Pulmonary effects of sulfur dioxide exposure and ipratropium bromide pretreatment in adults with nonallergic asthma

McManus, Michael S.; Koenig, Jane Q.; Altman, Leonard C.; Pierson, William E.

doi:10.1016/0091-6749(89)90074-2

Cited by 20 publications

(5 citation statements)

References 28 publications

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“…To our knowledge, this is the first published study to compare the respiratory effects of naturally occurring acid fog on nonatopic and atopic adult asthmatics. MCMANUS et al [19] reported that nonallergic asthmatics are more sensitive to short-term, low-level SO 2 exposure than are healthy, age-matched control subjects. As nonallergic asthma was more responsive than allergic asthma to ipratropium bromide [20], nonallergic asthmatics may have increased resting parasympathetic tone.…”

Section: Discussionmentioning

confidence: 99%

Acid fog and hospital visits for asthma: an epidemiological study

Tanaka

Honma²,

Nishi³

et al. 1998

Eur Respir J

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The aim of this study was to elucidate the adverse respiratory effects of naturally occurring acid fog. In total, 102 adult asthmatic patients (44 nonatopic and 58 atopic) were studied for a 2 yr period (January 1992 to December 1993) in Kushiro, a city with only a small industrial area, located in the northern-most island in Japan. Fog occurred on 378 out of 731 days, and the acidity of the fog ranged from pH 3.32 to 6.91 (mean pH 4.95). The association between hospital visits for asthma and meteorological factors or air pollutants was investigated. In nonatopic patients, fog, high ozone and water vapour pressure, low day-to-day temperature differences, low concentrations of atmospheric NO and NO2 contributed significantly (p<0.05) to increasing hospital visits. In atopic subjects, fog, high water vapour pressure, low levels of atmospheric NO2 and SO2 contributed significantly to hospital visits (p<0.05). In Poisson regression analysis the remaining factors of significance (p<0.01) for nonatopic asthma were fog and low NO and for atopic asthma were high water vapour pressure and low SO2 (p<0.05). A weak but significant correlation was observed between the number of hospital visits and the mean pH of the foggy day (r=-0.38, p<0.05) in nonatopic asthmatic patients, not in atopic asthma. On foggy days, gaseous air pollutant levels were significantly (p<0.01) lower than on fog-free days. It was concluded that, naturally occurring acid fog may have a weak bronchoconstrictive effect which appears to be more influential in nonatopic asthmatic subjects than in atopic subjects.

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Section: Discussionmentioning

confidence: 99%

Acid fog and hospital visits for asthma: an epidemiological study

Tanaka

Honma²,

Nishi³

et al. 1998

Eur Respir J

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“…The Comet Assay T has been established in recent publications by a number of authors from various fields of interest as a reliable method to detect DNA damage or to test DNA stability under adverse conditions [29][30][31][32]. On the other hand, this method is suitable for analyzing DNA repair and for quantifying antimutagenic effects as well [33][34][35].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Inflammatory Reactions and Genotoxic Effects after Exposure of Nasal Respiratory Epithelia to Benzene

Gosepath¹,

Grebneva²,

Brieger³

et al. 2003

ORL

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Background: The aim of this study was to identify inflammatory changes as well as genotoxic effects in cultivated human respiratory epithelial cells after in vitro exposure to benzene. Methods: Primary cell cultures of nasal respiratory mucosa were exposed to synthetic air enriched with 5,000 µg/m³ of benzene at an air/liquid interface over 8 h and then to synthetic air only over the following 24 h. Controls were continuously exposed to synthetic air over 32 h. To detect inflammatory reactions, release of prostaglandin E₂ was quantified using a competitive enzyme immunoassay. The Comet Assay was used to quantify the ratio of apoptotic cells with benzene-induced DNA fragmentation. Results: Prostaglandin release as well as DNA fragmentation increased after 8 h of exposure and remained elevated throughout the following 24 h but did not increase in controls. Conclusions: High concentrations of benzene induce an inflammatory response and possibly fragmentation of DNA in respiratory epithelial cells. These findings have to be discussed with respect to possible mutagenic or carcinogenic effects of benzene in nasal respiratory cells.

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“…Inhaled chemical substances are known to be potentially harmful to the respiratory mucosa (Kenney et al, 1994). Exposure of primary cultures of human respiratory epithelial cells in vitro has been established as an adequate method to investigate effects of air pollutants on respiratory mucosa Blasiak, 2002;Koren et al, 1990;McKinnon et al;McManus et al, 1989;Robson et al, 1992). In previous studies we evaluated acute effects of air pollutants on human respiratory mucosa after short-term exposure of 3 h Muttray et al, 1999) up to 24 h (Gosepath et al, 2003), as well as subacute effects of long-term exposures for up to 4 wk (Gosepath & Mann, 2000).…”

Section: Discussionmentioning

confidence: 99%

mRNA Induction and Cytokine Release of Inflammatory Mediators During In Vitro Exposure of Human Nasal Respiratory Epithelia to Acetaldehyde

Gosepath¹,

Brieger²,

Muttray³

et al. 2006

Inhalation Toxicology

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Acetaldehyde has been shown to be cytotoxic and carcinogenic to the upper respiratory tract epithelium of rodents following long-term exposure. Most animal studies have concentrated on carcinogenicity and DNA-protein cross-link formation, while less is known about potential dose- and time-dependent induction of aldehyde-induced rhinitis in humans. In this in vitro study, 22 primary cell cultures established from inferior turbinate tissue of healthy individuals were exposed to acetaldehyde concentrations of 50 (German MAK value) or 500 ppm for 4 or 24 h. mRNA expression and protein levels of cytokines and other inflammatory mediators were quantified at the end of the 4- and 24-h exposures. Controls were exposed to synthetic air. Quantitative polymerase chain reaction (Q-PCR) analysis was performed for interleukin (IL)-6, IL-8, IL-1beta, monocyte chemotactic protein (MCP)-1, tumor necrosis factor (TNF)-alpha, GMCSF, Cox-1, and Cox-2. Enzyme-linked immunosorbent assay (ELISA) was performed from culture supernatants for IL-6, IL-8, IL-1beta, MCP-1, TNF-alpha, and GMCSF. Significant inductions of IL-1beta, TNF-alpha, and Cox-1 and Cox-2 mRNA were observed following exposure to > or =50 ppm acetaldehyde for 4 h. IL-6 and MCP-1 were also induced following a 4-h exposure to 500 ppm acetaldehyde. For all these parameters, effects were significantly stronger at the higher concentration. After 24-h of exposure only Cox-2 remained significantly elevated at 500 ppm but not at 50 ppm, while all other mediators had been downregulated. The obtained data suggest that with exposure to 500 ppm and remarkably also at the level of the occupational exposure limit of 50 ppm, an immediate transient upregulation of inflammatory mediator mRNA is induced, possibly leading to subclinical inflammatory effects.

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Pulmonary effects of sulfur dioxide exposure and ipratropium bromide pretreatment in adults with nonallergic asthma

Cited by 20 publications

References 28 publications

Acid fog and hospital visits for asthma: an epidemiological study

Acid fog and hospital visits for asthma: an epidemiological study

Evaluation of Inflammatory Reactions and Genotoxic Effects after Exposure of Nasal Respiratory Epithelia to Benzene

mRNA Induction and Cytokine Release of Inflammatory Mediators During In Vitro Exposure of Human Nasal Respiratory Epithelia to Acetaldehyde

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