PubMed Health⌕ Search

Biomedical subjects

Emil J Bardana

Publications and source records attributed to Emil J Bardana.

8 recordsLinked to original sources

Inhalational mold toxicity: fact or fiction? A clinical review of 50 cases.

BACKGROUND: Three well-accepted mechanisms of mold-induced disease exist: allergy, infection, and oral toxicosis. Epidemiologic studies suggest a fourth category described as a transient aeroirritation effect. Toxic mold syndrome or inhalational toxicity continues to cause public concern despite a lack of scientific evidence that supports its existence. OBJECTIVES: To conduct a retrospective review of 50 cases of purported mold-induced toxic effects and identify unrecognized conditions that could explain presenting symptoms; to characterize a subgroup with a symptom complex suggestive of an aeroirritation-mediated mechanism and compare this group to other diagnostic categories, such as sick building syndrome and idiopathic chemical intolerance; and to discuss the evolution of toxic mold syndrome from a clinical perspective. METHODS: Eighty-two consecutive medical evaluations were analyzed of which 50 met inclusion criteria. These cases were critically reviewed and underwent data extraction of 23 variables, including demographic data, patient symptoms, laboratory, imaging, and pulmonary function test results, and an evaluation of medical diagnoses supported by medical record review, examination, and/or test results. RESULTS: Upper respiratory tract, lower respiratory tract, systemic, and neurocognitive symptoms were reported in 80%, 94%, 74%, and 84% of patients, respectively. Thirty patients had evidence of non-mold-related conditions that explained their presenting complaints. Two patients had evidence of allergy to mold allergens, whereas 1 patient exhibited mold-induced psychosis best described as toxic agoraphobia. Seventeen patients displayed a symptom complex that could be postulated to be caused by a transient mold-induced aeroirritation. CONCLUSION: The clinical presentation of patients with perceived mold-induced toxic effects is characterized by a disparate constellation of symptoms. Close scrutiny revealed a number of preexisting diagnoses that could plausibly explain presenting symptoms. The pathogenesis of aeroirritation implies completely transient symptoms linked to exposures at the incriminated site. Toxic mold syndrome represents the furtive evolution of aeroirritation from a transient to permanent symptom complex in patients with a psychogenic predisposition. In this respect, the core symptoms of toxic mold syndrome and their gradual transition to chronic symptoms related to nonspecific environmental fragrances and irritants appear to mimic what has been observed with other pseudodiagnostic categories, such as sick building syndrome and idiopathic chemical intolerance.

Adolescent↗

Indoor air quality and health does fungal contamination play a significant role?

Fungal contamination in buildings can vary greatly, and their presence in a dwelling does not necessarily constitute exposure. Measurement of mold spores and fragments varies depending on the methodology and instruments used. Meaningful comparison of data is rarely possible. The presence of a specific immune response to a fungal antigen only connotes that exposure to one or more related species has occurred, but not that there is a symptomatic clinical state. The response of individuals to indoor bioaerosols is complex and depends on age, gender, state of health, genetic makeup, and degree and time of bioaerosol exposure. In general, mold contamination in buildings is associated with incursion of water or moisture, which should be remedied as efficiently as possible. When disease occurs, it more likely is related to transient annoyance or irritational reactions. Allergic symptoms may be related to mold proliferation in the home environment. Because molds are encountered both indoors and outdoors, it is difficult to determine where the sensitivity initially arose and if the response is solely provoked by either an indoor or outdoor source. As an indoor allergen, mold is considered to be an infrequent participant in the induction of allergic disease when compared with housedust mites, animal dander, and cockroach allergens. Infection in healthy individuals is rare and usually is caused by an outdoor source. Building-related disease caused by mycotoxicosis has not been proved in the medical literature.

Air Pollution, Indoor↗

Psyllium-associated anaphylaxis and death: a case report and review of the literature.

BACKGROUND: Psyllium use has increased significantly in the United States in part due to its lipid-lowering property. The increased prevalence of consumption has led to its recognition as an emerging food allergen. OBJECTIVES: To report the case of a 42-year-old woman who experienced fatal anaphylaxis after ingesting a psyllium-based product and to review the literature. METHODS: The MEDLINE database was searched for articles from 1966 to 2002 using the keywords psyllium or ispaghula and each of the following: allergy, hypersensitivity, anaphylaxis, and asthma. Both English and non-English articles were included. RESULTS: Psyllium hypersensitivity has been well described in health care workers and pharmaceutical plant employees. Clinical manifestations of allergy range from upper respiratory tract symptoms on inhalation to anaphylaxis on ingestion. The prevalence of sensitization varies between these 2 groups. The allergenic epitope is not known. CONCLUSIONS: We present a case of psyllium hypersensitivity that resulted in death. There is a clear association between atopy and psyllium allergy. The case underscores the fact that even nonprescription "natural" products can be harmful to people with allergies.

Adult↗

Toxic mold: phantom risk vs science.

OBJECTIVE: To review the available literature on the subject of fungi (molds) and their potential impact on health and to segregate information that has scientific validity from information that is yet unproved and controversial. DATA SOURCES: This review represents a synthesis of the available literature in this area with the authors' collective experience with many patients presenting with complaints of mold-related illness. STUDY SELECTION: Pertinent scientific investigation on toxic mold issues and previously published reviews on this and related subjects that met the educational objectives were critically reviewed. RESULTS: Indoor mold growth is variable, and its discovery in a building does not necessarily mean occupants have been exposed. Human response to fungal antigens may induce IgE or IgG antibodies that connote prior exposure but not necessarily a symptomatic state. Mold-related disease has been discussed in the framework of noncontroversial and controversial disorders. CONCLUSIONS: When mold-related symptoms occur, they are likely the result of transient irritation, allergy, or infection. Building-related illness due to mycotoxicosis has never been proved in the medical literature. Prompt remediation of water-damaged material and infrastructure repair should be the primary response to fungal contamination in buildings.

Air Pollution, Indoor↗

8. Occupational asthma and allergies.

A diversity of airborne dusts, gases, fumes, and vapors can cause dose-related symptoms in individuals exposed in the workplace. More than 250 chemicals have been incriminated as a cause of occupational asthma (OA). The prevalence of OA ranges from 2% to 6% of the asthmatic population. Predisposing factors facilitating the development of OA include the work environment, climatic conditions, genetic proclivities, tobacco and recreational drug use, respiratory infection, and bronchial hyperresponsiveness. Pathogenetically, new-onset OA may be immunologic or nonimmunologic in origin. The immunologic variants are usually caused by high molecular-weight allergens such as grain dust and animal or fish protein. Symptoms ensue after a latent period of months to years. Nonimmunologic OA can be precipitated by a brief, high-level exposure to a potent irritant. Symptoms occur immediately or within a few hours of the exposure. In either instance, once the diagnosis is established, the worker should be removed from the workplace. If the diagnosis is made in a timely fashion, most workers experience improvement. Prevention is the best therapeutic intervention.

Asthma↗

The mechanisms, causes, and treatment of anaphylaxis.

Anaphylaxis is a severe life-threatening systemic reaction that offers many challenges to the clinician. The incidence of anaphylaxis is significant in the general population and an important cause of morbidity and mortality. While the most common causes of anaphylaxis include drugs, foods, and venoms, other important etiologies must be considered. The etiology of anaphylaxis is classically based on IgE mediated hypersensitivity but multiple mechanisms may be involved. The clinical presentation of anaphylaxis may be extremely variable with a broad differential diagnosis which will be outlined. Although the diagnosis of anaphylaxis can many times be based on a careful history and physical examination, there are laboratory and skin tests which may be helpful in establishing a diagnosis in some cases. The cornerstone of treatment of anaphylaxis remains epinephrine. Other supportive therapies will be discussed.

Anaphylaxis↗

Airway hyperreactivity: managing outcomes and new directions.

Bronchial hyperreactivity is defined as an increased sensitivity to bronchoconstrictor stimuli. It is regarded as the physiological hallmark of bronchial asthma. It is usually associated with a positive family history of asthma, atopy, and evaluated total serum immunoglobulin E. Its prevalence in the normal population ranges from 10 to 20%; it increases with age and is significantly associated with both allergic rhinitis and atopic dermatitis. The relationship between bronchial hyperreactivity and respiratory symptoms may be weak. Bronchial hyperreactivity varies in severity with allergen exposure, viral infection, exposure to pollutants, environmental avoidance measures, anti-inflammatory therapy, and immunotherapy.

Asthma↗