Transient epithelial loss in rat larynx after acute exposure to tobacco smoke

Lam, R.

doi:10.1016/0378-4274(80)90138-1

Cited by 12 publications

(6 citation statements)

References 6 publications

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“…In one report [62] a single exposure of rats to highly concentrated cigarette smoke resulted in a loss or necrosis of the larynx epithelial cells accompanied by acute inflammation and edema. Epithelial regeneration was rapid and was followed by development of hyperplasia within hours to days.…”

Section: Cigarette Smoke-induced Lung Inflammation In Rats 171mentioning

confidence: 97%

“…Although histopathological changes in the nose are mainly related to irritative volatile gas phase constituents, in the larynx they are generally particle driven [60,62]. This can be seen from the overall equal effects PP had on the larynx epithelium compared to 1R4F-high.…”

Section: Cigarette Smoke-induced Lung Inflammation In Rats 171mentioning

confidence: 97%

“…Previous investigations showed that the typical histopathological changes of the respiratory tract epithelia, i.e., hyperplasia, metaplasia, and=or atrophy, which are observed after subchronic inhalation of cigarette smoke, are mainly adaptive in nature and result from a local inflammatory response to the injury previously induced by cigarette smoke components [20,45,62]. In one report [62] a single exposure of rats to highly concentrated cigarette smoke resulted in a loss or necrosis of the larynx epithelial cells accompanied by acute inflammation and edema.…”

Section: Cigarette Smoke-induced Lung Inflammation In Rats 171mentioning

confidence: 99%

“…Epithelial regeneration was rapid and was followed by development of hyperplasia within hours to days. Repeated exposure to cigarette smoke over a period of weeks resulted in marked hyperplasia and metaplasia in the rat larynx, i.e., in lesions which are expected to be protective during the repeated insult by cigarette smoke [62].…”

Section: Cigarette Smoke-induced Lung Inflammation In Rats 171mentioning

confidence: 99%

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Lung Inflammation in Rats Following Subchronic Exposure to Cigarette Mainstream Smoke

Friedrichs

Miert²,

Vanscheeuwijck³

2006

Experimental Lung Research

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Female Sprague-Dawley rats were exposed to mainstream smoke from standard reference cigarettes and a nontobacco cellulose cigarette for 35 days. Whole smoke and smoke fractions were investigated. Lung inflammation was evaluated by differentiation of bronchoalveolar lavage cells and lymphocytes in thoracic lymph nodes. Histopathological changes in the nose and larynx were assessed. Results showed that the particulate phase of cigarette mainstream smoke is mostly responsible for inflammation in the lung (neutrophil increase up to 240-fold) and hyperplastic and metaplastic epithelial changes in the larynx, whereas irritative volatile constituents in the gas phase are mostly responsible for changes in the nose.

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Section: Cigarette Smoke-induced Lung Inflammation In Rats 171mentioning

confidence: 97%

Section: Cigarette Smoke-induced Lung Inflammation In Rats 171mentioning

confidence: 97%

Section: Cigarette Smoke-induced Lung Inflammation In Rats 171mentioning

confidence: 99%

Section: Cigarette Smoke-induced Lung Inflammation In Rats 171mentioning

confidence: 99%

See 2 more Smart Citations

Lung Inflammation in Rats Following Subchronic Exposure to Cigarette Mainstream Smoke

Friedrichs

Miert²,

Vanscheeuwijck³

2006

Experimental Lung Research

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“…A narrowly delineated region of ventral laryngeal epithelium is highly responsive to inhaled materials such as cobalt sulfate (1) and tobacco smoke in both acute (9,13) and sub-chronic (3)(4)(5)(6)14) exposures. Other inhaled materials (e.g., industrial chemicals, pharmaceuticals, and propellants) also produce histopathologic changes in the larynx (7).…”

mentioning

confidence: 99%

Histological Sectioning of the Rodent Larynx for Inhalation Toxicity Testing

et al. 1992

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In rodents, the larynx is a major site of histopathologic alteration following inhalation exposure to particulates, vapors, and aerosols. Specifically, the epithelial lining of a narrowly delineated region on the ventral floor of the larynges of rats and mice appears to be especially vulnerable to inhaled materials, and is recognized as a preferred site for histopathological evaluation in inhalation studies. This site is located at the base of the epiglottis, cranial to the ventral laryngeal diverticulum (ventral pouch (Fig. 1). The cranial half of the larynx is then embedded in paraffin (cut side down). The block of tissue is then slowly faced caudad to craniad until the ventral laryngeal diverticulum appears ventrally, and the arytenoid and &dquo;U&dquo; cartilages appear laterally (Fig. 2). Proceeding more

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Comparison of the inhalation toxicity of kretek (clove cigarette) smoke with that of American cigarette smoke. I. One day exposure

Clark¹

1989

Arch Toxicol

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The comparative acute toxicity of a branded American cigarette and kreteks (Indonesian cigarettes containing approximately 60% tobacco and 40% ground clove buds) was assessed by exposure of groups of ten male and ten female rats to three different but equivalent (in terms of total particulate matter) concentrations of smoke from each type of cigarette. The smoke was delivered "nose only" using an HRC Rodent Smoking Machine (Mark IV) within a single 1-h period, with a total delivery of 30 min smoke and a 15 min air-breathing period between the two smoke exposures. Comparison of the immediate response to smoke exposure was made by monitoring respiration during exposure and by observation of the animals immediately following exposure. At this level, the only differences observed were more severe signs of smoke intoxication in the American smoke exposed animals which, at least in part, was attributed to the higher concentrations of carbon monoxide (CO) to which these animals were exposed; CO concentrations in the American smoke atmospheres were 2-2.5 times higher than the corresponding kretek smoke atmospheres. Comparison of any delayed response was made by observation and measurement of body weight, food and water consumption for a sub-population maintained for 14 days following exposures. This comparison revealed no differences between the groups which could be attributed to the smoke exposures. Comparison of any lung changes induced were made at two intervals, 24 h and 14 days following smoke exposures. These intervals were selected to provide information on any damage to the lung attributable to the smoke exposures and any subsequent development or repair.(ABSTRACT TRUNCATED AT 250 WORDS)

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Transient epithelial loss in rat larynx after acute exposure to tobacco smoke

Cited by 12 publications

References 6 publications

Lung Inflammation in Rats Following Subchronic Exposure to Cigarette Mainstream Smoke

Lung Inflammation in Rats Following Subchronic Exposure to Cigarette Mainstream Smoke

Histological Sectioning of the Rodent Larynx for Inhalation Toxicity Testing

Comparison of the inhalation toxicity of kretek (clove cigarette) smoke with that of American cigarette smoke. I. One day exposure

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