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Occupational respiratory disease

U. Komine, K. Tsuji, and Y. Mori, Advances m the Prevention of Occupational Respiratory Diseases, New York Elsevier, 1998, pp. 1120-1126. [Pg.1011]

NIOSH. 1986. Acute and chronic respiratory effects of exposure to inhaled toxic agents. In Merchant JA, ed. Occupational respiratory diseases. Publication of the National Institute for Occupational Safety and Health, U.S. Department of Health and Human Services, 571-605. DHHS (NIOSH) publication no. 86-102. [Pg.195]

Medical Tests Used to Diagnose Lung Disease Types of Occupational Respiratory Disease... [Pg.163]

Recognition of Emerging Occupational Respiratory Disease in the Eood Industry Prevention of Known Occupational Respiratory Diseases in the Eood Industry References... [Pg.163]

VI. RECOGNITION OF EMERGING OCCUPATIONAL RESPIRATORY DISEASE IN THE FOOD INDUSTRY... [Pg.186]

Nagano, K., Nishizawa, T, Yamamoto, S. Matsushima, T. (1998) Inhalation carcinogenesis studies of six halogenated hydrocarbons in rats and mice. In Chiyotani, K., Hosoda, Y Aizawa, Y, eds, Advances in the Prevention of Occupational Respiratory Diseases, Amsterdam. Elsevier, pp. 741-746... [Pg.429]

Ghan-Yeung M and Malo JL (1995) Occupational respiratory diseases associated with forest products industries. In Harber P, Schenker M, and Balmes J (eds.) Occupational... [Pg.2857]

MEREDITH, S.K., TAYLOR, V.M. MCDONALD, J.C. (1991) Occupational respiratory disease in the United Kingdom 1989 a report to the British Thoracic Society and Society of Occupational Medicine by the SWORD project group. British Journal of Industrial Medicine, 48, 292-298. [Pg.5]

ROSS, D.J., SALLIE, B.A. MCDONALD, J.C. (1995) SWORD 94 surveillance of work-related and occupational respiratory disease in the UK. Occupational Medicine, 45, 175-178. [Pg.5]

The observation that T-cell immune responses may be involved in the pathogenesis of occupational respiratory diseases is supported by animal models (Dearman et al., 1992). Rodents can be easily sensitized to LMW chemicals such as acid anhydrides and diisocyanates. A murine model has been used to study the differential production of cytokines by helper T-cell subsets (Thl and Th2) after exposure to different reactive chemicals. It has been shown that under normal conditions Thl lymphocytes primarily secrete IL-2, interferon-/and tumour necrosis factor J3 (TNI -/ ) whereas Th2 lymphocytes secrete IL-4, IL-5, IL-10 and IL-13. A predominance of Th2 cells correlated with IgE-mediated immune responses, while a predominance of Thl cells was associated with cell-mediated immune responses (Dearman et al., 1992). These investigators demonstrated preferential activation of Th2 cells by phthalic anhydride (PA), trunellitic anhydride (TMA) and diphenyl-methylene diisocyanate, indicating that chemical structure may be important for determining the quality of immune response elicited (Dearman et al., 1992). [Pg.38]

The first element in risk assessment is knowledge of the chemical exposures of a workforce to see if a known sensitizer is present. A chemical becomes accepted as a cause of occupational asthma if there are at least two convincing clinical case reports from independent centres. Specialist clinicians are likely to be aware of the published literature at an early stage and may be a useful source of informal information. There is currently much interest in publishing lists of sensitizers. One is available in a recent textbook (Chan-Yeung and Malo, 1993). The Health and Safety Executive in the UK, the National Institute for Occupational Safety and Health in the USA and other agencies may publish lists with updates. Other sources of information on causes are reporting schemes such as SWORD (Surveillance of Work-related and Occupational Respiratory Disease) in the UK (Ross el al., 1995) and SENSOR (Sentinel Event Notification System for Occupational Risks) in some states in the USA (Matte et al., 1990). [Pg.68]

Occupationally related airway diseases, including asthma and chronic obstructive pulmonary disease (COPD), have emerged as having substantial public he th importance. Nearly 30% of COPD and adult asthma may be attributable to occupational exposure. Occupational asthma is now the most frequent occupational respiratory disease diagnosis. More than 20 million U.S. workers are exposed to substances that can cause airway diseases. [Pg.1167]

Commonly used items such as latex gloves can cause asthma and other lung ailments. Our respiratory system connects the mouth, nose, lungs, and tubes. Occupational respiratory disease is a medical term normally used to describe diseases caused by, or made worse by, something breathed in at work (eg, wood dust, stone dust, poultry dust, or fumes). [Pg.116]

Savonius B, Keskinen H, Tuppurainen M, Kanerva L (1993) Occupational respiratory disease caused by acrylics. Clin Exp Allergy 23 416-424... [Pg.649]


See other pages where Occupational respiratory disease is mentioned: [Pg.164]    [Pg.164]    [Pg.169]    [Pg.175]    [Pg.186]    [Pg.186]    [Pg.187]    [Pg.526]    [Pg.148]    [Pg.1]    [Pg.30]    [Pg.32]    [Pg.52]    [Pg.154]    [Pg.258]    [Pg.266]    [Pg.646]    [Pg.158]    [Pg.207]    [Pg.215]    [Pg.908]   
See also in sourсe #XX -- [ Pg.164 , Pg.169 , Pg.170 , Pg.171 , Pg.172 , Pg.173 , Pg.174 , Pg.175 ]

See also in sourсe #XX -- [ Pg.116 ]




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Occupational disease

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