Thank you for your inquiry.
The process by which commercial citric acid is made does involve aspergillus niger. However, the mold is filtered from the final product, and this product is treated with calcium hydroxide to yield calcium citrate, and citric acid is then formed by treatment with sulfuric acid. Therefore, it is highly unlikely that there is mold contained within citric acid preparations. And there is nothing that I could find in the medical literature which documents asthmatic responses to the ingestion of citric acid because of mold allergens contained within the commercial preparations.
There is, however, an abundance of lay literature on the Internet which postulates such a reaction. For your convenience and interest, I have copied below a link to an example of this lay literature.
Citric acid itself is a known asthmagenic substance and produces cough. In fact, inhalation of citric acid has been used to assay cough thresholds, and the mechanism of production of this reaction has been evaluated (see abstracts copied below). However, I have not seen, in the medical literature, any documentation that the ingestion of citric acid could produce such responses.
In summary based on the production process it appears unlikely that there is a significant quantity of preserved mold allergen in citric acid, and I could not find any medical literature reporting asthma from the ingestion of mold allergen within commercially available citric acid preparations.
If you did wish to investigate a link between the ingestion of citric acid and her symptoms, one thing that you might consider is to test the hypothesis that your patient is reacting to the ingestion of citric acid in foods is a blinded placebo-controlled oral challenge with pre and post pulmonary function tests.
Thank you again for your inquiry and we hope this response is helpful to you.
Eur J Med Res. 1997 Sep 29;2(9):384-8.
Citric acid-induced cough thresholds in normal subjects, patients with bronchial asthma, and smokers.
Schmidt D, Jörres RA, Magnussen H.
Krankenhaus Grosshansdorf, Zentrum für Pneumologie und Thoraxchirurgie, LVA-Freie und Hansestadt Hamburg, Wöhrendamm 80, Grosshansdorf D-22927, Germany.
Several challenge procedures have been developed to characterize the cough reflex in patients with airway diseases. This study was performed to compare the interindividual range of cough sensitivity in asthmatic and normal subjects as well as smokers using an identical method. Sixteen normal subjects, 20 patients with mild bronchial asthma, 6 patients with moderate to severe bronchial asthma, 9 current smokers, and 7 occasional smokers were included. In all subjects, methacholine challenges and standardized citric acid challenges were performed. Sensitivity of the cough reflex was expressed as cough threshold, i.e., as concentration at which coughing occurred. Reproducibility was assessed in 23 subjects. Within a concentration range of 0.625-320.0 mg/ml, inhaled citric acid caused cough in all subjects. Geometric mean (range) cough threshold was 13 (2.5-160) in normal subjects, 14 (5-40) in patients with mild, and 32 (20-40) mg/ml in patients with moderate to severe asthma, 40 (20-80) in current smokers, and 119 (80-160) in occasional smokers. Cough thresholds were reproducible within one doubling concentration. In normal subjects and patients with mild bronchial asthma, thresholds were not significantly different from each other but lower than those of the other groups (p<0.05 each). Cough thresholds in smokers and patients with moderate to severe asthma did also not differ significantly and were lower than in occasional smokers (p<0.05). There was no significant correlation between cough threshold, baseline FEV subset1 , and methacholine responsiveness. Our data indicate that (1) subjects with mild asthma showed on average similar cough thresholds as normal subjects, (2) there was a large variation in cough thresholds within groups, (3) the reproducibility of cough thresholds was within one doubling concentration, (4) cough thresholds did not correlate with methacholine responsiveness or baseline airway tone. In view of the prevalence of cough as a symptom of bronchial asthma, it appears that the determination of citric acid-induced cough thresholds does not yield additional diagnostic information in these subjects.
The American Journal of Medicine
Volume 111, Issue 8, Supplement 1 , Pages 18-24, 3 December 2001
Fabio L.M. Ricciardolo, MD, PhDMechanisms of citric acid-induced bronchoconstriction
In asthma patients, microaspiration of acid into the lower airways (ie, airway acidification) causes such respiratory responses as cough and bronchoconstriction. The mechanism of bronchoconstriction induced by airway acidification is unknown, although evidence is emerging that increasing proton concentrations in airway tissues can activate a subpopulation of primary sensory neurons, so-called capsaicin-sensitive primary sensory neurons, that contain such neuropeptides as the tachykinins substance P (SP) and neurokinin A (NKA). Protons activate a capsaicin-operated channel/receptor, located in the afferents of capsaicin-sensitive neurons, with the subsequent opening of ion channels that are permeable to sodium, potassium, and calcium ions. This event initiates a propagated action potential that antidromically depolarizes collateral fibers and triggers neuropeptide release from nerve fiber varicosities. The tachykinins SP and NKA, released from terminals of primary sensory neurons in peripheral tissues, cause all the major signs of inflammation (neurogenic inflammation) by means of activation of NK1 and NK2 receptors. Exposure of the airways to acidic solutions stimulates sensory nerve endings of capsaicin-sensitive sensory neurons and causes different airway responses, including bronchoconstriction. Recently, the NK2, and to a lesser extent the NK1, receptors have been shown to be involved with citric acid-induced bronchoconstriction in the guinea pig, which is in part mediated by endogenously released bradykinin. Tachykinins and bradykinin, released by airway acidification, could also modulate citric acid-induced bronchoconstriction by their ability to subsequently release the epithelially derived bronchoprotective nitric oxide (NO). Further study with selective tachykinin NK1 and NK2 agonists demonstrated that only the septide-insensitive tachykinin NK1 receptor releases NO. Thus, bronchoconstriction induced by citric acid inhalation in the guinea pig, mainly caused by the tachykinin NK2 receptor, is counteracted by bronchoprotective NO after activation of bradykinin B2 and tachykinin NK1 receptors in airway epithelium. If a similar mechanism is involved in the pathogenesis of bronchial asthma associated with gastroesophageal reflux in the respiratory tract, new therapeutic strategies should be investigated.
Can You Be Allergic to Additive Citric Acid but Not Natural Citric Acid?
Phil Lieberman, M.D.