Selected responses of hypertension-sensitive and resistant rats to inhaled acrolein

Kutzman, Raymond S.; Wehner, R. W.; Haber, S.B.

doi:10.1016/0300-483x(84)90155-0

Cited by 17 publications

(16 citation statements)

References 14 publications

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“…A susceptible rat strain succumbs to a high concentration of acrolein exposure for a short duration (300 mg/m 3 ×30 min) or to a lower concentration for a long duration (9.2 mg/m 3 ×6 h/d×62 d) (Supporting Information Table S2) 83–85. At lower concentrations, acrolein still produced histological features partially consistent with acute lung injury.…”

Section: Responsementioning

confidence: 99%

Acrolein – a pulmonary hazard

Bein

Leikauf

2011

Molecular Nutrition Food Res

181

128

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Acrolein is a respiratory irritant that can be generated during cooking and is in environmental tobacco smoke. More plentiful in cigarette smoke than polycyclic aromatic hydrocarbons (PAH), acrolein can adduct tumor suppressor p53 (TP53) DNA and may contribute to TP53-mutations in lung cancer. Acrolein is also generated endogenously at sites of injury, and excessive breath levels (sufficient to activate metalloproteinases and increase mucin transcripts) have been detected in asthma and chronic obstructive pulmonary disease (COPD). Because of its reactivity with respiratory-lining fluid or cellular macromolecules, acrolein alters gene regulation, inflammation, mucociliary transport, and alveolar-capillary barrier integrity. In laboratory animals, acute exposures have lead to acute lung injury and pulmonary edema similar to that produced by smoke inhalation whereas lower concentrations have produced bronchial hyperreactivity, excessive mucus production, and alveolar enlargement. Susceptibility to acrolein exposure is associated with differential regulation of cell surface receptor, transcription factor, and ubiquitin-proteasome genes. Consequent to its pathophysiological impact, acrolein contributes to the morbidly and mortality associated with acute lung injury and COPD, and possibly asthma and lung cancer.

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Section: Responsementioning

confidence: 99%

Acrolein – a pulmonary hazard

Bein

Leikauf

2011

Molecular Nutrition Food Res

181

128

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“…In other studies, Dahl rats exposed by inhalation to acrolein for up to 62 days had concentration-related histopathological changes in the trachea and lungs at 0.4 ppm (0.9 mg/m 3 ) (LOAEL), while no microscopic changes were observed in the nasal turbinates or other tissues examined (11). In contrast, slight microscopic changes in the nasal cavities have been observed in other strains of rats exposed by inhalation to 0.4 ppm (0.9 mg/m 3 ) acrolein (12)(13)(14)(15), with histopathological changes in the lungs and trachea and increased mortality at higher concentrations.…”

Section: Gomes Liteplo and Meekmentioning

confidence: 84%

Acrolein: Hazard Characterization and Exposure–response Analysis

Gomes

Liteplo

Meek

2001

Journal of Environmental Science and Health, Part C

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Acrolein has been assessed as a Priority Substance under the Canadian Environmental Protection Act. Adverse health effects associated with exposure to acrolein are primarily confined to the tissue of first contact and are concentration related. A tolerable concentration of 0.4 mg/m 3 has been derived, based upon the benchmark dose associated with a 5% increase in degenerative changes in the nasal respiratory epithelium of rats in a short-term inhalation study. For ingestion, a provisional tolerable concentration of 1.5 mg/L (7.5 mg/kg body weight per day) has been derived, based upon the benchmark dose associated with a 5% adverse response for non-neoplastic lesions in the gastrointestinal tract of rats in a subchronic oral study. 23

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“…Some of the identified studies did not have sufficient incidence data for modeling (Leach et al 1987; Lyon et al 1970). Of the other available studies (Cassee et al 1996; Costa et al 1986; Feron et al 1978; Kutzman et al 1984, 1985), we selected a data set from Costa et al (1986), which had a statistically significant dose–response relationship between acrolein exposure and both specific compliance (sC L ), calculated as dynamic compliance divided by forced residual capacity, and the ratio of residual volume to total lung capacity (RV/TLC). Both sC L and RV/TLC are normalized to an individual animal’s lung size, which corrects for inter-individual variability due to size for these measures.…”

Section: Methodsmentioning

confidence: 99%

Estimating Risk from Ambient Concentrations of Acrolein across the United States

Woodruff

Wells

Holt

et al. 2007

Environ Health Perspect

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BackgroundEstimated ambient concentrations of acrolein, a hazardous air pollutant, are greater than the U.S. Environmental Protection Agency (EPA) reference concentration throughout the United States, making it a concern for human health. However, there is no method for assessing the extent of risk under the U.S. EPA noncancer risk assessment framework.ObjectivesWe estimated excess risks from ambient concentrations of acrolein based on dose–response modeling of a study in rats with a relationship between acrolein and residual volume/total lung capacity ratio (RV/TLC) and specific compliance (sCL), markers for altered lung function.MethodsBased on existing literature, we defined values above the 90th percentile for controls as “adverse.” We estimated the increase over baseline response that would occur in the human population from estimated ambient concentrations of acrolein, taken from the U.S. EPA’s National-Scale Air Toxics Assessment for 1999, after standard animal-to-human conversions and extrapolating to doses below the experimental data.ResultsThe estimated median additional number of adverse sCL outcomes across the United States was approximately 2.5 cases per 1,000 people. The estimated range of additional outcomes from the 5th to the 95th percentile of acrolein concentration levels across census tracts was 0.28–14 cases per 1,000. For RV/TLC, the median additional outcome was 0.002 per 1,000, and the additional outcome at the 95th percentile was 0.13 per 1,000.ConclusionsAlthough there are uncertainties in estimating human risks from animal data, this analysis demonstrates a method for estimating health risks for noncancer effects and suggests that acrolein could be associated with decreased respiratory function in the United States.

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Selected responses of hypertension-sensitive and resistant rats to inhaled acrolein

Cited by 17 publications

References 14 publications

Acrolein – a pulmonary hazard

Acrolein – a pulmonary hazard

Acrolein: Hazard Characterization and Exposure–response Analysis

Estimating Risk from Ambient Concentrations of Acrolein across the United States

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