly produces daytime fatigue.

Oral allergy syndrome (profilin-mediated)

mild

Tingling, itching, or mild swelling of the lips, mouth, and throat after eating raw melons, tomatoes, bananas, or stone fruits may occur in profilin-sensitized patients.

When to see a doctor

White goosefoot pollen allergy produces the classic symptom complex of seasonal allergic rhinoconjunctivitis. The most prominent symptoms are sneezing, clear nasal discharge, nasal congestion, and intense itching of the eyes, nose, and palate. Because the pollen season is concentrated in late summer and early autumn, patients often describe a predictable pattern of worsening symptoms beginning in August and persisting until frost. In the Midwest and Great Plains, where goosefoot and ragweed seasons overlap almost perfectly, patients may experience particularly severe symptoms due to the combined pollen load. Distinguishing goosefoot-driven symptoms from ragweed-driven symptoms on clinical grounds alone is difficult; specific IgE testing or skin prick testing with regional weed panels is required for precise identification. Patients with profilin sensitization via Che a 1 may also experience oral allergy syndrome — tingling, itching, or mild swelling of the lips, mouth, and throat — when eating raw fruits and vegetables that contain profilins, including melons, tomatoes, bananas, and stone fruits. These symptoms are typically mild and self-limited. If you experience throat tightness, difficulty breathing, or facial swelling, seek emergency care immediately.

White Goosefoot Pollen and Asthma Risk

The relationship between white goosefoot pollen allergy and asthma follows the well-established epidemiological pattern linking allergic rhinitis to lower airway disease. Patients with untreated seasonal allergic rhinitis from weed pollens have a substantially elevated risk of developing asthma compared to non-atopic individuals — a progression often described as the atopic march. During the August–September peak pollen season, sensitized patients may experience increased cough, wheeze, chest tightness, and reduced peak expiratory flow rates. The profilin Che a 1, while primarily associated with rhinoconjunctivitis, can theoretically contribute to lower airway inflammation when pollen grains are small enough to reach the bronchial tree. Patients with known asthma who notice seasonal worsening during late summer should discuss weed pollen sensitization — including white goosefoot — with their allergist as a potential contributing factor.

If left untreated

Potential Complications of White Goosefoot Pollen Allergy

Untreated or poorly controlled white goosefoot pollen allergy can lead to several clinically significant complications over time. Chronic nasal mucosal inflammation impairs mucociliary clearance, creating conditions that favor secondary bacterial sinusitis — characterized by facial pain, thick discolored nasal discharge, fever, and reduced sense of smell. The persistent inflammation of the upper airway is also a recognized risk factor for the development of asthma, particularly in patients with a family history of atopy. Profilin sensitization via Che a 1 may produce oral allergy syndrome that, while typically mild, can cause significant dietary anxiety and restriction in affected patients. Rarely, profilin-mediated reactions can progress beyond the oral cavity to cause urticaria or bronchospasm, though systemic anaphylaxis from profilin alone is uncommon. The overlap of white goosefoot pollen season with ragweed, sagebrush, and other weed pollens can also lead to a cumulative pollen load that overwhelms standard pharmacotherapy, resulting in breakthrough symptoms and reduced quality of life during the late-summer months.

Chronic or recurrent sinusitis

Persistent nasal inflammation from untreated pollinosis impairs sinus drainage, predisposing patients to recurrent bacterial sinus infections that may require antibiotic treatment.

Asthma development or exacerbation

Long-term untreated allergic rhinitis is a major risk factor for new-onset asthma; existing asthma frequently worsens during the weed pollen season.

Oral allergy syndrome

Profilin cross-reactivity (Che a 1) may cause oral and pharyngeal symptoms with raw fruits and vegetables; typically mild but can restrict diet.

Sleep disturbance and daytime impairment

Nighttime nasal congestion from pollen-driven inflammation disrupts sleep architecture, leading to fatigue, reduced concentration, and impaired work or school performance.

03Why it happens

What Causes White Goosefoot Pollen Reactions?

The sensitization pathway for white goosefoot pollen allergy follows the classic Type I hypersensitivity model. When a genetically susceptible individual inhales Chenopodium album pollen grains, antigen-presenting cells in the respiratory mucosa process the pollen proteins and present them to naive T-helper cells, which differentiate into Th2 cells and drive B-cell class switching to produce Chenopodium-specific IgE antibodies. These IgE molecules bind to high-affinity receptors on mast cells and basophils, priming them for future encounters.

Common Species

White goosefoot / lamb's quarters

Chenopodium album

Epazote / Mexican tea

Chenopodium ambrosioides

Pitseed goosefoot

Chenopodium berlandieri

Quinoa (cultivated relative)

Chenopodium quinoa

White goosefoot pollen allergy is a Type I (IgE-mediated) hypersensitivity reaction. Inhaled pollen grains release Che a 1 profilin and other allergenic proteins onto the nasal and conjunctival mucosa. In sensitized individuals, these proteins cross-link specific IgE antibodies bound to mast cells, triggering degranulation with release of histamine, leukotrienes, and prostaglandins. The resulting inflammation produces rhinorrhea, sneezing, nasal congestion, and ocular itch. Che a 1's profilin structure means it shares epitopes with profilins from grasses, trees, and other weeds, explaining the broad cross-reactivity seen on allergy testing in goosefoot-sensitized patients.

Upon re-exposure during the July–October pollen season, white goosefoot pollen allergens cross-link the bound IgE on mast cells in the nasal and ocular mucosa, triggering degranulation and the release of histamine, leukotrienes, prostaglandins, and other inflammatory mediators. This cascade produces the classic symptoms of allergic rhinitis and conjunctivitis.

The primary characterized allergen, Che a 1, is a profilin — a small, highly conserved actin-binding protein found in all eukaryotic cells. Because profilins are structurally similar across the plant kingdom, Che a 1 sensitization frequently results in positive IgE tests to grass, tree, and other weed pollens, as well as to many raw fruits and vegetables. This cross-reactivity is clinically significant: a patient whose primary sensitization is to white goosefoot profilin may test positive to birch, timothy grass, and ragweed, not because they are independently sensitized to each, but because their IgE recognizes the shared profilin epitope.

Who's most affected

Risk factors to watch for

01

Residence in agricultural regions

White goosefoot is a dominant agricultural weed in the Midwest, Great Plains, and California's Central Valley, producing heavy pollen loads in these regions during late summer.

02

Existing profilin sensitization

Patients already sensitized to profilins from grass, tree, or other weed pollens are at elevated risk for cross-reactive white goosefoot sensitization via Che a 1.

03

Late-summer outdoor occupation or recreation

Farm workers, landscapers, and outdoor enthusiasts in goosefoot-heavy regions have high ambient pollen exposure during the July–October peak season.

04

Family history of atopy

A personal or family history of allergic rhinitis, asthma, or atopic dermatitis significantly increases the probability of developing pollen sensitization, including to white goosefoot.

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

How to Diagnose White Goosefoot Pollen Allergy

Diagnosing white goosefoot pollen allergy requires integrating the patient's seasonal symptom pattern with objective allergy testing. The clinical history is the starting point: a patient who reports predictable late-summer rhinitis symptoms — beginning in late July or August and persisting until the first frost — and who lives in or has visited the Midwest, Great Plains, or agricultural regions where Chenopodium album is abundant, has a pre-test probability high enough to warrant formal evaluation. Skin prick testing with a regional weed pollen panel that includes goosefoot or lamb's quarters extract can confirm sensitization. However, because Che a 1 is a profilin, a positive goosefoot test may reflect cross-reactive sensitization rather than primary goosefoot allergy. Component-resolved diagnostics — measuring specific IgE to profilin (Che a 1 or its equivalent markers) — can help distinguish genuine goosefoot sensitization from broader profilin-driven poly-sensitization. At-home allergy testing services such as Curex provide panels covering 40+ environmental allergens with results typically within 5 days and insurance coverage often available, allowing patients to map their weed pollen sensitization landscape before an in-person specialist visit.

Skin prick test with weed pollen panel

A standard weed pollen SPT panel including goosefoot/lamb's quarters, ragweed, sagebrush, and Russian thistle can identify sensitization. A positive goosefoot wheal confirms IgE-mediated reactivity.

Specific IgE blood testing (serology)

Serum IgE testing for Chenopodium album and profilin markers quantifies sensitization and can be performed while the patient remains on antihistamines.

Component-resolved diagnostics (profilin IgE)

Measuring specific IgE to profilin (rChe a 1 or rPhl p 12 as a marker) identifies whether the patient's sensitization is profilin-driven, which has implications for cross-reactivity and immunotherapy planning.

At-home testing

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06Treatment

Treatment Options for White Goosefoot Pollen Allergy

See how different approaches stack up for managing your allergy symptoms long-term.

Treatment for white goosefoot pollen allergy follows the evidence-based, stepwise approach used for all seasonal allergic rhinitis. The foundation is pharmacotherapy to control symptoms during the July–October pollen season, combined with practical avoidance measures to reduce pollen exposure. For patients with moderate-to-severe symptoms that are not adequately controlled with medication alone, or who wish to reduce their long-term reliance on daily pharmacotherapy, allergen immunotherapy offers the only disease-modifying option.

Because white goosefoot is a profilin-dominant allergen, immunotherapy planning should account for the broader sensitization profile. Patients with isolated goosefoot sensitization may benefit from goosefoot-specific immunotherapy, while those with profilin-driven poly-sensitization may require a broader weed pollen mix. Starting intranasal corticosteroids 1–2 weeks before the expected onset of the pollen season — typically in early July for most regions — provides superior symptom control compared to starting treatment after symptoms have already developed.

Pollen avoidance during peak season

Reducing outdoor exposure during high-count days, keeping windows closed, using HEPA air filtration indoors, and showering after outdoor activities reduces pollen load on mucosal surfaces.

Not applicable

Partial symptom reduction; complete avoidance is impractical for an abundant airborne weed pollen

Second-generation oral antihistamines

Non-sedating H1 receptor antagonists reduce sneezing, rhinorrhea, and ocular itch; most effective when taken daily throughout the pollen season rather than as-needed.

Zyrtec (cetirizine), Claritin (loratadine), Allegra (fexofenadine), Xyzal (levocetirizine)

Clinical trials show 50–60% reduction in total nasal symptom scores

Intranasal corticosteroids

First-line therapy for moderate-to-severe allergic rhinitis; reduce nasal mucosal inflammation, congestion, and discharge more effectively than oral antihistamines alone.

Flonase (fluticasone), Nasonex (mometasone), Nasacort (triamcinolone), Rhinocort (budesonide)

Meta-analyses demonstrate 30–40% greater symptom reduction compared to antihistamine monotherapy

Antihistamine eye drops

Topical ophthalmic antihistamines and mast cell stabilizers provide rapid relief of allergic conjunctivitis symptoms independent of oral medications.

Pataday (olopatadine), Alaway (ketotifen), Lastacaft (alcaftadine)

Fast onset (within minutes) with effective control of ocular itch and redness

Leukotriene receptor antagonists

Montelukast blocks the action of cysteinyl leukotrienes, reducing nasal congestion and inflammation; particularly useful in patients with co-existing asthma.

Singulair (montelukast)

Modest additive benefit when combined with antihistamines; less effective than intranasal corticosteroids as monotherapy

Allergen immunotherapy (weed pollen mix)

Sublingual or subcutaneous immunotherapy with goosefoot-containing weed pollen extracts provides long-term desensitization and is the only treatment that modifies the underlying allergic disease.

Standardized weed pollen allergen extracts including Chenopodium album

Clinical trials in weed pollen-sensitized populations show 60–80% reduction in symptom scores and medication use

Traditional

  • NoTreats root cause
  • NoLong-lasting relief
  • YesAt-home treatment
  • YesNo office visits
  • YesLow side effects
  • PartialEstimated cost

Allergy Shots (SCIT)

  • YesTreats root cause
  • YesLong-lasting relief
  • NoAt-home treatment
  • NoNo office visits
  • PartialLow side effects
  • PartialEstimated cost

Immunotherapy (SLIT)

Recommended
  • YesTreats root cause
  • YesLong-lasting relief
  • YesAt-home treatment
  • YesNo office visits
  • YesLow side effects
  • YesEstimated cost
Immunotherapy

Immunotherapy for White Goosefoot Pollen Allergy

Instead of masking symptoms, immunotherapy retrains your immune system.

For patients whose white goosefoot pollen allergy is not adequately controlled with pharmacotherapy — or who wish to reduce their long-term dependence on daily medications — allergen immunotherapy offers the only disease-modifying treatment. Both subcutaneous immunotherapy (allergy shots) and sublingual immunotherapy (allergy drops) have demonstrated efficacy in weed pollen-sensitized populations, with clinical trials showing 60–80% reduction in symptom scores and medication requirements over a 3–5 year treatment course. A key consideration for goosefoot immunotherapy is the profilin cross-reactivity of Che a 1. Patients with profilin-driven poly-sensitization — testing positive to multiple weed, grass, and tree pollens — may benefit from a broader immunotherapy formulation that addresses the shared profilin epitope rather than goosefoot alone. Component-resolved diagnostics can guide this decision by clarifying whether the patient's sensitization is primarily profilin-mediated or involves additional goosefoot-specific allergens. Sublingual immunotherapy drops, available through providers like Curex with plan-specific pricing (https://getcurex.com/learn/curex-pricing), allow patients to undergo desensitization at home without the weekly clinic visits required for allergy shots, and plans are typically covered by most insurance. In a real-world Curex study of 2,897 patients on at-home sublingual immunotherapy, clinically meaningful symptom improvement rose to 45% of patients by two years and quality-of-life improvement reached 90.7%, with adherence above 90% and no anaphylaxis reported. This convenience is particularly valuable for patients in agricultural regions where the July–October goosefoot season is long and pharmacotherapy alone may be insufficient.

1Step 1

Confirm sensitization profile

Skin prick testing or specific IgE serology with a regional weed pollen panel confirms goosefoot sensitization and identifies co-sensitizations.

2Step 2

Component-resolved diagnostics

Profilin-specific IgE testing clarifies whether sensitization is Che a 1-driven, which informs immunotherapy formulation and predicts cross-reactivity patterns.

3Step 3

Custom immunotherapy formulation

Allergen drops or shots are formulated based on the confirmed sensitization profile, including goosefoot and any co-reactive weed pollens.

4Step 4

3–5 year desensitization course

Gradually increasing allergen doses build immune tolerance; most patients experience significant improvement within the first 6–12 months of treatment.

“Clinical trials in weed pollen-allergic populations demonstrate 60–80% reduction in seasonal symptom scores and medication use with allergen immunotherapy”

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Living with it

Living With White Goosefoot Pollen Sensitivity

Managing white goosefoot pollen sensitivity is a seasonal challenge that, with the right combination of pharmacotherapy, environmental controls, and medical guidance, is entirely manageable. The key is recognizing the predictable pattern: symptoms that reliably begin in late July or August and persist until the first hard frost are characteristic of weed pollen allergy, and white goosefoot is a dominant contributor in much of the central and western United States. For patients in agricultural regions — the Midwest, Great Plains, and California's Central Valley — where goosefoot is an abundant field weed, the pollen load can be substantial. Creating a symptom diary that tracks daily severity alongside local pollen counts helps identify the specific triggers and provides valuable data for an allergist designing a treatment plan. Patients who also have grass or tree pollen allergies may experience overlapping seasons that extend symptoms from spring through fall, making a comprehensive pollen management strategy essential. For those pursuing immunotherapy, the 3–5 year commitment requires patience — but the long-term benefit of reduced medication dependence and sustained symptom control is well-documented in clinical trials. During the treatment period, continuing environmental controls and as-needed pharmacotherapy ensures that quality of life is maintained while immune tolerance develops.

  • Know your pollen season

    White goosefoot pollen peaks from August through September in most regions. Mark your calendar for early July to start preventive medications, and track local pollen counts to anticipate high-exposure days.

  • Address the full sensitization picture

    Because Che a 1 profilin cross-reacts broadly, patients with goosefoot allergy often test positive to multiple pollens. A comprehensive allergy evaluation identifies all relevant triggers and enables targeted treatment.

  • Plan outdoor activities strategically

    Pollen counts are typically highest in the early morning. Schedule outdoor exercise, gardening, or recreation for late afternoon or after rain, when pollen levels are lower.

When Does White Goosefoot Pollen Peak?

White goosefoot pollen season is a late-summer and early-autumn phenomenon across most of the United States. In the Midwest and Great Plains — where Chenopodium album is among the most abundant agricultural weeds — pollen release begins in mid-July, peaks in August and September, and tapers off with the first hard frost in October. In warmer regions such as the Southwest and California, the season can extend into November. This timing places white goosefoot squarely in the middle of the classic weed pollen season, overlapping significantly with ragweed (Ambrosia), sagebrush (Artemisia), Russian thistle (Salsola), and amaranth (Amaranthus). For patients in the central US, the August–September period often represents a perfect storm of multiple weed pollens, making it difficult to attribute symptoms to a single species without specific IgE testing. The profilin cross-reactivity of Che a 1 further complicates seasonal attribution, as patients may react to multiple pollens through a single sensitization pathway.

Summer

July - August

medium intensity

Fall

September - October

high intensity

Preventing White Goosefoot Pollen Reactions

Preventing white goosefoot pollen reactions requires a combination of environmental controls and proactive medical management during the July–October pollen season. Because Chenopodium album is an abundant agricultural and roadside weed, complete avoidance is impossible in affected regions — but reducing pollen exposure can meaningfully decrease symptom severity. During peak pollen season, keeping windows and doors closed, using air conditioning with HEPA filtration, and avoiding outdoor activities during mid-morning hours when pollen counts are highest significantly reduces indoor and personal pollen burden. After spending time outdoors, showering and changing clothes removes pollen that has accumulated on hair, skin, and fabric — preventing continued exposure indoors. Wearing wraparound sunglasses outdoors reduces pollen contact with the conjunctiva. Starting intranasal corticosteroids 1–2 weeks before the expected onset of the goosefoot pollen season — typically in early July for most of the central US — provides superior symptom control compared to waiting until symptoms develop. Monitoring local pollen counts through the National Allergy Bureau or weather apps allows patients to anticipate high-exposure days and adjust their activities and medication accordingly.

Monitor weed pollen counts

Use the National Allergy Bureau or a weather app to track local weed pollen levels and proactively limit outdoor exposure on high-count days during July–October.

Keep windows closed during pollen season

Close windows and use air conditioning with HEPA filtration during the late-summer and early-fall months to minimize indoor pollen infiltration.

Shower and change clothes after outdoor exposure

Pollen clings to hair, skin, and clothing; showering and changing after outdoor activities removes this reservoir and prevents continued indoor exposure.

Start medications before the season begins

Beginning intranasal corticosteroids 1–2 weeks before the expected goosefoot bloom in July reduces the initial inflammatory response and provides better overall symptom control.

Use HEPA air purifiers indoors

Portable HEPA air purifiers in bedrooms and living areas capture airborne pollen particles, reducing overnight exposure and improving sleep quality during the pollen season.

Long-term outlook

Outlook for White Goosefoot Pollen Allergy

The prognosis for white goosefoot pollen allergy is generally favorable with appropriate management. Seasonal allergic rhinitis from weed pollens is a chronic condition that tends to persist for years, but it is highly responsive to treatment. Most patients achieve adequate symptom control with a combination of intranasal corticosteroids and oral antihistamines during the July–October season, and the profilin-mediated oral allergy syndrome associated with Che a 1 is typically mild and self-limited. For patients who pursue allergen immunotherapy targeting goosefoot and co-reactive weed pollens, clinical trials demonstrate 60–80% long-term symptom reduction and decreased medication requirements. The 3–5 year treatment course produces sustained immune tolerance that persists for years after treatment completion in most patients. While white goosefoot pollen allergy is not typically a progressive or life-threatening condition, untreated chronic rhinitis does carry an elevated risk of asthma development and recurrent sinusitis — underscoring the importance of consistent management.

What to expect

Key takeaways

01

White goosefoot is a major late-summer weed pollen allergen across the Midwest, Great Plains, and agricultural regions of the US

02

Che a 1 profilin is the primary allergen, driving broad cross-reactivity with other pollens and some raw plant foods

03

Standard pharmacotherapy — intranasal corticosteroids plus antihistamines — provides effective symptom control for most patients during the July–October season

04

Allergen immunotherapy offers 60–80% long-term symptom reduction and is the only disease-modifying treatment for confirmed goosefoot pollen allergy

Diet

Diet and White Goosefoot Pollen Cross-Reactivity

Dietary cross-reactivity is a clinically relevant consideration for patients with white goosefoot pollen allergy, driven primarily by the profilin allergen Che a 1. Profilins are pan-allergens found in virtually all plant cells, meaning patients sensitized to Che a 1 may experience oral allergy syndrome — tingling, itching, or mild swelling of the lips, mouth, and throat — when eating raw fruits and vegetables that contain profilins. Commonly implicated foods include melons, watermelon, tomatoes, bananas, peaches, and cherries. These symptoms are typically heat-labile: cooking denatures profilin, so cooked or canned versions of the same foods are usually well-tolerated. Quinoa (Chenopodium quinoa) is a cultivated relative of white goosefoot in the same genus. While quinoa is a seed rather than a pollen, patients with significant Chenopodium pollen sensitization may theoretically react to quinoa protein, though documented cases of quinoa allergy in goosefoot-sensitized patients are rare in the published literature. Patients with known goosefoot allergy who wish to consume quinoa should discuss this with their allergist.

Foods to limit

  • Raw melons and watermelon (profilin-sensitized patients)

    Profilin cross-reactivity with Che a 1 may cause oral tingling and itching; cooked or processed melon products are typically tolerated.

  • Raw tomatoes (profilin-sensitized patients)

    Tomato profilin shares structural homology with Che a 1; cooking denatures the profilin and usually resolves symptoms.

  • Raw bananas (profilin-sensitized patients)

    Banana profilin may trigger oral allergy syndrome in goosefoot-sensitized individuals; ripe bananas may be more reactive than green ones.

  • Raw stone fruits (profilin-sensitized patients)

    Peach, nectarine, cherry, and plum profilins cross-react with Che a 1; canned or cooked versions are typically well-tolerated.

FAQ

Frequently Asked Questions

White goosefoot (Chenopodium album), also called lamb's quarters, is one of the most widespread and abundant weed species on Earth. It is an annual plant in the Amaranthaceae family that thrives in disturbed soils — agricultural fields, roadsides, construction sites, and gardens — across all 50 US states. It is particularly abundant in the Midwest, Great Plains, and California's Central Valley, where it is a dominant agricultural weed in corn, soybean, and wheat fields. The plant can grow up to six feet tall and produces enormous quantities of lightweight, wind-dispersed pollen from midsummer through early autumn. Its common name comes from the shape of its leaves, which resemble a goose's foot, and its mealy white coating on young leaves.

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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