Another ILO workshop on pneumoconiosis took me to Kuala Lumpur, for four days from 4 May, during the world's concern about Swine flu, which is now properly renamed as H1N1 influenza that seems like to have almost same, at most, features as usual influenza.
The quarantine control at Kuala Lumpur was swift and effective, and American friend of mine has told me that he has went through a bit more strict process because of the clusters in his homeland. Sheet of health information and thermography did the quick work on it.
My trip continued to visit Chenderawasih University, a corporation couterpart to Kochi University since 2004, to meet Rector and their staffs and talked about on-going collaboration. I gathered few words of Indonesian language, like Ikan Bakar, Udang, Cumi, Asam manis, or even Ena. Of course Terimakasi.
The visit have been very short but effective. I met future PhD students who are trying their best to get scholarship, as well as performing interesting studies from their own aspects. I hope to see them in my department in very near future.
Now I am writing this at Dempasar Airport waiting for my next flight that take me back to Osaka via Singapore.
2009年5月12日火曜日
2009年4月8日水曜日
New Fiscal Year
My labo has a new staff and two PhD students this year. Dr. Masamitsu Eitoku majors in basic biological studies on epigenetics and moved into our field of environmental medicine. He is a young and fresh researcher with honest mind. Situation in national universities in Japan is not ideal, but still we have place to conduct our researches and chances to get research grant.
One of the new students is from Thailand, who have known me since a couple of years ago when I went to Thailand on ILO mission for pneumooconioses workshop, and the other is from D. R. Congo. Now Ngatu is in the second year and will help these two new comers. Not many students are from Africa in KMS, only one other from Zimbabwe in the whole Kochi University. It seems my department will be the core for collaborating with African universities.
One of the new students is from Thailand, who have known me since a couple of years ago when I went to Thailand on ILO mission for pneumooconioses workshop, and the other is from D. R. Congo. Now Ngatu is in the second year and will help these two new comers. Not many students are from Africa in KMS, only one other from Zimbabwe in the whole Kochi University. It seems my department will be the core for collaborating with African universities.
2009年3月14日土曜日
2009年3月3日火曜日
Environmental Medicine
It is a bit hard to explain what the Environmental Medicine is. Of course it is a discipline of medicine that deals with pathologic environmental agents to human. Pathologic agents will be systematically devided into physical, chemical, biological and social environmental factors. The most severe effect of these agents or factors are usually observed in workplaces where these factors are used for industrial production purposes. So it is often referred to Occupational and Environmental Medicine. I am occupational physician, too.
Asbestos, one of the environmental carcinogen that causes lung cancer and mesothelioma, a rare cancer of pleura, is an example of bad occupational environment causing public nuisance. An asbestos-containing water pipe producing factory had spread life threatening agent in the midst of a big city named Amagasaki and nearly 100 citizens who lived near the factory suffered mesothelioma. This may have been prevented if the workplace hazard had been properly controlled.
Physicians and researchers in Environmental Medicine need to cover clinical medicine and toxicology regarding occupational and environmental hazard, principle of epidemiology and health policy regarding this issue. We need to see patients, workplaces, and communities. We need to act as clinicians and at the same time as public health practitioners. We need to see individuals and group of people. We need to do both.
As a clinician one has to see patients, diagnose, and treat. And as a public health practitioner, one has to seek the causative agent, prevent the same disease, and control the diseases. We are performing such tasks.
Asbestos, one of the environmental carcinogen that causes lung cancer and mesothelioma, a rare cancer of pleura, is an example of bad occupational environment causing public nuisance. An asbestos-containing water pipe producing factory had spread life threatening agent in the midst of a big city named Amagasaki and nearly 100 citizens who lived near the factory suffered mesothelioma. This may have been prevented if the workplace hazard had been properly controlled.
Physicians and researchers in Environmental Medicine need to cover clinical medicine and toxicology regarding occupational and environmental hazard, principle of epidemiology and health policy regarding this issue. We need to see patients, workplaces, and communities. We need to act as clinicians and at the same time as public health practitioners. We need to see individuals and group of people. We need to do both.
As a clinician one has to see patients, diagnose, and treat. And as a public health practitioner, one has to seek the causative agent, prevent the same disease, and control the diseases. We are performing such tasks.
2009年2月19日木曜日
Africa
Two of us in our department are going to attend the 23rd International Congress on Occupational Health due to be held in Cape Town, South Africa end of March. We, a graduate student Ngatu Nlandu, MD, and me, are both presenting research results on pneumoconiosis imaging. The day of presentation has been acturally not yet informed, and we also do not know whether we are presenting as an oral or a poster presentation or both. Well, that's life. We will both prepare powerpoint and a big sheet of poster.
Since his enrollment as PhD student, our department has got closer and closer to the African Continent. There have been a lot of correspondence with people there, we have also applied to many official and private grants for research project in Africa, and have done little investigation with the help from LIPS, a healthcare NGO that Ngatu has established in D. R. Congo. Also, we met Congolese medical doctors who stay in Japan and pursuing further educational oppotunities just like Ngatu. Hope our labo will give best support for them!
Since his enrollment as PhD student, our department has got closer and closer to the African Continent. There have been a lot of correspondence with people there, we have also applied to many official and private grants for research project in Africa, and have done little investigation with the help from LIPS, a healthcare NGO that Ngatu has established in D. R. Congo. Also, we met Congolese medical doctors who stay in Japan and pursuing further educational oppotunities just like Ngatu. Hope our labo will give best support for them!
2008年5月8日木曜日
Dpt Seminar
Professor T. Agatsuma gave lecuter on "Pragonimus and Pragonimiasis in India." The field study performed in Assam region in India revealed high prevalence of the parasite especially among young population in the area. It seemed intake of raw crab meat causes infection of the parasite and young children seemed to play around in the river nearby, catch the crabs with metacercaria and get infected. Pulmonary pragonimiasis seemed to be misdiagnosed as tuberculosis, which is also prevalent in the area and share the symptom of hemoptysis. Pragonimiasis is 100 % curable with prazyquantel.
The other topic today was "the 3 generation medical check-up" that has been performed in Saga region, Koroshio-cho, Kochi. Our department is co-organizing with Orthopedic department the community health programme for the elder inhabitants in the area with the help of school children in the same area. We are going to add "peer education" driven by Kochi Medical School students to give health education to the school children.
The other topic today was "the 3 generation medical check-up" that has been performed in Saga region, Koroshio-cho, Kochi. Our department is co-organizing with Orthopedic department the community health programme for the elder inhabitants in the area with the help of school children in the same area. We are going to add "peer education" driven by Kochi Medical School students to give health education to the school children.
2008年5月2日金曜日
Dpt Seminar: Journal Club
Update in Occupational and Environmental Respiratory Diseases 2007
Nawrot TS, Alfaro-Moreno E, Nemery B. AJRCCM 2008;177:696-700.
Most of the large population study use crude endpoints, such as mortality, self-reported respiratory symptoms, and simple pulmonary function tests. Integration of epidemiologic and toxicologic approach is needed to understand mechanism of the effect of air pollution on health.
Outdoor air pollution
Recent studies reinforce the previous findings showing the particulate matter’s (PM) adverse effect on children’s airway. A panel study of 200 asthmatic schoolchildren in a Mexico town near the US border showed FEV1 and exhaled NO were associated with the distance from the main road (Holguin, 07). Adult asthmatic patients were assessed by sputum and exhaled breath condensate after walking along the road with only diesel traffic and in the rural park with less traffic, showing the inflammatory changes in the former challenge (McCreanor 07). A cohort of 3,170 children aged 8 year-old at the baseline in Mexico City was followed up three years and revealed annual deficit in FEV1 of 11ml in girls and 15ml in boys for an increase of 36.4 mg/m3 (interquartile range, 24-h PM10 means averaged over 6 mo) in PM10 (Rojas-Martinez, 07).
The Harvard Six Cities Study (Dockery, 93) and others revealed the risk of death associated with air pollution is higher for cardiac diseases than for all other diseases, whose mechanism is not fully explained but the lung plays an important role more than mere portal organ for the entry of air pollutant and may mediate the effect to the heart.
Linking particulate levels in the air with markers of inflammation, coagulation and heart rate variability among 76 university students showed that CRP, PAI-1 and fibrinogen were associated with averaged 24-hour PM10 level and that heart rate variability was associated to 1 to3-day averaged PM10 (Chuang, 07). Longitudinal follow-up of postmenopausal women showed a 24% increase in the risk of developing a first-time cardiovascular event and a 76% increase in the risk of any death from cardiovascular cause for those live in the place with higher annual average PM2.5 of 10mg/m3 (Miller, 07). DEP is reported to cause clinically important ECG alteration among men with past myocardial infarction (Mill, 07).
Endothelial dysfunction seemed to be common event when explaining the cardiovascular effect caused by the particulate matter. PM is shown to have capability to induce expression of adhesion molecules, such as E-secletin, P-secletin, intracellular adhesion molecules (ICAM), vascular cell adhesion molecules (PCAM) (Alfaro-Moreno, 07; Nemmar, 07; Montiel-Davolos, 07). A randomized double-blinded crossover study, exposing human to DEP (300mgl m3) or to the filtered air, revealed no difference in the hemodynamic variables measured 24-hour after exposure but DEP induced a selective and persistent impairment of endothelium-dependent vasodilation (Tornqvist, 07).
Indoor air pollution
The assessment of indoor levels of PM2.5 and NO2 in the homes of 148 elderly patients with severe chronic COPD noted an association between poorer health status and indoor PM2.5 levels mainly explained by the smoker in the family (Osman, 07). Interestingly, 48-hour filtration of the indoor air improved microvascular function in 21 elderly couples (Brauner, 08).
Other indoor second-hand smoking occurs in other public spaces including pubs and bars, and those workers are reported to have improvement of pulmonary function test and QOL after comprehensive smoking bans (Schmidt, 07).
Few studies focused on chemical products used for the cleaning. Non-professional use of cleaning sprays at least once a week significantly increased the risk of new-onset asthma symptom or medication (RR, 1.49) and wheeze (RR, 1.39), irrespective of atopy using the European Community Respiratory Health Survey (ECRHS) (Zock, 07).
Occupational respiratory disease
Cleaning the medical instrument (OR, 2.22), general cleaning (OR, 2.02), use of powdered latex gloves in 90s OR, 2.17) and administration of aerosolized medications (OR, 1.72) (Delclos, 07). In the ECRHS, nursing was also identified as a high risk occupation of adult-onset asthma (Kogevinas, 07; Mirabelli, 07).The population attributable risk for adult asthma due to occupational exposure was estimated at 10 to 25%, corresponding to 250 to 300 new cases of work-related asthma per million people per year (Kogevinas, 07).
Clinicians consider “true” occupational asthma is due to specific sensitization to high-molecular-weight or low-molecular-weight agents (Nemery, 04). Risk factors and mechanism of sensitization of occupational asthma is not fully understood. A study of 581 workers at 128 spray-painting industry, where hexamethylene diisocyanate used much, showed exposure-response relationships for both work-related asthma, non-work-related COPD-like symptoms and for specific IgE sensitization, though the prevalence of specific IgE was as low as 0.4 to 4 % (Pronk, 07).
COPD may be caused or exacerbated by environmental and occupational factors. Chinese epidemiologic studies pointed out the domestic exposure to biomass fuel exhaust causes COPD (Liu, 07; Zhong, 07). The Lung Health Study that analyzed 5,724 participants showed ongoing exposure to fumes at work was associated with a more rapid decline in FEV1 in men with COPD (Harber, 07).
In “Popcorn worker’s lung”, a condition first described in microwave popcorn plant and diacetyl was identified as its causative agent, and some other cases obstructive impairment may due to occupational bronchiolitis obliterans (Kreiss, 07).
Asbestosis has common features of idiopathic pulmonary fibrosis and various growth factors (TNF-a, platelet-derived growth factor [PDGF], transforming growth factor-b), reactive oxygen species, and signal transduction pathways (MAPK). Asbestos-induced rat fibrosis model was used to show the recruitment and migration of bone marrow-derived cells into the areas of damaged lung (Spees, 07).
Hard metal lung disease a rare occupational lung disease with features of giant cell interstitial pneumonia (GIP), pathognomonic significance of GIP has been questioned (Blanc, 07). A sensitive electron probe microanalysis showed preferential presence of tungsten in the fibrotic areas of the lung, and immunochemical analysis showed macrophages may be instrumental in the pathogenesis of the disease (Moriyama, 07)
Nawrot TS, Alfaro-Moreno E, Nemery B. AJRCCM 2008;177:696-700.
Most of the large population study use crude endpoints, such as mortality, self-reported respiratory symptoms, and simple pulmonary function tests. Integration of epidemiologic and toxicologic approach is needed to understand mechanism of the effect of air pollution on health.
Outdoor air pollution
Recent studies reinforce the previous findings showing the particulate matter’s (PM) adverse effect on children’s airway. A panel study of 200 asthmatic schoolchildren in a Mexico town near the US border showed FEV1 and exhaled NO were associated with the distance from the main road (Holguin, 07). Adult asthmatic patients were assessed by sputum and exhaled breath condensate after walking along the road with only diesel traffic and in the rural park with less traffic, showing the inflammatory changes in the former challenge (McCreanor 07). A cohort of 3,170 children aged 8 year-old at the baseline in Mexico City was followed up three years and revealed annual deficit in FEV1 of 11ml in girls and 15ml in boys for an increase of 36.4 mg/m3 (interquartile range, 24-h PM10 means averaged over 6 mo) in PM10 (Rojas-Martinez, 07).
The Harvard Six Cities Study (Dockery, 93) and others revealed the risk of death associated with air pollution is higher for cardiac diseases than for all other diseases, whose mechanism is not fully explained but the lung plays an important role more than mere portal organ for the entry of air pollutant and may mediate the effect to the heart.
Linking particulate levels in the air with markers of inflammation, coagulation and heart rate variability among 76 university students showed that CRP, PAI-1 and fibrinogen were associated with averaged 24-hour PM10 level and that heart rate variability was associated to 1 to3-day averaged PM10 (Chuang, 07). Longitudinal follow-up of postmenopausal women showed a 24% increase in the risk of developing a first-time cardiovascular event and a 76% increase in the risk of any death from cardiovascular cause for those live in the place with higher annual average PM2.5 of 10mg/m3 (Miller, 07). DEP is reported to cause clinically important ECG alteration among men with past myocardial infarction (Mill, 07).
Endothelial dysfunction seemed to be common event when explaining the cardiovascular effect caused by the particulate matter. PM is shown to have capability to induce expression of adhesion molecules, such as E-secletin, P-secletin, intracellular adhesion molecules (ICAM), vascular cell adhesion molecules (PCAM) (Alfaro-Moreno, 07; Nemmar, 07; Montiel-Davolos, 07). A randomized double-blinded crossover study, exposing human to DEP (300mgl m3) or to the filtered air, revealed no difference in the hemodynamic variables measured 24-hour after exposure but DEP induced a selective and persistent impairment of endothelium-dependent vasodilation (Tornqvist, 07).
Indoor air pollution
The assessment of indoor levels of PM2.5 and NO2 in the homes of 148 elderly patients with severe chronic COPD noted an association between poorer health status and indoor PM2.5 levels mainly explained by the smoker in the family (Osman, 07). Interestingly, 48-hour filtration of the indoor air improved microvascular function in 21 elderly couples (Brauner, 08).
Other indoor second-hand smoking occurs in other public spaces including pubs and bars, and those workers are reported to have improvement of pulmonary function test and QOL after comprehensive smoking bans (Schmidt, 07).
Few studies focused on chemical products used for the cleaning. Non-professional use of cleaning sprays at least once a week significantly increased the risk of new-onset asthma symptom or medication (RR, 1.49) and wheeze (RR, 1.39), irrespective of atopy using the European Community Respiratory Health Survey (ECRHS) (Zock, 07).
Occupational respiratory disease
Cleaning the medical instrument (OR, 2.22), general cleaning (OR, 2.02), use of powdered latex gloves in 90s OR, 2.17) and administration of aerosolized medications (OR, 1.72) (Delclos, 07). In the ECRHS, nursing was also identified as a high risk occupation of adult-onset asthma (Kogevinas, 07; Mirabelli, 07).The population attributable risk for adult asthma due to occupational exposure was estimated at 10 to 25%, corresponding to 250 to 300 new cases of work-related asthma per million people per year (Kogevinas, 07).
Clinicians consider “true” occupational asthma is due to specific sensitization to high-molecular-weight or low-molecular-weight agents (Nemery, 04). Risk factors and mechanism of sensitization of occupational asthma is not fully understood. A study of 581 workers at 128 spray-painting industry, where hexamethylene diisocyanate used much, showed exposure-response relationships for both work-related asthma, non-work-related COPD-like symptoms and for specific IgE sensitization, though the prevalence of specific IgE was as low as 0.4 to 4 % (Pronk, 07).
COPD may be caused or exacerbated by environmental and occupational factors. Chinese epidemiologic studies pointed out the domestic exposure to biomass fuel exhaust causes COPD (Liu, 07; Zhong, 07). The Lung Health Study that analyzed 5,724 participants showed ongoing exposure to fumes at work was associated with a more rapid decline in FEV1 in men with COPD (Harber, 07).
In “Popcorn worker’s lung”, a condition first described in microwave popcorn plant and diacetyl was identified as its causative agent, and some other cases obstructive impairment may due to occupational bronchiolitis obliterans (Kreiss, 07).
Asbestosis has common features of idiopathic pulmonary fibrosis and various growth factors (TNF-a, platelet-derived growth factor [PDGF], transforming growth factor-b), reactive oxygen species, and signal transduction pathways (MAPK). Asbestos-induced rat fibrosis model was used to show the recruitment and migration of bone marrow-derived cells into the areas of damaged lung (Spees, 07).
Hard metal lung disease a rare occupational lung disease with features of giant cell interstitial pneumonia (GIP), pathognomonic significance of GIP has been questioned (Blanc, 07). A sensitive electron probe microanalysis showed preferential presence of tungsten in the fibrotic areas of the lung, and immunochemical analysis showed macrophages may be instrumental in the pathogenesis of the disease (Moriyama, 07)
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