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Chronic Inhalation of Nickel Oxide and Cigarette Smoke by Hamsters.

Date: 1975
Length: 1 page
2063594166
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Author
Busch, R.H.
Craig, D.K.
Olson, R.J.
Wehner, A.P.
Characteristic
EXTR, EXTRA
Master ID
2063594010/4240
Related Documents:
Site
R530
Area
CARCHMAN,RICHARD/OFFICE
Litigation
Iwoh/Produced
Type
SCRT, REPORT, SCIENTIFIC
Named Organization
American Industrial Hygiene Assn Journal
Univ of Ky
Date Loaded
07 Jun 1999

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Page 1: 2063594166 Log in for more options!
! I I I I I I I I I I I I I I I I I # 103 AUTHOR= WEHNER, A. P., R.H. BUSCH, R.J.OLSON, AND D.K. CRAIG DATE: 1975 TITLE: CHRONIC INHALATION OF NICKEL OXIDE AND CIGARETTE SMOKE BY HAMSTERS. CITATION: AMERICAN INDUSTRIAL HYGIENE ASSOCIATION JOURNAL 36:801-810 (1975) STUDY DESIGN: A group of 2-month old Syrian golden hamsters received life-span exposures to a respirable aerosol of NIO, 7 hours/day, 5 days/week. Half of the hamsters were exposed to cigarette smoke in a modified Hamburg II smoking machine twice before and once after the daily 7-hour dust or sham dust exposures. At each smoke exposure period, the animals received a continuous nose-only exposure of approximately lO minutes duration (cigarette used was University of Kentucky 1R1 research cigarette). A group of 51 hamsters, serving as "smoke controls" received 3 daily smoke exposures and a daily 7-hour sham dust exposure. An additional group of hamsters served as sham controls. RESULTS/FINDINGS: The first evidence of NiO effects on the lungs of hamsters exposed to this material consisted of NiO particulate accumulation on alveolar septa. The particulate material appeared to be located both intracellularly and extracellularly. The first site of accumulation was in macrophages aggregated adjacent to small blood vessels, lymphatic vessels and small bronchioles. Lesions characterized by the term pneumoconiosis include interstitial pneumonitis and diffuse granulamatous pneumonia which were frequently more severe in focal areas, fibrosis of alveolar septa, bronchial and bronchiolization of alveolar epithelium, squamous metaplasia and emphysema and/or atelectasis of varying degrees. Histopathologically, there was no marked difference between the NiO + smoke-exposed and NiO + sham-smoke exposed groups except for the presence of so-called "smoke cells" and a significant increase in laryngeal lesions in smoke-exposed hamsters. With the exception of pneumoconiosis, there was no significant difference in the incidence of respiratory tract lesions between the NiO + sham-smoke-exposed group and the sham controls, and between the NiO + smoke-exposed group and the smoke controls. CONCLUSIONS/COMMENTS: Under experimental conditions used in this study, inhaled NiO was neither carcinogenic nor particularly toxic in hamsters. Chronic cigarette smoke exposure, in combination with NiO or sham dust exposures, resulted in significantly lower body weights and increased survival time.

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