International Consensus Statement on Allergy and Rhinology: Allergic Rhinitis

In the paper

“The prevalence of “food-induced rhinitis” seems to be under 1%.157”

What the sources say

• Disputed

  The Discussion calls gustatory rhinitis a common phenomenon affecting a large portion of the population, contrary to a prevalence under 1%. The Food questionnaire section reports that hot chili peppers caused rhinorrhea in more than 60% of its 60 respondents; this is not a population-wide prevalence estimate, but it further contradicts the claimed figure. (LLM, conf=0.90)

  Checked by a reasoning model — may be wrong.

  cites [157] sourceExperimental — accuracy not yet measured

In the paper

“In both groups, 11% of individuals had a positive nasal challenge with Timothy grass.”

What the sources say

• Disputed

  The Nasal challenge section reports positive challenge results in 44% of group I and 42% of group III, not 11% in each. Table II gives 11% for each group only after a further assessment classified which challenge reactions indicated allergy; the citing sentence conflates that classification with a positive nasal challenge. (LLM, conf=0.87)

  Checked by a reasoning model — may be wrong.

  cites [856] sourceExperimental — accuracy not yet measured

In the paper

“Modern SPT of aeroallergens can be up to 25% more sensitive than sIgE serology depending on the patient population and the methodologies employed.793,930-934”

What the sources say

• ?Not checked — no full text of the sourcecites [793] source
• ?Not checked — no full text of the sourcecites [930] source
• Disputed

  The Results and Discussion (pages not available) report the opposite comparison in the children studied: SPT alone would have missed an average of 42% of sensitizations, versus 13% with sIgE serology alone. The paper finds discordance between the tests, but does not report SPT as up to 25% more sensitive. (LLM, conf=0.85)

  Checked by a reasoning model — may be wrong.

  cites [931] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [932] source
• Partly supported

  The Environmental and occupational disorders section says latex skin prick testing was more sensitive than serum-specific IgE assays for detecting natural rubber latex allergy in health care workers. The Study design section mentions aeroallergen skin tests, but the serum IgE tests measured latex; the paper does not establish the claimed comparison for aeroallergens or the ‘up to 25%’ figure. (LLM, conf=0.88)

  cites [933] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [934] source

In the paper

“No adverse events were reported, and there were no significant differences between outcome measures for both treatment arms.1729”

What the sources say

• Disputed

  The Results section (AEs; page not provided) reports 11 adverse events in each treatment group, contrary to the claim that none were reported. The abstract says no *severe* adverse events occurred, which is a narrower finding. (LLM, conf=0.95)

  Checked by a reasoning model — may be wrong.

  cites [1729] sourceExperimental — accuracy not yet measured

In the paper

“Despite improvement in asthma symptoms, objective measures using pulmonary function testing and peak expiratory flow have failed to demonstrate significant improvements.1804-1806”

What the sources say

• ?Not checked — no full text of the sourcecites [1804] source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [1805]
• Disputed

  The Results report statistically significant, though small, improvements in both morning and evening peak expiratory flow, contrary to the claim that peak expiratory flow failed to improve significantly. The FEV1 result was not statistically significant, and the Discussion says symptom scores could not be combined in the meta-analysis. Page numbers are unavailable in our copy. (LLM, conf=0.90)

  Checked by a reasoning model — may be wrong.

  cites [1806] sourceExperimental — accuracy not yet measured

In the paper

“A large population-based survey of AR patients demonstrated a strong correlation between AR disease severity and sleep disturbance.679”

What the sources say

• Disputed

  The Patient population section describes 63 carefully selected patients randomly allocated to vaccine or placebo, not a large population-based survey. Table III in the Discussion compares sleep-domain scores between treatment groups; it does not report a correlation between allergic rhinitis severity and sleep disturbance. Page numbers are unavailable in our copy. (LLM, conf=0.86)

  Checked by a reasoning model — may be wrong.

  cites [679] sourceExperimental — accuracy not yet measured

In the paper

“The prevention and early identification of occupational rhinitis during medical surveillance of exposed workers and of young apprentices may provide an excellent opportunity to prevent the development of occupational asthma.110,111”

What the sources say

• Supported

  The Abstract says rhinitis symptoms precede asthma and that early identification of rhinitis is crucial to preventing work-related asthma. The Understanding section recommends periodic medical surveillance during apprenticeship or work to detect occupational allergy and rhinitis early. (LLM, conf=0.94)

  cites [110] source
• ?Not checked — no full text of the sourcecites [111] source

In the paper

“Neurogenic nasal inflammation is mediated by neuropeptides such as substance P, neurokinin A, and calcitonin gene-related peptide. These mediators are released by sensory nerve fibers in the nose and result in vasodilation, edema, and inflammation.133”

What the sources say

• Supported

  The Neurogenic Inflammation section (p. 1) names substance P, neurokinin A, and calcitonin gene-related peptide in sensory neurons and says mediators released from sensory nerves produce vasodilation, edema, and other inflammation. The Chemical Irritant Receptors section (p. 2) specifically reports substance P release in the nose and links stimulation of nasal irritant receptors to neurogenic inflammation. (LLM, conf=0.89)

  cites [133] source

In the paper

“Chemicals known to cause sensitization of the respiratory tract include diisocyanates, acid anhydrides, some platinum salts, reactive dyes, glutaraldehyde, plicatic acid, and chroamine.118-120”

What the sources say

• ?Not checked — no full text of the sourcecites [118] source
• ?Not checked — no full text of the sourcecites [119] source
• Partly supported

  The Results tables list diisocyanates, several anhydrides, platinum salts, reactive dyes, glutaraldehyde, and chloramine T as occupational-asthma agents or inhalation sensitizers. Our copy does not identify plicatic acid or an agent named “chroamine”; the latter may be a misspelling of chloramine, but the paper does not establish that equivalence. (LLM, conf=0.87)

  cites [120] sourceExperimental — accuracy not yet measured

In the paper

“Pharmacologic treatment does not differ from that of non-occupational rhinitis.101”

What the sources say

• ?Could not verify

  Section 2.3.2 describes occupational rhinitis, and the Pharmacotherapy section discusses treatment of allergic rhinitis generally. Neither passage compares pharmacologic treatment for occupational and non-occupational rhinitis; searches for that comparison found no such statement in the available copy. (LLM, conf=0.68)

  cites [101] sourceExperimental — accuracy not yet measured

In the paper

“Approximately 2% of viral rhinitis episodes are secondarily infected by bacterial organisms such as Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis, with subsequent presentation of acute bacterial infection.138”

What the sources say

• Partly supported

  Section 2.2, “Clinical definition of rhinosinusitis in children” (page unavailable), says that a small percentage of patients with post-viral acute rhinosinusitis develop bacterial acute rhinosinusitis. It does not give a 2% rate for viral rhinitis episodes or name the three bacterial species; it also uses post-viral rhinosinusitis patients, rather than all viral rhinitis episodes, as the denominator. (LLM, conf=0.86)

  cites [138] sourceExperimental — accuracy not yet measured

In the paper

“In addition, nasal biopsies from these patients commonly show increased numbers of mast cells and prominent mast cell degranulation.177,178”

What the sources say

• Partly supported

  The Mast cells results and Mast cells and IgE+ cells discussion report increased epithelial mast cells in idiopathic rhinitis compared with controls, with most of those cells degranulated. However, the paper studied patients selected for idiopathic rhinitis, not specifically NARES; its Eosinophils discussion says not all idiopathic cases had increased eosinophils. The findings therefore support the mast-cell observations but not their attribution specifically to NARES patients. (LLM, conf=0.84)

  cites [177] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [178] source

In the paper

“This is considered a reflex response due to an adrenergic and cholinergic neural reaction of the nose.157”

What the sources say

• Partly supported

  The Discussion (page not available) proposes a neural reflex involving atropine-inhibitable parasympathetic nerves supplying the nasal mucosa and glands, supporting the reflex and cholinergic parts of the claim. It does not identify an adrenergic nasal reaction, so that added mechanism is unsupported. (LLM, conf=0.88)

  cites [157] sourceExperimental — accuracy not yet measured

In the paper

“For instance, in subjects with gustatory rhinitis, shortly after ingestion of hot or spicy foods, unilateral or bilateral watery rhinorrhea develops in the absence of nasal congestion, pruritus, or facial pain.”

What the sources say

• Partly supported

  The Discussion says watery rhinorrhea begins within minutes of eating hot or spicy foods and that subjects do not complain of congestion or pruritus. Nasal and food challenges reports bilateral rhinorrhea in all challenged subjects, but the copy does not establish unilateral rhinorrhea or address facial pain. (LLM, conf=0.87)

  cites [157] sourceExperimental — accuracy not yet measured

In the paper

“The absence of an IgE-mediated immune response differentiates vasomotor from allergic forms of rhinitis.101”

What the sources say

• Partly supported

  The Introduction (§2.1; page unavailable) associates allergic rhinitis with an IgE-mediated response. The paper places idiopathic rhinitis, sometimes called “vasomotor rhinitis,” among nonallergic conditions, but does not explicitly establish absence of IgE as its distinguishing criterion. It also cautions that vasomotor symptoms can occur in both allergic and nonallergic rhinitis. (LLM, conf=0.84)

  cites [101] sourceExperimental — accuracy not yet measured

In the paper

“This is likely due to age-related changes of the nasal mucosa,199 such as a decrease in mucosal blood flow and an increase in epithelial atrophy.213”

What the sources say

• ?Not checked — no full text of the sourcecites [199] source
• Supported

  The Abstract says decreased nasal blood flow leads to atrophy and drying of the nasal mucous membrane. The “Types of rhinitis in the elderly” section also links reduced blood flow to dryness and discusses clearing crusts. The paper uses “mucous membrane” rather than “epithelium,” but supports the attributed age-related changes. (LLM, conf=0.90)

  cites [213] source

In the paper

“Nasal dryness in the elderly population may also be caused by a decrease in intranasal temperature and humidity.200”

What the sources say

• Supported

  The ‘Nasal Humidification and Dryness’ section reports significantly lower nasal-cavity temperature and humidity in geriatric patients than in younger people. It says these findings likely explain dryness-related nasal irritation and crusting, supporting the claim’s hedged causal wording. (LLM, conf=0.92)

  cites [200] source

In the paper

“This makes the elderly population more vulnerable to symptoms such as rhinorrhea, nasal congestion, postnasal drip, dry nose, intranasal crusting, and decreased olfaction.199,200”

What the sources say

• ?Not checked — no full text of the sourcecites [199] source
• Supported

  The Classifications section (page not provided) lists congestion, rhinorrhea, and postnasal drip as rhinitis symptoms and says that, in older people, the symptom complex may also include intranasal crusting, olfactory loss, and nasal dryness. The Changes of the Aging Nose section further links aging to increased nasal drainage and postnasal drip, dryness and crusting, and declining olfaction. (LLM, conf=0.93)

  cites [200] source

In the paper

“Recent research has validated that the primary physiological mechanism that produces the sensation of ample nasal airflow is activation of trigeminal cool thermoreceptors, specifically TRPM8, by nasal mucosal cooling.224-228”

What the sources say

• Partly supported

  The Abstract and Conclusions identify nasal mucosal heat loss and trigeminal sensory input as important to perceived patency. But the Introduction describes TRPM8's role in nasal patency as possible, and the Discussion says TRPM8-targeting agents were not used in this pilot study. The paper therefore does not validate TRPM8 activation specifically as the primary mechanism. (LLM, conf=0.88)

  cites [224] sourceExperimental — accuracy not yet measured
• Partly supported

  The Discussion (page unavailable) reports that regional peak mucosal heat loss significantly contributes to perceived nasal patency. The Introduction and Discussion link cool trigeminal afferents and TRPM8 to cooling, but this study does not establish TRPM8 activation as the primary mechanism producing the sensation of ample airflow. (LLM, conf=0.88)

  cites [225] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [226] source
• Partly supported

  The Discussion (page not provided) says mucosal cooling is sensed by nasal thermoreceptors and contributes to perceived nasal patency. It does not identify those receptors as trigeminal or TRPM8, and it calls for future research on the relative contributions of cooling and other variables rather than establishing cooling as the primary mechanism. (LLM, conf=0.88)

  cites [227] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [228] source

In the paper

“Diagnosis should be suspected in patients with asthma, with increased peripheral blood eosinophil count (>10%) and pulmonary manifestations.238,248”

What the sources say

• ?Not checked — no full text of the sourcecites [238] source
• Partly supported

  Section 3 (recommendation 2; page not supplied) links asthma, eosinophilia and pulmonary infiltrates to EGPA evaluation. It does not give a >10% peripheral-blood eosinophil threshold, and its description of a straightforward diagnosis also includes sinus disease and evidence of vasculitis. The cited paper therefore supports suspicion in this clinical context, but not the claim's precise threshold. (LLM, conf=0.86)

  cites [248] sourceExperimental — accuracy not yet measured

In the paper

“AR shares several overlapping symptoms, namely rhinorrhea and nasal congestion, which may be confused with the subtypes of rhinosinusitis.264,265”

What the sources say

• Partly supported

  The Introduction and Diagnosis of AR sections identify watery rhinorrhea and nasal obstruction as AR symptoms. The Rhinosinusitis section discusses acute and chronic rhinosinusitis and mentions nasal obstruction in patients with both AR and acute rhinosinusitis, but it does not establish that both symptoms overlap with rhinosinusitis subtypes or that the conditions may be confused. (LLM, conf=0.82)

  cites [264] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [265] source

In the paper

“Treatment usually includes high doses of corticosteroids and immunosuppressants.248,251”

What the sources say

• Partly supported

  The treatment recommendations (p. 548) call for high-dose glucocorticoids during induction and an additional immunosuppressant for life- or organ-threatening EGPA. Recommendation 12 says glucocorticoids alone may be suitable without those manifestations, so the claim overgeneralizes the use of both drugs as usual treatment. (LLM, conf=0.87)

  cites [248] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [251] source

In the paper

“A longer duration of illness suggests bacterial ARS.137,138”

What the sources say

• Supported

  The Transition from Viral to Bacterial Infection section (pp. 9–10) says that bacterial infection becomes more likely as symptoms persist, and recommends diagnosing ABRS when symptoms last at least 10 days without improvement. It also cautions that viral symptoms can last beyond 10 days if they are gradually improving. (LLM, conf=0.90)

  cites [137] source
• ?Could not verify

  Section 2.2 distinguishes post-viral from bacterial acute rhinosinusitis and says only a small percentage of post-viral cases are bacterial. It does not say whether a longer illness makes bacterial ARS more likely; searches for illness duration and persistent symptoms found no passage addressing that link. (LLM, conf=0.73)

  cites [138] sourceExperimental — accuracy not yet measured

In the paper

“In general, viral ARS is present for less than 10 days.”

What the sources say

• Supported

  The Definition (p. 9) describes viral rhinosinusitis as symptoms lasting less than 10 days without worsening, supporting the general statement. The guideline also notes that viral symptoms can persist beyond 10 days while gradually decreasing in severity (Transition from Viral to Bacterial Infection, p. 10). (LLM, conf=0.90)

  cites [137] source
• ?Could not verify

  Section 2.2 identifies viral ARS with the common cold but gives no duration. Searches for “10 days,” “less than 10 days,” and the viral-versus-post-viral distinction found no passage in our copy establishing the claimed time limit. (LLM, conf=0.69)

  cites [138] sourceExperimental — accuracy not yet measured

In the paper

“The development of acute, moderate to severe symptoms, and nasal purulence may be consistent with ARS or RARS rather than AR.1,137,138”

What the sources say

• ?Not checked — no full text of the sourcecites [1] source
• Partly supported

  The guideline defines ARS by acute purulent nasal drainage accompanied by nasal obstruction or facial pain-pressure-fullness (Cardinal Symptoms of Acute Rhinosinusitis, p. 6). It defines RARS by four or more qualifying bacterial episodes per year (Recurrent Acute Rhinosinusitis, p. 21), so one episode of acute symptoms does not establish RARS. The cited passages do not establish moderate-to-severe symptoms as a distinguishing feature or directly compare this presentation with allergic rhinitis. (LLM, conf=0.84)

  cites [137] sourceExperimental — accuracy not yet measured
• Partly supported

  Sections 2.1 and 2.2 include nasal discharge and mucopurulent discharge in the clinical definition of rhinosinusitis, and section 2.2 discusses acute rhinosinusitis. The retrieved passages do not establish that moderate-to-severe symptoms or nasal purulence distinguish ARS or RARS from allergic rhinitis, and they do not address RARS specifically. (LLM, conf=0.83)

  cites [138] sourceExperimental — accuracy not yet measured

In the paper

“Conversely, AR is typically not associated with purulent or unilateral nasal discharge.”

What the sources say

• ?Not checked — no full text of the sourcecites [1] source
• ?Could not verify

  The Definition (p. 9) describes purulent discharge in acute rhinosinusitis, while Testing for Allergy (p. 26) discusses allergic rhinitis’s association with sinusitis. Neither passage characterizes discharge in allergic rhinitis as typically nonpurulent or nonunilateral. Searches for allergic-rhinitis symptoms and unilateral discharge found no passage addressing that claim. (LLM, conf=0.72)

  cites [137] sourceExperimental — accuracy not yet measured
• ?Could not verify

  The clinical definitions of rhinosinusitis (sections 2.1–2.2; page unavailable) list mucopurulent discharge as a possible sign of rhinosinusitis, but do not describe the usual discharge in allergic rhinitis. Searches for unilateral discharge and for a comparison with allergic rhinitis found no passage establishing that purulent or unilateral discharge is typically absent in allergic rhinitis. (LLM, conf=0.73)

  cites [138] sourceExperimental — accuracy not yet measured

In the paper

“Progressive worsening over a short period of time (ie, 5 days) is also suggestive of bacterial ARS.137,138”

What the sources say

• Partly supported

  The guideline’s “Transition from Viral to Bacterial Infection” section (p. 9) says that, between days 5 and 10, initial improvement followed by worsening (“double worsening”) is consistent with bacterial ARS. It does not say that progressive worsening over 5 days, without initial improvement, is suggestive of bacterial ARS. (LLM, conf=0.86)

  cites [137] sourceExperimental — accuracy not yet measured
• ?Could not verify

  Section 2.2 distinguishes post-viral from bacterial acute rhinosinusitis but does not say that worsening over five days suggests a bacterial cause. Searches for “5 days,” worsening symptoms, and bacterial diagnostic criteria found no passage addressing that indicator in our copy. (LLM, conf=0.72)

  cites [138] sourceExperimental — accuracy not yet measured

In the paper

“Fever is not included in other guidelines, due to its low specificity and sensitivity.137”

What the sources say

• Partly supported

  In “Transition from Viral to Bacterial Infection” (p. 10), the guideline says fever has about 50% sensitivity and specificity for ABRS and explains that it therefore did not include fever as a cardinal diagnostic sign. The same section says other guidelines do use high fever in criteria for severe presentations, so this source does not support the broader claim that fever is omitted from other guidelines generally. (LLM, conf=0.88)

  cites [137] sourceExperimental — accuracy not yet measured

In the paper

“AR symptoms are also exacerbated by exposure to allergens in a time dependent fashion.264”

What the sources say

• Supported

  The “Early and late reactions” section states that allergen exposure produces different reactions according to time sequence: sneezing and rhinorrhea develop within 30 minutes, while nasal obstruction appears approximately six hours later. This supports the claim that AR symptoms vary with time after allergen exposure. (LLM, conf=0.92)

  cites [264] source

In the paper

“Several studies, both in vivo and in vitro have confirmed the production of local IgE in the nasal mucosa of patients with AR.282-284”

What the sources say

• ?Not checked — no full text of the sourcecites [282] source
• ?Not checked — no full text of the sourcecites [283] source
• Partly supported

  The Discussion (page unavailable) describes nasal B cells locally producing IgE and reports mucosal allergen binding in allergic rhinitis subjects; the References also identify studies of local IgE production. Our copy does not establish the claim’s distinction that both in vivo and in vitro studies confirmed this finding. (LLM, conf=0.83)

  cites [284] sourceExperimental — accuracy not yet measured

In the paper

“The locally produced IgE plays a key role in ongoing inflammation by up-regulating FcεRI expression in mast cells.283-285”

What the sources say

• ?Not checked — no full text of the sourcecites [283] source
• Partly supported

  The Discussion (page unavailable) links localized nasal IgE production with mucosal allergic inflammation and reports allergen co-localization with mast cells. It does not say that locally produced IgE sustains inflammation by up-regulating FcεRI expression in mast cells; the paper instead suggests that inflammatory cells may help maintain IgE production. (LLM, conf=0.85)

  cites [284] sourceExperimental — accuracy not yet measured
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [285]

In the paper

“Whether AR will develop as a result of inhalant allergen exposure therefore depends largely upon the balance between Th1 and Th2 effector cells.274”

What the sources say

• Partly supported

  The Introduction says Th2 cells support allergic responses and describes atopic disease as an overly aggressive Th2 response to environmental antigens. It does not specifically say that allergic rhinitis after inhalant exposure depends largely on the Th1–Th2 balance; it cautions that atopic disorders do not simply reflect over-polarization of the T-cell response. No page number is available in our copy. (LLM, conf=0.85)

  cites [274] sourceExperimental — accuracy not yet measured

In the paper

“This stimulates IL-4, IL-5, and IL-13 production,274 which is characteristic of the Th2 response.”

What the sources say

• Partly supported

  The Introduction says Th2 cells express GATA-3 and produce IL-4, IL-5, and IL-13, supporting the cytokine profile attributed to a Th2 response. It does not say that activation of GATA-3 stimulates their production, so the causal part of the claim is not established by this copy. (LLM, conf=0.84)

  cites [274] sourceExperimental — accuracy not yet measured

In the paper

“Th2 differentiation also requires co-stimulation via the interaction of CD28 on T cells with CD80 and CD86 on antigen-presenting cells (APCs).278”

What the sources say

• Partly supported

  The Introduction and §1.5 identify CD28 as a T-cell costimulatory receptor and B7.1/B7.2 (CD80/CD86) as its ligands. They do not establish that this interaction is required specifically for Th2 differentiation; §1.5 notes that mice lacking CD28 or both ligands still produced reduced levels of effector cytokines. Page numbers are unavailable in our copy. (LLM, conf=0.83)

  cites [278] sourceExperimental — accuracy not yet measured

In the paper

“They also provide an important early stimulus toward a Th2-weighted immune response, through the secretion of thymic stromal lymphopoietin (TSLP).272,275,276”

What the sources say

• ?Not checked — no full text of the sourcecites [272] source
• ?Not checked — no full text of the sourcecites [275] source
• Supported

  The “Structural cells in allergic inflammation” section identifies TSLP as epithelial-cell-derived and says it induces dendritic-cell-mediated Th2-type allergic inflammation. This supports the paraphrase that epithelial cells provide a stimulus toward a Th2-weighted response through TSLP; the supplied passage does not give a page number. (LLM, conf=0.90)

  cites [276] source

In the paper

“An interesting recent development was the discovery of innate lymphoid cells (ILCs) as potential key players in the pathogenesis of Th2-type diseases such as AR, CRSwNP, and asthma.328-330”

What the sources say

• ?Not checked — no full text of the sourcecites [328] source
• Supported

  The Introduction describes ILC2s as important effectors in type 2 immunity and links them to allergic inflammation. The Chronic rhinosinusitis section suggests they contribute to nasal polyps; the Allergic rhinitis section discusses their possible role in AR and reports increased ILC2 activity in allergic asthma. The claim’s “potential” qualifier reflects the paper’s uncertainty about their exact role in AR. Page numbers are unavailable in our copy. (LLM, conf=0.88)

  cites [329] source
• Partly supported

  The Introduction reports increased ILC2s in allergic asthma and their accumulation in nasal polyps and sinus mucosa in chronic rhinosinusitis, supporting a potential role in asthma and CRSwNP. It also says increased innate type 2 responses were not observed in allergic rhinitis (AR). The Discussion suggests ILC2s may play a more prominent role in asthma than in AR, so the source does not support treating all three diseases alike. (LLM, conf=0.88)

  cites [330] sourceExperimental — accuracy not yet measured

In the paper

“Flow cytometry studies in nasal secretions have confirmed that aeroallergen exposure induces a Th2 inflammatory response in the nasal mucosa of LAR patients with increased eosinophils, basophils, mast cells, CD3+, and CD4+ T cells.300,301”

What the sources say

• Partly supported

  The Discussion (page unavailable) reports flow-cytometry evidence of increased nasal eosinophils, basophil–mast cells and CD3+ T cells in patients with seasonal idiopathic rhinitis who responded to pollen challenge. It does not report a significant increase in CD4+ T cells; the Results passage says no differences were found in the other measured values. The paper describes inflammation during seasonal pollen exposure, but does not establish that exposure induced a specifically Th2 response. (LLM, conf=0.88)

  cites [300] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [301] source

In the paper

“However, in recent years our understanding and appreciation of the important contributions of the nasal innate immune response to the pathogenesis of AR has grown substantially.320”

What the sources say

• Supported

  The Introduction describes the respiratory epithelium’s innate immune functions and its possible role in chronic airway inflammation, and identifies allergic rhinitis (AR) as a focus of the review. The Abstract says an increasing number of investigations have provided evidence for the importance of altered sinonasal epithelial homeostasis in upper-airway inflammation, supporting the claim of growing understanding. (LLM, conf=0.85)

  cites [320] source

In the paper

“In LAR, the presence of sIgE in nasal secretions has been confirmed after natural allergen exposure,300,301 NPT,300,301,303-305 and periods of non-exposure.300,301”

What the sources say

• Partly supported

  The Natural exposure to pollen (April–June) methods and Symptom score results report nasal sIgE in 7 of 32 patients with seasonal idiopathic rhinitis during pollen exposure. The Determinations made outside the pollen season section reports positive NAPT responses and says all patients with nasal sIgE had a positive NAPT. It does not report detecting sIgE in nasal secretions after NAPT or during non-exposure. (LLM, conf=0.86)

  cites [300] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [301] source

In the paper

“Intrinsic proteolytic activity of allergens may disrupt the nasal epithelial barrier, facilitating allergen penetration and chronic inflammation.321”

What the sources say

• Partly supported

  The Results (page unavailable) show that Bermuda grass pollen cysteine protease increased permeability of human airway epithelial cells; the paper also describes protease-bearing allergens facilitating allergen access. It did not test barrier disruption specifically in nasal epithelial cells or establish that this process leads to chronic inflammation, although it reports inflammatory responses and nasal eosinophil influx in mice. (LLM, conf=0.85)

  cites [321] sourceExperimental — accuracy not yet measured

In the paper

“The systemic allergic response is further characterized by increased expression of adhesion molecules, such as vascular cell adhesion molecule 1 and E-selectin on nasal and bronchial endothelium, which facilitates the migration of inflammatory cells into the tissue.352”

What the sources say

• Supported

  The Abstract (page unavailable) reports increased percentages of VCAM-1– and E-selectin–positive vessels in both nasal and bronchial tissue after nasal allergen provocation in patients with allergic rhinitis. The Discussion (page unavailable) links endothelial adhesion molecules to leukocyte recruitment and describes the response as generalized airway inflammation. (LLM, conf=0.90)

  cites [352] source

In the paper

“Although it was believed that IgE-producing B-cells reside in lymphoid follicles of the Waldeyer ring376 and antibodies were then transferred to the mucosa, newer evidence has identified B-cells and plasma cells capable of producing IgE in nasal tissue of AR patients.377”

What the sources say

• Supported

  The Discussion explicitly concludes that B-cells and plasma cells in the nasal mucosa of allergic rhinitis patients produce (specific) IgE. The biopsy findings described in the Abstract also identify IgE-positive B-cells and plasma cells in that tissue. Page numbers were not supplied. (LLM, conf=0.95)

  cites [377] source

In the paper

“Epithelial barrier leakiness, particularly tight junctions that seal the upper and lower respiratory mucosal epithelial surface, has been shown in asthma, AR and CRS.343,344”

What the sources say

• Partly supported

  The Discussion reports defective tight junctions in asthma, and the Results show a disrupted epithelial barrier in CRS, particularly CRS with nasal polyps. The paper mentions reduced barrier function in acute rhinovirus-associated rhinitis, but does not establish it in allergic rhinitis (AR); that part of the claim is unsupported. Page numbers were not provided in our copy. (LLM, conf=0.88)

  cites [343] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [344] source

In the paper

“Interestingly, cough is not induced in patients with rhinitis or healthy controls in simulated models of postnasal drip.349”

What the sources say

• Supported

  The Results (p. 3) report that cough did not increase significantly in either rhinitis patients or controls after either simulated-mucus challenge. The Conclusions (p. 6) state that the challenge did not trigger cough in either group. (LLM, conf=0.94)

  cites [349] source

In the paper

“Similarities are not only found in the acquired immune response, but also in the role of innate immunity like epithelial barrier function334 and innate lymphoid cells.332”

What the sources say

• ?Not checked — no full text of the sourcecites [334] source
• Supported

  The paper’s Abstract reports that allergen challenge increases innate lymphoid cells (ILC2) in people with allergic rhinitis and describes evidence suggesting a role for ILC2 in asthma. Citation 332 is attached to innate lymphoid cells; the separate epithelial-barrier claim carries citation 334. (LLM, conf=0.90)

  cites [332] source

In the paper

“In patients with AR, segmental bronchial or nasal provocation can induce allergic inflammation in both the nasal and bronchial mucosa.347-349”

What the sources say

• ?Not checked — no full text of the sourcecites [347] source
• ?Not checked — no full text of the sourcecites [348] source
• ?Could not verify

  The Discussion (p. 4) mentions nasal secretions collected after provocation, but does not say that provocation induces allergic inflammation in both nasal and bronchial mucosa. The paper examines symptoms after intranasal insertion of simulated mucus; searches for segmental bronchial provocation and bronchial mucosal inflammation found no passage addressing the claimed effect. (LLM, conf=0.76)

  cites [349] sourceExperimental — accuracy not yet measured

In the paper

“Corticosteroids have not, however, been shown to cause thinning of nasal epithelium.322,431”

What the sources say

• ?Could not verify

  The Discussion (pp. 7, 9) reports that intranasal steroids were associated with improved nasal epithelial barrier integrity, but barrier integrity is not epithelial thickness. A search for thinning, atrophy, and epithelial thickness found no passage assessing whether corticosteroids cause thinning. (LLM, conf=0.72)

  cites [322] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [431] source

In the paper

“Similarly, levels of chemokines such as thymus-regulated and activation-regulated chemokine (TARC, CCL17), macrophage derived chemokine (MDC, CCL22), eotaxin, RANTES, MCP-1, and macrophage inflammatory protein (MIP)-1α were elevated.388-391”

What the sources say

• Partly supported

  The Results section ('Effects of nasal allergen in placebo group compared with baseline'; page not provided) reports post-challenge increases in eotaxin, RANTES, MCP-1, and MIP-1α. The provided passages do not report increases in TARC/CCL17 or MDC/CCL22, so the source supports only four of the six listed chemokines. (LLM, conf=0.88)

  cites [388] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [389] source
• ?Not checked — no full text of the sourcecites [390] source
• ?Not checked — no full text of the sourcecites [391] source

In the paper

“Loss-of-function mutations and polymorphisms in genes coding for epithelial barrier markers such as filaggrin are associated with AR and eczema.427,428”

What the sources say

• ?Not checked — no full text of the sourcecites [427] source
• Partly supported

  The Methods section (page unavailable) lists FLG among genes associated with both allergic rhinitis (AR) and atopic dermatitis (eczema). It specifically links FLG polymorphisms and loss-of-function mutations to increased susceptibility to atopic dermatitis, but does not establish that those variants are associated with AR. (LLM, conf=0.86)

  cites [428] sourceExperimental — accuracy not yet measured

In the paper

“Proteolytic allergens directly disrupt the apical junctional complex via proteolysis, leading to barrier dysfunction.430”

What the sources say

• Partly supported

  The section on allergen recognition reports that the dust-mite allergen Der p disrupts airway epithelial tight junctions in a protease-dependent manner; the References annotation for study 29 says an allergen protease increased bronchial epithelial permeability. This supports the proposed barrier effect, but the copy does not establish that proteolytic allergens generally disrupt the entire apical junctional complex. (LLM, conf=0.83)

  cites [430] sourceExperimental — accuracy not yet measured

In the paper

“Penders et al.447 found that the presence of Clostridium difficile at 1 month of age was associated with an increased risk for allergic sensitization (odds ratio [OR] 1.54; 95% confidence interval [CI], 1.09 to 2.31) until the age of 2 years.”

What the sources say

• Partly supported

  The Results report that C. difficile colonisation at 1 month was associated with atopic sensitisation within the first 2 years of life, with an adjusted OR of 1.54. The cited confidence interval is incorrect: the Results give 95% CI 1.02–2.31, not 1.09–2.31. No page number is provided in our copy. (LLM, conf=0.93)

  cites [447] sourceExperimental — accuracy not yet measured

In the paper

“In a study of 29,662 children from the United States that used health care records to follow participants, the incidence of physician-diagnosed AR during the first year of life was 1%.”

What the sources say

• Supported

  The Methods (Cohort design; page not supplied) describe a U.S. birth cohort of 29,662 children followed using electronic medical records. Table 2 in Results (Age at diagnosis and overall incidence; page not supplied) reports rhinitis incidence of 0.1% at 0–5 months and 0.9% at 6–11 months, totaling 1% in the first year. (LLM, conf=0.94)

  cites [467] source

In the paper

“In the Cincinnati Childhood Allergen and Air Pollution Study (CCAAPS), 9% of the 12-month-old children with a parental history of respiratory allergy fulfilled the criteria of AR.465”

What the sources say

• Supported

  The Results (page not provided) report that 9% of infants in CCAAPS met the definition of allergic rhinitis. The Methods (page not provided) describe parental allergy-based eligibility and define infant allergic rhinitis using reported symptoms and a positive skin-prick test at approximately 12 months. (LLM, conf=0.91)

  cites [465] source

In the paper

“There is evidence that AR may start as early as during the first year of life.”

What the sources say

• Supported

  The Discussion reports allergic rhinitis in infants during the first year of life. The Methods define it as a rhinitis episode recorded during that year plus a positive aeroallergen skin-prick test at approximately 12 months. This supports the citing sentence’s cautious wording, although the Discussion notes that some symptoms could have been due to viral infection. (LLM, conf=0.92)

  cites [465] source

In the paper

“For instance, grass pollen, which is found across Europe, causes wide variations in atopic sensitizations across regions with different climates.480”

What the sources say

• Supported

  The Discussion reports widely differing grass-pollen sensitization rates across European regions, including 40.4% in Greece, 52.1% in Kosovo, and 97.46% in Northern Spain. The Abstract explains that climatic and geographic conditions affect pollen concentrations and that hypersensitivity differs by region. No page numbers are available in our copy. (LLM, conf=0.86)

  cites [480]

In the paper

“In a more recent meta-analysis of all studies performed according to the ISAAC-protocol (1,430,329 children aged 0 to 18 years), the overall prevalence of AR was 12.66%.473”

What the sources say

• Supported

  The Results (Description and final selection of studies; page unavailable) report 31 studies covering 1,430,329 children, and the Methods (Study selection; page unavailable) specify ages 0–18 and use of ISAAC questionnaires. The Results (Abstract; page unavailable) give an allergic rhinitis prevalence of 12.66%. The analysis included both official and non-official ISAAC studies using those questionnaires. (LLM, conf=0.93)

  cites [473] source

In the paper

“Most children with symptoms of AR early in life have persistent symptoms for several years.469-471”

What the sources say

• ?Not checked — no full text of the sourcecites [469] source
• Partly supported

  Table E4 (Extended Data) shows that 12 of 19 children with birch-pollen-related allergic rhinitis symptoms at age 4 also had symptoms at ages 8 and 16, supporting persistence in a majority over several years. The cited study examined birch-pollen-related rhinitis in one birth cohort, not allergic rhinitis generally, so the claim is broader than its evidence. (LLM, conf=0.85)

  cites [470] sourceExperimental — accuracy not yet measured
• Supported

  The Results report that 93 children (87%) with allergic rhinitis at age 4 still had it at age 8. This supports the claim that most children with early allergic rhinitis have symptoms persisting for several years. (LLM, conf=0.94)

  cites [471] source

In the paper

“Smaller studies over more limited geographic regions that examined PAR suggest increased sensitivity rates in urban settings and colder climates.476-479”

What the sources say

• ?Not checked — no full text of the sourcecites [476] source
• Partly supported

  The Results (section 2, page not provided) report higher overall allergic-rhinitis prevalence in urban than rural Guangzhou, while the Discussion reports a higher proportion of persistent allergic rhinitis in northern than southern regions and suggests climate as a possible explanation. The paper does not establish higher sensitivity rates specifically for perennial allergic rhinitis in either setting; its urban comparison concerns allergic rhinitis overall. (LLM, conf=0.86)

  cites [477] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [478] source
• ?Not checked — no full text of the sourcecites [479] source

In the paper

“In an accompanying GWAS on allergic sensitization, there was strong overlap between top hits for sensitization and self-reported allergies.487,493”

What the sources say

• Supported

  The paper’s main text (page not specified) compares its self-reported allergy associations with a companion allergic-sensitization study. All 22 loci had effects in the same direction, and 10 of its 16 genome-wide-significant loci had nominal support in the sensitization study, supporting the claimed strong overlap. (LLM, conf=0.92)

  cites [487] source
• Supported

  The paper reports that all 10 genome-wide significant SNPs for allergic sensitization were also associated with self-reported allergy symptoms in an independent companion study (section labeled Abstract; page not provided). This supports the claimed strong overlap between the top hits. (LLM, conf=0.94)

  cites [493] source

In the paper

“These associations suggest shared genetic mechanisms for AR and other allergy-related diseases, evidence further supported by the large-scale GWAS on self-reported cat, HDM, and pollen allergies (as well as AR), which revealed 16 shared susceptibility loci with strong association (p < 5 × 10−8; TLR-locus top hit).487”

What the sources say

• Supported

  The paper’s opening summary (page unavailable) reports a GWAS meta-analysis of self-reported cat, dust-mite, and pollen allergy, identifying 16 shared loci at P<5×10−8; the reported TLR-region association has the strongest P value listed. A later passage (page unavailable) reports an exploratory analysis of allergic-rhinitis symptoms. The citation supports the GWAS evidence in the citing sentence; the preceding reference to LRRC32 associations is the citing authors’ own framing. (LLM, conf=0.88)

  cites [487] source

In the paper

“However, many of the candidate genes reported in the literature have not been well-replicated across studies and populations.427,504”

What the sources say

• ?Not checked — no full text of the sourcecites [427] source
• Supported

  The Introduction reports poor reproducibility of previously reported allergic-rhinitis SNP associations across Swedish and Singapore Chinese populations. The Results and Discussion likewise find that very few of the 49 investigated SNPs were significantly associated with allergic rhinitis in those populations. The paper supports the claim in the context of allergic-rhinitis candidate-gene associations. (LLM, conf=0.90)

  cites [504] source

In the paper

“Notably, SNPs in genes involved in antigen presentation (for example HLA-DQA1), pathogen recognition (TLR2, TLR7, TLR8), IL signaling and proinflammation (IL13, IL18, and TSLP) are considered important susceptibility variants for AR.496-502”

What the sources say

• ?Not checked — no full text of the sourcecites [496]
• Partly supported

  The Results section (page unavailable) reports a tentative association between IL13 SNPs and birch-pollen sensitization in Swedish patients with allergic rhinitis. That is narrower than identifying IL13 as an important susceptibility gene for allergic rhinitis. The Methods section (page unavailable) does not list HLA-DQA1, TLR2, TLR7, TLR8, IL18, or TSLP among the genes tested, so this paper does not support those examples. (LLM, conf=0.84)

  cites [497] sourceExperimental — accuracy not yet measured
• Partly supported

  The Results report allergic-rhinitis-associated SNPs in the TLR7–TLR8 region in Swedish and Chinese populations. The Background says other studies failed to find an association between TLR2 variants and allergic rhinitis, and this paper does not establish TLR2 as a susceptibility gene. Its evidence therefore supports the TLR7/TLR8 portion of the multi-citation sentence, not the full pathogen-recognition list. (LLM, conf=0.88)

  cites [498] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [499] source
• Partly supported

  The Results report that the TLR2 R753Q variant was associated with increased atopic sensitization in German children, supporting the TLR2 portion of the claim. But Table 2 (shown in the indexed Discussion, page unavailable) shows no significant association with hay fever (P = 0.239), so this paper does not establish TLR2 as an allergic-rhinitis susceptibility variant. The other genes in the citing sentence are not attributed specifically to this source. (LLM, conf=0.90)

  cites [500] sourceExperimental — accuracy not yet measured
• Supported

  The Results report associations between TLR7/TLR8 SNP haplotypes and rhinitis, including associations observed in both study samples. This supports the TLR7/TLR8 portion of the multi-cited sentence; the other genes are not attributed specifically to this paper. (LLM, conf=0.91)

  cites [501] source
• ?Not checked — no full text of the sourcecites [502]

In the paper

“negative studies, (showing that early exposure to pets represents a risk factor for AR523,536-542)”

What the sources say

• ?Not checked — no full text of the sourcecites [523] source
• ?Not checked — no full text of the sourcecites [536] source
• ?Not checked — no full text of the sourcecites [537] source
• ?Not checked — no full text of the sourcecites [538] source
• ?Not checked — no full text of the sourcecites [539] source
• ?Not checked — no full text of the sourcecites [540] source
• Supported

  The Risk Factors section reports that having a dog at home in the first year of life was an independent risk factor for physician-diagnosed allergic rhinitis in the children studied. This supports citing the paper as an example of a study finding risk from early pet exposure; the finding specifically concerns dogs, not pets generally. (LLM, conf=0.92)

  cites [541] source
• ?Not checked — no full text of the sourcecites [542] source

In the paper

“These associations suggest shared genetic mechanisms for AR and other allergy-related diseases, evidence further supported by the large-scale GWAS on self-reported cat, HDM, and pollen allergies (as well as AR), which revealed 16 shared susceptibility loci with strong association (p < 5 × 10−8; TLR-locus top hit).487”

What the sources say

• Partly supported

  The paper’s opening summary (page not specified) reports a GWAS meta-analysis of self-reported cat, dust-mite, and pollen allergy that identified 16 shared loci at P<5×10−8; the TLR1/TLR6/TLR10-region locus has the strongest reported association. But allergic rhinitis was not one of the three phenotypes in that meta-analysis. The paper assessed rhinitis symptoms separately in an exploratory analysis, so the claim overstates its role in the 16-locus finding. (LLM, conf=0.89)

  cites [487] sourceExperimental — accuracy not yet measured

In the paper

“In addition to shared genetic effects between different allergy-related diseases, a significant overlap between susceptibility loci for allergy and autoimmune diseases has been observed.495”

What the sources say

• Supported

  The Introduction’s “Allergy and autoimmunity” section explicitly reports a large overlap: 12 of 18 genome-wide significant allergy loci also encompass variants associated with autoimmune diseases. This directly supports the cited claim. (LLM, conf=0.94)

  cites [495] source

In the paper

“Recent studies show that DNA methylation in children is very strongly influenced by well-known risk factors for allergic diseases such as maternal smoking during pregnancy505 and air pollution exposure.506”

What the sources say

• ?Not checked — no full text of the sourcecites [505] source
• Partly supported

  Citation 506 supports the air-pollution part of the sentence, not the separately cited maternal-smoking part. The Results report associations between prenatal NO2 exposure and methylation at a small number of sites, while the Discussion calls the evidence suggestive. That does not establish that children’s DNA methylation is very strongly influenced by air pollution. (LLM, conf=0.85)

  cites [506] sourceExperimental — accuracy not yet measured

In the paper

“However, 3 studies demonstrated that early exposure to fungal allergens is not associated with AR.465,542,557”

What the sources say

• Partly supported

  The Results (Table 2; page unavailable) show no statistically significant association between visible household mold and allergic rhinitis at age one. The study measured visible mold, not fungal allergen exposure, and its findings do not establish that no association exists. This source contributes one study to the citing sentence’s three-study claim. (LLM, conf=0.84)

  cites [465] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [542] source
• ?Not checked — no full text of the sourcecites [557] source

In the paper

“Despite several indepth reviews and a growing body of literature,561-563 no definitive and consensus may be drawn regarding risk-benefit of early inhalant allergen exposure, and further research is welcomed to address the unmet needs on this issue.”

What the sources say

• ?Could not verify

  The 'Putative risk and protective factors' section discusses mixed associations between childhood rhinitis and environmental exposures such as dust endotoxin and mould. It does not assess the risk-benefit of early inhalant allergen exposure or state whether a consensus exists on that question (searched: early inhalant allergen exposure, cat keeping, inhalant). (LLM, conf=0.73)

  cites [561] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [562] source
• Supported

  The Inhalant allergens section reports mixed findings for early house-dust allergen exposure: higher levels were linked to sensitization but not rhinitis symptoms, while an apparent inverse association with rhinoconjunctivitis disappeared after adjustment. The Conclusion says findings for environmental exposures are less consistent, supporting the claim that their risks and benefits are not settled. Page numbers are not available in our copy. (LLM, conf=0.86)

  cites [563] source

In the paper

“The relationship between sensitization to food allergens and the subsequent development of AR during childhood has been investigated in both population-based and high-risk cohorts.468,565-568”

What the sources say

• ?Not checked — no full text of the sourcecites [468] source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [565]
• ?Not checked — no full text of the sourcecites [566] source
• ?Not checked — no full text of the sourcecites [567] source
• Supported

  The Methods (Study Population) identify this as a population-based birth cohort followed to age 4. The Results (Association between Food, Inhalant Allergen Sensitization and Atopic Diseases) examine early food-allergen sensitization and later rhinitis. This source supports the population-based cohort part of the multi-citation sentence; it is not presented as a high-risk cohort. (LLM, conf=0.92)

  cites [568] sourceExperimental — accuracy not yet measured

In the paper

“However, 3 prospective cohort studies (the highest level of evidence identified for this topic) found no significant correlation.578-580”

What the sources say

• Supported

  The paper reports that, in its prospective birth cohort, high diesel-exhaust-particle exposure at age one was not significantly associated with allergic rhinitis at age four (p=0.09). This supports the finding for this cited study; the sentence’s count of three studies and evidence ranking are not findings attributed to this paper alone. (LLM, conf=0.87)

  cites [578] source
• ?Not checked — no full text of the sourcecites [579] source
• ?Not checked — no full text of the sourcecites [580] source

In the paper

“During the 1870s, Blackley found no hay fever among farmers and people living in deprived areas of cities.606”

What the sources say

• Partly supported

  In “Hay Fever’s Social Status,” Waite reports that Blackley found no hay-fever symptoms among the “farming classes.” The same passage attributes the negative inquiries in deprived city areas to Beard, not Blackley. (LLM, conf=0.90)

  cites [606] sourceExperimental — accuracy not yet measured

In the paper

“However, they did find a significant correlation between active smoking and non-allergic/chronic rhinitis.”

What the sources say

• Partly supported

  In Results > Active Smoking (page unavailable), the paper reports a significant association between active smoking and rhinitis under a fixed-effects analysis, but its analysis concerns allergic rhinitis, not non-allergic or chronic rhinitis. The random-effects analysis found no significant overall association with allergic rhinitis; the paper lists a study of nonallergic rhinitis in its References but does not report the claimed finding for that condition. (LLM, conf=0.84)

  cites [593] sourceExperimental — accuracy not yet measured

In the paper

“In contrast, the significant positive association between tobacco and the development of non-allergic/chronic rhinitis has been repeatedly identified.124,128,604”

What the sources say

• ?Not checked — no full text of the sourcecites [124] source
• Partly supported

  The Results and Conclusions report a significant positive association between smoking and rhinitis symptoms in adults, including those without allergic sensitization. The Discussion says this is consistent with another study linking smoking history to chronic sinusitis and nasal congestion. However, this paper examines rhinitis prevalence, not the development of diagnosed non-allergic or chronic rhinitis. (LLM, conf=0.86)

  cites [128] sourceExperimental — accuracy not yet measured
• Partly supported

  The Discussion (page unavailable) says epidemiologic studies suggest smoking may contribute to nonallergic rhinitis and reports an association with chronic rhinosinusitis. The Results find a significant association between tobacco exposure and rhinitis prevalence in children without allergic sensitization. The paper does not establish development of nonallergic or chronic rhinitis: its own outcome is prevalent rhinitis symptoms, and chronic rhinosinusitis is a different condition. (LLM, conf=0.83)

  cites [604] sourceExperimental — accuracy not yet measured

In the paper

“Some pediatric studies have identified a positive correlation between increased exposure to various pollutants and an increased diagnosis of AR during childhood.476,557,582-589”

What the sources say

• ?Not checked — no full text of the sourcecites [476] source
• ?Not checked — no full text of the sourcecites [557] source
• Supported

  The Results (page not provided) report that children living closer to a main road had a higher prevalence of diagnosed allergic rhinitis. The Methods (page not provided) explain that road proximity was used as a proxy for traffic-related air-pollution exposure; the study did not measure individual pollutants. (LLM, conf=0.88)

  cites [582] source
• Partly supported

  The Results (page not provided) report that more frequent truck traffic near homes was associated with rhinitis symptoms in children, and the Discussion reports an association between specific air pollutants and allergic rhinitis in Taiwanese schoolchildren. But this study used reported truck traffic as a proxy for exposure, did not measure pollutant levels, and assessed symptoms rather than an increased rate of diagnosed allergic rhinitis. (LLM, conf=0.88)

  cites [583] sourceExperimental — accuracy not yet measured
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [584]
• ?Not checked — no full text of the sourcecites [585] source
• ?Not checked — no full text of the sourcecites [586] source
• ?Not checked — no full text of the sourcecites [587] source
• Supported

  The Results (page unavailable) report significantly higher odds of a first allergic rhinitis occurrence in Taiwanese preschool children at higher pre-incident CO or NOX levels. This supports the claimed positive association between increased pollutant exposure and childhood allergic rhinitis diagnosis. (LLM, conf=0.93)

  cites [588] source
• Partly supported

  The Results (page unavailable) report higher odds of allergic-rhinitis treatment in children with greater exposure to BC, SO2, and NO2. The Statistical methods (page unavailable) say outcomes were identified by questionnaires about symptoms and treatment, not by confirmed diagnoses; the claim’s reference to increased diagnosis is therefore not established by this study. (LLM, conf=0.86)

  cites [589] sourceExperimental — accuracy not yet measured

In the paper

“Studies have shown that tobacco smoke exposure can propagate the development of atopic diseases via several mechanisms including direct surface damage to nasal mucosa, altered epigenetic mechanisms through histone acetylation, expression of microRNA, and DNA methylation.590,591”

What the sources say

• Supported

  The section “Mechanism of ETS on the development of childhood allergic diseases” explicitly lists surface damage, histone acetylation, microRNA expression, and DNA methylation as mechanisms linking tobacco-smoke exposure to allergic disease. It identifies the nose as part of the epithelial barrier, so “nasal mucosa” is a reasonable paraphrase in this context. (LLM, conf=0.90)

  cites [590] source
• ?Not checked — no full text of the sourcecites [591] source

In the paper

“Alternatively, it has also been shown that nicotine may exert an immunosuppressive effect on allergic disease by suppressing eosinophil trafficking and Th2 cytokine/chemokine responses.592”

What the sources say

• Supported

  The Abstract reports that nicotine suppressed eosinophil trafficking and Th2 cytokine/chemokine responses in allergen-sensitized and challenged rats. This directly supports the hedged claim about an immunosuppressive effect on allergic disease. (LLM, conf=0.94)

  cites [592] source

In the paper

“they do acknowledge that the protective effect of breastfeeding seen in patients less than 5 years of age may have been confounded by known protective effects of breast milk against viral respiratory infections.”

What the sources say

• Supported

  The Synthesis of study findings reports a reduced risk of allergic rhinitis associated with breastfeeding only below age 5. The Eczema and allergic rhinitis discussion (p. 48) says the apparent protection in younger children could reflect breast milk’s protection against viral infections rather than protection against allergic rhinitis; the Conclusion also raises this possibility for early-life allergic disease. (LLM, conf=0.91)

  cites [624] source

In the paper

“Pooling of estimates from the various studies found a nonsignificant protective effect of breastfeeding on the development of AR (OR 0.92; 95% CI, 0.84 to 1.01).”

What the sources say

• Supported

  The Synthesis of study findings reports that pooling 12 estimates for allergic rhinitis produced a nonsignificant protective association, with a random-effects odds ratio of 0.92 and a 95% confidence interval of 0.84–1.01. This is the result attributed to the review. (LLM, conf=0.95)

  cites [624] source

In the paper

“The protective farm effect seems to be stronger when exposed to farm animals and stables.522,649-655”

What the sources say

• ?Not checked — no full text of the sourcecites [522] source
• ?Not checked — no full text of the sourcecites [649] source
• ?Not checked — no full text of the sourcecites [650] source
• ?Not checked — no full text of the sourcecites [651] source
• Partly supported

  The Abstract reports protection against atopy in the mixed-farming region but not the crop-farming region, and the ‘Farming and atopy in children’ section suggests that contact with farm animals may explain the difference (page numbers unavailable). The paper does not assess exposure to stables or establish that animal exposure itself makes the protective effect stronger. (LLM, conf=0.85)

  cites [652] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [653] source
• ?Not checked — no full text of the sourcecites [654] source
• ?Not checked — no full text of the sourcecites [655] source

In the paper

“However, there was no association after 5 years of age (OR 1.05; 95% CI, 0.99 to 1.12).”

What the sources say

• Supported

  The Synthesis of study findings reports no association between breastfeeding and allergic rhinitis after age 5, with a pooled odds ratio of 1.05 (95% CI 0.99–1.12) from nine studies. This matches the cited sentence. (LLM, conf=0.95)

  cites [624] source

In the paper

“A large study based on questionnaire data for children aged 6 to 7 years from 31 countries and 13 to 14 years from 52 countries confirmed that the inverse association between the number of older siblings and prevalence of hay fever was strongest in more affluent countries.646”

What the sources say

• Supported

  Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [646] source

In the paper

“After stratification by age, a reduced risk of AR in patients under 5 years of age was associated with breastfeeding (OR 0.79; 95% CI, 0.63 to 0.98).”

What the sources say

• Supported

  The “Synthesis of study findings” section reports that, after stratification by age, breastfeeding was associated with reduced allergic rhinitis risk below age 5 (Fig. S10). The reported odds ratio and interval match the claim exactly. (LLM, conf=0.95)

  cites [624] source

In the paper

“More recently, 2 studies from Korea have reconfirmed the previously noted association between high SES and the development of AR.”

What the sources say

• ?Not checked — no full text of the sourcecites [478] source
• Supported

  The Conclusions state that high SES was a risk factor for allergic rhinitis, and the Results report higher allergic-rhinitis prevalence among adolescents with high family affluence and parental education. This Korean study supports the association attributed to it as one of the two studies; it does not need to establish what the other study found. (LLM, conf=0.91)

  cites [615] source

In the paper

“Furthermore, the productivity, practical/activity, emotional, social, and memory function of patients appear to be significantly impacted by AR.685-689”

What the sources say

• ?Not checked — no full text of the sourcecites [685] source
• ?Not checked — no full text of the sourcecites [686] source
• Partly supported

  The Abstract reports significant effects on emotional well-being, productivity, and cognitive functioning, and the Results (Burden of AR/C; page not provided) report interference with work or school performance. The copy does not specifically establish effects on social function or memory, and work or school interference does not fully substantiate the broader practical/activity function claim. (LLM, conf=0.85)

  cites [687] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [688] source
• ?Not checked — no full text of the sourcecites [689] source

In the paper

“The AIT RCTs have longer follow-up periods (12 to 18 months) and show similar results, with placebo patients either staying at their baseline QOL impairment, or improving to a lesser degree than the treatment arms.678,679”

What the sources say

• ?Not checked — no full text of the sourcecites [678] source
• Supported

  The RQLQ results report a significant difference in overall quality-of-life improvement between groups one year after treatment. Table III (displayed under Discussion; page unavailable) shows the placebo group's overall score changing only from 2.8 to 2.7, versus 2.8 to 1.9 in the active group. This paper supports the 12-month end of the cited trials' follow-up range. (LLM, conf=0.91)

  cites [679] source

In the paper

“For the adult population, there is level 1b evidence supporting the conclusion that AR negatively impacts sleep.705-709”

What the sources say

• ?Not checked — no full text of the sourcecites [705]
• ?Not checked — no full text of the sourcecites [706] source
• Supported

  The Methods describe a double-blind, placebo-controlled study of adults aged 18–48 with perennial allergic rhinitis. The Results report significantly fewer sleep problems with active treatment than with placebo (p = 0.0323), supporting the conclusion that allergic rhinitis-related nasal congestion adversely affects sleep. (LLM, conf=0.90)

  cites [707] source
• ?Not checked — no full text of the sourcecites [708] source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [709]

In the paper

“Comorbidities associated with AR, such as like rhinosinusitis, Eustachian tube dysfunction, and associated conductive hearing loss may further contribute to learning dysfunction.775,776”

What the sources say

• ?Not checked — no full text of the sourcecites [775]
• Supported

  The Introduction’s “Learning disabilities and problems at school” section explicitly says that sinusitis, Eustachian dysfunction, and associated conductive hearing loss may enhance learning dysfunction. The claim closely paraphrases that statement. (LLM, conf=0.95)

  cites [776] source

In the paper

“However, concerns regarding unnecessary exposure to ionizing radiation, with the risk for future cancer development, preclude recommendations for routine use.789,790”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [789]
• Supported

  The Discussion reports that CT radiation doses received by children and young adults were associated with increased risks of leukaemia and brain tumours. It also says CT scans should be performed only when clinically justified, supporting the concern about unnecessary exposure; it does not argue against clinically justified CT use. (LLM, conf=0.90)

  cites [790] source

In the paper

“Patient reported outcome measures (PROMs) can assess a number of different aspects of how AR affects patients.796”

What the sources say

• Partly supported

  The “Significance of PRO Instruments” section says patient-reported outcomes can measure symptoms, physical functioning, psychological and social well-being, and quality of life. The paper supports their ability to assess multiple aspects of a disease’s impact, but it does not discuss AR specifically. (LLM, conf=0.84)

  cites [796] sourceExperimental — accuracy not yet measured

In the paper

“Several of these instruments have been used extensively in many large clinical trials to determine the effectiveness of drugs and biologics for treating AR.797-802”

What the sources say

• Partly supported

  The Methods describe using TNSS, VAS, and MiniRQLQ to evaluate outcomes in this allergic-rhinitis immunotherapy trial, and the Results report 106 enrolled participants. The paper therefore supports use of several such instruments in a trial, but does not establish that they were used extensively across many large trials of AR drugs and biologics. (LLM, conf=0.86)

  cites [797] sourceExperimental — accuracy not yet measured
• Partly supported

  The Methods (Clinical endpoints and assessments; page unavailable) use TNSS and TOSS to evaluate the efficacy of a grass-pollen allergy vaccine. The paper does not establish that several validated instruments were used extensively across many large trials of AR drugs and biologics; its Discussion instead calls for larger studies of this vaccine. (LLM, conf=0.84)

  cites [798] sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [799] source
• ?Not checked — no full text of the sourcecites [800] source
• ?Not checked — no full text of the sourcecites [801] source
• ?Not checked — no full text of the sourcecites [802] source

In the paper

“This is lower than the pooled estimates of sensitivity (85-88%) and specificity (77%) for SPT, calculated from recent meta-analyses.830,854”

What the sources say

• Supported

  The Results, under “Primary analysis: diagnostic accuracy of skin-prick testing,” report pooled SPT sensitivity of 88.4% and specificity of 77.1%. A sensitivity analysis reports 85.0% and 77.3%, matching the cited ranges. No page number is provided in our copy. (LLM, conf=0.94)

  cites [830] source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [854]

In the paper

“Nevis et al.830 conducted a systematic review of 4 studies to determine the sensitivity and specificity of intradermal testing when used as a confirmatory test following negative SPT. Sensitivity ranged from 27% (95% CI, 10% to 57%) to 50% (sample sizes were too small to calculate CI), while specificity ranged from 69% (95% CI, 51% to 83%) to 100% (95% CI, 83% to 100%).”

What the sources say

• Supported

  The Results section, “Secondary analysis: diagnostic accuracy of intradermal testing,” reports a review of four studies and gives exactly these sensitivity and specificity ranges for intradermal testing after negative skin-prick results, including the confidence intervals and the reason one could not be estimated. (LLM, conf=0.95)

  cites [830] source