香港胸肺學會 美國胸肺學院港澳分會 Hong Kong Thoracic Society & ACCP (HK & Macau Chapter)

A Trimonthly joint communiqué of Hong Kong Thoracic Society & American College of Chest Physicians (Hong Kong and Macau Chapter)

聯合會員通訊

Newsletter

Circulation restricted to members only

Volume 15 Number 2 • Jun / Jul 2005

Contents

Council Members (2005-2007)

1 HKTS and ACCP (HK & Macau Chapter) Editorial Board

2 Editorial 2 Instruction to contributors

Special Event 3 Symposium on Avian Influenza – In Preparation for a Pandemic 5 The 45th Annual Meeting of Japanese Respiratory Society

Clinical Meeting Summary 6 Lady with “difficult” asthma 9 A 32-year-old man with bilateral lung shadow

Practical Corner 14 Questions for the next issue 15 What are atmospheric inversions and how will they affect the severity of air

pollution? 17 What are the pulmonary effects of cardioselective beta-blockers in asthma and COPD? 19 What is hygiene hypothesis?

Medical Statistics Corner 21 Medical biostatistics

Book Review Column 27 Clinical Atlas of Airway Diseases – Bronchoscopy, Radiology, and

Pathology

Diary of International Conferences 28

Forthcoming Clinical Meetings 29

Useful Websites 30

Chest Full Text On-Line 31

Membership News 31

Funds and Grants 32

HKTS

ACCP

Council of the Hong Kong Thoracic Society

Executive Committee of the American College of Chest Physicians (HK & Macau Chapter)

President Dr MOK Yun Wing, Thomas

Vice-President Dr TAM Cheuk Yin

Honorary Secretary Dr CHAN Wai Ming

Honorary TreasurerDr HO Chung Man, James

Council Members Prof HUI Shu Cheong, David

(Ex-President) Prof TSANG Wah Tak, Kenneth

Dr LAI Kei Wai, ChristopherProf LAM Wah Kit

Dr YAM Yin Chun, Loretta Dr CHAN Yuk Choi

Prof CHAN Mo Wah, Moira Dr YU Wai Cho

Dr PANG Joseph Dr HO Sheng Sheng

Dr YEE Kwok Sang, WilsonDr TSE Pak Yiu

Dr SO Kit Ying, Loletta Dr CHUI Wing Hung

Chief Editor:NewsletterDr KO Wai San, Fanny

Address for Correspondence Dr CHAN Wai Ming

Intensive Care Unit, Queen Mary Hospital Pokfulam, HK

President Dr WONG Poon Chuen

Vice-President Dr WONG Mo Lin, Maureen

Honorary Secretary/Treasurer Dr CHU Chung Ming

Executive Committee Members Dr CHAN Kin Sang (Ex-President) Prof LAM Wah Kit Dr CHAN Hok Sum Dr LAM Chak Wah Dr TAM Cheuk Ming Dr CHOO Kah Lin Dr CHAN Wai Man, Johnny Dr KWOK Kai Him, Henry Dr LAU Chun Wing

Governors Dr CHAN Chun Kwong, Jane Prof YIM Ping Chuen, Anthony Dr YEW Wing Wai

Regent Prof IP Sau Man, Mary

Address for Correspondence Dr CHU Chung Ming Department of Medicine, United Christian Hospital,Hong Kong

2 0 0 5 - 2 0 0 7

HHKKTTSS AACCCCPP

1

E ditorial Board

Editor Dr Fanny WS Ko

Deputy Editor Dr Johnny Chan

Board Members Dr Kah Lin CHOO

Dr James Ho Dr Sheng Sheng HO Dr Henry KWOK Dr Wai Kei LAM

Miss Barbara LAW Dr Loletta K Y SO

Dr Julie Wang Dr Matthew K Y WONG Dr Maureen M L WONG

Dr Wilson K S YEE

Address for Correspondence Dr Fanny WS Ko

Dept. of Medicine and Therapeutics Prince of Wales Hospital

Shatin N.T.

Hong Kong

Fax (852) 26375396

Email

fannyko@cuhk.edu.hk

Editorial The Symposium of Avian Influenza, jointly organized by the Hong Kong Thoracic Society and the American College of Chest Physicians (HK and Macau Chapter), sponsored by the Hong Kong Lung Foundation was held on April 16, 2005 with great success. Representative from Hong Kong had attended the 45th Japanese Respiratory Society Meeting in April 2005. We will report both events in this issue of the newsletter.

The new medical statistics corner introduced since last issue has received very good comments and we will thus continue this in the coming issues. Hope that you will enjoy reading the newsletter. The editorial board welcomes suggestions from all the readers for providing an informative and educational reading material to the members of our two local chest societies.

Instruction to Contributors We welcome contributions from invited guests and members of the Hong Kong Thoracic Society and the American College of Chest Physicians (Hong Kong and Macau Chapter). Articles should be prepared with suitable word processing software (eg Word 2000). Figures, table, pictures and photo- micrographs should be saved in the same file. Please do not use the auto-indexing features. The file could be sent either by e-mail or by post (on a floppy disc or CD) to the Chief Editor. Please indicate to the Chief Editor if the material has to be returned after the editing process. The article would be printed in the same way as it is submitted. The accuracy of the materials published is the responsibility of the contributors. The contributors must ensure that the materials submitted do not infringe copyright.

Disclaimer The opinions expressed in this newsletter are those of the author/s and do not necessarily reflect the official policies of the Hong Kong Thoracic Society, American College of Chest Physicians (Hong Kong and Macau Chapter), the institution with which the author(s) is/are affiliated, or the publisher.

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Symposium on Avian Influenza – In Preparation for a Pandemic

pecial Event

Drs David Hui and KS Chan

Co-Chairmen of the Organizing Committee

The Symposium on “Avian Influenza – In Preparation for a Pandemic” was held successfully on April 16, 2005 with attendance by more than 600 participants. This symposium was jointly organized by the Hong Kong Thoracic Society and the American College of Chest Physicians (Hong Kong and Macau Chapter), and sponsored by the Hong Kong Lung Foundation. The symposium kicked off with an opening speech by Dr. York Chow, the Secretary for Health, Welfare and Food Bureau of the Hong Kong Special Administrative Region. Distinguished speakers from Hong Kong and overseas, including representatives from Thailand which has managed 17 human avian flu cases since 2004, gathered in the Hong Kong Convention Centre on the Saturday afternoon. The programme was very rich and consisted of 3 sessions. The first session was on epidemiology and virology of Avian Flu and presented by two local experts Dr. Thomas Tsang and Professor Malik Peiris. The second session was on clinical features and management and was presented by Dr. Tawee Chotpitayasunondh (Thailand), Dr. David Hui, Dr. Wing-hong Seto and Dr. Loretta Yam. The third session was on public health issues and contingency plans. Dr. Supamit Chunsuttiwat (Thailand) shared with the audience the Thailand experience in public health control of H5N1 in poultry and humans, while Dr. Thomas Tsang and Dr. Shao-haei Liu presented the contingency plans on behalf of the Centre for Health Protection and Hospital Authority respectively. Professor Kenneth Tsang discussed the research aspects related to a clinic trial in preparation for avian flu pandemic. The meeting was concluded with a round table discussion chaired by Dr. Kin-sang Chan and Professor Wah-Kit Lam. Representatives from Thailand (Dr. Tawee Chotipitayasunondh, Dr. Supamit Chunsuttiwat), Malaysia (Professor Chong-kin Liam), Korea (Professor Young-soo Shim), Singapore (Professor Philip Eng) and Hong Kong (Dr. Chung-Ming Chu, Dr David Hui, Dr. Shao-haei Liu, Professor Malik Peiris, Professor Kenneth Tsang, Dr. Thomas Tsang and Dr. Loretta Yam) discussed on the relevant public health and treatment aspects in preparation for the pandemic.

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From left to right: Professor Malik Peiris., Dr. Thomas Tsang, Professor Young-soo Shim (chairman) and Dr. Thomas Mok (chairman) at the session Epidemiology and Virology

Dr. York Chow, the Secretary for Health, Welfare and Food Bureau of the Hong Kong Special Administrative Region, at the opening ceremony

From left to right: Dr. Loretta Yam, Dr. Wing-hong Seto, Dr David Hui, Professor Tawee Chotpitayasunondh, Dr. Poon-chuen Wong (Chairman) and Professor Philip Eng (Chairman) at the Clinical Features and Management

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Group photo from left to right: Front row --- Prof Wah-kit Lam, Professor Chong-kin Liam, Dr. Loretta Yam, Dr Tawee Chotpitayasunondh, Pofessor Young-soo Shim, Professor Philip Eng, Dr. Poon-chuen Wong. Back row --- Dr Supamit Chunsuttiwat, Professor Kenneth Tsang, Dr DavidHui, Professor Malik Peiris, Dr. Wing-hong Seto, Dr. Wai-ming Chan, Dr. Thomas Mok, Dr. Chung-ming Chu and Dr. Thomas Tsang

pecial Event

The 45th Annual Meeting of the Japanese Respiratory Society

Dr. Loletta KY So, Department of Medicine,

Pamela Youde Nethersole Eastern Hospital

The 45th JRS Meeting was held on 14–16 April 2005 in Makuhari of Chiba. Makuhari is located midway between central Tokyo and the Narita airport. Being a new urban city developed in the recent 15 years, it has modern amenities and facilities for participants to enjoy the meeting and organizers’ hospitality. The theme of meeting was “respiratory diseases as a mirror of external and internal environments” which covered a wide range of respiratory topics and drew the participation of many transpacific and transatlantic speakers. Presidents and delegates from the American Thoracic Society, European Respiratory Society and Asian Pacific Society of Respirology joined the local Japanese participants in filling the meeting halls and stages. Dr. Christopher KW Lai was among the invited experts and he enlightened the audiences on what we can do to reduce the burden of asthma in Asia Pacific. I am fortunate to have the opportunity of joining Dr. David CL Lam from the Queen Mary Hospital to attend the meeting as APSR Young Investigators. Dr. Lam presented his molecular research looking into the differential gene expressions in lung adenocarcinoma, and I spoke about the early and late outcomes of severe acute respiratory syndrome, an infectious hazard not experienced in Japan yet. We were encouraged by the enthusiasm of local participants in attending not only their domestic Japanese sessions but also the international English sessions with active responses. The meeting was enriched with a memorable welcoming reception hosted by the 45th JRS President, Professor Takayuki Kuriyama from the Chiba University, and a splendid sushi party where we met the 47th JRS President Professor Toshihiro Nukiwa from Sendai’s Tohoku University and enjoyed happy moments together as if we had advanced two years into 2007. This JRS meeting was again a reflection of boundless scientific links and international relationships in the field of respiratory medicine, and we owe our predecessors and pioneers a great deal in this regard.

Drs. David Lam, Loletta So and Christopher Lai (from left to right) in the sushi party where oishii sashimi and fine sake were served.

Professor Takayuki Kuriyama, the JRS President (in the middle) at the welcoming reception with Drs. David Lam (first left) and Loletta So (second right)

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linical Meeting Summary

Lady with “difficult” asthma

Dr. Thomas J.S. Lee

Department of Medicine, Tuen Mun Hospital

Our subject is a 28 years old Indonesian Chinese lady who presented to our hospital in April 2004 with shortness of breath associated with palpitations, coughs, sputum and fever. She had been in Hong Kong for 6 years, and had enjoyed good past health with no history or family history of atopy. She had 2 prior pregnancies before, which were complicated by pregnancy-induced hypertension, requiring induction of labour at term, and both resulted in normal vaginal delivery. She does not smoke or drink any alcohol, but her husband does smoke regularly. On physical examination, she was noted to be dyspnoeic, her temperature was 38.1°C, heart rate was 150/min, and there was generalized wheeze in her chest with right basal crepitations heard. Her other systems were otherwise normal. Her CXR showed right lower zone infiltrates. Her blood investigations results showed: WCC 29.4 x 109/L (92% polymorphs, eosinophil count was not raised), Hb 13.6 g/dl, Plt 237, ABG: pH 7.44, pCO2 4.52 kPa, pO2 11.07 kPa, SaO2 97%, liver & renal function was normal. She was treated as suffering from chest infection and suspected asthma with antibiotics and bronchodilators. Her symptoms improved and fever subsided so she was discharged planned for a pulmonary function test. She defaulted follow-up but was readmitted again in October and November 2004 with similar symptoms. She was treated with bronchodilators and steroids and her symptoms seemed to improve. A pulmonary function test showed a severe obstructive ventilatory limitation with insignificant bronchodilator response.

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Her lateral CXR showed a distal tracheal opacity.

CT thorax performed which showed a intra-luminal polypoid soft tissue mass at the distal trachea with near total luminal occlusion. She underwent emergency rigid bronchoscopy and the mass was debulked. She had an uneventful post-operative course. Histology of the mass showed a tumour with many tubular epithelial elements in sheets that was intermixed with a myxochondroid stroma. At the edges the epithelial cells seemed to stream into the stroma. There were also islands of squamous cell metaplasia. All these were consistent with the diagnosis of a pleomorphic adenoma of the trachea.

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HistologyHistologyTubular epithelial elements

Myxochondroidstroma

Primary tracheal tumours are rare in clinical practice and usually either squamous cell carcinoma, or adenoid cystic carcinoma. Tracheal pleomorphic adenoma is extremely rare. Only 28 cases have been reported in the literature to date with the patient’s age ranging from 15 to 80 years old. It is more common in male patients, occurring more in the upper third followed by middle and lower third of the trachea. 2 malignant cases have been reported, 1 from Japan, and 1 from Turkey. It is very similar to that found in the salivary glands and its pathogenesis is controversial. It may originate from the epithelial glands of the submucosal glands, but peripheral lesions in the lungs have also been reported, so it may have arise from primitive stem cells. Patients usually present with episodic coughs, dyspnoea on exertion, wheezing, haemoptysis, stridor, hoarseness, recurrent respiratory tract infections, and even

sphagia.

re foci of squamous metaplasia and the tumour cells re positive to S-100 protein, cytokeratin, glial fibrillary acidic protein, muscle

all, and well circumscribed tend to be benign, while those that re larger, more infiltrative or poorly circumscribed tend to recur but rarely

us foci, perineural invasion, and has growing atures.

References 1. Demirag F, Topcu

a case report and r2. Schneider P, Schi

Cardiothorac Sur 0(1):12-8. 3. Kim KH, Sung MW, Kim JW et al. Pleomorphic adenoma of the trachea. Otolaryngol Head Neck Surg

2000;123(1 Pt 1):4. Peretti G, Piazza

reconstruction. Ac5. Kiryu T, Kawagu . Pleomorphic adenoma of the trachea: a case report. Radiat Med

1998;16(3):205-7. 6. Paik SS, Jin YH, Park CK et al. Pleomorphic adenoma of the trachea. J Korean Med Sci 1997;12(6):564-6.

. Paik HC, Lim SH, Lee DY et al. Pleomorphic adenoma of the trachea--a case report. Yonsei Med J 1996;37(1):81-5.

. Heifetz SA, Collins B, Matt BH. Pleomorphic adenoma (benign mixed tumor) of the trachea. Pediatr Pathol ):563-74. hen CY, Chiang CH et al. Pleomorphic adenoma of the trachea: report of two cases..J Formos Med

10. Geka Gakkai Zasshi 1991;39(6):920-3.

dy Macroscopically, these tumours varies in size, they are sessile, of a whitish grey colour on the surface, firm and polypoid in shape. The cut surface is firm, gray in colour and may be slightly mucoid. Microscopically, they are seen to arise from the subepithelial tissues and are covered by respiratory and squamous epithelium. The glands are tubular and exhibits a varying amount of eosinophilic material. These epithelial elements are mixed with a myxochrondroid stroma which is rich in alcian blue-staininig mucopolysaccharide. There aaspecific actin, and vimentin. Tumours that are smametastasize. The main differential diagnosis is adenoid cystic carcinoma which is a more aggressive tumour, with amorphous periodic acid schiff positive tubular material with absence of cartilagenofe The treatment of choice is complete excision with cuffs of normal tissue to avoid recurrence. This would usually involve removing a section of the trachea followed by reanastomosis.

S, Kurul C et al. Malignant pleomorphic adenoma (malignant mixed tumor) of the trachea: eview of the literature. Eur Arch Otorhinolaryngol 2003;260(2):96-9. rren J, Muley T et al. Primary tracheal tumors: experience with 14 resected patients. Eur J g 2001 Jul;2

147-8. C, Berlucchi M et al. Pleomorphic adenoma: a case treated by laryngotracheal resection and ta Otorhinolaryngol Ital. 2000;20:54-61. chi S, Matsui E et al

7

81992;12(4

9. Yan HC, SAssoc 1991;90(11):1124-7. Takahashi H, Kubota M, Kitoh K et al. Nippon Kyobu

8

linical Meeting Summary

A 32-year-old man with bilateral lung shadow

Dr. SN Chan, Dr. LS Ip, Dr. PY Tse Department of Medicine, Tseung Kwan O Hospital

Case History Mr. Lam was 32 years old and was a non-smoker and non-drinker. He had childhood asthma but did not need regular follow up or medication for years. He presented with chronic productive cough for one month, associated with blood stained sputum and dyspnoea the week before admission. He complained of chest pain after severe cough, subjective weight loss and poor appetite. He did not have nasal congestion, night sweat, TB contact and recent travelling. On admission, he was stable and not in respiratory distress. The blood pressure was 99/56mmHg. Pulse rate was 100 beats per minute. Oxygen saturation was 92% on room air and body temperature was 37.5 ºc. On examination, there was bilateral basal crepitations on auscultation. There was no cardiac murmur or lower limb oedema. JVP was not elevated. CXR on admission showed multiple nodular shadows on bilateral lung fields (Fig.1).

Investigation results on admission: Haematology results: WBC: 15.4 x 10^9/L Neurtrophil ↑11.5 x 10^9/L (1.8-7.5 x 109/L)Lymphocyte 2 x 10^9/L (1-3.8 x 109/L) Eosinophil 0.6 x 10^9/L (0-0.5 x 109/L) Hb: 11 g/dL MCV: 90.5 fL PLT: 330 x 109/L Retic %: ↑7.6 ESR 33 mm/hr

Renal function test and electrolytes: Sodium 137 Potassium 3.5 Chloride 100 Urea 5.3 Creatinine 80 Spot glucose 6.5

Liver function test: Total protein 63 Albumin 39 Globulin 24 Bilirubin 13 ALP 69 ALT 13

He was given amoxycillin/clavulanate potassium, clarithromycin and tranexamic acid intravenously. Later the sputum culture, AFB smear and cytology were found to be negative. Six days after admission, he still complained of mild haemoptysis. Fever kicked up to 38.5ºc. He developed type I respiratory failure and required 50% of oxygen supplement. Haemoglobin level dropped to 7.7g/dL. CXR was repeated and showed increasing alveolar and nodular shadows(Fig.2). Computerized tomography for thorax with contrast was arranged which found a 4 x 5.5 cm filling defect in right atrium (Fig 3).

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Fig 1: CXR on admishadows on bilateral

t i as found. The iple nodular

ld.

Mr. Lam finally received an operation for the palliative excision of right atrial tumour. There was a large non-gelatinous tumour, arising from right atrium near the

llapsed changes. There was blood stained pleural effusion in oth pleural cavities and a straw colored pericardial effusion.

ssion: multiple nodular Fig 2: CXR on D6: Deteriorating CXR with lung field increasing alveolar and nodular shadow

Fig 3: CT thorax: A 4 x 5.5cm filling defec n right atrium w re were multand alveolar shadows on bilateral lung fie

superior vena cava entry (Fig.4). Both lungs were found to have patchy consolidation and cob

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Fig 4: Intra-operative photo of the right atria

After the operation, Mr. Lam was in critical condition and complicated with multi-organ failure. He succumbed two days after operation. Pathological examination:

ig 5: Capillaries and venule-like spaces Fig 6: Moderately pleomorphic tumor cells

in the less cellular ar

metastasis, likely

omplicated with pulmonary hemorrhage

l tumour

The atrial tumour was fleshywas found on microscopic efeature of malignancy (Fig. 5while the HHV8 staining wa

with extensive hemorrhage. Heterogeneous patternxamination. There was abnormal blood space with & 6). The CD31 and CD34 staining were positive

s negative. It was compatible with angiosarcoma.

Fea of tumor with abortive blood channel formation

Diagnosis: Cardiac angiosarcoma with pulmonary c

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Discussion: Primary malignant neoplasm of the heart is very rare. Angiosarcoma accounts for about one third of all malignant cardiac tumours. There is no specific predisposing factor identified. The age of onset ranges from 8 to 80 years old with mean at 40. There is slight male preponderance. About half of the cases have metastasis identified at the time of diagnosis. Right atrium is being the most commonly involved heart chamber. The initial presenting signs and symptoms are related to the location, size and extent of regional involvement, as well as to the presence or absence of metastasis. The most common site of metastasis is the lung, followed by the liver and the central nervous system. The presenting clinical features include pericardial effusion with cardiac tamponade, multiple lung metastases and diffuse pulmonary hemorrhage which, though is rare, should be considered in

rcoma to the lung.1, 2, 3, 4, 7

The tumour can be dark red, hemorrhagic and lobular or diffusely infiltrate the

ericardium and myocardium. Invasion of the superior and inferior vena cava,

nd formation of irregular anastomosing sinusoidal structures with papillary ohistochemically, the tumour has positive staining

infiltrations, pleural effusion, diffuse alveolar shadow or pneumothorax.5 ontrast CT scan of thorax can identify the intracardial filling defect which has w attenuation. The metastatic lung lesions can be either nodular or cystic.6

Two dimensional echocardiogram and MRI scan offer no more specific findings. Confirmatory diagnosis still relies on tissue biopsy. Tissue can be obtained through thoracotomy, transvenous biopsy under echocardiographic guidance. Surgical resection is the main state of therapy. Partial resection or orthotopic heart transplantation would be considered if complete resection is not possible. The tumour is not very responsive to either chemotherapy or radiotherapy though a combination of surgical resection, chemotherapy and radiotherapy has been tried with survival benefit. Overall, the prognosis is grave. The mean postoperative survival is about 10 months. Long term survival could be achieved in just few cases reported in literature.

patient with metastatic angiosa

ppulmonary artery and aortic root is not uncommon. Microscopically, the tumour shows vasoforming vascular channels lined by pleomorphic and atypical cells, aintraluminal tufting. Immunfor factor VIII-related antigen, vimentin, CD34 and CD31. Concerning the imaging modalities, chest radiograph is useful in identifying the metastatic lung lesions. The features include multiple nodules, linear

Clo

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References 1. Glancy DL, Morales C. Angiosarcoma of the heart. Am J Cardiol 1968;21:413-9. 2. Janigan DT, Husain A. Cardiac angiosarcomas. A review and a case report. Cancer

1986;57:852-9. 3. Hermann MA, Shan

clinicopathologic stu4. Butany J, Yu W. Ca review of the literature. Can J Cardiol. 2000

Feb;16(2):197-205. 5. Ashokakumar MP, J6. Ukihide T et al. Met7. Camilo A, Marie-Ch

Pulmonary Hemorrh Acknowledgement: W hology, QEH for lending the histological slides aintra-operative photos.

JB, Roberts WA, Robinson N

kerman RA, Edwards WD, Shub C, Schaff HV. Primary cardiac angiosarcoma: a dy of six cases. J Thorac Cardiovasc Surg 1992;103:655-64.

rdiac angiosarcoma: two cases and a

ay HR. Angiosarcoma in the Lung. Chest 1993;103:1531-33. astatic Angiosarcoma of the Lung: Spectrum of CT Findings. AJR 2003;180:1671-74. ristine A, Henry DT, Jeffrey LM. Metastatic Angiosarcoma Masquerading as Diffuse age. Arch Pathol Lab Med 2001 Dec;125:1562-65.

e’d like to thank Dr. Y.W. Tsang, Department of Patnd Dr. C.C. Ma, Department of Cardiothoracic Surgery, QEH for providing the

13

ractical Corner

ng the tions asked will be

give their brief discussions. In no way is it meant to be exhaustive or

ts. is

e comments, particularly when there is query on what had been published. Please send them to the editor email: fannyko@cuhk.edu.hk

Questions for the next issue:

This section serves to bombard the trainees with questions coveribasic concepts in respiratory medicine. Quesdiscussed in the next issue. Specialists and trainers are invited to

comprehensive, it only serves to highlight important concepSpecialists are welcome to offer questions (and the discussions) for thsection. Trainees are also welcome to giv

1 What are the ways to diagnose latent TB infection?

(from Dr. Ricky Lam, Northern District Hospital)

2 How would you work up a patient with suspected idiopathic pulmonary fibrosis? (from Dr. KC Wong, Kowloon Hospital)

3. What physical and aerodynamic properties of radon in making it an important etiology of lung cancer?

(from Dr. Henry Kwok, Ruttonjee Hospital)

14

ractical Corner

What are atmospheric inversions and how will they affect the severity of air pollution?

Dr. Henry Kwok Ruttonjee Hospital

tmospheric inversions are conditions in which the temperature of the

atmosphere increases with altitude in contrast to the normal decrease with the relatively warmer air near the ground will

e and will therefore bring with it the air pollutant emitted from the ground ures and vehicles. When atmospheric inversions occur, cold air underlies

rm r during the passa r by a cooler onshore breez d are thereby inhibited from when they reach the warmer, less dense air in the upper

rpollu osphere's lowest layer is trapped there and can be o g horizontal winds. Because the high-pressure syste rsion conditions and low wind speed , the resulting long residency of the pollutants over an industrial area

eare region. Inversions become

zed or densely settled areas here noxious pollutants can steadily accumulate to dangerous concentrations.

The two most important types of temperature inversions are: 1. Radiation inversions, which are normal nocturnal situations occurring in clear nights when absorbed daytime heat is radiated quickly out into space and the temperature of surface air drops below that of the air above them. Radiation inversions are usually short lived and will break up as soon as the morning sun warms the earth, reestablishing normal convection currents of warmer air rising up; 2. Subsidence inversions, which are caused when a layer of air within a high-pressure mass settles down over a region, compressed and thereby heated by the high pressure area above. They are particularly worrisome because they may remain in place for days. They are more common and last longer during the fall and winter months.

A

altitude. In the normal situation,risstructwa er air at higher altitudes. Atmospheric inversions may occu

ge of a cold front or result from the invasion of sea aie. Rising currents of cool air lose their buoyancy an rising further

laye s of a temperature inversion. During an atmospheric inversion, air tants released into the atmnly be removed by stronms often combine with atmospheric inves

usually results in episodes of severe smog. It should be noted that atmospheric inv rsions are natural occurrences and present no threat to human health if there

few sources of pollutants within the affected problematic only when they occur in industrialiw

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eadings zar P, Dominguez E. Meteorological phenomena affecting the presence of

air during winter. Int J Biometeorol. 2000 ;44:6-10. Lawrence EN. Atmospheric pollution during spells of low-level air temperature inversion. Atmos Environ. 1967;

3. Roberts L, Bate1957;16;269:57

Further r1. Carinanos P, Galan C, Alca

solid particles suspended in the2.

1:561-76. y JW. Atmospheric pollution, temperature inversion, and deaths from bronchitis. Lancet. 9.

ckers in asthma and COPD?

ractical Corner

What are the pulmonary effects of cardioselective beta-blo

Dr. MP Lee Department of Medicine, Queen Elizabeth Hospital

Beta-blockers have mortality benefits in several common cardiovascular disorders including ischaemic heart disease, congestive heart failure, arrhythmia, and hypertension. However, in the presence of co-existing obstructive airway diseases, physicians are often reluctant to prescribe this agents because of the fear of bronchospasm. Clinical studies in asthma Salpeter and colleagues had performed a meta-analysis by selected randomized, blinded, placebo-controlled trials of the effects of cardioselective beta-blockers in patients with reversible airway disease.1 Reactive airway disease was defined as asthma or COPD with a reactive component. The study evaluated 29 trials with 381 participants in whom treatment was given either as a single dose or for a longer duration lasting 3 days to 4 weeks. Compared to placebo, single dose of cardioselective beta-blockers was associated with a 7.46% reduction (95% CI, 5.59 to 9.32%) in FEV1, but with a 4.63% increase (95% CI, 2.47 to 6.78%) in FEV1 after beta2-agonist was given. There was no increase in respiratory symptoms reported in any of the studies. In the continued treatment trials the use of cardioselective beta-blockers as a group was not significantly different from placebo in terms of FEV1, symptoms or inhaler use. Most of these studies were carried out in patients with mild to moderate airway obstruction, and those with recent asthma exacerbations were often excluded. One study on survivors of myocardial infarction included 46,000 patients with concomitant asthma or COPD and showed a significant reduction in total mortality for those treated with beta-blockers compared with those who were not.2 Clinical studies in COPD Another meta-analysis evaluated cardioselective beta-blocker use in patients with documented COPD.3 Nineteen randomized, blinded, controlled trials with 267 participants were included, with study duration ranging from 2 days to 12 weeks. The pooled results showed no change in FEV1, respiratory symptoms, or beta-2 agonist inhaler use for single doses or continued treatment with cardioselective beta-blockers compared with placebo. Exacerbations and hospitalizations were recorded in all trials, but none occurred during the periods of study, in either group. Subgroup analyses revealed no difference in results for those with a reactive airway component. Furthermore, there was no difference in results for those with severe COPD, as demonstrated by a baseline FEV1 < 1.4 L or < 50% the normal predicted value.

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Drug Selection ve beta-blockers, or beta-1 blockers, have > 20 times more affinity eceptors than for beta-2 receptors, whereas nonselective beta-

blockers have equal affinity for both receptors.4 At therapeutic doses the beta-2

uation of their beta-blocking effects. Use of cardioselective beta-blockers without ISA (e.g. atenolol, metoprolol,

isoprolol and practolol) was associated with an increase in beta-2 agonist response that is maintained with continued treatment. This could be explained by an up-regulation or sensitization of beta-2 receptors. On the contrary, there is

treatment with beta-blockers with ISA (e.g. celiprolol and acebutolol) resulted in down-regulation of beta-2 receptors.

Cardioselectivity of beta-blockers can be lost at the higher dosage range. Formgren reported no effect on FEV1 at lower doses of practolol (200mg/d) and metoprolol (100mg/d).5 At higher doses (practolol 400mg/d; metoprolol

ummary here is substantial clinical evidence that cardioselective beta-blockers are safe

ts with mild to moderate asthma or COPD. These

References 1. Salpeter SR, O

disease: a meta- s. Ann Intern Med. 2002; 137: 715-725. 2. Gottlieb SS, McCarter RJ, Vogel RA. Effect of beta-blockade on mortality among high-risk and low-risk

patients after m al infarction. N Engl J Med. 1998;339:489-497. 3. Salpeter SR, Or ioselective β-blockers for chronic obstructive pulmonary

disease: a meta-4. Ablad B, Carlss

of the pharmaco5. Formgren H. T

asthmatics. Br J

Cardioselectifor beta-1 r

blocking effect, and therefore the risk of bronchoconstriction, is negligible. Intrinsic sympathomimetic activity (ISA) is present in varying degrees in some beta-blockers, which may result in an atten

b

evidence that

200mg/d) both beta-blockers reduced the FEV1 and some patients experienced a worsening of asthma as well. STand well tolerated in patiendrugs should be considered when strong indications are present in view of the mortality benefits e.g. unstable angina, myocardial infarction, congestive heart failure or tachyarrhythmia. It is preferred to choose cardioselective beta-blockers without ISA. Drugs should be initiated at low doses with close observation and, if tolerated, dosage can be titrated to achieve the desired clinical effect. Since no studies have yet been published that confirm the safety of cardioselective beta-blockers in patients with severe asthma or recent exacerbations, continued caution remains appropriate in these individuals.

rmiston TM, Salpeter EE. Cardioselective β-blockers in patients with reactive airway analysi

yocardimiston TM, Salpeter EE. Cardanalysis. Respiratory Medicine. 2003; 97: 1094-1101. on E, Dahlof C, et al. Pharmacology of betaadrenoceptor blocking drugs: some aspects logy of beta-adrenoceptor blockers. Drugs. 1976;11:100-111.

he effect of metoprolol and practolol on lung function and blood pressure in hypertensive Clin Pharmacol 1976; 3: 1007–1014.

6.

ractical

Corner

What is hygiene hypothesis?

Dr. Clarence CH Lee Private Pulmonologist

n to this phenomenon, such as better hygiene, fewer infections early in life due to antibiotic treatments and vaccinations, the loss of protective effects from rural life-style, environmental pollutions and

in dietary habits. Hygiene hypothesis is probably the most

een infection and allergic sensitization has come from studies of hepatitis A3. Martinez and co-workers showed that exposure of young children to older children at home and to other children at day-care centre protected against the development of asthma and frequent wheezing later in childhood4. Chu et al provided further support by elegantly demonstrating in mouse model that induced Mycoplasma pneumoniae infection before allergen sensitization reduced the bronchial hyperresponsiveness which was accompanied by Th1 responses5.

in the last decade6. Uncommitted

as IL-4, IL-5, and IL-

mption of the hygiene hypothesis is that newborn infants have a preponderance of Th2 cells. According to this hypothesis, it is the exposure of antigens in the early infancy that drives the development towards Th-1. The improved hygiene in the Western and developed countries results in fewer infections. It is thought that Th2 immunity, predominating from birth, dominates through critical childhood periods, resulting in the increased prevalence of atopy and asthma.

The prevalence of asthma and allergic diseases has been rising in recent decades1. The observed increase cannot be explained by genetics. Many explanations have been give

changes controversial one in this area. The concept of hygiene hypothesis was first proposed by Strachan in 1989, when he observed an inverse relationship between household size and hay fever2. He postulated that the higher incidence of infection in households with more siblings protected against the subsequent development of hay fever. Many studies have looked at the underlying mechanisms behind this hypothesis, such as childhood infections by measles, Mycobacterium tuberculosis, and hepatitis A; the role of environmental endotoxin; and the use of antibiotics in the first year. The results have been conflicting. Perhaps the most consistent supporting evidence of an inverse relationship betw

With more understanding of the immunological basis of asthma and atopy, hygiene hypothesis has gained great interestT helper cell (Th0 cell) can mature to either Th1 cell or Th2 cell under the influence of genetics and environment. Th1 cells produce cytokines interleukin (IL)-2, tumour necrosis factor (TNF) and interferon (IFN)-gamma that drive the B cells to produce defense immunoglobulins: IgM, IgA, and IgG. Th2 cells release pro-inflammatory cytokines such13 that stimulate the B cells to produce IgE, responsible for allergic inflammation. An essential assu

19

20

e are data contradicting the hypothesis. Respiratory infections, in iratory syncytial virus (RSV) bronchiolitis in infancy have been

found to be the most important risk factor for asthma and allergy in later childhood. A dose-response relationship between the frequency of ear infections and the prevalence of asthma in children was observed in a recent study7. There have been other criticisms8. It is unclear whether asthma is simply a Th2-driven disease. It is

ecreased bacterial exposure. On one hand, ced the prevalence of hay fever and atopy

provides support for hygiene hypothesis. On the other hand, the effects of dotoxins are dose-dependent. At high dose, endotoxin produces hypersensitivity

s the release of inflammatory cytokines. Whether endotoxin is protective or harmful may also be affected by the timing of exposure,

ntal cofactors and genetics. To conclude, the current status of hygiene hypothesis indicates the complexity of development of asthma and allergies9. It must be emphasized that hygiene hy s in s fo l ep y un s ap ha from developing asthma or allergies. Similarly, it is debatable to suggest parents to keep a pet, be it a dog or a cat, during the first ye f av r re o pr

References: 1. Global Initiatives For Asthma. National Institutes of Health. April 200. Available on www.ginasthma.com 2. Strachan DP. Hay fever, hyg3. Matricardi PM, Rosmini F, n

military students with antibod4. Ball TM, Castro-Rodriguez

during childhood. N Engl J M5. Chu HW, Honour JM, Raw t

2003; 123:390S 6. Busse WW, Lemanske RF J7. Eldeirawi K and Persky VW

aged 2 to 11 years. Chest 2008. Gelfand EW. The hygiene h

of the American Academy of 9. Strachan DP. Family size, in10. Wiess ST. Eating Dirt-The

However, therparticular resp

also unclear whether atopy results from dthe findings of endotoxin exposure redu

enpneumonitis and stimulate

the presence of any environme

pothesis fits better with the increasing trends in atopy rather than with the trend asthma. This is not surprising as atopy or exposure to allergens only accountr 40% of the attributable risks of asthma. More long-term longitudinaidemiological studies and basic immunology studies are needed to explore anidentified protective factors in this hypothesis. It is too early to talk about itplication in clinical practice. There are not enough grounds to advise parents tove more children to prevent them

ar of life of a baby. With the lessons from SARS and the imminent threat oian flu, the public awareness of personal hygiene has been raised. Eating dirt ondering children to have more infections are not practical recommendations tevent asthma and allergies10.

iene, and household size. BMJ 1989;299:1259-60. Ferrigno L et al. Cross-sectional retrospective study of prevalence of atopy among Italiaies against hepatitis A virus. BMJ 1997;314:999-1003. JA, Griffith KA et al. Siblings, day-care attendance, and the risk of asthma and wheezinged 2000; 343: 538-43. linson CA et al. A Murine Asthma model with Mycoplasma pneumoniae infection. Ches

r.. Advances in Immunology: Asthma. N Engl J Med 2001; 344:350-62. et al. History of ear infections and prevalence of asthma in a National sample of children4;125:1685-92. ypothesis revisited: Pros and Cons. Conference coverage of the 60th Aniversary MeetingAllergy, Asthma and Immunology, April 2003. fection, and atopy: the first decade of hygiene hypothesis. Thorax 2000;55:2-10. Hygiene Hypothesis and Allergic Diseases. N Engl J Med 2002 347:930-1.

edcial St

M

atistics Corner

edical Biostatistics

r. Julie Wang niversity Department of Medicine, Queen Mary Hospital

nticipating statistics as a set of formulae and numericals co

DU

A uld be quite boring and so etimes meaningless to us . However, it becomes much more interesting when you caow Ines In 1.ca2.- - - ns from small size sample. 3. Understanding the definition for confidence interval, confidence level, standard deviation and standard errors 4. Know how to estimate the confidence interval for a mean or a proportion under a one sample or two sample conditions.

1. What is Central Limit Theorem? Why is it so important? Under what situation can it be applied?

Before moving on to the application of statistical methods, we must make sure that the data is collected under random sampling, which is the obligatory condition for the estimation to hold true.

f n individuals from a population,

mn appreciate its underlying concepts, which is just like knowing a person by its n nature.

the following session, some basic concepts of why and how a parameter could be timated with a certain level of confidence are introduced.

the end of this chapter, you will be able to answer the following questions:

What is Central Limit Theorem? Why is it so important? Under what situation n it be applied? What is the difference between

normal population distribution the sampling distribution of means from large size sample, and

the sampling distribution of mea

A simple random sample (SRS) of size n consists ochosen in such a way that every set of n individuals has an equal chance to be the sample actually selected.

21

he sampling distribution of means is normal if the underlying population itself has a

sample means also gets loser to a normal distribution. This is true no matter what shape the population

Tnormal distribution. However, even when the population distribution is not normal, it turns out that as the sample size increases, the distribution ofcdistribution has, as long as the population has a finite standard deviation σ.

The above figure shows the central limit theorem in action: the distribution of sample means from a strongly nonnormal population becomes more normal as the sample size increases from (a) to (d).

22

23

Here, you can appreciate that whatever the underlying distribution a population parameter has, its population mean could be estimated using normal (z statistic) or near normal approximation (t statistic), when the sample size is adequately large.

2) What is the difference between normal population distribution, the sampling distribution of sample means from large size sample, and the sampling distribution of sample means from small size sample.

Normal population distribution

In a normal population distribution, a parameter X has its value lying across an interval, with each value being obtained from an individual observation in the population, where

mean = u ; standard deviation =σ

The sampling distribution of sample means from large size sample Upon drawing numerous SRS of size n, or some large size sample n from the normal population; by Central Limit Theorem, the sampling distribution of sample means x follows a normal distribution. Each value of x represents a sample mean, rather than an individual observation. The mean of this distribution equals the population mean of the parameter, while the standard deviation of it is called the standard error of the means. mean = u ; standard error =σ/√n The sampling distribution of sample means from small size sample If the SRS is of small sample size, the sampling distribution of sample means x will follow a t distribution. The mean here is x and standard error is s/√n. Both the x and s used here are estimated from the small sample data, which are just a rough estimation of the population parameter.

mean = x ;

The above conditions underlie the concepts why certain confidence intervals estimation are based on z statistics, whereas others uses t statistics.

3) Understanding the definition for confidence interval, confidence level, standard deviation and standard errors Confidence interval for the mean µ of the population is constructed upon the sampling distribution of the sample mean x, which is a range of numerical estimate

supposed to contain the true value of the population mean.

Here, the confidence level for a confidence interval represents the probability that the

interval containing the true value of the parameter. This probability level should be pre-determined , by choosing a value of z or t which corresponds to the desired confidence level, e.g. to construct a 99%, 95% and 90% confidence interval for x, z score of 2.576, 1.95 and 1.645 should be used respectively. If a 95% confidence interval for the estimated mean height of the population is ( 160, 180 ) cm; this means that when the sampling method is repeated many times, there is a 95% probability that the true value of the parameter will lie between 160 and 180cm. Standard error is the standard deviation of the sampling distribution of means, which indicates the variability of sample means. The value decreases as the size of n increase, which leads towards a more accurate estimate; while standard deviation of

rmal population represents the natural variations of a paramet , which is not a nction of n.

4) Kno val for a mean or a proportion under a one mple or two sample conditions. Listed below ome simple and very common interval finding methods for

sampling method will produce an

nofu

er

w how to estimate the confidence inter sa

are sillustration. The one-sample z confidence interval for a population mean or large size sample mean. Here, x is an estimate from the sample data, whileσ is known from population data.

The one-sample t confidence interval

data. for small size sample mean . Both x and s are estimates from sample

24

The two-sample t confidence interval for the difference in means of 2 small size samples ( SRS from 2 populations having

ormal distribution but different standard deviations). For example, if you want to stimate the difference in blood pressure of patients in clinic 1( geriatric clinic ) and

neclinic 2 ( pediatric clinic), where you do not expect them to have the same standard deviation in BP, the following method could be used.

The pooled two-sample t confidence interval for the difference in means of 2 small size samples ( SRS from 2 populations having normal distribution and the same standard deviations). This method could be applied if you want to estimate the difference in bone density of 2 groups of postmenopausal

omen who have been treated with alendronate vs calcium supplements, where the wstandard deviation of bone density is expected to be the same. Sp is the pooled standard deviation.

Large-sample confidence interval for a population proportion If you are interested to estimate the proportion of female newborn baby p in the population, with p= 0.5 from a SRS, the confidence interval is as follows:

Confidence interval for comparing two proportions

If you want to estimate the difference in proportion of female newborns between ountries 1 & 2, with p1 & p2 as the estimated proportion from 2 SRS, the onfidence interval is given below:

cc

25

Now you have some ideas that the confidence interval estimation for a parameter is actually dependent on the sampling distribution of means. In real life, the distribution of sample means encompasses much more sophisticated distribution pattern other than normal/near normal pattern, for instance, it could be i X2, F distribution or

ciprocal distribution. With the use of statistical software, these complicated arameter confidence interval could also be accurately calculated.

References: 1. DS Moore, GP McCabe. Introduction to the Practice of Statistics . Third Edition. Freeman. 2. JF Jekel, JG Elmore, DL Katz. Epidemiology Biostatistics and Preventive Medicine. W.B. Saunders 3. TD Swinscow. Statistics at Square One. BMJ.

n rep

Column

26

Publisher: Saunders Publication Date: 2004-11-05 ISBN: 0721600077

T

ook Review Column

his book provides an all-in-one reference for diagnosing diseases of the airway. It offers radiologic,

fnaiaorvtRt

Members of Hwill e

when ordering the boothrough McBarro

Enquiry and Ordering T(Free Delivery Ser

Note: Book ordering will be the two Thoracic Societ

bronchoscopic, and pathologic indings for the full range of neoplastic and on-neoplastic disorders, both common nd non-common. For each disease, it ncludes a case-based discussion, an natomical black and white drawing for rientation, two black and white adiographs, two colour bronchoscopic iews and a discussion of incidence, reatment, and prognosis. A bonus CD-OM provides a video-based introduction

o 16 invasive pulmonary procedures.

ong Kong Thoracic Society njoy 10% discount

k(s) under the “Book review column” n Book Co. 麥伯倫醫護圖書中心

el: (852) 2770 8521 Fax: (852) 2385 6236. vice to local hospitals included)

dealt with directly by McBarron Book Co and ies are not responsible for any liabilities.

27

nferences

iary of International Co

3 – 6 July, 2005 New Barcelona Spain

The 11th World Conference on Lung Cancer – International Association for the Study of Lung Cancer (IASLC)

.imedex.com/calendars/oncology.htmInfo: www

ember, 2005 15

gen

r – CHEST 20

Email: meetings@imedex.com

17-21 SeptCopenhaDenmark

th ERS Annual Congress Info: www.ersnet.org/ers

29 Octobe3 November, 2005 Montreal Canada

05 Info: www.chestnet.org/CHEST

11-14 November, 2005 Guangzhou China

10th Congr ss of the APSR 1st Joint Congress of the APSR/ACCP Info: www.a 5.

e

psr200005@a

eeting

com a.cmpmedica.com

The Society of Thoracic Surgeons ts.org ba.comEmail: sts@s

AAAI Meeting ww.aaaai.org/members/meetings/future_meetin

horacic.org.au

ting rs.or.jp

E-mail: apsr2 si

30 January – 1 February, 2006 New Orleans USA

42st Annual M ofInfo: www.s

3-7 March, 2006 Miami Beach, USA

62st Annual AInfo:http://w gs.stm

24-29 March, 2006 Canberra Australia

TSANZ ASM Info: www.t

1-3 June, 2006 Tokyo Japan

46th JRS MeeInfo: www.j

19-24 May, 2006 San Diego USA

American Th acic Society (ATS) International Conference Info: www.thoracic.org

or

28

orthcoming Clinical Meetings

Date Ho

July 21, 2005

sting Hospital / Centre

QMH, GH

September 15, 2005 PWH, AHNH

November 6, 2005 Autumn Respiratory Seminar

29

seful Websites

Medical Societies

Hong Kong Thoracic Society http://www.medicine.org.hk/hkts/home.htm

ACCP (HK & Macau Chapter) http://www.medicine.org.h

ociety http://www

ssociation http://www.lung.ca/

ng and Blood Institute http://www.nhlbi.nih.gov/

k/accp/home.htm

American College of Chest Physician http://www.chestnet.org/

American Thoracic S .thoracic.org/

British Thoracic Society http://www.brit-thoracic.org.uk/

Canadian Lung A

European Respiratory Society http://www.ersnet.org/

National Heart, Lu

Society of Critical Care Medicine (USA) http://www.sccm.org/home/sccm_home_set.html

American Association for Respiratory Care http://www.aarc.org/index.html

The Federation of Medical Societies of HK http://www.medicine.org.hk/fmshk/

Publications

American Journal of Respiratory and Critical Care Medicine http://ajrccm.atsjournals.org/

American Journal of Respiratory Cell and Molecular Biology http://ajrcmb.atsjournals.org/

Asian Medical News http://www.amn.com/

British Medical Journal http://www.bmj.com/

Canadian Respiratory Journal http://webserver.pulsus.com/Respir/home.htm

Allergy, Asthma & Immunology Online http://allergy.mcg.edu

Chest http://www.chestjournal.org/

Current Opinion in Pulmonary Medicine http://www.currentopinion.com

Lancet Interactive http://www.thelancet.com/

Medscape respiratory care http://respiratorycare.medscape.com/home/ topics/respiratorycare/respiratorycare.html

Morbidity and Mortality Weekly Report http://www2.cdc.gov/mmwr/

New England Journal of Medicine http://www.nejm.org/content/index.asp

Postgraduate Medical Journal http://www.postgradmedj.com/

Respiratory Care Online http://www.rcjournal.com/

Thorax http://www.thoraxjnl.com/

30

hest – Full Text On-Line

The Official Journal of ACCP is now on-line but is only available to subscribers (Fellows, members or affiliated members). Trainees

to join at r). should be d ir

be a Proof and detail of training (tentative period of training) is required. Any query can

to the Secreta acau Chapter) (see Browsing of infor CCP website:

.chestnet.org/m ries.html

are welcome a very privilege rate (US30 per yeaApplications irected to ACCP (USA) through thetrainers (who must Fellow of the ACCP).

be directedpage 1). mation is available on the Ahttp://www embership/catego

embership News

♦ As of May 2005, there a ry members, re 896 Members (233 Ordina6 Honorary members, Associate 51 Life members and 606

ry, ACCP (HK and M

members).

♦ To be eligible for Life membership, 3 years of full membership on is necessary. Please write to the

Honorary Secretary (D re Unit, Queen ulam, Hong Kong) and send with a cheque of

HK$2,000. Acceptan he Hong Kong Thoracic Society council meeting.

♦ is due to renew , please fill in the

lication/renewal (available at .fmshk.com

prior to the applicatir W M Chan, Intensive Ca

Mary Hospital, Pokfce will be decided in t

It app

your membershipform

http://www .hk/hkts/member.htm) and send to Dr Loletta So (address as on the form) with the subscription

r ass mbers respectively), (cheque payable to HONG KONG THORACIC SOCIETY LTD). Members who had t uld re-apply as new members. For enquiry, or checking your membership

re by email (loletta.so@hotmail.com) or fax (852 2468 6188) (Please supply your name Apology for not entertaining telephon

(HK$100/200 fo oicate/ordinary me

heir names deleted sho

status, please ach Dr Loletta So

and fax number). e enquiry.

31

u nds and Grants

Pneumoconiosis Compensation Board (PCFB) Research Fund

The Pneumoconiosis Compensation Board (PCFB) set up a research fund in 1996 with the purpose to support projects that are related to the prevention, diagnosis, assessment of disability and treatment of pneumoconiosis in Hong Kong. Individual or group are invited to apply. Interested parties may visit the website: www.pcfb.org.hk or contact the PCFB at Tel: 2541 0032, Fax: 2541 0211 or Email: contact@pcfb.org.hk.

Pneumoc

The Pneumoconiosis Compensation Board (PCFB) has recently established a n

healThis to encourage eligible applicants to attend overseas training programmes or conferences that are related to the topic of pneumoconiosis.

Inter2541 E-m

oniosis Compensation Board (PCFB) Training Grant

trai ing grant to facilitate health-care workers and occupational safety and th personnel to enhance their knowledge and skills in pneumoconiosis. scheme aims

A maximum grant of HK$ 100,000 will be allowed for a suitable course longer than 6 months, and HK$ 50,000 for a course of 6 months or less.

ested applicants may contact the Board Secretariat, Trophy Mak at 0032, or contact the PCFB at Tel: 2541 0032, Fax: 2541 0211 or ail: contact@pcfb.org.hk.

32