Asthma is a risk factor for acute chest syndrome and cerebral vascular accidents in children with sickle cell disease.

BACKGROUND: Asthma and sickle cell disease are common conditions that both may result in pulmonary complications. We hypothesized that children with sickle cell disease with concomitant asthma have an increased incidence of vaso-occlusive crises that are complicated by episodes of acute chest syndrome. METHODS: A 5-year retrospective chart analysis was performed investigating 48 children ages 3-18 years with asthma and sickle cell disease and 48 children with sickle cell disease alone. Children were matched for age, gender, and type of sickle cell defect. Hospital admissions were recorded for acute chest syndrome, cerebral vascular accident, vaso-occlusive pain crises, and blood transfusions (total, exchange and chronic). Mann-Whitney test and Chi square analysis were used to assess differences between the groups. RESULTS: Children with sickle cell disease and asthma had significantly more episodes of acute chest syndrome (p = 0.03) and cerebral vascular accidents (p = 0.05) compared to children with sickle cell disease without asthma. As expected, these children received more total blood transfusions (p = 0.01) and chronic transfusions (p = 0.04). Admissions for vasoocclusive pain crises and exchange transfusions were not statistically different between cases and controls. SS disease is more severe than SC disease. CONCLUSIONS: Children with concomitant asthma and sickle cell disease have increased episodes of acute chest syndrome, cerebral vascular accidents and the need for blood transfusions. Whether aggressive asthma therapy can reduce these complications in this subset of children is unknown and requires further studies.

Occupational lung disease related to cytophaga endotoxin exposure in a nylon plant.

Workers at a nylon plant developed pulmonary disease with systemic symptoms. Differentiating between humidifier fever and hypersensitivity pneumonitis (HP) is challenging. Cytophaga, an endotoxin-producing bacteria, was isolated from the plant air-conditioning system. A number of workers had systemic and pulmonary symptoms. Precipitins to Cytophaga endotoxin were identified. Several workers underwent lung biopsies demonstrating HP. Inhalation challenges with purified Cytophaga endotoxin were performed on three pairs of subjects: group 1, or employees with clinical features and biopsy consistent with HP; group 2, asymptomatic exposed workers with precipitins; and group 3, nonexposed healthy individuals. All subjects had fever and leukocytosis after inhalation challenge. Acute and/or late pulmonary function changes occurred in groups 1 and 2. Group 3 only had acute and transient pulmonary function changes. Cytophaga bacterial endotoxin is capable of inducing HP as well as humidifier fever.

Allergy and "toxic mold syndrome".

BACKGROUND: "Toxic mold syndrome" is a controversial diagnosis associated with exposure to mold-contaminated environments. Molds are known to induce asthma and allergic rhinitis through IgE-mediated mechanisms, to cause hypersensitivity pneumonitis through other immune mechanisms, and to cause life-threatening primary and secondary infections in immunocompromised patients. Mold metabolites may be irritants and may be involved in "sick building syndrome." Patients with environmental mold exposure have presented with atypical constitutional and systemic symptoms, associating those symptoms with the contaminated environment. OBJECTIVE: To characterize the clinical features and possible etiology of symptoms in patients with chief complaints related to mold exposure. METHODS: Review of patients presenting to an allergy and asthma center with the chief complaint of toxic mold exposure. Symptoms were recorded, and physical examinations, skin prick/puncture tests, and intracutaneous tests were performed. RESULTS: A total of 65 individuals aged 1 1/2 to 52 years were studied. Symptoms included rhinitis (62%), cough (52%), headache (34%), respiratory symptoms (34%), central nervous system symptoms (25%), and fatigue (23%). Physical examination revealed pale nasal mucosa, pharyngeal "cobblestoning," and rhinorrhea. Fifty-three percent (33/62) of the patients had skin reactions to molds. CONCLUSIONS: Mold-exposed patients can present with a variety of IgE- and non-IgE-mediated symptoms. Mycotoxins, irritation by spores, or metabolites may be culprits in non-IgE presentations; environmental assays have not been perfected. Symptoms attributable to the toxic effects of molds and not attributable to IgE or other immune mechanisms need further evaluation as to pathogenesis. Allergic, rather than toxic, responses seemed to be the major cause of symptoms in the studied group.

Toxic and other non-IgE-mediated effects of fungal exposures.

There are more than 100000 recognized species of fungi, comprising 25% of the biomass of the earth. Allergic, IgE-induced, manifestations of airborne fungi are common, whereas non-IgE manifestations are rare. Recently, much focus has been placed on the non-IgE-mediated effects of various molds, including hypersensitivity pneumonitis, infectious disease, and mycotoxicoses. Hypersensitivity pneumonitis is a clinical syndrome associated with systemic and interstitial lung disease that occurs in susceptible individuals following fungal inhalation. Most fungi are not pathogenic to man; however, certain fungi are capable of infecting immunocompetent individuals. Although mycotoxins and exposure to mycotoxins ("toxic mold syndrome") are implicated in causing numerous, nonspecific, systemic symptoms, currently, there is no scientific evidence to support the allegation that human health is affected by inhaled mycotoxins. However, if mold is discovered in a home, school, or office setting, the source should be investigated and appropriate remediation undertaken to minimize structural damage and potential allergic sensitization.