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  Occupational Exposure to Aerosols

Asthma risk and occupation as a respiratory therapist

Christiani DC, Kern DG.  Department of Environmental Health (Occupational Health Program), School of Public Health, Harvard University, Boston, MA 02115.  Am Rev Respir Dis 1993 Sep;148(3):671-674. 

In the modern hospital environment, many health care workers are exposed to hazardous substances. Among these hazards are respiratory sensitizers, irritants, and infectious agents. A previous cross-sectional study of Rhode Island respiratory therapists reported an excess risk of asthma after entry into that profession. Before the results of that study were published, we conducted a confirmatory mailed questionnaire survey of 2,086 Massachusetts respiratory therapists and 2,030 physical therapists and physical therapy assistants. Neither the survey questionnaire nor the accompanying cover letter revealed the focus of our investigation. A history of physician-diagnosed asthma was reported by 16% of respiratory therapists and 8% of control subjects. When analysis was restricted to those who developed asthma after entry into their profession, respiratory therapists still had a significant excess, 7.4 versus 2.8%. The odds ratio for respiratory therapy was 2.5 (95% Cl, 1.6 to 3.3) after adjustment for age, family history, atopic history, smoking, and gender. These results confirm the previous report of excess risk of asthma among respiratory therapists. This excess risk develops after entry into the profession and does not appear to be explained by bias or confounding. Efforts should be directed to identifying potential agents responsible for this form of occupational asthma.

Second Hand (S)-albuterol: RT exposure risk following racemic albuterol

Bettye Carnathan, RRT, Barbara Martin, PA-C, Gene Colice MD. Washington Hosp Ctr., Washington, DC. Respir Care 2001; 46; 1084.

Racemic albuterol (RAC), a 50:50 mix of (R)-albuterol[R] and (S)-albuterol [S], is commonly used by RTs. R confers all of the bronchodilatory effects, while S demonstrates proinflammatory properties in in vitro and in vivo models. S is metabolized 10-fold more slowly, resulting in higher plasma levels that remain in circulation much longer after RAC administration. RTs have a higher rate of developing asthma after entering their profession (7.4 vs 2.4%, respectively; Christiani, 1993). Whether exposure to nebulized medications such as RAC contribute to this, or some other occupational hazard is responsible, is unknown. This study was designed to determine if S and R are detectable in the plasma of RTs. Eligible subjects (at least 18 years old; no asthma or other lung disease; at least 4 hrs of RAC exposure on each of 4 study days) began the study after a 2-day work holiday. Blood was drawn for S and R levels at baseline, 2, 4, and 8 hrs after exposure on Days 1 and 4. Subjects (n=12; mean age 38 yrs) nebulized delivered were exposed to approximately 31 mg of RAC by nebulization or MDI (range 22-43 mg) for 4.3 hours (range 3.2-5.5 hours) each day. At baseline on Day 1, On Day 1,mean levels of R and S were below the limit of quantification (BLQ, <2 pg/mL) at baseline, but were detectable after 2 hrs and increased over the 8-hr period. S levels were 1.6-2.5-fold higher than R (Table). On Day 4, approximately 2416 hrs after the last exposure, baseline levels of S, but not R, were detectable (3.7 pg/mL). Peak flow improved or remained unchanged in most subjects, but decreased in 3/12 subjects by an average of 30 mL. R- and S-albuterol are detectable in RTs following administration of RAC. S achieves higher plasma levels that remain in the systemic circulation for a longer period of time.

Identification of airborne dissemination of epidemic multiresistant strains of Pseudomonas aeruginosa at a CF centre during a cross infection outbreak

AM Jones, JRW Govan, CJ Doherty, ME Dodd, BJ Isalska, TN Stanbridge and AK Webb Adult Cystic Fibrosis Centre, Wythenshawe Hospital, Manchester M23 9LT, UK.  Thorax 2003;58:525-527.

Background: Chronic Pseudomonas aeruginosa infection is a major cause of morbidity and mortality for individuals with cystic fibrosis (CF). P aeruginosa cross infection outbreaks have recently been reported at CF holiday camps and specialist centres. The mechanism of cross infection is unknown. A study was performed to look for the presence of epidemic strains of P aeruginosa in the environment of a CF centre during a cross infection outbreak and to examine their potential modes of spread between patients.  Methods: Microbiological sampling of the environment of the CF facility was performed, including room air sampling. Individual P aeruginosa strains were identified by bacterial fingerprinting. The typing patterns were compared with those of epidemic strains responsible for cross infection among the patients.  Results: Epidemic P aeruginosa strains were isolated from room air when patients performed spirometric tests, nebulisation, and airway clearance, but were not present in other areas of the inanimate environment of the CF centre.  Conclusions: Aerosol dissemination may be the most important factor in patient-to-patient spread of epidemic strains of P aeruginosa during recent cross infection outbreaks at adult CF centres.

A Major Outbreak of Severe Acute Respiratory Syndrome in Hong Kong

Lee N, Hui D, Wu A, Chan P, Cameron P, Joynt GM, Ahuja A, Yung MY, Leung CB, To KF, Lui SF, Szeto CC, Chung S, Sung JJ.  Department of Medicine, Chinese University of Hong Kong , Hong Kong , China .

Background: There has been an outbreak of the severe acute respiratory syndrome (SARS) worldwide. We report the clinical, laboratory, and radiologic features of 138 cases of suspected SARS during a hospital outbreak in Hong Kong . Methods: From March 11 to 25, 2003 , all patients with suspected SARS after exposure to an index patient or ward were admitted to the isolation wards of the Prince of Wales Hospital. Their demographic, clinical, laboratory, and radiologic characteristics were analyzed. Clinical end points included the need for intensive care and death. Univariate and multivariate analyses were performed. Results: There were 66 male patients and 72 female patients in this cohort, 69 of whom were health care workers. The most common symptoms included fever (in 100 percent of the patients); chills, rigors, or both (73.2 percent); and myalgia (60.9 percent). Cough and headache were also reported in more than 50 percent of the patients. Other common findings were lymphopenia (in 69.6 percent), thrombocytopenia (44.8 percent), and elevated lactate dehydrogenase and creatine kinase levels (71.0 percent and 32.1 percent, respectively). Peripheral air-space consolidation was commonly observed on thoracic computed tomographic scanning. A total of 32 patients (23.2 percent) were admitted to the intensive care unit; 5 patients died, all of whom had coexisting conditions. In a multivariate analysis, the independent predictors of an adverse outcome were advanced age (odds ratio per decade of life, 1.80; 95 percent confidence interval, 1.16 to 2.81; P=0.009), a high peak lactate dehydrogenase level (odds ratio per 100 U per liter, 2.09; 95 percent confidence interval, 1.28 to 3.42; P=0.003), and an absolute neutrophil count that exceeded the upper limit of the normal range on presentation (odds ratio, 1.60; 95 percent confidence interval, 1.03 to 2.50; P=0.04). Conclusions: SARS is a serious respiratory illness that led to significant morbidity and mortality in our cohort.

Quote from the publication: "We suspected that the infection was transmitted by droplets and possibly by fomites, and we therefore instituted both airborne precautions (e.g., use of the N-95 respirator) and contact precautions (e.g., use of gowns and gloves), as recommended by the CDC.  However, the use of a jet nebulizer to administer aerosolized albuterol in the index patient had probably aggravated the spread of the disease by droplet infections."

Chronic exposure to a beta 2-adrenoceptor agonist increases the airway response to methacholine

Witt-Enderby PA, Yamamura HI, Halonen M, Palmer JD, Bloom JW.  Department of Pharmacology, College of Medicine, University of Arizona Health Sciences Center , Tucson 85724. Eur J Pharmacol 1993 Sep 7;241(1):121-3. 

Scheduled chronic administration of beta 2-adrenoceptor agonist bronchodilators in patients with asthma recently has been reported to be associated with a worsening of symptoms and an increase in bronchial responsiveness. We wanted to determine whether a 28-day in vivo exposure to albuterol (beta 2-adrenoceptor agonist) altered the response of rabbit airways to the cholinergic agonist methacholine. We found, using in vitro tissue bath techniques, that in mainstem bronchi from rabbits given a 28-day exposure to albuterol, maximum contraction to methacholine was increased in the albuterol-treated group (control group = 1.10 +/- 0.11 g vs. treated group = 1.50 +/- 0.13 g, P < 0.05). The potency (EC75) was also increased in the albuterol-treated group. The potency for the control group was 5.6 microM (95% confidence limit: 2.3-13 microM) and was 1.7 microM (95% confidence limit: 1.1-2.8 microM, P < 0.05) for the albuterol-treated group. In a subgroup of animals, maximum contraction to KCl, a receptor-independent contractile stimulus, was not significantly different between the groups (control group = 0.79 +/- 0.23 g vs. treated group = 0.82 +/- 0.20 g). The potency (EC50) for KCl-induced contractions was also not significantly different between the groups: control = 12 mM (95% confidence limit: 3.3-44 mM) vs. treated 19 mM (95% confidence limit: 18-20 mM). These data demonstrate that chronic in vivo exposure to a beta 2-adrenoceptor agonist can alter the in vitro tissue bath response of airway smooth muscle to methacholine.

Asthma in respiratory therapists

Kern DG, Frumkin H.  Roger Williams General Hospital, Brown University Program in Medicine, Providence, Rhode Island.  Ann Intern Med. 1989 May 15;110(10):767-73.

STUDY OBJECTIVE: To test the hypothesis that work as a respiratory therapist is associated with an increased risk of developing asthma. DESIGN: Cross-sectional questionnaire study comparing respiratory therapists with controls (physical therapists and radiologic technologists). Subsequent validation of reported asthma with methacholine challenge studies. SUBJECTS: All respiratory therapists and physical therapists and a random 50% sample of radiologic technologists working in the state of Rhode Island as of June 1986. METHODS: All subjects received a mail questionnaire with questions about the presence or absence of asthma, time of onset, and important covariates. Responses were analyzed for all subjects, and again after excluding those subjects with pre-existing asthma. Subjects who reported physician-diagnosed asthma were asked to have methacholine challenge testing. RESULTS: Respondents included 194 respiratory therapists (response rate, 69.5%) and 517 controls (response rate, 75.3%). After excluding respiratory therapists from the hospital at which the hypothesis was generated, there were 34 respiratory therapists (18.7%) and 30 controls (5.8%) reporting physician-diagnosed asthma. After controlling for age, smoking status, family history, atopic history, and other covariates using logistic regression, respiratory therapy carried an odds ratio of 3.2 (95% CI, 1.9 to 5.5). With analysis restricted to those who developed asthma after entering their profession, the odds ratio for respiratory therapy was 4.6 (95% CI, 2.0 to 10.4). In the validation study, 10 of 14 respiratory therapists (71%) and 6 of 10 controls (60%) had evidence of bronchial hyperreactivity. CONCLUSIONS: These results suggest a previously unrecognized excess of asthma in respiratory therapists. The excess develops after entry into the profession, and does not appear to be explained by confounding, information bias, or selection bias.

Occupational asthma in the respiratory care worker

Alberts WM.  University of South Florida College of Medicine, Tampa, FL 33612.  Respir Care. 1993 Sep;38(9):997-1004.

No abstract available at this time.

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  Nebulizer Cleaning
(Compilation and comments by Jeff Pray, RCP)

Craven DE. et al. Contaminated medication nebulizers in mechanical ventilator circuits. American Journal of Medicine. 77(5):834-8, 1984 Nov. 

"Contaminated in-line medication nebulizers generate small-particle bacterial aerosols that may increase the risk of ventilator-associated pneumonia and therefore should be cleaned or disinfected after each treatment rather than every 24 hours."



Kelsen SG. McGuckin M. Kelsen DP. Cherniack NS. Airborne contamination of fine-particle nebulizers. JAMA. 237(21):2311-4, 1977 May 23.

"Nebulizers placed in a surgical intensive care unit that had higher numbers of bacteria and a predominance of Gram-negative organisms in background air had a significantly higher incidence of nebulizer contamination (33.0%) than did nebulizers placed in a non-patient-care area that had lower bacterial counts and a predominance of Gram-positive organisms (0%) (P less than .05). The present study indicates that airborne contamination of fine-particle reservoir nebulizers occurs when bacteria present in ambient air enter the nebulizer during its operation."



Vassal S, et al. Microbiologic contamination study of nebulizers after aerosol therapy in patients with cystic fibrosis. American Journal of Infection Control. 28(5):347-51, 2000 Oct.

"Regarding P aeruginosa alone, 38% of nebulizers were contaminated after an aerosol. The addition of Staphylococcus aureus to P aeruginosa (contamination rate of 31.8%) and other targeted bacteria led to an overall contamination rate for pathogenic flora of
63.6%. This rate was underestimated because of the unavoidable loss of bacteria during collection. This finding clearly demonstrates that any negligence during disinfection is associated with the risk of allowing the persistence of bacteria, which can be
nebulized in the patients’ lungs. CONCLUSION: This study demonstrates that in the absence of cleaning, nebulizers of patients with cystic fibrosis who are infected with P aeruginosa are likely to be contaminated by a pathogenic flora."




Hutchinson GR, et al. Home-use nebulizers: a potential primary source of Burkholderia cepacia and other colistin-resistant, gram-negative bacteria in patients with cystic fibrosis. [erratum appears in J Clin Microbiol 1996 Jun;34(6):1601]. Journal of Clinical Microbiology. 34(3):584-7, 1996 Mar. 

"Patients who followed recommended instructions for good nebulizer hygienic practice and paid particular attention to drying had minimal or no contamination of their nebulizers."




Cobben NA, et al. Outbreak of severe Pseudomonas aeruginosa respiratory infections due to contaminated nebulizers. Journal of Hospital Infection. 33(1):63-70, 1996 May.

"The data provided evidence for the relation between P. aeruginosa as a cause of infection and the contamination of the nebulizers."




Pegues CF,et al. Burkholderia cepacia respiratory tract acquisition: epidemiology and molecular characterization of a large nosocomial outbreak. Epidemiology & Infection.
116(3):309-17, 1996 Jun.

"Review of respiratory therapy procedures revealed opportunities for contamination of nebulizer reservoirs. This investigation suggests that careful adherence to standard procedures for administration of nebulized medications is essential to prevent nosocomial respiratory infections."




Struycken VH, et al. Problems in the use, cleaning and maintenance of nebulization equipment in the home situation. Nederlands Tijdschrift voor Geneeskunde. 140(12):654-8, 1996 Mar 23.

"Contamination by potentially pathogenic micro-organisms was present in 50% of the saline, medication cups and aerosols (Klebsiella, Enterobacter, Pseudomonas, Serratia, Escherichia coli)."



Takigawa K, et al. Nosocomial outbreak of Pseudomonas cepacia respiratory infection in immunocompromised patients associated with contaminated nebulizer devices. Kansenshogaku Zasshi - Journal of the Japanese Association for Infectious Diseases. 67(11):1115-25, 1993 Nov.

"From May 1990 to August 1991, 36 patients admitted to the Department of Internal Medicine in a medical school hospital with hematological malignancies or solid tumors, 
developed respiratory tract colonization with Pseudomonas cepacia. Sixteen (44.4%) of these patients developed pneumonia, and four (11.1%) died of respiratory failure due to P. cepacia pneumonia. Extensive survey of the hospital environment as well as 
equipment showed that nebulizer devices used by the patients for inhalation were contaminated with P. cepacia."  I think this article also appeared in CHEST 103(6):1706-9, 1993 Jun.




Burdge DR. Nakielna EM. Noble MA. Case-control and vector studies of nosocomial acquisition of Pseudomonas cepacia in adult patients with cystic fibrosis. Infection Control & Hospital Epidemiology. 14(3):127-30, 1993 Mar. 

"Reservoirs from nebulizers consistently grew P cepacia following therapy.  CONCLUSIONS: Respiratory equipment may be an important source of nosocomial acquisition of P cepacia in adult cystic fibrosis patients."




Wexler MR. Rhame FS. Blumenthal MN. Cameron SB. Juni BA. Fish LA. Transmission of gram-negative bacilli to asthmatic children via home nebulizers. Annals of Allergy. 66(3):267-71, 1991 Mar.

"Home use of nebulizers has increased in recent years, although adequate studies have not been performed to evaluate for possible contamination or transmission of potentially harmful bacteria. This study of 20 asthmatic children demonstrated that transmission of pathogenic bacteria occurs."

Mastro TD. Fields BS. Breiman RF. Campbell J. Plikaytis BD. Spika JS. Nosocomial Legionnaires' disease and use of medication nebulizers. Journal of Infectious Diseases. 163(3):667-71, 1991 Mar.

"These findings support the recommendation that only sterile fluids be used for filling or cleaning respiratory care equipment and suggest that this guideline is not universally followed."




Botman MJ. de Krieger RA. Contamination of small-volume medication nebulizers and its association with oropharyngeal colonization. Journal of Hospital Infection. 10(2):204-8, 1987 Sep.

"Inhalation therapy had a significant effect on colonization, with a relative risk of more than four. Age over 60 years also showed a significant association with
colonization. One-third of the nebulizers sampled were contaminated, 71% with Gram-negative bacilli. A direct route of contamination could be demonstrated in 28% of the patients."

Morris AH. Nebulizer contamination in a burn unit. American Review of Respiratory Disease. 107(5):802-8, 1973 May.



Le Brun PP. et al. A review of the technical aspects of drug nebulization. Pharmacy World & Science. 22(3):75-81, 2000 Jun.

"The efficacy of nebulizer therapy is influenced by a great number of factors, including the design of the device and the characteristics of the drug solution. Incorrect cleaning, maintenance and disinfection procedures may change the nebulizer performance in time, whereas patient factors can influence the lung deposition of the generated aerosol."



Standaert TA. et al. Effects of repetitive use and cleaning techniques of disposable jet nebulizers on aerosol generation. Chest. 114(2):577-86, 1998 Aug.

A multicenter study of particle size distribution and output using saline solution alone, 
tobramycin, gentamicin, or a mixture of albuterol and cromolyn said "The purpose of this study was to determine if significant changes in particle size distribution or output (mL/min) occurred with reuse" they also said "For each of the four solutes tested, there was no clinically significant change in performance for up to 100 cycles, when the nebulizers were properly cleaned between uses. Unwashed units containing tobramycin started to fail by 40 runs." They also said "the Pari LC had an output rate two to three times higher than the four disposable models." (but dosing per nebulizer is another 
discussion). They concluded: "CONCLUSIONS: When properly maintained, there was no trend of deterioration of performance with repeated use of disposable nebulizers. Microbial contamination was not addressed in this study and must be considered prior 
to recommendations for the reuse of disposable nebulizers."



Struycken VH. Problems in the use, cleaning and maintenance of nebulization equipment in the home situation. Nederlands Tijdschrift voor Geneeskunde. 140(12):654-8, 1996 Mar 23.

A study of home nebulizers said "In addition, we found that the aerodynamic mass median diameter increased considerably as the nebulizer became older. In 6/10 nebulizers the particle size was below 5 microns."

  Ventilator Circuits & Ventilator-Associated Pneumonia

Contaminated condensate in mechanical ventilator circuits: A risk factor for nosocomial pneumonia. Craven, et al. Am Rev Respir Dis 1984; 129:625-628.

Results of a survey of ventilator circuit practices in the United States. Craven, et al. Infect Control 1984; 5:353-355.

Pathogenesis and prevention of nosocomial pneumonia in the mechanically ventilated patient. Craven DE and Steger KA. Respir Care 1989; 34:85-97.

Patterns of colonization by Pseudomonas aeruginosa in intubated patients: a 3-year prospective study of 1,607 isolates using pulsed-field gel electrophoresis with implications for prevention of ventilator-associated pneumonia. Valles J, Mariscal D, Cortes P, Coll P, Villagra A, Diaz E, Artigas A, Rello J.  Intensive Care Med. 2004 Jul 9

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