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• W2000202810 abstract "Acrolein is an unsaturated aldehyde produced by combustion of many organic compounds. Massive exposure may lead to severe pulmonary disease and possibly death. We report a case of intoxication in a 2-year-old boy; an 18-month follow-up showed development of obstructive bronchiolar disease with diffuse bronchiectasis. Acrolein is an unsaturated aldehyde produced by combustion of many organic compounds. Massive exposure may lead to severe pulmonary disease and possibly death. We report a case of intoxication in a 2-year-old boy; an 18-month follow-up showed development of obstructive bronchiolar disease with diffuse bronchiectasis. computed tomography Acrolein is produced during the combustion of a variety of organic substances: house fires, cigarette smoking, burning fatty acid.1RE Gosselin and AI. Clinical toxicology of commercial products. 4th ed. Baltimore: Williams & Wilkins, 1976.Google Scholar Combustion of the lipids present in vegetable oil also produces acrolein. Dangerous inhalations usually are avoided because acrolein is a very powerful irritant. In contrast, very young children may be exposed to acrolein for a long time, and domestic accidents represent a potential but rare cause of intoxication. We report a case of a severe acrolein intoxication in a young boy who was confined in an area where acrolein was present due to the lack of parental care.Case ReportA previously healthy 27-month-old boy was admitted to the district hospital because of acute respiratory failure, after being confined for about 1 h in a kitchen where vegetable oil was burning on an electric hot plate and producing acrid smoke. The child was cyanotic, acutely dyspneic, and his respiratory rate was 58 breaths per minute; auscultation of the thorax revealed crackles. Intoxication by acrolein was suspected because of the nature of the smoke; the cooker was electric so carbon monoxide inhalation was unlikely. Arterial blood gas value analysis showed a pH level of 7.08, a PaO2 value of 47 mm Hg, and a PaCO2 level of 81 mm Hg. The chest x-ray film showed an alveolar consolidation with bat's wing distribution. The initial treatment consisted of oxygen therapy and administration of diuretics and antibiotics. Respiratory distress improved during the first hours, but hypoxemia persisted. No acetylcysteine treatment was given.Four weeks later, the child was transferred to our department. He still had tachypnea, had a productive cough, and needed continuous oxygen therapy (3 L/mn). Auscultation of the thorax revealed crackles and wheezing. A chest x-ray film showed notable regression of pulmonary opacities. Fiberoptic examination showed moderate but diffuse tracheobronchial inflammation. The results of functional follow-up are summarized in Table 1.Table 1Pulmonary Function Follow-UpTimne After ExposurePulmonary Function Data4 Weeks3 Months9 Months18 MonthsRespiratory rate58453530Oxygen saturation, %67808893Transfer factor of lung for carbon monoxide65%……92%Ratio of transfer factor of lung for carbon monoxide to functional residual capacity79%……66%Functional residual capacity, % of normal value11291…150Specific airway resistance, % of normal value568568…385 Open table in a new tab Three months after the exposure to acrolein, the productive cough was unchanged. There were moderate signs of bronchitis and general overinflation evidenced on the chest x-ray film. Computed tomography (CT) showed focal overinflation with decreased perfusion without any dominant localization (Fig 1). Bronchiectasis was not detected.Nine months after exposure, daily chest physiotherapy was still necessary, but oxygen was required only during the night. The chest x-ray film was unchanged and CT showed heterogeneous areas of overinflation with more marked focal emphysema. Some bronchiectasis and more diffuse thickened bronchial walls appeared in the lingula, middle lobe, and lower lobes.Eighteen months after the exposure, overnight transcutaneous saturation allowed the cessation of oxygen therapy. The clinical course was marked by occasional infections and permanent productive cough. Roentgenogram analysis showed bronchial thickening and massive overinflation. The CT scan showed patchy areas of emphysema, localized atelectasis, thickened bronchial walls, and diffuse bronchiectasis (Fig 2).FIGURE 2Ultrafast CT. Patchy areas of emphysema with decreased perfusion associated with obvious cylindric and varicose bronchectiasis (18 months after exposure).View Large Image Figure ViewerDownload (PPT)DiscussionAcrolein is produced by prolonged cooking of vegetable oil, and may therefore be a frequent source of domestic accidents involving young children. Acrolein affects protein structures by binding to sulfhydryl groups, which are very numerous in the nasal mucosa; this may explain the high irritant power of the molecule.2Beauchamp RD Andjelkovich DA Kligerman AD et al.A critical review of the literature on acrolein toxicity.CRC Crit Rev Toxicol. 1985; 14: 309-380Crossref Scopus (241) Google Scholar Glutathione protects against acrolein, probably because it contains sulfhydryl groups.3Lam CW Casanova M Heck HD Depletion of nasal mucosal glutathione by acrolein and enhancement of formaldehyde-induced-DNA protein cross linking by simultaneous exposure to acrolein.Arch Toxicol. 1985; 58: 67-71Crossref Scopus (67) Google Scholar Acrolein impairs α1-proteinase inhibitor activity and might be responsible for emphysematous lesions.4Gan JC Ansari GA Plausible mechanism of inactivation of plasma alphal-proteinase inhibitor by acrolein.Cancer Res. 1988; 55: 419-422Google Scholar In vivo, acrolein inhibits aldehyde dehydrogenase5Rikans LE The oxydation of acrolein by rat liver aldehyde deshydrogenase: relation to allyl alcohol hepatotoxieity. Drug Metab Dispos 1987 2187-2194Google Scholar and increases the rate of formation on toxic molecules including free radicals which are known to contribute to lung injury.6Schraufstätter IU Cochrane CG Oxydants.in: Cristal RG West JB Barnes PJ Cherniak NS Weibel ER The lung. Raven Press, New York1991: 1803-1806Google Scholar The effects of exposure to acrolein mostly have been studied in human volunteers and animals.2Beauchamp RD Andjelkovich DA Kligerman AD et al.A critical review of the literature on acrolein toxicity.CRC Crit Rev Toxicol. 1985; 14: 309-380Crossref Scopus (241) Google ScholarVolunteers have been exposed to small inhalations of acrolein; its characteristic smell was recognized before the appearance of nasal or conjunctival injury and these low concentrations did not cause detectable pulmonary lesions. In animals, massive inhalation initially induces pulmonary edema and destruction of the bronchial mucosa, and secondarily it causes severe bronchoconstriction and diffuse tracheobronchial hypersecretion.Few human cases have been reported. They include three occupational accidents in the chemical industry; two of them are polyintoxications and are therefore difficult to interpret.2Beauchamp RD Andjelkovich DA Kligerman AD et al.A critical review of the literature on acrolein toxicity.CRC Crit Rev Toxicol. 1985; 14: 309-380Crossref Scopus (241) Google Scholar In the third case, pulmonary edema was responsible for the initial respiratory distress,7Champeix J Catalina P Bronchopneumopathie aigue par vapeur d'acroleine.Arch Mal Prof. 1966; 27: 797-803Google Scholar and analysis of pulmonary function 18 months later showed persisting obstructive disease. No radiologic or CT features are available. Few cases of domestic intoxication previously have been described that resulted from excessive burning of a vegetable oil;8Gosselin B Wattel F Intoxication aigue par l'acroléine: une observation.Nouv Presse Med. 1979; 8: 5469-5472Google Scholar9Bauer K Czech K Porter A Schwere akzidentelle Acrolein-vergiftung in haushalt.Wien Klin Wchschr. 1977; 89: 243-244Google Scholar in one case, autopsy revealed diffuse and massive destruction of the mucosa responsible for complete obstruction of the pulmonary tree.8Gosselin B Wattel F Intoxication aigue par l'acroléine: une observation.Nouv Presse Med. 1979; 8: 5469-5472Google ScholarTo our knowledge, the case we report is the only observation of the development of diffuse bronchiectasis during the months following the exposure to acrolein. In our case, acute respiratory failure and respiratory acidosis initially were severe, but regressed within a few hours; bronchoconstriction and a productive cough were observed very early and remained unchanged despite salbutamol and corticosteroid treatment. The lesions of the small bronchial airways were permanent. The results of animal studies suggest that this probably was due to the massive desquamation.Findings of the clinical follow-up, characterized by chronic bronchorrhea, and the CT features illustrate the appearance of diffuse bronchiectasis and severe ventilation anomalies a few months after the exposure. The controlled normality of the carbon monoxide capacity transfer and the decreasing need for oxygen therapy argue against massive interstitial lesions. In this case, no treatment other than symptomatic measures was given on first admission. N-acetylcysteine has been shown in animal studies to have a protective effect.10Dawson JR Norbeck K The effectiveness of N-acetylcysteine in isolated hepatocytes against toxicity of paracetamol, acrolein and paraquat.Arch Toxicol. 1984; 55: 103-110Crossref Scopus (65) Google Scholar It is a precursor of glutathione and has antioxidant activity.11Heffner E Repine JE Pulmonary strategy of antioxidant defense.Am Rev Respir Dis. 1989; 140: 531-554Crossref PubMed Scopus (487) Google Scholar N-acetylcysteine administration may therefore be valuable in cases of acrolein intoxication. Acrolein is produced during the combustion of a variety of organic substances: house fires, cigarette smoking, burning fatty acid.1RE Gosselin and AI. Clinical toxicology of commercial products. 4th ed. Baltimore: Williams & Wilkins, 1976.Google Scholar Combustion of the lipids present in vegetable oil also produces acrolein. Dangerous inhalations usually are avoided because acrolein is a very powerful irritant. In contrast, very young children may be exposed to acrolein for a long time, and domestic accidents represent a potential but rare cause of intoxication. We report a case of a severe acrolein intoxication in a young boy who was confined in an area where acrolein was present due to the lack of parental care. Case ReportA previously healthy 27-month-old boy was admitted to the district hospital because of acute respiratory failure, after being confined for about 1 h in a kitchen where vegetable oil was burning on an electric hot plate and producing acrid smoke. The child was cyanotic, acutely dyspneic, and his respiratory rate was 58 breaths per minute; auscultation of the thorax revealed crackles. Intoxication by acrolein was suspected because of the nature of the smoke; the cooker was electric so carbon monoxide inhalation was unlikely. Arterial blood gas value analysis showed a pH level of 7.08, a PaO2 value of 47 mm Hg, and a PaCO2 level of 81 mm Hg. The chest x-ray film showed an alveolar consolidation with bat's wing distribution. The initial treatment consisted of oxygen therapy and administration of diuretics and antibiotics. Respiratory distress improved during the first hours, but hypoxemia persisted. No acetylcysteine treatment was given.Four weeks later, the child was transferred to our department. He still had tachypnea, had a productive cough, and needed continuous oxygen therapy (3 L/mn). Auscultation of the thorax revealed crackles and wheezing. A chest x-ray film showed notable regression of pulmonary opacities. Fiberoptic examination showed moderate but diffuse tracheobronchial inflammation. The results of functional follow-up are summarized in Table 1.Table 1Pulmonary Function Follow-UpTimne After ExposurePulmonary Function Data4 Weeks3 Months9 Months18 MonthsRespiratory rate58453530Oxygen saturation, %67808893Transfer factor of lung for carbon monoxide65%……92%Ratio of transfer factor of lung for carbon monoxide to functional residual capacity79%……66%Functional residual capacity, % of normal value11291…150Specific airway resistance, % of normal value568568…385 Open table in a new tab Three months after the exposure to acrolein, the productive cough was unchanged. There were moderate signs of bronchitis and general overinflation evidenced on the chest x-ray film. Computed tomography (CT) showed focal overinflation with decreased perfusion without any dominant localization (Fig 1). Bronchiectasis was not detected.Nine months after exposure, daily chest physiotherapy was still necessary, but oxygen was required only during the night. The chest x-ray film was unchanged and CT showed heterogeneous areas of overinflation with more marked focal emphysema. Some bronchiectasis and more diffuse thickened bronchial walls appeared in the lingula, middle lobe, and lower lobes.Eighteen months after the exposure, overnight transcutaneous saturation allowed the cessation of oxygen therapy. The clinical course was marked by occasional infections and permanent productive cough. Roentgenogram analysis showed bronchial thickening and massive overinflation. The CT scan showed patchy areas of emphysema, localized atelectasis, thickened bronchial walls, and diffuse bronchiectasis (Fig 2). A previously healthy 27-month-old boy was admitted to the district hospital because of acute respiratory failure, after being confined for about 1 h in a kitchen where vegetable oil was burning on an electric hot plate and producing acrid smoke. The child was cyanotic, acutely dyspneic, and his respiratory rate was 58 breaths per minute; auscultation of the thorax revealed crackles. Intoxication by acrolein was suspected because of the nature of the smoke; the cooker was electric so carbon monoxide inhalation was unlikely. Arterial blood gas value analysis showed a pH level of 7.08, a PaO2 value of 47 mm Hg, and a PaCO2 level of 81 mm Hg. The chest x-ray film showed an alveolar consolidation with bat's wing distribution. The initial treatment consisted of oxygen therapy and administration of diuretics and antibiotics. Respiratory distress improved during the first hours, but hypoxemia persisted. No acetylcysteine treatment was given. Four weeks later, the child was transferred to our department. He still had tachypnea, had a productive cough, and needed continuous oxygen therapy (3 L/mn). Auscultation of the thorax revealed crackles and wheezing. A chest x-ray film showed notable regression of pulmonary opacities. Fiberoptic examination showed moderate but diffuse tracheobronchial inflammation. The results of functional follow-up are summarized in Table 1. Three months after the exposure to acrolein, the productive cough was unchanged. There were moderate signs of bronchitis and general overinflation evidenced on the chest x-ray film. Computed tomography (CT) showed focal overinflation with decreased perfusion without any dominant localization (Fig 1). Bronchiectasis was not detected. Nine months after exposure, daily chest physiotherapy was still necessary, but oxygen was required only during the night. The chest x-ray film was unchanged and CT showed heterogeneous areas of overinflation with more marked focal emphysema. Some bronchiectasis and more diffuse thickened bronchial walls appeared in the lingula, middle lobe, and lower lobes. Eighteen months after the exposure, overnight transcutaneous saturation allowed the cessation of oxygen therapy. The clinical course was marked by occasional infections and permanent productive cough. Roentgenogram analysis showed bronchial thickening and massive overinflation. The CT scan showed patchy areas of emphysema, localized atelectasis, thickened bronchial walls, and diffuse bronchiectasis (Fig 2). DiscussionAcrolein is produced by prolonged cooking of vegetable oil, and may therefore be a frequent source of domestic accidents involving young children. Acrolein affects protein structures by binding to sulfhydryl groups, which are very numerous in the nasal mucosa; this may explain the high irritant power of the molecule.2Beauchamp RD Andjelkovich DA Kligerman AD et al.A critical review of the literature on acrolein toxicity.CRC Crit Rev Toxicol. 1985; 14: 309-380Crossref Scopus (241) Google Scholar Glutathione protects against acrolein, probably because it contains sulfhydryl groups.3Lam CW Casanova M Heck HD Depletion of nasal mucosal glutathione by acrolein and enhancement of formaldehyde-induced-DNA protein cross linking by simultaneous exposure to acrolein.Arch Toxicol. 1985; 58: 67-71Crossref Scopus (67) Google Scholar Acrolein impairs α1-proteinase inhibitor activity and might be responsible for emphysematous lesions.4Gan JC Ansari GA Plausible mechanism of inactivation of plasma alphal-proteinase inhibitor by acrolein.Cancer Res. 1988; 55: 419-422Google Scholar In vivo, acrolein inhibits aldehyde dehydrogenase5Rikans LE The oxydation of acrolein by rat liver aldehyde deshydrogenase: relation to allyl alcohol hepatotoxieity. Drug Metab Dispos 1987 2187-2194Google Scholar and increases the rate of formation on toxic molecules including free radicals which are known to contribute to lung injury.6Schraufstätter IU Cochrane CG Oxydants.in: Cristal RG West JB Barnes PJ Cherniak NS Weibel ER The lung. Raven Press, New York1991: 1803-1806Google Scholar The effects of exposure to acrolein mostly have been studied in human volunteers and animals.2Beauchamp RD Andjelkovich DA Kligerman AD et al.A critical review of the literature on acrolein toxicity.CRC Crit Rev Toxicol. 1985; 14: 309-380Crossref Scopus (241) Google ScholarVolunteers have been exposed to small inhalations of acrolein; its characteristic smell was recognized before the appearance of nasal or conjunctival injury and these low concentrations did not cause detectable pulmonary lesions. In animals, massive inhalation initially induces pulmonary edema and destruction of the bronchial mucosa, and secondarily it causes severe bronchoconstriction and diffuse tracheobronchial hypersecretion.Few human cases have been reported. They include three occupational accidents in the chemical industry; two of them are polyintoxications and are therefore difficult to interpret.2Beauchamp RD Andjelkovich DA Kligerman AD et al.A critical review of the literature on acrolein toxicity.CRC Crit Rev Toxicol. 1985; 14: 309-380Crossref Scopus (241) Google Scholar In the third case, pulmonary edema was responsible for the initial respiratory distress,7Champeix J Catalina P Bronchopneumopathie aigue par vapeur d'acroleine.Arch Mal Prof. 1966; 27: 797-803Google Scholar and analysis of pulmonary function 18 months later showed persisting obstructive disease. No radiologic or CT features are available. Few cases of domestic intoxication previously have been described that resulted from excessive burning of a vegetable oil;8Gosselin B Wattel F Intoxication aigue par l'acroléine: une observation.Nouv Presse Med. 1979; 8: 5469-5472Google Scholar9Bauer K Czech K Porter A Schwere akzidentelle Acrolein-vergiftung in haushalt.Wien Klin Wchschr. 1977; 89: 243-244Google Scholar in one case, autopsy revealed diffuse and massive destruction of the mucosa responsible for complete obstruction of the pulmonary tree.8Gosselin B Wattel F Intoxication aigue par l'acroléine: une observation.Nouv Presse Med. 1979; 8: 5469-5472Google ScholarTo our knowledge, the case we report is the only observation of the development of diffuse bronchiectasis during the months following the exposure to acrolein. In our case, acute respiratory failure and respiratory acidosis initially were severe, but regressed within a few hours; bronchoconstriction and a productive cough were observed very early and remained unchanged despite salbutamol and corticosteroid treatment. The lesions of the small bronchial airways were permanent. The results of animal studies suggest that this probably was due to the massive desquamation.Findings of the clinical follow-up, characterized by chronic bronchorrhea, and the CT features illustrate the appearance of diffuse bronchiectasis and severe ventilation anomalies a few months after the exposure. The controlled normality of the carbon monoxide capacity transfer and the decreasing need for oxygen therapy argue against massive interstitial lesions. In this case, no treatment other than symptomatic measures was given on first admission. N-acetylcysteine has been shown in animal studies to have a protective effect.10Dawson JR Norbeck K The effectiveness of N-acetylcysteine in isolated hepatocytes against toxicity of paracetamol, acrolein and paraquat.Arch Toxicol. 1984; 55: 103-110Crossref Scopus (65) Google Scholar It is a precursor of glutathione and has antioxidant activity.11Heffner E Repine JE Pulmonary strategy of antioxidant defense.Am Rev Respir Dis. 1989; 140: 531-554Crossref PubMed Scopus (487) Google Scholar N-acetylcysteine administration may therefore be valuable in cases of acrolein intoxication. Acrolein is produced by prolonged cooking of vegetable oil, and may therefore be a frequent source of domestic accidents involving young children. Acrolein affects protein structures by binding to sulfhydryl groups, which are very numerous in the nasal mucosa; this may explain the high irritant power of the molecule.2Beauchamp RD Andjelkovich DA Kligerman AD et al.A critical review of the literature on acrolein toxicity.CRC Crit Rev Toxicol. 1985; 14: 309-380Crossref Scopus (241) Google Scholar Glutathione protects against acrolein, probably because it contains sulfhydryl groups.3Lam CW Casanova M Heck HD Depletion of nasal mucosal glutathione by acrolein and enhancement of formaldehyde-induced-DNA protein cross linking by simultaneous exposure to acrolein.Arch Toxicol. 1985; 58: 67-71Crossref Scopus (67) Google Scholar Acrolein impairs α1-proteinase inhibitor activity and might be responsible for emphysematous lesions.4Gan JC Ansari GA Plausible mechanism of inactivation of plasma alphal-proteinase inhibitor by acrolein.Cancer Res. 1988; 55: 419-422Google Scholar In vivo, acrolein inhibits aldehyde dehydrogenase5Rikans LE The oxydation of acrolein by rat liver aldehyde deshydrogenase: relation to allyl alcohol hepatotoxieity. Drug Metab Dispos 1987 2187-2194Google Scholar and increases the rate of formation on toxic molecules including free radicals which are known to contribute to lung injury.6Schraufstätter IU Cochrane CG Oxydants.in: Cristal RG West JB Barnes PJ Cherniak NS Weibel ER The lung. Raven Press, New York1991: 1803-1806Google Scholar The effects of exposure to acrolein mostly have been studied in human volunteers and animals.2Beauchamp RD Andjelkovich DA Kligerman AD et al.A critical review of the literature on acrolein toxicity.CRC Crit Rev Toxicol. 1985; 14: 309-380Crossref Scopus (241) Google Scholar Volunteers have been exposed to small inhalations of acrolein; its characteristic smell was recognized before the appearance of nasal or conjunctival injury and these low concentrations did not cause detectable pulmonary lesions. In animals, massive inhalation initially induces pulmonary edema and destruction of the bronchial mucosa, and secondarily it causes severe bronchoconstriction and diffuse tracheobronchial hypersecretion. Few human cases have been reported. They include three occupational accidents in the chemical industry; two of them are polyintoxications and are therefore difficult to interpret.2Beauchamp RD Andjelkovich DA Kligerman AD et al.A critical review of the literature on acrolein toxicity.CRC Crit Rev Toxicol. 1985; 14: 309-380Crossref Scopus (241) Google Scholar In the third case, pulmonary edema was responsible for the initial respiratory distress,7Champeix J Catalina P Bronchopneumopathie aigue par vapeur d'acroleine.Arch Mal Prof. 1966; 27: 797-803Google Scholar and analysis of pulmonary function 18 months later showed persisting obstructive disease. No radiologic or CT features are available. Few cases of domestic intoxication previously have been described that resulted from excessive burning of a vegetable oil;8Gosselin B Wattel F Intoxication aigue par l'acroléine: une observation.Nouv Presse Med. 1979; 8: 5469-5472Google Scholar9Bauer K Czech K Porter A Schwere akzidentelle Acrolein-vergiftung in haushalt.Wien Klin Wchschr. 1977; 89: 243-244Google Scholar in one case, autopsy revealed diffuse and massive destruction of the mucosa responsible for complete obstruction of the pulmonary tree.8Gosselin B Wattel F Intoxication aigue par l'acroléine: une observation.Nouv Presse Med. 1979; 8: 5469-5472Google Scholar To our knowledge, the case we report is the only observation of the development of diffuse bronchiectasis during the months following the exposure to acrolein. In our case, acute respiratory failure and respiratory acidosis initially were severe, but regressed within a few hours; bronchoconstriction and a productive cough were observed very early and remained unchanged despite salbutamol and corticosteroid treatment. The lesions of the small bronchial airways were permanent. The results of animal studies suggest that this probably was due to the massive desquamation. Findings of the clinical follow-up, characterized by chronic bronchorrhea, and the CT features illustrate the appearance of diffuse bronchiectasis and severe ventilation anomalies a few months after the exposure. The controlled normality of the carbon monoxide capacity transfer and the decreasing need for oxygen therapy argue against massive interstitial lesions. In this case, no treatment other than symptomatic measures was given on first admission. N-acetylcysteine has been shown in animal studies to have a protective effect.10Dawson JR Norbeck K The effectiveness of N-acetylcysteine in isolated hepatocytes against toxicity of paracetamol, acrolein and paraquat.Arch Toxicol. 1984; 55: 103-110Crossref Scopus (65) Google Scholar It is a precursor of glutathione and has antioxidant activity.11Heffner E Repine JE Pulmonary strategy of antioxidant defense.Am Rev Respir Dis. 1989; 140: 531-554Crossref PubMed Scopus (487) Google Scholar N-acetylcysteine administration may therefore be valuable in cases of acrolein intoxication." @default.
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